1,1,2,2-Tetrachloroethane - PSL1

2.0 Summary of Information Critical to Assessment of "Toxic"

2.1 Identity, Properties, Production, and Uses

1,1,2,2-Tetrachloroethane (CAS # 79-34-5) is a colourless, nonflammable liquid at room temperature, having the molecular formula Cl₂CHCHCI₂ (Verschueren, 1983). It is a highly volatile, synthetic chemical having a relatively high vapour pressure (0.65 kPa at 20°C ) and water solubility (2900 mg/L at 20°C), and low partition coefficients (log K_oc= 1.66 and log K_ow = 2.39) (Verschueren, 1983; Chiou et al., 1979; Hansch and Leo, 1985).

1,1,2,2-Tetrachloroethane is produced by direct chlorination or oxychlorination of ethylene and is not usually purified but rather is used as an intermediate in the production of other chlorinated compounds (Archer, 1979). This chemical is detected and quantified in environmental samples by gas chromatography using either electron capture or mass spectrometric detectors.

1,1,2,2-Tetrachloroethane has not been produced in Canada since early 1985 (CPI, 1991a). At that time, 1,1,2,2-tetrachloroethane was manufactured at a facility in Shawinigan, Quebec for use as an intermediate in the production of trichloroethylene and tetrachloroethylene. These latter two substances have not been manufactured in Canada since 1986 and 1992, respectively (CPI, 1990; Dow Chemical Canada News Release, 1992)

Globally, 1,1,2,2-tetrachloroethane is used primarily as a feedstock in the production of tri- and tetra-chloroethylene (Archer, 1979). Small amounts of 1,1,2,2-tetrachloroethane are also used as specialty solvents.

2.2 Entry into the Environment

Since 1,1,2,2-tetrachloroethane is no longer produced in, or imported into Canada (CPI, 1991a), it is unlikely that any additional entry of this substance to the Canadian environment will occur through its production and use.

The manufacture of other chlorinated hydrocarbons, specifically vinyl chloride monomer (VCM), ethylene dichloride (EDC), and methyl chloroform, also generates detectable quantities of 1,1,2,2-tetrachloroethane as a by-product (U.S. EPA, 1981) and represents an indirect source of 1,1,2,2-tetrachloroethane release to the environment.

There is only one Canadian manufacturer of VCM and EDC, with plants located in Fort Saskatchewan, Alberta and in Sarnia, Ontario. Based on a Canadian VCM and EDC production of 416.8 and 922 kt, respectively, for 1990 (CPI, 1991b; CPI, 1991c), and a waste-to-product ratio of 0.008 (Tsang and Bisson, 1992), the total waste generated by these plants would be 10.7 kt. An analysis of the combined liquid waste streams from both the VCM plant and the EDC plant revealed a 1,1,2,2-tetrachloroethane content of 23% by weight, or 2.5 kt of 1,1,2,2- tetrachloroethane (Tsang and Bisson, 1992). These waste products are usually treated to recover the organic compounds present and then incinerated (McPherson et al., 1979). Since there is no market for 1,1,2,2-tetrachloroethane, however, no recovery process for 1,1,2,2-tetrachloroethane is undertaken (Dow Chemical Canada Inc., 1992). Assuming an incineration destruction efficiency of 99.99% (U.S. EPA, 1986), approximately 0.246 t (or 246 kg) of 1,1,2,2-tetrachloroethane from VCM and EDC wastes are emitted to the atmosphere every year.

Waste materials from the manufacture of methyl chloroform also contain small amounts of 1,1,2,2-tetrachloroethane. Estimates of quantities released from this source are not available; however, as of June 1992, methyl chloroform is no longer manufactured in Canada (Dow Chemical Canada Inc., 1992).

