Dataset Information

Ambient air pollution and prostate cancer risk in a population-based Canadian case-control study.

ABSTRACT: Ambient air pollution is a human carcinogen and a possible risk factor for prostate cancer.

Methods

We investigated associations between ambient concentrations particulate matter 2.5 (PM_2.5) and nitrogen dioxide (NO₂) and incident prostate cancer in a Canadian case-control study. Between 1994 and 1997, cases were identified from provincial cancer registries, and a population-based series of controls was recruited. Among men 50 years of age or older, risk factor and residential history data (1975 to 1994) were collected from 1,420 prostate cancer cases and 1,424 controls. Three methods were used to estimate the residential mean exposure to PM_2.5 and NO₂ during this period: (1) satellite-derived observations; (2) satellite-derived observations scaled with historical fixed-site measurements; and (3) a national land-use regression (LUR) model. Odds ratios (ORs) and their 95% confidence intervals (CIs) in relation to interquartile range (IQR) increases in PM_2.5 and NO₂ were estimated using logistic regression, adjusting for personal and contextual factors.

Results

We found positive associations between exposure to PM_2.5 and NO₂ over the previous 20 years and prostate cancer. An IQR increase in PM_2.5 (3.56 µg/m³ for satellite and 4.48 µg/m³ for scaled satellite observations) yielded ORs of 1.28 (95% CI = 1.07, 1.52) and 1.20 (95% CI = 1.03, 1.40), respectively. For NO₂, IQR increases (1.45 ppb for satellite, 15.18 ppb for scaled satellite-derived information, and 15.39 ppb for the national LUR) were associated with ORs of 1.09 (95% CI = 0.95, 1.24), 1.21 (95% CI = 1.02, 1.43), and 1.19 (95% CI = 1.03, 1.38), respectively.

Conclusions

Our findings support the hypothesis that ambient air pollution increases the risk of prostate cancer.

SUBMITTER: Youogo LMK

PROVIDER: S-EPMC9374191 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature

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Publications

Ambient air pollution and prostate cancer risk in a population-based Canadian case-control study.

Youogo Leslie Michele-Ange Kouam LMK Parent Marie-Elise ME Hystad Perry P Villeneuve Paul J PJ

Environmental epidemiology (Philadelphia, Pa.) 20220719 4

Ambient air pollution is a human carcinogen and a possible risk factor for prostate cancer.<h4>Methods</h4>We investigated associations between ambient concentrations particulate matter 2.5 (PM<sub>2.5</sub>) and nitrogen dioxide (NO<sub>2</sub>) and incident prostate cancer in a Canadian case-control study. Between 1994 and 1997, cases were identified from provincial cancer registries, and a population-based series of controls was recruited. Among men 50 years of age or older, risk factor and r ...[more]

PMID: 35975163

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Project description:BackgroundFew epidemiological studies of air pollution have used residential histories to develop long-term retrospective exposure estimates for multiple ambient air pollutants and vehicle and industrial emissions. We present such an exposure assessment for a Canadian population-based lung cancer case-control study of 8353 individuals using self-reported residential histories from 1975 to 1994. We also examine the implications of disregarding and/or improperly accounting for residential mobility in long-term exposure assessments.MethodsNational spatial surfaces of ambient air pollution were compiled from recent satellite-based estimates (for PM2.5 and NO2) and a chemical transport model (for O3). The surfaces were adjusted with historical annual air pollution monitoring data, using either spatiotemporal interpolation or linear regression. Model evaluation was conducted using an independent ten percent subset of monitoring data per year. Proximity to major roads, incorporating a temporal weighting factor based on Canadian mobile-source emission estimates, was used to estimate exposure to vehicle emissions. A comprehensive inventory of geocoded industries was used to estimate proximity to major and minor industrial emissions.ResultsCalibration of the national PM2.5 surface using annual spatiotemporal interpolation predicted historical PM2.5 measurement data best (R2 = 0.51), while linear regression incorporating the national surfaces, a time-trend and population density best predicted historical concentrations of NO2 (R2 = 0.38) and O3 (R2 = 0.56). Applying the models to study participants residential histories between 1975 and 1994 resulted in mean PM2.5, NO2 and O3 exposures of 11.3 μg/m3 (SD = 2.6), 17.7 ppb (4.1), and 26.4 ppb (3.4) respectively. On average, individuals lived within 300 m of a highway for 2.9 years (15% of exposure-years) and within 3 km of a major industrial emitter for 6.4 years (32% of exposure-years). Approximately 50% of individuals were classified into a different PM2.5, NO2 and O3 exposure quintile when using study entry postal codes and spatial pollution surfaces, in comparison to exposures derived from residential histories and spatiotemporal air pollution models. Recall bias was also present for self-reported residential histories prior to 1975, with cases recalling older residences more often than controls.ConclusionsWe demonstrate a flexible exposure assessment approach for estimating historical air pollution concentrations over large geographical areas and time-periods. In addition, we highlight the importance of including residential histories in long-term exposure assessments. For submission to: Environmental Health.

