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Published ahead of print on September 11, 2003, doi:10.1164/rccm.200305-684OC

Am. J. Respir. Crit. Care Med., Volume 168, Number 10, November 2003, 1199-1204

A more recent version of this article appeared on November 15, 2003
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Submitted on May 23, 2003
Accepted on September 9, 2003

NAD(P)H: Quinone Oxidoreductase and Glutathione S-Transferase M1 Polymorphisms and Childhood Asthma

Gloria L David1*, Isabelle Romieu2, Juan Jose Sienra-Monge3, William J Collins1, Matiana Ramirez-Aguilar2, Blanca Estela del Rio-Navarro3, Norma Isabel Reyes-Ruiz3, Richard W Morris1, Jacqueline M Marzec1, and Stephanie J London1

1 Health and Human Services, Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA, 2 National Institute of Public Health, Cuernavaca, Mexico, 3 Hospital Infantil de Mexico Frederico Gomez, Mexico City, Mexico

* To whom correspondence should be addressed. E-mail: davidbe1{at}niehs.nih.gov.

NAD(P)H: quinone oxidoreductase (NQO1) and glutathione S-transferase (GST)M1 are phase II enzymes important in response to oxidative stress, such as occurs during exposure to ozone. We examined the relationship between functionally significant polymorphisms in NQO1 (Pro187Ser) and GSTM1 (homozygous deletion) and asthma risk in children with high lifetime exposure to ozone. We enrolled asthmatic children from the allergy referral clinic at a public pediatric hospital in Mexico City, along with their parents. We assayed for the Pro187Ser polymorphism in NQO1 using a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay and for the presence of GSTM1 by PCR among 218 case-parent triads. We did not find strong evidence of an association between NQO1 genotype alone and asthma risk. However, among subjects with homozygous deletion of GSTM1, carriers of a serine allele were at significantly reduced risk of asthma compared to Pro/Pro homozygotes [Relative Risk (RR) = 0.4, 95% CI 0.2-0.8]. The P value for difference in RR for NQO1 by GSTM1 genotype = 0.013. These data are consistent with a protective effect of the NQO1 Ser allele in this population of GSTM1-null children with high ozone exposure.
Key words: case-parent triad, oxidative stress, environmental tobacco smoke




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