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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 in: | Environmental health 2023-01, Vol.22 (1), p.14-14, Article 14 |
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description | 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. |
doi_str_mv | 10.1186/s12940-022-00954-9 |
format | article |
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). 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.</description><identifier>ISSN: 1476-069X</identifier><identifier>EISSN: 1476-069X</identifier><identifier>DOI: 10.1186/s12940-022-00954-9</identifier><identifier>PMID: 36703205</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>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 ; 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 ; Outdoor air quality ; Oxidative stress ; Particulate matter ; Particulates ; Pollutants ; Pollution control ; Polymorphism ; Polymorphism, Genetic ; Prostaglandin F2a ; Prostaglandins ; Respiratory function ; Respiratory tract diseases ; Risk factors ; Sulfur dioxide ; Tumor necrosis factor-α ; Young Adult</subject><ispartof>Environmental health, 2023-01, Vol.22 (1), p.14-14, Article 14</ispartof><rights>2023. The Author(s).</rights><rights>COPYRIGHT 2023 BioMed Central Ltd.</rights><rights>2023. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c563t-dc10b8ff955c02f4f4f27bfe21897e420045fcf0f4118a82efee48695a9ab9e83</citedby><cites>FETCH-LOGICAL-c563t-dc10b8ff955c02f4f4f27bfe21897e420045fcf0f4118a82efee48695a9ab9e83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9881318/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2777783588?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36703205$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zeng, Xiang</creatorcontrib><creatorcontrib>Tian, Ge</creatorcontrib><creatorcontrib>Zhu, Jingfang</creatorcontrib><creatorcontrib>Yang, Fuyun</creatorcontrib><creatorcontrib>Zhang, Rui</creatorcontrib><creatorcontrib>Li, Huijun</creatorcontrib><creatorcontrib>An, Zhen</creatorcontrib><creatorcontrib>Li, Juan</creatorcontrib><creatorcontrib>Song, Jie</creatorcontrib><creatorcontrib>Jiang, Jing</creatorcontrib><creatorcontrib>Liu, Dongling</creatorcontrib><creatorcontrib>Wu, Weidong</creatorcontrib><title>Air pollution associated acute respiratory inflammation and modification by GSTM1 and GSTT1 gene polymorphisms: a panel study of healthy undergraduates</title><title>Environmental health</title><addtitle>Environ Health</addtitle><description>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.</description><subject>Adolescent</subject><subject>Air pollutants</subject><subject>Air Pollutants - adverse effects</subject><subject>Air pollution</subject><subject>Air Pollution - adverse effects</subject><subject>Asthma</subject><subject>Atmospheric models</subject><subject>Biomarkers</subject><subject>Chronic obstructive pulmonary disease</subject><subject>College students</subject><subject>Cytokines</subject><subject>Demographic aspects</subject><subject>Environmental health</subject><subject>Epidemiology</subject><subject>Exposure</subject><subject>Gene polymorphism</subject><subject>Genetic polymorphisms</subject><subject>Genotype</subject><subject>Genotypes</subject><subject>Glutathione</subject><subject>Glutathione S-Transferase</subject><subject>Glutathione transferase</subject><subject>Glutathione Transferase - genetics</subject><subject>GSTM1 protein</subject><subject>GSTT1 gene</subject><subject>GSTT1 protein</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - chemically induced</subject><subject>Interleukin 6</subject><subject>Interleukin 8</subject><subject>Interleukins</subject><subject>Longitudinal studies</subject><subject>Lung function</subject><subject>Lungs</subject><subject>Nitrogen dioxide</subject><subject>Outdoor air quality</subject><subject>Oxidative stress</subject><subject>Particulate matter</subject><subject>Particulates</subject><subject>Pollutants</subject><subject>Pollution control</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Prostaglandin F2a</subject><subject>Prostaglandins</subject><subject>Respiratory function</subject><subject>Respiratory tract diseases</subject><subject>Risk factors</subject><subject>Sulfur dioxide</subject><subject>Tumor necrosis factor-α</subject><subject>Young Adult</subject><issn>1476-069X</issn><issn>1476-069X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptUk1v1DAQjRCIlsIf4IAsceGSYjtO7HBAWlVQKhVxYJG4WRN_7HqVxMFOkPJL-Ls4m1K6CPng0cybN57nl2UvCb4kRFRvI6E1wzmmNMe4LlleP8rOCeNVjqv6--MH8Vn2LMYDxoSLqnyanRUVxwXF5Xn2a-MCGnzbTqPzPYIYvXIwGo1ATaNBwcTBBRh9mJHrbQtdByuy16jz2lmn1kQzo-uv28_kWEnRlqCd6c1CPnc-DHsXu_gOARqgNy2K46Rn5C3aG2jH_YymXpuwC6CnND4-z55YaKN5cXdfZN8-fthefcpvv1zfXG1uc1VWxZhrRXAjrK3LUmFqWTqUN9ZQImpuGMWYlVZZbFlSDAQ11hgmqrqEGpraiOIiu1l5tYeDHILrIMzSg5PHhA87CWF0qjVSQMWYAqsJsazUQvCyERUnABxUGpS43q9cw9R0RivTjwHaE9LTSu_2cud_yloIUpDlMW_uCIL_MZk4ys5FZdo2KeanKCnnmBBe0SJBX_8DPfgp9EmqBcW5KEoh_qJ2kBZI_-fTXLWQyg0vmGA4LZBQl_9BpaNN55TvjXUpf9JA1wYVfIzB2PsdCZaLNeVqTZmsKY_WlHVqevVQnfuWP14sfgMESOEO</recordid><startdate>20230127</startdate><enddate>20230127</enddate><creator>Zeng, Xiang</creator><creator>Tian, Ge</creator><creator>Zhu, Jingfang</creator><creator>Yang, Fuyun</creator><creator>Zhang, Rui</creator><creator>Li, Huijun</creator><creator>An, Zhen</creator><creator>Li, Juan</creator><creator>Song, Jie</creator><creator>Jiang, Jing</creator><creator>Liu, Dongling</creator><creator>Wu, Weidong</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T2</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8C1</scope><scope>8FE</scope><scope>8FG</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>L6V</scope><scope>M0S</scope><scope>M1P</scope><scope>M7S</scope><scope>PATMY</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20230127</creationdate><title>Air