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[Tetrachloroethylene: effect of low concentrations of 1,1,2,2-tetrachloroethylene (perchloroethylene) on the mouse. II. Study of tetrachloroethylene in various organs and demonstration of histological changes in the examined organs].

Perchlorethylene in subacute amounts in form of contaminated drinking-water was given to a group of NMRI-mice (group A = 0,05 mg PER/kg BW/d and group B = 0,1 mg PER/kg BW/d) over a period of seven weeks. The histologic changes of various organs and the perchlorethylene-residues in the examined organs have been determined. We only could establish the light-microscopic perceivable histologic changes in the spleen. Thus the pulpa cords were rich in erythrocytes and the area of the red pulpa contained plenty of blood-formation-centers with megakaryocytes. In the spleens of group B a siderin-storage in the red pulpa in macrophages could be established. These results are indicative for an increased hemolysis. In all of the examined organs, the heaviest accumulation of perchlorethylene we could be established in the spleen, whereby the concentration in the spleen amounted to several times as much as the residue-examinations of the other organs. In the liver for instance an insignificant amount of PER was stored. The erythrocytes and the fragments of them, that have been changed by the storage of PER are being decomposed in the spleen, and perchlorethylene reaches the spleen via the erythrocytes.

Administration, Oral↗

[Tetrachloroethylene: effect of low concentrations of 1,1,2,2-tetrachloroethylene (perchloroethylene) on organisms in the mouse. I. Laboratory chemical research].

Tetrachloroethylene in a concentration of 0.05 resp. 0.1 mg/kg bw/d was offered in drinking water to a group of NMRI-mice. Besides a decrease in bodyweight an increase in the relative weight of the spleen resp. of the kidneys could be determined. The liver and the brain remained uneffected. In the offered concentration, tetrachloroethylene influenced the lipoprotein metabolism in the liver in the sense of a chronic-alcohol-toxic liver change, whereas the liver cell was not destroyed in toto. The unchanged rate of the synthesis of liver cells could be established sufficiently through the normal serum-glutamate-pyruvate-transaminase, an unchanged serum electrophoresis as a measure for the efficiency of the protein synthesis of the liver cells, furthermore a swelling of the liver and/or an enlargement of the liver could not be diagnosed. The erythropoietic system was found to be most susceptible to tetrachloroethylene. We could detect a defect like in the case of hemolytic anemia, this manifested itself in a very high increase of the lactatdehydrogenase, in an increase of the LD-isoenzyme-1, as well as in the occurrence of reactive initial stages of erythrocytes in the bone marrow and in the moderate degree of a hyperchrome anemia in the peripheral blood-count.

Administration, Oral↗

Dose-excretion relationship in tetrachloroethylene-exposed workers and the effect of tetrachloroethylene co-exposure on trichloroethylene metabolism.

Personal monitoring of 8-hour time-weighted average intensity of exposure with diffuse samplers and analysis of shift-end urine for total trichloro-compounds (TTC) and other metabolites were conducted in two groups of workers in China, one (121 subjects) exposed to tetrachloroethylene (TETRA) alone, and the other (38 subjects) exposed to a mixture of TETRA and trichloroethylene (TRI). Urinalysis was also performed on samples from 103 non-exposed controls. A linear exposure-excretion relationship could be observed in both groups of workers. Comparison of these results with those of Japanese TETRA-workers suggested the presence of ethnic difference in TETRA metabolism. Urinary metabolite levels were markedly lower in the mixed (TETRA + TRI) exposure group as compared to previous findings in a group exposed to TRI alone. The observation indicates that metabolism of TRI is suppressed by the co-exposure to TETRA in humans.

Air Pollutants, Occupational↗

NTP Toxicology and Carcinogenesis Studies of Tetrachloroethylene (Perchloroethylene) (CAS No. 127-18-4) in F344/N Rats and B6C3F1 Mice (Inhalation Studies).

