A research on effects of tobacco dust on status of total thiol in bidi industry workers


  • Nagesh A. Bhalshankar Department of Biochemistry, Maharashtra Institute of Medical Science and Research, Latur, Maharashtra, India
  • Suresh S. Ugle Department of Biochemistry, Maharashtra Institute of Medical Science and Research, Latur, Maharashtra, India




Bidi workers, Thiobarbituric acid reactive substances, Total thiol


Background: Bidi industries workers handle tobacco ingredients during rolling of bidi and inhale tobacco dust and volatile component are present in the work environment. Tobacco absorbed by the body in tremendous amount leading to preventable cause of disease, disability and including chronic obstructive pulmonary disease, cardiovascular, carcinomas, premature death exposure among bidi workers. The goal of this study was to occupational exposure of tobacco dust on status of total thiol level in bidi workers.

Methods: Healthy controls - 30 subjects and 90 bidi workers were further subdivided on the basis of work experience in years as, Group-I: 5-9 years (30 subjects), Group-II: 10-14 years (30 subjects), Group-III: 15-19 years (30 subjects). Authors are measure total thiol concentration and thiobarbituric acid reactive substances. All the biochemical parameters measured in study group subjects were statistically compared with those estimated in controls.

Results: Highly significant decrease in levels of total thiol was found in all groups of bidi workers as compared to healthy controls (p<0.001) and serum thiobarbituric acid reactive substances levels were significantly elevated in all groups of bidi workers when compared with healthy controls (p<0.001). The study groups indicates that decline the total thiol gradually progresses with increase in exposure period to tobacco dust.

Conclusions: The study groups showed that decrease the total thiol level and increases the thiobarbituric acid reactive substances in all groups of bidi workers compared with healthy controls.


IARC. Monographs on the evaluation of the carcinogenic risk of chemicals to humans: Tobacco habits other than smoking; betal-quid and area-nut chewing; and some related nitrosamines. 1985;37:205-8.

Cheriamane D. Beedi rolling-its impact on workers health. Eur Resp J. 2014;44(Suppl 58).

Mittal S, Mittal A, Rengappa R. Ocular manifestations in bidi industry workers: Possible consequences of occupational exposure to tobacco dust. Indian J Ophthalmol. 2008;56(4):319.

Singh JK, Rana SV, Mishra N. Occupational health problems amongst women beedi rollers in Jhansi, Bundelkhand Region, Uttar Pradesh. J Ecophysiol Occupa Health. 2014;14(1/2):17.

Bagwe AN, Bhisey RA. Occupational exposure to tobacco and resultant genotoxicity in bidi industry workers. Mutat Res. 1993;299(2):103-9.

Kjærgaard SK, Pedersen OF, Frydenberg M, Schønheyder H, Andersen P, Bonde GJ. Respiratory Disease and lung function in tobacco industry. Arch Environment Health May/June. An Int J. 1989;44(3):164-70.

Speziale M, Fornaciai G, Monechi MV. Tobacco manufacturer, environmental and health studies. Med Lav. 1994;85(2):149-56.

ACGIH. Industrial Ventilation. 22edn, American Conference of Governmental Industrial Hygienists, Industrial Ventilation committee, Cincinnati, USA; 2007.

Ellman GL. Tissue sulfhydryl groups. Arch Biochem Biophys. 1959;82:70-7.

Hu ML. Measure of protein thiol group and glutathione in plasma. Method Enzyme. 1994;233:380-5.

Satoh K. Serum lipid peroxide in cerebrovascular disorders determined by a new colorimetric method. Clinica Chimica Acta. 1978;90:37-43.

Suryakar AN, Katkam RV, Dhadke VN, Bhogade RB. A study of oxidative stress in bidi industry workers from Solapur city. Int J Med Sci (India). 2010;3(1/2):1-5.

Swami S, Suryakar AN, Katkam RV, Kumbar KM. Absorption of nicotine induces oxidative stress among bidi workers. Indian J Public Health. 2006;50(4):231-5.

Crystal RG. Oxidants and respiratory tract epithelial injury: Pathogenesis and strategies for therapeutic interventation. Am J Med. 1991;91(3C):395-445.

Henson PE, Johnson. Tissue injury in inflammation: Oxidants, proteinases and cationic proteins. J Clin Invest. 1987;79:669-74.

Mahimkar MB, Bhisey RA. Occupational exposure to bidi tobacco increase chromosomal aberrations in tobacco processors. Mutat Res. 1995;334(2):139-44.

Bagwe AN, Bhisey RA. Occupational exposure to unburnt bidi tobacco elevates mutagenic burden among tobacco processors. Carcinogenesis. 1995;16(5):1095-9.

Pruijn FB, Bast A. Effects of free radicals on hormonally and non-hormonally regulated calcium homeostasis in rat liver microsomes and hepatocytes. Adv Biosci. 1989;76:83-97.

Schraufstatter IU, Hyslop PA, Hinshaw DB, Spragg RG, Sklar LA, Cochrane CG. Hydrogen peroxide-induced injury of cells and its prevention by inhibitors of poly (ADP-ribose) polymerase. Proc Natl Acad Sci USA. 1986;83:4908-12.

Crompton M, Costi A, Hayat L. Evidence for the presence of reversible Ca2+ dependent pore activated by oxidative stress in heart mitochondria. Biochem J. 1987;245:915-8.

Rossi R, Cardaioli E, Scloni A, Amiconi G, Di Simplicio P. Thiols group in proteins as endogenousreductants to determine glutathione-protein mixed disulphides in biological system. Biochem Biophys Acta. 1995:1243:230-8.

Raut AM, Suryakar AN, Mhaisekar D. A study of oxidative stress, thiol proteins and role of vitamin E supplementation in chronic obstructive pulmonary disease (COPD). Al Ameen J Med Sci. 2013;6:134-7.






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