1,1,2,2-Tetrachloroethane has also been found to enter the environment in air emissions and leachates from waste disposal sites (Lesage et al., 1990; Ghassemi et al., 1984; Harkov et al., 1985; Shah and Singh, 1988). Furthermore, 1,1,2,2-tetrachloroethane may be entering the Canadian environment by long- range atmospheric transport from other countries that continue to produce tri- and tetra-chloroethylene, vinyl chloride, and ethylene dichloride (SRI, 1988) and release 1,1,2,2-tetrachloroethane as a by-product (see Subsection 2.3.1). The contribution of these sources to the total release of 1,1,2,2-tetrachloroethane to the Canadian environment could not be estimated.

2.3 Exposure-related Information

2.3.1 Fate

Based on its vapour pressure, 1,1,2,2-tetrachloroethane is expected to exist entirely in the vapour phase in ambient air (Verschueren, 1983; Eisenreich et al., 1981). The principal removal process of 1,1,2,2-tetrachloroethane from the troposphere is expected to be photo-oxidation (Singh et al, 1982), although studies of competing fate processes have not been identified.

The calculated reaction rates of 1,1,2,2-tetrachloroethane with hydroxyl (OH) radicals derived from the Structure-Activity Relations (SAR) model of Atkinson (1987) [3 x 10^-13 cm³/(mol·s)] and from the model of Nimitz and Skaggs (1992) [5.4 x 10^-13 cm³/(mol·s)] are similar to the experimental value determined by Qiu et al. (1992) [2.3 x 10^-13 cm³/(mol·s)]. Therefore, using these reaction rates and assuming an atmospheric OH concentration representative of a moderately polluted area, the estimated atmospheric lifetime of 1,1,2,2-tetrachloroethane is between 43 calculated and 100 experimental days (Finlayson-Pitts and Pitts, 1986). Since the atmospheric lifetime of 1,1,2,2-tetrachloroethane is greater than one month, there is potential for long-range transport (LRT) of this compound. Further evidence of long-range transport is provided in a 1985 monitoring study by Class and Ballschmiter (1986) who detected 1,1,2,2-tetrachloroethane in the lower troposphere over the northern Atlantic Ocean.

In the stratosphere, 1,1,2,2-tetrachloroethane undergoes photolysis to produce chlorine radicals that may react with ozone (Callahan et al, 1979; Spence and Hanst, 1978). However, a simple method developed by Nimitz and Skaggs (1992), indicates that 1,1,2,2-tetrachloroethane is not expected to contribute significantly to the depletion of the stratospheric ozone layer. Based on either the experimental (Qiu et al., 1992) or predicted (Atkinson, 1987; Nimitz and Skaggs, 1992) rates of reaction between OH and 1,1,2,2-tetrachloroethane, the ozone depletion potential (ODP) for 1,1,2,2-tetrachloroethane is very much less than 0.001 relative to the chlorofluorocarbon, CFC- 11.

Volatilization is the major removal process of 1,1,2,2-tetrachloroethane from the aquatic environment (Dilling et al., 1975; Lyman et al., 1982). Based on a calculated Henry's Law constant of 47.6 Pa (Mackay and Shiu, 1981) and a modeling scenario representing a 1-m deep river flowing 1 m/s with a wind speed of 3 m/s at 25°C (Mackay and Leinonen, 1975), the volatilization half-life of 1,1,2,2-tetrachloroethane was estimated to be 6.2 hours (Lyman et al., 1982).

Neither hydrolysis nor biodegradation is considered a significant removal process for 1,1,2,2-tetrachloroethane at concentrations found in ambient surface waters; however, on the basis of experimental data, hydrolysis and biodegradation play a role in removing 1,1,2,2-tetrachloroethane from groundwater (Hallen et al., 1986; Haag and Mill, 1988; Agency for Toxic Substances and Disease Registry, 1989). When the hydrolysis rate was measured under experimental conditions similar to groundwater (e.g., higher ionic strength), the half-lives at pH 6.05, 7.01, and 9.0 were reported to be 573 days, 36 days, and 6.6 to 12.8 hours, respectively (Haag and Mill, 1988). Six weeks of simulated anaerobic growing conditions of landfills resulted in the dechlorination of 1,1,2,2-tetrachloroethane to lesser chlorinated ethanes and to chloroethenes including vinyl chloride (Hallen et al., 1986). Since anaerobic biodegradation depends on the availability and acclimation of micro-organisms capable of biodegrading 1,1,2,2-tetrachloroethane, it is, therefore, a site-specific process and as such would be an important degradation process where 1,1,2,2-tetrachloroethane or related chlorinated compounds have been discharged over time (Agency for Toxic Substances and Disease Registry, 1989).