Tetrachloroethylene is used primarily as a dry cleaning agent, an industrial solvent for fats, oils, tars, rubber, and gums, and a metal degreasing agent. Tetrachloroethylene had antihelminthic uses, particularly for hookworms (1.6-8 g/60 kg), and was formerly used in combination with some grain protectants and fumigants. Toxicology and carcinogenesis studies of tetrachloroethylene (99.9% pure) were conducted by inhalation exposure of groups of 50 male and 50 female F344/N rats and B6C3F1 mice 6 hours per day, 5 days per week, for 103 weeks. The exposure concentrations used (0, 200, or 400 ppm for rats and 0, 100, or 200 ppm for mice) were selected on the basis of results from 13-week inhalation studies in which groups of 10 rats and 10 mice of each sex were exposed to tetrachloroethylene at 100-1,600 ppm for 6 hours per day, 5 days per week. During the 13-week studies, 1,600 ppm tetrachloroethylene was lethal to 20%-70% of the rats and mice and reduced the final body weights of survivors. In rats, tetrachloroethylene at 200-800 ppm caused minimal to mild hepatic congestion. In dosed male and female mice, minimal to mild hepatic leukocytic infiltration, centrilobular necrosis, bile stasis (400-1,600 ppm), and mitotic alteration (200-1,600 ppm) were produced. Tetrachloroethylene exposure also caused minimal renal tubular cell karyomegaly in mice at concentrations as low as 200 ppm. During the 2-year studies, exposure to tetrachloroethylene did not consistently affect body weight gains in either rats or mice. Exposure at 400 ppm tetrachloroethylene reduced the survival of male rats (control, 23/50; low dose, 20/50; high dose, 12/50). This reduced survival may have been related to an increased incidence of mononuclear cell leukemia. Tetrachloroethylene at both exposure concentrations reduced the survival of male mice (46/50; 25/50; 32/50), whereas exposure at 200 ppm reduced female mouse survival (36/50; 31/50; 19/50). Early deaths in mice may have been related to the development of hepatocellular carcinomas. Both concentrations of tetrachloroethylene were associated with increased incidences of mononuclear cell leukemia in male rats (28/50; 37/50; 37/50). In female rats, tetrachloroethylene increased the incidence of leukemia (18/50; 30/50; 29/50) and decreased the time to occurrence of the disease. Tetrachloroethylene produced renal tubular cell karyomegaly in male and female rats, renal tubular cell hyperplasia in male rats, and renal tubular cell adenomas or adenocarcinomas (combined) in male rats (1/49; 3/49; 4/50). The incidence of the renal tubular cell tumors was not statistically significant; these uncommon tumors have been consistently found at low incidences in male rats in other 2-year studies of chlorinated ethanes and ethylenes. One low dose male rat had a kidney lipoma, and another had a nephroblastoma. Four high dose male and two high dose female rats had gliomas of the brain, whereas one control male and one control female had this tumor. In male and female mice, tetrachloroethylene caused dose-related increases in the incidences of hepatocellular neoplasms. In males, tetrachloroethylene at 200 ppm increased the incidence of hepatocellular adenomas (11/49; 8/49; 18/50) and at both concentrations increased the incidence of hepatocellular carcinomas (7/49; 25/49; 26/50). In female mice, tetrachloroethylene at both concentrations increased the incidences of hepatocellular carcinomas (1/48; 13/50; 36/50). Tetrachloroethylene also produced renal tubular cell karyomegaly in both sexes of mice, and one low dose male mouse had a tubular cell adenocarcinoma. In these inhalation studies, there were no neoplastic changes in the respiratory tracts of either species, but there was an increase in the incidence of squamous metaplasia in the nasal cavities in dosed male rats (0/50; 5/50; 5/50). Tetrachloroethylene was not mutagenic in Salmonella typhimurium strains TA98, TA100, TA1535, or TA1537 in the presence or absence of male Syrian hamster or male Sprague-Dawley rat liver S9. Tetrachloroethylene was not mutagenic in was not mutagenic in L5178Y/TK± mouse lymphoma cells with or without metabolic activation and did not induce sex-linked recessive lethal mutations in Drosophila melanogaster. Tetrachloroethylene did not induce sister-chromatid exchanges or chromosomal aberrations in Chinese hamster ovary cells in the presence or absence of metabolic activation. An audit of the experimental data was conducted for these 2-year studies on tetrachloroethylene. No data discrepancies were found that influenced the final interpretations. Under the conditions of these 2-year inhalation studies, there was clear evidence of carcinogenicity of tetrachloroethylene for male F344/N rats as shown by an increased incidence of mononuclear cell leukemia and uncommon renal tubular cell neoplasms. There was some evidence of carcinogenicity of tetrachloroethylene for female F344/N rats as shown by increased incidences of mononuclear cell leukemia. There was clear evidence of carcinogenicity for B6C3F1 mice as shown by increased incidences of both hepatocellular adenomas and carcinomas in males and of hepatocellular carcinomas in females. Synonyms: carbon bichloride; carbon dichloride; ethylene tetrachloride; per; perc; perchlor; perchlorethylene; perchloroethylene; perk; tetrachlorethylene; 1,1,2,2-tetrachloroethylene Trade names: Ankilostin; Antisal 1; Dee-Solv; Didakene; Dow-Per; ENT 1860; Fedel-Un; Nema; Perclene; Percosolv; Perklone; PerSec; Tetlen; Tetracap; Tetraleno; Tetravec; Tetroguer; Tetropil

