Draft Screening Assessment
Boric Acid, its Salts and its Precursors
Environment and Climate Change Canada
Table of Contents
- 1. Introduction
- 2. Scope of the Assessment
- 3. Substance Identity and Physical and Chemical Properties
- 4. Sources
- 5. Uses
- 6. Releases to the Environment
- 7. Environmental Fate and Behaviour
- 8. Potential to Cause Ecological Harm
- 8.1 Essentiality
- 8.2 Ecological effects assessment
- 8.3 Ecological exposure assessment
- 8.4 Characterization of ecological risk
- 9. Potential to Cause Harm to Human Health
- 10. Conclusion
- Appendix A: Lists of Boron-containing Substances that are Precursors or Non-precursors of Boric Acid
- Appendix B: Aquatic Ecotoxicological Data
- Appendix C: Soil Ecotoxicological Data
- Appendix D: Estimated Intakes from Environmental Media, Food and Drinking Water
- Appendix E: Estimated Intakes from the Use of Products
- Appendix F: Biomonitoring Data Tables
- Appendix G: Summary of Blood Boron Concentrations and Intake Concentrations in Various Human Exposure Studies
- Appendix H: Health Effects Data
List of Tables
- Table 3-1: Experimental physical and chemical property values for boric acid
- Table 4-1: Annual aggregate quantities of boric acid imported into Canada from 2009-2012 (CBSA 2013)
- Table 8-2: Concentrations of boron in surface waters of minimally impacted areas of Canada (2009-2012)
- Table 8-3: Summary of concentrations of boron in the Wabamun Lake area, Alberta
- Table 8-4: Summary of measured concentrations of boron in surface water near metal mines (Environment Canada 2014m)
- Table 8-5: Summary of measured concentrations of boron in surface waters in the vicinity of smelters and refineries
- Table 8-6: Summary of measured concentrations of boron near coal mines
- Table 8-7: Summary of measured concentrations of boron in the Athabasca River watershed
- Table 8-8: Predicted environmental concentrations of boron for the pulp and paper sector
- Table 8-9: Summary of predicted environmental concentrations as a result of wastewater effluent discharges, down-the-drain releases, land application of wastewater biosolids, and landfill leachate discharges
- Table 8-10: Summary of risk quotients obtained for different media and exposure scenarios for boric acid
- Table 9-1: Percentiles of usual dietary intakes (µg B/kg bw/d) for boron for the general Canadian population from food and water
- Table A-2: Substances considered non-precursors of boric acid
- Table B-1: Chronic toxicity data set used to develop the SSD-based water quality guideline (CCME 2009)
- Table B-2: Available sediment toxicity data
- Table C-1: Chronic toxicity data set used to develop the SSD for soil
- Table D-1: Average estimates of daily intake (μg B/kg bw/d) of boric acid by the general population in Canada through environmental media and food
- Table E-1: Arts, crafts and toys - Estimated intakes of boron for children playing with homemade modelling clay
- Table E-2: Cleaning products - Estimated intakes of boron from the use of cleaning products
- Table E-3: Cosmetics - Estimated intakes of boron from cosmetics applied dermally
- Table E-4: Cosmetics - Estimated intakes of boron for adults from cosmetics with potential for oral and mucosal exposure
- Table E-5: Natural health products - Estimated intakes of boron for adults taking oral supplements
- Table E-6: Swimming pool and spa products - Estimated intakes of boron from swimming pools
- Table F-1: Blood boron concentrations in humans - general population (µg/L)
- Table F-2: Blood boron concentrations in humans, high environmental exposure (µg/L)
- Table F-3: Blood boron concentrations in human supplement studies (µg/L)
- Table F-4: Blood boron concentrations in human worker studies (µg/L)
List of Figures
- Figure 3-1: Aqueous equilibrium of boric acid with the borate anion (B(OH)4-), pKa = 9.0 at 25°C
- Figure 8-1: Species sensitivity distribution (SSD) for boron based on chronic toxicity data for soil organisms. The Normal Model fit to data is shown on the graph along with the 95% confidence intervals.
- Figure 9-1: Blood boron concentrations as a function of daily intakes based on several exposure studies
Pursuant to section 68 or section 74 of the Canadian Environmental Protection Act, 1999 (CEPA), the Ministers of the Environment and Climate Change and of Health have conducted a screening assessment of boric acid, its salts and its precursors as part of the Substance Groupings Initiative of Canada’s Chemicals Management Plan (CMP). Substances in this assessment were identified as priorities for action, as they met categorization criteria under subsection 73(1) of CEPA or were included for assessment efficiency.
This screening assessment focuses on boric acid, and therefore includes boric acid, its salts and its precursors, i.e., boron-containing substances that release boric acid through all transformation pathways (e.g., hydrolytic, oxidative, digestive or metabolic) at environmentally or physiologically relevant conditions (i.e., pH and concentration). Boric acid, its salts and its precursors of commercial significance in Canada were considered in terms of their contribution to the combined exposure to boric acid but were not individually assessed. This assessment considers total exposure of humans and other living organisms to boric acid, whether it is present in environmental media (e.g., water, sediment, soil or air), food or products.
Boric acid has natural and anthropogenic sources. Natural sources of boric acid include sea-salt aerosols, soil dusts, volcanoes, biomass burning (e.g., forest fires), plant aerosols, and rock and soil weathering. Anthropogenic sources are also significant and include the manufacture, import and use of boric acid, its salts and its precursors in products and manufactured items. According to information reported under section 71 of CEPA for nine substances that were manufactured or imported above reporting thresholds in Canada in 2008 and information gathered by the Canada Border Services Agency (CBSA) (2009-2012), large quantities of boric acid, its salts and its precursors are imported annually into Canada (42 000-61 000 metric tons). The substances are used for a wide variety of products and applications, including fibreglass insulation, oil and gas extraction, fertilizers, cellulose insulation, gypsum boards, engineered wood products, pulp and paper manufacturing, rubber manufacturing, chemical manufacturing, metallurgical applications, cleaning products, cosmetics, drugs and natural health products (NHPs), swimming pool and spa chemicals, and surface finishing. Other anthropogenic sources include the incidental production and subsequent release of boric acid as a result of activities such as coal-fired power generation, metal mining (including base metals, precious metals and uranium), base metals and precious metals smelting and refining, coal mining, oil sands extraction and processing, oil and gas extraction, wastewater treatment (including the land application of biosolids), and waste disposal (landfill leachate).
Following releases to the environment, boric acid may enter water, air and soil media. Because of its high water solubility (49 grams per litre [g/L]), boric acid released to the aquatic environment is expected to remain in this compartment and to be highly bioavailable to aquatic organisms. Boric acid released to air is removed from the atmosphere and deposited to aquatic and terrestrial environments by wet (rain and snow) and dry deposition. In soil, boric acid is considered highly mobile, because it does not undergo redox reactions and its bioavailability is mainly influenced by adsorption reactions that may occur slowly. Generally, boric acid is not considered bioaccumulative in most aquatic organisms and especially not in invertebrates and fish, although bioaccumulation has been observed in some aquatic plants and algae. Evidence suggests that boric acid does not biomagnify in the environment.
Boron, absorbed as boric acid is a micronutrient for plants and other organisms such as fish and frogs. Boric acid may be taken up by aquatic organisms, and has been demonstrated to cause harm at moderately low concentrations as indicated by a long-term chronic predicted no effect concentration (PNEC) value of 1.5 milligrams of boron per litre (mg B/L). Considering the high bioavailability of anthropogenic boric acid added in soil compared to natural sources of boron, the added-risk approach focusing on anthropogenic added fraction only was used to characterize the effects of boric acid on soil organisms. Although certain soil-dwelling organisms are sensitive to boric acid, it is generally anticipated to cause harm at moderately low concentrations as a result of chronic exposure (i.e., PNECadded value of 6.08 mg B per kilogram [kg]).
Ecological exposure scenarios were developed for the various activities that represent significant sources of release of boric acid, its salts and its precursors to the environment. Exposure to boric acid was assessed based on modelled and measured concentrations of total or dissolved boron in environmental media, subsequently used to derive predicted environmental concentrations (PECs). Substance-specific exposure scenarios were developed to represent releases of boric acid from uses associated with the following sectors and activities: pulp and paper manufacturing, "down-the-drain releases" from specific uses (e.g., soaps and detergents, cosmetics, swimming pool chemicals), rubber manufacturing, electroplating, fiberglass insulation manufacturing, cellulose insulation manufacturing, gypsum board manufacturing, engineered wood manufacturing and fertilizer manufacturing. In addition, exposure was assessed for the following sectors based on their potential to release boric acid incidentally (as a by-product): coal-fired power generation, metal mining, base and precious metals smelting and refining, coal mining, oil sands extraction and processing, and wastewater and wastes management. Risk quotient (RQ) analyses were performed comparing aquatic concentrations of dissolved or total boron to effect concentrations. RQs were generally low. However, based on the high leachability of boron in slags from certain precious metal recovery operations and high RQs for aquatic organisms identified in the vicinity of one facility from the metal mining sector, it is reasonable to assume that other facilities engaged in similar activities could release elevated concentrations of boric acid to the aquatic environment.
Considering all available lines of evidence presented in this draft screening assessment, there is risk of harm to organisms, but not to the broader integrity of the environment, from boric acid, its salts and its precursors. Therefore, it is proposed to conclude that boric acid, its salts and its precursors meet the criteria under paragraph 64(a) of CEPA as they are entering or may enter the environment in a quantity or concentration or under conditions that have or may have an immediate or long-term harmful effect on the environment or its biological diversity. However, it is proposed to conclude that boric acid, its salts and its precursors do not meet the criteria under paragraph 64(b) of CEPA as they are not entering the environment in a quantity or concentration or under conditions that constitute or may constitute a danger to the environment on which life depends.
Boric acid, its salts and its precursors are considered to be toxicologically equivalent. Results from animal experiments demonstrate that boric acid adversely affects fertility, reproduction and development, and these adverse effects observed across species were very similar, both in nature and effective doses. A benchmark dose level (BMDL) of 2.90 mg B/kg of body weight per day (bw/d) for decreased testicular weight derived using two dog toxicity studies has previously been established as a point of departure by Health Canada. Additionally, a no observed adverse effect level (NOAEL) of 9.6 mg B/kg bw/d was noted in the rat for developmental effects. Given limitations in the available studies on humans, the effects noted in the animal studies were considered the critical effects for risk characterization.
Canadians are exposed to boric acid from environmental media, food, drinking water and products (this exposure was characterized through the use of biomonitoring data from Canadian and European studies). Total boron measured in blood in individuals provides a measure of integrated exposure for individuals, from all routes (oral, dermal, and inhalation) and all sources (including environmental media, food, and daily- or frequent-use products). Males have higher concentrations of boron in blood than females. For adults, there is a steady increase in the concentration of boron in blood with age; despite this trend in adults, blood boron concentrations are higher overall in children. Intake estimates from environmental media, food, drinking water and uses of certain product types were generated to characterize important sources of exposure. As boron is considered an essential micronutrient for plant growth, these estimates indicate, as expected, that naturally occurring boron in fruit, vegetables and to a lesser extent drinking water represent primary sources of exposure. Intake estimates from uses of boric acid in arts and craft materials, toys, cosmetics, cleaning products, NHPs, and swimming pool and spa products indicate that these may be significant sources of exposure to boric acid for the general population.
A comparison of estimates of intake predicted from biomonitoring data to critical effect levels in health effect studies results in margins of exposure that are potentially inadequate to address uncertainties in the exposure and health effects databases. Therefore, it is proposed to conclude that boric acid, its salts and its precursors meet the criteria under paragraph 64(c) of CEPA as they are entering or may enter the environment in a quantity or concentration or under conditions that constitute or may constitute a danger in Canada to human life or health.
It is proposed to conclude that boric acid, its salts and its precursors meet one or more of the criteria set out in section 64 of CEPA.
Pursuant to section 68 or section 74 of the Canadian Environmental Protection Act, 1999 (CEPA) (Canada 1999), the Minister of Environment and Climate Change and the Minister of Health conduct screening assessments of substances to determine whether these substances present or may present a risk to the environment or to human health.
The Substance Groupings Initiative is a key element of the Government of Canada’s Chemicals Management Plan (CMP). Fourteen substances were identified as priorities for assessment, given that they met the categorization criteria under section 73 of CEPA. Subsequently, boron-containing substances that may transform into boric acid (i.e., boric acid precursors), with the exception of polymers, were included for assessment efficiency.
This screening assessment considers boric acid, its salts and its precursors. Boric acid salts and precursors are substances that contain boron and have the potential to dissociate, dissolve or degrade to release boric acid, at environmentally and physiologically relevant conditions (i.e., pH and concentration). It is recognized that combined exposure of humans and other organisms to boric acid may occur from different pathways and sources. Exposure to boric acid may occur due to anthropogenic activities involving boron-containing substances, as well as incidental production and ambient background concentrations of boron. For the purposes of the human health assessment, "boric acid" will refer to boric acid, its salts and precursors; where relevant, specific substances containing boron will be explicitly identified by name or Chemical Abstracts Service Registry Number (CAS RN). For ease of comparison of the different sources of boric acid, all concentrations and doses described in this document have been adjusted to give amounts of boron in its elemental form.
Screening assessments focus on information critical to determining whether substances meet the criteria as set out in section 64 of CEPA, by examining scientific information to develop conclusions by incorporating a weight of evidence approach and precautionFootnote 1.
This draft screening assessment includes consideration of information on chemical properties, environmental fate, hazards, uses and exposure, including additional information submitted by stakeholders. Relevant data were identified up to March 2016. Empirical data from key studies as well as some results from models were used to reach proposed conclusions. When available and relevant, information presented in assessments from other jurisdictions was considered.
The assessment does not represent an exhaustive or critical review of all available data. Rather, it presents the most critical studies and lines of evidence pertinent to the proposed conclusion. Additional information used for this assessment is summarized separately in supporting documentation as referenced in the assessment below, which is available upon request.
This draft screening assessment was prepared by staff in the Existing Substances programs at Health Canada and Environment and Climate Change Canada, and incorporates input from other programs within these departments. The ecological and human health portions of this assessment have undergone external written peer review and/or consultation. Comments on the technical portions relevant to human health were received from Dr. Eric Hooker and Dr. Katherine Super, TetraTech Inc., and comments related to the relationship between blood boron concentrations and intake were received from Michael Dourson, Toxicology Excellence for Risk Assessment and Sean Hays, Summit Toxicology. Comments on the technical portions relevant to the environment were received from Dr. M.C. Harrass and from Dr. L Kaputska, LK Consultancy. Although external comments were taken into consideration, the final content and outcome of the screening assessment remain the responsibility of Health Canada and Environment and Climate Change Canada.
The critical information and considerations upon which the draft screening assessment is based are provided in this document.
2. Scope of the Assessment
This screening assessment focuses on boric acid, its salts and its precursors. There are many different salts of boric acid that dissociate to boric acid. There are also many substances that release boric acid as a result of relevant transformation pathways (e.g., hydrolytic, oxidative, digestive or metabolic) at environmentally or physiologically relevant conditions (i.e., pH and concentration); these are considered to be precursors of boric acid. Boron-containing substances other than polymers, were evaluated for their potential to be precursors of boric acid (see Appendix A). Precursors of boric acid include the following groups of boron-containing substances: oxygen compounds of boron (including boric acids, borates or boric acid salts and borate esters), boron halides, boranes (borohydrides) and organo-boron compounds. Not all boron-containing substances are precursors of boric acid; notable exceptions include elemental boron, borides (such as boron nitride or carbide) and inert substances (e.g., sodium borate silicates or borosilicate glass), which therefore fall outside the scope of this assessment.
This assessment considers the combined exposure of humans and other organisms from different pathways and sources of boric acid. The presence of boric acid in environmental media, food or products may result from natural or anthropogenic sources. Anthropogenic sources of boric acid include incidental production and release (i.e., as a by-product) of boric acid and its precursors as well as the import and use of these substances, and products or manufactured items containing these substances. Boric acid precursors of commercial significance in Canada were considered in terms of their contribution to the combined exposure of boric acid, but were not individually assessed. Where feasible, background or reference levels were differentiated from levels attributed to anthropogenic sources.
Measurements of boric acid in environmental media, products and humans are generally expressed in terms of boron (B) content, corresponding to a fraction (i.e., 17.5%) of the mass of boric acid on a molecular weight basis. Boron-containing substances that are precursors of boric acid under environmentally and physiologically relevant conditions and concentrations are toxicologically equivalent to boric acid. Therefore, concentrations and doses of boric acid reported in this assessment are expressed as the mass of boron per volume or mass of media, and environmental concentrations of boric acid are also generally reported in this manner. This assessment only considers effects associated with boric acid, and does not address other elements or moieties that may be present in certain complex boron-containing substances that may release these other elements or moieties (such as ammonium, cobalt, lithium, silver or zinc). These other elements or moieties may be addressed or may have already been addressed via other CMP initiatives.
Engineered nanomaterials containing boron or boron-containing substances were not explicitly considered in exposure scenarios of this assessment. However, measured boron concentrations could include boron-containing nanomaterials or other boron-containing substances.
3. Substance Identity and Physical and Chemical Properties
Because of its high ionization potential, the metalloid boron does not form B3+ cations, but covalently bonds with electronegative atoms (Cotton and Wilkinson 1999). It has a high affinity for oxygen and forms strong covalent boron-oxygen bonds (Ball et al. 2012). Therefore, it mainly exists in the environment as boric acid. Boric acid is a Lewis acid, which, unlike a Brönsted-Lowry acid, accepts hydroxide ions instead of releasing protons. The structure is displayed on the left side of the equation in Figure 3-1. In dilute solutions (less than or equal to 0.025M, or ~0.27 g B/L) (IPCS 1998), which encompasses the environmentally and physiologically likely range, boric acid is in equilibrium with the borate anion (B(OH)4-). However, based on the acid dissociation constant (pKa) value of 9.0 at 25°C, boric acid will predominantly exist in its neutral, undissociated form at environmentally and physiologically relevant pH values (5-8).
Physical and chemical properties determine the overall characteristics of a substance, and play an important role in determining the environmental fate of substances as well as their toxicity to humans and non-human organisms.
Properties such as water solubility and acid dissociation constant (Ka) are particularly relevant to the environmental fate and ecotoxicity of boric acid (Table 3-1), because they provide information on its bioavailability. Partition coefficients for boric acid (expressed as boron equivalent) pertaining to its partitioning between soil and water (Ksw) and suspended particles and water (Kspw) are discussed in Section 7.
Boric acid is considered highly soluble in water, with an extremely low log Kow (Table 3-1.). Pure boric acid is not volatile, as indicated by its low vapour pressure (9.9 x 10-5 Pa). Boric acid can be volatilized with steam from heated aqueous solutions (due to its dissolution into steam), or sublimed by high temperature processes (Ball et al. 2012; Schubert and Brotherton 2006). When heated, boric acid releases water in a stepwise fashion, forming various phases of metaboric acid (HBO2) as temperature increases, and eventually boron oxide (B2O3) (Cotton and Wilkinson 1999). Gaseous metaboric acid species are formed by the equilibration of water vapour with molten boron oxide at 600-1000°C (Schubert and Brotherton 2006).
|Property||Range of values|
|Physical state||-||White odourless crystalline solid||Borax Europe 2012|
|Borax Europe 2012; IPCS 1998; ECHA 2007-2014|
|Vapour pressure (Pa)||Generally considered negligible||9.9 x 10-5||Borax Europe 2012|
|Water solubility (g/L)||47.2-63.5|
|ATSDR 2010; Borax Europe 2012; IPCS 1998; ECHA 2007-2014|
|Borax Europe 2012; ECHA 2007-2014|
|ATSDR 2010; Borax Europe 2012; IPCS 1998; ECHA 2007-2014|
Abbreviations: Kow, octanol-water partition coefficient; pKa, acid dissociation constant.
Boric acid is considered highly soluble in water, with an extremely low log Kow (Table 3-1.). Pure boric acid is not volatile, as indicated by its low vapour pressure (9.9 x 10-5 Pa). Boric acid can be volatilized with steam from heated aqueous solutions (due to its dissolution into steam), or sublimed by high temperature processes (Ball et al. 2012; Schubert and Brotherton 2006). When heated, boric acid releases water in a stepwise fashion, forming various phases of metaboric acid (HBO2) as temperature increases, and eventually boron oxide (B2O3) (Cotton and Wilkinson 1999). Gaseous metaboric acid species are formed by the equilibration of water vapour with molten boron oxide at 600-1000°C (Schubert and Brotherton 2006).
4.1 Natural sources
Boron is a naturally occurring element in the terrestrial crust, with a concentration in the upper continental crust of approximately 10 mg/kg (Gupta 1993). Boron is not naturally found in its elemental form, but rather in the form of borosilicate minerals (the most abundant of which is tourmaline), boric acid or borates (Cotton and Wilkinson 1999; Holleman and Wiberg 2001). In the oceans, the average concentration of boron has been reported to be 4.5 mg B/L. Borate aerosols formed in the atmosphere via co-evaporation of boric acid with seawater, or the incursion of seawater into freshwaters, may be a significant source of boron in coastal areas (Argust 1998; Jahiruddin et al. 1998; Parks and Edwards 2005).
Global natural emissions to the atmosphere have been estimated to range between 1.1 × 109 and 3.1 × 109 kg B/year (Park and Schlesinger 2002). The main sources include sea-salt aerosols, soil dusts, volcanoes, biomass burning (e.g., forest fires) and plant aerosols. Atmospheric boron exists as gaseous or particulate boric acid, and may subsequently be introduced into surface water and soil as a result of wet and dry deposition. Naturally occurring boron is present in groundwater primarily as a result of leaching from rocks and soils containing borates and borosilicates WHO (2009). Rock and soil weathering constitute another important source of boron to the environment, estimated at 0.19 x 109 kg B/year (Park and Schlesinger 2002). The introduction of boron into surface water and soil as a result of these natural processes is reflected in the geochemical background concentrations in these media. Background concentrations are considered in this assessment (Section 8.3 and subsection 9.2.1) when estimating the exposure of ecological receptors and humans to boron substances.
4.2 Anthropogenic sources
4.2.1 Manufacture of boric acid precursors
There are no commercially valuable deposits of boron-containing minerals (i.e., borax, kernite, colemanite and ulexite) in Canada, with most mining activity taking place in the United States and Turkey and to a lesser degree in Chile, Argentina, Russia and Peru (USGS 2015). Furthermore, no evidence of the refinement of boron-containing minerals to other boric acid precursors was identified in Canada. Thus, for the purposes of this screening assessment, the term "manufacture" generally refers to incidental production, as described in the definition used by the National Pollutant Release Inventory (NPRI) of Environment and Climate Change Canada (NPRI 2014).
4.2.2 Import of boric acid precursors
Information regarding the import of boric acid was acquired through a notice issued pursuant to section 71 of CEPA (Canada 2009), through data obtained from the Canada Border Services Agency (CBSA) (CBSA 2013), and from voluntary data submissions received from stakeholders.
The DSL Inventory Update (DSL IU) Phase 1 initiative that was launched in 2009 (Canada 2009) (for the reporting year 2008) included two boric acids and seven boric acid precursors that fall under the scope of this assessment (see Table A-1 in Appendix A). The survey collected information on quantities of substances imported into Canada, and aided in the identification of key uses and sectors of interest for these substances. Additionally, a request was made to the CBSA to obtain information on the import activity of boric acid and boric acid precursors captured within Harmonized System (HS) codes for the years 2009-2012 on a company-by-company basis. Twelve HS codes (10-digit) were identified that correspond to boric acid and boric acid precursors; these codes and the corresponding total annual import quantities (Table 4-1) were obtained from the CBSA (2013). In addition, voluntary submissions were received from a number of stakeholders to determine quantities and uses of boric acid and its precursors in commerce in Canada and to provide other information relevant to exposure characterization.
High-level aggregation of the quantity of boric acid and its precursors imported into Canada over the period 2009-2012 was tallied (Table 4-1) (CBSA 2013) (further detail on quantities of boric acid precursors imported into Canada is available in Environment Canada 2014a). Results from CBSA (2013) indicate that the categories "oxides of boron and boric acid" and "disodium tetraborate - other hydrates" represented 70-91.5% of boric acid imported into Canada from 2009-2012. Only one substance captured within these HS codes, boron oxide (CAS RN 1303-86-2), has a boron content (31.1%) greater than boric acid (17.5%). However, based on results from the DSL IU Phase 1 survey of import quantities into Canada in 2008 and uses worldwide, quantities of boron oxide in commerce are much lower than those of boric acid (Ball et al. 2012; Environment Canada 2009a). Given that compounds of most commercial importance (e.g., borax pentahydrate and borax decahydrate) have boron contents lower than 17.5%, boron and other boric acid precursors corresponding to the other HS codes have boron contents on the order of, or lower than, that of boric acid. Therefore, the total import quantities recorded by the CBSA were assumed to correspond to boric acid for the purposes of calculating boron equivalents, thus simplifying the exposure characterization, while being a conservative assumption. Based on this assumption, between 42 000 000 and 61 000 000 kg of boric acid, approximately, were imported annually into Canada from 2009-2012.
|HS code nameFootnote Table 4-1a||HS code numbers||Quantity imported per year (kg) from 2009-2012|
|Oxides of boron and boric acid||2810000000,2810000010,2810000020||6 000 000-25 000 000|
|Disodium tetraborate - other hydrates||2840190000||26 000 000-31 000 000|
|Disodium tetraborate -anhydrous||2840110000||400 000-650 000|
|Natural borates and concen-trates||2528000000,2528100000,2528900000||1 500 000-13 000 000|
|Other borates, peroxo-borates of metals||2840200000,2840300090||1 500 000-4 500 000|
|Peroxo-borate (perborates)||2840300000,2840300010||50 000-200 000|
|TotalFootnote Table 4-1b||42 000 000-61 000 000|
4.2.3 Incidental manufacture of boric acid precursors
As noted in section 4.2.1, for the purpose of this assessment, the term "manufacture" also includes the incidental production of boric acid at any level of concentration as a result of the manufacturing, processing or other uses of other substances, mixtures or products. Therefore, sectors that may incidentally produce boric acid as a result of their activities and generate releases to the environment are considered in this draft screening assessment.
Information regarding the incidental manufacture of boric acid was also acquired through a notice issued pursuant to section 71 of CEPA (Canada 2009). Results of this survey identified a number of coal-fired power plants as incidental manufacturers of boron oxide (CAS RN 1303-86-2; Environment Canada 2009a), a substance known to transform into boric acid.
A number of sectors have been identified as potential incidental sources of boric acid to the environment (air, water, soil or sediment): coal-fired power generation, metal mining (including base metals, precious metals and uranium), base and precious metals smelting and refining, coal mining, oil sands extraction and processing, oil and gas extraction, pulp and paper manufacturing, and waste and wastewater management. Further details regarding some of these sectors are available in Environment Canada (2014b, 2014c, 2014d, 2014e, 2014f, 2014g). Other potential sources include iron and steel manufacturing, aluminium smelting and cement production (Environment Canada 2013a). Detailed exposure scenarios leading to predicted concentrations of boron in the environment are discussed later in this report (Section 8-3) for the sectors with the greatest expected releases of boric acid.
Consumption of boron minerals and chemicals worldwide is distributed among the following major uses: glass products and ceramics (72%), soaps and detergents (0.9%), flame retardants (0.9%) and a large number of uses that represent the remaining 26.2% (CEH 2011). Boron compounds are used extensively in a wide range of industrial applications, almost all of which involve boron-oxygen compounds (Schubert 2003) that are boric acid precursors. More than 140 different types of end-use applications are reported for borates (EU 2007a). Major uses also include fibreglass insulation, agricultural products (fertilizers and pest control products), cellulose insulation, cleaning products (soaps and detergents, as well as cleaning, polishing and toilet preparations), basic pharmaceutical products and preparations, various chemicals and chemical products (e.g., chemicals for metallurgy, antifreeze, brake fluids, buffers and lubricants), gypsum board and wood products (veneer and engineered wood), paper and paper products, and flame retardants (RPA 2008; Ball et al. 2012).
In Canada, the major uses of boric acid, and the sectors where use occurs, were identified as a result of the DSL IU for 2008, CBSA import data for 2009-2012, and other stakeholder engagement activities (Environment Canada 2009a, 2013b; CBSA 2013). Importers identified through the CBSA were attributed to a sector based on publicly available information regarding the importer’s primary activity, or by correlating the companies’ activity with information obtained through DSL IU submissions or voluntary stakeholder engagement. As a result, the major uses and sectors implicated in Canada include: cellulose and fibreglass insulation manufacturing, industrial and consumer cleaning products, personal care products, other chemicals (water softeners and swimming pool chemicals), gypsum board manufacturing, engineered wood products manufacturing, oil and gas extraction (e.g., hydraulic fracturing fluids), agriculture (fertilizers), pulp and paper manufacturing and packaging, rubber manufacturing, chemical manufacturing (e.g., lubricants), metallurgical applications (e.g., slag stabilization and analytical chemicals), and surface finishing (e.g., the cleaner and buffer in electroplating). Further detail is available in Environment Canada (2014a). For the purpose of this document, a personal care product is defined as a substance or mixture of substances that is/are generally recognized by the public for use in daily cleansing or grooming. Depending on both how the product is represented for sale and its composition, personal care products may fall into one of three regulatory categories in Canada: cosmetics, drugs or natural health products (NHPs).
The use of boric acid in NHPs, drugs, cosmetics, pest control products, fertilizers, and toys is regulated in Canada. For commercially available children’s toys, compliance and enforcement of the existing prohibition on boron will continue as a part of the regular enforcement of the Toys Regulations under the Canada Consumer Product Safety Act. With respect to NHPs, the use of boric acid, its salts and its precursors in such products is regulated under the Natural Health Products Regulations and Food and Drugs Act (Canada 1985a, 2003). Boron compounds are present as medicinal ingredients and non-medicinal ingredients in currently licensed NHPs (LNHPD 2013). The Natural and Non-prescription Health Products Directorate’s (NNHPD’s) Multi-vitamin/Mineral Supplements monograph outlines the following source materials for boron in NHPs: boracic acid/orthoboric acid, borax/disodium tetraborate/sodium biborate/sodium borate/sodium pyroborate/sodium tetraborate, boron aspartate, boron citrate, boron glycinate, boron hydrolyzed animal protein (HAP) chelate, boron hydrolyzed vegetable protein (HVP) chelate, calcium borate/calcium pyroborate/calcium tetraborate, calcium borogluconate/calcium diborogluconate, calcium fructoborate and magnesium borate; whereas the Natural Health Products Ingredients Database lists borax, boric acid, boron aspartate, boron citrate, boron-enriched yeast, boron glycinate, boron HAP chelate, boron HVP chelate, calcium borate, calcium borogluconate, calcium fructoborate, lignite, magnesium borate and sodium borate as source ingredients for boron (Health Canada 2007a, 2007b; NHPID 2014).
In 2007, the NNHPD published the document Boron as a Medicinal Ingredient in Oral Natural Health Products, which evaluates the risks and benefits associated with the use of boron as a medicinal ingredient in oral NHPs, setting a maximum limit in multi-vitamin/mineral supplements of 700 micrograms per day (µg/d), for adults only (Health Canada 2007b). A maximum daily dose of 3.36 mg B/d was set for products making bone mineralization-type claims associated not with the presence of boron but rather with other medicinal ingredients (e.g., vitamin D and calcium) (Health Canada 2007b). This higher maximum daily dose as compared to that for multi-vitamin/mineral supplements was based on the expectation that these types of products, with claims that are more therapeutic in nature, would be intended for older adults and that these products would be labelled as contraindicated for pregnant and breastfeeding women and as advising consultation with a health care practitioner prior to use in the case of an estrogen-dependent cancer (Health Canada 2007b).
Boron compounds are also listed in the Drug Product Database as being found in human and veterinary drugs. For human drugs, it is used primarily as an ingredient in ophthalmic products and contact lens disinfectants, and otic and topical products; and it is used in the form of injectable solutions for veterinary drugs (DPD 2014). Under the Food and Drugs Act, Food and Drugs Regulations (Part C, Drugs, subsection c.01.028 b), drugs containing boric acid or sodium borate as a medicinal ingredient shall carry a cautionary statement to the effect that the drug should not be administered to a child under three years of age (Canada 1978, 1985a).
Boric acid, its salts and its precursors are used as ingredients in many cosmetics notified to Health Canada under the Cosmetic Regulations of the Food and Drugs Act (2012 email from the Consumer Product Safety Directorate, Health Canada, to the Existing Substances Risk Assessment Bureau, Health Canada; unreferenced). They are present in a wide variety of cosmetic products and are most common in skin lotion/moisturizer and skin cleanser products. Boric acid and its salts are included on the List of Prohibited and Restricted Cosmetic Ingredients (more commonly referred to as the Cosmetic Ingredient Hotlist or simply the Hotlist), an administrative tool that Health Canada uses to communicate to manufacturers and others that products containing certain substances are unlikely to be classified as a cosmetic under the Food and Drugs Act, and that certain substances, when present in a cosmetic at certain concentrations, may contravene the general prohibition found in section 16 of the Food and Drugs Act or a provision of the Cosmetic Regulations (Canada 2014; Health Canada 2014a). The current listing for boric acid and its salts does not include all precursors of boric acid and it describes a concentration limit of 5% for boric acid and its salts (CAS RN 10043-35-3 and 11113-50-1, including sodium borate 1303-96-4). Under the Cosmetic Regulations, the label of cosmetics (containing boric acid and its salts) are required to carry cautionary statements to this effect: “Do not use on broken or abraded skin. Not to be used by children under three years of age.” A warning is not required when boric acid is used as a pH adjuster and the concentration is equal to or less than 0.1%. Other boric acid precursors are described in Hotlist entries: phenyl mercuric borate is described as prohibited in cosmetics; and sodium perborate, a peroxide-generating compound, is subject to data submission and cautionary label statements associated with peroxide-generating compounds.
In Canada, several boric acid salts and precursors, including boric acid, borax (pentahydrate), borax (disodium tetraborate decahydrate), disodium octaborate tetrahydrate and zinc borate, are active ingredients in pest control products. The use of boric acid and its salts as a pesticide is regulated under the Pest Control Products Act (Canada 2002). Health Canada’s Pest Management Regulatory Agency [PMRA] has published a proposed re-evaluation decision for boric acid and its salts (Health Canada 2012). Boric acid salts and precursors are present in products used to control a broad range of insects and fungi in structures, wood and wood products including antisapstain, joinery and millwork applications, remedial wood preservation, and cockroach and ant control products. As well, boric acid salts and precursors are registered for use as a wood composite preservative and material preservative for the manufacturing of paints, coatings, plastics and rubber (Health Canada 2012). In addition, borax, disodium tetraborate, boric acid, boric acid disodium salt pentahydrate and sodium borohydrate are included on the PMRA list of formulants as List 3 formulants and thus may be present in other pest control products (Health Canada 2010). For example, some algaecide and sanitizer pool products regulated under the Pest Control Products Act contain boron as a formulant, which, when used according to label directions, results in a final concentration range in pool/spa water of 5 parts per trillion (ppt) to 1 part per million (ppm), depending on the use.
Boron is a recognized plant micronutrient and is regulated as a fertilizer under the Fertilizers Act (Canada 1985b). Boric acid, borax, sodium calcium borate (ulexite), calcium borate, sodium calcium borate, sodium pentaborate, boron polyamide and ammonium polyborate are all boron-containing substances in registered agricultural products. Approximately 80 registered agricultural products contain boron-containing substances in Canada (2012 email from the Fertilizer Program, Canadian Food Inspection Agency to Risk Management Bureau, Health Canada; unreferenced).
In Canada, boric acid and salts of boric acid in toys are specifically regulated under section 22 of the Toys Regulations of the Canada Consumer Product Safety Act (Canada 2010, 2011). A toy must not contain boric acid and salts of boric acid if they could, under reasonably foreseeable circumstances, become accessible to a child or, if they are used as a filling, could be released upon breakage or leakage. In 1997, Health Canada published a hazard assessment of boric acid in toys (Craan et al. 1997). For commercially available children’s toys, compliance and enforcement of the existing prohibition on boron will continue as a part of the regular enforcement of the Toys Regulations under the Canada Consumer Product Safety Act.
Boric acid, its salts and its precursors are present in food packaging materials, including as a component of adhesives, paper and paperboard food packaging materials, and in flocculants/retention aids that are used in the production of paper. Boron is used as an additive in ethylene-vinyl acetate-vinyl alcohol copolymers (EVOH) and poly(ethylene/methacrylic acid) resin as a component of alkyd systems (level of less than 7.5%) and epoxy primers (level of less than 23%) in coatings for food plants on non-food contact surfaces (2013 email from Food Directorate to Risk Management Bureau, Health Canada, unreferenced).
6. Releases to the Environment
6.1 Releases to air
Co-evaporation of boric acid from industrial process waters at sufficiently high temperatures is anticipated, and is dependent on the amount of boron in the process water (Parks and Edwards 2005). Additional anthropogenic sources of boric acid and its precursors to air include the combustion of fossil fuels (especially coal), the manufacture of fibreglass and glass, and most metallurgical processes (Environment Canada 2013a; Eriksson et al. 1981; Goodarzi 2013; Sakata et al. 2010; Temple et al. 1978; Van Limpt 2007). Emissions to air of boric acid are generally in gaseous and particulate forms of boron oxide, metaboric acid or boron halides that further transform into boric acid (Environment Canada 2009a; Park and Schlesinger 2002; Van Limpt 2007). Windblown particulate matter (PM) from dry tailings (from coal mining or oil sands extraction and processing) or ash piles from coal combustion may be a potential atmospheric source of boric acid (Environment Canada 2014b, 2014e, 2014f).
6.2 Releases to water and sediments
Boric acid releases to water may include (but are not limited to) releases from coal-fired power plants (ash ponds and power plant effluents), oil sands extraction and processing (tailing ponds seepage and run-off to surface waters), coal mining (run-off to surface waters and seepage from tailing ponds), oil and gas extraction (leaks and spills), pulp and paper mills (effluent and landfill leachate), wastewater treatment systemsFootnote 2 (effluent) and landfills (leachate), metal mining and base metals smelters (effluents), agricultural run-off to surface waters, surface finishing (effluent), rubber products manufacturing (effluent), and building products manufacturing (e.g., effluent from gypsum board, fibreglass insulation and wood products manufacturing facilities) (Environment Canada 2014a, 2014b, 2014c, 2014d, 2014e, 2014f, 2014g, 2014h).
6.3 Releases to soil
Dry and wet deposition of atmospheric boric acid originating from anthropogenic air emissions and the application of biosolids are potential sources of boric acid to soil.
7. Environmental Fate and Behaviour
7.1 Environmental distribution
Based on the non-volatility of boric acid (due to negligible vapour pressure), it is expected to be emitted to air principally in PM. However, using an impregnated filter sampling technique, Fogg and Duce (1985) estimated that gaseous boron may represent up to 95% of total boron measured in air, and hypothesized the dominant chemical form to be boric acid. Residence times of 19-36 days and 2-6 days for gaseous and particulate boric acid, respectively, were calculated. A second study conducted by Anderson et al. (1994) using a similar sampling protocol also found high percentages of gaseous boric acid in the atmosphere versus particulate boric acid. The two sampling techniques involved the use of KOH-impregnated cellulose filters for the capture of smaller particles, molecular aggregates, or gases collectively referred to as gaseous boric acid. Since the size of suspended particles in the atmosphere ranges from 0.002-100 microns (µm), approximately (Baird 1999), these studies could have overestimated the percentage of gaseous boric acid compared to the percentage of boric acid adsorbed to suspended particles or dissolved in atmospheric condensed phases. Flue gas measurements taken in a full-scale coal combustion process equipped with selective catalytic reduction (SCR), an electrostatic precipitator (ESP) and flue-gas desulphurization (FGD) showed vapour- and particulate-phases boron concentrations to be comparable (within one order of magnitude) prior to reaching pollution control systems (Cheng et al. 2009). It is expected that gaseous-phase boric acid as well as particulate boric acid emitted to the atmosphere will travel for a certain distance but will be removed from the atmosphere and deposited to terrestrial or aquatic environments by wet (rain and snow) and dry deposition (Anderson et al. 1994; Fogg and Duce 1985; Kot 2009; Zhao and Liu 2010).
7.1.2 Water and sediment
Generally, if released to water, most boric acid is expected to remain in the water column, where it is considered highly mobile, given its high water solubility (47.2-63.5 g B/L) (see section 3). At environmentally and physiologically relevant concentrations, boric acid [B(OH)3] is in a pH-dependent equilibrium with borate anions [B(OH)4-] (CCME 2009). At acidic pH, undissociated boric acid is the predominant species, whereas at alkaline pH (i.e., above the pKa of 9.0) the borate anion is predominant (Howe 1998; Parks and Edwards 2005). Both species are highly soluble and stable, because they do not undergo oxido-reduction reactions or biotransformation (Kot 2009). In natural waters (pH 6-8), polyborates and other minor complexes with transitional metals and fluoride may also exist (Basset 1980; Kot 2009). Complexation of boric acid with environmentally important cations (i.e., Al3+, Fe3+, Ca2+, Mg2+) is generally considered insignificant (Parks and Edwards 2005). Boric acid and borate ions may form complexes with organic matter (Power and Woods 1997; Chauveheid and Denis 2004; Parks and Edwards 2005), and have been observed to sorb weakly to dissolved organic matter in wastewater and to clays (Banerji 1969; Gu and Lowe 1990; Keren and Communar 2009; Parks and Edwards 2005). Adsorption to suspended solids has been hypothesized to explain elevated boron concentration observed in sediment porewater of North Carolina lakes continuously receiving effluent containing coal combustion residues (Ruhl et al. 2009). However, limited sorption to sludge has been confirmed in a number of Canadian wastewater treatment systems(e.g., median removal rate of 2.2%) (Environment Canada 2013c). This indicates that while sorption to suspended solids in solution could occur, removal of boric acid from solution is generally low. Sorption to clays and the co-precipitation of boron via sorption onto ferric iron compounds in sediment has been observed (Butterwick et al. 1989; Hart et al. 2005; Kot 2009). However, based on a low sediment-water (Ksdw) partition coefficient value (log Ksdw = 0.29) (Gerke 2011a) and a low tendency to form complexes with environmentally common cations, boric acid will generally tend to remain in the water column. Therefore, sediments are not anticipated to be a significant sink in freshwater ecosystems. Additionally, boric acid in sediments may reflux into the water column in addition to potential resuspension through bioturbation, dredging, seasonal floods, or mixing by turnover events. For example, low boron concentrations in the sediment of a river in Italy where elevated boron concentrations were observed in the water column (i.e., 1.1 mg B/L) were hypothesized to be caused by the leaching of adsorbed boron on soil minerals (Bonanno 2011).
