3.32 Health effects of smoking other substances

Last updated: March 2015

Suggested citation: Bellew, B, Greenhalgh, EM & Winstanley, MH. 3.32 Health effects of smoking other substances. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-32-health-effects-of-smoking-other-substances

 

This section is not intended to provide a comprehensive overview of drug use other than tobacco, but to demonstrate that the deliberate inhalation of smoke from the combustion of any matter is injurious to the health. The health effects of smoking any substance will depend on various factors, including the age at which smoking commences, the duration for which the body is exposed to the smoke, and the concentration and nature of constituents of the material smoked.

The scientific literature describing the health effects of smoking tobacco is comprehensive but the same cannot generally be said of other smoked substances, particularly where use is illegal. For example, in the case of marijuana, its illegality has militated against broad-based population studies, although data gathering has improved with its growing public acceptance (see Chapter 1, Section 1.10). Lack of adequate funding for medical and epidemiological research is a factor in some countries where smoking of substances other than tobacco may be more widespread. Another reason that these other forms of smoking have been under-researched is that the relatively small numbers of users and the scattered pattern of their geographical distribution make systematic study more challenging. Despite these issues the evidence base is sufficient to allow important conclusions on the adverse health effects of smoking these other substances on their own or in various combinations with tobacco. Here we cover the findings with regard to the smoking of herbal and other non-tobacco cigarettes, cannabis, kreteks and bidis.

3.32.1 Herbal and other non-tobacco cigarettes

Herbal and other non-tobacco cigarettes may erroneously be considered as a safer alternative to smoking, or an aid to quitting smoking, and are actively promoted as such by some manufacturers.1 However, even cigarettes that do not contain tobacco or nicotine may still produce toxic substances including carcinogens. Recent research has examined DNA damage response arising from exposure of human lung cells to smoke from tobacco- and nicotine-free cigarettes (made from lettuce and herbal extracts). This exposure led to formation of double-strand DNA breaks that are potentially carcinogenic; there was a dose–response relationship between exposure to the smoke and the severity of ensuing DNA damage response. The study concluded that smoking tobacco and nicotine-free cigarettes is at least as hazardous as smoking cigarettes containing tobacco and nicotine.2

A 2009 study conducted in China tested the claim by the tobacco industry in that country that herbal cigarettes are less harmful than regular cigarettes. Four discriminating biomarkers were analysed from urine samples provided by 135 herbal cigarette smokers and 143 regular smokers. Importantly, the researchers found a concern about their health to be one of the main reasons that smokers switched from regular to herbal cigarettes and they reported increased consumption after doing so. The researchers found no significant difference in the levels of the four biomarkers between smokers of herbal cigarettes and smokers of regular cigarettes, concluding that herbal cigarettes did not deliver less carcinogens than regular cigarettes and that the Chinese tobacco industry should avoid misleading the public by promoting herbal cigarettes as safer products.3 An analysis of 'vegetable-based cigarettes' manufactured in France and sold in Austria were found to yield levels of carbon monoxide at least as high as those produced by conventional cigarettes. Analysis of other constituents of the smoke was not made, although initial studies had shown that combustion may have produced carcinogens and other noxious chemicals.4 Investigations of a different brand of 'non-nicotine, non-tar' herbal cigarettes popular in the Philippines has also shown significant yields of tar and carbon monoxide.5 Smokers attempting to use herbal cigarettes as an adjunct to quitting are therefore exposing themselves to dangerous tar and carbon monoxide levels, without actually increasing their chance of quitting.

