Chromosome aberrations and sister chromatid exchanges in styrene‐exposed workers with reference to their smoking habits

Watanabe, Toshiaki; Endo, Akira; Kumai, Miho; Ikeda, Masayuki

doi:10.1002/em.2860050308

Cited by 44 publications

(8 citation statements)

References 49 publications

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“…However, other workers who have studied solvent-exposed cohorts have noted that the combination of smoking and solvent exposure may be genotoxic. In 18 workers Watanabe et al [1983] noted a significant elevation in SCE frequency in the smokers exposed to styrene, while the SCE level in the non-smoking workers was not different than controls. Fredga et al [1982] observed that the SCE frequency in fuel-exposed personnel who smoked was above similar controls, while the non-smoking, exposed workers had SCE levels essentially similar to non-smoking controls.…”

Section: Discussionmentioning

confidence: 80%

“…Haglund et al [ 19801 completed [Toftgard and Gustafsson, 19801, elevations in SCE attributable to recent exposure (within weeks) may have gone undetected in both studies. Bias of this sort (misclassification) might also explain the lack of consistency between studies in the detection of an increase of SCE in smoking workers (an elevation in SCE similar to that reported by Fredga et al [1982], Maki-Paakkanen et al [1984], and Watanabe et al [1983]). …”

Section: Discussionmentioning

confidence: 92%

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Effects of cigarette smoking and solvent exposure on sister chromatid exchange frequency in painters

Kelsey

Wiencke

Little

et al. 1988

Environ and Mol Mutagen

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A cross-sectional study of sister chromatid exchange frequency (SCE) in peripheral blood lymphocytes from 117 members of the International Brotherhood of Painters and Allied Tradesman was conducted in union locals in two major U.S. cities. Chronic solvent exposure intensity and duration were estimated from interviewer-administered-questionnaire data. SCE for all of the workers in the study were scored by one reader. A second reader determined the SCE frequency from a random sample of 30 workers. No significant difference in SCE frequency was associated with reader or time of reading. Age, coffee and alcohol intake and chronic solvent exposure (both intensity and duration, estimated over the working lifetime and over the year prior to study for each worker) did not significantly elevate SCE. The effect of smoking on SCE frequency, assessed by analysis of variance controlling for other possible confounding factors, showed that smoking increased SCE frequency (P less than .0001). The SCE frequency in the smoking, solvent-exposed (estimated as lifetime exposure) painters was 6.75 SCE/cell; in the non-smoking, solvent-exposed workers the SCE frequency was 5.73 SCE/cell; the controls had SCE levels of 6.84 SCE/cell (smokers) and 5.90 SCE/cell (non-smokers), respectively. These observations are consistent with other work suggesting that chronic solvent exposure in the paint trade is not associated with an elevation in SCE in peripheral blood lymphocytes. However, further work is necessary to address adequately the question of the genotoxicity of acute solvent exposure in these workers.

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Section: Discussionmentioning

confidence: 80%

Section: Discussionmentioning

confidence: 92%

Effects of cigarette smoking and solvent exposure on sister chromatid exchange frequency in painters

Kelsey

Wiencke

Little

et al. 1988

Environ and Mol Mutagen

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“…Six out of 20 exposed workers were smokers, with a mean consumption o f eight (ran ge [3][4][5][6][7][8][9][10][11][12][13] cigarett es per day. Eleven out of 22 referents were smo kers, with a mean consumption of 12 (range [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] cigar ettes per da y. Of th e exposed subjects 13 had had radiographic examinations du ring the last year, and th ree regularly took drug s (theophyllin, terbutalin, pidolol , insulin).…”

Section: Subjects and Samplingmentioning

confidence: 99%

Cytogenetic and hematological effects in plastics workers exposed to styrene.

Hagmar¹,

Högstedt²,

Welinder³

et al. 1989

Scand J Work Environ Health

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“…It has been shown that concomitant exposure to aromatic solvents and polycyclic aromatic hydrocarbons (PAHs) in cigarette smoke and combustion emissions may result in a toxic interaction between these two xenobiotics (Watanabe et al, 1983). In epidemiologic studies, petroleumprocessing industry workers had a higher incidence of both sister chromatid exchange (SCE) and chromosomal aberrations in lymphocytes (Simenova et al, 1989), while solvent-exposed smoking painters had high levels of lymphatic SCE (Kelsey et al, 1989).…”

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confidence: 99%

EFFECT OF LOW-LEVEL SHORT-TERM o-XYLENE INHALATION ON BENZO[a]PYRENE (BaP) METABOLISM AND BaP-DNA ADDUCT FORMATION IN RAT LIVER AND LUNG MICROSOMES

Park

Schatz²

1999

Journal of Toxicology and Environmental Health, Part A

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o-Xylene is a commonly used solvent that alters mixed-function oxidase (MFO) activity in an organ- and isozyme-specific pattern following intraperitoneal (ip) administration. Similar MFO alterations have been observed after ip or inhalation exposure to other methyl benzenes. These MFO alterations shifted the metabolism of the carcinogen benzo[a]pyrene (BaP) toward formation of toxication metabolites in lung. The purpose of this study was to determine whether o-xylene inhalation caused similar MFO changes and whether these alterations were reflected in altered BaP metabolism and BaP-DNA adduct formation. o-Xylene (300 ppm, 6 h) decreased the activity of arylhydrocarbon hydroxylase (AHH) in lung. CYP2B1 activity (benzyloxyresorufin O-dealkylase; BROD), which is responsible for metabolism of BaP to relatively nontoxic metabolites, was decreased in lung, as was, to a lesser extent, CYP1A1 (ethoxyresorufin O-dealkylase; EROD), which is responsible for metabolism of BaP to reactive/toxic metabolites. The BROD/EROD ratio, an indirect indicator of the pattern of BaP toxication/detoxication, was decreased in lung, suggesting that BaP metabolism is shifted toward toxication. No MFO alterations were observed in liver. In lung microsomes, o-xylene increased formation of 7,8-BaP-diol, while 9,10-BaP-diol, 3-OH BaP, and 9-OH BaP were decreased. In liver, o-xylene increased 9-OH BaP formation, while 4,5- and 9,10-diols as well as total diols were decreased. The toxication/detoxication ratios for BaP individual and total metabolite groups were increased in lung microsomes and unaltered in liver. The major BaP-DNA adduct, BaP diol epoxide-N2-deoxyguanosine, was increased in lung but decreased in liver microsomes from o-xylene-exposed rats. Four minor BaP-DNA adducts were formed in lung and three in liver, only one of which (liver adduct 3) was decreased. The o-xylene-induced increase in BaP adduct formation in lung and decrease in liver indicate that coexposure to organic solvents such as the methyl benzenes may alter the carcinogenesis of BaP, or other PAHs, in an organ-specific fashion.

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Chromosome aberrations and sister chromatid exchanges in styrene‐exposed workers with reference to their smoking habits

Cited by 44 publications

References 49 publications

Effects of cigarette smoking and solvent exposure on sister chromatid exchange frequency in painters

Effects of cigarette smoking and solvent exposure on sister chromatid exchange frequency in painters

Cytogenetic and hematological effects in plastics workers exposed to styrene.

EFFECT OF LOW-LEVEL SHORT-TERM o-XYLENE INHALATION ON BENZO[a]PYRENE (BaP) METABOLISM AND BaP-DNA ADDUCT FORMATION IN RAT LIVER AND LUNG MICROSOMES

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