Lorraine B Ware1,2, Zhiguo Zhao3, Tatsuki Koyama3, Addison K May4, Michael A Matthay5,6, Fred W Lurmann7, John R Balmes5,8, Carolyn S Calfee5,6. 1. 1 Department of Medicine and. 2. 2 Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee. 3. 3 Department of Biostatistics and. 4. 4 Division of Trauma and Surgical Critical Care, Vanderbilt University, Nashville, Tennessee. 5. 5 Department of Medicine and. 6. 6 Department of Anesthesia and Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California. 7. 7 Sonoma Technology Inc., Petaluma, California; and. 8. 8 Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, Berkeley, California.
Abstract
RATIONALE: The contribution of air pollution to the risk of acute respiratory distress syndrome (ARDS) is unknown. METHODS: We studied 1,558 critically ill patients enrolled in a prospective observational study at a tertiary medical center who lived less than 50 km from an air quality monitor and had an ARDS risk factor. Pollutant exposures (ozone, NO2, SO2, particulate matter < 2.5 μm, particulate matter < 10 μm) were assessed by weighted average of daily levels from the closest monitors for the prior 3 years. Associations between pollutant exposure and ARDS risk were evaluated by logistic regression controlling for age, race, sex, smoking, alcohol, insurance status, rural versus urban residence, distance to study hospital, and Acute Physiology and Chronic Health Evaluation II. MEASUREMENTS AND MAIN RESULTS: The incidence of ARDS increased with increasing ozone exposure: 28% in the lowest exposure quartile versus 32, 40, and 42% in the second, third, and fourth quartiles (P < 0.001). In a logistic regression model controlling for potential confounders, ozone exposure was associated with risk of ARDS in the entire cohort (odds ratio, 1.58 [95% confidence interval, 1.27-1.96]) and more strongly associated in the subgroup with trauma as their ARDS risk factor (odds ratio, 2.26 [95% confidence interval, 1.46-3.50]). There was a strong interaction between ozone exposure and current smoking status (P = 0.007). NO2 exposure was also associated with ARDS but not independently of ozone exposure. SO2, particulate matter less than 2.5 μm, and particulate matter less than 10 μm were not associated with ARDS. CONCLUSIONS: Long-term ozone exposure is associated with development of ARDS in at-risk critically ill patients, particularly in trauma patients and current smokers. Ozone exposure may represent a previously unrecognized environmental risk factor for ARDS.
RATIONALE: The contribution of air pollution to the risk of acute respiratory distress syndrome (ARDS) is unknown. METHODS: We studied 1,558 critically illpatients enrolled in a prospective observational study at a tertiary medical center who lived less than 50 km from an air quality monitor and had an ARDS risk factor. Pollutant exposures (ozone, NO2, SO2, particulate matter < 2.5 μm, particulate matter < 10 μm) were assessed by weighted average of daily levels from the closest monitors for the prior 3 years. Associations between pollutant exposure and ARDS risk were evaluated by logistic regression controlling for age, race, sex, smoking, alcohol, insurance status, rural versus urban residence, distance to study hospital, and Acute Physiology and Chronic Health Evaluation II. MEASUREMENTS AND MAIN RESULTS: The incidence of ARDS increased with increasing ozone exposure: 28% in the lowest exposure quartile versus 32, 40, and 42% in the second, third, and fourth quartiles (P < 0.001). In a logistic regression model controlling for potential confounders, ozone exposure was associated with risk of ARDS in the entire cohort (odds ratio, 1.58 [95% confidence interval, 1.27-1.96]) and more strongly associated in the subgroup with trauma as their ARDS risk factor (odds ratio, 2.26 [95% confidence interval, 1.46-3.50]). There was a strong interaction between ozone exposure and current smoking status (P = 0.007). NO2 exposure was also associated with ARDS but not independently of ozone exposure. SO2, particulate matter less than 2.5 μm, and particulate matter less than 10 μm were not associated with ARDS. CONCLUSIONS: Long-term ozone exposure is associated with development of ARDS in at-risk critically illpatients, particularly in traumapatients and current smokers. Ozone exposure may represent a previously unrecognized environmental risk factor for ARDS.
Entities:
Keywords:
acute lung injury; air pollution; ozone; pulmonary edema
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