Cigarettes combining herbs and tobacco have been produced in China since 1959, and they are now manufactured in South Korea, Taiwan and Thailand.6 These cigarettes are commonly promoted with messages implying that they are aids in quitting, are less harmful than conventional cigarettes, or with claims for active health benefits such as raising immunity or protecting the kidneys. There is no reliable published literature to support any health claims for herbal-tobacco cigarettes,6 and at least one report (from the tobacco industry) has indicated that the tar and nicotine level of Chinese herbal-tobacco cigarettes is very high.7

3.32.2 Cannabis (marijuana, hash, ganja)

The main forms of cannabis are marijuana, hashish and hashish oil. Marijuana comprises the dried leaves, flowering tops and stems of the hemp plant Cannabis sativa. The more concentrated resin from the flowers is called hashish. Cannabis is usually smoked as a cigarette (joint) or in a pipe (bong).8 The substance in cannabis that causes the user to experience a 'high' is THC (tetrahydrocannabinol), which binds to receptors in the brain. Recent studies have reported the emergence of synthetic cannabinoids; these compounds are more potent than traditional cannabis and have been widely used to deliver products with psychoactive properties while circumventing drug legislation. As a result, authorities around the world are now beginning to exert control by either naming individual compounds or using generic legislation.9 Some early research indicates that synthetic forms of cannabis may be more likely to provoke psychosis in vulnerable individuals.10

Cannabis is the most frequently used illegal drug in Australia, with data published by the Australian Institute of Health and Welfare in 2011 indicating that about 1.9 million people had used the drug in a 12-month period. Between 2007 and 2010 the proportion of people in Australia who had used cannabis in the previous 12 months increased from 9.1% to 10.3%; among cannabis users, 20.9% said they used it once a week or more. More than half of people in Australia aged 30–39 years had used cannabis at some time in their lives, a proportion that was higher than in any other age group and was similar for both males and females. The highest proportion of males who had used cannabis in the last 12 months was for those aged 20–29 years (25%), and for females for those aged 18–19 years (19.3%). Fewer than 1 in 10 (8.8%) teenagers aged 12–17 years had used cannabis in the previous 12 months, but this proportion more than doubled to 1 in 5 (21.3%) among those aged 18–29 years.11 Continued use may lead to both physical and behavioural addiction, especially among regular, heavy users, and those who start using the substance at an earlier age.12

A comprehensive review of the adverse effects of cannabis use was recently undertaken.13 The authors of the review concluded that the effects of cannabis are dose dependent; adverse effects most frequently reported in the literature are mental slowness, impaired reaction times, and accentuation of anxiety. Users can feel dependent on cannabis, but this dependence is usually psychological. Withdrawal symptoms tend to occur within 48 hours following cessation of regular cannabis use, and include increased irritability, anxiety, nervousness, restlessness, sleep difficulties and aggression. Symptoms subside within two to 12 weeks. Serious psychological disorders have been reported with high levels of intoxication. The relationship between poor school performance and early, regular and frequent cannabis use seems to be a vicious circle, in which each sustains the other. Many research studies have examined the possible long-term effects of cannabis on memory, but results to date are inconclusive. Longitudinal studies of the influence of cannabis on depressive thoughts or suicidal ideation have yielded conflicting results and are also inconclusive. Several longitudinal studies have shown a statistical association between psychotic illness and self-reported cannabis use, but methodological problems (particularly the unknown reliability of self-reported data) make it difficult to draw definitive conclusions about causation. Therefore the question as to whether cannabis use causes psychosis cannot yet be answered conclusively because of the limitations in the current evidence.13 This latter finding is supported by another robust review of cohort studies into cannabis and psychosis, conducted by McLaren and colleagues.14 Consistent with these study findings, a 2009 systematic review by Le Bec and colleagues noted that cannabis use may be an independent risk factor for the development of psychotic disorders, with the level of risk increasing by an estimated factor of 1.2–2.8.15 Hall and Degenhardt's review, published in The Lancet in 2009, is also consistent with the studies cited above; with a focus on adverse health effects of greatest potential public health impact (those most likely to occur and to affect a large number of cannabis users) these researchers concluded that the most probable adverse effects were: (i) a dependence syndrome, (ii) increased risk of motor vehicle crashes, (iii) impaired respiratory function, (iv) cardiovascular disease, and (v) adverse effects of regular use on adolescent psychosocial development and mental health.16 Studies have concluded that the provision of advice to vulnerable individuals that cannabis may cause acute psychotic effects (especially at high doses) is appropriate.13, 15 There is evidence supporting an association between cannabis use and the development of major depression, anxiety and panic disorders.12 Cannabis use is linked to a 50% increased risk of a later depression spell (age ≥17 years) from early-onset use of cannabis (age <17 years).17 Recent Australian Institute of Health and Welfare population surveillance data provide corroborative support for these findings, noting the apparent relationship between a person's cannabis use and his or her mental health. For people in Australia aged 18 years or older, those who had reported using cannabis in the previous 12 months (18.7%) or in the previous month (20.5%) were more likely to have been diagnosed or treated for a mental illness than people who had not used it in the previous 12 month (11.3%); those who had used cannabis in the previous month (19.1%) or previous 12 months (16.3%) were more likely to report high or very high levels of psychological distress compared with those who had not recently used cannabis (9.1%).11

