Appendices of the Screening Assessment Report

Ethene, 1,1-dichloro-
(1,1-Dichloroethene)

Chemical Abstracts Service Registry Number
75-35-4

Environment Canada
Health Canada
June 2013

Appendices

Appendix 1: Concentrations of 1,1-DCE in different media

Table A1. Concentration of 1,1-DCE in ambient air
LocationSampling periodNumber of samplesDetection limit (μg/m3)Concentration[1](μg/m3)Reference
Windsor, OntarioJanuary 23 to March 25, 2006

July 3 to August 26, 2006
214

214
0.046Arithmetic mean and median: 0.023[3] (all ND)

Arithmetic mean and median: 0.023[3] (all ND)
Health Canada 2010b
Windsor, OntarioJanuary 24 to March 19, 2005

July 4 to August 27, 2005
201

216
0.152Arithmetic mean and median: 0.076[3] (all ND)

Arithmetic mean and median: 0.076[3] (all ND)
Health Canada 2010b
Regina, Saskatchewan (full set)January 8 to March 16, 2007

June 20 to August 29, 2007
94 (winter; only 24-h canisters reported)

97 (summer; 5-day canisters)
0.012Arithmetic mean and median: 0.006[3] (all ND)

Arithmetic mean and median: 0.006[3] (Range: 0.006 – 0.014)
Health Canada 2010a
Canada-wide sites (43 locations)January to December 200818960.0260.013[3]NAPS 2008
Ottawa, Ontario (residential areas)Nov 20, 2002 to Mar 11, 2003740.011Arithmetic mean: 0.05
Median: 0.005
(Range: 0.005 –0.83)
(detected in 13 of 74 samples)
Zhu et al. 2005
Canada-wide sites1989–19969128ns0.06 [ND–0.78]; 8% > detection limit)[4]NAPS 2004
Montréal, Quebec (urban)19931600.2
(0.05 ppbv)[2]
0.03 [ND–0.30] (14% > detection limit)Environment Canada 1995
Montréal, Quebec (suburban)1993240.2
(0.05 ppbv)[2]
0.00 [ND–0.04] (0% > detection limit)Environment Canada 1995
Sainte-Françoise, Quebec (rural)1993340.2
(0.05 ppbv)[2]
0.02 [ND–0.12] (6% > detection limit)Environment Canada 1995
Montréal, Quebec (urban)19921660.2
(0.05 ppbv)[2]
0.00 [ND–0.02] (0% > detection limit)Environment Canada 1995
Montréal, Quebec (urban)1991910.2
(0.05 ppbv)[2]
0.01 [ND–0.22] (4% > detection limit)Environment Canada 1995
Montréal, Quebec (urban)19901100.2
(0.05 ppbv)[2]
0.00 [ND–0.11] (2% > detection limit)Environment Canada 1995
Montréal, Quebec (urban)1989760.2
(0.05 ppbv)[2]
0.03 [ND–0.44] (13% > detection limit)Environment Canada 1995
Greater Vancouver Regional District1989–19924730.2
(0.05 ppbv)[2]
0.05 (4% > detection limit)[3]Environment Canada 1994
Canada
(sites unspecified)
1989–199011000.2
(0.05 ppbv)[2]
0.06 (9% > detection limit)[3]Environment Canada 1994
Windsor, OntarioJuly 1987 to October 1990124nsns [ND–0.3] (10 of 124 samples > detection limit)Environment Canada 1992
Walpole Island, OntarioJanuary 1988 to October 199061nsns [ND–0.2] (8 of 61 samples > detection limit)Environment Canada 1992
Toronto, Ontario (downtown)June–August 1990160.4
(MQL = 2.1)
1.9OME 1991d
Toronto, Ontario (residential)June–August 199070.4
(MQL = 2.1)
0.4OME 1991d
Canada (residential homes)February–March 198766 ng/tube (collection vial)0.3 [ND–1]Chan et al. 1990
Canada (residential homes)November–December 1986126 ng/tube (collection vial)3.2 [ND–7]Chan et al. 1990
[1] Value in parentheses indicates range of concentrations when available.
[2] Value presented for the detection limit is the target or typical detection limit reported for volatile organic compounds.
[3] Mean calculated with values below detection set to 0.5*Method Detection Limit
[4] Values below detection limit set to 0.05 µg/m3
MQL = method quantifiable limit
ns = not specified
ND = not detected
Table A2. Concentration of 1,1-DCE in indoor air
LocationSampling periodNumber of samplesDetection limit (μg/m3)Concentration[1](μg/m3)Reference
Windsor, Ontario (personal breathing-zone air)January 24 to March 19, 2005

July 4 to August 27, 2005
225

207
0.152Winter
AM: 0.076
Median: 0.076
P-95: 0.076
R: All ND Summer
AM: 0.077
Median: 0.076
P-95: 0.076
R: 0.076 – 0.400
Health Canada 2010b
Windsor, OntarioJanuary 23 to March 25, 2006

July 3 to August 26, 2006
224

211
0.046Winter
AM: 0.025
Median: 0.023
P-95: 0.023
R: 0.023 – 0.463 Summer
AM: 0.025
Median: 0.023
P-95: 0.023
R: 0.023 – 0.103
Health Canada 2010b
Windsor, OntarioJanuary 24 to March 19, 2005

