Experimental exposure to wood smoke: effects on airway inflammation and oxidative stress

Background:Particulate air pollution affects cardiovascular and pulmonary disease and mortality. A main hypothesis about the mechanisms involved is that particles induce inflammation in lower airways, systemic inflammation and oxidative stress.Objectives:To examine whether short-term exposure to woo...

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Published in:Occupational and environmental medicine (London, England) England), 2008-05, Vol.65 (5), p.319-324
Main Authors: Barregard, L, Sällsten, G, Andersson, L, Almstrand, A-C, Gustafson, P, Andersson, M, Olin, A-C
Format: Article
Language:English
Subjects:
Adult
adverse effects
Air
Air cleanliness
Air pollution
analysis
Biological and medical sciences
Biological Markers
Biomarkers
Biomarkers - metabolism
Breath tests
Bronchitis
Bronchitis - chemically induced
Bronchitis - physiopathology
Chemical hazards
chemically induced
Diesel exhaust
Environmental pollutants toxicology
Exposure
Female
Humans
Hydrocarbons
Hypotheses
Indoor environments
Inhalation Exposure
Inhalation Exposure - adverse effects
Lung
Lung - metabolism
Lung - physiopathology
Lungmedicin och allergi
Male
Medical sciences
metabolism
Middle Aged
Nitric Oxide
Nitric Oxide - metabolism
Outdoor air quality
Oxidative Stress
Oxides
Particle Size
Particulate matter
physiopathology
Proteins
Pulmonary alveoli
Respiratory Medicine and Allergy
Respiratory tract
Smoke
Smoke - adverse effects
Smoke - analysis
Toxicology
Urine
Uteroglobin
Uteroglobin - metabolism
Wood
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cited_by cdi_FETCH-LOGICAL-b516t-3ff68e53c1f03553bea0406fdbfae68b505f8885c6a5d0172b8e5282816ee63a3
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container_title Occupational and environmental medicine (London, England)
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creator Barregard, L
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Gustafson, P
Andersson, M
Olin, A-C
description Background:Particulate air pollution affects cardiovascular and pulmonary disease and mortality. A main hypothesis about the mechanisms involved is that particles induce inflammation in lower airways, systemic inflammation and oxidative stress.Objectives:To examine whether short-term exposure to wood smoke in healthy subjects affects markers of pulmonary inflammation and oxidative stress.Methods:13 subjects were exposed first to clean air and then to wood smoke in a chamber during 4-hour sessions, 1 week apart. The mass concentrations of fine particles at wood smoke exposure were 240–280 μg/m3, and number concentrations were 95 000–180 000/cm3, about half of the particles being ultrafine (
doi_str_mv 10.1136/oem.2006.032458
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A main hypothesis about the mechanisms involved is that particles induce inflammation in lower airways, systemic inflammation and oxidative stress.Objectives:To examine whether short-term exposure to wood smoke in healthy subjects affects markers of pulmonary inflammation and oxidative stress.Methods:13 subjects were exposed first to clean air and then to wood smoke in a chamber during 4-hour sessions, 1 week apart. The mass concentrations of fine particles at wood smoke exposure were 240–280 μg/m3, and number concentrations were 95 000–180 000/cm3, about half of the particles being ultrafine (&lt;100 nm). Blood and breath samples were taken before and at various intervals after exposure to wood smoke and clean air and examined for exhaled nitric oxide and Clara cell protein in serum and urine, and malondialdehyde in exhaled breath condensate.Results:Exposure to wood smoke increased alveolar nitric oxide 3 hours post-exposure while malondialdehyde levels in breath condensate were higher both immediately after and 20 hours after exposure. Serum Clara cell protein was increased 20 hours after exposure.Conclusions:Wood smoke at levels that can be found in smoky indoor environments caused an inflammatory response and signs of increased oxidative stress in the respiratory tract, especially in the lower airways.