Biologic monitoring of exposure to chemical mutagens in the occupational environment

Sorsa, Marja; Hemminki, Kari; Vainio, Harri

doi:10.1002/1520-6866(1990)2:2<137::aid-tcm1770020204>3.0.co;2-4

Cited by 38 publications

(8 citation statements)

References 84 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Evidence is accumulating for a positive association between low-dose exposures to genotoxic agents and the production of alterations in the sensitivity threshold of a biomarker [Bender et al, 1988;Sorsa et al, 1982]. With regard to DEB-induced SCEs, the present study revealed a suggestive but nonsignificant gene-environment interaction between the GSTT1 genotype and occupational benzene exposure among women.…”

Section: Discussionmentioning

confidence: 41%

Benzene exposure, glutathione S-transferase theta homozygous deletion, and sister chromatid exchanges

Xu¹,

Wiencke

Niu

et al. 1998

Am. J. Ind. Med.

View full text Add to dashboard Cite

Recent studies have shown a strong positive correlation between chromosomal aberrations and future cancer risk. Sister chromatid exchange (SCE) has been widely applied in monitoring early biological effects to assess human genetic risk of cancer at the population level. We studied 45 Chinese workers (23 in the painting workshop of a glass factory with occupational exposure to benzene, and 22 fitters and planers in the punching and planing machine workshops of a nearby shipyard without such an exposure) to examine the association between occupational exposure to benzene and SCE frequency in peripheral blood lymphocytes. We also sought to investigate whether the glutathione S‐transferase class θ gene (GSTT1) affects individual susceptibility to cytogenetic damage induced by in vivo exposure to benzene or in vitro exposure to diepoxybutane. The time‐weighted average concentrations of benzene were 0.71 ppm in the exposed group and 0.03 ppm in the non‐exposed group. Controlling for age, gender and educational level, cigarette smoking was significantly associated with increased SCE frequencies (P < 0.05), while GSTT1 genotype was significantly associated with DEB‐induced SCEs (P < 0.01). There was no relationship between benzene exposure and baseline or DEB‐induced SCEs. After stratification by smoking status, the GSTT1 deletion was a significant predictor of DEB‐induced SCEs for both smokers (P < 0.05) and nonsmokers (P < 0.01). A significant benzene‐GSTT1 interaction was found in nonsmokers (P < 0.05). Our study suggests that GSTT1 is an important determinant of heterogeneity in individual susceptibility to chromosomal damage associated with exposure to benzene. Am. J. Ind. Med. 33:157–163, 1998. © 1998 Wiley‐Liss, Inc.

show abstract

Section: Discussionmentioning

confidence: 41%

Benzene exposure, glutathione S-transferase theta homozygous deletion, and sister chromatid exchanges

Xu¹,

Wiencke

Niu

et al. 1998

Am. J. Ind. Med.

View full text Add to dashboard Cite

show abstract

“…The measurement of urinary mutagenicity (Ames test) has been used to detect absorption of potentially mutagenic compounds as a non-specific biological marker of exposure. 15 It has been used together with HpU determination to assess the exposure of coke oven workers to genotoxicants. 7 16 There are several studies of the exposure to PAHs in which biomakers of biological effect measuring different kinds of genetic damage in peripheral blood lymphocytes have been used.…”

mentioning

confidence: 99%

Association between urinary 1-hydroxypyrene and genotoxic effects in coke oven workers

Siwinska

2004

Occup Environ Med

View full text Add to dashboard Cite

Aims: To investigate whether current occupational exposure of coke oven workers to polycyclic aromatic hydrocarbons (PAHs) results in genotoxic effects measured in peripheral blood lymphocytes and whether these biomarkers are associated with the biomarkers of exposure. Methods: Blood and urine samples were collected immediately after a shift at the end of a working week from 50 coke oven workers and 50 control workers not exposed to PAHs. Methods included: (1) biomarkers of exposure: urinary 1-hydroxypyrene (HpU), urinary mutagenicity by the plate Salmonella test with strains TA98 and YG1024 after metabolic activation, expressed as mutagenic rate (MR98 and MR1024, respectively), urinary cotinine; and (2) biomarkers of biological effects in peripheral blood lymphocytes (PBL): sister chromatid exchanges (SCE/cell), cells of high frequency of SCE (% HFC), micronuclei (MN/1000 cells), chromosomal aberrations (CA/100 cells), and DNA damage by the Comet assay. Results: Occupational exposure to PAH resulted in significantly increased levels of HpU and mutagenic effect of urine. Median values of these biomarkers in coke oven workers were: 9.0 mmol/mol creatinine for HpU, 2.7 for MR98, and 8.2 for MR1024, compared to the controls: HpU = 0.6 mmol/mol creatinine, MR98 = 1.2, and MR1024 = 5.5. Occupational exposure caused significant induction of SCE, HFC, and MN in coke oven workers: median SCE = 5.9, HFC = 12.0%, MN = 6.0 compared to the controls: 3.9, 5.0%, and 3.0, respectively. No effect of occupational exposure was found in relation to CA and DNA damage measured with the Comet assay. HpU concentration was positively associated with SCE and HFC. The concentration of urinary 1-hydroxypyrene corresponding to a 5% probability of increased SCE was 1.0 mmol/mol creatinine. Conclusions: The occupational exposure to PAHs resulted in measurable biological effects (SCE, HFC, MN). In coke oven workers an increased level of SCE was not observed below the level of 1.0 mmol HpU/ mol creatinine.

