Environmental Erectile Dysfunction: Can the Environment Really Be Hazardous to Your Erectile Health?
Department of Urology, The Johns Hopkins Hospital, 600 N Wolfe Street, Marburg 407, Baltimore, MD 21287-2411 (e-mail: firstname.lastname@example.org).
ABSTRACT: The proposal that exposures to environmental or occupational substances may affect erection ability is a tenable one and would add to a growing list of pathogenic risk factors associated with erectile dysfunction. Several lines of evidence gained by clinical epidemiologic and biomedical research investigations lend support. Several environmental toxicants to include lead, organic solvents, and pesticides have been implicated as possibly hazardous agents. Effects on the nervous and hormonal systems have been proposed as the leading mechanisms by which environmental toxicants adversely impact erectile function. Synthesis of the current evidence supports a possible risk association between environmental exposures and erectile dysfunction. However, scientific support is lacking to establish a direct causal association at this time. More scientific work is needed to identify specific environmental agents that may harm erectile function and define their exact mechanisms of action in this regard.
Erection physiology as a scientific field has evolved enormously over the past 2 decades in various ways. In terms of risk parameters and pathophysiologic concepts associated with erectile dysfunction, the disorder has now come to be viewed as being mainly organic in etiology and associated in most cases with identifiable physical or medical conditions. Currently recognized pathogenic risk factors include clinical disease states, trauma to the pelvic or genital region, iatrogenic medical and surgical interventions, and even self-imposed lifestyle or behavioral factors. Considerations for the latter include physical inactivity, unhealthy dietary habits, alcohol abuse, and active cigarette smoking. A relatively new concept in the determination of potential risk factors for erectile dysfunction is the possibility that exposures to harmful biological or chemical substances existing in one's surroundings constitute a pathogenic basis for this sexual dysfunction.
The concept of environmental erectile dysfunction is hardly preposterous. The suspicion that environmental or occupational exposures may affect sexual function resembles widespread concerns of possibly adverse health effects of cigarette smoking and alcohol consumption on erectile function detailed by the recent reports of the United States Surgeon General (Burnett, 2004) and the Board of Science and Education and Tobacco Control Resource Center of the British Medical Association (Editorial Board of Science and Education, 2004). Further, the premise that environmental exposures constitute a pathogenic basis for erectile dysfunction is analogous to perspectives in the field of male reproductive function suggesting that certain pesticides, solvents, and related chemical agents may affect fertility (Lancranjan et al, 1975; Landrigan et al, 1983; Toppari et al, 1996; Cheek and McLachlan, 1998).
The intent of this presentation is to investigate and evaluate findings from the medical literature on the subject matter of environmental erectile dysfunction. The exercise involves a review of various sources that serve to implicate environmental agents either in the development or progression of the inability to attain or maintain erection satisfactory for sexual intercourse. For the most part, the information included in this summary derives from both clinical epidemiologic as well as biomedical research studies specific to this line of inquiry. The level of analysis herein pertains mainly to whether environmental exposures constitute a risk association for erectile dysfunction, although a brief glimpse of the data scrutinized in the manner of a causation analysis is also included.
A central component of epidemiologic investigation is the accrual of observational data regarding a subject matter of investigation. This strategy is no less important in exploring the association between environmental exposures and the occurrence of erectile dysfunction. The approach largely applies self-reporting and the use of subjective instruments (eg, logs, questionnaires, and sexual function inventories), which offer assessments of substance exposure and erectile performance. This approach differs from the application of objective, quantitative measurements of these variables. A special concern associated with retrospective, subjective study design is that it often relies on the individual's perception of environmental exposure and its level (eg, dosage effect). This situation refers to the potential limitation of information bias, possibly toward underestimating the effects of the environmental exposure. Some studies have applied external indicators (eg, known location and duration of exposure) in an effort to document the exposure risk, although the exact exposure conditions (eg, intensity and frequency) frequently are elusive. With respect to erectile function assessment, a single-item assessment (eg, “Do you experience difficulty getting and/or maintaining an erection that is rigid enough for satisfactory sexual intercourse?”) has gained prominence particularly for population-based epidemiologic studies (Derby et al, 2000). This manner of data collection may also introduce the possibility of information bias, probably toward underreporting. Furthermore, it may fail to disclose the severity of the erectile impairment. Nonetheless, the findings generally remain insightful as to the probable significance of the problem affecting the general population.
