Science Journal of Public Health
Volume 6, Issue 2, March 2018, Pages: 43-49
Received: Dec. 13, 2017;
Accepted: Jan. 12, 2018;
Published: Jan. 25, 2018
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Duangkamol Viroonudomphol, Faculty of Nursing, Siam University, Bangkok, Thailand
Pornpimon Poomrittikul, Faculty of Nursing, Siam University, Bangkok, Thailand
Tharntip Jirakanjana, Faculty of Nursing, Siam University, Bangkok, Thailand
Siriwan Tribanyatkul, Pramongkutklaw Hospital, Bangkok, Thailand
Saowanee Kanjanachumpon, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand
Disease risk due to smoking is not limited to smokers only. Passive smoking (exposure to environmental tobacco smoke) is associated with adverse health effect especially in cardiovascular disease. Side-stream cigarette smoke, a major component of secondhand smoke induces reactive oxygen species with promote oxidative stress. This paper summarizes the cardiovascular effects of tobacco smoke. According to the results of the alternative level of biochemistry substances, Cholesterol (C), HDL- Cholesterol (HDL-C), LDL-Cholesterol (LDL-C), Triglyceride (TG), Malondialdehyde (MDA), Conjugate diene (CD), vitamin B12, folate and Homocysteine (Hcy). The results showed that vitamin B12 and Hcy of smokers were significantly higher than those of non-smokers while C, LDL-C, TG and folate were significantly lower than those of non-smokers. More detail of smoking group, the industrial tobacco smokers had HDL-C and vitamin B12 lower than those in non-smokers whereas passive smokers and local handmade tobacco smokers had serum HDL-C and vitamin B12 higher than those in non-smokers. For serum C, LDL-C, TG and folate of all groups of smokers were significantly lower than non-smokers. The industrial tobacco smokers had serum MDA significantly higher than non-smokers but passive smokers and local handmade tobacco smokers had serum MDA lower than non-smokers. The industrial tobacco smokers and passive smokers had serum Hcy significantly higher than non-smokers but local handmade tobacco smokers had serum Hcy lower than non-smokers.
Homocysteine and Lipid Peroxidation in Active and Passive Smoking, Science Journal of Public Health.
Vol. 6, No. 2,
2018, pp. 43-49.
apps.who.int/gho/data/node.main.65 and United Nations. World Population prospects 1990. New York: United Nation; 1991, 226-31.
WHO report on the global tobacco epidemic (2013). Tobacco fact sheet No. 339 update July 2013, http://www.who.int/mediacentre/factsheets/fs339/en/.
World Bank. Development in practice-curbing the epidemic: governments and the economics of tobacco control. Washington DC. World Bank. 1999 pp. 32-3.
US Department of Health and Human Services. The health consequences of involuntary exposure to tobacco smoke: A report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2006. Available from http://www.cdc.gov/tobacco/data_statistics/sgr/sgr_2006/index/htm.
X. Lv, J. Sun, Y. Bi, et al., (2015) “Risk of all cause mortality and cardiovascular disease associated with secondhand smoke exposure: A systematic review and meta-analysis,” International Journal of Cardiology 199, 106-115. Available from http://www.ncbi.nlm.nih.gov/pubmed/15911719.
DS. Celemajor, MR. Adams, P. Clarkson et al., (1996) “Passive smoking and impaired endothelium-dependent arterial dilatation in healthy adults,” N Eng J Med 334, 150-154.
EJ. Neufeld, SM. Mietus, AS. Beiser, AL. Baker, JW. Newbuger, (1997) “Passive cigarette smoking and reduce HDL cholesterol levels in children with high-risk lipid profiles,” Circulation 96, 1403-1407.
SG. Kavita, GN. Meeta, MG. Priyada and Gonsa RN, (2013) “Effect of smoking on lipid profile,” JCRR 5, 36-42.
Y. He, B. Jiang, ZH. Wan, QS. Zheng and LS. Li, (2007) “Study on the relationship between passive smoking and blood lipid, fibrinogen and viscosity among women who never smoke,” Zhonghua Liu Xing Bing Xue Za Zhi 28,1167-1170.
DE. Wilcken, (2002) “Homocysteine, smoking and vascular disease,” Eur Heart J 23, 1559-1560.
R. Meenakshisundaram, C. Rajendiran and P. Thirumalai Kolunthu Subramanian, (2010) “Lipid and lipoprotein profiles among middle aged male smokers: a study from southern India,” Tobacco Induced Diseases 8, 11-15.
M. F. McCarty, (2000) “Increased homocyst (e) ine associated with smoking, chronic inflammation, and aging may reflect acute-phase induction of pyridoxal phosphatase activity,” Medical Hypotheses 55, 289-293.
K. Pagin, J. Hou, R. L. Goldenberg, S. P. Cliver, and T. Tamura, (2001) “Effect of smoking on serum concentrations of total homocysteine and B vitamins in mid-pregnancy,” Clinica Chimica Acta 306,103-9.
K. S. McCully, (1969) “Vascular pathology of homocysteinemia: Implications for the pathogenesis of arteriosclerosis,” The American Journal of pathology 56, 111-128.