In an anoxic sediment-water system (pH unreported), the half-life of 1,1,2,2-tetrachloroethane due to both chemical hydrolysis and biotic degradation was 6.6 days (Jafvert and Wolfe, 1987). In contrast, the hydrolytic half-life of 1,1,2,2-tetrachloroethane in sediment-extracted pore water was 29 days in a laboratory study where 1,1,2,2-tetrachloroethane was in contact with low-carbon sediment at a pH of 7 and at 25°C (commonly associated with groundwater) (Haag and Mill, 1988).

1,1,2,2-Tetrachloroethane is not expected to adsorb appreciably to soil, suspended solids, or sediment, based on its partition coefficients. This is confirmed by two partitioning experiments in which the sorption coefficient of 1,1,2,2-tetrachloroethane in a silt loam soil and in a low organic carbon soil were found to be 46 and 0.05, respectively (Chiou et al., 1979; Whitehead, 1987). 1,1,2,2-Tetrachloroethane would be expected to leach readily from soil surfaces into the subsurface soil and groundwater (Agency for Toxic Substances and Disease Registry, 1989). Sorption may be significant in dry soils having a high clay content (Agency for Toxic Substances and Disease Registry, 1989). When subsurface soil conditions (anaerobic, methanogenic) were simulated in a laboratory with a continuous influent concentration of 27 µg/L for four months, 97% of the 1,1,2,2-tetrachloroethane was dehydrohalogenated to 1,1,2-trichloroethane (Bouwer and McCarty, 1983).

1,1,2,2-Tetrachloroethane has a low bioaccumulation potential. A measured bioconcentration factor (BCF) of 8 and a depuration half-life in tissues of less than one day were observed in freshwater bluegill (Lepomis macrochirus) exposed to 9.6 µg/L of 1,1,2,2-tetrachloroethane for 14 days (Barrows et al., 1980). The experimental BCF is consistent with the calculated BCF of 21 to 72 estimated by regression analysis with K_ow (Veith et al., 1980). Similarly, in another study in which rainbow trout (Oncorhynchus mykiss) were exposed to up to 1 mg/L of 1,1,2,2-tetrachloroethane, 1,1,2,2-tetrachloroethane was found to partition preferentially to fatty tissue by approximately 8 times that in blood; exposed trout were close to steady-state in 48 hours (Nichols et al., 1991).

2.3.2 Concentrations

1,1,2,2-Tetrachloroethane was detected in Canadian ambient and indoor air, surface waters, and groundwaters but not detected in food. No studies were identified that measured 1,1,2,2-tetrachloroethane in human breast milk, precipitation, sediments, soil, and aquatic or terrestrial biota in Canada.

Based on preliminary results of a pilot study, the mean concentration of 1,1,2,2-tetrachloroethane in indoor air in approximately 750 homes from 10 provinces across Canada in 1991 was 1.8 µg/m³, with a maximum single value of 11 µg/m³ (Otson et al., 1992).