Observational case series qualify as an attempt to link environmental exposures as a health risk factor associated with impaired erectile function. However, it is recognized that such epidemiologic evidence is limited by not having true comparison groups. Despite these limitations, case series are informative in providing some early insight into a possible risk association. These provide a foundation for a more robust study design for this purpose.
Perhaps the earliest citation handling this subject matter can be attributed to Espir and colleagues (1970). These investigators documented impaired erectile function in 4 farm workers in Great Britain who had used herbicides and pesticides in association with their agricultural work over a 1-year interval. Organophosphorus chemicals were identified as the hazardous agent with implications that these chemicals disrupted testosterone metabolism (Peck, 1970). An interesting observation was that all 4 men recovered erectile function upon discontinuing their occupational activity.
Oliva and associates (2002) investigated the erectile dysfunction risk in agricultural and industrial workers in Argentina exposed to chemical and physical environmental agents in their region. The investigators evaluated the health complaint of erectile impairment in 199 men, finding that 56 (28%) had been exposed to pesticides or solvents with median exposure times of 12 and 14 years, respectively. This population was confirmed to carry confounding lifestyle and medical risk factors for erectile dysfunction, such as a 31% rate of cigarette smoking, a 33% rate of alcohol abuse, an 11% rate of diabetes mellitus, a 34% rate of hypertension, a 16% rate of cardiovascular diseases, and a 22% rate of use of therapeutic drugs.
Park and colleagues (2005) identified methyl bromide as having a risk association with erectile dysfunction. In a single case report, the investigators described a patient with erectile dysfunction whose occupation involved working in the fumigation department at a public food quarantine station for 12 years. The patient was diagnosed with a peripheral sensory-motor polyneuropathy, consistent with the known neurotoxicity associated with this fumigant. The patient had discontinued his occupational activity but failed to recover spontaneous erectile function afterwards.
Cross-sectional, random surveys of a sample population offer increasingly valid appraisals of the effects of potential environmental toxicants on erectile function. This level of investigation has served to document the widely ranging occupational hazards of chemical compounds primarily along the lines of reproductive ability while also allowing an assessment of adverse effects on sexual function. An early study by Lancranjan and associates (1975) served to evaluate the long-term occupational exposure to lead in this regard. The investigators performed a comprehensive clinical and toxicological assessment of 100 workmen who had a mean occupational exposure of 8.5 (1–23) years working at a storage battery plant in Bucharest, as well as 50 technicians and office workers of this plant who worked in annex work rooms in a lead-polluted environment for a mean interval of 6 (1–27) years. In their evaluation of fertility in these men, the investigators found by sexual history that “pathologic erections” occurred at a rate of 33% in the lead-exposed workmen compared with a 14% rate for coworkers, who were identified to have a physiologic, nontoxic absorption of lead.
Another questionnaire-based investigation suggested the importance of organic solvents in the development of erectile dysfunction. Sabroe and Olsen (1979) studied the health problem responses of 478 members of the carpenters/cabinetmakers trade union in the Aarhus area of Denmark. These investigators found a significantly higher percentage rate of erectile dysfunction in lacquerers (12.3%) when compared with that of former lacquerers (7.4%), which was also significantly greater than that of non-lacquerers (1.4%) after controlling for differences in age, smoking habits, and exposure to dust. The investigators implicated short-term toxic effects associated with organic solvents on the nervous system as the basis for this and other health complaints of the workers.
