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Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review
The contribution of environmental teratogens to embryonic and fetal loss.
Clinical Obstetrics and Gynecology 1994 September
Environmental causes of human malformations account for approximately 10% of malformations, and less than 1% of all human malformations are related to prescription drug exposure, chemicals, or radiation. Malformations caused by drugs and other therapeutic agents are important, however, because these exposures are preventable. As we better understand the mechanisms of teratogenesis from all etiologies, we may learn how best to predict and test for teratogenicity and apply this knowledge to the prevention of human birth defects. Spontaneous abortions account for a much higher percentage of reproductive failure than do congenital malformations, but a very high proportion of aborted fetuses are malformed or defective. Therefore, the consequences of abortion are much different than the consequences of having a survival malformed infant, from both the medical and psychologic perspectives. We are less certain about the contribution of environmental, physical, and chemical agents to the incidence of spontaneous abortion. Although we realize that spontaneous abortions are a significant medical and emotional burden to a family, a surviving malformed infant can be greater burden to that family. We do not have an accurate picture of the contribution of environmental agents to the incidence of spontaneous abortion. At the present time, it would appear that only a very small proportion of abortions can be attributed to exposure to environmental toxicants during pregnancy (Tables 1 and 2). Conversely, it is the scientific and medical community's responsibility to prevent the introduction and use of agents that cause unwanted embryonic and fetal loss. Because the teratogenic and abortigenic effects of environmental agents differ, one cannot conclude that an agent is an abortifacient because it is teratogenic, nor can one conclude that an agent is not an abortifacient because it is not teratogenic (Table 2).
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