Occupational exposure to metal-rich particulate matter modifies the expression of repair genes in foundry workers
Foundry workers are exposed to numerous occupational health hazards, which may result in increased risk of cancer, respiratory disease, and other diseases. Oxidative stress is known to be involved in the pathogenesis of such diseases. The present study aimed to investigate the association between mu...
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| Veröffentlicht in: | Toxicology and industrial health 2021-08, Vol.37 (8), p.504-512 |
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| creator | Panjali, Zahra Hahad, Omar Rajabi, Fatemeh Maddah, Saeid Zendehdel, Rezvan |
| description | Foundry workers are exposed to numerous occupational health hazards, which may result in increased risk of cancer, respiratory disease, and other diseases. Oxidative stress is known to be involved in the pathogenesis of such diseases. The present study aimed to investigate the association between multiple occupational exposures in foundry workers and expression of deoxyribonucleic acid (DNA) repair genes as a biomarker of oxidative DNA damage. The study sample comprised 17 foundry workers and 27 matched control subjects. Expression of 8-oxoguanine DNA glycosylase-1 (OGG1), inosine triphosphate pyrophosphate (ITPA), and MutT homolog 1 (MTH1) in peripheral blood was examined using the real-time polymerase chain reaction method. Air sampling to determine exposure to metal-rich particulate matter and measurement of extremely low-frequency electromagnetic fields (ELF-EMFs) were conducted according to the National Institute for Occupational Safety and Health standard methods. Personal air sampling revealed that occupational exposure to particulate matter exceeded the threshold limit values (TLVs) in 76% of the workstations, whereas ELF-EMF exposure appeared to be lower than the TLV. ITPA was significantly upregulated in foundry workers compared with control subjects, whereas no significant difference was observed for OGG1 and MTH1. Moreover, ITPA was strongly and positively correlated with the concentration of metal-rich particulate matter in foundry workers. No significant correlation was found between ELF-EMF exposure and expression of DNA repair genes. DNA repair gene expression may be a sensitive biomarker for occupational exposures, which suggests an involvement of oxidative stress in metal-induced toxicity. Further studies are needed to determine the role of DNA repair gene expression in response to occupational/environmental hazards. |
| doi_str_mv | 10.1177/07482337211021202 |
| format | Article |
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Oxidative stress is known to be involved in the pathogenesis of such diseases. The present study aimed to investigate the association between multiple occupational exposures in foundry workers and expression of deoxyribonucleic acid (DNA) repair genes as a biomarker of oxidative DNA damage. The study sample comprised 17 foundry workers and 27 matched control subjects. Expression of 8-oxoguanine DNA glycosylase-1 (OGG1), inosine triphosphate pyrophosphate (ITPA), and MutT homolog 1 (MTH1) in peripheral blood was examined using the real-time polymerase chain reaction method. Air sampling to determine exposure to metal-rich particulate matter and measurement of extremely low-frequency electromagnetic fields (ELF-EMFs) were conducted according to the National Institute for Occupational Safety and Health standard methods. Personal air sampling revealed that occupational exposure to particulate matter exceeded the threshold limit values (TLVs) in 76% of the workstations, whereas ELF-EMF exposure appeared to be lower than the TLV. ITPA was significantly upregulated in foundry workers compared with control subjects, whereas no significant difference was observed for OGG1 and MTH1. Moreover, ITPA was strongly and positively correlated with the concentration of metal-rich particulate matter in foundry workers. No significant correlation was found between ELF-EMF exposure and expression of DNA repair genes. DNA repair gene expression may be a sensitive biomarker for occupational exposures, which suggests an involvement of oxidative stress in metal-induced toxicity. Further studies are needed to determine the role of DNA repair gene expression in response to occupational/environmental hazards.