The National Institute for Occupational Safety and Health (NIOSH) in the United States initiated similar lines of investigation into the risk of environmental factors associated with occupation on reproductive ability. Under such auspices, Landrigan and associates (1983) carried out an initial interview involving 39 randomly selected male chemical workers employed at a large manufacturing plant in Alabama in 1981 who were exposed to the stilbene derivative 4,4′-diaminostilbene-2,2′-disulfonic acid (DAS), an intermediate used for the production of optical brightening agents. Among these workers, 14 (36%) reported erectile dysfunction, and of 28 exposed workers who underwent hormonal evaluation, 8 (29%) were found to have reduced serum testosterone measurements (<300 mg/mL). The hormonal abnormalities suggested to the investigators that the adverse health effects likely were associated with the estrogenic activity of the chemical exposure.
NIOSH released an official report in 1990 known as The Health Hazard Evaluation representing a formal questionnaire survey conducted during 1981–1983 among men working in the area of the aforementioned chemical plant that manufactured DAS (Quinn et al, 1990). Among 44 men aged 20–57 comprising the study population, 11 (25%) reported current or previous erectile dysfunction, which developed after beginning work at the plant (averaging 4.7 years of employment). Low levels of serum testosterone (<350 ng/dL) were identified in 16 (37%) of 43 men who underwent hormonal testing.
The second report of the NIOSH Health Hazard Evaluation derived from a questionnaire-based survey of sexual function conducted in 1991 among 30 male workers who currently manufactured DAS, 20 former DAS workers, and 35 workers who manufactured plastics additives in a different manufacturing area (ie, unexposed workers; Whelan et al, 1996). Adjusting for age, the investigators described a greater likelihood for currently exposed workers than unexposed workers to score in the lowest quartile for “physiologic competence” (a measure of erection ability; adjusted OR × 1.9, 95% CI × 0.6 to 6.4) and “activity/performance factor II” (a measure of ejaculatory function; adjusted OR × 5.8, 95% CI × 1.3 to 27.3). Currently exposed workers were also more likely than unexposed workers to score in the lowest quartile for “sexual interest” (adjusted OR × 1.9, 95% CI × 0.5 to 7.2). Former DAS workers reported problems associated with “activity/performance factors I and II” (measures of quality of erection and ejaculatory function, respectively; adjusted OR × 2.2, 95% CI × 0.5 to 10.1 and adjusted OR × 6.7, 95% CI × 1.2 to 35.9, respectively) compared to unexposed workers.
Another questionnaire-based study explored the potentially toxic effects of carbon disulfide on sexual function. Vanhoorne and colleagues (1994) followed up on earlier observations of possible sexual dysfunction in male viscose rayon factor workers in Belgium finding that among 116 exposed workers, 18 (15.7%) reported erectile dysfunction compared with 3 of 79 (3.8%) of nonexposed workers.
Besides industrial exposures, additional work in the field has promoted a direct risk association between agricultural exposures and erectile dysfunction. Amr and associates (1997) conducted an epidemiologic investigation in an agricultural region in Egypt exploring whether pesticides (eg, carbamates, pyrethroids, and organophosphates) frequently used in this region exert adverse effects on erectile function. The study population consisted of randomly selected workers, 208 pesticide formulators and 172 pesticide applicators, whose responses to standardized health questionnaires were compared to those of 223 unexposed control subjects (72 from an urban textile factory who were matched with the pesticide formulators and 151 from a rural area who were matched with the pesticide applicators). The groups were otherwise matched for age and socioeconomic and educational levels. The formulators were directly exposed to pesticides for at least 40 hr per week for at least 9 months of the year for at least 2 consecutive years, and the applicators were exposed for at least 2 consecutive years during standard farm work. Erectile dysfunction was documented to occur at a significantly greater rate in the exposed group (pesticide formulators) than in the unexposed control group, 26.9% vs 4.2%, respectively. Both pesticide formulators and applicators demonstrated a significantly greater frequency of psychiatric disorders compared with that of the control group.
