Results from the BACH survey, a population-based random sample of 2301 men, reveal an association between smoking and ED. A dose-response effect was observed with increasing pack-years of smoking, with exposure to ≥ 20 pack-years being associated with ED after adjusting for major ED risk factors such as older age, CVD, and diabetes. The association between passive smoking and ED is not statistically significant; however, the magnitude of the effect of passive smoking is comparable to 10–19 pack-years of smoking exposure.
The observed association between smoking and ED and dose-response with increased cumulative exposure is consistent with reports from previous studies across different countries. Increased risk of ED among current smokers who smoke ≥ 20 cigarettes per day compared to never smokers was reported by studies conducted in Australia [11
] (adjusted OR = 1.39; 95%CI, 1.05, 183), China [12
] (adjusted OR = 1.47; 95%CI, 1.00, 2.16), Canada [13
] (adjusted OR for 25–50 pack-years was 2.11, 95%CI, 1.02, 4.36), Italy (adjusted OR for 10–20 yr of smoking was 1.6, 95%CI, 1.2, 2.0, with a similar OR for ≥ 20 years of smoking), [14
] and a cross-national survey of Brazil, Italy, Japan, and Malaysia [10
] (adjusted OR for ≥ 30 cigarettes/d was 2.3, 95%CI, 1.19, 4.49). Findings from the BACH study show a similar effect of cumulative pack-years among both former and current smokers with an adjusted OR of 1.70 (95%CI, 1.04, 2.77) for ≥ 20 pack-years of smoking. Compared to never smokers, a significant trend of increasing ED risk was observed across pack-years of smoking (). Similar finding were reported by a study using data from the Olmsted County Study (OCS), with a statistically significant multivariate-adjusted OR of 1.60 (95%CI, 1.04, 2.46) for men with ≥ 29 pack-years of smoking, and a dose-response pattern with increasing pack-years [9
]. Longitudinal data from the MMAS show that the incidence of ED is twice as high among smokers compared to nonsmokers over a 9-yr period [7
]. Similarly, data from the HPFS show an increased risk of ED, over a follow-up period of 14 yr, for both former smokers (relative risk = 1.2; 95%CI, 1.1, 1.3) and current smokers (relative risk = 1.5; 95%CI, 1.3-1.7).
Few studies have reported on the effect of passive smoking on ED. Results from the present study indicate a moderate, statistically nonsignificant, increase in risk of ED with exposure to passive smoking. This effect was comparable to a cumulative exposure of 10–19 pack-years (). Longitudinal results from the MMAS study show that men exposed to passive smoking were at twice the risk of developing ED over a 9-yr follow-up period [7
]. Although the effect of current smoking was adjusted for in the analysis of MMAS data, former smokers were not excluded from the passive smoking group, thus potentially overestimating the effect of passive smoking. These results suggest that although the increased risk in ED with passive smoking is small, long-term chronic exposure to passive smoking may have adverse effects on erectile function.
Although the association between smoking, ED, and CVD has been previously documented [7
], indicating vascular damage as the likely pathway between smoking and ED, the role of passive smoking in the etiology of ED is not known. Animal models suggest that long-term exposure to passive smoke leads to impaired endothelial function, possibly due to reduced penile oxide synthase activity [16
]. However, small studies of short-term exposure to passive smoke among healthy nonsmokers have not confirmed a direct effect of passive smoking on endothelial function [29
], suggesting that assessment of chronic exposure to passive smoke is warranted.
This study has many strengths; however, there are some important limitations. The BACH survey is a community-based random sample across a broad age range (30–79 yr) and includes large numbers of minority participants representative of both the black (African American) and Hispanic populations. ED is assessed using the IIEF-5, a validated instrument for ED assessment widely used in both clinical and epidemiologic studies. A limitation of the use of the IIEF-5 instrument is recall bias among men who had not engaged in sexual activities in the 4 wk preceding completion of the questionnaire (about 40% of men), potentially resulting in greater misclassification in this group. Results of analyses restricted to sexually active men showed a similar pattern but were statistically nonsignificant, largely due to the decreased sample size. The BACH study is presently a cross-sectional design; thus, incidence of ED related to smoking could not be assessed. Additionally, because data on duration since smoking cessation were not collected, the impact of quitting cigarette smoking on erectile function could not be assessed. Full information on smoking cessation will be collected in BACH follow-up studies. Self-reported smoking status and retrospective pack-year calculation may also result in reporting and misclassification bias. Previous studies of the validity of self-reported smoking have shown that prevalence rates of self-reported smoking match well with those of from contemporaneous smoking behavior [20
]. Although retrospective pack-year calculation may result in misclassification, categorizing pack-years into smoking groups reduces this bias [21
]. The BACH study was limited geographically to the Boston area. However, comparison of sociodemographic and health-related variables from the BACH survey with other large regional (Boston BRFSS) and national (National Health and Nutrition Examination Survey, National Health Interview Survey, national BRFSS) studies have shown that BACH estimates are comparable on health-related variables.