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HPRT and glycophorin A mutations in foundry workers: relationship to PAH exposure and to PAH-DNA adducts
Mutations were evaluated in workers in an iron foundry with exposure to polycyclic aromatic hydrocarbons (PAHs), measured by personal and area monitoring, ranging from
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| Published in: | Carcinogenesis (New York) 1993-05, Vol.14 (5), p.969-973 |
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| container_title | Carcinogenesis (New York) |
| container_volume | 14 |
| creator | Perera, F.P. Tang, D.L. O'Neill, J.P. Bigbee, W.L. Albertini, R.J. Santella, R. Ottman, R. Tsai, W.Y. Dickey, C. Mooney, L.A. Savela, K. Hemminki, K. |
| description | Mutations were evaluated in workers in an iron foundry with exposure to polycyclic aromatic hydrocarbons (PAHs), measured by personal and area monitoring, ranging from |
| doi_str_mv | 10.1093/carcin/14.5.969 |
| format | article |
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Mutation at the hypoxanthine guanine phosphoribosyl transferase (HPRT) and glycophorin A (GPA) loci (measures of molecular effect in lymphocytes and erythrocytes respectively) were assessed to demonstrate their relationship to external exposure at lower levels than previously analyzed in foundry workers at this plant (<50–200 ng/m3). The relationship between mutations and PAH - DNA adducts measured by immunoassay (as a measure of the biologically effective dose) was also investigated. The markers were analyzed for dose-response and interindividual variability. Workers were classified into three exposure categories (low, medium and high). PAH-DNA adduct values for the low, medium and high exposure groups were 5.19, 6.10 and 9.57×10−8 nucleotides respectively (r = 0.28; P = 0.08). HPRT mutant frequencies (adjusted for age and cloning efficiency) for the low, medium and high exposure groups were 1.04, 1.13 and 1.82×10−6 cells respectively and demonstrated an upward trend with increasing exposure that was of borderline significance (r = 0.46, P = 0.06). In contrast, HPRT mutations were highly correlated with PAH-DNA adducts (r = 0.67; P = 0.004). Interindividual variability in mutant frequencies ranged from 1.5- to 4.5-fold within the three exposure categories. With respect to GPA variants, NN frequency (Vf) in erythrocytes (which reflects chromosomal loss and duplication, recombination or gene conversion) was not positively correlated with PAH exposure. The level of NØ Vf (arising from small-scale structural mutations in the GPA gene or from larger-scale chromosomal rearrangements or deletions) increased slightly, but not significantly, over the three exposure groups from 8.2 to 10.7 to 11.8/106 cells (P = 0.32). Interindividual variation in GPA NN Vf ranged from 2- to 18-fold and in GPA NØ from 4- to 5-fold. NN and NØ Vf were highly correlated (P = 0.001) but no correlation was seen between GPA and HPRT or between GPA and PAH-DNA adducts. Thus, the most interesting and novel finding is that, even at relatively low exposures to PAH, HPRT mutations were increased in parallel with PAH-DNA adducts. The observed association between PAH-DNA adducts and HPRT gene mutation in humans is consistent with experimental data for PAHs. These results support the use of both biomonitoring and personal ambient monitoring in further molecular epidemiology studies.</description><identifier>ISSN: 0143-3334</identifier><identifier>EISSN: 1460-2180</identifier><identifier>DOI: 10.1093/carcin/14.5.969</identifier><identifier>PMID: 8504491</identifier><identifier>CODEN: CRNGDP</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>adducts ; Adult ; Biological and medical sciences ; Cohort Studies ; DNA ; DNA - blood ; exposure ; Female ; Glycophorin - genetics ; glycophorin A ; Host-tumor relations. Immunology. Biological markers ; Humans ; hypoxanthine phosphoribosyl transferase ; Hypoxanthine Phosphoribosyltransferase - genetics ; Iron ; Leukocytes - metabolism ; Male ; man ; Medical sciences ; Middle Aged ; Mutagenesis ; mutation ; Occupational Exposure ; polycyclic aromatic hydrocarbons ; Polycyclic Compounds - blood ; Tumors</subject><ispartof>Carcinogenesis (New York), 1993-05, Vol.14 (5), p.969-973</ispartof><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-ef116114e6aa03d79e68d0e2eb241f0fc8f0d67429a4bedb244d23afc21fb1ce3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4754548$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8504491$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Perera, F.P.