Follow-up biological and genotoxicological monitoring of acrylonitrile- and dimethylformamide-exposed viscose rayon plant workers
In order to investigate the genotoxic effects of occupational acrylonitrile (ACN) and dimethylformamide (DMF) exposures, clinical serum and urine parameters and genotoxicological endpoints such as chromosome aberration (CA), sister chromatid exchange (SCE), high frequency SCE (HFC), cell cycle kinet...
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Veröffentlicht in: | Environmental and molecular mutagenesis 1998, Vol.31 (4), p.301-310 |
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creator | Major, J. Hudák, Aranka Kiss, Gabriella Jakab, M. G. Szaniszló, Judith Náray, M. Nagy, I. Tompa, Anna |
description | In order to investigate the genotoxic effects of occupational acrylonitrile (ACN) and dimethylformamide (DMF) exposures, clinical serum and urine parameters and genotoxicological endpoints such as chromosome aberration (CA), sister chromatid exchange (SCE), high frequency SCE (HFC), cell cycle kinetics, and UV‐induced unscheduled DNA synthesis (UDS) were followed up three times during a 20‐month period in peripheral blood lymphocytes (PBL) of 26 workers (13 maintainers and 13 fiber producers) occupationally exposed to ANC and/or DMF in a viscose rayon plant, 26 matched control subjects, and six industrial controls (all males). Six of the 26 exposed subjects were hospitalized because of liver dysfunction that had developed due to inhalative DMF exposure. The rate of smoking was estimated on the basis of serum thiocyanate (SCN) levels. Average peak air ACN and DMF concentrations were over the maximum concentration limits at the time of both investigations. Urine ACN and monomethyl‐formamide (MMF) excretions of the exposed subjects were almost doubled after work shifts. An increase in lymphocyte count (in months 0 and 7), and severe alterations in the liver function were observed in the exposed subjects. In PBLs the proliferative rate index (PRI) was already increased in month 0 compared with the controls. In each study, significant increases in CA and SCE frequencies, as well as increases in UDS were found in PBLs of the exposed subjects. The frequencies of chromatid breaks and acentric fragments further increased in month 7 and remained constantly elevated in month 20. Increased yields of both chromatid and chromosome‐type exchange aberrations first appeared in month 20, when HFCs were 2.72 times more frequent in fiber producers than in maintainers. The role of some important biological confounding factors (age, white blood cell count, and hematocrit) and lifestyle confounding factors (smoking and drinking habits) were subjected to an analysis of variance during the second study. Increased CA, SCE, and UDS were found both in control and exposed smokers when current smoking was established on the basis of the serum SCN levels. The cytogenetic data suggest that occupational exposures to ACN and DMF induce considerable genotoxic consequences and may increase the cancer risk in the exposed human populations. Environ. Mol. Mutagen. 31:301–310, 1998 © 1998 Wiley‐Liss, Inc. |
doi_str_mv | 10.1002/(SICI)1098-2280(1998)31:4<301::AID-EM1>3.0.CO;2-L |
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G. ; Szaniszló, Judith ; Náray, M. ; Nagy, I. ; Tompa, Anna</creator><creatorcontrib>Major, J. ; Hudák, Aranka ; Kiss, Gabriella ; Jakab, M. G. ; Szaniszló, Judith ; Náray, M. ; Nagy, I. ; Tompa, Anna</creatorcontrib><description>In order to investigate the genotoxic effects of occupational acrylonitrile (ACN) and dimethylformamide (DMF) exposures, clinical serum and urine parameters and genotoxicological endpoints such as chromosome aberration (CA), sister chromatid exchange (SCE), high frequency SCE (HFC), cell cycle kinetics, and UV‐induced unscheduled DNA synthesis (UDS) were followed up three times during a 20‐month period in peripheral blood lymphocytes (PBL) of 26 workers (13 maintainers and 13 fiber producers) occupationally exposed to ANC and/or DMF in a viscose rayon plant, 26 matched control subjects, and six industrial controls (all males). Six of the 26 exposed subjects were hospitalized because of liver dysfunction that had developed due to inhalative DMF exposure. The rate of smoking was estimated on the basis of serum thiocyanate (SCN) levels. Average peak air ACN and DMF concentrations were over the maximum concentration limits at the time of both