The risk association between environmental exposures and erectile dysfunction can be further characterized by several specific risk relationships. Type of exposure, dose-response effect, effect of risk factor covariates, and effects of discontinuation of exposure represent such disease correlates. As suggested by the aforementioned section, various types of environmental exposure apparently correlate with erectile dysfunction. Passive exposure to cigarette smoke, which contains numerous pollutants, represents a further example of a type of environmental exposure that has been shown to be a risk factor for erectile dysfunction. According to a prospective analysis of the Massachusetts Male Aging Study, the odds of incident erectile dysfunction were more than doubled for passive exposure to cigarette smoke, if present both at home and at work, compared to non-exposure (adjusted OR × 2.07, 95% CI × 1.04 to 4.13; Feldman et al, 2000). In contrast, passive exposure at home or at work alone did not increase the odds of incident erectile dysfunction in nonsmokers, but each increment of exposure did increase the estimated likelihood of erectile dysfunction in smokers (Feldman et al, 2000). According to the Boston Area Community Health survey, men passively exposed to cigarette smoke had a moderate, statistically nonsignificant increase in erectile dysfunction (adjusted OR × 1.33, 95% CI × 0.69 to 2.55) when compared to never smokers not exposed to passive smoking (Kupelian et al, 2007).
A dose-response effect is characterized by a relationship demonstrated between the amount of exposure to an environmental toxicant and the extent of erectile dysfunction. Support for this concept is provided in the medical literature. Among 150 men with lead exposure categorized as being “poisoned” or having “moderate,” “slight,” or “physiologic” absorption, rates of pathologic erections were 48%, 33%, 22%, and 14%, respectively (Lancranjan et al, 1975). Among viscose rayon workers, those who were chemically exposed to carbon disulfide with a high cumulative exposure index score (ie, amount and duration of exposure >300 mg/m3 × years) manifested a significantly higher erectile dysfunction rate (20%) than that (9.1%) for men with a low cumulative index score (<300 mg/m3 × years; Vanhoorne et al, 1994). In a similar way, a direct correlation between duration of exposure and frequency of erectile dysfunction was found among Egyptian pesticide formulators (Amr et al, 1997). For exposure durations of ≤5 years, ≤10 years, ≥15 years, or ≥20 years, erectile dysfunction rates were 12.2%, 17.8%, 35%, and 35.8%, respectively, with statistically significant differences shown for the 2 longer durations compared to the shorter durations. In another study which applied a logistic regression analysis and a reference group of men with normal erectile function to calculate strength of association, objectively confirmed erectile dysfunction was found to be greater in men who were frequently exposed to pesticides (OR × 8.4) than in men who were so exposed only occasionally (OR × 4.4; Oliva et al, 2002).
As an additional risk relationship, one could suggest that exposure discontinuation leading to erectile function recovery implies that environmental exposure adversely affects erectile function. Accordingly, it was shown that farm workers who had developed erectile dysfunction after exposure to toxic chemicals recovered erectile function after discontinuing their occupations (Espir et al, 1970). On the other hand, a fumigator intoxicated by occupational methyl bromide did not recover erections after discontinuing his occupation (Park et al, 2005). The discrepancy may be explained by the differences in the amount of chemical exposure occurring in these 2 examples, the former consisting of 1 year of exposure and the latter consisting of 12 years of exposure. The inference is that exposure discontinuation after a significant lifetime interval or extent may fail to modify the frequency of erectile dysfunction. Those experiencing long-term exposure to chemical agents may proceed to develop an irreversible situation of erectile impairment.
Objective criteria largely derived from clinical investigation offer a meaningful basis to evaluate a link between environmental exposures and erectile dysfunction. The supposition is that quantitative measurements can be obtained to assist with the evaluation. These measurements may include indices of the integrity of erectile function among individuals exposed to environmental toxicants. They may also include assays or other measurement levels of actual chemical exposures related to impaired erectile function.