Boron exists in soils in four main forms: water soluble, adsorbed, organically bound, and fixed in the clay and mineral lattices (Gupta 1993). Boron that is bound and fixed in clay and minerals (e.g., tourmaline) is insoluble and non-bioavailable in the long-term. Adsorbed or organically bound boron is also insoluble but may be released via desorption and organic matter degradation (Gupta 1993) as boric acid. Measurements of boron in soil differ depending on whether total boron or hot-water-soluble boron is measured (Gupta 1993). The total boron content of a particular soil is not a reliable indicator of available boron (Sah and Brown 1997), and the most common method for extracting available boron (as boric acid) is by hot water or from a saturated soil to water extract (Gupta 1993). Generally, less than 5% of the total background concentration of boron in soils is in a form that is bioavailable to plants (Gupta 1993), and plants absorb boron as molecular boric acid (Gupta et al. 1985).
In soils, boric acid is highly mobile, consistent with its low soil-water partitioning coefficient (log Ksw = -1.06-2.2) (Buchter et al. 1989; Elrashidi and O’Connor 1982; Equilibrium Environmental Inc. 2012; Janik et al. 2010; Majidi et al. 2010; Sauve et al. 2000; Singh 1971), and is expected to follow the water flux (Kot 2009). Boric acid does not undergo oxidation-reduction or volatilization reactions in soils, and therefore its concentration in soil solution is mainly controlled by adsorption reactions (Goldberg 1997). The main factors affecting boric acid adsorption in soil and its bioavailability are soil moisture, soil solution pH, soil texture (coarse vs. fine), soil content (organic matter, clays, metal hydroxides), and temperature (Goldberg 1997). The adsorption of boron reaches a maximum at pH 9, coinciding with an increase of the concentration of borate anions, which have more affinity with clays than boric acid (Keren and Bingham 1985). Adsorption to metal hydroxides (e.g., aluminium and iron oxides), clay minerals and organic matter generally occurs via ligand exchange, as summarized by Goldberg (1997). Mg-borates precipitates have been observed in soil samples from sites with high boron concentrations (Paliewicz et al 2015). Therefore, the bioavailability of boric acid in soil generally decreases as the fraction of these soil components increases. While multiple studies show evidence of sorption of boron (presumably boric acid) to soil, Mertens et al. (2011) recently observed that boric acid concentration in soil solutions of soil amended with boric acid did not decrease by ageing (a period of five months), indicating that added boric acid is not quickly bound and is highly mobile. Because of its incorporation into silicate structures or biomass, boron naturally present in soil was determined to be much less soluble and therefore much less bioavailable than boric acid added to soil by amendment (Mertens et al. 2011).
7.2 Environmental persistence
A metalloid ion like boric acid is considered infinitely persistent because it cannot degrade any further, though it can transform into different chemical species or partition among different phases within an environmental medium. In other words, boron will be present in the environment indefinitely, generally as boric acid or the borate anion. Biodegradation and photodegradation are not applicable to boric acid or other inorganic boron-containing substances.
7.3 Potential for bioaccumulation
The bioaccumulation of metalloids is of potential concern because of the possibility of reaching internal body concentrations that can cause harm to the organisms accumulating these substances in their tissues or to the predators that eat these organisms. Accumulation of metalloids depends on their uptake process, which depends on the forms of the metalloid that are bioavailable and its depuration process once in the organism. Boric acid is considered highly bioavailable in the environment because of its high water solubility and relatively inert behaviour (e.g., absence of redox reactions).
7.3.1 Water and sediment
Generally, boric acid is not considered bioaccumulative in most aquatic organisms, particularly in invertebrates and fish, although bioaccumulation has been observed in some aquatic plants and algae.
Bioconcentration factors (BCFs) ranging from 23-766 (geometric mean of 75) have been measured in filamentous algae from the lower San Joaquin River and some of its tributaries (Saiki et al. 1993). Studying remediation of boron-polluted waters with duckweed (Lemna gibba), Del-Campo Marín and Oron (2007) also reported moderately high BCF values of 1100-2400 at boron concentrations in water of 0.3-1 mg/L. Lower BCF values of 500 and less than 300 were observed in duckweed exposed to higher boron concentrations (e.g., 1.0-2.5 mg/L and greater than 5 mg/L) (Del-Campo Marin and Oron 2007). However, the bioaccumulation of boric acid in algae may be species-specific, because similar results were not duplicated in studies conducted with another species of duckweed (Spirodella polyrrhiza) and with the algae Chlorella pyrenoidosa (Fernandez et al. 1984; Davis et al. 2002).
Bioaccumulation of boric acid in invertebrates and fish is low. In invertebrates, Saiki et al. (1993) observed bioaccumulation factor (BAF) values of 16 (range of 7-60) in chironomids, 14 (range of 8-60) in amphipods, and 10 (range of 6-38) in crayfish. Low or no bioaccumulation was also observed in pacific oysters by Thompson et al. (1976). Average boron concentrations in some streams and biota in Turkey varied from 8.6-16.7 mg/L in water and 1.98-2.84 mg/kg in invertebrates, leading to BAF values (based on boron concentrations in water and the whole-body levels in organisms) of 0.085-0.15 (Arslan 2013). Low BAF values ranging from 0.176-8.7 were also observed for aquatic invertebrates in a stream in Turkey where organisms were exposed to high concentrations of boron in surface water (1.61-3.45 mg B/L) and sediment (15.7-32.3 mg B/kg) (Emiroglu et al. 2010). Boric acid does not bioaccumulate in fish, as indicated by BAF values of less than 0.1 in Chinook Salmon (Oncorhynchus tshawytscha) (Hamilton and Wiedmeyer 1990) and BCF values of 0.3 in Fathead Minnows (Pimephales promelas) and Green Sunfish (Lepomis cyanellus) (Suloway et al. 1983). Slightly higher BAF values were observed for Lake Whitefish (Coregonus clupeaformis) (51.5), Northern Pike (Esox Lucius) (63), Lake Cisco (Coregonus artedi) (64), Lake Trout (Salvelinus namaycush) (75) and White Sucker (Catostomus commersonii) (198) (Tsui and McCart 1981). BAFs calculated for fish from streams where boron concentrations ranged from 8.6-16.7 mg/L varied from 0.57-0.92 based on boron concentrations in water and in the muscle, liver and gills of Marmara chub (Squalius cii ) (Arslan 2013). Low bioaccumulation potential in fish was also observed by Emiroglu et al. (2010), with the BAF calculated for European chub (Leuciscus cephalus) using concentrations measured in muscle, liver, gills and head, ranging from 0.78-41. In addition, low BAF values are reported for mosquitofish (BAF of 4), Bluegill (Lepomis macrochirus) (BAF of 2) and Largemouth Bass (Micropterus salmoides) (BAF of 0.7) (Saiki et al. 1993).
The studies conducted by Saiki et al. (1993) and Emiroglu et al. (2010) clearly determine that boric acid does not biomagnify in the environment, because concentrations of boron measured in organisms decrease with increasing trophic levels.
In terms of bioavailability for plants, generally less than 5% of the total boron background in soils is in available form (hot water-soluble) (Gupta 1993). Bioavailable boron is absorbed by roots as undissociated boric acid (Hu and Brown 1997; Mengel and Kirkby 1982; Marschner 1995). Dicotyldeon plants (e.g., legumes) in general require 4-7 times more boron (20-70 mg/kg) than monocotyledons (graminae) (5-10 mg/kg) (Bergmann 1988, 1995; Marschner 1995). According to Kabata-Pendias (2011), the average boron concentrations are 0.7-4.3 mg/kg in grains, 5-7.4 mg/kg in grasses and 14-40 mg/kg in clover. Shacklette et al. (1978) showed that trees and shrubs (usually containing 50-500 mg/kg of boron) generally contain 2-10 times more boron than vegetables.
Boric acid may bioaccumulate in some terrestrial plants. Dos Santos et al. (2010) reported that boron concentrations in shoots of kenaf (Hybiscus canabinnus), mustard (Brassica juncea), turnip (Raphunus sativus) and amaranth (Amaranthus crentus) range from 63-93 mg/kg, whereas the concentrations of soluble and total boron in soil were 3.8 and 6.4 mg/kg, respectively. Therefore, for these species, bioaccumulation potential is low. At boron concentrations in irrigation water of 5 mg/L, mean levels of boron in shoots of wheat (Triticum aestivum), tomato (Solanum lycopersicum) and silver beet (Beta vulgaris) were greater, ranging from 701-1110 mg/kg (Ayars et al. 1990, 1993). Therefore, for some plants, boric acid bioaccumulation can be high, which is in line with the fact that boron is an essential nutrient for plants (see Section 8.1).
8. Potential to Cause Ecological Harm
Boron absorbed primarily as boric acid is an essential micronutrient for plant growth, development, and seed quality (Brown et al. 1999; Dordas et al. 2007; Hu and Brown 1997; Marschner 1995; Pilbeam and Kirkby 1983). There are indications of the involvement of boron in cell wall structure (Hu and Brown 1994; Brown et al. 2002), cell membrane integrity (Marschner 1995; Schon and Blevins 1990), sugar metabolism (Marschner 1995), biological membrane bindings, conversion of glucose-l-phosphate sugars to starch, and metabolism of nucleic acids (Cakmak and Römheld 1997). Boron plays a role in nitrogen fixation (Bolaños et al. 1996; Bellaloui et al. 2009), phenolic metabolism (Marschner 1995; Bellaloui et al. 2012a, 2012b), ion uptake (Marschner 1995; Goldbach 1985), and plasma-membrane-bound H+-ATPase (Schon and Blevins 1990; Camacho-Cristóbal and González-Fontes 2007; Camacho-Cristóbal et al. 2008).
Boron is an essential micronutrient for the development and reproduction of the African Clawed Frog (Xenopus laevis) (Fort et al. 1998, 2002). Abnormal development of the gut, craniofacial region and eye, visceral edema, kinking of the tail musculature, and an increase in the proportion of necrotic eggs and less viable embryos were observed in frogs that were administered a low boron diet compared to frogs given a diet supplemented with boric acid (Fort et al. 1998, 2002). Tests conducted with low boron-concentration water and water supplemented with boric acid show that boron is essential for Zebrafish (Danio rerio) embryo development and stimulates the growth of embryonic Rainbow Trout (Oncorhynchus mykiss) via its ability to bind to cellular cis-diols such as ribose (Eckhert 1998; Rowe and Eckhert 1999). The essentiality thresholds for Rainbow Trout and Zebrafish were determined to be approximately 0.1 mg B/L and 2 x 10-3 mg B/L, respectively (Rowe et al. 1998).
8.2 Ecological effects assessment
Many empirical studies are available on the acute and chronic toxicity of boric acid to aquatic organisms such as micro-organisms (ciliates), algae, invertebrates, fish, plants and amphibians. Results of aquatic toxicity testing for boric acid are generally reported as boron equivalent (mg B/L). Details are available in Environment Canada (2014i). Chronic toxicity data are of greater relevance and weighted more heavily as a line of evidence than acute data in this assessment, because they are a more sensitive indicator of potential for harm from long-term exposures. Given the persistence of boric acid, long-term exposures are particularly pertinent. Chronic data are therefore used to derive a critical toxicity value (CTV), which is a quantitative expression of a low toxic effect (e.g., IC25) that relates to the most sensitive toxicity endpoint for receptor organisms in the medium of interest.
Acute toxicity studies were identified for 35 species, including two algae species, one aquatic plant species, 15 invertebrate species, 15 fish species and two amphibian species. Acute toxicity endpoints range from a three-day no observed effect concentration (NOEC) (teratogenesis at hatching) of 0.109 mg B/L for Largemouth Bass embryos at hatching to a 96-hour lethal concentration (LC50) of 979 mg B/L for mosquitofish and a 48-hour LC50 of 1376 mg B/L for midges (Birge and Black 1977; Black et al. 1993; Maier and Knight 1991). Data from these studies are not included or discussed further in this assessment, because they are not used to derive a CTV.
Chronic toxicity studies were identified for 40 species, including five algae species, eight plant species, eight invertebrate species, seven fish species, seven amphibian species, two species of zooplankton, one species of cyanobacteria, one species of protozoan, and one species of bacteria. Chronic toxicity endpoint values ranged from a 32-day lowest observed effect concentration (LOEC) (survival and teratogenesis) of 0.1 mg B/L for Rainbow Trout (embryo larval stages) in lab-reconstituted water to a 32-day LC50 of 138 mg B/L for Rainbow Trout as well (Black et al. 1993; Birge and Black 1977). A full data set is available in Environment Canada (2014i). A lower chronic 28-day NOEC (survival and teratogenesis) of 0.001 mg B/L for embryo-larval stages of Rainbow Trout is generally considered unreliable (EU 2007a). Indeed, this result is several orders of magnitude lower than other toxicity studies, and the effects observed on Rainbow Trout may have resulted from boron deficiency (i.e., a level lower than the essentiality threshold of 0.1 mg B/L proposed by Rowe et al. 1998).
The importance of water quality characteristics and toxicity-modifying factors on boric acid aquatic toxicity is not well understood, and generally appears less significant than for other metalloids or metals (e.g., copper) (Black et al. 1993; Dethloff et al. 2009). Toxicity tests on Rainbow Trout performed with natural waters indicate higher toxicity threshold concentrations (up to 180 times greater) than those observed with reconstituted water (Black et al. 1993), indicating that the composition of the natural waters lessens boron toxicity to fish and possibly other aquatic organisms. The toxicity of boron to aquatic organisms in laboratory settings (added as boric acid) is generally not significantly modified by water hardness (Birge and Black 1977; Dethloff et al. 2009; Hamilton and Buhl 1990; Maier and Knight 1991; Soucek et al. 2011). However, a protective effect has been observed in certain acute toxicity tests conducted with invertebrate water flea species such as Daphnia magna and Hyalella azteca (MELP 1996)or Ceriodaphnia dubia, allwith very hard waters (greater than 500 mg/L as calcium carbonate [CaCO3]) (Dethloff et al. 2009). Similarly, increasing sodium, chloride or sulfate concentrations do not significantly affect the toxicity of boron to aquatic organisms (added as boric acid) (Dethloff et al. 2009; Maier and Knight 1981), although protective effects of chloride have been observed with Hyalella azteca (Soucek et al. 2011). Complexation of boric acid and borates with organic compounds (e.g., a-hydroxy carboxylic acids) and adsorption to PM have been hypothesized as potential modifying factors for boron toxicity to aquatic organisms (Black et al. 1993). Dissolved organic carbon (DOC) has been shown to decrease the acute toxicity of boron to Ceriodaphnia dubia above 2 mg/L of DOC (Dethloff et al. 2009).
In 2009, the Canadian Council of Ministers of the Environment (CCME) published acute and chronic Canadian Water Quality Guidelines (WQGs) for Boron for the Protection of Aquatic Life (CCME 2009) based on the CCME protocol (CCME 2007). The long-term (chronic) WQG was developed using a statistical approach, because the minimum data requirements for a species sensitivity distribution (SSD) were met. A total of 28 data points (NOEC, effective concentration [EC10], maximum acceptable toxicant concentration [MATC] and LOEC data) for fish, invertebrates, plants and algae, and amphibians, generated using boric acid or boric acid-equivalent compounds, were used to derive the WQGs. The data set used in the chronic WQG is presented in Table B-1 (Appendix B). Long-term exposure guidelines are intended to protect all forms of aquatic life for indefinite exposure periods (greater than or equal to 7-day exposures for fish and invertebrates, greater than or equal to 24-hour exposures for aquatic plants and algae) (CCME 2009). Therefore, the long-term WQG for boron of 1.5 mg B/L (i.e., a hazardous concentration to 5% of species [HC5], corresponding to the 5thpercentile of the SSD) for freshwater was selected as the predicted no effect concentration (PNEC) to characterize risk to aquatic organisms in this assessment. This PNEC value is comparable or more protective than recent HC5 values of 1.7 and 3.8 calculated with SSDs using chronic aquatic toxicity data (Borax Europe 2012; EU 2007a). Assessment factors (AFs) were applied to these latter values in the PNEC derivation process.
Recent aquatic toxicity studies, or studies that were unavailable for the 2009 WQG derivation, were systematically reviewed to confirm the protective nature of the water quality objective. Additional chronic boric acid toxicity results for one amphibian, three invertebrates, one fish and one algal species were all above the chronic PNEC value of 1.5 mg B/L (6.6-34.6 mg B/L), confirming that the PNEC adequately protects a wide variety of freshwater organisms (Fort 2011; Hall et al. 2014; Hansveit et al. 2001; Soucek et al. 2011; US EPA 2010).
Sediment toxicity data are limited for boric acid. Data for benthic organisms were identified for freshwater midges (Chironomus riparius), the aquatic Blackworm (Lumbriculus variegatus) and the Fatmucket mussel (Lampsilis siliquoidea) (Gerke et al. 2011a, 2011b; Hall et al. 2014; Hooftman et al. 2000a). Toxicity values based on whole-sediment concentrations ranged from a 28-day NOEC value of 37.8 mg B/kg for the freshwater midge to a 21-day LC25(survival) of 363.1 mg B/kg for the Fatmucket mussel (Gerke et al. 2011a; Hall et al. 2014). Toxicity values based on porewater concentrations ranged from a 21-day NOEC (growth) of 10 mg B/L for the Fatmucket mussel to a 28-day LOEC (emergence) value of 59 mg B/L for the freshwater midge (Hooftman et al. 2000a; Hall et al. 2014) (see Appendix B-2).
Due to its high water solubility, boric acid is rapidly depleted from spiked sediments (Borax Europe 2012; Gerke et al. 2011a; Hall et al. 2014). In the test study conducted by Gerke et al (2011a), the test chambers were prepared two days prior to study initiation when midges were added, for a total duration of 30 days. On the 30th day of the study, the boron load in overlying water had increased to 75% of the total load from 31% on day 2, for a concentration in overlying water of 20.9 mg B/L. This concentration is almost identical to a 28-day NOEC of 20.4 mg B/L obtained by Gerke et al. (2011b) in a second study using spiked water only, and comparable to a 28-day NOEC value of 32 mg B/L measured by Hooftman et al. (2000a) for the same species. Therefore, the chronic toxicity observed for the freshwater midge may be mostly explained by the boron concentrations measured in the water column (Borax Europe 2012), and not by exposure to boron in sediment. To generate accurate sediment toxicity data, the overlying water must also be spiked at concentrations matching those of the targeted porewater exposures, as carried out by Hall et al. (2014) forthe aquatic worm (L. variegatus). The worm growth endpoint showed much variability (possibly due to the fragmentation mode of worm reproduction) and is considered less reliable than the survival endpoint (Hall et al. 2014). Results for the Fatmucket mussel indicate that the primary route of boric acid exposure was through the aqueous phase, not the solid phase (Hall et al. 2014).
Due to the low partitioning of aqueous boric acid to sediment (see section 7.1.2) and the limited sediment toxicity studies available for boric acid, exposure via this media is given a low weight as a line of evidence. Therefore, a PNEC value is not calculated for benthic organisms.
Many empirical studies are available on the acute and chronic toxicity of boric acid to terrestrial organisms such as plants, invertebrates and soil micro-organisms. Acute and chronic soil toxicity data are available for 15 invertebrate species spanning nine different families; 26 plant species, including monocotyledons, dicotyledons and herbaceous plants and trees; and soil micro-organisms addressing two key soil biochemical processes (carbon transformation and nitrification). No studies aiming to establish the efficacy of boric acid as a pesticide (e.g., to control ants or termites) are included in this dataset (available in Environment Canada 2014j). Exposure to boric acid in soil is expected to be long term because of its persistence, and, therefore, chronic data are of greater relevance than acute data in this assessment because they are a more sensitive indicator of potential for harm from long-term exposures. All concentrations reported in soil toxicity studies and reports were converted into concentrations of boron equivalence to simplify comparison with exposure concentrations used in characterizing risk. The data were then used to derive a CTV. Robust Study Summaries (RSSs) were completed for all studies from which the toxicity data were used to derive the CTV (these RSSs are available upon request).
Reliable chronic data were identified for 25 species, including 13 invertebrate species and 12 plant species. The species were exposed to varying concentrations of boric acid in different types of North American, European and artificial soils. Individual chronic toxicity values for invertebrates (4-63 days NOEC/NOAEC [NOAEC = no observed adverse effect concentration], LOEC/LOAEC [LOAEC = lowest observed adverse effect concentration] and EC/IC10-50) [IC = inhibitory concentration]) ranged from 1.43-630 mg B/kg (Amorim et al. 2012; Becker et al. 2011; Becker-Van Slooten et al. 2003; Environment Canada 2014k; ESG International Inc. and Aquatera Environmental Consulting Ltd. 2003; Huguier et al. 2013; Moser and Becker 2009a, 2009b, 2009c, 2009d, 2009e; Moser and Scheffczyk 2009; Owojori et al. 2011; Princz and Scroggins 2003; Princz et al. 2010; Smit et al. 2012; Stantec Consulting Ltd. and Aquaterra Environmental Consulting 2004). Individual chronic toxicity values for plants (14-90 days NOEC, LOEC and EC/IC10-50) ranged from 1.75-242 mg B/kg (Anaka et al. 2007; Bagheri et al. 1994; Becker et al. 2011; Environment Canada 2014k; Forster and Becker 2009; Gestring and Soltanpour 1987; Hosseini et al. 2007; Miller 2013). Toxicity symptoms in plants include yellowing, spotting or drying of leaf tissues (Gupta 1985). Further detail is available in Environment Canada (2014j).
The toxicity of boric acid to soil organisms depends on its bioavailability in the dissolved fraction of soil solution. Soil moisture has been determined to be the most important soil property (among soil moisture content, background boron, clay content and cation exchange capacity) for explaining boron bioavailability and toxicity to plants (Mertens et al. 2011). Adsorption reactions (see Section 7.1.3) are dependent on soil moisture and also pH, soil texture and soil content. Differences in soil toxicity values of approximately a factor of two for E. albidus and F. candida in LUFA Speyer and Organisation for Economic Co-operation and Development (OECD) standard soils were explained by a reduction in boron bioavailability, presumably because of adsorption given that OECD soil has greater organic matter and clay content than LUFA soil (Amorim et al. 2012). However, the impacts of soil ageing (up to five months) and sorption on the bioavailability of boric acid to plants in soil amended with boric acid were recently found to be minimal, indicating that added boric acid was not quickly bound (Mertens et al. 2011). This suggests that the effects of toxicity-modifying factors on the toxicity of boric acid in soil are generally low (less than one order of magnitude) or slow-occurring, and consequently they are not further considered in this assessment to characterize effects. Additionally, because the fraction of bioavailable boron in natural background concentration is low (see Section 7.1.3), the possible contribution of natural background concentration to the toxic effects of boric acid in soil organisms is considered negligible compared to boric acid concentrations added to soil as a result of anthropogenic activities, which are much more bioavailable. Based on these considerations, the added risk approach, which assumes that only the anthropogenic added fraction of boron (as boric acid) in soil may contribute to risk, was used to characterize the effects of boric acid on soil organisms (ICMM 2007a). Therefore, the PNEC derived for soil organisms focuses on the added fraction of boric acid in soil only and is referred to as a PNECadded.
The large data set available for boric acid meets the minimum criteria of species of the CCME (2006) and Metals Environmental Risk Assessment Guidance (MERAG) (ICMM 2007b), allowing derivation of a CTV using an SSD. The data used to develop the SSD are presented in Table C-1 (Appendix C) and include a total of 23 species (11 invertebrate and 12 plant species). The preferred endpoints to be used in the SSD were chosen following guidance from the CCME for the derivation of WQGs (CCME 2007) and include, in decreasing order of preference, EC10, EC/IC20, IC25 and NOECs. When more than one value for an endpoint was available for a single species (including data for different soils), the geometric mean of the toxicity values was calculated and used in the SSD. When a single value was available for a number of endpoints (e.g., biomass, growth) within one study, the lowest endpoint toxicity value for a given species was selected.
The software SSD Master v3.0 (SSD Master 2010) was used to plot the SSD (Figure 8-1). Several cumulative distribution functions (CDFs) (Normal, Logistic, Gompertz and Fisher-Tippett) were fit to the data using regression methods. Model fit was assessed using statistical and graphical techniques. The best model was selected based on consideration of goodness-of-fit and model feasibility. Model assumptions were verified graphically and with statistical tests. The Normal Model provided the best fit of the models tested upon visual inspection, the lowest levels of statistical variability (residuals), even distribution of the residuals, and lowest confidence interval spread. The Extreme Value Model had a slightly better Anderson-Darling Statistic test value (A2) = 0.254 (p less than 0.05) compared to a (A2) = 0.259 (p less than 0.05) for the Normal Model. However, the confidence interval spread of the Extreme Value was greater (i.e., 2.78-5.06) and the Normal Model was preferred. The HC5 of the SSD plot is 6.08 mg B/kg with lower and upper confidence limits of 5.42 and 6.82 mg B/kg, respectively.
The HC5 of 6.08 mg B/kg calculated from the SSD is selected as the CTV for soil organisms. This value is based on a chronic SSD that covers multiple species and taxa, and therefore no assessment factor is used to derive the added PNEC for soil organisms. Hence, the PNECadded for soil organisms is 6.08 mg B/kg.
8.3 Ecological exposure assessment
Environmental concentrations of boric acid are reported as concentrations of boron in a particular medium.
8.3.1 Ambient/background concentrations in Canada
18.104.22.168 Surface waters
Concentrations, where available, of recent total and dissolved boron measured in water bodies across Canada (Table 8-1) indicate that while some of the high concentrations may be related to the contribution from point-source anthropogenic releases, concentrations up to the 50th percentile should be representative of the regional biogeochemical background concentration (ICMM 2007c). These data were collected between 2009 and 2012 as part of Environment Canada’s Monitoring and Surveillance Program under the CMP (Environment Canada 2013c).
|Location||Concentration range (µg/L)||Median (µg B /L)||Reference|
|Pacific and Yukon RegionFootnote Table 8-2a||ND-100||5.75|
(dissolved = 3.43)
|Environment Canada 2013c|
|Prairie and Northern RegionFootnote Table 8-2b||2.8-43.6|
(dissolved = 2.9-78.6)
(dissolved = 13.61)
|Environment Canada 2013c|
|Ontario Region (Hudson’s Bay)Footnote Table 8-2c||1.2-806|
(dissolved = 1.2-729)
(dissolved = 29.48)
|Environment Canada 2013c|
|Ontario Region (Erie-Superior-Ontario)Footnote Table 8-2d||0.1-65.7||8.70||Environment Canada 2013c|
|Quebec RegionFootnote Table 8-2e||0.8-23.4||6.25||Environment Canada 2013c|
|Atlantic RegionFootnote Table 8-2f||0.3-347||3.59||Environment Canada 2013c|
Concentrations of total boron or extractable boron in soils of Canadian provinces are dependent on soil types, soil origin and pH (Parks and Edwards 2005). Higher concentrations of boron may be found in clay, loam or soils rich in organic matter than in sandy soil (Gupta 1967). The highest background concentrations are found in sedimentary rocks, particularly those originating from clay-rich marine sediments (Butterwick et al. 1989). Boron retention in soil depends on boron concentration in the soil solution, soil pH, texture, organic matter, cation exchange capacity, type of clay and mineral coating on the clay (see Section 7.1.3). Less than 5% of the total boron in soils is bioavailable to plants (Gupta 1993).
The U.S. Geological Survey (USGS 1984) reported an average boron concentration of 33 mg/kg (range less than 20-300 mg/kg) in surface soils from the conterminous United States, with concentrations slightly higher in the eastern U.S. Boron concentrations in soil are also high in California. In Canada, there is less data available on the concentration of total boron in soil, but median total boron concentrations reported for a limited number of sites sampled throughout Canada (20) between 1962-1973 range from 10.7-30 mg B/kg (Agriculture and Agri-Food Canada 2013). It is unknown whether agricultural activities occurred at these sites prior to sampling. In British Columbia, total boron concentrations in soil range from 1-90 mg/kg, with median concentrations from 1-26 mg/kg; concentrations are high in the Peace River area, and are considered deficient in the rest of B.C. (BC MOE 2005). In New Brunswick, the baseline boron soil concentration, characterized as 97th percentile boron soil concentration, is reported as 8 mg/kg (Government of New Brunswick 2005). In Alberta, extractable boron (hot water) measured in soil from 42 benchmark sites across the province ranged from 0.29-2.32 mg/kg with a mean of 0.92 mg/kg (Penny 2004). In the Flin Flon soil study, extractable boron ranged from 0.1-19 mg/kg from residential surface soils around east and west Flin Flon and Channing, Manitoba, and Creighton, Saskatchewan (Intrinsik 2010).
8.3.2 Exposure scenarios and predicted environmental concentrations
Exposure scenarios were developed for various activities that represent significant sources of release of boric acid and its precursors to the environment. These scenarios are presented in this section by sectors of activity. For each scenario, predicted environmental concentrations (PECs) expressed as elemental boron are estimated in order to assess exposure to boric acid for ecological receptors. Depending on the environmental media to which releases of boric acid are expected to occur, PECs are estimated for surface water or soil. PECs were not developed for air, because boric acid released to this medium is expected to be removed from this compartment by wet and dry deposition and to be ultimately deposited on soil or in water bodies. PECs were also not developed for sediment, because boric acid released to freshwater environments tends to remain in the water column due to its high water solubility.
PECs for the aquatic environment were primarily estimated using adequate data on measured concentrations of boron in relevant environmental media when available, as they provide evidence for exposure to organisms in Canada from specific sectors of activity (Sections 22.214.171.124-126.96.36.199). Although based on measured concentrations, these concentrations are labelled as "predicted" because measurements taken from specific sites for a sector of activity are used to represent the sector as a whole. The adequacy of measured environmental concentrations was assessed considering factors such as distance between sampling sites and source of release, the year the samples were collected, analytical method used, and number of available measurements. When available, preference was given to dissolved boron concentrations instead of total boron concentrations, because they comprise the fraction of boron that is most bioavailable. When it was not specified whether concentrations were reported for total or dissolved boron, the concentrations were assumed to be dissolved in order to be conservative (i.e., assuming high bioavailability). This assumption has minimal consequence to the final results, because dissolved and total boron measurements are generally almost identical, thus confirming the high bioavailability of boric acid in surface water. PECs consist of ranges of concentrations for individual sites, or ranges of arithmetic means or medians for multiple sites. When data were available, these PECs were compared to concentrations from designated "reference" or "unexposed" sites to confirm that the measured concentrations observed at the exposed sites were the results of anthropogenic releases.
When measured concentrations of boron in the aquatic environment were deemed inadequate or not available PECs were estimated. These PECs were determined based on a tiered approach, i.e., using conservative assumptions for the first calculations and then refining these assumptions where a potential concern is identified, to increase the realism of the scenario. For many industrial sectors, the main medium of potential environmental concern is surface water, because boric acid is expected to be released from industrial facilities directly to surface water (direct discharges) or indirectly through off-site wastewater treatment systems (indirect discharges). For each of these sectors, estimated aquatic concentrations (EACs) are the environmental concentrations resulting from the releases of these facilities or activities (e.g., down-the-drain-releases) and were calculated as a range across the related releases and exposure conditions. When data were modelled for direct discharges, a range of PECs for a particular sector was obtained by adding the median (50th percentile) background concentration of boron in water to the range of the related EACs (i.e., PEC range = EAC range + median background concentration). When data were estimated for indirect discharges, a range of PECs for a particular sector was obtained by adding, to the range of the related EAC, both the median background concentration of boron in water and the range of boron concentrations resulting from "down-the-drain" releases (i.e., releases from consumer use; see Section 188.8.131.52). As a conservative approach, the highest median background concentration (0.031 mg/L [Table 8-1]) was used.
For the soil compartment, measured concentrations in the vicinity of a site were compared to concentrations from designated "reference" or "unexposed" sites representing regional background conditions, when data were available (Section 184.108.40.206). When designated background concentrations were unavailable, environmental concentrations representing only the anthropogenic addition of boron in soil as a result of a specific activity were estimated. These concentrations are referred to as PECadded, because they ignore the potential contribution of bioavailable boric acid from naturally occurring boron soil background concentration. However, the availability of non-anthropogenic metals in soil is generally low, and because the bioavailable fraction of boron in soil is known to be low (less than 5% [Gupta 1993]), assuming a default bioavailability in soil equal to zero is considered reasonable (Struijs et al. 1997). Conservative assumptions were nevertheless used to generate soil PECadded values, including the use of a high soil-water partitioning coefficient value (i.e., log Ksw = 2.2) as well as assuming no loss via run-off, leaching or uptake by plants in modelling. PECadded values were generated to estimate the addition of boric acid in soil expressed as boron, resulting from air emissions (sections 220.127.116.11, 18.104.22.168 and 22.214.171.124) or from biosolids application (Section 126.96.36.199). Further details are available in Environment Canada (2014b, 2014f, 2014h).
188.8.131.52 Exposure scenario for power generation using coal
Boron is naturally present in coal, in concentrations ranging from 16-217 mg B/kg in Canadian coal, with the highest concentrations usually found in lignite and sub-bituminous coal used for power generation in Saskatchewan and Alberta (Goodarzi 2013). The combustion of boron-containing coal to generate electricity releases boron to the environment. Boron is emitted to air in particulate and gaseous forms, which can be expected to be deposited or washed out by rain and snow to terrestrial and aquatic ecosystems. Additionally, boron may be released to the aquatic environment by discharges from power plant wastewater effluents, fly ash and bottom ash containment areas (i.e., ash lagoons), coal piles, or groundwater seepage from containment areas. Additional information on boron releases associated with this sector can be found in Environment Canada (2014b).
An exposure scenario was developed for the Wabamun Lake area located within the North Saskatchewan River watershed, based on boron concentrations measured in various environmental media. This area is used as a realistic worst-case scenario to assess releases from coal-fired power plants in Canada. A number of water quality surveys were conducted by the Alberta Ministry of the Environment at Wabamun Lake in 2002 and 2005 (Alberta Environment 2002, 2003a, 2003b, 2006), and measured boron concentrations revealed relatively high amounts of boron (Table 8-3). Several coal mines are located in the Wabamun Lake area and in the vicinity of the power plants, and therefore measured concentrations in the lake water may include contributions from both coal-fired power generation and coal mining industrial activities. Soil samples were collected as part of an air deposition survey conducted in the Wabamun Lake area between 1994 and 1997 by the Geological Survey of Canada (GSC) (GSC 2002); no adequate designated soil background concentrations were identified for comparison. Generally, the low cumulative deposition rate of boron around Wabamun Lake (18.44 grams per hectare accumulated over four years), and the lack of apparent correlation between soil concentrations and boron measurements in moss used to monitor metal deposition, suggest that boron concentrations in soil in the region may be largely due to geogenic sources. In order to assess increases of boron in soil as a result of air emissions, the added soil concentrations were estimated over a period of 50 years using the cumulative deposition rate calculated by the GSC (2002) and a model converting soil deposition to soil concentration (Environment Canada 2014l). Added boron concentrations in soil as a result of air emissions over a period of 50 years were estimated to be relatively low (Table 8-3).
|Medium and units||PEC range (mg/L)||PEC median (mg/L or mg/kg)||Sample size (n=)||Sampling period||Reference|
|Water||0.786-1.0||0.884||116||1996-2005||Alberta Environment 2002, 2003a, 2003b, 2006|
|Soil||-||0.322Footnote Table 8-3a||-||2002||GSC 2002; Environment Canada 2014l|
184.108.40.206 Metal mining
Mining activities can include both ore extraction via open-pit or underground mining, and ore processing at a milling facility (commonly referred to as a mill). Ore typically consists of small amounts of valuable minerals in close association with much larger amounts of waste minerals of no economic value (gangue). The valuable ore minerals are separated (liberated) from the gangue in milling operations to obtain higher quality metal. Major steps in ore processing at milling facilities include grinding and crushing, chemical/physical separation and dewatering (Environment Canada 2009b). While boron compounds are not mined in Canada, boron is ubiquitous in nature and may be found in ores at varying concentrations. For example, boron can be associated with “vein-type” gold mineralization (Boyle 1974; Closs and Sado 1981). Additionally, borates are used in precious metals recovery (Borax 2013), where they serve as fluxes during fire assaying of ore or final refining of precious metals (Paliewicz et al2015). Smelting of precious metals concentrates may take place in a small furnace located within the milling facility of precious metals mining operations (Paliewicz et al 2015; U.S. EPA 1994). Less than four companies indicated purchasing between 10 000 – 100 000 kg of a boric acid precursor, and less than four companies indicated purchasing between 1000 and 10 000 kg of the same precursor for the year 2012, as a result of voluntary stakeholder engagement activities (Environment Canada 2013b). Because borates may be a major ingredient of fluxes in precious metal recovery (12-50 wt%) (Bugbee 1981), high concentrations of boron may be found in the slags generated by this activity (Paliewicz et al 2015). Laboratory leachability tests conducted on pulverized slags samples from three Canadian mining operations, show that a significant amount of boron (3-12 wt% of the initial mass of solid slag) may be released within 24-hr (Paliewicz et al 2015). Therefore, boric acid could be released into the environment as a result of the mining and production of metal concentrates.
Samples were collected by AMEC (2005) from a tailings area that received wastes from a former milling facility that processed an estimated 60 000 000 kg of boron-containing slag and refinery bricks (75% slag; 25% brick) for a precious metal refinery in addition to gold ore (Paliewicz et al 2015). Sampling results showed boron concentrations of up to 242 mg/L in local groundwater, and up to 9.1 mg/L in locally discharged surface water (AMEC 2005). As described in Paliewicz et al (2015), the AMEC (2005) study did not examine boron-concentrations in the river adjacent to the tailings area, but determined from the drainage pattern of the tailings area that the river flowing in the vicinity of the site was likely receiving discharges from the tailings area as surface runoff, groundwater seepage, or decanted dam water (AMEC 2005).
Reports from Environment and Climate Change Canada for 118 metal ore mining and milling sites that conduct environmental effects monitoring (EEM) under the Metal Mining Effluent Regulations (MMER) were reviewed (Environment Canada 2014m). Measurements of boron concentrations in effluent or in the receiving environment where effluent is discharged were available for 70 sites (approximately 60% of all sites) from 2004-2013, including four sites in the Quebec region, seven sites in the Atlantic region, 10 sites in the Pacific region, 22 sites in the Ontario region, and 27 sites in the Northern-Prairie region. Based on available data for monitoring of effluent and the exposure area, 54 sites showed low boron concentrations (less than or equal to 0.2 mg B/L), nine sites showed moderate boron concentrations (greater than 0.2-0.5 mg B/L), five sites showed high boron concentrations in the exposure area (greater than 0.5-1.4 mg B/L), and one site showed extremely high concentrations in the exposure area (greater than 10 mg B/L) (Table 8-4) (Environment Canada 2014m). The concentrations reported in the effluent at one site (less than 0.7 mg B/L) could not be interpreted, because of a high detection limit.
Of the sites showing high boron concentrations in the exposure area, site 1 is an integrated base metal mine and smelter, site 2 is a uranium mine, site 3 is a uranium ore processing mill, site 4 comprises a number of base metals and precious metals mines discharging into a common waterbody, site 5 is a former metal ore processing mill, and site 6 is a mill that processes a range of ores and feeds. Further details are available in Environment Canada (2014c).
|Site and type of facility||Reference or exposed area||PEC range (mg total B/L)||Sample size (n=)||Sampling period|
|65 mining sites||Exposed area||Negligible - less than or equal to 0.5||-||2004-2013|
|Site 1 - mine and smelter||Exposed areaFootnote Table 8-4a||1.02-1.17||5||2011|
|Site 1 - mine and smelter||Reference||less than 0.01||5||2011|
|Site 2 - mine||Exposed areaFootnote Table 8-4b||0.29-0.56||2||2004|
|Site 2 - mine||Reference||0.003-0.023||3||2004|
|Site 3 - mill||Exposed area||0.22-1.3||5||2011|
|Site 3 - mill||Reference||less than 0.010-0.010||8||2011|
|Site 4 - multiple mines||Exposed area||0.168-0.907||29||2003-2010|
|Site 4 - multiple mines||Reference||0.03-0.14||39||2003-2010|
|Site 5 - mill||Exposed area||0.047-0.687||6||2004-2007|
|Site 5 - mill||Reference||0.013-0.016||2||2004-2007|
|Site 6 - mill||Exposed area||14.6-20.1||14||2010-2013|
|Site 6 - mill||Reference||less than 0.01||14||2010-2013|
220.127.116.11 Base metals and precious metals smelting and refining
A number of Canadian facilities involved in the smelting or refining of base and precious metals reported using boric acid precursors in their processes. Less than four companies whose primary sector of activity is base metal smelting reported importing between 50 000 and 100 000 kg of a boric acid precursor in 2008 (Environment Canada 2009a). Less than four companies indicated purchasing between 100 000 and 1 000 000 kg of a boric acid precursor, and less than four companies indicated purchasing between 1000 and 10 000 kg of another boric acid precursor for the year 2012, as a result of voluntary stakeholder engagement activities (Environment Canada 2013b). In base metal smelting and gold metallurgy, borates are used as flux, dissolving metallic oxide impurities that may be subsequently removed with slags, and also as a cover flux to protect metals against oxidation (Borax 2013; Cole and Ferron 2002). Slags generated at certain processing steps from some base metals smelting facilities such as lead smelters, may contain up to 25 wt% of boron oxide (Jaeck 1989). Based on Paliewicz et al (2015), it is inferred that the leachability of boron (as boric acid) from these slags could be significant. Boron may also be present in the various ores and concentrate being processed. Releases of boron to the environment from base and precious metals smelting and refining facilities may occur via air emissions (Environment Canada 2013a) or effluent releases to the aquatic environment as a result of processing activities
Results from studies conducted near a smelter in British Columbia and two smelters in Manitoba indicate that air emissions may not contribute significantly to boron levels in soils or in water bodies located near smelters (exposed areas), because those levels are generally comparable to levels from reference (unexposed) areas (CEI 2003; Intrinsik Environmental Sciences Inc. et al. 2011; Jacques Whitford 2008; Jones and Henderson 2006; Jones and Phillips 2003; Stantec 2009). Further details are available in Environment Canada (2014d).
