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SHORT COMMUNICATION
Year : 2012  |  Volume : 56  |  Issue : 1  |  Page : 57-60  

Risk for oral cancer associated to smoking, smokeless and oral dip products


1 Department of Public Health, School of Health, Hormozgan University of Medical Sciences, Bandarabbas, Iran
2 Department of Chemistry, University of Pune, Maharashtra, India
3 Department of Oncology, Morbai Naraindas Budhrani Cancer Institute, Inlaks and Budhrani Hospital, Pune, Maharashtra, India

Date of Web Publication6-Jun-2012

Correspondence Address:
Abdoul Hossain Madani
Department of Public Health, School of Health, Hormozgan University of Medical Sciences, Bandarabbas
Iran
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DOI: 10.4103/0019-557X.96977

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   Abstract 

Oral cancer is one of the most common life threatening diseases in India. Tobacco and alcohol are considered to be the most risk factors for oral cancer. This study was conducted to investigate the association of tobacco and poly-ingredient oral dip products with oral cancer. A case-control study of 350 cases and 350 controls, over a period of 19 months, between February 2005 and September 2006 was carried out in Pune, India. The self-reported information about the consumption of tobacco, poly-ingredient oral dip products, alcohol, dietary habits and demographic status were collected by a researcher made questionnaire. Univariate and multivariate analysis were used to identify the risk of substances abuse. The frequency of smoking, smokeless and oral dip products in cases were significantly higher than controls (P < 0.0001). Among smoking types, bidi (P < 0.0001, OR = 4.1 95% CI = 2.4 - 6.9), of smokeless types, chewing tobacco (P < 0.0001, OR = 8.3, 95% CI = 5.4 - 13.0) and mishiri (P < 0.0001, OR = 3.3, 95% CI =2.1 - 5.4), and of oral dip products, consumption of gutkha (P < 0.0001, OR = 12.8, 95% CI =7.0 - 23.7) and supari (P < 0.0001, OR = 6.6, 95% CI =3.0 - 14.8) indicated strong association with oral cancer upon adjustment. This study provides strong evidence that gutkha, supari -areca nut- chewing tobacco (tobacco flakes), bidi smoking and mishiri (tobacco powder, which applied as a tooth and gum cleaner) are independent risk for oral cancer.

Keywords: Tobacco, Oral dip products, Oral cancer


How to cite this article:
Madani AH, Dikshit M, Bhaduri D. Risk for oral cancer associated to smoking, smokeless and oral dip products. Indian J Public Health 2012;56:57-60

How to cite this URL:
Madani AH, Dikshit M, Bhaduri D. Risk for oral cancer associated to smoking, smokeless and oral dip products. Indian J Public Health [serial online] 2012 [cited 2014 Nov 1];56:57-60. Available from: http://www.ijph.in/text.asp?2012/56/1/57/96977

Whereas in most countries, cigarettes and water pipe smoking are the main form of tobacco use, [1],[2] in India, where oral cancer is a striking incidence, [3] only less than one-fifth (19%) of tobacco consumed is in the form of cigarettes. Over half of all tobacco consumed in India is smoked as bidi (Indian specific non-filtered cigarette) and about one-fourth of tobacco consumption is in smokeless form, such as chewing tobacco and mishiri (tooth cleaner applied tobacco). [4] Moreover, areca nut, seed of the fruit of the oriental palm Areca catechu, is common to use in India and other South Asian countries. The basic forms of areca nut usage can be classified as the traditional form and the recent form. In the traditional form, naturally crud areca nut is used, wrapped in leaves of Piper betel, with lime, saffron and additives such as catechu, cinnamon, cloves. This preparation is referred as betel quid or paan. Since 1970's and 80's, the areca nut industries, using traditional Indian technology, along with the tobacco industry has developed products similar to betel quid, ready for immediate consumption, packed in small, beautiful and convenient sachets. This product without tobacco is known as 'panmasala' while the product with tobacco is known as 'gutkha'. The other forms of areca nut include indigenous preparations like supari (a naturally crud areca nut without adding other ingredients). [5] There are several outstanding issues to be clarified, including the determination of which type of tobacco and which kind of oral dip substances are precisely associated with oral cancer. Moreover, what is the estimation of the magnitude of the effect of tobacco and poly-ingredient oral dip products on oral cancer? Thus, in this study, we investigated how tobacco and poly-ingredient oral dip products consumption was associated with the oral cancer.