</description><identifier>ISSN: 0748-2337</identifier><identifier>EISSN: 1477-0393</identifier><identifier>DOI: 10.1177/07482337211021202</identifier><identifier>PMID: 34247554</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>8-Hydroxyguanine ; Adult ; Air sampling ; Biomarkers ; Biomarkers - blood ; Case-Control Studies ; Deoxyribonucleic acid ; DNA ; DNA Damage ; DNA glycosylase ; DNA Glycosylases - blood ; DNA repair ; DNA Repair Enzymes - blood ; Electromagnetic fields ; Electromagnetic Fields - adverse effects ; Environmental hazards ; Exposure ; Gene expression ; Genes ; Health hazards ; Health risks ; Homology ; Humans ; Iran ; LF electromagnetic fields ; Low frequency ; Male ; Metal concentrations ; Metallurgy ; Metals, Heavy - adverse effects ; Middle Aged ; Occupational exposure ; Occupational Exposure - adverse effects ; Occupational Exposure - analysis ; Occupational health ; Occupational safety ; OGG1 protein ; Oxidative Stress ; Particulate emissions ; Particulate matter ; Particulate Matter - adverse effects ; Particulate Matter - analysis ; Pathogenesis ; Peripheral blood ; Phosphoric Monoester Hydrolases - blood ; Polymerase chain reaction ; Pyrophosphatases - blood ; Repair ; Respiratory diseases ; Toxicity ; Workstations</subject><ispartof>Toxicology and industrial health, 2021-08, Vol.37 (8), p.504-512</ispartof><rights>The Author(s) 2021</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c368t-dc084d26781ccfc8f503276be8159460f73118e030cd17ca6a28f517235ea1013</citedby><cites>FETCH-LOGICAL-c368t-dc084d26781ccfc8f503276be8159460f73118e030cd17ca6a28f517235ea1013</cites><orcidid>0000-0002-3850-7670 ; 0000-0002-1886-6713</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/07482337211021202$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/07482337211021202$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,780,784,21819,27924,27925,43621,43622</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34247554$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Panjali, Zahra</creatorcontrib><creatorcontrib>Hahad, Omar</creatorcontrib><creatorcontrib>Rajabi, Fatemeh</creatorcontrib><creatorcontrib>Maddah, Saeid</creatorcontrib><creatorcontrib>Zendehdel, Rezvan</creatorcontrib><title>Occupational exposure to metal-rich particulate matter modifies the expression of repair genes in foundry workers</title><title>Toxicology and industrial health</title><addtitle>Toxicol Ind Health</addtitle><description>Foundry workers are exposed to numerous occupational health hazards, which may result in increased risk of cancer, respiratory disease, and other diseases. Oxidative stress is known to be involved in the pathogenesis of such diseases. The present study aimed to investigate the association between multiple occupational exposures in foundry workers and expression of deoxyribonucleic acid (DNA) repair genes as a biomarker of oxidative DNA damage. The study sample comprised 17 foundry workers and 27 matched control subjects. Expression of 8-oxoguanine DNA glycosylase-1 (OGG1), inosine triphosphate pyrophosphate (ITPA), and MutT homolog 1 (MTH1) in peripheral blood was examined using the real-time polymerase chain reaction method. Air sampling to determine exposure to metal-rich particulate matter and measurement of extremely low-frequency electromagnetic fields (ELF-EMFs) were conducted according to the National Institute for Occupational Safety and Health standard methods. Personal air sampling revealed that occupational exposure to particulate matter exceeded the threshold limit values (TLVs) in 76% of the workstations, whereas ELF-EMF exposure appeared to be lower than the TLV. ITPA was significantly upregulated in foundry workers compared with control subjects, whereas no significant difference was observed for OGG1 and MTH1. Moreover, ITPA was strongly and positively correlated with the concentration of metal-rich particulate matter in foundry workers. No significant correlation was found between ELF-EMF exposure and expression of DNA repair genes. DNA repair gene expression may be a sensitive biomarker for occupational exposures, which suggests an involvement of oxidative stress in metal-induced toxicity. Further studies are needed to determine the role of DNA repair gene expression in response to occupational/environmental hazards.</description><subject>8-Hydroxyguanine</subject><subject>Adult</subject><subject>Air sampling</subject><subject>Biomarkers</subject><subject>Biomarkers - blood</subject><subject>Case-Control Studies</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Damage</subject><subject>DNA glycosylase</subject><subject>DNA Glycosylases - blood</subject><subject>DNA repair</subject><subject>DNA Repair Enzymes - blood</subject><subject>Electromagnetic fields</subject><subject>Electromagnetic Fields - adverse effects</subject><subject>Environmental hazards</subject><subject>Exposure</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Health hazards</subject><subject>Health risks</subject><subject>Homology</subject><subject>Humans</subject><subject>Iran</subject><subject>LF electromagnetic fields</subject><subject>Low frequency</subject><subject>Male</subject><subject>Metal concentrations</subject><subject>Metallurgy</subject><subject>Metals, Heavy - adverse effects</subject><subject>Middle Aged</subject><subject>Occupational exposure</subject><subject>Occupational Exposure - adverse effects</subject><subject>Occupational Exposure - analysis</subject><subject>Occupational health</subject><subject>Occupational safety</subject><subject>OGG1 protein</subject><subject>Oxidative Stress</subject><subject>Particulate emissions</subject><subject>Particulate matter</subject><subject>Particulate Matter - adverse effects</subject><subject>Particulate Matter - analysis</subject><subject>Pathogenesis</subject><subject>Peripheral