Elevated boron concentrations are reported in the effluent of a number of smelters, including three combined mining and smelting sites that conduct EEM (Ouellet et al. 2013; Environment Canada 2014m). However, boron concentrations in receiving aquatic environments in exposed areas downstream of smelter effluent discharges are generally comparable to boron concentrations measured in reference sites (Table 8-5). The samples from Site 1 (also discussed in the metal mining sector exposure characterization in subsection 18.104.22.168), where elevated dissolved boron concentration was measured (1.17 mg B/L), consist of partially diluted effluent (75% effluent) (Environment Canada 2014m). Further details are available in Environment Canada (2014d).
|Site||Reference or exposed area||PEC range (mg B/L)||Sample size (n=)||Sampling period||Reference|
|Site 1||Exposed||1.02-1.17||5||2011||Environment Canada 2014m|
|Site 1||Reference||less than 0.01||5||2011||Environment Canada 2014m|
|Site 2||Exposed||0.03-0.07||3||2011||Environment Canada 2014m|
|Site 2||Reference||0.002-0.006||5||2011||Environment Canada 2014m|
|Site 3||ExposedFootnote Table 8-5a||0.016-0.054||13||2011||Environment Canada 2014m|
|Site 3||Referencea||0.032-0.044||2||2011||Environment Canada 2014m|
|Site 4||Exposeda (far-field)||Negligible - 2.7 x 10-3||58||1996-1997||Ryan 2005|
|Site 4||Referencea||Negligible - 2.4 x 10-3||58||1996-1997||Ryan 2005|
22.214.171.124 Coal mining
The mining of coal reserves may lead to the release of boron naturally present in coal (16-217 mg B/kg) into the environment (Goodarzi 2013). Releases to the aquatic environment may occur as a result of discharges and seepage from tailing ponds, mining dewatering activities, surface water run-off from disturbed areas, and leaching from exposed coal-bearing materials or waste rock piles (BC MOE 1978; Craw et al. 2006; NRC 1981; Seierstad et al. 1983). Further details are available in Environment Canada (2014e).
Most coal mines in Canada are located in Alberta (nine in total) and British Columbia (10). A total of two areas in these provinces were selected for exposure scenarios based on their number of mines and the availability of studies reporting environmental concentrations of boron: the Elk River watershed in British Columbia, and the McLeod and Smoky River watersheds in western Alberta. Results from the studies show that, in some cases, boron concentrations were slightly elevated downstream of mine activities compared to select reference areas (Casey 2005; Frenette 2007) (see Table 8-6).
|Medium and units||PEC range||Number of samples (n=)||Sampling period||Reference|
|Water (mg B/L), exposed area||0.004-0.061||92||1998-2007||Casey 2005; Frenette 2007|
|Water (mg B/L), reference area||0-0.017||64||1998-2007||Casey 2005; Frenette 2007|
126.96.36.199 Oil sands extraction and processing
Boron occurs naturally in the bitumen found in Athabasca oil sands deposits in northern Alberta and in formation waters and reservoir rock that may be disturbed during extraction/mining of the deposits (Hitchon et al. 1977; Williams et al. 2001; Frank et al. 2014). Elevated boron concentrations (0.128-3.7 mg B/L) have been reported in oil sands process waters (OSPW) from surface mining operations, which are stored in tailing ponds (Frank et al. 2014; Gupta 2009; Holden et al. 2013; Redfield et al. 2004; Renault et al. 1998; Puttaswamy et al. 2010; Renault et al. 2001; Van Den Heuvel et al. 1999) and higher concentrations have been reported in OSPW from underground (in-situ) operations (76.6-196 mg B/L) (Williams et al. 2001). Bitumen extraction and processing generates large amounts of coke, and elevated boron concentrations have been measured in coke leachate (495-749 mg B/L) (Puttaswamy et al. 2010). Releases of boron to the aquatic environment may occur as a result of surface water run-off from mining areas and seepage from tailing ponds and OSPW storage ponds (Frank et al. 2014; Pollet and Bendell Young 2000).
Atmospheric deposition via wet and dry process has also been identified as a source of boron to soil in the Athabasca oil sands region (Bari et al. 2014). Boron concentrations in samples collected using four bulk samplers over a three-month period in winter 2012 were greater near oil sands extraction and processing sites, with a maximum average daily deposition rate of 3.6 µg/m2/d within a 20-km radius, compared to deposition rates of 0.4 and 0.3 µg/m2/d at distant monitoring stations (48 and 68 km away, respectively) (Bari et al. 2014). Over a 50-year period, such a deposition rate would lead to an added boron concentration in soil of 0.92 mg B/kg (Table 8-7) (Environment Canada 2014l). Further details are available in Environment Canada (2014f).
Concentrations of total and dissolved boron available for multiple monitoring stations situated on the Athabasca River and many of its tributaries from the Regional Aquatics Monitoring Program (RAMP) and the Joint Canada-Alberta Oil Sands Environmental Monitoring program are generally low (Table 8-7) (JOSM 2014; RAMP 2014). RAMP designates its monitoring stations as "baseline" stations situated upstream of focal projects at the time of sampling, or as "test" stations located downstream of focal projects at the time of sampling (RAMP 2013). Baseline stations may reasonably be considered representative of "unexposed" conditions and test stations representative of "exposed" conditions; however, because oil sands development has been occurring for many decades in a large area, it can be difficult to clearly identify background (or reference) stations within the Athabasca River watershed. A dissolved boron concentration above 1 mg B/L (i.e., 1.7 mg B/L) was detected in only one instance, at a test station (MAR-2A) located on the MacKay River in winter 2010 (RAMP 2014). The second-highest dissolved boron concentration measured at this site is 0.193 mg B/L (also measured in the winter), with a median concentration (from 2009-2012) of 0.059 mg B/L (n=14). Although the cause of the elevated boron concentration measured at station MAR-2A is unknown, based on the large dataset available this measurement seems to be an isolated event.
|Medium and units||PEC range and 95thpercentile||Number of samples (n=)||Sampling period||Reference|
|Water (mg B/L), unexposed stationFootnote Table 8-7a||0.004-0.892 (0.167)||392||1997-2012||RAMP 2014|
|Water (mg B/L), exposed stationa||0.004-1.72 (0.164)||589||1997-2012||RAMP 2014|
|Water (mg B/L)Footnote Table 8-7b||0.0001-0.172||332||2003-2011||JOSM 2014|
|Soil (mg B/kg)Footnote Table 8-7c||0.92||-||2012||Bari et al. 2014; Environment Canada 2014l|
188.8.131.52 Oil and gas extraction
A number of boric acid precursors are used in oil and gas extraction activities, including drilling and hydraulic fracturing. The quantities of a number of boric acid precursors imported into Canada by oilfield service companies (involved in drilling and hydraulic fracturing activities) ranged between approximately 1 000 000-10 000 000 and 10 000 000-50 000 000 kg yearly between 2009 and 2012 (CBSA 2013). They generally serve as crosslinkers to maintain fluid viscosity as temperature increases down the well (FracFocus 2014; US EPA 2012a). Releases of boric acid to the environment may occur as a result of the transportation and on-site storage of boric acid precursors, the preparation of drilling muds and hydraulic fracturing fluids, and the storage, treatment and disposal of flowback fluid and produced water (CCA 2014). Flowback fluid consists of the chemical additives that were mixed into the fracturing fluid and the formation water that may be high in dissolved solids (CCA 2014). Produced water is water trapped in underground formations that is brought to the surface with the oil and gas (CSUR 2014). Boron has been measured in flowback fluid and produced water in Canada (0.05-30.6 mg B/L), due primarily to natural sources found in the oil and gas formations (Cheung et al. 2009; MDDEP 2010a).
Provinces and territories are the primary regulators of oil and gas exploration and extraction, including chemical use, water use, water storage and disposal of wastewater (including flowback fluids and produced water). Flowback fluids and produced water are recovered and stored in lined surface ponds or storage tanks, and are either treated for re-use or disposed of. Wastewater disposal occurs either on-site or off-site through injection into a deep wastewater disposal well or at a waste treatment facility (CCA 2014). The wastewater management option that is authorized depends on the geological characteristics of the site where the activity occurs and the provincial or territorial regulatory requirements.
Given the activities taking place in Canada to identify substances that are used in hydraulic fracturing and to monitor ongoing activities in other jurisdictions, and given existing provincial and territorial regulations, these uses will not be considered further in this assessment at this time. As information evolves, future activities may be considered by Environment and Climate Change Canada and Health Canada.
Boron, an essential micronutrient for plants, is applied to soils to address nutrient deficiencies and is incorporated into some fertilizer pre-mixes to prevent nutrient deficiencies (Shubert 2003; [personal communication from CFIA 2014; unreferenced]). Boric acid precursors are used in Canada as boron micronutrients in fertilizers (see Section 5). According to CBSA (2013), between 1 000 000 and 2 400 000 kg of boric acid precursors were imported yearly into Canada between 2009 and 2012 by companies whose primary activity is agricultural chemicals.
Elevated boron concentrations in surface waters (median 3.1 mg B/L) and river waters (median 1.1 mg B/L) have been observed in the western San Joaquin Valley in California as a result of agricultural drain-water management practices, where shallow-lying saline groundwater (with elevated concentrations of boron) is directed away from fields to ensure crop productivity (Eisler 1990; Klasing and Pilch 1988; Ohlendorf 2002). Monitoring data for boron in surface water in Canada near intensive agricultural areas are scarce. However, water samples collected in July 2008 at 20 sites (including agricultural drainage ditches and streams) in Creston Valley, British Columbia (the central Kootenay region’s most significant agricultural area) found boron levels to be below the detection limit of 0.05 mg B/L (Davies 2008).
184.108.40.206 Pulp and paper manufacturing
Between 2008 and 2012, multiple companies in the pulp and paper sector reported importing, purchasing or using boric acid precursors in their processes (CBSA 2013; Environment Canada 2009a, 2013a). Quantities imported or used yearly by a number of companies between 2008 and 2012 ranged from 0-100 kg to 100 000-1 000 000 kg of boric acid precursors (CBSA 2013; Environment Canada 2009a, 2013b). The substances are used as reducing agents to bleach wood pulps and recycled fibers (Ni et al. 2001; Wasshausen et al. 2006), and may be used in partial borate autocausticizing (Mao et al. 2006; Tran et al. 1999). Given that boron is an essential nutrient for plants and trees (Reiman and De Caritat 1998), it is naturally found in the raw materials (cell wall structure) processed in this sector. Therefore, boron releases to the environment might also occur from pulp and paper mills that do not directly use boric acid precursors in their manufacturing processes, but these releases are anticipated to be small. However, mills that use boron-containing substances are anticipated to release greater amounts to the environment, because the capture and removal of boron from wastewater treatment systems is low (Bryant and Pagoria 2004). Releases to surface water from pulp and paper mills’ final effluents were identified as the principal source of boron to the environment for this sector.
Measured concentrations of boron in surface waters across Canada (obtained as part of the EEM program) for three pulp and paper mills (Environment Canada 2014m) are relatively low (Table 8-8). Due to the scarcity of environmental concentrations of boron available in receiving water bodies downstream of mills (exposed areas), PECs were also derived using available concentration data in mills’ effluents. Average or median effluent concentrations were identified for 46 mills in Canada, and range from non-detected to 4.01 mg B/L (Environment Canada 2014m; Kovacs et al. 2007; Martel et al. 2010; MDDEP 2010b; NCASI 2006; UBC 1996). A high boron concentration value of 30.6 mg B/L reported in the final combined effluent of one facility (NCASI 2006) was determined to be erroneous. The correct average effluent concentration in effluent over the three-day monitoring event at the facility was 1.3 mg B/L (personal communication from MDDELCC 2014; unreferenced). Further details are available in Environment Canada (2014g). PECs were estimated for this sector by applying a default dilution factor of 10 to the average or median effluent concentrations reported at each facility and by adding the default background value of 0.031 mg B/L (see 8.3.2) to the resulting diluted effluent concentrations (see Table 8-8).
Because facilities using boron-containing substances are not necessarily captured in the available monitoring data, exposure modelling was also conducted for this sector. There are about 100 active mills in Canada that manufacture pulp (chemical, mechanical, thermo-mechanical and recycled), newsprint, printing/writing paper, tissue/towel paper, and paperboard. To account for differences in release rates for the purpose of aquatic PEC calculations, these mills were divided into two groups: 34 tissue, towel and paperboard mills, and 66 pulp, paper and newsprint mills.
Conservative EACs for this sector were modelled using the highest release rates for each group based on available measured boron concentrations in mill effluents. These measured concentrations were obtained from 25 of the 100 active mills over the period 2001-2003 (NCASI 2006), and are assumed to be representative of the pulp and paper sector in Canada. The EACs of boron are in the range of 0.013-1.07 mg/L for tissue, towel and paperboard mills, and 0.029-1.4 mg/L for pulp, paper and newsprint mills. This corresponds to PECs ranging from 0.044-1.10 and 0.06-1.43 when considering background levels (see Table 8-8). Further details are available in Environment Canada (2014h).
|Medium and units||PEC range||Number of samples (n=)||Sampling period||Reference|
|Water (mg B/L), reference stationFootnote Table 8-8a||0.011-0.05||11||2009||Environment Canada 2014m|
|Water (mg B/L), exposed stationa||0.011-0.05||16||2009||Environment Canada 2014m|
|Water based on effluent concentration (mg B/L)Footnote Table 8-8b||0.031-0.431||200||1994-2004||Kovacs et al. 2007; Martel et al. 2010; MDDEP 2010b; NCASI 2006; personal communication from MDDELCC 2014 (unreferenced); UBC 1996|
|Water, modelled (mg B/L)||0.044-1.43||-||-||Environment Canada 2014h|
220.127.116.11 Wastewater, down the drain releases, biosolids application and waste management
Wastewater treatment systems in municipalities represent a common point of entry for substances to surface water through effluent discharges. Also, the land application of wastewater biosolids is a potential point of entry to soil.
Empirical monitoring data are available for a number of wastewater treatment systems. For example, data were collected under the CMP monitoring program for 15 facilities located across Canada from January 2011 to November 2012 (Environment Canada 2013c). A total of 72 influent samples, 18 primary effluent samples, and 72 final effluent samples were analyzed for total boron. Boron was detected in all but nine samples, with concentrations ranging from less than 0.0011-2.1 mg B/L in the influent and less than 0.0011-1.94 mg B/L in the final effluent. Median influent and effluent concentrations were 0.152 and 0.153 mg B/L, respectively. Assuming a dilution factor of 10, a range of concentrations in receiving water of less than 0.00011-0.194 mg B/L is obtained for down-the-drain releases or their combination with industrial releases, and a range of PECs from 0.031-0.225 mg B/L is obtained when adding the aquatic background (i.e., 0.031 mg B/L) (see Table 8-9). Median removal of boron from influent to final effluent was negative 2.2% (i.e., effluent concentrations were greater than influent concentrations), indicating that little removal usually takes place. The increased boron concentration in effluent may be caused by the release of boron bound to organic matter following its degradation in biological treatments. Maximal removal of 83% observed at one facility could not be explained. Additional data for concentrations of boron in treated wastewater effluents identified for other locations throughout Canada between 1978 and 2012 range from less than 0.01-0.7 mg B/L (Cain and Swain 1980; CWWA 2001; MDDEP 2001; Environment Canada 2013b; Swain et al. 1998).
Because releases of boron-containing substances to wastewater treatment systems are not necessarily captured in the available monitoring data, exposure modelling was also conducted for this sector. Several uses of boron-containing substances potentially resulting in down-the-drain releases contributing to the cumulative aquatic exposure to boron have been identified in Canada (CBSA 2013; Environment Canada 2009a, 2013b). Categories of products subject to down-the-drain releases include soaps and detergents, cosmetics, eye and personal care, swimming pool chemicals and veterinary products. Based on Canadian import data between 2009 and 2012 from companies involved in these categories of products, and U.S. annual quantities (for comparison purposes) for soaps and detergents, the annual quantity of substances used in products subject to down-the-drain releases is estimated to be approximately 650 000 kg B/year (Ball et al. 2012; CBSA 2013). A calculation combining information on quantities of boron reaching wastewater treatment systems and on removal efficiency for different wastewater treatment types (i.e., primary and secondary) with their effluent flows across Canada as well as receiving water bodies was used to estimate EACs. EACs calculated for these products range from negligible to 0.194 mg B/L, resulting in PECs ranging from 0.032-0.225 mg B/L, when adding background (0.031 mg B/L). The modelled PECs are similar to the PECs derived from measured concentrations in wastewater treatment effluents. Further details are available in Environment Canada (2014h).
Boron was also detected in most samples (64 of 81) of primary sludge, secondary sludge, and biosolids collected as part of CMP monitoring activities (Environment Canada 2013c). Concentrations in primary sludge, secondary sludge and biosolids ranged from less than 0.03 to less than 76 mg/kg dw (median of less than 0.05 mg/kg dw), less than 0.002-16.4 mg/kg dw (median of 6.03 mg/kg dw), and 0.03-445 mg/kg dw (median of 14.1 mg/kg dw), respectively (Environment Canada 2013c). The maximum concentration of 445 mg/kg could not be explained. Biosolids from wastewater treatment systems are sent to landfills, incinerated or spread on agricultural land. The equation below was used to estimate the input of boron to soils via spreading of biosolids containing boron.
PECadded = boron concentration in biosolids x application rate x number of years ÷ mixing depth x soil density
To simulate a worst-case scenario, a maximum application rate of 8300 kg dry weight per hectare (dw/ha) per year (based on the highest existing provincial regulatory limit; Environment Canada 2006), a mixing depth of 0.2 m (plough depth; ECHA 2012) and a soil density of 1200 kg/m3 were used (Williams 1999), along with the highest concentration of boron measured in biosolids (37.6 mg/kg dw) from wastewater treatment systems in Canada, that are not incinerated. A period of 10 consecutive years was chosen as a length of accumulation (ECHA 2012). The cumulative boron concentration in soil at the end of this period is calculated to be 1.3 mg/kg dw. This PECadded value is based on the assumption that boron will not leach or run off, nor be taken up by plants and removed through harvest, and is therefore conservative considering the high water solubility of boric acid.
Boric acid contained in products, manufactured items or other materials (e.g., contaminated soils) that are disposed of in landfills may leach out and end up in landfill leachate. Monitoring data were collected at 13 larger landfills across Canada between 2008 and 2013 under the CMP monitoring program. Total and dissolved boron concentrations were measured in leachate before and after treatment (when available). Before any treatment, total boron concentrations in leachate ranged from 0.001-42.1 mg B/L (median of 3.8 mg B/L; n=109) (Conestoga-Rovers and Associates 2015). Five of the 13 landfills treat their leachate on-site before either sending it to a wastewater treatment system or releasing it to the environment. For these landfills, total boron concentrations in leachate after treatment were 3.1-34.9 mg B/L (median of 15.3 mg B/L; n=25). Removal rates were generally low (11.3%), and in a few cases the concentration of boron in leachate was greater after treatment (Conestoga-Rovers and Associates 2015).
For landfills that send their leachate (treated or not) to a wastewater treatment system, the dilution of the leachate in the system’s influent and dilution of the system’s effluent in the receiving watercourse are expected to result in concentrations of boron below the levels of concern (PNEC) for aquatic ecosystems. Three landfills, however, release their leachate (treated or not) to the environment, to wetlands, a filtering marsh or directly to a river. Total boron concentrations measured in leachate (post-treatment if available) from 2008-2011 ranged from 0.8-5 mg B/L (n=6), from 3.1-6.1 mg B/L (n=6), and from 3.8-6.2 mg B/L (n=3). Using a dilution factor of 10 and adding 0.031 mg B/L for background yielded PECs of 0.11-0.65 mg B/L for all three sites.
|Medium and units||PEC range||Number of samples (n=)||Sampling period||Reference|
|Water, from treated wastewater effluent concentrations (mg B/L)Footnote Table 8-9a||0.031-0.225||-||1978-2012||Environment Canada 2013c|
|Water, modelled for down-the-drain releases (mg B/L)||0.032-0.225||Environment Canada 2014h|
|Water, from landfill leachate concentrations (mg B/L)a||0.11-0.65||15||2008-2011||Conestoga-Rovers and Associates 2015|
|Soil (mg B/kg dw), from biosolids application||1.3||-||2009||Environment Canada 2013c|
18.104.22.168 Rubber sector
Less than four rubber manufacturing companies imported between 10 000-100 000 to 100 000-1 000 000 kg/yr of boric acid precursors yearly into Canada from 2009-2012 (CBSA 2013), typically used as flame retardant in rubber products (Ball et al. 2012). Releases of boric acid from this sector are anticipated to be to the aquatic environment: facilities either release boric acid in their effluent to the receiving environment directly (direct dischargers) or indirectly via wastewater treatment systems (indirect dischargers).
EACs were calculated for direct dischargers and indirect dischargers, assuming that the maximum yearly quantity of boric acid imported into Canada for this sector is used at a single facility. EACs ranged from negligible (0.038 mg B/L for indirect dischargers) to a range of 0.03-0.29 mg B/L for direct dischargers. This leads to aquatic PECs of 0.032- 0.26 mg B/L for indirect dischargers upon addition of the natural background concentration (0.031 mg B/L) and the concentration range (7.7 x 10-4-0.194 mg B/L) resulting from down-the-drain releases, and PECs of 0.06-0.32 mg B/L for direct dischargers with the addition of the natural background concentration only (0.031 mg B/L). Further details are available in Environment Canada (2014h).
22.214.171.124 Surface finishing
Boric acid precursors are imported into and used in Canada by surface finishing facilities (i.e., electroplating) (CBSA 2013; Environment Canada 2009a, 2013b), to clean substrate surface prior to plating and as a buffer in plating solutions. Boric acid also serves other purposes such as promoting plating deposition and reducing passive film formation (Tsuru et al. 2002).
The highest annual known use quantity of boric acid precursors at an electroplating facility in Canada was reported to be in the range of 10 000-100 000 kg/yr (Environment Canada 2013b). The upper end value of 100 000 kg/yr was used to estimate the largest quantity used at a single facility discharging its treated wastewater to an off-site wastewater treatment system in a municipality, leading to an EAC of 0.095 mg B/L. When considering sources of down-the-drain releases and default background, a conservative aquatic PEC range of 0.13-0.32 mg B/L is obtained for this sector. Further details are available in Environment Canada (2014h).
126.96.36.199 Fibreglass insulation manufacturing
Large quantities of boric acid precursors (1 000 000-10 000 000 to 10 000 000-50 000 000 kg) were annually imported, used or purchased by insulation fibreglass manufacturers in Canada from 2008-2012 (CBSA 2013; Environment Canada 2014n). The substances are used as flux to lower glass batch melting temperatures (Borax 2014a), increase mechanical strength and drawing quality (Woods 1994), impart decompressibility (Etimine 2014), and increase product insulation performance (Borax 2014a).
Impact upon vegetation as a result of boric acid precursors’ air emissions has been observed in the vicinity of fibreglass manufacturing plants in Canada and Norway (Temple and Linzon 1976; Temple et al. 1978; Eriksson et al. 1981). Symptoms specific to boron toxicity observed on deciduous trees can include chlorosis and dark intercostal necrotic lesions of leaves (Eriksson et al. 1981; Temple et al. 1978). Emissions from the glass melting process can be particulates (boron oxides) or gaseous (as boric acid) (US EPA 1995; NPI 1998), and up to 15% of the boron added may volatilize during the manufacturing process (Wallenberger 2010). Emissions led to increased concentrations of boron in soil (a water-soluble boron concentration of 14.8 mg/L) and foliage (a maximum concentration of boron in foliage of 989 ppm) at the monitoring station located closest (150 m) to the Canadian facility (Temple et al. 1978). Uptake of boron was through direct absorption of gaseous or particulate boron into the foliage and from uptake of residual soluble boron in soil (Temple et al. 1978). Boric acid precursors were eliminated from the manufacturing process in the Canadian facility in 1973, bringing an end to emissions of boric acid precursors for this particular facility (Temple et al 1978).
Given that emissions of boric acid precursors and their uptake have been shown to harm vegetation, a conservative exposure scenario was developed to estimate increases in boron soil concentration related to the air emissions and resulting soil deposition of boron from currently operating fibreglass manufacturing sites (effects associated with direct absorption of boric acid precursors into foliage could not be modelled and are not captured by this analysis). A worst-case scenario was developed for a large Canadian facility using conservative emission rates and the program AERMOD, leading to a maximum steady-state PECadded in soil of 1.3 mg B/kg based on continuous release for 100 years (Environment Canada 2014l). Further details are available in Environment Canada (2014h).
Additionally, elevated boron concentrations (total boron of up to 114 mg B/kg and hot-water-soluble boron of up to 26.4 mg B/kg) have been observed in soil samples collected on the property of one facility that uses borax (Ontario MOE 2012). These elevated concentrations were hypothesized to be related to the presence of outdoor stockpiles of crushed glass (cullet) on the property or releases linked to a loading dock used to accept raw materials including borax (Ontario MOE 2012). Elevated soil concentrations seen on-site are, however, believed to be limited to property boundaries.
188.8.131.52 Generic scenarios
Boric acid is used for purposes in addition to those already discussed. According to the CBSA (2013), these other uses can be broadly divided into large and small industrial users. The category of large industrial users comprises two main sectors having an annual cumulative import quantity of more than 1 million kg of boric acid precursors: agriculture products manufacturing, and construction products manufacturing (fibreglass insulation, cellulose insulation, engineered wood products and gypsum board). Boric acid and other precursors are used as flame retardant in cellulose insulation and engineered wood products (Borax 2014a; Lea 2000; Levan and Tran 1990). Boric acid is added during the manufacture of gypsum board to improve manufacturing processes, increase strength and enhance resistance to fire (Borax 2014b). Functions of boric acid precursors in agriculture and fibreglass insulation manufacturing are presented in sections 184.108.40.206 and 220.127.116.11, respectively. The category of small industrial users comprises various uses, with each having an annual import quantity well below 1 million kg (PECs were not estimated for these uses, but are expected to be lower than those from large users).
A total of 53 facilities were identified from import data obtained from the CBSA (CBSA 2013) and collected through a DSL IU (Environment Canada 2009a) for the large users’ category. The facilities were further divided into three quantity groups:
- Group I (21 facilities): use quantity per facility = 1000-100 000 kg/yr
- Group II (28 facilities): use quantity per facility = 100 000-1 000 000 kg/yr
- Group III (4 facilities): use quantity per facility = 1 000 000-10 000 000 kg/yr
Conservative EACs were calculated for indirect discharges to the environment from these manufacturing activities, by combining the daily release of boron based on the maximum use quantity of boric acid precursors selected for each group with daily dilution water volumes. Calculated EACs ranged from 0.12 x 10-3-0.5 mg B/L, leading to PECs ranging from 0.032-0.725 mg B/L when adding background concentrations and sources of down-the-drain releases. Further details are available in Environment Canada (2014h).
8.4 Characterization of ecological risk
The approach taken in this ecological screening assessment was to examine the scientific literature, and develop conclusions based on a weight-of-evidence approach and using precaution as required under CEPA. Lines of evidence considered include results from risk quotient (RQ) analyses of key exposure scenarios, as well as information on fate, persistence, bioaccumulation, toxicity, and potential sources of boric acid releases to the Canadian environment. This section first presents the results of RQ analysis for exposure scenarios based on the various anthropogenic activities that may represent significant sources of release of boric acid to the environment. The PECs in the aquatic environment were based on measurements of boron in water or were modelled using conservative assumptions. Soil PECaddeds were estimated by modelling the added concentration of boron in soil as a result of the deposition of boron on soil from air emissions or from land application of biosolids.
8.4.1 Risk quotient analysis
RQ analyses, integrating measured boron concentrations and realistic worst-case orconservative estimates of exposure with toxicity information, were performed for the aquatic environment and, in some cases, the terrestrial environment, to determine whether there is potential for boric acid to cause ecological harm in Canada. The exposure scenarios presented in Section 8.3.2 yielded negligible PECs ranging from negligible to 20.1 mg B/L in the aquatic environment and PECadded of 0.322 to 1.3 mg B/kg in soil. PNECs were derived for the aquatic environment (1.5 mg B/L), and a PNECadded value was derived for the terrestrial environment (6.08 mg B/kg) (see sections 8.2.1 and 8.2.3).
While the majority of the resulting RQs (PEC/PNEC) based on PEC ranges are below 1, RQ exceedances were identified in the aquatic environment for the metal mining sector and oil sands extraction and processing sector (Table 8-10). RQs within the metal mining sector were low for 68 sites (<0.6), while moderately high RQs of 0.68 - 0.78 and 0.15 - 0.86 were calculated for two sites (one mine / smelter and a uranium mill). However, elevated RQs of 9.7–13.4 were calculated at one milling site based on 14 samples over a 4 year period (2010-2013) indicative of high risk associated with aquatic releases of boric acid at this location.
Given that the oil sands extraction and processing sector’s upper range PEC value of 1.72 mg B/L may reasonably be considered an outlier datapoint (see 18.104.22.168), the 95thpercentile PEC value was used for comparison to the PNEC value, resulting in an RQ of 0.11. Although the upper end of the RQs for the pulp and paper sector is close to 1 (0.95), it is based on conservative assumptions for boron releases and limited to one site only, with the next-highest estimated RQ being 0.69. With the further refining of the pulp and paper exposure scenario, lower estimates for the RQs can be derived, although this is deemed not necessary at this time.
|Sector||Medium||PNEC water (mg B/L);|
PNECadded soil (mg B/kg)
|Range of PECsFootnote Table 8-10a water|
PECadded soil (mg B/kg)
|Range of RQs|
|Smelting and refining||Water||1.5||Negligible-1.17||0-0.78|
|Oil sands extraction and processing||Water||1.5||0.0001-1.7; .16Footnote Table 8-10b||0-1.13; .11Footnote Table 8-10c|
|Oil sands extraction and processing||Soil||6.08||0.92||0.15|
|Agriculture||Water||1.5||less than 0.05||0|
|Pulp and paper||Water||1.5||0.011-1.43||0.007-0.95|
|Wastewater and down-the-drain releases||Water||1.5||0.031-0.225||0.02-0.15|
|Waste management (landfill leachate)||Water||1.5||0.11-0.65||0.07-0.43|
8.4.2 Consideration of lines of evidence and conclusion
This screening assessment includes all substances having the potential to dissolve, dissociate or degrade to release boric acid through various transformation pathways that can potentially contribute to the combined exposure of ecological receptors to boric acid (boric acid precursors). Sources of boric acid include activities involving boric acid precursors (including the 14 boron-containing substances that had been identified as meeting the categorization criteria) having the potential to release boric acid, as well as incidental manufacture and natural/ambient background concentration of boric acid. Efforts were made throughout this ecological assessment to focus on all sources of boric acid and link assessment endpoints and exposure scenarios to the industrial activities involving them, to the extent possible. Data on manufacture, import and use of specific substances were used, where possible, to model releases in order to estimate PECs. As well, other anthropogenic incidental sources of boric acid to the environment were systematically included, using sector analyses and through the use of monitoring data to estimate PECs.
Once released into the environment, boric acid is expected to be persistent in water, soil and sediment. Boric acid has been demonstrated to have low to moderate toxicity to sensitive aquatic and terrestrial organisms. The bioaccumulation potential of boric acid is low in most organisms, and does not generally lead to levels causing harm to sensitive species at body concentrations higher than required for essentiality.
This assessment of boric acid and its precursors examined exposures from a wide range of sources covering multiple substances that could contribute to loadings of boric acid in the environment. Generally, the data indicate that anthropogenic releases of boric acid, either through the import and inferred uses of boric acid and its precursors or as a result of incidental releases from a number of industrial activities, are not expected to result in concentrations of boric acid at levels higher than effects threshold concentrations in the Canadian environment (water and soil) for most sectors of activity. However, one location or area of concern for aquatic organisms was identified for metal mining, with high RQs for that site (an ore milling facility) ranging from 9.7–13.4, and RQs of up to 0.78 and 0.86 were also calculated for two other sites within this sector including one combined mine and smelter site and one uranium mill. Based on these findings and other supporting information from Paliewicz et al (2015) regarding the high leachability of boron in slags from precious metal recovery, it is reasonable to assume that other facilities engaged in similar activities could release elevated concentrations of boric acid to the aquatic environment.
Considering all lines of evidence above, there is a risk of harm to organisms, but not to the broader integrity of the environment, from boric acid, its salts and its precursors. It is therefore proposed to conclude that boric acid, its salts and its precursors meet the criteria under paragraph 64(a) of CEPA as they are entering or may enter the environment in a quantity or concentration or under conditions that have or may have an immediate or long-term harmful effect on the environment or its biological diversity. However, it is proposed to conclude that boric acid, its salts and its precursors do not meet the criteria under paragraph 64(b) of CEPA as they are not entering the environment in a quantity or concentration or under conditions that constitute or may constitute a danger to the environment on which life depends.
8.4.3 Uncertainties in evaluation of ecological risk
Boric acid is a well-characterized substance in terms of its ecotoxicological properties. The CCME water quality guideline published in 2009 was found to appropriately represent the aquatic PNEC for boric acid, because a review of the literature concluded that no studies published since that time have presented evidence for higher toxicity. Some uncertainty was noted in the data for effects to sediment organisms. Experimental difficulties were noted in achieving and maintaining exposure concentrations within sediment, due to the tendency of boric acid to partition back into the water phase. Based on the NOEC values for spiked water tests being much larger than the aquatic PNEC, the aquatic PNEC was deemed to be protective of sediment organisms exposed to pore-water concentrations of boric acid. Because of the low partitioning of added boric acid to soil, the absence of soil-aging effects, and the low bioavailability of boron in natural soil, the added risk approach was used to derive a soil PNECadded. The added risk approach assumes that only the anthropogenic added fraction of boric acid contributes to risks, thereby ignoring the possible contribution of natural background concentration to toxic effects. Although the contribution of natural background concentration to toxic effects is anticipated to be low, conservative assumptions (e.g., no loss via run-off, leaching, or uptake by plants) were used when generating model soil PECadded as a precaution. A rich dataset of high-quality chronic soil-toxicity studies for 23 species, including many boreal species found in Canada, was employed to derive the soil PNECadded from a species sensitivity distribution. The dataset met species coverage requirements suggested by domestic (CCME) and international (MERAG) guidance. Uncertainty in the ecological effects data is expected to be low.
Due to widespread use across a majority of sectors, including incidental manufacture in many sectors, uncertainties were noted in the exposure component of the ecological risk assessment. Exposure scenarios were developed for the major sectors that either use boric acid precursors or that are implicated in their incidental manufacture. Major sectors were identified on the basis of quantity of substances used, or of high concentrations identified in available monitoring data, given that these variables were more likely to be directly correlated with releases to the environment. Although some uncertainty is introduced by this approach, PECs for the remaining uses were calculated using a very conservative generic scenario.
Import data from the CBSA were used to supplement findings from the DSL IU and voluntary stakeholder engagement, in order to characterize the sectors with the largest involvement with boric acid precursors by quantity. Importers were assigned to a sector by making assumptions about the importer’s primary activity based on publicly available information or by correlating with DSL IU submissions or voluntary stakeholder engagement. An additional uncertainty arises from the fact that the CBSA data are organized by HS codes, which in several cases describe groups of substances (e.g., metal borates). Thus, in some instances, an HS code-based import quantity could comprise unknown quantities of several different substances. To address this uncertainty, and because quantities required conversion to boron equivalents for comparison to the derived PNECs, a conservative assumption was made that all HS code-based import quantities would be treated as boric acid. Boric acid has the highest boron content (17.5%) among the major commercial boron-containing substances (e.g., borax pentahydrate, borax decahydrate), while the majority of other boric acid precursors are also below this value.
PEC calculations for sectors using boric acid precursors were performed under the assumption that users from different sectors were not releasing to the same wastewater treatment facility or surface water body. If the maximum modelled aquatic PEC values were added for multiple sectors, a resulting combined PEC could potentially exceed the aquatic PNEC. However, based on the CBSA data (which contains addresses), voluntary stakeholder engagement, and DSL IU results, it can be concluded that such “combined release” would be unlikely to result in ecological risk at present. Some uncertainty remains, with the potential for relocation of users or introduction of new users to result in combined releases. However, from a probabilistic standpoint, it appears a rare occurrence for multiple users to all be at the maximum of the exposure distribution for their sector at the same time and place. Additionally, the exposure calculations were conservative.
Aquatic concentrations of boron in the receiving environment (i.e. downstream from effluent discharge) were available for approximately 60% of metal mining sites. While this does not present a full picture of boron releases from the mining sector in Canada, the available data is recent and considered highly reliable. There is however uncertainty, and therefore potential concern, for sites similar to the site showing high risk and those with RQs approaching one.
One measured environmental concentration at one location for the oil sands extraction and processing sector was in excess of the aquatic PNEC. The value was reasonably assumed to represent statistical outliers, because 95th percentiles and/or median values were found to be well below the aquatic PNEC. This was only the case for this sector, and the outlier was deemed to carry insufficient weight to alter the ecological conclusion. However, environmental concentrations should continue to be measured and analyzed for this sector to ensure that high concentration values truly are, and remain, outliers.
Overall, uncertainty in the exposure characterization may be larger than the effects characterization for the ecological risk assessment. However, based on mitigation by a number of conservative assumptions, the impact on the conclusion is minimal.
9. Potential to Cause Harm to Human Health
9.1 Health effects assessment
Boric acid, it salts and its precursors are considered toxicologically equivalent. As such, dose levels between studies conducted with boric acid, its salts or its precursors were standardized to boron equivalents. Given that the health effects of boric acid have previously been reviewed by Health Canada’s PMRA (Health Canada 2012), the scope of this section is limited to a review of the human studies that were not included in the PMRA Re−evaluation of Boric Acid and its Salts, which focused on pesticidal applications.
Health Canada (2012) previously established a benchmark dose level (BMDL) of 2.90 mg B/kg bw/d, which was derived from two dog toxicity studies. This BMDL was based on testicular weight changes with histological indications of toxicity. Other assessments (WHO 2003, 2009; US EPA 2004; ATSDR 2010; EFSA 2013) are based on a no observed adverse effect level (NOAEL) of 9.6 mg B/kg bw/d that is based on developmental toxicity in a rat study (see Appendix H).
A number of boric acid precursors were classified by the European Union (European Commission 2008) as Category 1 reproductive toxicants. In addition, sodium perborate monohydrate and tetrahydrate were classified as causing "risk of serious damage to eyes," and sodium tetraborates were classified as eye irritants under European Commission guidelines 67/548/EEC (European Commission 2009).
Toxicokinetics of boric acid
Boric acid and borates were readily and near completely absorbed by humans and rats following oral ingestion, as indicated by the changes of boron levels in urine, blood and tissues. In human volunteers, over 90% of the administered dose was excreted in the urine over a 96-hour period after oral exposure (Schou et al. 1984; Jansen et al. 1984a). In rats, 95% and 4% of the administered dose was recovered from urine and feces, respectively, within 24 hours of exposure (Vanderpool et al. 1994). A 100% inhalation absorption rate as worst-case assumption was applied by ATSDR (2010) and Austria (2008a) for the risk assessment of boron compounds.
Borates have been demonstrated as being able to penetrate damaged or abraded skin (Draize and Kelley 1959; Nielsen 1970; Stüttgen et al. 1982; EU 2007a). Wester et al. (1998a) reported on the in vivo percutaneous absorption of boric acid precursors. Volunteers (eight per group) were dosed (non-occluded) with boric acid (5%), borax (5%) or disodium tetraborate decahydrate (10%) in aqueous solution. Both pre-treatment urine on days 1-4 and post−treatment urine up to day 17 were collected. On days 5 and 12, the test chemical was applied to the back area of individuals; the day 12 exposure was pre-treated with sodium lauryl sulphate to mimic potentially irritated skin. The chemical remained on the skin for 24 hours, at which point the remaining chemical was removed via skin washes. The dermal absorption rate was calculated based on comparing applied dose to detected boron levels in 24−hour urine samples that were collected daily for 17 days. Chemical losses to outside clothing and bedding were not corrected in the reported study results. The mean percentage absorbed (standard deviation) was reported to be 0.226% (± 0.125), 0.210% (± 0.194) and 0.122% (± 0.108) for boric acid, borax and disodium octaborate, respectively (Wester et al. 1998a). Based on the amount of test chemical recovered from the skin washes, the average corrected dermal absorption ranged from approximately 2-4% for the three groups and two doses studied.
In addition to in vivo absorption, Wester et al. (1998b) studied the in vitro percutaneous absorption of boric acid (0.05-5%), borax (5%) and disodium octaborate tetrahydrate (10%) through human skin. The study reported permeability coefficient (Kp) values ranging from 1.4×10-6-5.0×10-4 centimetres per hour (cm/h).
These studies have been considered by the European Commission Scientific Committee on Consumer Safety (SCCS 2010a, 2010b) and Health Canada (2012) to estimate dermal penetration or establish default dermal absorption values. The SCCS derived a dermal absorption of 0.5% based on Wester et al. (1998a), which is two standard deviations above the 0.226% absorption reported for boric acid. In Health Canada (2012a), due to limitations in the studies including a low mass balance recovery, a dermal absorption of 50% was used. In the current assessment, dermal absorption is estimated using a range of dermal absorption values, i.e., 0.5% at the low end and 10% at the high end, to account for the above-noted study limitations. In addition, the current assessment uses the highest reported Kp (5.0×10-4 cm/h) from Wester et al. (1998b) to estimate exposure in infinite-dose scenarios (e.g., swimming in pools). In the absence of adequate studies to quantify absorption across broken skin, absorption across broken or abraded skin was considered to be 100% in this assessment.