pollution associated acute respiratory inflammation and modification by GSTM1 and GSTT1 gene polymorphisms: a panel study of healthy undergraduates</title><author>Zeng, Xiang ; Tian, Ge ; Zhu, Jingfang ; Yang, Fuyun ; Zhang, Rui ; Li, Huijun ; An, Zhen ; Li, Juan ; Song, Jie ; Jiang, Jing ; Liu, Dongling ; Wu, Weidong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c563t-dc10b8ff955c02f4f4f27bfe21897e420045fcf0f4118a82efee48695a9ab9e83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Adolescent</topic><topic>Air pollutants</topic><topic>Air Pollutants - adverse effects</topic><topic>Air pollution</topic><topic>Air Pollution - adverse effects</topic><topic>Asthma</topic><topic>Atmospheric models</topic><topic>Biomarkers</topic><topic>Chronic obstructive pulmonary disease</topic><topic>College students</topic><topic>Cytokines</topic><topic>Demographic aspects</topic><topic>Environmental health</topic><topic>Epidemiology</topic><topic>Exposure</topic><topic>Gene polymorphism</topic><topic>Genetic polymorphisms</topic><topic>Genotype</topic><topic>Genotypes</topic><topic>Glutathione</topic><topic>Glutathione S-Transferase</topic><topic>Glutathione transferase</topic><topic>Glutathione Transferase - genetics</topic><topic>GSTM1 protein</topic><topic>GSTT1 gene</topic><topic>GSTT1 protein</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammation - chemically induced</topic><topic>Interleukin 6</topic><topic>Interleukin 8</topic><topic>Interleukins</topic><topic>Longitudinal studies</topic><topic>Lung function</topic><topic>Lungs</topic><topic>Nitrogen dioxide</topic><topic>Outdoor air quality</topic><topic>Oxidative stress</topic><topic>Particulate matter</topic><topic>Particulates</topic><topic>Pollutants</topic><topic>Pollution control</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Prostaglandin F2a</topic><topic>Prostaglandins</topic><topic>Respiratory function</topic><topic>Respiratory tract diseases</topic><topic>Risk factors</topic><topic>Sulfur dioxide</topic><topic>Tumor necrosis factor-α</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zeng, Xiang</creatorcontrib><creatorcontrib>Tian, Ge</creatorcontrib><creatorcontrib>Zhu, Jingfang</creatorcontrib><creatorcontrib>Yang, Fuyun</creatorcontrib><creatorcontrib>Zhang, Rui</creatorcontrib><creatorcontrib>Li, Huijun</creatorcontrib><creatorcontrib>An, Zhen</creatorcontrib><creatorcontrib>Li, Juan</creatorcontrib><creatorcontrib>Song, Jie</creatorcontrib><creatorcontrib>Jiang, Jing</creatorcontrib><creatorcontrib>Liu, Dongling</creatorcontrib><creatorcontrib>Wu, Weidong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health and Safety Science Abstracts (Full archive)</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Engineering Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Engineering Database</collection><collection>Environmental Science Database</collection><collection>Publicly Available Content (ProQuest)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>Environmental health</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zeng, Xiang</au><au>Tian, Ge</au><au>Zhu, Jingfang</au><au>Yang, Fuyun</au><au>Zhang, Rui</au><au>Li, Huijun</au><au>An, Zhen</au><au>Li, Juan</au><au>Song, Jie</au><au>Jiang, Jing</au><au>Liu, Dongling</au><au>Wu, Weidong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Air pollution associated acute respiratory inflammation and modification by GSTM1 and GSTT1 gene polymorphisms: a panel study of healthy undergraduates</atitle><jtitle>Environmental health</jtitle><addtitle>Environ Health</addtitle><date>2023-01-27</date><risdate>2023</risdate><volume>22</volume><issue>1</issue><spage>14</spage><epage>14</epage><pages>14-14</pages><artnum>14</artnum><issn>1476-069X</issn><eissn>1476-069X</eissn><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
). 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.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>36703205</pmid><doi>10.1186/s12940-022-00954-9</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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source | Open Access: PubMed Central; Publicly Available Content (ProQuest) |
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 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 Outdoor air quality Oxidative stress Particulate matter Particulates Pollutants Pollution control Polymorphism Polymorphism, Genetic Prostaglandin F2a Prostaglandins Respiratory function Respiratory tract diseases Risk factors Sulfur dioxide Tumor necrosis factor-α Young Adult |
title | Air pollution associated acute respiratory inflammation and modification by GSTM1 and GSTT1 gene polymorphisms: a panel study of healthy undergraduates |
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