Draft Screening Assessment Phthalate Substance Grouping

Environment and Climate Change Canada
Health Canada

October 2017

(PDF Format-1584KB)

Table of contents

• Synopsis
• 1. Introduction
• 2. Identity of substances
• 3. Physical and chemical properties
• 4. Sources
• 5. Uses
• 6. Releases to the environment
• 7. Environmental fate and behaviour
  • 7.1 Environmental distribution
  • 7.2 Environmental persistence
  • 7.3 Potential for bioaccumulation
• 8. Potential to cause ecological harm
  • 8.1 Ecological effects assessment
  • 8.2 Ecological exposure assessment
  • 8.3 Characterization of ecological risk
• 9. Potential to cause harm to human health
• 10. Conclusion
• References
• Appendices

List of Tables

• Table 2-1. Substances considered in the Phthalate Substance Grouping screening assessment
• Table 4-1. Information on Canadian quantities (for the year 2012) for phthalates in the Phthalate Substance Grouping submitted pursuant to a CEPA section 71 survey
• Table 4-2. Information on Canadian quantities (for the year 2012) for additional phthalates submitted pursuant to a CEPA section 71 survey
• Table 5-1. Summary of Canadian uses for selected additional phthalates, as reported pursuant to a CEPA section 71 survey^a
• Table 5-2. Summary of Canadian uses for selected additional phthalates, as reported pursuant to a CEPA section 71 survey^a (continued)
• Table 5-3. Notifications in Canada for selected additional phthalates^a
• Table 8-1. Available empirical phthalate effects data^a for aquatic organisms
• Table 8-2. In silico predictions of estrogen receptor (ER) and androgen receptor (AR) binding capabilities of phthalates
• Table 8-3. Critical toxicity values and predicted no-effect concentrations for phthalates in the aquatic compartment
• Table 8-4. Near-field predicted environmental concentrations for phthalates
• Table 8-5. Risk quotients (RQs) for Phthalate Substance Grouping and DEHP
• Table 8-6. Summary of lines of evidence and levels of uncertainty
• Table 9-1. Biomonitoring daily intakes (μg/kg bw/day) for BBP
• Table 9-2. Concentrations of BBP in cosmetics and personal care products
• Table 9-3. Biomonitoring daily intakes (μg/kg bw/day) for DBP
• Table 9-4. Percent content of DBP in various soft vinyl toys and childcare articles available in Canada
• Table 9-5. Concentrations of DBP in cosmetics and personal care products
• Table 9-6. Estimates of dermal exposure from nail polish use^a
• Table 9-7. Biomonitoring daily intakes (μg/kg bw/day) for DEHP
• Table 9-8. Percent content of DEHP in various toys and childcare articles available in Canada
• Table 9-9. Concentrations of DEHP in cosmetics and personal care products
• Table 9-10. Summary results of reproductive and/or developmental effects studies based on oral exposure to DMP
• Table 9-11. Summary results of reproductive and/or developmental effects studies based on dermal exposure to DMP
• Table 9-12. Summary table of critical systemic effects after dermal exposure to DMP
• Table 9-13. Summary of levels of evidence of associations between short-chain phthalates and health outcomes
• Table 9-14. Summary of critical effect levels for reproductive and/or developmental effects after oral exposure to DIBP
• Table 9-15. Summary of new DCHP developmental studies identified since the publication of the MCP SOS report. Effects from gestational exposure to DCHP in male offspring (mg/kg-bw/day)
• Table 9-16. Summary of new literature of DCHP identified since the publication of the MCP SOS report
• Table 9-17. Summary of critical effect levels for reproductive and/or developmental effects after oral exposure to DCHP
• Table 9-18. Summary table of critical systemic effects after oral exposure to DCHP
• Table 9-19. Summary of critical effect levels after oral exposure to DBzP using MBzP as closest analogue
• Table 9-20. Summary of critical effect levels for reproductive and/or developmental effects after oral exposure to B84P
• Table 9-21. Summary table of critical systemic effects after oral exposure to B84P
• Table 9-22. Summary of critical effect levels for reproductive and/or developmental effects after oral exposure to DIHepP
• Table 9-23. Summary table of critical systemic effects after oral exposure to DIHepP
• Table 9-24. Effects from gestational exposure to B79P in male offspring (mg/kg-bw/day)
• Table 9-25. Reproductive effects from exposure to B79P in adult males (mg/kg-bw/day)
• Table 9-26. Summary of critical effects levels for reproductive and/or developmental effects after oral exposure to B79P
• Table 9-27. Summary table of critical systemic effects after oral exposure to B79P
• Table 9-28. Effects from gestational exposure to DINP in male offspring (mg/kg-bw/day)
• Table 9-29. Summary of critical effect levels for reproductive and/or developmental effects after oral exposure to DINP
• Table 9-30. Summary of new studies identified since the publication of DINP SOS report
• Table 9-31. Summary table of critical non-cancer effects after oral exposure to DINP
• Table 9-32. Summary of levels of evidence of associations between medium-chain phthalates in the Phthalate Substance Grouping and health outcomes
• Table 9-33. Effects from gestational exposure to BBP in male offspring (mg/kg-bw/day)
• Table 9-34. Summary of critical effect levels for reproductive and or developmental effects after oral exposure to BBP
• Table 9-35. Key studies with effects from gestational exposure to DBP in male offspring (mg/kg-bw/day)
• Table 9-36. Key studies with effects from exposure to DBP in prepubertal/pubertal males (mg/kg-bw/day)
• Table 9-37. Effects from exposure to DBP in adults males (mg/kg-bw/day)
• Table 9-38. Summary of critical effect level for reproductive and/or developmental effects in mature adult male rats after oral exposure to DBP
• Table 9-39. Key studies with effects from gestational exposure to DEHP in male offspring (mg/kg-bw/day)
• Table 9-40. Key studies of effects from exposure to DEHP in (pre)pubertal males (mg/kg-bw/day)
• Table 9-41. Effects from exposure to DEHP in adults males (mg/kg-bw/day)
• Table 9-42. Key studies with effects from gestational exposure to DnHP in male offspring (mg/kg-bw/day)
• Table 9-43. Effects from exposure to DnHP in mature adult males (mg/kg-bw/day)
• Table 9-44. Effects from gestational exposure to DIOP in male offspring (mg/kg-bw/day)
• Table 9-45. Summary of critical effect levels for reproductive and/or developmental effects after oral exposure to DIOP based on its analogue
• Table 9-46. Summary of levels of evidence of associations between additional phthalates and health outcomes
• Table 9-47. Summary of critical systemic effects after oral exposure to DIDP
• Table 9-48. Summary of critical systemic effects associated with oral exposure to DUP
• Table 9-49. Summary of levels of evidence of associations between long-chain phthalates and health outcomes
• Table 9-50. Summary of MOEs to DMP for subpopulations with highest exposure
• Table 9-51. Summary of MOEs to DIBP for relevant subpopulations with highest exposure
• Table 9-52. Summary of MOEs to DCHP for relevant subpopulations with highest exposure
• Table 9-53. Summary of MOEs to DMCHP for relevant subpopulations with highest exposure
• Table 9-54. Summary of MOEs to DBzP for relevant subpopulations with highest exposure
• Table 9-55. Summary of MOEs to B84P for relevant subpopulations with highest exposure
• Table 9-56. Summary of MOEs to DIHepP for relevant subpopulations with highest exposure
• Table 9-57. Summary of MOEs to B79P for relevant subpopulations with highest exposure
• Table 9-58. Summary of MOEs to DINP for subpopulations with highest exposure
• Table 9-59. Hazard index values for subpopulations with the highest exposure
• Table 9-60. Summary of MOEs to DIDP for subpopulations with highest exposure
• Table 9-61. Summary of MOEs to DUP for subpopulations with highest exposure
• Table 9-62. Sources of uncertainty in the cumulative risk characterization
• Table A-1. Substance identity and key physico-chemical properties
• Table B-1. Cumulative risk based on narcosis
• Table D-1a. Central tendency and (upper-bounding) estimates of daily intake of BBP by various age groups (μg/kg bw/day)
• Table D-1b. Probabilistic estimates of daily intake of BBP from food (μg/kg bw/day)
• Table D-2a. Central tendency and (upper-bounding) estimates of daily intake of DBP by various age groups (μg/kg bw/day)
• Table D-2b. Probabilistic estimates of daily intake of DBP from food (μg/kg bw/day)
• Table D-3a. Central tendency and (upper-bounding) estimates of daily intake of DEHP by various age groups (μg/kg bw/day)
• Table D-3b. Probabilistic estimates of daily intake of DEHP from food (μg/kg bw/day)
• Table D-4a. Central tendency and (upper-bounding) estimates of daily intake of DnHP by various age groups (μg/kg bw/day)
• Table D-4b. Probabilistic estimates of daily intake of DnHP from food (μg/kg bw/day)
• Table D-5. Central tendency and (upper-bounding) estimates of daily intake of DIOP by various age groups (μg/kg bw/day)
• Table F-1. Summary of biomonitoring daily intakes for relevant subpopulations with highest exposure - phthalates in the Phthalate Substance Grouping
• Table F-2. Summary of biomonitoring daily intakes for relevant subpopulations with highest exposure - additional phthalates
• Table F-3. Summary of daily intakes for relevant subpopulations with highest exposure from environmental media and food - phthalates in the Phthalate Substance Grouping
• Table F-4. Summary of daily intakes for relevant subpopulations with highest exposure from environmental media and food - additional phthalates
• Table F-5. Critical effect levels for medium-chain phthalates in the Phthalate Substance Grouping
• Table F-6. Critical effect levels for additional phthalates
• Table F-7. Individual HQs and total HI for pregnant women and women of childbearing age
• Table F-8. Individual HQs and total HI for infants
• Table F-9. Individual HQs and total HI for children

Synopsis

Pursuant to sections 68 and 74 of the Canadian Environmental Protection Act, 1999 (CEPA), the Minister of the Environment and the Minister of Health have conducted a screening assessment of 14 phthalate esters (phthalates), known collectively as the Phthalate Substance Grouping. Substances in this grouping were identified as priorities for assessment under the Substance Groupings Initiative of the Government of Canada's Chemicals Management Plan (CMP), because they met categorization criteria under section 73 of CEPA or were considered a priority because of human health concerns. This screening assessment follows the August 2015 publication of four state of the science (SOS) reports and an approach document for cumulative risk assessment of phthalates, and it presents information relevant to concluding on the substances in this grouping under section 64 of CEPA.

