Sam E Wing1, Gretchen Bandoli2, Donatello Telesca3, Jason G Su4, Beate Ritz5. 1. Department of Epidemiology, Fielding School of Public Health, University of California, Los Angeles, 650 Charles E Young Dr S, Los Angeles, CA 90095, USA. Electronic address: samwing@ucla.edu. 2. Department of Pediatrics, University of California, San Diego, 9500 Gilman Drive #0828 La Jolla, CA 92093, USA. Electronic address: gbandoli@ucsd.edu. 3. Environmental Health Sciences Division, School of Public Health, University of California, Berkeley 50 University Hall #7360, Berkeley, CA 94720, USA. Electronic address: dtelesca@ucla.edu. 4. Department of Biostatistics, Fielding School of Public Health, University of California, Los Angeles, 650 Charles E Young Dr S, Los Angeles, CA 90095, USA. Electronic address: jasonsu@berkeley.edu. 5. Department of Epidemiology, Fielding School of Public Health, University of California, Los Angeles, 650 Charles E Young Dr S, Los Angeles, CA 90095, USA. Electronic address: britz@ucla.edu.
Abstract
BACKGROUND: Chronic health effects of traffic-related air pollution, like nitrogen dioxide (NO2), are well-documented. Animal models suggested that NO2 exposures dysregulate cortisol function. OBJECTIVES: We evaluated the association between traffic-related NO2 exposure and adolescent human cortisol concentrations, utilizing measures of the cortisol diurnal slope. METHODS: 140 adolescents provided repeated salivary cortisol samples throughout one day. We built a land use regression model to estimate chronic NO2 exposures based on home and school addresses. We then generated model-based estimates of the association between cortisol and NO2 exposure one year prior to cortisol sampling, examining changes in cortisol diurnal slope. The final model was adjusted other criteria pollutants, measures of psychosocial stress, anthropometry, and other demographic and covariates. RESULTS: We observed a decrease in diurnal slope in cortisol for adolescents exposed to the estimated 75th percentile of ambient NO2 (high exposure) relative to those exposed at the 25th percentile (low exposure). For a highly exposed adolescent, the log cortisol was lower by 0.06 µg/dl at waking (95% CI: -0.15, 0.02), 0.07 µg/dl at 30 min post waking (95% CI: -0.15, 0.02), and higher by 0.05 µg/dl at bedtime (95% CI: 0.05, 0.15), compared to a low exposed adolescent. For an additional interquartile range of exposure, the model-based predicted diurnal slope significantly decreased by 0.12 (95% CI: -0.23, -0.01). CONCLUSIONS: In adolescents, we found that increased, chronic exposure to NO2 and the mixture of pollutants from traffic sources was associated with a flattened diurnal slope of cortisol, a marker of an abnormal cortisol response which we hypothesize may be a mechanism through which air pollution may affect respiratory function and asthma in adolescents.
BACKGROUND: Chronic health effects of traffic-related air pollution, like nitrogen dioxide (NO2), are well-documented. Animal models suggested that NO2 exposures dysregulate cortisol function. OBJECTIVES: We evaluated the association between traffic-related NO2 exposure and adolescent humancortisol concentrations, utilizing measures of the cortisol diurnal slope. METHODS: 140 adolescents provided repeated salivary cortisol samples throughout one day. We built a land use regression model to estimate chronic NO2 exposures based on home and school addresses. We then generated model-based estimates of the association between cortisol and NO2 exposure one year prior to cortisol sampling, examining changes in cortisol diurnal slope. The final model was adjusted other criteria pollutants, measures of psychosocial stress, anthropometry, and other demographic and covariates. RESULTS: We observed a decrease in diurnal slope in cortisol for adolescents exposed to the estimated 75th percentile of ambient NO2 (high exposure) relative to those exposed at the 25th percentile (low exposure). For a highly exposed adolescent, the log cortisol was lower by 0.06 µg/dl at waking (95% CI: -0.15, 0.02), 0.07 µg/dl at 30 min post waking (95% CI: -0.15, 0.02), and higher by 0.05 µg/dl at bedtime (95% CI: 0.05, 0.15), compared to a low exposed adolescent. For an additional interquartile range of exposure, the model-based predicted diurnal slope significantly decreased by 0.12 (95% CI: -0.23, -0.01). CONCLUSIONS: In adolescents, we found that increased, chronic exposure to NO2 and the mixture of pollutants from traffic sources was associated with a flattened diurnal slope of cortisol, a marker of an abnormal cortisol response which we hypothesize may be a mechanism through which air pollution may affect respiratory function and asthma in adolescents.
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