Conclusions
PM2.5 exposure contributes to significant dysregulation of the SAE transcriptome of smokers, linking pollution and airway epithelial biology in the risk of development of respiratory disease in susceptible individuals.
Methods
From 2009 to 2012, healthy nonsmoker (n = 29) and smoker (n = 129) residents of New York City underwent bronchoscopy with SAE brushing (2.6 ± 1.3 samples/subject; total of 405 samples). SAE gene expression was assessed by Affymetrix HG-U133 Plus 2.0 microarray. New York City PM2.5 levels (Environmental Protection Agency data) were averaged for the 30 days before bronchoscopy. A linear mixed model was used to assess PM2.5-related gene dysregulation accounting for multiple clinical and methodologic variables. Measurements and main
Results
Thirty-day mean PM2.5 levels varied from 6.2 to 18 μg/m3. In nonsmokers, there was no dysregulation of SAE gene expression associated with ambient PM2.5 levels. In marked contrast, n = 219 genes were significantly dysregulated in association with PM2.5 levels in the SAE of smokers. Many of these genes relate to cell growth and transcription regulation. Interestingly, 11% of genes were mitochondria associated. Conclusions: PM2.5 exposure contributes to significant dysregulation of the SAE transcriptome of smokers, linking pollution and airway epithelial biology in the risk of development of respiratory disease in susceptible individuals.