Background: Epidemiological evidence on the association between ambient air pollution and brain tumor risk is sparse and inconsistent. Methods: In 12 cohorts from six 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 282,194 subjects from 12 cohorts, 466 developed malignant brain tumors during 12 years of follow-up. Six of the cohorts had also data on nonmalignant brain tumor, where among 106,786 subjects, 366 developed brain tumor: 176 nonmalignant and 190 malignant. We found a positive, statistically non-significant association between malignant brain tumor and PM2.5 absorbance (Hazard Ratio and 95% Confidence Interval: 1.67; 0.89-3.14 per 10 -5/m 3), 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/m 3) 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
