• Michael Joffe.
• Department of Epidemiology and Public Health, Imperial College London, London, UK. m.joffe@imperial.ac.uk
• Br. Med. Bull. 2003 Jan 1; 68: 477047-70.

AbstractWhile it has long been known that female fertility is impaired by oestrogen exposure, it is unclear whether environmental pollutants with weak oestrogenic effects are sufficiently potent and prevalent to have biological effects in humans. Male fertility, or sperm concentration at least, appears to have deteriorated, and there is substantial spatial variation at both national and global level, as well as a genetic component. Sperm morphology and motility are implicated too. There is good evidence for an increase in testicular cancer, and possibly in other conditions that certain spatial characteristics plus evidence on heritability suggest are linked to impaired spermatogenesis. A candidate agent would need to have started increasing in the early 20th century. Weak environmental oestrogens are not responsible. Candidates include agents affecting endogenous maternal oestrogen levels, environmental anti-androgens (although these cannot explain the epidemiological findings), and dioxin and related compounds. Genetic damage should be considered as a unifying hypothesis, possibly focused on the Y-chromosome.

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