Air pollutants such as NO2 and PM2.5 have consistently been linked to mortality, but only few previous studies have addressed associations with long-term exposure to black carbon (BC) and ozone (O3). We investigated the association between PM2.5, PM10, BC, NO2, and O3 and mortality in a Danish cohort of 49,564 individuals who were followed up from enrollment in 1993-1997 through 2015. Residential address history from 1979 onwards was combined with air pollution exposure obtained by the state-of-the-art, validated, THOR/AirGIS air pollution modelling system, and information on residential traffic noise exposure, lifestyle and socio-demography. We observed higher risks of all-cause as well as cardiovascular disease (CVD) mortality with higher long-term exposure to PM2.5, PM10, BC, and NO2. For PM2.5 and CVD mortality, a hazard ratio (HR) of 1.29 (95% CI: 1.13-1.47) per 5 μg/m3 was observed, and correspondingly HRs of 1.16 (95% CI: 1.05-1.27) and 1.11 (95% CI: 1.04-1.17) were observed for BC (per 1 μg/m3) and NO2 (per 10 μg/m3), respectively. Adjustment for noise gave slightly lower estimates for the air pollutants and CVD mortality. Inverse relationships were observed for O3. None of the investigated air pollutants were related to risk of respiratory mortality. Stratified analyses suggested that the elevated risks of CVD and all-cause mortality in relation to long-term PM, NO2 and BC exposure were restricted to males. This study supports a role of PM, BC, and NO2 in all-cause and CVD mortality independent of road traffic noise exposure.

Vehicle engine exhaust includes ultrafine particles with a large surface area and containing absorbed polycyclic aromatic hydrocarbons, transition metals and other substances. Ultrafine particles and soluble chemicals can be transported from the airways to other organs, such as the liver, kidneys, and brain. Our aim was to investigate whether air pollution from traffic is associated with risk for other cancers than lung cancer. We followed up 54,304 participants in the Danish Diet Cancer and Health cohort for 20 selected cancers in the Danish Cancer Registry, from enrolment in 1993-1997 until 2006, and traced their residential addresses from 1971 onwards in the Central Population Registry. We used modeled concentration of nitrogen oxides (NO_x) and amount of traffic at the residence as indicators of traffic-related air pollution and used Cox models to estimate incidence rate ratios (IRRs) after adjustment for potential confounders. NO_x at the residence was significantly associated with risks for cervical cancer (IRR, 2.45; 95% confidence interval [CI], 1.01;5.93, per 100 μg/m³ NO_x) and brain cancer (IRR, 2.28; 95% CI, 1.25;4.19, per 100 μg/m³ NO_x). This hypothesis-generating study indicates that traffic-related air pollution might increase the risks for cervical and brain cancer, which should be tested in future studies.

The hypothesis that exposure to traffic-related air pollution increases the risk of developing cancer during childhood was investigated. The authors enrolled 1,989 children reported to the Danish Cancer Registry with a diagnosis of leukemia, tumor of the central nervous system, or malignant lymphoma during 1968–1991 and 5,506 control children selected at random from the entire childhood population. The residential histories of the children were traced from 9 months before birth until the time of diagnosis of the cases and a similar period for the controls. For each of the 18,440 identified addresses, information on traffic and the configuration of streets and buildings was collected. Average concentrations of benzene and nitrogen dioxide (indicators of traffic-related air pollution) were calculated for the relevant period, and exposures to air pollution during pregnancy and during childhood were calculated separately. The risks of leukemia, central nervous system tumors, and all selected cancers combined were not linked to exposure to benzene or nitrogen dioxide during either period. The risk of lymphomas increased by 25% (p for trend = 0.06) and 51% (p for trend = 0.05) for a doubling of the concentration of benzene and nitrogen dioxide, respectively, during the pregnancy. The association was restricted to Hodgkin's disease.