J Toppari, J C Larsen, Peter Christiansen, Alexander Giwercman, P Grandjean, L J Guillette, B Jégou, T K Jensen, P Jouannet, N Keiding, H Leffers, J A McLachlan, O Meyer, Jørn Müller, E Rajpert-De Meyts, T Scheike, R Sharpe, J Sumpter, N E Skakkebaek
Male reproductive health has deteriorated in many countries during the last few decades. In the 1990s, declining semen quality has been reported from Belgium, Denmark, France, and Great Britain. The incidence of testicular cancer has increased during the same time incidences of hypospadias and cryptorchidism also appear to be increasing. Similar reproductive problems occur in many wildlife species. There are marked geographic differences in the prevalence of male reproductive disorders. While the reasons for these differences are currently unknown, both clinical and laboratory research suggest that the adverse changes may be inter-related and have a common origin in fetal life or childhood. Exposure of the male fetus to supranormal levels of estrogens, such as diethlylstilbestrol, can result in the above-mentioned reproductive defects. The growing number of reports demonstrating that common environmental contaminants and natural factors possess estrogenic activity presents the working hypothesis that the adverse trends in male reproductive health may be, at least in part, associated with exposure to estrogenic or other hormonally active (e.g., antiandrogenic) environmental chemicals during fetal and childhood development. An extensive research program is needed to understand the extent of the problem, its underlying etiology, and the development of a strategy for prevention and intervention.
|Journal||Environmental Health Perspectives|
|Volume||104 Suppl 4|
|Number of pages||63|
|Publication status||Published - 1 Aug 1996|