Journal Article↗

Cardiopulmonary toxicity of tetrachloroethylene.

Tetrachloroethylene (1,1,2,2-tetrachloroethene) is a widely used organic solvent capable of producing adverse renal, hepatic, and central nervous system effects. The cardiac effects of tetrachloroethylene, thus far unexplored, were studied in several species. To standardize the dosimetry, tetrachloroethylene was prepared for intravenous injection in solutions of Tween 80, which had no demonstrable cardiotoxicity. In rabbits under urethane and in cats and dogs under pentobarbital, tetrachloroethylene increased the vulnerability of the ventricles to epinephrine-induced extra-systoles, bigeminal rhythms, and tachycardia. The mean threshold doses of tetrachloroethylene were 10 mg/kg in rabbits, 24 mg/kg in cats, and 13 mg/kg in dogs. In rabbits this threshold dose for cardiac arrhythmias correspond to blood levels between 2.2 and 3.6 microgram/ml. Animals demonstrating a reflex bradycardia to vasopressor doses of epinephrine were relatively resistant to the arrhythmogenic action of tetrachloroethylene. Ventricular arrhythmias occurred in less than 30% of the animals after tetrachloroethylene alone. In cats higher doses of tetrachloroethylene (40 mg/kg) produced acute pulmonary edema. Tetrachloroethylene (30-40 mg/kg) decreased left intraventricular dP/dt (max) in dogs, without significantly increasing left intraventricular end-diastolic pressure, although there was a transient decrease in arterial blood pressure that accompanied the early phase of myocardial depression. These results are being used as the basis for studies of the chronic effects of tetrachloroethylene on cardiac performance.

Animals↗

[Metabolism of tetrachloroethylene in guinea pigs (author's transl)].

Tetrachloroethylene oxide was chemically prepared from tetrachloroethylene, and the metabolites of the oxide in guinea pigs were analyzed by gaschromatography and Fujiwara reaction. The results obtained are as follows: 1) Trichloroacetic acid appeared in gaschromatogram after injection of tetrachloroethylene oxide, but trichloroethanol did not. 2) The metabolites analyzed by Fujiwara reaction after injection of tetrachloroethylene oxide were composed of large proportion of trichloroacetic acid and small proportion of trichloroethanol. 3) The ratio of trichloroacetic acid to trichloroethanol in the urine in case of tetrachloroethylene oxide was relatively similar to that of tetrachloroethylene. 4) The effects of pH (2.0 and 10.0) and temperature (4 degrees C and 37 degrees C) on the urinary metabolites suggest that the substance equivalent to trichloroethanol by Fujiwara reaction in metabolites may not be a real one. 5) Toxicity of tetrachloroethylene oxide seems to be much higher as compared with that of tetrachloroethylene in consideration of the maximum allowable dose in guinea pigs. 6) It is supposed from our experiments that tetrachloroethylene oxide is an intermediary metabolite of tetrachloroethylene.