July 4 to August 27, 2005
232

217
0.152Winter
AM: 0.076
Median: 0.076
P-95: 0.076
R: 0.076 – 0.185 Summer
AM: 0.085
Median: 0.076
P-95: 0.076
R: 0.076 – 1.380
Health Canada 2010b
Regina, Saskatchewan[2] (full set; 5-day data)January 8 to March 16, 2007

June 20 to August 29, 2007
89

101
0.012Winter
AM: 0.009
Median: 0.006
P-95: 0.027
R: 0.006 – 0.083 Summer
AM: 0.007
Median: 0.006
P-95: 0.023
R: 0.006 – 0.033
Health Canada 2010a
Ottawa, Ontario (detected in 34 of 75 homes)Nov 20, 2002 to Mar 11, 2003750.011AM: 0.27
Median: 0.005
P-95: 0.99
R: 0.005 – 4.05
Zhu et al. 2005
International locations (literature review of 50 studies)1978–1990n = 50 studiesnsMean: 1–< 5Brown et al. 1994
Toronto, Ontario (office)June–August 199080.4
(MQL = 2.1)
Mean: 5OME 1991d
Toronto, Ontario (domestic)June–August 199040.4
(MQL = 2.1)
Mean: 5.4OME 1991d
Canada (residential homes)November–December 1986126 ng/tube (collection vial)Mean: 8.4
Range: ND–77
Chan et al. 1990
Canada (residential homes)February/March 198766 ng/tube (collection vial)Mean: 3.8
Range: ND–13
Chan et al. 1990
Woodland, California (residential homes)June 19901280.78 (MQL)not quantifiable in any sampleCARB 1992
North Carolina (Research Triangle Park area – residential homes)Summer15nsDetected in 4 of 15 homes, with a mean of 12.06 and a range of 0.46–23.9 µg/m3Pleil et al. 1985
North Carolina (Research Triangle Park area – residential homes)Winter16nsDetected in 4 of 16 homes, with a mean of 1.81 and a range of 1.3–2.5 µg/m3Pleil et al. 1985
United States (various sites)1970–19872120nsMean: 5.02 µg/m3Shah and Heyerdahl 1988
[1] Mean calculated with values below detection set to 0.5*Method Detection Limit
[2] 5-day canister data were selected as they represent time-weighted average over longer period than 24-h canisters.R = range
P-95 = 95th percentile
AM = arithmetic mean
MQL = method quantifiable limit
ns = not specified
ND = not detected
Table A3. Concentration of 1,1-DCE in drinking water and groundwater
LocationSampling periodNumber of samplesDetection limit (μg/L)Mean concentration[1] (μg/L)Reference
DRINKING WATER
Victoria, British Columbia200820.1NDCity of Victoria 2008
Vancouver, British ColumbiaAugust 19, 200830.5NDCity of Vancouver 2008
Toronto, OntarioJanuary–December 2008nsnsNDTDWS 2008
Niagara Falls, OntarioNovember 6, 200810.41NDCity of Niagara Falls 2008
Saskatoon, Saskatchewan200810.2NDCSWTP 2008
London, OntarioJune 10, 200810.41NDCity of London 2008
Kitchener, OntarioJanuary–November 200860.5NDOME 2008
Kingston, Ontario200820.1NDUtilities Kingston 2008
Hamilton, OntarioFebruary–November 2008ns0.2NDBCOS 2008
Edmonton, Alberta2008nsnsNDEPCOR 2008
Barrie, Ontario200614nsND –“< 0.41”CBWO 2008
Montréal, Quebec2006ns0.07NDVille de Montreal 2006
Calgary, Alberta2003ns0.5NDCCW 2003
Ottawa, Ontario2003350.52NDCOWQS 2003
Québec, QuebecFebruary–November 20024ns< 0.2 (< 0.1 to < 0.4)Ville de Québec 2002
United States1985–2001n = 1096 (public well samples)MDL 0.047 (Connor et al. 1998)< 0.16 (median of all samples) 0.20 (median of samples with detection)Zogorski et al. 2006
United States1985–2001n = 2400 (domestic well samples)MDL 0.047 (Connor et al. 1998)<0.18 (median of all samples) 0.026 (median of samples with detection)Zogorski et al. 2006
Toronto, Ontario1986 and 19872 (tap water)
7 (bottled water)
0.04tap water - ND
bottled water - ND
City of Toronto 1990
Ontario (water treatment plants, various locations)198744 treatment plants0.1raw - ND
treated - ND
distribution water - ND
OME 1988, 1989
29 Alberta municipal drinking water supplies1978–1985nsnsns (detected in one of 29 municipal supplies at a max concentration of 1.4 µg/LHealth Canada 1994a
10 Ontario water treatment plants (Great Lakes locations)July–August 1982
January–February 1983
April–May 1983
42 raw
42 treated
[0.1–0.4] [2]raw - 0 [ND]
treated- &lt; 0.1 [ND–trace (1 sample at less than 0.1)]
Otson 1987
Canada-wide (29 municipalities, 30 water treatment plants)August–September 197930 raw
30 treated
5.0 (MQL)raw - 0 [ND]
treated - < 1 [ND–~20]
Otson et al. 1982b
Canada-wide (29 municipalities, 30 water treatment plants)November–December 197930 raw
30 treated
5.0 (MQL)raw - 0 [ND]
treated - 0 [ND]
Otson et al. 1982b
United States (EPA survey)nsnsnsdetected in 3% of drinking water supplies; 0.3 µg/L (0.2–0.5 µg/L)US EPA 1985 (cited in ATSDR 1994)
GROUNDWATER
United States1985–20013497ns< 0.20 (median for all samples) 0.068 (median for samples with detection)Zogorski et al. 2006
Ottawa, OntarioMay 198837nsdetected in 43% of samples [0.9–60]Lesage et al. 1990
United States (community-based groundwater sources, nationwide survey)ns9450.2 (MQL)detected in 2.3% of samples (max. 6.3 µg/L, subset median values, 0.28–1.2 µg/L)Rajagopal and Li 1991 [cited in ATSDR 1994] Westrick et al. 1984 [cited in ATSDR 1994]
United States, Ground Water Supply Survey1982466nsdetected in 9 samples; 0.3 µg/L (median)Cotruvo 1985 [cited in ATSDR 1994]
[1] Value in parentheses indicates range of concentrations when available.
[2] Value presented for the detection limit is the target or typical detection limit reported for volatile organic compounds.MDL – method detection limit
MQL - method quantifiable limit
ns = not specified; ND = not detected
Table A4. Concentration of 1,1-DCE in foodstuffs
Item sampledSampling periodNo. of samplesDetection limitMean concentration (μg/kg)Reference
FOOD

