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Jorma Toppari,^1,2 John Chr. Larsen,³ Peter Christiansen,¹ Aleksander Giwercman,¹ Philippe Grandjean,⁴ Louis J. Guillette Jr.,⁵ Bernard Jégou,⁶ Tina K. Jensen,¹ Pierre Jouannet,⁷ Niels Keiding,⁸ Henrik Leffers,¹ John A. McLachlan,⁹ Otto Meyer,¹⁰ Jørn Müller,¹ Ewa Rajpert-De Meyts,¹ Thomas Scheike,^1,8 Richard Sharpe,¹¹ John Sumpter,¹² and Niels E. Skakkebæk^1,13

¹Department of Growth and Reproduction, Juliane Marie Center, National University Hospital, Copenhagen, Denmark; ²Departments of Pediatrics and Physiology, University of Turku, Turku, Finland; ³National Food Agency, Søborg, Denmark; ⁴Department of Environmental Medicine, Odense University, Odense, Denmark; ⁵Department of Zoology, University of Florida, Gainesville, Florida; ⁶GERM-INSERM U 435, Campus de Beaulieu, 35042 Rennes Cedex, France; ⁷Université Paris V, Groupe Hospitalier Cochin, Paris, France; ⁸Department of Biostatistics, University of Copenhagen, The Panum Institute, Copenhagen, Denmark; ⁹Tulane/Xavier Center for Bioenvironmental Research, Department of Pharmacology, Tulane University, New Orleans, Louisiana; ¹⁰Institute of Toxicology, Department of General Toxicology, Søborg, Denmark; ¹¹MRC Unit of Reproductive Biology, Edinburgh, United Kingdom; ¹²Department of Biology and Biochemistry, Brunel University, Uxbridge, Middlesex, United Kingdom

Abstract

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. -- Environ Health Perspect 104(Suppl 4) :741-803 (1996)

Key words: male reproduction, reproductive disorders, semen quality, testicular neoplasms, environment, estrogenic chemicals, endocrine disruptors, exposure, pesticides