• John P Reilly, Zhiguo Zhao, ShashatyMichael G SMGS1 Division of Pulmonary, Allergy, and Critical Care.2 Center for Translational Lung Biology, and., Tatsuki Koyama, Jason D Christie, Paul N Lanken, Chunxue Wang, John R Balmes, Michael A Matthay, Carolyn S Calfee, and Lorraine B Ware.
• 1 Division of Pulmonary, Allergy, and Critical Care.
• Am. J. Respir. Crit. Care Med. 2019 Jan 1; 199 (1): 627062-70.

RationaleExposure to air pollution has molecular and physiologic effects on the lung that may increase the risk of acute respiratory distress syndrome (ARDS) after injury.ObjectivesTo determine the association of short- and long-term air pollutant exposures and ARDS risk after severe trauma.MethodsWe analyzed data from a prospective cohort of 996 critically ill patients presenting with acute trauma and an injury severity score greater than 15. Exposures to ozone, nitrogen dioxide, sulfur dioxide, carbon monoxide, and particulate matter less than 2.5 μm were assessed by weighted averages of daily levels from all monitors within 50 km of the geocoded location of a patient's residence. Patients were followed for 6 days for the development of ARDS according to Berlin Criteria. The association between each exposure and ARDS was determined via multivariable logistic regression adjusting for potential confounders.Measurements And Main ResultsARDS developed in 243 (24%) patients. None of the short-term exposures averaged over the 3 days before presentation was associated with ARDS, except sulfur dioxide, which demonstrated a nonlinear association. Nitrogen dioxide, sulfur dioxide, and particulate matter less than or equal to 2.5 μm in aerodynamic diameter exposure over the 6 weeks before presentation was significantly associated with ARDS (P < 0.05). All long-term exposures (3 yr) were associated with ARDS (P < 0.01) in adjusted models, despite exposure levels largely below U.S. and European Union air quality standards.ConclusionsLong-term low- to moderate-level air pollutant exposure is associated with a greater risk of developing ARDS after severe trauma and represents a novel and potentially modifiable environmental risk factor for ARDS.

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