Ville-Mercier, Quebec

Ice cream
Cheese and butter
Beef and veal
Pork/cured pork
Lamb chops
Poultry
Eggs
Organ meats
Luncheon meats
Canned meats
Marine fish
Freshwater fish
Canned fish
Shellfish
Canned meat soups
Canned pea and tomato soups
Dehydrated soups
Bread
Flour and cakes
Cereals
Pies
Pasta
Potatoes and vegetables
Rice and vegetables
Beets and tomatoes
Fruits
Juices and canned fruit
Oils and fats
Peanut butter

January 199345.0 μg/kgNDETL 1993

Ville-Mercier, Quebec

Dairy
Coffee and tea
Soft drinks
Alcohols
Water

January 199341.0 μg/LNDETL 1993

United Kingdom

Biscuits
Marshmallow
Swiss roll
Snack biscuits
Crisps and snack foods
Whole turkey
Black pudding
Smoked cheese
Liver pate
Cooked sausage

ns

ns

 

1 μg/kg< 1
< 1
< 1
< 1
< 1
< 1
6
< 1
5
5
MAFF 1980

United States (food simulants)

heptane (0.5-mm film)
corn oil (0.5-mm film)
water (0.5-mm film)

Note: 0.5-mm film is equivalent thickness to plastic wrap used for food applications.

1977n = 4
n = 5
n = 4
5–10 ppb39 ppb (34–44 ppb)
34 ppb (18–41 ppb)
25 ppb (24–27 ppb)
Hollifield and McNeal 1978
Great Britain (potato crisps)1979n = 40.005 ppm0.019 ppm (0.010–0.025 ppm)Gilbert et al. 1980

Great Britain

Biscuits
Cakes
Snack products
Cheeses
Cooked meats:
Black pudding (n = 1)
Liver pate (n = 1)
Polony (n = 1)
Bacon and liver pate (n = 1)

October 1978n = 7
n = 1
n = 3
n =1
0.005 ppm

ND
ND
ND
ND

0.005–0.01 ppm
0.005–0.01 ppm
ND
ns

Gilbert et al. 1980

Japan

Sausage
Fish sausage
Boiled fish paste
Cheese

August 2004n = 130.001 µg/g0.008 µg/g
0.005 µg/g
0.003 µg/g
0.0095 µg/g
Ohno and Kawamura 2006
ND - not detected, below detection limit
ns - not specified
Table A5. Concentration of 1,1-DCE in soil
LocationSampling periodNo. of samplesDetection limit (ng/g)[2]Mean concentration[1] (ng/g)Reference
SOIL
Ontario regions – urban parklandns (~1993)59MDL[4] = 20.074 [0.039–0.12][3]OMEE 1993
Ontario regions – rural parkland (not including northwest region)ns (~1993)85MDL[4] = 20.016 [0.010–0.024][3]OMEE 1993
Ontario regions – rural parkland (northwest region)ns (~1993)17MDL[4] = 20.097 [0.063–0.098][3]OMEE 1993
[1] Value in parentheses indicates range of concentrations when available.
[2] The method detection limit is defined as three times the within-run analytical standard deviation and is considered only an estimate that may vary with time (OMEE 1993).
[3] The ranges are derived from the Ontario Typical Range Model released in 1993.
[4] Method detection limit (MDL).

