Screening Assessment

Petroleum Sector Stream Approach

Low Boiling Point Naphthas
[Site-restricted]

Chemical Abstracts Service Registry Numbers
64741-54-4
64741-55-5
64741-64-6
64741-74-8
64742-22-9
64742-23-0
64742-73-0
68410-05-9
68410-71-9
68410-96-8
68476-46-0
68477-89-4
68478-12-6
68513-02-0
68514-79-4
68606-11-1
68783-12-0
68919-37-9
68955-35-1
101795-01-1

Environment Canada
Health Canada

September 2011

(PDF Version - 1,824 KB)

Table of Contents

• Synopsis
• Introduction
• Substance Identity
• Physical and Chemical Properties
• Sources
• Uses
• Releases to the Environment
• Environmental Fate
• Persistence and Bioaccumulation Potential
• Potential to Cause Ecological Harm
• Potential to Cause Harm to Human Health
• Conclusion
• References
• Appendix 1: Description of the Nine Groups of Petroleum Substances
• Appendix 2: Process Flow Diagrams for Low Boiling Point Naphthas
• Appendix 3: Data Tables for Site-restricted Low Boiling Point Naphthas
• Appendix 4: Summary of Health Effects Information from Pooled Toxicological Data for LBPNs

Synopsis

Pursuant to section 74 of the Canadian Environmental Protection Act, 1999 (CEPA 1999), the Ministers of the Environment and of Health have conducted a screening assessment of the following site-restricted low boiling point naphthas (LBPNs):

These substances were identified as high priorities for action during the categorization of the DSL, as they were determined to present the greatest potential or intermediate potential for exposure of individuals in Canada and were considered to present a high hazard to human health. Some of the components of these substances met the ecological categorization criteria for persistence, bioaccumulation potential and inherent toxicity to non-human organisms, but none of them met all of the criteria. These substances were included in the Petroleum Sector Stream Approach (PSSA) because they were related to the petroleum sector and are all complex mixtures.

LBPNs are a group of complex petroleum mixtures that generally serve as blending constituents in gasoline or are intermediate products of distillation or extraction processes, which subsequently undergo further refining. Final fuel products usually consist of a mixture of LBPNs as well as other high-quality hydrocarbons that have been isolated during processing at refinery or upgrader facilities. The compositions of LBPNs vary depending on the source of crude oil or bitumen. As such, LBPNs are considered to be of Unknown or Variable composition, Complex reaction products or Biological materials (UVCBs). In order to predict overall behaviour of these complex substances for purposes of assessing the potential for ecological effects, representative structures have been selected from each chemical class in the mixture.

Based on the available information, all of these LBPNs are likely to have high proportions of C₄–C₆ hydrocarbons that are considered to be persistent in air, based on criteria defined in the Persistence and Bioaccumulation Regulations of CEPA 1999.

None of the LBPNs considered here contain components that are considered to be bioaccumulative based on criteria in the Persistence and Bioaccumulation Regulations of CEPA 1999.

Experimental and modelled ecotoxicological data indicate that many of these LBPNs are moderately toxic to aquatic organisms. It is likely that the toxicity observed in experimental studies is due to the presence of mono- and di-aromatic and alkylated aromatic hydrocarbons; however, the lack of data on the proportions of these components makes it impossible to confirm.

Site-restricted LBPNs were identified as a high priority for action because they were considered to present a high hazard to human health. A critical effect for the initial categorization of site-restricted LBPN substances was carcinogenicity, based primarily on classifications by other international agencies. Furthermore, benzene, a genotoxic carcinogen, is known to be a constituent of LBPN substances. Several studies also confirmed skin tumour development in mice following repeated dermal application of LBPN substances. However, LBPNs demonstrated limited evidence of genotoxicity in in vivo and in vitro assays, as well as limited potential to adversely affect reproduction and development. Information on additional LBPN substances in the PSSA that are similar from a processing and physical-chemical perspective was considered for characterization of human health effects.

The LBPNs considered in this screening assessment have been identified as site-restricted (i.e., they are a subset of LBPNs that are not expected to be transported off refinery or upgrader facility sites). According to information submitted under section 71 of CEPA 1999, and other sources of information, these LBPNs are consumed on-site or are blended into substances leaving the site under different CAS RNs. In addition, a number of regulatory and non-regulatory measures are already in place in Canada, which minimize releases of site-restricted petroleum sector substances, including provincial/territorial operating permit requirements, and best practices and guidelines put in place by the petroleum industry at refinery and upgrader facilities. Accordingly, environmental and general population exposure to these substances is not expected, and therefore harm to human health or the environment is not expected.

Therefore, it is concluded that these site-restricted LBPNs 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, or that constitute or may constitute a danger in Canada to human life or health.

Based on the information available, it is concluded that site-restricted LBPNs listed under CAS RNs 64741-54-4, 64741-55-5, 64741-64-6, 64741-74-8, 64742-22-9, 64742-23-0, 64742-73-0, 68410-05-9, 68410-71-9, 68410-96-8, 68476-46-0, 68477-89-4, 68478-12-6, 68513-02-0, 68514-79-4, 68606-11-1, 68783-12-0, 68919-37-9, 68955-35-1 and 101795-01-1 do not meet any of the criteria set out in section 64 of CEPA 1999.

Because these substances are listed on the DSL, their import and manufacture in Canada are not subject to notification under subsection 81(1) of CEPA 1999. Given the potential hazardous properties of these substances, there is concern that new activities that have not been identified or assessed could lead to these substances meeting the criteria set out in section 64 of the Act. Therefore, application of the Significant New Activity provisions of the Act to these substances if being considered, so that any proposed new manufacture, import or use of these substances outside a petroleum refinery or upgrader facility is subject to further assessment, to determine if the new activity requires further risk management consideration.

Introduction

The Canadian Environmental Protection Act, 1999 (CEPA 1999) (Canada 1999) requires the Minister of the Environment and the Minister of Health to conduct screening assessments of substances that have met the categorization criteria set out in the Act to determine whether these substances present or may present a risk to the environment or to human health.

Based on the information obtained through the categorization process, the Ministers identified a number of substances as high priorities for action. These include substances that

• met all of the ecological categorization criteria, including persistence (P), bioaccumulation potential (B) and inherent toxicity to aquatic organisms (iT), and were believed to be in commerce in Canada; and/or
• met the categorization criteria for greatest potential for exposure (GPE) or presented an intermediate potential for exposure (IPE) and had been identified as posing a high hazard to human health based on classifications by other national or international agencies for carcinogenicity, genotoxicity, developmental toxicity or reproductive toxicity.

A key element of the Government of Canada’s Chemicals Management Plan (CMP) is the Petroleum Sector Stream Approach (PSSA), which involves the assessment of approximately 160 petroleum substances that are considered high priorities for action. These substances are primarily related to the petroleum sector and are considered to be of Unknown or Variable composition, Complex reaction products or Biological materials (UVCBs).

Screening assessments focus on information critical to determining whether a substance meets the criteria as set out in section 64 of CEPA 1999. Screening assessments examine scientific information and develop conclusions by incorporating a weight of evidence approach and precaution.^[1]

Grouping of Petroleum Substances

The high-priority petroleum substances fall into nine groups of substances based on similarities in production, toxicity and physical-chemical properties (Table A1.1 in Appendix 1). In order to conduct screening assessments, each high-priority petroleum substance was placed into one of five categories (“streams”) depending on its production and uses in Canada:

0 - substances concluded not to be relevant to the petroleum sector and/or not in commerce;
1 - site-restricted substances, which are substances that are not expected to be transported off refinery, upgrader or natural gas processing facility sites^[2];
2 - industry-restricted substances, which are substances that may leave a petroleum-sector facility and may be transported to other industry facilities (for example, for use as a feedstock, fuel or blending component), but that do not reach the public market in the form originally acquired;
3 - substances that are primarily used by industries and consumers as fuels;
4 - substances that may be present in products available to the consumer.

An analysis of the available data determined that approximately 70 high-priority petroleum substances are site-restricted under stream 1, as described above. These occur within four of the nine groupings: heavy fuel oils, gas oils, petroleum and refinery gases, and low boiling point naphthas (LBPNs).

These site-restricted substances were identified as GPE or IPE during the categorization exercise, based on their production volumes reported in the Domestic Substances List (DSL). However, according to information submitted under section 71 of CEPA 1999, voluntary industry submissions, an in-depth literature review, and a search of material safety data sheets, these substances are consumed on-site or are blended into substances leaving the site under different Chemical Abstracts Service Registry Numbers (CAS RNs) (which will also be addressed under the CMP).

This screening assessment addresses 20 site-restricted LBPNs captured under CAS RNs 64741-54-4, 64741-55-5, 64741-64-6, 64741-74-8, 64742-22-9, 64742-23-0, 64742-73-0, 68410-05-9, 68410-71-9, 68410-96-8, 68476-46-0, 68477-89-4, 68478-12-6, 68513-02-0, 68514-79-4, 68606-11-1, 68783-12-0, 68919-37-9, 68955-35-1 and 101795-01-1. The remaining high-priority LBPNs (under 25 different CAS RNs) will be assessed separately, as they belong to streams 2, 3 or 4 (as described above). Health effects were assessed using toxicological data pooled across all 45 LBPN CAS RNs.

Included in this screening assessment is the consideration of information on chemical properties, hazards, uses and exposure, including the additional information submitted under section 71 of CEPA 1999. Data relevant to the screening assessment of these substances were identified in original literature, review and assessment documents, stakeholder research reports and from recent literature searches, up to July 2010 for the ecological section of the document and up to November 2009 for the health effects section. Key studies were critically evaluated; modelling results were used to reach conclusions.

Characterizing risk to the environment involves the consideration of data relevant to environmental behaviour, persistence, bioaccumulation and toxicity, combined with an estimation of exposure to potentially affected non-human organisms from the major sources of release to the environment. Conclusions regarding risk to the environment are based on an estimation of environmental concentrations resulting from releases and the potential for a negative impact on non-human organisms. As well, other lines of evidence of environmental hazard are taken into account. The ecological portion of the screening assessment summarizes the most pertinent data on environmental behaviour and effects, and does not represent an exhaustive or critical review of all available data. Environmental models and comparisons with similar petroleum mixtures have been used in the assessment.

Evaluation of risk to human health involves consideration of data relevant to estimation of exposure (non-occupational) of the general population, as well as information on health hazards (based principally on the weight of evidence assessments of other agencies that were used for prioritization of the substance). Decisions for human health are based on the nature of the critical effect and/or margins between conservative effect levels and estimates of exposure, taking into account confidence in the completeness of the identified databases on both exposure and effects, within a screening context. The screening assessment does not represent an exhaustive or critical review of all available data. Rather, it presents a summary of the critical information upon which the conclusion is based.

This screening assessment was prepared by staff in the Existing Substances Programs at Health Canada and Environment Canada and incorporates input from other programs within these departments. The human health and ecological portions of this assessment have undergone external written peer review/consultation. Comments on the technical portions relevant to human health were received from scientific experts selected and directed by Toxicology Excellence for Risk Assessment (TERA), including Patricia Nance (TERA), Dr. Bob Benson (U.S. Environmental Protection Agency), Dr. Stephen Embso-Mattingly (NewFields Environmental Forensics Practice, LLC), Dr. Michael Jayjock (The Lifeline Group) and Dr. Donna Vorhees (Science Collaborative).

Additionally, the draft of this screening assessment was subject to a 60-day public comment period. While external comments were taken into consideration, the final content and outcome of the screening assessment remain the responsibility of Health Canada and Environment Canada.

The critical information and considerations upon which the screening assessment is based are summarized below.

Substance Identity

LBPNs are a group of complex liquid mixtures containing volatile components and are produced by the refining or upgrading of crude oils or bitumen. Their composition varies depending on the sources of crude oil or bitumen and the processing steps involved.

Physical and Chemical Properties

The physical and chemical properties of LBPNs vary depending on the sources of crude oil or bitumen and the processing steps involved. LBPNs are volatile liquid hydrocarbons with a typical boiling point range from -20°C to 230°C (CONCAWE 2005). A summary of data on the physical and chemical properties of site-restricted LBPNs is presented in Table 1.

Table 1. General physical and chemical properties of site-restricted LBPNs

These LBPNs are complex mixtures with components that predominantly fall in the C₄–C₁₂ carbon range: alkanes, cycloalkanes, aromatics and, if they are subject to a cracking process, alkenes as well (CONCAWE 2005). Some of the LBPNs in this report are heavily aromatic (up to 65%), others contain up to 40% alkenes, while all of the others are heavily aliphatic in composition, up to 100%. Depending on the specific refining and distillation processes involved, the chemical composition of several CAS RNs is quite restricted, comprising almost exclusively (for example) C₄–C₆ aliphatics or C₇–C₁₂ isoalkanes. Others have a much broader range of constituent hydrocarbons, some (for example) being composed of a full spectrum of C₄–C₁₂ aliphatics and aromatics (see Table A3.1 in Appendix 3 for the detailed analysis of CAS RN 68919-37-9).

In order to predict the overall properties and behaviour of a complex petroleum substance, representative structures were chosen from each chemical class within the mixture (see Table A3.2 in Appendix 3). Nineteen structures were chosen from the database in PetroTox (2009) based on boiling point ranges for each LBPN, the amount of data on each structure and the middle of the boiling point range of similar structures. As the composition of most LBPNs is not well defined, representative structures could not be chosen based on their proportion in the mixture. This lack of general compositional data resulted in the selection of representative structures for alkanes, isoalkanes, alkenes, one- and two-ring cycloalkanes, and one- and two-ring aromatics ranging from C₄–C₁₂. Physical and chemical data were assembled from scientific literature and from the EPIsuite (2008) group of environmental models.

Water solubilities range from very low for the longest-chain alkanes to high for the simplest mono-aromatic. In general, the aromatic compounds are more soluble than the same-sized alkanes, isoalkanes and cycloalkanes. This indicates that the components likely to remain in water are the one- and two-ring aromatics (C₆–C₁₂). The C₉–C₁₂ alkanes, isoalkanes and one- and two-ring cycloalkanes are likely to be attracted to sediments based on their low water solubilities and moderate to high log octanol–water partition coefficient (K_ow) and log organic carbon–water partition coefficient (K_oc) values.

Experimental and modelled vapour pressures for representative structures are moderate to very high and decrease with increasing molecular size. This suggests that losses from soil and water will likely be high and that the air will be the ultimate receiving environment for most of the components of LBPNs.

Sources

Site-restricted LBPNs are produced in Canadian refineries and upgraders. The CAS RN descriptions (NCI 2006), typical process flow diagrams (Figures A2.1-A2.20 in Appendix 2) (Hopkinson 2008), and information collected under section 71 of CEPA 1999 (Environment Canada 2008, 2009) indicate that these 20 LBPNs are intermediate streams within both refineries and upgraders or are blended to make other products under a new CAS RN (Figures A2.5, A2.6 and A2.20 show blending streams). As such, these LBPNs are not expected to be transported off of facility sites. Quantities produced were reported under section 71 of CEPA 1999 (Environment Canada 2008, 2009) by the petroleum refining and upgrading industry but are considered to be confidential. However, these data are not critical to this screening assessment, since release to the environment is not expected.

CAS RN 64741-54-4 and CAS RN 64741-55-5 refer to products of a catalytic cracking process (Figures A2.1 and A2.2 in Appendix 2).

CAS RN 64741-64-6 represents a bottom substance from distillation of alkylation products (Figure A2.3 in Appendix 2).

CAS RN 64741-74-8 often refers to an overhead distillate from a fractionation column in a thermal cracking unit (coking or visbreaking) (Figures A2.4a and A2.4b in Appendix 2).

CAS RN 64742-22-9 and CAS RN 64742-23-0 refer to a heavy naphtha and a light naphtha, respectively. Both are treated by an alkali solvent to remove acid compounds via a neutralization reaction (Figures A2.5 and A2.6 in Appendix 2).

CAS RN 64742-73-0 represents a bottom substance discharged from a distillation column fed with hydrodesulphurized light naphtha (Figures A2.7a and A2.7b in Appendix 2).

CAS RN 68410-05-9 refers to a product of the atmospheric distillation tower (Figure A2.8 in Appendix 2).

CAS RN 68410-71-9 refers to a raffinate from an extraction column where aromatic compounds are removed from the product of a catalytic reforming process (Figure A2.9 in Appendix 2).

CAS RN 68410-96-8 refers to a bottom residue discharged from a stabilization column treated with the product of a hydrotreating process of straight-run heavy naphtha (Figures A2.10a and A2.10b in Appendix 2).

CAS 68476-46-0 represents a distillate derived from the main distillation column (Figure A2.11 in Appendix 2).

CAS RN 68477-89-4 refers to an overhead product (C₅ and less) from a distillation column treated with the product of a catalytic cracking process (Figure A2.12 in Appendix 2).

CAS RN 68478-12-6 refers to a bottom product from a distillation column where isobutane is separated from n-butane and heavier compounds (Figures A2.13a and A2.13b in Appendix 2).

CAS RN 68513-02-0 represents an overhead distillate from a fractionation column in a coking unit (Figure A2.14a and A2.14b in Appendix 2).

CAS RN 68514-79-4 refers to a bottom substance discharged from a distillation column fed with hydrotreated heavy naphtha from a hydrofiner-powerformer process (Figure A2.15 in Appendix 2).

CAS RN 68606-11-1 refers to a side distillate coming directly from an atmospheric distillation column; it is normally blended into gasoline products (Figure A2.16 in Appendix 2).

CAS RN 68783-12-0 is a generic description of naphthas produced from various distillation processes in a refinery, including straight-run naphthas from an atmospheric distillation column, naphtha distillates from cracking units (catalytic cracking, thermal cracking, hydrocracking) and naphtha upgrading units (isomerization, alkylation, polymerization, reformer) (Figures A2.17a and A2.17b in Appendix 2).

CAS RN 68919-37-9 and CAS RN 68955-35-1 represent a bottom substance of a distillation column fed with effluent from a catalytic reforming process (Figures A2.18 and A2.19 in Appendix 2).

CAS RN 101795-01-1 refers to a product after mercaptans and other acid compounds are removed by a sweetening process (Figure A2.20 in Appendix 2).

Uses

According to the information collected through the Notice with respect to certain high priority petroleum substances (Environment Canada 2008) and the Notice with respect to potentially industry-limited high priority petroleum substances (Environment Canada 2009), published under section 71 of CEPA 1999, the LBPN substances listed in this screening assessment were identified as either being consumed at the facility or blended into substances leaving the site under different CAS RNs. Although these substances were identified by multiple use-codes established during the development of the DSL, it has been determined from information submitted under section 71 of CEPA 1999 (Environment Canada 2008, 2009), voluntary submissions from industry, an in-depth literature review and a search of material safety data sheets that these site-restricted LBPNs are not expected to be transported off refinery or upgrader facility sites.

Releases to the Environment

Potential releases of LBPN substances from refineries and upgraders can be characterized as either controlled or unintentional releases. Controlled releases are planned releases from pressure relief valves, venting valves and drain systems that occur for safety purposes or maintenance, are considered part of routine operations and occur under controlled conditions. Unintentional releases are typically characterized as unplanned releases due to spills or leaks from various equipment, valves, piping, flanges, etc. resulting from equipment failure, poor maintenance, lack of proper operating practices, adverse weather conditions or other unforeseen factors. Refinery and upgrader operations are highly regulated and regulatory requirements established under various jurisdictions, as well as voluntary non-regulatory measures implemented by the petroleum industry, are in place to manage these releases (SENES 2009).

Controlled Releases

The site-restricted LBPN CAS RNs in this screening assessment originate from distillation or extraction columns in refineries or upgraders, as either a distillate or a residue (bottom product). Thus, the potential locations for the controlled release of LBPNs are relief valves, venting valves or drain valves on the piping (e.g., columns and vessels) in the vicinity of the equipment.

Under typical operating conditions, controlled releases of site-restricted LBPNs would be captured in a closed system,^[3] according to defined procedures, and then returned to the processing facility. In cases where the amount of the substance is small or its concentration is dilute, the site-restricted LBPN is sent to the facility wastewater treatment plant. In both cases, exposure of the general population or the environment is not expected from the site-restricted LBPN substances under the CAS RNs listed in this screening assessment, as they are not expected to be transported off refinery or upgrader facility sites.

Unintentional Releases

Unintentional releases (including fugitive releases) occur from equipment (e.g., pumps, storage tanks), seals, valves, piping, flanges, etc., during processing and handling of petroleum substances, and can be greater in situations of poor maintenance or operating practice. Regulatory and non-regulatory measures are in place to reduce these events (SENES 2009). Rather than being specific to one substance, these measures are developed in a more generic way in order to reduce unintentional releases of all substances in the petroleum sector.

For the Canadian petroleum industry, requirements at the provincial/territorial level typically prevent or manage the unintentional releases of petroleum substances and streams within a facility (through the use of operating permits) (SENES 2009).

At the federal level, unintentional releases of some petroleum substances are addressed under the Fisheries Act; the Petroleum Refinery Liquid Effluent Regulations and Guidelines set the discharge limits of oil and grease, phenol, sulphides, ammonia nitrogen and total suspended matter, as well as testing requirements for acute toxicity in the final petroleum effluents entering Canadian waters.

Additionally, existing occupational health and safety legislation specifies measures to reduce occupational exposures of employees, and some of these measures also serve to reduce unintentional releases (CanLII 2001).

Non-regulatory measures (e.g., guidelines, best practices) are also in place at petroleum sector facilities to reduce unintentional releases. Such control measures include appropriate material selection during the design and setup processes; regular inspection and maintenance of storage tanks, pipelines and other process equipment; the implementation of leak detection and repair or other equivalent programs; the use of floating roofs in above-ground storage tanks to reduce the internal gaseous zone; and the minimal use of underground tanks, which can lead to undetected leaks (SENES 2009).

Environmental Fate

Given that these are site-restricted LBPNs which are not expected to be transported off refinery or upgrader facility sites, only general data on the environmental behaviour of these CAS RNs are presented in the screening assessment.

Persistence and Bioaccumulation Potential

Environmental Persistence

No empirical data are available on the degradation of LBPNs as complex mixtures. However, estimates can be derived from analyzing the biodegradation of the components of LBPNs. Aerobic biodegradation data for individual isoalkanes (C₉–C₁₂) from an Organisation for Economic Co-operation and Development (OECD) 301F ready biodegradation test indicate that they will be 22% degraded (ultimate biodegradation) over a period of 28 days (ECB 2000e). This equates to a degradation half-life of approximately 78 days in water, assuming that degradation follows first-order kinetics. Numerous researchers have found that the degree of branching in an isoalkane increases its resistance to biodegradation (Atlas 1981). However, Prince et al. (2007a, 2007b) reported that C₆–C₁₀ components (alkanes, isoalkanes, alkenes, cycloalkanes, one-ring aromatics and two-ring aromatics) in a formulated gasoline had relatively short median half-lives (primary biodegradation)--ranging from 3 to 17 days--in freshwater, salt water and sewage effluent (see Table A3.3 in Appendix 3). They hypothesized that primary biodegradation half-lives were shorter for hydrocarbons in a gasoline mix than for individual components, because indigenous micro-organisms degrade hydrocarbons most effectively when they are presented as a mixed suite of hydrocarbon substrates that allows microbes to use intermediates from different pathways to balance their overall metabolism.

A quantitative structure–activity relationship (QSAR)–based weight of evidence approach (Environment Canada 2007) was also applied using primary biodegradation model BIOHCWIN (2008), the ultimate biodegradation model BIOWIN (2009) and the atmospheric degradation model AOPWIN (2008). BIOWIN (2009) is a general biodegradation estimation model for organic compounds that estimates a variety of biodegradation rates, such as primary and ultimate biodegradation. Primary biodegradation is the transformation of a parent compound to an initial metabolite. Ultimate biodegradation is the transformation of a parent compound to carbon dioxide and water, mineral oxides of any other elements present in the test compound, and new cell material (EPIsuite 2008). The key persistence metric is ultimate biodegradation.

Using an extrapolation ratio of 1:1:4 for water:soil:sediment biodegradation half-lives (Boethling et al. 1995), the half-lives in soil and sediment can be extrapolated from the half-life estimations in water.

The results of the BIOHCWIN (2008) model indicate that the components of LBPNs have primary degradation half-lives in water ranging from 3.1 to 55.9 days (see Table A3.4 in Appendix 3). Outputs from BIOWIN (2009) indicate that most components of LBPNs undergo ultimate degradation in a period of “weeks” or less, although a time frame of “weeks to months” is indicated for a few of the heavier components (“weeks to months” is equated to a half-life of 37.5 days by Aronson et al. 2006). Using an extrapolation ratio of 1:1:4 for water:soil:sediment biodegradation half-lives (Boethling et al. 1995), the ultimate degradation half-life in soil for the heavy components is also < 182 days, and the half-life in sediments is < 365 days.

In air, empirical data (Atkinson 1990) show that butane, isobutane, pentane and isopentane are persistent (see Table A3.5a in Appendix 3), with half-lives ranging from 2 to 3.4 days. Predicted atmospheric oxidation half-lives (AOPWIN 2008) for representative structures confirm these data; as well, AOPWIN (2008) predicted that benzene and hexane have half-lives of equal to or greater than 2 days (5.5 days and 2 days, respectively) (see Table A3.5b in Appendix 3). The atmosphere would be an important environmental compartment for these LBPNs due to the high volatility of most of the components.

For all of the LBPNs considered in this report, the C₄-C₆ components that are highly persistent based on criteria in the Persistence and Bioaccumulation Regulations of CEPA 1999 (Canada 2000) likely make up a large proportion of the mixture (see Tables A3.6a, b and c in Appendix 3). For CAS RNs 64742-22-9 and 68410-71-9, it is assumed that they also contain significant proportions of these persistent components, although there are no data to enable an estimate of their compositions. There is nothing to suggest that they would not contain persistent components.

Potential for Bioaccumulation

Because no experimental bioaccumulation or bioconcentration data for these LBPNs as mixtures were available, empirical data for the representative structures found in LBPNs and a predictive approach were applied using a bioconcentration factor (BCF) model (BCFBAF 2008). The BCFBAF program incorporates the generic QSAR model of Arnot and Gobas (2003). As well, experimental data for similar substances were considered.

Both experimentally derived and modelled log K_ow values for representative structures of the LBPNs (Table A3.2, Appendix 3) suggest that these components have a moderate to high potential to bioaccumulate in biota.

Correa and Venables (1985) exposed a tropical fish (Mugil curema) to naphthalene (a C₁₀ di-aromatic) in water for 96 hours and found rapid uptake with slower depuration. BCFs in muscle were 81 to 567. A whole fish BCF of 145 was calculated for this species.

The Arnot-Gobas kinetic model (BCFBAF 2008) estimates bioaccumulation factor (BAF) values for the nineteen representative structures ranging from 10–9605 (Table A3.7, Appendix 3). Four of the nineteen components have predicted BAF values in excess of 5000. These representative structures include C₁₂ alkanes, C₁₂ isoalkanes, C₁₂ alkenes and C₁₂ 1-ring cycloalkanes. However, experimental data do not indicate significant bioaccumulation by mono-aromatics and di-aromatics (Table 3.8, Appendix 3), with the highest measured BAF being 230 litres per kilogram (L/kg).

The results of the BCF model calculations (see also Table A3.7 in Appendix 3) indicate a generally low bioconcentration potential of these representative structures, with values from 10–2180.

Studies on the bioconcentration potential of many of the representative structures in LBPNs have been conducted in Japan (Table A3.9, Appendix 3) (JNITE 2010). None of the substances considered had a BCF ≥ 5000.

Tolls and van Dijk (2002) measured the BCF value for a C₁₂ isoalkane at between 880 and 3500 L/kg, which is consistent with the modelled BCF value for 2,3-dimethyl decane (1910 L/kg), but not the BAF (8232 L/kg). There is some supporting evidence of low BAF values, in that some n-alkanes of around C₁₂ and some C₁₀–C₁₂ aromatics and alkylated aromatics are bioaccumulative at low to moderate levels in mussels (Boehm and Quinn 1977) and fish (Colombo et al. 2007) via diet. However, the research data on the accumulation of n-alkanes and polycyclic aromatic hydrocarbons (PAHs) in this size range are contrary to the high BAFs predicted by the BAF model (Correa and Venables 1985; Niimi and Dookhran 1989; Wan et al. 2007; Takeuchi et al. 2009). This is likely due to the slower estimated metabolism rate of these compounds or faster estimated uptake rates used in the kinetic mass-balance model compared with the field data.

In this assessment, laboratory, field and modelled data are available for the C₁₂ linear and cyclic fractions. In the case of the BCF, both empirical and modelled data agree and suggest a low potential for bioconcentration from water. In the case of accumulation from all exposures including the diet (BAF), greater weight has been placed on the field data because the field data inherently account for factors that are sources of uncertainty in model estimates. The field BAF data indicate that none of the components of these LBPNs would be bioaccumulative based on criteria in the Persistence and Bioaccumulation Regulations of CEPA 1999.

Potential to Cause Ecological Harm

Ecological Effects Assessment

A - In the Aquatic Compartment

Experimental aquatic toxicity data were obtained for some of the LBPN CAS RNs considered here (see Table A3.10 in Appendix 3), whereas others were extrapolated from results for similar types of LBPNs. Moderate toxicity (median lethal loading [LL₅₀] values of 4.5–32 milligrams [mg]/L) was seen with the water-accommodated fractions in shrimp, Daphnia magna, Rainbow Trout and Fathead Minnows (Adema and van den Bos Bakker 1986; PPSC 1995a; CONCAWE 1996; ECB 2000g, 2000h, 2000k). It is likely that the mono-aromatic and di-aromatic hydrocarbons and alkylated aromatics are largely responsible for the toxicity seen in the tests, as C₉–C₁₂ alkanes and isoalkanes are known not to be especially toxic to aquatic organisms (ECB 2000e). Algae appear to be some of the most sensitive organisms to whole products in water; one algal no-observed-adverse-effect level (NOAEL) was below 1 mg/L, although the median effective concentration (EC₅₀) for growth was 880 mg/L (ECB 2000i). Empirical tests with water-accommodated fractions of LBPNs did not indicate that the substances tested were highly hazardous to aquatic organisms.

CONCAWE developed an aquatic toxicity model specific to petroleum hydrocarbon mixtures, called PetroTox (2009). PetroTox assumes toxicological action via narcosis and therefore accounts for additive effects according to the toxic unit approach (PetroTox 2009). It models the toxicity of petroleum hydrocarbons dissolved in the water fraction for C₅–C₄₁ compounds; compounds smaller than C₅ are considered by the model to be too volatile to remain in water long enough to impart any significant aquatic toxicity, and compounds greater than C₄₁ are assumed to be too hydrophobic and immobile to impart any toxicity. PetroTox generates estimates of toxicity as an LL₅₀ rather than a median lethal concentration (LC₅₀), due to the insolubility of petroleum substances in water. The LL₅₀ is the amount of petroleum substance needed to generate a water-accomodated fraction (WAF) that is toxic to 50% of the test organisms. It is not a measure of the concentration of the petroleum components in the WAF.

