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British Medical Journal May 1971
Topics: Adult; Humans; Male; Substance-Related Disorders; Swimming; Trichloroethylene; Ventricular Fibrillation
PubMed: 5575245
DOI: 10.1136/bmj.2.5757.334-a -
British Medical Journal Feb 1969
Topics: Adult; Humans; Male; Occupational Diseases; Peripheral Nervous System Diseases; Psychophysiologic Disorders; Taste; Trichloroethylene; Trigeminal Nerve
PubMed: 4303442
DOI: 10.1136/bmj.1.5641.422 -
British Medical Journal May 1969
Topics: Adult; Humans; Male; Nervous System Diseases; Occupational Diseases; Trichloroethylene
PubMed: 5780469
DOI: 10.1136/bmj.2.5652.315-c -
British Medical Journal Apr 1969
Topics: Humans; Nervous System Diseases; Occupational Diseases; Trichloroethylene
PubMed: 5775443
DOI: 10.1136/bmj.2.5649.118-d -
Environmental Health Perspectives Mar 2013In support of the Integrated Risk Information System (IRIS), the U.S. Environmental Protection Agency (EPA) completed a toxicological review of trichloroethylene (TCE)... (Review)
Review
BACKGROUND
In support of the Integrated Risk Information System (IRIS), the U.S. Environmental Protection Agency (EPA) completed a toxicological review of trichloroethylene (TCE) in September 2011, which was the result of an effort spanning > 20 years.
OBJECTIVES
We summarized the key findings and scientific issues regarding the human health effects of TCE in the U.S. EPA's toxicological review.
METHODS
In this assessment we synthesized and characterized thousands of epidemiologic, experimental animal, and mechanistic studies, and addressed several key scientific issues through modeling of TCE toxicokinetics, meta-analyses of epidemiologic studies, and analyses of mechanistic data.
DISCUSSION
Toxicokinetic modeling aided in characterizing the toxicological role of the complex metabolism and multiple metabolites of TCE. Meta-analyses of the epidemiologic data strongly supported the conclusions that TCE causes kidney cancer in humans and that TCE may also cause liver cancer and non-Hodgkin lymphoma. Mechanistic analyses support a key role for mutagenicity in TCE-induced kidney carcinogenicity. Recent evidence from studies in both humans and experimental animals point to the involvement of TCE exposure in autoimmune disease and hypersensitivity. Recent avian and in vitro mechanistic studies provided biological plausibility that TCE plays a role in developmental cardiac toxicity, the subject of substantial debate due to mixed results from epidemiologic and rodent studies.
CONCLUSIONS
TCE is carcinogenic to humans by all routes of exposure and poses a potential human health hazard for noncancer toxicity to the central nervous system, kidney, liver, immune system, male reproductive system, and the developing embryo/fetus.
Topics: Animals; Carcinogenicity Tests; Carcinogens; Humans; Trichloroethylene
PubMed: 23249866
DOI: 10.1289/ehp.1205879 -
Anaesthesia Oct 1963
Topics: Air; Anesthesia; Anesthesia, Inhalation; Ether; Ethers; Humans; Trichloroethylene
PubMed: 14071375
DOI: 10.1111/j.1365-2044.1963.tb13571.x -
Anaesthesia Jul 1975
Topics: Air Pollution; Anesthesia, General; Anesthetics; History, 20th Century; Methods; Trichloroethylene
PubMed: 1096662
DOI: No ID Found -
Environmental Health Perspectives May 2000This article addresses the evidence that trichloroethylene (TCE) or its metabolites might mediate tumor formation via a mutagenic mode of action. We review and draw... (Review)
Review
This article addresses the evidence that trichloroethylene (TCE) or its metabolites might mediate tumor formation via a mutagenic mode of action. We review and draw conclusions from the published mutagenicity and genotoxicity information for TCE and its metabolites, chloral hydrate (CH), dichloroacetic acid (DCA), trichloroacetic acid (TCA), trichloroethanol, S-(1, 2-dichlorovinyl)-l-cysteine (DCVC), and S-(1, 2-dichlorovinyl) glutathione (DCVG). The new U.S. Environmental Protection Agency proposed Cancer Risk Assessment Guidelines provide for an assessment of the key events involved in the development of specific tumors. Consistent with this thinking, we provide a new and general strategy for interpreting genotoxicity data that goes beyond a simple determination that the chemical is or is not genotoxic. For TCE, we conclude that the weight of the evidence argues that chemically induced mutation is unlikely to be a key event in the induction of human tumors that might be caused by TCE itself (as the parent compound) and its metabolites, CH, DCA, and TCA. This conclusion derives primarily from the fact that these chemicals require very high doses to be genotoxic. There is not enough information to draw any conclusions for trichloroethanol and the two trichloroethylene conjugates, DCVC and DCVG. There is some evidence that DCVC is a more potent mutagen than CH, DCA, or TCA. Unfortunately, definitive conclusions as to whether TCE will induce tumors in humans via a mutagenic mode of action cannot be drawn from the available information. More research, including the development and use of new techniques, is required before it is possible to make a definitive assessment as to whether chemically induced mutation is a key event in any human tumors resulting from exposure to TCE.
Topics: Animals; Carcinogens, Environmental; Dose-Response Relationship, Drug; Genes; Humans; Mutagens; Neoplasms; Risk Assessment; Trichloroethylene; United States; United States Environmental Protection Agency
PubMed: 10807553
DOI: 10.1289/ehp.00108s2215 -
IARC Monographs on the Evaluation of... 1995
Review
Topics: Animals; Carcinogenicity Tests; Carcinogens; Humans; Solvents; Trichloroethylene
PubMed: 9139130
DOI: No ID Found -
British Journal of Anaesthesia Sep 1965
Review
Topics: Anesthesia, Inhalation; Animals; Humans; Trichloroethylene
PubMed: 5320090
DOI: 10.1093/bja/37.9.681