DNA repair and metabolic gene polymorphisms affect genetic damage due to diesel engine exhaust exposure
Diesel engine exhaust (DEE) is a complex mixture of toxic gases, halogenated aromatic hydrocarbons, alkyl polycyclic aromatic hydrocarbons, polycyclic aromatic hydrocarbons, benzene derivatives, metals and diesel exhaust particles (DEPs) generated from the incomplete combustion of diesel fuel. Many...
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| creator | León-Mejía, Grethel Quintana-Sosa, Milton de Moya Hernandez, Yurina Rodríguez, Ibeth Luna Trindade, Cristiano Romero, Marco Anaya Luna-Carrascal, Jaime Ortíz, Ludis Oliveros Acosta-Hoyos, Antonio Ruiz-Benitez, Martha Valencia, Karen Franco Rohr, Paula da Silva, Juliana Henriques, João Antônio Pêgas |
| description | Diesel engine exhaust (DEE) is a complex mixture of toxic gases, halogenated aromatic hydrocarbons, alkyl polycyclic aromatic hydrocarbons, polycyclic aromatic hydrocarbons, benzene derivatives, metals and diesel exhaust particles (DEPs) generated from the incomplete combustion of diesel fuel. Many of the compounds in this mixture can cause oxidative damage to DNA and are considered carcinogenic for humans. Further, chronic DEE exposure increases risks of cardiovascular and pulmonary diseases. Despite these pervasive health risks, there is limited and inconsistent information regarding genetic factors conferring susceptibility or resistance to DEE genotoxicity. The present study evaluated the effects of polymorphisms in two base excision repair (BER) genes (
OGG1 Ser326Cys
and
XRCC1 Arg280His
), one homologous recombination (HRR) gene (
XRCC3 Thr241Met
) and two xenobiotic metabolism genes (
GSTM1
and
GSTT1
) on the genotoxicity profiles among 123 mechanics exposed to workplace DEE. Polymorphisms were determined by PCR-RFLP. In comet assay, individuals with the
GSTT1
null genotype demonstrated significantly greater % tail DNA in lymphocytes than those with non-null genotype. In contrast, these null individuals exhibited significantly lower frequencies of binucleated (BN) cells and nuclear buds (NBUDs) in buccal cells than non-null individuals. Heterozygous
hOGG1 326
individuals (
hOGG1 326 Ser/Cys
) exhibited higher buccal cell NBUD frequency than
hOGG1 326 Ser/Ser
individuals. Individuals carrying the
XRCC3 241 Met/Met
polymorphism also showed significantly higher buccal cell NBUD frequencies than those carrying the
XRCC3 241 Thr/Thr
polymorphism. We found a high flow of particulate matter with a diameter of |
| doi_str_mv | 10.1007/s11356-020-08533-6 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2405801713</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2405801713</sourcerecordid><originalsourceid>FETCH-LOGICAL-c412t-336d65ed7d561a05ad4a7c386e190ea2a91df1a1deb26db633a9d45e1a02974c3</originalsourceid><addsrcrecordid>eNp9kDtPwzAUhS0EoqXwBxiQJWaDX3HqsSpPqYIFZsuJb9JUzQM7kei_xzQFNqY7nO-cK30IXTJ6wyhNbwNjIlGEckroPBGCqCM0ZYpJkkqtj9GUaikJE1JO0FkIGxpJzdNTNBGcSyV5MkXl3csCe-hs5bFtHK6ht1m7rXJcQgO4a7e7uvXdugp1wLYoIO_3SR8JZ2tbAnYD4L7FroIAWwxNWcUifK7tEPp4uzYMHs7RSWG3AS4Od4beH-7flk9k9fr4vFysSC4Z74kQyqkEXOoSxSxNrJM2zcVcAdMULLeauYJZ5iDjymVKCKudTCCyXKcyFzN0Pe52vv0YIPRm0w6-iS8NlzSZU5YyESk-UrlvQ_BQmM5XtfU7w6j5dmtGtyYaM3u3RsXS1WF6yGpwv5UfmREQIxBi1JTg_37_M_sFDRiFKw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2405801713</pqid></control><display><type>article</type><title>DNA repair and metabolic gene polymorphisms affect genetic damage due to diesel engine exhaust exposure</title><source>SpringerLink Journals - AutoHoldings</source><creator>León-Mejía, Grethel ; Quintana-Sosa, Milton ; de Moya Hernandez, Yurina ; Rodríguez, Ibeth Luna ; Trindade, Cristiano ; Romero, Marco Anaya ; Luna-Carrascal, Jaime ; Ortíz, Ludis Oliveros ; Acosta-Hoyos, Antonio ; Ruiz-Benitez, Martha ; Valencia, Karen Franco ; Rohr, Paula ; da Silva, Juliana ; Henriques, João Antônio Pêgas</creator><creatorcontrib>León-Mejía, Grethel ; Quintana-Sosa, Milton ; de Moya Hernandez, Yurina ; Rodríguez, Ibeth Luna ; Trindade, Cristiano ; Romero, Marco Anaya ; Luna-Carrascal, Jaime ; Ortíz, Ludis Oliveros ; Acosta-Hoyos, Antonio ; Ruiz-Benitez, Martha ; Valencia, Karen Franco ; Rohr, Paula ; da Silva, Juliana ; Henriques, João Antônio Pêgas</creatorcontrib><description>Diesel engine exhaust (DEE) is a complex mixture of toxic gases, halogenated aromatic hydrocarbons, alkyl polycyclic aromatic hydrocarbons, polycyclic aromatic hydrocarbons, benzene derivatives, metals and diesel exhaust particles (DEPs) generated from the incomplete combustion of diesel fuel. Many of the compounds in this mixture can cause oxidative damage to DNA and are considered carcinogenic for humans. Further, chronic DEE exposure increases risks of cardiovascular and pulmonary diseases. Despite these pervasive health risks, there is limited and inconsistent information regarding genetic factors conferring susceptibility or resistance to DEE genotoxicity. The present study evaluated the effects of polymorphisms in two base excision repair (BER) genes (
OGG1 Ser326Cys
and
XRCC1 Arg280His
), one homologous recombination (HRR) gene (
XRCC3 Thr241Met
) and two xenobiotic metabolism genes (
GSTM1
and
GSTT1
) on the genotoxicity profiles among 123 mechanics exposed to workplace DEE. Polymorphisms were determined by PCR-RFLP. In comet assay, individuals with the
GSTT1
null genotype demonstrated significantly greater % tail DNA in lymphocytes than those with non-null genotype. In contrast, these null individuals exhibited significantly lower frequencies of binucleated (BN) cells and nuclear buds (NBUDs) in buccal cells than non-null individuals. Heterozygous
hOGG1 326
individuals (
hOGG1 326 Ser/Cys
) exhibited higher buccal cell NBUD frequency than
hOGG1 326 Ser/Ser
individuals. Individuals carrying the
XRCC3 241 Met/Met
polymorphism also showed significantly higher buccal cell NBUD frequencies than those carrying the
XRCC3 241 Thr/Thr
polymorphism. We found a high flow of particulate matter with a diameter of < 2.5 μm (PM
2.5
) in the workplace. The most abundant metals in DEPs were iron, copper, silicon and manganese as detected by transmission electron microscopy–energy-dispersive X-ray spectroscopy (TEM-EDX). Scanning electron microscopy (SEM-EDS) revealed particles with diameters smaller than PM
2.5
, including nanoparticles forming aggregates and agglomerates. Our results demonstrate the genotoxic effects of DEE and the critical influence of genetic susceptibility conferred by DNA repair and metabolic gene polymorphisms that shed light into the understanding of underlying mechanisms.</description><identifier>ISSN: 0944-1344</identifier><identifier>EISSN: 1614-7499</identifier><identifier>DOI: 10.1007/s11356-020-08533-6</identifier><identifier>PMID: 32246425</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Agglomerates ; Aquatic Pollution ; Atmospheric Protection/Air Quality Control/Air Pollution ; Base excision repair ; Benzene ; Bioassays ; Carcinogens ; Chromosome aberrations ; Comet assay ; Damage detection ; Deoxyribonucleic acid ; Diesel ; Diesel engines ; Diesel fuels ; DNA ; DNA damage ; DNA repair ; Earth and Environmental Science ; Ecotoxicology ; Electron microscopy ; Environment ; Environmental Chemistry ; Environmental Health ; Environmental science ; Exhaust emissions ; Exhaust gases ; Exposure ; Gene polymorphism ; Genes ; Genetic factors ; Genotoxicity ; GSTM1 protein ; GSTT1 protein ; Halogenated hydrocarbons ; Health risks ; Heavy metals ; Homologous recombination ; Homologous recombination repair ; Homology ; Lung diseases ; Lymphocytes ; Manganese ; Metabolism ; Microscopy ; Nanoparticles ; Nuclear fuels ; Occupational exposure ; Particulate matter ; Polycyclic aromatic hydrocarbons ; Polymerase chain reaction ; Polymorphism ; Repair ; Research Article ; Resistance factors ; Restriction fragment length polymorphism ; Scanning electron microscopy ; Transmission electron microscopy ; Waste Water Technology ; Water Management ; Water Pollution Control ; X-ray spectroscopy</subject><ispartof>Environmental science and pollution research international, 2020-06, Vol.27 (16), p.20516-20526</ispartof><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2020</rights><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-336d65ed7d561a05ad4a7c386e190ea2a91df1a1deb26db633a9d45e1a02974c3</citedby><cites>FETCH-LOGICAL-c412t-336d65ed7d561a05ad4a7c386e190ea2a91df1a1deb26db633a9d45e1a02974c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11356-020-08533-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11356-020-08533-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32246425$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>León-Mejía, Grethel</creatorcontrib><creatorcontrib>Quintana-Sosa, Milton</creatorcontrib><creatorcontrib>de Moya Hernandez, Yurina</creatorcontrib><creatorcontrib>Rodríguez, Ibeth Luna</creatorcontrib><creatorcontrib>Trindade, Cristiano</creatorcontrib><creatorcontrib>Romero, Marco Anaya</creatorcontrib><creatorcontrib>Luna-Carrascal, Jaime</creatorcontrib><creatorcontrib>Ortíz, Ludis Oliveros</creatorcontrib><creatorcontrib>Acosta-Hoyos, Antonio</creatorcontrib><creatorcontrib>Ruiz-Benitez, Martha</creatorcontrib><creatorcontrib>Valencia, Karen Franco</creatorcontrib><creatorcontrib>Rohr, Paula</creatorcontrib><creatorcontrib>da Silva, Juliana</creatorcontrib><creatorcontrib>Henriques, João Antônio Pêgas</creatorcontrib><title>DNA repair and metabolic gene polymorphisms affect genetic damage due to diesel engine exhaust exposure</title><title>Environmental science and pollution research international</title><addtitle>Environ Sci Pollut Res</addtitle><addtitle>Environ Sci Pollut Res Int</addtitle><description>Diesel engine exhaust (DEE) is a complex mixture of toxic gases, halogenated aromatic hydrocarbons, alkyl polycyclic aromatic hydrocarbons, polycyclic aromatic hydrocarbons, benzene derivatives, metals and diesel exhaust particles (DEPs) generated from the incomplete combustion of diesel fuel. Many of the compounds in this mixture can cause oxidative damage to DNA and are considered carcinogenic for humans. Further, chronic DEE exposure increases risks of cardiovascular and pulmonary diseases. Despite these pervasive health risks, there is limited and inconsistent information regarding genetic factors conferring susceptibility or resistance to DEE genotoxicity. The present study evaluated the effects of polymorphisms in two base excision repair (BER) genes (
OGG1 Ser326Cys
and
XRCC1 Arg280His
), one homologous recombination (HRR) gene (
XRCC3 Thr241Met
) and two xenobiotic metabolism genes (
GSTM1
and
GSTT1
) on the genotoxicity profiles among 123 mechanics exposed to workplace DEE. Polymorphisms were determined by PCR-RFLP. In comet assay, individuals with the
GSTT1
null genotype demonstrated significantly greater % tail DNA in lymphocytes than those with non-null genotype. In contrast, these null individuals exhibited significantly lower frequencies of binucleated (BN) cells and nuclear buds (NBUDs) in buccal cells than non-null individuals. Heterozygous
hOGG1 326
individuals (
hOGG1 326 Ser/Cys
) exhibited higher buccal cell NBUD frequency than
hOGG1 326 Ser/Ser
individuals. Individuals carrying the
XRCC3 241 Met/Met
polymorphism also showed significantly higher buccal cell NBUD frequencies than those carrying the
XRCC3 241 Thr/Thr