The Chemical Abstracts Service Registry Numbers (CAS RN^{Footnote 1}), Domestic Substances List (DSL) names and acronyms for phthalates in the Phthalate Substance Grouping screening assessment are listed in the table below.

Phthalates in the Phthalate Substance Grouping assessment were divided into short-chain, medium-chain and long-chain subgroups, depending on the length of the carbon backbone in the ester side-groups. The primary basis for the subgroups from a health hazard perspective was a structure activity relationship (SAR) analysis using studies related to certain events in the mode of action for phthalate-induced androgen insufficiency during male reproductive development in the rat. From an ecological perspective, subgrouping was based primarily on differences in log K_ow and water solubility and their resulting effects on bioaccumulation and ecotoxicity. Phthalates within each subgroup are likely to have similar chemical properties, while toxicological properties are largely, but not exclusively, similar. The above table also identifies the subgroup to which each phthalate in the grouping was assigned.

Fourteen additional phthalates on the Domestic Substances List were included within the scope of the screening assessment in the context of their potential to contribute to cumulative risk from combined exposure to phthalates. Substance identity information for the additional phthalates considered in this assessment is provided in the table below. Thirteen of the 14 additional phthalates were not assessed individually and therefore no conclusion under section 64 of CEPA is made regarding them. The remaining substance, DEHP, was previously assessed in 1994. However, at that time, there was insufficient information to provide an ecological conclusion. Information has since become available to support a conclusion on its potential to cause harm to the environment.

Results from a CEPA section 71 survey for 2012 determined that 6 of the 28 phthalates being considered in the assessment (DINP, DIDP, DUP, DEHP, D911P and DIUP) were manufactured in and/or imported into Canada in quantities greater than 10 million kg/year, while 7 (BCHP, CHIBP, DBzP, DMCHP, BIOP, DnHP and DPrP) were below the reporting threshold of 100 kg/year. Manufacture and import quantities for the remaining 15 phthalates were in the range of 10 000 to 1 000 000 kg/year. Phthalates are used in a variety of consumer, commercial and industrial products in Canada, including plastics, paints and coatings, adhesives and sealants, automotive parts, electronics, and personal care products.

Water is expected to be the primary receiving medium for phthalates, although some release into air may also occur. When released into the environment, short-chain phthalates are predicted to distribute into water, air and soil, while long-chain phthalates will distribute mainly into soil and sediment with lesser proportions present in the water column. Substances in the medium-chain subgroup exhibit a range of physical-chemical properties; therefore the predicted distribution among environmental media varies across the substances.

Phthalates biodegrade and are not expected to persist in the environment, although degradation rates vary with phthalate molecular size and physicochemical properties, substrate concentration and environmental conditions. Degradation proceeds more slowly under low oxygen conditions, such as may occur in sediment and soil, potentially increasing exposure times for organisms residing in these media. As well, information on Canadian phthalate use and release patterns suggests that exposure to phthalates in the Canadian environment may be continuous. Because of their rapid biodegradation, exposure to phthalates will be greatest for organisms inhabiting areas close to release sites.

In the environment, phthalates are bioavailable but do not have high bioaccumulation and biomagnification potential given a high rate of biotransformation in biota. Most long-chain phthalates demonstrate low hazard potential in aquatic and terrestrial species, while short- and medium-chain phthalates exhibit moderate to high hazard potential. While narcosis is an important mode of toxic action for phthalates, particularly under short-term exposure, there is strong evidence that some phthalates may also elicit longer-term chronic adverse effects through other, specific modes of action. In particular, some phthalates may have the ability to affect the normal functioning of endocrine systems in organisms. While strong in vivo evidence of effects on endocrine systems in aquatic organisms has only been demonstrated for a small number of medium-chain phthalates, evidence suggests that many medium-chain phthalates and some short-chain and long-chain phthalates possess properties that could allow them to adversely influence endocrine activity under some conditions.

Results from an analysis of risk quotients comparing estimated potential exposures for individual phthalates (predicted environmental concentration [PEC]) with their potential for adverse effects (predicted no-effect concentration [PNEC]) determined that 13 phthalates in the Phthalate Substance Grouping present a low risk of causing adverse effects to aquatic species given current exposure levels in the Canadian environment. Two phthalates, B79P and DEHP, have the potential to cause adverse effects in populations of aquatic organisms in Canada at current exposure levels.

In addition, tissue residue analyses were conducted for phthalates having dietary uptake as the primary exposure pathway. The results indicated that maximum tissue concentrations based on solubility limits will be lower than levels associated with adverse acute or chronic lethality effects due to narcosis. A cumulative risk analysis using the Sum of Internal Toxic Units (ITUs) approach determined a total ITU value of 0.2. This value was considered to be conservative as it assumed maximum internal tissue concentrations and highest predicted exposure levels for each of the 28 phthalates examined in the assessment. The results indicate there is no ecological concern due to cumulative effects based on lethality and a narcotic mode of action.

For the general population in Canada, exposure estimates derived from biomonitoring data, when available, were compared to environmental media and food exposure estimates. The principal source of exposure to DMP is expected to be breast milk and food, with indoor air and dust also acting as contributors. Dermal and inhalation (aerosol) exposure to cosmetics and personal care products were also evaluated for adults and infants. Sources of exposure for medium-chain phthalates are indoor air, dust, food and breast milk. Given the information received indicating that a portion of these substances in manufactured items may come in contact with skin, exposure scenarios were identified to characterize dermal exposure for adults and infants. Finally, DIBP and DINP may also be present in children's toys and articles; therefore, oral exposure from mouthing these products was also evaluated. The principal source of exposure to DIDP and DUP for the general population is expected to be house dust (oral ingestion) as well as food and beverages for DIDP (oral ingestion). Exposure scenarios were identified to characterize dermal exposure for adults and children for both long-chain phthalates.

With regard to human health, the health effects data for medium-chain phthalates shows that there is evidence of effects in animal studies that include developmental, reproductive and systemic effects related to the liver and kidneys. Of these, depending on the phthalate in question, the critical effect for risk characterization is developmental effects on males, as the available evidence is strongest for effects on the development of the reproductive system, such as indications of feminization in males, reproductive tract malformations, and effects on fertility related to a relatively well-studied mode of action called the "rat phthalate syndrome" (RPS). This syndrome has been associated with the lowest levels of exposure to this subgroup examined to date in animal studies. The health effects database for short-chain and long-chain phthalate esters shows no evidence of adverse effects on the development of the reproductive system in males. The critical levels selected for risk characterization for DMP were mainly related to mild changes in brain weights after chronic dermal exposure. The health effects database for long-chain phthalates shows that the critical effect for risk characterization is effects on the liver.

Comparisons of estimates of exposure to the 10 medium-chain phthalates in the Phthalate Substance Grouping from various sources, such as environmental media, food, contact with plastic articles (PVC, polyurethane, polyester, etc.), toys and/or personal care products, as well as biomonitoring levels (if available) for all age groups with the appropriate critical effect levels, result in margins of exposures (MOEs) that are considered adequate to address uncertainties in the exposure and health effects databases. Further, these margins are also considered protective of potential reproductive effects not only in males exposed at older life stages but also in females, in addition to effects in other organ systems. Comparisons of estimates of exposure to DMP from environmental media, food, and personal care products, as well as biomonitoring levels for all age groups, with the appropriate critical effect levels, result in MOEs that are considered adequate to address uncertainties in the exposure and health effects databases. Comparisons of estimates for exposure to DIDP and DUP from various sources such as environmental media, food and contact with plastic articles as well as from biomonitoring levels, as available, with critical effect levels results in margins that are considered adequate to address uncertainties in the exposure and health effects databases. Those margins are also protective of potential limited developmental and reproductive effects of DIDP and DUP toxicity not only in males, but also in females as well as other systemic effects.

Results of the CEPA section 71 industry survey indicate that CHIBP, BCHP and BIOP are not currently in use above the reporting threshold of 100 kg, and the likelihood of exposure to the general population in Canada is considered to be low. Hence, the potential risk to human health is considered to be low for these three substances.

On the basis of the information available, there is evidence that phthalates in the medium-chain subgroup have a common mode of action, as they elicit effects on the developing male reproductive system indicative of RPS. Although the MOEs associated with the original 10 medium-chain phthalates included in this assessment are currently considered adequate on an individual substance basis, these MOEs do not address potential risk from concurrent exposure to these and other similar phthalates. As mentioned above, an additional 5 phthalates (BBP, DBP, DEHP, DnHP, and DIOP) were considered in the evaluation of cumulative risk for human health given information indicating that their mode of action is likely to be similar to that of phthalates in the medium-chain subgroup, as well as evidence that they may represent a potential for exposure to the general population of Canada.