Absorbed boron is distributed rapidly and evenly throughout the body’s soft tissues, with slight accumulation in bone (2-3 times higher than soft tissue), as demonstrated in experimental rats and occupationally exposed workers (Culver et al. 1993, 1994; Jansen et al. 1984a, 1984b; Treinen and Chapin 1991; Ku et al. 1991). Studies indicate that boric acid has a strong affinity for cis-hydroxyl groups (this effect is reversible and concentration-dependent) (WHO 1998), which may explain the higher concentrations of boric acid in bone (EU 2007a).
Boric acid is not metabolized in animals or humans due to the high energy level required (523 kilojoules per mole [kJ/mol]) to break the boron-oxygen bond (Emsley 1989). Other inorganic borates convert to boric acid at physiological pH in the aqueous layer overlying the mucosal surfaces prior to absorption.
In humans, rats and rabbits, boron is mainly excreted in urine in an ionized form, regardless of the route of administration, with only 2-5% lost in feces (Jansen et al. 1984b; Usuda et al. 1998; Draize and Kelley 1959). Reabsorption of boron from kidney tubules may occur in humans at low doses (Murray and Schlekat 2004). The elimination half-life was estimated to be approximately one hour for mice and less than 12 hours for rats (Farr and Konikowski 1963; Ku et al. 1991, 1993a, 1993b). At the high dose level, the urinary boron clearance was slightly higher in pregnant than non-pregnant rats (US Borax 2000; Vaziri et al. 2001). The mean plasma half-life of boric acid was determined to be 13.4 hours (a range of 4.0-27.8 hours) in humans who were accidentally exposed to boric acid (Litovitz et al. 1988). Similarly, pregnant women clear boron more effectively than non-pregnant women (1.02 ± 0.55 vs 0.80 ± 0.31 mL/min/kg-bw, respectively), which is consistent with increased measures of renal function in humans during pregnancy (Pahl et al. 2001). There is evidence to suggest that boron is able to cross the placenta (Grella et al. 1976; Harari et al. 2012).
Acute toxicity, irritation and sensitization
Symptoms of acute oral toxicity found in humans typically include depression, ataxia, convulsions and death. Eye irritation and respiratory symptoms were significantly associated with workers exposed to boron dust (boric acid, borax or boron oxide) (Garabrant et al. 1984; Wegman et al. 1991, 1994; Cain et al. 2004, 2008).
Human epidemiological studies and case reports
Similar to the opinion issued by the Committee for Risk Assessment of the European Chemicals Agency (ECHA) (ECHA 2014), the current evaluation has determined that the available epidemiology studies are not of sufficient quality to select points of departure for risk assessment. The studies have shortcomings, including small sample size, limited consideration of confounders, and limited evaluation of health end-points. Indications of toxicity were noted in many animal studies, in the form of histopathological changes in the testes; similar investigations are not available with human subjects. Although the suite of human studies demonstrate less overt toxicity than animal studies, they were conducted at lower exposure levels and therefore do not reduce confidence in the animal database. Thus, the limitations in these studies preclude their use in the quantification of risk.
In several studies where boron has been administered to human volunteers, there have been suggestions of a beneficial effect on calcium retention, lean body mass and free testosterone levels (Naghii et al. 2011; Hasbahceci et al. 2013; Nielsen et al. 1987). However, in some studies, doses as low as 3 mg/d (assumed to be 43 µg/kg bw/d based on an assumed body weight of 70 kg) resulted in changes in blood pressure and the shape of the QRS complex (from electrocardiogram recordings) (Hunt et al. 1997). Other authors have reported an increase in menopause symptoms (hot flashes and night sweats) in women dosed with 2.5 mg boron per day (plasma boron concentrations were elevated to a mean of 0.053 µg/mL from the control concentration of 0.034 µg/mL). Changes in circulating oestradiol and white blood cell counts were also noted in this study (Nielsen and Penland 1999). The endocrine modulation effects of boron supplementation are of concern, and these endocrine effects have not been adequately investigated in animal experiments.
In worker studies, several authors reported an absence of toxicological effects from high boron exposures. However, some authors have identified a range of health outcomes, including abortions, delayed pregnancy and an alteration in male-to-female offspring sex ratio. Although the overall database is insufficient to identify points of departure for risk characterization, as noted below there are potential indications of adverse health outcomes from high boron exposures.
Reproductive history, including (primarily) infertility, parity of sex in offspring, birth defects, spontaneous abortions, prenatal mortality and developmental disabilities, were investigated by interview or questionnaire among workers in boron industries within the United States, Turkey and China (reviewed by Scialli et al. 2010). A survey by Whorton et al. (1994a, 1994b) conducted in 542 married, male boron workers from Boron, California showed that the live birth rates in the wives of boron workers were significantly higher than the U.S. Standardized Birth Ratio after adjusting confounders (529 vs. 466.6, p less than 0.01). However, an excess of female offspring numbers almost reached statistical significance in boron workers compared to that of the national standard (52.7% in workers vs. 48.8% of the national standard). As noted below, changes in offspring sex ratio represent the most common finding in human studies; however, it is of unknown toxicological significance.
In a study of female boron workers (Whorton et al. 1992, cited in US EPA IRIS 2004, no detail available), a reduced offspring delivery rate was recorded in 68 participants (34.5 expected, 32 delivered). Although the reduction was not significant, the United States Environmental Protection Agency (U.S. EPA) (US EPA 2004) claimed that this may indicate a deficiency in birth rate. Another study of 904 female workers in semiconductor industries, by Swan et al. (1995), showed that the risk of spontaneous abortion was increased among subgroups that experienced a low level of boron exposure at work compared with other workers without exposure. Several studies were conducted by Sayli and colleagues in boron-exposed populations in Turkey to investigate the correlation between boron exposure and impaired fertility in subpopulations living in regions with varied boron concentrations in the environment; there were no significant differences in primary infertility rates reported in residents living in different regions (2.34% in high-boron regions vs. 2.62% in low-boron regions) (Sayli 1998), but the sex ratio (male: female) at birth in the high-boron regions was reported to be lower than that of regions far away from the high boron area (0.995 vs. 1.37). The female-favoured sex ratio of offspring was also identified in a follow-up study by Sayli et al. (1998). As part of Sayli’s investigation, a survey conducted by Tüccar et al. (1998) did not reveal significant differences in spontaneous abortion rate or stillbirth rate among subgroups in high- or low-boron regions. Similarly, Sayli (2001, 2003), Sayli et al. (2003) and Cöl et al. (2000) did not identify a significant difference in infertility rate or reproductive history between boron workers and non−boron workers in Turkey. However, a similar survey conducted among wives of 945 boron workers and wives of 249 control workers from a boron plant in Liaoning, China (Liu et al. 2005a) revealed that the prevalence of spontaneous abortion (5.74% in workers vs. 3.30% in controls, p less than 0.05) and delayed pregnancy (5.07% vs. 3.07%, not significant) among the wives of boron workers were all higher than those of local control groups after adjusting for the potential confounders. The sex ratio at birth among workers was slightly lower than that of controls and the provincial and national ratios (1.09, 1.18, 1.12 and 1.16, respectively). In another study conducted at the same mining site in China, although not statistically significant, boron workers showed greater delay in pregnancy among wives of 936 boron workers compared to that of 251 controls (9.42% in workers and 4.62% in controls; Chang et al. 2006). The number of spontaneous miscarriages was found to be higher among boron workers (7.71% vs. 4.92%), whereas the sex ratio was lower in boron workers (52.45% male offspring among boron workers vs. 54.35% among controls). Daily boron exposure was estimated as 0.06-51.07 mg in boron workers and 0.005-0.016 mg in comparison groups in this study, based on occupational exposure limit via inhalation route. A slightly lower, but not statistically significant, sex ratio at birth was also reported in the offspring of men living in the area of Northern France where the boron drinking-water level was approximately 0.30 mg B/L compared to the men from a relatively low-boron area (Yazbeck et al. 2005).
Despite the general methodological limitations and the variation in considering the lifestyle, social and cultural influences in the epidemiological studies discussed above, the altered sex ratio at birth (female-favoured) was observed in several studies among high boron-exposure groups. Although the mechanism by which boron exposure may change the sex ratio has not yet been established, studies in humans and animals reviewed by Terrell et al. (2011) on several reproductive toxicants, including boron, have found an association between the reduction in the number of male births and chemical exposure.
The relationship between boron exposure and sperm parameters, such as sperm count, sperm motility and morphology, sperm DNA integrity and X- to Y-bearing sperm ratio, was investigated in various studies among boron workers in Russia, Turkey and China. The results of an early Russian study showed that reduced sperm count, sperm motility and elevated fructose content of seminal fluid were found in 6 of 28 male boron workers exposed to 22-80 mg/m3 of borax vapour and aerosol via inhalation for more than 10 years; however, the number of pregnancies among their wives was not affected (Tarasenko et al. 1972). Sperm quality and blood hormone levels were further inspected in 102 boron workers and 102 controls in Bandirma, Turkey by Duydu et al. (2011) and Basaran et al. (2012). There were no significant differences in blood hormone levels (FSH, LH or testosterone) or sperm parameters between the high- and low-blood boron groups (P > 0.05). In addition, the DNA integrity of sperm, as indicated by the tail intensity between the groups, was statistically not different (P > 0.05) for both alkaline and neutral COMET assays (Duydu et al. 2012). The highest daily boron exposure in air, water and food was estimated as a mean of 14.45 ± 6.57 mg/d (range 3.32-35.62) in boron workers. However, the daily boron intake derived from urine boron analysis in a similar study in Turkey was reported as 1.4 mg B/d and 6.5 mg B/d in control and exposure groups, respectively (Korkmaz et al. 2011). A sperm parameter study has also been conducted in northern Chile, in communities with high boron levels in drinking water. Espinoza-Navarro et al. (2010) found that the sperm mortality among 102 healthy young male residents was low, but only 38.3% of participants had sperm quality sufficient to meet criteria established by the World Health Organization (WHO) (1999).
A study conducted in Liaoning, China by Liu et al (2005b) found that the sperm viability, motility, path velocity and progressive velocity in 60 boron workers were significantly lower than that of nine controls, even after confounder adjustment. The mean daily intake of boron (diet, water ± air dust) was estimated as 19.79 mg/d (equivalent to 0.28 mg B/kg bw/d) in boron workers and 1.53 mg/d in controls. However, similar health effects were not identified in extended cohorts in later studies by the same author (Liu et al. 2006a, 2006b). The reproductive history and sperm quality in a cohort in the same area in China were later investigated again by Robbins et al. (2010) and Robbins (2008). The only effect noted was a lower ratio of Y- to X-bearing sperm in boron workers compared to men not working in the boron industry. However, the correlations between the biological boron measures and the Y:X-bearing sperm ratios within groups were not statistically significant (Robbins et al. 2010). The total daily boron exposure was estimated as (mean ± SD) 41.2 ± 37.4, 4.3 ± 3.1 and 2.3 ± 3.0 mg in boron workers, community controls and remote area controls, respectively (Robbins et al. 2008). The highest estimated boron daily intake derived from these studies was 41.2 mg/d (equivalent to 0.6 mg B/kg bw/d).
Boron exposure via inhalation in humans is mainly limited to the occupational setting. A cross-sectional study of respiratory effects was performed by Ury (1966) in male workers at the borax plant in California, and the result showed that, among the 629 men who experienced over a year of work-related exposure to sodium borate dehydrate dust, 82 showed some evidence of respiratory effects. Occupational exposure to boron oxide and/or boric acid via inhalation also induced eye irritation, dryness of mouth, nose or throat, sore throat, and productive cough.
Essentiality in humans
The body of evidence has yet to establish a clear biological function for boron in humans (IOM 2001). The use of boron as a dietary supplement has not been endorsed by the U.S. Food and Nutrition Board/Institute of Medicine (ATSDR 2010); the European Food Safety Authority concluded that the cause and effect relationships have not been established between the consumption of boron and the maintenance of normal bone or joints, maintenance of normal thyroid function, or contribution to normal cognitive function (EFSA 2011a, 2011b); and boron has not been established to be an essential nutrient for humans, nor has a biochemical function for boron been identified in most animal species studied or in humans (EFSA 2004).
Early case reports have shown death in newborns within five days of ingesting less than 3 g of boric acid (Young 1949, cited in Health Canada 2012). Boron-induced convulsions and seizures have been associated with infants accidentally exposed to honey-borax mixture in their diet at 429-1287 mg/d for 4-10 weeks or at 125 mg borax for over three months (O’Sullivan and Taylor 1983; Gordon et al. 1973). Repeated dermal application of baby powder containing boric acid induced cutaneous lesions, seizures and gastrointestinal disturbances in infant poisoning cases (Goldbloom and Goldbloom 1953). Dermatitis, alopecia and indigestion were observed in patients receiving 5 mg B/kg bw/d or more (route not clear) when boron was used for the chronic treatment (over two years) of epilepsy. When the dose was reduced to 2.5 mg B/kg bw/d, the toxic signs and symptoms disappeared (Culver and Hubbard 1996).
9.2 Exposure assessment
Given that boric acid is a naturally occurring substance and is ubiquitous in environmental media, it is present in food, drinking water, air, soil and dust. Boric acid is also a common ingredient in a wide range of products used by Canadians. All of these sources contribute to total daily exposure. As noted previously, measurements of boric acid in environmental media, products and humans in this assessment are expressed in terms of total boron, and exposure estimates are expressed as mass of boron per mass of body weight (bw).
Environmental media, food and drinking water
Boron concentrations in ambient air are less commonly measured than other inorganic elements. In Canada, Health Canada has conducted studies that reported concentrations of total boron present in PM collected in indoor, outdoor and personal air samples. Specifically, boron air concentrations are available for Windsor, Ontario; Halifax, Nova Scotia; and Calgary and Edmonton, Alberta. Median concentrations of boron measured in indoor and outdoor fine PM samples (PM1) collected in residential areas of Edmonton, Calgary and Halifax were less than 5 nanograms per cubic metre (ng/m3 ) (n=262) (Health Canada 2013a, 2013b, 2013c). The median and 95th percentile concentrations of boron in coarse PM samples (PM10) measured in Windsor in 2005 and 2006 were 5.3 and 17.6 ng/m3 in personal samples, 5.3 and 21.0 ng/m3in indoor samples, and 12.1 and 34.3 ng/m3 in outdoor samples, respectively (Rasmussen et al. 2013). Overall, boron concentrations measured in PM in residential areas are low-in the ng/m3 range.
Soil and dust
There are over 200 minerals containing boron oxide, with the four most important boron-containing minerals being borax, kernite, colemite and ulexite (USGS 2013). The highest concentrations of boron are found in sediments and sedimentary rock, particularly clay-rich marine sediments (Moss and Nagpal 2003). Boron is naturally released to soil by rainfall, weathering of boron-containing minerals, desorption from clays, and decomposition of boron-containing organic matter (ATSDR 2010). Most boron compounds are transformed to borates in soil due to the presence of moisture; borates themselves are not further degraded in soil (ATSDR 2010). Boron is an essential nutrient for plant growth, and boron is taken up by plants as boric acid (Penny 2004). Boron retention in soil depends on boron concentration in the soil solution, soil pH, texture, organic matter, cation exchange capacity, type of clay, and mineral coating on the clay. Anthropogenic sources of boron to soil include the application of boron-containing fertilizers; application of fly ash, wastewater or biosolids as a soil amendment; the use of wastewater for irrigation; and land disposal of boron-containing industrial wastes (ATSDR 2010). There are limited data characterizing the concentration of boron in soil in Canada. Reported total boron soil concentrations from residential, agricultural and industrial areas range from 1-90 mg/kg (BC MOE 2005; Agriculture and Agri-Food Canada 2013; Government of New Brunswick 2005; Penny 2004; Jacques Whitford AXYS 2008). Average boron soil concentration in the United States is 33 mg/kg, ranging from less than 20-300 mg/kg (USGS 1984). These data are discussed in more detail in Section 22.214.171.124.
Nationally representative bioaccessible boron concentrations from Canadian homes were available from the Canadian House Dust Study (Rasmussen et al. 2013). This study reported bioaccessible boron concentrations (measured in simulated stomach fluids) ranging from 7-2091 mg/kg with a median concentration of 65.3 mg/kg (n=1025) (Rasmussen et al. 2013). Sources of boron in household dust include the use of boric acid in building materials (e.g., wood, cellulose insulation), products that contain boron substances (e.g., cleaning products, pesticides), and tracked-in soil.
Food and drinking water
The most common source of daily exposure for Canadians is ingestion of boron from food. Boron is an microessential nutrient for plant growth, meaning boron enters the food chain through plants. According to research, within the intestinal tract, most ingested boron is believed to convert to boric acid, the normal end product of hydrolysis of most boron compounds, and is available for absorption (Hunt et al. 1997, 2004; Hunt 2006). The natural boron content of foods varies considerably depending on various factors, including the concentration of boron in the underlying soil, the soil properties, and the requirements of the plant. Little is known about the speciation or bioavailability of boron in natural foodstuffs (Hunt et al. 2004). Anthropogenic inputs of boron into the food chain include intentional inputs from the use of boron-containing fertilizers and unintentional inputs from food packaging (in adhesives, paper and paperboard). Industrial point sources (e.g., leaching) and agricultural run-off can also be a source of boron in the food chain.
Total boron was measured in over 30 000 food samples collected as part of various monitoring programs conducted by the Canadian Food Inspection Agency (CFIA), including the National Chemical Residue Monitoring Program (2008-2009 and 2009-2010), the Children’s Food Project (2008-2009 and 2010-2011) and the Food Safety Action Plan (2009-2013) (as described in CFIA 2014). The highest average total boron concentrations in foods, as purchased, were in baking ingredients at 25 µg/g, nut butters at 16 µg/g, herbs and spices at 14 µg/g, beverages at 12 µg/g, seed butters (sunflower and tahini) at 10 µg/g, and vegetable proteins at 10 µg/g. Fruits and vegetables had average concentrations of 3 and 4 µg/g, respectively, while grains, dairy and meat all had lower average concentrations of 1.5, 0.2 and 0.06 µg/g, respectively (CFIA 2014). Boron is present in breast milk; an average concentration of 30 µg/L total boron was measured in breast milk from 10 mothers in Newfoundland (Hunt et al. 2004).
In Canada, total boron is commonly measured at water treatment facilities and in distribution systems for drinking water. Total boron concentration data were available from Newfoundland and Labrador, New Brunswick, Quebec, Ontario, Manitoba, Saskatchewan and the Yukon Territory (2013 email from the Water and Air Quality Bureau, Health Canada, to the Existing Substances Risk Assessment Bureau, Health Canada; unreferenced). Typical concentrations of total boron ranged from less than 5 to 150 µg/L. In over 30 000 samples reported, there were 2 exceedances of the Health Canada drinking water guideline of 5000 µg/L. Concentrations of total boron in well water may be higher and more variable than in surface waters, due to natural leaching from rocks (Health Canada 1990). Boron concentrations in groundwater (and hence well water) are typically higher in regions composed of sedimentary rocks (these conditions are present in the Prairie provinces).
Probabilistic dietary intake estimates for the general population were derived by Health Canada’s Food Directorate, using concentrations of total boron in food commodities collected from 2009-2013 and from provincial drinking water data. Consumption estimates were based on data from the Canadian Community Health Survey, Cycle 2.2 on Nutrition (Statistics Canada 2004), including intake of drinking water. When possible, the CFIA imported and domestic mean boron concentration values were combined. In the case of drinking water, log-normal distributions were fitted to the water concentration data for each of the provinces, and boron concentration values were randomly generated from log-normal distributions with the parameter estimates for the corresponding province (NL, NB, QC, ON, MB, SK, YT).
Median dietary intakes (food and drinking water) ranged from 20.4-91.7 µg B/kg bw/d, and 95th percentile intakes ranged from 41.5-182.6 µg B/kg bw/d (Table 9-1). The highest dietary intakes occurred in children aged 1-3, while the lowest dietary intakes occurred in males aged 71 and older. Fruits (e.g., apples), fruit juice and vegetables (e.g., carrots, tomatoes) were the primary contributors to dietary intake, accounting for 41-62% of dietary intake depending on the age group. Drinking water (tap and bottled) accounted for 3-16% of dietary intake. Intake for breastfed infants (aged less than 6 months) is estimated to be 3.0 µg B/kg bw/d. Although the concentration of boron in some other food categories was higher (e.g., for baking ingredients and nut butters), the consumption levels for fruits and vegetables render them the highest contributor to dietary exposure.
These estimated dietary intakes in Canadians are similar to earlier estimates generated by Clarke and Gibson (1988) based on the analysis of boron in 1-day diet composites in 22 premenopausal women. The estimates are similar to, but slightly higher than, estimated dietary intakes in the United States based on the Continuing Survey of Food Intakes by Individuals, 1994-1996 (Rainey et al. 2002; IOM 2001), and intakes in the United Kingdom based on the 1994 UK Total Diet Study (Ysart et al. 1999). Fruits, beverages, vegetables and grains were the primary contributors to boron intake in the United States (Rainey et al. 2002).
|Sex/Age group||Median µg/kg bw/d|
(95% CIFootnote Table 9-1a)
|95th percentile µg/kg bw/d|
|M/F: 6 mo. -1 yr.||50.9 (44.6, 63.0)||82.6 (68.7, 119.5)|
|M/F: 1-3 yrs.||91.7 (89.0, 94.8)||182.6 (173.3, 198.3)|
|M/F: 4-8 yrs.||63.6 (62.3, 65.2)||121.7 (116.2, 129.2)|
|M: 9-13 yrs.||37.8 (36.7, 39.1)||77.2 (72.9, 87.4)|
|F: 9-13 yrs.||36.2 (35.0, 37.5)||70.5 (65.9, 80.5)|
|M: 14-18 yrs.||26.2 (25.4, 27.1)||53.2 (49.8, 59.1)|
|F: 14-18 yrs.||25.4 (24.6, 26.2)||52.0 (48.5, 58.0)|
|M: 19-30 yrs.||23.0 (22.1, 24.2)||45.0 (41.2, 53.5)|
|F: 19-30 yrs.||24.7 (23.8, 25.9)||48.6 (44.7, 54.6)|
|M: 31-50 yrs.||20.8 (20.0, 21.7)||43.3 (39.6, 51.1)|
|F: 31-50 yrs.||23.4 (22.6, 24.3)||51.2 (48.0, 59.7)|
|M: 51-70 yrs.||21.1 (20.5, 21.8)||43.7 (40.9, 49.0)|
|F: 51-70 yrs.||23.2 (22.5, 23.8)||47.4 (44.4, 52.8)|
|M: 71+ yrs.||20.4 (19.7, 21.4)||41.5 (38.8, 50.2)|
|F: 71+ yrs.||22.1 (21.4, 23.0)||45.1 (42.4, 52.4)|
Intake estimates from environmental media, food and drinking water
Average intake estimates from environmental media, food and drinking water were derived for the general Canadian population, based on concentrations of total boron measured in food, drinking water, air, soil and dust (presented in Appendix D). Based on these estimates, average daily intake of boron for the general public ranges from 3-92 µg B/kg bw/d, and, of these, naturally occurring boron in fruit, vegetables and to a lesser extent, drinking water is the primary source of total daily intake for the general public. Fruits and vegetables account for approximately 40-60% of dietary intake, while drinking water accounts for 3-16%. Air, soil and dust are negligible sources.
Based on a search of material safety data sheets (MSDSs), the U.S. Household Products Database, the GoodGuide, notifications under the Cosmetic Regulations, the Licenced Natural Health Products Database, and concentration data of boron in arts and crafts and toys, boric acid is found in thousands of products available to Canadians. Several targeted studies demonstrate an increase in blood boron concentrations following the use of products containing boric acid or precursors of boric acid (Wallace et al. 2002; Nielsen and Penland 1999; Hunt et al. 1997; Green and Ferrando 1994; Edwall et al. 1979).
The presense of boric acid in some products, including adhesives and sealants, arts and crafts materials, cleaning products, cosmetics, fertilizers, NHPs, paints and coatings, swimming pool and spa products, science education kits, textiles and toys (HPD 1993-; GoodGuide 2014; 2012 email from Consumer Product Safety Directorate, Health Canada to Existing Substances Risk Assessment Bureau, Health Canada [unreferenced]; 2013 email from Risk Management Bureau, Health Canada to Existing Substances Risk Assessment Bureau, Health Canada [unreferenced]; 2013 email from Food Directorate to Risk Management Bureau, Health Canada [unreferenced]; KEMI 2014), can result in direct exposure to Canadians during use. Other uses, including boron as a flame retardant in building materials, cellulose and fiberglass insulation, cotton mattresses, engineered wood and gypsum board (RPA 2008; Ball et al. 2012), are more likely to result in indirect exposure to the general public, via household dust and indoor air as a result of use or presence of products in the home. Other uses, such as boron in glass and ceramics (CEH 2011), are considered to result in negligible exposure to boric acid.
Thousands of products on the market contain boric acid, and, therefore, for the purposes of this screening assessment, direct exposure to boric acid was quantified for five product categories that were considered to have a significant contribution to exposure and/or were frequently used. These categories include arts and crafts materials and toys, cleaning products, cosmetics, NHPs, and swimming pool and spa products. For each category, sentinel products were selected to characterize exposure potential for the general public; sentinel product intake estimates, by category, are presented in the following subsection.
Arts and crafts materials and toys
Boric acid can be a component of many arts and crafts materials. The U.S. Art and Crafting Materials Institute (ACMI) measured soluble boron (using ASTM standard D5517) in marker inks (range 8.3-1400 ppm), technical drawing inks (1400 ppm), ceramic glazes (67-40 000 ppm), pencils (27-650 ppm), coloured sand (525 ppm), paints and enamels including acrylic, gouache, watercolour, water colours and oils (13-8300 ppm), colours and pigments including encaustic and acrylic (1600-17 400 ppm), and glue (380-1800 ppm) (Stopford 2013). Many of these products, such as marker inks, ceramic glazes, pencils and glue, are marketed to children or to teachers for use by children.
Boric acid can also be a component of some commercially-made toys. Soluble boron has been quantified in plastic putty, modelling clay and modelling dough by the ACMI, ranging from 225-1300 ppm (Stopford 2013). In Canada, boric acid and salts of boric acid are specifically prohibited in toys under section 22 of the Toys Regulations of the Canada Consumer Product Safety Act (Canada 2010, 2011). Health Canada conducts periodic sampling and testing to verify compliance with its regulations, by targeting products that may be more likely to not meet health and safety requirements due to characteristics that are observed. Health Canada compliance testing conducted from 2002-2009 found measurable boric acid in play dough, glue and paint samples. In 2002, 85% of the clay, modelling dough, putty and glue samples analyzed had detectable boric acid concentrations, ranging from less than 4 ppm-49 000 ppm (Health Canada 2002). Boric acid was also detected in science kits. In 2004 and 2009, boric acid was detected in clay and plasticine at concentrations of 27-40 300 ppm (Health Canada 2004, 2009b, 2009c). For commercially available children’s toys, compliance and enforcement of the existing prohibition on boron will continue as a part of the regular enforcement of the Toys Regulations under the Canada Consumer Product Safety Act.
Borax is a precursor of boric acid and is a common ingredient in make-your-own crafts and toys, including crystal formations, slime and play dough (The Dial Corporation 2014). Online sources provide recipes and ideas for making these crafts at home, school, birthday parties or science fairs (American Chemical Society 2014; PBS 2014; About Education 2014; Government of Canada 2014). Borax is available to consumers in grocery and hardware stores in Canada. When making crafts or toys, powdered borax is typically mixed in a bowl by hand with glue or water.
To evaluate potential exposure to adults and children using arts and craft materials and playing with toys containing boric acid, a sentinel scenario was generated. Exposure during children’s use of homemade modelling clay was selected as a potentially high-exposure scenario. When playing with modelling clays or slimes, there is potential for oral and dermal exposure from the ingestion of small quantities of the material, via incidental hand-to-mouth activities or intentional consumption. Dermal intake estimates for a child playing with 350 g of homemade modelling clay ranged from 69-1381 µg/kg bw/event. Oral intake for a child from ingestion of 100 mg-5 g of modelling clay was 56-2819 µg/kg bw/event. Estimated intakes of boric acid from the use of arts, crafts and toys are presented in Appendix E.
Boric acid may be found in a variety of cleaning products. Based on a search of MSDSs, the U.S. Household Products Database and GoodGuide, boric acid was found in over 200 cleaning products and borax was found as an ingredient in 244 household cleaning products, including air fresheners, all-purpose cleaners, bleach products, fabric treatments, glass and surface cleaners, household chemicals, household cleaners, kitchen cleaners, laundry products, laundry detergents and stain removers (HPD 1993-; GoodGuide 2014). The cleaning products generally fall into five main categories: all-purpose cleaners; dishwashing detergents; floor, carpet and furniture cleaning products; laundry detergents; and toilet bowl cleaners. Some products, such as some laundry detergents, are marketed as baby products. Overall, the concentration of boron found in products was highly variable, ranging from 0.01-11% (this includes products containing 100% borax). The products occur in a variety of formulation types, including powders, solid tablets, pastes, putties, liquids and aerosols, and are either ready-to-use or require dilution in water.
Exposures can occur during mixing, loading or applying of cleaning products. Application methods can vary depending on the formulation type and the use pattern, and therefore a single product can have a wide variety of potential exposure scenarios. For example, powdered borax can be applied directly to hard surfaces as an abrasive cleaner, diluted in water to clean hard surfaces (such as floors, countertops, furniture), diluted in water to steam-clean carpets, added as a powder to automatic dishwashers or washing machines, or added to water for hand-washing of laundry or dishes. There is also potential for post-application exposure to residues following the use of cleaning products, including exposure to residues on dishes, clothing, floors and furniture. Given the variation in types of cleaning products, concentrations of boron, formulation types and application methods, there are numerous potential exposure scenarios.
To evaluate potential exposure to people from the use of cleaning products, several sentinel scenarios were developed: ready-to-use spray cleaner, dishwashing detergent, floor cleaners, and hand-washing laundry with detergent. These products and scenarios were considered to represent high-exposure scenarios or have the potential for frequent use. Application of a ready-to-use general purpose cleaner (0.7% boron) on hard surfaces results in dermal exposure estimates ranging from 10-199 µg B/kg bw/d. Hand-washing dishes with a product containing 0.14% boron results in dermal exposure estimates from 4-86 µg B/kg bw/d; loading automatic dishwashers would result in lower exposure for the user. Hand-washing a floor with a ready-to-use floor cleaning product containing 1.75% boron could result in dermal estimates ranging from 27-542 µg B/kg bw/d and post-application dermal exposure to a toddler crawling on the floor of 8-160 µg B/kg bw/d and another 120 µg B/kg bw/d from oral hand-to-mouth exposure. Loading powdered laundry products containing 11.4% boron was estimated to result in 0.02 µg B/kg bw/d via the inhalation route of exposure. Estimated intakes of boric acid from the use of cleaning products are presented in Appendix E.
Some cleaning products are formulated as tablets (e.g., laundry and dishwashing detergents), which mitigates exposure to the user during loading and application. However, these types of formulations present a reasonably foreseeable accidental exposure to boric acid for young children through mouthing or ingestion.
Boric acidFootnote 4 is an ingredient in approximately 1100 cosmetics notified to Health Canada under the Cosmetic Regulations (2015, email from the Consumer Product Safety Directorate, Health Canada, to the Existing Substances Risk Assessment Bureau, Health Canada; unreferenced). Boric acid is an ingredient in anti-wrinkle preparations, baby products, barrier creams, bath preparations, body make-up, deodorant, douches, eye lotions, eye make-up, face make-up, fragrances, genital lubricants, hair bleaches, hair conditioners, hair dyes, hair grooming products, hair shampoo, hair straighteners, hair waving preparations, massage oils, mouthwash, shaving preparation, skin cleansers, skin moisturizers, and tanning preparations. Of all cosmetic product types, boric acid is most commonly found in skin moisturizers and skin cleansers.
Borax was identified as an ingredient in approximately 400 cosmetics in the GoodGuide, which is a resource for information on consumer products in the United States (GoodGuide 2014).
To evaluate potential exposure to users of cosmetics, daily intake estimates were generated for products with the potential for dermal, oral and mucosal exposure. Body creams, body soaps and diaper creams were selected as sentinel products to represent potential intake of boric acid from the use of dermally applied cosmetics. Mouthwash, lipstick and genital lubricants were selected to represent orally and mucosally applied cosmetics. These products were selected as sentinels as they are considered to result in high exposure relative to other cosmetics and have the potential for daily or frequent exposure. In the 1950s, cases of infant poisoning were reported from the use of products containing boric acid used to treat damaged skin from diaper rash (MacGillivray and Fraser 1953; Fisher et al. 1958). These reports demonstrate the potential for systemic exposure to boric acid following use on abraded skin. The GoodGuide identifies borax (a precursor to boric acid) as an ingredient in 15 baby care products sold in the United States, including diaper creams, and therefore diaper creams were evaluated as a sentinel product given that they may be used on broken or abraded skin.
Daily intake estimates were generated using the maximum permissible concentrations (this value reflects the maximum concentration of 5% boric acid, equivalent to 0.87% boron, outlined in the Hotlist restriction) and frequency of use per day data. When relevant, dermal absorption estimates of 0.5 and 10% were incorporated for non-abraded skin, whereas absorption across broken or abraded skin and mucosal membranes was considered to be 100%. Although the Hotlist entry for boric acid describes a maximum limit of 5%, there are cosmetic products available to Canadians (such as powdered hand soaps) that contain 60-100% borax, equivalent to up to 65% boric acid (The Dial Corporation 2013; GoodGuide 2014; HPD 1993). It should be noted that current market data indicates that concentrations of boric acid in diaper creams, and other cosmetic baby products, sold in Canada are much lower than the level of 5% (i.e., less than 0.1%) (2015 email from the Consumer Product Safety Directorate, Health Canada, to the Risk Management Bureau, Safe Environments Directorate, Health Canada; unreferenced).
Intake estimates for body lotions, skin cleansers and diaper creams are estimated to range from 0.03-1399 µg B/kg bw/d. Intake estimates for mouthwash, lipstick and genital lubricants range from 2-740 µg B/kg bw/d. Estimated intakes of boric acid from the use of cosmetics are presented in Appendix E.
Natural health products
BoronFootnote 5 is present in over 700 licensed NHPs in Canada, both as a medicinal and non-medicinal ingredient (LNHPD 2014). Most commonly, boron is used as a medicinal ingredient in multi-vitamin/mineral supplements (intended for adult use up to a maximum daily dose of 700 µg B/d), and to a lesser extent in multiple-ingredient joint health products (up to a maximum of 3360 µg B/d [Health Canada 2007a, 2007b, 2014b]). Boron is present in a smaller number of licenced products for oral (in addition to the ones mentioned above), dermal, ophthalmic and vaginal use, including homeopathic medicines, oral antiseptic rinses, toothpaste, ointments and skin lotions, sunscreens, yeast infections, eye drops and eye washes (LNHPD 2014).
To evaluate potential exposure to users of NHPs, daily intake estimates were generated for users of multi-vitamin/mineral supplements and multiple-ingredient joint health products, which were selected as sentinel products because they result in high exposure and are used daily. Numerous studies document an increase in boron blood concentrations following the use of oral supplements containing boron (Wallace et al. 2002; Hunt et al. 1997; Nielsen and Penland 1999).
Intake estimates for adults consuming multi-vitamin/mineral supplements and multiple-ingredient joint health products, based on the maximum permitted concentrations, are 10 and 47 µg B/kg bw/d, respectively. Estimated intakes of boric acid from the use of NHPs are presented in Appendix E.
Swimming pool and spa products
Swimming pool and spa products may contain boric acid. As pesticides, algaecide and sanitizer pool products containing boron, present as a formulant, are regulated under the Pest Control Products Act (Canada 2002). However, other swimming pool and spa products which are not pesticides, including performance products and water conditioners available to Canadians, may contain boron. Target concentrations of 30-50 ppm B are frequently recommended to make water feel soft, improve water clarity and make water easier to maintain (Nisus Corporation 2010; Haviland Consumer Products, Inc. 2007). To evaluate potential exposure to people swimming in pools or using spas containing boron, total intake estimates (combined oral and dermal) were derived for all age groups (infants through to adults) swimming in pools. Estimates were based on algorithms from the U.S. EPA (2003) SWIMODEL using a maximum dermal Kp of 5.0 × 10-4 cm/h (Wester et al. 1998b) and the recommended concentration of boron in pool water of 50 ppm. Combined (oral and dermal) exposure estimates from swimming ranged from 36-518 µg B/kg bw/event (Appendix E). Oral intake accounted for the majority of intake.
Boron has been measured in a wide variety of human tissues, including whole blood, serum, plasma, red blood cells, platelets, urine, breast milk, hair, nails, semen, placenta, and cord blood. Studies examining worker exposure to boron have demonstrated that serum, whole blood, urine and semen are all good biomarkers of boron exposure and are all highly correlated with total daily boron intake (Xing et al. 2008; Robbins et al. 2010; Duydu et al. 2011). In a study conducted in Turkey, whole blood boron concentrations were considered much more reliable indicators of boron exposure (and were used to reclassify exposed and unexposed participants) than the initial classification based on estimates of intake from environmental media (Duydu et al. 2011). Blood boron (serum, plasma, whole blood) concentrations have been used as an indicator of boron status and excessive boron intake in numerous supplementation studies, and blood is considered a relatively reliable biomarker of exposure related to potential health effects (Nielsen 2009). Whole blood boron concentrations are slightly higher than serum because low concentrations of boron are found in red blood cells and platelets. Based on these reasons, blood boron concentrations were evaluated as a method of quantifying boron exposure in the Canadian population. Blood boron concentrations in humans are presented in Appendix F.
Although boron has not been included in large-scale biomonitoring initiatives such as the Canadian Health Measures Survey or National Health and Nutrition Examination Survey, blood boron concentrations have been measured in several smaller population studies, studies on trace-element analysis, supplementation studies, and occupational exposure studies. The most comprehensive dataset on blood boron concentrations in Canadians originates from the Alberta biomonitoring program. Blood boron was measured in pooled serum samples from over 50 599 pregnant women and 1373 children (Alberta Health and Wellness 2008; Government of Alberta 2010). Serum samples were pooled into 158 pools stratified by age, geographical location, and season. Average blood boron concentrations ranged from 13-34 µg/L in pregnant women and 29-33 µg/L in children (Alberta Health and Wellness 2008; Government of Alberta 2010). Blood samples from different subjects were pooled prior to laboratory analysis, and therefore the variability between individuals was lost. These pooled data provide reliable estimates of average population-level exposure in pregnant women and children, but do not provide information on the overall distributions of exposure, most importantly the upper end of the exposure distribution. The only other blood boron concentration data in Canadians originate from studies conducted by Clarke and colleagues (1987a, 1987b, 2004), in which average concentrations in 12 individuals were measured at 30.8 ± 5.6 µg/L with a range of 15.3-79.5 µg/L. Other population-level studies conducted in the United States and Europe reported average blood boron concentrations similar to those found in the Alberta data and Clarke et al. (1987a), ranging from 11-56.7 µg/L, with the exception of France where the average blood boron concentration in a study of 180 males was much higher at 126 µg/L (Ferrando et al. 1993; Pahl et al. 2001; Abou-Shakra et al. 1989; Rodushkin et al. 1999; Vanhoe et al. 1993; Heitland and Köster 2006; Yazbeck et al. 2005; Goulle et al. 2005; Hasbachecei et al. 2013). Maximum values of 170.4 and 195 µg/L, respectively, were reported from studies in the United Kingdom (n=50) and northern Germany (n=130) (Abou-Shakra et al. 1989; Heitland and Köster 2006). Given that there are limited data on the upper tails of the exposure distribution (e.g., maximum, 95th percentiles) in Canadians, the maximum data from the United Kingdom and Germany (170.4 and 195 µg/L) and the average concentration from France (126 µg/L) will be considered as surrogate data to represent the upper tail of the exposure distribution for Canadians.
Age and sex trends have been observed in the overall dataset. In a study of mother-infant pairs in northern Argentina and Chile, boron was found to transfer from the mother to the developing fetus via the placenta, and later via breast milk (transfer was greater via the placenta) (Harari et al. 2012). In Alberta, average blood boron concentrations were significantly higher in children under age 13 than in pregnant women. There are no blood concentration data for children under age 2, so it is unknown if blood concentrations would be higher or lower in this age group. In adults, an increase in blood boron concentrations with age was observed in studies conducted in Alberta, Turkey and Japan (Alberta Health and Wellness 2008; Hasbachecei et al. 2013; Usuda et al. 1997). In the same Japanese study, blood boron concentrations increased in adult males from 20 to 49 years, followed by a plateau, followed by a second increase at age 70; in females there was a continuous steady rise in blood boron concentrations from age 20 onward; and, overall, blood boron concentrations were significantly higher in males than females.
Boron concentrations vary in different biological media. For example, boron was found at much higher concentrations in semen than blood in a series of worker exposure studies in China (Robbins et al. 2010; Scialli et al. 2010; Xing et al. 2008).
Blood boron concentrations can also vary by geographical location, which in some cases can be explained by variations in the boron concentrations in environmental media and in diet. Blood boron concentrations are markedly higher in populations living in northern Argentina and Chile than other parts of the world, with averages ranging from 22-901 µg/L, resulting from high boron content in the soil and drinking water (Barr et al. 1993, 1996; Harari et al. 2012). Blood boron concentrations as high as 2000 µg/L have been reported in Chileans in this region (Barr et al. 1996). Elevated blood boron concentrations in a Japanese population, with a geometric means of 79.8 and 67.9 µg/L for males and females, respectively, were attributed to differences in dietary intake-including the consumption of green tea, which has a high boron content (Usuda et al. 1997). In Canada, blood boron concentrations were higher in women from southern Alberta than central and northern Alberta (Alberta Health and Wellness 2008); the reasons for this are unknown.
