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Genetic susceptibility to the respiratory effects of air pollution

Genetic susceptibility to the respiratory effects of air pollution
Genetic susceptibility to the respiratory effects of air pollution
There is large variation between individuals in their response to air pollutants. This review summarises the existing evidence that genetic factors influence the mechanisms of lung injury caused by air pollutants. Genetic association studies have compared the adverse effects of air pollutants between subjects with specific genotypes in biologically relevant genes. In human studies of ozone exposure, polymorphisms in oxidative stress genes (NQO1, GSTM1, GSTP1) modify respiratory symptoms, lung function, biomarkers and risk of asthma. Inflammatory gene polymorphisms (TNF) influence the lung function response to ozone, and the effect of different levels of ozone on the development of asthma. Polymorphisms in oxidative stress genes (GSTM1, GSTP1) alter the response to combined exposure to ragweed pollen and diesel exhaust particles. Importantly, polymorphisms in an oxidative stress gene (GSTM1) have predicted patients with asthma who benefit from antioxidant supplementation in Mexico City, which has chronically high ozone exposure. Genetic linkage studies of families have not been feasible for studying the effects of air pollution in humans, but some progress has been made with pedigrees of specially bred mice, in identifying chromosomal regions linked to effects of ozone or particles. A high priority now, in addition to avoiding exposure in the most susceptible people, is to clearly identify the most effective and safe chemopreventive agents for individuals who are genetically susceptible to the adverse effects of air pollution (eg, antioxidants to be taken during high ozone levels) WEB/URL: PM:18511640;
phenotype, lung, sulfur dioxide, genetic, genetics, antioxidants, adverse effects, oxidative stress, genetic predisposition to disease, variation (genetics), humans, particulate matter, chemically induced, lung diseases, air pollutants, nitrogen dioxide, respiration disorders, air pollution, polymorphism, asthma, toxicity, ozone, stress
0040-6376
555-563
Yang, I. A.
e39eb959-ba98-45a8-a8f7-81d5b8142be4
Fong, K. M.
21396746-7519-49fa-8304-2bc8d46e62f1
Zimmerman, P. V.
3faec5b7-17d2-4eec-809a-8e175c3b0ba6
Holgate, S. T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc
Holloway, J. W.
4bbd77e6-c095-445d-a36b-a50a72f6fe1a
Yang, I. A.
e39eb959-ba98-45a8-a8f7-81d5b8142be4
Fong, K. M.
21396746-7519-49fa-8304-2bc8d46e62f1
Zimmerman, P. V.
3faec5b7-17d2-4eec-809a-8e175c3b0ba6
Holgate, S. T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc
Holloway, J. W.
4bbd77e6-c095-445d-a36b-a50a72f6fe1a

Yang, I. A., Fong, K. M., Zimmerman, P. V., Holgate, S. T. and Holloway, J. W. (2008) Genetic susceptibility to the respiratory effects of air pollution. Thorax, 63 (6), 555-563. (doi:10.1136/thx.2007.079426).

Record type: Article

Abstract

There is large variation between individuals in their response to air pollutants. This review summarises the existing evidence that genetic factors influence the mechanisms of lung injury caused by air pollutants. Genetic association studies have compared the adverse effects of air pollutants between subjects with specific genotypes in biologically relevant genes. In human studies of ozone exposure, polymorphisms in oxidative stress genes (NQO1, GSTM1, GSTP1) modify respiratory symptoms, lung function, biomarkers and risk of asthma. Inflammatory gene polymorphisms (TNF) influence the lung function response to ozone, and the effect of different levels of ozone on the development of asthma. Polymorphisms in oxidative stress genes (GSTM1, GSTP1) alter the response to combined exposure to ragweed pollen and diesel exhaust particles. Importantly, polymorphisms in an oxidative stress gene (GSTM1) have predicted patients with asthma who benefit from antioxidant supplementation in Mexico City, which has chronically high ozone exposure. Genetic linkage studies of families have not been feasible for studying the effects of air pollution in humans, but some progress has been made with pedigrees of specially bred mice, in identifying chromosomal regions linked to effects of ozone or particles. A high priority now, in addition to avoiding exposure in the most susceptible people, is to clearly identify the most effective and safe chemopreventive agents for individuals who are genetically susceptible to the adverse effects of air pollution (eg, antioxidants to be taken during high ozone levels) WEB/URL: PM:18511640;

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More information

Published date: 2008
Keywords: phenotype, lung, sulfur dioxide, genetic, genetics, antioxidants, adverse effects, oxidative stress, genetic predisposition to disease, variation (genetics), humans, particulate matter, chemically induced, lung diseases, air pollutants, nitrogen dioxide, respiration disorders, air pollution, polymorphism, asthma, toxicity, ozone, stress

Identifiers

Local EPrints ID: 70872
URI: http://eprints.soton.ac.uk/id/eprint/70872
ISSN: 0040-6376
PURE UUID: 0ff3e893-2ab3-4ece-b2aa-11a88d4b828f
ORCID for J. W. Holloway: ORCID iD orcid.org/0000-0001-9998-0464

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Date deposited: 10 Mar 2010
Last modified: 14 Mar 2024 02:41

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Contributors

Author: I. A. Yang
Author: K. M. Fong
Author: P. V. Zimmerman
Author: S. T. Holgate
Author: J. W. Holloway ORCID iD

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