A cumulative risk assessment, using a conservative, lower-tiered hazard index (HI) approach has been conducted and indicates no concern for potential cumulative risk of medium-chain phthalates for the general Canadian population, specifically the more sensitive subpopulations (pregnant women/women of childbearing age, infants, and children) at current exposure levels. The HI values for the three subpopulations with the highest estimated exposure levels are all below 1. Hence, further refinement to a higher-tiered assessment is not necessary at this time.

Overall proposed conclusion

Considering all available lines of evidence presented in this draft screening assessment, there is low risk of harm to organisms and the broader integrity of the environment from 13 of the phthalates in the Phthalate Substance Grouping (DMP, DIBP, CHIBP, BCHP, DCHP, DBzP, DMCHP, DIHepP, BIOP, B84P, DINP, DIDP and DUP); however, there is risk of harm to organisms, but not to the broader integrity of the environment, from 1 phthalate included in the Phthalate Substance Grouping, B79P, and from 1 additional phthalate, DEHP. DEHP was previously assessed by Environment Canada and Health Canada in 1994 under the Priority Substances Assessment Program. The assessment concluded that DEHP is harmful to human health in Canada. However, a conclusion for potential harm to the environment could not be determined at that time because of insufficient information.

It is proposed to conclude that 13 of the 14 substances in the Phthalate Substance Grouping do not meet the criteria under paragraphs 64(a) or (b) of CEPA as they are not entering 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 or that constitute or may constitute a danger to the environment on which life depends. It is proposed to conclude that the remaining substance in the Phthalate Substance Grouping, B79P, as well as DEHP, 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 B79P and DEHP 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.

It is proposed to conclude that all 14 phthalates in the Phthalate Substance Grouping do not meet the criteria under paragraph 64(c) of CEPA as they are not entering the environment in a quantity or concentration or under conditions that constitute or may constitute a danger in Canada to human life or health.

Therefore, it is proposed to conclude that B79P and DEHP meet one or more of the criteria set out in section 64 of CEPA. B79P and DEHP have been determined to not meet the persistence and bioaccumulation criteria as set out in the Persistence and Bioaccumulation Regulations of CEPA.

1. Introduction

Pursuant to sections 68 and 74 of the Canadian Environmental Protection Act, 1999 (CEPA) (Canada 1999), the Minister of the Environment and the Minister of Health have conducted a screening assessment of 14 phthalate esters (phthalates), known collectively as the Phthalate Substance Grouping. Substances in this grouping were identified as priorities for assessment under the Substance Groupings Initiative of the Government of Canada's Chemicals Management Plan (CMP) because they met categorization criteria under section 73 of CEPA and/or were considered a priority because of human health concerns (ECCC, HC [modified 2007]).

Certain substances within this grouping have been identified by other jurisdictions as a concern given their potential reproductive and developmental effects in humans. Some phthalates may have common health or ecological effects of concern, so the potential for cumulative risk from combined exposure to these substances was addressed by considering an additional 14 phthalates. The additional 14 phthalates did not meet categorization criteria and were therefore not identified as priorities for assessment. However, they were selected for inclusion in the evaluation of cumulative risk on the basis of information indicating that their mode of action is likely to be similar to that of phthalates in the grouping, as well as evidence that they may represent a potential for exposure to the general population of Canada and to the Canadian environment. Four of the additional phthalates (DBP, BBP, DEHP and DnOP) were previously assessed, on an individual basis, in the First or Second Priority Substances Lists (PSL1 and PSL2) (Environment Canada and Health Canada 1993, 1994a,b, 2000). DBP and BBP were determined to not present a risk to the environment or to human health. DnOP was found to not present a risk to the environment; however, at the time of the assessment, the available information was not sufficient to allow a conclusion in terms of human health. A subsequent report published by Health Canada in 2003 concluded that DnOP did not pose a risk to human health. DEHP was determined to present a risk to human health in Canada; however, there was insufficient information to conclude on the potential for risk to the environment.

Screening assessments focus on information critical to determining whether substances meet the criteria as set out in section 64 of CEPA^{Footnote 2}. This is done by examining scientific information and incorporating a weight-of-evidence approach and precaution. This draft screening assessment considered information about chemical properties, environmental fate, hazards, uses and exposure, including information submitted by stakeholders. Relevant data were identified up to April 2016 for the ecological portion and up to July 2016 for the health portion of this draft screening assessment. 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. This draft screening assessment presents the critical information and considerations on which the proposed conclusion is based.

This screening assessment follows the August 2015 publication of four state of the science (SOS) reports (Environment Canada, Health Canada 2015a,b,c,d) for the 14 substances in the Phthalate Substance Grouping, and of a document entitled Proposed Approach for Cumulative Risk Assessment of Certain Phthalates under the Chemicals Management Plan (Environment Canada, Health Canada 2015e). These documents were released ahead of the screening assessment in order to allow for the receipt of comments and suggestions from interested parties relating to the proposed cumulative risk assessment approach. Comments received during the 60-day public comment period were taken into consideration during the preparation of this draft screening assessment. The screening assessment summarizes the information presented in the four SOS reports and incorporates relevant new information. As well, the assessment presents risk characterizations for phthalates in the grouping, including analysis of the potential for cumulative risk (ecological risk and risk to human health), and provides proposed conclusions under section 64 of CEPA.

This draft screening assessment was prepared by staff in the Existing Substances Programs at Environment and Climate Change Canada and Health Canada and incorporates input from other programs within these departments. The ecological and human health portions of this draft screening assessment have undergone external written peer review and/or consultation. Comments on the technical portions relevant to the environment were received from Dr. Thomas Backhaus (Faust & Backhaus Environmental Co., Germany), Sonja Bissegger (Royal Military College of Canada), Dr. Valerie Langlois (Royal Military College of Canada), Dr. Lynn McCarty (L.S. McCarty Scientific Research & Consulting, Canada), and Patricia Schmieder (U.S. Environmental Protection Agency). Comments on the technical portions relevant to human health were received from Linda Teuschler (Private consultant - retired from US EPA), Donna Vorhees (The Science Collaborative), Bernard Gadagbui (Toxicology Excellence for Risk Assessment), and Dr. Raymond York (RG York & Associates). While external comments were taken into consideration, the final content and outcome of the screening assessment remain the responsibility of Environment and Climate Change Canada and Health Canada.

The draft screening assessment presents the critical information and considerations on which the proposed conclusions are based. Additional details are provided in the SOS reports and cumulative risk assessment (CRA) document referred to above.

2. Identity of substances

The phthalate esters (phthalates) examined in this draft screening assessment are listed in Table 2-1. Structurally, these phthalates are comprised of a benzene ring with two ester side groups in the ortho position.

Substances in the Phthalate Substance Grouping were divided into short-chain, medium-chain and long-chain subgroups, depending on the length of the carbon backbone (i.e., the longest straight chain of carbons) in their ester side-groups. Short-chain phthalates are those with a carbon backbone length of 1 or 2, medium-chain phthalates have a backbone length of 3 to 7 carbons and long-chain phthalates have a backbone length of 8 carbons or greater. The nature of the ester side-groups, which can be linear, branched or cyclic, determines both the identity of the particular phthalate and its physical and toxicological properties.

The primary basis for the subgroups from a health hazard perspective was a structure activity relationship (SAR) analysis using studies related to important events in the mode of action for phthalate-induced androgen insufficiency during male reproductive development in the rat. The effects of phthalate esters for these important events appear to be structure-dependent and highly related to the length and nature of their alkyl chain. From an ecological perspective, subgrouping was based primarily on differences in log K_ow and water solubility and their resulting effects on bioaccumulation and ecotoxicity. For the purposes of the health review, DINP was included with the medium-chain phthalates subgroup, while for the purposes of the ecological review, it was considered to align more closely with the long-chain phthalate subgroup.

The chemical structure, molecular weights, water solubilities and octanol-water partition coefficients (log K_ow) for phthalates in the Phthalate Substance Grouping are listed in Appendix A. Additional information is provided in Environment Canada, Health Canada (2015a,b,c,d,e), Environment and Climate Change Canada (ECCC 2016) and Health Canada (2016a,b).

In some cases, a read-across approach using data from analogues and the results of quantitative structure-activity relationship (QSAR) models were used to inform the ecological and human health assessments. Model results and descriptions of methods used for analogue selection are provided in Environment Canada, Health Canada (2015a,b,c,d) and Health Canada (2016a,b).

3. Physical and chemical properties

The chemical properties of substances in the Phthalate Substance Grouping are primarily determined by the molar volume of the substance and the length of the alkyl side-chains substituted on the diester groups (Cousins et al. 2003). Substances in the grouping are oily liquids at typical ambient temperatures. Melting points for substances in the grouping vary between -64°C and 66°C, and boiling points are between 205°C and 463°C. Therefore, some phthalates in the grouping have the potential to be present in the solid state at low temperatures in the environment. In general, water solubility and vapour pressure decrease with increasing molar volume and alkyl side-chain length, while the tendency to adsorb to organic materials and particulates increases. For example, the short-chain phthalate DMP has very high water solubility (4000 mg/L), moderate vapour pressure (0.4 Pa) and low partition coefficients (log K_ow 1.6, log K_oc between 1.9 and 2.5), while the long-chain phthalate DIDP has very low water solubility and vapour pressure (1.7 × 10^-4 mg/L, 6.7 × 10^-5 Pa) and high to very high partition coefficients (log K_ow greater than 8, log K_oc5.5). Medium-chain phthalates display a range of chemical property values intermediate between those of short- and long-chain phthalates. Detailed information about chemical property values for substances in the Phthalate Substance Grouping is provided in the SOS reports (Environment Canada, Health Canada 2015a,b,c,d).