Several targeted studies demonstrate an increase in blood boron concentrations following the use of products containing boric acid or precursors to boric acid (Wallace et al. 2002; Nielsen and Penland 1999; Hunt et al. 1997; Green and Ferrando 1994; Edwall et al. 1979). For example, supplement use can result in significant increases in blood boron concentrations. Multiple studies conducted in the general population, peri- and post-menopausal women, and weightlifters examined blood boron concentrations before and after supplement use. In one study, baseline blood concentrations averaging 14 µg/L peaked at 136 µg/L 4 hours after ingestion of an 11.6 mg boron dose. At 6 hours, blood concentrations were still elevated at 124 µg/L (Wallace et al. 2002). Three other studies found 1.5-1.7-fold increases in plasma boron concentrations following 2.5 and 3 mg doses from supplements (Hunt et al. 1997; Nielsen and Penland 1999; Green and Ferrando 1994). The use of other products containing boron can also result in elevated blood boron concentrations. In one study, blood boron increased four-fold following use of a mouthwash and remained elevated over the baseline for 24 hours after use (Edwall et al. 1979). In addition, there was a low rate of accumulation of blood boron following repeated use of the mouthwash over a one-week period.
Blood boron concentration data are available to characterize exposure to Canadians from studies conducted in Canada, the United States and Europe. Total boron measured in blood in individuals provides a measure of integrated exposure for individuals, from all routes (oral, dermal and inhalation) and all sources (including environmental media, diet, and frequent or daily use products to which they were exposed). Males have higher concentrations of boron in blood than females. For adults, there is a steady increase in the concentration of boron in blood with age; despite this trend in adults, blood boron concentrations are higher overall in children.
The Alberta Biomonitoring Program (Alberta Health and Wellness 2008; Government of Alberta 2010) provides average estimates of exposure from over 50 000 pregnant women and over 1000 children, both of which are populations of concern for the identified health effects of boric acid. Average blood boron concentrations from the Alberta biomonitoring studies (34 µg/L) are considered adequate to represent average concentrations in Canadians and are representative of exposures in children and adults (Alberta Health and Wellness 2008; Government of Alberta 2010). Given that there are no adequate Canadian data to characterize upper-percentile blood boron concentrations, the maximum values from the United Kingdom and Germany (170.4 and 195 µg/L, respectively) as well as the average concentration from France (126 µg/L) support the use of 195 µg/L to represent the upper tail (e.g., 95thpercentile) of the exposure distribution for the general Canadian public (Yazbeck et al. 2005; Abou-Shakra et al. 1989; Heitland and Köster 2006). Biomonitoring data are often considered the "gold standard" in exposure assessment, and, in this case, sufficient high-quality biomonitoring data exist to adequately characterize exposure to the Canadian population, including sub-populations of interest (e.g., children and pregnant women). These blood boron concentrations will be carried forward to risk characterization in order to represent exposure to Canadians.
Although the whole blood biomonitoring data provide a measure of integrated exposure from all routes and sources for the general population, including food, drinking water, dust, soil and products containing boron, not all products available to Canadians or every potential exposure source are captured in these studies. In addition, biomonitoring data are unable to identify sources of exposure. Accordingly, average intake estimates were derived for the general Canadian population in order to identify the main sources of intake.
Based on exposure modelling intake estimates, food, drinking water and products were determined to be primary contributors to total daily intake, whereas soil, dust and air were minor contributors. Fruits, vegetables, in particular, are important sources of dietary intake. Representative, high-quality Canadian data were available to characterize exposure to boron in air, soil, dust, food and drinking water, resulting in high confidence intake estimates. Average daily intakes from environmental media, food and drinking water ranged from 3-92 µg B/kg bw/d.
Based on modelling intake estimates for products containing boric acid (and precursors), products may be significant contributors to total daily intake. Systemic exposure was estimated for users of products containing boric acid, including arts and crafts, toys, cleaning products, cosmetics, NHPs, and swimming pool and spa products. Intakes for sentinel products were estimated to range from 0.03-2819 µg B/kg bw/d. Intake estimates from some products greatly exceed average daily intake from environmental media, food and drinking water. However, overall confidence in the intake estimates from products is low to moderate, due to uncertainties in adequate algorithms for estimating intake, selection of sentinel products, dermal absorption and the lack of information on directions for use of specific products, frequency of use and concentration.
Relationship of blood boron to boron intakes
Several human studies have identified blood boron concentration as an indicator of boron intakes (Neilsen and Penland 1999; Neilsen 2009; Hunt 1997; WHO 1998). A regression correlation between boron oral intakes and blood (whole blood, plasma, serum) boron concentrations was derived by Health Canada to facilitate the estimation of intake from available blood boron data obtained from biomonitoring studies. Details of the regression approach are described below.
Toxicokinetic data indicate that the blood boron concentrations reach steady-state levels effectively post-exposure (Treinen and Chapin 1991). Absorbed boron is distributed rapidly and evenly throughout the body’s soft tissues, with slight accumulation in bone (2-3 times higher). A three-compartment model used to describe blood and urine concentration of boric acid following oral and intravenous exposure in male volunteers suggests that additional compartments were needed to describe the initial rapid elimination of boron following intake and a gradual release after three days of intake (Jansen et al. 1984a, 1984b). This model may also suggest that accumulation of boron depends on the rate to deplete body stores and the renal clearance. A non-linear relationship between boron intake and blood concentrations was suggested by Dourson et al. (1998) after reviewing human and rat studies. When additional new data were applied to this original observed function, the consistency for mean blood boron concentrations and exposure doses was within the expected variability. As a result, a power function adjusted from the Dourson et al. (1998) original observation was used to describe the correlation between the mean blood boron concentrations and daily boron intake in humans in this assessment.
Studies on boron exposure (i.e., dietary, supplements or drinking water) were selected when deriving the regression correlation, because those sources of exposure are more relevant for the general population (see Appendix G). In dietary supplementation studies, individuals were supplemented with known concentrations of boron, and blood boron concentrations were monitored at regular intervals (Nielsen and Penland 1999; Hunt et al. 1997; Green and Ferrando 1994; Wallace et al. 2002). Intake estimates from supplementation studies include boron exposure from both supplements and diets. Because boron is well absorbed and is excreted in urine, Neilson and Penland (1999) estimated boron intakes based on urinary boron excretion. In Hunt et al. (1997), the blood boron concentration was presented as µmoles per litre, with the molecular weight of 10.8 g/mol applied to calculate blood boron concentration in µg/L. In Green and Ferrando (1994), the average plasma boron concentrations were calculated based on the individual plasma data. For individuals with plasma boron concentrations below or equal to limits of detection, half of the limit was assumed.
In drinking water studies, blood boron concentrations were monitored in people living in northern Chile, an area with naturally high concentrations of boron in drinking water and soil (Appendix G) (Barr et al. 1993; Harari et al. 2012). Barr et al. (1993) calculated the daily intake of boron based on the boron concentrations in drinking water; the dietary intakes were not considered. Harari et al. (2012) did not estimate the boron intakes, and only provided the boron concentration in drinking water. An average water consumption rate of 1.8 L per day was assumed when estimating boron intakes, a rate consistent with the value assumed in Barr et al. (1993). Similar to Barr et al (1993), Harari et al. (2012) did not include a dietary component in deriving intake estimates.
Workplace exposure to boron arises primarily from dust, and assumptions on particle size, pulmonary disposition and bioavailability may bias the exposure estimates under occupational settings compared with the general population. Therefore, only the control groups (local community controls and remote background controls) from occupational studies were included in the regression correlation. The community controls were individuals from the same community as boron workers, but without workplace boron exposure, while the remote-area background controls were individuals from another community where background boron exposure levels were low. As indicated in Appendix G, all oral intakes were converted to mg B/kg bw/d. When the body weights were not provided in the study, an average body weight of 70 kg was applied for all cohorts, except for Chinese cohorts. In general, body weights of Chinese people are lower than the other ethnic groups, and therefore an average body weight of 60 kg was applied. When the blood boron concentrations were presented in a weight/weight (wt/wt) basis, the blood density was assumed as 1 g/mL to convert blood boron concentrations from wt/wt to weight/volume (wt/v).
Based on the regression analysis, the mathematical correlation between blood boron concentrations and the oral intakes of boron is shown in Figure 9-1, and can be explained as follows:
Blood concentration (µg/L) = 1008.8 (daily intake)0.7339
where daily intake is in mg B/kg bw/d.
9.3 Characterization of risk to human health
Results from animal experiments demonstrate that boric acid adversely affects fertility, reproduction and development. These effects observed across species were very similar, both in nature and effective doses. The lowest point of departure in the animal database was a BMDL of 2.90 mg B/kg bw/d for decreased testicular weight, derived from dog studies (which have limitations in quality). The other notable point of departure is an NOAEL of 9.6 mg B/kg bw/d identified in rats, based on fetal toxicity in the absence of maternal toxicity. Given that the dog is a more sensitive animal model, and because the rat developmental toxicity study was limited to a 20-day in utero exposure with limited examinations of fetal or maternal toxicity, there are limitations with the use of this endpoint for risk characterization as well. Given the limitations in the available animal database, margins of exposure were derived from the BMDL of 2.90 mg B/kg bw/d as per the PMRA (Health Canada 2012).
Given that no additional animal studies have been conducted since the publication of the PMRA risk assessment (Health Canada 2012), epidemiological data were assessed to determine if adequate studies were available to derive points of departure for risk characterization. It was concluded that the epidemiological studies in humans are collectively insufficient to demonstrate the absence of an adverse effect of boron exposure in humans, due to several limitations in design. The Committee for Risk Assessment of the ECHA (ECHA 2014) concluded that the toxicity data from four species (dog, rat, mice and rabbit) provide clear evidence of adverse effects on sexual function, fertility and development. The methodological limitations in human studies limit their utility, but do not contradict the animal data (ECHA 2014). As such, effects observed in animals are considered relevant to humans and are used for the risk assessment.
Canadians are exposed to naturally occurring and anthropogenic boric acid from environmental media, food, drinking water and products. Intake estimates indicate that naturally occurring boron in fruits, vegetables and, to a lesser extent, drinking water are primary sources of exposure. Estimates of intakes from uses of boric acid in some arts, crafts, toys, cleaning products, cosmetics, NHPs and swimming pool and spa products indicate that these may be significant sources of exposure to the general population.
With the availability of biomonitoring data, exposure to boric acid was characterized using predicted daily intakes based on the measurement of total boron concentrations in the blood of Canadians and Europeans. Total boron blood concentrations are a measure of integrated exposure to all precursors of boric acid, from all routes (oral, dermal and inhalation), and all sources (including environmental media, food, and daily- or frequent-use products). Average and upper percentile (e.g., 95th) blood boron concentrations for Canadians are considered to be 34-195 µg/L based on measured data from the Alberta biomonitoring program and European data. Using the relationship between blood boron concentrations and intake estimates, as described in section 9.2.2, where blood concentration (µg/L) = 1008.8 (daily intake in mg/kg bw/d)0.7339 , average and upper-percentile blood concentrations of 34 and 195 µg/L correspond to intakes of 10 and 107 µg B/kg bw/d, respectively.
Risk to human health for boric acid was characterized based on a comparison of predicted intake estimates based on blood boron concentrations to the critical health effect. The margins of exposure between average and upper percentile intakes derived from average and upper percentile biomonitoring data and the critical effect (2.90 mg B/kg bw/d) are 290 and 27 respectively. These margins of exposure are considered potentially inadequate to address uncertainties in the exposure and health effects databases.
9.4 Uncertainties in the characterization of risk to human health
The human health effects database does not measure the same range of toxicological endpoints noted in the animal database, reducing the ability to make species-sensitivity comparisons. Although cardiovascular and endocrine effects were noted in several human supplement studies, there is inadequate information available to accurately characterize the risks of these possible health effects.
The animal database mainly consists of older studies with inherent limitations. Administered doses in animal studies have a degree of uncertainty, because the background boron concentration in animal feed and/or stability and homogeneity analyses of administered doses were not conducted for many studies in the animal database. The dog studies have been criticized for lack of good laboratory practice (the studies were conducted prior to Good Laboratory Practice implementation), and there is some concern regarding the dose relationship with regards to testicular atrophy due to the animals’ age. For a fulsome discussion of the limitations of this study see (Austria 2008a). Given that the rat study is only conducted over a 20 day dosing regime, has limited examinations not limited to fetal development, and does not examine the most sensitive organ at the most sensitive life stage identified in the dog studies, there is uncertainty about extrapolation of this study to assess developing male reproductive function. Several endpoints of potential concern reported in humans (cardiovascular, endocrine, cancer and testicular toxicity) are not fully characterized in the animal database, and therefore there is uncertainty about adequacy of the database to fully characterize health effects associated with boric acid. Conducting toxicity studies to fully address these concerns could reduce database uncertainty and allow for refinement of the risk characterization.
It remains unclear to what extent boron bioavailability could be reduced by the natural boron complexes that form in plant materials, and any matrix effects that occur as a result. The current screening assessment does not specify a target margin of exposure (MOE), or chronic reference dose. Rather, the assessment presents the achieved margins of exposure to the proposed point of departure (POD) for testicular toxicity (BMDL based on combined data from two 90-day dog studies). The screening assessment refers to the Health Canada pesticide re-evaluation under the Pest Control Products Act (PCPA) (Health Canada 2012), which identified, for boron, a target MOE of 300 to the POD. It is acknowledged that other organizations have derived lower target MOEs based on the publically available boron database, and then applying various adjustment factors to the standard uncertainty factors. Of note, target MOEs between 25 and 60 were applied to the POD of 9.6 mg B/kg bw/d from the rat developmental toxicity study (EFSA 2013; EGVM 2003; IOM 2001; WHO 1998), mainly through a refinement constructed on human pharmacokinetic variability factors. For example, by subdividing the intraspecies default UF of 10 into 3.2 for toxicokinetics and 3.2 for toxicodynamics, and using the glomerular filtration rate data in pregnant women as also reported by Dourson et al. (1998), EFSA (2013) and EGVM (2003) adjusted the toxicokinetic subfactor to 1.8, resulting in a chemical-specific intraspecies UF of 6 (3.2 x 1.8 = 5.72) and an overall UF of 60. WHO (1998), also by subdividing the UF into toxicokinetics and toxicodynamics, reduced the default interspecies UF of 10 based on half-life similarities in the elimination of boron between rats and humans; however, clearance has been reported as being more important than half-life for comparison of toxicant elimination (Zhao et al. 1999). Another recent article from Dourson and collaborators (Hasegawa et al., 2013) proposes 0.13 mg B/kg bw/d as the most appropriate cRfD boron, applying an UF of 78 to a rat developmental POD of 10.3 mg B/kg bw/d.
The pesticide assessment (Health Canada 2012) did not agree with refining the intraspecies factor, given the inadequacy and large variability in the human data on which these refinements were based (Health Canada 2012). Additional human data/information examined during the current assessment further indicating the large degree of human variability supports the Health Canada 2012 interpretation of the human pharmacokinetic data. Thus, while there remains uncertainty as to the most appropriate level of conservatism required for the screening assessment, it is important to note that the proposed conclusion of this screening assessment would remain the same with the use of any one of the target MOEs suggested by other regulatory bodies.
There is uncertainty about whether homeostatic capacity may be exceeded by environmental media exposure levels. However, in the absence of definitive studies, the risk characterization for boron focused on total exposure based on biomonitoring data.
Boron is not included in the Canadian Health Measures Survey or National Health and Nutrition Examination Survey, which provide robust population-level exposure estimates (> 5000 participants per cycle, data from two or more cycles could be combined for analysis). The Alberta biomonitoring data include > 50 000 pregnant women and > 1300 children, but due to the study design (pooled serum), there are no data to describe exposure in the upper tails (95th percentile) of the distribution. In addition, in other studies men have been found to have higher exposure and are not included in the Alberta study. Data from the United States and Europe were evaluated to enable the evaluation of risks in individuals with the highest exposures, but differences in study design (e.g., pooled serum vs. individual samples, e.g., target population [general population studies vs. supplement vs. occupational]) and analytical methods (colorimetric vs. neutron activation analysis mass spectrometry [NAA-MS] vs. inductively coupled plasma mass spectrometry [ICP-MS]) made comparisons between studies difficult. It is uncertain to what degree the European biomonitoring data are representative of Canadian exposure to boron, although average concentrations are similar, increasing confidence in the use of this data for Canadians. It is possible that the upper percentile (e.g., 95th) blood concentrations in Canadians were not captured in the European datasets, and the extent to which exposure from products is captured in the biomonitoring data is uncertain. The inclusion of boron in a national population-level biomonitoring study (e.g., the Canadian Health Measures Survey), and targeted studies on users of products containing boric acid or precursors of boric acid, would reduce uncertainty in the exposure characterization.
There is uncertainty associated with the intake estimates for users of products containing boric acid, due to a lack of data on product use (e.g., frequency, amount of product used, market share and target market), of adequate exposure models to predict intake from product use, and of targeted exposure studies. There is uncertainty regarding the characterization of dermal absorption, because the available studies have several limitations, including poor mass balance and only one route of elimination measured. Additional data, such as dermal absorption (e.g., OECD test guideline for in vitro human and rat, and in vivo rat) and targeted exposure studies, would reduce uncertainty in the exposure assessment.
There is moderate to high confidence in the regression correlation developed between daily intake of boron and steady-state blood boron concentration, as presented in subsection 9.2.2. A similar analysis of blood boron concentrations as a function of administered dose has been conducted by Dourson et al. (1998), and the relationship between blood boron concentrations and exposure doses was previously used to characterize risk of boron exposure (Bolt et al. 2012). This current evaluation expands upon earlier work by Dourson et al. (1998) to include additional human studies with exposure sources relevant to the general Canadian population (e.g., dietary supplement studies and control groups from occupational studies). Given that the current correlation is derived from relevant intake data, exposure sources were considered relevant to the general Canadian population.
Considering all available lines of evidence presented in this draft screening assessment, there is risk of harm to organisms, but not to the broader integrity of the environment, from boric acid, its salts and its precursors. It is proposed to conclude that boric acid, its salts and its precursors meet the criteria under paragraph 64(a) of CEPA, as they are entering or may enter the environment in a quantity or concentration or under conditions that have or may have an immediate or long-term harmful effect on the environment or its biological diversity. However, it is proposed to conclude that boric acid, its salts and its precursors do not meet the criteria under paragraph 64(b) of CEPA, as they are not entering the environment in a quantity or concentration or under conditions that constitute or may constitute a danger to the environment on which life depends.
Based on margins of exposure between adverse health effects and intake estimates considered inadequate to address uncertainties in the exposure and health effects database, it is proposed to conclude that boric acid, its salts and its precursors meet the criteria under paragraph 64(c) of CEPA, as they are entering or may enter the environment in a quantity or concentration or under conditions that constitute or may constitute a danger in Canada to human life or health.
Abou-Shakara FR, Havercroft JM, Ward NI. 1989. Lithium and boron in biological tissues and fluids. Trace Elemen Med 6:142-146 [cited in Green et al. 1994].
About Education. 2014. Slime Recipe - How to Make Borax and White Glue Slime [Internet] [cited 2014 Dec.]. Available from: http://chemistry.about.com/od/chemistryactivities/ss/slimerecipe.htm
Agriculture and Agri-Food Canada. 2013. Boron concentrations in Canadian soils. Unpublished, submitted to Environment Canada under the Chemicals Management Plan.
Alberta Environment. 2002. Lake Wabamun water quality and sediment survey. Preliminary report. Edmonton (AB): Alberta Environment. ISBN 0-7785-2296-0. 37 p. Available from: http://environment.gov.ab.ca/info/library/5811.pdf
Alberta Environment. 2003a. Spatial variability of water quality in Wabamun Lake (July 2002). Draft Report, Environmental Monitoring and Evaluation Branch, Alberta Environment.
Alberta Environment. 2003b. Wabamun Lake water quality 1982 to 2001. Science and Standards Branch, Alberta Environment.
Alberta Environment. 2006. Wabamun Lake Oil Spill August 2005: Data report for Water and Sediment Quality in the Pelagic Area of the Lake (August 4-5 to September 15, 2005). Edmonton (AB): Alberta Environment. ISBN 0-7785-4589-X. 99 p. Available from: http://environment.gov.ab.ca/info/posting.asp?assetid=7657&categoryid=5
Alberta Health and Wellness. 2008. The Alberta Biomonitoring Program: Chemical Biomonitoring in Serum of Pregnant Women in Alberta. Edmonton (AB): Alberta Health and Wellness. ISBN 978-0-7785-6695-3 [cited 2013 May 2]. Available from: http://www.health.alberta.ca/documents/Chemical-Biomonitoring-2008.pdf
AMEC 2005. Geotechnical and environmental tailings closure assessment McIntyre tailings dam. AMEC America’s Limited Earth & Environmental Div, Lively, Ontario [cited in Paliewicz et al 2015]
American Chemical Society. 2014. Time for Slime. [Internet] [cited 2014 Dec.]. Available from: http://www.acs.org/content/acs/en/education/whatischemistry/adventures-in-chemistry/experiments/slime.html
Amorim JB, Natal-da-Luz T, Sousa JP, Loureiro S, Becker L, Römbke J, Soares AMVM. 2012. Boric acid as reference substance: pros, cons and standardization. Ecotoxicology 21:919-924.
Anaka A, Wickstrom M, Siciliano SD. 2007. Increased sensitivity and variability of phytotoxicity responses in arctic soils to a reference toxicant, boric acid. Environ Toxicol Chem 27(3):720-726.
Anderson DL, Kitto ME. 1994. Sources and atmospheric distribution of particulate and gas-phase boron. Atmos Environ 28(8):1401.
ANZECC. 2000. Australia and New Zealand Environment and Conservation Council and the Agriculture and Resource Management Council of Australia and New Zealand. Australian and New Zealand Guidelines for Fresh and Marine Water Quality. Volumes 1, 2 & 3.
[ANSES] French Agency for Food, Environmental and Occupational Health & Safety. 2012. OPINION of the French Agency for Food, Environmental and Occupational Health & Safety on assessing the need for a revision of the classification of boric acid. Available from: www.anses.fr/Documents/REACH2011sa0301.pdf
ARCHE 2010. Boron effects assessment in the terrestrial compartment, Final report 27 July 2010.
Argust P. 1998. Distribution of Boron in the Environment. Biol Trace Elemen Res 66:131-143.
Arslan N. 2013. Invisible face of boron pollution in fluvial ecosystem: the level in the tissues of sentinel and nectonic organisms. AMBIO 42:715-723.
[ATSDR] Agency for Toxic Substances and Disease Registry. 2010. Toxicological Profile for boron. Atlanta (GA): U.S. Department of Health and Human Services, Public Health Service. Available from: www.atsdr.cdc.gov/toxprofiles/tp26.pdf
Austria. 2008a. Annex XV Transitional Report-Boric Acid. Submitted by Austria, December 1, 2008. Documentation of the work done under the Existing Substance Regulation (EEC) No. 793/93 and submitted to the European Chemicals Agency according to Article 136(3) of Regulation (EC) No. 1907/2006. Published by the European Chemicals Agency. Available from: https://echa.europa.eu/documents/10162/13630/trd_austria_boric_acid_en.pdf
Austria. 2008b. Annex XV Transitional Report-Disodium Tetraborate Anhydrous. Submitted by Austria, December 1, 2008. Documentation of the work done under the Existing Substance Regulation (EEC) No. 793/93 and submitted to the European Chemicals Agency according to Article 136(3) of Regulation (EC) No. 1907/2006. Published by the European Chemicals Agency. Available from: http://echa.europa.eu/doc/trd_substances/disodium_tetraborate_anhydrous/ann_xv_trd/trd_austria_trisodiumtet raborate.pdf
Ayars JE, Hoffman GJ, Schrale G. 1990. Strategies to reduce salt load in drainage water. In: Proceedings of the 1990 National Conference IrDiv/ASCE. Durango (CO). Pp. 331-338. [Cited in: Nable RO, Bañuelos GS, Paull JC. 1997. Boron toxicity. Plant Soil 193:181-198.]
Ayars JE, Hutmacher RB, Schoneman RA, Vail SS, Pflaum T. 1993. Long term use of saline water for irrigation. Irrigation Sci 14:27-34. [Cited in: Nable RO, Bañuelos GS, Paull JC. 1997 Boron toxicity. Plant Soil 193:181-198.]
Baird 1999. Environmental Chemistry, second edition. New York (NY): W.H. Freeman and Company. ISBN 0-7167-3153-3
Bagheri A, Rathjen AJ, Paull JG. 1994. The response of Pisum sativum L. germplasm to high concentrations of soil boron. Euphytica 75:9-17.
Ball RW, Harrass MC, Culver BD. 2012. Boron. Patty's Toxicology 45:885-934. Sixth Edition, Volume 1, John Wiley & Sons, Inc. Available from: http://onlinelibrary.wiley.com/doi/10.1002/0471435139.tox045.pub2/abstract
Banerji. 1969. Boron adsorption on soils and biological sludges and its effects on endogenous respiration. Proceedings of the 24th Industrial Waste Conference, Engineering Extension Series No.135, Engineering Technical Reports Collection, Purdue University, p. 1118-1127 [Internet]. Available from: http://earchives.lib.purdue.edu/u?/engext
Bari MA, Kindzierski WB, Cho S. 2014. A wintertime investigation of atmospheric deposition of metals and polycyclic aromatic hydrocarbons in the Athabasca oil sands region, Canada. Sci Total Environ 485-486: 180.
Barr RD, Clarke WB, Clarke RM, Venturelli J, Norman GR, Downing RG. 1993. Regulation of lithium and boron levels in normal human blood: environmental and genetic considerations. J Lab Clin Med 121(4):614-9.
Barr RD, Barton SA, Schull WJ. 1996. Boron levels in man: Preliminary evidence of genetic regulation and some implications for human biology. Med Hypoth 46:286-289.
Başaran N, Duydu Y, Bolt HM. 2012. Reproductive toxicity in boron exposed workers in Bandirma, Turkey. J Trace Elem Med Bio 26:165-167.
Basset RL. 1980. A critical evaluation of the thermodynamic data for boron ions, ion pairs, complexes, and poly anions in aqueous solution at 298.15 K 1 bar. Geochim Cosmochim Acta 44:1151 [cited in Kot 2009].
[BC MOE] British Columbia Ministry of Environment. 1978. Kootenay air and water quality study phase II. Water quality in the Elk and Flathead River Basins. Water Investigations Branch.
[BC MOE] British Columbia Ministry of Environment. 2005. Soil Quality Database. Technical Guidance on Contaminated Sites. British Columbia Ministry of Environment [Internet]. Available from: http://www.env.gov.bc.ca/epd/remediation/guidance/technical/soil/cariboo.htm
Becker L, Scheffezyk A, Forster B, Oehlmann J, Princz J, Rombke J, Moser T. 2011. Effects of boric acid on various microbes, plants, and soil invertebrates. J Soils Sediments 11:238-248.
Becker-Van Slooten K, Campiche S, Tarradellas J. 2003. Research in support of the Environment Canada Collembolan toxicity test method with Folsomia candida for assessment of contaminated soils, final report. Prepared for Method Development and Applications Section, Environmental Technology Centre, Environment Canada, by Laboratory of Environmental Chemistry and Ecotoxicology (CECOTOX), Ecole polytechnique federale de Lausanne (EPFL), ENAC-ISTE.
Bellaloui N, Abbas HK, Gillen AM, Abel CA. 2009. Effect of glyphosate-boron application on seed composition and nitrogen metabolism in glyphosate-resistant soybean. J Agri Food Chem 57:9050-9056.
Bellaloui N, Mengistu A, Fisher DK, Abel CA. 2012a. Soybean seed composition as affected by drought and Phomopsis in phomopsis-susceptible and resistant genotypes. J Crop Imp 26:428-453.
Bellaloui N, Mengistu A, Zobiole LHS, Shier WT. 2012b. Resistance to toxin-mediated fungal infection: Role of lignins, isoflavones, other seed phenolics, sugars, and boron in the mechanism of resistance to charcoal rot disease in soybean. Toxin Rev 31:16-26.
Bergmann W. 1988. Ernährungsstörungen bei Kulturpflanzen. Entstehung, visuelle und analytische diagnose. Fischer Verlag, Jena, Germany [cited in Marschner 1995].
Bergmann W, Bruchlos P, Marks G. 1995. The toxic limiting value of boron. Tenside Surfact Det 32(3):229-237.
[BfR] Bundesinstitut fur Risikobewertung. 2005. Borsaure in Hupfknete. Gesundheitliche Bewertung Nr. 014/2005 des BfR vom 27. Oktober 2004 [Internet]. [In German, cited Feb. 2015]. Available from: http://www.bfr.bund.de/cm/343/borsaeure_in_huepfknete.pdf
Birge WJ, Black JA. 1977. Sensitivity of vertebrate embryos to boron compounds. EPA-560/1-76-008. Washington (DC): Office of Toxic Substances, U.S. EPA.
Black JA, Barnum JB, Birge WJ. 1993. An integrated assessment of the effects of boron to the rainbow trout. Chemosphere 26:1383-1413.
Bolaños L, Brewin NJ, Bonilla I. 1996. Effects of boron on rhizobium-legume cell-surface interactions and node development. Plant Physiol 110:1249-1256.
Bolt HM, Başaran N, Duydu Y. 2012. Human environmental and occupational exposures to boric acid: reconciliation with experimental reproductive toxicity data. J Toxicol Environ Health A 75(8-10): 508-14.
Bonanno G. 2011. Trace element accumulation and distribution in the organs of Phragmites australis (common reed) and biomonitoring applications. Ecotoxicol Environ Safe 74:1057.
Borax. 2013. Borates in metallurgical applications [Internet]. Available from: http://www.google.ca/url?sa=t&rct=j&q=&esrc=s&frm=1&source=web&cd=1&ved=0CDkQFjAA&url=http%3A%2F%2Fwww.borax.com%2Fdocs%2Feuf_pdfs%2Feuf-borates-boratesinmetallurgicalapplications.pdf%3Fsfvrsn%3D2&ei=SMXrUpu_LOuzsATD1IHwAw&usg=AFQjCNGxabWVCZKFQruL1yKxCB3B7JnV6Q&bvm=bv.60444564,d.cWc
Borax. 2014a. Insulation [Internet]. Available from http://www.borax.com/market/insulation.aspx
Borax. 2014b. Borates in gypsum board [Internet]. Available from: http://www.borax.com/markets/other-uses/other-uses
Borax Europe. 2012. Joint chemical safety report: Boric acid. EC Number: 233-139-2, CAS Number: 10043-35-3. Prepared for the European Chemicals Agency (ECHA) for REACH.
Boyle. 1974. Elemental Associations in Mineral Deposits and Indicator Elements of Interest in Geochemical Prospecting (Revised). Geological Survey of Canada. Paper 74-45, 40 p.
Brown PH, Bellaloui N, Dandekar AM, Hu H. 1999. Transgenically enhanced sorbitol synthesis facilitates fhloem boron transport and increases tolerance of tobacco to boron deficiency. Plant Physiol 119:17-20.
Brown PH, Bellaloui N, Wimmer MA, Bassil ES, Ruiz J, Hu H, Pfeffer H, Dannel F, Romheld V. 2002. Boron in plant biology. Plant Biol 4:205-223.
Bryant CW, Pagoria PS. 2004. The fate of metals in forest industry wastewater treatment systems. Water Sci Technol 50(3):21-28.
Buchter BD, Amacher MC, Hinz C, Iskandar IK, Selim HM. 1989. Correlation of Freundlich Kd and n retention parameters with soils and elements. Soil Sci 148(5):370.
Bugbee EE. 1981. A textbook of fire assaying. Wiley, New York City
Butterwick L, De Oude N, Raymond K. 1989. Safety assessment of boron in aquatic and terrestrial environments. Ecotoxicol Environ Safe 17:339-371.
Cain RT, Swain LG. 1980. Fraser River Estuary Study. Water Quality. Municipal Effluents. Province of British Columbia.
Cain WS, Jalowayski AA, Kleinman M, Lee N-S, Lee B-R, Ahn B-H, Magruder K, Schmidt R, Hillen BK, Warren CB et al. 2004. Sensory and associated reactions to mineral dusts: sodium borate, calcium oxide, and calcium sulfate. J Occup Environ Hyg 1:222-236.
Cain WS, Jalowayski AA, Schmidt R, Kleinman M, Magruder K, Lee KC, Culver BD. 2008. Chemesthetic responses to airborne mineral dusts: Boric acid compared to alkaline materials. Int Arch Occup Environ Health 81:337-345.
Cakmak L, Römheld V. 1997. Boron deficiency-induced impairments of cellular function in plants. Plant Soil 193:71-83.
Camacho-Cristóbal JJ, González-Fontes A. 2007. Boron deficiency decreases plasmalemma H+-ATPase expression and nitrate uptake, and promotes ammonium assimilation into asparagine in tobacco roots. Planta 226:443-451.
Camacho-Cristóbal JJ, Rexach J, González-Fontes A. 2008. Boron in plants: deficiency and toxicity. J Integr Plant Biol 50:1247-1255.
Canada. 1978. Food and Drug Regulations, C.R.C., c. 870. Available from: www.canlii.org/en/ca/laws/regu/crc-c-870/latest/crc-c-870.html
Canada. 1985a. Food and Drugs Act, R.S.C. 1985, c. F-27. Available from: www.canlii.org/ca/sta/f-27/whole.html
Canada. 1985b. Fertilizers Act, R.S.C. 1985, c. F-10. Available from: http://laws-lois.justice.gc.ca/eng/acts/F-10/
Canada. 1999. Canadian Environmental Protection Act, 1999. S.C. 1999, c. 33, Part III, vol. 22, no. 3. Available from: http://www.gazette.gc.ca/archives/p3/1999/g3-02203.pdf
Canada. 2002. Pest Control Products Act. S.C. 2002, c.28. Available from: http://laws-lois.justice.gc.ca/eng/acts/P-9.01/
Canada. 2003. Natural Health Products Regulations. SOR/2003-196. Available from: http://laws-lois.justice.gc.ca/eng/regulations/sor-2003-196/
Canada. 2009. Canadian Environmental Protection Act, 1999: Notice with respect to certain inanimate chemicals (substances) on the Domestic Substances List. Canada Gazette, Part I: Vol. 143, No. 40 - October 3, 2009. Available from: http://www.gazette.gc.ca/rp-pr/p1/2009/2009-10-03/html/notice-avis-eng.html#d101
Canada. 2010. Canada Consumer Product Safety Act, S.C. 2010, c.21. Available from: http://laws-lois.justice.gc.ca/eng/acts/C-1.68/
Canada. 2011. Toys Regulations. SOR/2011-17. Available from: http://laws-lois.justice.gc.ca/eng/regulations/sor-2011-17/index.html
Canada. 2014. Cosmetic Regulations, C.R.C., c. 869. Available from: http://laws-lois.justice.gc.ca/eng/regulations/C.R.C.,_c._869/index.html
Casey R. 2005. Results of aquatic studies in the McLeod and Upper Smoky River systems. Prepared for: Science and Standards Branch, Alberta Environment [Internet]. Available from: http://environment.gov.ab.ca/info/posting.asp?assetid=7743&categoryid=5
[CBSA] Canada Border Services Agency. 2013. Information gathered on the import of commodities corresponding to the codes HS 281000, HS 284011, HS 284019, HS 284030, HS 284020, HS 252800, HS 252810 and HS 252890. Confidential information.
[CCA] Council of Canadian Academies. 2014. Environmental impacts of shale gas extraction in Canada. The expert panel on harnessing science and technology to understand the environmental impacts of shale gas extraction [Internet]. Available from: http://www.scienceadvice.ca/en/assessments/completed/shale-gas.aspx
[CCME] Canadian Council of Ministers of the Environment. 2006. A protocol for the derivation of Environmental and Human Health Soil Quality Guidelines.
[CCME] Canadian Council of Ministers of the Environment. 2007. A protocol for the derivation of water quality guidelines for the protection of aquatic life 2007. In: Canadian environmental quality guidelines, 1999, Canadian Council of Ministers of the Environment, 1999.
[CCME] Canadian Council of Ministers of the Environment. 2009. Scientific criteria document for the development of the Canadian Water Quality Guidelines for Boron. PN 1437, ISBN 978-1-896997-89-6 PDF.
CEH. 2011. CEH Marketing Research Report: Boron Minerals and Chemicals.
[CEI] Cantox Environmental Inc. 2003. Ecological Risk Assessment for Teck Cominco Operations at Trail, British Columbia; Terrestrial Risk Modelling Level of Refinement # 2. Prepared for Teck Cominco Metals Ltd.
[CFIA] Canadian Food Inspection Agency. 2014. Chemical Residues in Food [Internet]. Date modified: 2014-05-23 [cited 2014 April]. Available from: http://www.inspection.gc.ca/food/chemical-residues-microbiology/chemical-residues/eng/1324258929171/1324264923941
Chang BL, Robbins WA, Wei F, Xun L, Wu G, Li N, Elashoff DA. 2006. Boron workers in China: exploring work and lifestyle factors related to boron exposure. AAOHN J 54(10):435-443.
Chauveheid E, Denis M. 2004. The boron-organic carbon correlation in water. Water Res 38:1663.
Cheng CM, Hack P, Chu P, Chang YN, Lin TY, Ko CS, Chiang PH, He CC, Lai YM, Pan WP. 2009. Partitioning of mercury, arsenic, selenium, boron and chloride in a full-scale coal combustion process equipped with selective catalytic reduction, electrostatic precipitation and flue gas desulfurization systems. Energy Fuels 2009(23):4805-4816.
Cheung K, Sanei H, Klassen P, Mayer B, Goodarzi F. 2009. Produced fluids and shallow groundwater in coalbed methane (CBM) producing regions of Alberta, Canada: Trace element and rare earth element geochemistry. Int J Coal Geol 77:338-349.
Clarke BC, Gibson RS. 1988. Lithium, boron and nitrogen in 1-day diet composites and a mixed-diet standard. J Food Comp Anal 1:209-220.
Clarke WB, Koekebakker M, Barr RD, Downing RG, Fleming RF. 1987a. Analysis of ultratrace lithium and boron by neutron activation and mass-spectrometric measurement of 3He and 4He. Appl Radiat Isotopes 38(9):735-743.
Clarke WB, Webber CE, Koekebakker M, Barr RD. 1987b. Lithium and boron in human blood. J Lab Clin Med 109(2):155−158.
Clarke WB, Guscott R, Downing RG, Lindstrom RM. 2004. Endogenous lithium and boron red cell-plasma ratios: normal subjects versus bipolar patients not on lithium therapy. Biol Trace Elem Res 97(2):105-116.
Closs LG, Sado EV. 1981. Geochemistry of Soils and Glacial Sediments Near Gold Mineralization in the Beardmore-Geraldton Area. District of Thunder Bay. Ministry of Natural Resources, Ontario Government.
Cöl M, Sayli BS, Genc Y, Ercevik E, Elhan AH, Keklik A. 2000. An assessment of fertility in boron exposed workers in Turkey: an epidemiological approach. Turk J Med Res 18:10-6. [Cited in Scialli et al. 2010, detail found in EBA_comments_Annex_XV_100104_final.sflb.pdf].
Cole S and Ferron CJ 2002. A review of the beneficiation and extractive metallurgy of the platinum group elements, highlighting recent process innovations, SGS Minerals Services, Technical Paper 2002-03
Conestoga-Rovers and Associates. 2013. Landfill Monitoring Data - Correlation, Trends, and Perspectives. Report Number 9. Unpublished report prepared for Environment Canada. 435 p.
[ConsExpo] Consumer Exposure Model [Internet]. 2006. Version 4.1. Bilthoven (NL): Rijksinstituut voor Volksgezondheid en Milieu [National Institute for Public Health and the Environment] [cited 2014 Nov. ]. Available from: www.rivm.nl/en/healthanddisease/productsafety/ConsExpo.jsp#tcm:13-42840
Cotton FA, Wilkinson G. 1999. Advanced Inorganic Chemistry,5th Ed. New York (NY): John Wiley & Sons.
Craan AG, Myres AW, Green DW. 1997. Hazard assessment of boric acid in toys. Regul Toxicol Pharm 26:271-280.
Craw D, Rufaut CG, Haffert L, Todd A. 2006. Mobilisation and attenuation of boron during coal mine rehabilitation, Wangaloa, New Zealand. Sci Total Environ 368:444.
[CSUR] Canadian Society for Unconventional Resources. 2014. Water disposal [Internet]. Available from: http://www.csur.com/resources/fact-sheets
Culver BD, Hubbard SA. 1996. Inorganic boron health effects in humans: an aid to risk assessment and clinical judgment. J Trace Elem Exp Med 9:175-184.
Culver BD, Shen P, Taylor TH, Feldstein AL, Anton-Culver H, Strong PL. 1993. Absorption of boron by sodium borate and boric acid production workers. Report to US Borax, August 11 [cited in Rio Tinto Borax 2005].
Culver BD, Shen PT, Taylor TH, Lee-Feldstein A, Anton-Culver H, Strong PL. 1994. The relationship of blood-and urine-boron exposure in borax-workers and usefulness of urine-boron as an exposure marker. Environ Health Perspect 102(7):133-137.
[CWWA] Canadian Water and Wastewater Association. 2001. National Survey of Wastewater Treatment Plants. Final Report. Submitted to Environment Canada, National Pollutant Release Inventory (NPRI).
Davies. 2008. Effectiveness evaluation, Creston Valley, BC. Ministry of Environment, Kootenay Region, Environmental Protection Division.
Davis SM, Drake KD, Maier KJ. 2002. Toxicity of boron to duckweed, Spirodella polyrrhiza. Chemosphere 48:615-620.
Del-Campo Marin CM, Oron G. 2007. Boron removal by the duckweed Lemna gibba: A potential method for the remediation of boron-polluted waters. Water Res 41:4579.
Dethloff GM, Stubblefield WA, Schlekat CE. 2009. Effects of water quality parameters on boron toxicity to Ceriodaphnia dubia. Arch Environ Contam Toxicol 57:60.
Dordas C, Apostolides G, Goundra O. 2007. Boron application affects seed yield and seed quality of sugar beets. J Agr Sci 145:377-384.
dos Santos GCG, Rodella AA, Abreu CA, Coscione AR. 2010. Vegetable species for phytoextraction of boron, copper, lead, manganese and zinc from contaminated soil. Sci Agric 67(6):713 -719. ISSN 0103-9016. Available from: http://dx.doi.org/10.1590/S0103-90162010000600014.
Dourson M, Maier A, Meek B, Renwick A, Ohanian E, Poirier K. 1998. Boron tolerable intake re-evaluation of toxicokinetics for data-derived uncertainty factors. Biol Trace Elem Res 66:453-463.