investigations. Urine ACN and monomethyl‐formamide (MMF) excretions of the exposed subjects were almost doubled after work shifts. An increase in lymphocyte count (in months 0 and 7), and severe alterations in the liver function were observed in the exposed subjects. In PBLs the proliferative rate index (PRI) was already increased in month 0 compared with the controls. In each study, significant increases in CA and SCE frequencies, as well as increases in UDS were found in PBLs of the exposed subjects. The frequencies of chromatid breaks and acentric fragments further increased in month 7 and remained constantly elevated in month 20. Increased yields of both chromatid and chromosome‐type exchange aberrations first appeared in month 20, when HFCs were 2.72 times more frequent in fiber producers than in maintainers. The role of some important biological confounding factors (age, white blood cell count, and hematocrit) and lifestyle confounding factors (smoking and drinking habits) were subjected to an analysis of variance during the second study. Increased CA, SCE, and UDS were found both in control and exposed smokers when current smoking was established on the basis of the serum SCN levels. The cytogenetic data suggest that occupational exposures to ACN and DMF induce considerable genotoxic consequences and may increase the cancer risk in the exposed human populations. Environ. Mol. Mutagen. 31:301–310, 1998 © 1998 Wiley‐Liss, Inc.</description><identifier>ISSN: 0893-6692</identifier><identifier>EISSN: 1098-2280</identifier><identifier>DOI: 10.1002/(SICI)1098-2280(1998)31:4<301::AID-EM1>3.0.CO;2-L</identifier><identifier>PMID: 9654238</identifier><identifier>CODEN: EMMUEG</identifier><language>eng</language><publisher>New York: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Acrylonitrile - toxicity ; Biological and medical sciences ; Case-Control Studies ; Cell Cycle ; cell cycle kinetics ; Chemical and industrial products toxicology. Toxic occupational diseases ; Chromosome Aberrations ; clinical laboratory parameters ; Dimethylformamide - toxicity ; Humans ; Male ; Medical sciences ; Mutagens ; Occupational Exposure ; Risk Assessment ; Sister Chromatid Exchange ; Smoking ; Textiles ; Toxicology ; Various organic compounds</subject><ispartof>Environmental and molecular mutagenesis, 1998, Vol.31 (4), p.301-310</ispartof><rights>Copyright © 1998 Wiley‐Liss, Inc.</rights><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2F%28SICI%291098-2280%281998%2931%3A4%3C301%3A%3AAID-EM1%3E3.0.CO%3B2-L$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2F%28SICI%291098-2280%281998%2931%3A4%3C301%3A%3AAID-EM1%3E3.0.CO%3B2-L$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,4010,27904,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2315173$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9654238$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Major, J.</creatorcontrib><creatorcontrib>Hudák, Aranka</creatorcontrib><creatorcontrib>Kiss, Gabriella</creatorcontrib><creatorcontrib>Jakab, M. G.</creatorcontrib><creatorcontrib>Szaniszló, Judith</creatorcontrib><creatorcontrib>Náray, M.</creatorcontrib><creatorcontrib>Nagy, I.</creatorcontrib><creatorcontrib>Tompa, Anna</creatorcontrib><title>Follow-up biological and genotoxicological monitoring of acrylonitrile- and dimethylformamide-exposed viscose rayon plant workers</title><title>Environmental and molecular mutagenesis</title><addtitle>Environ. Mol. Mutagen</addtitle><description>In order to investigate the genotoxic effects of occupational acrylonitrile (ACN) and dimethylformamide (DMF) exposures, clinical serum and urine parameters and genotoxicological endpoints such as chromosome aberration (CA), sister chromatid exchange (SCE), high frequency SCE (HFC), cell cycle kinetics, and UV‐induced unscheduled DNA synthesis (UDS) were followed up three times during a 20‐month period in peripheral blood lymphocytes (PBL) of 26 workers (13 maintainers and 13 fiber producers) occupationally exposed to ANC and/or DMF in a viscose rayon plant, 26 matched control subjects, and six industrial controls (all males). Six of the 26 exposed subjects were hospitalized because of liver dysfunction that had developed due to inhalative DMF exposure. The rate of smoking was estimated on the basis of serum thiocyanate (SCN) levels. Average peak air ACN and DMF concentrations were over the maximum concentration limits at the time of both investigations. Urine ACN and monomethyl‐formamide (MMF) excretions of the exposed subjects were almost doubled after work shifts. An increase in lymphocyte count (in months 0 and 7), and severe alterations in the liver function were observed in the exposed subjects. In PBLs the proliferative rate index (PRI) was already increased in month 0 compared with the controls. In each study, significant increases in CA and SCE frequencies, as well as increases in UDS were found in PBLs of the exposed subjects. The frequencies of chromatid breaks and acentric fragments further increased in month 7 and remained constantly elevated in month 20. Increased yields of both chromatid and chromosome‐type exchange aberrations first appeared in month 20, when HFCs were 2.72 times more frequent in fiber producers than in maintainers. The role of some important biological confounding factors (age, white blood cell count, and hematocrit) and lifestyle confounding factors (smoking and drinking habits) were subjected to an analysis of variance during the second study. Increased CA, SCE, and UDS were found both in control and exposed smokers when current smoking was established on the basis of the serum SCN levels. The cytogenetic data suggest that occupational exposures to ACN and DMF induce considerable genotoxic consequences and may increase the cancer risk in the exposed human populations. Environ. Mol. Mutagen. 31:301–310, 1998 © 1998 Wiley‐Liss, Inc.</description><subject>Acrylonitrile - toxicity</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>Cell Cycle</subject><subject>cell cycle kinetics</subject><subject>Chemical and industrial products toxicology. Toxic occupational diseases</subject><subject>Chromosome Aberrations</subject><subject>clinical laboratory parameters</subject><subject>Dimethylformamide - toxicity</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mutagens</subject><subject>Occupational Exposure</subject><subject>Risk Assessment</subject><subject>Sister Chromatid Exchange</subject><subject>Smoking</subject><subject>Textiles</subject><subject>Toxicology</subject><subject>Various organic compounds</subject><issn>0893-6692</issn><issn>1098-2280</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUuP0zAUhSMEGoaBn4CUBUIzCxe_4iYFIQ2ZBxWFDi-xvHJsp2MmiYud0nbJP8ehVTcjsbJ9fXx8dL4kKQgeEYzpq9Ov03J6RnCRI0pzfEqKIj9jZMLfMEwmk_PpBbr8SN6yER6V89cUzR4kxwf1w-QY5wVDQhT0cfIkhJ8YE8ILepQcFSLjlOXHyZ8r1zRujVbLtLKucQurZJPKTqcL07nebaw6TFvX2d552y1SV6dS-W0zTLxtDPr3RNvW9Lfbpna-la3VBpnN0gWj0982qLhJvdy6Ll02suvTtfN3xoenyaNaNsE8268nyfery2_lezSbX0_L8xlSPCMEUZFTxUmhmJbM8EpXptZaVZXmNOeZFDirBeMy00woUmWSS15UOs8rhnNdS3aSvNz5Lr37tTKhhzaGMk3MYtwqABEZEWMqovDzTqi8C8GbGpbettJvgWAYsAAMWGAoGoaiYcACjACHiAUgYoGIBRhgKOdAYRY9n-8_X1Wt0QfHPYd4_2J_L0OsuvayUzYcZJSRjIxZlN3sZOvY-fZerv_Gup9qOEZLtLO0oTebg6X0dyDGbJzBj0_XUH75wMRFfgPv2F8Xg8Yg</recordid><startdate>1998</startdate><enddate>1998</enddate><creator>Major, J.</creator><creator>Hudák, Aranka</creator><creator>Kiss, Gabriella</creator><creator>Jakab, M. G.</creator><creator>Szaniszló, Judith</creator><creator>Náray, M.</creator><creator>Nagy, I.</creator><creator>Tompa, Anna</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>7T2</scope><scope>7U2</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>1998</creationdate><title>Follow-up biological and genotoxicological monitoring of acrylonitrile- and dimethylformamide-exposed viscose rayon plant workers</title><author>Major, J. ; Hudák, Aranka ; Kiss, Gabriella ; Jakab, M. G. ; Szaniszló, Judith ; Náray, M. ; Nagy, I. ; Tompa, Anna</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4511-2682c419c3da3e4bdbefddcbbd42845a605f634a5d36c1b5a4a49bd88b308dfa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Acrylonitrile - toxicity</topic><topic>Biological and medical sciences</topic><topic>Case-Control Studies</topic><topic>Cell Cycle</topic><topic>cell cycle kinetics</topic><topic>Chemical and industrial products toxicology. Toxic occupational diseases</topic><topic>Chromosome Aberrations</topic><topic>clinical laboratory parameters</topic><topic>Dimethylformamide - toxicity</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mutagens</topic><topic>Occupational Exposure</topic><topic>Risk Assessment</topic><topic>Sister Chromatid Exchange</topic><topic>Smoking</topic><topic>Textiles</topic><topic>Toxicology</topic><topic>Various organic compounds</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Major, J.</creatorcontrib><creatorcontrib>Hudák, Aranka</creatorcontrib><creatorcontrib>Kiss, Gabriella</creatorcontrib><creatorcontrib>Jakab, M. G.