Publication date: 

1 Feb 2019

Ref: 

Environ Int. 2019 Feb;123:124-131

Author(s): 

Van Veldhoven K, Kiss A, Keski-Rahkonen P, Robinot N, Scalbert A, Cullinan P, Chung KF, Collins P, Sinharay R, Barratt BM, Nieuwenhuijsen M, Rodoreda AA, Carrasco-Turigas G, Vlaanderen J, Vermeulen R, Portengen L, Kyrtopoulos SA, Ponzi E, Chadeau-Hyam M, Vineis P.

Publication type: 

Article

Abstract: 

Exposure to traffic-related air pollution (TRAP) has been associated with adverse health outcomes but underlying biological mechanisms remain poorly understood. Two randomized crossover trials were used here, the Oxford Street II (London) and the TAPAS II (Barcelona) studies, where volunteers were allocated to high or low air pollution exposures. The two locations represent different exposure scenarios, with Oxford Street characterized by diesel vehicles and Barcelona by normal mixed urban traffic. Levels of five and four pollutants were measured, respectively, using personal exposure monitoring devices. Serum samples were used for metabolomic profiling. The association between TRAP and levels of each metabolic feature was assessed. All pollutant levels were significantly higher at the high pollution sites. 29 and 77 metabolic features were associated with at least one pollutant in the Oxford Street II and TAPAS II studies, respectively, which related to 17 and 30 metabolic compounds. Little overlap was observed across pollutants for metabolic features, suggesting that different pollutants may affect levels of different metabolic features. After observing the annotated compounds, the main pathway suggested in Oxford Street II in association with NO2 was the acyl-carnitine pathway, previously found to be associated with cardio-respiratory disease. No overlap was found between the metabolic features identified in the two studies.