A systematic review conducted to assess risk of cannabis-related mortality examined the scientific literature published between 1990 and 2008; it found that evidence published to date is insufficient to assess whether the all-cause mortality rate is elevated among cannabis users in the general population. Nonetheless, case–control study evidence does suggest that some adverse health outcomes may be elevated among heavy cannabis users, namely, fatal motor vehicle accidents, and possibly respiratory and brain cancers. The evidence as to whether regular cannabis use increases the risk of suicide is unclear.18 There is evidence that babies born to women who have smoked marijuana during pregnancy have a greater probability of experiencing developmental problems, evident from early schooling through to adolescence12 and that prenatal exposure may have long-term effects, specifically on attentional skills.19

Mixing tobacco with cannabis elevates the amount of THC administered while smoking; a recent study found that tobacco increases the amount of THC inhaled per gram of cannabis from 32.70 +/– 2.29 mg/g for a 100% cannabis cigarette to 58.90 +/– 2.30 mg/g for a 25% cannabis cigarette. This indicates that tobacco increases the vaporisation efficiency of THC by as much as 45%.20 Recent laboratory studies have compared mainstream and sidestream cannabis and tobacco smoke condensates for their genotoxicity (level of damage or mutation caused to DNA). The cannabis condensates were all found to be more toxic to cells and more mutagenic than the matched tobacco condensates. For tobacco, the resulting genetic damage appeared to be dose dependent, whereas for marijuana it did not.21 Cannabis smoke contains a higher concentration of carcinogens than tobacco smoke, and because of a user's tendency to inhale deeply and hold the smoke in for longer, exposure of the lung and airways to toxic chemicals may be far greater per joint of cannabis than per typical tobacco cigarette.8, 22. Long-term, heavy users of cannabis show a higher frequency of inflammatory and pre-cancerous changes to the bronchial tubes than non-users. A recent review of the evidence concludes that there are good grounds for believing that chronic smoking of cannabis carries a significant risk of cancer.12 There is some evidence of a possible link between cannabis use and testicular cancer; in a hospital-based case–control study, patients with nonseminoma (testicular germ cell cancer) were three times more likely than controls to be frequent cannabis users (OR 3.1; 95% CI, 1.2–8.2).23 Recent research examining the possible link between cannabis use and head and neck cancers did not rule out completely the possibility of moderately increased risk; however large increases in risk levels for these specific cancers have not as yet been detected.24