polymorphism. We found a high flow of particulate matter with a diameter of < 2.5 μm (PM
2.5
) in the workplace. The most abundant metals in DEPs were iron, copper, silicon and manganese as detected by transmission electron microscopy–energy-dispersive X-ray spectroscopy (TEM-EDX). Scanning electron microscopy (SEM-EDS) revealed particles with diameters smaller than PM
2.5
, including nanoparticles forming aggregates and agglomerates. Our results demonstrate the genotoxic effects of DEE and the critical influence of genetic susceptibility conferred by DNA repair and metabolic gene polymorphisms that shed light into the understanding of underlying mechanisms.</description><subject>Agglomerates</subject><subject>Aquatic Pollution</subject><subject>Atmospheric Protection/Air Quality Control/Air Pollution</subject><subject>Base excision repair</subject><subject>Benzene</subject><subject>Bioassays</subject><subject>Carcinogens</subject><subject>Chromosome aberrations</subject><subject>Comet assay</subject><subject>Damage detection</subject><subject>Deoxyribonucleic acid</subject><subject>Diesel</subject><subject>Diesel engines</subject><subject>Diesel fuels</subject><subject>DNA</subject><subject>DNA damage</subject><subject>DNA repair</subject><subject>Earth and Environmental Science</subject><subject>Ecotoxicology</subject><subject>Electron microscopy</subject><subject>Environment</subject><subject>Environmental Chemistry</subject><subject>Environmental Health</subject><subject>Environmental science</subject><subject>Exhaust emissions</subject><subject>Exhaust gases</subject><subject>Exposure</subject><subject>Gene polymorphism</subject><subject>Genes</subject><subject>Genetic factors</subject><subject>Genotoxicity</subject><subject>GSTM1 protein</subject><subject>GSTT1 protein</subject><subject>Halogenated hydrocarbons</subject><subject>Health risks</subject><subject>Heavy metals</subject><subject>Homologous recombination</subject><subject>Homologous recombination repair</subject><subject>Homology</subject><subject>Lung diseases</subject><subject>Lymphocytes</subject><subject>Manganese</subject><subject>Metabolism</subject><subject>Microscopy</subject><subject>Nanoparticles</subject><subject>Nuclear fuels</subject><subject>Occupational exposure</subject><subject>Particulate matter</subject><subject>Polycyclic aromatic hydrocarbons</subject><subject>Polymerase chain reaction</subject><subject>Polymorphism</subject><subject>Repair</subject><subject>Research Article</subject><subject>Resistance factors</subject><subject>Restriction fragment length polymorphism</subject><subject>Scanning electron microscopy</subject><subject>Transmission electron microscopy</subject><subject>Waste Water Technology</subject><subject>Water Management</subject><subject>Water Pollution Control</subject><subject>X-ray 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repair and metabolic gene polymorphisms affect genetic damage due to diesel engine exhaust exposure</title><author>León-Mejía, Grethel ; Quintana-Sosa, Milton ; de Moya Hernandez, Yurina ; Rodríguez, Ibeth Luna ; Trindade, Cristiano ; Romero, Marco Anaya ; Luna-Carrascal, Jaime ; Ortíz, Ludis Oliveros ; Acosta-Hoyos, Antonio ; Ruiz-Benitez, Martha ; Valencia, Karen Franco ; Rohr, Paula ; da Silva, Juliana ; Henriques, João Antônio Pêgas</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c412t-336d65ed7d561a05ad4a7c386e190ea2a91df1a1deb26db633a9d45e1a02974c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Agglomerates</topic><topic>Aquatic Pollution</topic><topic>Atmospheric Protection/Air Quality Control/Air Pollution</topic><topic>Base excision repair</topic><topic>Benzene</topic><topic>Bioassays</topic><topic>Carcinogens</topic><topic>Chromosome aberrations</topic><topic>Comet assay</topic><topic>Damage detection</topic><topic>Deoxyribonucleic