Animals↗

Induction of rat liver drug-metabolizing enzymes by tetrachloroethylene.

The effect of tetrachloroethylene on Phase I and II drug-metabolizing enzymes in rat liver was examined. Rats were treated orally with tetrachloroethylene daily for five days, at doses of 125, 250, 500, 1,000 and 2,000 mg/kg. The higher doses (> 500 mg/kg) of tetrachloroethylene induced the hepatic microsomal 7-pentoxyresorufin O-depentylase and 7-benzyloxyresorufin O-debenzylase activities associated with the CYP2B subfamily. 7-ethoxyresorufin O-deethylase activity was also induced about 2-fold compared with that of control rats at 500, 1,000, and 2,000 mg/kg dose levels of tetrachloroethylene. However, 7-ethoxycoumarin O-deethylase and 7-methoxyresorufin O-demethylase activities were increased significantly at only the 1,000 mg/kg dose level of tetrachloroethylene (1.4- and 1.5-fold). Although other cytochrome P450-mediated monooxygenase activities such as nitrosodimethylamine N-demethylase, aminopyrine N-demethylase and erythromycin N-demethylase were also induced by tetrachloroethylene, the relative induction to control activity was lower than those of 7-pentoxyresorufin O-depentylase and 7-benzyloxyresorufin O-debenzylase. Western immunoblotting showed that the levels of CYP2B1 and CYP2B2 proteins in liver microsomes were increased at doses of 1,000 and 2,000 mg/kg of tetrachloroethylene. In addition to cytochrome P450-mediated monooxygenases, there was significant induction of the Phase II drug-metabolizing enzymes, DT-diaphorase, glutathione S-transferase activities towards 1-chloro-2,4-dinitrobenzene and 1,2-dichloro-4-nitrobenzene, and UDP-glucuronyltransferase activities towards 4-nitrophenol and 7-hydroxycoumarin. The results indicate that tetrachloroethylene induces both Phase I (CYP2B-mediated monooxygenase) and Phase II drug-metabolizing enzymes (DT-diaphorase, glutathione S-transferase and UDP-glucuronyltransferase) in the rat liver.

Administration, Oral↗

Assessment of urban population exposure to trichloroethylene and tetrachloroethylene by means of biological monitoring.

Exposure of the general population to trichloroethylene and tetrachloroethylene under normal environmental conditions, achieved with biological monitoring, was assessed, and the possible influence of these compounds via drinking water on the body burden was revealed. A total of 79 subjects with no known solvent exposure was selected, by stratified sampling, from the residents of the city of Zagreb. Trichloroethylene and tetrachloroethylene were determined in blood, and trichloroethanol and trichloroacetic acid were determined in plasma and urine. Drinking water samples were also analyzed for trichloroethylene and tetrachloroethylene. Concentrations of trichloroethylene and tetrachloroethylene in blood, trichloroacetic acid in plasma, trichloroacetic acid in urine, trichloroethylene in drinking water, and tetrachloroethylene in drinking water were as follows: < 0.015 to 0.090 micrograms/l, < 0.010 to 0.239 micrograms/l, 8.6 to 148.1 micrograms/l, 1.67 to 102.3 micrograms/24 h, < 0.05 to 22.93 micrograms/l, and 0.21 to 7.80 micrograms/l, respectively. The variation in all results presented is probably a reflection of different environmental contamination with trichloroethylene and tetrachloroethylene in the different city areas. Correlation analyses revealed significant relationships between trichloroethylene and tetrachloroethylene in blood (r = .402, p = .0004); trichloroacetic acid in urine and in plasma (r = .522, p = .0000); and trichloroethylene and tetrachloroethylene in drinking water (r = .800, p = .0000). A division of all parameters into a subgroup (n = 58), taking drinking water concentrations of trichloroethylene above 3 micrograms/l as a basis, demonstrated the same significant relationships as mentioned above.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effect of dry-cleaned clothes on tetrachloroethylene levels in indoor air, personal air, and breath for residents of several New Jersey homes.