A range of moderate aquatic toxicity predictions was obtained from the PetroTox (2009) model. The LL₅₀ predictions were in the same range as observed in the empirical tests, from 0.5–154 mg/L (see Tables A3.11a and b in Appendix 3). Some of the CAS RNs were predicted to have relatively high toxicity to some aquatic organisms: 64741-64-6, 64742-22-9, 68513-02-0 and 68783-12-0. The most sensitive organism from the PetroTox (2009) tests was Rhepoxynius abronius, a marine amphipod known to be sensitive to sediment pollutants. However, PetroTox (2009) predicts toxicity only from water-soluble components, not those that would likely be attracted to sediments.

B - In Other Environmental Compartments

Selected endpoints (mortality and reproduction) from studies on small mammals used to evaluate human health effects were also used to bound terrestrial toxicity. Analysis was limited to site-restricted LBPN CAS RNs, obtained from the summary of studies used to evaluate human health effects (see Appendix 4).

Rats exhibited an LD₅₀ of 3500 milligrams per kilogram of body weight (mg/kg-bw) when orally dosed with CAS RN 68955-35-1 (API 2008a). CAS RN 64741-55-5 delivered via inhalation at 9041 mg per cubic metre (mg/m³) was considered to be a no-observed-adverse-effect-concentration (NOAEC) for systemic toxicity in rats using a reproductive/developmental toxicity testing protocol (Shreiner et al. 1999; API 2008a). An oral NOAEL of 2000 mg/kg-bw/day was determined for CAS RN 64741-55-5 for reproductive and developmental toxicity in rats (Stonybrook Laboratories, Inc. 1995), and an oral NOAEL of 50 mg/kg-bw/day was determined for CAS RN 68513-74-8 for reproductive and developmental toxicity in rabbits (this was the highest dose tested) (Miller and Schardein 1981). These values do not indicate that these CAS RNs are highly hazardous to terrestrial mammals for these particular endpoints and exposure routes.

Ecological Exposure Assessment

Because the LBPNs in this report have been identified as site-restricted, indicating that they are not expected to be transported off refinery or upgrader facility sites, the potential for release to the ecosystem is negligible, and exposure is not expected.

Characterization of Ecological Risk

Most of the LBPNs in this report are only moderately toxic to aquatic organisms through their water-soluble components, although the PetroTox model suggests that LBPNs 64741-64-6, 64742-22-9, 68513-02-0 and 68783-12-0 have higher toxicity to some aquatic organisms.

All of these LBPNs contain large proportions of components that are considered to be persistent in the atmosphere based on criteria in the Persistence and Bioaccumulation Regulations.

Based on the available field BAF data none of the components of these LBPNs would be bioaccumulative based on criteria in the Persistence and Bioaccumulation Regulations of CEPA 1999.

Based on information obtained from a variety of sources (voluntary industry submissions, an in-depth literature review, and a search of material safety data sheets), the LBPNs considered in this screening assessment have been identified as site-restricted - i.e., they are not expected to be transported off refinery or upgrader facility sites. These LBPNs are consumed on-site or are blended into other substances leaving the site under different CAS RNs. Measures (including provincial/territorial operating permit requirements, and best practices and guidelines put in place by the petroleum industry) are in place to minimize releases from refineries and upgrader facilities. As a result of these factors, the likelihood of exposure, and potential for risk, of organisms in the environment to LBPNs under these CAS RNs is considered to be low.

Uncertainties in Evaluation of Ecological Risk

As the site-restricted LBPNs are UVCBs, their specific chemical compositions are not well defined. LBPN streams under the same CAS RN can vary significantly in the number, identity and proportion of constituent compounds, depending on operating conditions, feedstocks and processing units.

Modelling of the physical and chemical properties of LBPNs, as well as their persistence, bioaccumulation and toxicity, is based on representative structures. The physical and chemical properties of 19 representative structures were used to estimate the overall behaviour of the LBPNs. Given that a variety of representative structures may be derived for the same LBPN, it is recognized that structure-related uncertainties exist for these substances. However, the limited number of hydrocarbons theoretically present in LBPNs (based on boiling point ranges and carbon ranges) reduces this uncertainty. The lack of specific proportions of representative structures in CAS RNs also creates uncertainty in estimating certain properties, such as toxicity.

As these substances are classified as site-restricted, environmental releases and exposures are expected to be negligible. However, CAS RN specific monitoring data were not identified to verify this assumption.

The lack of data on the composition of two of the CAS RNs (68410-05-9 and 68410-96-8) resulted in uncertainty regarding their behaviour in the environment, including persistence.

Potential to Cause Harm to Human Health

Health Effects Assessment

Given the limited number of studies available that evaluated the health effects of site-restricted LBPNs, an adequately representative toxicological data set specifically for the site-restricted LBPNs could not be obtained. Therefore, to characterize the toxicity of these site-restricted substances, additional LBPNs in the PSSA that are similar from both a process perspective as well as a physical and chemical perspective were also evaluated for their toxicological effects. As both the site-restricted and the additional LBPN substances have similar physical and chemical as well as toxicological properties, the toxicological data across CAS RNs were used to construct a toxicological profile to represent all LBPNs. Accordingly, the toxicity of LBPNs is represented as a group, not by individual CAS RNs.

Appendix 4 contains a summary of available health effects information on LBPNs in experimental animals. A summary of key studies selected to represent the toxicity of site-restricted LBPNs follows.

LBPNs have low acute toxicity by the oral (median lethal dose [LD₅₀] in rats > 2000 mg/kg-bw), inhalation (LD₅₀ in rats > 5000 mg/m³) and dermal (LD₅₀ in rabbits > 2000 mg/kg-bw) routes of exposure (CONCAWE 1992; Rodriguez and Dalbey 1994a, 1994b, 1994c, 1994d; API 2008a). This oral LD₅₀ value is lower than the 5000 mg/kg-bw value identified in CONCAWE (1992) and API (2008a). Most LBPNs are mild to moderate eye and skin irritants in rabbits, with the exception of heavy catalytic cracked and heavy catalytic reformed naphthas, which have higher primary skin irritation indices (API 1980a, 1985a, 1985b, 1985c, 1986a, 1986b, 1986c, 1986d, 2008a; CONCAWE 1992; Rodriguez and Dalbey 1994e, 1994f, 1994g, 1994h, 1994i). LBPNs do not appear to be skin sensitizers, but a poor response in the positive control was also noted in these studies (API 1980a, 1985b, 1986a, 1986b, 1986c, 1986d, 1986e, 1986f).

The lowest-observed-adverse-effect concentration (LOAEC) and lowest-observed-adverse-effect level (LOAEL) values identified following short-term (2–89 days) and subchronic (greater than 90 days) exposure to the LBPN substances are listed in Table 2. These values were determined for a variety of endpoints after considering the toxicity data for all LBPNs in the PSSA. Most of the studies were carried out by the inhalation route of exposure. Renal effects, including increased kidney weight, renal lesions (renal tubule dilation, necrosis) and hyaline droplet formation, observed in male rats exposed orally or by inhalation to most LBPNs, were considered species- and sex-specific (Carpenter et al. 1975; Halder et al. 1984, 1985; Phillips and Egan 1984; Research and Environmental Division 1984; Gerin et al. 1988; Schreiner et al. 1998, 1999, 2000a; McKee et al. 2000; API 2005, 2008b, 2008c). These effects were determined to be due to a mechanism of action not relevant to humans--specifically, the interaction between hydrocarbon metabolites and alpha-2-microglobulin, an enzyme not produced in substantial amounts in female rats, mice and other species, including humans. The resulting nephrotoxicity and subsequent carcinogenesis in male rats were therefore not considered in deriving LOAEC/LOAEL values.

Table 2. LOAECs/LOAELs identified for a variety of endpoints in experimental animals following short-term or subchronic exposure to LBPNs

Only a limited number of studies of short-term and subchronic duration were identified for site-restricted LBPNs. The lowest LOAEC identified in these studies, via the inhalation route, is 5475 mg/m³, based on a concentration-related increase in liver weight in both male and female rats following a 13-week exposure to light catalytic cracked naphtha (API 1987a). Shorter exposures of rats to this test substance resulted in nasal irritation at 9041 mg/m³ (Schreiner et al. 1999; API 2008a). No systemic toxicity was reported following dermal exposure to light catalytic cracked naphtha, but skin irritation and accompanying histopathological changes were increased, in a dose-dependent manner, at doses as low as 30 mg/kg-bw per day when applied 5 days per week for 90 days in rats (Mobil 1988a).

No non-cancer chronic toxicity studies (≥ 1 year) were identified for site-restricted LBPNs and very few non-cancer chronic toxicity studies were identified for other LBPNs. An LOAEC of 200 mg/m³ was noted in a chronic inhalation study that exposed mice and rats to unleaded gasoline (containing 2% benzene). This inhalation LOAEC was based on ocular discharge and ocular irritation in rats. At the higher concentration of 6170 mg/m³, increased kidney weight was observed in male and female rats (increased kidney weight was also observed in males only at 870 mg/m³). Furthermore, decreased body weight in male and female mice was also observed at 6170 mg/m³ (MacFarland et al. 1984). A LOAEL of 714 mg/kg-bw was identified for dermal exposure based on local skin effects (inflammatory and degenerative skin changes) in mice following application of naphtha for 105 weeks. No systemic toxicity was reported (Clark et al. 1988).

Although few genotoxicity studies were identified for the site-restricted LBPNs, the genotoxicity of several other LBPN substances has been evaluated using a variety of in vivo and in vitro assays. While in vivo genotoxicity assays were negative overall, the in vitro tests exhibited mixed results as described below.

For in vivo genotoxicity tests, LBPNs exhibited negative results for chromosomal aberrations and micronuclei induction (API 1985d, 1985e, 1985f, 1985g, 1985h, 1985i, 1986i; Gochet et al. 1984; Khan 1984; Khan and Goode 1984), but exhibited positive results in one sister chromatid exchange assay (API 1988a), although this result was not considered definitive for clastogenic activity as no genetic material was unbalanced or lost (API 2008a). Mixtures that were tested, which included a number of light naphthas, displayed mixed results (i.e., both positive and negative for the same assay) for chromosomal aberrations and negative results for the dominant lethal mutation assay (API 1977a). Unleaded gasoline (containing 2% benzene) was tested for its ability to induce unscheduled deoxyribonucleic acid (DNA) synthesis (UDS) and replicative DNA synthesis (RDS) in rodent hepatocytes and kidney cells. UDS and RDS were induced in mouse hepatocytes via oral exposure and RDS was induced in rat kidney cells via oral and inhalation exposure (Loury et al. 1986, 1987). Unleaded gasoline (benzene content not stated) exhibited negative results for chromosomal aberrations and the dominant lethal mutation assay (API 1977b, 1977c, 1980b; Dooley et al. 1988; Conaway et al. 1984) and mixed results for atypical cell foci in rodent renal and hepatic cells (Short et al. 1989; Standeven et al. 1994, 1995; Standeven and Goldsworthy 1993).

For in vitro genotoxicity studies, LBPNs were negative for six out of seven Ames tests, and were also negative for UDS and for forward mutations (Riccio and Stewart 1991; Blackburn 1981; Blackburn et al. 1986, 1988; Gochet et al. 1984; Brecher 1984a; Brecher and Goode 1984a; Papciak and Goode 1984). LBPNs exhibited mixed or equivocal results for the mouse lymphoma and sister chromatid exchange assays, as well as for cell transformation (API 1985d, 1985j, 1985k, 1985l, 1985m, 1985n, 1985o, 1985p, 1986j, 1986k, 1986l, 1987b, 1988b; Kirby et al. 1979; Gochet et al. 1984; Brecher 1984b; Brecher and Goode 1984b; Tu and Sivak 1981; Jensen and Thilager 1978; Roy 1981) and positive results for one bacterial DNA repair assay (Haworth 1978). Mixtures that were tested, which included a number of light naphthas, displayed negative results for the Ames and mouse lymphoma assays (API 1977a). Gasoline exhibited negative results for the Ames test battery, the sister chromatid exchange assay and for one mutagenicity assay (API 1977b; Farrow et al. 1983; Dooley et al. 1988; Conaway et al. 1984; Richardson et al. 1986). Mixed results were observed for UDS and the mouse lymphoma assay (API 1977b, 1988c; Farrow et al. 1983; Conaway et al. 1984; Dooley et al. 1988; Loury et al. 1986, 1987).

While the majority of in vivo genotoxicity results for LBPN substances are negative, the potential for genotoxicity of LBPNs as a group cannot be discounted based on the mixed in vitro genotoxicity results.

No inhalation studies assessing the carcinogenicity of the site-restricted LBPNs were identified. Only unleaded gasoline has been examined for its carcinogenic potential, in several inhalation studies (MacFarland et al. 1984; Short et al. 1989; Standeven and Goldsworthy 1993; Standeven et al. 1994, 1995). In one study, rats and mice were exposed to 0, 200, 870 or 6170 mg/m³ of a 2% benzene formulation of the test substance, via inhalation, for approximately 2 years. A statistically significant increase in hepatocellular adenomas and carcinomas, as well as a non-statistical increase in renal tumours, were observed at the highest dose in female mice. A dose-dependent increase in the incidence of primary renal neoplasms was also detected in male rats, but this was not considered to be relevant to humans, as discussed previously (MacFarland et al. 1984). In other studies, no renal cell tumours were observed after 1 year in male and female rats exposed to lower concentrations (0, 27, 183 or 791 mg/m³) for 24 or 65–67 weeks (Short et al. 1989). Carcinogenicity was also assessed for unleaded gasoline, via inhalation, as part of initiation/promotion studies. In these studies, unleaded gasoline did not appear to initiate tumour formation, but did show renal cell and hepatic tumour promotion ability, when rats and mice were exposed, via inhalation, for durations ranging from 13 weeks to approximately 1 year using an initiation/promotion protocol (Short et al. 1989; Standeven and Goldsworthy 1993; Standeven et al. 1994, 1995). However, further examination of data relevant to the composition of unleaded gasoline demonstrated that this is a highly-regulated substance; it is expected to contain a lower percentage of benzene and has a discrete component profile when compared to other substances in the LBPN group.

Both the European Commission and the International Agency for Research on Cancer (IARC) have classified LBPN substances as carcinogenic. All of these substances were classified by the European Commission (2008) as Category 2 (R45: may cause cancer) (benzene content ≥ 0.1% by weight). IARC has classified gasoline, an LBPN, as a Group 2B carcinogen (possibly carcinogenic to humans) and “occupational exposures in petroleum refining” as Group 2A carcinogens (probably carcinogenic to humans). In both IARC classifications, several LBPN substances, including some that are site-restricted, were included: CAS RNs 64741-46-4, 64741-54-4, 64741-55-5, 64741-64-6, 64741-74-8 and 68919-37-9 were identified by IARC as major components of gasoline, while CAS RNs 64741-41-9, 64741-46-4, 64741-54-4, 64741-55-5, 64741-63-5, 64741-64-6, 64741-68-0, 64741-69-1, 64741-74-8, 64742-82-1, 68410-05-9 and 68919-37-9 were listed in “occupational exposures in petroleum refining” (IARC 1989a, b).

