Journal of the National Cancer Institute · 2026
Outdoor air pollution and prostate cancer risk in the NIH-AARP diet and health study.
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Post Lydia Marcus, Hurwitz Lauren, Fisher Jared A, Kaufman Joel D, Koutros Stella, Jones Rena R
Аннотация
BACKGROUND: Outdoor air pollution, including fine particulate matter (PM2.5), is an established carcinogen, yet few studies evaluate its associations with prostate cancer risk and findings are mixed.
METHODS: We used spatiotemporal prediction models to estimate annual average historical residential PM2.5 (1980 to 2017) and NO2 (1990 to 2017) concentrations for N = 289,299 men aged ≥50 years in the NIH-AARP Diet and Health Study, enrolled from six states and two metro areas in 1995 to 1996, followed through 2018. We used Cox regression to estimate hazard ratios and 95% confidence intervals (HR [CI]) of associations between 5-year average PM2.5 and NO2 and incident prostate cancer, overall and by tumor aggressiveness (ie, advanced [n = 5,791], high-grade [ie, Gleason score ≥8, n = 5,793], fatal [n = 3,057]). We evaluated interactions with hypothesized effect modifiers.
RESULTS: Historical PM2.5 and NO2 concentrations were not associated with prostate cancer risk overall (PM2.5 HR10-year lag per 5 µg/m3=1.00 [0.98-1.02], NO2 HR10-year lag per 10 ppb = 1.00 [0.98-1.01]). Some positive trends were observed for aggressive disease (eg, high-grade PM2.5 HR10-year lag=1.03 [0.99-1.09], advanced: NO2 HR10-year lag=1.04 [0.99-1.08]). Stratified analyses also showed stronger associations for aggressive disease among Hispanic men (eg, high-grade: NO2 HR = 1.25 [1.05-1.48], pint=0.01). Heterogeneity was also evident by urbanicity (high-grade: pint=0.01, PM2.5 and NO2) and state (advanced: pint=0.05, NO2), potentially reflecting air pollution mixture heterogeneity.
CONCLUSIONS: In this large U.S. cohort, historical residential PM2.5 or NO2 concentrations were not associated with prostate cancer risk overall; however, risk was elevated in some subgroups and for aggressive outcomes. Future evaluation of air pollution mixture components may clarify observed subgroup differences.
METHODS: We used spatiotemporal prediction models to estimate annual average historical residential PM2.5 (1980 to 2017) and NO2 (1990 to 2017) concentrations for N = 289,299 men aged ≥50 years in the NIH-AARP Diet and Health Study, enrolled from six states and two metro areas in 1995 to 1996, followed through 2018. We used Cox regression to estimate hazard ratios and 95% confidence intervals (HR [CI]) of associations between 5-year average PM2.5 and NO2 and incident prostate cancer, overall and by tumor aggressiveness (ie, advanced [n = 5,791], high-grade [ie, Gleason score ≥8, n = 5,793], fatal [n = 3,057]). We evaluated interactions with hypothesized effect modifiers.
RESULTS: Historical PM2.5 and NO2 concentrations were not associated with prostate cancer risk overall (PM2.5 HR10-year lag per 5 µg/m3=1.00 [0.98-1.02], NO2 HR10-year lag per 10 ppb = 1.00 [0.98-1.01]). Some positive trends were observed for aggressive disease (eg, high-grade PM2.5 HR10-year lag=1.03 [0.99-1.09], advanced: NO2 HR10-year lag=1.04 [0.99-1.08]). Stratified analyses also showed stronger associations for aggressive disease among Hispanic men (eg, high-grade: NO2 HR = 1.25 [1.05-1.48], pint=0.01). Heterogeneity was also evident by urbanicity (high-grade: pint=0.01, PM2.5 and NO2) and state (advanced: pint=0.05, NO2), potentially reflecting air pollution mixture heterogeneity.
CONCLUSIONS: In this large U.S. cohort, historical residential PM2.5 or NO2 concentrations were not associated with prostate cancer risk overall; however, risk was elevated in some subgroups and for aggressive outcomes. Future evaluation of air pollution mixture components may clarify observed subgroup differences.