Appendices of the Screening Assessment Report Ethane, 1,2-dibromo- (1,2-Dibromoethane) Chemical Abstracts Service Registry Number 106-93-4 Environment Canada Health Canada Juin 2013
Appendices
- Appendix 1: Robust Study Summaries for Ecotoxicity Studies
- Appendix 2: Concentrations of 1,2-dibromoethane in ambient air
- Appendix 3: Concentrations of 1,2-dibromoethane in indoor air
- Appendix 4: Concentrations of 1,2-dibromoethane in water
- Appendix 5: Concentrations of 1,2-dibromoethane in food
- Appendix 6: Concentrations of 1,2-dibromoethane in soil
- Appendix 7: Summary of health effects information for 1,2-dibromoethane
Appendix 1: Robust Study Summaries for Ecotoxicity Studies
For determination of the reliability of experimental data for key ecological endpoints (i.e., inherent toxicity to aquatic organisms, bioaccumulation potential, persistence), an evaluation approach has been developed, which is analogous to that of Klimisch et al. (1997). It involves the use of a standardized Robust Study Summary form, including a scoring system to quantitatively evaluate the studies.
The Robust Study Summary (RSS) is an adaptation of the OECD Robust Study Summary templates (OECD 2009). It consists of a checklist of items or criteria relating to identity of the substance, experimental protocol or method, test organism, specific test design/conditions, ecological relevance, and results. Most items are weighted according to their criticality to the quality and reliability of the study. The most important or critical items (which describe parameters/factors that have the most direct influence on the quality of the study) have been given a higher weight (5 points), while the less critical items have been given a lower score (1 or 2 points). For each item, the evaluator must indicate whether the item has been addressed appropriately in the study by answering “yes”, “no” or “non-applicable (n/a)”.Specific information relating to the items is also provided the RSS as well.
Once answers to all the items have been provided in the template, an overall Robust Study Summary score for the study is calculated as:
Overall Study Score (%) = ∑ WYes / WYes+No × 100%
Where:
WYes = weight of applicable “Yes” answers;
WYes+No = weight of applicable “Yes” and “No” answers.
The overall score’s corresponding reliability code and category is determined using the four categories adapted from the Klimisch approach and based on the score ranges as described in Table A.
| Reliability Code | Reliability Category | Overall Study Score Range |
|---|---|---|
| 1 | High confidence | ≥ 80% |
| 2 | Satisfactory confidence | 60 – 79% |
| 3 | Low confidence | 40 – 59% |
| 4 | Not acceptable | < 40% |
| No | Item | Weight | Yes/No | Specify |
|---|---|---|---|---|
| 1 | Reference: Holcombe GW, Benoit DA, Hammermeister DE, Leonard EN, Johnson RD. 1995. Acute and long-term effects of nine chemicals on the Japanese medaka (Oryzias latipes). Arch Environ Contamin Toxicol 28:287-297. | |||
| 2 | Substance identity: CAS RN | n/a | Y | |
| 3 | Substance identity: 1,2-dibromoethane | n/a | Y | |
| 4 | Chemical composition of the substance | 2 | Y | |
| 5 | Chemical purity | 1 | Y | |
| 6 | Persistence/stability of test substance? | 1 | Y | |
| Method | ||||
| 7 | Reference | 1 | Y | |
| 8 | OECD, EU, national, or other standard method? | 3 | - | Not applicable |
| 9 | Justification of the method/protocol if a non-standard method was used | 2 | Y | |
| 10 | GLP (good laboratory practice) | 3 | - | Not applicable |
| Test organism | ||||
| 11 | Organism identity: medaka | n/a | Y | |
| 12 | Latin or both Latin and common names reported? | 1 | N | |
| 13 | Life cycle age / stage of test organism | 1 | Y | 28–43 days old for acute tests |
| 14 | Length and/or weight | 1 | Y | 18–71 mg |
| 15 | Sex | 1 | N | |
| 16 | Number of organisms per replicate | 1 | Y | 10 |
| 17 | Organism loading rate | 1 | Y | |
| 18 | Food type and feeding periods during the acclimation period | 1 | Y | |
| Test design / conditions | ||||
| 19 | Test type (acute or chronic) | n/a | Y | Both |
| 20 | Experiment type (laboratory or field) | n/a | Y | Lab |
| 21 | Exposure pathways (food, water, both) | n/a | Y | Water |
| 22 | Exposure duration | n/a | Y | Acute 96h |
| 23 | Negative or positive controls (specify) | 1 | Y | |
| 24 | Number of replicates (including controls) | 1 | Y | |
| 25 | Nominal concentrations reported? | 1 | Y | |
| 26 | Measured concentrations reported? | 3 | Y | |
| 27 | Food type and feeding periods during the long-term tests | 1 | Y | |
| 28 | Were concentrations measured periodically (especially in the chronic test)? | 1 | Y | |
| 29 | Were the exposure media conditions relevant to the particular chemical reported? (e.g., for the metal toxicity – pH, DOC/TOC, water hardness, temperature) | 3 | Y | |
| 30 | Photoperiod and light intensity | 1 | Y | |
| 31 | Stock and test solution preparation | 1 | Y | |
| 32 | Was solubilizer/emulsifier used if the chemical was poorly soluble or unstable? | 1 | - | Not applicable |
| 33 | If solubilizer/emulsifier was used, was its concentration reported? | 1 | - | Not applicable |
| 34 | If solubilizer/emulsifier was used, was its ecotoxicity reported? | 1 | - | Not applicable |
| 35 | Monitoring intervals (including observations and water quality parameters) reported? | 1 | N | |
| 36 | Statistical methods used | 1 | Y | |
| Information relevant to the data quality | ||||
| 37 | Was the endpoint directly caused by the chemical's toxicity, not by the organism’s health (e.g. when mortality in the control > 10%) or physical effects (e.g. “shading effect”)? | n/a | Y | |
| 38 | Was the test organism relevant to the Canadian environment? | 3 | Y | |
| 39 | Were the test conditions (pH, temperature, DO, etc.) typical for the test organism? | 1 | Y | |
| 40 | Do system type and design (static, semi-static, flow-through; sealed or open; etc.) correspond to the substance's properties and organism's nature/habits? | 2 | Y | |
| 41 | Was pH of the test water within the range typical for the Canadian environment (6 to 9)? | 1 | Y | |
| 42 | Was temperature of the test water within the range typical for the Canadian environment (5 to 27°C)? | 1 | Y | |
| 43 | Was toxicity value below the chemical’s water solubility? | 3 | Y | |
| Results | ||||
| 44 | Toxicity values (specify endpoint and value) | n/a | Y | |
| 45 | Other endpoints reported – e.g., BCF/BAF, LOEC/NOEC (specify)? | n/a | N | |
