1. Chemical and Physical Data

1.2. Structural and molecular formulae and molecular weight

2. Production, Use, Occurrence and Analysis

2.1. Production and use

(a) Production

1,1,2-Trichloroethane is produced in the USA by the chlorination of ethylene (see IARC, 1987a). In a two-stage manufacturing process, this initially yields 1,2-dichloroethane (see IARC, 1987b); subsequent chlorination yields 1,1,2-trichloroethane and hydrochloric acid. In an alternative production method, ethylene is combined with hydrochloric acid and oxygen at 280–370 °C on a catalyst of cupric chloride and potassium chloride to yield 1,1,2-trichloroethane and other chlorinated ethanes (Reed et al., 1988). 1,1,2-Trichloroethane has also been made by the chlorination of vinyl chloride (see IARC, 1987c) in a liquid phase at 300–320°C (Thomas et al., 1982).

There is only one producer in the USA, with an annual production estimated to be 186 000 tonnes (Reed et al., 1988). 1,1,2-Trichloroethane is also produced by one company each in France and the UK (Chemical Information Services Ltd, 1988).

(b) Use

Over 95% of the 1,1,2-trichloroethane produced in the USA is used as an intermediate in the production of vinylidene chloride (see IARC, 1987d). Vinylidene chloride is made by dehydrochlorination of 1,1,2-trichloroethane with an aqueous suspension of calcium hydroxide at about 320°C or with lime or sodium hydroxide (Wiseman, 1972; Reed et al., 1988). 1,1,2-Trichloroethane has two minor uses: as a solvent for the coating laid down on films and as a chemical intermediate or process solvent in pharmaceutical manufacture. It has been used as a solvent for fats, oils, waxes and resins and, in small amounts, as a solvent for chlorinated rubber and adhesives (US Environmental Protection Agency, 1980; Sax & Lewis 1987; Strobel & Grummt, 1987).

(c) Regulatory status and guidelines

Occupational exposure limits and guidelines for 1,1,2-trichloroethane are presented in Table 1.

Table 1.

Occupational exposure limits and guidelines for 1,1,2-trichloroethane.

2.3. Analysis

Selected methods for the analysis of 1,1,2-trichloroethane in air and water are identified in Table 2. The US Environmental Protection Agency methods for analysing water (Methods 8010 and 8240) have also been applied to liquid and solid wastes. Volatile components of solid-waste samples are first extracted with methanol prior to purge-and-trap concentration and analysis by gas chromatography-electrolytic conductivity detection (Method 8010) or gas chromatography- mass spectrometry (Method 8240). The detection limit using Method 8010 is 0.02 μg/l, and the practical quantification limit using Method 8240 is 5 μg/l for groundwater and 5 μg/kg for soil/sediment samples (US Environmental Protection Agency, 1986a,b). Method 624 has also been adapted to the analysis of 1,1,2-trichloroethane in fish, with an estimated detection limit of 10 μg/kg (Easley et al.,1981).

Table 2.

Methods for the analysis of 1,1,2-trichloroethane.

3. Biological Data Relevant to the Evaluation of Carcinogenic Risk to Humans

3.1. Carcinogenicity studies in animals (Table 3)

Table 3.

Summary of carcinogenicity studies of 1,1,2-trichloroethane in experimental animals.

(a) Oral administration

Mouse: Groups of 50 male and 50 female B6C3F₁ mice, five weeks of age, received technical-grade 1,1,2-trichloroethane (one batch; purity, 99, 91 and 95% in three analyses over a one-year period [impurities unspecified]) in corn oil by gavage on five consecutive days per week for 78 weeks. Low-dose and high-dose animals received, respectively, 150 and 300 mg/kg bw per day for eight weeks and then 200 and 400 mg/kg bw per day for 70 weeks, followed by 12–13 weeks without treatment, after which the experiment was terminated. The time-weighted average doses were 195 and 390 mg/kg bw per day, respectively [calculated over seven days per week]. Groups of 20 male and 20 female mice either received corn oil alone and served as matched vehicle controls or remained untreated and served as matched untreated controls. At least 50% of the male mice in each group were alive at week 86; 50% of the female mice were still alive after 90, 89, 58 and 81 weeks in the untreated control, vehicle control, low-dose and high-dose groups, respectively. The incidence of hepatocellular neoplasms [reported as carcinomas] was increased significantly (p < 0.01) in all treated groups: males—2/17 (untreated controls, 2/20 vehicle controls, 18/49 low-dose animals and 37/49 high-dose animals; in females-2/20 untreated controls, 0/20 vehicle controls, 16/48 low-dose animals and 40/45 high-dose animals. Adrenal phaeochromocytomas were present in 8/48 high-dose males and in 12/43 high-dose females, but in no other group (National Cancer Institute, 1978).