Project description:Few epidemiologic studies have evaluated the effects of air pollution on the risk of Parkinson disease (PD).We investigated the associations of long-term residential concentrations of ambient particulate matter (PM) < 10 ?m in diameter (PM10) and < 2.5 ?m in diameter (PM2.5) and nitrogen dioxide (NO2) in relation to PD risk.Our nested case-control analysis included 1,556 self-reported physician-diagnosed PD cases identified between 1995 and 2006 and 3,313 controls frequency-matched on age, sex, and race. We geocoded home addresses reported in 1995-1996 and estimated the average ambient concentrations of PM10, PM2.5, and NO2 using a national fine-scale geostatistical model incorporating roadway information and other geographic covariates. Air pollutant exposures were analyzed as both quintiles and continuous variables, adjusting for matching variables and potential confounders.We observed no statistically significant overall association between PM or NO2 exposures and PD risk. However, in preplanned subgroup analyses, a higher risk of PD was associated with higher exposure to PM10 (ORQ5 vs. Q1 = 1.65; 95% CI: 1.11, 2.45; p-trend = 0.02) among women, and with higher exposure to PM2.5 (ORQ5 vs. Q1 = 1.29; 95% CI: 0.94, 1.76; p-trend = 0.04) among never smokers. In post hoc analyses among female never smokers, both PM2.5 (ORQ5 vs. Q1 = 1.79; 95% CI: 1.01, 3.17; p-trend = 0.05) and PM10 (ORQ5 vs. Q1 = 2.34; 95% CI: 1.29, 4.26; p-trend = 0.01) showed positive associations with PD risk. Analyses based on continuous exposure variables generally showed similar but nonsignificant associations.Overall, we found limited evidence for an association between exposures to ambient PM10, PM2.5, or NO2 and PD risk. The suggestive evidence that exposures to PM2.5 and PM10 may increase PD risk among female never smokers warrants further investigation. Citation: Liu R, Young MT, Chen JC, Kaufman JD, Chen H. 2016. Ambient air pollution exposures and risk of Parkinson disease. Environ Health Perspect 124:1759-1765;?http://dx.doi.org/10.1289/EHP135.

Project description:BackgroundAlthough growing evidence links air pollution to stroke incidence, less is known about the effect of air pollution on atrial fibrillation (AF), an important risk factor for stroke.ObjectivesWe assessed the associations between air pollution and incidence of AF and stroke. We also sought to characterize the shape of pollutant-disease relationships.MethodsThe population-based cohort comprised 5,071,956 Ontario residents, age 35–85 y and without the diagnoses of both outcomes on 1 April 2001 and was followed up until 31 March 2015. AF and stroke cases were ascertained using health administrative databases with validated algorithms. Based on annual residential postal codes, we assigned 5-y running average concentrations of fine particulate matter ([Formula: see text]), nitrogen dioxide ([Formula: see text]), and ozone ([Formula: see text]) from satellite-derived data, a land-use regression model, and a fusion-based method, respectively, as well as redox-weighted averages of [Formula: see text] and [Formula: see text] ([Formula: see text]) for each year. Using Cox proportional hazards models, we estimated the hazard ratios (HRs) and 95% confidence intervals (95% CIs) of AF and stroke with each of these pollutants, adjusting for individual- and neighborhood-level variables. We used newly developed nonlinear risk models to characterize the shape of pollutant–disease relationships.ResultsBetween 2001 and 2015, we identified 313,157 incident cases of AF and 122,545 cases of stroke. Interquartile range increments of [Formula: see text], [Formula: see text], [Formula: see text], and [Formula: see text] were associated with increases in the incidence of AF [HRs (95% CIs): 1.03 (1.01, 1.04), 1.02 (1.01, 1.03), 1.01 (1.00, 1.02), and 1.01 (1.01, 1.02), respectively] and the incidence of stroke [HRs (95% CIs): 1.05 (1.03, 1.07), 1.04 (1.01, 1.06), 1.05 (1.03, 1.06), and 1.05 (1.04, 1.06), respectively]. Associations of similar magnitude were found in various sensitivity analyses. Furthermore, we found a near-linear association for stroke with [Formula: see text], whereas [Formula: see text], [Formula: see text]-, and [Formula: see text] relationships exhibited sublinear shapes.ConclusionsAir pollution was associated with stroke and AF onset, even at very low concentrations. https://doi.org/10.1289/EHP4883.

Dataset Information

Ambient air pollution and prostate cancer risk in a population-based Canadian case-control study.

Methods

Results

Conclusions

Publications

Ambient air pollution and prostate cancer risk in a population-based Canadian case-control study.

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