LBPNs potentially contain the volatile component benzene. The most likely average benzene concentration in naphthas is approximately 1%, and measured benzene concentrations ranged from non-detected in isomerized naphthas to 20% in reformates (UN 2009). Benzene was assessed by the Government of Canada under CEPA, 1988 (Canada 1993) and was determined to be harmful to human health based on carcinogenicity. This substance was subsequently added to the List of Toxic Substances - Schedule 1 of CEPA 1999. Other organizations have drawn similar conclusions. IARC classified benzene as a Group 1 carcinogen (carcinogenic to humans) (IARC 1987, 2004, 2007) and the European Commission has recommended that all LBPNs containing ≥ 0.1% benzene by weight be classified as Category 2 carcinogens, even in the absence of stream-specific experimental animal data (ECB 2007; CONCAWE 2005; UN 2009). This is consistent with the approach used to categorize petroleum streams during the categorization exercise conducted for substances on the DSL under CEPA 1999 (Health Canada 2008).

Several studies were conducted on experimental animals to investigate the dermal carcinogenicity of LBPNs. The majority of these studies were conducted through exposure of mice to doses ranging from 694–1351 mg/kg-bw, for durations ranging from 1 year to the animals’ lifetime or until a tumour persisted for 2 weeks. Given the route of exposure, the studies specifically examined the formation of skin tumours. Results for carcinogenicity via dermal exposure are mixed. Both malignant and benign skin tumours were induced with heavy catalytic cracked naphtha, light catalytic cracked naphtha, light straight-run naphtha and naphtha (API 1986m, 1986n; Blackburn et al. 1986, 1988; Witschi et al. 1987; Clark et al. 1988; Broddle et al. 1996). Significant increases in squamous cell carcinomas were also observed when mice were dermally treated with Stoddard solvent (US EPA 1984), but the latter was administered as a mixture (90% test substance), and the details of the study were not available. In contrast, insignificant increases in tumour formation or no tumours were observed when light alkylate naphtha, heavy catalytic reformed naphtha, sweetened naphtha, light catalytically cracked naphtha or unleaded gasoline was dermally applied to mice (API 1986m, 1986n, 1986o, 1988d; Skisak et al. 1994; Broddle et al. 1996). Negative results for skin tumours were also observed in male mice dermally exposed to sweetened naphtha using an initiation/promotion protocol (Skisak et al. 1994).

Therefore, after consideration of the carcinogenicity data set, there is evidence for carcinogenicity for some LBPN substances in experimental animals following dermal exposure. There also appears to be evidence of tumour formation in rodents following inhalation exposure to gasoline. However, no inhalation studies examining site-restricted, or other, LBPN substances were identified.

No reproductive or developmental toxicity was observed for the majority of LBPN substances evaluated. Most of these studies were carried out by inhalation exposure in rodents.

NOAEC values for reproductive toxicity following inhalation exposure ranged from 1701 mg/m³ (CAS RN 8052-41-3) to 27 687 mg/m³ (CAS RN 64741-63-5) for the LBPNs group evaluated, and from 7690 mg/m³ to 27 059 mg/m³ for the site-restricted light catalytic cracked and full-range catalytic reformed naphthas (API 1978, 2008a, 2008b, 2008c, 2008d; Phillips and Egan 1981; Schreiner 1984; McKee et al. 1990; Dalbey et al. 1996; Bui et al. 1998; Schreiner et al. 1999, 2000b; Roberts et al. 2001). However, a decreased number of pups per litter and higher frequency of post-implantation loss were observed following inhalation exposure of female rats to hydrotreated heavy naphtha (CAS RN 64742-48-9) at a concentration of 4679 mg/m³, 6 hours per day, from gestational days 7–20 (Hass et al. 2001). For dermal exposures, NOAEL values of 714 mg/kg-bw (CAS RN 8030-30-6) and 1000 mg/kg-bw per day (CAS RN 68513-02-0) were noted (Clark et al. 1988; ARCO 1994). For oral exposures, no adverse effects on reproductive parameters were reported when rats were given site-restricted light catalytic cracked naphtha at 2000 mg/kg on gestational day 13 (Stonybrook Laboratories, Inc. 1995).

For most LBPNs, no treatment-related developmental effects were observed by the different routes of exposure (API 1977d, 1978, 2008b, 2008c, 2008d; Litton Bionetics 1978; Miller and Schardein 1981; Phillips and Egan 1981; Schreiner 1984; Clark et al. 1988; Mobil 1988b; ARCO 1994; Stonybrook Laboratories 1995; Dalbey et al. 1996; Bui et al. 1998; Schreiner et al. 1999, 2000b; Roberts et al. 2001). However, developmental toxicity was observed for a few naphthas. Decreased fetal body weight and an increased incidence of ossification variations were observed when rat dams were exposed to light aromatized solvent naphtha, by gavage, at 1250 mg/kg-bw per day (Bio/Dynamics, Inc. 1991c). In addition, pregnant rats exposed by inhalation to hydrotreated heavy naphtha at 4679 mg/m³ delivered pups with higher birth weights. Cognitive and memory impairments were also observed in the offspring (Hass et al. 2001).

Although a number of epidemiological studies have reported increases in the incidence of a variety of cancers, the majority of these studies are considered to contain incomplete or inadequate information. Limited data, however, are available for skin cancer and leukemia incidence, as well as mortality among petroleum refinery workers (Hendricks et al. 1959; Lione and Denholm 1959; McCraw et al. 1985; Divine and Barron 1986; Nelson et al. 1987; Wong and Raabe 1989). IARC (1989b) therefore concluded that there is limited evidence supporting the view that working in petroleum refineries entails a carcinogenic risk (Group 2A carcinogen). IARC (1989a) also classified gasoline as a Group 2B carcinogen; it considered the evidence for carcinogenicity in humans from gasoline to be inadequate and noted that published epidemiological studies had several limitations, including a lack of exposure data and the fact that it was not possible to separate the effects of combustion products from those of gasoline itself. Similar conclusions were drawn from other reviews of epidemiological studies for gasoline (US EPA 1987a, 1987b). Thus, the evidence gathered from these epidemiological studies is considered to be inadequate to conclude on the effects of human exposure to LBPN substances.

Characterization of Risk to Human Health

Site-restricted LBPNs were identified as a high priority for action because they were considered to present a high hazard to human health. A critical effect for the initial categorization of site-restricted LBPN substances was carcinogenicity, based primarily on classifications by other international agencies. These substances are classified by the European Commission (2008) as Category 2 (benzene content ≥0.1% by weight), and by IARC as Group 2A and 2B (IARC 1989a, b). However, the LBPNs considered in this report have been identified as site-restricted (i.e., indicating that they are not expected to be transported off refinery or upgrader facility sites), and therefore general population exposure is not expected. Accordingly, the likelihood of exposure to Canadians is considered to be low; hence, the risk to human health is likewise considered to be low.

Uncertainties in Evaluation of Risk to Human Health

As the site-restricted LBPNs are considered to be UVCBs, their specific compositions are not well defined. LBPN streams under the same CAS RN can vary significantly in the number, identity and proportion of constituent compounds, depending on operating conditions, feedstocks and processing units. Consequently, it is difficult to obtain a truly representative toxicological dataset for individual CAS RNs. For this reason, all available toxicological data on LBPN substances with similar processing as well as physical and chemical properties were pooled across CAS RNs to develop a comprehensive toxicity profile. Specific physical and chemical properties of some LBPN substances were not available; therefore, properties of representative LBPNs were used as needed.

The scope of this screening assessment does not involve full investigation of the mode of induction of effects.

The PSSA screening assessments evaluate substances that are complex mixtures (UVCBs) composed of a number of components in various proportions due to the source of the crude oil or bitumen and its subsequent processing. Monitoring information or provincial release limits from petroleum facilities target broad releases (such as oils and greases) to water or air. These widely encompassing release categories do not allow for detection of individual complex mixtures or production streams. As such, the monitoring of broad releases cannot provide sufficient data to associate a detected release with a specific substance identified by a CAS RN, and the proportion of releases attributed to individual CAS RNs cannot be defined.

Conclusion

Based on the available information, all of the LBPNs in this report are likely to have high proportions of C₄–C₆ hydrocarbons that are considered to be persistent in air, based on criteria in the Persistence and Bioaccumulation Regulations of CEPA 1999.

Based on the available information, none of the LBPNs considered here contain components that are considered to be bioaccumulative based on criteria in the Persistence and Bioaccumulation Regulations of CEPA 1999.

Based on the information presented in this screening assessment, the basis for initial categorization for human health hazard was carcinogenicity. Genotoxicity assays in vivo were essentially negative. Mixed results, however, were obtained in vitro, suggesting that some LBPNs have the potential to be mutagenic. LBPNs also appear to have limited potential to adversely affect reproduction and development.

The LBPNs listed in this screening assessment (64741-54-4, 64741-55-5, 64741-64-6, 64741-74-8, 64742-22-9, 64742-23-0, 64742-73-0, 68410-05-9, 68410-71-9, 68410-96-8, 68476-46-0, 68477-89-4, 68478-12-6, 68513-02-0, 68514-79-4, 68606-11-1, 68783-12-0, 68919-37-9, 68955-35-1 and 101795-01-1) are restricted to refinery and/or upgrader facilities; therefore, exposure of the general population and the environment is not expected. It is concluded that these site-restricted LBPNs 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; that constitute or may constitute a danger to the environment on which life depends; or that constitute or may constitute a danger in Canada to human life or health.

It is therefore concluded that these site-restricted LBPNs do not meet the criteria set out in section 64 of CEPA 1999.

Because these substances are listed on the DSL, their import and manufacture in Canada are not subject to notification under subsection 81(1) of CEPA 1999. Given the potential hazardous properties of these substances, there is concern that new activities that have not been identified or assessed could lead to these substances meeting the criteria set out in section 64 of the Act. Therefore, application of the Significant New Activity provisions of the Act to these substances if being considered, so that any proposed new manufacture, import or use of these substances outside a petroleum refinery or upgrader facility is subject to further assessment, to determine if the new activity requires further risk management consideration.

References

Adema DMM, van den Bos Bakker GH. 1986. Aquatic toxicity of compounds that may be carried by ships (Marpol 1973, Annex II). A progress report for 1986 from TNO to the Dutch Ministry of Housing, Physical Planning and the Environment. Delft (NL): TNO. Report No.: 86/326a. [cited in CONCAWE 2001].

[AOPWIN] Atmospheric Oxidation Program for Windows [Estimation Model]. 2008. Version 1.92a. Washington (DC): US Environmental Protection Agency, Office of Pollution Prevention and Toxics; Syracuse (NY): Syracuse Research Corporation. Exposure Assessment Tools and Models.

[API] American Petroleum Institute. 1977a. Letter from American Petroleum Institute to US Environmental Protection Agency regarding submission of 8(E) information on 3 commercial solvents with attachments. Washington (DC): American Petroleum Institute. EPA/OTS Document No. 88-7700010. NTIS/OTS0200393. [Abstract]. [cited in TOXLINE 2009].

[API] American Petroleum Institute. 1977b. Mutagenicity evaluation of unleaded gasoline (L5178Y mouse lymphoma assay and Ames test). Washington (DC): American Petroleum Institute. API Report No. 28-30173. [cited in API 2002, 2008a].

[API] American Petroleum Institute. 1977c. Rat bone marrow cytogenesis analysis, unleaded gasoline [5 daily intraperitoneal doses]. Washington (DC): American Petroleum Institute. API Report No. 26-60099. [cited in CONCAWE 1992].

[API] American Petroleum Institute. 1977d. Teratology study in rats. Stoddard solvent final report. Washington (DC): American Petroleum Institute. FYI-AX-0183-0232 IN. [cited in ATSDR 1995a].

[API] American Petroleum Institute. 1978. Teratology study in rats, unleaded gasoline. Washington (DC): American Petroleum Institute. API Report No. 26-60014. [cited in API 2008a].

[API] American Petroleum Institute. 1980a. Acute toxicity tests. API PS-6 unleaded motor gasoline. Washington (DC): American Petroleum Institute. API Report No. 27-32130. [cited in CONCAWE 1992; API 2008a].

[API] American Petroleum Institute. 1980b. Mutagenicity evaluation of gasoline, API PS-6 fuel in the mouse dominant lethal assay. Washington (DC): American Petroleum Institute. API Report No. 28-31344. [cited in CONCAWE 1992; API 2002, 2008a].

[API] American Petroleum Institute. 1985a. Acute oral toxicity study in rats, acute dermal toxicity study in rabbits, primary dermal irritation study in rabbits, primary eye irritation study in rabbits, API 83-05 full range catalytic reformed naphtha (CAS #68955-35-1). Washington (DC): American Petroleum Institute. API Report No. 32-31474. [cited in CONCAWE 1992; API 2008a].

[API] American Petroleum Institute. 1985b. Acute oral toxicity study in rats, acute dermal toxicity study in rabbits, primary dermal irritation study in rabbits, primary eye irritation study in rabbits, dermal sensitization study in guinea pigs. API sample 83-06 heavy catalytically reformed naphtha (CAS #64741-68-0). Washington (DC): American Petroleum Institute. API Health and Environmental Science Department Report 32-32860. [cited in CONCAWE 1992].

[API] American Petroleum Institute. 1985c. Acute oral toxicity study in rats, acute dermal toxicity study in rabbits, primary dermal irritation study in rabbits and primary eye irritation study in rabbits of API sample 83-04 light catalytically reformed naphtha. Washington (DC): American Petroleum Institute. API Medical Research Publication 32-31473. [cited in CONCAWE 1992].

[API] American Petroleum Institute. 1985d. Mutagenic evaluation studies in the bone marrow cytogenetics assay (inhalation) and in the mouse lymphoma forward mutation assay, light catalytic cracked naphtha 81-03. Washington (DC): American Petroleum Institute. API Report No. 32-31300. [cited in CONCAWE 1992; API 2003b, 2008a].

[API] American Petroleum Institute. 1985e. Acute in vivo cytogenetics assay in male and female rats of API sample 83-19, light alkylate naphtha. Washington (DC): American Petroleum Institute. API Report No. 32-32409. [cited in CONCAWE 1992; API 2003c, 2008a].

[API] American Petroleum Institute. 1985f. Activity of API 81-04, light catalytic cracked naphtha, in the acute (IP) in vivo cytogenetics assay in male and female rats. Washington (DC): American Petroleum Institute. API Report No. 32-32288. [cited in CONCAWE 1992; API 2003b, 2008a].

[API] American Petroleum Institute. 1985g. Mutagenicity evaluation of 83-04 (light catalytic reformed naphtha) in the bone marrow cytogenetics assay (IP). Washington (DC): American Petroleum Institute. API Report No. 33-31092. [cited in CONCAWE 1992; API 2003a, 2008a].

[API] American Petroleum Institute. 1985h. Mutagenicity evaluation of 83-06 (heavy catalytic reformed naphtha) in the bone marrow cytogenetics assay (IP). Washington (DC): American Petroleum Institute. API Report No. 32-30494. [cited in API 2003a, 2008a].

[API] American Petroleum Institute. 1985i. Mutagenicity evaluation of 83-05 (full range catalytic reformed naphtha) in the bone marrow cytogenetics assay (IP). Washington (DC): American Petroleum Institute. API Report No. 32-32289. [cited in CONCAWE 1992; API 2003a, 2008a].

[API] American Petroleum Institute. 1985j. L5178Y +/- mouse lymphoma assay, API 81-08 sweetened naphtha. Washington (DC): American Petroleum Institute. API Report No. 32-31233. [cited in CONCAWE 1992; API 2003d, 2008a].

[API] American Petroleum Institute. 1985k. L5178Y +/- mouse lymphoma assay, API 83-19 light alkylate naphtha. Washington (DC): American Petroleum Institute. API Report No. 32-32746. [cited in CONCAWE 1992; API 2003c, 2008a].

