Abstract
SummaryThis paper summarises the main findings on congenital anomalies and environmental pollution. The lines of evidence for environmental causes of congenital anomalies are listed. These are based on clinical, epidemiological, laboratory and wildlife studies. The data show that not only are a (limited) number of pollutants (e.g. lead, methyl mercury) well known teratogens, but also that the number of daily environmental exposures associated with congenital anomalies is increasing. This latter applies, among others, to lead and nitrates in drinking water, living near waste deposit sites and non- occupational exposure to pesticides.The increasing incidence of hypospadias and cryptorchidism in a number of industrialised countries is noticeable. The “testicular dysgenesis syndrome” (TDS) theory links the epidemiological data with environmental causes and hypothesises one unifying mechanism for which the experimental evidence is significant.Core concepts related to the mechanisms of teratology are reviewed. They include dose-response relationships, exposure windows, latency periods and multicausality in the underlying factors of congenital anomalies. The discussion shows that at different points during recent years, teratology underwent important paradigmatic shifts.The concluding part of the paper deals with the question: which data are of primary importance for the stakeholders in the discussion on pollution and congenital anomalies: the prenatal health advisors, lawyers, policy makers and the media? Each of these groups has specific agendas and corresponding needs for information. Although main guidelines for handling this information exist, much more research is needed, e.g. on case studies from the past, and on effectiveness and efficiency of information transfer.
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