Air pollution associated acute respiratory inflammation and modification by GSTM1 and GSTT1 gene polymorphisms: a panel study of healthy undergraduates

Epidemiological evidence has linked air pollution with adverse respiratory outcomes, but the mechanisms underlying susceptibility to air pollution remain unclear. This study aimed to investigate the role of glutathione S-transferase (GST) polymorphism in the association between air pollution and lun...

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Published inEnvironmental health Vol. 22; no. 1; pp. 14 - 12
Main Authors Zeng, Xiang, Tian, Ge, Zhu, Jingfang, Yang, Fuyun, Zhang, Rui, Li, Huijun, An, Zhen, Li, Juan, Song, Jie, Jiang, Jing, Liu, Dongling, Wu, Weidong
Format Journal Article
LanguageEnglish
Published London BioMed Central 27.01.2023
BioMed Central Ltd
BMC
Subjects
Adolescent
Air pollutants
Air Pollutants - adverse effects
Air pollution
Air Pollution - adverse effects
Asthma
Atmospheric models
Biomarkers
Chronic obstructive pulmonary disease
College students
Cytokines
Demographic aspects
Earth and Environmental Science
Environment
Environmental Health
Epidemiology
Exposure
Gene polymorphism
Genetic polymorphisms
Genotype
Genotypes
Glutathione
Glutathione S-Transferase
Glutathione transferase
Glutathione Transferase - genetics
GSTM1 protein
GSTT1 gene
GSTT1 protein
Health aspects
Humans
Inflammation
Inflammation - chemically induced
Interleukin 6
Interleukin 8
Interleukins
Longitudinal studies
Lung function
Lungs
Nitrogen dioxide
Occupational Medicine/Industrial Medicine
Outdoor air quality
Oxidative stress
Particulate matter
Particulates
Pollutants
Pollution control
Polymorphism
Polymorphism, Genetic
Prostaglandin F2a
Prostaglandins
Public Health
Respiratory function
Respiratory tract diseases
Risk factors
Sulfur dioxide
Tumor necrosis factor-α
Young Adult
China
United States > US
Japan
Oxidative stress
Air pollution
Inflammation
Lung function
Air pollutants
Glutathione S-Transferase
Online AccessGet full text
ISSN1476-069X
1476-069X
DOI10.1186/s12940-022-00954-9

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Abstract Epidemiological evidence has linked air pollution with adverse respiratory outcomes, but the mechanisms underlying susceptibility to air pollution remain unclear. This study aimed to investigate the role of glutathione S-transferase (GST) polymorphism in the association between air pollution and lung function levels. A total of 75 healthy young volunteers aged 18–20 years old were recruited for six follow-up visits and examinations. Spirometry was conducted to obtain lung function parameters such as forced vital capacity (FVC), and forced expiratory volume in 1 s (FEV 1 ). Nasal fluid concentrations of interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and 8-epi-prostaglandin F2α (8-epi-PGF2a) were measured using ELISA kits. Linear mixed-effect models were used to evaluate the association of air pollutants with respiratory outcomes. Additionally, polymorphisms of glutathione S-transferase mu 1 (GSTM1) and glutathione S-transferase theta 1 (GSTT1) were estimated to explore its role in the association between air pollutants and lung function. We found that short-term exposure to atmospheric particulates such as PM 2.5 and PM 10 can cause an increase in nasal biomarkers of inflammation, oxidative stress, and lung function, while air gaseous pollutant exposure is linked with decreased lung function, except for CO. Stratification analyses showed that an increase in nasal inflammatory cytokines caused by exposure to atmospheric particulates is more obvious in subjects with GSTM1 -sufficient ( GSTM1 + ) than GSTM1 -null ( GSTM1 − ), while elevated lung function levels due to air particles are more significant in subjects with the genotype of GSTM1 − when compared to GSTM1 + . As for air gaseous pollutants, decreased lung function levels caused by O 3 , SO 2 , and NO 2 exposure is more manifest in subjects with the genotype of GSTM1 − compared to GSTM1 + . Taken together, short-term exposure to air pollutants is associated with alterations in nasal biomarkers and lung function levels in young healthy adults, and susceptible genotypes play an important mediation role in the association between exposure to air pollutants and inflammation, oxidative stress, and lung function levels.