</creatorcontrib><creatorcontrib>Tang, D.L.</creatorcontrib><creatorcontrib>O'Neill, J.P.</creatorcontrib><creatorcontrib>Bigbee, W.L.</creatorcontrib><creatorcontrib>Albertini, R.J.</creatorcontrib><creatorcontrib>Santella, R.</creatorcontrib><creatorcontrib>Ottman, R.</creatorcontrib><creatorcontrib>Tsai, W.Y.</creatorcontrib><creatorcontrib>Dickey, C.</creatorcontrib><creatorcontrib>Mooney, L.A.</creatorcontrib><creatorcontrib>Savela, K.</creatorcontrib><creatorcontrib>Hemminki, K.</creatorcontrib><title>HPRT and glycophorin A mutations in foundry workers: relationship to PAH exposure and to PAH-DNA adducts</title><title>Carcinogenesis (New York)</title><addtitle>Carcinogenesis</addtitle><description>Mutations were evaluated in workers in an iron foundry with exposure to polycyclic aromatic hydrocarbons (PAHs), measured by personal and area monitoring, ranging from <5 to 60 ng/m3 of benzo[a]pyrene (B[a]P). Mutation at the hypoxanthine guanine phosphoribosyl transferase (HPRT) and glycophorin A (GPA) loci (measures of molecular effect in lymphocytes and erythrocytes respectively) were assessed to demonstrate their relationship to external exposure at lower levels than previously analyzed in foundry workers at this plant (<50–200 ng/m3). The relationship between mutations and PAH - DNA adducts measured by immunoassay (as a measure of the biologically effective dose) was also investigated. The markers were analyzed for dose-response and interindividual variability. Workers were classified into three exposure categories (low, medium and high). PAH-DNA adduct values for the low, medium and high exposure groups were 5.19, 6.10 and 9.57×10−8 nucleotides respectively (r = 0.28; P = 0.08). HPRT mutant frequencies (adjusted for age and cloning efficiency) for the low, medium and high exposure groups were 1.04, 1.13 and 1.82×10−6 cells respectively and demonstrated an upward trend with increasing exposure that was of borderline significance (r = 0.46, P = 0.06). In contrast, HPRT mutations were highly correlated with PAH-DNA adducts (r = 0.67; P = 0.004). Interindividual variability in mutant frequencies ranged from 1.5- to 4.5-fold within the three exposure categories. With respect to GPA variants, NN frequency (Vf) in erythrocytes (which reflects chromosomal loss and duplication, recombination or gene conversion) was not positively correlated with PAH exposure. The level of NØ Vf (arising from small-scale structural mutations in the GPA gene or from larger-scale chromosomal rearrangements or deletions) increased slightly, but not significantly, over the three exposure groups from 8.2 to 10.7 to 11.8/106 cells (P = 0.32). Interindividual variation in GPA NN Vf ranged from 2- to 18-fold and in GPA NØ from 4- to 5-fold. NN and NØ Vf were highly correlated (P = 0.001) but no correlation was seen between GPA and HPRT or between GPA and PAH-DNA adducts. Thus, the most interesting and novel finding is that, even at relatively low exposures to PAH, HPRT mutations were increased in parallel with PAH-DNA adducts. The observed association between PAH-DNA adducts and HPRT gene mutation in humans is consistent with experimental data for PAHs. These results support the use of both biomonitoring and personal ambient monitoring in further molecular epidemiology studies.