The toxicity of constituents of cedar and pine woods to pulmonary epithelium
Identifieur interne : 002013 ( Istex/Checkpoint ); précédent : 002012; suivant : 002014The toxicity of constituents of cedar and pine woods to pulmonary epithelium
Auteurs : Garrison H. Ayars [États-Unis] ; Leonard C. Altman [États-Unis] ; Charles E. Frazier [États-Unis] ; Emil Y. Chi [États-Unis]Source :
- 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
Affiliations:
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Ayars</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Seattle, Wash.</wicri:regionArea><wicri:noRegion>Wash.</wicri:noRegion></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 wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Seattle, Wash.</wicri:regionArea><wicri:noRegion>Wash.</wicri:noRegion></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 wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Seattle, Wash.</wicri:regionArea><wicri:noRegion>Wash.</wicri:noRegion></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 wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Seattle, Wash.</wicri:regionArea><wicri:noRegion>Wash.</wicri:noRegion></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><affiliations><list><country><li>États-Unis</li></country></list><tree><country name="États-Unis"><noRegion><name sortKey="Ayars, Garrison H" sort="Ayars, Garrison H" uniqKey="Ayars G" first="Garrison H." last="Ayars">Garrison H. Ayars</name></noRegion><name sortKey="Altman, Leonard C" sort="Altman, Leonard C" uniqKey="Altman L" first="Leonard C." last="Altman">Leonard C. Altman</name><name sortKey="Chi, Emil Y" sort="Chi, Emil Y" uniqKey="Chi E" first="Emil Y." last="Chi">Emil Y. Chi</name><name sortKey="Frazier, Charles E" sort="Frazier, Charles E" uniqKey="Frazier C" first="Charles E." last="Frazier">Charles E. Frazier</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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