Several volatile organic compounds, including tetrachloroethylene, have been found to be nearly ubiquitous in residential indoor environments during previous TEAM studies. Eleven homes in New Jersey were monitored over three or five days to examine the effect of bringing freshly dry-cleaned clothes into the home on indoor air levels and personal exposures to tetrachloroethylene. Indoor air, personal air, and breath concentrations were measured over multiple 12-hrs periods before and after dry-cleaned clothes were introduced into nine of the homes. No dry-cleaned clothes were introduced into the two remaining homes. Outdoor air tetrachloroethylene concentrations were measured at six of the eleven homes. Indoor/outdoor concentration ratios and source strengths were calculated at the six homes with outdoor measurements. Elevated indoor air levels and human exposures to tetrachloroethylene were measured at seven of the nine homes with dry-cleaned clothes. Indoor air concentrations reached 300 micrograms/m3 in one home and elevated indoor levels persisted for at least 48 hrs in all seven homes. Indoor/outdoor tetrachloroethylene concentration ratios exceeded 100 for the four homes with both dry-cleaned clothes and outdoor measurements. Maximum source strengths ranged from 16 to 69 mg/hr in these homes and did not directly correspond to the number of dry-cleaned garments brought into the home. Breath levels of tetrachloroethylene increased two to six-fold for participants living in seven homes with increased indoor air levels. Indoor air, personal air, and breath tetrachloroethylene concentrations were significantly related (0.05 level) to the number of garments introduced divided by the home volume.

Air Pollutants↗

Bioassay of tetrachloroethylene for possible carcinogenicity.

The bioassay of U.S.P.-grade tetrachloroethylene for possible carcinogenicity was conducted using Osborne-Mendel rats and B6C3F1 mice. Tetrachloroethylene in corn oil was administered by gavage at either of two dosages to groups of 50 male and 50 female animals of each species, 5 days a week, over a period of 78 weeks followed by an observation period of 32 weeks for rats and 12 weeks for mice. Initial dosage levels for the chronic bioassay were selected on the basis of a preliminary subchronic toxicity test. Subsequent dosage adjustments were made during the course of the chronic bioassay. The high and low time-weighted average dosages of tetrachloroethylene in the chronic study were 941 and 471 mg/kg/day for the male rats, 949 and 474 mg/kg/day for the female rats, 1,072 and 536 mg/kg/day for the male mice, and 772 and 386 mg/kg/day for the female mice. For each species, 20 animals of each sex were placed on test as vehicle controls. These animals were gavaged with corn oil at the same time that dosed animals were gavaged with tetrachloroethylene mixtures. Twenty animals of each sex were placed on test as untreated controls for each species. These animals received no gavage treatments. No significant increased incidence of neoplastic lesions was observed in treated rats. In both dosed and control rats, respiratory disease was observed with increasing frequency for the latter part of the first year until termination of the bioassay. Lesions indicative of pneumonia were observed in nearly all rats at necropsy. A high incidence of toxic nephropathy was observed in treated rats. Toxic nephropathy was noted in rats that died early in the study (as early as week 20 for male rats and week 28 for female rats). Mortality of rats was dose-related. Fifty percent of the high dose males had died by week 44 and 50 percent of the high dose females had died by week 66. In both male and female mice, administration of tetrachloroethylene was associated with a significantly increased incidence of hepatocellular carcinoma. Hepatocellular carcinomas were observed in 2/17 (12 percent) untreated control males, 2/20 (10 percent) vehicle control males, 32/49 (65 percent) low dose males, 27/48 (56 percent) high dose males, 2/20 (10 percent) untreated control females, 0/20 vehicle control females, 19/48 (40 percent) low dose females, and 19/48 (40 percent) high dose females. Hepatocellular carcinomas metastasized to the kidney in one untreated control male and to the lung in three low dose males, one low dose female, and one high dose female. Toxic nephropathy, similar to that observed in rats, was also observed in treated but not control mice. Fisher exact tests indicated a highly significant increased incidence of hepatocellular carcinoma for each dosed group compared to each control group. Cochran-Armitage tests showed a highly significant positive association between increased dosage and elevated tumor incidence. Time-adjusted analyses, based on Kaplan and Meier survival curves, indicated that the estimated probability of observing hepatocellular carcinoma by week 91 was 1.00 in a dosed male mouse and 0.938 in a dosed female mouse. The results of the bioassay of tetrachloroethylene in Osborne-Mendel rats do not allow an evaluation of the carcinogenicity of this compound due to the high rate of early death among the treated animals. However, under the condition of this study, tetrachloroethylene is a liver carcinogen in B6C3F1 mice of both sexes.

