RESUMEN
Testicular cancer is one of the commonest cancers in men of working age, and is increasing in incidence in Europe and North America. One suggested mechanism of causation is that there is impaired differentiation of germ cells in the pre- or perinatal period, followed by malignant transformation in later life, possibly by a hormonal mechanism. Endocrine disrupting chemicals [EDCs] have been a major focus of interest for etiological research into tes-ticular cancer because they interact with various hormonal pathways. Several EDCs including bisphenol A, phthalates, metals, polychlorinated biphenyls, and organochlorines have been investigated, but there are few studies and those that exist have not been able to assess exposure well. In addition, several studies, particularly those with better exposure assessment, have suggested that workers in electrical occupations have increased risks of testicular cancer. Electromagnetic radiation may have subthermal effects or may disrupt hormone release. Chronodisruption such as due to shift-work could potentially increase the risk of testicular cancer via disruption of hormonal cycles, but only one study has so far investigated this possibility. Lastly, solvent exposure, particularly to dimethylformamide, has been suggested to be associated with testicular cancer, but almost all these studies are based on job title only, with no specific assessment of solvent exposure. In conclusion, there is little evidence available on which to base definitive statements about occupational causes of testicular cancer. Future studies need to improve exposure assessment and develop ways to adjust for possible prenatal factors