GSTM1 and GSTP1 and respiratory health in asthmatic children exposed to ozone

Romieu, Isabelle; Ramírez-Aguilar, Matiana; Sienra-Monge, Juan-Jose; Moreno-Macías, Hortensia; Río-Navarro, Blanca Estela Del; David, Gloria L.; Marzec, Jacqui; Hernández-Ávila, Mauricio; London, Stephanie J.

doi:10.1183/09031936.06.00114905

Cited by 129 publications

(94 citation statements)

References 34 publications

(34 reference statements)

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“…We found that children with the GSTM1-null or the GSTP1 Val/Val genotype had greater increases in difficulty breathing in relation to ozone than other children (22). Increases were enhanced among children with both of these genotypes.…”

Section: Interaction Between Genetics and Ozone In Relation To Asthmamentioning

confidence: 57%

Gene-Air Pollution Interactions in Asthma

London

2007

Proceedings of the American Thoracic Society

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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 geneenvironment 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.

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Section: Interaction Between Genetics and Ozone In Relation To Asthmamentioning

confidence: 57%

Gene-Air Pollution Interactions in Asthma

London

2007

Proceedings of the American Thoracic Society

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“…Therefore, the GSTM1 null genotype would be expected to affect the individual's response to O 3 exposure, possibly causing increased susceptibility to oxidative injury. Since 2001, the results of several field studies showed that the GSTM1 null genotype is associated with greater acute lung function response and/or respiratory symptom response to O 3 -induced oxidative stress [21][22][23]. Other studies have suggested that the GSTM1 null genotype may play a significant role in the development of asthma in response to oxidative stress [24,25].…”

mentioning

confidence: 99%

Effects of antioxidant enzyme polymorphisms on ozone-induced lung function changes

Chen¹,

Arjomandi²,

Tager³

et al. 2007

European Respiratory Journal

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Chronic exposure to ozone (O 3 ) can cause changes in lung function that may reflect remodelling of small airways. It is likely that antioxidant enzyme function affects susceptibility to O 3 . The aim of the present study was to determine whether polymorphisms in antioxidant enzyme (GSTM1, GSTP1 and NQO1) genes affect the risk of lung function changes related to chronic exposure to O 3 .In total, 210 young adults who participated in a previous study, which showed a relationship between lifetime exposure to O 3 and decreased lung function, were genotyped. Multivariable linear regression was used to model sex-specific associations between genotypes and O 3 -related lung function changes, adjusting for height, weight, lifetime exposure to nitrogen dioxide and particles with a 50% cut-off aerodynamic diameter of 10 mm, and self-identified race/ethnicity.The GSTM1-null/NQO1 Pro187Pro-combination genotype was significantly associated with increased risk of an O 3 -related decrease in mean forced expiratory flow between 25-75% of forced vital capacity in females (parameter estimate¡SE -75¡35 mL?s -1 ), while the GSTP1 Val105 variant genotypes were significantly associated with greater risk of an O 3 -related decrease in mean forced expiratory flow at 75% of forced vital capacity in males (-81¡31 mL?s -1). GSTM1-null status was not significantly associated with any O 3 -related changes in lung function in either sex.The current authors conclude that the effects of antioxidant enzyme gene polymorphisms on the risk of decreased lung function related to chronic exposure to ozone may be modified by sexspecific factors.

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“…GST genindeki polimorfizm, inflamasyona ve oksidatif strese karşı verilecek cevaba ve hava kirliliğinin ortaya çıkardığı olumsuz etkilerin artışına yol açabilir. Meksika'da yapılan bir çaışmada GST gen polimorfizmi olan astımlı çocuklarda ozon maruziyetinin daha fazla olduğu, bunun da dispnede ve nazal inflamasyonda artışa neden olduğu belirtilmiştir (38).…”

Section: Buket Mermit çIlingirunclassified

Hava Ki̇rli̇li̇ği̇ Ve Akci̇ğer

Çilingir¹

2016

J Contemp Med

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Air pollution has an expeditious growing for the last century depending mostly on industrialization and civic life. Elements causing air pollution have been divided into two groups; indoor pollutants and outdoor pollutants. These elements spread out to lung, and then through whole body by circulation and affects every organ. Children, old people, people who has genetical susceptibility or chronic disease are affected more easily. Pollution leads to deterioration of pulmonary functions, increase in respiratory infections increase in chronic obstructive pulmonary disease and asthma development and exacerbations and finally rises lung cancer generation. People must be trained in order to decrease air pollution and exposure. Even so the main solution is refinement of the public health and environment policies..

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GSTM1 and GSTP1 and respiratory health in asthmatic children exposed to ozone

Cited by 129 publications

References 34 publications

Gene-Air Pollution Interactions in Asthma

Gene-Air Pollution Interactions in Asthma

Effects of antioxidant enzyme polymorphisms on ozone-induced lung function changes

Hava Ki̇rli̇li̇ği̇ Ve Akci̇ğer

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