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Published ahead of print on October 14, 2004, doi:10.1164/rccm.200402-194OC

Am. J. Respir. Crit. Care Med., Volume 171, Number 2, January 2005, 171-176

A more recent version of this article appeared on January 15, 2005
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Submitted on February 18, 2004
Accepted on October 14, 2004

Association of Tumour Necrosis Factor-{alpha} polymorphisms and Ozone-induced Change in Lung Function

Ian A Yang1*, Olaf Holz2, Rudolf A Jorres3, Helgo Magnussen2, Sheila J Barton1, Santiago Rodriguez1, Julie A Cakebread1, John W Holloway1, and Stephen T Holgate1

1 Asthma Genetics Laboratory, Human Genetics and Infection , Inflammation and Repair Divisions, University of Southampton, Southampton, United Kingdom, 2 Center for Pneumology and Thoracic Surgery, Hospital Grosshansdorf, Grosshansdorf, Germany, 3 Center for Pneumology and Thoracic Surgery, Hospital Grosshansdorf, Grosshansdorf, Germany; Occupational and Environmental Medicine, Ludwig-Maximilians-University, Munich, Germany

* To whom correspondence should be addressed. E-mail: Ian_Yang{at}health.qld.gov.au.

Ozone is a major air pollutant with adverse health effects which exhibit marked inter-individual variability. In mice, regions of genetic linkage with ozone-induced lung injury include the tumour necrosis factor-{alpha} (TNF), lymphotoxin-{alpha} (LTA), Toll-like receptor 4 (TLR4), superoxide dismutase (SOD2) and glutathione peroxidase (GPX1) genes. We genotyped polymorphisms in these genes in 51 individuals who had undergone ozone challenge. Mean change in FEV1 with ozone challenge, as % of baseline, was -3% in TNF -308G/A or A/A individuals, compared to -9% in G/G individuals (P=0.024). When considering TNF haplotypes, the smallest change in FEV1 with ozone exposure was associated with the TNF haplotype comprising LTA +252G / TNF -1031T / TNF -308A / TNF -238G. This association remained statistically significant after correction for age, sex, disease and ozone concentration (P=0.047). SOD2 or GPX1 genotypes were not associated with lung function, and the TLR4 polymorphism was too infrequent to analyse. The results of this study support TNF as a genetic factor for susceptibility to ozone-induced changes in lung function in humans, and has potential implications for stratifying health risks of air pollution.
Key words: air pollution, polymorphism (genetics), tumour necrosis factor-alpha




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