Environment Canada has been monitoring volatile organic chemicals in the ambient air of 12 Canadian cities since 1989 and has detected 1,1,2,2-tetrachloroethane at all sites with a detection frequency of approximately 50%. In 1989 and 1990, the mean concentrations at these Canadian sites ranged from non-detectable (below 0.1 µg/m³) to 0.25 µg/m³, with a maximum single value of 0.86 µg/m³ in Ottawa, Ontario (Environment Canada, 1992). In contrast, 1,1,2,2-tetrachloroethane was infrequently detected (18%) above the detection limit of 0.1 µg/m³ in 385 samples from several cities in Ontario between 1989 and 1991 (OME, 1992a; 1992b; 1992c). In addition, a report to the International Joint Commission focused on the ambient air quality of five sites in the vicinity of the Ontario/Michigan border during 1987 and 1988 and found only one sample (N=1825) above the minimum detectable level of 0.02 µg/m³ at a concentration of 0.76 µg/m³ (D-W/PH-S APAB, 1990).

1,1,2,2-Tetrachloroethane was not detected in more than 2000 samples of drinking water in Ontario in 1991 (detection limit 0.05 µg/L) (Lachmaniuk, 1991) or in 171 samples of drinking water from across New Brunswick in 1990 (detection limit 1.0 µg/L) (Ecobichon and Allen, 1990). It was found only once in treated drinking water in a 1979 survey of 30 potable water treatment facilities across Canada at a concentration of 1 µg/L (quantitation limit 1 µg/L) (Otson et al., 1982).

In 1985, numerous volatile chemicals were monitored in the St. Clair River and 1,1,2,2-tetrachloroethane was identified downstream of Sarnia, Ontario (COARGLWQ, 1986). The levels of 1,1,2,2-tetrachloroethane ranged from non-detectable (1.0 µg/L) to 4.0 µg/L for surface waters, and to 2.0 µg/L for bottom waters. In a 1981 survey of the Welland River in Ontario, concentrations ranged from non-detectable (0.005 µg/L) to 0.06 µg/L (Kaiser and Comba, 1983).

1,1,2,2-Tetrachloroethane is not frequently detected in groundwater and appears primarily in leachates from hazardous waste sites. Laboratory organic solvents were the primary wastes deposited in a Gloucester, Ontario landfill site and, although the site has been abandoned since 1980, concentrations of 1,1,2,2-tetrachloroethane in groundwater were reported to range between 5 and 15 µg/L in 1988 (Lesage et al., 1990). A hazardous waste site in Ville Mercier, Quebec had a maximum 1,1,2,2-tetrachloroethane concentration of 1600 µg/L in groundwater in 1988 (Pakdel et al., 1992).

1,1,2,2-Tetrachloroethane has not been detected in two surveys of samples of 34 food groups in Canada (detection limits of 1.0 µg/L for liquids in both surveys, and 50 and 5 µg/kg for solid food in the first and second survey, respectively) (Enviro-Test Laboratories, 1991; 1992), or in a survey of 231 food items in the U.S. (quantitation limits of 13 or 20 µg/kg) (Daft, 1988). No data were identified on levels of 1,1,2,2-tetrachloroethane in human breast milk in Canada or elsewhere.

2.4 Effects-related Information

2.4.1 Experimental Animals and In Vitro

Based on limited data, 1,1,2,2-tetrachloroethane does not appear to be highly acutely toxic in experimental species. Hepatic effects, including congestion, fatty degeneration, histological changes, alterations in levels of enzymes, and increased DNA synthesis have been reported in rodents following short-term inhalation or ingestion of 1,1,2,2-tetrachloroethane in the few available, principally limited, studies (Horiuchi et al., 1962; Gohlke and Schmidt, 1972; Schmidt et al., 1972; Hanley et al., 1988).

Only a few limited studies have been identified on the effects in experimental animals following subchronic exposure to 1,1,2,2-tetrachloroethane. Ingestion of up to 316 mg/[kg (b.w.)·day] had no effects on body weight gain or mortality in mice, while doses of 100 (females) or 178 (males) mg/[kg (b.w.)·day] and above resulted in decreased body weight gain in rats in subchronic studies preliminary to longer term bioassays (no other endpoints appear to have been examined) (National Cancer Institute, 1978).

