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In stark contrast to impressive gains in health and longevity in industrialized countries, male reproductive health appears to be in decline (Sharpe and Skakkebæk, 2003; Skakkebæk et al, 2006). This is believed to be because of early, primarily prenatal exposure to environmental endocrine disruptors. In particular, estrogenic compounds are a likely underlying cause of these declines in sperm count and increased incidence of testicular cancer (Sharpe and Skakkebæk, 2003).
I would like to propose that exposure to radioactive fallout generated by testing nuclear weapons represents another potential mechanism of the decline in male reproductive health. The arms race after World War II involved atmospheric testing of nuclear weapons in desert regions of the United States, the Soviet Union, and Africa that introduced massive amounts of radioactive compounds into the upper layer of the atmosphere. This material was gradually distributed over the entire Northern Hemisphere, with gravity sedimentation and rains leading to its removal and deposition on the soil and vegetation. Most of the radioactive material that was widely deposited was strontium 90 (90Sr), a high-energy beta emitter with a half-life of nearly 29 years, which readily enters the food chain and becomes deposited in bone.
Although the resulting exposure of the general population to radiation was below the levels known to be toxic or mutagenic, I suggest that exposure to these low doses, especially during embryonic and fetal development, may have impacted adult testicular function and cancer risk. In the context of this hypothesis, it is of interest that the particularly striking reductions in sperm count and increases in the incidence of testicular cancer were reported from Denmark and other northern European countries, where relatively rainy weather is conducive to removal of solid particles from the atmosphere, and a dairy industry creates favorable conditions for the transfer of 90Sr from radioactive fallout via vegetation, cows, and milk to humans. However, other etiological factors may have also been involved, because incidence of testicular cancer in Denmark increased before the period of intensive testing of nuclear weapons (Moller, 1993).
From the available information, it is difficult and perhaps impossible to know what stages of male development are most vulnerable to the exposure to low radiation doses and whether mutagenic or epigenetic effects in women and transgenerational effects of radiation could have also been involved (Barber et al, 2002). Men who are currently diagnosed with reduced sperm count and/or quality or develop testicular cancer include children of individuals who have been exposed in utero to the radioactive fallout and grandchildren of individuals who were exposed as adults.
It is hoped that the hypothesis proposed in this letter may encourage novel directions of research.
Acknowledgments
Sincere thanks to Dr Serge Volovik for his assistance and most helpful discussions.
References
Barber R, Plumb MA, Boulton E, Roux I, Dubrova YE. Elevated
mutation rates in the germ line of first- and second-generation offspring of
irradiated male mice. Proc Natl Acad Sci U S A. 2002; 99: 6877
–6882.
Møller H. Clues to the aetiology of testicular germ cell tumours from descriptive epidemiology. Eur Urol. 1993; 23: 8 –13.[Medline]
Sharpe RM, Skakkebæk NE. Male reproductive disorders and the role of endocrine disruption: advances in understanding and identification of areas for future research. Pure Appl Chem. 2003; 75: 2023 –2038.[CrossRef]
Skakkebæk NE, Jorgensen N, Main KM, Rajpert-De Meyts E, Leffers H, Andersson AM, Juul A, Carlsen E, Mortensen GK, Jensen TK, Toppari J. Is human fecundity declining? Int J Androl. 2006; 29: 2 –11.[CrossRef][Medline]
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