Toxicant developmental

Lead is known to cause reproductive and developmental toxicity. Decreased sperm counts and abnormal sperm development have been reported in male workers heavily exposed to lead. Increased incidences of spontaneous abortion have been reported in female lead workers as well as in the wives of male lead workers (13). Lead crosses the placenta and has been found to cause irreversible neurologic impairment to the fetus at maternal blood levels as... 

GL32 Safety Developmental toxicity test Studies to evaluate the safety of residues of veterinary drugs in human food Developmental toxidly testing... 

Short- to medium-term exposures have shown neurotoxicity, developmental toxicity, immunotoxicity, and endocrine disruption to be relevant end-points, although the degree of each of these toxic end-points differs across the group as a whole. 

Developmental toxicity is shown by the disubstituted methyl-, butyl-, and octyltins, but not by the corresponding monosubstituted compounds. The major reported effect is teratogenicity, with effects on fetuses shown at doses close to maternally toxic ones in most cases. NOAELs for dimethyltin, dibutyltin, and dioctyltin are 10 (10), 2.5 (1.0), and 45 (30) mg/kg body weight per day for teratogenicity (maternal toxicity NOAELs in parentheses). 

The predominant toxic end-points vary among the different organotins and include neurotoxicity, reproductive and developmental toxicity, immunotoxicity,... 

Animal data consistently show dibutyltin dichloride to cause dose-dependent developmental toxicity, such as fetal deaths, birth defects, and reductions in fetal weight. 

Faqi et al. (2001) studied the developmental toxicity inNMRI mice of an octyltin stabilizer ZK 30.434, a mixture of 80% dioctyltin diisooctylthioglycolate and... 

Monomethyltin Rat MMTC 8 weeks at 0, 30, 150, and 750 mg/kg diet = 0, 1.5, 7.5, and 37.5 mg/kg body weight Fertility, developmental toxicity, and maternal toxicity (screening) NOAEL = 7.5 Appel Waalkens-Berendsen (2004a)... 

Monobutyltin Rat MBTC Gestation days 7-17at0, 50, 100, 200, and 400 mg/kg body weight Maternal toxicity thymic atrophy dose-dependent developmental toxicity fetuses with visceral or skeletal abnormalities NOAEL >400 Noda etal. (1992)... 

Short- to medium-term exposure has shown neurotoxicity, developmental toxicity, immunotoxicity, and endocrine disruption to be relevant end-points. Table 24 summarizes the critical studies for each compound and identifies NOAELs or LOAELs. The degree of each of the toxic end-points differs across the group as a whole. For example, tributyltin is well established as an aromatase inhibitor, and dibutyltin appears to have some potency also (exact characterization of the endocrine disrupting capacity of dibutyltin alone is difficult because of the presence of tributyltin as an impurity). Monobutyltin and mono- and dioctyltins have no aromatase inhibiting capacity in in vitro tests. No data are available for this end-point for the methyltins. 

Organotin Neurotoxicity Developmental toxicity Endocrine disruption Immunotoxicity... 

Ema M, Kurosaka R, Amano H, Ogawa Y (1995) Comparative developmental toxicity of butyltin trichloride, dibutyitin dichloride and tributyitin chloride in rats. Journal of Applied Toxicology, 15(4) 297-302. 

No acute oral MRL was derived for methyl parathion because data regarding the most sensitive effect that was observed after acute oral exposure are conflicting. Increased pup mortality and altered behavior occurred in offspring of rats exposed to 1 mg/kg/day methyl parathion during, but no effects on pup survival or on sensitive electrophysiological indices of neurotoxicity were seen at virtually the same dose, 0.88 mg/kg/day, in a similar developmental toxicity study. 

No studies were located regarding developmental toxicity in humans after oral exposure to methyl parathion. 

No dose-response relationship can be established for the developmental toxicity of methyl parathion from the available database. All reliable LOAEL values in rats for developmental effects for the acute- and intermediate-duration categories are recorded in Table 3-3 and plotted in Figure 3-2. 

Developmental Toxicity—The occurrence of adverse effects on the developing organism that may result from exposure to a chemical prior to conception (either parent), during prenatal development, or postnatally to the time of sexual maturation. Adverse developmental effects may be detected at any point in the life span of the organism. 

Kelce, W.R., Monosson, E., and Gamcsik, M.P. et al. (1994). Environmental hormone disrupters—evidence that Vinclozolin developmental toxicity is mediated by antiandrogenic metabolites. Toxicology and Applied Pharmacology 126, 276-285. 

Gomez J, Macina OT, Mattison DR, Zhang YP, Klopman G, Rosenkrantz HS. Structural determinants of developmental toxicity in hamsters. Teratol 1999 60 190-205. 

Studies in animals indicate that trichloroethylene can act as a developmental toxicant, especially at doses also resulting in maternal toxicity. Significant decreases in litter size have been reported in rats treated by gavage... 

Fort DJ, Stover EL, Rayburn JR, et al. 1993. Evaluation of the developmental toxicity of trichloroethylene and detoxification metabolites usingXenopus. Teratogenesis Carcinog Mutagen 13 35-45. 

Narotsky MG, Kavlock RJ. 1995. A multidisciplinary approach to toxicological screening 11. Developmental toxicity. J Toxicol Environ Health 45 145-171. 

Narotsky MG, Weller EA, Chinchilli VM, et al. 1995. Nonadditive developmental toxicity in mixtures of trichloroethylene, di(2-ethylhexyl) phthalate, and heptachlor in a 5 x 5 x 5 design. Fund Appl Toxicol 27 203-216. 

Raybum JR, DeYoimg DJ, Bantle JA. 1991. Altered developmental toxicity caused by three carrier solvents. J Appl Toxicol 11 253-260. 

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