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Association of Maternal Air Pollution Exposure and Infant Lung Function Is Modified by Genetic Propensity to Oxidative Stress
The association between air pollution and poor respiratory health outcomes is well established. Children are particularly at risk from air pollution, especially during the prenatal period as their organs and systems are still undergoing crucial development. This study investigated maternal exposure...
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Published in: | Children (Basel) 2024-07, Vol.11 (8), p.937 |
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creator | Vilcins, Dwan Lee, Wen Ray Pham, Cindy Tanner, Sam Knibbs, Luke D Burgner, David Blake, Tamara L Mansell, Toby Ponsonby, Anne-Louise Sly, Peter D Barwon Infant Study Investigator Group |
description | The association between air pollution and poor respiratory health outcomes is well established. Children are particularly at risk from air pollution, especially during the prenatal period as their organs and systems are still undergoing crucial development. This study investigated maternal exposure to air pollution during pregnancy and oxidative stress (OS), inflammation, and infant lung function at 4 weeks of age.
Data from the Barwon Infant Study were available for 314 infants. The exposure to NO
and PM
were estimated. Infant lung function (4 weeks) was measured by multiple-breath washout. Glycoprotein acetyls (GlycA) (36 weeks prenatal), cord blood, and OS biomarkers were measured in maternal urine (28 weeks). A genetic pathway score for OS (gPFSox) was calculated. Linear regression was used and potential modification by the OS genotype was tested.
There was no relationship between maternal exposure to air pollution and infant lung function, or with GlycA or OS during pregnancy. We found an association in children with a genetic propensity to OS between NO
and a lower functional residual capacity (FRC) (β = -5.3 mls, 95% CI (-9.3, -1.3),
= 0.01) and lung clearance index (LCI) score (β = 0.46 turnovers, (95% CI 0.10, 0.82),
= 0.01).
High prenatal exposure to ambient NO
is associated with a lower FRC and a higher LCI score in infants with a genetic propensity to oxidative stress. There was no relationship between maternal exposure to air pollution with maternal and cord blood inflammation or OS biomarkers. |
doi_str_mv | 10.3390/children11080937 |
format | article |
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Data from the Barwon Infant Study were available for 314 infants. The exposure to NO
and PM
were estimated. Infant lung function (4 weeks) was measured by multiple-breath washout. Glycoprotein acetyls (GlycA) (36 weeks prenatal), cord blood, and OS biomarkers were measured in maternal urine (28 weeks). A genetic pathway score for OS (gPFSox) was calculated. Linear regression was used and potential modification by the OS genotype was tested.
There was no relationship between maternal exposure to air pollution and infant lung function, or with GlycA or OS during pregnancy. We found an association in children with a genetic propensity to OS between NO
and a lower functional residual capacity (FRC) (β = -5.3 mls, 95% CI (-9.3, -1.3),
= 0.01) and lung clearance index (LCI) score (β = 0.46 turnovers, (95% CI 0.10, 0.82),
= 0.01).
High prenatal exposure to ambient NO
is associated with a lower FRC and a higher LCI score in infants with a genetic propensity to oxidative stress. There was no relationship between maternal exposure to air pollution with maternal and cord blood inflammation or OS biomarkers.</description><identifier>ISSN: 2227-9067</identifier><identifier>EISSN: 2227-9067</identifier><identifier>DOI: 10.3390/children11080937</identifier><identifier>PMID: 39201872</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Age ; air pollutants ; Air pollution ; Airway management ; Babies ; Biomarkers ; children’s health ; environmental health ; Genes ; Infants ; Inflammation ; lung function ; Nitric oxide ; Nitrogen dioxide ; NMR ; Nuclear magnetic resonance ; Outdoor air quality ; Oxidative stress ; Pediatrics ; Pregnancy ; Womens health</subject><ispartof>Children (Basel), 2024-07, Vol.11 (8), p.937</ispartof><rights>COPYRIGHT 2024 MDPI AG</rights><rights>2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2024 by the authors. 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c413t-ba6b030eea990e4c2e8d760b0a98a8c5a406ecbee269609f3e0833c74004bf4f3</cites><orcidid>0000-0002-8304-4302 ; 0000-0001-6305-2201 ; 0000-0002-1282-6331 ; 0000-0002-6581-3657 ; 0000-0003-0271-9230 ; 0000-0002-1900-9801</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/3097885705/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/3097885705?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39201872$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vilcins, Dwan</creatorcontrib><creatorcontrib>Lee, Wen Ray</creatorcontrib><creatorcontrib>Pham, Cindy</creatorcontrib><creatorcontrib>Tanner, Sam</creatorcontrib><creatorcontrib>Knibbs, Luke D</creatorcontrib><creatorcontrib>Burgner, David</creatorcontrib><creatorcontrib>Blake, Tamara L</creatorcontrib><creatorcontrib>Mansell, Toby</creatorcontrib><creatorcontrib>Ponsonby, Anne-Louise</creatorcontrib><creatorcontrib>Sly, Peter D</creatorcontrib><creatorcontrib>Barwon Infant Study Investigator Group</creatorcontrib><creatorcontrib>Barwon Infant Study Investigator Group</creatorcontrib><title>Association of Maternal Air Pollution Exposure and Infant Lung Function Is Modified by Genetic Propensity to Oxidative Stress</title><title>Children (Basel)</title><addtitle>Children (Basel)</addtitle><description>The association between air pollution and poor respiratory health outcomes is well established. Children are particularly at risk from air pollution, especially during the prenatal period as their organs and systems are still undergoing crucial development. This study investigated maternal exposure to air pollution during pregnancy and oxidative stress (OS), inflammation, and infant lung function at 4 weeks of age.
