PubMed · 6346560
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L B Holmes. 1983. Teratogen update: bendectin.. https://doi.org/10.1002/tera.1420270216
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BACKGROUND: Studies in animals indicate that natural forms of vitamin A are teratogenic. Synthetic retinoids chemically similar to vitamin A cause birth defects in humans; as in animals, the defects appear to affect tissues derived from the cranial neural crest. METHODS: Between October 1984 and June 1987, we identified 22,748 pregnant women when they underwent screening either by measurement of maternal serum alpha-fetoprotein or by amniocentesis. Nurse interviewers obtained information on the women's diet, medications, and illnesses during the first trimester of pregnancy, as well as information on their family and medical history and exposure to environmental agents. We obtained information on the outcomes of pregnancy from the obstetricians who delivered the babies or from the women themselves. Of the 22,748 women, 339 had babies with birth defects; 121 of these babies had defects occurring in sites that originated in the cranial neural crest. RESULTS: For defects associated with cranial-neural-crest tissue, the ratio of the prevalence among the babies born to women who consumed more than 15,000 IU of preformed vitamin A per day from food and supplements to the prevalence among the babies whose mothers consumed 5000 IU or less per day was 3.5 (95 percent confidence interval, 1.7 to 7.3). For vitamin A from supplements alone, the ratio of the prevalence among the babies born to women who consumed more than 10,000 IU per day to that among the babies whose mothers consumed 5000 IU or less per day was 4.8 (95 percent confidence interval, 2.2 to 10.5). Using a smoothed regression curve, we found an apparent threshold near 10,000 IU per day of supplemental vitamin A. The increased frequency of defects was concentrated among the babies born to women who had consumed high levels of vitamin A before the seventh week of gestation. CONCLUSIONS: High dietary intake of preformed vitamin A appears to be teratogenic. Among the babies born to women who took more than 10,000 IU of preformed vitamin A per day in the form of supplements, we estimate that about 1 infant in 57 had a malformation attributable to the supplement.
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In studies of delayed effects of environmental exposures there is a need for accurate reconstruction of exposure, to the environmental factor under study, for a large number of individuals. There is also a need for similar assessments of exposure to possible confounding factors for the same population. In general, such reconstruction is not possible but it is often possible to make an estimate of exposures as they would have likely occurred. This requires selection of populations and circumstances which allow such estimates to be made. For each environmental exposure and for each disease outcome to be evaluated it is likely that the optimum exposure assessment methodology will be different. In each case these opportunities will have to be identified, tested and validated to the extent possible. Exposures will almost always have to be assessed retrospectively, if for no other reason than that prospective designs would not yield results for long periods of time after the initiation of the study. Examples are presented for the case of residential radon progeny exposure and associated excess lung cancer, where the delay is of the order of decades, and for the case of the possible teratogenic effects associated with living in the proximity of sites in which hazardous wastes are stored. In the latter case the delay is much shorter.