4. Sources

Anthropogenic activities are the major source of phthalates in the environment. An industry survey issued pursuant to section 71 of CEPA was conducted in 2013 to obtain information on quantities in commerce in 2012 for substances in the Phthalate Substance Grouping and for the additional phthalates in Canada (Canada 2013). Results are presented in Tables 4-1 and 4-2 (Environment Canada 2014). Because of the targeted nature of the survey, reported use quantities may not fully reflect all uses in Canada.

5. Uses

The results of a CEPA section 71 industry survey for 2012 included information on uses for 21 phthalates (Environment Canada 2014). No information was available for the other 7 substances.

Canadian uses identified for phthalate substances included in the Phthalate Substance Grouping are summarized in the SOS reports (Environment Canada, Health Canada 2015a,b,c,d). For the additional phthalates, Canadian uses are identified in Tables 5-1, 5-2 and 5-3. Additionally, international uses of phthalates can also be found in the SOS documents (Environment Canada, Health Canada 2015a,b,c,d).

6. Releases to the environment

There are no known major natural sources of phthalates, and releases to the environment are associated with anthropogenic activities. Releases may occur during the manufacture and processing of phthalates, including transportation and storage, as well as during production, use and disposal of products that contain phthalates (e.g., release of phthalates into wastewater systems from use of cosmetics). Phthalates are not chemically bound to polymer matrices during processing activities and can migrate to the surface of polymer products over time. The rate of this migration is expected to be slow and will be counteracted by chemical and physical attractive forces that work to hold the phthalates within polymers. Given their consumer and industrial applications, releases of phthalates to the environment are expected to occur primarily to air and to water.

Information on releases of phthalates in Canada is limited. Six phthalates (DMP and five of the additional phthalates, i.e., DEP, DBP, BBP, DEHP and DnOP) are reportable to the National Pollutant Release Inventory (NPRI), where all reported releases were to air (NPRI 2010-2014). For the section 71 survey, many submissions indicated no or unknown releases (Environment Canada 2014).

Further discussion on the potential for environmental release is provided in Environment Canada, Health Canada (2015a,b,c,d).

7. Environmental fate and behaviour

7.1 Environmental distribution

The EQC Level III fugacity model (New EQC 2011) was used to predict the environmental mass-fraction distributions of the short-, medium-, and long-chain phthalates. Environmental distribution trends were largely driven by the phthalates' capacity to solubilize in water, volatilize or adsorb to particles, where smaller more soluble substances tended to be associated with the air and aquatic media, and larger substances with limited water solubility tended to adsorb to sediment or remain in soil. The EQC model results show that the short-chain phthalates distribute into water, soil and air, but not into sediment, the medium-chain phthalates distribute more evenly between water and sediment, and the long-chain phthalates distribute mainly into sediment, with a lesser proportion remaining in water. Soil was predicted to be an important receiving compartment for the medium- and long-chain phthalates (that is, if released to air or soil, the medium- and long-chain phthalates primarily remain in soil). The results from the Level III fugacity modelling showing percent distribution into water, soil and sediment based on simulated release into each compartment are summarized in ECCC (2016).

On the basis of the known uses and releases of phthalates (see Sections 5 and 6), water is considered to be the key receiving environmental compartment of phthalates.

7.2 Environmental persistence

The degradation of phthalates is well-characterized, and phthalates are known to be degraded by abiotic and biotic processes. Numerous studies have been conducted for the short-chain phthalates DMP and DEP, the medium-chain phthalates DIBP, DCHP, B79P, BBP, DBP and DEHP, and the long-chain phthalates DIDP, DUP and DINP. Many of these studies have been used to characterize the less-studied phthalates, including the medium-chain phthalates BCHP, CHIBP, DBzP, DMCHP, BIOP, B84P, 79P, DIOP, DnHP, DPrP and DIHepP, and the long-chain phthalates 610P, D911P, D911P-2, DTDP, DIUP and DnOP. Summaries of degradation studies and QSAR modelling are available in the SOS reports (Environment Canada, Health Canada 2015a,b,c,d) and in ECCC (2016).

Abiotically, phthalates undergo hydrolysis, which tends to be slow, and relatively fast photolysis (Peterson and Staples 2003). It is biodegradation-particularly in aerobic conditions, by micro-organisms, including the green microalgae species (Chang et al. 2005; Yan and Pan 2004; Yan et al. 2002), phytoplankton (Li et al. 2007) and fungi (Ganji et al. 1995; Sivamurthy et al. 1991; Engelhardt et al. 1977; Kim and Lee 2005; Lee et al. 2007; Kim et al. 2002a, 2003, 2007)-that contributes most to the breakdown of these substances in the environment. The observed biodegradation rates vary and are influenced by the molecular size and physicochemical properties of phthalates, substrate concentration and environmental conditions. The (Q)SAR model-generated data are in agreement with the experimental data. The biodegradation of phthalate esters releases monoalkyl phthalate esters (MPEs) into the environment (McConnell 2007). Most studies suggest that biodegradation rates of MPEs proceed faster than those of phthalate esters (Peterson and Staples 2003). MPEs were shown to be quickly degraded in natural sediments (Otton et al. 2008).

Studies have demonstrated that phthalates with shorter side-chains can be readily biodegraded and mineralized, whereas phthalates with longer side-chains tend to be somewhat less biodegradable (Wang et al. 2000; Chang et al. 2004; Zeng et al. 2004; Lertsirisopon et al. 2006; Liang et al. 2008). The differences in biodegradability among phthalates are attributed to the steric effects of the side-chains, where binding of hydrolytic enzymes can become hindered, resulting in limited hydrolysis. Differences in phthalate isomers can also influence rates of degradation, as phthalate-hydrolyzing enzymes are structurally specific (Liang et al. 2008).

The short-chain phthalate DMP has a long modelled half-life in air. Its measured concentrations in biota in Hudson's Bay and in air and water of the Norwegian Arctic indicate that it has some potential for long-range transport (Morin 2003). Medium- and long-chain phthalates are not persistent in air, and modelling results suggest that they are unlikely to have the potential for long-range transport (see Environment Canada, Health Canada 2015a,b,c,d), although DEHP, DBP, DIBP, DnBP, and DINP and the short-chain phthalate DEP can be associated with fine particles in areas close to emission sources (Ma et al. 2014; Ruzicková et al. 2016). DIBP was also found in biota in the Arctic (Morin 2003). Fine particle transport is considered a plausible explanation for the observed presence of DMP and DIBP in remote areas.

Phthalates have been detected in fresh water worldwide and tend to adsorb to sediments (Chang et al. 2005). In surface water, most phthalates are readily biodegradable (Furtmann 1994). In sediments, both aerobic and anaerobic microorganisms can degrade phthalates (Hashizume et al. 2002; Chang et al. 2004; Kim et al. 2008). However, despite their inherent biodegradability, phthalates can exhibit long half-lives in sediments because of the high degree of sorption driven by their hydrophobicity (Kickham et al. 2012). In aerobic biodegradation studies conducted according to the Organisation for Economic Cooperation and Development (OECD) guidelines and where wastewater treatment system sludge is used as substrate, phthalates were found to be both inherently and readily biodegradable (Environment Canada, Health Canada 2015a,b,c,d). The apparent variability in test results can be attributed to the differences in experimental protocols, concentrations of the test substance, and the substrate.

In soil, the patterns for biodegradation rates are generally very similar to those in water (Peterson and Staples 2003). Environmental conditions, such as temperature, soil moisture and oxygen levels, as well as initial substance concentrations and soil type, all have an impact on the biodegradation rate (Peterson and Staples 2003; Madsen et al. 1999; Scheunert et al. 1987). For example, half-lives for DEHP in different types of soil ranged from 2 days in loam soil to 69.3 days in sand (Rüdel et al. 1993; Shanker et al. 1985; Roslev et al. 1998; Peterson and Staples 2003) and were up to 77 days in bioremediated soil from an industrial site in Brazil (Ferreira and Morita 2012).

7.3 Potential for bioaccumulation

Bioaccumulation data for the substances in the Phthalate Substance Grouping and certain additional phthalates that were used for read-across (i.e., BBP and DEHP) are provided in the SOS reports (Environment Canada, Health Canada 2015a,b,c,d). Bioaccumulation data for other additional phthalates or obtained after the SOS reports were published are in agreement with the data presented in the SOS reports and are summarized in ECCC (2016).

Phthalates are bioavailable in the environment and certain phthalates have been measured in biota. The experimental and modelled bioaccumulation data and measurements of phthalate metabolites in aquatic organisms suggest that phthalates are effectively metabolized and thus do not tend to significantly bioaccumulate. Measured bioconcentration factors (BCFs) and bioaccumulation factors (BAFs) for aquatic species range from as low as 1 to over 3000 L/kg, with the majority of the reported values below 1000 L/kg. Biotransformation rates were found to be in the range of less than 1 to 3.5 day^-1. Data for sediment- and soil-dwelling organisms were also available for some phthalates and indicated that bioaccumulation in these media is not significant. Field studies confirm that phthalates do not biomagnify in the food chain (summarized in Environment Canada, Health Canada 2015a,,b,c,d).

8. Potential to cause ecological harm

8.1 Ecological effects assessment

Detailed summaries of the available effects studies for substances in the Phthalate Substance Grouping and for a number of additional phthalates and the related critical body residue calculations are presented in the SOS reports (Environment Canada, Health Canada 2015a,b,c,d), and results of additional studies, including those newly available, are tabulated in ECCC (2016). Results from toxicity studies on rodents considered as surrogates for piscivorous mammals, such as mink and otters, are presented in Health Canada (2015) and in the Human Health Effects section of this screening assessment. An analysis of the overall ecological effects dataset for phthalates, observations related to their modes of action, and key ecological effects are summarized below. Emphasis is placed on aquatic organisms, given that water is considered to be the key receiving environmental compartment of phthalates. Data on both freshwater and marine organisms are considered collectively, with no distinction made between them, as there is no reason to suspect that one or the other would have greater sensitivity to phthalates.