[API] American Petroleum Institute. 1985l. Mutagenicity evaluation of API sample 83-04 in the mouse lymphoma forward mutation assay. Final report. Washington (DC): American Petroleum Institute. API Medical Research Publication 32-32168. [cited in CONCAWE 1992; API 2003a, 2008a].

[API] American Petroleum Institute. 1985m. L5178Y +/- mouse lymphoma assay, API 83-16 heavy catalytic reformed naphtha. Washington (DC): American Petroleum Institute. API Report No. 32-32460. [cited in API 2008a].

[API] American Petroleum Institute. 1985n. Mutagenicity evaluation in the mouse lymphoma forward mutation assay, API 83-06 heavy catalytically reformed naphtha. Washington (DC): American Petroleum Institute. API Report No. 33-32640. [cited in API 2003a].

[API] American Petroleum Institute. 1985o. L5178Y TK +/- mouse lymphoma assay of API 81-04. Washington (DC): American Petroleum Institute. API Medical Research Publication 32-31710. [cited in CONCAWE 1992; API 2003b].

[API] American Petroleum Institute. 1985p. L5178Y +/- mouse lymphoma assay, API 83-05 full range catalytic reformed naphtha. Washington (DC): American Petroleum Institute. API Report No. 32-32459. [cited in CONCAWE 1992; API 2003a, 2008a].

[API] American Petroleum Institute. 1986a. Acute oral toxicity in rats, acute dermal toxicity study in rabbits, primary dermal irritation study in rabbits, primary eye irritation study in rabbits, dermal sensitization study in guinea pigs on API 83-19, light alkylate naphtha (CAS #64741-66-8). Washington (DC): American Petroleum Institute. API Report No. 33-30594. [cited in CONCAWE 1992; API 2008a].

[API] American Petroleum Institute. 1986b. Acute oral toxicity in rats, acute dermal toxicity study in rabbits, primary dermal irritation study in rabbits, primary eye irritation study in rabbits, dermal sensitization study in guinea pigs on API 83-20, light catalytic cracked naphtha (CAS #64741-55-5). Washington (DC): American Petroleum Institute. API Report No. 33-32722. [cited in CONCAWE 1992; cited in API 2008a].

[API] American Petroleum Institute. 1986c. Acute oral toxicity in rats, acute dermal toxicity study in rabbits, primary dermal irritation study in rabbits, primary eye irritation study in rabbits, dermal sensitization study in guinea pigs on API 81-08, sweetened naphtha (CAS #64741-87-3). Washington (DC): American Petroleum Institute. API Report No. 30-31990. [cited in CONCAWE 1992; API 2008a].

[API] American Petroleum Institute. 1986d. Acute oral toxicity in rats, acute dermal toxicity study in rabbits, primary dermal irritation study in rabbits, primary eye irritation study in rabbits, dermal sensitization study in guinea pigs. API sample 83-18 heavy catalytically cracked naphtha (CAS #64741-54-4). Final report. Washington (DC): American Petroleum Institute. API Health and Environmental Science Department Report No. 33-30593. [cited in CONCAWE 1992].

[API] American Petroleum Institute. 1986e. Dermal sensitization study in guinea pigs with full range catalytic reformed naphtha (API 83-05). Washington (DC): American Petroleum Institute. API Report No. 33-30498. [cited in CONCAWE 1992; API 2008a].

[API] American Petroleum Institute. 1986f. Dermal sensitization study in guinea pigs. API sample 83-04 light catalytically cracked reformed naphtha (CAS 64741-63-5). Final report. API Health and Environmental Science Department Report No. 33-30496. [cited in CONCAWE 1992].

[API] American Petroleum Institute. 1986g. 28-day dermal toxicity study in the rabbit. API sample 83-18 heavy catalytically cracked naphtha (CAS 64741-54-4). Study conducted by Tegeris Laboratories. Washington (DC): American Petroleum Institute. API Medical Research Publication No. 32-32748. [cited in CONCAWE 1992].

[API] American Petroleum Institute. 1986h. 28-day dermal toxicity study in the rabbit. API sample 83-05 full range catalytically reformed naphtha (CAS 68955-35-1). Study conducted by Tegeris Laboratories. Washington (DC): American Petroleum Institute. API Health and Environmental Science Department Report No. 33-30598. [cited in CONCAWE 1992].

[API] American Petroleum Institute. 1986i. Mutagenicity evaluation in the bone marrow cytogenetics assay with API 81-08 (IP). Washington (DC): American Petroleum Institute. API Report No. 33-31093. [cited in CONCAWE 1992; API 2003d, 2008a].

[API] American Petroleum Institute. 1986j. L5178Y TK +/- mouse lymphoma assay. API 83-06 heavy catalytically reformed naphtha (CAS 64741-68-0). Washington (DC): American Petroleum Institute. API Report No. 33-31641. [cited in API 2003a].

[API] American Petroleum Institute. 1986k. L5178Y +/- mouse lymphoma assay, API 81-04 light catalytic cracked naphtha. Washington (DC): American Petroleum Institute. API Report No. 32-30498. [cited in API 2008a].

[API] American Petroleum Institute. 1986l. Mutagenicity of API sample 83-18 heavy catalytic cracked naphtha (petroleum) (CAS 64741-54-4) in a mouse lymphoma mutation assay. Final report. Washington (DC): American Petroleum Institute. API Health and Environmental Science Department Report No. 33-32804. [cited in CONCAWE 1992].

[API] American Petroleum Institute. 1986m. Lifetime dermal carcinogenesis/chronic toxicity screening bioassay of refinery streams in C3H/HeJ mice. Twenty-fourth month progress report (weeks 101-104). Washington (DC): American Petroleum Institute. API Study No. PS-36. PRI Study No. AP-135r.

[API] American Petroleum Institute. 1986n. Lifetime dermal carcinogenesis/chronic toxicity screening bioassay of refinery streams in C3H/HeJ mice. Thirty-first month progress report (weeks 131-134). Washington (DC): American Petroleum Institute. API Study No. PS-36. PRI Study No. AP-135r.

[API] American Petroleum Institute. 1986o. Lifetime dermal carcinogenesis/chronic toxicity screening bioassay of refinery streams in C3H/HeJ mice. Twelve month toxicity evaluation report. Washington (DC): American Petroleum Institute. API Study No. PS-36. PRI Study No. API-135r.

[API] American Petroleum Institute. 1987a. 13-week subchronic inhalation study of light catalytic cracked naphtha (81-03) in rats. Washington (DC): American Petroleum Institute. API Report No. 34-33173. [cited in API 2008a].

[API] American Petroleum Institute. 1987b. L5178Y +/- mouse lymphoma assay, API 83-20 light catalytic cracked naphtha. Washington (DC): American Petroleum Institute. API Report No. 34-30633. [cited in CONCAWE 1992; API 2003b, 2008a].

[API] American Petroleum Institute. 1988a. In vivo sister chromatid exchange assay in B6C3F1 mice, with API 81-03 (light catalytic cracked naphtha). Washington (DC): American Petroleum Institute. API Report No. 36-30044. [cited in CONCAWE 1992; API 2003b, 2008a].

[API] American Petroleum Institute. 1988b. Sister chromatid exchange assay in Chinese hamster ovary (CHO) cells with API 81-03 (light catalytic cracked naphtha). Washington (DC): American Petroleum Institute. API Report No. 36-30045. [cited in CONCAWE 1992; API 2003b, 2008a].

[API] American Petroleum Institute. 1988c. In vitro unscheduled DNA synthesis in rat hepatocytes - gasoline. Washington (DC): American Petroleum Institute. API Report No. 35-32431. [cited in API 2008a].

[API] American Petroleum Institute. 1988d. Short term dermal tumorigenesis study of selected petroleum hydrocarbons in male CD-1 mice initiation and promotion phases (draft final report) with attachments and cover letter 052688. Washington (DC): American Petroleum Institute. NTIS/OTS0000547-1.

[API] American Petroleum Institute. 2001a. Gasoline blending streams test plan. Submitted to US Environmental Protection Agency. Washington (DC): American Petroleum Institute, Petroleum HPV Testing Group.

[API] American Petroleum Institute. 2001b. Robust summary of information on group 6: low benzene naphthas. Washington (DC): American Petroleum Institute. Report No. AR201-13437B.

[API] American Petroleum Institute. 2002. Robust summary of information on gasoline. Washington (DC): American Petroleum Institute.

[API] American Petroleum Institute. 2003a. Robust summary of information on aromatic naphthas. Washington (DC): American Petroleum Institute.

[API] American Petroleum Institute. 2003b. Robust summary of information on olefinic naphthas. Washington (DC): American Petroleum Institute.

[API] American Petroleum Institute. 2003c. Robust summary of information on paraffinic naphthas. Washington (DC): American Petroleum Institute.

[API] American Petroleum Institute. 2003d. Robust summary of information on naphthenic naphthas. Washington (DC): American Petroleum Institute.

[API] American Petroleum Institute. 2005. Baseline gasoline vapor condensate. Micronucleus assay in a 13-week whole-body inhalation toxicity study in rats with neurotoxicity assessments and 4-week in vivo genotoxicity and immunotoxicity assessments. HLS Study No. 00-6125, Volume IV, Appendix X. East Millstone (NJ): Huntingdon Life Sciences Laboratories; and Suffolk (GB): Huntingdon Eye Research Centre. [cited in API 2008a].

[API] American Petroleum Institute. 2008a. Gasoline blending streams category assessment document. Final 8-21-08. Submitted to the US Environmental Protection Agency. Consortium Registration No. 1100997. Washington (DC): American Petroleum Institute, Petroleum HPV Testing Group.

[API] American Petroleum Institute. 2008b. OECD 422 inhalation combined repeated dose toxicity study with the reproductive/developmental toxicity screening test of heavy straight run naphtha (CAS # 64741-41-9). Wilmington (DE): Haskell Laboratories. Project No. DuPont-18331. [cited in API 2008a].

[API] American Petroleum Institute. 2008c. Baseline gasoline vapor condensate. A 2-generation whole-body inhalation reproductive study in rats. HLS Study No. 00-4207. East Millstone (NJ): Huntingdon Life Sciences Laboratories. [cited in API 2008a].

[API] American Petroleum Institute. 2008d. Baseline gasoline vapor condensate. Whole-body inhalation developmental toxicity study in rats with baseline gasoline vapor condensate. EMBSL No. MRD-00-695: 169534. Annandale (NJ): ExxonMobil Biomedical Sciences Inc. [cited in API 2008a].

[ARCO] Atlantic Richfield Company. 1994. Developmental toxicity screen in rats administered test article F-250. ARCO Study No. ATX-93-0024 (Merox Feed); UBTL Study No. 66869. Los Angeles (CA): Atlantic Richfield Company. [cited in API 2008a].

Arnot JA, Gobas FA. 2003. A generic QSAR for assessing the bioaccumulation potential of organic chemicals in aquatic food webs. QSAR Comb Sci 22(3):337–345 [Internet]. [cited 2007 Mar 15]. Molecular Informatics [restricted access]

Aronson D, Boethling R, Howard P, Stiteler W. 2006. Estimating biodegradation half-lives for use in chemical screening. Chemosphere 63:1953-1960.

Atkinson R. 1990. Gas-phase tropospheric chemistry of organic compounds: a review. Atmos Environ 24A:1–41.

Atlas R. 1981. Microbial degradation of petroleum hydrocarbons: an experimental perspective. Microbiol Rev 45(1):180–209.

[ATSDR] Agency for Toxic Substances and Disease Registry. 1995a. Toxicological profile for Stoddard solvent. Atlanta (GA): US Department of Health and Human Services, Public Health Service. [cited 2009 Apr 17].

[ATSDR] Agency for Toxic Substances and Disease Registry. 1995b. Toxicological profile for automotive gasoline. Atlanta (GA): US Department of Health and Human Services, Public Health Service. [cited 2009 Apr 17].

[BCFBAF] BioConcentration Factor Program for Windows [Estimation Model]. 2008. Version 4.00. Washington (DC): US Environmental Protection Agency, Office of Pollution Prevention and Toxics; Syracuse (NY): Syracuse Research Corporation. Exposure Assessment Tools and Models.

Bio/Dynamics Inc. 1991a. A subchronic (3 month) oral toxicity study in the rat with LX-1006-01 via gavage (final report) with attachments and cover letter dated 042491 (sanitized). EPA Document No. 86-910000807S. NTIS/OTS0529439. [Abstract]. [cited in TOXLINE 2009].

Bio/Dynamics Inc. 1991b. A subchronic (3-month) oral toxicity study in the dog with LX1106-01 via capsule administration (final report) with attachments and cover letters dated 042491 (sanitized). EPA Document No. 86-91000808S. NTIS/OTS0529440. [Abstract]. [cited in TOXLINE 2009].

Bio/Dynamics Inc. 1991c. A teratology study in rats with LX1106-01 (final report) with attachments and cover letter dated 042491 (sanitized). EPA/OTS Document No. 86-910000809S. NTIS/OTS0529441. [Abstract]. [cited in TOXLINE 2009].

[BIOHCWIN] Biodegradation of Petroleum Hydrocarbons Program for Windows [Estimation Model]. 2008. Version 1.01a. Washington (DC): US Environmental Protection Agency, Office of Pollution Prevention and Toxics; Syracuse (NY): Syracuse Research Corporation. Exposure Assessment Tools and Models.

[BIOWIN] Biodegradation Probability Program for Windows [Estimation Model]. 2009. Version 4.10. Washington (DC): US Environmental Protection Agency, Office of Pollution Prevention and Toxics; Syracuse (NY): Syracuse Research Corporation. Exposure Assessment Tools and Models.

Blackburn GR. 1981. An Ames Salmonella/mammalian microsome mutagenesis assay for the determination of potential mutagenicity of rerun tower overheads from an olefins/aromatics plant. Study No. 1781-80. Princeton (NJ): Mobil Environmental and Health Sciences Laboratory. [cited in US EPA 2004].

Blackburn GR, Deitch RA, Schreiner CA, Mackerer CR. 1986. Predicting carcinogenicity of petroleum distillation fractions using a modified Salmonella mutagenicity assay. Cell Biol Toxicol 2(1):63–84.

Blackburn GR, Deitch RA, Roy TA, Johnson SW, Schreiner CA, Mackerer CR. 1988. Estimation of dermal carcinogenic potency of petroleum fractions using a modified Ames assay. In: Cooke M, Dennis AJ, editors. Proceedings of the 10th Annual Symposium on Polynuclear Aromatic Hydrocarbons: a decade of progress. Columbus (OH): Battelle Press. p. 83–97. [Abstract]. [cited in TOXLINE 2009].

Boehm P, Quinn J. 1977. The persistence of chronically accumulated hydrocarbons in the Hard Shell Clam (Mercenaria mercenaria). Mar Biol 44:227–233.

Boethling RS, Howard PH, Beauman JA, Larosche ME. 1995. Factors for intermedia extrapolations in biodegradability assessment. Chemosphere 30(4):741–752.

Brecher S. 1984a. Hepatocyte primary culture/DNA repair test of hydrogenated pyrolysis gasoline. Project No. 2097. Prepared for Gulf Oil Chemicals Co., Houston (TX). Pittsburgh (PA): Gulf Life Sciences Center. [cited in US EPA 2004].

Brecher S. 1984b. Transformation test of hydrogenated pyrolysis gasoline. Project No. 2098. Prepared for Gulf Oil Chemicals Co., Houston (TX). Pittsburgh (PA): Gulf Life Sciences Center. [cited in US EPA 2004].

Brecher S, Goode JW. 1984a. Hepatocyte primary culture/DNA repair test of heavy aromatic distillate. Project No. 2056. Prepared for Gulf Oil Chemicals Co., Houston (TX). Pittsburgh (PA): Gulf Life Sciences Center. [cited in API 2001b].

