Carbon di-sulfide (CS2) induced chromosomal alterations and apoptosis in circulated blood lymphocytes of personnel working in viscose industry

Manikantan Pappuswamy, Rajkumar Sundrama, Karishankar K, Thirunavukkarasu P

Abstract


Circulated blood lymphocytes (PBL) of 41 workers occupationally exposed to Carbon di-sulfide (CS2) exposed from viscose industry were investigated to collect data on the effects and to find a possible relationship between in-vivo CS2 induced apoptosis and genotoxic effects. The subjects were divided into three groups: 41 subjects exposed to CS2 together with various confounding factors, another 41subjects inhabitants of Viscose industry partially exposed to CS2 in longperiods. The results were compared with 41 control subjects without known occupational exposure. Ambient air concentrations of CS2 were measured in different work places. Measures of genotoxicity included the determination of the frequencies of chromosomal aberrations (CA), sister-chromatid exchange (SCE), HPRT mutations (variant frequency, VF) and the measurement of UV-induced unscheduled DNA-repair synthesis (UDS). The percentages of premature centromere division (PCD) and of cells with a high frequency of SCE (HF/SCE) were also scored. Apoptosis and cell proliferation were determined by flow cytometry. In both CS2 exposed groups, the apoptotic activity and the CA levels in PBLs were significantly higher than in controls. The CA was mostly breaks of the chromatid type. In the second group, which was partially exposed to CS2, CA were slightly lower in comparison with group I fully exposed to CS2 and other confounding factors, which may be attributed to a different rate of elimination of damaged lymphocytes as a consequence of CS2 induced apoptotic activity. In conclusion, the results demonstrate that exposure to CS2 induces apoptosis and CA, indicating an excess cancer risk among subjects occupationally exposed to CS2. The results also emphasize the importance of the measurement of occupationally exposed pollutants, such as CS2, in order to avoid genotoxic effects in the workers also habit of cigarette smoking and alcohol consumption among the viscose workers had a synergistic effect on inducing cancer risk.


Full Text:

PDF (FULL TEXT)

References


Albertini R J, Anderson D, Douglas GR, et al (2000). IPCS guidelines for the monitoring of genotoxic effects of carcinogens in human. Mutat Res, 463(2), 111–172.

Bao Y S, Zheng Q, Jiang H (1996). Toxic effects of carbon disulfide on mouse oocytes (Abstract). Teratology, 53(2), 101-02.

Beauchamp RO, Bus JS, Popp JA, et al (1983). A critical review of the literature on carbon disulfide toxicity. Crit Rev Toxicol, 11(3), 169-278.

Bianchi V, Nuzzo F, Abbondandalo A, et al (1982). Scintillometric determination of DNA repair in human cell lines: a critical appraisal. Mutat Res 93, 447–463.

Biro A, Pallinger E, Major J, et al (2002). Lymphocyte phenotype analysis and chromosome aberration frequency of workers occupationally exposed to styrene, benzene, polycyclic aromatic hydrocarbons or mixed solvents. Immunol Lett 81, 133–140.

Carrano AV, Natarajan AT (1988). Considerations on population monitoring using cytogenetic techniques. Mutat Res, 204, 379–406.

Collins A, Dusinska M, Franklin M, et al (1997). Comet assay in human biomonitoring studies reliability, validation and applications. Environ Mol Mutagen 30, 139-46.

Countryman P, Heddle J (1976). The production of micronuclei from chromosome aberrations in irradiated cultures of human lymphocytes. Mutat Res, 41(2-3), 321-332.

Cox C, Hee SS, Tolos WP (1998). Biological monitoring of workers exposed to carbon disulfide. Am J Ind Med, 33(1), 48–54.

Daemen E, van Risseghem M, De Bacquer D, et al (1999). Preliminary external quality assessment for the biological monitoring of carbon disulfide with urinary 2- thiothiazolidine-4-carboxylic acid. Ann Occup Hyg, 43, 125-30.

Dusinska M, Collins AR (2008). The comet assay in human biomonitoring: gene–environment interactions. Mutagenesis, 23, 191-205.

Fairbairn DW, Olive PL, O’Neill KL (1995). The comet assay: a comprehensive review. Mutat Res, 33, 37-59.