AbstractList Epidemiological evidence has linked air pollution with adverse respiratory outcomes, but the mechanisms underlying susceptibility to air pollution remain unclear. This study aimed to investigate the role of glutathione S-transferase (GST) polymorphism in the association between air pollution and lung function levels. A total of 75 healthy young volunteers aged 18-20 years old were recruited for six follow-up visits and examinations. Spirometry was conducted to obtain lung function parameters such as forced vital capacity (FVC), and forced expiratory volume in 1 s (FEV.sub.1). Nasal fluid concentrations of interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-[alpha] (TNF-[alpha]), and 8-epi-prostaglandin F2[alpha] (8-epi-PGF2a) were measured using ELISA kits. Linear mixed-effect models were used to evaluate the association of air pollutants with respiratory outcomes. Additionally, polymorphisms of glutathione S-transferase mu 1 (GSTM1) and glutathione S-transferase theta 1 (GSTT1) were estimated to explore its role in the association between air pollutants and lung function. We found that short-term exposure to atmospheric particulates such as PM.sub.2.5 and PM.sub.10 can cause an increase in nasal biomarkers of inflammation, oxidative stress, and lung function, while air gaseous pollutant exposure is linked with decreased lung function, except for CO. Stratification analyses showed that an increase in nasal inflammatory cytokines caused by exposure to atmospheric particulates is more obvious in subjects with GSTM1-sufficient (GSTM1.sup.+) than GSTM1-null (GSTM1.sup.-), while elevated lung function levels due to air particles are more significant in subjects with the genotype of GSTM1.sup.- when compared to GSTM1.sup.+. As for air gaseous pollutants, decreased lung function levels caused by O.sub.3, SO.sub.2, and NO.sub.2 exposure is more manifest in subjects with the genotype of GSTM1.sup.- compared to GSTM1.sup.+. Taken together, short-term exposure to air pollutants is associated with alterations in nasal biomarkers and lung function levels in young healthy adults, and susceptible genotypes play an important mediation role in the association between exposure to air pollutants and inflammation, oxidative stress, and lung function levels. Keywords: Air pollution, Air pollutants, Inflammation, Oxidative stress, Lung function, Glutathione S-Transferase
Epidemiological evidence has linked air pollution with adverse respiratory outcomes, but the mechanisms underlying susceptibility to air pollution remain unclear. This study aimed to investigate the role of glutathione S-transferase (GST) polymorphism in the association between air pollution and lung function levels. A total of 75 healthy young volunteers aged 18-20 years old were recruited for six follow-up visits and examinations. Spirometry was conducted to obtain lung function parameters such as forced vital capacity (FVC), and forced expiratory volume in 1 s (FEV ). Nasal fluid concentrations of interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and 8-epi-prostaglandin F2α (8-epi-PGF2a) were measured using ELISA kits. Linear mixed-effect models were used to evaluate the association of air pollutants with respiratory outcomes. Additionally, polymorphisms of glutathione S-transferase mu 1 (GSTM1) and glutathione S-transferase theta 1 (GSTT1) were estimated to explore its role in the association between air pollutants and lung function. We found that short-term exposure to atmospheric particulates such as PM and PM can cause an increase in nasal biomarkers of inflammation, oxidative stress, and lung function, while air gaseous pollutant exposure is linked with decreased lung function, except for CO. Stratification analyses showed that an increase in nasal inflammatory cytokines caused by exposure to atmospheric particulates is more obvious in subjects with GSTM1-sufficient (GSTM1 ) than GSTM1-null (GSTM1 ), while elevated lung function levels due to air particles are more significant in subjects with the genotype of GSTM1 when compared to GSTM1 . As for air gaseous pollutants, decreased lung function levels caused by O , SO , and NO exposure is more manifest in subjects with the genotype of GSTM1 compared to GSTM1 . Taken together, short-term exposure to air pollutants is associated with alterations in nasal biomarkers and lung function levels in young healthy adults, and susceptible genotypes play an important mediation role in the association between exposure to air pollutants and inflammation, oxidative stress, and lung function levels.