| 46 | Other adverse effects (e.g. carcinogenicity, mutagenicity) reported? | n/a | N | |
| 47 | Score: ... % | 36/39 = 92% | ||
| 48 | EC reliability code: | 1 | ||
| 49 | Reliability category (high, satisfactory, low): | High | ||
| 50 | Comments | |||
| No | Item | Weight | Yes/No | Specify |
|---|---|---|---|---|
| 1 | Reference: Kszos LA, Talmage SS, Morris GW, Konetsky BK, Rottero T. 2003. Derivation of aquatic screening benchmarks for 1,2-dibromoethane. Arch Environ Toxicol 45:66-71. | |||
| 2 | Substance identity: CAS RN | n/a | Y | |
| 3 | Substance identity: 1,2-dibromoethane | n/a | Y | |
| 4 | Chemical composition of the substance | 2 | Y | |
| 5 | Chemical purity | 1 | - | Not specified but not needed |
| 6 | Persistence/stability of test substance? | 1 | Y | |
| Method | ||||
| 7 | Reference | 1 | Y | |
| 8 | OECD, EU, national, or other standard method? | 3 | - | Not applicable |
| 9 | Justification of the method/protocol if a non-standard method was used | 2 | Y | |
| 10 | GLP (good laboratory practice) | 3 | - | Not applicable |
| Test organism | ||||
| 11 | Organism identity: Daphnia magna, Ceriodaphnia dubia and Pimephales promelas(fathead minnow) | n/a | Y | |
| 12 | Latin or both Latin and common names reported? | 1 | Y | |
| 13 | Life cycle age / stage of test organism | 1 | Y | Fish (5 days old) |
| 14 | Length and/or weight | 1 | N | |
| 15 | Sex | 1 | N | |
| 16 | Number of organisms per replicate | 1 | Y | 8 |
| 17 | Organism loading rate | 1 | Y | 5 concentrations on D. magna and C. dubia 4 concentrations on fish |
| 18 | Food type and feeding periods during the acclimation period | 1 | Y | |
| Test design / conditions | ||||
| 19 | Test type (acute or chronic) | n/a | Y | Acute |
| 20 | Experiment type (laboratory or field) | n/a | Y | Lab |
| 21 | Exposure pathways (food, water, both) | n/a | Y | water |
| 22 | Exposure duration | n/a | Y | 48 h for D. magma and C. dubia 98 h for fathead minnow |
| 23 | Negative or positive controls (specify) | 1 | Y | Negative control |
| 24 | Number of replicates (including controls) | 1 | Y | 4 (for D. magna and C. dubia) 8 (fathead minnow) |
| 25 | Nominal concentrations reported? | 1 | Y | 5 for D. magna and C. dubia 4 for P. promelas |
| 26 | Measured concentrations reported? | 3 | Y | |
| 27 | Food type and feeding periods during the long-term tests | 1 | Y | Feeding fish with brine shrimp nauplii 2 h prior to test solution renewal in 48 h |
| 28 | Were concentrations measured periodically (especially in the chronic test)? | 1 | Y | At least 2 times |
| 29 | Were the exposure media conditions relevant to the particular chemical reported? (e.g., for the metal toxicity – pH, DOC/TOC, water hardness, temperature) | 3 | Y | |
| 30 | Photoperiod and light intensity | 1 | Y | |
| 31 | Stock and test solution preparation | 1 | Y | |
| 32 | Was solubilizer/emulsifier used if the chemical was poorly soluble or unstable? | 1 | - | Not applicable |
| 33 | If solubilizer/emulsifier was used, was its concentration reported? | 1 | - | Not applicable |
| 34 | If solubilizer/emulsifier was used, was its ecotoxicity reported? | 1 | - | Not applicable |
| 35 | Monitoring intervals (including observations and water quality parameters) reported? | 1 | Y | |
| 36 | Statistical methods used | 1 | Y | |
| Information relevant to the data quality | ||||
| 37 | Was the endpoint directly caused by the chemical's toxicity, not by organism’s health (e.g. when mortality in the control > 10%) or physical effects (e.g. “shading effect”)? | n/a | Y | |
| 38 | Was the test organism relevant to the Canadian environment? | 3 | Y | |
| 39 | Were the test conditions (pH, temperature, DO, etc.) typical for the test organism? | 1 | Y | |
| 40 | Do system type and design (static, semi-static, flow-through; sealed or open; etc.) correspond to the substance's properties and organism's nature/habits? | 2 | Y | |
| 41 | Was pH of the test water within the range typical for the Canadian environment (6 to 9)? | 1 | Y | |
| 42 | Was temperature of the test water within the range typical for the Canadian environment (5 to 27°C)? | 1 | Y | |
| 43 | Was toxicity value below the chemical’s water solubility? | 3 | Y | |
| Results | ||||
| 44 | Toxicity values (specify endpoint and value) | n/a | Y | |
| 45 | Other endpoints reported – e.g., BCF/BAF, LOEC/NOEC (specify)? | n/a | N | |
| 46 | Other adverse effects (e.g. carcinogenicity, mutagenicity) reported? | n/a | N | |
| 47 | Score: ... % | 37/39 = 95% | ||
| 48 | EC Reliability code: | 1 | ||
| 49 | Reliability category (high, satisfactory, low): | High | ||
| 50 | Comments | |||
| No | Item | Weight | Yes/No | Specify |
|---|---|---|---|---|
| 1 | Reference: Hawkins WE, Walker WW, James MO, Manning CS, Barnes DH, Heard CS, Overstreet RM. 1998. Carcinogenic effects of 1,2-dibromoethane (ethylene dibromide; EDB) in Japanese medaka (Oryzias latipes). Mutat Res 399(2):221-32. | |||
| 2 | Substance identity: CAS RN | n/a | N | |
| 3 | Substance identity: 1,2-dibromoethane | n/a | Y | |
| 4 | Chemical composition of the substance | 2 | N | Not specified but not needed |
| 5 | Chemical purity | 1 | N | Not specified but not needed |
| 6 | Persistence/stability of test substance? | 1 | N | |
| Method | ||||
| 7 | Reference | 1 | Y | |
| 8 | OECD, EU, national, or other standard method? | 3 | - | Not applicable |
| 9 | Justification of the method/protocol if a non-standard method was used | 2 | Y | |
| 10 | GLP (good laboratory practice) | 3 | - | Not applicable |
| Test organism | ||||
| 11 | Organism identity: Japanese medaka |
n/a | Y | |
| 12 | Latin or both Latin and common names reported? | 1 | N | |
| 13 | Life cycle age / stage of test organism | 1 | Y | Fish (7 days old) |
| 14 | Length and/or weight | 1 | N | |
| 15 | Sex | 1 | N | |
| 16 | Number of organisms per replicate | 1 | Y | 350 |
| 17 | Organism loading rate | 1 | Y | 1 static control 1 flow-through control 3 test concentrations |
| 18 | Food type and feeding periods during the acclimation period | 1 | Y | |
| Test design / conditions | ||||
| 19 | Test type (acute or chronic) | n/a | Y | Chronic |
| 20 | Experiment type (laboratory or field) | n/a | Y | Lab |
| 21 | Exposure pathways (food, water, both) | n/a | Y | Water |
| 22 | Exposure duration | n/a | Y | 73-97 days |
| 23 | Negative or positive controls (specify) | 1 | Y | Negative control |
| 24 | Number of replicates (including controls) | 1 | Y | 350 |