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Appendix 2: Upper-bounding Deterministic Estimate of 1,1-DCE Daily Intake

Upper-bounding Deterministic Estimate of 1,1-DCE Daily Intake (μg/kg-bw per day)
Route of ExposureEstimated intake (μg/kg-bw per day) of 1,1-DCE by various age groups
0–6 months[1],[2],[3]0.5–4 yr[4]5–11 yr[5]12–19 yr[6]20–59 yr[7]60+ yr[8]
Formula fedNot formula fed
Ambient air[9]2.66 × 10-35.70 × 10-34.44 × 10-32.53 × 10-32.17 × 10-31.89 × 10-3
Indoor air[10]1.86 × 10-23.99 × 10-23.11 × 10-21.77 × 10-21.52 × 10-21.32 × 10-2
Drinking water[11]5.55 × 10-21.39 × 10-26.71 × 10-36.71 × 10-33.50 × 10-32.93 × 10-32.89 × 10-3
Food and beverages[12]1.3100.8590.5490.3200.2400.196
Soil[13]<0.001<0.001<0.001<0.001<0.001<0.001
Total intake7.67 × 10-21.3400.9110.5910.3440.2600.214
Maximum total intake from all routes of exposure:1.34

Abbreviations: ND, not detected; ns, not specified; ppbv, parts per billion by volume.
[1] No data were available for the presence of 1,1-DCE in breast milk, although it has been qualitatively detected in two related studies of breast milk from four cities across the United States, detection limits unspecified (Erickson et al. 1980; Pellizzari et al. 1982).
[2] Assumed to weigh 7.5 kg, to breathe 2.1 m3 of air per day, drink 0.8 L of water per day (formula fed) or 0.3 L/day (not formula-fed) and ingest 30 mg of soil per day (Health Canada 1998).
[3] For exclusively formula-fed infants, intake from water is synonymous with intake from food. The concentration of 1,1-DCE in water used to reconstitute formula was the detection limit (0.52 µg/L) of a study of distribution water and raw and treated water located at two treatment plants in Ottawa, Ontario, in 2003 (COWQS 2003). No data on concentrations of 1,1-DCE in formula milk were identified for Canada. Approximately 50% of not-formula-fed infants are introduced to solid foods by 4 months of age and 90% by 6 months of age (NHW 1990 in Health Canada 1998).
[4] Assumed to weigh 15.5 kg, to breathe 9.3 m3 of air per day, drink 0.7 L of water per day and ingest 100 mg of soil per day (Health Canada 1998).
[5] Assumed to weigh 31.0 kg, to breathe 14.5 m3 of air per day, drink 1.1 L of water per day and ingest 65 mg of soil per day (Health Canada 1998).
[6] Assumed to weigh 59.4 kg, to breathe 15.8 m3 of air per day, and to drink 1.2 L of water per day and ingest 30 mg of soil per day (Health Canada 1998).
[7] Assumed to weigh 70.9 kg, to breathe 16.2 m3 of air per day, drink 1.5 L of water per day and ingest 30 mg of soil per day (Health Canada 1998).
[8] Assumed to weigh 72.0 kg, to breathe 14.3 m3 of air per day, drink 1.6 L of water per day and ingest 30 mg of soil per day (Health Canada 1998).
[9] The median concentration of 1,1-DCE in outdoor air in Windsor, Ontario for 2005 of 0.076 µg/m3 was used in deriving the intake estimate (Health Canada 2010b). This data point was selected as it represents the highest median concentration across recent Canadian outdoor air studies. Canadians are assumed to spend 3 h per day outdoors (Health Canada 1998). The critical data were identified from a dataset of studies of ambient air (Zhu et al. 2005; NAPS 2008; Health Canada 2010a, 2010b; Environment Canada 1992, 1994, 1995; OME 1991d; Chan et al. 1990).
[10] The median concentration of 1,1-DCE in indoor air in Windsor, Ontario during 2005 of 0.076 µg/m3 was used in deriving the intake estimate (Health Canada 2010b). This data point was selected as it represents the highest median concentration across recent Canadian indoor air studies. Canadians are assumed to spend 21 h per day indoors (Health Canada 1998). The critical data were identified from a dataset of indoor air studies from Canada and international sites, primarily the United States (Health Canada 2010a, 2010b; Zhu et al. 2005; Brown et al. 1994; OME 1991d; CARB 1992; Chan et al. 1990; Pleil et al. 1985; Shah and Heyerdahl 1988).
[11] The detection limit (0.52 μg/L) of a study of distributed water and raw and treatment water located at two treatment plants in Ottawa, Ontario, in 2003 (n = 35 samples) was used as the most conservative estimate of exposure. Consumption estimates are for “total tap water” (Health Canada 1998). The critical data were identified from a dataset of drinking water studies from Canada and the United States (CBWO 2008; City of Victoria 2008; City of Vancouver 2008; TDWS 2008; City of Niagara Falls 2008; CSWTP 2008; City of London 2008; OME 2008; Utilities Kingston 2008; BCOS 2008; EPCOR 2008; Ville Montréal 2006; CCW 2003; COWQS 2003; Ville de Québec 2002; City of Toronto 1990; Zogorski et al. 2006; OME 1988, 1989; Health Canada 1994; Otson et al. 1982b; Otson 1987; US EPA 1985).
[12] In the absence of detected amounts in foods analyzed in Canada (ETL 1991, 1992, 1993), estimates of intakes for some food groups were based on studies conducted in Japan and the United Kingdom. The intake analysis is based on the following selected food groups (Health Canada 1998):

[13] The weighted average of Ontario urban parkland, rural parkland (not including northwest region) and rural parkland (northwest region) soil of 0.046 μg/kg solids of 161 samples was used in generating the intake estimate (OMEE 1993).

