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Smoking and ambient air pollution affect lung function decline via different oxidative stress related genes in the general population

09.07.2012

The article “Different Genes Interact with Particulate Matter and Tobacco Smoke Exposure in Affecting Lung Function Decline in the General Population” by Curjuric I, Imboden M, Nadif R et al. has been published by PLOSOne on July 6th 2012.


In this study, investigators from the SAPALDIA cohort study at SwissTPH and international collaborating partners have analyzed how exposure to active tobacco smoking and ambient air pollution over an 11 year period interact with genes involved in oxidative stress response, and compared the patterns of interaction between exposures.


Oxidative stress is known to be a central component of respiratory health effects induced by both exposures. In contrast, the genes found to affect lung function decline in recently performed large, genome wide studies were rarely related to oxidative stress, possibly because these studies investigated gene main effects only. Based on this rationale, 152 genes involved in oxidative stress response were preselected and analyzed in terms of their interaction on the gene and pathway level with cumulative tobacco smoke and ambient air pollution exposure in to 669 SAPALDIA participants with available genetic, exposure and health data.


Only a small overlap in genes interacting with tobacco smoke versus ambient air pollution exposure was found. Genes interacting with ambient air pollution were more directly involved in handling oxidative stress exposure (scavengers or endogenous producers of free radicals), whereas those interacting with tobacco smoke exposure more often constituted cell signaling and apoptosis genes.


These results are consistent with previous evidence from exposure studies in human and mouse cell lines showing a stratified cellular response depending on imposed level of oxidative stress. The present study highlights the importance of considering gene-environment interactions in respiratory disease development as well as the potential inherent to pathway analysis techniques in genome wide data.


Link to the article:
http://dx.doi.org/10.1371/journal.pone.0040175


Link to the SAPALDIA study:
http://www.sapaldia.net/en/


Corresponding author:
Prof. Dr. Nicole Probst-Hensch
Swiss TPH
Deputy Head of Epidemiology and Public Health Department
Socinstrasse 57
Postfach
4002 Basel, Switzerland