Brecher S, Goode JW. 1984b. BALB/3T3 transformation test: heavy aromatic distillate. Project No. 2057. Prepared for Gulf Oil Chemicals Co., Houston (TX). Pittsburgh (PA): Gulf Life Sciences Center. [cited in API 2001b].

Broddle WD, Dennis MW, Kitchen DN, Vernot EH. 1996. Chronic dermal studies of petroleum streams in mice. Fundam Appl Toxicol 30(1):47–54.

Bui QQ, Burnett DM, Breglia RJ, Koschier FJ, Lapadula ES, Podhasky PI, Schreiner CA, White RD, Dalbey WE, Feuston MH. 1998. Toxicity evaluation of petroleum blending streams: reproductive and developmental effects of a distillate from light alkylate naphtha. J Toxicol Environ Health A 53(2):121–133.

Buryskova B, Blaha L,Vrskova D, Simkova K, Marsalek B. 2006. Sublethal toxic effects and induction of glutathione S-transferase by short chain chlorinated paraffins (SCCPs) and C-12 alkane (dodecane) in Xenopus laevis frog embryos. Acta Vet Brno 75:115–122.

Canada. 1993. Benzene [Internet]. Ottawa (ON): Environment Canada; Health Canada. (Priority substances list assessment report).

Canada. 1999. Canadian Environmental Protection Act, 1999. S.C., 1999, c. 33. Canada Gazette, Part III, Vol. 22, No. 3.

Canada. 2000. Canadian Environmental Protection Act, 1999: Persistence and Bioaccumulation Regulations, P.C. 2000-348, 23 March 2000, SOR/2000-107. Canada Gazette, Part II, Vol. 34, No. 7.

[CanLII] Canada Legal Information Institute [databases on the Internet]. 2001– . Ottawa (ON): Canadian Legal Information Institute. [cited 2009 Dec 2]. Search Engine CanLII Databases.

Carpenter CP, Kinkead ER, Geary DL, Sullivan LJ, King JM. 1975. Petroleum hydrocarbon toxicity studies. III. Animal and human response to vapors of Stoddard solvent. Toxicol Appl Pharmacol 32(2):282–297.

Chu I, Poon R, Valli V, Yagminas A, Bowers WJ, Seegal R, Vincent R. 2005. Effects of an ethanol–gasoline mixture: results of a 4-week inhalation study in rats. J Appl Toxicol 25(3):193–199.

Clark CR, Walter MK, Ferguson PW, Katchen M. 1988. Comparative dermal carcinogenesis of shale and petroleum-derived distillates. Toxicol Ind Health 4(1):11–22.

Clark DG, Butterworth ST, Martin JG, Roderick HR, Bird MG. 1989. Inhalation toxicity of high flash aromatic naphtha. Toxicol Ind Health 5(3):415–428. [cited as original article and in Edwards et al. 1997].

Colombo J, Cappelletti N, Migoya M, Speranza E. 2007. Bioaccumulation of anthropogenic contaminants by detritivorous fish in the Río de la Plata estuary: 1--Aliphatic hydrocarbons. Chemosphere 68:2128–2135.

Conaway CC, Schreiner CA, Cragg ST. 1984. Mutagenicity evaluation of petroleum hydrocarbons. In: MacFarland HN, Holdsworth CE, MacGregor JA, Call RW, Lane ML, editors. Applied toxicology of petroleum hydrocarbons. Princeton (NJ): Princeton Scientific Publishers. p. 89–107. [cited in IARC 1989a].

[CONCAWE] CONservation of Clean Air and Water in Europe. 1992. Gasolines. Prepared by CONCAWE’s Petroleum Products and Health Management Groups. Brussels (BE): CONCAWE. Product Dossier No. 92/103.

[CONCAWE] CONservation of Clean Air and Water in Europe. 1996. Acute aquatic toxicity of gasolines: report on CONCAWE test programme. Prepared by CONCAWE’s Petroleum Products and Health Management Groups. Brussels (BE): CONCAWE. Product Dossier No. 96/57.

[CONCAWE] CONservation of Clean Air and Water in Europe. 2001. Environmental classification of petroleum substances--summary data and rationale. Prepared by CONCAWE’s Petroleum Products and Health Management Groups. Brussels (BE): CONCAWE. Product Dossier No. 01/54.

[CONCAWE] CONservation of Clean Air and Water in Europe. 2005. Classification and labelling of petroleum substances according to the EU dangerous substances directive (CONCAWE recommendations July 2005). Prepared by CONCAWE’s Petroleum Products and Health Management Groups. Brussels (BE): CONCAWE. Product Dossier No. 6/05.

Correa M, Venables B. 1985. Bioconcentration of naphthalene in tissues of the white mullet (Mugil curema). Environ Toxicol Chem 4:227-231.

Dalbey WE, Feuston MH, Yang JJ, Kommineni CV, Roy TA. 1996. Light catalytically cracked naphtha: subchronic toxicity of vapors in rats and mice and developmental toxicity screen in rats. J Toxicol Environ Health 47(1):77–91.

Daubert T, Danner R. 1989. Physical and thermodynamic properties of pure chemicals data compilation. Washington (DC): Taylor & Francis.

Divine BJ, Barron V. 1986. Texaco mortality study. II. Patterns of mortality among white males by specific job groups. Am J Ind Med 10:371–381. [cited in IARC 1989b].

Dooley JF, Skinner MJ, Roy TA, Blackburn GR, Schreiner CA, Mackerer CR. 1988. Evaluation of the genotoxicity of API reference unleaded gasoline. In: Cooke M, Dennis AJ, editors. Proceedings of the 10th Annual Symposium on Polynuclear Aromatic Hydrocarbons: a decade of progress. Columbus (OH): Battelle Press. p. 179–194. [cited in IARC 1989a; ATSDR 1995b].

[DOSE] The Dictionary of Substances and their Effects [database on the Internet]. 1999. 2nd ed. [cited 2009 Apr 17]. Cambridge (GB): RSC Publishing.

[ECB] European Chemicals Bureau. 2000a. IUCLID dataset for naphtha (petroleum), heavy catalytic cracked. CAS No. 64741-54-4. European Commission, European Chemicals Bureau. [cited 2008 Mar].

[ECB] European Chemicals Bureau. 2000b. IUCLID dataset for naphtha (petroleum), light catalytic cracked. CAS No. 64741-55-5. European Commission, European Chemicals Bureau. [cited 2008 Mar].

[ECB] European Chemicals Bureau. 2000c. IUCLID dataset for full range alkylate naphtha. CAS No. 64741-64-6. European Commission, European Chemicals Bureau. [cited 2008 Mar].

[ECB] European Chemicals Bureau. 2000d. IUCLID dataset for naphtha (petroleum), light thermal cracked. CAS No. 64741-74-8. European Commission, European Chemicals Bureau. [cited 2008 Mar].

[ECB] European Chemicals Bureau. 2000e. IUCLID dataset for naphtha (petroleum), hydrodesulfurized light. CAS No. 64742-73-0. European Commission, European Chemicals Bureau. [cited 2008 Mar].

[ECB] European Chemicals Bureau. 2000f. IUCLID dataset for distillates (petroleum) hydrotreated middle, intermediate boiling. CAS No. 68410-96-8. European Commission, European Chemicals Bureau. [cited 2008 Mar].

[ECB] European Chemicals Bureau. 2000g. IUCLID dataset for hydrocarbons, C3-11, catalytic cracker distillates. CAS No. 68476-46-0. European Commission, European Chemicals Bureau. [cited 2008 Mar].

[ECB] European Chemicals Bureau. 2000h. IUCLID dataset for distillates (petroleum), depentanizer overheads. CAS No. 68477-89-4. European Commission, European Chemicals Bureau. [cited 2008 Mar].

[ECB] European Chemicals Bureau. 2000i. IUCLID dataset for residues (petroleum), butane splitter bottoms. CAS No. 68478-12-6. European Commission, European Chemicals Bureau. [cited 2008 Mar].

[ECB] European Chemicals Bureau. 2000j. IUCLID dataset for petroleum products, hydrofiner-powerformer reformates. CAS No. 68514-79-4. European Commission, European Chemicals Bureau. [cited 2008 Mar].

[ECB] European Chemicals Bureau. 2000k. IUCLID dataset for gasoline, straight-run, topping-plant. CAS No. 68606-11-1. European Commission, European Chemicals Bureau. [cited 2008 Mar].

[ECB] European Chemicals Bureau. 200l. IUCLID dataset for naphtha (petroleum), unsweetened. CAS No. 68783-12-0. European Commission, European Chemicals Bureau. [cited 2008 Mar].

[ECB] European Chemicals Bureau. 2000m. IUCLID dataset for naphtha (petroleum) full range reformed. CAS No. 68919-37-9. European Commission, European Chemicals Bureau. [cited 2008 Mar].

[ECB] European Chemicals Bureau. 2000n. IUCLID dataset for catalytic reformed naphtha. CAS No. 68955-35-1. European Commission, European Chemicals Bureau. [cited 2008 Mar].

[ECB] European Chemicals Bureau. 2000o. IUCLID dataset for naphtha (petroleum), sweetened light. CAS No. 101795-01-1. European Commission, European Chemicals Bureau. [cited 2008 Mar].

[ECB] European Chemicals Bureau. 2007. Guidelines for setting specific concentration limits for carcinogens in annex 1 of directive 67/548/EEC. Inclusion of potency considerations. European Commission, European Chemicals Bureau: Commission Working Group on the Classification and Labelling of Dangerous Substances.

Edwards DA, Andriot MD, Amoruso MA, Tummey AC, Bevan CJ, Tveit A, Hayes LA, Youngren SH, Nakles DV. 1997. Development of fraction specific reference doses (RfDs) and reference concentrations (RfCs) for total petroleum hydrocarbons (TPH). Prepared for Chevron, British Petroleum and the Total Petroleum Hydrocarbon Criteria Working Group. Total Petroleum Hydrocarbon Criteria Working Group Series, Vol. 4. Amherst (MA): Amherst Scientific Publishers.

Environment Canada. 2007. Guidance for conducting ecological assessments under CEPA, 1999: science resource technical series, draft module on QSARs. Draft document. Available from: Environment Canada, Existing Substances Division.

Environment Canada. 2008. Data for petroleum sector stream substances collected under the Canadian Environmental Protection Act, 1999, Section 71: Notice with respect to certain high priority petroleum substances. Data prepared by: Environment Canada, Oil, Gas and Alternative Energy Division.

Environment Canada. 2009. Data for petroleum sector stream substances collected under the Canadian Environmental Protection Act, 1999, Section 71: Notice with respect to potentially industry-limited high priority petroleum substances. Data prepared by: Environment Canada, Oil, Gas and Alternative Energy Division.

[EPIsuite] Estimation Programs Interface Suite for Microsoft Windows [Estimation Model]. 2008. Version 3.4. Washington (DC): US Environmental Protection Agency, Office of Pollution Prevention and Toxics; Syracuse (NY): Syracuse Research Corporation. Exposure Assessment Tools and Models.

European Commission. 2008. Commission Directive 2008/58/EC of 21 August 2008. Official Journal of the European Union. 15.9.2008. European Commission. [cited 2009 Apr 17].

Farrow MG, McCarroll N, Cortina T, Draus M, Munson A, Steinberg M, Kirwin C, Thomas W. 1983. In vitro mutagenicity and genotoxicity of fuels and paraffinic hydrocarbons in the Ames, sister chromatid exchange, and mouse lymphoma assays. Toxicologist 3(1):36. [cited in IARC 1989a].

Gerin M, Viau C, Talbot D, Greselin E. 1988. Aviation gasoline: comparative subchronic nephrotoxicity study in the male rat. Toxicol Lett 44:13–19.

Gochet B, De Meester C, Leonard A, DeKnudt G. 1984. Lack of mutagenic activity of white spirit. Int Arch Occup Environ Health 53(4):359–364.

Halder CA, Warne TM, Hartoum NS. 1984. Renal toxicity of gasoline and related petroleum naphthas in male rats. Adv Mod Environ Toxicol 7:73–88.

Halder CA, Holdsworth CE, Cockrell BY, Piccirillo VJ. 1985. Hydrocarbon nephropathy in male rats: identification of the nephrotoxic components of unleaded gasoline. Toxicol Ind Health 1(3):67–87. [cited in CONCAWE 1992].

Hansch C, Leo A, Hoekman D. 1995. Exploring QSAR. Hydrophobic, electronic, and steric constants. ACS Professional Reference Book. Washington (DC): American Chemical Society.

Hass U, Ladefoged O, Lam HR, Ostergaard G, Lund SP, Simonsen L. 2001. Behavioural effects in rats after prenatal exposure to dearomatized white spirit. Pharmacol Toxicol 89(4):201–207.

Haworth SR. 1978. Bacterial DNA repair assay of Mobil Chemical Company Compound MCTR-125-78 (MRI #110). E.G. and G. Mason Research Institute. Rockville (MD) for Mobil Chemical Co., Edison (NJ). [cited in US EPA 2004].

Health Canada. 2008. Results of the Health-Related Components of Categorization of the Domestic Substances List under CEPA 1999. [cited 2010 Feb 11].

Hendricks NV, Berry CM, Lione JG, Thorpe JJ. 1959. Cancer of the scrotum in wax pressman. I. Epidemiology. Arch Ind Health Occup Med 19:524–529. [cited in IARC 1989b].

[HENRYWIN] Henry’s Law Constant Program for Microsoft Windows [Estimation Model]. 2008. Version 3.20. Washington (DC): US Environmental Protection Agency, Office of Pollution Prevention and Toxics; Syracuse (NY): Syracuse Research Corporation. Exposure Assessment Tools and Models.

Hopkinson R. 2008. Priority substances under Environment Canada’s Chemicals Management Plan for the petroleum sector. Richmond (BC): Levelton Consultants Ltd.

Howard P, Boethling R, Jarvis W, Meylan W, Michalenko E. 1991. Handbook of environmental degradation rates. Boca Raton (FL): Lewis Publishers.

[HSDB] Hazardous Substances Data Bank [database on the Internet]. 1983– . Bethesda (MD): National Library of Medicine (US). [cited 2009 Nov 12].

[IARC] IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. 1987. Overall evaluations of carcinogenicity: an updating of IARC monographs volumes 1 to 42. IARC Monogr Eval Carcinog Risks Hum Suppl 7:38–74.

[IARC] IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. 1989a. Gasoline. IARC Monogr Eval Carcinog Risks Hum 45:159–201.

[IARC] IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. 1989b. Occupational exposures in petroleum refining. IARC Monogr Eval Carcinog Risks Hum 45:39–117.

[IARC] IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. 2004. Overall evaluations of carcinogenicity to humans: as evaluated in IARC Monographs volumes 1–88 (a total of 900 agents, mixtures and exposures). Lyon (FR): International Agency for Research on Cancer. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans.

[IARC] IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. 2007. Agents reviewed by the IARC monographs. Volumes 1–100A (alphabetical order). Lyon (FR): International Agency for Research on Cancer.

[IPCS] International Programme on Chemical Safety. 1996. White spirit. Geneva (CH): World Health Organization. (Environmental Health Criteria 187). Jointly sponsored by the United Nations Environment Programme, the International Labour Organization and the World Health Organization. [cited 2009 Aug 23].

Jensen EM, Thilager AK. 1978. C3H 10T1/2 cell transformation assay. Mobil Chemical Co. Compound MCTR-125-78 (MRI #110). Rockville (MD): E.G. and G. Mason Research Institute. [cited in US EPA 2004].

