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 FÊm 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 282 194 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 106 786 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.

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

Ricceri F.;Sacerdote C.;Migliore E.;Vineis P.;
2018-01-01

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 FÊm 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 282 194 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 106 786 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.
2018
20
3
420
432
air pollution; brain cancer; brain tumor; traffic; Adult; Air Pollution; Brain Neoplasms; Cohort Studies; Environmental Exposure; Europe; Female; Follow-Up Studies; Humans; Incidence; Male; Middle Aged; Particulate Matter; Prognosis; Risk Factors
Andersen Z.J.; Pedersen M.; Weinmayr G.; Stafoggia M.; Galassi C.; Jorgensen J.T.; Sommar J.N.; Forsberg B.; Olsson D.; Oftedal B.; Aasvang G.M.; Schwarze P.; Pyko A.; Pershagen G.; Korek M.; Faire U.D.; Ostenson C.-G.; Fratiglioni L.; Eriksen K.T.; Poulsen A.H.; Tjonneland A.; Brauner E.V.; Peeters P.H.; Bueno-De-Mesquita B.; Jaensch A.; Nagel G.; Lang A.; Wang M.; Tsai M.-Y.; Grioni S.; Marcon A.; Krogh V.; Ricceri F.; Sacerdote C.; Migliore E.; Vermeulen R.; Sokhi R.; Keuken M.; De Hoogh K.; Beelen R.; Vineis P.; Cesaroni G.; Brunekreef B.; Hoek G.; Raaschou-Nielsen O.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/1766511
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