ETS exposure in pregnant women adversely affects pregnancy by increasing fetal mortality and preterm delivery at higher exposure levels and slowing fetal growth across all levels of ETS exposure.

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Bisphenol A (BPA) exposure has been documented in pregnant women, but consequences for development are not yet widely studied in human populations. This review presents research on the consequences for offspring of BPA exposure during pregnancy. Extensive work in laboratory rodents has evaluated survival and growth of the conceptus, interference with embryonic programs of development, morphological sex differentiation, sex differentiation of the brain and behavior, immune responsiveness, and mechanism of action. Sensitive measures include RAR, aryl hydrocarbon receptor, and Hox A10 gene expression, anogenital distance, sex differentiation of affective and exploratory behavior, and immune hyperresponsiveness. Many BPA effects are reported at low doses (10-50 µg/kg d range) by the oral route of administration. At high doses (>500,000 µg/kg d) fetal viability is compromised. Much of the work has centered around the implications of the estrogenic actions of this agent. Some work related to thyroid mechanism of action has also been explored. BPA research has actively integrated current knowledge of developmental biology, concepts of endocrine disruption, and toxicological research to provide a basis for human health risk assessment.

Environmental tobacco smoke ( ETS ) exposure has been studied in relation to many diseases. The ability of a study to find an association between exposure and disease is, in part, determined by the accuracy of the exposure measure. This study examined how accurately one question, the number of smokers in the household, asked at birth, predicts ETS exposure in pregnant nonsmokers as assessed by serum cotinine. Blood specimens, drawn at 15 -19 weeks gestation, from 783 women who participated in a prenatal screening program in California in 1992 were analyzed for cotinine. Serum cotinine was significantly correlated with the number of smokers in the household ( r = 0.35, P < 0.001, geometric mean cotinine ( nanograms per milliliter ) for 0 smokers = 0.06, 1 smoker = 0.18, 2 or more smokers = 0.29 ). Using multiple regression, the number of smokers in the household accounted for 11% of the variation in serum cotinine. Cotinine concentrations were twice as high in women living with one or more smokers compared to women not living with a smoker, when reported exposure ( 0 or >0 h ) at home, work and other places was similar. Thus, the number of household smokers can account for a statistically significant amount of variation in serum cotinine and omission of this information would result in an underestimation of ETS exposure. Although use of this question alone does not provide an adequate estimation of ETS exposure as determined by serum cotinine, the results of this study indicate that this question is an important component of assessing ETS exposure.

Purpose of Review Cannabis exposure during critical windows of development may have intergenerational physiological consequences disrupting epigenetic programming and marks. This review examines the literature relating to pre-gestational and prenatal cannabinoid exposure and its effect on genes and molecular pathways related to the development of psychiatric disease. Recent Findings Developmental cannabis exposure alters epigenetic processes with functional gene consequences. These include potentially heritable alterations in genes and molecular pathways critical for brain development and associated with autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), schizophrenia, addiction, and other psychiatric diseases. Summary Cannabis consumption and mental health illness in adolescents and young adults are increasing in the United States (U.S.), and recent studies suggest that cannabis consumption during critical periods of brain development could contribute to mental health illness through epigenetic mechanisms. These findings warrant future studies and consideration by regulators and health communicators. Keywords Cannabis. Δ 9-THC. Epigenetics. Prenatal exposure. DOHaD. DNA methylation This article is part of the Topical Collection on Topical Collection on Environmental Epigenetics

Restraint has been used as a procedure to study the effects of stress on gestation outcome in rodents. The effects of restraint could potentially be used as a model for the impact of general stress produced by high doses of toxicants and other interventions. In mice, restraint in the peri-implantation period leads to implantation failure, and restraint at appropriate times in organogenesis produces cleft palate, supernumerary ribs, and resorption. In rats, there is some evidence for an association with restraint for implantation failure, but not for the morphological anomalies. Restraint in late gestation alters adult sexual behavior of male rat offspring, but consequences for their fertility are not known. Intrauterine growth retardation is not commonly associated with gestational restraint. In the few studies where they have been directly compared, different restraint procedures produced graded, qualitatively different, or no effects. Adrenocortical hormones have been implicated as mediating the effect of restraint on cleft palate, but not on supernumerary ribs, implantation failure, or sexual differentiation. Given the variety of restraint procedures and the varying species-dependent consequences, it is not possible to infer a generalizable pattern of developmental effects due to gestational stress from the restraint literature. As an alternative approach, contemporary methods in gene expression and developmental biology could profitably be applied to understanding different patterns of stress-mediated effects of toxicant exposures on intrauterine development. Birth Defects Res B 71:26-36, 2004. r 2004 Wiley-Liss, Inc.

Progesterone is a potent, multi-faceted endocrine agent with an expanding therapeutic profile and a minimal scientific database for evaluating safe use during pregnancy.