The study design was a hospital-based case-control, conducted at Pune Cancer Institute, India. After obtaining the institutional ethics committee approval, a total of 700 age and gender grouping matched subjects, including 350 cases and 350 controls were selected using schedule sampling.

Cases were the newly diagnosed patients with cancer of oral cavity, aged above 18 years. To confirm the diagnosis, inclusion and exclusion criteria were implemented through physical and histopathological examination and classified by the standard International Classification of Diseases (ICD10) criterion. The controls were selected from the relatives, friends and caretakers of the cases, who were accompanied the patients at the hospital and were healthy and did not reportedly have cancer. A written consent forms were obtained from each participant and at the well-situated, a trained interviewer interviewed the case and control participants.

An investigator-made structured questionnaire was used to obtain complete information on demographical characteristics, tobacco and oral dipping- related behavioral features. Medical record was obtained from patients' record files, preserved in Morbai Naraindas Budhrani Cancer Institute.

The significance of difference between the proportions of qualitative characteristics is tested using Chi-square test of independence of attributes. The quantitative risk assessment was done by calculating the odds ratios (OR) with 95% confidence intervals. All the associations were adjusted for potential confounders such as, other tobacco types, oral dip products, alcohol, non-vegetarian habit, education, occupation, age and gender. The entire data were analyzed using a statistical package for social sciences (SPSS) version 13. In the first place, the variables were analyzed by univariate regression models. Finally, a multiple logistic regression model was obtained with the variables having statistical significance.

In general, overall smoking and smokeless tobacco as well as drinking alcohol, and non-vegetarian diet habit were significantly different between cases and controls (P = 0.001 for all, respectively). Smoking further categorized into 3 sub-types viz. filtered, non-filtered cigarette and bidi; the prevalence of all types were significantly different for cases compared to controls (P = 0.001 for all, respectively). Similarly, the oral dip products further categorized in to sub-types viz, chewing tobacco, mishiri, pan parag, gutkha, supari, and betel quid (paan); all except betel quid, (P = 0.112), and pan parag (P = 0.621), shown significantly difference by cases compared to controls [Table 1].
Table 1: Distribution of subjects by selected habits towards tobacco, alcohol and diet

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Univariate analysis revealed that, in terms of oral dipping products, the risk was 7.3 for consumption of gutkha (OR = 7.3; 95% CI, 4.5 - 12.1), 5.3 for consumption of chewing tobacco (OR = 5.3; 95% CI, 3.7 - 7.6) and 4 for consumption of supari (pure areca nut) (OR = 4.0; 95% CI, 2.1 - 7.8). However, the lower risk was found for mishiri (OR = 2.2; 95% CI, 1.5 - 3.1). In the case of smoking, only bidi smoking was significant risk (OR = 4.1; 95% CI, 2.4 - 6.9) [Table 2].
Table 2: Crude and adjusted odds ratios of tobacco and oral dip products

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Conversely, no significant risk of filtered cigarette and betel quid (paan) was found in this study.

Multivariate analysis model approved the risk of studied tobacco and oral dipping products after adjusting for possible confounders like alcohol, non-vegetarian habit, education, monthly household income, occupation, and other tobacco types (by adjusted OR). Hence, in this study, hierarchy of risk was gutkha (OR = 12.8; 7.0 - 23.7), chewing tobacco (OR = 8.3; 5.4 - 13.0), supari (OR = 6.6; 3.0 - 14.8), bidi (OR = 4.1; 2.4 - 6.9), mishiri (OR = 3.3; 2.1 - 5.4) [Table 2].