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Appendix 3: Summary of health effects information for 1,1-dichloroethene

Summary of health effects information for 1,1-dichloroethene
EndpointLowest effect levels[1] / Results
Acute toxicity

Lowest inhalation LC50 (mouse) = 200 mg/m3 (Zeller et al. 1979a, 1979b, 1979c, 1979d)

[Additional studies: Carpenter et al. 1949; Siegel et al. 1971; Jaeger et al. 1973, 1974; Klimisch and Freisberg, 1979a, 1979b; Zeller et al. 1979a, 1979b, 1979c, 1979d]

Lowest oral LD50 (mouse) = 194 mg/kg-bw (Jones and Hathway 1978a)

[Additional studies: Jenkins et al. 1972; Andersen and Jenkins 1977; Ponomarkov and Tomatis 1980]

Short-term repeated-dose toxicity

Lowest inhalation LOEC (rat) = 200 mg/m3: fatty changes and focal liver cell necrosis (4 weeks) (Plummer et al. 1990); changes to the liver and kidneys (7 days, with observation period to 28 days) (Maltoni and Patella 1983)

[Additional studies: Gage 1970; Short et al. 1977; Oesch et al. 1983; Norris and Reitz 1984]

Lowest oral LOEL (gavage) (rat) = 200 mg/kg-bw (2 times per week): increased serum sorbitol dehydrogenase and aminotransferases indicative of hepatotoxicity (4 weeks) (Siegers et al. 1983)

[Additional studies: NTP 1982; Maltoni and Patella 1983]

Subchronic toxicity

Lowest inhalation LOEC (rat) = 100 mg/m3: minimal, reversible liver cell cytoplasmic vacuolation (90 days) (Norris 1977; Quast et al. 1977)

[Additional studies: Lazarev 1960; Prendergast et al. 1967]

Lowest oral LOEL (rat) = 19 mg/kg-bw per day: minimal, recoverable liver cell cytoplasmic vacuolation (90 days) (Norris 1977; Quast et al. 1977)

[Additional studies: NTP 1982; Quast et al. 1983]

Chronic toxicity/ carcinogenicity

Lowest inhalation LOAEC (mice) = 40 mg/m3: significant increases in kidney damage (regressive changes and/or abscesses and nephritis in males) (52 weeks) (Maltoni et al. 1984, 1985)

[Additional studies: Lee et al. 1977; Rampy et al. 1977, 1978; Viola and Caputo 1977; Hong et al. 1981; Quast et al. 1986; Cotti et al. 1988]

Lowest oral LOEL (rat) = 5 mg/kg-bw per day: increased incidence of chronic renal inflammation in male and female F344/N rats, 2-year gavage study (NTP 1982)

[Additional studies: Ponomarkov and Tomatis 1980; Quast et al. 1983; Maltoni et al. 1984, 1985]

Inhalation study in Swiss mice: 0, 10 or 25 ppm (0, 40 or 100 mg/m3; conversion by IPCS 1990) for 52 weeks; significantly increased incidence of renal adenocarcinomas (0/126, 0/25 and 28/119 for the control, low and high concentrations, respectively) in males at 100 mg/m3; mammary carcinomas (3/185, 6/30 and 16/148 for the control, low and high concentrations, respectively) in females and pulmonary adenomas (12/331, 14/58 and 41/288 for the control, low and high concentrations, respectively) in males and females were not clearly exposure-related (Maltoni et al. 1984, 1985)

No significant increases in tumours considered to be related to exposure were observed in rats or hamsters in inhalation bioassays or in any species in studies by oral, dermal or subcutaneous routes of exposure (Lee et al. 1977, 1978; Rampy et al. 1977, 1978; Viola and Caputo 1977; Van Duuren et al. 1979; Hong et al. 1981; NTP 1982; Quast et al. 1983, 1986; Maltoni et al. 1984, 1985).

Dermal initiation–promotion study in female mice: initiation with 1,1-DCE; promotion by phorbol myristate acetate for 428–576 days, beginning 14 days after exposure to 1,1-DCE; 8/30 treated mice with lung papillomas versus 9/120 controls (Van Duuren et al. 1979)

Developmental toxicity

Lowest inhalation LOAEC (mouse) = 60 mg/m3: significant increase in the mean number of fetuses with an unossified incus and incompletely ossified sternebrae (gestation days 6–16); maternal LOEC = 119 mg/m3, based upon decrease in weight gain (Short et al. 1977)

[Additional studies: Murray et al. 1979]

Lowest oral LOEL (maternal, rat) = 14 mg/kg-bw per day; dams: minimal hepatocellular fatty change; reversible, accentuated hepatic lobular pattern; pups: no effects were observed (three-generation study) (Nitschke et al. 1983)

Note: Although 0.02 mg/kg-bw per day (rat) was the lowest identified oral LOAEL (Dawson et al. 1993), based on several factors, the US EPA (2002a) could not conclude that exposure to 1,1-DCE caused these effects.