</description><subject>adducts</subject><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Cohort Studies</subject><subject>DNA</subject><subject>DNA - blood</subject><subject>exposure</subject><subject>Female</subject><subject>Glycophorin - genetics</subject><subject>glycophorin A</subject><subject>Host-tumor relations. Immunology. Biological markers</subject><subject>Humans</subject><subject>hypoxanthine phosphoribosyl transferase</subject><subject>Hypoxanthine Phosphoribosyltransferase - genetics</subject><subject>Iron</subject><subject>Leukocytes - metabolism</subject><subject>Male</subject><subject>man</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mutagenesis</subject><subject>mutation</subject><subject>Occupational Exposure</subject><subject>polycyclic aromatic hydrocarbons</subject><subject>Polycyclic Compounds - blood</subject><subject>Tumors</subject><issn>0143-3334</issn><issn>1460-2180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><recordid>eNo9kMFv0zAUhy0EGmVw5oTkA-KW1i92nJhb1TIKmrYxbdLExXLtZxqWxpmdiPW_J5Cqp6f3vu_9Dj9C3gObA1N8YU20dbsAMS_mSqoXZAZCsiyHir0kMwaCZ5xz8Zq8Sek3YyB5oc7IWVUwIRTMyG5zc3tHTevor-ZgQ7cLsW7pku6H3vR1aBMdVx-G1sUD_RPiI8b0mUZsJrqrO9oHerPcUHzuQhoi_g-bbtn6akmNc4Pt01vyypsm4bvjPCf3F1_uVpvs8vrrt9XyMrNcsT5DDyABBEpjGHelQlk5hjlucwGeeVt55mQpcmXEFt14FS7nxtsc_BYs8nPyacrtYngaMPV6XyeLTWNaDEPSIKUQea5GcTGJNoaUInrdxXpv4kED0_-61VO3GoQu9Njt-PHhGD1s9-hO_rHMkX88cpOsaXw0ra3TSRNlIQpRjVo2aXXq8fmETXzUsuRloTcPP_XFWsD3Hw9rveJ_AZijkqA</recordid><startdate>19930501</startdate><enddate>19930501</enddate><creator>Perera, F.P.</creator><creator>Tang, D.L.</creator><creator>O'Neill, J.P.</creator><creator>Bigbee, W.L.</creator><creator>Albertini, R.J.</creator><creator>Santella, R.</creator><creator>Ottman, R.</creator><creator>Tsai, W.Y.</creator><creator>Dickey, C.</creator><creator>Mooney, L.A.</creator><creator>Savela, K.</creator><creator>Hemminki, K.</creator><general>Oxford University Press</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>7T3</scope><scope>7TM</scope><scope>7TV</scope><scope>7U2</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope></search><sort><creationdate>19930501</creationdate><title>HPRT and glycophorin A mutations in foundry workers: relationship to PAH exposure and to PAH-DNA adducts</title><author>Perera, F.P. ; Tang, D.L. ; O'Neill, J.P. ; Bigbee, W.L. ; Albertini, R.J. ; Santella, R. ; Ottman, R. ; Tsai, W.Y. ; Dickey, C. ; Mooney, L.A. ; Savela, K. ; Hemminki, K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-ef116114e6aa03d79e68d0e2eb241f0fc8f0d67429a4bedb244d23afc21fb1ce3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>adducts</topic><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Cohort Studies</topic><topic>DNA</topic><topic>DNA - blood</topic><topic>exposure</topic><topic>Female</topic><topic>Glycophorin - genetics</topic><topic>glycophorin A</topic><topic>Host-tumor relations. Immunology. Biological markers</topic><topic>Humans</topic><topic>hypoxanthine phosphoribosyl transferase</topic><topic>Hypoxanthine Phosphoribosyltransferase - genetics</topic><topic>Iron</topic><topic>Leukocytes - metabolism</topic><topic>Male</topic><topic>man</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Mutagenesis</topic><topic>mutation</topic><topic>Occupational Exposure</topic><topic>polycyclic aromatic hydrocarbons</topic><topic>Polycyclic Compounds - blood</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Perera, F.P.</creatorcontrib><creatorcontrib>Tang, D.L.</creatorcontrib><creatorcontrib>O'Neill, J.P.</creatorcontrib><creatorcontrib>Bigbee, W.L.</creatorcontrib><creatorcontrib>Albertini, R.J.</creatorcontrib><creatorcontrib>Santella, R.</creatorcontrib><creatorcontrib>Ottman, R.</creatorcontrib><creatorcontrib>Tsai, W.Y.</creatorcontrib><creatorcontrib>Dickey, C.</creatorcontrib><creatorcontrib>Mooney, L.A.</creatorcontrib><creatorcontrib>Savela, K.</creatorcontrib><creatorcontrib>Hemminki, K.</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>Human Genome Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Pollution Abstracts</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><jtitle>Carcinogenesis (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Perera, F.P.</au><au>Tang, D.L.</au><au>O'Neill, J.P.</au><au>Bigbee, W.L.