[DPD] Drug Product Database [database on the Internet]. 2014. Ottawa (ON): Health Canada [cited 2014 May]. Available from: www.hc-sc.gc.ca/dhp-mps/prodpharma/databasdon/index-eng.php
Draize JH, Kelley EA. 1959. The urinary excretion of boric acid preparations following oral administration and topical applications to intact and damaged skin of rabbits. Toxicol Appl Pharm 1:267-276.
Duydu Y, Başaran N, Üstündağ A, Aydin S, Ündeğer Ü, Ataman OY, Aydos K, Düker Y, Ickstadt K, Waltrup BS et al. 2011. Reproductive toxicity parameters and biological monitoring in occupationally and environmentally boron-exposed persons in Bandirma, Turkey. Arch Toxicol 85(6):589-600.
Duydu Y, Başaran N, Üstündağ A, Aydın S, Ündeğer Ü, Ataman OY, Aydos K, Düker Y, Ickstadt K, Waltrup BS et al. 2012. Assessment of DNA integrity (COMET assay) in sperm cells of boron-exposed workers. Arch Toxicol 86(1):27-35.
Dyer SD. 2001. Determination of the aquatic PNEC0.05 for boron. Chemosphere 44:369-376.
[ECETOC] European Centre for Ecotoxicology and Toxicology of Chemicals. 1995. Reproductive and general toxicology of some inorganic borates and risk assessment for human beings. Technical Report No. 65. Brussels (BE): European Centre for Ecotoxicology and Toxicology of Chemicals.
[ECHA] European Chemicals Agency. ©2007-2014. Registered Substances database. Search results for CAS RN 10043-35-3. Helsinki (FI): ECHA [cited 2014 Feb.]. Available from: www.echa.europa.eu/information-on-chemicals/registered-substances
[ECHA] European Chemicals Agency. 2010. Annex XV dossier. Proposal for identification of a substance as substance of very high concern (SVHC). Substance name: Boric acid. EC Number: 233-139-2/234- 343-4. CAS RN: 10043-35-3/11113- 50-1. Helsinki: European Chemicals Agency.
[ECHA] European Chemicals Agency. 2012. Guidance on information requirements and chemical safety assessment. Chapter R.16: Environmental exposure estimation, Version 2.1. Helsinki (FI): European Chemicals Agency. Available from: http://echa.europa.eu/documents/10162/13632/information_requirements_r16_en.pdf
[ECHA] European Chemicals Agency. 2014. Committee for Risk Assessment. Opinion proposing harmonised classification and labelling at EU level of boric acid, CAS RN 10043-35-3. CLH-O-0000003738-64-03/D. Adopted 14 March 2014.
Eckhert CD. Boron stimulates embryonic trout growth. 1998. J Nutr 128(12):2488-2493.
Edwall L, Karlén B, Rosén A. 1979. Absorption of boron after mouthwash treatment with Bocosept. Eur J Clin Pharmacol 15(6):417-20.
[EFSA] European Food Safety Authority. 2004. Opinion of the Scientific Panel on Dietetic Products, Nutrition and Allergies on a request from the Commission related to the Tolerable Upper Intake Level of Boron (Sodium Borate and Boric Acid). Request N° EFSA-Q-2003-018.
[EFSA] European Food Safety Authority. 2011a. Scientific Opinion on the substantiation of health claims related to boron and prevention and treatment of prostate cancer (ID 221), maintenance of normal thyroid function (ID 222) and contribution to normal cognitive function (ID 223) pursuant to Article 13(1) of Regulation (EC) No 1924/2006. Available from: http://www.efsa.europa.eu/en/efsajournal/doc/2209.pdf
[EFSA] European Food Safety Authority. 2011b. Scientific Opinion on the substantiation of health claims related to boron and maintenance of bone (ID 218, 219) and maintenance of joints (ID 219, 220) pursuant to Article 13(1) of Regulation (EC) No 1924/20061. Available from: http://www.efsa.europa.eu/en/efsajournal/doc/1261.pdf
[EFSA] European Food Safety Authority. 2013. Scientific opinion on the re-evaluation of boric acid (E284) and sodium tetraborate (borax) (E 285) as food additives. EFSA panel on food additive and nutrient sources added to food (ANS). EFSA Journal 11(10):3407.
EGVM 2003. Safe Upper Levels for Vitamins and Minerals. Expert Group on Vitamins and Minerals. URL: http://cot.food.gov.uk/sites/default/files/vitmin2003.pdf [Accessed 2016-01-04].
Eisler R . 1990. Boron hazards to fish, wildlife, and invertebrates: a synoptic review. U.S. Fish and Wildlife Service., Biological Report 85(1.20). 32 p.
Elrashidi MA, O'Connor GA. 1982. Boron sorption and desorption in soils. Soil Sci Soc Am J 46:27.
Emiroglu O, Cicek A, Arslan N, Aksan S, Ruzgar M. 2010. Boron concentration in water, sediment and different organisms around large borate deposits of Turkey. Bull Environ Contam Toxicol 84:427.
Emsley J. 1989. The Elements. Oxford (UK): Clarendon Press. p. 32 [cited in Ball 2012].
Environment Canada. 2006. Guidance for conducting ecological assessments under CEPA 1999: Science resource technical series, technical guidance module: Sludge amendment. Working document. Gatineau (QC): Environment Canada, Ecological Assessment Division.
Environment Canada. 2007. Ecological categorization of substances on the Domestic Substances List (DSL) [Internet]. [Updated and reviewed 2007 May]. Available from: www.ec.gc.ca/substances/ese/eng/dsl/cat_index.cfm
Environment Canada. 2009a. Data for certain inanimate substances (chemicals) collected under the Canadian Environmental Protection Act, 1999, section 71: Notice with respect to certain inanimate substances (chemicals) on the Domestic Substances List. Data prepared by: Environment Canada, Health Canada; Existing Substances Program.
Environment Canada 2009b. Environmental Code of Practice for Metal Mines. Mining Section, Mining and Processing Division, Public and Resources Sectors Directorate, Environmental Stewardship Branch. Available from: https://www.ec.gc.ca/lcpe-cepa/documents/codes/mm/mm-eng.pdf
Environment Canada. 2013a. Fenceline Metals in Air Measurements. Estimated Releases of Boron, Selenium and Cobalt. Unpublished data from 1991-2011. March 2013 email from Emissions Research and Measurement Section, Environmental Science and Technology Centre, Science and Technology Branch.
Environment Canada. 2013b. Voluntary submissions obtained as part of the CMP 2 Grouping initiative, boron-containing substances grouping. Year 2013.
Environment Canada. 2013c. Data obtained from CMP monitoring program for the Grouping initiative, boron-containing substances grouping. Year 2013.
Environment Canada. 2014a. Supporting documentation: Additional information on the Canadian sources and uses of boron-containing substances. Gatineau (QC): Environment Canada. Information in support of the Draft Screening Assessment for Boric acid, its salts and its precursors. Available from: email@example.com
Environment Canada. 2014b. Supporting documentation: Releases and exposure characterization for the coal-fired power generation sector. Gatineau (QC): Environment Canada. Information in support of the Draft Screening Assessment for Boric acid, its salts and its precursors. Available from: firstname.lastname@example.org
Environment Canada. 2014c. Supporting documentation: Releases and exposure characterization for the metal mining sector. Gatineau (QC): Environment Canada. Information in support of the Draft Screening Assessment for Boric acid, its salts and its precursors. Available from: email@example.com
Environment Canada. 2014d. Supporting documentation: Releases and exposure characterization for the base metals and precious metals smelting and refining sector. Gatineau (QC): Environment Canada. Information in support of the Draft Screening Assessment for Boric acid, its salts and its precursors. Available from: firstname.lastname@example.org
Environment Canada. 2014e. Supporting documentation: Releases and exposure characterization for the coal mining sector. Gatineau (QC): Environment Canada. Information in support of the Draft Screening Assessment for Boric acid, its salts and its precursors. Available from: email@example.com
Environment Canada. 2014f. Supporting documentation: Releases and exposure characterization for the oil sands mining sector. Gatineau (QC): Environment Canada. Information in support of the Draft Screening Assessment for Boric acid, its salts and its precursors. Available from: firstname.lastname@example.org
Environment Canada. 2014g. Supporting documentation: Releases and exposure characterization for the pulp and paper sector. Gatineau (QC): Environment Canada. Information in support of the Draft Screening Assessment for Boric acid, its salts and its precursors. Available from: email@example.com
Environment Canada. 2014h. Supporting documentation: Ecological modelled exposure analysis of boron-containing substances. Gatineau (QC): Environment Canada. Information in support of the Draft Screening Assessment for Boric acid, its salts and its precursors. Available from: firstname.lastname@example.org
Environment Canada. 2014i. Supporting documentation: Summary Table of aquatic toxicity data. Gatineau (QC): Environment Canada. Information in support of the Draft Screening Assessment for Boric acid, its salts and its precursors. Available from: email@example.com
Environment Canada. 2014j. Supporting documentation: Summary Table of terrestrial toxicity data. Gatineau (QC): Environment Canada. . Information in support of the Draft Screening Assessment for Boric acid, its salts and its precursors. Available from: firstname.lastname@example.org
Environment Canada. 2014k. Unpublished terrestrial toxicity data submitted by Method Development and Applications Section, Environmental Technology Centre, Environment Canada.
Environment Canada. 2014l. Soil PEC calculation spreadsheet. Spreadsheet calculations to convert soil deposition rates to soil concentrations. Ecological Assessment Division.
Environment Canada. 2014m. Unpublished confidential reports submitted to Environment Canada under the Environmental Effects Monitoring (EEM) Program of the Metal Mining Effluent Regulations (MMER) and Pulp and Paper Effluent Regulations (PPER). Gatineau (QC): Environment Canada, Forestry Products and Fisheries Act Division.
Environment Canada. 2014n. Voluntary information obtained as part of the CMP 2 Grouping initiative, boron-containing substances grouping. Year 2014.
Environment Canada and Health Canada. 2014. Supporting documentation: Scoping Document for Boron-containing substances. Gatineau (QC): Environment Canada. Information in support of the Draft Screening Assessment for Boric acid, its salts and its precursors. Available from: email@example.com
Environment Canada and Health Canada. 2014. Supporting documentation: Scoping Document: Precursors of Boric acid. Gatineau (QC): Environment Canada. Information in support of the Draft Screening Assessment for Boric acid, its salts and its precursors. Available from firstname.lastname@example.org
Equilibrium Environmental Inc. 2012. Sulfate adsorption and desorption properties of Alberta soils and their relevance to transport properties and leaching / redistribution rates. Final report.
Eriksson J, Bergholm J, Kvist K. 1981. Injury to vegetation caused by industrial emissions of boron compounds. Silva Fenn 15 (4):459.
ESG International Inc. and Aquatera Environmental Consulting Ltd. 2003. Assessment of the biological test methods for terrestrial arthropods: further refinement of the Collembola test method using Onychiurus Folsomi. Prepared for Method Development and Applications Section, Environmental Technology Centre, Environment Canada.
Espinoza-Navarro O, Cortés S, Monreal J, Ferreccio C. 2010. Spermograms of healthy young subjects living in Arica, Chile. Rev Med Chile138(12):1510-1516 (full text available in Spanish). [Cited in ECHA 2014].
Etimine. 2014. Boron Usage, Glass and Glass Fibers [Internet]. Available from: http://www.etiproducts.com/boron-in-glass-and-glass-fibre-13s.htm
[EU] European Union. 2007a. Risk Assessment Report (EURAR). Disodium tetraborate, anhydrous boric acid, boric acid, crude natural. CAS No. 1330-43-4, 11113-50-1, 10043-35-3. Risk assessment. Substance Evaluation Report, Draft 19, October 2007. Austria.
[EU] European Union. 2007b. Risk Assessment Report (EURAR). Perboric acid, sodium salt, CAS No. 11138-47-9. Risk Assessment with Addendum 2007. Institute of Health and Consumer Protection (IHCP). Italy.
European Commission. 2008. Regulation (EC) No 1272/2008 of the European parliament and of the council of 16 December 2008 on classification, labelling and packaging of substances and mixtures, amending and repealing Directives 67/548/EEC and 1999/45/EC, and amending Regulation (EC) No 1907/2006.
European Commission. 2009. Boric acid, Product-type 8 (Wood preservative). Annex I, the Netherlands. Finalised in the Standing Committee on Biocidal Products at its meeting on 20 February 2009 in view of its inclusion in Annex I to Directive 98/8/EC.
Farr LE, Konikowski T. 1963. The renal clearance of sodium pentaborate in mice and men. Clin Chem 9:771-726.
Fernandez E, Sanchez E, Bonilla I, Mateo P, Ortega P. 1984. Effect of boron on the growth and cell composition of Chlorella pyrnoidosa. Phyton 44:125−131.
Ferrando AA, Green NR, Barnes KW, Woodward B. 1993. Microwave digestion preparation and ICP determination of boron in human plasma. Biol Trace Elem Res 37:17−25.
Fisher RS, Freimuth HC. 1958. Blood boron levels in human infants. J Invest Dermatol 30:85-86.
Fogg TR, Duce RA. 1985. Boron in the troposphere-distribution and fluxes. J Geophys Res 20:3781−3796.
Förster B, Becker L. 2009. Boric acid: Terrestrial plant seedling emergence test. According to ISO 11269-2 Soil Quality, Determination of the effects of pollutants on soil flora, Part 2: Effects of chemicals on the emergence and growth of higher plants (2005). ECT Oekotoxikologie GmbH, for Reach Consortium for Borates c/o Industrial Minerals Association - Europe (IMA-Europe), Brussels (BE).
Fort DJ. 2011. Amphibian reproduction study (Xenopus laevis). Testing laboratory: Fort Environmental Laboratories, Inc. (In-life testing), 515 South Duncan Street, Stillwater (OK) 74074; and ABC Laboratories Inc. (Analytical Chemistry), 7200 E. ABC Lane, Columbia (MO) 65202. Report no: RIOT01-00232. Owner company: RTM, 2500 W. Higgins Road, Suite 1000, Hoffman Estates (IL) 60169. Report date: 2011-02-21.
Fort DJ, Propst TL, Stover EL, Strong PL, Murray FJ. 1998. Adverse reproductive and developmental effects in Xenopusfrom insufficient boron. Biol Trace Elem Res 66(1-3):237−259.
Fort DJ, Rogers RL, McLaughlin DW, Sellers CM, Schlekat CL. 2002. Impact of boron deficiency on Xenopus laevis: a summary of biological effects and potential biochemical roles. Biol Trace Elem Res 90(1-3):117−142.
FracFocus. 2014. What chemicals are used. FracFocus Chemical Disclosure Registry [Internet]. Available from: http://fracfocus.org/chemical-use/what-chemicals-are-used
Frank RA, Roy JW, Bickerton G, Rowland ST, Headley JV, Scarlett AG, West CE, Peru KM, Parrott JL, Conly FM et al. 2014. Profiling oil sands mixtures from industrial developments and natural groundwaters for source identification. Enviro Sci Technol 48(5):2660−2670.
Frenette JL. 2007. An evaluation of benthic invertebrate communities as an indicator of stream ecosystem health below active coal mines in the Elk river watershed.
Garabrant DH, Bernstein L, Peters JM, Smith TJ. 1984. Respiratory and eye irritation from boron oxide and boric acid dusts. J Occup Med 26(8):584−586 [cited in ATSDR 2010].
Garabrant DH, Bernstein L, Peters JM, Smith T, Wright WE. 1985. Respiratory effects of borax dust. Brit J Ind Med 42:831−837 [cited in ATSDR 2010].
Gerke A. 2011a. Boric acid: chronic toxicity in whole sediment to freshwater midge, Chironomus riparius using spiked sediment. Testing laboratory: ABC Laboratories, Inc. Report no: Study No. 65474. Owner company: REACH Consortium for Borates. Report date: 2011-01-31.
Gerke A. 2011b. Boric acid: chronic toxicity in whole sediment to freshwater midge, Chironomus riparius using spiked water. Testing laboratory: ABC Laboratories, Inc. Report no: Study No. 65475. Owner company: REACH Consortium for Borates. Report date: 2011-01-31.
Gestring WD, Soltanpour PN. 1987. Comparison for soil tests for assessing boron toxicity to Alfalfa. Soil Sci Soc Am J 51:1214−1219.
Goldbach H. 1985. Influence of boron nutrition on net uptake and efflux of 32P and 14C-glucose in Helianthus annuus roots and cell cultures of Daucus carota. J Plant Physiol 118:431-438.
Goldberg S. 1997. Reactions of boron with soils. Plant Soil 193:35−48.
Goldbloom RB, Goldbloom A. 1953. Boric acid poisoning: report of four cases and a review of 109 cases from the world literature. J Pediatr 43:631−643 [cited in UK FSA 2002].
Goodarzi F. 2013. Characteristics and elemental composition of milled coals, bottom and fly ashes from power plants in Alberta and Nova Scotia. Unpublished reported prepared by FG and Partners Ltd., Calgary (AB) and submitted to Environment Canada, January 2013. 108 p.
GoodGuide Inc. 2014. GoodGuide [Internet] [cited 2014 Dec.]. Available from: http://www.goodguide.com/products?filter=borax
Gordon AS, Prichard JS, Freedman MH. 1973. Seizure disorders and anemia associated with chronic borax intoxication. Can Med Assoc J 108:719−721, 724.
Goulle JP, Mahieu L, Castermant J, Neveu N, Bonneau L, Laine G, Bouige D, Lacroix C. 2005. Metal and metalloid multi-elementary ICP-MS validation in whole blood, plasma, urine and hair reference values. Forensic Sci Int 153:39-44.
Government of Alberta. 2010. Alberta Biomonitoring Program. Chemicals in Serum of Children in Southern Alberta 2004-2006. Influence of Age Comparison to Pregnant Women [cited 2013 May 2]. Available from: http://www.health.alberta.ca/documents/Chemical-Biomonitoring-2010.pdf
Government of Canada. 2014. Science Funfest. Science.gc.ca [Internet] [cited 2014 Dec.]. Available from: http://www.science.gc.ca/default.asp?lang=en&n=03E9C1FB-1
Government of New Brunswick. 2005. Belledune Area Health Study, Appendix A - Human Health Risk Assessment. Department of Health and Wellness, Government of New Brunswick [cited 2014 July]. Available from: http://www2.gnb.ca/content/dam/gnb/Departments/h-s/pdf/en/Publications/BelleduneAppendixA.pdf
Green NR, Ferrando AA. 1994. Plasma Boron and the Effects of Boron Supplementation in Males. Environ Health Perspect 102(Suppl 7):73−77.
Grella P, Tambuscio B, Suma V. 1976. Boric acid and poisoning during pregnancy: Description of one case. Acta Anaesthesiol Italica 27:745−748 [in Italian] [cited in ECHA 2010].
[GSC] Geological Survey of Canada. 2002. Open file 4171: The deposition of trace elements on the land/surface soil in the Wabamun Lake area, Alberta, Canada. Ottawa (ON). 66 p. Available from: http://geopub.rncan.gc.ca/moreinfo_e.php?id=213042&_h=ca
Gu B, Lowe LE. 1990. Studies on the adsorption of boron on humic acids. Can J Soil Sci 70:305−311 [cited in Keren and Communar 2009].
Guhl W. 1992a. Laboratory river models and their relevance to the real environment. Presentation at Joint Meeting of SETAC-Europe, Potsdam (DEU), 22−24 June 1992 [cited in Dyer 2001].
Guhl W. 1992b. Okologischesspekte von bor. SOFW J 118(18/92):1159−1168 [cited in Dyer 2001].
Gupta UC. 1967. A simplified method for determining hot-water soluble boron in podzol soils. Soil Sci 103(6):424-428 [cited in Parks and Edwards 2005].
Gupta UC. 1993. Boron and its role in crop production. CRC Press Inc., ISBN 0-8493-6582-1.
Gupta UC. 2009. Effects of oil sands process-affected water and substrates on wood frog (Rana sylvatica) eggs and tadpoles. Thesis submitted to the College of Graduate Studies and Research, in partial fulfillment of the requirements for the degree of Master of Science in the Toxicology Graduate Program at the University of Saskatchewan, Saskatoon (SK), Canada.
Gupta UC, Jame YW, Campbell CA, Leyshon AJ, Nicholaichuk W. 1985. Boron toxicity and deficiency: A review. Can J Soil Sci 65(3):381-409.
Hall S, Lockwood R, Harrass MC. 2014. Application of a unique test design to determine the chronic toxicity of boron to the aquatic worm lumbriculus variegatus and fatmucket mussel lampsilis siliquoidea. Arch Environ Contam Toxicol 66:58.
Hamilton SJ, Buhl KJ. 1990. Acute toxicity of boron, molybdenum and selenium to fry of chinook salmon and coho salmon. Arch Environ Contam Toxicol 19:366.
Hamilton S, Wiedmeyer RH. 1990. Concentrations of boron, molybdenum and selenium in chinook salmon. T Am Fish Soc 119:500.
Hansveit R, Schoonmade JA, Akdemir A. 2001. The assessment of the effects of Boric Acid, manufacturing grade, on the nitrogen transformation activity of soil microorganisms (OECD 216 Guideline). Department of Environmental Toxicology. Schoemakerstraat 97. For Borax Europe Limited, UK.
Harari F, Roncob AM, Conchac G, Llanosb M, Grandéra G, Castrob F, Palma B, Nermella B, Vahtera M. 2012. Early-life exposure to lithium and boron from drinking water. Reprod Toxicol 34:552-560.
Hart RJ, Taylor HE, Antweiler RC, Graham DD, Fisk GG, Rigins SG. 2005. Sediment chemistry of the Colorado River Delta of Lake Powell, Utah. Open-file report 2005-1178. U.S. Department of the Interior, U.S. Geological Survey, Denver [cited in Kot 2009].
Hasbahceci M, Cipe G, Kadioglu H, Aysan E, Muslumanoglu M. 2013. Reverse relationship between blood boron level and body mass index in humans: does it matter for obesity? Biol Trace Elem Res 153:141-144.
Haviland Consumer Products, Inc. 2007. MSDS Document, Product ProTeam Supreme [cited 2014 Dec.]. Available from: http://www.proteampoolcare.com/images/uploads/SUPREME.pdf
Health Canada. 1990. Boron [Internet]. Ottawa (ON): Health Canada [cited 2015 Jan.]. Available from: http://www.hc-sc.gc.ca/ewh-semt/pubs/water-eau/boron-bore/index-eng.php
Health Canada. 1995. Investigating human exposure to contaminants in the environment: A handbook for exposure calculations.
Health Canada. 1998. Exposure factors for assessing total daily intake of priority substances by the general population of Canada. Unpublished report. Ottawa (ON): Health Canada, Environmental Health Directorate.
Health Canada. 2002. Project Report: Roll-up report for the determination of boric acid in toys. Product Safety Laboratory, Ottawa (ON): Health Canada. Project #2002-0699 [unpublished data].
Health Canada. 2004. Report of Analysis or Test. Product Safety Laboratory, Ottawa (ON): Health Canada. Date of Report 2004-05-18, Sample No. 1004553 [unpublished data].
Health Canada. 2007a. Multi-Vitamin/Mineral Supplement Monograph [Internet]. Ottawa (ON): Health Canada [cited 2014 April]. Available from: http://webprod.hc-sc.gc.ca/nhpid-bdipsn/atReq.do?atid=multi_vitmin_suppl
Health Canada. 2007b. Boron as a Medicinal Ingredient in Oral Natural Health Products [Internet]. Ottawa (ON): Natural Health Products Directorate, Health Canada [cited 2014 Nov.]. Available from: http://www.hc-sc.gc.ca/dhp-mps/pubs/natur/boron-bore-eng.php
Health Canada. 2009a. Categorization of substances on the Domestic Substances List [Internet]. Ottawa (ON): Health Canada [modified 2009 Sept.]. Available from: www.hc-sc.gc.ca/ewh-semt/contaminants/existsub/categor/index-eng.php
Health Canada. 2009b. Report of Analysis or Test. Product Safety Laboratory, Ottawa (ON): Health Canada. Date of Report 2009-04-30, Sample No. 1009120 [unpublished data].
Health Canada. 2009c. Report of Analysis or Test. Product Safety Laboratory, Ottawa (ON): Health Canada. Date of Report 2009-04-30, Sample No. 1009121 [unpublished data].
Health Canada. 2010. PMRA List of Formulants. Ottawa (ON): Pest Management Regulatory Agency, Health Canada. 31 August 2010.
Health Canada. 2012. Proposed Re-evaluation Decision. PRVD 2012-03. Boric Acid and its Salts (Boron). Ottawa (ON): Pest Management Regulatory Agency, Health Canada.16 October 2012.
Health Canada. 2013a. ICPMS data from Edmonton Indoor Air Quality Study (2010). Water and Air Quality Bureau, Health Canada (personal communication, unpublished data).
Health Canada. 2013b. ICPMS data from Calgary Spatial Study (2010, 2011). Water and Air Quality Bureau, Health Canada (personal communication, unpublished data).
Health Canada. 2013c. ICPMS data from Halifax Spatial Study (2010, 2011). Water and Air Quality Bureau, Health Canada (personal communication, unpublished data).
Health Canada. 2014a. The Cosmetic Ingredient Hotlist April 2014 [Internet]. Ottawa (ON): Consumer Product Safety Directorate, Health Canada [cited 2014 April]. Available from: http://www.hc-sc.gc.ca/cps-spc/cosmet-person/hot-list-critique/hotlist-liste-eng.php
Health Canada. 2014b. Multiple Ingredient Joint Health Products [Internet]. Ottawa (ON): Natural and Non-prescription Health Products Directorate, Health Canada. June 13, 2014 [cited 2014 Nov.]. Available from: http://webprod.hc-sc.gc.ca/nhpid-bdipsn/atReq.do?atid=multiple.joint.health
Heitland P, Köster HD. 2006. Biomonitoring of 37 trace elements in blood samples from inhabitants of northern Germany by ICP-MS. J Trace Elem Med Bio 20:253-262.
[HERA] Human and Environmental Risk Assessment. 2005. Human & Environmental Risk Assessment on Ingredients of Household Cleaning Products: Guidance document methodology. Available from: http://www.heraproject.com/files/HERA%20TGD%20February%202005.pdf
Hickey CW. 1989. Sensitivity of four New Zealand cladoceran species and Daphnia magna to aquatic toxicants. New Zeal J Mar Fresh 23:131-137.
Hitchon B, Levinson AA, Horn MK. 1977. Bromide, Iodide and Boron in Alberta formation waters. Edmonton (AB): Alberta Research Council.
Holden AA, Haque SE, Mayer KU, Ulrich AC. 2013. Biogeochemical processes controlling the mobility of major ions and trace metals in aquitard sediments beneath an oil sand tailing pond: Laboratory studies and reactive transport modeling. J Contam Hydrol 151:55.
Holleman AF, Wiberg E. 2001. Inorganic Chemistry. New York (NY): Academic Press [cited in Parks and Edwards 2005].
Hooftman RN, Van Drongelen-Sevenhuijsen D, de Haan HPM. 2000a. Toxicity test with boric acid, manufacturing grade and the midge larva Chironomus riparius using spiked sediment (Guideline: OECD draft document, May 1998). TNO report V99.1146, TNO Nutrition and Food Research Institute, Department of Environmental Toxicology, The Netherlands.
Hooftman RN, van Drongelen-Sevenhuijsen D, de Haan HPM. 2000b. Early life stage test under semi-static conditions with boric acid, manufacturing grade and the zebra fish Brachydanio rerio(OECD Guideline no. 210). The Netherlands: TNO Nutrition and Food Research Institute. TNO Report V99-168, Unpublished Report to Borax Europe, Ltd.
Hosseini SM, Maftoun M, Karimian N, Ronaghi A, Emam Y. 2007. Effect of zinc x boron interaction on plant growth and tissue nutrient concentration of corn. J Plant Nutr 30:773-781.
Howe PD. 1998. A review of boron effects in the environment. Bio Trace Elem Res 66:153.
[HPD] Household Products Database [database on the Internet]. 1993- . Bethesda (MD): National Library of Medicine (U.S.) [cited 2013 Nov.]. Available from: http://householdproducts.nlm.nih.gov/
Hu H, Brown PH. 1994. Localization of boron in cell walls of squash and tobacco and its association with pectin: evidence for a structural role of boron in the cell wall. Plant Physiol 105:681-689.
Hu H, Brown PH. 1997. Absorption of boron by plant roots. Plant Soil 193:49-58.
Huguier P, Manier N, Meline C, Bauda P, Pandard P. 2013. Improvement of the carnorhabditis elegans growth and reproduction test to assess the ecotoxicity of soils and complex matrices. Environ Toxicol Chem 32(9):2100.
Hunt C. 2006. Dietary boron: progress in establishing essential roles in human and animal physiology. In: Guyaguler T, Karakas S, Ozdemir Z, Karakas A, Bukulmez A, Sonmezer O, editors. Proc. 3rd Int. Boron Symposium, November 2-4, 2006, Ankara (Tur), p. 3-10.
Hunt CD, Friel JK, Johnson LK. 2004. Boron concentrations in milk from mothers of full-term and premature infants. Am J Clin Nutr 80:1327-33.
Hunt CD, Herbel JL, Nielsen FH. 1997. Metabolic responses of postmenopausal women to supplemental dietary boron and aluminum during usual and low magnesium intake: boron, calcium, and magnesium absorption and retention and blood mineral concentrations. Am J Clin Nutr 65:803-13.
[ICMM] International Council on Mining & Metals 2007a. Risk Characterization: General Aspects, Metals Environmental Risk Assessment Guidance (MERAG) Fact sheet 01. London, UK, 22 p
[ICMM] International Council on Mining & Metals. 2007b. Effects assessments: data compilation, selection and derivation of PNEC values for the risk assessment of different environmental compartments (water, STP, soil, sediment), Metals Environmental Risk Assessment Guidance (MERAG) Fact sheet 03. London (UK), 33 p.
[ICMM] International Council on Mining and Metals. 2007c, Exposure assessment, Metals Environmental Risk Assessment Guidance (MERAG), Factsheet no. 2. London (UK), 50 p.
Intrinsik Environmental Sciences Inc., Swansin Environmental Strategies Ltd., Delphinium Holdings Inc., Teck Metals Ltd. 2011. Terrestrial ecological risk assessment for the Teck Metals Ltd. Smelter at Trail, BC. Main report, revised May 2011. 162 p. Available from: http://www.teck.com/Generic.aspx?PAGE=Teck+Site%2fDiversified+Mining+Pages%2fZinc+Pages%2fTrail+Pages%2fEcological+Risk+Assessment&portalName=tc
[IOM] Institute of Medicine. 2001. U.S. Food and Nutrition Board. Dietary Reference Intakes: Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington (DC): Institute of Medicine.
[IPCS] International Programme on Chemical Safety. 1998. Environmental Health Criteria 204 Boron. United Nations Environment Programme, International Labour Organization, World Health Organization [Internet]. Available from: http://www.inchem.org/documents/ehc/ehc/ehc204.htm
Jacques Whitford AXYS. 2008. FINAL Metals in Soil Flin Flon. Project No. 1022002.01. In: Intrinsik Environmental Sciences Inc. 2010. Human health risk assessment of Flin Flon, Manitoba, and Creighton, Saskatchewan. Appendix B, Metals in Soil [accessed 2014 July]. Available from: http://flinflonsoilsstudy.com/wp-content/uploads/2013/07/AppxBMetalsinSoil.pdf
Jahiruddin M, Smart R, Wade AJ, Neal C, Cresser MS. 1998. Factors regulating the distribution of boron in water in the River Dee catchment in north east Scotland. Sci Total Environ 210/211:53-62.
Janik L, Forrester S, Kirby JK, McLaughlin MJ. 2010. Predicting metal partitioning in soils of the GEMAS sampling program using isotopic and infrared spectroscopic techniques. Solid-solution partitioning of boron in soils. Testing laboratory: CSIRO. Owner company: REACH Consortium for Borates. Report date 2010-04-30 [cited in Borax Europe 2012].
Jansen JA, Andersen J, Schou JS. 1984a. Boric acid single dose pharmacokinetics after intravenous administration to man. Arch Toxicol 55:64-67 [cited in US EPA 2002].
Jansen JA, Schou JS, Aggerback A. 1984b. Gastrointestinal absorption and in vitro release of boric acid from water emulsifying ointments. Food Chem Toxicol 22:49-53 [cited in US EPA 2002].
Jones G, Henderson V. 2006. Metal Concentrations in Soils and Produce from Gardens in Flin Flon, Manitoba, 2002. Report No. 2006-01, Manitoba Conservation.
Jones G, Phillips F. 2003. Metal Concentrations in Surface Soils of Thompson, Manitoba, September 2001. Manitoba Conservation Report No. 03-01.
[JOSM] Joint Canada-Alberta Implementation Plan for Oil Sands Monitoring. 2014. Canada-Alberta Oil Sands Environmental Monitoring Information Portal [Internet]. Available from: http://jointoilsandsmonitoring.ca/default.asp?lang=En&n=68413213-1
Kabata-Pendias A. 2011. Trace elements in soils and plants. 4th ed. Boca Raton (FL): CRC Press, c2011. 520 p.
[KEMI] Swedish Chemicals Agency. 2014. Hazardous chemicals in textiles - report of a government assignment. A Report from the Swedish Chemicals Agency. Report No 6/14. Stockholm (SWE) [accessed 2014 Nov.]. Available from: http://www.kemi.se/Documents/Publikationer/Trycksaker/Rapporter/Report6-14-Chemicals-in-textiles.pdf
Keren R, Bingham FT. 1985. Boron in water, soils and plants. Adv Soil Sci 1:230.
Keren R, Communar G. 2009. Boron sorption on wastewater dissolved organic matter: pH effect. Soil Sci Soc Am J 73(6):2021.
Klasing SA, Pilch SM. 1988. Agricultural drainage water contamination in the San Joaquin Valley: a public health perspective for selenium, boron and molybdenum [cited in Eisler 1990].
Kliegel W. 1980. Bor in biologie, medizin, und pharmazie. Springer-Verlag Berlin, Heidelberg, New York. ISBN 3-540-934 11-0. 900 p. [cited in Austria 2008a].
Korkmaz M, Yenigün M, Bakırdere S, Ataman OY, Keskin S, Müezzinoğlu T, Lekili M. 2011. Effects of chronic boron exposure on semen profile. Biol Trace Elem Res 143: 738-750.
Kot FS. 2009. Boron sources, speciation and its potential impact on health. Rev Environ Sci Biotechnol 8:3-28.
Kovacs T, Hewitt M, MacLatchy D, Martel P, McMaster M, Parrot J, Van Der Kraak G, Van Den Heuvel MR. 2007. Cycle 4 National Investigation of Cause Project, Final Report.
Ku WW, Chapin RE, Moseman RF, Brink RE, Pierce KD, Adams KY. 1991. Tissue disposition of boron in male Fischer rats. Toxicol Appl Pharmacol 111:145-151.
Ku WW, Chapin RE, Wine RN, Gladen BC. 1993a. Testicular toxicity of boric acid (BA): Relationship of dose to lesion development and recovery in the F344 rat. Reprod Toxicol 7: 305-319.
Ku WW, Shih LM, Chapin RE. 1993b. The effects of boric acid (BA) on testicular cells in culture. Reprod Toxicol 7(4):321-31.
Laposata MM, Dunson WA. 1998. Effects of boron and nitrate on hatching success of amphibian eggs. Arch Environ Contam Toxicol 35:615-619.
Lea D. 2000. Building a Greener New Jersey Conference, Cellulose Insulation Manufacturers Association, October 4, 2000 [Internet]. Available from: http://www.cellulose.org/HomeOwners/InsulationTechnicalDataResearch.php
LeVan SL, Tran HC. 1990. The role of boron in flame-retardant treatments. In: Hamel M, editor. First International Conference on Wood Protection with Diffusible Preservatives. Proceedings 47355, Nashville (TN), November 28-30, p 39-41.
Litovitz TL, Klein-Schwartz W, Oderda GM, Schmitz BF. 1988. Clinical manifestations of toxicity in a series of 784 boric acid ingestions. Am J Emerg Med 6:209-213 [cited in US EPA 2002].
Liu P, Wang C, Hu J, Xun L, Robbins WA, Wu G, Wei F. 2005a. Preliminary study on pregnancy outcome of spouses of boron workers. Chin J Public Health 21(5):567-8 [in Chinese].
Liu P, Hu W, Xun L, Robbins WA, Wu G, Wei F. 2005b. Preliminary study on sperm quality of boron-exposed workers. J Environ Health 22(2):90-92 [in Chinese].
Liu P, Hu W, Wei F, Xu J, Wu G, Xun L, Robbins WA. 2006a. Effect of boron exposure on human semen quality. Chin J Public Health 22(8):940-942 [in Chinese].
Liu P, Hu W, Xu J, Robbins WA, Xun L, Wu G, Wei F. 2006b. Influence of boron exposure on male semen quality. China Environ Sci 26(1):43-47 [in Chinese].
[LNHPD] Licensed Natural Health Products Database [database on the Internet]. 2014. Version 1.0. Ottawa (ON): Health Canada [cited 2014 May]. Available from: webprod3.hc-sc.gc.ca/lnhpd-bdpsnh/index-eng.jsp
MacGillivray PC, Fraser MS. 1953. Boric acid poisoning in infancy arising from the treatment of napkin rash. Arch Dis Child 28:484-489.
Maier KJ, Knight AW. 1991. The toxicity of waterborne boron to Daphnia magna and Chironomus decorus and the effects of water hardness and sulfate on boron toxicity. Arch Environ Contam Toxicol 20:282-287.
Majidi A, Rahnemaie R, Hassani A, Malakouti MJ. 2010. Adsorption and desorption processes of boron in calcareous soils. Chemosphere 80:733.
Mao X, Kim J, Tran H, Kochesfahani SH. 2006. Effect of chloride and potassium on borate autocausticizing reactions during black liquor combustion. Pulp & Paper Canada 107(10):33.
Marschner H. 1995. Mineral nutrition of higher plants. 2nd ed. London (UK): Academic Press. 889 p.
Martel P, Hewitt M, Kovacs T, MacLatchy D, McMaster M, O'Connor B, Parrott J, Van Den Heuvel MR, Van Der Kraak GV. 2010. Cycle 5 National Investigation of Cause project [Internet]. Available from: http://publications.gc.ca/site/eng/458431/publication.html
Martinez F, Mateo P, Bonilla I, Fernandez-Valiente E, Garate A. 1986. Growth of Anacystis nidulans in relation to boron supply. Israel J Bot 35:17-21.
[MDDEP] Ministère du Développement durable, de l'Environnement et des Parcs. 2001. Evaluation du potentiel toxique des effluents des stations d'epuration municipales du Quebec. Rapport final.
[MDDEP] Ministère du Développement durable, de l'Environnement et des Parcs. 2010a. Résultats de la caractérisation de 13 eaux usées non traitées, résultant de la fracturation hydraulique (Jan 2008 à juillet 2010).
[MDDEP] Ministère du Développement durable, de l'Environnement et des Parcs. 2010b. Évaluation des rejets usées des usines de pâtes et papier du Quebec en fonction du milieu récepteur.
MELP. 1996. Unpublished data on boron toxicity on Oncorhynchus kisutch, Hyalella azteca, Eohaustorius washingtonianus and Microtox. Ministry of Environment, Lands and Parks [cited in Moss and Nagpal 2003].
MELP. 1997. Unpublished data on boron toxicity on Selenastrum capricornutum and Strongylocentrus droebachiensis. Ministry of Environment, Lands and Parks [cited in Moss and Nagpal 2003].
Mengel K, Kirkby EA. 1982. Principles of plant nutrition. 3rd ed. Worblaufen-Bern (CHE): International Potash Institute.
Mertens J, Van Laer L, Salaets P, Smolders E. 2011. Phytotoxic doses of boron in contrasting soils depend on soil water content. Plant Soil 342:73-82.
Miller J. 2013. Inter-laboratory validation of Environment Canada's new test method for measuring soil toxicity using plants native to the Canadian boreal region. Miller Environmental Sciences Inc., prepared for Biological Assessment and Standardization Section, Science and Technology Branch, Environment Canada, Ottawa (ON).
Moser TH, Becker L. 2009a. Boric acid reproduction toxicity to the earthworm Eisenia fetida in artificial soil based on the OECD Guideline No 222 for the Testing of Chemicals, Earthworm Reproduction Test (Eisenia fetida/Eisenia andrei), adopted April 13, 2004; and the International Standard ISO 11268-2 Part 2 (1998): Soil quality - Effects of pollutants on earthworms (Eisenia fetida) - Part 2: Determination of effects on reproduction. ECT Oekotoxikologie GmbH, Germany. Prepared for the REACH Consortium for Borates c/o Industrial Minerals Association - Europe (IMA-Europe), Brussels (BEL).
Moser TH, Becker L. 2009b. Boric acid: Acute and reproduction toxicity to the nematode species Caenorhabditis elegans in LUFA 2.2 soil based on the International Standard ISO 10872 (2009), Water quality - Determination of the toxic effect of sediment and soil samples on growth, fertility and reproduction of Caenorhabditis elegans (Nematoda), ECT Oekotoxikologie GmbH, Germany. Prepared for the REACH Consortium for Borates c/o Industrial Minerals Association - Europe (IMA-Europe), Brussels (BEL).
Moser TH, Becker L. 2009c. Boric acid: Reproduction toxicity to the enchytraeid species Enchytraeus crypticus in artificial soil based on the OECD Guideline No 220 for the testing of chemicals, Enchytraeid Reproduction Test, ECT Oekotoxikologie GmbH, Germany. Prepared for the REACH Consortium for Borates c/o Industrial Minerals Association - Europe (IMA-Europe), Brussels (BEL).
Moser TH, Becker L. 2009d. Boric acid: Reproduction toxicity to the enchytraeid species Enchytraeus luxuriosus in artificial soil based on the OECD Guideline No. 220 for the testing of chemicals, Enchytraeid Reproduction Test, ECT Oekotoxikologie GmbH, Germany. Prepared for the REACH Consortium for Borates c/o Industrial Minerals Association - Europe (IMA-Europe), Brussels (BEL).
