HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by London, S. J. Search for Related Content PubMed PubMed Citation Articles by London, S. J.

Gene–Air Pollution Interactions in Asthma

¹ Epidemiology Branch and Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina

Correspondence and requests for reprints should be addressed to Stephanie London, M.D., Dr.P.H., P.O. Box 12233, MD A3-05, Research Triangle Park, NC 27709. E-mail: London2{at}niehs.nih.gov

ABSTRACT

Genetic and environmental factors interact to cause asthma. However, genetic studies have generally ignored environmental factors and environmental studies have generally ignored genetics. Thus, there are few examples from the literature of specific gene–environment interactions in relation to asthma. The clearest examples of genetic interactions for inhaled pollutants exist for endotoxin, environmental tobacco smoke, and ozone. Endotoxin–genetic interactions in asthma are the focus of two other manuscripts from this conference, so this review focuses on environmental tobacco smoke and ozone. In the sparse literature, there is evidence for the role of specific genes involved in oxidative stress, notably GSTM1 and TNF, in the respiratory responses to ozone and environmental tobacco smoke. There are few data on genes involved in innate immune pathways, which are crucial in response to endotoxin and may play a role in response to ozone and environmental tobacco smoke. Genes involved in oxidative stress may interact with both air pollutants and diet in relation to asthma phenotypes. Future directions to advance the field include whole genome association studies, better assessment of exposure and phenotypes, and consideration of joint interactions with diet and other co-factors that influence individual susceptibility.

Key Words: asthma • genetic • air pollution • tobacco smoke pollution • single nucleotide polymorphism

This article has been cited by other articles:

				T. S. Nawrot and I. Adcock The Detrimental Health Effects of Traffic-related Air Pollution: A Role for DNA Methylation? Am. J. Respir. Crit. Care Med., April 1, 2009; 179(7): 523 - 524. [Full Text] [PDF]

				B. L. Heidenfelder, D. M. Reif, J. R. Harkema, E. A. Cohen Hubal, E. E. Hudgens, L. A. Bramble, J. G. Wagner, M. Morishita, G. J. Keeler, S. W. Edwards, et al. Comparative Microarray Analysis and Pulmonary Changes in Brown Norway Rats Exposed to Ovalbumin and Concentrated Air Particulates Toxicol. Sci., March 1, 2009; 108(1): 207 - 221. [Abstract] [Full Text] [PDF]

				T Islam, K Berhane, R McConnell, W J Gauderman, E Avol, J M Peters, and F D Gilliland Glutathione-S-transferase (GST) P1, GSTM1, exercise, ozone and asthma incidence in school children Thorax, March 1, 2009; 64(3): 197 - 202. [Abstract] [Full Text] [PDF]