Data from the Barwon Infant Study were available for 314 infants. The exposure to NO
and PM
were estimated. Infant lung function (4 weeks) was measured by multiple-breath washout. Glycoprotein acetyls (GlycA) (36 weeks prenatal), cord blood, and OS biomarkers were measured in maternal urine (28 weeks). A genetic pathway score for OS (gPFSox) was calculated. Linear regression was used and potential modification by the OS genotype was tested.
There was no relationship between maternal exposure to air pollution and infant lung function, or with GlycA or OS during pregnancy. We found an association in children with a genetic propensity to OS between NO
and a lower functional residual capacity (FRC) (β = -5.3 mls, 95% CI (-9.3, -1.3),
= 0.01) and lung clearance index (LCI) score (β = 0.46 turnovers, (95% CI 0.10, 0.82),
= 0.01).
High prenatal exposure to ambient NO
is associated with a lower FRC and a higher LCI score in infants with a genetic propensity to oxidative stress. There was no relationship between maternal exposure to air pollution with maternal and cord blood inflammation or OS biomarkers.</description><subject>Age</subject><subject>air pollutants</subject><subject>Air pollution</subject><subject>Airway management</subject><subject>Babies</subject><subject>Biomarkers</subject><subject>children’s health</subject><subject>environmental health</subject><subject>Genes</subject><subject>Infants</subject><subject>Inflammation</subject><subject>lung function</subject><subject>Nitric oxide</subject><subject>Nitrogen dioxide</subject><subject>NMR</subject><subject>Nuclear magnetic resonance</subject><subject>Outdoor air quality</subject><subject>Oxidative stress</subject><subject>Pediatrics</subject><subject>Pregnancy</subject><subject>Womens health</subject><issn>2227-9067</issn><issn>2227-9067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpdkk1PGzEQhldVq4Io954qS730Ejr-2LV9qiIENBIIpLbnldceB0cbO7V3ETnw37skFAHywdbM-z4zI09VfaZwwrmG7_Y29C5jpBQUaC7fVYeMMTnT0Mj3L94H1XEpKwCgnNVMyY_VAdcMqJLssHqYl5JsMENIkSRPrsyAOZqezEMmN6nvx13m7H6TypiRmOjIInoTB3I5xiU5H6PdKRaFXCUXfEBHui25wIhDsOQmpw3GEoYtGRK5vg9uKnWH5NeQsZRP1Qdv-oLHT_dR9ef87Pfpz9nl9cXidH45s4LyYdaZpgMOiEZrQGEZKicb6MBoZZStjYAGbYfIGt2A9hxBcW6lABCdF54fVYs91yWzajc5rE3etsmEdhdIedmaPLXbYwsNE8I3EqXUwlmqHdYARnSm5r5mbmL92LM2Y7dGZzEO2fSvoK8zMdy2y3TXUsprpgWfCN-eCDn9HbEM7ToUi31vIqaxtBy0lpo19FH69Y10lcbH_9mppFK1hHpSnexVSzNNEKJPU2E7HYfrYFNEH6b4XIEUTCjFJgPsDTanUjL65_YptI_L1b5drsny5eXYz4b_q8T_AZVuzSs</recordid><startdate>20240731</startdate><enddate>20240731</enddate><creator>Vilcins, Dwan</creator><creator>Lee, Wen Ray</creator><creator>Pham, Cindy</creator><creator>Tanner, Sam</creator><creator>Knibbs, Luke D</creator><creator>Burgner, David</creator><creator>Blake, Tamara L</creator><creator>Mansell, Toby</creator><creator>Ponsonby, Anne-Louise</creator><creator>Sly, Peter D</creator><creator>Barwon Infant Study Investigator Group</creator><general>MDPI AG</general><general>MDPI</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>NAPCQ</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-8304-4302</orcidid><orcidid>https://orcid.org/0000-0001-6305-2201</orcidid><orcidid>https://orcid.org/0000-0002-1282-6331</orcidid><orcidid>https://orcid.org/0000-0002-6581-3657</orcidid><orcidid>https://orcid.org/0000-0003-0271-9230</orcidid><orcidid>https://orcid.org/0000-0002-1900-9801</orcidid></search><sort><creationdate>20240731</creationdate><title>Association of Maternal Air Pollution Exposure and Infant Lung Function Is Modified by Genetic Propensity to Oxidative Stress</title><author>Vilcins, Dwan ; Lee, Wen Ray ; Pham, Cindy ; Tanner, Sam ; Knibbs, Luke D ; Burgner, David ; Blake, Tamara L ; Mansell, Toby ; Ponsonby, Anne-Louise ; Sly, Peter D ; Barwon Infant Study Investigator Group</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c413t-ba6b030eea990e4c2e8d760b0a98a8c5a406ecbee269609f3e0833c74004bf4f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Age</topic><topic>air pollutants</topic><topic>Air pollution</topic><topic>Airway management</topic><topic>Babies</topic><topic>Biomarkers</topic><topic>children’s health</topic><topic>environmental health</topic><topic>Genes</topic><topic>Infants</topic><topic>Inflammation</topic><topic>lung function</topic><topic>Nitric oxide</topic><topic>Nitrogen dioxide</topic><topic>NMR</topic><topic>Nuclear