Penile Tumescence Studies. As a noninvasive diagnostic technique to quantify erection physiology objectively, nocturnal penile tumescence (NPT) monitoring is used. The evaluation takes place during the naturally occurring cycle of sleep-related penile erections, with the knowledge that spontaneous episodes of tumescence normally accompany rapid eye movement (REM) sleep. Further, it is understood that men having organic erectile dysfunction display diminished measurable tumescence (Levine and Lenting, 1995). Oliva and colleagues (2002) applied NPT in a study of Argentinean agricultural and industrial workers in an attempt to establish objectively their erectile impairment. The evaluation established the risk of having a flat erectile pattern to be significantly increased for pesticide exposure (OR × 7.1, 95% CI × 1.5 to 33.0) and solvent exposure (OR × 12.2, 95% CI × 1.2 to 124.8) compared with that of nonexposure (Oliva et al, 2002). The possibility that physical factors could also contribute to erectile dysfunction was suggested by the finding of a slightly elevated risk to a nonsignificant degree from exposure to heat compared with the exposure groups (OR × 1.7, 95% CI × 0.3 to 9.4; Oliva et al, 2002).
Clinical Toxicologic Assessment. The assay of environmental chemicals in the tissues of individuals suspected to be exposed to such agents who report erectile dysfunction offers an elegant approach to study their possible roles in the etiology of this sexual dysfunction. Such an evaluation equates to applying biomarkers for environmental chemical exposures. In a clinic-based, case-control study conducted in Kingston, Ontario, Polsky and associates (2007) explored whether organochlorines, which are related to such pollutants as polychlorinated biphenyls and chlorinated pesticides and are measurable in blood, are associated with erectile dysfunction risk. Plasma levels of an assortment of these compounds were no different among 101 men presenting with erectile dysfunction and 234 comparable control subjects after adjusting for age, total lipids, and health condition confounders. Results from this study would imply that environmental chemicals are uninvolved in erectile dysfunction risk. However, it is importantly noted that the study represented a small population of individuals, and conceivably a study of larger size, as suggested by the investigators, may reveal the actual risk. Understandably, this assessment may be applicable to the general population without excluding the risk encountered by individuals having a more significant level of toxic exposure to environmental chemicals.
The study of the effect of lead on reproductive ability among workers in a storage plant in Bucharest included an evaluation of the levels of toxic absorption of lead and lead-containing metabolites in blood and urine, a basic hematologic screen, and measurement of urinary 17-ketosteroid (17-KS) levels as a measure of Leydig cell function (Lancranjan et al, 1975). The pathologic lead-exposed groups demonstrated toxicologic abnormalities to a greater extent and higher rates of erection difficulties in contrast to control subjects. The analysis suggested that such parameters may serve as indicators of erectile impairment in lead-exposed individuals. However, a relationship was not found between the level of lead absorption and 17-KS elimination, despite the observation of abnormal fertility parameters in lead-exposed workers. The investigators were led to suggest that the likely toxic effects of the heavy metal on body organs including the testes are exerted by mechanisms other than functional disruption of the hypothalamic-pituitary-gonadal axis.
A clinic-based case-control study performed in Cairo, Egypt also served as a toxicologic evaluation of chronic lead exposure impacting erectile function. The investigation pertained to 34 men presenting with erectile dysfunction who were scheduled to undergo penile prosthesis surgery (Anis et al, 2007). Among these 34 patients, 16 (47%) and none of the clinically matched control subjects had elevated serum levels of lead (>25 g/dL). The serum lead level significantly correlated with cavernous tissue lead level in the patient group, in which lead granule deposition was identified histologically in cavernous tissue at the time of surgery. Higher serum levels of reactive oxygen species and lower levels of antioxidants were further confirmed, indicating the presence of oxidative stress in individuals with a high serum lead level compared with those having a low serum lead level. The analysis supported lead toxicity as a risk factor for erectile dysfunction while also further suggesting the pathogenic basis of lead exposure to be related to oxidative stress mechanisms.