Comparing smoking with smokeless and other oral dipping products, it showed that smokeless tobacco users and oral dipping consumers were more at risk to develop oral cancer. This finding confirmed the previous results from India [6],[7] as well as in some case-control studies in other countries. [8],[9] Smokeless tobacco and poly-ingredient oral dipping products may have a stronger effect than smoking because of the direct contact of the ingredient carcinogens with the oral epithelium. However, the etiologic role of these factors is not well understood, and further methods for modifying them need to be developed.

It is very interesting to know that 112 out of 350 (32%) of cases used gutkha while only 21 out of 350 (6%) of controls used this substance with a maximum association of 12.8, in development of oral cancer. This result confirm prior findings that have shown gutkha as the strong risk for oral submucous fibrosis (OSMF) [10] compared to supari (crude areca nut) and other products . Betel quid (areca nut, tobacco, catechu and lime wrapped in betel leaf), approximately weighing 3.5 - 4 grams has 70 %moisture, and dry weight of areca nut and tobacco is only 1.14 grams, whereas the gutkha sachet, weighing 3.5 gram, has only 7% moisture and dry weight is 3.26 grams. [9] Since habitual chewers tend to consume more dry weight of areca nut and tobacco when they use gutkha, they probably develop more fibrosis of the oral mucosa, particularly the disorder, afflicting quite earlier as well.

In this study, a great risk of oral cancer was found in consumers chewing tobacco, which is used with or without lime and kept in the mouth for different duration of time, depending on the personal habits. Present study confirmed the previous findings that showed chewing tobacco as the strong risk factor for oral cancer. [6],[7]

Chewing of supari; pure areca nut, has also been implicated as one of the ingredients that can cause oral cancer. Van Wyck et al[11] have shown evidence on the carcinogenicity of areca nut, where 68% of South African Indians with cheek cancer are areca nut chewers, who do not smoke or drink. Similarly, there is a strong cause and effect relationship between areca nut chewing and oral submucous fibrosis in the South African and Indian studies. [11] Conversely, Stich reported that in Guam, where areca nut is chewed alone or with leaf only, there is apparently no increase in oral cancer. [12] It may be due to the procedure of preparing the product.

Smoking in general, appears to increase the risk of oral cancer, but similar to other studies in India, [6],[7] no association was found between filtered cigarette smoking and the risk of oral cancer . An increased risk of oral cancer amongst bidi smokers was observed compared to never bidi smokers, which corroborated the finding of earlier studies. [6],[7] It is possible because, firstly, the most prevalence type of smoking in the population was bidi. Secondly, it might also indicate the qualitative difference between bidi and cigarette smoking, due to the additional burning of the dried temburi leaf. Moreover, in India, bidi smoking being affordable to mass of population, is most common than cigarette smoking. These aspects may explain bidi being a factor for an increased risk of oral cancer in India.

In this study, no significant effect of betel quid was seen in association with oral cancer. It may be explained by the protective effects of betel leaf, main ingredient of betel quid, to the oral mucosa against the harmful alkaloids present in the areca nut in betel quid chewers, because betel leaf is known to be rich in beta-carotene, which have the capacity to quench free radicals that are toxic. [13]

Limitations of the study:Likely, the present study has faced overmatching because of selecting controls of relatives, friends and caretakers instead of population source. A combination of population-based and other control source like relatives, friends and caretakers might be a more appropriate approach to reduce the weakness of case-control study. Similar to the other case-control studies, main limitation of this study was recall bias. To minimize the recall bias, a well-situation was prepared for the participants and a trained interviewer asked them to first think about the year before, then to go back to further rear years. Moreover, using researcher-made questionnaire was a potential limitation of this study as well. Another limitation that should be mentioned is that the subjects were derived from a hospital and, therefore, may not approximate the relative risk for the general population. As cases and controls were not matched according to education / awareness, there was another limitation for present study.