[JNITE]. 2010. Japanese National Institute of Technology and Evaluation. Official Bulletin of Economy, Trade and Industry. Database accessed September 2010. Biodegradation and Bioconcentration of the Existing Chemical Substances under the Chemical Substances Control Law.

Jonsson G, Bechmann RK, Bamber SD, Baussant T. 2004. Bioconcentration, biotransformation, and elimination of polycyclic aromatic hydrocarbons in Sheepshead minnows (Cyprinodon variegates) exposed to contaminated seawater. Environ Toxicol Chem 23:1538-1548.

Khan SH. 1984. Micronucleus test of hydrogenated pyrolysis gasoline. Project No. 2096. Prepared for Gulf Oil Chemicals Co., Houston (TX). Pittsburgh (PA): Gulf Life Sciences Center. [cited in US EPA 2004].

Khan SH, Goode JW. 1984. Micronucleus test in mouse bone marrow: heavy aromatic distillate administered orally for 2 days. Project No. 2005. Prepared for Gulf Oil Chemicals Co., Houston (TX). Pittsburgh (PA): Gulf Life Sciences Center. [cited in API 2001b].

Kirby PE et al. 1979. An evaluation of mutagenic potential of MCTR-125-78 (MRI #110) employing the L5178Y TK+/- mouse lymphoma assay. Prepared for Mobil Chemical Co., Edison (NJ). Rockville (MD): E.G. and G. Mason Research Institute. [cited in US EPA 2004].

[KOWWIN] Octanol–Water Partition Coefficient Program for Microsoft Windows [Estimation Model]. 2008. Version 1.67a. Washington (DC): US Environmental Protection Agency, Office of Pollution Prevention and Toxics; Syracuse (NY): Syracuse Research Corporation. Exposure Assessment Tools and Models.

Lam HR, Ostergaard G, Guo SX, Ladefoged O, Bondy SC. 1994. Three weeks’ exposure of rats to dearomatized white spirit modifies indices of oxidative stress in brain, kidney, and liver. Biochem Pharmacol 47(4):651–657.

Lapin C, Bui Q, Breglia R, Koschier F, Podhasky P, Lapadula E, Roth R, Schreiner C, White R, Clark C et al. 2001. Toxicity evaluation of petroleum blending streams: inhalation subchronic toxicity/neurotoxicity study of a light catalytic cracked naphtha distillate in rats. Int J Toxicol 20(5):307-319. [cited in PubMed 1997; API 2008a].

Lione JG, Denholm JS. 1959. Cancer of the scrotum in wax pressman. II. Clinical observations. Arch Ind Health Occup Med 19:530–539. [cited in IARC 1989b].

Litton Bionetics. 1978. Teratology study in rats: unleaded gasoline. Final report submitted to American Petroleum Institute, Washington (DC). Kensington (MD): Litton Bionetics Inc. [cited in ATSDR 1995b].

Loury DJ, Smith-Oliver T, Strom S, Jirtle R, Michalopoulos G, Butterworth BE. 1986. Assessment of unscheduled and replicative DNA synthesis in hepatocytes treated in vivo and in vitro with unleaded gasoline or 2,2,4-trimethylpentane. Toxicol Appl Pharmacol 85(1):11–23.

Loury DJ, Smith-Oliver T, Butterworth BE. 1987. Assessment of unscheduled and replicative DNA synthesis in rat kidney cells exposed in vitro or in vivo to unleaded gasoline. Toxicol Appl Pharmacol 87(1):127–140.

Lykke AW, Stewart BW. 1978. Fibrosing alveolitis (pulmonary interstitial fibrosis) evoked by experimental inhalation of gasoline vapours. Experientia 34(4):498. [cited in DOSE 1999].

MacFarland HN, Ulrich CE, Holdsworth CE, Kitchen DN, Halliwell WH, Blum SC. 1984. A chronic inhalation study with unleaded gasoline vapour. Int J Toxicol 3(4):231–248.

McAuliffe C. 1963. Solubility in water of C1–C9 hydrocarbons. Nature 200:1092–1093. [cited in HSDB 2009].

McAuliffe C. 1966. Solubility in water of paraffin, cycloparaffin, olefin, acetylene, cycloolefin and aromatic hydrocarbons. J Phys Chem 70:1267–1275. [cited in HSDB 2009].

McCraw DS, Joyner RE, Cole P. 1985. Excess leukemia in a refinery population. J Occup Med 27:220–222. [cited in IARC 1989b].

McKee RH, Wong ZA, Schmitt S, Beatty P, Swanson M, Schreiner CA, Schardein JL. 1990. The reproductive and developmental toxicity of high flash aromatic naphtha. Toxicol Ind Health 6(3/4):441–460.

McKee RH, Trimmer GW, Whitman FT, Nessel CS, Mackerer CR, Hagemann R, Priston RAJ, Riley AJ, Cruzan G, Simpson BJ, Urbanus JH. 2000. Assessment in rats of the reproductive toxicity of gasoline from a gasoline vapor recovery unit. Reprod Toxicol 14:337–353.

Miller LG, Schardein JL. 1981. Rerun tower overheads: teratology study in rabbits (MCTR-171-79). IRDC Study No. 450-011a. Prepared for Mobil Corporation, Princeton (NJ). Mattawan (MI): International Research and Development Corporation. [cited in US EPA 2001, 2004].

[Mobil] Mobil Environmental and Health Science Laboratory. 1988a. Thirteen week dermal administration of light catalytically cracked naphtha (LCCN) to rats. Study No. 50381. Princeton (NJ): Mobil Corporation. [cited in API 2008a].

[Mobil] Mobil Environmental and Health Science Laboratory. 1988b. Developmental toxicity screen in rats exposed dermally to light catalytically cracked naphtha (LCCN). Study No. 50341. Princeton (NJ): Mobil Corporation. [cited in API 2008a].

[MPBPWIN] Melting Point Boiling Point Program for Microsoft Windows [Estimation Model]. 2008. Version 1.43. Washington (DC): US Environmental Protection Agency, Office of Pollution Prevention and Toxics; Syracuse (NY): Syracuse Research Corporation. Exposure Assessment Tools and Models.

[NCI] National Chemical Inventories [database on a CD-ROM]. 2006. Columbus (OH): American Chemical Society, Chemical Abstracts Service. [cited 2009 Dec 9]. National Chemical Inventory (NCI) System Requirements.

Neff J, Cox B, Dixit D, Anderson J. 1976. Accumulation and release of petroleum-derived aromatic hydrocarbons by four species of marine animals. Mar Biol 38:279–89.

Nelson NA, Van Peenen PFD, Blanchard AG. 1987. Mortality in a recent oil refinery cohort. J Occup Med 29:610–612. [cited in IARC 1989b].

Niimi A, Dookhran G. 1989. Dietary absorption efficiencies and elimination rates of polycyclic aromatic hydrocarbons (PAHs) in rainbow trout (Salmo gairdneri). Environ Toxicol Chem 8:719-722.

Papciak MS, Goode JW. 1984. CHO/HGPRT test: heavy aromatic distillate. Project No. 2054. Prepared for Gulf Oil Chemicals Co., Houston (TX). Pittsburgh (PA): Gulf Life Sciences Center. [cited in API 2001b].

[PCKOCWIN] Organic Carbon Partition Coefficient Program for Windows [Estimation Model]. 2009. Version 2.00. Washington (DC): US Environmental Protection Agency, Office of Pollution Prevention and Toxics; Syracuse (NY): Syracuse Research Corporation. Exposure Assessment Tools and Models.

[PetroTox] A tool for the hazard assessment of petroleum substances. 2009. Version 3.01. HydroQual, Inc., for CONservation of Clean Air and Water in Europe (CONCAWE).

Phillips RD, Egan GF. 1981. Teratogenic and dominant lethal investigation of two hydrocarbon solvents. Toxicologist 1(1):15. [Abstract]. [cited in IPCS 1996; US EPA 1998].

Phillips RD, Egan GF. 1984. Subchronic inhalation exposure of dearomatized white spirit and C10–C11 isoparaffinic hydrocarbon in Sprague-Dawley rats. Fundam Appl Toxicol 4(5):808–818.

[PPSC] Petroleum Product Stewardship Council. 1995a. Static-renewal 96-hour acute toxicity study of the water accommodated fraction (WAF) of whole light alkylate product to fathead minnow. Study conducted by Stonybrook Laboratories Inc. Study No. 65908. Washington (DC): Petroleum Product Stewardship Council. [cited in CONCAWE 2001].

[PPSC] Petroleum Product Stewardship Council. 1995b. Static-renewal 48-hour acute toxicity study of the water accommodated fraction (WAF) of whole light alkylate product to Daphnia magna. Study conducted by Stonybrook Laboratories Inc. Study No. 65907. Washington (DC): Petroleum Product Stewardship Council. [cited in CONCAWE 2001].

Prince R, Parkerton T, Lee C. 2007a. The primary aerobic biodegradation of gasoline hydrocarbons. Environ Sci Technol 41:3316–3321.

Prince R, Parkerton T, Lee C. 2007b. The primary aerobic biodegradation of gasoline. Supplementary information. Environ Sci Technol 41:3316–3321.

PubMed [database on the Internet]. 1997– . Bethesda (MD): National Library of Medicine (US). [revised 2009 Apr 23; cited 25 Apr 2009].

Rector DE, Steadman BL, Jones RA, Siegel J. 1966. Effects on experimental animals of long-term inhalation exposure to mineral spirits. Toxicol Appl Pharmacol 9(2):257–268.

Research and Environmental Division. 1984. Follow-up to TSCA Section 8(E) on Isopar C and Varsol 40 with cover letter dated 011884. EPA Document No. 88-8400586. NTIS/OTS0200630. [Abstract]. [cited in TOXLINE 2009].

Riccio ES, Stewart KR. 1991. Salmonella–Escherichia coli/microsome plate incorporation assay of hydrogenated pyrolysis gasoline. SRI Study No. 2545-A03-91. Sponsor Study No. 91-66. Prepared for Chevron Environmental Health Center, Richmond (CA). Menlo Park (CA): SRI International. [cited in US EPA 2004].

Richardson KA, Wilmer JL, Smith-Simpson D, Skopek TR. 1986. Assessment of the genotoxic potential of unleaded gasoline and 2,2,4-trimethylpentane in human lymphoblasts in vitro. Toxicol Appl Pharmacol 82(2):316–322. [cited in IARC 1989a].

Riley AJ, Collings AJ, Browne NA, Grasso P. 1984. Response of the upper respiratory tract of the rat to white spirit vapour. Toxicol Lett 22(2):125–131.

Roberts L, White R, Bui Q, Daughtrey W, Koschier F, Rodney S, Schreiner C, Steup D, Breglia R, Rhoden R et al. 2001. Developmental toxicity evaluation of unleaded gasoline vapour in the rat. Reprod Toxicol 15(5):487–494.

Rodriguez SC, Dalbey WE. 1994a. Acute oral toxicity of dripolene in Sprague-Dawley rats. Study No. 65642. Prepared for Mobil Chemical Co., Edison (NJ). Princeton (NJ): Stonybrook Laboratories. [cited in US EPA 2004].

Rodriguez SC, Dalbey WE. 1994b. Acute oral toxicity of pyrolysis gasoline in Sprague-Dawley rats. Study No. 65636. Prepared for Mobil Chemical Co., Edison (NJ). Princeton (NJ): Stonybrook Laboratories. [cited in US EPA 2004].

Rodriguez SC, Dalbey WE. 1994c. Dermal toxicity of dripolene in the New Zealand white rabbit. Study No. 65643. Prepared for Mobil Chemical Co., Edison (NJ). Princeton (NJ): Stonybrook Laboratories. [cited in US EPA 2004].

Rodriguez SC, Dalbey WE. 1994d. Dermal toxicity of pyrolysis gasoline in the New Zealand white rabbit. Study No. 65637. Prepared for Mobil Chemical Co., Edison (NJ). Princeton (NJ): Stonybrook Laboratories. [cited in US EPA 2004].

Rodriguez SC, Dalbey WE. 1994e. Acute dermal irritation/corrosion of dripolene in the New Zealand white rabbit. Study No. 65644. Prepared for Mobil Chemical Co., Edison (NJ). Princeton (NJ): Stonybrook Laboratories. [cited in US EPA 2004].

Rodriguez SC, Dalbey WE. 1994f. Acute dermal irritation/corrosion of pyrolysis gasoline in the New Zealand white rabbit. Study No. 65639. Prepared for Mobil Chemical Co., Edison (NJ). Princeton (NJ): Stonybrook Laboratories. [cited in US EPA 2004].

Rodriguez SC, Dalbey WE. 1994g. Ocular irritation of dripolene in the New Zealand white rabbit. Study No. 65644. Prepared for Mobil Chemical Co., Edison (NJ). Princeton (NJ): Stonybrook Laboratories. [cited in US EPA 2004].

Rodriguez SC, Dalbey WE. 1994h. Acute dermal irritation/corrosion of dripolene in the New Zealand white rabbit. Study No. 65645. Prepared for Mobil Chemical Co., Edison (NJ). Princeton (NJ): Stonybrook Laboratories. [cited in US EPA 2004].

Rodriguez SC, Dalbey WE. 1994i. Ocular irritation of pyrolysis gasoline in the New Zealand white rabbit. Study No. 65638. Prepared for Mobil Chemical Co., Edison (NJ). Princeton (NJ): Stonybrook Laboratories. [cited in US EPA 2004].

Roy TA. 1981. Analysis of rerun tower bottom oil by combined capillary gas chromatography/mass spectrometry. Study No. 1272-81. Princeton (NJ): Mobil Oil Co., Toxicology Division. [cited in US EPA 2004].

[RTECS] Registry of Toxic Effects of Chemical Substances [database on the Internet]. 2008b. Ligroine. RTECS No. O16180000. CAS No. 8032-32-4. [updated 2008 Nov[cited 2009 Nov 31]]. Hamilton (ON): Canadian Centre for Occupational Health and Safety.

Salem H, Katz SA, editors. 2006. Inhalation toxicology. 2nd ed. Boca Raton (FL): CRC Press, Taylor & Francis Group.

Savolainen H, Pfaffli P. 1982. Neurochemical effects of extended exposure to white spirit vapour at three concentration levels. Chem Biol Interact 39(1):101–110.

Schreiner CA. 1984. Petroleum and petroleum products: a brief review of studies to evaluate reproductive effects. In: Christian MS, Galbraith WM, Voytek P, Mehlman MA, editors. Advances in modern environmental toxicology. Vol. III. Assessment of reproductive and teratogenic hazards. Princeton (NJ): Princeton Scientific Publishers Inc. p. 29–45.

Schreiner CA, Lapadula E, Breglia R, Bui Q, Burnett D, Koschier F, Podhasky P, White R, Mandella R, Hoffman G. 1998. Toxicity evaluation of petroleum blending streams: inhalation subchronic toxicity/neurotoxicity study of a light alkylate naphtha distillate in rats. J Toxicol Environ Health A 55(4):277–296.

Schreiner C, Bui Q, Breglia R, Burnett D, Koschier F, Podhasky P, Lapadula E, White R, Schroeder RE. 1999. Toxicity evaluation of petroleum blending streams: reproductive and developmental effects of light catalytic cracked naphtha distillate in rats. J Toxicol Environ Health A 58(6):365–382.

Schreiner C, Bui Q, Breglia R, Burnett D, Koschier F, Lapadula E, Podhasky P, White R. 2000a. Toxicity evaluation of petroleum blending streams; inhalation subchronic toxicity/neurotoxicity study of a light catalytic reformed naphtha distillate in rats. J Toxicol Environ Health A 60(7): 489–512. [abstract in PubMed 2009].

