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5 Reproductive and Developmental Toxicity
Pages 182-212

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From page 182...
... . A study of male mice exposed to trichloroethylene via inhalation found significantly increased percentages of abnormal sperm at the highest test 182
From page 183...
... (2002) used an inhibitory CYP2E1 monoclonal antibody to demonstrate that the enzyme CYP2E1 is involved in trichloroethylene metabolism to chloral in both the testes and epididymides.
From page 184...
... . The authors concluded that exposure to trichloroethylene leads to impairment of sperm's fertilizing ability, which may be attributed to the trichloroethylene metabolites chloral hydrate and trichloroethanol (Xu et al.
From page 185...
... (2001) reported that a mixture of drinking water pollutants, including trichloroethylene, caused alterations in mating desire and ability, sperm quality, and Leydig cell function in rabbits.
From page 186...
... No effect on fertilization was found with trichloroethylene at concentrations up to 1,000 ppm. Dichloroacetic acid and trichloroacetic acid each showed a dose-related decrease in the percent of eggs fertilized that was significant at 1,000 and 100 mg/kg, respectively.
From page 187...
... neonates exhibited a dose-related increase across groups. The authors concluded that oral exposure to trichloroethylene at doses below those that cause maternal toxicity did not affect fertility or pregnancy outcome and that the accumulation of trichloroethylene and trichloroacetic acid in ovaries, adrenal glands, and uteri had no impact on mating success.
From page 188...
... (1979) compared the effects of timing of exposure to trichloroethylene on reproductive outcomes of female Long-Evans hooded rats exposed to trichloroethylene by inhalation at concentrations of 1,800 200 ppm.
From page 189...
... . Thus, trichloroacetic acid appears to be more potent than dichloroacetic acid in causing cardiac teratogenicity, although both compounds exhibited dose-response relationships.
From page 190...
... They found an increased incidence of cardiac malformations with trichloroacetic acid at a concentration of 2,730 ppm (10.53% versus 2.15% in the cumulative control group; P = 0.0001 for fetuses and P = 0.0004 for affected litters)
From page 191...
... and the metabolites trichloroacetic acid (300 mg/kg/day) and dichloroacetic acid (300 mg/kg/day)
From page 192...
... . The trichloroethylene metabolites dichloroacetic acid, trichloroacetic acid, trichloroethanol, and oxalic acid have also tested positive in the FETAX assay, but each was significantly less toxic than trichloroethylene.
From page 193...
... , or one of four chlorinated compounds (trichloroacetic acid, dichloroacetic acid, chloral hydrate, and trichloroacetyl chloride)
From page 194...
... 1991] ; and smooth muscle -actin and transforming growth factor 3 [Nakajima et al.
From page 195...
... Trichloroacetic acid was not teratogenic at 1,000 M. At 2,000 M, increased neural tube defects and fewer somites were observed.
From page 196...
... Direct extrapolation of the results of direct embryo culture studies is limited because maternal absorption, excretion, and metabolism do not occur in in vitro systems. In addition, no conceptuses were exposed simultaneously to multiple haloacetic acids, all of which are frequently low-level water disinfection products, or to other common coexposure chemicals, including compounds metabolically upstream and downstream of the haloacetic acids, such as trichloroethylene and chloral hydrate.
From page 197...
... evaluations of spermatogenesis and sexual function among men with occupational exposure to high concentrations of trichloroethylene or trichloroethylene-related compounds. The following discussion provides a qualitative overview of the epidemiologic evidence.
From page 198...
... Trichloroethylene exposure appears to be associated with significantly smaller male infants, whether measured as a continuous variable or as a dichotomous variable (ATSDR 1998; Sonnenfeld et al.
From page 199...
... A full study is planned to include all confirmed cases of birth defects and childhood cancers and an assessment of exposure to trichloroethylene and other drinking water contaminants by modeling the water system.
From page 200...
... . The relative risk of congenital anomalies considered as a single entity was 3.1 (95 % CI = 1.1, 10.4)
From page 201...
... . However, the relationships between central nervous system and neural tube defects and trichloroethylene exposure were not monotonic, only the continuous variable was associated.
From page 202...
... An increased frequency of congenital heart disease was suspected in Tucson, Arizona, in 1973. In 1981, drinking water contaminated with trichloroethylene (up to 270 ppb [approximately 0.009 mg/kg/day for a 60 kg adult]
From page 203...
... The proportion of mothers who were both older and had presumed trichloroethylene exposure was more than 6-fold greater among case infants (with congenital heart defects) than among control infants (3.3% versus 0.5%)
From page 204...
... In analyses that adjusted for multiple demographic factors, the relative risk of poor growth in the eastern study area was greater than in the controls. The ORs were 1.44 (95% CI = 1.13-1.83)
From page 205...
... was increased in both groups relative to WHO norms, but the low-exposure group had higher sperm density than the high-exposure group. When the sperm densities were compared with urinary trichloroacetic acid quartile levels, the incidence of hyperspermia (>120 million per mL of ejaculate)
From page 206...
... Seminal fluid from all eight subjects contained trichloroethylene, chloral, and trichloroethanol, whereas dichloroacetic acid and trichloroacetic acid were present in only two and one sample, respectively. Neither trichloroethylene nor its metabolites was detected in the five control male seminal fluid samples.
From page 207...
... Spontaneous abortion was associated with increased paternal exposure to solvents in general (adjusted OR = 2.3, 95% CI = 1.1, 5.0)
From page 208...
... Cleft palate as an isolated anomaly was associated with trichloroethylene exposure (OR = 6.7, 95% CI = 0.9, 49.7)
From page 209...
... Although the evidence suggests that trichloroethylene can generate such effects, the lowest-observed-adverse-effect level for human risk assessment remains unclear. Some information suggests that certain human subpopulations might be at increased risk because age, genetic polymorphisms, or disease (see Chapter 9)
From page 210...
... 1988) , suggest that trichloroethylene, or one or more of its metabolites (trichloroacetic acid and dichloroacetic acid)
From page 211...
... Recommendations: Additional studies evaluating a lowest-observed-adverse-effect level and mode of action for trichloroethylene-induced develop mental effects are needed to determine the most appropriate species for human modeling. More information is needed on metabolic activation in the avian model to evaluate interspecies differences, tissue-specific concentrations of trichloroethylene and its metabo lites, and human data with better ascertainment of congenital heart disease and improved quantitative assessment of trichloroethylene exposures.
From page 212...
... 212 ASSESSING THE HUMAN HEALTH RISKS OF TRICHLOROETHYLENE or permanent is unclear. The mode of action is unclear and might or might not relate to hormonal alterations.


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