At acute exposure levels, phthalates have been shown to act through diester toxicity, which is a non-specific mode of action similar to baseline (non-polar) narcosis and polar narcosis, but resulting in slightly higher toxicity (Veith and Broderius 1987; Veith and Broderius 1990; Adams et al. 1995). The body of data shows that under longer-term exposures many phthalates also act through specific modes of action (MoAs). These MoAs are well documented in mammalian studies for the medium-chain phthalates, notably androgen-dependent effects affecting development of the male reproductive tract (reviewed in Health Canada 2015). In aquatic organisms, studies with exposures to phthalates of lower chain lengths, i.e., the short- and a number of medium-chain phthalates, show an array of apical and non-apical effects. Non-apical effects have been linked to estrogen and thyroid-mediated cellular pathways; however, the androgen-dependent responses have not been extensively studied in non-mammalian organisms. Non-apical responses implicated in development, reproduction, and cellular stress have been identified for certain short- and medium-chain phthalates, as well as the long-chain phthalate DnOP (Mathieu-Denoncourt et al. 2015). It is noted that for certain well-studied phthalates (e.g., BBP, DBP, DEHP) there is often variability or inconsistency among studies and model results in the observed effects or responses, such as changes in vitellogenin (VTG) levels or model estimates of receptor binding affinities. While this is likely due to the differences in design of assays and studies, it makes it a challenge to elucidate the precise MoA(s) underlying the observed effects.

8.1.1 Toxicity to aquatic organisms

Water solubility and log K_ow are important parameters that affect bioavailability of a substance in environmental media, thereby influencing its toxicity. Substances with very low water solubilities are likely to be less bioavailable in the environment through direct water uptake, with more likely exposure through the diet. Log K_ow can be an important parameter in predicting acute toxicity for many MoAs, e.g., non-polar narcosis, polar narcosis, ester narcosis, but not for others characterized by reactive mechanisms, including electrophile MoAs. Interestingly, log K_ow was also observed to correlate with a receptor-based MoA, i.e., estrogen receptor (ER) binding affinity. For a series of industrial chemicals including phthalates, the binding affinity to rainbow trout ER was found to increase linearly with log K_ow values in the range of 1.6 to 4.6 (DMP to DBP and BBP) and to remain nearly constant at greater lipophilicity, as seen for DnHP with a log K_ow of 6.6(Hornung et al. 2014). Phthalates with higher log K_ow(e.g., DEHP, DnOP) did not bind to the ER. For long-chain phthalates, which are characterized by very low water solubilities and high log K_ow values, diester toxicity seems to be the prevalent acute mode of action. It has been suggested that phthalates with alkyl chains of six or more carbons do not cause intrinsic toxicity to aquatic organisms as the rapid metabolism and low water solubility prevent the critical toxicity body burden from being reached (Bradlee and Thomas 2003). Indeed, for many of the phthalates with carbon backbones of 8 or more carbons, no acute effects have been observed below solubility limits, and the calculated tissue residues were low, not exceeding thresholds for lethal effects (see Table 8-3). However, for the poorly soluble medium-chain phthalates with backbones of 6 or 7 carbons, e.g., DEHP and B79P, high toxicities have been noted (summarized in Environment Canada, Health Canada 2015b; ECCC 2016).

An analysis of the available effects data for aquatic organisms was conducted for each phthalate. A simplified schematic is presented in Table 8-1, where data availability is noted for each substance from in vivo standard testing and studies characterizing effects linked to estrogen-, androgen-, and the thyroid-mediated pathways either in vivo or in vitro. In silico tools, including ER Expert System (ERES) (version 3) [Schmieder et al. 2014; personal communication, external peer review by US EPA, Office of Research and Development, National Health and Environmental Effects Research Laboratory Mid-Continent Ecology Division, April 2016 (ERES binding predictions 4-20-16 Excel spreadsheet), unreferenced] and TIMES (2014) have also been used to identify receptor binding potential of phthalates. In silico-determined binding potential of phthalates is presented in Table 8-2 for rainbow trout ER (from ERES version 3) and rodent ER (including both parent compounds and their metabolites) and androgen (AR) receptor (TIMES 2014). According to the TIMES (2014) model, metabolites of certain long-chain phthalates showed affinity for the ER, while their parent compounds were predicted to have no binding affinity for the ER.

Large data gaps were found in ecological effects information for phthalates, even though certain phthalates, such as DEHP, BBP and DBP, have been relatively well studied. Of particular importance is the lack of studies characterizing the relative potency of phthalates across the subgroups. The few studies that look at effects in the same biological system include only a small subset of phthalates, and since different endpoints are characterized, a direct comparison is not possible. Mankidy et al. (2013) observed that DEHP was more potent than BBP, on the basis of potency as an agonist of the aryl hydrocarbon receptor (AhR), whereas Zhou et al. (2011a) established a potency order of DBP greater than DEP greater than DMP greater than DnOP greater than DEHP based on abalone metamorphosis. Another limitation found in many studies is the tendency to conduct them at exposure concentrations that are high or that exceed water solubility limits, which makes interpretation of results complicated and results in little relevance to environmental conditions. It is noted that in the few in vivo studies performed at very low exposure concentrations (in the range of 10^-4 to 10^-3 mg/L), such as those for DEHP (Oehlmann et al. 2009; Carnevali et al. 2010; Corradetti et al. 2013), deleterious effects continue to be observed. The key data gap is the lack of aquatic effects studies for phthalates conducted at environmentally relevant exposure concentrations and within solubility limits, which characterize modes of action, particularly related to the androgen-mediated pathways, and that could be linked to population-level effects.

Below is a brief summary of some of the available effects data for the short-, medium-, and long-chain phthalates that describes both standard studies and those describing specific MoAs. It is meant to highlight effect levels across phthalate subgroups, as observed based on standard and non-standard testing. Available ecological effects information has been previously summarized in detail in Environment Canada, Health Canada (2015a,b,c,d), and additional and newly published studies are noted in ECCC (2016).

Standard toxicity testing indicates that the soluble short-chain phthalates have low acute and chronic toxicity to fish, invertebrates, and algae. For DMP and DEP, fish acute median lethal concentration (LC₅₀) values were in the range of 10 to 120 mg/L (summarized in ECCC 2016). Similarly, LC50 values and median effective concentration (EC₅₀) values for effects such as immobility and changes in biomass, on mysid shrimp, daphnids and algae and malformations in tadpoles were noted at exposure concentrations generally greater than 10 mg/L (summarized in Environment Canada, Health Canada 2015a; ECCC 2016; Mathieu-Denoncourt et al. 2016). In contrast, studies with abalone suggest that this species is particularly sensitive to DMP and DEP exposure, with adverse effects established through modes of action other than narcosis. For DMP, effects on larval settlement were noted at an exposure concentration of 0.05 mg/L (Yang et al. 2009), and a no observed effect concentration (NOEC) for metamorphosis was determined as 0.02 mg/L, with a 50% reduction in metamorphosis at 0.2 mg/L (Liu et al. 2009). In terms of reproductive effects, DMP-treated abalone sperm were found to exhibit dose-dependent decreases in fertilization efficiency, morphogenesis and hatchability at exposure concentrations between 0.01 mg/L and 0.1 mg/L (Zhou et al. 2011b). At an exposure concentration of 0.2 mg/L, DEP was found to reduce metamorphosis rates, and at 2 mg/L it resulted in increased abnormality rates of abalone embryos and reduced hatching rates (Zhou et al. 2011a).

For the medium-chain phthalates, moderate to high toxicity has been observed in numerous studies with aquatic organisms (summarized in Environment Canada, Health Canada 2015b; ECCC 2016). Results indicate that those with side-chain backbones of six or fewer carbons-i.e., DBP, BBP, DCHP, DEHP and B79P-are highly hazardous to fish, invertebrates, and algae, where LC50 and effects such as behavioral abnormalities in fish, reproductive effects in daphnids, and effects on biomass in algae were observed at an exposure concentration of less than 1 mg/L. Secondary effects linked to estrogenic, thyroid-, or anti-androgenic modes of action are also relatively well documented for these substances, although inconsistent responses have been observed for alteration of VTG levels in studies with BBP and DEHP. BBP was shown to displace estradiol from the hepatic estrogen receptor, to inhibit ER binding, to either alter VTG production in rainbow trout following intra-peritoneal injection (Christiansen et al. 2000) or to have no impact on VTG levels in studies with fathead minnow (Study Submission 2014d; Harries et al. 2000), to impact gonadal histology (Study Submission 2014d) and to reduce spermatogonia of fathead minnows (ECHA 2009; ECHA c2007-2015). BBP also exhibited a small but significant increase in the expression of mRNA of the androgen receptor in developing fish embryos (Mankidy et al. 2013).