Experimental studies in which environmental chemical exposures are controlled provide an additional approach to ascertain the consequences of environmental factors on erectile function. Such studies commonly apply rigorous scientific methodology (eg, random allocation of subjects to experimental and control groups, use of different control groups, and application of blinding procedures to reduce bias), and as such offer the most robust data from which to draw conclusions regarding risk associations. As one would suspect, such ideal studies in which environmental exposures are controllably delivered to humans are nearly impossible to conduct. However, an informative perspective may derive from examining results from several experiments testing the effects of cigarette smoking on erectile function in humans. These experiments, which mainly consisted of either acute exposure or exposure discontinuation study designs, showed direct temporal and dosing level effects of cigarette smoking on various erectile parameters (Abber et al, 1986; Gilbert et al, 1986; Glina et al, 1988; Levine and Gerber, 1990; Guay et al, 1998).
Animal models offer another experimental approach for investigating the association between environmental chemical exposure and erectile dysfunction. Brien and associates (2000) studied the effects of dichlorodiphenyldichloroethylene (p,p′-DDE), a prominent and persistent metabolite of the insecticide dichlorodiphenyltrichloroethane (commonly known as DDT), on erectile function in a rat model of apomorphine-induced erections. The investigators found that animals given a single intraperitoneal dose of the chemical agent manifested a decline in erectile function for at least 2 weeks compared with control rats. However, they were able to reverse the erectile dysfunction in p,p′- DDE—treated rats using high doses of testosterone. The investigators concluded that p,p′-DDE exerts a deleterious effect on penile erection, presumably by interference with androgen-mediated mechanisms. The conclusion is consistent with the known action of this chemical agent as an androgen receptor antagonist and supports altered steroid hormone function resulting from certain chemical exposures as a proximate basis for environmental erectile dysfunction.
Available observational, clinical, and experimental data all support a possible risk association between environmental exposures and erectile dysfunction (Table). The next inference is whether chemical exposures actually cause erectile dysfunction. This suggestion must be carefully evaluated. Several criteria require consideration prior to establishing causation per se. The application of causality criteria is notably associated with the evaluation of the first report of the Surgeon General's Advisory Committee on Smoking and Health (US Dept of Health, Education, and Welfare, 1964). Such criteria, as further articulated by Hill (1965), consist of consistency, specificity, strength, temporality, and coherence. Consistency implies that similar findings result from repeated studies that examine an association in the context of different clinical settings, subjects, eligibility criteria, and exposure opportunities. Specificity refers to a dose-response effect with an assessment that establishes independence of a potential risk variable. Strength refers to the relative risk estimation, which is generally calculated. Temporality acknowledges that the effect occurs with the onset of the exposure and, supposedly, the effect is diminished with cessation of the exposure. Coherence means that a biological mechanism has been explored and considered to be tenable. Satisfaction of these criteria would strongly support the proposal that environmental exposures qualify as a causal basis for erectile dysfunction.
With regard to the consistency of the association, both case series and population-based studies of environmental exposures establishing rates of erectile dysfunction among individuals lend meaningful support for causation. Population-based studies afford a more accurate observational basis for this determination than do uncontrolled case series. In view of the relative paucity of these population-based studies, a definitive conclusion at this time cannot be made.
The description of dose-response relationships for several exposures that show a correlative effect of greater amount of exposure and greater extent of erectile dysfunction also contributes to these considerations. The strength of the association currently rests on limited available information. Temporality of the association is also fairly limited although data derived from observational and experimental studies in this area of study would suggest that erectile dysfunction occurs in a temporal sequence following exposures to environmental chemicals. Further, data are available to suggest that erectile function is recoverable after the offending exposure is removed, at least in the case that exposure removal occurs only after an appreciably limited extent of lifetime exposure.