Epidemiological evidence has linked air pollution with adverse respiratory outcomes, but the mechanisms underlying susceptibility to air pollution remain unclear. This study aimed to investigate the role of glutathione S-transferase (GST) polymorphism in the association between air pollution and lung function levels. A total of 75 healthy young volunteers aged 18–20 years old were recruited for six follow-up visits and examinations. Spirometry was conducted to obtain lung function parameters such as forced vital capacity (FVC), and forced expiratory volume in 1 s (FEV 1 ). Nasal fluid concentrations of interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and 8-epi-prostaglandin F2α (8-epi-PGF2a) were measured using ELISA kits. Linear mixed-effect models were used to evaluate the association of air pollutants with respiratory outcomes. Additionally, polymorphisms of glutathione S-transferase mu 1 (GSTM1) and glutathione S-transferase theta 1 (GSTT1) were estimated to explore its role in the association between air pollutants and lung function. We found that short-term exposure to atmospheric particulates such as PM 2.5 and PM 10 can cause an increase in nasal biomarkers of inflammation, oxidative stress, and lung function, while air gaseous pollutant exposure is linked with decreased lung function, except for CO. Stratification analyses showed that an increase in nasal inflammatory cytokines caused by exposure to atmospheric particulates is more obvious in subjects with GSTM1 -sufficient ( GSTM1 + ) than GSTM1 -null ( GSTM1 − ), while elevated lung function levels due to air particles are more significant in subjects with the genotype of GSTM1 − when compared to GSTM1 + . As for air gaseous pollutants, decreased lung function levels caused by O 3 , SO 2 , and NO 2 exposure is more manifest in subjects with the genotype of GSTM1 − compared to GSTM1 + . Taken together, short-term exposure to air pollutants is associated with alterations in nasal biomarkers and lung function levels in young healthy adults, and susceptible genotypes play an important mediation role in the association between exposure to air pollutants and inflammation, oxidative stress, and lung function levels.
Epidemiological evidence has linked air pollution with adverse respiratory outcomes, but the mechanisms underlying susceptibility to air pollution remain unclear. This study aimed to investigate the role of glutathione S-transferase (GST) polymorphism in the association between air pollution and lung function levels. A total of 75 healthy young volunteers aged 18-20 years old were recruited for six follow-up visits and examinations. Spirometry was conducted to obtain lung function parameters such as forced vital capacity (FVC), and forced expiratory volume in 1 s (FEV.sub.1). Nasal fluid concentrations of interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-[alpha] (TNF-[alpha]), and 8-epi-prostaglandin F2[alpha] (8-epi-PGF2a) were measured using ELISA kits. Linear mixed-effect models were used to evaluate the association of air pollutants with respiratory outcomes. Additionally, polymorphisms of glutathione S-transferase mu 1 (GSTM1) and glutathione S-transferase theta 1 (GSTT1) were estimated to explore its role in the association between air pollutants and lung function. We found that short-term exposure to atmospheric particulates such as PM.sub.2.5 and PM.sub.10 can cause an increase in nasal biomarkers of inflammation, oxidative stress, and lung function, while air gaseous pollutant exposure is linked with decreased lung function, except for CO. Stratification analyses showed that an increase in nasal inflammatory cytokines caused by exposure to atmospheric particulates is more obvious in subjects with GSTM1-sufficient (GSTM1.sup.+) than GSTM1-null (GSTM1.sup.-), while elevated lung function levels due to air particles are more significant in subjects with the genotype of GSTM1.sup.- when compared to GSTM1.sup.+. As for air gaseous pollutants, decreased lung function levels caused by O.sub.3, SO.sub.2, and NO.sub.2 exposure is more manifest in subjects with the genotype of GSTM1.sup.- compared to GSTM1.sup.+. Taken together, short-term exposure to air pollutants is associated with alterations in nasal biomarkers and lung function levels in young healthy adults, and susceptible genotypes play an important mediation role in the association between exposure to air pollutants and inflammation, oxidative stress, and lung function levels.
Epidemiological evidence has linked air pollution with adverse respiratory outcomes, but the mechanisms underlying susceptibility to air pollution remain unclear. This study aimed to investigate the role of glutathione S-transferase (GST) polymorphism in the association between air pollution and lung function levels. A total of 75 healthy young volunteers aged 18–20 years old were recruited for six follow-up visits and examinations. Spirometry was conducted to obtain lung function parameters such as forced vital capacity (FVC), and forced expiratory volume in 1 s (FEV1). Nasal fluid concentrations of interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and 8-epi-prostaglandin F2α (8-epi-PGF2a) were measured using ELISA kits. Linear mixed-effect models were used to evaluate the association of air pollutants with respiratory outcomes. Additionally, polymorphisms of glutathione S-transferase mu 1 (GSTM1) and glutathione S-transferase theta 1 (GSTT1) were estimated to explore its role in the association between air pollutants and lung function. We found that short-term exposure to atmospheric particulates such as PM2.5 and PM10 can cause an increase in nasal biomarkers of inflammation, oxidative stress, and lung function, while air gaseous pollutant exposure is linked with decreased lung function, except for CO. Stratification analyses showed that an increase in nasal inflammatory cytokines caused by exposure to atmospheric particulates is more obvious in subjects with GSTM1-sufficient (GSTM1+) than GSTM1-null (GSTM1−), while elevated lung function levels due to air particles are more significant in subjects with the genotype of GSTM1− when compared to GSTM1+. As for air gaseous pollutants, decreased lung function levels caused by O3, SO2, and NO2 exposure is more manifest in subjects with the genotype of GSTM1− compared to GSTM1+. Taken together, short-term exposure to air pollutants is associated with alterations in nasal biomarkers and lung function levels in young healthy adults, and susceptible genotypes play an important mediation role in the association between exposure to air pollutants and inflammation, oxidative stress, and lung function levels.
