In utero environmental exposures and reproductive endpoints

Abstract

The etiology of age at menarche, infertility, and endometriosis, three common reproductive outcomes is largely unknown. Environmental chemicals exhibiting endocrine disrupting behavior have recently been implicated in a number of reproductive disorders, however little research has been done to examine the potential effects of these chemicals on adult reproductive health when the woman is exposed in utero. This research focuses on the effects of exposure to cigarette smoke and diethylstilbesterol (DES) experienced in utero and three reproductive outcomes: age at menarche, infertility, and endometriosis. Using data from over 5,000 women enrolled in the National Cooperative DES and Adenosis Study (DESAD) and a subsequent follow-up we were able to ascertain in utero exposures from the mother and subsequent health outcomes from the daughters later in life. Overall, we found no suggestion for a delay or advance in age at menarche for women who were exposed in utero to tobacco smoke. Furthermore, we found null results for the associations between in utero tobacco smoke and self-reported infertility and endometriosis. This is in contrast to a few earlier studies which have found effects. We determined that women exposed in utero to DES had a 70% increase in the odds for developing endometriosis compared to women who were unexposed after controlling for age. We also used these data to determine whether self-reported age at menarche later in life is a reliable measure. Women were asked around the age of puberty to report their age at menarche, and they were queried on this same information approximately twenty years later. We found that self-report of age at menarche later in life is not reliable when exact age at menarche is required, but the reliability is good within a year of the first reported age at menarche. The only covariates slightly associated with discordant responses were young age (14 years). These three papers add to a small body of literature and address critical data gaps regarding the potential effects of the intrauterine environment on later reproductive health. These findings stress the importance of limiting potentially harmful exposures to pregnant women, as health effects may not only be seen at birth, but also years into adulthood. Furthermore our finding with respect to DES highlights the possibility that other endocrine disrupting chemicals, both pharmaceutical and those found in our environment may have similar adverse reproductive effects

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