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. 2018 Feb 19;20(3):420-432.
doi: 10.1093/neuonc/nox163.

Long-term exposure to ambient air pollution and incidence of brain tumor: the European Study of Cohorts for Air Pollution Effects (ESCAPE)

Affiliations

Long-term exposure to ambient air pollution and incidence of brain tumor: the European Study of Cohorts for Air Pollution Effects (ESCAPE)

Zorana J Andersen et al. Neuro Oncol. .

Abstract

Background: Epidemiological evidence on the association between ambient air pollution and brain tumor risk is sparse and inconsistent.

Methods: In 12 cohorts from 6 European countries, individual estimates of annual mean air pollution levels at the baseline residence were estimated by standardized land-use regression models developed within the ESCAPE and TRANSPHORM projects: particulate matter (PM) ≤2.5, ≤10, and 2.5-10 μm in diameter (PM2.5, PM10, and PMcoarse), PM2.5 absorbance, nitrogen oxides (NO2 and NOx) and elemental composition of PM. We estimated cohort-specific associations of air pollutant concentrations and traffic intensity with total, malignant, and nonmalignant brain tumor, in separate Cox regression models, adjusting for risk factors, and pooled cohort-specific estimates using random-effects meta-analyses.

Results: Of 282194 subjects from 12 cohorts, 466 developed malignant brain tumors during 12 years of follow-up. Six of the cohorts also had data on nonmalignant brain tumor, where among 106786 subjects, 366 developed brain tumor: 176 nonmalignant and 190 malignant. We found a positive, statistically nonsignificant association between malignant brain tumor and PM2.5 absorbance (hazard ratio and 95% CI: 1.67; 0.89-3.14 per 10-5/m3), and weak positive or null associations with the other pollutants. Hazard ratio for PM2.5 absorbance (1.01; 0.38-2.71 per 10-5/m3) and all other pollutants were lower for nonmalignant than for malignant brain tumors.

Conclusion: We found suggestive evidence of an association between long-term exposure to PM2.5 absorbance indicating traffic-related air pollution and malignant brain tumors, and no association with overall or nonmalignant brain tumors.

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Figures

Fig. 1
Fig. 1
Adjusted associations between malignant brain tumor and PM2.5, PM2.5 absorbance, PM10, and PMcoarse (main Model 3) in 10 European cohorts (CEANS [pooled data from the 4 cohorts from Stockholm, Sweden: SNAC-K, SALT/Twin gene, 60 y/IMPROVE, and SDPP], HUBRO, DCH, EPIC-NL [pooled data from 2 cohorts: EPIC-MORGEN and EPIC-PROSPECT], VHM&PP, and EPIC-Turin) result from cohort-specific analyses and random-effects analyses.
Fig. 2
Fig. 2
Adjusted associations between malignant brain tumor and NO2, NOx, and traffic intensity on the nearest road (main Model 3) in 12 European cohorts (aEPIC-Umeå, CEANS [pooled data from the 4 cohorts from Stockholm, Sweden: SNAC-K, SALT/Twin gene, 60 y/IMPROVE, and SDPP], HUBRO, DCH, EPIC-NL [pooled data from 2 cohorts: EPIC-MORGEN and EPIC-PROSPECT], VHM&PP, EPIC-Varese, and EPIC-Turin) result from cohort-specific analyses and random-effects analyses.

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