Most toxicity studies for DCHP in fish, amphibians, invertebrates and algae were conducted at exposure concentrations above the substance's water solubility limit (ECHA c2007-2014b; Mathieu-Denoncourt et al. 2015; Mathieu-Denoncourt et al. 2016). Two Daphnia studies, within the water solubility limit for DCHP, showed effects at low exposure concentrations, but only with chronic exposure (21-day EC₅₀ and NOEC for loss of mobility at 0.68 and 0.18 mg/L, respectively) (ECHA c2007-2014b). For DBP, 96-hour LC₅₀s of less than 1 mg/L to 7.3 mg/L in fish were determined (Buccafusco et al. 1981; Mayer and Ellersieck 1986; CMA 1984; Hudson et al. 1981; Adams et al. 1995). DBP did not induce VTG in rainbow trout or zebrafish at concentrations up to 1 mg/L (Van den Belt et al. 2003). DBP exposure concentrations in the range of 0.005 to 0.5 mg/L in different studies increased larval mortality and teratogenicity (Ortiz-Zarragitia et al. 2006), increased activity of anti-oxidant enzymes and immune-related enzymes (Xu et al. 2013), and altered plasma 11-ketotestosterone and spiggin levels (Aoki 2010; Aoki et al. 2011). For DEHP, Carnevali et al. (2010) found a significant reduction in fecundity of female zebrafish exposed to nominal concentrations ranging from 2 × 10^-5 to 0.40 mg/L. Corradetti et al. (2013) also found that exposure to DEHP at a concentration of 2 × 10^-4 mg/L impaired reproduction in zebrafish by inducing a number of changes, including reduced embryo production. Histological changes in fish spermatozoa and gonads (indication of intersex) and retardation of oocyte development following exposure to DEHP have also been reported (Ye et al. 2013; Kim et al. 2002b; Norman et al. 2007). While B79P studies on fish and algae were conducted at concentrations above the substance's water solubility limit, two studies on daphnids indicate that B79P is highly toxic. An acute EC50 of 0.3 mg/L and a chronic NOEC for reproduction of 0.039 mg/L were determined (ECHA c2007-2014c). It is noted that these endpoints are consistent with the modelled data for aquatic species, in the range of 0.0045 mg/L for fish to 0.05 mg/L for daphnids (summarized in Environment Canada, Health Canada 2015b). (Q)SAR modelling indicates that B79P also has ER binding potential (see Table 8-1).

No evidence of toxicity was seen in standard testing for the medium-chain phthalates with longer carbon backbones-i.e., DIHepP and B84P-or for the long-chain phthalates up to their water solubility limits (summarized in Environment Canada, Health Canada 2015b-d). However, for phthalates DIDP and DINP, results from in vitro laboratory testing provide preliminary indications that DIDP and DINP might influence normal endocrine activity in mammalian species by altering the production of steroid hormones in the presence of an endocrine-active substance (Mlynarcíková et al. 2007; Chen et al. 2014). In a multigenerational feeding study with Japanese medaka, effects in hepatic microsomal testosterone metabolism were observed for DINP and DIDP; however, consistent adverse effects on embryo mortality, hatching success or survival were not observed (Patyna et al. 2006). Similarly, malformation and alterations in gene expression related to androgen axis were also not observed in Xenopus tadpoles following exposure to DINP (de Solla and Langlois 2014). In silico results from the Estrogen Receptor Expert System (ERES) model with trout ER (Schmieder et al. 2014; personal communication, external peer review by US EPA, Office of Research and Development, National Health and Environmental Effects Research Laboratory Mid-Continent Ecology Division, April 2016; unreferenced) suggest no ER binding affinity for the long-chain phthalates parent compounds (see Table 8-2).

The available aquatic effects data for the medium- and long-chain phthalates with very low water solubilities and high log K_ow values-i.e., DIHepP, DINP, D911P, D911P-2, DIDP, DIUP, DTDP, DUP, B84P and DIOP-were above water solubility limits. It is noted that for these substances, dietary exposure is likely the more relevant route of uptake in the environment. Therefore, for DIHepP, B84P, DINP, DIDP and DUP, tissue residues (TRs) were calculated using substance-specific bioaccumulation factors (BAFs), molecular weights and water solubilities. The TR represents the internal whole body concentration of a phthalate resulting from exposure at its limit of solubility in water, taking into account its toxicokinetics as approximated by the BAF. The calculated TR values for medium-chain phthalates ranged from 5.4 × 10^-3 mmol/kg (1.96 mg/kg) for DIHepP to 0.13 mmol/kg (59.1 mg/kg) for B84P and were low for the long-chain phthalates DINP at 2.6 × 10^-4 mmol/kg (0.12 mg/kg), DIDP at 1.5 × 10^-5 mmol/kg (0.007 mg/kg), and DUP at 5.8 × 10^-8 mmol/kg (0.000028 mg/kg). Critical body residues (CBR) associated with acutely lethal baseline narcosis in small aquatic organisms typically range from about 2 to 8 mmol/kg, while those for chronic exposures range from 0.2 to 0.8 mmol/kg (McCarty and Mackay 1993). The calculated internal concentrations for the subset of the medium-chain and long-chain phthalates indicate that these phthalates are unlikely to reach levels sufficient to cause acute or chronic lethal effects toxicity in aquatic organisms, as the CBR thresholds are not surpassed. It is noted that CBR thresholds have not been developed for other modes of action including diester toxicity, and baseline narcosis is therefore assumed for those phthalates with TR calculations. It is recognized that somewhat lower CBR thresholds may be associated with other MoA(s), and thus baseline narcosis MoA may underestimate the potential toxicity, particularly under chronic exposure. Nonetheless, an overlap between CBRs for narcosis and diester toxicity is expected; accordingly, the narcosis CBR is considered appropriate for use with phthalates.

8.1.1.1 Predicted no-effect concentrations for the aquatic compartment

When experimental data were not available, modelled and analogue data were used to select critical toxicity values for the short- and medium-chain phthalates (summarized in Environment Canada, Health Canada 2015a,b). Predicted no-effect concentrations (PNECs), obtained by dividing critical toxicity values (CTVs) by the appropriate assessment factors (AFs), were then calculated and ranged from 0.00007 mg/L (DEHP) to 0.19 mg/L (DIBP). The CTVs, AFs and calculated PNECs for each phthalate are presented in Table 8-3. When PNECs could not be derived, TR to CBR comparisons were made. PNECs for the additional phthalates, which are not being assessed, ranged from 0.003 mg/L to 0.33 mg/L and can be found in ECCC (2016).

8.1.2 Toxicity to sediment-dwelling organisms

Sediment toxicity data are very limited for phthalates. Data for the short-chain phthalate DEP indicate low toxicity. Data for the medium-chain phthalates DBP and DEHP also indicate low toxicity (Call et al. 2001b; Brown et al. 1996). BBP, however, was found to be highly toxic to sediment-dwelling organisms (in water exposure studies) (Call et al. 2001a). For those medium-chain phthalates where PNECs in sediment could be calculated, they ranged from 0.76 mg/kg dw (B79P) to 97.8 mg/kg dw (DMCHP) , and were well below the calculated values for maximum saturation in sediment (where maximum saturation in sediment was calculated using the substance's water solubility, organic carbon-water partition coefficient (K_oc), and a default value of 0.04 for Canadian sediment organic carbon content). Tissue residue calculations were done for those medium-chain phthalates where effects data were above water solubility limits or not available. The highest calculated tissue residue in sediment-dwelling organisms was for DIHepP at 0.05 mmol/kg, which indicates that internal concentrations for medium-chain phthalates are unlikely to reach levels sufficient to cause acute or chronic lethal effects. In sediment toxicity studies for the long-chain phthalates, no adverse effects were observed up to the highest concentrations tested, even including those concentrations which exceeded maximum saturation limits for the substances under the study conditions The calculated maximum tissue residue for DIDP, for example, was 0.008 mmol/kg, which is below levels sufficient to cause acute or chronic toxicity by narcosis MoA.

8.1.3 Toxicity to soil-dwelling organisms

Limited soil toxicity studies available for some short-chain phthalates (e.g., DMP) and medium-chain phthalates (e.g., BBP) indicate that these phthalates are not highly toxic to soil-dwelling organisms (summarized in Environment Canada, Health Canada 2015a,b). For the long-chain phthalates, CBR analyses for DINP and DIDP indicated that, up to soil saturation limits, internal concentrations of these substances are unlikely to reach levels sufficient to cause adverse effects (summarized in Environment Canada, Health Canada 2015c,d).

8.1.4 Toxicity to wildlife

Exposure of wildlife to short-chain phthalates via inhalation was evaluated, as these substances have a relatively high residence time in air (summarized in Environment Canada, Health Canada 2015e). An inhalation study for rats exposed to DEP (SCCNFP 2002) was used to derive a PNEC of 49 mg/m³.

Toxicity of phthalates to wildlife via food web exposure was not assessed quantitatively. Studies on secondary poisoning of wildlife were not found in the literature. Also, as noted previously in this report, phthalates are rapidly biotransformed in vertebrates and have low bioaccumulation and biomagnification potential. Therefore, exposure through the food web is not expected to pose a concern.

8.2 Ecological exposure assessment

Certain phthalates have been measured in environmental media including air, water, sediment, soil and biota in Canada and worldwide. Measured concentrations for the Phthalate Substance Grouping were presented in the SOS reports (Environment Canada, Health Canada 2015a,b,c,d). Measured concentrations for the additional phthalates in Canadian environmental media are summarized in ECCC (2016).

Information on phthalate concentrations in wastewater in Canada was obtained through a sampling campaign carried out by ECCC's Monitoring and Surveillance Program in 2014-2016. Samples of influent and effluent of on-site wastewater treatment systems at 5 industrial facilities involved in the manufacture or use of phthalates were collected and analyzed, along with samples of influent and effluent of the off-site wastewater treatment systems (WWTS)^{Footnote 3} to which the industrial sites direct their effluents. In addition to these 5 industrial sites and corresponding WWTS, the influents and effluents of 11 other Canadian WWTS were sampled and analyzed (personal communication; unpublished environmental surveillance data received in 2015 by Ecological Assessment Division, ECCC, from Aquatic Contaminants Research Division, ECCC; unreferenced). Detection limits ranged from 0.0001 μg/L to 20.7 μg/L for individual phthalates. Two phthalates, DIOP and CHIBP, were not detected in any effluent samples. Most removal efficiencies for on-site treatment were greater than 50%, with half being greater than 90% and the lowest being less than 6%. Most removal efficiencies for off-site treatment were greater than 50%, with less than one tenth being greater than 90% and the lowest being less than 8%.

