Association between a Composite Lifestyle Risk Score and Urinary Polycyclic Aromatic Hydrocarbon Levels in a Pilot Nigerian Male Cohort: A Multicenter Cross-Sectional Study

Abstract

Background: Polycyclic aromatic hydrocarbons (PAHs) from dietary, occupational, domestic, and tobacco sources contribute to the cumulative internal PAH burden. Whether a composite lifestyle score integrating these exposures predicts urinary PAH concentrations in sub-Saharan African populations with high baseline dietary PAH exposure remains unknown. Objective: The objective of this study is to examine the association between a four-component composite lifestyle PAH risk score (range 0–4) and total urinary PAH biomarker concentrations in Nigerian men with prostate diseases, and to evaluate whether smoking history modifies this association. Methods: This multicenter cross-sectional pilot study enrolled 25 men (15 prostate cancer, 10 benign prostatic hyperplasia) from two tertiary hospitals in southeastern Nigeria (January–August 2025). The composite lifestyle risk score summed four binary components: smoking history, above-median dietary PAH score, high-risk occupation, and physical inactivity. Total urinary PAH (sum of 16 EPA-priority congeners) was quantified by gas chromatography with flame ionisation detection (GC-FID). Notably, analysis was performed on unconjugated parent PAH without enzymatic hydrolysis or creatinine correction. Spearman rank correlations and linear regression models assessed score–biomarker associations; smoking-stratified analyses evaluated effect modification. Results: Of 25 participants, 11 (44.0%) were former smokers and 14 (56.0%) were never smokers. Median total urinary PAH was 24.3 mg/L (interquartile range [IQR] 6.75–88.86). The composite lifestyle score (mean 2.33 ± 0.97; range 1–4) showed no significant overall association with urinary PAH (Spearman ρ = −0.147, p = 0.524). Smoking-stratified analysis revealed opposing directional trends: among former smokers, higher lifestyle scores showed a non-significant positive trend with urinary PAH (ρ = +0.512, p = 0.089), while among never smokers the trend was inverse (ρ = −0.287, p = 0.366). Individual dietary components showed significant inverse associations with urinary PAH, consistent with the dietary PAH paradox described in preliminary analyses of this cohort. Conclusions: In this pilot study of 25 Nigerian men with prostate diseases, a composite lifestyle risk score did not significantly predict urinary PAH concentrations, although wide confidence intervals preclude definitive conclusions. Smoking history emerged as a qualitative effect modifier producing opposing directional associations—a hypothesis-generating finding that warrants confirmation in adequately powered, smoking-stratified study designs. These findings underscore the need for population-specific public health strategies that prioritise smoking cessation, dietary PAH reduction through modified food preparation practices, and occupational safety measures to mitigate carcinogenic PAH exposure in high-risk sub-Saharan African communities.