M. Naruszenewicz, E. Mirkiewicz, A. J. Olszewski, and K. S. McCully, (1994) “Thiolation of low-density lipoprotein by homocysteine-thiolactone sauses increased aggregation and interaction with cultured macrophages,” Nutrition, Metabolism and Cardiovascular Disease 4, 70-77.
W. J. Vermaak, H. C. Barnard, G. M. Potgieter, and H. D. Theron, (1987) “Vitamin B6 and coronary artery disease. Epidemiological observations and case studies,” Atherosclerosis 63, 235-238.
K. Robinson, E. L. Mayer, D. P. Miller, et al., (1995) “Hyperhomocysteinemia and low pyridoxal phosphate. Common and independent reversible risk factors for coronary artery disease,” Circulation 92, 2825-2830.
R. L. Stedman, (1968) “The chemical composition of tobacco and tobacco smoke,” Chemistry Reviews 68, 53-207.
D. F. Church, and W. A. Pryor, (1985) “Free-radical chemistry of cigarette smoke and its toxicological implications,” Environmental Health Perspectives 64, 111-126.
Office of Environmental Health Hazard Assessment CEPA. (1997) “Health Effects of Exposure to Environmental Tobacco Smoke,” Final Draft for Scientific, Public and SRP Reviews 8, 71.
J. A. Buge, and S. D. Aust, (1978) “Microsomal lipid peroxidation,” Methods in Enzymology 52, 302-310.
R. B. Mansour, S. Lassoued, B. Gargouri, E. A. Gaid, and F. Fakkhfakh, (2008) “Increased levels of autoantibodies against catalase and superoxide dismutase associated with oxidative stress in patients with rheumatoid arthritis and systemic lupus erythematosus,” Scandinavian Journal of Rheumatology 37, 103-108.
J. S. Nosanchuk, J Chang, and Bennett, J. M. (1978) “The analytic basis for the use of platelet estimates from periperal blood smears. Laboratory and clinical applications” American Journal of Clinical Pathology. Apr; 69 (4), 383-387.
T. Katayama, Y. Iwasaki, N. Sakodam, and M. Yoshioka, (2008) “The etiology of ‘smoker’s paradox’ in acute myocardial infarction with special emphasis on the association with inflammation,” International Heart Journal 49, 13-24.
I. Kawachi, G. A. Colditz, F. E. Speizer, et al., (1997) “A prospective study of passive smoking and coronary heart disease” Circulation 95, 2374-2379.
H. Refsum, P. M. Ueland, O. Nygard, and S. E. Vollset, (1998) “Homocysteine and cardiovascular disease,” Annual Review of Medicine 49, 31-62.
C. A. Northrop-Clewes, and D. I. Thurnham, (2000) “Monitoring micronutrients in cigarette smokers,” Clinica Chimica Acta 377 (1-2), 14-38.
R. M. Ortega, A. M. Lopez-Sobaler, Gonzalez-Gross, M. Met al., (1994) “Influence of smoking of folate intake and blood folate concentration s in a group of elderly Spanish men,” The Journal of the American College of Nutrition 13, 68-72.
CJ., M. Piyathilake, Hine, R. J Richards, E. W. and Krumdieck, C. L. (1994). “Local and systemic effect” -566.
Sobczak, A (2003) “The effects of tobacco smoke on the homocysteine level a risk factor of atherosclerosis,” Addition Biology June 8,147-158.
M. Milman, and M. (1999) “Relationship between serum ferritin and risk factors for ischemic heart disease in 2235 Danes aged 30-60 years” The Journal of Internal Medicine 245 (5), 423-433.
S. Kim, H Shun, and C. Keen, (2003) “Influence of smoking on markers of oxidative stress and serum mineral concentrations in teenage girls in Korea,” Nutrition 19 (3), 240-243.
C. L. Relton, M. S. Pearce, and L. Parker, (2005) “The influence of erythrocyte folate and serum B12 status on birth weight” British Journal of Nutrition 93,593-599.
J. Selhub, P. F. Jacques, P. W. Wilson, D. and I. H. Rosenberg, (1993) “Vitamin status and intake as primary determinants of homocysteinemia in an elderly population” The Journal of the American Medical Association 270, 2693-2698.
C. I. Vardavas, M. K. Linardakis, C. M. Hatzis, N. Malliaraki, Malliaraki, W. H. and Kafatos, A. G., (2008) “Smoking status in relation to serum folate and dietary vitamin intake,” Tobacco Induced Diseases Sep 9, 4-8.
S. Voutilainen, T. H. Rissanen, J. Virtanen, T. A. Lakka, and Salonen, J. T., (2001) “Low dietary folate intake is associated with an excess incidence of acute coronary events,” the Kuopio Ischemic Heart Disease Risk Factor Study Circulation 103, 2674-2680.
P. Padrao, N. Lunet, A. C. Santos, and H. Barros, (2007) “Smoking, alcohol, and dietary choices: evidence from the Portuguese National Health Survey,” BMC Public Health. 7, 138.
R. M. Ortega, A. M. Requejo, et al., (2004) “Smoking and passive smoking as conditioners of folate status in young women” The Journal of the American College of Nutrition,” 365-371.
Clark. J. D., 3rd, J. D. W. G. LeBlanc, et al., (2008). “Inflammatory markers and secondhand tobacco smoke exposure among U. S. workers,” American Journal of Industrial Medicine 51, 626-632.