Dataset Information

Ambient air pollution and sickle cell disease-related emergency department visits in Atlanta, GA.

ABSTRACT:

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. Associations between daily air pollution levels for 8 urban air pollutants 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 and corresponding SCD ED visits [e.g., rate ratio of 1.022 (95% CI: 1.002, 1.043) per interquartile range increase in carbon monoxide]. Age stratified analyses indicated stronger associations with traffic pollutants among children (0-18 years), as compared to older age strata. Associations involving other pollutants, including ozone and particulate matter and for models of individuals >18 years old, were consistent a null hypothesis of no association.

Discussion

This analysis represents the first North American study to examine acute risk among individuals with SCD to urban air pollution and provide evidence of urban air pollution, especially from traffic sources, as a trigger for acute exacerbations. These findings are consistent with a hypothesis that biological pathways, including several centrally associated with oxidative stress, may contribute towards enhanced susceptibility in individuals with SCD.

SUBMITTER: Blumberg AH

PROVIDER: S-EPMC7847665 | biostudies-literature |

REPOSITORIES: biostudies-literature

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