acid</topic><topic>Diesel</topic><topic>Diesel engines</topic><topic>Diesel fuels</topic><topic>DNA</topic><topic>DNA damage</topic><topic>DNA repair</topic><topic>Earth and Environmental Science</topic><topic>Ecotoxicology</topic><topic>Electron microscopy</topic><topic>Environment</topic><topic>Environmental Chemistry</topic><topic>Environmental Health</topic><topic>Environmental science</topic><topic>Exhaust emissions</topic><topic>Exhaust gases</topic><topic>Exposure</topic><topic>Gene polymorphism</topic><topic>Genes</topic><topic>Genetic factors</topic><topic>Genotoxicity</topic><topic>GSTM1 protein</topic><topic>GSTT1 protein</topic><topic>Halogenated hydrocarbons</topic><topic>Health risks</topic><topic>Heavy metals</topic><topic>Homologous recombination</topic><topic>Homologous recombination repair</topic><topic>Homology</topic><topic>Lung diseases</topic><topic>Lymphocytes</topic><topic>Manganese</topic><topic>Metabolism</topic><topic>Microscopy</topic><topic>Nanoparticles</topic><topic>Nuclear fuels</topic><topic>Occupational exposure</topic><topic>Particulate matter</topic><topic>Polycyclic aromatic hydrocarbons</topic><topic>Polymerase chain reaction</topic><topic>Polymorphism</topic><topic>Repair</topic><topic>Research Article</topic><topic>Resistance factors</topic><topic>Restriction fragment length polymorphism</topic><topic>Scanning electron microscopy</topic><topic>Transmission electron microscopy</topic><topic>Waste Water Technology</topic><topic>Water Management</topic><topic>Water Pollution Control</topic><topic>X-ray spectroscopy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>León-Mejía, Grethel</creatorcontrib><creatorcontrib>Quintana-Sosa, Milton</creatorcontrib><creatorcontrib>de Moya Hernandez, Yurina</creatorcontrib><creatorcontrib>Rodríguez, Ibeth Luna</creatorcontrib><creatorcontrib>Trindade, Cristiano</creatorcontrib><creatorcontrib>Romero, Marco Anaya</creatorcontrib><creatorcontrib>Luna-Carrascal, Jaime</creatorcontrib><creatorcontrib>Ortíz, Ludis Oliveros</creatorcontrib><creatorcontrib>Acosta-Hoyos, Antonio</creatorcontrib><creatorcontrib>Ruiz-Benitez, Martha</creatorcontrib><creatorcontrib>Valencia, Karen Franco</creatorcontrib><creatorcontrib>Rohr, Paula</creatorcontrib><creatorcontrib>da Silva, Juliana</creatorcontrib><creatorcontrib>Henriques, João Antônio Pêgas</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Ecology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Pollution Abstracts</collection><collection>Toxicology Abstracts</collection><collection>ABI/INFORM 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Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>León-Mejía, Grethel</au><au>Quintana-Sosa, Milton</au><au>de Moya Hernandez, Yurina</au><au>Rodríguez, Ibeth Luna</au><au>Trindade, Cristiano</au><au>Romero, Marco Anaya</au><au>Luna-Carrascal, Jaime</au><au>Ortíz, Ludis Oliveros</au><au>Acosta-Hoyos, Antonio</au><au>Ruiz-Benitez, Martha</au><au>Valencia, Karen Franco</au><au>Rohr, Paula</au><au>da Silva, Juliana</au><au>Henriques, João Antônio Pêgas</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>DNA repair and metabolic gene polymorphisms affect genetic damage due to diesel engine exhaust exposure</atitle><jtitle>Environmental science and pollution research international</jtitle><stitle>Environ Sci Pollut Res</stitle><addtitle>Environ Sci Pollut Res Int</addtitle><date>2020-06-01</date><risdate>2020</risdate><volume>27</volume><issue>16</issue><spage>20516</spage><epage>20526</epage><pages>20516-20526</pages><issn>0944-1344</issn><eissn>1614-7499</eissn><abstract>Diesel engine exhaust (DEE) is a complex mixture of toxic gases, halogenated aromatic hydrocarbons, alkyl polycyclic aromatic hydrocarbons, polycyclic aromatic hydrocarbons, benzene derivatives, metals and diesel exhaust particles (DEPs) generated from the incomplete combustion of diesel fuel. Many of the compounds in this mixture can cause oxidative damage to DNA and are considered carcinogenic for humans. Further, chronic DEE exposure increases risks of cardiovascular and pulmonary diseases. Despite these pervasive health risks, there is limited and inconsistent information regarding genetic factors conferring susceptibility or resistance to DEE genotoxicity. The present study evaluated the effects of polymorphisms in two base excision repair (BER) genes (
