Working Group Report 3: Sensitivity to organic dusts-atopy and gene polymorphisms
Working Group 3 (Sensitivity to Organic Dusts—Atopy and Gene Polymorphisms) was convened to review the current understanding of how effects of inhaled organic dust may be modified by genetic factors—both those that increase as well as those that may reduce susceptibility. Furthermore, the group was...
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Veröffentlicht in: | American journal of industrial medicine 2004-10, Vol.46 (4), p.416-418 |
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description | Working Group 3 (Sensitivity to Organic Dusts—Atopy and Gene Polymorphisms) was convened to review the current understanding of how effects of inhaled organic dust may be modified by genetic factors—both those that increase as well as those that may reduce susceptibility. Furthermore, the group was asked to suggest areas that require more investigation in this field. The discussion focused on individual sensitivity to inhaled agents as the most important determinant of inter‐individual heterogeneiety in responses to exposures. Genetic modifiers are known for a number of pathologic conditions (including asthma, atopy, chronic obstructive pulmonary disease, and hypersensitivity pneumonitis) associated with inhalation of organic dusts; modifiers are likely to be identified for a number of other disease states. Further studies are required to delineate more precisely the contribution (and the role in inflammatory cascade modulation) of these known polymorphims, as well as to identify novel genetic factors. Am. J. Ind. Med. 46:416–418, 2004. © 2004 Wiley‐Liss, Inc. |
doi_str_mv | 10.1002/ajim.20065 |
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Furthermore, the group was asked to suggest areas that require more investigation in this field. The discussion focused on individual sensitivity to inhaled agents as the most important determinant of inter‐individual heterogeneiety in responses to exposures. Genetic modifiers are known for a number of pathologic conditions (including asthma, atopy, chronic obstructive pulmonary disease, and hypersensitivity pneumonitis) associated with inhalation of organic dusts; modifiers are likely to be identified for a number of other disease states. Further studies are required to delineate more precisely the contribution (and the role in inflammatory cascade modulation) of these known polymorphims, as well as to identify novel genetic factors. Am. J. Ind. Med. 46:416–418, 2004. © 2004 Wiley‐Liss, Inc.</description><identifier>ISSN: 0271-3586</identifier><identifier>EISSN: 1097-0274</identifier><identifier>DOI: 10.1002/ajim.20065</identifier><identifier>PMID: 15376221</identifier><identifier>CODEN: AJIMD8</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Asthma - diagnosis ; Asthma - etiology ; Asthma - genetics ; Biological and medical sciences ; Chemical and industrial products toxicology. Toxic occupational diseases ; cytokines ; Cytokines - genetics ; Cytokines - immunology ; Dust ; Humans ; Hypersensitivity, Immediate - diagnosis ; Hypersensitivity, Immediate - etiology ; Hypersensitivity, Immediate - genetics ; Inorganic dusts (pneumoconiosises) and organic dusts (byssinosis etc.) ; Medical sciences ; Occupational Exposure - adverse effects ; Occupational Exposure - analysis ; pathogen-associated molecular patterns (PAMP) ; polymorphism ; Polymorphism, Genetic ; Sensitivity and Specificity ; toll-like receptor-4 (TLR-4) ; Toxicology</subject><ispartof>American journal of industrial medicine, 2004-10, Vol.46 (4), p.416-418</ispartof><rights>Copyright © 2004 Wiley‐Liss, Inc.</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4245-31f6928fd69881004c2461bffbbfb12e8273d31916f9b485d0ff2c58fc89af9a3</citedby><cites>FETCH-LOGICAL-c4245-31f6928fd69881004c2461bffbbfb12e8273d31916f9b485d0ff2c58fc89af9a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fajim.20065$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fajim.20065$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>309,310,314,780,784,789,790,1417,23930,23931,25140,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16179497$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15376221$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kline, Joel N.