| 25 | Nominal concentrations reported? | 1 | Y | 1 flow-through control 3 test concentrations |
| 26 | Measured concentrations reported? | 3 | Y | |
| 27 | Food type and feeding periods during the long-term tests | 1 | Y | Very detailed |
| 28 | Were concentrations measured periodically (especially in the chronic test)? | 1 | Y | Twice every week |
| 29 | Were the exposure media conditions relevant to the particular chemical reported? (e.g., for the metal toxicity – pH, DOC/TOC, water hardness, temperature) | 3 | Y | |
| 30 | Photoperiod and light intensity | 1 | N | |
| 31 | Stock and test solution preparation | 1 | Y | |
| 32 | Was solubilizer/emulsifier used if the chemical was poorly soluble or unstable? | 1 | - | Not applicable |
| 33 | If solubilizer/emulsifier was used, was its concentration reported? | 1 | - | Not applicable |
| 34 | If solubilizer/emulsifier was used, was its ecotoxicity reported? | 1 | - | Not applicable |
| 35 | Monitoring intervals (including observations and water quality parameters) reported? | 1 | Y | |
| 36 | Statistical methods used | 1 | Y | |
| Information relevant to the data quality | ||||
| 37 | Was the endpoint directly caused by the chemical's toxicity, not by organism’s health (e.g. when mortality in the control > 10%) or physical effects (e.g. “shading effect”)? | n/a | Y | |
| 38 | Was the test organism relevant to the Canadian environment? | 3 | Y | |
| 39 | Were the test conditions (pH, temperature, DO, etc.) typical for the test organism? | 1 | Y | |
| 40 | Do system type and design (static, semi-static, flow-through; sealed or open; etc.) correspond to the substance's properties and organism's nature/habits? | 2 | Y | |
| 41 | Was pH of the test water within the range typical for the Canadian environment (6 to 9)? | 1 | Y | |
| 42 | Was temperature of the test water within the range typical for the Canadian environment (5 to 27°C)? | 1 | Y | |
| 43 | Was toxicity value below the chemical’s water solubility? | 3 | Y | |
| Results | ||||
| 44 | Toxicity values (specify endpoint and value) | n/a | Y | |
| 45 | Other endpoints reported – e.g., BCF/BAF, LOEC/NOEC (specify)? | n/a | N | |
| 46 | Other adverse effects (e.g. carcinogenicity, mutagenicity) reported? | n/a | Y | |
| 47 | Score: ... % | 35/40 = 87.5% | ||
| 48 | EC Reliability code: | 1 | ||
| 49 | Reliability category (high, satisfactory, low): | High | ||
| 50 | Comments | |||
Appendix 2: Concentrations of 1,2-dibromoethane in ambient air
| Location | Sampling period | Number of samples | Detection limit (μg/m3) | Mean concentration (μg/m3)[1] | Reference |
|---|---|---|---|---|---|
| Halifax, Nova Scotia | January to April, 2009 | 287 | 0.025 | ND (ND-0.025) | Health Canada 2012 |
| June to September, 2009 | 324 | 0.025 | ND (ND-0.026) | Health Canada 2012 | |
| Windsor, Ontario | January 23 to March 25, 2006 | 214 | 0.15 | ND | Health Canada 2010b |
| July 3 to August 26, 2006 | 214 | ND | |||
| Windsor, Ontario | January 24 to March 19, 2005 | 201 | 0.123 | ND | Health Canada 2010b |
| July 4 to August 27, 2005 | 216 | ND | |||
| Regina, Saskatchewan | January 8 to March 16, 2007 | 94(winter; 24-h canisters) | 0.054 | ND | Health Canada 2010a |
| June 20 to August 29, 2007 | 97 (summer; 5-day canisters) | ND | |||
| 43 Canadian sites | January to December 2008 | 10–119 (total of 1896 samples) | 0.012 | 0.006[3](0.002–0.013) [detected in 7 samples] | NAPS 2008 |
| Twenty-nine Canadian cities | 2004–2009 | - | - | 0–0.060 | Environment Canada 2009b |
| Twenty-nine Canadian cities | 1998–2002 | - | - | < 0.012–0.143 | Environment Canada 2004 |
| 40 Canadian sites | January to December 2003 | 14–145 (total of 1854 samples) | 0.012 | (ND–0.11) [detected in 458 samples] |
2003 personal communication from Analysis and Air Quality Division, Environment Canada to Existing Substances Division; unreferenced |
| Ottawa, Ontario (vicinity of 75 homes) | Fall 2002 | 75 | 0.018 | ND | Zhu et al. 2005 |
| 50 Canadian sites | January 1998 to December 2002 | 14–293 (total of 8275 samples) | 0.012 | (0.002–0.143) [detected in 6766 samples] |
2002 personal communication from Analysis and Air Quality Division, Environment Canada to Existing Substances Division; unreferenced |
| 37 Canadian sites | 2000 | 9–62 (total of 1573 samples) | 0.012 | 0.06 (0.01–0.12) | 2001 personal communication from Analysis and Air Quality Division, Environment Canada to Existing Substances Division; unreferenced |
| Montréal, Quebec (urban) | 1993 | 160 | 0.38[2](0.05 ppbv) | 0.02 (ND–0.67) [6% > detection limit] |
Environment Canada 1995 |
| Brossard, Quebec (suburban) | 1993 | 24 | 0.38[2](0.05 ppbv) | ND | Environment Canada 1995 |
| Sainte-Françoise, Quebec (rural) | 1993 | 34 | 0.38[2](0.05 ppbv) | ND | Environment Canada 1995 |
| Montréal, Quebec (urban) | 1992 | 166 | 0.38[2](0.05 ppbv) | 0.01 (ND–1.73) [1% > detection limit] |
Environment Canada 1995 |
| Montréal, Quebec (urban) |
1991 | 91 | 0.38[2](0.05 ppbv) | 0.03 (ND–0.48) [10% > detection limit] | Environment Canada 1995 |
| Montréal, Quebec (urban) | 1990 | 110 | 0.38[2](0.05 ppbv) | ND–0.12 [1% > detection limit] |
Environment Canada 1995 |
| Montréal, Quebec (urban) | 1989 | 79 | 0.38[2](0.05 ppbv) | 0.03 (ND–0.43) [11% > detection limit] | Environment Canada 1995 |
| Modelled local air dispersion (at 100 m from the source) | - | - | - | 0.3774 | SCREEN3 1995 |
| Windsor, Ontario | 1988–1992 | 410 | 0.1 | ND–0.80 [ND 80% of the time] | OMEE 1994 |
| Greater Vancouver Regional District | 1989–1992 | 473 | 0.38[2](0.05 ppbv) | 0.06[3] [4% > detection limit] | Environment Canada 1994 |
| Canada-wide | 1989–1990 | 1100 | 0.38[2](0.05 ppbv) | 0.06[3] [5% > detection limit] | Environment Canada 1994 |
| Walpole Island, Ontario | 1989–1991 | 94 | 0.1 | ND–0.76 | OMEE 1994 |
| Walpole Island, Ontario | January 1988 to October 1990 | 61 | 0.1 | ND–0.80 [above detection limit in 9 samples] | Environment Canada 1992 |
| Windsor, Ontario | July 1987 to October 1990 | 123 | 0.1 | ND–0.4 [above detection limit in 7 samples] | Environment Canada 1992 |
| Canadian urban sites | 1989 | 17 | 0.1 | ND | Environment Canada 1991 |
| Kitchener, Ontario | April 16 to May 24, 1989 | 10 | ns | (ND–0.30) | CMHC 1989 |
| North and South Atlantic Ocean | 1985 | 0 | 0 | 0.020 | Class and Ballschmiter 1988 |
| Seven U.S. cities | 1980 | - | - | 0.122–2.822 | Singh et al. 1982 |
Abbreviations: ND, not detected; ns, not specified; ppbv, parts per billion by volume.