blood</subject><subject>Phosphoric Monoester Hydrolases - blood</subject><subject>Polymerase chain reaction</subject><subject>Pyrophosphatases - blood</subject><subject>Repair</subject><subject>Respiratory diseases</subject><subject>Toxicity</subject><subject>Workstations</subject><issn>0748-2337</issn><issn>1477-0393</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kD1PwzAQhi0EoqXwA1iQJeYUn53Y6YgqvqRKXWCOXOfSpiRxajuC_nsStcCAmG64531P9xByDWwKoNQdU3HKhVAcgHHgjJ-QMcRKRUzMxCkZD_toAEbkwvstY0zKhJ-TkYh5rJIkHpPd0piu1aG0ja4ofrbWdw5psLTGoKvIlWZDW-1CabpKB6S1DgEdrW1eFiV6GjY4xBx633dQW1CHrS4dXWPTr8uGFrZrcrenH9a9o_OX5KzQlcer45yQt8eH1_lztFg-vczvF5ERMg1Rblga51yqFIwpTFokTHAlV5hCMoslK5QASJEJZnJQRkvNewYUFwlqYCAm5PbQ2zq769CHbGs713_pM57I3lYqY95TcKCMs947LLLWlbV2-wxYNkjO_kjuMzfH5m5VY_6T-LbaA9MD4PUaf8_-3_gF8L-E7Q</recordid><startdate>202108</startdate><enddate>202108</enddate><creator>Panjali, Zahra</creator><creator>Hahad, Omar</creator><creator>Rajabi, Fatemeh</creator><creator>Maddah, Saeid</creator><creator>Zendehdel, Rezvan</creator><general>SAGE Publications</general><general>Sage Publications Ltd</general><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>7QF</scope><scope>7QQ</scope><scope>7SC</scope><scope>7SE</scope><scope>7SP</scope><scope>7SR</scope><scope>7T2</scope><scope>7TA</scope><scope>7TB</scope><scope>7U5</scope><scope>7U7</scope><scope>8BQ</scope><scope>8FD</scope><scope>C1K</scope><scope>F28</scope><scope>FR3</scope><scope>H8D</scope><scope>H8G</scope><scope>JG9</scope><scope>JQ2</scope><scope>K9.</scope><scope>KR7</scope><scope>L7M</scope><scope>L~C</scope><scope>L~D</scope><orcidid>https://orcid.org/0000-0002-3850-7670</orcidid><orcidid>https://orcid.org/0000-0002-1886-6713</orcidid></search><sort><creationdate>202108</creationdate><title>Occupational exposure to metal-rich particulate matter modifies the expression of repair genes in foundry workers</title><author>Panjali, Zahra ; 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Oxidative stress is known to be involved in the pathogenesis of such diseases. The present study aimed to investigate the association between multiple occupational exposures in foundry workers and expression of deoxyribonucleic acid (DNA) repair genes as a biomarker of oxidative DNA damage. The study sample comprised 17 foundry workers and 27 matched control subjects. Expression of 8-oxoguanine DNA glycosylase-1 (OGG1), inosine triphosphate pyrophosphate (ITPA), and MutT homolog 1 (MTH1) in peripheral blood was examined using the real-time polymerase chain reaction method. Air sampling to determine exposure to metal-rich particulate matter and measurement of extremely low-frequency electromagnetic fields (ELF-EMFs) were conducted according to the National Institute for Occupational Safety and Health standard methods. Personal air sampling revealed that occupational exposure to particulate matter exceeded the threshold limit values (TLVs) in 76% of the workstations, whereas ELF-EMF exposure appeared to be lower than the TLV. ITPA was significantly upregulated in foundry workers compared with control subjects, whereas no significant difference was observed for OGG1 and MTH1. Moreover, ITPA was strongly and positively correlated with the concentration of metal-rich particulate matter in foundry workers. No significant correlation was found between ELF-EMF exposure and expression of DNA repair genes. DNA repair gene expression may be a sensitive biomarker for occupational exposures, which suggests an involvement of oxidative stress in metal-induced toxicity. Further studies are needed to determine the role of DNA repair gene expression in response to occupational/environmental hazards.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>34247554</pmid><doi>10.1177/07482337211021202</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-3850-7670</orcidid><orcidid>https://orcid.org/0000-0002-1886-6713</orcidid></addata></record> |
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| subjects | 8-Hydroxyguanine Adult Air sampling Biomarkers Biomarkers - blood Case-Control Studies Deoxyribonucleic acid DNA DNA Damage DNA glycosylase DNA Glycosylases - blood DNA repair DNA Repair Enzymes - blood Electromagnetic fields Electromagnetic Fields - adverse effects Environmental hazards Exposure Gene expression Genes Health hazards Health risks Homology Humans Iran LF electromagnetic fields Low frequency Male Metal concentrations Metallurgy Metals, Heavy - adverse effects Middle Aged Occupational exposure Occupational Exposure - adverse effects Occupational Exposure - analysis Occupational health Occupational safety OGG1 protein Oxidative Stress Particulate emissions Particulate matter Particulate Matter - adverse effects Particulate Matter - analysis Pathogenesis Peripheral blood Phosphoric Monoester Hydrolases - blood Polymerase chain reaction Pyrophosphatases - blood Repair Respiratory diseases Toxicity Workstations |
| title | Occupational exposure to metal-rich particulate matter modifies the expression of repair genes in foundry workers |
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