Gastroschisis and endocrine disruptors

Abstract

Endocrine disruptors have been linked to a variety of human and animal disorders showing ongoing increases in frequency, but analysis is often complicated by retrospective issues of definition and ascertainment. Gastroschisis, a congenital abdominal wall defect with 10 to 20 fold or greater increases over the past half century, has origins linked to an estrogenic thrombophilia, suggesting a relationship to estrogen disruption. With this, a distinct morphology and other features make it particularly suited for retrospective studies. Early reports show ongoing increases starting in the U.S. and North-East Europe during the early 1960s. Exogenous and endogenous factors modify risks, which are primarily related to thrombophilia, although other mechanisms, especially vascular, may have a role. These factors can interact, often vary from study to study, and include geographic, genetic, ethnic and racial influences. Increases in other prenatal defects with similar origins indicate more than just an idiosyncratic effect limited to a single disorder. Findings suggest that a single agent is responsible for increases, although other factors can modify its effects. The same agent may affect other conditions through other mechanisms related to endocrine disruptors, which would be supported by a similar epidemiology. Bisphenol A is a possible candidate in terms of mechanisms, timing, increases, and distribution.