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Published ahead of print on June 7, 2004, doi:10.1164/rccm.200312-1763OC

Am. J. Respir. Crit. Care Med., Volume 170, Number 4, August 2004, 388-394

A more recent version of this article appeared on August 15, 2004
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Submitted on December 23, 2003
Accepted on May 20, 2004

Glutathione S Transferase Variants and their Interaction with Smoking on Lung Function

Jian-Qing He1, John E Connett2, Nicholas R Anthonisen3, Peter D Pare1, and Andrew J Sandford1*

1 University of British Columbia, The James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, St. Paul's Hospital, Vancouver, British Columbia, Canada, 2 Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis, MN, USA, 3 Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada

* To whom correspondence should be addressed. E-mail: asandford{at}mrl.ubc.ca.

We studied glutathione S transferase (GST) polymorphisms in 1098 whites with the lowest (n = 544, FEV1 % predicted = 62.6±0.1) and the highest (n = 554, FEV1% predicted = 91.8±0.1) lung function at the beginning of the Lung Health Study. Homozygosity for GSTP1 105Val was significantly more frequent in the low than in the high function group (13.2% versus 9.3%), with an odds ratio (OR) (95%CI) = 1.69 (1.11-2.61), p = 0.016, after adjustment for confounding variables. Subjects with 105Val homozygotes had higher rates of lung function decline in the high function group (p = 0.017). The frequencies of GSTM1, GSTT1 null genotypes were similar between the high and low function groups; but subjects with the GSTT1 null genotype had faster decline of lung function in the low function group (p = 0.032). In addition, there was a significant interaction of GSTT1 genotype and pack-years on lung function. When comparing individuals with GSTT1 null genotype with wild type, the adjusted OR (95%CI) was 3.49 (1.48-8.39), p = 0.005 in mild smokers (≤25 pack years). We conclude that GST genotypes are risk factors for rapid decline or low lung function in smokers with mild to moderate airflow obstruction.
Key words: Genetic polymorphism, cigarette smoking, glutathione S transferase, forced expiratory volume in one second (FEV1), gene-environment interaction




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