Prenatal exposure

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. 

Qrandjean P, Weihe P, White RF, Debes F, Araki S, Yokoyama K, Murata K, Sorensen N, Dahl R, Jorgensen PJ. 1997. Cognitive deficit in 7-year-old children with prenatal exposure to methyhnercury. Neurotoxicol Teratol 19 417 28. 

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. 

In most of these studies, prenatal exposure was generally estimated through maternal and/or cord blood lead concentrations. Exposure of the mothers can be assumed to have been primarily through the oral route, but with contribution from the inhalation route as well. The most relevant studies are discussed below, along with results from a few investigations of different markers for lead exposure. 

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. 

In rodents, a greater proportion of nervous system development takes place postnatally than in humans. Accordingly, rodent studies of developmental neurobehavioral toxicity that extend exposure into the early postnatal period are probably more analogous to human prenatal exposure than are rodent studies that use only prenatal exposure. 

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. 

Bellinger DC, Needleman HL, Leviton A, et al. 1984. Early sensory-motor development and prenatal exposure to lead. Neurobehav Toxicol Teratol 6 387-402. 

Bonithon-Kopp C, Huel G, Moreau T, et al. 1986b. Prenatal exposure to lead and cadmium and psychomotor development of the child at 6 years. Neurobehav Toxicol Teratol 8 307-310. 

Kristensen P, Eilertsen E, Einarsdottir E, et al. 1995. Fertility in mice after prenatal exposure to benzo[a]pyrene and inorganic lead. Environ Health Perspect 103 588-590. 

Nayak BN, Ray M, Persaud TVN. 1989a. Maternal and fetal chromosomal aberrations in mice following prenatal exposure to subembryotoxic doses of lead nitrate. Acta Anat 135 185-188. 

Rabe A, French JH, Sinha B, et al. 1985. Functional consequences of prenatal exposure to lead in immature rats. Neuroloxicology 6 43-54. 

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)... 

Zhao G, Xu Y, Li W, Han G, Ling B (2007) Prenatal exposures to persistent organic pollutants as measured in cord blood and meconium from three localities of Zhejiang, China. Sci Total Environ 377(2-3) 179-191. doi 10.1016/j.scitotenv.2007.02.006... 

There is some evidence from animal studies that cannabis can lead to reduced sperm production and impaired ovulation (Bloch, 1983). Furthermore, it has been reported that prenatal exposure to cannabis leads to significant impairment of... 

Crammer, J.S., D.L. Avery, R.R. Grady, and J.I. Kitoy. 1978. Postnatal endocrine dysfunction resulting from prenatal exposure to carbofuran, diazinon or chlordane. Jour. Environ. Pathol. Toxicol. 2 357-369. 

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. 

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