Glutathione S transferase deficiency and passive smoking increase childhood asthma
Open accessAbstract
BACKGROUND: It has been suggested that the genetically determined deficiency of glutathione S transferase (GST) enzymes involved in the detoxification of environmental tobacco smoke (ETS) components may contribute to the development of asthma. METHODS: A large population of German schoolchildren (n = 3054) was genotyped for deficiencies of the GST isoforms M1 and T1. The association between GSTM1 and GSTT1 genotypes and asthma as well as atopy was investigated with respect to current and in utero ETS exposure. RESULTS: In children lacking the GSTM1 allele who were exposed to current ETS the risk for current asthma (OR 5.5, 95% CI 1.6 to 18.6) and asthma symptoms such as wheeze ever (OR 2.8, 95% CI 1.3 to 6.0), current wheezing (OR 4.7, 95% CI 1.8 to 12.6) and shortness of breath (OR 8.9, 95% CI 2.1 to 38.4) was higher than in GSTM1 positive individuals without ETS exposure. Hints of an interaction between ETS exposure and GSTM1 deficiency were identified. In utero smoke exposure in GSTT1 deficient children was associated with significant decrements in lung function compared with GSTT1 positive children not exposed to ETS. CONCLUSIONS: GSTM1 and GSTT1 deficiency may increase the adverse health effects of in utero and current smoke exposure.
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Subsequent research has demonstrated increased airway resistance and decreased lung function after in utero smoke exposure in children with GSTTI and GSTP1 alleles.
“Subsequent research has demonstrated physiologic changes, including increased airway resistance and decreased lung function after in utero smoke exposure in children with GSTTI and GSTP1 alleles.86,88”
From Impact of Tobacco Smoke and Nicotine Exposure on Lung Development (2016) · cites this paper as [88]
The Results (page not provided) report decreased lung-function measurements in children with a GSTT1 null genotype exposed to smoke in utero. The paper studied GSTM1 and GSTT1, not GSTP1, and the cited passages do not report increased airway resistance. (LLM, conf=0.89)
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- Authors
- Kabesch, M.
- Affiliations
- Ludwig-Maximilians-Universität München (DE)
- Corresponding author
- Kabesch, M
- ORCID
- Kabesch, M
- Venue
- Thorax
- Publisher
- BMJ
- Published
- 2004-07-01
- Volume
- 59
- Issue
- 7
- Pages
- 569-573
- ISSN
- 0040-6376 (ISSN-L)
- PMC
- PMC1747082
- OpenAlex
- W1981676959
- Cited by
- 209
- References
- 30
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 1 · 2023: 3 · 2022: 2 · 2021: 7 · 2020: 3 · 2019: 7 · 2018: 6 · 2017: 2 · 2016: 8 · 2015: 7 · 2014: 8 · 2013: 15 · 2012: 15
- FWCI
- 5.57
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Thorax (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Glutathione Transferases and Polymorphisms
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Keywords
- GSTM1, GSTT1, childhood asthma, passive smoking, environmental tobacco smoke, wheezing, atopy, lung function, gene-environment interaction, detoxification
- MeSH terms
- Asthma, Child, Cross-Sectional Studies, Female, Forced Expiratory Volume, Gene Frequency, Genotype, Glutathione Transferase, Humans, Male, Pregnancy, Prenatal Exposure Delayed Effects, Respiratory Sounds, Risk Factors, Tobacco Smoke Pollution, Vital Capacity
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