Benign prostatic hyperplasia (BPH) is increasingly prevalent among aging male populations and is often accompanied by a lower urinary tract symptoms (LUTS). This study aimed to comprehensively analyze the impact of air pollution and lifestyle on the incidence of BPH and LUTS. In a prospective study-based U.K. Biobank (UKB) cohort, every 1 μg/m3 increase of PM2.5 was associated with a 2.18% increased risk of BPH (P = 0.0029). Furthermore, PM2.5–10, PM10, NO2, and NOX also showed similar risk effects. As for mixed exposures, the weighted quantile sum (WQS) and quantile g-computation (qgcomp) method indicated that for each additional unit, the risk of BPH increased by 3.53% (P = 0.0265) and 2.20% (P < 0.0001). Analyses of LUTS in males showed that for each additional unit of mixed exposure, the risk of LUTS increased by 6.78% (P < 0.0001) and 9.17% (P < 0.0001). A cross-country cohort in western China was also replicated. As for single air pollutant exposure, the risk of BPH increased by 2.77% (P < 0.0001) for every 1 μg/m3 increase of PM2.5. The other single and mixed pollutants also remained dangerous. Further analysis revealed that each additional 1 μg/m3 of PM2.5 increased 2.34% risk of LUTS (P = 0.0014). The other pollutants also remained dangerous. The same applies to other single and mixed pollutants. The restricted cubic spline (RCS) curve found that there was a dose–response relationship between PM2.5 concentration and BPH risk (P = 0.0169) and determined that 9.83 μg/m3 was the risk threshold for BPH. Compared with participants’ exposure to low PM2.5 and low-fat diet, participants with high PM2.5 exposure and high-fat diet had 16% increased risk of BPH (P < 0.0001). Mediation analysis identified 34 lipid-related metabolites as potential mediators. This study emphasizes the significance of environmental and lifestyle factors in the prevention and management of BPH.
Wei et al. (2026) studied this question.