Rat: Groups of 50 male and 50 female Osborne-Mendel rats, six weeks of age, received technical-grade 1,1,2-trichloroethane (see above) in corn oil by gavage on five consecutive days a week for 78 weeks. Low-dose and high-dose groups received, respectively, 35 and 70 mg/kg bw per day for 20 weeks, then 50 and 100 mg/kg bw per day for 58 weeks and were left untreated for the subsequent 34–35 weeks. The time-weighted average doses were 46 and 92 mg/kg bw per day [calculated over seven days per week]. Groups of 20 male and 20 female rats either received corn oil alone and served as matched vehicle controls or remained untreated and served as matched untreated controls. At least 50% of the male rats in untreated, low-dose and high-dose control groups survived more than 96 weeks; 50% of the females in the untreated control, low-dose and high-dose groups survived more than 105 weeks. Vehicle control groups had unexpectedly poor survival, with only 5% (1/20) of males and 20% (4/20) of females still alive at the end of the study; the authors did not, therefore, include them in statistical comparisons. No statistically significant increase in tumour incidence was found, either in males or in females (National Cancer Institute, 1978).

In a screening assay based on the production of γ-glutamyltranspeptidase-positive foci in rat liver, 10 male Osborne-Mendel rats (weighing 180– 230 g when received and observed for a further five days before the start of the experiment) were given a single dose of 0.52 mmol/kg bw ([69.4 mg] maximum tolerated dose) 1,1,2-trichloroethane (98% pure) in corn oil by gavage 24 h following a two-thirds partial hepatectomy. Ten male rats given 2 ml/kg bw corn oil following partial hepatectomy served as vehicle controls. Six days after partial hepatectomy, the rats were given 0.05% (w/w) phenobarbital in the diet for seven weeks; they were then transferred to their regular diet for seven more days, at which time they were sacrificed. The number of foci/cm² liver in rats given 1,1,2-trichloroethane was not greater than that in the vehicle controls [numbers of foci not reported]. In further studies, groups of 10 male rats were given a single initiating dose of 30 mg/kg bw N-nitrosodiethylamine in 5 ml water or water alone by intraperitoneal injection 24 h after a two-thirds partial hepatectomy. Six days later, the rats were given 0.52 mmol/kg bw 1,1,2-trichloroethane in corn oil or corn oil alone by gavage on five days per week for seven weeks. In rats initiated with N-nitrosodiethylamine, 1,1,2-trichloroethane significantly increased the incidence of γ-glutamyltranspeptidase-positive foci/cm² liver: control (N-nitrosodiethylamine plus corn oil), 1.6 ± 0.3 (SD); treated, 6.3 ± 2.2 (p < 0.05, Student’s t test). In rats not initiated with N-nitrosodiethylamine, 1,1,2-trichloroethane also produced a significant increase in the number of foci/cm² liver: control (water plus corn oil), 0.4 ± 0.2; treated, 4.4 ± 1.3 (p < 0.05) (Story et al., 1986).

(b) Subcutaneous injection

Rat: Groups of 50 male and 50 female Sprague-Dawley rats [200–250 g] were given 15.37 or 46.77 μmol [2.05 or 6.24 mg] 1,1,2-trichloroethane (> 99% pure) in 0.25 ml dimethylsulfoxide by subcutaneous injection once a week for two years. Groups of 35 male and 50 female rats given 0.25 ml dimethylsulfoxide on the same dosing schedule served as vehicle controls; groups of the same size without treatment served as untreated controls. The median survival time was: males—untreated control, 100 weeks; vehicle control, 87 weeks; low-dose, 90 weeks-high-dose, 85 weeks; females—untreated control, 91 weeks; vehicle control, 95 weeks; low-dose, 86 weeks; high-dose, 83 weeks. Sarcomas occurred at various sites in none of the untreated controls, in 2/35 and 3/50 vehicle control, in 4/50 and 3/50 low-dose and in 8/50 and 5/50 high-dose rats. The proportion of low- or high-dose rats with sarcomas was not significantly larger than that of vehicle controls (Norpoth et al., 1988).

