Personal exposure to traffic-related air pollutants and relationships with respiratory symptoms and oxidative stress: A pilot cross-sectional study among urban green space workers.

Exposure to ambient air pollution has been associated with various adverse health effects including respiratory, cardiovascular and neurological diseases. Exposure data for some specific pollutants and settings are however still insufficient and mechanisms underlying negative health outcomes are not fully elucidated. This pilot study aimed to assess individual exposure to three traffic-related air pollutants, black carbon (BC), polycyclic aromatic hydrocarbons (PAHs) and benzene, and the relationship with respiratory and oxidative stress outcomes in a cross-sectional sample of 48 green space workers in Brussels, Belgium. Participants were followed during four consecutive working days in 2016-2017 during which their individual exposure to BC, PAHs, benzene and more generally air pollution was measured using aethalometers, urinary biomarkers (1-hydroxypyrene, 1-naphthol, 2-naphthol, S-phenylmercapturic acid) and questionnaires. Data on respiratory health and oxidative stress were collected using questionnaires and respiratory/urinary biomarkers (exhaled nitric oxide [NO], 8-hydroxydeoxyguanosine [8-OHdG]). Associations between exposure and health outcomes were investigated using comparison tests and linear regression models, after stratification by present-day smoking status. Spatial variation in BC exposure was high, with concentrations varying between 0.26 and 5.69 μg/m. The highest levels were recorded during transport and, to a lesser extent, in green spaces located in the vicinity of roads with high traffic intensity. Concentrations of PAHs and benzene biomarkers did not systematically exceed the limits of detection. Among smokers, respiratory inflammation increased linearly with exposure to BC measured over the four days of follow-up (β = 8.73, 95% CI: 4.04, 13.41). Among non-smokers, oxidative stress increased linearly with BC measured on the fourth day (β = 2.88, 95% CI: 1.52, 4.24). Despite some limitations, this work supports the hypothesis that BC induces respiratory inflammation and oxidative stress. It also highlights the value of this compound as well as exhaled NO and urinary 8-OHdG biomarkers to detect early/mild effects of air pollution.