Concentrations of the different phthalates found in the effluent of the 16 WWTS were used to calculate predicted environmental concentrations (PECs) in the receiving water near the WWTS discharge point. PECs were calculated using the following equation:

PEC = C_eff / DF

Where

PEC: predicted environmental concentration in the receiving water body, μg/L
C_eff: phthalate concentration in the WWTS effluent, μg/L
DF: receiving water dilution factor (ratio of the WWTS effluent flow to the flow of the receiving water body), dimensionless.

In the risk quotient approach^{Footnote 4} the 10^th percentile flow of the receiving water body was used to calculate the DF. A 10^th percentile flow is used to represent conditions during approximately the lowest flow over 30-day periods, which are equivalent to typical chronic toxicity test durations. The 30-day low flows are expected and assumed to occur consecutively (summer). The resulting environmental concentrations are then compared directly to an effects concentration. Additionally, to estimate concentrations of phthalates near the point of release (near-field), the DF was limited to 10.

Taking into account the longer period of time required for phthalates to accumulate in an organism's tissues, the DF for the cumulative approach was calculated using the 50^thpercentile flow of the receiving water body. The 50^thpercentile flow is used as it is deemed to more appropriately reflect the average environmental concentrations that would lead to accumulation in the organism's tissues. The use of this longer averaging period is also considered more appropriate for cumulative effects, as the highest concentrations of phthalates (used in the cumulative approach) occur at different times and locations. Short-term releases of aggregated quantities of phthalates are not expected to occur. In the case of the cumulative approach, no limit to the DF was set because the cumulative approach is not restricted to the area (near-field) where the release occurs.

PECs for industrial users and manufacturers of phthalates that were not covered by the sampling campaign were calculated using emission factors obtained from similar industrial sites where monitoring data were available. Removal rates for on-site or off-site WWTS that were not sampled were also estimated using the monitoring data for WWTS with similar types of treatment. In these cases, PECs were calculated using the following equation:

PEC = (Q × C × E × (1 - R)) / (N × F × DF)

Where

PEC: predicted environmental concentration in the receiving waterbody, μg/L
Q: total yearly quantity of substance manufactured or used at an industrial site, kg/yr-site
C: conversion factor from kg to μg, 1 x 10⁹μg/kg
E: emission factors, fraction
R: WWTS removal rate, fraction
N: number of annual release days, d/yr
F: effluent flow, L/d
DF: receiving water dilution factor (ratio of the WWTS effluent flow to the flow of the receiving water body), dimensionless.

In the risk quotient approach, the 10^th percentile flow of the receiving water body was used to calculate the DF. To estimate concentrations of phthalates near the point of release (near-field), the DF was limited to 10. Taking into account the longer period of time required for phthalates to accumulate in an organism's tissues, the DF for the cumulative approach was calculated using the 50^th percentile flow. Also, no limit to the DF was set because the cumulative approach is not restricted to the area (near-field) where the release occurs.

Table 8-4 shows the ranges of near-field PECs developed from the monitoring and modelling discussed above. Approximately 600 PECs have been generated this way. Of the quantities manufactured or used that were reported under the s.71 survey for 2012, 95% have been accounted for by the monitoring and modelling. The remaining 5% are small volume uses and uses that are not expected to lead to significant aquatic release. The three substances with the highest PECs were B79P (3.8 μg/L), DINP (3.4 μg/L), and DCHP (3.2 μg/L).

An analysis of the locations where both industrial and municipal monitoring was available suggests that phthalate loading from the known industrial phthalates manufacturers or users generally accounted for less than 10% of the total phthalate loading in the off-site WWTS influents. There were only two cases (DUP and B79P) where it was possible to link the presence of phthalate in a WWTS influent to an industrial user or manufacturer. This suggests that a large part of the phthalates found in the influents of off-site WWTS may be coming from other sources, such as wastewater from residential and commercial sources, industrial sources not captured by the s. 71 survey reporting requirements, or landfill leachate.

Out of the 16 off-site WWTS that were part of the sampling campaign, 3 are receiving and treating leachate from nearby landfills. For each phthalate in each of the WWTS, a per capita influent loading was estimated. Except for 1 phthalate (DUP), where an industrial source has been identified, it was found that the average per capita loading of phthalates for a WWTS that receives landfill leachate was 2 to 9 times higher than the average per capita loading of phthalates for a WWTS that did not receive leachate. This suggests that landfill leachate may represent a non-negligible source of phthalates in WWTS influent. However, because the total quantity of phthalates entering landfills through end-of-life products, manufactured items or other materials is not known, and because concentrations of phthalates in landfill leachate were not measured, it is not presently possible to confirm or quantify the contribution of landfill leachate as a source of phthalates to WWTSs.

8.3 Characterization of ecological risk

8.3.1 General considerations

Phthalates are released both during various industrial activities and continuously through consumer use of products and manufactured items that contain phthalates, with environmental releases occurring primarily to water via off-site wastewater treatment systems. Phthalates are not chemically bound to polymer matrices, so they can migrate slowly to the polymer surface, and then possibly enter the environment. Phthalates will biodegrade rapidly and are not expected to be recalcitrant in the environment. Degradation may be slightly slower under anaerobic conditions, thereby increasing the duration of exposure to organisms. According to information about releases and the predicted distribution in the environment, aquatic and soil-dwelling organisms close to release sites will have the highest potential for exposure. Phthalate concentrations are expected to decrease with increasing distance from points of release; however, long-range atmospheric transport potential has been identified for the short-chain phthalate DMP (Morin 2003). There is also evidence that other phthalates are transported in the atmosphere on fine particles (Ruzicková et al. 2016).

The aquatic compartment is thought to be the key receiving environmental compartment for all phthalates. Releases to the aquatic compartment are continuous, and even the long-chain phthalates, which are highly hydrophobic, are detected in water. Distribution of phthalates between environmental media depends primarily on which medium they are emitted to and also on their water solubility and partition coefficients. Short-chain and some medium-chain phthalates are expected to reside predominantly in water, and the long-chain and other medium-chain phthalates are expected to partition to sediments and adsorb to particles. Toxicity data available for soil- and sediment-dwelling organisms indicate that effects are not likely to occur at environmentally relevant concentrations. No toxicity below solubility limits or soil/sediment saturation levels was found for long-chain phthalates and some of the larger medium-chain phthalates (e.g., DIHepP, B84P). The focus of this assessment is therefore on aquatic organisms, for which deleterious effects from phthalate exposure have been observed. Acute effects of short- and medium-chain phthalates in aquatic organisms range from high (LC₅₀ of 0.08 mg/L) to moderate (LC₅₀ of 10 mg/L).

8.3.2 Cumulative risk assessment using grouping and additional phthalates

Where similar chemicals are potentially exerting combined effects on organisms through a common mode of action (MoA), it is appropriate to consider assessing risk from the cumulative exposure, rather than considering risk from each individual substance separately. In determining whether to conduct a cumulative risk assessment (CRA), the most important consideration is whether there is co-occurrence of the substances in one or more environmental media. In the case of phthalates, there are several lines of evidence to suggest the potential for co-occurrence in the environment. These include their uses, releases, degradation processes, and presence in wastewater treatment system effluents. The selection of which CRA method to use depends on whether there is a common MoA among the substances. There is sufficient evidence that, under short-term exposures, all phthalates are acting through narcosis and can be considered together in a CRA based on concentration addition (CA).

The selection of the specific CRA method depends on what types of data are available to characterize the effect and exposure concentrations of each substance. The Sum of Internal Toxic Units method was chosen from among the various CA methods available. This approach involves summing toxic units on the basis of internal toxic units (i.e., concentrations in organism tissues), rather than on the basis of external (i.e., water) exposure concentrations of substances. This is also referred to as a CBR approach.

The sum of internal toxic units (ITU_mix) for a group of substances is calculated using the equation shown below. For this CRA, the internal toxic unit for each substance is estimated by multiplying its estimated concentration in water (PECi) by the bioaccumulation factor (BAFi), and dividing by the critical body residue (CBR) associated with chronic lethality in aquatic organisms (0.2 mmol/kg for narcosis; McCarty and Mackay 1993), multiplying CBRi by MWi (the molecular weight of the substance), and finally applying an assessment factor (AF). An AF of 5 was applied because the CBR is based on lethality, so the AF is intended to extrapolate from median lethal effects to sublethal low- or no-level effects. A larger factor was not deemed necessary since the CBR is already for chronic (long-term) exposure.

Further detail about CRA methods, including the Sum of Internal Toxic Units (ITU) method, are found in a separate document (Environment Canada, Health Canada 2015e).

All 28 phthalates (the 14 substances in the Phthalate Substance Grouping and 14 additional phthalates) were included in a CRA calculation. Although no effects are typically observed for the long-chain phthalates when tested individually up to their solubility limits, they are the highest volume phthalates in Canadian commerce, and monitoring data shows that some of them are present in wastewater effluents and surface waters at high concentrations. The approach chosen (ITU method) accounts for the possibility that they might still be contributing to cumulative effects based on lethality due to the narcosis MoA. Support for this approach is provided by Mayer and Reichenberg (2006), who found that highly hydrophobic substances that do not demonstrate narcotic effects on their own could still contribute to the toxicity of complex mixtures.