Cannabis use has been linked to the development of cardiovascular symptoms, particularly in the predisposed.12 Smoking cannabis has a significant impact on lung structure and function; it causes airflow obstruction, impaired large airways function and hyperinflation (overexpansion of the lungs due to reduced elasticity), the effects worsening as the amount smoked increases. Research has shown one joint of cannabis to be equivalent to between 2.5 and 5 tobacco cigarettes in terms of airflow obstruction, probably for the most part due to differences in the way cannabis is smoked (deeper and longer inhalations), as well as the fact that a joint is generally smoked without a filter and down to a smaller butt length, and that the smoke is generated at a higher temperature.22 Cannabis smokers also experience respiratory symptoms including wheezing, coughing, phlegm production and chest tightness.22 Over the longer term, using both cannabis and tobacco has an additive effect on respiratory symptoms and lung function. This means that in users of both substances, respiratory symptoms are increased and lung function is worsened to a greater extent than if just one of the two drugs is used.25 A recent study found that concurrent use of cannabis and tobacco was associated with a two-fold risk of respiratory symptoms (OR 2.39; 95% CI, 1.58–3.62) and an almost three-fold risk of chronic obstructive pulmonary disease (OR 2.90; 95% CI, 1.53–5.51) if the lifetime dose exceeded 50 cannabis cigarettes. The research concluded that these increased risks of respiratory symptoms and of chronic obstructive pulmonary disease were related to a synergistic interaction between cannabis and tobacco.26

3.32.3 Bidis (beedis, beedies, biris)

Bidis are small, thin, hand-rolled cigarettes consisting of sun-dried and cured tobacco flakes rolled up in a piece of dried tendu or temburni leaf (from plants native to Asia). They may be flavoured with a variety of sweet or fruit essences (e.g. chocolate, cherry and mango) or unflavoured, and are secured at either end with colourful threads.36 Bidi use is most prevalent in India, Bangladesh, Nepal, Sri Lanka, Pakistan and the Maldives.37, 38 Up to 56% of men in South Asian countries smoke bidis.39 Smoke from a bidi contains 3–5 times the amount of nicotine as a regular cigarette and places users at risk for nicotine addiction.40 The compounds added to provide flavouring (such as clove, cinnamon, vanilla, cardamom, strawberry, mango, grape, lemon-lime and chocolate) are also present in high levels and may contribute to long-term damage to health, particularly in the case of cloves.41 Bidi smoking increases the risk of oral cancer,42-44 lung cancer,45-47 stomach cancer, and oesophageal cancer;39,48 is associated with a more than three-fold increased risk for coronary heart disease and acute myocardial infarction (heart attack);39, 49 is associated with a nearly four-fold increased risk for chronic bronchitis;39 and is also associated with emphysema.50 Bidi use in pregnancy is associated with perinatal mortality.51 Tobacco factory employees who hand-roll bidis are chronically exposed to potentially toxic levels of tobacco via inhalation of dust and flakes, and through the skin.39

Bidis are smoked by 2.4% of high school and 1.6% of middle school students in the US.35 Consumption patterns in Australia are not known.

Recent news and research

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References

1. Honeyrose Products. Corporate website. Ipswich, UK: Honeyrose Products, 2007 viewed 20 June 2007. Available from: http://www.honeyrose.co.uk/index.html

2. Jorgensen ED, Zhao H, Traganos F, Albino AP and Darzynkiewicz Z. DNA damage response induced by exposure of human lung adenocarcinoma cells to smoke from tobacco- and nicotine-free cigarettes. Cell Cycle 2010;9(11):2170-6. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20404482

3. Gan Q, Yang J, Yang G, Goniewicz M, Benowitz N and Glantz S. Chinese 'herbal' cigarettes are as carcinogenic and addictive as regular cigarettes. Cancer Epidemiology, Biomarkers & Prevention 2009;18(12):3497–501. Available from: http://cebp.aacrjournals.org/content/18/12/3497.long

4. Groman E, Bernhard G, Blauensteiner D and Kunze U. A harmful aid to stopping smoking Letter. The Lancet 1999;353:466-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/9989723