Moser TH, Becker L. 2009e. Boric acid: Acute toxicity to the carabid beetle Poecilus cupreus (Coleoptera, Carabidae) using an extended laboratory test (dose-response) in LUFA 2.1 soil based on the IOBC/WPRS 2000, ECT Oekotoxikologie GmbH, Germany. Prepared for the Reach Consortium for Borates c/o Industrial Minerals Association - Europe (IMA-Europe), Brussels (BEL).
Moser TH, Scheffczyk A. 2009. Boric acid: acute and reproduction toxicity to the predatory mite Hypoaspis(Geolaelaps) aculeiferCanestrini (Acari: Laelapidae) in artificial soil with 5% peat, based on the OECD Guideline No 226 for the testing of chemicals, Predatory mite Hypoaspis (Geolaps) aculeifer reproduction test in soil, adopted October 3, 2008, ECT Oekotoxikologie GmbH, Germany. Prepared for the Reach Consortium for Borates c/o Industrial Minerals Association - Europe (IMA-Europe), Brussels (BEL).
Moss SA, Nagpal NK. 2003. Ambient Water Quality Guidelines for Boron. Water Protection Section, Ministry of Water, Land and Air Protection, British Columbia. ISBN 0-7726-5048-9 [cited 2014 July]. Available from: http://www.env.gov.bc.ca/wat/wq/BCguidelines/boron/boron.pdf
Murray FJ, Schlekat CE. 2004. Comparison of risk assessments of boron: alternate approaches to chemical-specific adjustment factors. Hum Ecol Risk Assess 10:57-68 [cited in EFSA 2013].
Naghii MR, Mofid M, Asgari AR, Hedayati M, Daneshpour MS. 2011. Comparative effects of daily and weekly boron supplementation on plasma steroid hormones and proinflammatory cytokines. J Trace Elem Med Biol 25(1):54-8.
[NCASI] National Council for Air and Stream Improvement. 2006. Unpublished confidential report submitted to Environment Canada. Gatineau (QC): Environment Canada, Forestry Products and Fisheries Act Division.
[NHPID] Natural Health Products Ingredients Database [database on the Internet]. 2014. Ottawa (ON): Health Canada [cited 2014 May]. Available from: http://webprod.hc-sc.gc.ca/nhpid-bdipsn/search-rechercheReq.do
Ni Y, Somerville J, Van Heiningen ARP. 2001. Bleaching of recycled fibers by adding sodium borohydride to a peroxide reinforced oxygen stage. Tappi J 84(6).
Nielsen FS. 2009. Micronutrients in Parenteral Nutrition: Boron, Silicon, and Fluoride. Gastroenterology 137:S55-S60.
Nielsen GH. 1970. Percutaneous absorption of boric acid form boron-containing preparations in rats. Acta Pharmacol Tox 28:413-424.
Nielsen FH, Penland JG. 1999. Boron supplementation of peri-menopausal women affects boron metabolism and indices associated with macromineral metabolism, hormonal status and immune function. J Trace Elem Exp Med 12:251-261.
Nielsen FH, Hunt CD, Mullen L, Hunt JR. 1987. Effect of dietary boron on mineral, estrogen, and testosterone metabolism in postmenopausal women. FASEB J 1:394-7.
Nisus Corporation. 2010. Pool Proof Hexaborate Water Harmonizer. MSDS [cited 2014 Dec.]. Available from: http://nisuscorp.com/images/uploads/documents-specimen-labels/label_msds_poolproof.pdf
[NPI] National Pollutant Inventory. 1998. Emission Estimation Technique Manual for Glass and Glass Fibre Manufacturing. Australia: Queensland Department of Environment.
[NPRI] National Pollutant Release Inventory. 2014. Glossary of terms and expressions used by the NPRI. Gatineau (QC): Environment Canada [cited 2014 March]. Available from: http://www.ec.gc.ca/inrp-npri/default.asp?lang=en&n=9264E929-1#b
[NRC] National Research Council. 1981. Coal Mining and Ground-Water Resources in the United States. A report prepared by the Committee on the Groundwater Resources in relation to Coal Mining. Board on Mineral and Energy Resources, Commission on Natural Resources, National Research Council.
Ohlendorf HM. 2002. The birds of Kesterson Reservoir: a historical perspective. Aquat Toxicol 57:1-10.
[Ontario MOE] Ontario Ministry of the Environment. 2012. Record of Site Condition # 206387. Record of Site Condition, Under Part XV.1 of the Environmental Protection Act [Internet]. Available from: http://www.ontario.ca/environment-and-energy/records-site-condition
O'Sullivan K, Taylor M. 1983. Chronic boric acid poisoning in infants. Arch Dis Child 58:737-739 [cited in ATSDR 2010].
Ouellet JD, Dube MG, Niyogi S. 2013. Influence of elevated alkalinity and natural organic matter (NOM) on tissue-specific metal accumulation and reproductive performance in fathead minnows during chronic, multi-trophic exposures to a metal mine effluent. Ecotoxicol Environ Safe 95:104-112.
Owojori O, Healey J, Princz J, Siciliano S. 2011. Can avoidance behavior of the mite Oppia nitens be used as a rapid toxicity test for soils contaminated with metals or organic chemicals? Environ Toxicol Chem 30(11):2594-2601.
Pahl MV, Culver BD, Strong PL, Murray FJ, Vaziri ND. 2001. The effect of pregnancy on renal clearance of boron in humans: a study based on normal dietary intake of boron. Toxicol Sci 60(2):252-256.
Paliewicz CC., Sirbescu MLC., Sulatycky T., van Hees EH. 2015. Environmentally Hazardous Boron in Gold Mine Tailings, Timmins, Ontario, Canada, Mine Water Environ, 34, 162
Park H, Schlesinger WH. 2002. Global biogeochemical cycle of boron. Global Biogeochem Cy 16:1072-1082.
Parks JL, Edwards M. 2005. Boron in the environment. Environ Sci Technol 35:81-114.
[PBS] Public Broadcasting Service. 2014. PBS Parents, Crafts for Kids [Internet] [cited 2014 Dec.]. Available from: http://www.pbs.org/parents/crafts-for-kids/
Pellerin E, Macey K. 2001. Canadian PHED Tables version 7. Ottawa (ON): Pest Management Regulatory Agency, Health Canada. August 21, 2001 [unpublished report].
Penny D. 2004. The Micronutrient and Trace Element Status of Forty-Three Soil Quality Benchmark Sites in Alberta. Prepared for the AESA Soil Quality Monitoring Program, Alberta Agriculture, Food and Rural Development, Conservation and Development Branch, Edmonton (AB). 87 p. [cited 2014 July]. Available from: http://www1.agric.gov.ab.ca/$department/deptdocs.nsf/all/aesa8874
Pilbeam DJ, Kirkby EA. 1983. The physiological role of boron in plants. J Plant Nutr 6:563-582.
Pollet I, Bendell-Young LI. 2000. Amphibians as indicators of wetland quality in wetlands formed from oil sands effluent. Environ Toxicol Chem 19(10):2589.
Power PP, Woods WG. 1997. The chemistry of boron and its speciation in plants. Plant Soil 193:1-13.
Princz J, Scroggins R. 2003. Toxicological comparison of different soil test options - earthworm lethality, avoidance and reproduction. Poster.
Princz J, Behan-Pelletier VM, Scroggins RP, Siciliano SD. 2010. Oribatid mites in soil toxicity testing - the use of Oppia nitens (C.L. Koch) as a new test species. Environ Toxicol Chem 29(4):971-979.
Procter and Gamble. 1979. Unpublished data - Fathead minnow toxicity testing using boric acid [cited in Moss and Nagpal 2003].
Puttaswamy N, Turcotte D, Liber K. 2010. Variation in toxicity response of Ceriodaphnia dubia to Athabasca oil sands coke leachates. Chemosphere 80:489-497.
Rainey CJ, Nyquist LA, Coughlin JR, Downing RG. 2002. Dietary boron intake in the United States: CSFII 1994-1996. J Food Compos Anal 15:237-250.
[RAMP] Regional Aquatics Monitoring Program. 2013. 2012 Technical Report [Internet]. Available from: http://www.ramp-alberta.org/ramp/results/report.aspx
[RAMP] Regional Aquatics Monitoring Program. 2014. Monitoring Database. Searched for acid sensitive lakes, water quality and sediment quality data [cited 2014 March]. Available from: http://www.ramp-alberta.org/ramp/data.aspx
Rasmussen et al. 2013. Preliminary Data from the Windsor Exposure Assessment Study and the Canadian House Dust Study. Exposure and Biomonitoring Division, Health Canada [personal communication, unpublished data].
Redfield EB, Durnie SM, Zwiazek JJ. 2004. Effects of hypoxia on ion accumulation in wild raspberry (Rubus idaeus) exposed to water released from saline oil sands mine tailings. Environ Exp Bot 52(1):1-9.
Reimann C, de Caritat P. 1998. Chemical Elements in the Environment. Factsheet for the Geochemist and Environmental Scientist.
Renault S, Lait C, Zwiazek JJ, MacKinnon M. 1998. Effect of high salinity tailings waters produced from gypsum treatment of oil sands tailings on plants of the boreal forest. Environ Pollut 102:177-184.
Renault S, Croser C, Franklin JA, Zwiazek JJ, MacKinnon M. 2001. Effects of consolidated tailings water on red-osier dogwood (Cornus stolonifera Michx) seedlings. Environ Pollut 113:27-33.
Rio Tinto. 2015. Consumer Exposure Scenarios. Consumer Use of Modelling Clays [Internet]. 20 Mule Team Borax, Part of Rio Tinto [cited 2015 March 2]. Available from: http://www.borax.com/docs/consumer-exposure-scenarios/esc7--consumer-use-of-modelling-clays.pdf?sfvrsn=2
Rio Tinto Borax. 2005. Hazard Assessment of Borates. Update February 2005.
[RIVM] Rijksinstituut voor Volksgezondheid en Milieu [National Institute for Public Health and the Environment (NL)]. 2002. Children's Toys Fact Sheet: To assess the risks for the consumer. Report No: 612810012/2002.
[RIVM] Rijksinstituut voor Volksgezondheid en Milieu [National Institute for Public Health and the Environment (NL)]. 2006. Cleaning products fact sheet: To assess the risks for the consumer. Report No. 320104003/2006.
[RIVM] Rijksinstituut voor Volksgezondheid en Milieu [National Institute for Public Health and the Environment (NL)]. 2008. Chemicals in Toys. A general methodology for assessment of chemical safety of toys with a focus on elements. Updated version for ConsExpo 4 [Internet]. Bilthoven (NL): RIVM (National Institute for Public Health and the Environment). Report No.: 320003001/2008. Available from: http://www.rivm.nl/bibliotheek/rapporten/320003001.pdf
Robbins WA. 2008. Male reproductive effects from occupational exposure to boron: final progress report to NIOSH; 2008. Unpublished data [cited in Scialli et al. 2010].
Robbins WA, Wei F, Elashoff DA, Wu G, Xun L, Jia J. 2008. Y:X sperm ratio in boron exposed men. J Androl 29(1):115-121.
Robbins WA, Xun L, Jia J, Kennedy N, Elashoff DA, Ping L. 2010. Chronic boron exposure and human semen parameters. Reprod Toxicol 29:184-90.
Rodushkin I, Odman F, Branth S. 1999. Multielement analysis of whole blood by high resolution inductively coupled plasma mass spectrometry. Fresen J Anal Chem 364:338-346.
Rowe RI, Bouzan C, Nabili S, Eckhert CD. 1998. The response of trout and zebrafish embryos to low and high boron concentrations is U-Shaped. Biol Trace Elem Res 66:261-270.
Rowe RI, Eckhert CD. 1999. Boron is required for zebrafish embryogenesis. J Exp Biol 202:1649-1654.
RPA. 2008. Assessment of the risk to consumers from borates and the impact of potential restrictions on their marketing and use. Final report. Prepared for the European Commission Directorate General (DG) Enterprise and Industry.
Ruhl L, Vengosh A, Dwyer GS, Hsu-Kim H, Schwartz G, Romanski A, Smith SD. 2009. The impact of coal combustion residue effluent on water resources: A North Carolina example. Environ Sci Technol 46:12226-12233.
Ryan AL. 2005. Measurement of Low-level Metals in the Columbia River at Birchbank and Waneta, Environment Canada Pacific and Yukon Region.
Sah RN, Brown PH. 1997. Techniques for boron determination and their application to the analysis of plant and soil samples. Plant Soil 193:15-33.
Sakata M, Natsumi M, Tani Y. 2010. Isotopic evidence of boron in precipitation originating from coal burning in Asian continent. Geochem J 44:113-123.
Saiki MK, Jennings MR, Brumbaugh WG. 1993. Boron, molybdenum and selenium in aquatic food chains from the lower San Joaquin River and its tributaries, California. Arch Environ Contam Toxicol 24:307-319.
Sauve S, Hendershot W, Allen HE. 2000. Solid-solution partitioning of metals in contaminated soils: Dependence on pH, total metal burden, and organic matter. Environ Sci Technol 34:1125-1131.
Sayli BS. 1998. An assessment of fertility in boron-exposed Turkish subpopulations. 2. Evidence that boron has no effect on human reproduction. Biol Trace Elem Res 66:409-422.
Sayli BS. 2001. Assessment of fertility and infertility in boron-exposed Turkish subpopulation. 3. Evaluation of fertility among sibs and in “borate families.” Biol Trace Elem Res 81:255-267.
Sayli BS. 2003. Low frequency of infertility among workers in a borate processing facility. Biol Trace Elem Res 93:19-29.
Sayli BS, Tuccar E, Elhan AH. 1998. An assessment of fertility in boron-exposed Turkish subpopulations. Reprod Toxicol 12(3):297-304.
Sayli BS, Çöl M, Elhan AH, Genç Y. 2003. Assessment of fertility and infertility in boron-exposed Turkish subpopulations 6: relevant data from all centers. J Ankara Med School 25(4):165-174.
[SCCS] Scientific Committee on Consumer Safety. European Commission. 2010a. Opinion on boron compounds. Available from: http://ec.europa.eu/health/scientific_committees/consumer_safety/docs/sccs_o_027.pdf
[SCCS] Scientific Committee on Consumer Safety. European Commission. 2010b. Opinion on sodium perborate and perboric acid. Available from: http://ec.europa.eu/health/scientific_committees/consumer_safety/docs/sccs_o_031.pdf
Schets FM, Schijven JF, de Roda Husman AM. 2011. Exposure assessment for swimmers in bathing waters and swimming pools. Water Res 45:2392-2400.
Schon MK, Blevins DG. 1990. Foliar boron applications increase the final number of branches and pods on branches of field-grown soybeans. Plant Physiol 92:602-607.
Schou JS, Jansen JA, Aggerbeck B. 1984. Human pharmacokinetics and safety of boric acid. Arch Toxicol 7:232-235.
Schubert DM. 2003. Borates in industrial use. Structure and bonding, Vol. 105. Springer-Verlag Berlin Heidelberg.
Schubert DM, Brotherton RJ. 2006. Boron: Inorganic Chemistry. Encyclopedia of Inorganic and Bioinorganic Chemistry, John Wiley & Sons, Ltd.
Scialli AR, Bonde JP, Brüske-Hohlfeld I, Culver BD, Li Y, Sullivan FM. 2010. An overview of male reproductive studies of boron with an emphasis on studies of highly exposed Chinese workers. Reprod Toxicol 29(1):10-24.
Seierstad AJ, Adams VD, Lamarra VA, Hoefs NJ, Hinchee RE. 1983. The evaluation of metals and other substances released into coal mine accrual waters on the Wasatch Plateau Coal Field, Utah. Utah Water Research Laboratory, Utah State University, Logan (UT). Water Quality Series UWRL/Q-83/09.
Shacklette HT, Erdman JA, Harms TF. 1978. Trace elements in plant foodstuffs. In: Oehme FW, editor. Toxicity of Heavy Metals in the Environment, Part I. New York (NY): Marcel Dekker.
Singh M. 1971. Equilibrium adsorption of boron in soils and clays. Geoderma 5:209-217.
Smit CE, Moser Th, Rombke J. 2012. A new OECD test guideline for the predatory soil mite Hypoaspis aculeifer: Results of an international ring test. Ecotoxicol Environ Safe 82:56-62.
Solvay. 2002. Production of sodium perborate, medical surveillance date-respiratory effects. Unpublished data. Brussels (BEL): Solvay S.A. [cited in EURAR 2007b].
Soucek DJ, Dickinson A, Koch BT. 2011. Acute and chronic toxicity of boron to a variety of freshwater organisms. Environ Toxicol Chem 30(8):1906-1914.
[SSD Master] Determination of Hazardous Concentrations with Species Sensitivity Distributions [computer model]. 2010. Version 3. Ottawa (ON): Intrinsik Science.
Stantec. 2009. Metals in surface water, sediment, fish and blueberry samples collected near Flin Flon, Manitoba and Creighton, Saskatchewan. File No. 160960429, report prepared for Hudson Bay Mining and Smelting.
Stantec Consulting Ltd and Aquaterra Environmental Consulting. 2004. Developmental studies in support of Environment Canada's biological test methods for measuring soil toxicity using earthworms. Prepared for Method Development and Applications Section, Environmental Technology Centre, Environment Canada.
Statistics Canada. 2004. Canadian Community Health Survey - Nutrition (CCHS). Detailed information for 2004 (cycle 2.2). Ottawa (ON): Statistics Canada. Available from: http://www23.statcan.gc.ca/imdb/p2SV.pl?Function=getSurvey&SDDS=5049&lang=en&db=imdb&adm=8&dis=2
Stokinger HE. 1981. Boron. In: Clayton GD, Clayton FE, editors. Patty's Industrial Hygiene and Toxicology - Vol. 2B: Toxicology, 3rd ed. New York (NY): Wiley. p. 2978-3005 [cited in UK FSA 2002].
Stopford W. 2013. Boron in Art and Craft Materials. Durham (NC): Art and Creative Materials Institute [personal communication, unpublished data].
Struijs J, van de Meent D, Peijnenburg WJGM, van den Hoop MAGT, Crommentuijn T. 1997. Added risk approach to derive maximum permissible concentrations for heavy metals: How to take natural background levels into account. Ecotoxicol Environ Safe 37:112.
Stüttgen G, Siebel T, Aggerbeck B. 1982. Absorption of boric acid through human skin depending on the type of vehicle. Arch Dermatol Res 272:21-29 [cited in SCCS 2010a].
Suloway JJ, Roy WR, Skelly TM, Dickerson DR, Schuller RM, Griffin RA. 1983. Chemical and toxicological properties of coal fly ash. Champaign (IL): Illinois State Geological Survey (Publication NTIS PB84-116110).
Swan SH, Beaumont JJ, Hammond SK, VonBehren J, Green RS, Hallock MF, Woskle SR, Hines CJ, Schenker MB. 1995. Historical cohort study of spontaneous abortion among fabrication workers in the semiconductor health study: agent-level analysis. Am J Ind Med 28:751-769 [cited in US EPA 2004].
Swain LG, Walton DG, Phippen B, Lewis H, Brown S, Bamford G, Newsom D, Lundman I. 1998. Water quality assessment and objectives for the Fraser River from Hope to Sturgeon and Roberts Banks. First Update, Technical Appendix, Ministry of Environment, Lands and Parks, Province of British Columbia.
Tarasenko NY, Kasparov AA, Strongina OM. 1972. Effect of boric acid on the generative function in males. Gigiena Truda y Professionalnye Zabolevaniya 16(11):13-16 [cited in Austria 2008a human study; rat study was cited in ANSES 2012].
Taylor M. 1997. Letter to M. Dourson, TERA, Cincinnati (OH). August 28, 1997 [cited in US EPA 2002].
Temple PJ, Linzon SN. 1976. Boron as a phytotoxic air pollutant. JAPCA 26(5).
Temple PJ, Linzon SN, Smith ML. 1978. Fluorine and boron effects on vegetation in the vicinity of a fibreglass plant. Water Air Soil Poll 10:163-174.
Terrell ML, Hartnett KP, Marcus M. 2011. Can environmental or occupational hazards alter the sex ratio at birth? A systematic review. Emerging Health Threats 12:1-18.
The Dial Corporation. 2014. 20 Mule Team Borax [Internet] [cited 2014 Dec.]. Available from: http://www.20muleteamlaundry.com/
Thompson JAJ, Davis JC, Drew RE. 1976. Toxicity, uptake and survey studies of boron in the marine environment. Water Res 10:869-875.
Tran H, Mao X, Cameron J, Bair CM. 1999. Autocausticizing of smelt with sodium borates. Pulp & Paper Canada 100(9):35.
Treinen KA, Chapin RE. 1991. Development of testicular lesions in F344 rats after treatment with boric acid. Toxicol Appl Pharmacol 107:325-335.
Tsui PTP, McCart PJ. 1981. Chlorinated hydrocarbon residues and heavy metals in several fish species from the Cold Lake area in Alberta, Canada. Int J Environ Anal Chem 10:277-285.
Tsuru Y, Nomura M, Foulkes FR. 2002. Effects of boric acid on hydrogen evolution and internal stress in films deposited from a nickel sulfamate bath. J Appl Electrochem 32:629-634.
Tüccar E, Elhan AH, Yavuz Y, Şayli BS. 1998. Comparison of infertility rates in communities from boron-rich and boron-poor territories. Biol Trace Elem Res 66:401-407.
[UBC] University of British Columbia. 1996. Fraser River pulp mill effluents: Interpretation of Northwood effluent characterization data, Final Report, DOE FRAP 1997-10. Prepared for Fraser Pollution Abatement Office, Environment Canada.
[UK FSA] Food Standards Agency of UK. 2002. Expert Group on Vitamins and Minerals. Available from: www.food.gov.uk/multimedia/webpage/vitandmin/CachedSimilar
Ury HK. 1966. Interim Report on the 1963 Respiratory Disease Survey at Boron, CA. Air Pollution Medical Studies Unit, Bureau of Chronic Diseases, California State Dept. of Public Health [cited in US EPA 2002].
US Borax. 2000. UCI boric acid clearance study reports and associated data: rat and human studies. April 4, 2000 [cited in US EPA 2002].
[US EPA] United States Environmental Protection Agency. 1994. Technical Resource Document, Extraction and beneficiation of ores and minerals, Volume 2, Gold, EPA 530-R-94-013, NTIS PB94-170-305, U.S. Environmental Protection Agency, Office of Solid Waste, Special Waste Branch
[US EPA] United States Environmental Protection Agency. 1995. AP-42, 5th Edition, Volume 11, Mineral Products Industry, Chapter 11.15 Glass Fiber Manufacturing [Internet]. Available from: http://www.epa.gov/ttnchie1/ap42/
[US EPA] United States Environmental Protection Agency. 2002. Toxicological review of boron and compounds (CAS No. 7440-42-8). In Support of Summary Information on Integrated Risk Information (IRIS). Washington (DC): National Center for Environmental Assessment. Available from: http://www.epa.gov/iris
[US EPA] United States Environmental Protection Agency. 2003. User's Manual Swimmer Exposure Assessment Model (SWIMODEL) Version 3.0. Washington (DC): Office of Pesticides Programs, Antimicrobials Division. Available from: http://www.epa.gov/oppad001/swimodelusersguide.pdf
[US EPA] United States Environmental Protection Agency. 2004. Toxicological review of boron and compounds (CAS No. 7440-42-8). In Support of Summary Information on Integrated Risk Information (IRIS). Washington (DC): National Center for Environmental Assessment. Available from: http://www.epa.gov/iris
[US EPA] United States Environmental Protection Agency. 2010. Final report on acute and chronic toxicity of nitrate, nitrite, boron, manganese, fluoride, chloride and sulfate to several aquatic animal species. EPA 905-5-10-002.
[US EPA] United States Environmental Protection Agency. 2011. Exposure Factors Handbook: 2011 Edition. EPA/600/R-090/052F. Washington (DC): Office of Research and Development, National Center for Environmental Assessment.
[US EPA] United States Environmental Protection Agency. 2012a. Study of the potential impacts of hydraulic fracturing on drinking water resources. Progress Report. Washington (DC): Office of Research and Development, National Center for Environmental Assessment.
[US EPA] United States Environmental Protection Agency. 2012b. Standard Operating Procedures for Residential Pesticide Exposure Assessment. Washington (DC): Health Effects Division, Office of Pesticide Programs, Office of Chemical Safety and Pollution Prevention. Available from: http://www.epa.gov/pesticides/science/USEPA-OPP-HED_Residential%20SOPs_Oct2012.pdf
[USGS] United States Geological Survey. 1984. Element concentrations in soils and other surficial materials of the conterminous United States. Alexandria (VA): U.S. Geological Survey. Geological Survey Professional Paper 1270 [cited 2014 July]. Available from: http://pubs.usgs.gov/pp/1270/pdf/PP1270_508.pdf
[USGS] United States Geological Survey. 2015. Mineral Commodity Summaries. U.S. Geological Survey, U.S. Department of the Interior [Internet]. Available from: http://minerals.usgs.gov/minerals/pubs/mcs/2015/mcs2015.pdf
Usuda K, Kono K, Yoshida Y. 1997. Serum boron concentration from inhabitants of an urban area in Japan: Reference value and interval for the health screening of boron exposure. Biol Trace Elem Res 56:167-178.
Usuda K, Kono K, Orita Y, Dote T, Iguchi K, Nishiura H, Tominaga M, Tagawa T, Goto E, Shirai Y. 1998. Serum and urinary boron levels in rats after single administration of sodium tetraborate. Arch Toxicol 72:468-474.
Van Den Heuvel MR, Power M, MacKinnon MD, Van Meer T, Dobson EP, Dixon DG. 1999. Effects of oil sands related aquatic reclamation on yellow perch (Perca flavescens). I. Water quality characteristics and yellow perch physiological and population responses. Can J Fish Aquat Sci 56:1213-1225.
Vanderpool RA, Hof D, Johnson PE. 1994. Use of inductively coupled plasma-mass spectrometry in boron-10 stable isotope experiments with plants, rats, and humans. Environ Health Perspect 102(Suppl 7):13-20.
Van Limpt JAC. 2007. Modeling of evaporation processes in glass melting furnaces, ISBN: 978-90-386-1147-1
Vanhoe H, Dams R, Vandecasteele C, Versieck J. 1993. Determination of boron in human serum by inductively coupled plasma mass spectrometry after a simple dilution of the sample. Anal Chim Acta 281:401-411.
Vaziri ND, Oveisi F, Culver BD, Pahl MV, Anderson ME, Strong PL, Murray FJ. 2001. The effect of pregnancy on renal clearance of boron in rats given boric acid orally. Toxicol Sci 60:257-263.
Wallace JMW, Hannon−Fletcher MPA, Robson PJ, Gilmore WS, Hubbard SA, Strain JJ. 2002. Boron supplementation and activated factor VII in healthy men. Eur J Clin Nutr 56(11):1102-7.
Wallenberger FT. 2010. Chapter 1, Commercial and Experimental Glass Fibers. In: Wallenberger FT, Bingham PA (editors). Fiberglass and Glass Technology. Energy-friendly Compositions and Applications. DOI 10.1007/978-1-4419-0736-3_1, Springer Science + Business Media, LLC 2010.
Wang W. 1986. Toxicity tests of aquatic pollutants by using common duckweed. Environ Pollut (Series B) 11:1-14.
Wasshausen J, Rangamannar G, Amyotte R, Cordy B. 2006. “Premix”: A novel process for improved bleaching of mechanical pulps using a mixture of reductive agents. Pulp & Paper Canada 107:3.
Wegman DH, Eisen EA, Smith RG. 1991. Acute and chronic respiratory effects of sodium borate particulate exposures. Unpublished report to U.S. Borax Research Corporation [cited in Austria 2008b].
Wegman DH, Eisen EA, Hu X, Woskie SR, Smith RG, Garabrant DH. 1994. Acute and chronic respiratory effects of sodium borate particulate exposures. Environ Health Perspect 102(Suppl 7):119-128.
Wester RC, Hui X, Hartway T, Maibach HI, Bell K, Schell MJ, Northington DJ, Strong P, Culver BD. 1998a. In vivo percutaneous absorption of boric acid, borax and disodium octaborate tetrahydrate in humans compared to in vitro absorption in human skin from infinite to finite doses. Toxicol Sci 45:42-51.
Wester RC, Hartway T, Maibach HI, Schell MJ, Northington DJ, Culver BD, Strong P. 1998b. In vitro percutaneous absorption of boric acid, borax and disodium octaborate tetrahydrate in human skin. A summary. Biol Trace Elem Res 66:111-120.
[WHO] World Health Organization. 1998. Environmental Health Criteria 204. Boron. Geneva (CHE): World Health Organization, International Programme on Chemical Safety. Available from: http://www.inchem.org/documents/ehc/ehc/ehc204.htm
[WHO] World Health Organization. 1999. Laboratory Manual for the examination of human semen and spermcervical mucus interaction. 4th ed. Cambridge (UK): Cambridge University Press.
[WHO] World Health Organization. 2003. Boron in Drinking-water: Background document for the development of WHO Guidelines for Drinking-water Quality. Guidelines for drinking-water quality (WHO/SDE/WSH/03.04/54).
[WHO] World Health Organization. 2009. Boron in Drinking-water: Background document for the development of WHO Guidelines for Drinking-water Quality. Guidelines for drinking-water quality (WHO/HSE/WSH/09.01/2). Available from: http://whqlibdoc.who.int/hq/2009/WHO_HSE_WSH_09.01_2_eng.pdf?ua=1
Whorton D, Haas J, Trent L. 1992. Reproductive effects of inorganic borates on male employees: birth rate assessment report. Prepared for United States Borax & Chemical Corporation. Document No. 6966001 [cited in US EPA 2002].
Whorton MD, Haas J, Trent L. 1994a. Reproductive effects of inorganic borates on male employees: birth rate assessment. Environ Health Perspect 102(Suppl 7):129-131 [cited in US EPA 2002].
Whorton MD, Haas JL, Trent L, Wong O. 1994b. Reproductive effects of sodium borates on male employees: birth rate assessment. Occup Environ Med 51:761-767.
Wiley HW. 1904. Influence of food preservatives and artificial colours on digestion and health, I-Boric acid and borax. U.S. Department of Agriculture, Bureau of Chemistry, Bulletin 84, Part I, 1-477, Washington (DC) [cited in ECETOC 1995].
Williams JH. 1999. Regulations on additions of sludge-borne metals to soil and their adaptation to local conditions. In: L'Hermite P, editor. Treatment and use of sewage sludge and liquid agricultural wastes. London (UK): Elsevier Applied Science. p. 243-250.
Williams LB, Wieser ME, Fennell J, Hutcheon I, Hervig RL. 2001. Application of boron isotopes to the understanding of fluid-rock interactions in a hydrothermally stimulated oil reservoir in the Alberta Basin, Canada. Geofluids 1:229-240.
Wilson R, Jones-Otazo H, Petrovic S, Bitchell I, Bonvalot Y, Williams D, Richardson MG. 2013. Revisiting dust and soil ingestion rates based on hand-to-mouth transfer. Hum Ecol Risk Assess 19(1):158-188.
Wong LC, Heimbach MD, Truscott DR, Duncan BD. 1964. Boric acid poisoning: Report of 11 cases. Can Med Assoc J 90:1018-1023 [cited in ATSDR 2010].
Woods WG. 1994. An introduction to boron: history, sources, users and chemistry. Environ Health Perspect 102(Suppl 7):5-11.
Xing X, Wu G, Wei F, Liu P, Wei H, Wang C, Xu J, Xun L, Jia J, Kennedy N et al. 2008. Biomarkers of environmental and workplace boron exposure. J Occup Environ Hyg 5:141−147.
Yazbeck C, Kloppmann W, Cottier R, Sahuquillo J, Debotte G, Huel G. 2005. Health impact evaluation of boron in drinking water: a geographical risk assessment in Northern France. Environ Geochem Hlth 27:419−427.
York M, Griffiths HA, Whittle E, Basketter DA. 1996. Evaluation of a human patch test for the identification and classification of skin irritation potential. Contact Dermatitis 34:204−212 [cited in EURAR 2007b].
Young EG, Smith RP, MacIntosh OC. 1949. Boric acid as a poison report of six accidental deaths in infants. Can Med Assoc J 5:447−450. DACO: 5.12 [cited in Health Canada 2012a].
Ysart G, Millar P, Crews H, Robb P, Baxter M, de L'Argy C, Lofthouse S, Sargent C, Harrison N. 1999. Dietary exposure estimates of 30 elements from the UK Total Diet Study. Food Addit Contam 16(9):391−403.
Zhao ZQ, Liu CQ. 2010. Anthropogenic inputs of boron into urban atmosphere: Evidence from boron isotopes of precipitations in Guiyang City, China. Atmos Environ 44:4165−4171.
Appendix A: Lists of Boron-containing Substances that are Precursors or Non-precursors of Boric Acid
Fourteen substances were identified as priorities for further action during categorization. Given that the screening assessment focuses on a common moiety of concern (boric acid), all boron-containing substances on the Domestic Substances List (DSL) (and associated hydrated forms that do not appear on the DSL), other than polymers, were subsequently evaluated for their potential to be precursors of boric acid (Environment Canada and Health Canada 2014). Substances determined to be precursors are listed in Table A-1, and those found to be non-precursors are listed in Table A-2. Additional substances were identified as potential contributors to boric acid in the environment (e.g., hydrated forms of substances on the DSL, which are not listed on the DSL because they are considered mixtures; boron-containing substances on other Canadian inventories; or other substances in commerce in Canada that may be boric acid precursors) and are included in the lists below and further discussed in Environment Canada and Health Canada (2014). Most of these additional substances of interest are captured within Harmonized System (HS) codes for which import data were requested of the Canada Border Services Agency (CBSA).
|CAS RN||Chemical name||Chemical class||Inventory|
|10043-35-3Footnote Table A-1a||Boric acid (H3BO3)||Boric acids||DSL|
|11113-50-1||Boric acid (crude natural)||Boric acids||DSL|
|13460-50-9||Boric acid (HBO2)||Boric acids||DSL|
|13460-51-0||Metaboric acid||Boric acids||ICL|
|1303-86-2||Boron oxide (B2O3)||Boric acids||DSL|
|11138-47-9||Perboric acid, sodium salt||Borates||DSL|
|10332-33-9||Perboric acid (HBO(O2)), sodium salt monohydrate||Borates||DSL|
|10486-00-7||Perboric acid (HBO(O2)), sodium salt tetrahydrate||Borates||ICL (hydrate)|
|7632-04-04a||Perboric acid (HBO(O2)), sodium salt||Borates||DSL|
|13840-56-7||Boric acid (H3BO3), sodium salt||Borates||DSL|
|1333-73-9||Boric acid, sodium salt||Borates||DSL|
|13453-69-5a||Boric acid (HBO2), lithium salt||Borates||DSL|
|20786-60-1||Boric acid (H3BO3), potassium salt||Borates||DSL|
|7775-19-1||Boric acid (HBO2), sodium salt||Borates||DSL|
|16800-11-6||Sodium metaborate dihydrate (Na2B2O4.4H2O)||Borates||DSL (hydrate)|
|10555-76-7||Sodium metaborate tetrahydrate (Na2B2O4.8H2O)||Borates||DSL (hydrate)|
|13701-64-9||Boric acid (HBO2), calcium salt||Borates||DSL|
|13709-94-9||Boric acid (HBO2), potassium salt||Borates||DSL|
|13701-59-2||Boric acid (HBO2), barium salt||Borates||DSL|
|22694-75-3||Boric acid (H3BO3), triammonium salt||Borates||ICL|
|11128-98-6||Boric acid, ammonium salt||Borates||ICL|
|27522-09-4||Boric acid (H3BO3), ammonium salt||Borates||ICL|
|1330-43-4a||Boron sodium oxide (B4Na2O7)||Borates||DSL|
|12267-73-1||Boron sodium oxide (B4Na2O7), hydrate (1:?)||Borates||DSL (hydrate)|
|12045-88-4||Sodium tetraborate pentahydrate (borax pentahydrate)||Borates||DSL (hydrate)|
|12179-04-3||Sodium tetraborate pentahydrate||Borates||DSL (hydrate)|
|12767-90-7a||Boron zinc oxide (B6Zn2O11)||Borates||DSL|
|1332-07-6a||Boric acid, zinc salt||Borates||DSL|
|12447-61-9||Boron zinc oxide (B6Zn2O11) hydrate (2:15)||Borates||DSL (hydrate)|
|12280-01-2||Zinc triborate monohydrate||Borates||DSL (hydrate)|
|138265-88-0||Boron zinc hydroxide oxide (B12Zn4(OH)14O15)||Borates||DSL (hydrate)|
|149749-62-2||Zinc borate (4ZnO.B2O3.H2O)||Borates||DSL (hydrate)|
|10192-46-8||Boric acid (H3BO3), zinc salt (2:3)||Borates||ICL|
|12007-60-2a||Boron lithium oxide (B4Li2O7)||Borates||DSL|
|12007-89-5a||Ammonium boron oxide ((NH4)B5O8)||Borates||DSL|
|12046-04-7||Borate(5-), bis[m-oxotetraoxodiborato (4-)]-, ammonium tetrahydrogen, dihydrate, (T-4)-||Borates||DSL (hydrate)|
|12229-12-8||Ammonium pentaborate tetrahydrate||Borates||DSL (hydrate)|
|12271-95-3a||Boron silver oxide (B4Ag2O7)||Borates||DSL|
|12008-41-2||Boron sodium oxide (B8Na2O13)||Borates||DSL|
|12280-03-4||Boron sodium oxide (B8Na2O13), tetrahydrate||Borates||DSL (hydrate)|
|1332-77-0||Boron potassium oxide (B4K2O7)||Borates||DSL|
|12045-78-2||Boron potassium oxide (B4K2O7), tetrahydrate||Borates||DSL (hydrate)|
|11128-29-3||Boron potassium oxide (B5KO8)||Borates||DSL|
|12229-13-9||Boron potassium oxide (B5KO8), tetrahydrate||Borates||DSL (hydrate)|
|1318-33-8||Colemanite (CaH(BO2)3.2H2O)||Borates||Substance of commercial importance|
|12291-65-5||Colemanite (CaH(BO2)3.2H2O)||Borates||Substance of commercial importance|
|1319-33-1||Ulexite (CaNaH12(BO3)5.2H2O)||Borates||Substance of commercial importance|
|68457-13-6a||Cobalt, borate neodecanoate complexes||Borates||DSL|
|68442-99-9||Manganese, borate neodecanoate complexes||Borates||DSL|
|102-24-9||Boroxin, trimethoxy-||Borate esters||DSL|
|102-98-7||Mercurate(2-), [orthoborato(3-)-.κ.O]phenyl-, hydrogen (1:2)||Borate esters||ICL|
|121-43-7||Boric acid (H3BO3), trimethyl ester||Borate esters||DSL|
|150-46-9||Boric acid (H3BO3), triethyl ester||Borate esters||DSL|
|2467-16-5||Boric acid (H3BO3), tricyclohexyl ester||Borate esters||DSL|
|2665-13-6||1,3,2-Dioxaborinane, 2,2'-[(1-methyl-1,3-propanediyl)bis(oxy)]bis[4-methyl-||Borate esters||DSL|
|5743-34-0||D-Gluconic acid, cyclic 4,5-ester with boric acid (H3BO3), calcium salt (2:1)||Borate esters||DSL|
|6273-99-0||Mercury, [.μ.-[orthoborato(2-)-.κ.O:.κ.O']]diphenyldi-||Borate esters||ICL|
|7091-41-0||2,4,8,10-Tetraoxa-3,9-diboraspiro[5.5]undecane, 3,9-bis(4-methylphenyl)-||Borate esters||DSL|
|14697-50-8||1,3,2-Dioxaborinane, 2,2'-oxybis[4,4,6-trimethyl-||Borate esters||DSL|
|51136-86-8||Hexanoic acid, 2-ethyl-, trianhydride with boric acid (H3BO3)||Borate esters||DSL|
|67859-60-3||Boroxin, tris[(2-ethylhexyl)oxy]-||Borate esters||DSL|
|68130-12-1||Boric acid, 2-aminoethyl ester||Borate esters||ICL|
|68298-96-4||Ethanol, 2,2’-iminobis-, monoester with boric acid||Borate esters||DSL|
|89325-22-4||9-Octadecenoic acid (Z)-, (2-hydroxy-1,3,2-dioxaborolan-4-yl)methyl ester||Borate esters||DSL|
|71889-05-9||Benzenemethanol, 4-amino-α-(4-amino-3,5-dimethylphenyl)-α-(2,6-dichlorophenyl)-3,5-dimethyl-, monoester with boric acid (H3BO3)||Borate esters||DSL|
|10377-81-8||Ethanol, 2-amino-, monoester with boric acid||Borate esters (monoalkanolamine borate)||DSL|
|26038-87-9||Boric acid (H3BO3), compd. with 2-aminoethanol||Borate esters (monoalkanolamine borate)||DSL|
|26038-90-4||Boric acid (H3BO3), compd. with 1-amino-2-propanol||Borate esters (monoalkanolamine borate)||DSL|
|68003-13-4||Boric acid (H3BO3), compd. with 1-amino-2-propanol (1:1)||Borate esters (monoalkanolamine borate)||ICL|
|68586-07-2||Boric acid (H3BO3), compd. with 2-aminoethanol (1:1)||Borate esters (monoalkanolamine borate)||DSL|
|68797-44-4||Boric acid (H3BO3), compd. with 2-aminoethanol (1:3)||Borate esters (monoalkanolamine borate)||DSL|
|93964-50-2||Boric acid (H3BO3), compd. with 2-amino-2-methyl-1-propanol||Borate esters (monoalkanolamine borate)||DSL|
|10049-36-2||Boric acid (H3BO3), compd. with 2,2’,2’’-nitrilotris[ethanol]||Borate esters (trialkanolamine borate)||DSL|
|10220-75-4||Boric acid (H3BO3), compd. with 2,2’,2’’-nitrilotris[ethanol] (1:1)||Borate esters (trialkanolamine borate)||DSL|
|64612-24-4||Boric acid (H3BO3), compd. with 2,2’-iminobis[ethanol] (1:1)||Borate esters (dialkanolamine polyborate)||DSL|
|67952-33-4||Boric acid (H3BO3), compd. with 2,2’-iminobis[ethanol]||Borate esters (dialkanolamine polyborate)||DSL|
|68425-66-1||Boric acid, compd. with 2,2’-iminobis[ethanol]||Borate esters (dialkanolamine polyborate)||DSL|
|68954-07-4||Boric acid, reaction products with diethanolamine||Borate esters (dialkanolamine polyborate)||DSL|
|68512-53-8||Boric acid (H3BO3), reaction products with ethanolamine and triethanolamine||Borate esters (monoalkanolamine / trialkanolamine polyborate)||DSL|
|75-23-0||Boron, (ethanamine)trifluoro-, (T-4)-||Boron halides||DSL|
|109-63-7||Boron, trifluoro[1,1’-oxybis[ethane]]-, (T-4)-||Boron halides||DSL|
|368-39-8||Oxonium, triethyl-, tetrafluoroborate(1-)||Boron halides||DSL|
|456-27-9||Benzenediazonium, 4-nitro-, tetrafluoroborate(1-)||Boron halides||DSL|
|592-39-2||Boron, trifluoro(piperidine)-, (T-4)-||Boron halides||DSL|
|2145-24-6||Benzenediazonium, 4-sulfo-, tetrafluoroborate(1-)||Boron halides||DSL|
|7445-38-7||Boron, trifluoro[N-(phenylmethyl) benzenemethanamine]-, (T-4)-||Boron halides||DSL|
|7637-07-2||Borane, trifluoro-||Boron halides||DSL|
|10294-33-4||Borane, tribromo-||Boron halides||DSL|
|10294-34-5||Borane, trichloro-||Boron halides||DSL|
|13755-29-8||Borate(1-), tetrafluoro-, sodium||Boron halides||DSL|
|13814-96-5a||Borate(1-), tetrafluoro-, lead(2++) (2:1)||Boron halides||DSL|
|13814-97-6||Borate(1-), tetrafluoro-, tin(2++) (2:1)||Boron halides||DSL|
|13826-83-0a||Borate(1-), tetrafluoro-, ammonium||Boron halides||DSL|
|14075-53-7||Borate(1-), tetrafluoro-, potassium||Boron halides||DSL|
|14486-19-2a||Borate(1-), tetrafluoro-, cadmium (2:1)||Boron halides||DSL|
|16872-11-0||Borate(1-), tetrafluoro-, hydrogen||Boron halides||DSL|
|16903-52-9||Borate(1-), trifluorohydroxy-, hydrogen, (T-4)-||Boron halides||DSL|
|34762-90-8||Boron, trichloro(N,N-dimethyl-1-octanamine)-, (T-4)-||Boron halides||DSL|
|36936-37-5||Benzeneethanaminium, 4-[[4-[ethyl[2-hydroxy-3-(trimethylammonio)propyl]amino]-2-methylphenyl]azo]-N,N,N-trimethyl-β-oxo-, bis[tetrafluoroborate(1-)]||Boron halides||DSL|
|72140-65-9||Sulfonium, (2-cyano-1-methylethyl)dodecylethyl-, tetrafluoroborate(1-)||Boron halides||DSL|
|74-94-2||Boron, trihydro(N-methylmethanamine)-, (T-4)-||Boranes||DSL|
|7337-45-3||Boron, trihydro(2-methyl-2-propanamine)-, (T-4)-||Boranes||DSL|
|12386-10-6||Methanaminium, N,N,N-trimethyl-, octahydrotriborate(1-)||Boranes||DSL|
|16940-66-2||Borate(1-), tetrahydro-, sodium||Boranes||DSL|
|98-80-6||Boronic acid, phenyl-||Organoboron compounds||DSL|
|143-66-8||Borate(1-), tetraphenyl, sodium||Organoboron compounds||DSL|
|3262-89-3||Boroxin, triphenyl||Organoboron compounds||DSL|
|13331-27-6||Boronic acid, (3-nitrophenyl)-||Organoboron compounds||DSL|
|66472-86-4||Boronic acid, (3-aminophenyl)-, sulfate (2:1)||Organoboron compounds||DSL|
|39405-47-5||Dextrin, reaction products with boric acid||UVCBs||DSL|
|58450-10-5||D-gluco-Heptonic acid, (2ξ)-, ester with boric acid (H3BO3), sodium salt||UVCBs||DSL|
|68411-21-2||Boric acid (HB5O8), sodium salt, reaction products with propylene glycol||UVCBs||DSL|
|68411-22-3||Phosphoric acid, reaction products with aluminum hydroxide and boric acid (H3BO3)||UVCBs||DSL|
|68610-78-6||Acetic acid, anhydride, reaction products with boron trifluoride and 1,5,9-trimethyl-1,5,9-cyclododecatriene||UVCBs||DSL|
|68855-38-9||Formic acid, reaction products with boron trifluoride and [1S-(1α,3aβ,4α,8aβ)]-decahydro-4,8,8-trimethyl-9-methylene-1,4-methanoazulene||UVCBs||DSL|
|69898-30-2||Starch, base-hydrolyzed, borated||UVCBs||DSL|
|72066-70-7||Sulfite liquors and cooking liquors, spent, borated||UVCBs||DSL|
|90530-04-4||2-Propanol, reaction products with boron trifluoride and 5-ethylidenebicyclo[2.2.1]hept-2-ene||UVCBs||DSL|
|91770-03-5||Fatty acids, tall-oil, reaction products with boric acid (H3BO3) and diethanolamine||UVCBs||DSL|
|91782-44-4||1,2-Ethanediol, reaction products with boron sodium oxide (B4Na2O7)||Organics||DSL|
|93924-91-5||Boric acid (H3BO3), reaction products with 2,2’-[(C16-18 and C16-18-unsaturated alkyl)imino]bis[ethanol]||UVCBs||DSL|
|121053-02-9||Sulfonic acids, petroleum, calcium salts, overbased, reaction products with acetic acid, boric acid and 12-hydroxyoctadecanoic acid||UVCBs||DSL|
|124751-09-3||Caseins, reaction products with ammonium hydroxide, boron sodium oxide (B4Na2O7), sodium hydroxide and trisodium phosphate||UVCBs||DSL|
|125328-30-5||Starch, acid-hydrolyzed, borated||UVCBs||DSL|
|127087-85-8||Boric acid (H3BO3), reaction products with 2-(butylamino)ethanol and diethanolamine||UVCBs||DSL|
|129783-46-6||Borate(1-), tetrafluoro-, hydrogen, reaction products with 2-(ethylthio)ethanol||UVCBs||DSL|
Abbreviations: ICL, In-Commerce List; UVCB, Substance of Unknown or Variable composition, Complex reaction products or Biological materials.