[Additional studies: Murray et al. 1979]

Genotoxicity and related endpoints: in vivo

Chromosomal aberrations

Positive results:
Hamster, bone marrow (Hofmann and Peh 1976) [inhalation; 120 or 400 mg/m3, 6 hours/day, 5 days/week, 6 weeks]

Negative results:
Rat, bone marrow (Rampy et al. 1977) [inhalation; 100 or 300 mg/m3, 6 hours/day, 5 days/week, 6 months]; mouse, bone marrow (Cerna and Kypenova 1977)[intraperitoneal injection for 5 days]

DNA adduct formation
Positive results:

CD1-mice [inhalation; 40 or 200 mg/m3, 6 hours], Sprague-Dawley rats [inhalation, 40 mg/m3, 6 hours], liver and kidney (Reitz et al. 1980)

Dominant lethal test
Negative results:

Mouse (Andersen and Jenkins 1977) [inhalation; 50 ppm (198 mg/m3), 6 hours/day, 5 days]; rat (Short et al. 1977)[inhalation; 55 ppm (218 mg/m3), 6 hours/day, 5 days/week, 11 weeks]

Micronuclei test
Negative results:

Mouse, bone marrow [oral, 200 mg/kg-bw]; mouse, fetal erythrocytes [oral, 100 mg/kg-bw] (Sawada et al. 1987)

Non-mammalian sex-linked recessive lethal assay

Negative results:
Drosophila (Foureman et al. 1994) [oral, 20 000 or 25 000 ppm, 72 hours; or injection, 5000 ppm, 24 hours]

Unscheduled DNA synthesis
Positive results:

CD-1 mice, liver and kidney (Reitz et al.1980) [inhalation; 200 mg/m3, 6 hours]

Genotoxicity and related endpoints: in vitro

Aneuploidy
Positive results:

Saccharomyces cerevisiae,with and without activation (Koch et al. 1988)

Chromosomal aberrations
Positive results:

Chinese hamster lung cells, with activation (Sawada et al. 1987)

Negative results:
Chinese hamster lung cells, without activation (Sawada et al.1987); Chinese hamster fibroblast CHL cells (Ishidate 1983); Chinese hamster DON-6 cells (Sasaki et al. 1980)

Gene conversion
Positive results:

S. cerevisiae,without activation(Koch et al.1988); S. cerevisiae,with activation(Bronzetti et al.1981)

Negative reults:
S. cerevisiae,without activation(Bronzetti et al. 1981); S. cerevisiae, with activation(Koch et al.1988)

Mutagenicity
Positive results:

Salmonella typhimurium BA13/BAL13, with activation (Roldan-Arjona et al.1991)
S. typhimurium TA100, with activation (Bartsch et al. 1975, 1979; Baden et al. 1976, 1978, 1982; Jones and Hathway 1978b; Simmon and Tardiff 1978; Waskell 1978; Oesch et al.1983; Strobel and Grummt 1987; Malaveille et al.1997)
S. typhimurium TA100, without activation (Baden et al. 1976, 1978, 1982; Cerna and Kypenova 1977; Waskell 1978; Strobel and Grummt 1987)
S. typhimurium TA1535, with activation (Baden et al.1977; Jones and Hathway 1978b; Oesch et al.1983)
S. typhimurium TA1535, without activation (Cerna and Kypenova 1977)
S. typhimurium TA1537, with activation (Oesch et al.1983)
S. typhimurium TA1538, without activation (Cerna and Kypenova 1977)
S. typhimurium TA98, with activation (Oesch et al.1983; Strobel and Grummt 1987)
S. typhimurium TA98, without activation (Cerna and Kypenova 1977)
S. typhimurium TA92, with activation (Oesch et al.1983)
S. typhimurium TA97, with activation (Strobel and Grummt 1987)
Escherichia coli K12, with activation (Oesch et al.1983)
E. coli K12, without activation (Greim et al. 1975)
E. coli WP2,with activation (Oesch et al.1983)
S. cerevisiae, with activation (Bronzetti et al.1981; Koch et al.1988);
S. cerevisiae, without activation (Koch et al.1988)
Mouse lymphoma L5178Y T/K +/- cells, with activation (McGregor et al.1991)

Negative results:
S. typhimurium BA13/BAL13, without activation (Roldan-Arjona et al.1991)
S. typhimurium TA100, with activation (Mortelmans et al. 1986)
S. typhimurium TA100, without activation (Bartsch et al. 1975, 1979; Simmon and Tardiff 1978; Oesch et al.1983; Mortelmans et al. 1986)
S. typhimurium TA104, with and without activation(Strobel and Grummt 1987)
S. typhimurium TA1535, with activation (Mortelmans et al. 1986)
S. typhimurium TA1535, without activation (Baden et al.1977; Oesch et al.1983; Mortelmans et al. 1986)
S. typhimurium TA1537, with activation (Mortelmans et al. 1986)
S. typhimurium TA1537, without activation (Oesch et al.1983; Mortelmans et al. 1986)
S. typhimurium TA98, with activation (Mortelmans et al. 1986)
S. typhimurium TA98, without activation (Oesch et al.1983; Mortelmans et al. 1986; Strobel and Grummt 1987)
S. typhimurium TA92, without activation (Oesch et al.1983)
S. typhimurium TA97, without activation (Strobel and Grummt 1987)
E. coli K12, without activation (Oesch et al.1983)
E. coli WP2,without activation (Oesch et al.1983)
Chinese hamster lung V79 cells, hprt locus, with and without activation (Drevon and Kuroki 1979)
Chinese hamster lung V79 cells, ouabain resistance, with and without activation (Drevon and Kuroki 1979)

Sister chromatid exchange
Positive results:

Chinese hamster lung cells, with activation (Sawada et al.1987); Chinese hamster ovary cells (McCarroll et al.1983)

Negative results:
Chinese hamster lung cells, without activation (Sawada et al.1987)

Unscheduled DNA synthesis

Positive results:
Rat, hepatocytes (Costa and Ivanetich 1982)  