</au><au>Albertini, R.J.</au><au>Santella, R.</au><au>Ottman, R.</au><au>Tsai, W.Y.</au><au>Dickey, C.</au><au>Mooney, L.A.</au><au>Savela, K.</au><au>Hemminki, K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HPRT and glycophorin A mutations in foundry workers: relationship to PAH exposure and to PAH-DNA adducts</atitle><jtitle>Carcinogenesis (New York)</jtitle><addtitle>Carcinogenesis</addtitle><date>1993-05-01</date><risdate>1993</risdate><volume>14</volume><issue>5</issue><spage>969</spage><epage>973</epage><pages>969-973</pages><issn>0143-3334</issn><eissn>1460-2180</eissn><coden>CRNGDP</coden><abstract>Mutations were evaluated in workers in an iron foundry with exposure to polycyclic aromatic hydrocarbons (PAHs), measured by personal and area monitoring, ranging from <5 to 60 ng/m3 of benzo[a]pyrene (B[a]P). Mutation at the hypoxanthine guanine phosphoribosyl transferase (HPRT) and glycophorin A (GPA) loci (measures of molecular effect in lymphocytes and erythrocytes respectively) were assessed to demonstrate their relationship to external exposure at lower levels than previously analyzed in foundry workers at this plant (<50–200 ng/m3). The relationship between mutations and PAH - DNA adducts measured by immunoassay (as a measure of the biologically effective dose) was also investigated. The markers were analyzed for dose-response and interindividual variability. Workers were classified into three exposure categories (low, medium and high). PAH-DNA adduct values for the low, medium and high exposure groups were 5.19, 6.10 and 9.57×10−8 nucleotides respectively (r = 0.28; P = 0.08). HPRT mutant frequencies (adjusted for age and cloning efficiency) for the low, medium and high exposure groups were 1.04, 1.13 and 1.82×10−6 cells respectively and demonstrated an upward trend with increasing exposure that was of borderline significance (r = 0.46, P = 0.06). In contrast, HPRT mutations were highly correlated with PAH-DNA adducts (r = 0.67; P = 0.004). Interindividual variability in mutant frequencies ranged from 1.5- to 4.5-fold within the three exposure categories. With respect to GPA variants, NN frequency (Vf) in erythrocytes (which reflects chromosomal loss and duplication, recombination or gene conversion) was not positively correlated with PAH exposure. The level of NØ Vf (arising from small-scale structural mutations in the GPA gene or from larger-scale chromosomal rearrangements or deletions) increased slightly, but not significantly, over the three exposure groups from 8.2 to 10.7 to 11.8/106 cells (P = 0.32). Interindividual variation in GPA NN Vf ranged from 2- to 18-fold and in GPA NØ from 4- to 5-fold. NN and NØ Vf were highly correlated (P = 0.001) but no correlation was seen between GPA and HPRT or between GPA and PAH-DNA adducts. Thus, the most interesting and novel finding is that, even at relatively low exposures to PAH, HPRT mutations were increased in parallel with PAH-DNA adducts. The observed association between PAH-DNA adducts and HPRT gene mutation in humans is consistent with experimental data for PAHs. These results support the use of both biomonitoring and personal ambient monitoring in further molecular epidemiology studies.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>8504491</pmid><doi>10.1093/carcin/14.5.969</doi><tpages>5</tpages></addata></record> |
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| subjects | adducts Adult Biological and medical sciences Cohort Studies DNA DNA - blood exposure Female Glycophorin - genetics glycophorin A Host-tumor relations. Immunology. Biological markers Humans hypoxanthine phosphoribosyl transferase Hypoxanthine Phosphoribosyltransferase - genetics Iron Leukocytes - metabolism Male man Medical sciences Middle Aged Mutagenesis mutation Occupational Exposure polycyclic aromatic hydrocarbons Polycyclic Compounds - blood Tumors |
| title | HPRT and glycophorin A mutations in foundry workers: relationship to PAH exposure and to PAH-DNA adducts |
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