</creatorcontrib><creatorcontrib>Doekes, Gert</creatorcontrib><creatorcontrib>Bønløkke, Jakob</creatorcontrib><creatorcontrib>Hoffman, Hans Jürgen</creatorcontrib><creatorcontrib>Essen, Susanna Von</creatorcontrib><creatorcontrib>Zhai, Rihong</creatorcontrib><title>Working Group Report 3: Sensitivity to organic dusts-atopy and gene polymorphisms</title><title>American journal of industrial medicine</title><addtitle>Am. J. Ind. Med</addtitle><description>Working Group 3 (Sensitivity to Organic Dusts—Atopy and Gene Polymorphisms) was convened to review the current understanding of how effects of inhaled organic dust may be modified by genetic factors—both those that increase as well as those that may reduce susceptibility. Furthermore, the group was asked to suggest areas that require more investigation in this field. The discussion focused on individual sensitivity to inhaled agents as the most important determinant of inter‐individual heterogeneiety in responses to exposures. Genetic modifiers are known for a number of pathologic conditions (including asthma, atopy, chronic obstructive pulmonary disease, and hypersensitivity pneumonitis) associated with inhalation of organic dusts; modifiers are likely to be identified for a number of other disease states. Further studies are required to delineate more precisely the contribution (and the role in inflammatory cascade modulation) of these known polymorphims, as well as to identify novel genetic factors. Am. J. Ind. Med. 46:416–418, 2004. © 2004 Wiley‐Liss, Inc.</description><subject>Asthma - diagnosis</subject><subject>Asthma - etiology</subject><subject>Asthma - genetics</subject><subject>Biological and medical sciences</subject><subject>Chemical and industrial products toxicology. Toxic occupational diseases</subject><subject>cytokines</subject><subject>Cytokines - genetics</subject><subject>Cytokines - immunology</subject><subject>Dust</subject><subject>Humans</subject><subject>Hypersensitivity, Immediate - diagnosis</subject><subject>Hypersensitivity, Immediate - etiology</subject><subject>Hypersensitivity, Immediate - genetics</subject><subject>Inorganic dusts (pneumoconiosises) and organic dusts (byssinosis etc.)</subject><subject>Medical sciences</subject><subject>Occupational Exposure - adverse effects</subject><subject>Occupational Exposure - analysis</subject><subject>pathogen-associated molecular patterns (PAMP)</subject><subject>polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Sensitivity and Specificity</subject><subject>toll-like receptor-4 (TLR-4)</subject><subject>Toxicology</subject><issn>0271-3586</issn><issn>1097-0274</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEtP3DAAhC3UqmyXXvoDKl_KoVLAr9gxN4RgoVqKeAluluPYiyGJg5205N83dLfl1tNcvpnRDACfMdrDCJF9_eibPYIQz7fADCMpMkQEewdmk-CM5gXfBh9TekQIY8bZB7CNcyo4IXgGLu9CfPLtCi5iGDp4ZbsQe0gP4LVtk-_9T9-PsA8wxJVuvYHVkPqU6T50I9RtBVe2tbAL9diE2D341KQd8N7pOtlPG52D25Pjm6PTbHmxODs6XGaGEZZnFDsuSeEqLotimsEMYRyXzpWlKzGxBRG0olhi7mTJirxCzhGTF84UUjup6RzsrnO7GJ4Hm3rV-GRsXevWhiEpLHJE5bR0Dr6tQRNDStE61UXf6DgqjNTrger1QPXnwAn-skkdysZWb-jmsQn4ugF0Mrp2UbfGpzeOYyGZFBOH19wvX9vxP5Xq8PvZ-d_ybO3xqbcv_zw6PikuqMjV3Y-Furnm9_cCLdUJ_Q2snpdH</recordid><startdate>200410</startdate><enddate>200410</enddate><creator>Kline, Joel N.</creator><creator>Doekes, Gert</creator><creator>Bønløkke, Jakob</creator><creator>Hoffman, Hans Jürgen</creator><creator>Essen, Susanna Von</creator><creator>Zhai, Rihong</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</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>7U7</scope><scope>C1K</scope></search><sort><creationdate>200410</creationdate><title>Working Group Report 3: Sensitivity to organic dusts-atopy and gene polymorphisms</title><author>Kline, Joel N. ; Doekes, Gert ; Bønløkke, Jakob ; Hoffman, Hans Jürgen ; Essen, Susanna Von ; Zhai, Rihong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4245-31f6928fd69881004c2461bffbbfb12e8273d31916f9b485d0ff2c58fc89af9a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Asthma - diagnosis</topic><topic>Asthma - etiology</topic><topic>Asthma - genetics</topic><topic>Biological and medical sciences</topic><topic>Chemical and industrial products toxicology. Toxic occupational diseases</topic><topic>cytokines</topic><topic>Cytokines - genetics</topic><topic>Cytokines - immunology</topic><topic>Dust</topic><topic>Humans</topic><topic>Hypersensitivity, Immediate - diagnosis</topic><topic>Hypersensitivity, Immediate - etiology</topic><topic>Hypersensitivity, Immediate - genetics</topic><topic>Inorganic dusts (pneumoconiosises) and organic dusts (byssinosis etc.)</topic><topic>Medical sciences</topic><topic>Occupational Exposure - adverse effects</topic><topic>Occupational Exposure - analysis</topic><topic>pathogen-associated molecular patterns (PAMP)</topic><topic>polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Sensitivity and Specificity</topic><topic>toll-like receptor-4 (TLR-4)</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kline, Joel N.</creatorcontrib><creatorcontrib>Doekes, Gert</creatorcontrib><creatorcontrib>Bønløkke, Jakob</creatorcontrib><creatorcontrib>Hoffman, Hans Jürgen</creatorcontrib><creatorcontrib>Essen, Susanna Von</creatorcontrib><creatorcontrib>Zhai, Rihong</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>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>American journal of industrial medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kline, Joel N.</au><au>Doekes, Gert</au><au>Bønløkke, Jakob</au><au>Hoffman, Hans Jürgen</au><au>Essen, Susanna Von</au><au>Zhai, Rihong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Working Group Report 3: Sensitivity to organic dusts-atopy and gene polymorphisms</atitle><jtitle>American journal of industrial medicine</jtitle><addtitle>Am. J. Ind. Med</addtitle><date>2004-10</date><risdate>2004</risdate><volume>46</volume><issue>4</issue><spage>416</spage><epage>418</epage><pages>416-418</pages><issn>0271-3586</issn><eissn>1097-0274</eissn><coden>AJIMD8</coden><abstract>Working Group 3 (Sensitivity to Organic Dusts—Atopy and Gene Polymorphisms) was convened to review the current understanding of how effects of inhaled organic dust may be modified by genetic factors—both those that increase as well as those that may reduce susceptibility. Furthermore, the group was asked to suggest areas that require more investigation in this field. The discussion focused on individual sensitivity to inhaled agents as the most important determinant of inter‐individual heterogeneiety in responses to exposures. Genetic modifiers are known for a number of pathologic conditions (including asthma, atopy, chronic obstructive pulmonary disease, and hypersensitivity pneumonitis) associated with inhalation of organic dusts; modifiers are likely to be identified for a number of other disease states. Further studies are required to delineate more precisely the contribution (and the role in inflammatory cascade modulation) of these known polymorphims, as well as to identify novel genetic factors. Am. J. Ind. Med. 46:416–418, 2004. © 2004 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>15376221</pmid><doi>10.1002/ajim.20065</doi><tpages>3</tpages></addata></record> |
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subjects | Asthma - diagnosis Asthma - etiology Asthma - genetics Biological and medical sciences Chemical and industrial products toxicology. Toxic occupational diseases cytokines Cytokines - genetics Cytokines - immunology Dust Humans Hypersensitivity, Immediate - diagnosis Hypersensitivity, Immediate - etiology Hypersensitivity, Immediate - genetics Inorganic dusts (pneumoconiosises) and organic dusts (byssinosis etc.) Medical sciences Occupational Exposure - adverse effects Occupational Exposure - analysis pathogen-associated molecular patterns (PAMP) polymorphism Polymorphism, Genetic Sensitivity and Specificity toll-like receptor-4 (TLR-4) Toxicology |
title | Working Group Report 3: Sensitivity to organic dusts-atopy and gene polymorphisms |
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