Overview
Air pollution is a pervasive global health threat that extends beyond the lungs. A growing body of evidence indicates that ambient pollutants can affect the urinary tract and male reproductive health, increasing the risk of urinary tract infections (UTIs) and male reproductive system infections (MRSIs) such as prostatitis and orchiepididymitis. A large prospective cohort study using the UK Biobank cohort provides new, clinically validated insights into how long-term exposure to key pollutants relates to these infections over up to 15 years of follow-up.
Study design and exposure assessment
The UK Biobank study followed nearly 376,000 participants (after exclusions) from 2006–2010, tracking incident UTIs and MRSIs identified via validated hospital records and ICD-10 codes. Long-term exposure to air pollutants was estimated for 2010 using land-use regression models based on ESCAPE data. The pollutants included PM2.5, PM10, PMcoarse (2.5–10 μm), NO2, and NOx. By leveraging individual-level exposure estimates and clinically defined outcomes, the researchers aimed to overcome prior limitations seen in smaller, cross-sectional studies.
Key findings: UTIs and air pollution
Across fully adjusted models, higher exposure to the studied pollutants was consistently associated with an increased risk of UTIs. Notably:
- A 5 μg/m3 rise in PM2.5 or PMcoarse corresponded to a 43% and 17% higher UTI risk, respectively.
- A 10 μg/m3 rise in PM10 was linked to about a 24% higher UTI risk.
- NO2 and NOx also showed meaningful associations, with each 10 μg/m3 NO2 increase and each 20 μg/m3 NOx increase raising UTI risk by ~10% and ~9%, respectively.
Nonlinear exposure-response curves (restricted cubic splines) indicated that risks rose more sharply at higher pollutant levels, particularly for PM2.5. Stratified analyses suggested the strongest pollutant-related increases occurred among older adults and women for PMcoarse, though most pollutants showed positive associations across subgroups.
Key findings: MRSIs and air pollution
For MRSIs, associations with long-term air pollution exposure were also evident. Specifically:
- PM2.5: a 5 μg/m3 increase was associated with a 30% higher MRSI risk.
- PM10: a 10 μg/m3 increase correlated with a 24% higher risk.
- NO2 and NOx showed significant, albeit smaller, associations (NO2: ~12% per 10 μg/m3; NOx: ~8% per 20 μg/m3).
The exposure–response curves for MRSIs revealed nonlinear patterns, with noticeable risk increases once PM2.5 exceeded around 12.5 μg/m3. Subgroup analyses highlighted that age, BMI, smoking, diet, and income could modify some pollutant effects, though the overall direction of risk remained positive across most groups.
Interpretation of mechanisms
The study discusses several plausible pathways by which air pollution could influence UTIs and MRSIs. Systemic oxidative stress and inflammation, driven by fine particles and NOx, may compromise mucosal barriers and urinary tract tissues. Heavy metals carried by PM10/PMcoarse could contribute nephrotoxicity, while inflammatory cascades triggered by inhaled pollutants might promote susceptibility to infections in distant organs, including the urinary tract and prostate. These mechanisms align with observed non-linear relationships, suggesting heightened vulnerability at higher exposure levels.
Strengths and limitations
Strengths include the prospective design, a large, well-characterized cohort, clinically validated outcomes, and individualized exposure assessment. However, limitations exist. Exposure was measured at baseline and may not capture changes over time; other pollutants (ozone, CO, SO2) were not analyzed; and residual confounding remains possible despite extensive covariate adjustment. The authors note potential collinearity concerns are minimal in their models, and sensitivity analyses supported the robustness of findings.
Public health implications
These findings strengthen the case for air quality improvements as a means to reduce infectious disease burden beyond respiratory outcomes. Policymakers should consider integrated strategies that lower ambient pollution levels, particularly in urban and industrialized settings, to potentially ease pressures on healthcare systems from UTIs and MRSIs. Clinicians and public health practitioners may also factor environmental exposure into risk assessment and prevention efforts for urogenital infections.
Conclusion
With its large sample and clinically validated outcomes, the UK Biobank analysis provides compelling evidence that long-term exposure to ambient air pollutants is associated with higher incidence of UTIs and MRSIs. The study highlights nonlinear exposure-response patterns and suggests that environmental health policies should incorporate urogenital infection risk alongside traditional cardiovascular and respiratory concerns.