</description><identifier>ISSN: 1351-0711</identifier><identifier>ISSN: 1470-7926</identifier><identifier>EISSN: 1470-7926</identifier><identifier>DOI: 10.1136/oem.2006.032458</identifier><identifier>PMID: 17704195</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd</publisher><subject>Adult ; adverse effects ; Air ; Air cleanliness ; Air pollution ; analysis ; Biological and medical sciences ; Biological Markers ; Biomarkers ; Biomarkers - metabolism ; Breath tests ; Bronchitis ; Bronchitis - chemically induced ; Bronchitis - physiopathology ; Chemical hazards ; chemically induced ; Diesel exhaust ; Environmental pollutants toxicology ; Exposure ; Female ; Humans ; Hydrocarbons ; Hypotheses ; Indoor environments ; Inhalation Exposure ; Inhalation Exposure - adverse effects ; Lung ; Lung - metabolism ; Lung - physiopathology ; Lungmedicin och allergi ; Male ; Medical sciences ; metabolism ; Middle Aged ; Nitric Oxide ; Nitric Oxide - metabolism ; Outdoor air quality ; Oxidative Stress ; Oxides ; Particle Size ; Particulate matter ; physiopathology ; Proteins ; Pulmonary alveoli ; Respiratory Medicine and Allergy ; Respiratory tract ; Smoke ; Smoke - adverse effects ; Smoke - analysis ; Toxicology ; Urine ; Uteroglobin ; Uteroglobin - metabolism ; Wood</subject><ispartof>Occupational and environmental medicine (London, England), 2008-05, Vol.65 (5), p.319-324</ispartof><rights>2008 BMJ Publishing Group</rights><rights>2008 INIST-CNRS</rights><rights>Copyright: 2008 2008 BMJ Publishing Group</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b516t-3ff68e53c1f03553bea0406fdbfae68b505f8885c6a5d0172b8e5282816ee63a3</citedby><cites>FETCH-LOGICAL-b516t-3ff68e53c1f03553bea0406fdbfae68b505f8885c6a5d0172b8e5282816ee63a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://oem.bmj.com/content/65/5/319.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttps://oem.bmj.com/content/65/5/319.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,230,314,780,784,885,3196,23571,27924,27925,58238,58471,77472,77503</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=20259863$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17704195$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://gup.ub.gu.se/publication/88113$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Barregard, L</creatorcontrib><creatorcontrib>Sällsten, G</creatorcontrib><creatorcontrib>Andersson, L</creatorcontrib><creatorcontrib>Almstrand, A-C</creatorcontrib><creatorcontrib>Gustafson, P</creatorcontrib><creatorcontrib>Andersson, M</creatorcontrib><creatorcontrib>Olin, A-C</creatorcontrib><title>Experimental exposure to wood smoke: effects on airway inflammation and oxidative stress</title><title>Occupational and environmental medicine (London, England)</title><addtitle>Occup Environ Med</addtitle><description>Background:Particulate air pollution affects cardiovascular and pulmonary disease and mortality. A main hypothesis about the mechanisms involved is that particles induce inflammation in lower airways, systemic inflammation and oxidative stress.Objectives:To examine whether short-term exposure to wood smoke in healthy subjects affects markers of pulmonary inflammation and oxidative stress.Methods:13 subjects were exposed first to clean air and then to wood smoke in a chamber during 4-hour sessions, 1 week apart. The mass concentrations of fine particles at wood smoke exposure were 240–280 μg/m3, and number concentrations were 95 000–180 000/cm3, about half of the particles being ultrafine (&lt;100 nm). Blood and breath samples were taken before and at various intervals after exposure to wood smoke and clean air and examined for exhaled nitric oxide and Clara cell protein in serum and urine, and malondialdehyde in exhaled breath condensate.Results:Exposure to wood smoke increased alveolar nitric oxide 3 hours post-exposure while malondialdehyde levels in breath condensate were higher both immediately after and 20 hours after exposure. Serum Clara cell protein was increased 20 hours after exposure.Conclusions:Wood smoke at levels that can be found in smoky indoor environments caused an inflammatory response and signs of increased oxidative stress in the respiratory tract, especially in the lower airways.</description><subject>Adult</subject><subject>adverse effects</subject><subject>Air</subject><subject>Air cleanliness</subject><subject>Air pollution</subject><subject>analysis</subject><subject>Biological and medical sciences</subject><subject>Biological Markers</subject><subject>Biomarkers</subject><subject>Biomarkers - metabolism</subject><subject>Breath tests</subject><subject>Bronchitis</subject><subject>Bronchitis - chemically induced</subject><subject>Bronchitis - physiopathology</subject><subject>Chemical hazards</subject><subject>chemically induced</subject><subject>Diesel exhaust</subject><subject>Environmental pollutants toxicology</subject><subject>Exposure</subject><subject>Female</subject><subject>Humans</subject><subject>Hydrocarbons</subject><subject>Hypotheses</subject><subject>Indoor environments</subject><subject>Inhalation Exposure</subject><subject>Inhalation Exposure - adverse effects</subject><subject>Lung</subject><subject>Lung - metabolism</subject><subject>Lung - physiopathology</subject><subject>Lungmedicin och allergi</subject><subject>Male</subject><subject>Medical sciences</subject><subject>metabolism</subject><subject>Middle Aged</subject><subject>Nitric Oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Outdoor air quality</subject><subject>Oxidative Stress</subject><subject>Oxides</subject><subject>Particle Size</subject><subject>Particulate matter</subject><subject>physiopathology</subject><subject>Proteins</subject><subject>Pulmonary alveoli</subject><subject>Respiratory Medicine and Allergy</subject><subject>Respiratory tract</subject><subject>Smoke</subject><subject>Smoke - adverse effects</subject><subject>Smoke - analysis</subject><subject>Toxicology</subject><subject>Urine</subject><subject>Uteroglobin</subject><subject>Uteroglobin - metabolism</subject><subject>Wood</subject><issn>1351-0711</issn><issn>1470-7926</issn><issn>1470-7926</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><recordid>eNqFkUtv1DAUhSMEoqWwZgWyhGCByNSP8WPYoWkHEBVsymNnOcl1lWkSB9-Emf57HGU0ldiwsn3P53t9fLLsOaMLxoQ6D9AuOKVqQQVfSvMgO2VLTXO94uph2gvJcqoZO8meIG4pZUIL_jg7YVrTJVvJ0-zX5b6HWLfQDa4hsO8DjhHIEMguhIpgG27hPQHvoRyQhI64Ou7cHak737i2dUM91bqKhH1dpdMfIDhEQHyaPfKuQXh2WM-y75vL6_Wn_Orbx8_rD1d5IZkacuG9MiBFyTwVUooCHF1S5avCO1CmkFR6Y4wslZMVZZoXieaGG6YAlHDiLHs398Ud9GNh-2TGxTsbXG1vxt6m0s1oEawx6ccS_mbG-xh-j4CDbWssoWlcB2FEy6kyZslVAl_9A27DGLtkxTJtGF-x9JhEnc9UGQNiBH-cz6idErIpITslZOeE0o2Xh75j0UJ1zx8iScDrA-CwdI2PritrPHKccrkyanLyYua2OIR4r6cZktNJz2e9xgH2R93FW6u00NJ-_bG2F1_k5mJz_dNOht_OfNFu_-viL4m5v3s</recordid><startdate>20080501</startdate><enddate>20080501</enddate><creator>Barregard, L</creator><creator>Sällsten, G</creator><creator>Andersson, L</creator><creator>Almstrand, A-C</creator><creator>Gustafson, P</creator><creator>Andersson, M</creator><creator>Olin, A-C</creator><general>BMJ Publishing Group Ltd</general><general>BMJ Publishing Group</general><general>BMJ</general><general>BMJ Publishing Group LTD</general><scope>BSCLL</scope><scope>IQODW</scope><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>7RV</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>AEUYN</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>L6V</scope><scope>M0S</scope><scope>M1P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>PATMY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>7T2</scope><scope>7TV</scope><scope>7U2</scope><scope>C1K</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>F1U</scope></search><sort><creationdate>20080501</creationdate><title>Experimental exposure to wood smoke: effects on airway inflammation and oxidative stress</title><author>Barregard, L ; Sällsten, G ; Andersson, L ; Almstrand, A-C ; Gustafson, P ; Andersson, M ; Olin, A-C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b516t-3ff68e53c1f03553bea0406fdbfae68b505f8885c6a5d0172b8e5282816ee63a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adult</topic><topic>adverse effects</topic><topic>Air</topic><topic>Air cleanliness</topic><topic>Air pollution</topic><topic>analysis</topic><topic>Biological and medical sciences</topic><topic>Biological Markers</topic><topic>Biomarkers</topic><topic>Biomarkers - metabolism</topic><topic>Breath tests</topic><topic>Bronchitis</topic><topic>Bronchitis - chemically induced</topic><topic>Bronchitis - physiopathology</topic><topic>Chemical hazards</topic><topic>chemically induced</topic><topic>Diesel exhaust</topic><topic>Environmental pollutants toxicology</topic><topic>Exposure</topic><topic>Female</topic><topic>Humans</topic><topic>Hydrocarbons</topic><topic>Hypotheses</topic><topic>Indoor