OGG1 Ser326Cys
and
XRCC1 Arg280His
), one homologous recombination (HRR) gene (
XRCC3 Thr241Met
) and two xenobiotic metabolism genes (
GSTM1
and
GSTT1
) on the genotoxicity profiles among 123 mechanics exposed to workplace DEE. Polymorphisms were determined by PCR-RFLP. In comet assay, individuals with the
GSTT1
null genotype demonstrated significantly greater % tail DNA in lymphocytes than those with non-null genotype. In contrast, these null individuals exhibited significantly lower frequencies of binucleated (BN) cells and nuclear buds (NBUDs) in buccal cells than non-null individuals. Heterozygous
hOGG1 326
individuals (
hOGG1 326 Ser/Cys
) exhibited higher buccal cell NBUD frequency than
hOGG1 326 Ser/Ser
individuals. Individuals carrying the
XRCC3 241 Met/Met
polymorphism also showed significantly higher buccal cell NBUD frequencies than those carrying the
XRCC3 241 Thr/Thr
polymorphism. We found a high flow of particulate matter with a diameter of < 2.5 μm (PM
2.5
) in the workplace. The most abundant metals in DEPs were iron, copper, silicon and manganese as detected by transmission electron microscopy–energy-dispersive X-ray spectroscopy (TEM-EDX). Scanning electron microscopy (SEM-EDS) revealed particles with diameters smaller than PM
2.5
, including nanoparticles forming aggregates and agglomerates. Our results demonstrate the genotoxic effects of DEE and the critical influence of genetic susceptibility conferred by DNA repair and metabolic gene polymorphisms that shed light into the understanding of underlying mechanisms.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>32246425</pmid><doi>10.1007/s11356-020-08533-6</doi><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0944-1344 |
| ispartof | Environmental science and pollution research international, 2020-06, Vol.27 (16), p.20516-20526 |
| issn | 0944-1344 1614-7499 |
| language | eng |
| recordid | cdi_proquest_journals_2405801713 |
| source | SpringerLink Journals - AutoHoldings |
| subjects | Agglomerates Aquatic Pollution Atmospheric Protection/Air Quality Control/Air Pollution Base excision repair Benzene Bioassays Carcinogens Chromosome aberrations Comet assay Damage detection Deoxyribonucleic acid Diesel Diesel engines Diesel fuels DNA DNA damage DNA repair Earth and Environmental Science Ecotoxicology Electron microscopy Environment Environmental Chemistry Environmental Health Environmental science Exhaust emissions Exhaust gases Exposure Gene polymorphism Genes Genetic factors Genotoxicity GSTM1 protein GSTT1 protein Halogenated hydrocarbons Health risks Heavy metals Homologous recombination Homologous recombination repair Homology Lung diseases Lymphocytes Manganese Metabolism Microscopy Nanoparticles Nuclear fuels Occupational exposure Particulate matter Polycyclic aromatic hydrocarbons Polymerase chain reaction Polymorphism Repair Research Article Resistance factors Restriction fragment length polymorphism Scanning electron microscopy Transmission electron microscopy Waste Water Technology Water Management Water Pollution Control X-ray spectroscopy |
| title | DNA repair and metabolic gene polymorphisms affect genetic damage due to diesel engine exhaust exposure |
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