Smoking enhances asbestos-induced genotoxicity, relative involvement of chromosome 1: a study using multicolor FISH with tandem labeling

Our plain-English summary of Smoking enhances asbestos-induced genotoxicity, relative involvement of chromosome 1: a study using multicolor FISH with tandem labeling, by M. Lohani, E. Dopp, H.H. Becker, et al (Toxicology Letters, 2002).

The study

• Authors: M. Lohani, E. Dopp, H.H. Becker, K. Seth, D. Schiffmann, Q. Rahman
• Journal: Toxicology Letters
• Published: 2002;136(1):55-63
• Cited by: 7 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Several experimental and epidermological studies have indicated augmentation of asbestos induced diseases by cigarette smoke by the mechanisms, which are still unknown. To determine whether smoking affects genetic system of the cells and further modifies asbestos induced genotoxicity, whole blood from non-smokers and smokers was exposed to asbestos fibres separately in vitro and micronucleus test was performed. The number of micronuclei was found to be significantly higher (P<0 05) in cases of smoker's lymphocytes, asbestos exposed non-smokers lymphocytes as well as asbestos exposed smokers lymphocytes, as compared with unexposed non-smokers lymphocytes. Further we investigated involvement of chromosome 1 in the damaging process using multicolor FISH technique. FISH is fast and reliable method, distinguishing both structural and numerical alterations. The centric/pericentric regions of chromosome 1 (cen-q12) were labeled, as the pericentric heterochromatin region 1 (q12) is quite large, highly repetitive and prone to breakage. Multicolor FISH assay suggested that the genetic damage by asbestos fibres mainly involve chromosome 1 but in case of cigarette smoking the damage is not strictly connected to chromosome 1 only, but also involves damage to other chromosomes. Further the study suggested that smoking makes genetic system of the cells more vulnerable to the deleterious effects of asbestos.

In plain English

This laboratory study tested whether smoking makes blood cells more vulnerable to asbestos-caused genetic damage. The authors took blood from six healthy smokers (20 to 30 cigarettes a day for 15 to 20 years) and six non-smokers matched for age, sex and socio-economic conditions. They exposed the cells in culture to chrysotile or crocidolite asbestos at two concentrations. They counted micronuclei, which the authors treated as a sign of genetic damage. They also used a fluorescent labeling method (FISH) to look for breaks and extra copies of chromosome 1. Unexposed smokers' cells had significantly more micronuclei than unexposed non-smokers' cells. Micronuclei rose with asbestos dose and were highest in smokers' cells given the higher crocidolite dose. Chromosome 1 breaks and extra copies were significantly higher in all asbestos-exposed cells than in unexposed cells. Unexposed smokers' and non-smokers' cells did not differ significantly on this measure. The authors concluded that asbestos damage mainly involved chromosome 1, that smoking damage seemed, from comparing the two tests, to involve other chromosomes too, and that prolonged smoking makes cells more vulnerable to asbestos.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Laboratory (in vitro) experiment: blood lymphocytes from smokers and non-smokers were exposed to asbestos in culture and tested with the micronucleus assay and multicolor FISH for chromosome 1
• Who was studied: Blood from six healthy smokers (20 to 30 cigarettes per day for the last 15 to 20 years) and six non-smoker volunteers of the same age, sex and socio-economic conditions. The article does not state where or when the blood was collected.
• Exposure: Crocidolite and chrysotile asbestos fibres were added to cell cultures at two concentrations, printed as 10 and 50 mg/ml, with 48 h incubation for the FISH cultures. The donors' own cigarette smoking was the second factor compared.
• Main results:
  • Unexposed (control) lymphocytes from smokers had significantly more micronuclei than unexposed lymphocytes from non-smokers (P less than 0.001)
  • Micronuclei increased with asbestos dose
  • At the lower concentration (10), micronuclei per 1000 cells for chrysotile and crocidolite were printed as '62.489/5.96' and '63.329/3.91' in non-smokers' cells and '68.279/6.92' and '75.109/6.90' in smokers' cells. Given the scanning damage, these appear to be means with spreads, which would read as about 62.48, 63.32, 68.27 and 75.10, but the article does not confirm this reading.
  • At the higher concentration (50), micronuclei per 1000 cells for chrysotile and crocidolite were printed as '78.289/6.93' and '80.729/6.10' in non-smokers' cells and '85.139/5.89' and '91.29/8.0' in smokers' cells. The maximum number of micronuclei was in smokers' cells exposed to crocidolite at 50.
  • In the FISH test of chromosome 1, unexposed smokers' cells had slightly more total breaks and hyperdiploidy than unexposed non-smokers' cells (total breaks 13.09 vs 10.37 per thousand cells), but the difference was not significant
  • Breaks and hyperdiploidy of chromosome 1 were significantly higher (P less than 0.001) in all asbestos-exposed cells, from both non-smokers and smokers, than in unexposed cells. The maximum was in smokers' cells exposed to crocidolite at 50 (total breaks 42.12 per thousand cells).
  • After asbestos treatment, the most common damage in both smokers' and non-smokers' cells was breakage between the alpha and classical satellite regions of chromosome 1
  • Crocidolite caused more micronuclei, breaks and aneuploidies than chrysotile
  • The authors inferred that smoking-related damage seems to involve other chromosomes as well. They based this on the smaller smoker vs non-smoker difference in the chromosome 1 FISH test than in the micronucleus test.
  • The authors described the micronucleus results as suggesting a close to additive effect of asbestos exposure in smokers' blood
• The authors' conclusion: The authors concluded three things. Asbestos damage mainly involves chromosome 1. Cigarette smoke damage seems to involve other chromosomes too. Prolonged smoking makes cells more sensitive and vulnerable to asbestos.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Chrysotile, Crocidolite.

Medical terms in this study, explained in our Lexicon: Genotoxicity, Fluorescence In Situ Hybridization (FISH), Micronuclei.

Related studies

• Reduction of chrysotile asbestos-induced genotoxicity in human peripheral blood lymphocytes by garlic extract — K. Bhattacharya, S. Yadava, et al. (2004)
• Diallylsulfide attenuates asbestos-induced genotoxicity — M. Lohani, S. Yadav, et al. (2003)
• Induction of micronuclei, hyperdiploidy and chromosomal breakage affecting the centric/pericentric regions of chromosomes 1 and 9 in human amniotic fluid cells after treatment with asbestos and ceramic fibers — E. Dopp, M. Schuler, et al. (1997)
• A study of the effect of chrysotile fiber surface composition on genotoxicity in vitro — M.J. Keane, J.W. Stephens, et al. (1999)
• The utility of the in vitro micronucleus test for evaluating the genotoxicity of natural and manmade nano-scale fibres — P. Fowler, A. Homan, et al. (2016)
• Chromosomal aberrations induced by chrysotile and crocidolite in human lymphocytes in vitro — F. Valerio, M. de Ferrari, et al. (1983)

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