Metabolism1,1-DCE is rapidly absorbed following inhalation and oral exposures. The major route of excretion for unchanged 1,1-DCE is through the lung. Intraperitoneal (i.p.) administration of 125 mg/kg 14C-1,1-DCE to mice resulted in the highest concentrations of covalent binding (based on protein content) in the kidney, lung and liver. The covalent binding and cellular damage in kidney, lung and liver correlated with the high concentration of CYP2E1 Oxidation of 1,1-DCE by CYP2E1 should produce three metabolites: 1,1-DCE epoxide, 2-chloroacetyl chloride, and 2,2-dichloroacetaldehyde.The epoxide, and perhaps to a lesser extent the chloroacetaldehyde, are believed to be associated with the tissue reactivity and toxic effects in tissues that ensue after significant depletion of GSH. 1,1-DCE does  not bioaccumulate in tissues to a significant extent. When the inhalation exposure was less than 100 ppm, the estimated amount of epoxide formed was fivefold lower in humans than in rats (US EPA 2002b).
Epidemiology

Cohort of 138 U.S. workers exposed to 1,1-DCE, where vinyl chloride was not used as a copolymer. Twenty-seven workers were lost to follow-up but considered to be alive in the analyses. Fifty-five people had less than 15 years since first exposure, and only five deaths were observed. The authors indicate no finding was statistically attributable to exposure to 1,1-DCE (Ott et al. 1976).

Cohort of 629 males (447 German and 182 foreign workers) employed at two plants in the Federal Republic of Germany that had produced 1,1-DCE since 1955. Vital status was ascertained for 97% of the 447 German workers. Of the 182 foreign workers, 65 had worked for less than one year, and only 24% (44) were traced. Observed deaths were compared with local and regional rates, without making allowance for a latent period. Within the study period (approximately 20 years), 39 deaths were observed, where 57 [local] and 36 [regional] would have been expected. Five cases of lung carcinoma were observed, whereas 3.9 [local] and 2.2 [regional] were expected; this result was not statistically significant. Workers in the factory were also potentially exposed to vinyl chloride and acrylonitrile (Thiess et al. 1979).

The International Agency for Research on Cancer Working Group noted that both Ott et al. (1976) and Thiess et al. (1979) suffered from the limited size of cohorts, the short observation period and the small numbers of deaths from specific causes. The fact that no allowance was made for latent period may have resulted in an overestimation of the expected numbers and an underestimation of risk.

In an attempt to identify the specific exposure associated with an excess lung cancer risk noted previously in a U.S. synthetic chemicals plant, Waxweiler et al. (1981) considered 19 chemicals, one of which was 1,1-DCE. Company personnel assigned a rank of exposure to 1,1-DCE (from 0 to 5) to each job in the plant for each year since its opening in 1942. These exposure data were then linked with detailed, individual work histories to obtain an individual estimate for each of the 4806 male workers employed at the plant. The doses calculated were the product of the exposure rank of the job and the number of days worked at that job. Cumulative doses for 45 workers who had died of lung cancer during the study period of 1942–1973 were then compared to expected doses based on the cumulative exposure of subcohorts of fellow workers matched individually to the cases by year of birth and age of hire into the plant. This comparison failed to suggest any specific association between exposure to 1,1-DCE in the plant and excess lung cancer risk.

[1] LC50 = median lethal concentration; LD50 = median lethal dose; LOEC = lowest-observed-effect concentration; LOEL = lowest-observed-effect level; LOAEL = lowest-observed-adverse-effect level; LOAEC = lowest-observed-adverse-effect concentration

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Appendix 4: Robust Study Summaries for Ecotoxicity Studies

