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 Permissions Request Permissions Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science 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 Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Senn, O. Articles by Probst-Hensch, N. M. Search for Related Content PubMed PubMed Citation Articles by Senn, O. Articles by Probst-Hensch, N. M.

₁-Antitrypsin deficiency and lung disease: risk modification by occupational and environmental inhalants

¹ Dept of Molecular Epidemiology/Cancer Registry, University of Zurich, and ² Dept of Pneumology, University Hospital of Zurich, Zurich, Switzerland.

CORRESPONDENCE: N. M. Probst-Hensch, Dept of Molecular Epidemiology/Cancer Registry, University of Zurich, Vogelsangstrasse 10, 8091 Zurich, Switzerland. Fax: 41 442555636. E-mail: nicole.probst{at}usz.ch

Keywords: ₁-Antitrypsin, ₁-antitrypsin deficiency, gene–environment interaction, occupational disorder, occupational exposure, passive smoking

Received: February 24, 2005
Accepted June 9, 2005

Chronic obstructive pulmonary disease (COPD) is a prevalent and preventable disease associated with high morbidity and mortality. Severe and intermediate ₁-antitrypsin (AAT) deficiency (serum levels <11 and 11–20 µmol·L^–1, respectively) increase the risk of COPD in active smokers. However, little is known about the interaction of severe and intermediate AAT deficiency with modifiable COPD risk factors other than active smoking.

In this study, a MEDLINE search was carried out for studies investigating the combined effect of environmental inhalants (occupation and passive smoking) and AAT deficiency in the lung. A total of 18 studies using established methods for the assessment of AAT deficiency were included in this review.

Occupational exposures and passive smoking affected lung function decline or prevalence of respiratory symptoms in four out of five studies investigating subjects with severe AAT deficiency, and in eight out of 13 studies with a focus on intermediate AAT deficiency. While study designs mostly prohibited formal assessment of effect modification, an interaction between intermediate AAT deficiency and passive smoking was identified in two studies with children. Additional study limitations included small sample size, poor adjustment for confounding and misclassification of environmental exposure as well as AAT activity.

In conclusion, population-based epidemiological studies with associated biobanks are needed to identify gene–environment interactions and population subgroups susceptible to ₁-antitrypsin deficiency.

This article has been cited by other articles:

				A. M. Wood, R. M. Harrison, S. Semple, J. G. Ayres, and R. A. Stockley Outdoor air pollution is associated with disease severity in {alpha}1-antitrypsin deficiency Eur. Respir. J., August 1, 2009; 34(2): 346 - 353. [Abstract] [Full Text] [PDF]

				D. M.v. Leeuwen, E. v. Agen, R. W.H. Gottschalk, R. Vlietinck, M. Gielen, M. H.M.v. Herwijnen, L. M. Maas, J. C.S. Kleinjans, and J. H.M.v. Delft Cigarette smoke-induced differential gene expression in blood cells from monozygotic twin pairs Carcinogenesis, March 1, 2007; 28(3): 691 - 697. [Abstract] [Full Text] [PDF]