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  • Title: Five epidemiological studies on transport and asthma: objectives, design and descriptive results.
    Author: Zmirou D, Gauvin S, Pin I, Momas I, Just J, Sahraoui F, Le Moullec Y, Brémont F, Cassadou S, Albertini M, Lauvergne N, Chiron M, Labbé A, VESTA Investigators.
    Journal: J Expo Anal Environ Epidemiol; 2002 May; 12(3):186-96. PubMed ID: 12032815.
    Abstract:
    A case-control study was conducted in five French metropolitan areas in order to assess the role of traffic-related air pollution in the occurrence of childhood asthma. This paper presents the study design and describes the distribution of key exposure variables. A set of 217 pairs of matched 4- to 14-year-old cases and controls were investigated (matching criteria: city, age, and gender). Current and past environmental smoke exposures, indoor allergens or air pollution sources, and personal and family atopy were assessed by standard questionnaires. When possible, direct measurements were done to check the validity of this information, on current data: skin prick tests, urine cotinine, house dust mites densities, personal exposures to, and home indoor concentrations of NO(x) and PM(2.5). Cumulative exposure to traffic-related pollutants was estimated through two indices: "traffic density" refers to a time-weighted average of the traffic density-to-road distance ratio for all home and school addresses of each child's life; "air pollution" index combines lifelong time-activity patterns and ambient air concentration estimates of NO(x), using an air dispersion model of traffic exhausts. Average current PM(2.5) personal exposure is 23.8 microg/m3 (SD=17.4), and average indoor concentrations=22.5 microg/m3 (18.2); corresponding values for NO(2) are 31.4 (13.9) and 36.1 (21.4) microg/m3. Average lifelong calculated exposures to traffic-related NO(x) emissions are 62.6 microg/m3 (43.1). The five cities show important contrasts of exposure to traffic pollutants. These data will allow comparison of lifelong exposures to indicators of traffic exhausts between cases and controls, including during early ages, while controlling for a host of known enhancers or precipitators of airway chronic inflammation and for possible confounders.
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