magnetic resonance</topic><topic>Outdoor air quality</topic><topic>Oxidative stress</topic><topic>Pediatrics</topic><topic>Pregnancy</topic><topic>Womens health</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vilcins, Dwan</creatorcontrib><creatorcontrib>Lee, Wen Ray</creatorcontrib><creatorcontrib>Pham, Cindy</creatorcontrib><creatorcontrib>Tanner, Sam</creatorcontrib><creatorcontrib>Knibbs, Luke D</creatorcontrib><creatorcontrib>Burgner, David</creatorcontrib><creatorcontrib>Blake, Tamara L</creatorcontrib><creatorcontrib>Mansell, Toby</creatorcontrib><creatorcontrib>Ponsonby, Anne-Louise</creatorcontrib><creatorcontrib>Sly, Peter D</creatorcontrib><creatorcontrib>Barwon Infant Study Investigator Group</creatorcontrib><creatorcontrib>Barwon Infant Study Investigator Group</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Nursing and Allied Health Journals</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Nursing & Allied Health Premium</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Children (Basel)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vilcins, Dwan</au><au>Lee, Wen Ray</au><au>Pham, Cindy</au><au>Tanner, Sam</au><au>Knibbs, Luke D</au><au>Burgner, David</au><au>Blake, Tamara L</au><au>Mansell, Toby</au><au>Ponsonby, Anne-Louise</au><au>Sly, Peter D</au><au>Barwon Infant Study Investigator Group</au><aucorp>Barwon Infant Study Investigator Group</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association of Maternal Air Pollution Exposure and Infant Lung Function Is Modified by Genetic Propensity to Oxidative Stress</atitle><jtitle>Children (Basel)</jtitle><addtitle>Children (Basel)</addtitle><date>2024-07-31</date><risdate>2024</risdate><volume>11</volume><issue>8</issue><spage>937</spage><pages>937-</pages><issn>2227-9067</issn><eissn>2227-9067</eissn><abstract>The association between air pollution and poor respiratory health outcomes is well established. Children are particularly at risk from air pollution, especially during the prenatal period as their organs and systems are still undergoing crucial development. This study investigated maternal exposure to air pollution during pregnancy and oxidative stress (OS), inflammation, and infant lung function at 4 weeks of age.
Data from the Barwon Infant Study were available for 314 infants. The exposure to NO
and PM
were estimated. Infant lung function (4 weeks) was measured by multiple-breath washout. Glycoprotein acetyls (GlycA) (36 weeks prenatal), cord blood, and OS biomarkers were measured in maternal urine (28 weeks). A genetic pathway score for OS (gPFSox) was calculated. Linear regression was used and potential modification by the OS genotype was tested.
There was no relationship between maternal exposure to air pollution and infant lung function, or with GlycA or OS during pregnancy. We found an association in children with a genetic propensity to OS between NO
and a lower functional residual capacity (FRC) (β = -5.3 mls, 95% CI (-9.3, -1.3),
= 0.01) and lung clearance index (LCI) score (β = 0.46 turnovers, (95% CI 0.10, 0.82),
= 0.01).
High prenatal exposure to ambient NO
is associated with a lower FRC and a higher LCI score in infants with a genetic propensity to oxidative stress. There was no relationship between maternal exposure to air pollution with maternal and cord blood inflammation or OS biomarkers.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>39201872</pmid><doi>10.3390/children11080937</doi><orcidid>https://orcid.org/0000-0002-8304-4302</orcidid><orcidid>https://orcid.org/0000-0001-6305-2201</orcidid><orcidid>https://orcid.org/0000-0002-1282-6331</orcidid><orcidid>https://orcid.org/0000-0002-6581-3657</orcidid><orcidid>https://orcid.org/0000-0003-0271-9230</orcidid><orcidid>https://orcid.org/0000-0002-1900-9801</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Age air pollutants Air pollution Airway management Babies Biomarkers children’s health environmental health Genes Infants Inflammation lung function Nitric oxide Nitrogen dioxide NMR Nuclear magnetic resonance Outdoor air quality Oxidative stress Pediatrics Pregnancy Womens health |
title | Association of Maternal Air Pollution Exposure and Infant Lung Function Is Modified by Genetic Propensity to Oxidative Stress |
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