Histopathological damage was reported in the liver, kidney, testicles, and thyroid gland of rats administered oral doses of 3.2 to 50 mg/[kg (b.w.)·day] of 1,1,2,2-tetrachloroethane for periods ranging from 2 to 150 days (Gohlke et al., 1977), although the poor documentation of results in this study precludes validation of an effect level. Exposure to 50 mg/m³ for approximately 5 weeks resulted in neurological effects, and alterations in biochemical parameters and organ weights in rats, although no "morphological changes" were noted upon examination (the nature and extent of which were unspecified) (Schmidt et al., 1975). Hepatic effects, including a transient increase in DNA synthesis, reversible histopathological changes, and an increase in relative liver weight were reported in female Sprague-Dawley rats exposed to 560 mL/m³ (890 000 mg/m³) for 15 weeks (Truffert et al., 1977); however, the results of this study are inconsistent with those of other investigations, as the concentration to which the animals were exposed was extremely high, and would likely have been lethal.

The chronic toxicity of 1,1,2,2-tetrachloroethane has not been extensively investigated; available studies are not adequate to determine an effect level for non-neoplastic effects. An increase in the incidence of hepatocellular carcinomas was reported in male and female B6C3F₁ mice administered time-weighted average daily doses of 142 or 284 mg/[kg (b.w.)·day] of 1,1,2,2-tetrachloroethane in corn oil by gavage for 78 weeks (1/18, 13/50, and 44/49 in males, and 0/20, 30/48, and 43/47 in females in the vehicle controls, low and high dose group, respectively) (National Cancer Institute, 1978). There were no significant increases in the incidence of any type of tumor in male or female Osborne-Mendel rats similarly administered 62 or 108 mg/[kg (b.w.)·day] and 43 or 76 mg/[kg (b.w.)·day] of 1,1,2,2-tetrachloroethane, respectively, for 78 weeks, although there were two males with hepatocellular carcinomas and one with a hepatic neoplastic nodule in the high dose group (National Cancer Institute, 1978). Intraperitoneally administered 1,1,2,2-tetrachloroethane did not increase the number of pulmonary adenomas per animal in a limited bioassay designed to investigate the potential of the compound to induce these tumors in mice; however, mortality was high in this study (Theiss et al., 1977).

Increased adrenocorticotropic hormone activity of the hypophysis was observed in rats exposed to 13.3 mg/m³ of 1,1,2,2-tetrachloroethane by inhalation for up to 325 days; there was also a reversible decrease in body weight, an increase in lipid content of the liver, and alterations in hematological parameters, which were only significantly different from controls at one point in time during the study (Schmidt et al., 1972). However, histopathological effects were apparently not examined in this study.

1,1,2,2-Tetrachloroethane acted as a potent promoter in rats initiated with diethylnitrosamine in an initiation/promotion bioassay in rats (Milman et al., 1988; Story et al., 1986). Although inadequately tested in vivo (results have been negative or equivocal), some potential for genotoxicity of 1,1,2,2-tetrachloroethane has been demonstrated in vitro, as mixed results have been reported for induction of gene mutation and conversions in prokaryotic systems in the presence of metabolic activation, and chromosomal aberrations and cell transformation in mammalian cells. 1,1,2,2-tetrachloroethane is reported to bind to cellular macromolecules, including DNA, RNA and proteins of several organs in rodents following in vivo exposure (Colacci et al., 1987; Mitoma et al., 1985; Hanley et al., 1988), although it has been suggested that this results from uptake of carbon atoms during normal biosynthetic pathways (Hanley et al., 1988).

Liver tumors induced by some chemicals in mice appear to be of limited relevance for assessing hazard to humans. However, little information has been identified on the mechanism(s) of liver tumor induction in mice exposed to 1,1,2,2-tetrachloroethane.