3.2. Other relevant data

(a) Experimental systems

(i) Absorption, distribution, excretion and metabolism

The blood/gas partition coefficient (at 37°C) of 1,1,2-trichloroethane in rats was 58 (Gargas et al., 1989), and the blood serum/gas partition coefficient (at 25 °C) in humans was 56 (Morgan et al., 1972); these findings predict that this compound is readily absorbed by inhalation.

1,1,2-Trichloroethane is absorbed through mouse skin (Tsuruta, 1975): when 5.4 mmol (0.5 ml) of undiluted 1,1,2-trichloroethane were applied to a 2.92-cm² area of mouse skin, 5.7 μmol (763 μg) were absorbed after 15 min, 0.015 μmol (2 μg) was eliminated in expired air, and the balance was retained in the body. The percutaneous absorption rate was 130 nmol/min per cm² of skin. Skin absorption was confirmed in guinea-pigs (Jakobson et al., 1977).

In mice exposed to 1000 ppm (5445 mg/m³) 1,1,2-trichloroethane by whole-body inhalation for 1 h, the highest concentrations of the halocarbon immediately after exposure were found in fat, followed by liver and kidney (Takahara, 1986).

In dogs given undiluted 1,1,2-trichloroethane (0.375 or 0.75 mmol/kg, 50 or 100 mg/kg) intravenously, about 20 or 30%, respectively, was eliminated in the expired air within 60 min (Hobara et al., 1981).

The metabolic kinetic constants for 1,1,2-trichloroethane in rats exposed in vivo by inhalation to 501 ppm [2.7 g/m³] for 6 h were K_m = 0.75 mg/l (5.63 μM) and V_max = 7.70 mg/kg per h (57.7 μmol/kg per h) (Gargas & Andersen, 1989).

¹⁴C-l,l,2-Trichloroethane (0.75–1.5 mmol/kg, 100–200 mg/kg) was given in olive oil to mice by intraperitoneal injection, and the elimination of radiolabel was followed for three days (Yllner, 1971); 73–87% of the dose was eliminated in the urine, 0.1–2% in the feces and 16–22% in expired air, largely (60%) as ¹⁴C-carbon dioxide. Several urinary metabolites were identified: chloroacetic acid (6–31% of urinary radioactivity), free S-carboxymethylcysteine (29–46%), conjugated S-carboxymethylcysteine (3–10%), thiodiacetic acid (38–42%), 2,2-dichloroethanol (1–2%), oxalic acid (about 0.5%) and trichloroacetic acid (1.4–2.3%). The latter compound may be formed from an impurity or may be a metabolite of 1,1,2-trichloroethane.

Thiodiglycolic acid (about 20% of the dose) was identified as a urinary metabolite of 1,1,2-trichloroethane given intraperitoneally (40 or 160 μmol [5.3 or 21.3 mg]/rat) in corn oil to rats (Norpoth et al., 1988).

Daily oral doses of 1,1,2-trichloroethane (0.52 mmol/kg [70 mg/kg] to rats and 2.24 μmol/kg [300 mg/kg] to mice) on five days per week for four weeks followed by a single dose of ¹⁴C-1,1,2-trichloroethane in corn oil resulted in elimination of about 7–9 or 3–5% of the dose in the expired air as 1,1,2-trichloroethane and volatile metabolites or as ¹⁴C-carbon dioxide, respectively, by 48 h (Mitoma et al., 1985). The excreta contained about 75% of the administered radiolabel, and 2–4% was retained in the carcass. S-Carboxymethylcysteine, thiodiacetic acid and chloro-acetic acid were identified as urinary metabolites in both rats and mice.

1,1,2-Trichloroethane is metabolized by rat hepatic cytochromes P450 to chloroacetic acid (Ivanetich & Van den Honert, 1981) and to inorganic chloride (Van Dyke & Wineman, 1971; Van Dyke & Gandolfi, 1975).

When ¹⁴C-1,1,2-trichloroethane was incubated in air with primary cultures of rat hepatocytes isolated from phenobarbital-treated rats, covalent binding of 1,1,2-trichloroethane metabolites to protein (about 1.6 nmol/mg protein per 30 min) and to lipid (about 5 nmol/mg lipid phosphorus) was detected (DiRenzo et al., 1984).

