1191
EDITORIALS
after the year 2000 Cigarette smoking is now regarded as a form of drug Nicotine
use
addiction. A landmark in this process was the 1988 report of the US Surgeon General, who concluded that addiction to nicotine resembles addiction to drugs such as heroin, cocaine, and alcohol.1 What distinguishes nicotine from other widely abused drugs is that its effects are subtle and do not cause socially
disruptive intoxication, provoke violence, or impair performance. Yet deaths due to tobacco far outnumber those caused by all other drugs. The central paradox is that, while people smoke for nicotine they die mainly from the tar and other unwanted components in the smoke. Why have governments persisted in allowing the manufacture, extensive advertising, and promotion of such a lethally contaminated drug delivery system as the cigarette, while putting so little pressure on the tobacco industry to develop more purified forms of nicotine delivery? The pressure for change has come instead from the pharmaceutical industry, driven by the search for more effective aids to smoking cessation. The initial development of nicotine chewing gum has now been followed by other products. Nicotine skin patches maintain stable blood nicotine concentrations over 4-16 h,2 whereas nicotine vapour inhalers mimic the rapid absorption from cigarette smoking.3At least five pharmaceutical companies have skin patches at various stages of testing, and clinical use of such patches is licensed in some countries. Other products undergoing clinical trials include a nasal nicotine spray, nicotine lozenges, and a nicotine vapour puffer.4 Although these nicotine replacement products are marketed as aids to stopping smoking, with further refinement some may also have potential for long-term use and, if permitted, might eventually replace tobacco on the open market. If a strategy were adopted to sanction and encourage the use of purified nicotine products as substitutes for smoking, and at the same time impose
stringent regulations on permissible constituents of cigarette smoke and progressively lower limits for deliveries of harmful components such as nitrosamines and nitrogen oxides, as well as of tar and carbon monoxide, the virtual elimination of smoking could become a more realistic health promotion target. It could also be achieved more quickly. The question is whether policy-makers will consider such a strategy and whether the antismoking movement would support or oppose it. Is a new strategy needed? Are existing programmes sufficient? There has been some progress in many countries. In the UK, for example, the prevalence of cigarette smoking has declined steadily from 46% in 1972 to 32 % in 1988, an average rate of about 1 % per yearsBut progress worldwide has been swamped by the rapid increase in smoking in developing countries. Progress with tar reduction programmes is likewise slow. The modest aims of the Tar Yield Directive of the EC Council of Health Ministers on Nov 13,1989, have been hailed as an important measure. The Directive sets a limit for tar yields of 15 mg by the end of 1992, and 12 mg by the end of 1997. Greece has derogation allowing higher yields until 2007. Overall, on the basis of current approaches and policies, there seems little prospect of averting Peto’s estimate of 10 million premature deaths throughout the world each 6 year during the next century as a result of tobacco use.6 The core of the problem lies in the addictiveness of nicotine. It is nicotine that people cannot easily do without, not tobacco; it is nicotine dependence that slows the progress of existing programmes. As a drug delivery system the modem cigarette is a highly efficient device for getting nicotine to the brain, but by pharmaceutical standards it is also a very "dirty" one, the nicotine being contaminated with nitrosamines and other carcinogens in the tar, as well as with carbon monoxide and other harmful gases. Thus it seems logical to offer either a cleaner product or, better still, an acceptable source of more pure, less contaminated nicotine. The principle is the same as that of the UK low-tar programme,7,8 albeit a gigantic step-too big it for regulatory authorities and health seems professions in the USA. In 1988, a major US tobacco company released details of a highly innovative type of cigarette that heats rather than burns tobacco.9 The smoke particles were virtually tar-free, consisting mainly of water, glycerol, and a small amount of propylene glycol. The nicotine yield was low-0-3 mg. Apart from a carbon monoxide yield of 10-6 mg, amounts of other noxious gases were negligible compared with conventional cigarettes, as was the biological activity in extensive tests.9,10 In terms of the aims for product modification laid down by the UK Independent Scientific Committee on Smoking and Health,this would seem a near-perfect low-tar cigarette, and there is no doubt that it would be less harmful than most other brands on the market. Far from welcoming it in the USA, the American
1192
Medical
Association, the Heart and Lung Association, the American Cancer Society, and others combined to petition and speak against it at a special
Hearing before a Subcommittee of the House of Representatives." Eventually the product was labelled as a nicotine delivery system and attempts to market it as a tobacco product were abandoned by the company, who meanwhile remain free to promote