|CAS RN||Chemical name||Chemical class||Inventory|
|50815-87-7||Sodium borate silicate||Borates||DSL|
|59794-15-9||Calcium borate silicate||Borates||DSL|
|65997-17-3||Glass, oxide, chemicals||Borates||DSL/ICL|
|10043-11-5||Boron nitride (BN)||Borides||DSL|
|12008-21-8||Lanthanum boride (LaB6), (OC-6-11)-||Borides||DSL|
|12045-63-5||Titanium boride (TiB2)||Borides||DSL|
|12069-32-8||Boron carbide (B4C)||Borides||DSL|
Appendix B: Aquatic Ecotoxicological Data
|Group||Species name (common name)||Endpoint and duration||Response||Effects concentra-tion mg B/L (geomean)||Reference|
|Algae||Elodea canadensis (American Waterweed)||NOEC||Growth||1.0||ANZECC 2000|
|Algae||Spirodela polyrhiza(duckweed)||10-d MATC||Frond production||1.8 (geomean; n=2)||Davis et al. 2002|
|Algae||Chlorella pyrenoidosa (green algae)||14-d NOEC||Growth or cell composition||2.0 (geomean; n=2)||ANZECC 2000;|
Fernandez et al. 1984
|Fish||Oncorhynchus mykiss (Rainbow Trout)||87-d NOEC||Embryo survival||2.1||Black et al. 1993|
|Fish||Ictalurus punctatus (Channel Catfish)||9-d MATC||Survival||2.4 (geomean; n=8)||Birge and Black 1977|
|Plant||Phragmites australis (Common Reed)||4-mo NOEC||Growth||4.0||Bergmann 1995|
|Fish||Micropterus salmoides(Largemouth Bass)||11-d MATC||Teratogenesis||4.1 (geomean; n=2)||Black et al. 1993|
|Algae||Chlorella vulgaris (green algae)||NOEC||Population growth||5.2||ANZECC 2000|
|Invertebrate||Daphnia magna (water flea)||NOEC||Reproduction||6.0||ANZECC 2000|
|Protozoa||Opercularia bimarginata||72-hr NOEC||Growth, reproduction||10.0||Guhl 1992a|
|Fish||Danio rerio (Zebrafish)||34-d MATC||Mortality, growth condition||10.0||Hooftman et al. 2000b|
|Algae||Selenastrum capricornutum(green algae)||72-hr LOEC||Growth||12.3||MELP 1997|
|Invertebrate||Ceriodaphnia dubia (water flea)||14-d MATC||Growth, reproduction||13.4||Hickey 1989|
|Invertebrate||Entosiphon sulcatum(zooplankton)||72-hr NOEC||Growth||15.0||Guhl 1992a|
|Fish||Carassius auratus(Goldfish)||7-d MATC||Survival and teratogenesis||15.6 (geomean; n=8)||Birge and Black 1977|
|Fish||Pimephales promelas (Fathead Minnow)||30-d MATC||Growth reduction||18.3 (geomean; n=2)||Procter and Gamble 1979|
|Invertebrate||Chironomus decorus(Midge)||96-hr NOEC||Growth||20.0||Maier and Knight 1991|
|Ciliate||Paramecium caudatum||72-hr NOEC||Growth, reproduction||20.0||Guhl 1992a|
|Amphibian||Rana pipiens (Leopard Frog)||7-d MATC||Survival and teratogenesis||20.4 (geomean; n=8)||Birge and Black 1977;|
Butterwick et al. 1989;
|Algae||Scenedesmus subspicatus(green algae)||96-hr EC10||Growth||30.0||Guhl 1992b|
|Algae||Myriophyllum spicatum (Spiked or Eurasian Watermilfoil)||NOEC||Growth||34.2||ANZECC 2000|
|Amphibian||Bufo fowleri (Fowler's Toad)||7-d MATC||Survival and teratogenesis||48.6||Birge and Black 1977|
|Algae||Aspergillus nidulans(blue-green algae)||NOEC||Growth or organic constituents||50.0||Martinez et al. 1986|
|Amphibian||Bufo americanus (American Toad)||43-d LOEC||Proportion of eggs hatching||50.0||Laposata and Dunson 1998|
|Algae||Lemna minor (duckweed)||7-d NOEC||Growth||60.0||Wang 1986|
|Amphibian||Ambystoma jeffersonianium(Jefferson’s Salamander)||17 to 25-d MATC||Proportion of deformed hatchlings||70.7 (geomean; n=2)||Laposata and Dunson 1998|
|Amphibian||Ambystoma maculatum (Spotted Salamander)||38 to 44-d MATC||Proportion of deformed hatchlings||70.7 (geomean; n=2)||Laposata and Dunson 1998|
|Amphibian||Rana sylvatica (Wood Frog)||13 to 23-d MATC||Proportion of eggs hatched||70.7 (geomean; n=2)||Laposata and Dunson 1998|
|Group||Species name (common name)||Endpoint and duration||Response||Effects concentration||Reference|
|28-d NOEC||MultipleFootnote Table B-2a||37.8 mg B/kg||Gerke et al. 2011aFootnote Table B-2b|
|Invertebrate||Chironomus riparius||28-d LOEC||Multiplea||greater than 37.8 mg B/kg||Gerke et al. 2011ab|
|Invertebrate||Chironomus riparius||28-d NOEC||Survival, emergence||20.4 mg B/L||Gerke et al. 2011bFootnote Table B-2c|
|Invertebrate||Chironomus riparius||28-d LOEC||Survival, emergence||43.3 mg B/L||Gerke et al. 2011bc|
|Invertebrate||Chironomus ripari us||28-d EC10||Survival||43 mg B/L||Gerke et al. 2011bc|
|Invertebrate||Chironomus riparius||28-d EC50||Survival||46.5 mg B/L||Gerke et al. 2011bc|
|Invertebrate||Chironomus riparius||28-d EC10||Emergence||40.8 mg B/L||Gerke et al. 2011bc|
|Invertebrate||Chironomus riparius||28-d EC50||Emergence||50.2 mg B/L||Gerke et al. 2011bc|
|Invertebrate||Chironomus riparius||28-d NOEC||MultipleFootnote Table B-2d||43.3 mg B/L||Gerke et al. 2011bc|
|Invertebrate||Chironomus riparius||28-d LOEC||Multipled||greater than 43.3 mg B/L||Gerke et al. 2011bc|
|Invertebrate||Chironomus riparius||28-d NOEC||Mortality, emergence||180 mg B/kg||Hooftman et al. 2000a|
|Invertebrate||Chironomus riparius||28-d LOEC||Mortality, emergence||320 mg B/kg||Hooftman et al. 2000a|
|Invertebrate||Chironomus riparius||28-d LC50||Mortality||278 mg B/kg||Hooftman et al. 2000a|
|Invertebrate||Chironomus riparius||28-d NOEC||Mortality, emergence||32 mg B/L||Hooftman et al. 2000a|
|Invertebrate||Chironomus riparius||28-d LOEC||Mortality, emergence||59 mg B/L||Hooftman et al. 2000a|
|Invertebrate||Chironomus riparius||28-d LC50||Mortality||49 mg B/L||Hooftman et al. 2000a|
|21-d NOEC||Survival||254.9 mg B/kg||Hall et al. 2014|
|Invertebrate||Lampsilis siliquoidea||21-d IC25||Survival||363.1 mg B/kg||Hall et al. 2014|
|Invertebrate||Lampsilis siliquoidea||21-d NOEC||Survival||31.6 mg B/L||Hall et al. 2014|
|Invertebrate||Lampsilis siliquoidea||21-d IC25||Survival||45.0 mg B/L||Hall et al. 2014|
|Invertebrate||Lampsilis siliquoidea||21-d NOEC||Growth||80.6 mg B/kg||Hall et al. 2014|
|Invertebrate||Lampsilis siliquoidea||21-d IC25||Growth||310.6 mg B/kg||Hall et al. 2014|
|Invertebrate||Lampsilis siliquoidea||21-d NOEC||Growth||10 mg B/L||Hall et al. 2014|
|Invertebrate||Lampsilis siliquoidea||21-d IC25||Growth||38.5 mg B/L||Hall et al. 2014|
|28-d NOEC||Survival||100.8 mg B/kg||Hall et al. 2014|
|Invertebrate||Lumbriculus variegatus||28-d NOEC||Survival||12.5 mg B/L||Hall et al. 2014|
|Invertebrate||Lumbriculus variegatus||28-d IC25||Survival||12.7 mg B/L||Hall et al. 2014|
|Invertebrate||Lumbriculus variegatus||28-d NOEC||Growth||201.6 mg B/kg||Hall et al. 2014|
|Invertebrate||Lumbriculus variegatus||28-d IC25||Growth||235.5 mg B/kg||Hall et al. 2014|
|Invertebrate||Lumbriculus variegatus||28-d NOEC||Growth||25 mg B/L||Hall et al. 2014|
|Invertebrate||Lumbriculus variegatus||28-d IC25||Growth||25.9 mg B/L||Hall et al. 2014|
Appendix C: Soil Ecotoxicological Data
|Group||Species name (common name)||Endpoint and duration||Response||Effects concentration mg B/kg (geomean)||Reference|
|Invertebrate||Folsomia candida(springtail)||28 to 42-d EC10||Reproduction||5.5||Amorim et al. 2012|
|Plant (monocot)||Zea mays (corn)||70-d EC10||Growth (yield shoot)||7.2||ARCHE 2010; Hosseini et al. 2007|
|Invertebrate||Enchytraeus albidus (White Worm)||28 to 42-d EC10||Reproduction||8.5 (geomean, n=2)||Amorim et al. 2012|
|Plant (monocot)||Elymus lanceolatus (Northern Wheatgrass)||21-d IC20||Emergence||9.6||Anaka et al. 2007|
|Plant (monocot)||Avena sativa (oat)||14-d EC10||Shoot biomass||11||Förster and Becker 2009|
|Plant (dicot)||Medicago sativa sp (Alfalfa)||45-d NOEC||Yield shoot||13.35 (geomean; n=12)||Gestring and Soltanpour 1987|
|Plant (dicot)||Brassica napus(Rapeseed)||14-d EC10||Shoot biomass||13.9||Förster and Becker 2009|
|Invertebrate||Enchytraeus luxuriosus(earthworm)||28-d EC10||Reproduction||17||Moser and Beker 2009d|
|Invertebrate||Enchytraeus crypticus(earthworm)||28-d EC10||Reproduction||22.5||Moser and Beker 2009c|
|Invertebrate||Hypoaspis aculeifer(Predatory Mite)||14-d EC10||Reproduction||22.7||Moser and Scheffczyk 2009|
|Invertebrate||Onychiurus folsomi||35-d EC20||Reproduction||24.1 (geomean; n=2)||ESG International Inc. and Aquatera Environmental Consulting Ltd. 2003|
|Invertebrate||Eisenia andrei(earthworm)||56 to 63-d IC20||Reproduction (juvenile dry mass)||24.8 (geomean; n=6)||Stantec and Aquaterra Consulting 2004|
|Plant (tree)||Picea glauca (White Spruce)||35-d IC25||Root length||27.7 (geomean n=3)||Environment Canada 2014|
|Plant (tree)||Betula papyrifera (Paper Birch)||28-d IC25||Root length||28.25 (geomean; n=3)||Environment Canada 2014|
|Plant (monocot)||Calamagrostis canadensis(Bluejoint Reedgrass)||14-d IC25||Root length||36.45 (geomean; n=4)||Environment Canada 2014|
|Plant (tree)||Populus tremuloides (White Poplar)||21-d IC25||Root length||42.7 (geomean; n=3)||Environment Canada 2014|
|Invertebrate||Poecilus cupreus (ground beetle)||21-d EC10||Feeding rate||47.5||Moser and Becker 2009e|
|Plant (eudicot)||Solidago canadensis (Canada Goldenrod)||21-d IC25||Shoot length||48.1 (geomean; n=3)||Environment Canada 2014|
|Invertebrate||Dendrodrilus rubidus(earthworm)||56-d IC25||Reproduction||58.8 (geomean; n=2)||Environment Canada 2014|
|Plant (tree)||Picea mariana (Black Spruce)||35-d IC25||Root length||60.2 (geomean; n=5)||Environment Canada 2014|
|Plant (tree)||Pinus banksiana (Jack Pine)||14-d IC25||Root length||61.1 (geomean; n=3)||Environment Canada 2014|
|Invertebrate||Eisenia fetida (Tiger Worm)||56-d EC10||Reproduction||70.1||Moser and Becker 2009a|
|Invertebrate||Caenorhabditis elegans(nematode)||4-d EC10||Reproduction||86.7||Moser and Becker 2009b|
Appendix D: Estimated Intakes from Environmental Media, Food and Drinking Water
|Route of exposure||0-6 months breast fedFootnote Table D-1a,Footnote Table D-1b||0.5-4 yearsFootnote Table D-1c||5-11 yearsFootnote Table D-1d||12-19 yearsFootnote Table D-1e||20-59 yearsFootnote Table D-1f||60+ yearsFootnote Table D-1g|
|AirFootnote Table D-1h||0.001||0.003||0.002||0.001||0.001||0.001|
|Food and waterFootnote Table D-1i||3.0||91.7||63.6||26.2||24.7||23.2|
|SoilFootnote Table D-1j||NA||0.030||0.022||0.001||0.001||0.001|
|DustFootnote Table D-1k||0.331||0.173||0.065||0.002||0.002||0.002|
NA: not applicable
Appendix E: Estimated Intakes from the Use of Products
|Scenario||Age group||Body weight (kg)||Boron concentration (%)||Product amount||Dermal absorption (%)||Intake (µg/kg bw/d)|
|Direct ingestion from playing with modelling clayFootnote Table E-1a||6 m to 4 yr||15.5||0.874|
(5% boric acid)
|100 mg to 5 g ingested||n/a||56-2819|
|Dermal exposure from playing with modelling clayFootnote Table E-1b||6 m to 4 yr||15.5||0.874|
(5% boric acid)
|350 g||0.5 and 10||69-1381|
|Product||Scenario||Age group||Boron concentration (%)||Dermal intake (µg/kg bw/d)||Inhalation intake (µg/kg bw/d)||Oral intake (µg/kg bw/d)|
|General purpose cleaner (liquid)Footnote Table E-2a||Surface cleaning (application)||Adult||0.742||10–199||na||na|
|Dishwashing detergent (liquid)Footnote Table E-2b||Hand- washing (application)||Adult||0.148||4–86||na||na|
|Floor cleaner (liquid)Footnote Table E-2c||Hand-washing (application)||Adult||1.759||27–542||na||na|
|Floor cleaner (liquid)Footnote Table E-2d,Footnote Table E-2e||Post-application dermal from crawling on floor and oral hand-to-mouth||Toddler||1.759||8–160||na||120|
|Laundry detergent (powder)Footnote Table E-2f||Laundry additive (loading)||Adult||11.4||na||0.02||na|
na = not applicable.
|Product||Age group||Amount appliedFootnote Table E-3a (g)||Frequency per daya||Retention factora||Dermal absorption (%)||Intake (µg/kg bw/d)Footnote Table E-3b|
|Body cream||20-59||4.4||1.1||1||0.5, 10||3-6|
|Body cream||5-11||2.2||1.1||1||0.5, 10||3-68|
|Body cream||0.5-4||1.4||1.7||1||0.5, 10||7-134|
|Body cream||less than 0.5||1.4||1.7||1||0.5, 10||14-277|
|Skin cleanser||20-59||11.3||1.37||0.01||0.5, 10||0.1-1.9|
|Skin cleanser||5-11||6.48||0.42||0.01||0.5, 10||0.04-0.8|
|Skin cleanser||0.5-4||3.76||0.42||0.01||0.5, 10||0.04-0.9|
|Skin cleanser||less than 0.5||0.873||0.64||0.01||0.5, 10||0.03-0.65|
|Diaper cream||less than 0.5||0.3||4||1||100||1399|
|Product||Concentration (% B)Footnote Table E-4a||Amount ingested / available for absorptionFootnote Table E-4b||Frequency per dayb||Intake (µg/kg bw/d)Footnote Table E-4c|
|Genital lubricant||0.525||10 g||1b||740|
|Product||Amount of boron in oral supplement (µg)Footnote Table E-5a||Intake (µg/kg bw/d)Footnote Table E-5b|
|Joint health supplement||3360||47|
(kg)Footnote Table E-6a
area (cm2)Footnote Table E-6b
|Oral ingestion rate|
(L/hr)Footnote Table E-6c
|Dermal intakeFootnote Table E-6d|
|Oral intakeFootnote Table E-6e|
(µg/kg bw/ event)
|Total intakeFootnote Table E-6f|
|20-59 yr||70.9||18 200||0.025||10||26||36|
|60+ yr||72.0||18 200||0.025||9||26||36|
Appendix F: Biomonitoring Data Tables
|Population||Age group||Sex||n||Mean ± SD µg/L||Range µg/L||Reference|
|Alberta, pregnant women, serum||less than 25-31+||F||151 pools|
mean of pools
|na||Alberta Health and Wellness 2008|
|Alberta, pregnant women, serum||18-25||F||54 pools||21.5||na||Government of Alberta 2010|
|Alberta, pregnant women, serum||26-30||F||50 pools||24||na||Government of Alberta 2010|
|Alberta, pregnant women, serum||31+||F||47 pools||25||na||Government of Alberta 2010|
|Alberta, children, serum||less than 5-13|
means of pools
|na||Government of Alberta 2010|
|Alberta, children, serum||less than or equal to 5|
(2 - less than or equal to 5)
|M+F||3 pools||31.5||na||Government of Alberta 2010|
|Alberta, children, serum||6-13||M+F||3 pools||30.5||na||Government of Alberta 2010|
|Canada, healthy volunteers, whole blood||Adult||na||12||30.8 ± 5.6||15.3-79.5||Clarke et al. 1987a|
|Canada, healthy volunteers, blood||Adult||M+F||7||97 ± 22||na||Clarke et al. 1987b|
|Canada, healthy volunteers (controls),|
|Adult||M+F||7||23 ± 2||na||Clarke et al. 2004|
|Canada, healthy volunteers (controls), plasma||Adult||M+F||7||28 ±2||na||Clarke et al. 2004|
|U.S., plasma||Na||na||12||25 ± 7||14-39||Ferrando et al. 1993|
|U.S., non-pregnant women, plasma||18-40||F||15||22 ± 13||na||Pahl et al. 2001|
|U.S., pregnant women, plasma||18-40||F||16||23 ± 15||na||Pahl et al. 2001|
|UK, whole blood||na||na||50||56.7||8.4-170.4||Abou-Shakra et al. 1989|
|UK, serum||na||na||50||22.3||8.3-48.1||Abou-Shakra et al. 1989|
|Sweden, athletes, blood||16-36||M+F||31||11 ± 7||6-33||Rodushkin et al. 1999|
|Belgium, serum||23-51||M+F||12||13.9 ± 6.9||4.1-25.8||Vanhoe et al. 1993|
|Northern Germany, blood||18-70||M+F||130||42||12-195||Heitland and Köster 2006|
|Northern France, plasma||21.2 (mean)||M||180||126.11 ± 106.27||Na||Yazbeck et al. 2005|
|France, whole blood||na||na||100||Median 26||P5-P95|
|Goulle et al. 2005|
|France, plasma||na||na||100||Median 36||P5-P95|
|Goulle et al. 2005|
|Turkey, plasma||44 (mean)||M+F||80||11.3 ± 7.9 to 18.3 ± 19.5 means by body mass index||Na||Hasbachecei et al. 2013|
|Japan, serum||less than 20-80+||F||583||GM 67.9||19.6-211.3||Usuda et al. 1997|
|Japan, serum||less than 20||M||45||GM 63.8||24.6-156.6||Usuda et al. 1997|
|Japan, serum||20-29||M||45||GM 66.5||23.5-189.0||Usuda et al. 1997|
|Japan, serum||30-39||M||32||GM 75.2||27.7-166.3||Usuda et al. 1997|
|Japan, serum||40-49||M||41||GM 86.5||33.7-210.2||Usuda et al. 1997|
|Japan, serum||50-59||M||71||GM 83.9||33.4-192.4||Usuda et al. 1997|
|Japan, serum||60-69||M||111||GM 85.1||31.8-237.8||Usuda et al. 1997|
|Japan, serum||70-79||M||38||GM 87.7||34.3-213.2||Usuda et al. 1997|
|Japan, serum||80+||M||14||GM 95.9||35.9-210.6||Usuda et al. 1997|
|Japan, serum||less than 20-80+||M||397||GM 79.8||23.5-237.8||Usuda et al. 1997|
|Japan, serum||less than 20||F||51||GM 59.4||19.6-151.6||Usuda et al. 1997|
|Japan, serum||20-29||F||104||GM 59.2||21.8-133.8||Usuda et al. 1997|
|Japan, serum||30-39||F||88||GM 63.0||25.2-181.6||Usuda et al. 1997|
|Japan, serum||40-49||F||93||GM 67.5||23.8-180.2||Usuda et al. 1997|
|Japan, serum||50-59||F||89||GM 72.1||25.3-187.5||Usuda et al. 1997|
|Japan, serum||60-69||F||87||GM 75.0||27.0-211.3||Usuda et al. 1997|
|Japan, serum||70-79||F||49||GM 82.0||35.9-134.9||Usuda et al. 1997|
|Japan, serum||80+||F||22||GM 82.4||43.9-169.9||Usuda et al. 1997|
Abbreviations: SD, standard deviation; na, not available; GM, geometric mean.
Assumed blood density 1g/mL when converting weight/weight (wt/wt) to weight/volume (wt/vol).
|Population||Age group||Sex||n||Mean ± SD µg/L||Range µg/L||Reference|
|Northern Chile, whole blood||16–86||M+F||38||22–659|
means by community
|na||Barr et al. 1993|
|Northern Chile, siblings, plasma||na||na||19||253–901||na||Barr et al. 1996|
|Northern Chile, mothers 2–4 weeks after delivery, whole blood||28 (mean)||F||7||GM 430||210–1500||Harari et al. 2012|
|Northern Argentina, mothers 2–4 weeks after delivery, plasma||25 (mean)||F||24||GM 380||125–1360||Harari et al. 2012|
|Santiago control location, mothers 2–4 weeks after delivery, plasma||30 (mean)||F||11||GM 35||21–66||Harari et al. 2012|
Abbreviations: SD, standard deviation; na, not available; GM, geometric mean.
Assumed blood density 1g/mL when converting wt/wt to wt/v.
|Population||Age group||Sex||n||Mean ± SD µg/L||Range µg/L||Reference|
|11.6 mg dose plasma||45-65||M||15||0 hr 14 ± 10|
4 hr 136 ± 20
6 hr 124 ± 20
|na||Wallace et al. 2002|
|Placebo, plasma||45-65||M||15||8-16||na||Wallace et al. 2002|
|Peri-menopausal women, 2.5 mg dose plasma||Older adult||F||19||53 ± 12||28-75||Nielsen and Penland 1999|
|Peri-menopausal women, placebo, plasma||Older adult||F||24||34 ± 10||20-67||Nielsen and Penland 1999|
|Post-menopausal women, 3 mg dose plasma||48-82||F||11||95 ± 56||Hunt et al. 1997|
|Post-menopausal women, placebo, plasma||48-82||F||11||64 ± 45||Hunt et al. 1997|
|Weightlifters, 2.5 mg dose plasma||Adults||M||10||32.9Footnote Table F-3a||less than 12-77||Green and Ferrando 1994|
|Weightlifters, placebo, plasma||Adults||M||9||8.4||less than 12-17||Green and Ferrando 1994|
Abbreviations: SD, standard deviation; na, not available; GM, geometric mean.
Assumed blood density 1g/mL when converting wt/wt to wt/v.
|Population||Age group||Sex||n||Mean ± SD µg/L||Range µg/L||Reference|
|China, remote background community, control, serum||Adult||M||23||39.1||8.20– 72.1||Scialli et al. 2010|
|China, local community, control (environmental exposure), serum||Adult||M||15||114||3.29–348||Scialli et al. 2010|
|China, workers, boron plant (occupational airborne and environmental exposure), serum||Adult||M||75||252||22.8–2482||Scialli et al. 2010|
|China, workers, Pengxiang plant (highest occupational airborne exposure and environmental exposure), serum||Adult||M||16||1558 ± 1041||na||Scialli et al. 2010|
|Turkey, workers, control, whole blood||26–52||M||49||less than LOQ (less than 48.5)||less than LOQ||Duydu et al. 2011|
|Turkey, workers, low exposure, whole blood||23–50||M||72||72.94 +/- 15.43||48.46– 99.91||Duydu et al. 2011|
|Turkey, workers, medium exposure, whole blood||32–50||M||44||121.68 +/- 15.62||100.51 –146.01||Duydu et al. 2011|
|Turkey, workers, high exposure, whole blood||28–53||M||39||223.80 +/- 69.49||152.82– 152.82||Duydu et al. 2011|
Appendix G: Summary of Blood Boron Concentrations and Intake Concentrations in Various Human Exposure Studies
|Exposure type||Mean intake (mg B/kg bw/d)||Mean blood concentration ± SD or (min-max) (µg/L)||Reference|
|Supplement study (placebo)||0.017Footnote Table Gac||34 ± 10||Nielsen and Penland 1999|
|Supplement||0.047aFootnote Table Gc||53 ± 12||Nielsen and Penland 1999|
|Supplement study (placebo)||0.005c||64 ± 45Footnote Table Ge||Hunt et al. 1997|
|Supplement||0.049c||95 ± 56e||Hunt et al. 1997|
|Supplement||0.032c||32.9 (less than or equal to 12-77)Footnote Table Gf||Green and Ferrando 1994|
|Supplement||0.133c||124 ± 20Footnote Table Gg||Wallace et al. 2002|
|Drinking water (northern Chile)||0.010a||22 ± 2g||Barr et al. 1993|
|Drinking water||0.020a||68 ± 34g||Barr et al. 1993|
|Drinking water||0.040a||52 ± 15g||Barr et al. 1993|
|Drinking water||0.06a||347 ± 163g||Barr et al. 1993|
|Drinking water||0.24a||585 ± 166g||Barr et al. 1993|
|Drinking water||0.300a||450 ± 87g||Barr et al. 1993|
|Drinking water||0.39a||659 ± 337g||Barr et al. 1993|
|Drinking water, mother-infant (Argentina)||0.13aFootnote Table Gd||GM 430 (210-1500)||Harari et al. 2012|
|Drinking water, mother-infant (northern Chile, Arica)||0.20ad||GM 380 (125-1360)||Harari et al. 2012|
|Drinking water, mother-infant (Chile, capital [Santiago])||0.005ad||GM 35 (21-66)||Harari et al. 2012|
|Worker study, China (remote control)||0.02Footnote Table Gbh||39.1 (8.20-72.1)||Scialli et al. 2010|
|Worker study, China (2004 community control)||0.07bFootnote Table Gh||114 (3.29-348)||Scialli et al. 2010|
Appendix H: Health Effects Data
|Key animal study||Protocol||Result|
|90-day dietary, dog||5/sex/dose, borax|
Dose levels in boron equivalents: 0.0, 0.4, 5.0, 46.2 mg B/kg bw/d
|NOAEL (mg/kg bw/d): provisional female: 46.2, male: 5.0|
greater than or equal to 0.4 mg/kg bw: dose-related in abs+rel testis wt, but not seen in 2-yr dog at this dose level.
greater than or equal to 5.0 mg/kg bw: all 5 male had artifactual distortion of the tubules in the outer 1/3 of the gland. The males also had a greater proportion of small and solid epithelial nests (thyroid) and female adrenal cortex was distinctly widened (considered non-adverse).
@ 46.2 mg/kg bw: severe testicular atrophy in all dogs, complete degeneration of the spermatogenic epithelium in 4/5 dogs, with partial degeneration in 1 male (dog died on day 68, congestion of kidneys and small and large intestines), interstitial cells and Leydig-like cells. Abs testicular wt 40–44%, rel to bw and brain wt .
Liver, spleen, kidney: hemosiderin pigment accumulation from the breakdown of RBC. Effect more severe in male, but number of animals affected not given.
Supplemental (no ovary data, poor reporting of control data, no individual path. reports).
No sperm analysis.
(Study No. 1237735, cited in Health Canada 2012)
|90-day dietary, dog||5/sex/dose, boric acid|
Dose levels in boron equivalents: 0.0, 0.46, 4.2, 35 mg B/kg bw/d; dose levels for male calculated from actual test article intake and converted into boron equivalent intake.
|NOAEL (mg/kg bw/d): provisional female: 35.0, male: 4.2|
greater than or equal to 4.2 mg/kg bw: in abs and rel (to body weight) testes wt, but not seen in 2-yr dog at this dose level, testes of all 5 male had artifactual distortion of the tubules in the outer 1/3 of the gland. The male had in small and solid epithelial thyroid nests (2 with squamous metaplasia).
@ 35 mg/kg bw: rel thyroid (male). Severe testicular atrophy in all males. Degeneration of the spermatogenic epithelium was generally complete except in one dog where some activity remained in 2/3 of tubules, in interstitial tissue. female: of lymphoid infiltration and atrophy of the thyroid.
Supplemental (no ovary data, poor reporting of control data, no individual path. reports).
No sperm analysis.
(Study No. 1249382, cited in Health Canada 2012)
|Teratology dietary feeding study, Sprague-Dawley rat, boric acid||Gestation day 0-20|
30/dose, teratogenic evaluation
30/dose, postnatal evaluation
Dose levels in boron equivalents: 0, 3.3, 6.3, 9.6, 13.3, 25.0 mg B/kg bw/d
|Developmental NOAEL: 9.6 mg/kg bw/d (the conclusive developmental NOAEL that could not be set in the previous studies).|
No maternal toxicity: as in the previous CNS study, there were no maternal effects after correcting for gravid uterine wt: "No maternal deaths occurred and no distinctive treatment-related clinical signs of toxicity were observed during either study (this study and the original NTP developmental study)."
Phase I (teratogenic evaluation (gd 20))
greater than or equal to 9.6 mg/kg bw: in short rib XIII
greater than or equal to 13.3 mg/kg bw: in wavy rib, in fetal BW
Phase II (postnatal)
There was recovery from the in fetal BW.
@ 25 mg/kg bw: in short rib XIII (postnatal day 21)
Supplemental NTP study to support the 1990 NTP study.
Fetal and offspring sensitivity.
(Cited in Health Canada 2012)
|Poisoning case/short-term study||Oral exposure (some source doses were not able to convert to boron- equivalent doses)||Accidental single ingestion of approx. 5 g of sodium perborate bleach (95%) often led to vomiting, diarrhoea and abdominal pain (Kliegel 1980).|
In a case study of seven infants (aged 6-16 weeks at the end of the exposure) exposed to borax in a honey-borax mixture in their diet at 429–1287 mg/d (equivalent to 9.6–33 mg B/kg-bw/d, Taylor 1997) for 4-10 weeks, seizures, convulsions and other milder effects were observed.
Early case reports have shown that death in newborns occurred within five days of ingesting less than 3 g of boric acid (Young et al. 1949).
One 4.5-month-old infant who ingested (via pacifier dipped in honey and borax mixture) approx. 125 g borax over three months induced a seizure disorder (accumulated exposure); the tested blood boron level was 1.64 mg/100 mL (Gordon et al. 1973).
The lowest lethal doses for humans exposed to boric acid were 640 mg/kg-bw by oral exposure, 8600 mg/kg-bw by dermal exposure, and 29 mg/kg-bw by intravenous injection (Stokinger 1981).
The potential lethal doses in humans for boric acid reported by Litovitz et al. (1988) were 3-6 g total for infants and 15-20 g total for adults.
Degenerative changes in parenchymal cells with oliguria and albuminuria were demonstrated in two newborn infants after ingestion of 505 and 765 mg B/kg-bw/d as boric acid in an evaporated milk formula over a period of 3-05 days. Five infants who ingested formula accidentally prepared with 2.5% aqueous solution of boric acid (no daily dose provided) became lethargic, developed vomiting and diarrhea, and died within three days of exposure (Wong et al. 1964).
12 young male volunteers were dosed up to 870 mg B/d of boric acid or borax equivalent for 4 days-2 weeks, resulting in a loss of appetite, a feeling of fullness and uneasiness in the stomach, or nausea. Similar reversible adverse effects were observed at a diet-dose level of 0.5 g of B/d (87 mg B/day) for 50 days (Wiley 1904).
Epilepsy patients receiving 5 or more mg B/kg bw/d (over two years [route unspecified]) developed dermatitis, alopecia and indigestion. When the dose was reduced to 2.5 mg B/kg bw/d, the signs and symptoms disappeared (Culver and Hubbard 1996).
|Poisoning case/short- term study||Dermal exposure (some source doses were not able to convert to boron- equivalent doses)||Accidental misuse in the preparation of baby formula (1-14 g boric acid in the formula) and the topical use of pure boric acid powder for infants has led to poisonings (Austria 2008a). Repeated dermal application of boric acid containing baby powder induced cutaneous lesions (erythema over the entire body, excoriation of the buttocks, and desquamation) gastrointestinal disturbances, and seizures (Goldbloom and Goldbloom 1953).|
|Eye and respiratory irritation||113 boron workers and 214 controls exposed to mean total level of 4.1 mg/m3 boron oxide or 4.1 mg/m3 boric acid (equivalent to 1.3 and 0.7 mg B/m3)||Boron exposure was significantly associated with respiratory symptoms and eye irritation (dryness of mouth, nose or throat; sore throat; and reproductive cough) (Garabrant et al. 1984). The follow-up study of 629 workers confirmed this finding. The author concluded that borax dust is an acute respiratory irritant at exposures of 4.4 mg/m3(0.6 mg B/m3 or more), which is a level of respiratory irritation that produces chronic bronchitis without impairment of pulmonary function. At an exposure level of 4.0 mg/m3, eye irritation was noted in over 5% of participants (Garabrant et al. 1985).|
|Eye and respiratory irritation||Boron workers (number not defined) exposed to boron dust for 6h/day, at 5.72 mg/m3 of total dust (equivalent to 0.44 mg B/m3, 1.0-10.0 mg/m3 of total dust)||The acute irrigative effects and chronic pulmonary function analyses of the incidence and severity of irritant symptoms in boron workers indicated that exposure-response relationships were presented for each symptom. The exposure – response trends were statistically significant (p less than 0.05), except for eye irritation (Wegman et al. 1991, 1994).|
|Respiratory irritation||12 subjects, exposed to 5, 10, 20, 30 and 40 mg/m3borax dust or 10 mg/m3 boric acid dust for 20 min while performing moderate exercise.||Sensory perception was judged among subjects by level of feeling or irritation in the eye, nose and throat at 5-min intervals. At 10 mg/m3 (1.5 mg B/m3 borax or 1.75 mg B/m3 boric acid), nasal secretion increased in participants (Cain et al. 2004, 2008).|
|Eye irritation||Sodium perborate|
(no protocol provided)
|Sodium perborate induced reversible eye irritation, and irritative effects on the mucosa of the nose were reported in boron workers (Solvay 2002).|
|Skin irritation||Sodium perborate monohydrate, 26 volunteers (aged 18-65),|
0.2 g sodium perborate on a 25 mm pad,
from 15 min to 4 h.
|0.2 g sodium perborate on a 25 mm pad was applied on the upper, outer arm of subjects progressively from 15 min to 4 h, in a sequential single-patch test. 1/26 tested volunteers showed a positive skin reaction, while 21/ 26 reacted to the positive control (sodium dodecyl sulfate). The material was evaluated as non-irritant to human skin (York et al. 1996).|
|Human epidemiological study||Several epidemiological studies investigated the potential impact of boron compounds on fertility and sperm quality in boron workers and a sub-population living in boron-rich areas of the United States, Turkey and China. However, due to the methodological deficiencies (small sample size for the population studied, unsuitable measurement means, improperly characterized exposure, and inconsistency in confounding adjustment), these studies were unable to confirm the absence of an effect in humans. The studies were reviewed in this assessment report; see text for details.|
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