Table A6. Robust Study Summary – Aquatic Toxicity – Alga
No.ItemWeightYes/NoSpecify
1Reference: Brack W, Rottler H. 1994. Toxicity testing of highly volatile chemicals with green algae – a new assay. Environ Sci Pollut Res 1(4):223–228.
2Substance identity: 75-35-4n/a[1]Y 
3Substance identity: 1,1-dichloroethenen/aYThe test substance name
4Chemical composition of the substance2YThe test substance name
5Chemical purity1Y> 99%
6Persistence/stability of test substance in aquatic solution reported?1YData are available but not included in the study. See Table 4a
Method
7Reference1NNew approach test
8OECD, EU, national, or other standard method?3YBased on OECD tests
9Justification of the method/protocol if a non-standard method was used2Y 
10GLP (good laboratory practice)3Nn/a
Test organism
11Organism identity: Chlamydomonas reinhardtiin/aYGreen alga
12Latin or both Latin and common names reported?1YGreen alga
13Life cycle age / stage of test organism1 n/a
14Length and/or weight1 n/a
15Sex1 n/a
16Number of organisms per replicate1 n/a
17Organism loading rate1 NA[2]
18Food type and feeding periods during the acclimation period1YLight, CO2 source
Test design / conditions
19Test type (acute or chronic)n/aYAcute
20Experiment type (laboratory or field)n/aYLab
21Exposure pathways (food, water, both)n/aYWater
22Exposure durationn/aY72 hrs
23Negative or positive controls (specify)1YNegative
24Number of replicates (including controls)1Y 
25Nominal concentrations reported?1N 
26Measured concentrations reported?3Y 
27Food type and feeding periods during the long-term tests1 n/a
28Were concentrations measured periodically (especially in the chronic test)?1Y 
29Were the exposure media conditions relevant to the particular chemical reported? (e.g. for the metal toxicity – pH, DOC/TOC, water hardness, temperature)3Y 
30Photoperiod and light intensity1Y 
31Stock and test solution preparation1Y 
32Was solubilizer/emulsifier used if the chemical was poorly soluble or unstable?1  n/a
33If solubilizer/emulsifier was used, was its concentration reported?1  n/a
34If solubilizer/emulsifier was used, was its ecotoxicity reported?1  n/a
35Monitoring intervals (including observations and water quality parameters) reported?1Y 
36Statistical methods used1Y 
Information relevant to the data quality
37Was 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/aY 
38Was the test organism relevant to the Canadian environment?3Y 
39Were the test conditions (pH, temperature, DO, etc.) typical for the test organism?1Y 
40Do system type and design (static, semi-static, flow-through; sealed or open; etc.) correspond to the substance's properties and organism's nature/habits?2Y 
41Was pH of the test water within the range typical for the Canadian environment (6 to 9)?1Y 
42Was temperature of the test water within the range typical for the Canadian environment (5 to 27°C)?1Y 
43Was toxicity value below the chemical’s water solubility?3Y 
Results
44Toxicity values (specify endpoint and value)n/aEC10, EC50Growth
45Other endpoints reported - e.g. BCF/BAF, LOEC/NOEC (specify)?n/aN 
46Other adverse effects (e.g. carcinogenicity, mutagenicity) reported?n/aN 
47Score: ... %35/40 = 87.5
48EC reliability code:1
49Reliability category (high, satisfactory, low):High Confidence
50Comments 
[1] n/a – not applicable.
[2] NA – not available.
Table A7. Robust Study Summary – Terrestrial Toxicity – Mammals
No.ItemWeightYes/NoSpecify
1Reference: Prendergast J, Jones R, Jenkins Jr L, Siegel J. 1967. Effects on experimental animals of long-term inhalation of trichloroethylene, carbon tetrachloride, 1,1,1-trichloroethane, dichlorofluoromethane and 1,1-dichloroethylene. Toxicol Appl Phamacol 10:270–289.
2Substance identity: CAS RNn/a[1]N 
3Substance identity: 1,1-dichloroethenen/aYThe test substance name
4Chemical composition of the substance2YThe test substance name
5Chemical purity1YReagent grade
6Persistence/stability of test substance?1YData are available but not included in the study. See Table 4a
Method
7Reference1Y 
8OECD, EU, national, or other standard method?3N 
9Justification of the method/protocol if a non-standard method was used2Y 
10GLP (good laboratory practice)3 NA[2]
Test organism
11Organism identity: rats (Sprague-Dawley or Long-Evans), guinea pigs (Hartley), squirrel monkeys, rabbits (New Zealand albino), beagle dogsn/aY 
12Latin or both Latin and common names reported?1N 
13Life cycle age / stage of test organism1N 
14Length and/or weight1YTrends noted
15Sex1 n/a to study
16Number of organisms per replicate1Y 
17Organism loading rate1Y 
18Food type and feeding periods during the acclimation period1Y 
Test design / conditions
19Test type (acute or chronic)n/aY90-day inhalation or "work week" inhalation
20Experiment type (laboratory or field)n/aYLab
21Exposure pathways (food, water, both)n/aYAir
22Exposure durationn/aY90-day or 5-day
23Negative or positive controls (specify)1YNegative
24Number of replicates (including controls)1Y 
25Nominal concentrations reported?1N 
26Measured concentrations reported?3YContinuous
27Food type and feeding periods during the long-term tests1Y 
28Were concentrations measured periodically (especially in the chronic test)?1YContinuous
29Were the exposure media conditions relevant to the particular chemical reported? (e.g. for the metal toxicity – pH, DOC/TOC, water hardness, temperature)3Y 
30Photoperiod and light intensity1 n/a to study 
31Stock and test solution preparation1Y 
32Was solubilizer/emulsifier used if the chemical was poorly soluble or unstable?1 n/a
33If solubilizer/emulsifier was used, was its concentration reported?1 n/a
34If solubilizer/emulsifier was used, was its ecotoxicity reported?1 n/a
35Monitoring intervals (including observations and water quality parameters) reported?1Y 
36Statistical methods used1Y 
Information relevant to the data quality
37Was 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/aY 
38Was the test organism relevant to the Canadian environment?3Y 
39Were the test conditions (pH, temperature, DO, etc.) typical for the test organism?1Y 
40Do system type and design (static, semi-static, flow-through; sealed or open; etc.) correspond to the substance's properties and organism's nature/habits?2Y 
41Was pH of the test water within the range typical for the Canadian environment (6 to 9)?1 n/a in air
42Was temperature of the test water within the range typical for the Canadian environment (5 to 27°C)?1 n/a in air
43Was toxicity value below the chemical’s water solubility?3 n/a in air
Results
44Toxicity values (specify endpoint and value)n/aY90-day LC50
45Other endpoints reported - e.g. BCF/BAF, LOEC/NOEC (specify)?n/aYNOEL = 101 mg/m3; LOEL = 189 mg/m3
46Other adverse effects (e.g. carcinogenicity, mutagenicity) reported?n/aN 
47Score: ... %30/36 = 83.3
48EC reliability code:1
49Reliability category (high, satisfactory, low):High Confidence
50Comments 
[1] n/a – not applicable.
[2] NA – not available.

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