Abstract Epidemiological evidence has linked air pollution with adverse respiratory outcomes, but the mechanisms underlying susceptibility to air pollution remain unclear. This study aimed to investigate the role of glutathione S-transferase (GST) polymorphism in the association between air pollution and lung function levels. A total of 75 healthy young volunteers aged 18–20 years old were recruited for six follow-up visits and examinations. Spirometry was conducted to obtain lung function parameters such as forced vital capacity (FVC), and forced expiratory volume in 1 s (FEV1). Nasal fluid concentrations of interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and 8-epi-prostaglandin F2α (8-epi-PGF2a) were measured using ELISA kits. Linear mixed-effect models were used to evaluate the association of air pollutants with respiratory outcomes. Additionally, polymorphisms of glutathione S-transferase mu 1 (GSTM1) and glutathione S-transferase theta 1 (GSTT1) were estimated to explore its role in the association between air pollutants and lung function. We found that short-term exposure to atmospheric particulates such as PM2.5 and PM10 can cause an increase in nasal biomarkers of inflammation, oxidative stress, and lung function, while air gaseous pollutant exposure is linked with decreased lung function, except for CO. Stratification analyses showed that an increase in nasal inflammatory cytokines caused by exposure to atmospheric particulates is more obvious in subjects with GSTM1-sufficient (GSTM1 +) than GSTM1-null (GSTM1 − ), while elevated lung function levels due to air particles are more significant in subjects with the genotype of GSTM1 − when compared to GSTM1 +. As for air gaseous pollutants, decreased lung function levels caused by O3, SO2, and NO2 exposure is more manifest in subjects with the genotype of GSTM1 − compared to GSTM1 +. Taken together, short-term exposure to air pollutants is associated with alterations in nasal biomarkers and lung function levels in young healthy adults, and susceptible genotypes play an important mediation role in the association between exposure to air pollutants and inflammation, oxidative stress, and lung function levels.
Epidemiological evidence has linked air pollution with adverse respiratory outcomes, but the mechanisms underlying susceptibility to air pollution remain unclear. This study aimed to investigate the role of glutathione S-transferase (GST) polymorphism in the association between air pollution and lung function levels. A total of 75 healthy young volunteers aged 18-20 years old were recruited for six follow-up visits and examinations. Spirometry was conducted to obtain lung function parameters such as forced vital capacity (FVC), and forced expiratory volume in 1 s (FEV1). Nasal fluid concentrations of interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and 8-epi-prostaglandin F2α (8-epi-PGF2a) were measured using ELISA kits. Linear mixed-effect models were used to evaluate the association of air pollutants with respiratory outcomes. Additionally, polymorphisms of glutathione S-transferase mu 1 (GSTM1) and glutathione S-transferase theta 1 (GSTT1) were estimated to explore its role in the association between air pollutants and lung function. We found that short-term exposure to atmospheric particulates such as PM2.5 and PM10 can cause an increase in nasal biomarkers of inflammation, oxidative stress, and lung function, while air gaseous pollutant exposure is linked with decreased lung function, except for CO. Stratification analyses showed that an increase in nasal inflammatory cytokines caused by exposure to atmospheric particulates is more obvious in subjects with GSTM1-sufficient (GSTM1+) than GSTM1-null (GSTM1-), while elevated lung function levels due to air particles are more significant in subjects with the genotype of GSTM1- when compared to GSTM1+. As for air gaseous pollutants, decreased lung function levels caused by O3, SO2, and NO2 exposure is more manifest in subjects with the genotype of GSTM1- compared to GSTM1+. Taken together, short-term exposure to air pollutants is associated with alterations in nasal biomarkers and lung function levels in young healthy adults, and susceptible genotypes play an important mediation role in the association between exposure to air pollutants and inflammation, oxidative stress, and lung function levels.Epidemiological evidence has linked air pollution with adverse respiratory outcomes, but the mechanisms underlying susceptibility to air pollution remain unclear. This study aimed to investigate the role of glutathione S-transferase (GST) polymorphism in the association between air pollution and lung function levels. A total of 75 healthy young volunteers aged 18-20 years old