For the ITU calculations, the highest PEC determined for each phthalate was used, resulting in a conservative assumption that the highest concentrations of all phthalates were co-occurring at the same site. The CBR value used (in the denominator) was 0.2 mmol/kg for chronic lethal exposures (McCarty and Mackay 1993). The results of the ITU calculations are shown in Appendix B (Table B-1). The sum of internal toxic units across the 28 phthalates, prior to application of an assessment factor, is 0.033. The highest toxic unit in the mixture is for BBP (0.02). Ten phthalates account for approximately 95% of the cumulative risk based on narcosis: BBP, D911P, DCHP, B79P, DIOP, DINP, DEHP, DBP, DEP, and DIHepP (Appendix B, Figure B-1).

When the AF of 5 is applied to the sum of ITUs, the final ITU_mix is 0.2 (0.033 x 5). This indicates that there is low risk from the mixture. An examination of contributions of the various phthalates to the mixture toxicity indicates that the overall toxicity is largely dominated by one substance, BBP (see Appendix B1).

8.3.3 Calculation of individual risk quotients and consideration of endocrine effects

In the SOS reports (Environment Canada, Health Canada 2015a,b,c,d), risk quotient (RQ) analyses for the aquatic medium were done for the short-chain and some of the medium-chain phthalates. For the other medium-chain and the long-chain phthalates, their low water solubility and high hydrophobicity suggest that dietary exposure will be the major route of exposure for organisms, rather than the surrounding medium. For this reason, tissue residues were calculated on the basis of bioaccumulation factors and water solubility and compared with the critical body residues (CBRs) for narcosis to estimate the potential for the substance to reach internal concentrations that are sufficiently high to cause effects through baseline narcosis. None of the individual RQ or CBR results for substances in the Phthalate Substance Grouping indicated a risk of harm to aquatic organisms through narcotic effects. It should be noted that the CBRs were conservative because they were calculated using the maximum water solubility for each substance and assumed 100% bioavailability; they would be even lower if actual environmental concentrations had been used instead of water solubility limits.

The ITU approach used in this assessment employs lethality CBRs based on data for narcotic chemicals. However, effects from specific modes of action, including endocrine activity, may occur at lower exposure levels than narcotic effects. A cumulative approach based on endocrine activity is not presently viable given the data limitations. Therefore, in addition to the cumulative risk assessment based on narcosis, risk quotients (RQs) were also calculated, using CTVs based on endocrine effects where these data were available (see Table 8-5). Although RQs were presented for the Grouping phthalates in the SOS reports, these were recalculated for this assessment using more recent PNECs and PECs, specifically those shown in Tables 8-3 and 8-4. These results, presented in Table 8-5, indicate that there is a risk to aquatic organisms from B79P and from the additional phthalate DEHP. Risk quotients for the additional phthalates, which are not being assessed, ranged from 1.2 x 10^-3 to 0.58 and can be found in ECCC (2016).

The RQ based on endocrine effects calculated for DEHP indicates potential risk to aquatic organisms. The RQ for B79P, based on limited evidence for B79P in daphnids and supported by QSAR modelling, suggests that the substance is highly hazardous and indicates potential risk to aquatic organisms.

8.3.4 Consideration of the lines of evidence and conclusion

Phthalates examined in this screening assessment are not persistent, although all biodegrade more slowly under low oxygen conditions, and short-chain phthalates such as DMP may remain resident in air for periods of longer than two days and may be found in areas far from the source of release. Phthalates are used in a variety of consumer, commercial and industrial applications, creating the potential for widespread release into the Canadian environment. Some phthalates, in particular DINP and the long-chain phthalates DIDP and DUP, are manufactured and/or imported in large quantities. Constant release of phthalates into the environment may result in continuous exposure for organisms residing in near-field receiving media. Phthalates are released mainly into air and water, and while all phthalates are predicted to distribute into water, only short-chain phthalates such as DMP are predicted to distribute appreciably to air. Therefore, water is the primary medium of concern for the phthalates being considered in this assessment.

Phthalates are bioavailable but do not have high bioaccumulation potential because of high rates of biotransformation in biota. Long-chain phthalates demonstrate low toxicity to aquatic organisms, while short- and medium-chain phthalates exhibit moderate to high toxicity. Phthalates are efficiently metabolized, with the formation of less toxic metabolites that can be readily excreted. Narcosis is an important mode of toxic action for phthalates. However, there is strong evidence that some phthalates may also elicit effects through other modes of action. In particular, some phthalates may have the ability to adversely affect the normal functioning of endocrine systems, such as gonadal development, in organisms. While in vivo evidence of effects on the endocrine system has only been definitively demonstrated for a small number of phthalates, such as DEHP, an analysis of in vivo, in vitro, and in silico data suggests that many phthalates possess properties that could allow them to adversely influence endocrine activity under some conditions. There are considerable in vivo data for medium-chain phthalates in mammals indicating endocrine effects on the development of the male reproductive tract. Given that pathways are highly conserved within vertebrates, it might be expected that, if tested, many of the data-poor medium-chain phthalates could also show effects on endocrine systems in aquatic species, such as fish.

An analysis of risk quotients determined that one phthalate included in the Phthalate Substance Grouping, B79P, and one additional phthalate, DEHP, have the potential to cause harm to aquatic organisms in Canada. Risk quotients for the remaining phthalates indicate low to moderate potential for risk to aquatic organisms in Canada.

Key lines of evidence presented in this draft screening assessment included hazardous properties of phthalates, where observed effects on aquatic organisms such as lethality and disturbances of reproduction and development can occur at low exposure levels, their continual releases and presence in the environment, and exposure analyses and the resulting risk quotients. On the basis of these lines of evidence and precaution, two phthalates, DEHP and B79P, are considered to have potential to cause ecological harm in Canada and are proposed to meet the criteria under section 64(a) of CEPA. DEHP was assessed by Environment Canada and Health Canada in 1994 under the Priority Substances Assessment Program. The assessment concluded that DEHP posed a risk to human health in Canada, but was not able to conclude on the potential for risk to the environment due to insufficient information. Sufficient data were gathered in the course of this assessment to now conclude on the potential for DEHP to cause ecological harm in Canada.

In addition to DEHP and B79P, certain short- and medium-chain phthalates (i.e., DMP, DEP, DPrP, DIBP, BCHP, DCHP, DBzP, DMCHP, BIOP, DBP, BBP, DnHP, and DINP), as well as the long-chain phthalate DnOP, may be highly hazardous because of their potential for effects on the endocrine system. However, under current exposure levels, these substances are not expected to pose a risk. The remaining phthalates in the grouping, primarily the long-chain phthalates, are considered to have low potential to cause ecological harm in Canada. The other 13 additional phthalates were only considered for purposes of informing the CRA and were not assessed as individual substances; therefore, no conclusion is made about the ecological harm of the individual additional phthalates.

8.3.5 Uncertainties in evaluation of ecological risk

Key uncertainties and a qualitative analysis of weight of evidence are presented in Table 8-6. This qualitative analysis served to determine the overall confidence in the decision-making process that led to the proposed assessment conclusion. The level of uncertainty was judged on the basis of the abundance, quality and suitability of data. The analysis also included consideration of the relevance of each line of evidence and the qualitative assessment of the weight for each line of evidence to determine their impact on the overall conclusion. Qualifiers used in the analysis ranged from low to high.

The nature and extent of the potential for phthalates evaluated in this assessment to cause adverse effects on the endocrine system in aquatic organisms is a key uncertainty. Effects on endocrine systems have been extensively studied for a few phthalates, but large data gaps remain for the majority of them. Additionally, there are inconsistent/variable study methodologies and sometimes conflicting results. Certain longer chain phthalates (greater than C7) may have some minor endocrine activity, or might enhance the activity of other endocrine-active substances, but the evidence does not seem to indicate that this is a significant effect for these phthalates. Consequently, while an analysis of data for endocrine activities (see Tables 8-1 and 8-2) suggests that many phthalates can potentially influence endocrine activity, the results were not sufficient to support a conclusion, under section 64 of CEPA, for all phthalates under assessment. However, phthalates with evidence for endocrine activity will be flagged for further evaluation in the event of a change to exposure conditions (for example, through increased use quantities) or receipt of additional toxicity information.

The lack of in vivo aquatic toxicity data on effects in endocrine systems is also an important uncertainty in the assessment. These data are not available for many of the phthalates examined in this assessment and would be particularly useful for the medium-chain phthalates as substances in this subgrouping exhibit the highest aquatic toxicity and are therefore expected to be more reactive than the short- and long-chain phthalates. Also, for those phthalates that have been tested for effects to the endocrine system, there is often a lack of testing at low, environmentally relevant concentrations. Therefore, although research is ongoing, it is currently unknown whether they might still cause adverse effects at concentrations found in the environment.

There are very limited empirical effects data of phthalates for soil- and sediment-dwelling organisms. Measurements of phthalates in soils and sediments have also been limited. Although available data suggest low concern for these environmental media, a more robust dataset would help characterize effects in these media more clearly.

There is uncertainty with respect to the sources of phthalates in the aquatic environment. For DEHP, modelling suggests that aquatic releases from industrial users (i.e., plastic products manufacturers) may be a potential source. Furthermore, considering the measured concentrations of phthalates in WWTS that receive both domestic and industrial wastewaters, the contribution of industrial activities may not be the main source of phthalates in most cases. Rather, the main sources are potentially linked to contribution from consumer or commercial inputs or landfill leachate, but it is not possible to specifically attribute the sources.

Date modified:

2017-10-12