Journal Article↗

Health surveillance of workers exposed to tetrachloroethylene in dry-cleaning shops.

Behavioral, renal, hepatic and pulmonary tests were applied to 22 subjects exposed to tetrachloroethylene in 6 dry-cleaning shops. The results were compared with those obtained in 33 subjects non-occupationally exposed to organic solvents. The intensity of exposure was monitored by personal environmental monitoring and by urine analysis for trichloroacetic acid and expired air and venous blood analysis for tetrachloroethylene. The time-weighted average exposure to tetrachloroethylene amounted to 21 ppm (range 9 to 38 ppm). The correlation between the concentration of tetrachloroethylene in ambient air sampled with the charcoal tube method and with a passive dosimeter indicates that the latter can correctly estimate the time-weighted average exposure to the solvent. In view of the long biological half-life of tetrachloroethylene, the internal dose may be better estimated by measuring its concentration in blood 16 h after the end of exposure (i.e. before resuming work the next morning). The present study suggests that if the blood concentration of tetrachloroethylene does not exceed 1 mg/l, 16 h after the end of exposure, the time-weighted average exposure is likely to have been below 50 ppm. Exposure to such level for 6 years on the average does not seem to exert any adverse effect on the central nervous system, the liver and the kidney.

Adolescent↗

Factors influencing tetrachloroethylene concentrations in residences above dry-cleaning establishments.

Indoor air quality has been increasingly recognized as a significant public health problem. Proximity to industrial or commercial sources contributes to contamination in homes. Air sampling was conducted at 12 residences in 8 buildings that housed dry cleaners and 6 residential control sites. The authors found that concentrations of tetrachloroethylene, a dry-cleaning solvent, were elevated significantly in residences located in buildings that also housed dry-cleaning establishments (mean = 2.0 mg/m3) relative to their concentrations in control residences (mean = < 0.07 mg/m3 [p < .001]). Tetrachloroethylene concentrations remained elevated when the cleaners were closed on weekends (p < .01). The authors verified that colorimetric detector tubes were a useful screening tool for residences. Also identified were factors that could affect tetrachloroethylene concentrations. The use of exhaust fans and the implementation of required inspection and maintenance requirements by dry cleaners were associated significantly with reduced tetrachloroethylene concentrations in residences (p < .01). In all cases, tetrachloroethylene concentrations exceeded "minimal risk levels" posited by the Agency for Toxic Substances Disease Registry for chronic exposure to tetrachloroethylene. Residents who live in buildings that house dry cleaners may be exposed at concentrations that are of public health concern. Measures that might reduce this exposure were also identified.

Air Pollution, Indoor↗

Urinary excretion of tetrachloroethylene (perchloroethylene) in experimental and occupational exposure.

