Published ahead of print on November 5, 2004, doi:10.1164/rccm.200407-888OC Am. J. Respir. Crit. Care Med., Volume 171, Number 2, January 2005, 165-170 A more recent version of this article appeared on January 15, 2005
Submitted on July 9, 2004 Microsomal Epoxide Hydrolase, Endotoxin, and Lung Function Decline in Cotton Textile WorkersJingqing Hang1,1 Shanghai Putuo District People's Hospital, Shanghai, China; Occupational Health Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA, 2 Occupational Health Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA, 3 Shanghai Putuo District People's Hospital, Shanghai, China, 4 Occupational Health Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA; Department of Medicine, Pulmonary and Critical Care Unit, Massachusetts General Hospital/Harvard Medical School, Boston, MA, USA * To whom correspondence should be addressed. E-mail: dchristi{at}hsph.harvard.edu.
Occupational exposure to endotoxin in organic dust may induce lung function decline. Microsomal epoxide hydrolase (mEH) detoxifies reactive oxygen species generated by endotoxin exposure, and polymorphisms of this gene are associated with altered enzyme activity. We investigated the associations between mEH polymorphisms, endotoxin exposure, and lung function decline in a 20-year prospective study of 265 workers exposed to endotoxin and 234 controls. mEH Tyr113His and His139Arg polymorphisms were genotyped by the 5' nuclease assay, and the data were analyzed using multivariate linear regression models, adjusting for important covariates. Overall, the annual decline rate of forced expiratory volume in 1 second (FEV1) was 29.47 ml during the 20 years' follow up. Endotoxin exposure was associated with faster lung function decline among genotypes associated with slower enzyme activity: estimates (standard error) of annual FEV1 decline rate for endotoxin exposure were -2.33 (2.07), -2.81 (1.66) and -6.73 (2.83) ml for Tyr/Tyr, Tyr/His, and His/His genotype groups, respectively, for the Tyr113His polymorphism; and -1.82 (2.58) and -4.27 (1.33) ml for Arg/Arg + His/Arg and His/His genotypes, respectively, for the His139Arg polymorphism. We conclude that mEH polymorphisms modify the association between occupational endotoxin exposure and longitudinal lung function decline. Key words: mEH, polymorphis, occupational lung disease, chronic obstructive pulmonary disease
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