Coherence of the association seems likely based on proposals of plausible biological mechanisms that could be suggested to impact on the physiologic basis of penile erection. Leading possibilities in this regard include hormonal derangements and neurotoxicity. For the former, a host of environmental toxicology studies have centered on the threat of various compounds on male reproductive health, homeostasis, and physical development (Toppari et al, 1996; Cheek and McLachlan, 1998). Such compounds have been collectively termed “endocrine disrupters” as defined by the United States Environmental Protection Agency (Ginsburg, 1996) and include: pesticides (eg, 2,4-dichlolorophenoxyacetic acid [2,4-D], dichlorodiphenyltrichloroethane [DDT], and dieldrin), plasticizers (eg, styrene, phenols, and phythalates), and industrial chemicals (eg, polychlorinated biphenyls [PCBs] and dioxins) (Colborn et al, 1993; Korach, 1993; Brotons et al, 1995). In light of the documented anti-androgenic or estrogenic properties of many of these environmental chemicals, it is conceivable that they negatively impact erectile function in ways ranging from altering penile smooth muscle function to interfering with neurotransmission of erectile responses (Mills et al, 1996; Burnett, 2003; Traish and Guay, 2006). With regard to the latter consideration of possible neurotoxicity associated with environmental chemicals, it remains entirely possible that these chemicals in some cases operate as neurotoxins. Various compounds (eg, di-isopropyl fluorophosphates and organophosphorus insecticides) are known to produce toxic effects by inhibiting cholinesterase and acetylcholinesterase activity, thereby causing an accumulation of acetylcholine and eventually persistent depolarization at cholinergic nerve endings (Edson, 1955; Durham and Hayes, 1962). Accordingly, neurotoxins may well impair the neurogenic mechanisms involved in penile erection. These concepts are attractive to consider. However, experimental studies establishing the exact biological basis for erectile dysfunction resulting from specific environmental chemical effectors remain lacking at this time.
It is acknowledged that confounding issues could hinder assessments of causation in this field of study. One concern pertaining to population-based studies is whether a potentially toxic exposure is so pervasive in a certain community of interest that it introduces a magnitude of risk that is artifactually increased. This circumstance describes prevalence bias. The assignment of risk for a certain chemical exposure considered to have public health significance would require the study of a sufficiently large population base with appropriate control groups. As a related concern associated with such epidemiologic studies, it is entirely possible that a particular exposure may produce consequences which secondarily affect penile erection. An example of misattribution would be that of chemically exposed workers who experience psychological and general health ill-effects that subsequently hamper sexual interest and activity. Use of validated questionnaires specific for erection ability may serve optimally to evaluate environmental exposures as a primary risk factor.
This evaluation of the potential relationship between environmental exposures and erectile dysfunction suggests the possibility of a risk association. Enough intriguing information currently exists to raise a strong consideration for this possibility. The excitement of this risk association follows emerging lines of thought that erectile dysfunction is a public health concern associated with various potential risk factors. The consideration that environmental chemical exposures may contribute to erectile dysfunction underscores the potential public health significance of erectile dysfunction in general. It is acknowledged that limited information currently exists in this field of investigation to make any well-supported conclusions about the actual impact on chemical exposures that negatively affect erectile function. Indeed, the current scope of evidence remains insufficient to establish a direct causal association. Further scientific investigation is definitely needed. Specific areas of study would include additional observational studies, particularly those having a longitudinal design, which apply rigorous outcomes assessments, as well as basic scientific studies, which define biological mechanisms for the risk association. In the meantime, while further investigation and evidenced-based recommendations regarding this possible health risk are awaited, individuals may wish to limit environmental exposures to chemical agents with toxicity effects that may be hazardous to erectile health.