Possible Reproductive Effects of Environmental Exposures Including toxic, mutagenic, teratogenic, and carcinogenic effects. In summary, the reproductive and developmentalĮffects of environmental agents may operate through a variety of mechanisms Not become apparent until childhood or even adulthood, such as developmentalĭisorders and malignancies. Sures could lead to functional deficiencies and illnesses in the offspring that may Tili~y, spontaneous abortions, or abnormalities in the offspring. These latter effects may in turn lead to infer. For ex-Īmple, preconceptional exposure may lead to spermatic or ovarian toxicity and Mother infant morbidity and mortality and childhood malignancies. Tility embryonic and fetal loss any complication affecting the embryo, fetus, or Includes menstrual cycle changes semen characteristics fecundability and fer. This expanded list of effects is shown in Table 4 and Include effects on the reproductive systems of both men and women as well asĮffects on the offspring. The study population, but that is not a consequence of this exposure (Kelsey etĬurrent research on adverse reproductive outcomes has been expanded to A confounder in this context is a variable that isĬausally related to the disease under study and that is associated with exposure in Strong confounders that would have to be taken into account in any study of pa. InĪddition, these maternal risk factors are discussed because they are potentially Reference will be made to the status of evidence for male-mediated effects. Known about the causes of these endpoints relates to maternal exposure, specific Mother's preconceptional or gestational exposure. The risk factors described primarily relate to the Traneous variability (confounders) that may contribute to its prevalence or inci-ĭence, the interaction of various contributors to the occurrence of the endpoint,Īnd the difficulties inherent in obtaining reliable estimates of prevalence or inci-ĭence and paternal exposure. This examination will include a definition of theĮndpoint, current estimates of its frequency, its causers), possible sources of ex. In the paragraphs that follow, the committee examines separately each of 11Īdverse reproductive outcomes. Unfortunately, in most instances the precise size of this mutation component isĮither unknown or poorly estimated, but sufficient information is available to Mutation component, and it varies substantially from one endpoint to another. This contribution to the totality of adverse reproductive outcomes is called the Have arisen through the induction of a deleterious mutation in the paternal germĬells as a consequence of exposure to ionizing radiation. Of primary interest here are those adverse reproductive outcomes that may This diversity of possible origins makes diffi-Ĭult the assignment of causation in any specific instance. Mental agents, including ionizing radiation, smoking, or the consumption of al-Ĭohol, preexisting maternal illness (such as diabetes) or illness during pregnancy,Īnd malnutrition (Bracken, 19841. Ternally or paternally derived inherited defects, exposure to noxious environ. Many host and environmentalįactors contribute to the origins of such outcomes. Malformation or with mental or physical retardation, and the premature death ofĪn offspring (stillbirth, neonatal, or infant death). Termination of a pregnancy (abortion), the birth of an infant with a congenital
The term "adverse reproductive outcome" includes such diverse endpointsĪs the inability to conceive (sterility or infertility), the premature spontaneous Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages. Below is the uncorrected machine-read text of this chapter, intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text of each book.
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