5. Calafat AM, Polzin GM, Saylor J, Richter P, Ashley DL and Watson CH. Determination of tar, nicotine, and carbon monoxide yields in the mainstream smoke of selected international cigarettes. Tobacco Control 2004;13:45-51. Available from: http://tc.bmj.com/cgi/content/abstract/13/1/45

6. Chen A, Glantz SA and Tong E. Asian herbal-tobacco cigarettes: 'not medicine but less harmful'? Tobacco Control 2007;16:e3. Available from: http://tobaccocontrol.bmj.com/cgi/reprint/16/2/e3.pdf

7. Zimmerman C. Herbal cigarettes: blending ancient Chinese medicine. Tobacco Reporter 1991;March:29.

8. National Institute on Drug Abuse. NIDA Infofacts. Marijuana. Rockville, Maryland: US Department of Health and Human Services, 2006. Available from: http://www.drugabuse.gov/infofacts/marijuana.html

9. Hudson S and Ramsey J. The emergence and analysis of synthetic cannabinoids. Drug Testing and Analysis 2011;3(7-8):466-78. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21337724

10. Every-Palmer S. Synthetic cannabinoid JWH-018 and psychosis: an explorative study. Drug and Alcohol Dependence 2011;Epub ahead of print. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21316162

11. Australian Institute of Health and Welfare. 2010 National Drug Strategy Household Survey report. Drug statistics series no. 25, cat. no. PHE 145. Canberra: AIHW, 2011. Available from: http://www.aihw.gov.au/WorkArea/DownloadAsset.aspx?id=10737419578&libID=10737419577

12. Kalant H. Adverse effects of cannabis on health: an update of the literature since 1996. Progress in Neuro-psychopharmacology & Biological Psychiatry 2004;28(5):849–63. Available from: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TBR-4CY0JSM-2&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=95a842fef02272cc8b862ad11cc89cb8

13. Adverse effects of cannabis; inform psychologically vulnerable patients of the risk of serious, dose-dependent disorders. Prescrire International 2011;20(112):18-23. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21462790

14. McLaren JA, Silins E, Hutchinson D, Mattick RP and Hall W. Assessing evidence for a causal link between cannabis and psychosis: a review of cohort studies. International Journal on Drug Policy 2010;21(1):10-19. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19783132

15. Le Bec PY, Fatseas M, Denis C, Lavie E and Auriacombe M. Cannabis and psychosis: search of a causal link through a critical and systematic review. L'Encephale 2009;35(4):377-85. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19748375

16. Hall W and Degenhardt L. Adverse health effects of non-medical cannabis use. The Lancet 2009;374(9698):1383-91. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19837255

17. de Graaf R, Radovanovic M, van Laar M, Fairman B, Degenhardt L, Aguilar-Gaxiola S, et al. Early cannabis use and estimated risk of later onset of depression spells: epidemiologic evidence from the population-based World Health Organization World Mental Health Survey Initiative. American Journal of Epidemiology 2010;172(2):149-59. Available from: http://aje.oxfordjournals.org/content/172/2/149.long

18. Calabria B, Degenhardt L, Hall W and Lynskey M. Does cannabis use increase the risk of death? Systematic review of epidemiological evidence on adverse effects of cannabis use. Drug and Alcohol Review 2010;29(3):318-30. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20565525

19. Williams JH and Ross L. Consequences of prenatal toxin exposure for mental health in children and adolescents: a systematic review. European Child & Adolescent Psychiatry 2007;16(4):243-53. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17200791

20. Van der Kooy F, Pomahacova B and Verpoorte R. Cannabis smoke condensate II: influence of tobacco on tetrahydrocannabinol levels. Inhalation Toxicology 2009;21(2):87–90. Available from: http://informahealthcare.com/doi/full/10.1080/08958370802187296

21. Maertens RM, White PA, Rickert W, Levasseur G, Douglas GR, Bellier PV, et al. The genotoxicity of mainstream and sidestream marijuana and tobacco smoke condensates. Chemical Research in Toxicology 2009;22(8):1406–14. Available from: http://pubs.acs.org/doi/abs/10.1021/tx9000286

