ArticleBritish journal of industrial medicine1993
Sister chromatid exchanges in lymphocytes of petroleum retailers.
Article in British journal of industrial medicine, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed, 11 citations in OpenAlex.
- Evaluation of genotoxic effects of benzene and its derivatives in workers of gas stations.Environmental monitoring and assessment · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Occupational exposure to petroleum vapour was assessed in workers employed in suburban petroleum retail outlets. Urinary output of thioethers provided a non-specific estimate of exposure to chemicals metabolised via a mercapturic acid pathway. Urinary d-glucaric acid (DGA) excretion was taken as an estimate of hepatic enzyme activity. Sister chromatid exchange frequency in lymphocytes was used as an indicator of genotoxic response to exposure. Workers were classified according to their employment at self service (where customers operate petrol pumps) or at driveway attended service stations (at which an employee operates the pumps), and according to exposure to cigarette smoke on the basis of urinary cotinine excretion. Prework and postwork urine samples of workers employed at driveway attended petrol stations contained more thioether than did those of self serve workers. When classified according to smoking behaviour there were no statistically significant differences, although thioether excretion tended to be higher in smokers than in nonsmokers. Urinary DGA excretion was similar in the two exposure groups. Cigarette smokers excreted more DGA, however, than nonsmokers. Sister chromatid exchange frequencies were higher in driveway attendants than in self serve personnel. When the influence of cigarette smoking was investigated there was a significant increase of sister chromatid exchange with combined exposure to petrol and cigarette smoking, but not with either factor alone. Correlation analysis showed that urinary cotinine concentrations were positively associated with urinary excretion of thioether and DGA, indicating that cigarette smoke induces the activity of hepatic enzymes and acts as a source of substrates metabolised through a thioether pathway. In conclusion it seems that exposure to petroleum vapour causes increased sister chromatid exchange in circulating lymphocytes of cigarette smokers, possibly as a result of enhanced hepatic conversion of vapour components to reactive metabolites. Urinary thioether output does not clearly discriminate between workers exposed to different amounts of petroleum vapour at retail outlets.
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