show abstract

“…Protein Adduct. Analysis of serum or red cells for mutagen-protein adducts [Sorsa et al, 1982;Tice, 1984;Van Sittert and de Jong, 1985;Garner, 1985;Tannenbaum and Skipper, 19861. RBC Protein.…”

Section: Willingness To Share Resultsmentioning

confidence: 99%

“…The scientific literature demonstrates a diversity of opinion on the ability of mutagenicity tests to indicate individual exposure [Irr, 1984;Rudolph, 1984;Sandberg, 1980;Schechter, 1983;Sorsa et al, 1982;Wolff, 1982, 19831. There have been a limited number of studies examining the correlation between mutagenicity test results and either a history of cancer or an increased risk of cancer [Bazopoulou-Kyrkanidou et al, 1986;Caderni et al, 1982;Cervenka et al, 1979;Holly et al, 1986;Irr, 1984;Jung et al, 1982;Knuutila et al, 1978;Minnich et al, 1976;Mitra et al, 1982;Morris et al, 19841.…”

Section: Significance Of Test Resultsmentioning

confidence: 99%

Recontacting subjects in mutagen‐exposure‐monitoring studies: II. Results of a questionnaire study of mutagenesis researchers, with review of the pertinent literature

Busch

Easterling

Leventhal

et al. 1988

Environ and Mol Mutagen

View full text Add to dashboard Cite

A questionnaire on the attitudes of mutagenesis researchers regarding the health significance of and the use of data from tests of human mutagen exposure or genetic damage was completed by 71 of 312 (23%) individuals who had been participants in meetings or organizations concerned with mutagenesis research. On a point scale of 0 to 10, with 0 indicating strong disagreement, 5 indicating uncertainty, and 10 indicating strong agreement, the average respondent felt (8.31 +/- 2.27) that data indicating a probable health hazard should be shared automatically with the subjects, but was also moderately concerned about psychological distress of subjects learning of study results indicating abnormally high mutagen exposure (6.14 +/- 2.57) or genetic damage (6.94 +/- 2.48). The average respondent felt that follow-up of subjects could improve the quality of mutagen-exposure-monitoring studies (8.33 +/- 1.49), disagreed that subjects whose laboratory data suggested unusually severe exposure or damage should not be asked about possible sources of exposure (1.15 +/- 1.32), and disagreed that it was ethical to follow up but not discuss results with subjects having laboratory evidence of abnormal mutagen exposure (3.78 +/- 3.43) or genetic damage (3.06 +/- 3.17) to see how many developed cancer relative to a control group. Fifteen specific tests for measuring mutagen exposure or genetic damage were rated on a scale of 0 to 10, with 0 being "totally experimental" and 10 being "absolutely diagnostic of degree of exposure or genetic damage." Values ranged from 6.13 +/- 2.67 for karyotyping leukocytes to 3.43 +/- 2.43 for quantifying frequency of rare red cells with mutant protein. This study may help in decision making regarding follow-up of mutagen-exposed subjects.

show abstract

Biologic monitoring of exposure to chemical mutagens in the occupational environment

Cited by 38 publications

References 84 publications

Benzene exposure, glutathione S-transferase theta homozygous deletion, and sister chromatid exchanges

Benzene exposure, glutathione S-transferase theta homozygous deletion, and sister chromatid exchanges

Association between urinary 1-hydroxypyrene and genotoxic effects in coke oven workers

Recontacting subjects in mutagen‐exposure‐monitoring studies: II. Results of a questionnaire study of mutagenesis researchers, with review of the pertinent literature

Contact Info

Product

Resources

About