|
|
||||||||
1-antitrypsin and tobacco smoke exposure
1 University Children's Hospital Munich, Munich, 2 Children's Hospital, Technical University Dresden, 3 Clinical Laboratory Becker, Olgemöller & Partner, Munich, 4 Dept of Epidemiology, University of Ulm, Ulm and 5 Dept of Epidemiology and Social Medicine, University of Muenster, Muenster, Germany
CORRESPONDENCE: E. von Mutius, Lindwurmstr.4, D-80337, München, Germany. Fax: 49 8951604452. E-mail: Erika.Von.Mutius@kk-I.med.uni-muenchen.de
Keywords:
1-Antitrypsin, children, environmental tobacco smoke, epidemiology, pulmonary function
Received: December 13, 2000
Accepted January 17, 2002
This Work was supported by the Bundesministerium für Bildung, Forschung und Technologie (German Ministry for the Sciences and Technology) and the Center for Environment and Health (Project Environment and Health, Baden-Württemberg).
Exposure to environmental tobacco smoke (ETS) and other air pollutants has been associated with small decrements in lung function. The susceptibility to pollution exposure may, however, vary substantially between individuals. Children with an impaired protease-antiprotease balance may be particularly vulnerable. Therefore this study aimed to investigate the effects of ETS exposure on children with reduced levels of
Random samples of school children (aged 911 yrs) (n=3,526) were studied according to the International Study of Asthma and Allergies in Childhood (ISAAC) phase II protocol, including parental questionnaires, pulmonary function and allergy testing. Blood samples were obtained to measure plasma levels of
Children with low levels of
These findings suggest that school children with low levels of
1-antitrypsin (
1-AT).
1-AT and to genotype for pleomorphic protein inhibitor (Pi)Z and PiS alleles.
1-AT (
116 mg·dL1) showed significant, albeit small decrements in baseline lung function. When exposed to ETS, pronounced decrements of pulmonary function, particularly in measures of mid- to end-expiratory flow rates, were seen in these children as compared to exposed children with normal levels of
1-AT. The mean levels of % predicted±se in both groups were: maximum expiratory flow at 50% of vital capacity 79.4±7.2 versus 99.0±1.5, maximum expiratory flow at 25% of vital capacity 67.4±10.0 versus 100.3±2.1, maximal midexpiratory flow 73.7±8.6 versus 99.9±1.7.
1-antitrypsin are at risk of developing pronounced decrements in pulmonary function, particularly if they are exposed to environmental tobacco smoke. Parents of children with heterozygous
1-antitrypsin deficiency resulting in significantly reduced blood concentrations should be advised to prevent their children from being exposed to environmental tobacco smoke and dissuade them from taking up smoking.
This article has been cited by other articles:
![]() |
T. Yoshida and R. M. Tuder Pathobiology of Cigarette Smoke-Induced Chronic Obstructive Pulmonary Disease Physiol Rev, July 1, 2007; 87(3): 1047 - 1082. [Abstract] [Full Text] [PDF] |
||||
![]() |
J Genuneit, G Weinmayr, K Radon, H Dressel, D Windstetter, P Rzehak, C Vogelberg, W Leupold, D Nowak, E von Mutius, et al. Smoking and the incidence of asthma during adolescence: results of a large cohort study in Germany Thorax, July 1, 2006; 61(7): 572 - 578. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Moshammer, G. Hoek, H. Luttmann-Gibson, M. A. Neuberger, T. Antova, U. Gehring, F. Hruba, S. Pattenden, P. Rudnai, H. Slachtova, et al. Parental Smoking and Lung Function in Children: An International Study Am. J. Respir. Crit. Care Med., June 1, 2006; 173(11): 1255 - 1263. [Abstract] [Full Text] [PDF] |
||||
![]() |
O. Senn, E. W. Russi, M. Imboden, and N. M. Probst-Hensch {alpha}1-Antitrypsin deficiency and lung disease: risk modification by occupational and environmental inhalants Eur. Respir. J., November 1, 2005; 26(5): 909 - 917. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Dahl, C. P. Hersh, N. P. Ly, C. S. Berkey, E. K. Silverman, and B. G. Nordestgaard The protease inhibitor PI*S allele and COPD: a meta-analysis Eur. Respir. J., July 1, 2005; 26(1): 67 - 76. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. E. J. Wadsworth, L. E. Vinall, A. L. Jones, R. J. Hardy, D. B. Whitehouse, S. L. Butterworth, W. S. Hilder, J. U. Lovegrove, and D. M. Swallow Alpha1-Antitrypsin as a Risk for Infant and Adult Respiratory Outcomes in a National Birth Cohort Am. J. Respir. Cell Mol. Biol., November 1, 2004; 31(5): 559 - 564. [Abstract] [Full Text] [PDF] |
||||
![]() |
C P Hersh, M Dahl, N P Ly, C S Berkey, B G Nordestgaard, and E K Silverman Chronic obstructive pulmonary disease in {alpha}1-antitrypsin PI MZ heterozygotes: a meta-analysis Thorax, October 1, 2004; 59(10): 843 - 849. [Abstract] [Full Text] [PDF] |
||||
![]() |
M Kabesch, C Hoefler, D Carr, W Leupold, S K Weiland, and E von Mutius Glutathione S transferase deficiency and passive smoking increase childhood asthma Thorax, July 1, 2004; 59(7): 569 - 573. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Nicolai, D. Carr, S.K. Weiland, H. Duhme, O. von Ehrenstein, C. Wagner, and E. von Mutius Urban traffic and pollutant exposure related to respiratory outcomes and atopy in a large sample of children Eur. Respir. J., June 1, 2003; 21(6): 956 - 963. [Abstract] [Full Text] [PDF] |
||||
![]() |
G M Corbo, F Forastiere, N Agabiti, V Dell'Orco, R Pistelli, G Massi, C A Perucci, and S Valente Passive smoking and lung function in {alpha}1-antitrypsin heterozygote schoolchildren Thorax, March 1, 2003; 58(3): 237 - 241. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |