The toxicity of constituents of cedar and pine woods to pulmonary epithelium
Identifieur interne : 001600 ( Istex/Corpus ); précédent : 001599; suivant : 001601The toxicity of constituents of cedar and pine woods to pulmonary epithelium
Auteurs : Garrison H. Ayars ; Leonard C. Altman ; Charles E. Frazier ; Emil Y. ChiSource :
- The Journal of Allergy and Clinical Immunology [ 0091-6749 ] ; 1989.
English descriptors
- Teeft :
- Abietic, Abietic acid, Abietic acids, Acid, Acute bronchospastic syndrome, Airway, Airway epithelium, Allergy, Allergy clin, Allergy clin immunol, Alveolar epithelial cells, Alveolar epithelium, Arachidonic acid, Asthma, Basal cell layer, Bronchial epithelium, Causative agent, Cedar, Cedar asthma, Cedar wood, Cedar workers, Cell lysis, Chronic bronchitis, Chronic lung disease, Clin, Clin allergy, Colophony, Colophony fumes, Control subjects, Cultured explant, Desquamated cells, Desquamation, Direct toxicity, Dose response, Electronic workers, Epithelial, Epithelial cell lysis, Epithelial cells, Epithelium, Exfoliated cells, Explants, Grand island, Immunologic mechanism, Infectious diseases, Instilled intratracheally, Intermittent addition, Light micrograph, Lysis, Major constituent, Maximum release, Media control, Microtiter plates, Newborn calf serum, Occupational asthma, Occupational exposure, Original magnification, Overnight incubation, Percent lysis, Pine resin, Pine wood, Pine woods, Plicatic, Plicatic acid, Progressive lysis, Pulmonary epithelium, Pulmonary function, Putative toxins, Respir, Respiratory disease, Significant cause, Similar locations, Target cells, Time course, Toxicity, Toxin, Tracheal, Tracheal explants, Vanox microscope, Volume number.
Abstract
Abstract: Occupational exposure to cedar and pine woods and pine resin (colophony) can cause asthma and chronic lung disease. Prior studies suggest that plicatic and abietic acids are responsible for the asthmatic reactions that occur in cedar-wood and colophony workers; however, the etiologic mechanism(s) of the chronic lung disease is unknown. To determine if plicatic acid from cedar wood and abietic acid from pine resin could directly damage lung cells, we exposed monolayers of rat type II and human A549 alveolar epithelial cells, intact rat lungs, and rat tracheal explants to solutions of plicatic and abietic acids. As indices of injury, we measured lysis of alveolar epithelial cells with a 51Cr technique, quantitative desquamation of epithelial cells from tracheal explants, and histologic alterations in tracheal explants and intact lungs. Plicatic and abietic acids both caused dose- and time-dependent lysis of alveolar epithelial cells. Instillation of plicatic and abietic acids into rat lungs produced bronchial epithelial sloughing. Abietic acid also caused destruction of the alveolar epithelium. The addition of either acid to rat tracheal explants caused epithelial desquamation that was dose- and time-dependent. Our results suggest that plicatic acid, a unique constituent of cedar wood, and abietic acid, the major constituent in pine resin, can produce lytic damage to alveolar, tracheal, and bronchial epithelial cells. We hypothesize that repeated occupational exposure to these substances might promote the chronic lung damage observed in some cedar- and pine-wood workers and in electronic workers exposed to colophony.
Url:
DOI: 10.1016/0091-6749(89)90073-0
Links to Exploration step
ISTEX:F9E29AD3A29998073C9412418AA061F1E1A010A0Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>The toxicity of constituents of cedar and pine woods to pulmonary epithelium</title><author><name sortKey="Ayars, Garrison H" sort="Ayars, Garrison H" uniqKey="Ayars G" first="Garrison H." last="Ayars">Garrison H. Ayars</name><affiliation><mods:affiliation>Seattle, Wash., USA</mods:affiliation></affiliation></author><author><name sortKey="Altman, Leonard C" sort="Altman, Leonard C" uniqKey="Altman L" first="Leonard C." last="Altman">Leonard C. Altman</name><affiliation><mods:affiliation>Seattle, Wash., USA</mods:affiliation></affiliation></author><author><name sortKey="Frazier, Charles E" sort="Frazier, Charles E" uniqKey="Frazier C" first="Charles E." last="Frazier">Charles E. Frazier</name><affiliation><mods:affiliation>Seattle, Wash., USA</mods:affiliation></affiliation></author><author><name sortKey="Chi, Emil Y" sort="Chi, Emil Y" uniqKey="Chi E" first="Emil Y." last="Chi">Emil Y. Chi</name><affiliation><mods:affiliation>Seattle, Wash., USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:F9E29AD3A29998073C9412418AA061F1E1A010A0</idno><date when="1989" year="1989">1989</date><idno type="doi">10.1016/0091-6749(89)90073-0</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-ZRLCNGHJ-M/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">001600</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001600</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">The toxicity of constituents of cedar and pine woods to pulmonary epithelium</title><author><name sortKey="Ayars, Garrison H" sort="Ayars, Garrison H" uniqKey="Ayars G" first="Garrison H." last="Ayars">Garrison H. Ayars</name><affiliation><mods:affiliation>Seattle, Wash., USA</mods:affiliation></affiliation></author><author><name sortKey="Altman, Leonard C" sort="Altman, Leonard C" uniqKey="Altman L" first="Leonard C." last="Altman">Leonard C. Altman</name><affiliation><mods:affiliation>Seattle, Wash., USA</mods:affiliation></affiliation></author><author><name sortKey="Frazier, Charles E" sort="Frazier, Charles E" uniqKey="Frazier C" first="Charles E." last="Frazier">Charles E. Frazier</name><affiliation><mods:affiliation>Seattle, Wash., USA</mods:affiliation></affiliation></author><author><name sortKey="Chi, Emil Y" sort="Chi, Emil Y" uniqKey="Chi E" first="Emil Y." last="Chi">Emil Y. Chi</name><affiliation><mods:affiliation>Seattle, Wash., USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">The Journal of Allergy and Clinical Immunology</title><title level="j" type="abbrev">YMAI</title><idno type="ISSN">0091-6749</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1989">1989</date><biblScope unit="volume">83</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="610">610</biblScope><biblScope unit="page" to="618">618</biblScope></imprint><idno type="ISSN">0091-6749</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0091-6749</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Abietic</term><term>Abietic acid</term><term>Abietic acids</term><term>Acid</term><term>Acute bronchospastic syndrome</term><term>Airway</term><term>Airway epithelium</term><term>Allergy</term><term>Allergy clin</term><term>Allergy clin immunol</term><term>Alveolar epithelial cells</term><term>Alveolar epithelium</term><term>Arachidonic acid</term><term>Asthma</term><term>Basal cell layer</term><term>Bronchial epithelium</term><term>Causative agent</term><term>Cedar</term><term>Cedar asthma</term><term>Cedar wood</term><term>Cedar workers</term><term>Cell lysis</term><term>Chronic bronchitis</term><term>Chronic lung disease</term><term>Clin</term><term>Clin allergy</term><term>Colophony</term><term>Colophony fumes</term><term>Control subjects</term><term>Cultured explant</term><term>Desquamated cells</term><term>Desquamation</term><term>Direct toxicity</term><term>Dose response</term><term>Electronic workers</term><term>Epithelial</term><term>Epithelial cell lysis</term><term>Epithelial cells</term><term>Epithelium</term><term>Exfoliated cells</term><term>Explants</term><term>Grand island</term><term>Immunologic mechanism</term><term>Infectious diseases</term><term>Instilled intratracheally</term><term>Intermittent addition</term><term>Light micrograph</term><term>Lysis</term><term>Major constituent</term><term>Maximum release</term><term>Media control</term><term>Microtiter plates</term><term>Newborn calf serum</term><term>Occupational asthma</term><term>Occupational exposure</term><term>Original magnification</term><term>Overnight incubation</term><term>Percent lysis</term><term>Pine resin</term><term>Pine wood</term><term>Pine woods</term><term>Plicatic</term><term>Plicatic acid</term><term>Progressive lysis</term><term>Pulmonary epithelium</term><term>Pulmonary function</term><term>Putative toxins</term><term>Respir</term><term>Respiratory disease</term><term>Significant cause</term><term>Similar locations</term><term>Target cells</term><term>Time course</term><term>Toxicity</term><term>Toxin</term><term>Tracheal</term><term>Tracheal explants</term><term>Vanox microscope</term><term>Volume number</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Occupational exposure to cedar and pine woods and pine resin (colophony) can cause asthma and chronic lung disease. Prior studies suggest that plicatic and abietic acids are responsible for the asthmatic reactions that occur in cedar-wood and colophony workers; however, the etiologic mechanism(s) of the chronic lung disease is unknown. To determine if plicatic acid from cedar wood and abietic acid from pine resin could directly damage lung cells, we exposed monolayers of rat type II and human A549 alveolar epithelial cells, intact rat lungs, and rat tracheal explants to solutions of plicatic and abietic acids. As indices of injury, we measured lysis of alveolar epithelial cells with a 51Cr technique, quantitative desquamation of epithelial cells from tracheal explants, and histologic alterations in tracheal explants and intact lungs. Plicatic and abietic acids both caused dose- and time-dependent lysis of alveolar epithelial cells. Instillation of plicatic and abietic acids into rat lungs produced bronchial epithelial sloughing. Abietic acid also caused destruction of the alveolar epithelium. The addition of either acid to rat tracheal explants caused epithelial desquamation that was dose- and time-dependent. Our results suggest that plicatic acid, a unique constituent of cedar wood, and abietic acid, the major constituent in pine resin, can produce lytic damage to alveolar, tracheal, and bronchial epithelial cells. We hypothesize that repeated occupational exposure to these substances might promote the chronic lung damage observed in some cedar- and pine-wood workers and in electronic workers exposed to colophony.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>plicatic</json:string><json:string>abietic</json:string><json:string>abietic acid</json:string><json:string>epithelial</json:string><json:string>colophony</json:string><json:string>plicatic acid</json:string><json:string>lysis</json:string><json:string>tracheal</json:string><json:string>abietic acids</json:string><json:string>explants</json:string><json:string>epithelium</json:string><json:string>airway</json:string><json:string>occupational asthma</json:string><json:string>cedar</json:string><json:string>asthma</json:string><json:string>allergy</json:string><json:string>tracheal explants</json:string><json:string>clin</json:string><json:string>respir</json:string><json:string>toxicity</json:string><json:string>pine resin</json:string><json:string>desquamation</json:string><json:string>light micrograph</json:string><json:string>original magnification</json:string><json:string>alveolar epithelial cells</json:string><json:string>chronic lung disease</json:string><json:string>putative toxins</json:string><json:string>cedar wood</json:string><json:string>epithelial cells</json:string><json:string>volume number</json:string><json:string>toxin</json:string><json:string>cell lysis</json:string><json:string>occupational exposure</json:string><json:string>major constituent</json:string><json:string>pine woods</json:string><json:string>pulmonary epithelium</json:string><json:string>desquamated cells</json:string><json:string>percent lysis</json:string><json:string>clin allergy</json:string><json:string>acid</json:string><json:string>pine wood</json:string><json:string>direct toxicity</json:string><json:string>acute bronchospastic syndrome</json:string><json:string>newborn calf serum</json:string><json:string>grand island</json:string><json:string>intermittent addition</json:string><json:string>overnight incubation</json:string><json:string>microtiter plates</json:string><json:string>respiratory disease</json:string><json:string>maximum release</json:string><json:string>chronic bronchitis</json:string><json:string>cedar workers</json:string><json:string>vanox microscope</json:string><json:string>instilled intratracheally</json:string><json:string>similar locations</json:string><json:string>time course</json:string><json:string>dose response</json:string><json:string>epithelial cell lysis</json:string><json:string>infectious diseases</json:string><json:string>target cells</json:string><json:string>media control</json:string><json:string>bronchial epithelium</json:string><json:string>exfoliated cells</json:string><json:string>basal cell layer</json:string><json:string>airway epithelium</json:string><json:string>significant cause</json:string><json:string>electronic workers</json:string><json:string>cultured explant</json:string><json:string>causative agent</json:string><json:string>cedar asthma</json:string><json:string>immunologic mechanism</json:string><json:string>colophony fumes</json:string><json:string>arachidonic acid</json:string><json:string>control subjects</json:string><json:string>alveolar epithelium</json:string><json:string>allergy clin</json:string><json:string>pulmonary function</json:string><json:string>allergy clin immunol</json:string><json:string>progressive lysis</json:string></teeft></keywords><author><json:item><name>Garrison H. Ayars MD</name><affiliations><json:string>Seattle, Wash., USA</json:string></affiliations></json:item><json:item><name>Leonard C. Altman MD</name><affiliations><json:string>Seattle, Wash., USA</json:string></affiliations></json:item><json:item><name>Charles E. Frazier PhD</name><affiliations><json:string>Seattle, Wash., USA</json:string></affiliations></json:item><json:item><name>Emil Y. Chi PhD</name><affiliations><json:string>Seattle, Wash., USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>AM : Alveolar macrophage</value></json:item></subject><arkIstex>ark:/67375/6H6-ZRLCNGHJ-M</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: Occupational exposure to cedar and pine woods and pine resin (colophony) can cause asthma and chronic lung disease. Prior studies suggest that plicatic and abietic acids are responsible for the asthmatic reactions that occur in cedar-wood and colophony workers; however, the etiologic mechanism(s) of the chronic lung disease is unknown. To determine if plicatic acid from cedar wood and abietic acid from pine resin could directly damage lung cells, we exposed monolayers of rat type II and human A549 alveolar epithelial cells, intact rat lungs, and rat tracheal explants to solutions of plicatic and abietic acids. As indices of injury, we measured lysis of alveolar epithelial cells with a 51Cr technique, quantitative desquamation of epithelial cells from tracheal explants, and histologic alterations in tracheal explants and intact lungs. Plicatic and abietic acids both caused dose- and time-dependent lysis of alveolar epithelial cells. Instillation of plicatic and abietic acids into rat lungs produced bronchial epithelial sloughing. Abietic acid also caused destruction of the alveolar epithelium. The addition of either acid to rat tracheal explants caused epithelial desquamation that was dose- and time-dependent. Our results suggest that plicatic acid, a unique constituent of cedar wood, and abietic acid, the major constituent in pine resin, can produce lytic damage to alveolar, tracheal, and bronchial epithelial cells. We hypothesize that repeated occupational exposure to these substances might promote the chronic lung damage observed in some cedar- and pine-wood workers and in electronic workers exposed to colophony.</abstract><qualityIndicators><score>9.319</score><pdfWordCount>4403</pdfWordCount><pdfCharCount>28466</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>9</pdfPageCount><pdfPageSize>540 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>243</abstractWordCount><abstractCharCount>1652</abstractCharCount><keywordCount>1</keywordCount></qualityIndicators><title>The toxicity of constituents of cedar and pine woods to pulmonary epithelium</title><pmid><json:string>2926083</json:string></pmid><pii><json:string>0091-6749(89)90073-0</json:string></pii><genre><json:string>research-article</json:string></genre><serie><title>Proc Natl Acad Sci USA</title><language><json:string>unknown</json:string></language><volume>82</volume><pages><first>4633</first><last>4637</last></pages></serie><host><title>The Journal of Allergy and Clinical Immunology</title><language><json:string>unknown</json:string></language><publicationDate>1989</publicationDate><issn><json:string>0091-6749</json:string></issn><pii><json:string>S0091-6749(00)X0233-3</json:string></pii><volume>83</volume><issue>3</issue><pages><first>610</first><last>618</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1989</json:string><json:string>15S</json:string></date><geogName></geogName><orgName><json:string>Department of Internal Medicine</json:string><json:string>National Institutes of Health DE</json:string><json:string>Forintek, Inc.</json:string><json:string>GIBCG Laboratories</json:string><json:string>Department of Pathology, University of Washington, Seattle, Wash</json:string><json:string>Grand Island Biologic Co.</json:string><json:string>Forintek, Inc., Vancouver</json:string><json:string>Olympus Corp.</json:string><json:string>Bioproducts, Inc.</json:string><json:string>Department of Medicine, RM</json:string><json:string>Tetko, Inc.</json:string><json:string>Fluke Chemical Co.</json:string><json:string>Packard Instruments, Inc.</json:string><json:string>Sigma Chemical Co.</json:string><json:string>W Scientific Corp.</json:string><json:string>Collaborative Research, Lexington, Mass</json:string><json:string>American Type Tissue Culture Collection, Rockville, Md</json:string><json:string>University of Washington</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>M. Specific</json:string><json:string>Goralie Baker</json:string><json:string>M. Maximal</json:string><json:string>H. Metabolism</json:string><json:string>Leonard C. Altman</json:string><json:string>Falcon Labware</json:string><json:string>M. Fate</json:string><json:string>K. Symptoms</json:string><json:string>T. Tine</json:string><json:string>Emil Y. Chi</json:string><json:string>E. Frazier</json:string><json:string>S. Clinical</json:string><json:string>Joan Blackbum</json:string></persName><placeName><json:string>Columbia</json:string><json:string>Monterey</json:string><json:string>Toxicity</json:string><json:string>Canada</json:string><json:string>Seattle</json:string><json:string>America</json:string><json:string>N.Y.</json:string><json:string>York</json:string><json:string>WA</json:string><json:string>Grand Island</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Ayars et al.</json:string><json:string>Dobbs et al.</json:string><json:string>Fisher et al.</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-ZRLCNGHJ-M</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - immunology</json:string><json:string>2 - allergy</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - allergy</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and Microbiology</json:string><json:string>3 - Immunology</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Immunology and Allergy</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string><json:string>4 - pneumologie</json:string></inist></categories><publicationDate>1989</publicationDate><copyrightDate>1989</copyrightDate><doi><json:string>10.1016/0091-6749(89)90073-0</json:string></doi><id>F9E29AD3A29998073C9412418AA061F1E1A010A0</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-ZRLCNGHJ-M/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-ZRLCNGHJ-M/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-ZRLCNGHJ-M/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a">The toxicity of constituents of cedar and pine woods to pulmonary epithelium</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>elsevier</p></licence></availability><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M"></p><date>1989</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note><note>Supported by National Institutes of Health DE 0 8229 and RO1 ESO 2366.</note><note type="content">Section title: Original article</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">The toxicity of constituents of cedar and pine woods to pulmonary epithelium</title><author xml:id="author-0000"><persName><forename type="first">Garrison H.</forename><surname>Ayars</surname></persName><roleName type="degree">MD</roleName><note type="biography">From the Division of Allergy and Infectious Diseases, Department of Internal Medicine, University of Washington, Seattle, Wash.</note><affiliation>From the Division of Allergy and Infectious Diseases, Department of Internal Medicine, University of Washington, Seattle, Wash.</affiliation><affiliation>Seattle, Wash., USA</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Leonard C.</forename><surname>Altman</surname></persName><roleName type="degree">MD</roleName><note type="biography">Reprint requests: Leonard C. Altman, MD, Division Allergy and Infectious Diseases, Department of Medicine, RM-13, University of Washington, Seattle, WA 98195.</note><note type="biography">From the Division of Allergy and Infectious Diseases, Department of Internal Medicine, University of Washington, Seattle, Wash.</note><affiliation>Reprint requests: Leonard C. Altman, MD, Division Allergy and Infectious Diseases, Department of Medicine, RM-13, University of Washington, Seattle, WA 98195.</affiliation><affiliation>From the Division of Allergy and Infectious Diseases, Department of Internal Medicine, University of Washington, Seattle, Wash.</affiliation><affiliation>Seattle, Wash., USA</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Charles E.</forename><surname>Frazier</surname></persName><roleName type="degree">PhD</roleName><note type="biography">From the Division of Allergy and Infectious Diseases, College of Forest Resources, University of Washington, Seattle, Wash.</note><affiliation>From the Division of Allergy and Infectious Diseases, College of Forest Resources, University of Washington, Seattle, Wash.</affiliation><affiliation>Seattle, Wash., USA</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Emil Y.</forename><surname>Chi</surname></persName><roleName type="degree">PhD</roleName><note type="biography">From the Division of Allergy and Infectious Diseases, The Department of Pathology, University of Washington, Seattle, Wash.</note><affiliation>From the Division of Allergy and Infectious Diseases, The Department of Pathology, University of Washington, Seattle, Wash.</affiliation><affiliation>Seattle, Wash., USA</affiliation></author><idno type="istex">F9E29AD3A29998073C9412418AA061F1E1A010A0</idno><idno type="ark">ark:/67375/6H6-ZRLCNGHJ-M</idno><idno type="DOI">10.1016/0091-6749(89)90073-0</idno><idno type="PII">0091-6749(89)90073-0</idno></analytic><monogr><title level="j">The Journal of Allergy and Clinical Immunology</title><title level="j" type="abbrev">YMAI</title><idno type="pISSN">0091-6749</idno><idno type="PII">S0091-6749(00)X0233-3</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1989"></date><biblScope unit="volume">83</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="610">610</biblScope><biblScope unit="page" to="618">618</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1989</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Occupational exposure to cedar and pine woods and pine resin (colophony) can cause asthma and chronic lung disease. Prior studies suggest that plicatic and abietic acids are responsible for the asthmatic reactions that occur in cedar-wood and colophony workers; however, the etiologic mechanism(s) of the chronic lung disease is unknown. To determine if plicatic acid from cedar wood and abietic acid from pine resin could directly damage lung cells, we exposed monolayers of rat type II and human A549 alveolar epithelial cells, intact rat lungs, and rat tracheal explants to solutions of plicatic and abietic acids. As indices of injury, we measured lysis of alveolar epithelial cells with a 51Cr technique, quantitative desquamation of epithelial cells from tracheal explants, and histologic alterations in tracheal explants and intact lungs. Plicatic and abietic acids both caused dose- and time-dependent lysis of alveolar epithelial cells. Instillation of plicatic and abietic acids into rat lungs produced bronchial epithelial sloughing. Abietic acid also caused destruction of the alveolar epithelium. The addition of either acid to rat tracheal explants caused epithelial desquamation that was dose- and time-dependent. Our results suggest that plicatic acid, a unique constituent of cedar wood, and abietic acid, the major constituent in pine resin, can produce lytic damage to alveolar, tracheal, and bronchial epithelial cells. We hypothesize that repeated occupational exposure to these substances might promote the chronic lung damage observed in some cedar- and pine-wood workers and in electronic workers exposed to colophony.</p></abstract><textClass><keywords scheme="keyword"><list><head>Abbreviations</head><item><term>AM</term><term>Alveolar macrophage</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1989">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-ZRLCNGHJ-M/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>YMAI</jid><aid>89900730</aid><ce:pii>0091-6749(89)90073-0</ce:pii><ce:doi>10.1016/0091-6749(89)90073-0</ce:doi><ce:copyright type="unknown" year="1989"></ce:copyright></item-info><head><ce:article-footnote><ce:label>☆</ce:label><ce:note-para>Supported by National Institutes of Health DE 0 8229 and RO1 ESO 2366.</ce:note-para></ce:article-footnote><ce:dochead><ce:textfn>Original article</ce:textfn></ce:dochead><ce:title>The toxicity of constituents of cedar and pine woods to pulmonary epithelium</ce:title><ce:author-group><ce:author><ce:given-name>Garrison H.</ce:given-name><ce:surname>Ayars</ce:surname><ce:degrees>MD</ce:degrees><ce:cross-ref refid="FN1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Leonard C.</ce:given-name><ce:surname>Altman</ce:surname><ce:degrees>MD</ce:degrees><ce:cross-ref refid="COR1"><ce:sup>∗</ce:sup></ce:cross-ref><ce:cross-ref refid="FN1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Charles E.</ce:given-name><ce:surname>Frazier</ce:surname><ce:degrees>PhD</ce:degrees><ce:cross-ref refid="FN2"><ce:sup>∗∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Emil Y.</ce:given-name><ce:surname>Chi</ce:surname><ce:degrees>PhD</ce:degrees><ce:cross-ref refid="FN3"><ce:sup>∗∗∗</ce:sup></ce:cross-ref></ce:author><ce:affiliation><ce:textfn>Seattle, Wash., USA</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Reprint requests: Leonard C. Altman, MD, Division Allergy and Infectious Diseases, Department of Medicine, RM-13, University of Washington, Seattle, WA 98195.</ce:text></ce:correspondence><ce:footnote id="FN1"><ce:label>∗</ce:label><ce:note-para>From the Division of Allergy and Infectious Diseases, Department of Internal Medicine, University of Washington, Seattle, Wash.</ce:note-para></ce:footnote><ce:footnote id="FN2"><ce:label>∗∗</ce:label><ce:note-para>From the Division of Allergy and Infectious Diseases, College of Forest Resources, University of Washington, Seattle, Wash.</ce:note-para></ce:footnote><ce:footnote id="FN3"><ce:label>∗∗∗</ce:label><ce:note-para>From the Division of Allergy and Infectious Diseases, The Department of Pathology, University of Washington, Seattle, Wash.</ce:note-para></ce:footnote></ce:author-group><ce:date-received day="11" month="3" year="1988"></ce:date-received><ce:date-accepted day="3" month="8" year="1988"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Occupational exposure to cedar and pine woods and pine resin (colophony) can cause asthma and chronic lung disease. Prior studies suggest that plicatic and abietic acids are responsible for the asthmatic reactions that occur in cedar-wood and colophony workers; however, the etiologic mechanism(s) of the chronic lung disease is unknown. To determine if plicatic acid from cedar wood and abietic acid from pine resin could directly damage lung cells, we exposed monolayers of rat type II and human A549 alveolar epithelial cells, intact rat lungs, and rat tracheal explants to solutions of plicatic and abietic acids. As indices of injury, we measured lysis of alveolar epithelial cells with a <ce:sup loc="pre">51</ce:sup>Cr technique, quantitative desquamation of epithelial cells from tracheal explants, and histologic alterations in tracheal explants and intact lungs. Plicatic and abietic acids both caused dose- and time-dependent lysis of alveolar epithelial cells. Instillation of plicatic and abietic acids into rat lungs produced bronchial epithelial sloughing. Abietic acid also caused destruction of the alveolar epithelium. The addition of either acid to rat tracheal explants caused epithelial desquamation that was dose- and time-dependent. Our results suggest that plicatic acid, a unique constituent of cedar wood, and abietic acid, the major constituent in pine resin, can produce lytic damage to alveolar, tracheal, and bronchial epithelial cells. We hypothesize that repeated occupational exposure to these substances might promote the chronic lung damage observed in some cedar- and pine-wood workers and in electronic workers exposed to colophony.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="abr"><ce:section-title>Abbreviations</ce:section-title><ce:keyword><ce:text>AM</ce:text><ce:keyword><ce:text>Alveolar macrophage</ce:text></ce:keyword></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>The toxicity of constituents of cedar and pine woods to pulmonary epithelium</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>The toxicity of constituents of cedar and pine woods to pulmonary epithelium</title></titleInfo><name type="personal"><namePart type="given">Garrison H.</namePart><namePart type="family">Ayars</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Seattle, Wash., USA</affiliation><description>From the Division of Allergy and Infectious Diseases, Department of Internal Medicine, University of Washington, Seattle, Wash.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Leonard C.</namePart><namePart type="family">Altman</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Seattle, Wash., USA</affiliation><description>Reprint requests: Leonard C. Altman, MD, Division Allergy and Infectious Diseases, Department of Medicine, RM-13, University of Washington, Seattle, WA 98195.</description><description>From the Division of Allergy and Infectious Diseases, Department of Internal Medicine, University of Washington, Seattle, Wash.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Charles E.</namePart><namePart type="family">Frazier</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Seattle, Wash., USA</affiliation><description>From the Division of Allergy and Infectious Diseases, College of Forest Resources, University of Washington, Seattle, Wash.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Emil Y.</namePart><namePart type="family">Chi</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Seattle, Wash., USA</affiliation><description>From the Division of Allergy and Infectious Diseases, The Department of Pathology, University of Washington, Seattle, Wash.</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1989</dateIssued><copyrightDate encoding="w3cdtf">1989</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Occupational exposure to cedar and pine woods and pine resin (colophony) can cause asthma and chronic lung disease. Prior studies suggest that plicatic and abietic acids are responsible for the asthmatic reactions that occur in cedar-wood and colophony workers; however, the etiologic mechanism(s) of the chronic lung disease is unknown. To determine if plicatic acid from cedar wood and abietic acid from pine resin could directly damage lung cells, we exposed monolayers of rat type II and human A549 alveolar epithelial cells, intact rat lungs, and rat tracheal explants to solutions of plicatic and abietic acids. As indices of injury, we measured lysis of alveolar epithelial cells with a 51Cr technique, quantitative desquamation of epithelial cells from tracheal explants, and histologic alterations in tracheal explants and intact lungs. Plicatic and abietic acids both caused dose- and time-dependent lysis of alveolar epithelial cells. Instillation of plicatic and abietic acids into rat lungs produced bronchial epithelial sloughing. Abietic acid also caused destruction of the alveolar epithelium. The addition of either acid to rat tracheal explants caused epithelial desquamation that was dose- and time-dependent. Our results suggest that plicatic acid, a unique constituent of cedar wood, and abietic acid, the major constituent in pine resin, can produce lytic damage to alveolar, tracheal, and bronchial epithelial cells. We hypothesize that repeated occupational exposure to these substances might promote the chronic lung damage observed in some cedar- and pine-wood workers and in electronic workers exposed to colophony.</abstract><note>Supported by National Institutes of Health DE 0 8229 and RO1 ESO 2366.</note><note type="content">Section title: Original article</note><subject><genre>Abbreviations</genre><topic>AM : Alveolar macrophage</topic></subject><relatedItem type="host"><titleInfo><title>The Journal of Allergy and Clinical Immunology</title></titleInfo><titleInfo type="abbreviated"><title>YMAI</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1989</dateIssued></originInfo><identifier type="ISSN">0091-6749</identifier><identifier type="PII">S0091-6749(00)X0233-3</identifier><part><date>1989</date><detail type="volume"><number>83</number><caption>vol.</caption></detail><detail type="issue"><number>3</number><caption>no.</caption></detail><extent unit="issue-pages"><start>A3</start><end>A45</end></extent><extent unit="issue-pages"><start>A49</start><end>A56</end></extent><extent unit="issue-pages"><start>A63</start><end>A70</end></extent><extent unit="issue-pages"><start>A80</start><end>A84</end></extent><extent unit="issue-pages"><start>A88</start><end>A102</end></extent><extent unit="issue-pages"><start>563</start><end>710</end></extent><extent unit="pages"><start>610</start><end>618</end></extent></part></relatedItem><identifier type="istex">F9E29AD3A29998073C9412418AA061F1E1A010A0</identifier><identifier type="ark">ark:/67375/6H6-ZRLCNGHJ-M</identifier><identifier type="DOI">10.1016/0091-6749(89)90073-0</identifier><identifier type="PII">0091-6749(89)90073-0</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-ZRLCNGHJ-M/record.json</uri></json:item></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/MersV1/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001600 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 001600 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= MersV1
|flux= Istex
|étape= Corpus
|type= RBID
|clé= ISTEX:F9E29AD3A29998073C9412418AA061F1E1A010A0
|texte= The toxicity of constituents of cedar and pine woods to pulmonary epithelium
}}
| This area was generated with Dilib version V0.6.33. |  |