Ambient Air Pollution and Acute Sickle Cell Disease Exacerbation in Atlanta, Ga : Environmental Epidemiology

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Abstracts of the 2019 Annual Conference of the International Society for Environmental Epidemiology, August 25-28 2019, Utrecht, the Netherlands

Ambient Air Pollution and Acute Sickle Cell Disease Exacerbation in Atlanta, Ga

J, Sarnat1; A, Blumberg1; S, Ebelt Sarnat1; D, Liang1

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Environmental Epidemiology 3():p 350, October 2019. | DOI: 10.1097/01.EE9.0000609864.70291.df
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OPS 50: Air pollution and health care utilization, Room 117, Floor 1, August 28, 2019, 10:30 AM - 12:00 PM

Background. Sickle cell disease (SCD) is an inherited, autosomal recessive blood disorder, among the most prevalent genetic diseases, globally. While the genetic and hemolytic dynamics of SCD have been well-characterized, the etiology of SCD-related pathophysiological processes is unclear. Although limited, observational evidence suggests that environmental factors, including urban air pollution, may play a role. Objectives. We assessed whether daily ambient air pollution concentrations are associated with corresponding emergency department (ED) visit counts for acute SCD exacerbations in Atlanta, Georgia, during a 9-year (2005-2013) period. We also examined heterogeneity in response by age and sex. Methods. ED visit data were from 41 hospitals in the 20-county Atlanta, GA area. Ambient pollutant measurements, including daily information for 8 air pollutants of interest: carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), and fine particulate matter (PM2.5), sulfate (SO42-), elemental carbon (EC), and organic carbon (OC). Associations of daily air pollution levels and counts of SCD related ED visits were estimated using Poisson generalized linear models. Results. We observed positive associations between pollutants generally indicative of traffic emissions (CO, NO2, EC) and corresponding SCD ED visits [e.g., rate ratio of 1.022 (95% CI: 1.002, 1.043) per interquartile range increase in CO]. Age stratified analyses indicated stronger associations with traffic pollutants among children (0-18 years), as compared to older age strata. It is possible that several biological pathways may be involved in the observed findings and may contribute towards enhanced susceptibility. Notably, vaso-occlusion and hemolysis, primary pathophysiologic features involved in acute SCD response, are associated with dysregulated arginine-nitric oxide metabolism. Conclusions. This analysis represents the largest US epidemiological study to examine enhanced acute risk among individuals with SCD to urban air pollution health effects and add to the emerging evidence of enhanced susceptibility to components of urban air pollution, among those with SCD.

Copyright © 2019 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of Environmental Epidemiology. All rights reserved.