Fielder RJ, Shillaker R O; (1981) Great Britain. Health and Safety Executive ; Great Britain. Health and Safety Commission, 1981. Advisory Committee on Toxic Substances. London : H.M.S.O. Toxicity review, 3.

Ghittori S, Maestri L, Contardi I, et al (1998). Biological monitoring of workers exposed to carbon disulfide (CS2) in a viscose rayon fibers factory. Am J Ind Med, 33(5), 478–84.

Guidotti TL, Hoffman H (1999). Indicators of cardiovascular risk among workers exposed to high intermittent levels of carbon disulphide. Occup Med (Lond) 49, 507-511.

Hagmar L, Brøgger A, Hansteen IL, et al (1994). Cancer risk in humans predicted by increased levels of chromosomal aberrations in lymphocytes: Nordic study group on the health risk of chromosome damage. Cancer Res, 54, 2919-22.

Hoffman P, Klapperstuck M (1990). Effects of carbon disulfide on cardiovascular function after acute and subacute exposure of rats. Biomed Biochem Acta, 49, 121-8.

Huang CC, Chu CC, Wu TN, et al (2002). Clinical course in patients with chronic carbon disulfide polyneuropathy. Clin Neurol and Neurosur, 104(2), 115–20.

Izmerov NF (1983). Carbon disulfide. Moscow, Centre of International Projects (GKNT), Scientific reviews of Soviet literature on toxicity and hazards of chemicals, No. 41.

Jakab MG, Major J, Tompa A (1996). HPRT mutation frequencies in control human populations in Hungary. Occup and Environ Med, 2, 317-328.

Keil DE, Padgett EL, Barnes D.B, et al (1996). Role of decomposition products in sodium methyldithiocarbamate-induced immunotoxicity. J Toxicol Env Health, 47, 479–492.

Korinth G, Goen T, Ulm K, et al (2003). Cardiovascular function of workers exposed to carbon disulphide. Int Arch Occup Env Health, 76(1), 81–85.

Lancranjan I, Popescu HI, Klepsch I (1969). Changes of the gonadic function in chronic carbon disulfide poisoning. Med Lav, 60, 556-71.

Le JY, Fu XM (1996). Human sperm chromosome analysis study on human sperm chromosome mutagenesis induced by carbon disulfide. Biomed Environ Sci, 9: 37-40.

Liss G, Finkelstein M (1996). Mortality among workers ex-posed to carbon disulfide. Archive Environ Health, 51, 193-200.

Major J, Jakab MG, Tompa A (1996). Genotoxicological investigation of hospital nurses occupationally exposed to ethylene-oxide: I. Chromosome aberrations, sister-chromatid exchanges, cell cycle kinetics, and UV-induced DNA synthesis in peripheral blood lymphocytes. Environ Mol Mutagen, 27, 84–92.

Manikantan P, BalachandarV, Sasikala K, et al (2009). DNA damage in viscose factory workers occupationally exposed to carbon di-sulfide using buccal cell comet assay. Braz J Oral Sci, 8 (4), 197-200.

Marzin D (1999). New approaches to estimating the mutagenic potential of chemicals. Cell Biol Toxicol, 15, 359-365.

Medeiros MG, Rodrigues AS, Batoreu MC (2003). Elevated levels of DNA–protein cross links and micronuclei in peripheral lymphocytes of tannery workers exposed to trivalent chromium. Mutagenesis, 18,19–24.

Mehes K, Bajnoczky K (1981). Non-random centromere division: analysis of G-banded human chromosomes. Acta Biologica Hungarica, 32, 55–59.

Moller P (2006). The alkaline Comet assay: towards validation in biomonitoring of DNA damaging exposures. Clin Pharmacol Toxicol, 98, 336-45.

Moorhead PS, Nowell PC, Mellman WJ, (1960). Chromosome preparation of leukocytes cultured from human peripheral blood. Exp Cell Res, 20, 613–616.

Nishiwaki Y, Takebayashi T, O’Uch T, et al (2004). Six-year observational cohort study of the effect of carbon disulphide on brain MRI in rayon manufacturing workers. J Occup Env Med, 61, 225-32.

Perry P, Wolff S (1974). New Giemsa method for the differential staining of sister chromatids. Nature, 251, 156–158.