22. Aldington S, Williams M, Nowitz M, Weatherall M, Pritchard A, McNaughton A, et al. The effects of cannabis on pulmonary structure, function and symptoms. Thorax 2007;62:1058-63. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17666437

23. Trabert B, Sigurdson AJ, Sweeney AM, Strom SS and McGlynn KA. Marijuana use and testicular germ cell tumors. Cancer 2011;117(4):848-53. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20925043

24. Berthiller J, Lee Y, Boffetta P, Wei Q, Sturgis E, Greenland S, et al. Marijuana smoking and the risk of head and neck cancer: pooled analysis in the INHANCE Consortium. Cancer Epidemiology, Biomarkers & Prevention 2009;18(5):1544–51. Available from: http://cebp.aacrjournals.org/cgi/content/full/18/5/1544

25. Taylor D and Hall W. Respiratory health effects of cannabis: position statement of the Thoracic Society of Australia and New Zealand. International Medical Journal 2003;33:310-13. Available from: http://www.thoracic.org.au/cannabispositionpaper.pdf

26. Tan W, Lo C, Jong A, Xing L, Fitzgerald M, Vollmer W, et al. Marijuana and chronic obstructive lung disease: a population-based study. Canadian Medical Association Journal 2009;180(8):814–20. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2665947/?tool=pubmed

27. Lawrence S and Collin J. Competing with kreteks: transnational tobacco companies, globalisation, and Indonesia. Tobacco Control 2004;13(suppl. 2):ii96-ii103. Available from: http://tobaccocontrol.bmj.com/cgi/reprint/13/suppl_2/ii96

28. Malson J, Lee E, Murty R, Moolchan E and Pickworth W. Clove cigarette smoking: biochemical, physiological, and subjective effects. Pharmacology, Biochemistry and Behavior 2003;74:739-45 Available from: http://www.ncbi.nlm.nih.gov/pubmed/12543240

29. Stanfill SB, Brown CR, Yan XJ, Watson CH and Ashley DL. Quantification of flavor-related compounds in the unburned contents of bidi and clove cigarettes. Journal of Agriculture and Food Chemistry 2006;54(22):8580-8. Available from: http://pubs.acs.org/doi/abs/10.1021/jf060733o

30. Polzin GM, Stanfill SB, Brown CR, Ashley DL and Watson CH. Determination of eugenol, anethole, and coumarin in the mainstream cigarette smoke of Indonesian clove cigarettes. Food and Chemistry Toxicology 2007;45(10):1948-53. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17583404

31. Guidotti TL, Laing L and Prakash UB. Clove cigarettes. The basis for concern regarding health effects. Western Journal of Medicine 1989;151(2):220-8. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1026937/pdf/westjmed00120-0106.pdf

32. Mangunnegoro H and Sutoyo D. Environmental and occupational lung diseases in Indonesia. Respirology 1996;1:85-93. Available from: http://www.ncbi.nlm.nih.gov/pubmed/9434323

33. American Medical Association Council on Scientific Affairs. Council report: evaluation of the health hazard of clove cigarettes. Journal of the American Medical Association 1988;260:3641-4. Available from: http://www.ncbi.nlm.nih.gov/pubmed/3057254

34. Soetiarto F. The relationship between habitual clove cigarette smoking and a specific pattern of dental decay in male bus drivers in Jakarta, Indonesia. Caries Research 1999;33(3):248-50. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10207202

35. Centers for Disease Control and Prevention. Tobacco Use Among Middle and High School Students–United States, 2000–2009. Morbidity and Mortality Weekly Report 2010;59(33):1063-8. Available from: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5933a2.htm

