Prenatal exposure effect

Hansen E, Meyer O. 1980. Neurobehavioral effects of prenatal exposure to parathion-methyl on rats. Acta Morphol Acad Sci Hung 28 210. 

Embryotoxicity and Fetotoxicity—Any toxic effect on the conceptus as a result of prenatal exposure to a chemical the distinguishing feature between the two terms is the stage of development during which the insult occurs. The terms, as used here, include malformations and variations, altered growth, and in utero death. 

Information from wel1-control 1 ed animal studies that focus on the effects of prenatal exposure to single and polydrug use will be of great value. Further evaluation of the fine motor movements that appear to be clearly neurological ly deviant in the PCP-exposed infants is essential. The emerging socialization skills during the second year of life also need more detailed evaluations. 

Barr, H. M., Streissguth, A. P., Darby, B. L., Sampson, P. D., Prenatal exposure to alcohol, caffeine, tobacco, and aspirin Effects on fine and gross motor performance in 4-year-old children. Developmental-Psychology 26(3), 339-348, 1990. 

Recent studies have focused on neurobehavioral effects of exposure of the developing organisms to lead. Studies concerned primarily with the effects of prenatal exposure are presented in the section on developmental effects (Section 2.2.3. 6), while studies concerned primarily with postnatal exposure are discussed here. 

Developmental Effects. Evidence from human studies on congenital anomalies as an end point (Emhart et al. 1985, 1986 McMichael et al. 1986 Needleman et al. 1984) indicate no association between prenatal exposure to low levels of lead and the occurrence of major congenital anomalies. This conclusion is further supported by developmental toxicity studies conducted in rats and mice these studies provide no evidence that lead compounds (acetate or nitrate) are teratogenic when exposure is by natural routes (i.e., inhalation, oral, dermal). Intravenous or intraperitoneal injection of lead compounds (acetate, chloride, or nitrate) into pregnant rats, mice, or hamsters, however, has produced malformations in several studies reviewed by EPA (1986a). 

Animal studies support he human evidence of neurobehavioral toxicity from prenatal exposure to low levels of lead. In an extensive review of the literature, Davis et al. (1990) discussed similarities between human effects and those in animals. The authors concluded that qualitatively "... the greatest similarities between human and animal effects involve cognitive and relatively complex behavioral processes such as learning." They further reported that quantitative relationships for PbB levels across species that cause developmental neurobehavioral effects are 10-15 pg/dL in children, <15 pg/dL in primates, and <20 pg/dL in rodents. 

In contrast to the animal studies for prenatal exposure, animal studies for postnatal exposure report effects at blood lead levels similar to those associated with effects in humans. 

Winneke G, Beginn U, Ewert T, et al. 1984. [Understanding of subclinical lead effects on the nervous system of children with known prenatal exposure in Nordenhami], Schriftenr Ver Wasser Boden Lufthyg 59 215-230. (German)... 

Spyker, J.M. and D.L. Avery. 1977. Neurobehavioral effects of prenatal exposure to the organophosphate diazinon in mice. Jour. Toxicol. Environ. Health 3 989-1002. 

Developmental Effects. Developmental effects associated with exposure of humans to endrin have not been reported. Prenatal exposure of animals to concentrations of endrin sufficient to cause maternal toxicity has resulted in a statistically significant increase in the incidence of fused ribs, cleft palate, exencephaly, microencephaloceles, and open eyes in hamsters and mice. Effects were not necessarily reproducible between studies. Adverse developmental effects generally have not been observed in rats (Kavlock et al. 1981) except for temporary increase in locomotor activity of pups (Gray et al. 1981) and delayed ossification at doses which resulted in maternal toxicity (Goldenthal 1978a). Developmental effects were found primarily in one species. It is unknown if these effects would occur in humans. 

ChemoffN, Kavlock RJ, Hanisch RC, et al. 1979a. Perinatal toxicity of endrin in rodents. I. Fetotoxic effects of prenatal exposure in hamsters. Toxicology 13 155-165. 

Gray LE Jr, Kavlok RJ, Ostby J, et al. 1986. An evaluation of figure-eight maze activity and general behavioral development following prenatal exposure to forty chemicals Effects of cytosine arabinoside, dinocap, nitrofen, and vitamin A. Neurotoxicology 7(2) 449-462. 

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