In summary, the statistical data of this study provide strong evidence that oral dipping products could be in a straight line responsible for developing oral cancer. The hierarchy of importance of effects was related to gutkha, chewing tobacco, supari, bidi and mishiri, respectively. The public should be aware of the high risk of oral cancer, attributed to use above mentioned substances. Further studies are required in other parts of India to demonstrate the similar effects of these consumptions. There is a need for appropriate prevention and planning strategies for gutkha, supari and chewing tobacco consumption as well as for bidi smoking.

 
   References Top

1.Sedigheh-Sadat T, Teamur A, Shahram Z. Water pipe smoking and health-related quality of life: A population-based study. Arch Iran Med 2009;12:232-7.  Back to cited text no. 1
    
2.Hays RD, Smith AW, Reeve BB, Spritzer KL, Marcus SE, Clauser SB. Cigarette smoking and health-related quality of life in Medicare beneficiaries. Health Care Finance Rev 2008;29:57-67.  Back to cited text no. 2
    
3.Khandekar SP, Bagdey PS, Tiwari RR. Oral cancer and some epidemiological factors: A hospital based study. Indian J Community Med 2006;31:154-9.  Back to cited text no. 3
    
4.Panchamukhi PR, Woolery T, Nayantara SN. Economics of bidis in India. In: Gupta PC, Asma S, editors. Bidi Smoking and Public Health. Ministry of Health and Family Welfare, Government of India, 2008. p. 167-95.  Back to cited text no. 4
    
5.Rooban T, Elizabeth J, Anusa R, Girish KG. Health hazards of chewing areca nut and products containing areca nut. Calicut Med J 2005;3:e3.  Back to cited text no. 5
    
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7.Znaor A, Brennan P, Gajalakshmi V, Mathew A, Shanta V, Varghese C, et al. Independent and combined effects of tobacco smoking, chewing and alcohol drinking on the risk of oral, pharyngeal and esophageal cancers in Indian men. Int J Cancer 2003;105:681-6.   Back to cited text no. 7
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8.Bundgaard T, Wildt J, Frydenberg M, Elbrønd O, Nielsen JE. Case-control study of squamous cell cancer of the oral cavity in Denmark. Cancer Causes Control 1995;6:57-67.   Back to cited text no. 8
    
9.Macfarlane GJ, Zheng T, Marshall JR, Boffetta P, Niu S, Brasure J, et al. Alcohol, tobacco, diet and the risk of oral cancer: A pooled analysis of three case-control studies. Eur J Cancer 1995;31:181-7.   Back to cited text no. 9
    
10.Babu S, Bhat RV, Kumar PU, Sesikaran B, Rao KV, Aruna P, et al. A comparative clinico-pathological study of oral submucous fibrosis in habitual chewers of panmasala and betel quid. Clin Toxicol 1996;34:317-22.   Back to cited text no. 10
    
11.Van Wyck CW, Stander I, Padayachee A, Grobler-Rabie AF. The areca nut chewing habit and oral squamous cell carcinoma in South African Indians. S Afr Med J 1993;83:425-9.   Back to cited text no. 11
    
12.Stich HF, Rosin MP, Brunnermann KD. Oral lesions, genotoxicity and nitrosamines in betel quid chewers with no obvious increase in oral cancer risk. Cancer Lett 1986;31:15-25.  Back to cited text no. 12
    
13.Young SC, Wang CJ, Lin JJ, Peng PL, Hsu JL, Chou FP. Protection effect of piper betel leaf extract against carbon tetrachloride-induced liver fibrosis in rats. Arch Toxicol 2007;81:45-55.  Back to cited text no. 13
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    Tables

  [Table 1], [Table 2]


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