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Perspectives and Editorials |
Oliva A, Giami A, Multigner L. Environmental agents and
erectile dysfunction: a study in a consulting population. J
Androl.2002
;23:546–550.
The investigators have constructed an interesting hypothesis, that occupational exposure to chemical and physical environmental agents constitutes a risk factor for erectile dysfunction, and they tested this hypothesis with an elegant study. The genesis of their study borrows from concepts that were developed in the field of male reproductive function with concerns that certain pesticides, solvents, and related chemical agents may affect fertility, but erectile ability as well. The impetus to carry out this study also derives from early citations of men presenting to clinics with erectile dysfunction reporting occupational exposure to environmental chemicals. This study also takes on an evaluation of the mythical contention that heat may also be an environmental risk factor for erectile dysfunction. In exploring occupational and environmental risk factors, these investigators have gone beyond the often cited medical correlates that have appeared recently, such as cardiovascular disease, diabetes mellitus, and neurological illnesses. Thus, their study carries a certain novelty. The focus is on exposure risks for erectile dysfunction, similar to increased interest in smoking and alcohol consumption as possible risk factors for erectile dysfunction.
The investigators should be applauded for producing a solid clinical and epidemiologic study. The study used a small population of men who presented with erectile dysfunction to an andrology clinic in Argentina, who then underwent a comprehensive evaluation for their erectile disorder, and whose clinical, demographic, and occupational historical information was subjected to rigorous epidemiologic analysis. A highlight of the investigation was the application of nocturnal penile tumescence testing and rigidity using RigiScan as an objective assessment of erectile ability. Thus, the subjective complaint of the disorder was not relied on in order to ascertain the significance of the problem. It is noteworthy that 29 of the 199 individuals in the study (15%) were considered normal by this determination as a result. The approach carries certain potential limitations. Whereas it may assess nocturnal erection as a surrogate for sexual-related erectile ability, the concern exists that the presence of nocturnal erections does not always equate with those needed for sexual function. False positives may occur in the event of psychological or interpersonal variables, vascular steal syndrome, and sensory neuropathies, among others.
Some discussion is warranted with regard to the epidemiologic component of the study. In general, the epidemiologic analysis is rigorous, with an analysis that draws out some important relationships despite the relatively small size of the population studied. There is an assessment of relative risk, based on a calculation of odds ratios according to the different types of exposure in correlation with the degree of abnormality found with nocturnal penile tumescence testing. There are, however, several limitations from the epidemiologic perspective that should be acknowledged. Because the study involved a consulting population, there is the concern of inherent selection bias. The study was not population-based, but it was more like a case series because the evaluation did not represent the entire population, and represented only those who presented with complaints of erectile dysfunction. Data retrieval was retrospective in nature. It relied on patient interviews and recollection of the characteristics of exposure, such as whether there was exposure, how much was sustained, and when this occurred. Only a prospective evaluation with other validated techniques to define the type and amount of exposure with longitudinal assessment would allow utmost confidence in establishing the occupational and environmental risk. It is noteworthy to mention that a randomized controlled trial in which exposure could be completely regulated offers the optimal assessment, but it is obvious that such an investigation would hardly be feasible.
A unique feature of the investigation is the high amount of exposure to environmental agents sustained by the population at hand. The investigators indicate that about 40% of the men in the study were exposed to either chemical or physical environmental agents. This prevalence, as acknowledged by the investigators, relates to the given region of the study in which industrial and agricultural work predominates. In some respects, this feature offers an opportunity to assess the extent to which environmental agents are responsible for erectile dysfunction in this unique population. On the other hand, there is a concern that confounding variables may be introduced by such a homogeneous background. Is it the environmental exposure that constitutes the risk or some other characteristic of this highly exposed population? A study based on a population with this high level of exposure also runs the risk that a definitive estimate from these data of erectile dysfunction probability from chemical agent exposure may be skewed. Data in the article indicate that patients with organic erectile dysfunction had a higher prevalence of exposure to pesticides or solvents than patients in the nonorganic erectile dysfunction group, which therefore supports these concerns.
The estimation of risk factors for erectile dysfunction might reasonably comply with the causality criteria promoted by the First Surgeon General's Advisory Committee on Smoking and Health in 1964, which evaluated the significance of the association between cigarette smoking and a condition in the host (US Department of Health, Education, and Welfare, 1964). Several criteria to be considered with respect to an association include consistency, specificity, strength, temporality, and coherence. Consistency is met by repeated studies that examine different clinical settings, subjects, eligibility criteria, and exposure opportunities. Specificity implies a dose-response effect with an assessment that establishes independence of a potential risk variable. Strength pertains to relative risk estimation. Temporality implies that the effect occurs with the onset of the exposure and, conceivably, the effect is diminished with cessation of the exposure. Coherence means that a biological mechanism has been explored and found to be tenable. In light of these issues, this study provides a useful initiation to an analysis of occupational and environmental risk factors for erectile dysfunction, which will need to be fortified by additional studies that support all of the necessary criteria before causality can be affirmed.
Overall, this article is solid for bringing attention to occupational and environmental risk factors that may lead to erectile dysfunction. It expands concepts of potential risk factors for the disorder. Certainly, more investigation is needed. A true population-based, longitudinal assessment would be most valuable. Further assessment of the mechanism of the effect would be most interesting with further scientific exploration. There may be antiandrogenic properties of certain environmental agents, or perhaps these serve as neurotoxins. As further information is gathered, recommendations may nonetheless be issued, based on the awareness of a possible link between environmental agents and erectile dysfunction. Similar concerns have arisen with regard to the smoking risk for erectile dysfunction that has prompted the Sexual Medicine Society of North America to issue a policy statement recently that smoking is a risk factor for erectile dysfunction. With prevailing wisdom, the discontinuation or avoidance of smoking may preserve a man's erectile ability. Similar beliefs could apply to an argument to limit occupational and environmental agent exposure. This issuance is all the more compelling, given recent epidemiologic results showing that a high lifetime exposure to cigarette smoking may not reverse the effect of erectile dysfunction (Derby et al, 2000).
References
Derby CA, Mohr BA, Goldstein I, Feldman HA, Johannes CB, McKinlay JB. Modifiable risk factors and erectile dysfunction: can life-style changes modify risk? Urology.2000 :56:302 -306.[Medline]
US Department of Health, Education, and Welfare. Smoking and Health; Report of the Advisory Committee to the Surgeon General of the Public Health Service. Washington, DC: HEW, Public Health Service; 1964. DHEW publication 1103.
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