conventional cigarettes to the 50 million Americans who still smoke after decades of antismoking policies. There is no cause for complacency in the UK. In 1980, when the Committee on Safety of Medicines licensed the medical use of nicotine chewing gum as an aid to stopping smoking, the decision was based on the usual grounds of safety and efficacy. Not long afterwards the Advisory Committee on Borderline Substances ruled against its use on National Health Service prescriptions, one of the reasons being their doubts about its efficacy, a matter on which they were not competent to judge. The chewing gum (’Nicorette’) was thus the only prescription-only medicine not available on the NHS. From May 1, the 2 mg dose of Nicorette but not the 4 mg dose has been available over the counter. Meanwhile, other less pure and untested nicotine-containing lozenges based on tobacco extracts were allowed to be promoted and sold without medical prescription or evidence of clinical
efficacy Y These examples of regulatory decisions in two countries do not augur well for the initiation of any strategy to replace smoking with a purer source of nicotine. For such a strategy to succeed, it would need to be radical. Suitable nicotine replacement products would have to be made as acceptable and palatable as possible, advertised, actively promoted with health authority endorsement, and given tax advantages over tobacco. Support from the antismoking movement, coupled with progressive restrictions on tobacco might ultimately lead to an effective ban on smoking in public places, which is feasible only if an alternative is available. As tobacco is phased out the emphasis could shift to avoidance of nicotine, if by then it proves to be an unacceptable burden to health. What are the risks of nicotine itself? It has no known role in tobacco-related cancers, neither is it implicated in chronic obstructive lung disease. The possibility of endogenous formation of carcinogenic nitrosamines from nicotine metabolites has been suggested.13 However, this has not been documented and, if it occurs, the amounts would be negligible compared with those present in tobacco and formed when tobacco is burned. While the negligible cardiovascular risks in primary pipe and cigar smokers who have never smoked cigarettes14 may be reassuring as far as slow buccal absorption is concerned, there are various mechanisms through which rapid nicotine absorption from cigarettes might interact with carbon monoxide to exacerbate cardiovascular disease. For example, propranolol largely abolishes the deleterious effects of smoking on mortality following a first heart attack,
indicating that adrenergic mechanisms are involved.15 This observation strongly implicates nicotine, which is the only major smoke component with effects on adrenergic systems. Thus the view of the Chairman and a member of the UK Independent Scientific Committee on Smoking and Health may be oversanguine. They state "That nicotine has a role in the cause of cardiovascular disease has its adherents, but the evidence is not compelling". 16 There is no good reason why a switch from tobacco products to less harmful nicotine delivery systems should not be encouraged. Smoking-related deaths after the year 2000 would fall steadily and substantially if this can be achieved. There is no compelling objection to the recreational and even addictive use of nicotine provided it is not shown to be physically, psychologically, or socially harmful to the user or to
others.
1. Nicotine addiction:
a report of the Surgeon General. Washington, DC: US Department of Health and Human Services, 1988. 2. Abelin T, Buehler A, Muller P, et al. Controlled trial of transdermal nicotine patch in tobacco withdrawal. Lancet 1989; i: 7-10. 3. Feyerabend C, Russell MAH. A rapid gas-liquid chromatographic method for the determination of cotinine and nicotine in biological fluids. J Pharm Pharmacol 1990; 42: 450-52. 4. Russell MAH, Jarvis MJ, Sutherland G, Feyerabend C. Nicotine replacement in smoking cessation: absorption of nicotine vapor from smoke-free cigarettes. JAMA 1987; 257: 3262-65. 5. Office of Population Censuses and Surveys. General Household Survey 1988. London: HM Stationery Office, 1990. 6. Peto R. 7th World Conference on Tobacco and Health, Perth, Western
Australia, 1-5 April, 1990. 7. Fourth Report of the Independent Scientific Committee on Smoking
and
Health. London: HM Stationery Office, 1988. 8. Wald N, Froggatt P, eds. Nicotine, smoking and the low tar programme. Oxford: Oxford University Press, 1989. 9. RJ Reynolds Tobacco Company. Chemical and biological studies on new cigarette prototypes that heat instead of bum tobacco. Winston-Salem, NC: RJ Reynolds Tobacco Co, 1988. 10. DeBethizy JD, Borgerding MF, Doolittle DJ, et al. Chemical and biological studies of a cigarette that heats rather than burns tobacco. J Clin Pharmacol 1990; 30: 755-63. 11. US House of Representatives. Subcommittee on Health and Environment Hearing. Serial no 100-68, July 29, 1988. Washington, DC: US Government Printing Office, 1988. 12. Belcher M, Jarvis MJ, Sutherland G. Nicotine absorption and dependence on an over-the-counter aid to stop smoking. Br Med J
1989; 289: 570. Nicotine, a tobacco-specific precursor for carcinogens. In. Wald N, Froggatt P, eds. Nicotine, smoking and the low tar programme. Oxford: Oxford University Press, 1989: 29-40. 14. Doll R. Prospects for prevention. Br Med J 1983; 286: 445-53. 15. Jafri SM, Tilley BC, Peters R, Schultz LR, Goldstein S. Effects of
13. Hoffman D.
cigarette smoking and propanolol in survivors of acute myocardial infarction. Am J Cardiol 1990; 65: 271-76. 16. Froggatt P, Wald N. The role of nicotine in the tar reduction programme. In: Wald N, Froggatt P, eds. Nicotine, smoking and the low tar programme. Oxford: Oxford University Press, 1989: 229-35.