Although several of the metabolites of 1,1,2,2-tetrachloroethane, including trichloroethylene, tetrachloroethylene, trichloroacetic acid, and dichloroacetic acid, have been demonstrated to be carcinogenic in experimental animals (e.g., National Toxicology Program, 1986; 1988; 1990; National Cancer Institute, 1977; Maltoni et al., 1986; 1988; Herren-Freund et al., 1987; Bull et al., 1990; DeAngelo et al., 1991), mechanistic studies have been conducted which indicate that some of the tumors induced by these substances may not be relevant to humans, or at least that humans are less susceptible. Paolini et al., (1992) have suggested that the formation of free radicals produced by reductive metabolism of 1,1,2,2-tetrachloroethane observed in mice administered 300 or 600 mg/kg (b.w.) of the compound by intraperitoneal injection, along with marked changes in heme turnover and activities of hepatic microsomal oxygenases, may contribute to hepatotoxicity through lipid peroxidation. The metabolites trichloroacetic acid and dichloroacetic acid have been demonstrated to induce lipid peroxidation to a similar degree in mice and rats, with the latter having greater lipoperoxidative activity (Larson and Bull, 1992). Such damage may play a role in the aetiology of liver tumors observed in mice. Bull (personal communication, 1992) has suggested that the 1,1,2,2-tetrachloroethane-induced liver tumors in mice are likely due to the ability of dichloroacetic acid (the major metabolite of 1,1,2,2-tetrachloroethane) to cause hepatic damage distinct from peroxisome proliferation, such as focal necrosis associated with intense cellular proliferation (Larson and Bull, 1992). It has also been hypothesized that a compensatory increase in hepatic DNA synthesis following hepatic injury or altered homeostasis may act in concert with genetic predisposition in B6C3F₁ mice to enhance the rate of spontaneous tumor formation in this strain (Hanley et al., 1988).

Available data are insufficient to evaluate the effect of exposure to 1,1,2,2-tetrachloroethane on the reproduction or development of experimental animals. Histological changes in the testes have been reported in rats administered 8 mg/[kg b.w.)·day] in peanut oil by gavage (Gohlke et al., 1977), but not consistently in rats exposed to 13.3 mg/m³ (Schmidt et al., 1972; Gohlke and Schmidt, 1972), or a single monkey exposed to 6980 to 27 920 mg/m³ (Horiuchi et al., 1962), although it should be noted that the experimental protocol and results were poorly documented in these studies. Immunological effects, the significance of which is unclear, have been reported in rabbits following inhalation of 10 or 100 mg/m³ of 1,1,2,2-tetrachloroethane for 8 months (Shmuter, 1977; Kulinskaya and Verlinskaya, 1972). Neurotoxic effects have been noted in several species following acute or short-term exposure to 1,1,2,2-tetrachloroethane, e.g., at concentrations as low as 200 ppm (1396 mg/m³) for 6 hours (Horvath and Frantik, 1973).

2.4.2 Humans

No significant increase in mortality due to any specific cause was noted in a limited epidemiological investigation in a population of 1099 men exposed to unknown concentrations of tetrachloroethane (probably the 1,1,2,2-isomer), although non-statistically significant increases in mortality due to cancers of the genital organs, leukemia and aleukemia, and other lymphatic cancers were reported (Norman et al., 1981). The prevalence of tremors was reported to increase with airborne concentration of 1,1,2,2-tetrachloroethane (up to 98 ppm or 684 mg/m³) in a group of 380 workers in India exposed for varying durations, although no information was presented on the prevalence of these signs in an unexposed group (Lobo-Mendonca, 1963).

2.4.3 Ecotoxicology

Although terrestrial organisms would be the most likely of environmental biota to be exposed to 1,1,2,2-tetrachloroethane, ecotoxicological studies were found only for aquatic organisms.

Toxicity bioassays were conducted by Blum and Speece (1991) on three groups of environmental bacteria: methanogens (anaerobes from an enrichment culture maintained for >10 years); aerobic heterotrophs (seed bacteria obtained from the mixed liquor of an activated sludge wastewater treatment plant); and Nitrosomonas (seed bacteria obtained from the mixed liquor of an activated sludge plant that treats meat-packing, rendering, and hide-curing wastewater). Inhibition of gas production (methanogens), oxygen uptake (aerobic heterotrophs), and ammonia consumption (Nitrosomonas) were the endpoints used in this study to evaluate toxicity. Varying degrees of sensitivities were exhibited; however, Nitrosomonas were more sensitive than methanogens (IC₅₀ value of 4.1 mg/L), and significantly more sensitive than aerobic heterotrophs(IC₅₀ 130 mg/L of 1,1,2,2-tetrachloroethane), having an IC₅₀ value of 1.4 mg/L.