[1] Values in parentheses indicate range of concentrations when available.
[2] Value given for the detection limit is the target or typical detection limit reported for volatile organic compounds.
[3] Values below the detection limit set at one-half the detection limit.
[1] Values in parentheses indicate range of concentrations when available.
[2] Value given for the detection limit is the target or typical detection limit reported for volatile organic compounds.
[3] Values below the detection limit set at one-half the detection limit.
Appendix 3: Concentrations of 1,2-dibromoethane in indoor air
| Location | Sampling period | Number of samples | Detection limit (μg/m3) | Mean concentration (μg/m3)[1] | Reference |
|---|---|---|---|---|---|
| Halifax, Nova Scotia | January to April, 2009 | 312 | 0.025 | ND | Health Canada 2012 |
| June to September, 2009 | 331 | 0.025 | ND | Health Canada 2012 | |
| Windsor, Ontario (personal breathing-zone air) | January 24 to March 19, 2005 | 225 | 0.123 | ND | Health Canada 2010b |
| July 4 to August 27, 2005 | 207 | ND (ND–0.190) | |||
| Windsor, Ontario | January 24 to March 19, 2005 | 232 | 0.123 | ND | Health Canada 2010b |
| July 4 to August 27, 2005 | 217 | ND | |||
| Windsor, Ontario | January 23 to March 25, 2006 | 224 | 0..15 | ND | Health Canada 2010b |
| July 3 to August 26, 2006 | 211 | ND | |||
| Regina, Saskatchewan (5-day canister data were selected, as they represent time-weighted average over longer period than 24-h canisters) | January 8 to March 16, 2007 | 97(winter) | 0.054 | ND | Health Canada 2010a |
| June 20 to August 29, 2007 | 101 (summer) | ND [maximum 0.080] | |||
| Ottawa, Ontario (75 homes) |
Fall 2002 | 75 | 0.018 | ND | Zhu et al. 2005 |
| International locations (literature review of 50 studies) | 1978–1990 | 50 studies | ns | 1 – <5 | Brown et al. 1994 |
| Canada-wide | August–October and January–March 1983–1984 | 10 | 0.4 | ND | Otson 1986 |
| Woodlands, California, USA (residential) | June 1990 | 128 | ns | Not quantifiable | Cal EPA 1992 |
| Kanawha Valley, West Virginia, USA (residential) | August 1987 | 35 | 8.5 | 6.06 [maximum 23.53; 29% > detection limit] | Cohen et al. 1989 |
Abbreviations: ND, not detected; ns, not specified.
[1] Values in parentheses indicate range of concentrations when available.
[1] Values in parentheses indicate range of concentrations when available.
Appendix 4: Concentrations of 1,2-dibromoethane in water
| Location | Sampling period | Number of samples | Detection limit (μg/L) | Mean concentration (μg/L) | Reference |
|---|---|---|---|---|---|
| Victoria, British Columbia (drinking water) | 2008 | 2 | 0.005 | ND | City of Victoria 2008 |
| Ontario, Canada (drinking water) | January 1, 2005 to December 31, 2006 | 2901 | 0.1 | ND | Ontario MOE 2006 |
| Montréal, Quebec (drinking water) | 2006 | ns | 0.04 | ND | Ville de Montreal 2006 |
| Nova Scotia, Canada (drinking water) | June 2002 to May 2005 | 24 | 1 | ND | NSEL 2005 |
| Ottawa, Ontario (drinking water) | 2003 | 19 | 0.10 | ND | COWQS 2003 |
| United States | 1985–2001 | 462 (public well samples) | ns | < 0.10 (median for all samples) | Zogorski et al. 2006 |
| United States | 1985–2001 | 2085 (domestic well samples) | ns | < 0.04 (median for all samples); 0.55 (median for samples with detection) |
Zogorski et al. 2006 |
| United States | 1985–2001 | 2851 (groundwater) | ns | < 0.10 (median for all samples); 0.72 (median for samples with detection) |
Zogorski et al. 2006 |
| Lemieux Island, Ottawa, Ontario | 1987 | 48 (raw and treated) | 50 | Not quantifiable at detection limit | Ontario MOE 1988 |
| Toronto, Ontario | November–December 1988 | 7 (bottled) 27 (tap) |
0.04 | Not quantifiable at detection limit | City of Toronto 1990 |
| New Jersey, USA (surface water) |
1977–1979 | - | - | 0.2 (maximum) | Page 1981 |
| Oil refining and manufacturing facility, Sugar Creek, Missouri, USA (surface water) |
1975 or earlier | - | - | 1.05 – 1.13 | Going and Long 1975 |
| Pincher Creek, Alberta, at 50 m from the source (surface water) |
- | - | - | 16–21[a] 2–3[b] |
ChemSim 2003 |
| North and South Atlantic Ocean (marine water) |
1985 | - | - | 0.00002 | Class and Ballschmiter 1988 |
| Site of a chemical plant, Ontario (groundwater) |
1997 | - | - | 5.0 | Environment Canada 2001b |
| Three U.S. states[c] (groundwater) |
1981 – 1987 | - | - | Detected | Pignatello and Cohen 1990 |
| Six U.S. states[d] (groundwater) |
1988 or earlier | - | - | 14 (maximum) 9 (median) |
Williams et al. 1988 |
| New Jersey, USA (groundwater) |
1977–1979 | - | - | 48 (maximum) | Page 1981 |
Abbreviations: ND, not detected; ns, not specified.
[a] Most conservative scenarios: modelled value based on the assumption that the total amount reported in Canada is used at the Pincher Creek, Alberta, facility, with or without sewage treatment plant removal.
[b] More realistic scenarios (less conservative): modelled value based on the assumption that the total amount reported in Canada is divided among eight facilities, with or without sewage treatment plant removal.
[c] Arizona, Wisconsin and Florida.
[d] California, Connecticut, Georgia, Massachusetts, New York and Washington.
[a] Most conservative scenarios: modelled value based on the assumption that the total amount reported in Canada is used at the Pincher Creek, Alberta, facility, with or without sewage treatment plant removal.
[b] More realistic scenarios (less conservative): modelled value based on the assumption that the total amount reported in Canada is divided among eight facilities, with or without sewage treatment plant removal.
[c] Arizona, Wisconsin and Florida.
[d] California, Connecticut, Georgia, Massachusetts, New York and Washington.