</creatorcontrib><creatorcontrib>Szaniszló, Judith</creatorcontrib><creatorcontrib>Náray, M.</creatorcontrib><creatorcontrib>Nagy, I.</creatorcontrib><creatorcontrib>Tompa, Anna</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>Health and Safety Science Abstracts (Full archive)</collection><collection>Safety Science and Risk</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Environmental and molecular mutagenesis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Major, J.</au><au>Hudák, Aranka</au><au>Kiss, Gabriella</au><au>Jakab, M. G.</au><au>Szaniszló, Judith</au><au>Náray, M.</au><au>Nagy, I.</au><au>Tompa, Anna</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Follow-up biological and genotoxicological monitoring of acrylonitrile- and dimethylformamide-exposed viscose rayon plant workers</atitle><jtitle>Environmental and molecular mutagenesis</jtitle><addtitle>Environ. Mol. Mutagen</addtitle><date>1998</date><risdate>1998</risdate><volume>31</volume><issue>4</issue><spage>301</spage><epage>310</epage><pages>301-310</pages><issn>0893-6692</issn><eissn>1098-2280</eissn><coden>EMMUEG</coden><abstract>In order to investigate the genotoxic effects of occupational acrylonitrile (ACN) and dimethylformamide (DMF) exposures, clinical serum and urine parameters and genotoxicological endpoints such as chromosome aberration (CA), sister chromatid exchange (SCE), high frequency SCE (HFC), cell cycle kinetics, and UV‐induced unscheduled DNA synthesis (UDS) were followed up three times during a 20‐month period in peripheral blood lymphocytes (PBL) of 26 workers (13 maintainers and 13 fiber producers) occupationally exposed to ANC and/or DMF in a viscose rayon plant, 26 matched control subjects, and six industrial controls (all males). Six of the 26 exposed subjects were hospitalized because of liver dysfunction that had developed due to inhalative DMF exposure. The rate of smoking was estimated on the basis of serum thiocyanate (SCN) levels. Average peak air ACN and DMF concentrations were over the maximum concentration limits at the time of both investigations. Urine ACN and monomethyl‐formamide (MMF) excretions of the exposed subjects were almost doubled after work shifts. An increase in lymphocyte count (in months 0 and 7), and severe alterations in the liver function were observed in the exposed subjects. In PBLs the proliferative rate index (PRI) was already increased in month 0 compared with the controls. In each study, significant increases in CA and SCE frequencies, as well as increases in UDS were found in PBLs of the exposed subjects. The frequencies of chromatid breaks and acentric fragments further increased in month 7 and remained constantly elevated in month 20. Increased yields of both chromatid and chromosome‐type exchange aberrations first appeared in month 20, when HFCs were 2.72 times more frequent in fiber producers than in maintainers. The role of some important biological confounding factors (age, white blood cell count, and hematocrit) and lifestyle confounding factors (smoking and drinking habits) were subjected to an analysis of variance during the second study. Increased CA, SCE, and UDS were found both in control and exposed smokers when current smoking was established on the basis of the serum SCN levels. The cytogenetic data suggest that occupational exposures to ACN and DMF induce considerable genotoxic consequences and may increase the cancer risk in the exposed human populations. Environ. Mol. Mutagen. 31:301–310, 1998 © 1998 Wiley‐Liss, Inc.</abstract><cop>New York</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>9654238</pmid><doi>10.1002/(SICI)1098-2280(1998)31:4<301::AID-EM1>3.0.CO;2-L</doi><tpages>10</tpages></addata></record> |
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subjects | Acrylonitrile - toxicity Biological and medical sciences Case-Control Studies Cell Cycle cell cycle kinetics Chemical and industrial products toxicology. Toxic occupational diseases Chromosome Aberrations clinical laboratory parameters Dimethylformamide - toxicity Humans Male Medical sciences Mutagens Occupational Exposure Risk Assessment Sister Chromatid Exchange Smoking Textiles Toxicology Various organic compounds |
title | Follow-up biological and genotoxicological monitoring of acrylonitrile- and dimethylformamide-exposed viscose rayon plant workers |
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