were recruited for six follow-up visits and examinations. Spirometry was conducted to obtain lung function parameters such as forced vital capacity (FVC), and forced expiratory volume in 1 s (FEV1). Nasal fluid concentrations of interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and 8-epi-prostaglandin F2α (8-epi-PGF2a) were measured using ELISA kits. Linear mixed-effect models were used to evaluate the association of air pollutants with respiratory outcomes. Additionally, polymorphisms of glutathione S-transferase mu 1 (GSTM1) and glutathione S-transferase theta 1 (GSTT1) were estimated to explore its role in the association between air pollutants and lung function. We found that short-term exposure to atmospheric particulates such as PM2.5 and PM10 can cause an increase in nasal biomarkers of inflammation, oxidative stress, and lung function, while air gaseous pollutant exposure is linked with decreased lung function, except for CO. Stratification analyses showed that an increase in nasal inflammatory cytokines caused by exposure to atmospheric particulates is more obvious in subjects with GSTM1-sufficient (GSTM1+) than GSTM1-null (GSTM1-), while elevated lung function levels due to air particles are more significant in subjects with the genotype of GSTM1- when compared to GSTM1+. As for air gaseous pollutants, decreased lung function levels caused by O3, SO2, and NO2 exposure is more manifest in subjects with the genotype of GSTM1- compared to GSTM1+. Taken together, short-term exposure to air pollutants is associated with alterations in nasal biomarkers and lung function levels in young healthy adults, and susceptible genotypes play an important mediation role in the association between exposure to air pollutants and inflammation, oxidative stress, and lung function levels.
ArticleNumber 14
Audience Academic
Author Jiang, Jing
Li, Huijun
Zhu, Jingfang
Song, Jie
An, Zhen
Zeng, Xiang
Li, Juan
Liu, Dongling
Yang, Fuyun
Zhang, Rui
Tian, Ge
Wu, Weidong
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/36703205$$D View this record in MEDLINE/PubMed
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Issue 1
Keywords Oxidative stress
Air pollution
Inflammation
Lung function
Air pollutants
Glutathione S-Transferase
Language English
License 2023. The Author(s).
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  start-page: 112
  issue: 1
  year: 2020
  ident: 954_CR7
  publication-title: Am J Respir Crit Care Med
  doi: 10.1164/rccm.201902-0286OC
– volume: 41
  start-page: 713
  issue: 5
  year: 2021
  ident: 954_CR3
  publication-title: J. Appl. Toxicol.
  doi: 10.1002/jat.4138
– volume: 755
  start-page: 142522
  issue: Pt 1
  year: 2021
  ident: 954_CR43
  publication-title: Sci Total Environ.
  doi: 10.1016/j.scitotenv.2020.142522
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Snippet Epidemiological evidence has linked air pollution with adverse respiratory outcomes, but the mechanisms underlying susceptibility to air pollution remain...
Abstract Epidemiological evidence has linked air pollution with adverse respiratory outcomes, but the mechanisms underlying susceptibility to air pollution...
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SubjectTerms Adolescent
Air pollutants
Air Pollutants - adverse effects
Air pollution
Air Pollution - adverse effects
Asthma
Atmospheric models
Biomarkers
Chronic obstructive pulmonary disease
College students
Cytokines
Demographic aspects
Earth and Environmental Science
Environment
Environmental Health
Epidemiology
Exposure
Gene polymorphism
Genetic polymorphisms
Genotype
Genotypes
Glutathione
Glutathione S-Transferase
Glutathione transferase
Glutathione Transferase - genetics
GSTM1 protein
GSTT1 gene
GSTT1 protein
Health aspects
Humans
Inflammation
Inflammation - chemically induced
Interleukin 6
Interleukin 8
Interleukins
Longitudinal studies
Lung function
Lungs
Nitrogen dioxide
Occupational Medicine/Industrial Medicine
Outdoor air quality
Oxidative stress
Particulate matter
Particulates
Pollutants
Pollution control
Polymorphism
Polymorphism, Genetic
Prostaglandin F2a
Prostaglandins
Public Health
Respiratory function
Respiratory tract diseases
Risk factors
Sulfur dioxide
Tumor necrosis factor-α
Young Adult
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Title Air pollution associated acute respiratory inflammation and modification by GSTM1 and GSTT1 gene polymorphisms: a panel study of healthy undergraduates
URI https://link.springer.com/article/10.1186/s12940-022-00954-9
https://www.ncbi.nlm.nih.gov/pubmed/36703205
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https://pubmed.ncbi.nlm.nih.gov/PMC9881318
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Volume 22
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