Appendix 5: Concentrations of 1,2-dibromoethane in food
| Item sampled | Sampling period | Number of samples | Detection limit (μg/kg) | Mean concentration[1] (μg/kg) | Reference |
|---|---|---|---|---|---|
| Greece (domestic honey) | 2004 | 25 | 0.8 | Quantified in only two samples: 75 ± 3 and 12 ± 0.5 |
Tananaki et al. 2005 |
| Greece (honey) | 2003 | 142 | 0.8 | Maximum 132.5 | Tananaki et al. 2006 |
| 2004 | 737 | Maximum 331.2 | |||
| 2005 | 266 | Maximum 95.2 | |||
| fir honey | 2003–2005 | 24 | Maximum 12.7 | ||
| blossom honey | 60 | Maximum 10.5 | |||
| thymus honey | 49 | Maximum 2.9 | |||
| pine honey | 283 | Maximum 16.0 | |||
| United States (sweet cucumber pickles) |
September–October 1991 to July– August 2001 | 1 | 0.5 | 13 | US FDA 2003 |
| United States | April 1982 to April 1986 | 16 | LOQ 1.0[2] |
Gunderson 1988a | |
| - cottage cheese | 0.9 (ND–2.7) | ||||
| - popcorn in oil | 0.4 (ND–1.3) | ||||
| - onion rings, breaded/fried | 0.3 (ND–1.0) | ||||
| - frozen fried chicken | 0.6 (ND–1.9) | ||||
| - honey, bottled | 0.7 (ND–2.0) | ||||
| - chocolate cake/icing | 4.0 (ND–11.9) | ||||
| - yellow cake | 2.8 (ND–8.4) | ||||
| - doughnuts | 2.2 (ND–6.5) | ||||
| - cookies, chocolate chip | 2.4 (ND–7.3) | ||||
| - cookies, sandwich | 0.6 (ND–1.9) | ||||
| - apple pie, frozen | 0.3 (ND–1.0) | ||||
| - carbonated soda | 0.003 (ND–0.0084) | ||||
| Florida (grapefruit) | April–June 1987 | 5 | 0.5 | Pulp: 1.84 (ND–5.3) Peel: 3.12 (0.6–10.0) Seeds: 336 (ND–591) |
Nakamura et al. 1989 |
| Israel (grapefruit) | April–June 1987 | 2 | 0.5 | Pulp: 0.95 (0.6–1.3) Peel: ND Seeds: 776 (521–1031) |
Nakamura et al. 1989 |
| Philippines (mango) | April–June 1987 | 6 | 0.5 | Pulp: 1.57 (ND–2.8) Peel: 4.4 (2.7–6.3) Seeds: 2.47 (ND–4.1) |
Nakamura et al. 1989 |
| Mexico (mango) | April–June 1987 | 4 | 0.5 | Pulp: 4.1 (ND–7.9) Peel: 6.4 (ND–15.6) Seeds: 58 (2.3–137) |
Nakamura et al. 1989 |
| Hawaii (papaya) | April–June 1987 | 10 | 0.5 | Pulp: 0.75 (ND–2.4) Peel: 0.66 (ND–1.5) Seeds: 1.0 (ND–3.0) |
Nakamura et al. 1989 |
| Taiwan (lychee) | April–June 1987 | 6 | 0.5 | Pulp: 2.77 (ND–10.0) Peel: 6.8 (2–23.2) Seeds: 12.9 (2.2–47.2) |
Nakamura et al. 1989 |
| China (lychee) | April–June 1987 | 1 | 0.5 | Pulp: 0.9 Peel: 4.3 Seeds: 9.7 |
Nakamura et al. 1989 |
| United States (found in one sample of peanut butter and one sample of whiskey) |
1988 | 231 samples (derived from US FDA market basket collection) | ns | Whiskey (80 proof): 2 Peanut butter: 11 |
Daft 1988 |
| United States | 1980 | Rains and Holder 1981 | |||
| - flour | 22 | 5 | 807 (ND–4200) | ||
| - biscuits | 22 | 0.5 | 36 (ND–260) | ||
| Japan (wheat; authors note that processing and market circulation would likely decrease levels) | 1985 | 3 | 0.5 | 1.11 (0.74–1.70) | Konishi et al. 1986 |
| United States | 1985 |
Clower et al. 1986 | |||
| - flour, enriched | 3 | 2 | 24 | ||
| - flour, unbleached pastry | 3 | 140 | |||
| - meal, corn | 3 | 55 | |||
| - wheat, whole grain red winter | 3 | 167 | |||
| United States (cooked rice) | 1984 | 4 | 0.4 | 2.5 (ND–8.3) | Clower et al. 1985 |
| Saskatoon, Saskatchewan (flour) |
1984 | 10 | ns | 81 (4.1–405.3) | McKay 1986 |
Abbreviations: ND, not detected; ns, not specified.
[1] Values in parentheses indicate range of concentrations when available.
[2] The limit of quantitation (LOQ) was obtained from a related total diet study of eight U.S. FDA market baskets during the period from April 1982 to April 1984 (Gunderson 1988b). The Gunderson (1988a) study incorporated the results of Gunderson (1988b) and included an additional two years of sampling (April 1984 to April 1986).
[1] Values in parentheses indicate range of concentrations when available.
[2] The limit of quantitation (LOQ) was obtained from a related total diet study of eight U.S. FDA market baskets during the period from April 1982 to April 1984 (Gunderson 1988b). The Gunderson (1988a) study incorporated the results of Gunderson (1988b) and included an additional two years of sampling (April 1984 to April 1986).
Appendix 6: Concentrations of 1,2-dibromoethane in soil
| Location | Sampling period | No. of samples | Detection limit (ng/g)[1] | Mean Concentration (ng/g)[2] | Reference |
|---|---|---|---|---|---|
| Site of a chemical plant, Ontario | 1997 | - | - | 3 m depth: 4.24 × 106 (dry weight) 0.8 m depth: 1.19× 10[4] (dry weight) 0.2–0.76 m depth: 80 (dry weight) |
Environment Canada 2001b |
| Ontario regions (rural parkland, soil) | ca. 1993 | 59 | MDL 4.0 | 0.032[3](0.012–0.390)[4] [dry weight] |
OMEE 1993 |
| Ontario (soil) | 1986 | 5 | MDL 0 | 0.032[3](0.012–0.390)[4] [dry weight] |
OMEE 1993 |
| Port Credit, Ontario (soil) | 1987 | 8 | MDL 0.2 [wet weight] |
ND | Golder Associates 1987 |
| Oakville/ Burlington, Ontario (soil) | 1986 | 8 | MDL 0.2–10 [wet weight] |
ND | Golder Associates 1987 |
Abbreviations: MDL, method detection limit; ND, not detected.
[1] The MDL is defined as 3 times the within-run analytical standard deviation and is considered only an estimate that may vary with time (OMEE 1993).
[2] The limit of quantitation (LOQ) was obtained from a related total diet study of eight U.S. FDA market baskets during the period from April 1982 to April 1984 (Gunderson 1988b). The Gunderson (1988a) study incorporated the results of Gunderson (1988b) and included an additional two years of sampling (April 1984 to April 1986).
[3] The concentration is the 97.5th percentile Ontario typical range value. This concentration is two standard deviations above the mean value.
[4] The ranges are derived from the Ontario typical range model released in 1993 (to replace the previous "upper limit of normal" contaminant guidelines).
[1] The MDL is defined as 3 times the within-run analytical standard deviation and is considered only an estimate that may vary with time (OMEE 1993).
[2] The limit of quantitation (LOQ) was obtained from a related total diet study of eight U.S. FDA market baskets during the period from April 1982 to April 1984 (Gunderson 1988b). The Gunderson (1988a) study incorporated the results of Gunderson (1988b) and included an additional two years of sampling (April 1984 to April 1986).
[3] The concentration is the 97.5th percentile Ontario typical range value. This concentration is two standard deviations above the mean value.
