Journal
AMERICAN JOURNAL OF EPIDEMIOLOGY
Volume 165, Issue 9, Pages 1015-1022Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/aje/kwk109
Keywords
androgens; DDT; developmental biology; dichlorodiphenyl dichloroethylene; endocrine system diseases; genitalia; male; prenatal exposure delayed effects
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Funding
- Intramural NIH HHS Funding Source: Medline
- NIEHS NIH HHS [N01-ES-15468, Z01 ES044009-05] Funding Source: Medline
- NINDS NIH HHS [R01 NS044623-05] Funding Source: Medline
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The insecticide 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) is still used for disease control in some areas, resulting in high levels of human exposure. The main degradation product of DDT is 1,1-dichloro-2,2bis(p-chlorophenyl)ethylene (DDE), an antiandrogen. In animal experiments, in utero exposure to DDE decreases anogenital distance in male offspring. In these models, anogenital distance serves as a measure of fetal androgen action. The authors designed the present study to examine the hypothesis that in utero exposure to DDE decreases anogenital distance in newborn human males. A cross-sectional study of 781 newly delivered male infants was conducted in 2002-2003 in Chiapas, Mexico, where DDT had recently been used for malaria control. Measurements of anogenital distance and penile dimensions were taken, and a sample of the mother's blood was drawn. In this population, the range of serum DDE levels was large (0.8-398 pg/liter). The authors, using two-sided tests, found no evidence that exposure in utero to DDE was related to reduced androgen action as reflected by anogenital distance or penile dimensions at birth. If DDE has important antiandrogenic action in humans, it may be manifest only at higher levels of exposure or via effects on other outcomes.
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