Schreiner C, Bui Q, Breglia R, Burnett D, Koschier F, Podhasky P, White R, Hoffman G, Schroeder R. 2000b. Toxicity evaluation of petroleum blending streams: reproductive and developmental effects of light catalytic reformed naphtha distillate in rats. J Toxicol Environ Health A 60(3):169–184.

[SENES] SENES Consultants Limited. 2009. Review of current and proposed regulatory and non-regulatory management tools pertaining to selected petroleum substances under the Chemicals Management Plan. Report to Health Canada.

Shell Research Ltd. 1980. Group research report TLGR.79.141. The inhalation toxicity of SHELLSOL A to rats following 13 weeks’ exposure. Unpublished data submitted to US Environmental Protection Agency, Washington (DC), on July 8, 1988 (OPTS-41009). [cited in Clark et al. 1989].

Short BG, Steinhagen WH, Swenberg JA. 1989. Promoting effects of unleaded gasoline and 2,2,4-trimethylpentane on the development of atypical cell foci and renal tubular cell tumors in rats exposed to N-ethyl-N-hydroxyethylnitrosamine. Cancer Res 49(22):6369–6378.

Simpson BJ. 2005. Analysis of petroleum hydrocarbon streams on the Health Canada CEPA/DSL Draft Maximal List. Report to the Canadian Petroleum Products Institute.

Skisak CM, Furedi-Machacek EM, Schmitt SS, Swanson MS, Vernot EH. 1994. Chronic and initiation/promotion skin bioassays of petroleum refinery streams. Environ Health Perspect 102(1):82–87.

Standeven AM, Goldsworthy TL. 1993. Promotion of preneoplastic lesions and induction of CYP2B by unleaded gasoline vapour in female B6C3F1 mouse liver. Carcinogenesis 14(10):2137–2141.

Standeven AM, Wolf DC, Goldsworthy TL. 1994. Interactive effects of unleaded gasoline and estrogen on liver tumor promotion in female B6C3F1 mice. Cancer Res 54(5):1198–1204.

Standeven AM, Wolf DC, Goldsworthy TL. 1995. Promotion of hepatic preneoplastic lesions in male B6C3F1 mice by unleaded gasoline. Environ Health Perspect 103(7–8):696–700.

Stewart BW, LeMesurier SM, Lykke AW. 1979. Correlation of biochemical and morphological changes induced by chemical injury to the lung. Chem Biol Interact 26(3):321–338. [cited in DOSE 1999].

Stonybrook Laboratories, Inc. 1995. Teratogenicity study in rats exposed orally to a single dose of a refinery stream. Study No. 65371. Princeton (NJ): Stonybrook Laboratories, Inc. [cited in API 2008a].

[Syncrude] Syncrude Canada Limited. 2006. MSDS: Untreated Coker Naphtha. Fort McMurray (AB): Syncrude Canada Limited.

Takeuchi I, Miyoshi N, Mizukawa K, Takada H, Ikemoto T, Omori K, Tsuchiya K. 2009. Biomagnification profiles of polycyclic aromatic hydrocarbons, alkylphenols and polychlorinated biphenyls in Tokyo Bay elucidated by δ¹³C and δ¹⁵N isotope ratios as guides to trophic web structure. Mar Pollut Bull 58:663–671.

Tolls J, van Dijk J. 2002. Bioconcentration of n-dodecane and its highly branched isomer 2,2,4,6,6-pentamethylheptane in fathead minnows. Chemosphere 47:1049–1057.

[TOXLINE] Toxicology Literature Online [database on the Internet]. 1974– . Bethesda (MD): National Library of Medicine (US). [revised 2009 Apr 18; cited 2009 Apr 21].

Tu AS, Sivak A. 1981. BALB-c/3T3 neoplastic transformation assay on 0818802, 08188003 and 08188005 (rerun tower overheads). ALD Reference No. 86374. Study No. 1771-80. Prepared for Mobil Oil Corporation, Princeton (NJ). Cambridge (MA): Arthur D. Little, Inc. [cited in US EPA 2004].

[UN] United Nations. 2009. Development of guidance on the application of GHS criteria. Geneva (CH): United Nations, Committee of Experts on the Transport of Dangerous Goods and on the Globally Harmonized System of Classification and Labelling of Chemicals.

[US EPA] US Environmental Protection Agency. 1984. Estimating concern levels for concentrations of chemical substances in the environment. Washington (DC): US Environmental Protection Agency, Office of Pollution Prevention and Toxics, Economics, Health and Environmental Review Division, Environmental Effects Branch. [cited in US EPA 1998].

[US EPA] US Environmental Protection Agency. 1987a. Evaluation of the carcinogenicity of unleaded gasoline. Washington (DC): US Environmental Protection Agency. Report No. EPA/600/6-87/001. [cited in CONCAWE 1992].

[US EPA] US Environmental Protection Agency. 1987b. Notice of proposed rulemaking on gasoline. 52 FR 31162, August 19, 1987. Washington (DC): US Environmental Protection Agency. [cited in CONCAWE 1992].

[US EPA] US Environmental Protection Agency. 1998. Cleaner technologies substitutes assessment: professional fabricare processes. Prepared for the Economics, Exposure and Technology Division, Office of Pollution Prevention and Toxics, US Environmental Protection Agency, Washington (DC), by Abt Associates Inc. Contract Nos. 68-W-9805 and 68-W6-0021.

[US EPA] US Environmental Protection Agency. 2001. High benzene naphthas robust summaries. Prepared for the Higher Production Volume (HPV) Chemical Challenge Program, US Environmental Protection Agency, Washington (DC), by Olefins Panel HPV Work Group of the American Chemistry Council. EPA Reference No. AR201-13436B.

[US EPA] US Environmental Protection Agency. 2004. High benzene naphthas robust summaries: mammalian toxicity (Attachment 1C). Prepared for the Higher Production Volume (HPV) Chemical Challenge Program, US Environmental Protection Agency, Washington (DC), by Olefins Panel HPV Work Group of the American Chemistry Council. EPA Reference No. 201-15727B.

Verschueren K. 2001. Handbook of environmental data on organic chemicals. 4th ed. Vols. 1–2. New York (NY): John Wiley & Sons. p. 1269.

Wan Y, Jin X, Hu J, Jin F. 2007. Trophic dilution of polycyclic aromatic hydrocarbons (PAHs) in a marine food web from Bohai Bay, North China. Environ Sci Technol 41:3109–3114.

Witschi HP, Smith LH, Frome EL, Pequet-Goad ME, Griest WH, Ho C-H, Guerin MR. 1987. Skin tumorigenic potential of crude and refined coal liquids and analogous petroleum products. Fundam Appl Toxicol 9(2):297–303.

Wong O, Raabe GK. 1989. Critical review of cancer epidemiology in petroleum industry employees, with a quantitative meta-analysis by cancer site. Am J Ind Med 15:283–310. [cited in IARC 1989b].

[WSKOWWIN] Water Solubility for Organic Compounds Program for Microsoft Windows [Estimation Model]. 2008. Version 1.41a. Washington (DC): US Environmental Protection Agency, Office of Pollution Prevention and Toxics; Syracuse (NY): Syracuse Research Corporation. Exposure Assessment Tools and Models.

Zellers JE. 1985. Four week repeated dose dermal toxicity study in rats using heavy aromatic distillate. Project No. 2063. Prepared for Gulf Oil Chemicals Co., Houston (TX). Pittsburgh (PA): Gulf Life Sciences Center. [cited in API 2001b].

Zhou S, Heras H, Ackman RG. 1997. Role of adipocytes in the muscle tissue of Atlantic salmon (Salmo salar) in the uptake, release and retention of water-soluble fraction of crude oil hydrocarbons. Mar Biol 127:545–553.

Appendix 1: Description of the Nine Groups of Petroleum Substances ^[4]

Table A1.1. Description of the nine groups of petroleum substances

Appendix 2: Process Flow Diagrams for Low Boiling Point Naphthas ^[4]

(Please see the PDF version to get better image quality)

Figure A2.1. Process flow diagram for CAS RN 64741-54-4 (Hopkinson 2008)

CAS RN 64741-54-4 is shown to be a processing intermediate formed after processing in the FCCU (fluid catalytic cracking unit) in a refinery.

Figure A2.2. Process flow diagram for CAS RN 64741-55-5 (Hopkinson 2008)

CAS RN 64741-55-5 is shown to be a processing intermediate formed after processing in the FCCU in a refinery.

Figure A2.3. Process flow diagram for CAS RN 64741-64-6 (Hopkinson 2008)

CAS RN 64741-64-4 is shown to be a processing intermediate formed in an alkylation unit in a refinery.

Figure A2.4a. Process flow diagram for CAS RN 64741-74-8, refinery (Hopkinson 2008)

CAS RN 64741-74-8 is shown to be a processing intermediate (distillate) formed after fractionation in a thermal cracking unit (coking or visbreaking) in a refinery.

Figure A2.4b. Process flow diagram for CAS RN 64741-74-8, upgrader (Hopkinson 2008)

CAS RN 64741-74-8 is shown to be a processing intermediate (distillate) formed after fractionation in a thermal cracker (coker) in an upgrader.

Figure A2.5. Process flow diagram for CAS RN 64742-22-9 (Hopkinson 2008)

CAS RN 64742-22-9 is shown to be formed after distillate sweetening (sulfur removal), treating and blending in a refinery to remove acids from heavy naphtha.

Figure A2.6. Process flow diagram for CAS RN 64742-23-0 (Hopkinson 2008)

CAS RN 64742-23-0 is shown to be formed after treating and blending in a refinery to remove acids from light naphtha.

Figure A2.7a. Process flow diagram for CAS RN 64742-73-0, refinery (Hopkinson 2008)

CAS RN 64742-73-0 is shown to be a processing intermediate (bottom substance) formed after hydrotreating in a refinery.

Figure A2.7b. Process flow diagram for CAS RN 64742-73-0, upgrader (Hopkinson 2008)

CAS RN 64742-73-0 is shown to be formed after hydrotreating in an upgrader.

Figure A2.8. Process flow diagram for CAS RN 68410-05-9 (Hopkinson 2008)

CAS RN 68470-05-9 is a light product shown to be a processing intermediate formed after distillation in a refinery.

Figure A2.9. Process flow diagram for CAS RN 68410-71-9 (Hopkinson 2008)

CAS RN 68410-71-9 is shown to be a processing intermediate (raffinate) from an extraction column where aromatic compounds are removed from the product stream following catalytic reforming in a refinery.

Figure A2.10a. Process flow diagram for CAS RN 68410-96-8, refinery (Hopkinson 2008)

CAS RN 68410-96-8 is shown to be a processing intermediate after hydrotreating heavy straight-run naphtha in a refinery.

Figure A2.10b. Process flow diagram for CAS RN 68410-96-8, upgrader (Hopkinson 2008)

CAS RN 68410-96-8 is shown to be formed after hydrotreating heavy straight-run naphtha in an upgrader.

Figure A2.11. Process flow diagram for CAS RN 68476-46-0 (Hopkinson 2008)

CAS RN 68476-46-0 is shown to be a processing intermediate (distillate) formed after catalytic cracking in a refinery.

Figure A2.12. Process flow diagram for CAS RN 68477-89-4 (Hopkinson 2008)

CAS RN 68477-89-4 is shown to be a processing intermediate formed from a distillation column overhead product treated with a catalytic cracking process in a refinery.

Figure A2.13a. Process flow diagram for CAS RN 68478-12-6, gas plant (Hopkinson 2008)

In a gas plant, distillation is not necessary due to the volatility of the compounds. CAS RN 68478-12-6 is shown to be formed after processing in the deethanizer/depropanizer/debutanizer to separate isobutene from heavier compounds.

Figure A2.13b. Process flow diagram for CAS RN 68478-12-6, refinery (Hopkinson 2008)

CAS RN 68478-12-6 is shown to be a bottom product from a gas separation unit in a refinery.

Figure A2.14a. Process flow diagram for CAS RN 68513-02-0, refinery (Hopkinson 2008)

CAS RN 68513-02-0 is shown to be a processing intermediate that represents an overhead distillate stream from a fractionation column in a coking unit.

Figure A2.14b. Process flow diagram for CAS RN 68513-02-0, upgrader (Hopkinson 2008)

CAS RN 68513-02-0 is shown to be a processing intermediate formed after fractionation in a coking unit.

Figure A2.15. Process flow diagram for CAS RN 68514-79-4 (Hopkinson 2008)

CAS RN 68514-79-4 is shown to be a processing intermediate formed after hydrofining or powerfining in a refinery.

Figure A2.16. Process flow diagram for CAS RN 68606-11-1 (Hopkinson 2008)

CAS RN 68606-11-1 is shown to be a processing intermediate coming directly from the atmospheric distillation column in a refinery.

Figure A2.17a. Process flow diagram for CAS RN 68783-12-0, refinery (Hopkinson 2008)

CAS RN 68783-12-0 is shown to be a processing intermediate produced from various distillation processes in a refinery.

Figure A2.17b. Process flow diagram for CAS RN 68783-12-0, upgrader (Hopkinson 2008)

CAS RN 68783-12-0 is shown to be a processing intermediate that describes naphthas formed after various processes in an upgrader.

Figure A2.18. Process flow diagram for CAS RN 68919-37-9 (Hopkinson 2008)

CAS RN 68919-37-9 is shown to be a processing intermediate that is represented as a product of a distillation column fed with effluent from a catalytic reforming process.

Figure A2.19. Process flow diagram for CAS RN 68955-35-1 (Hopkinson 2008)

CAS RN 68955-35-1 is shown to be a processing intermediate from a distillation column fed with effluent from a catalytic reforming process.

Figure A2.20. Process flow diagram for CAS RN 101795-01-1 (Hopkinson 2008)

CAS RN 101795-01-1 is formed after mercaptans and other acid compounds are removed through sweetening.

Appendix 3: Data Tables for Site-restricted Low Boiling Point Naphthas

Table A3.1. Detailed hydrocarbon analysis of CAS RN 68919-37-9 (%) (API 2003a)

Table A3.2. Physical and chemical properties of representative structures contained in low boiling point naphthas^{[1], [2]}

Table A3.3. Primary degradation half-lives in soil of hydrocarbons from a formulated gasoline (Prince et al. 2007a, 2007b)

Table A3.4. Modelled data for primary (BIOHCWIN 2008)^[1], ultimate (BIOWIN 2009)^[2] biodegradation of representative structures of low boiling point naphthas

Table A3.5a. Empirical data for photodegradation of components of low boiling point naphthas in air (Atkinson 1990)

Table A3.5b. Atmospheric degradation of representative structures for low boiling point naphthas (AOPWIN 2008)

Table A3.6. Potential presence of representative structures for low boiling point naphthas that are persistent in air

(a)

(b)

Table A3.7. Fish BAF and BCF predictions for low boiling point naphthas using the Arnot-Gobas kinetic model (BCFBAF 2008) with corrections for metabolism

Table A3.8. Comparisons of experimental BAFs and modelled BAFs (BCFBAF 2008) for selected aromatic hydrocarbons

Table A3.9. Comparisons of experimental BCFs and modelled BCFs (BCFBAF 2008) on some representative structures of gas oils

Table A3.10. Empirical data for aquatic toxicity of low boiling point naphthas

Table A3.11. Modelled data for toxicity of low boiling point naphthas to aquatic organisms [Acute LL₅₀ (mg/L)] (PetroTox 2009)

(a)

(b)

Appendix 4: Summary of Health Effects Information from Pooled Toxicological Data for LBPNs

Footnotes

Date modified:

2013-09-24