[4] The ranges are derived from the Ontario typical range model released in 1993 (to replace the previous "upper limit of normal" contaminant guidelines).
Appendix 7: Summary of health effects information for 1,2-dibromoethane
| Endpoint | Lowest effect levels[1] / Results |
|---|---|
| Laboratory animals and in vitro | |
| Acute toxicity | Lowest oral LD50(rabbit) = 55 mg/kg-bw (Rowe et al. 1952) Lowest inhalation LC50(rat) = 3080 mg/m3 (Rowe et al. 1952) [Additional studies: Koptagel and Bulut 1998] |
| Short-term repeated-dose toxicity |
Lowest oral LOEL (mice) = 125 mg/kg-bw per day based on increased cholesterol levels and increased in vitro phagocytosis of pooled cultured cells from 2–3 dosed animals at 125 mg/kg-bw per day and higher doses. Ethylene bromide (in corn oil) was injected intragastrically at doses of 100, 125, 160 or 200 mg/kg-bw per day for 14 days (n = 10 per treatment) (Ratajczak et al. 1994). |
| Subchronic toxicity | Lowest oral LOEL (mice) = 125 mg/kg-bw per day based on alterations in in vivo serum and hematology parameters and in vitro lymphocyte response. Ethylene bromide (in corn oil) was injected intragastrically at doses of 31.25, 62.5 or 125 mg/kg-bw per day, 5 days a week for 12 weeks (n = 6–9 per treatment) (Ratajczak et al. 1995). Lowest inhalation LOEC (rats) = 77 mg/m3 based on epithelial hyperplasia of the nasal turbinates at 77 and 307 mg/m3. Rats were exposed to ethylene bromide at doses of 0, 3, 10 or 40 ppm (equivalent to 0, 23, 77 or 307 mg/m3 as per IPCS 1996), 6 hr/day, 5 days per week for 13 weeks (n = 10 per treatment) (Nitschke et al. 1981). [Additional studies: Reznik et al. 1980] |
| Chronic toxicity/ carcinogenicity |
Oral (gavage) carcinogenicity bioassay in rats: Males were exposed to a time-weighted average of 0, 38 or 41 mg/kg-bw per day (5 days/week for up to 49 weeks). Females were exposed to 0, 37 or 39 mg/kg-bw per day (5 days/week for up to 61 weeks). Both sexes initially received 0, 40 or 80 mg/kg-bw per day of 1,2-dibromoethane, but, due to excessive mortality, the exposure levels and the overall duration of the study were reduced. In both sexes, there were significant increases in the incidence of squamous cell carcinomas of the forestomach in exposed groups (0/20 for both male and female controls, 45/50 for low-dose males, 33/50 for high-dose males, 40/50 for low-dose females, 29/50 for high-dose females). In males in the low-dose group, there was a significant increase in the incidence of hemangiosarcomas of the circulatory system (0/20 controls, 11/50 low dose); after time-adjusted analysis in high-dose females, there was a significant increase in the incidence of hepatocellular carcinomas (0/20 controls, 5/25 high dose) (NCI 1978). Oral (gavage) carcinogenicity bioassay in mice:Mice were exposed to time-weighted average doses of 0, 62 or 107 mg/kg-bw per day (5 days/week for 53 weeks). Mortality was high in all treated groups and due to this, all males and high-dose females were sacrificed at wk 78 (25 wks after dosing ceased). Low-dose females were sacrificed at wk 90. There were significant increases in the incidence of squamous cell carcinomas of the forestomach (males: vehicle control, 0/20; low dose, 45/50; high dose, 29/49; females: vehicle control, 0/20; low dose, 46/49; high dose, 28/50) and in alveolar/bronchiolar adenomas (males: control, 0/20; high dose, 10/47; females: control, 0/20; low dose, 11/43) (NCI 1978). [Additional study: Van Duuren et al. 1985 (drinking water): evidence of carcinogenicity was observed] Inhalation carcinogenicity bioassay in rats: Rats were exposed by inhalation to 0, 10 or 40 ppm (equivalent to 0, 77 or 308 mg/m3) 6 h/day, 5 days/week, for 88–103 weeks). High mortality at the high concentration (90% in males, 84% in females) resulted in sacrifice of the remaining high-dose animals at wks 88 (males) or 91 (females). There were significant increases in the incidence of nasal cavity carcinomas at high doses (males: controls, 0/50; high dose, 21/50; females: controls, 0/50; high dose, 25/50) and adenocarcinomas at both doses (males: controls, 0/50; low dose, 20/50; high dose, 28/50; females: controls, 0/50; low dose, 20/50; high dose, 29/50) and adenomas at low doses (males: control, 0/50; low dose, 11/50; females: controls, 0/50; low dose, 11/50). There was a significant increase in the incidence of hemangiosarcomas of the circulatory system in the high-dose groups of both sexes (males: controls, 0/50; high dose, 15/50; females: controls, 0/50; high dose, 5/50). Female rats had a significantly increased incidence of mammary gland fibroadenomas (controls, 4/50; low dose, 29/50; high dose, 24/50), and the highest-dose females exhibited significant levels of alveolar/bronchiolar adenomas combined with carcinomas (controls, 0/50; high dose, 5/47). Male rats had a significant increase in the incidence of tunica vaginalis mesotheliomas at both doses (controls, 0/50; low dose, 7/50; high dose, 25/50) and nasal cavity adenomatous polyps at the low dose (controls, 0/50; low dose, 18/50) (NTP 1982). Inhalation carcinogenicity bioassay in mice: Mice were exposed by inhalation to 0, 10, or 40 ppm (equivalent to 0, 77 or 308 mg/m3) 6 h/day, 5 days/week, for 78–103 weeks). High mortality in both treated and control males resulted in sacrifice of all remaining males at wk 78. In females, high mortality was observed only at the high concentration (86%), and all remaining females at this concentration were sacrificed at wk 90. There were significantly increased incidences of alveolar/bronchiolar carcinomas (males: control, 0/41; high dose, 19/46; females: control, 1/49; high dose, 37/50) and adenomas (males: controls, 0/41; high dose, 11/46; females: controls, 3/49; high dose, 13/50) in the highest-dose groups of both sexes. In dosed females, there was also a significantly increased incidence of hemangiosarcomas of the circulatory system (controls, 0/50; low dose, 11/50; high dose, 23/50), subcutaneous fibrosarcomas (controls, 0/50; low dose, 5/50; high dose, 11/50), nasal cavity carcinomas (controls, 0/50; high dose, 6/50) and mammary gland adenocarcinomas (controls, 2/50; low dose, 14/50; high dose, 8/50) (NTP 1982). [Additional studies: Stinson et al. 1981; Wong et al. 1982: evidence of carcinogenicity was observed in both studies] Dermal