(ii) Toxic effects

The single-dose oral LD₅₀s (in 10% Emulphor in water) of 1,1,2-trichloroethane in male and female CD-I mice were estimated to be 378 and 491 mg/kg bw, respectively (White et al., 1985). Six-hour LC₅₀ values of 1654 (9 g/m³) and 416 ppm (2.3 g/m³) 1,1,2-trichloroethane by whole-body inhalation have been reported for male Sprague-Dawley rats and for mice [sex and strain not specified], respectively (Bonnet et al., 1980). Percutaneous applications of undiluted 1,1,2-trichloroethane at doses of 0.5 or 2.0 ml/3.1 cm² skin to male and female guinea-pigs resulted in 100% mortality; 0.25 ml was lethal for 25% of the animals (Wahlberg, 1976). Intraperitoneal administration of 0.25–2.0 ml/animal 1,1,2-trichloroethane to male and female guinea-pigs was also lethal to all animals (Wahlberg & Boman, 1979). Signs of toxicity included sedation, gastric irritation, lung haemorrhage and liver and kidney damage (White et al., 1985).

Daily administration of 3.8 or 38 mg/kg bw 1,1,2-trichloroethane by gavage (in 10% Emulphor in water) to male and female CD-I mice for 14 days had no significant toxic effect (Sanders et al., 1985; White et al., 1985).

Administration of 0.02, 0.2 or 2 g/l 1,1,2-trichloroethane in the drinking-water of male and female CD-1 mice for 90 days [calculated daily doses: males—4.4,46 or 305 mg/kg bw; females—3.9,44 or 384 mg/kg bw] resulted in body weight reduction, depressed peritoneal macrophage function and decreased liver glutathione levels in males; decreased haematocrit and haemoglobin levels in females; and increased serum alkaline phosphatase activities and decreased haemagglutination titres in males and females at some doses. No other significant toxic effect was observed (Sanders et al., 1985; White et al., 1985).

1,1,2-Trichloroethane significantly increased the total number of enzyme-altered foci in livers of Osborne-Mendel rats when administered after treatment with N-nitrosodiethylamine (Milman et al., 1988; see also section 3.1).

(iii) Effects on reproduction and prenatal toxicity

In a developmental toxicity screening study, 1,1,2-trichloroethane given orally in corn oil at a dose that killed 3/30 pregnant mice caused no developmental toxicity in offspring of survivors (Seidenberg et al., 1986).

(iv) Genetic and related effects (Table 4)

Table 4.

Genetic and related effects of 1,1,2-trichloroethane.

The genetic and related effects of 1,1,2-trichloroethane have been reviewed (Infante & Tsongas, 1982).

1,1,2-Trichloroethane did not induce mutation in Salmonella typhimurium. It caused chromosome malsegregation in Aspergillus nidulans and morphological transformation of BALB/c 3T3 cells. 1,1,2-Trichloroethane bound to DNA in vitro (DiRenzo et al., 1982) and to DNA, RNA and protein of various organs following treatment of rodents in vivo (Mazzullo et al., 1986). Strong S-phase induction but no unscheduled DNA synthesis was observed in livers of treated mice.

A study in which a negative response was reported in S. typhimurium and positive responses in tests for unscheduled DNA synthesis in rat hepatocytes and for transformation in BALB/c 3T3 cells could not be evaluated [details not given] (Milman et al., 1988).

(b) Humans

(i) Absorption, distribution, excretion and metabolism

When ³⁸Cl-1,1,2-trichloroethane was administered by inhalation at a dose of about 5 mg/subject in a single breath to human volunteers [subject weight and gender not stated], about 3% of the administered radiolabel was eliminated in the breath within 1 h. Urinary excretion of ³⁸C1 amounted to < 0.01% of the dose/min (Morgan et al., 1970).

(ii) Toxic effects

No data were available to the Working Group.

(iii) Effects on reproduction and prenatal toxicity

No data were available to the Working Group.

(iv) Genetic and related effects

No data were available to the Working Group.

4. Summary of Data Reported and Evaluation

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Footnotes

1

In square brackets, spectrum number in compilation

2

Calculated from: mg/m³ = (molecular weight/24.45) × ppm, assuming standard temperature (25°C) and pressure (760 mm Hg)

1

(For) definition of the italicized terms, see Preamble, pp. 30–33.