Mendelian randomization evaluates the causal impact of air pollutants on benign prostatic hyperplasia, suggesting an association with NO₂ exposure.
An increasing number of studies have investigated the relationship between air pollution and human health, yielding significant findings. However, few studies have explored the relationship between air pollution and prostate health. Mendelian randomization was employed to evaluate the causal relationships between 5 major air pollutants and benign prostatic hyperplasia. Univariate Mendelian randomization (UVMR) was used to test the primary causal relationships, whereas multivariate Mendelian randomization (MVMR) was applied to construct risk-adjusted models, enhancing the robustness of the causal inference. Finally, we further assessed the potential mediating role of the gut microbiome in the relationships identified. We found a significant positive causal association between NO₂ and benign prostatic hyperplasia (OR = 2.39, 95% CI = 1.17–4.91, P = .01). The results of the MVMR analysis are consistent with UVMR (OR = 2.01, 95% CI = 1.05–3.85, P = .03). Additionally, we identified significant positive associations between several gut microbial species and benign prostatic hyperplasia. However, further mediated Mendelian randomization analyses did not reveal a mediating effect in the causal relationship between NO₂ and benign prostatic hyperplasia. Mendelian randomization analysis showed that there is a genetic causal relationship between air pollution and benign prostatic hyperplasia, and high exposure to NO 2 will increase the risk of benign prostatic hyperplasia.
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Xia et al. (2025) studied this question.
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