Mutagens in human urine: effects of cigarette smoking and diet

Sasson, Isaac M.; Coleman, Daniel T.; LaVoie, Edmond J.; Hoffmann, Dietrich; Wynder, Ernst L.

doi:10.1016/0165-1218(85)90078-3

Cited by 33 publications

(4 citation statements)

References 31 publications

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“…71 More extensive studies are needed in order to quantify the contribution of ETS exposure to urinary mutagenicity, which is primarily dominated by dietary factors. 80 Markers for biological effects related to ETS exposure By definition, biological effect markers are not specific for the underlying exposure but reflect at NANYANG TECH UNIV LIBRARY on May 31, 2015 het.sagepub.com Downloaded from physiological or toxicological responses to a great number of factors. Therefore, it is extremely important to control for confounding factors when applying these markers in population studies.…”

Section: Mutagensmentioning

confidence: 99%

Biomonitoring exposure to environmental tobacco smoke (ETS): A critical reappraisal

Scherer

Richter²

1997

Hum Exp Toxicol

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1 The most frequently used biomarkers for exposure to environmental tobacco smoke (ETS) are cotinine and thiocyanate in body fluids, carboxyhaemoglobin in red blood cells (COHb) and carbon monoxide in the expired air. Although not ideal, cotinine in blood, saliva or urine is an established biomarker for ETS exposure within the past 1-3 days. Comparison with cotinine concentrations in cigarette smokers reveals that passive smokers take up less than 1/100 of the nicotine dose of smokers. 2 Biomonitoring data available for the ETS-related exposure to genotoxic substances comprise uptake of benzene, polycyclic aromatic hydrocarbons (PAH), aromatic amines, tobacco-specific nitrosamines (TSNA), electrophilic compounds giving rise to ur inary thioethers, mutagens causing urinary mutagenic activity and the formation of various DNA adducts. With the exception of TSNA, these biomarkers are related to chemicals occurring ubiquitously in the environment and in the food. As a consequence, the background levels in unexposed nonsmokers are high compared to the observed increases (if any) associated with ETS exposure. 3 Some markers of biological effects, which, by defini tion, are non-specific with regard to the underlying exposure, have also been investigated in relation to ETS exposure. These markers comprise cytogenetic effects, aryl hydrocarbon hydroxylase (AHH) induc tion, urinary hydroxyproline excretion and various factors indicative of cardiovascular risks. The avail able data suggest that passive smoking is associated with a small induction of placental AHH and also with effects on cardiovascular risk markers. The latter findings in particular may be confounded by other risk factors, which have been observed to be more frequent in passive smokers than in unexposed nonsmokers.

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Section: Mutagensmentioning

confidence: 99%

Biomonitoring exposure to environmental tobacco smoke (ETS): A critical reappraisal

Scherer

Richter²

1997

Hum Exp Toxicol

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“…Ames (Biochemistry Department, University of California, Berkeley). The strains were stored and tested before use for the maintenance of characteristics and for the sensitivity to standard mutagens as described by Maron and Ames [1983], with some modifications [Dunkel et al, 1984;Sasson et al, 1985;Warren and Rogers, 19821. S9 was prepared from 5-week-old Sprague-Dawley rats treated with Aroclor 1254 (200 mg/kg), and was routinely used in assays at a final concentration of 3%.…”

Section: Bacterial Tester Strains and S9mentioning

confidence: 99%

Comparison of three assays for genetic effects of antineoplastic drugs on cancer patients and their nurses

Krepinsky¹,

Bryant

Davison

et al. 1990

Environ and Mol Mutagen

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Three assays have been compared for their ability to detect genetic damage caused by antineoplastic drugs in cancer patients and possible damage in the nurses who administered these drugs. The assays were sister chromatid exchanges (SCE) and chromosomal aberrations in peripheral blood lymphocytes, and the Salmonella/mammalian microsome assay on urine. Three comparisons were made: 1) patients before versus after treatment; 2) the administering nurses immediately after their work period versus after a few days off that followed (work and off-work); 3) the exposed nurses versus other nurses who did not administer antineoplastic drugs (controls). The SCE assay detected the treatments in all eight patients from whom complete data were obtained, and was positive in two nurses with a long history of smoking. The Salmonella/mammalian microsome assay detected eight of ten treatments in patients but failed to detect smokers. Four of nine patients receiving treatment were detected by the analysis of chromosomal aberrations. The SCE assay did not distinguish between the work and off-work samples in either the exposed or control nurses. The exposed nurses, as a group, had slightly fewer SCEs than the controls due to the two smokers detected in the latter group. Chromosomal aberration was the only assay which showed significant difference between the two samples of the exposed nurses and, consequently, between the exposed and control nurses. These differences, however, arose primarily from a higher frequency of aberrations found among the exposed nurses in samples taken after a few days away from work, rather than at the end of their work period. There is no evidence that the increase was connected to occupational exposure.

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“…The behavioral risk factors for cervical cancer reported in the medical literature include early age of initiating sexual intercourse Hulka, 1982;Rotkin, 1973), multiparity , multiple partners Green 1979;Hulka, 1982;Parkin et al, 1985;Vyslouzilova et al, 1997), a sexual partner with multiple partners (Harris et al, 1980;Peters et al, 1986;Terris et al, 1967;Vyslouzilova et al, 1997), frequent sexually transmitted infections, including human papillomavirus (HPV) (Harris et al, 1980;Peters et al, 1986;Terris et al, 1967;Vyslouzilova et al, 1997), and smoking of cigarettes (Clarke et al, 1982;de Vet et al, 1994;Hellberg et al, 1986;LaVecchia et al, 1986;Lyon et al, 1983;Nischan et al, 1988;Sasson et al, 1985;Stellman et al, 1980;Trevathan et al, 1983). Epidemiological data about these risk factors is provided in detail in Chapter 7.…”

Section: Behavioral Risksmentioning

confidence: 99%

Cercival Cancer: From Etiology to Prevention

2004

Cancer Prevention — Cancer Causes

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Mutagens in human urine: effects of cigarette smoking and diet

Cited by 33 publications

References 31 publications

Biomonitoring exposure to environmental tobacco smoke (ETS): A critical reappraisal

Biomonitoring exposure to environmental tobacco smoke (ETS): A critical reappraisal

Comparison of three assays for genetic effects of antineoplastic drugs on cancer patients and their nurses

Cercival Cancer: From Etiology to Prevention

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