carcinogenicity bioassay in mice: Female mice were given 0, 25 or 50 mg/mouse in acetone, dermally, 3 times a week for 440–594 days (equivalent to 357 or 714 mg/kg-bw per day, respectively; as per Health Canada 1994). There was a significant increase in the incidence of benign lung papillomas at both dose levels (low dose, 24/30; high dose, 26/30) and a significant increase in the incidence of combined squamous skin papillomas and carcinomas (3/30), as well as skin papillomas (5/30) at the high dose(Van Duuren et al. 1979). Lowest non-neoplastic oral (gavage) effect level(rats) = 38 (male) and 37 (female) mg/kg-bw per day, based on hyperkeratosis and acanthosis of the forestomach in females, degenerative changes in the liver, cortical cell degeneration of the adrenal gland and testicular atrophy in males (lowest dose tested, carcinogenic dose) (NCI 1978) Lowest non-neoplastic inhalation concentration(rats) = 77 mg/m3, based on toxic nephropathy and testicular degeneration in males, retinal atrophy and adrenal cortex degeneration in females and increases in hepatic necrosis in both sexes (lowest dose tested, carcinogenic dose; NTP 1982). [Additional studies: Stinson et al. 1981; NTP 1982; Wong et al. 1982] |
| Reproductive toxicity | Lowest oral (feed) LOEL (bulls) = 2 mg/kg-bw per day for 12 months (followed by 4 mg/kg-bw every 2 days for 10–12 months), based on reversible low sperm density, poor motility and altered spermatozoa morphology (Amir and Volcani 1965) Oral (gavage) at 38 mg/kg-bw per day for 49 weeks caused testicular atrophy in male rats (NCI 1978) [Additional study: Shivanandappa et al. 1987] Lowest inhalation LOEC (rats) = 77 mg/m3, based on testicular degeneration in males rats in a 88–103-week study (NTP 1982) Reproductive effects were reported in male or female rats following inhalation exposure to 0, 19, 39 or 89 ppm (equivalent to 146, 300 or 684 mg/m3 as per IPCS 1996) in males or 0, 20, 39 or 80 ppm (equivalent to 154, 300, or 614 mg/m3 as per IPCS 1996) in females for 10 or 3 weeks, respectively. In male rats, a reduction in testicular weight; decreased serum testosterone levels; atrophy of testes, epididymis, prostate and seminal vesicles; and changes in reproductive behaviour were reported only in the high-dose group. Also, female rats in the high-dose group showed abnormal estrous cycle until several days after cessation of exposure. Mortality occurred in both sexes in the high-dose group (Short et al. 1979). |
| Developmental toxicity | Lowest inhalation LOEC (rats) = 51.2 mg/m3, based on decreased maternal body weight and improved rotorod performance and T-maze brightness discrimination acquisition in offspring (Smith and Goldman 1983) [Additional study: Short et al. 1978] |
| Genotoxicity and related endpoints: in vitro | GENE MUTATION Positive results: Salmonella typhimurium TA98 (+/-S9), TA100 (+/-S9), TA100 (GSH-) (−S9, +GSH), TA100 (GSTA1-1 or GST1-1) (−S9), TA100W (Strr, 8AGr) (−S9), TA102 (activation not specified), TA1530 (−S9), TA1535 +/-S9), TA1535 (GST1-1) (−S9), TA2638 (activation not specified), G46 (−S9), BA13 +/-S9) (Ames and Yanofsky 1971; Von Buselmaier et al. 1972; Brem et al. 1974; McCann et al. 1975; Rosenkranz 1977; Rannug and Beije 1979; Elliott and Ashby 1980; Shiau et al. 1980; Stolzenberg and Hine 1980; van Bladeren et al. 1980, 1981; Barber et al. 1981; Principe et al. 1981; Barber and Donish 1982; Kerklaan et al. 1983, 1985; Moriya et al. 1983; Buijs et al. 1984; Dunkel et al. 1985; Tennant et al. 1986, 1987; Hughes et al. 1987; Zoetemelk et al. 1987; Ong et al. 1989; Roldán-Arjona et al. 1991; Zeiger et al. 1992; Simula et al. 1993; Novotná and Duverger-van Bogaert 1994; Thier et al. 1996; Watanabe et al. 1998) Escherichia coli WP2 (+/-S9), WP2/pKM101 (activation not specified), WP2 uvrA/pKM101 (activation not specified), CHY832 (−S9), 343/286 (+/-S9), K12 (+/-S9), KI201 (−S9), KI211 (−S9), uvrB5 (Scott et al. 1978; Hemminki et al. 1980; Izutani et al. 1980; Moriya et al. 1983; Hayes et al. 1984; Mohn et al. 1984; Dunkel et al. 1985; Foster et al. 1988; Watanabe et al. 1998) Bacillus subtilis TKJ5211, TKJ6321 (+S9) (Shiau et al. 1980) Streptomyces coelicolor (−S9, spot test) (Principe et al. 1981) Aspergillus nidulans (Scott et al. 1978; Principe et al. 1981) Neurospora crassa ad-3 (forward mutation) (De Serres and Malling 1983) Mouse L5178Y (+/-S9) (Clive et al. 1979; Tennant et al. 1986, 1987) Chinese hamster CHO-K1(+/-S9) (Tan and Hsie 1981; Brimer et al. 1982) Human cell line AHH-1, TK6 (−S9) (Crespi et al. 1985) Human cell line EUE (−S9) (Ferreri et al. 1983) E. coli lacZ reversion assay (Josephy et al. 2006) Negative results: Salmonella typhimurium TA98 (+/-S9), TA100 (+/-S9), TA1537 (+/-S9), TA1538 (+/-S9), E503 (Brem et al. 1974; Alper and Ames 1975; Shiau et al. 1980; Principe et al. 1981; Wildeman and Nazar 1982; Moriya et al. 1983; Dunkel et al. 1985; Tennant et al. 1986) Serratia marcescens a21 (−S9) (Von Buselmaier et al. 1972) Escherichia coli 343/113 (−S9) (Mohn et al. 1984) Streptomyces coelicolor (−S9, plate method) (Principe et al. 1981) UNSCHEDULED DNA SYNTHESIS Positive results: Rat hepatocytes (Williams et al. 1982; Tennant et al. 1986; Working et al. 1986) Rat spermatocytes (Working et al. 1986) Opossum lymphocytes (Meneghini 1974) Human lymphocytes (+/-S9) (Perocco and Prodi 1981) Mouse (C3Hf×101)F1 germ cells (Sega and Sotomayor 1980) SISTER CHROMATID EXCHANGE Positive results: Chinese hamster V79 cl-15 (−S9) (Tezuka et al. 1980) Chinese hamster ovary (+/-S9) (Tennant et al. 1987; Ivett et al. 1989) Human lymphocytes (−S9) (Tucker et al. 1984; Ong et al. 1989) CHROMOSOMAL ABERRATIONS Positive results: Chinese hamster V79 cl-15 (−S9) (Tezuka et al. 1980) Chinese hamster ovary (+/-S9) (Tennant et al. 1987; Ivett et al. 1989) MICRONUCLEI INDUCTION Positive results: Human lymphocytes (Channarayappa et al. 1992) DNA DAMAGE Positive results: Escherichia coli polA1−/polA+(−S9) (Brem et al. 1974) Human nasal mucosa cells, rat ethmoidal mucosa, rat nasal mucosa cells (Holzer et al. 2008) Negative results: Bacilis subtilis TKJ5211, TKJ6321 (+/-S9) (Shiau et al. 1980) SOS INDUCTION Positive results: Salmonella typhimurium TA1535/pSK1002 (+/-S9), NM5004 expressing GST 5-5 (Ong et al. 1987; Oda et al. 1996) Escherichia coli (Ohta et al. 1984; Quillardet et al. 1985) Negative