Poirier MC (1997). DNA adducts as exposure biomarkers and indicators of cancer risk. Environ Health Persp, 105 (Suppl. 4), 907-12.

Rojas E, Valverde M, Sordo, et al (1996). DNA damage in exfoliated buccal cells of smokers assessed by the single cell gel electrophoresis assay. Mutat Res, 370, 115-20.

Ruijten M, Sallé HJA, Verbrek MM, et al (1990). Special nerve functions and colour discrimination in workers with long-term low-level exposure to carbon disulphide. Br J Ind Med, 47, 589-595.

Ruijten M W M M, Sallé H J A, Verbek M M (1993). Verification of effects on the nervous system of low level occupational exposure to CS2. Br J Ind Med, 50, 301- 307.

Sills RC, Harry GJ, Valentine W, et al (2005). Interdisciplinary neurotoxicity inhalation studies: carbon disulfide and carbonyl sulfide research in F344 rats. Environ Toxicol Pharmacol, 207 (2 suppl): 245-50.

Strauss GH, Albertini RJ (1979). Enumeration of 6-thioguanine-resistant peripheral blood lymphocytes in man as a potential test for somatic cell mutations arising in vivo. Mutat Res, 61, 353–379.

Struwe W, Sprinzl G (1984). Transmission von H2S und CS2 (Transmission of H2S and CS2). Vienna, Ősterreichisches Bundesinstitut für Gesundheitswesen.

Sulsky SI, Hooven FH, Burch MT, (2002). Critical review of the epidemiological literature on the potential cardiovascular effects of occupational carbon disulfide exposure. ‎Int Arch Occup Envi 75, 365-80.

Swaen GM, Braun C, Slangen JJ (1994). Mortality of Dutch workers exposed to carbon disulfide. Int Arch Occup Envi, 66,103-10.

Tan Xiaodong, Chen Guanmin, Peng Xiaoxia, et al (2004). Cross-Sectional Study of Cardiovascular Effects of Carbon Disulfide Among Chinese Workers of a Viscose Factory. Int J Hyg Environ Health, 206, 217–25.

Tang GH, Xuan DF (2003). Detection of DNA damage induced by carbon disulfide in mice sperm with single-cell gel electrophoresis assay. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi, 21(6), 440-3.

Tates AD, Grummt T, Tornquist M, et al (1991). Biological and chemical monitoring of occupational exposure to ethylene oxide. Mutat Res, 250, 483–487.

Tompa A, Sapi E (1989). Detection of 6-thioguanine resistance in human peripheral blood lymphocytes (PBL) of industrial workers and lung cancer patients. Mutat Res, 210, 345-351.

Tsai CH, Lee WJ, Chen CY, (2002). Formation of Solid Sulfur by Decomposition of Carbon Disulfide in the Oxygen-Lean Cold Plasma Environment. Ind Eng Chem Res, 41, 1412-1418.

Valverde M, del Carmen López M, López I, et al (1998). DNA damage in leukocytes and buccal and nasal epithelial cells of individuals exposed to air pollution in Mexico City. Environ Mol Mutagen 30, 147-52.

Van Er PEJ, Brons PPT, Boezeman JBM, et al (1988). A rapid flow cytometeric method for bivariate bromodeoxyuridine/DNA analysis using simultaneous proteolytic enzyme digestion and acid denaturation. Cytometry, 9, 627–630.

Vanhoorne M, Comhaire F, De Bacquer D (1994). Epidemiological study of the effects of carbon disulfide on male sexuality and reproduction. Arch Environ Health, 49(4), 273–78.

Wang Q, Fu K, Wu Q (1999). Effects on fertility and menstrual cycle of female workers exposed to carbon disulfide. Chinese J Pub Health, 15, 215-7.

Wang YF, Shiu YF (2000). Investigation on eye injury of workers exposed to CS2. J Lab Clin Med, 17, 89.




DOI (PDF (FULL TEXT)): http://dx.doi.org/10.22034/APJCB.2018.3.1.11

Refbacks

  • There are currently no refbacks.


Copyright (c) 2017 Asian Pacific Journal of Cancer Biology

Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.


 

  

PORTICO

 

Asia Pacific Organization for Cancer Prevention 

West Asia Organization for Cancer Prevention