Fifteen human volunteers were exposed to tetrachloroethylene (perchloroethylene, tetrachloroethene) vapor at 3.6-316 mg/m3 for 2-4 hr at rest (10 cases) and during light physical exercise (5 cases). Subsequently, 55 workers who were occupationally exposed to tetrachloroethylene in eight commercial dry cleaning facilities were studied (median value, 66 mg/m3; geometric standard deviation, 3.15 mg/m3). In both the experimentally exposed subjects and occupationally exposed workers the urinary concentration of tetrachloroethylene showed a linear relationship to the corresponding environmental time-weighted average concentration. The findings indicate that the urinary concentration of tetrachloroethylene can be used as an appropriate biological exposure indicator. In occupationally exposed subjects performing moderate work, the urinary tetrachloroethylene concentration corresponding to the time-weighted average of the threshold limit value proved to be 120 mcg/L and its 95% lower confidence limit (biological threshold) 100 mcg/L. The effects of workload on the tetrachloroethylene urinary elimination are also accounted for.

Adult↗

Trichloroethylene, tetrachloroethylene, nitrates, and other chemicals in well water in the Fresno-Clovis Metropolitan Area.

In this study, the author examined the spatial and temporal distribution of tetrachloroethylene, trichloroethylene, nitrate, and several other organic and inorganic chemicals in large community wells in the Fresno-Clovis Metropolitan Area and estimated the lifetime cancer risk associated with exposure to tetrachloroethylene and trichloroethylene. By 1992-1993, investigators found the industrial solvent tetrachloroethylene in 34 wells and found trichloroethylene in 16 wells. All wells had detectable levels of nitrate. In addition, investigators found radon, arsenic, cadmium, iron, manganese, trihalomethanes, and several other volatile organic chemicals in the wells, but only radon and arsenic posed a significant health risk. In 1995, 16 wells were closed because chemicals were found in them. Twenty-six of 248 (10.5%) active wells and 24 of 43 (55.8%) closed wells contained multiple contaminants, excluding nitrate. Between 1988 and 1993, concentrations of trichloroethylene, tetrachloroethylene, and nitrates increased in selected wells. Daily, monthly, and bimonthly variations in the concentrations of tetrachloroethylene, trichloroethylene, and nitrate were often considerable. Granulated activated carbon filtration reduced trichloroethylene levels in well water by 91%-95%, and the author examined its usefulness as a remedial measure. Estimated lifetime cancer risks for tetrachloroethylene and trichloroethylene were 1 excess cancer death per 9.5 million people and 1 excess death per 250 million, respectively. The author also included recommendations for the conduct of further epidemiological and environmental studies.

Arsenic↗

ras proto-oncogene activation in dichloroacetic acid-, trichloroethylene- and tetrachloroethylene-induced liver tumors in B6C3F1 mice.

The frequency and mutation spectra of proto-oncogene activation in hepatocellular neoplasms induced by tetrachloroethylene, trichloroethylene and dichloroacetic acid were examined to help define the molecular basis for their carcinogenicity. H-ras codon 61 activation was not significantly different among dichloroacetic acid- and trichloroethylene-induced and combined historical and concurrent control hepatocellular tumors (62%, 51% and 69% respectively). The mutation spectra of H-ras codon 61 mutations showed a significant decrease in AAA and increase in CTA mutations for dichloroacetic acid- and trichloroethylene-induced tumors when compared to combined controls. The H-ras codon 61 mutation frequency for tetrachloroethylene-induced tumors was significantly lower (24%) than that of combined controls and also that of the two other chemicals. Mutations at codons 13 and 117 plus a second exon insert contributed 4% to the total H-ras frequencies for trichloroethylene and tetrachloroethylene. There was also a higher incidence of K-ras activation (13%) in tetrachloroethylene-induced tumors than in the other chemically induced or control tumors. Four liver tumors were found to contain insertions of additional bases within the second exon of K- or H-ras. These findings suggest that exposure to dichloroacetic acid, trichloroethylene and tetrachloroethylene provides a selective growth advantage to spontaneously occurring mutations in codon 61 of H-ras and, at the same time, is responsible for a small number of unique molecular lesions suggestive of either a random genotoxic mode of action or a non-specific result of secondary DNA damage. However, the absence of ras activation in many of the liver neoplasms suggests that alternative mechanisms are also important in B6C3F1 mouse hepatocarcinogenesis.

Animals↗