results: Salmonella typhimurium TA1535/pSK1002 (−S9) (Oda et al. 1996) MITOTIC GENE CONVERSION Positive results: Saccharomyces cerevisiae ade2, trp5 (Fahrig 1974) SOMATIC SEGREGATION Positive results: Aspergillus nidulans diploid 35×17 (−S9) (Crebelli et al. 1984) CELL PROLIFERATION Positive results: Human lymphocytes (Channarayappa et al. 1992) DNA STRAND BREAKS Positive results: Rat hepatocytes (Sina et al. 1983) Rat testicular cells (Bradley and Dysart 1985) Rat and human testicular cells (Bjørge et al. 1996) DNA BINDING Positive results: Calf thymus DNA (Arfellini et al. 1984; Colacci et al. 1985; Prodi et al. 1986) Rat hepatocytes (Inskeep et al. 1986; Cmarik et al. 1990) Human hepatocytes (Cmarik et al. 1990) Negative results: Escherichia coli Q13 (+/-S9) and mouse Ehrlich ascites (+/-S9) (Kubinski et al. 1981) CELL TRANSFORMATION Positive results: Balb/c 3T3 mouse cells (Perocco et al. 1991; Colacci et al. 1995) Negative results: Balb/c 3T3 mouse cells (−S9) (Tennant et al. 1986) |
| Genotoxicity and related endpoints: in vivo | GENE MUTATION Positive results: Drosophila melanogaster (Graf et al. 1984; Ballering et al. 1993) Salmonella typhimurium G46 host-mediated (Von Buselmaier et al. 1972) Negative results: Serratia marcescens host-mediated (Von Buselmaier et al. 1972) Silk worm (Sugiyama 1980) RECOMBINATION Positive results: Drosophila melanogaster (Graf et al. 1984; Ballering et al. 1993) SEX-LINKED RECESSIVE LETHAL MUTATIONS Positive results: Drosophila melanogaster (Vogel and Chandler 1974; Kale and Baum 1979a, 1979b, 1981, 1982, 1983; Yoshida and Inagaki 1986; Ballering et al. 1993, 1994; Foureman et al. 1994; Kale and Kale 1995) CHROMOSOMAL ABERRATIONS Negative results: Mouse (intraperitoneal) bone marrow (Krishna et al. 1985) (IARC reports weakly positive) (IARC 1999) Mouse (intraperitoneal) bone marrow (NTP 1993) DNA STRAND BREAKS Positive results: Rat hepatocytes (Nachtomi and Sarma 1977; Kitchin and Brown 1994) Mouse hepatocytes (White 1982; Storer and Conolly 1983) Rat testicular cells (Bradley and Dysart 1985) MICRONUCLEI Positive results: Mouse (peripheral blood) (Witt et al. 2000) Negative results: Mouse (Krishna et al. 1985; Asita et al. 1992) DNA BINDING Positive results: Mouse (liver, stomach, kidney, lung) (Arfellini et al. 1984; Prodi et al. 1986) Mouse hepatocyte DNA (Kim and Guengerich 1990) Mouse (liver, kidney) (Watanabe et al. 2007) Rat (liver, stomach, kidney, lung) (Arfellini et al. 1984; Prodi et al. 1986) Rat hepatocyte DNA (Inskeep et al. 1986; Kim and Guengerich 1990) Rat (liver, kidney) (Watanabe et al. 2007) SPECIFIC LOCUS TEST Negative results: Mouse (Russell 1986; Barnett et al. 1992) SISTER CHROMATID EXCHANGE Negative results: Mouse (intraperitoneal) bone marrow (Krishna et al. 1985) Mouse (intraperitoneal) bone marrow (NTP 1992) DOMINANT LETHAL Negative results: Rat (Short et al. 1979; Teramoto et al. 1980; Teaf et al. 1990) Mouse (Epstein et al. 1972; Teramoto et al. 1980; Barnett et al. 1992) DNA REPAIR EXCLUSIVE OF UNSCHEDULED DNA SYNTHESIS Negative results: Mouse hepatocytes (White et al. 1981) UNSCHEDULED DNA SYNTHESIS Positive results: Rat hepatocytes (Working et al. 1986) Negative results: Rat spermatocytes (Working et al. 1986; Bentley and Working 1988) DNA DAMAGE Positive results: Mouse (stomach, liver, kidney, bladder, lung) (Sasaki et al. 1998) |
| Humans | |
| Acute toxicity | Estimated fatal dose in adult male and female (human) = 1.5 ml or 3240 mg (46 mg/kg-bw for a 70-kg person). Effects observed included nausea, vomiting, abdominal pain and signs of hepatotoxicity, nephrotoxicity, nervous system toxicity and cardiotoxicity in male and female patients (Singh et al 2007 - review of 64 cases of acute 1,2-dibromoethane poisoning). Estimated inhalation lethal concentration (human) = 154 mg/m3 for more than 30 min (IPCS 1996) [Additional studies: Alexeeff et al. 1990 ; Peoples et al. 1978; Letz et al. 1984; Jacobs 1985; Sarawat et al. 1986; Singh et al. 1993; Prakash et al. 1999; Raman and Sain 1999; Mehrotra et al. 2001] |
| Chronic toxicity/ carcinogenicity |
Mortality assessed in employees occupationally exposed to 1,2-dibromoethane in two production units while working as still and reactor operators (level of exposure was not provided in secondary accounts). In the first production unit, there were 2 deaths from malignant neoplasms (3.6 expected), and in the second production unit, there were 5 deaths from malignant neoplasms (2.2 expected). However, employees of the second production unit were also exposed to other chemicals, and overall there was no increase in total deaths or malignant neoplasms with increased exposure (Ott et al. 1980). [Additional study: Ter Haar 1980] |
| Reproductive and developmental toxicity | Lowest inhalation LOEC = 0.46 mg/m3based on significantly decreased sperm velocity and semen volume in male forestry workers (occupational time-weighted average) in male forestry workers. Forestry workers engaged in applying or spraying of 1,2-dibromoethane emulsion (4% 1,2-dibromoethane by volume) were examined following short-term inhalation and dermal exposure (Schrader et al. 1988; IPCS 1996). Male forestry workers conducting fumigation (n = 46) with 1,2-dibromoethane for 5 years, showed significant decreases in sperm count, number of viable sperms and increase in sperms with abnormal morphology. 1,2-Dibromoethane concentration ranged from a geometric mean of 88 ppb to peak concentration of up to 262 ppb (equivalent to 0.68 mg/m3to 2.0 mg/m3 as per IPCS 1996) for 8-hr time-weighted average. The authors did not report exposure to any other chemicals in the forestry workers engaged in the application or spraying activities (Ratcliffe et al. 1987). [Additional studies: Ter Haar 1980; Wong et al. 1985; Dobbins 1987;Schrader et al. 1987] |
| Genotoxicity and related endpoints | Negative results: Chromosomal aberrations and sister chromatid exchange were not detected in men who worked in papaya-packing plants and used 1,2-dibromoethane to fumigate the fruit. These workers were exposed to mean concentrations ranging from 0.12 to 1.35 mg/m3(Steenland et al. 1986). [Additional study: Steenland et al. 1985] |
[1] LC50 = median lethal concentration; LD50 = median lethal dose; LOEC = lowest-observed-effect concentration; LOEL = lowest-observed-effect level.