Based on bioluminescence, the five-minute IC₅₀ was 5.4 mg/L of 1,1,2,2- tetrachloroethane in a Microtox test using Photobacterium phosphoreum (Blum and Speece, 1991).

Only two acute toxicity studies on freshwater invertebrates were identified, both of which used first instar Daphnia magna (<24 hours old) under static test conditions. Unfed and fed D. magna had similar measured 48-h LC ₅₀ values of 62 and 57 mg/L of 1,1,2,2-tetrachloroethane, respectively (Richter et al., 1983). Using complete immobilization as the endpoint, the 48-h EC₅₀ values were 23 and 25 mg/L, for unfed and fed D. magna, respectively. LeBlanc (1980) conducted a similar test at 22°C and reported a nominal 24-h and 48-h LC ₅₀ value and corresponding 95% confidence limits of 18 (12 to 24) and 9.3 (6.8 to 13) mg/L, respectively.

Chronic 28-day toxicity tests were conducted on Daphnia magna to determine the lowest-observable-effect-concentration (LOEC) and the no-observable-effect-concentration (NOEC) based on reproductive impairment. The measured 28-day LOEC and NOEC values were 14.4 and 6.9 mg/L of 1,1,2,2-tetrachloroethane under flow-through conditions (Richter et al., 1983). Occasionally, the animals were observed in a comatose state, demonstrating the narcotic properties of 1,1,2,2-tetrachloroethane.

Numerous acute toxicity studies have been conducted on a variety of freshwater fish species and, in general, 96-h LC ₅₀ values were very similar. The response of 30-day-old fathead minnows (Pimephales promelas) to acute exposures of 1,1,2,2-tetrachloroethane was investigated by Veith et al. (1983), Walbridge et al. (1983), and Geiger et al. (1985). Under flow-through conditions, the measured 96-h LC₅₀ s were found to be 20.3, 20.4, and 20.3 mg/L (Veith et al., 1983; Walbridge et al., 1983; Geiger et al., 1985). The acute toxicity of 1,1,2,2-tetrachloroethane to juvenile (2 to 4 month) flagfish (Jordanella floridae) was investigated by the Aquatic Toxicity Research Group (ATRG, 1988) and then repeated by Smith et al. (1991) using both flow-through and static-renewal test systems. The measured 96-h LC₅₀ for the flow-through toxicity test was 18.5 mg/L of 1,1,2,2-tetrachloroethane; the nominal LC₅₀ value in a static-renewal 96-h toxicity test was 26.8 mg/L.

No valid acute toxicity studies of marine fish were identified.

Chronic toxicity studies under flow-through test conditions were conducted on the early life-stages of flagfish (Jordanella floridae) by ATRG (1988) and then later repeated by Smith et al. (1991). Egg hatchability was unaffected at a measured 1,1,2,2-tetrachloroethane concentration of 22.0 mg/L, the highest concentration tested in both studies. The measured LOEC for reduced 10-day larval survival was 10.6 and 7.2 mg/L and the LOEC for 28-day juvenile survival was 11.7 and 8.5 mg/L (ATRG, 1988; Smith et al., 1991). The effects of 1,1,2,2-tetrachloroethane on the growth of 1-week-old fry over a 28-day exposure period were not statistically significant, even at the highest concentration tested (11.7 mg/L).

No studies were identified on the effects on wild birds or mammals. The limited number of toxicity studies involving laboratory mammals were not used to extrapolate to wildlife as the endpoints chosen were considered insufficient to assess potential risks to wildlife populations.