Reproductive toxicity prenatal exposure

Other types of reproductive toxicity studies, e.g., the prenatal developmental toxicity study, the reproduction/developmental toxicity screening study, and the developmental neurotoxicity study (Section 4.10.3) may give some indications of general toxicological effects arising from repeated exposure over a relatively limited period of the animal s life span as clinical signs of toxicity and... 

The reproductive/developmental toxicity screening test can provide initial information on possible effects on reproduction and/or development and may make it possible to identify a substance as being toxic to reproduction, i.e., the test gives a clear positive result. However, this test offers only limited means of detecting postnatal manifestations of prenatal exposure or effects that may be induced during postnatal exposure. In addition, because of the study design (e.g., relatively small numbers of animals per dose level, relatively short smdy duration), the test will not provide evidence for definite claims of no effects. 

Prenatal exposure of rats and rabbits to doses of methylacrylonitrile that did not induce toxicity in the adults also did not induce developmental toxicity in the fetus. Methylacrylonitrile was also determined not to be a selective reproductive toxin. In a continuous breeding study in rats, doses that caused decreases in epididymal sperm density of Fi... 

Previous reproductive toxicology studies in laboratory animals examining the effects of prenatal exposure to fumonisin demonstrated a potential risk to the developing fetus. Studies using an aqueous extract of contaminated maize-culture material of F. verticillioides reported that fumonisin was developmentally toxic in hamsters (Floss et al., 1994 Penner et al., 1998). In addition, purified fumonisin Bi was shown experimentally to cause fetal toxicity in rats and mice (Collins et al., 1998 Reddy et al., 1996). In another study, pregnant CD1 mice treated with a semipurified extract... 

For male and female reproductive toxicity, exposure assessments should consider the duration and period of exposure during development (prenatal, prepubescent, and reproductive) and physiological state in females (pregnancy, lactation, peri- and postmenopausal). 

Data on the toxicity and disposition of JP-8 in animals are sparse, and no data are available for humans. No reproductive toxicity studies have been done in experimental animals. One adequate study demonstrated developmental toxicity in rats treated orally at 1,500-2,000 mg/kg/d (Cooper and Mattie 1996). A study in a second species should be supplemented with a multiple-generation reproductive toxicity study in rats or mice, including an evaluation of postnatal endpoints, such as developmental neurotoxicity, immunotoxicity, and hematological, hepatic, and renal effects, that could result from prenatal exposures. 

Restricting women of childbearing age from the lead industry workforce for most of the twentieth century because of concerns about fetal exposures and toxic hazards to prenatal populations clearly reduced the prevalence and incidence of reproductive and developmental toxicity. Paternal exposures to lead in terms of reproductive competence indices has continued, based on occupational epidemiology data from several databases. 

Based on the observations of reproductive toxicity (including endocrine disruption) in wildlife and domestic animals, as well as ongoing concerns about reproductive dysgenesis in human populations and the observed effects of industrial accidents involving MIC and dioxins, there has been increasing interest in the effects of prenatal exposures of humans to suspected endocrine disrupters and other reproductive toxicants. However, when impaired reproductive function is discovered in adults, it is difficult to comment with complete certainty on the relative contributions of prenatal versus postnatal exposures to reproductive toxicants. There is a wide array of pesticides and other organic environmental... 

---