environments</topic><topic>Inhalation Exposure</topic><topic>Inhalation Exposure - adverse effects</topic><topic>Lung</topic><topic>Lung - metabolism</topic><topic>Lung - physiopathology</topic><topic>Lungmedicin och allergi</topic><topic>Male</topic><topic>Medical sciences</topic><topic>metabolism</topic><topic>Middle Aged</topic><topic>Nitric Oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Outdoor air quality</topic><topic>Oxidative Stress</topic><topic>Oxides</topic><topic>Particle Size</topic><topic>Particulate matter</topic><topic>physiopathology</topic><topic>Proteins</topic><topic>Pulmonary alveoli</topic><topic>Respiratory Medicine and Allergy</topic><topic>Respiratory tract</topic><topic>Smoke</topic><topic>Smoke - adverse effects</topic><topic>Smoke - analysis</topic><topic>Toxicology</topic><topic>Urine</topic><topic>Uteroglobin</topic><topic>Uteroglobin - metabolism</topic><topic>Wood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Barregard, L</creatorcontrib><creatorcontrib>Sällsten, G</creatorcontrib><creatorcontrib>Andersson, L</creatorcontrib><creatorcontrib>Almstrand, A-C</creatorcontrib><creatorcontrib>Gustafson, P</creatorcontrib><creatorcontrib>Andersson, M</creatorcontrib><creatorcontrib>Olin, A-C</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><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>ProQuest Nursing and Allied Health Journals</collection><collection>ProQuest Health &amp; 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A main hypothesis about the mechanisms involved is that particles induce inflammation in lower airways, systemic inflammation and oxidative stress.Objectives:To examine whether short-term exposure to wood smoke in healthy subjects affects markers of pulmonary inflammation and oxidative stress.Methods:13 subjects were exposed first to clean air and then to wood smoke in a chamber during 4-hour sessions, 1 week apart. The mass concentrations of fine particles at wood smoke exposure were 240–280 μg/m3, and number concentrations were 95 000–180 000/cm3, about half of the particles being ultrafine (&lt;100 nm). Blood and breath samples were taken before and at various intervals after exposure to wood smoke and clean air and examined for exhaled nitric oxide and Clara cell protein in serum and urine, and malondialdehyde in exhaled breath condensate.Results:Exposure to wood smoke increased alveolar nitric oxide 3 hours post-exposure while malondialdehyde levels in breath condensate were higher both immediately after and 20 hours after exposure. Serum Clara cell protein was increased 20 hours after exposure.Conclusions:Wood smoke at levels that can be found in smoky indoor environments caused an inflammatory response and signs of increased oxidative stress in the respiratory tract, especially in the lower airways.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd</pub><pmid>17704195</pmid><doi>10.1136/oem.2006.032458</doi><tpages>6</tpages></addata></record>
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identifier ISSN: 1351-0711
ispartof Occupational and environmental medicine (London, England), 2008-05, Vol.65 (5), p.319-324
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source BMJ Journals - NESLi2; JSTOR
subjects Adult
adverse effects
Air
Air cleanliness
Air pollution
analysis
Biological and medical sciences
Biological Markers
Biomarkers
Biomarkers - metabolism
Breath tests
Bronchitis
Bronchitis - chemically induced
Bronchitis - physiopathology
Chemical hazards
chemically induced
Diesel exhaust
Environmental pollutants toxicology
Exposure
Female
Humans
Hydrocarbons
Hypotheses
Indoor environments
Inhalation Exposure
Inhalation Exposure - adverse effects
Lung
Lung - metabolism
Lung - physiopathology
Lungmedicin och allergi
Male
Medical sciences
metabolism
Middle Aged
Nitric Oxide
Nitric Oxide - metabolism
Outdoor air quality
Oxidative Stress
Oxides
Particle Size
Particulate matter
physiopathology
Proteins
Pulmonary alveoli
Respiratory Medicine and Allergy
Respiratory tract
Smoke
Smoke - adverse effects
Smoke - analysis
Toxicology
Urine
Uteroglobin
Uteroglobin - metabolism
Wood
title Experimental exposure to wood smoke: effects on airway inflammation and oxidative stress
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