36. Centers for Disease Control and Prevention. Bidis and kreteks. Factsheet. Atlanta, Georgia: Office on Smoking and Health, CDCP, 2011 viewed 29 July 2011. Available from: http://www.cdc.gov/tobacco/data_statistics/fact_sheets/tobacco_industry/bidis_kreteks/index.htm

37. Shafey O, Dolwick S and Guindon G. Tobacco control country profiles. Atlanta, Georgia: American Cancer Society, World Health Organization, International Union Against Cancer, 2003. Available from: http://www.cancer.org/docroot/PRO/content/PRO_1_1_Tobacco_Control_Country_Profiles.asp

38. Rahman M, Nurullah Awal AS, Fukui T and Sakamoto J. Prevalence of cigarette and bidi smoking among rickshaw pullers in Dhaka city. Preventive Medicine 2007;44(3):218-22. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17173963

39. Rahman M and Fukui T. Bidi smoking and health. Public Health 2000;114:123-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10800151

40. Delnevo CD, Pevzner ES, Hrywna M and Lewis MJ. Bidi cigarette use among young adults in 15 states. Preventive Medicine 2004;39(1):207-11. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15208004

41. Stanfill S, Calafat A, Brown C, Polzin G, Chiang J, Watson C, et al. Concentrations of nine alkenylbenzenes, coumarin, piperonal and pulegone in Indian bidi cigarette tobacco. Food and Chemical Toxicology 2003;41:303-17. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12480305

42. Pednekar MS, Gupta PC, Yeole BB and Hebert JR. Association of tobacco habits, including bidi smoking, with overall and site-specific cancer incidence: results from the Mumbai cohort study. Cancer Causes & Control 2011;22(6):859-68. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21431915

43. Jayalekshmi PA, Gangadharan P, Akiba S, Koriyama C and Nair RR. Oral cavity cancer risk in relation to tobacco chewing and bidi smoking among men in Karunagappally, Kerala, India: Karunagappally cohort study. Cancer Science 2011;102(2):460-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21129124

44. Rahman M, Sakamoto J and Fukui T. Calculation of population attributable risk for bidi smoking and oral cancer in south Asia. Preventive Medicine 2005;40(5):510-4. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15749132

45. Prasad R, Ahuja RC, Singhal S, Srivastava AN, James P, Kesarwani V, et al. A case-control study of bidi smoking and bronchogenic carcinoma. Annals of Thoracic Medicine 2010;5(4):238-41. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20981185

46. Prasad R, Singhal S and Garg R. Bidi smoking and lung cancer. Bioscience Trends 2009;3(2):41–3. Available from: http://www.biosciencetrends.com/action/downloaddoc.php?docid=198

47. Jayalekshmy PA, Akiba S, Nair MK, Gangadharan P, Rajan B, Nair RK, et al. Bidi smoking and lung cancer incidence among males in Karunagappally cohort in Kerala, India. International Journal of Cancer 2008;123(6):1390-7. Available from: http://onlinelibrary.wiley.com/doi/10.1002/ijc.23618/pdf

48. Sankaranarayanan R, Duffy SW, Padmakumary G, Nair SM, Day NE and Padmanabhan TK. Risk factors for cancer of the oesophagus in Kerala, India. International Journal of Cancer 1991;49(4):485-9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/1917146

49.. Pais P, Pogue J, Gerstein H, Zachariah E, Savitha D, Jayprakash S, et al. Risk factors for acute myocardial infarction in Indians: a case-control study. The Lancet 1996;348(9024):358-63. Available from: http://www.ncbi.nlm.nih.gov/pubmed/8709733

50. Gupta PC and Asma S. Bidi smoking and public health. New Delhi: Ministry of Health and Family Services, Government of India, 2008. Available from: http://mohfw.nic.in/WriteReadData/l892s/file16-29724885.pdf

51. Centers for Disease Control and Prevention. Bidi use among urban youth-Massachusetts, March-April 1999. Morbidity and Mortality Weekly Reports 1999;48:796-9. Available from: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm4836a2.htm

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