The autistic dimension A child usually begins to speak at about twelve months. During that first year an internal map of the world is constructed from a mass of incoming sensory data. Once a certain degree of thought, based on this experience, is achieved, the child goes on to acquire a range of communication skills of which language is the most important. Cognitive development therefore depends on the evolution of thought processes that are
EDITORIALS
after the year 2000 Cigarette smoking is now regarded as a form of drug Nicotine
use
addiction. A landmark in this process was the 1988 report of the US Surgeon General, who concluded that addiction to nicotine resembles addiction to drugs such as heroin, cocaine, and alcohol.1 What distinguishes nicotine from other widely abused drugs is that its effects are subtle and do not cause socially
disruptive intoxication, provoke violence, or impair performance. Yet deaths due to tobacco far outnumber those caused by all other drugs. The central paradox is that, while people smoke for nicotine they die mainly from the tar and other unwanted components in the smoke. Why have governments persisted in allowing the manufacture, extensive advertising, and promotion of such a lethally contaminated drug delivery system as the cigarette, while putting so little pressure on the tobacco industry to develop more purified forms of nicotine delivery? The pressure for change has come instead from the pharmaceutical industry, driven by the search for more effective aids to smoking cessation. The initial development of nicotine chewing gum has now been followed by other products. Nicotine skin patches maintain stable blood nicotine concentrations over 4-16 h,2 whereas nicotine vapour inhalers mimic the rapid absorption from cigarette smoking.3At least five pharmaceutical companies have skin patches at various stages of testing, and clinical use of such patches is licensed in some countries. Other products undergoing clinical trials include a nasal nicotine spray, nicotine lozenges, and a nicotine vapour puffer.4 Although these nicotine replacement products are marketed as aids to stopping smoking, with further refinement some may also have potential for long-term use and, if permitted, might eventually replace tobacco on the open market. If a strategy were adopted to sanction and encourage the use of purified nicotine products as substitutes for smoking, and at the same time impose
stringent regulations on permissible constituents of cigarette smoke and progressively lower limits for deliveries of harmful components such as nitrosamines and nitrogen oxides, as well as of tar and carbon monoxide, the virtual elimination of smoking could become a more realistic health promotion target. It could also be achieved more quickly. The question is whether policy-makers will consider such a strategy and whether the antismoking movement would support or oppose it. Is a new strategy needed? Are existing programmes sufficient? There has been some progress in many countries. In the UK, for example, the prevalence of cigarette smoking has declined steadily from 46% in 1972 to 32 % in 1988, an average rate of about 1 % per yearsBut progress worldwide has been swamped by the rapid increase in smoking in developing countries. Progress with tar reduction programmes is likewise slow. The modest aims of the Tar Yield Directive of the EC Council of Health Ministers on Nov 13,1989, have been hailed as an important measure. The Directive sets a limit for tar yields of 15 mg by the end of 1992, and 12 mg by the end of 1997. Greece has derogation allowing higher yields until 2007. Overall, on the basis of current approaches and policies, there seems little prospect of averting Peto’s estimate of 10 million premature deaths throughout the world each 6 year during the next century as a result of tobacco use.6 The core of the problem lies in the addictiveness of nicotine. It is nicotine that people cannot easily do without, not tobacco; it is nicotine dependence that slows the progress of existing programmes. As a drug delivery system the modem cigarette is a highly efficient device for getting nicotine to the brain, but by pharmaceutical standards it is also a very "dirty" one, the nicotine being contaminated with nitrosamines and other carcinogens in the tar, as well as with carbon monoxide and other harmful gases. Thus it seems logical to offer either a cleaner product or, better still, an acceptable source of more pure, less contaminated nicotine. The principle is the same as that of the UK low-tar programme,7,8 albeit a gigantic step-too big it for regulatory authorities and health seems professions in the USA. In 1988, a major US tobacco company released details of a highly innovative type of cigarette that heats rather than burns tobacco.9 The smoke particles were virtually tar-free, consisting mainly of water, glycerol, and a small amount of propylene glycol. The nicotine yield was low-0-3 mg. Apart from a carbon monoxide yield of 10-6 mg, amounts of other noxious gases were negligible compared with conventional cigarettes, as was the biological activity in extensive tests.9,10 In terms of the aims for product modification laid down by the UK Independent Scientific Committee on Smoking and Health,this would seem a near-perfect low-tar cigarette, and there is no doubt that it would be less harmful than most other brands on the market. Far from welcoming it in the USA, the American
1192
Medical
Association, the Heart and Lung Association, the American Cancer Society, and others combined to petition and speak against it at a special
Hearing before a Subcommittee of the House of Representatives." Eventually the product was labelled as a nicotine delivery system and attempts to market it as a tobacco product were abandoned by the company, who meanwhile remain free to promote
conventional cigarettes to the 50 million Americans who still smoke after decades of antismoking policies. There is no cause for complacency in the UK. In 1980, when the Committee on Safety of Medicines licensed the medical use of nicotine chewing gum as an aid to stopping smoking, the decision was based on the usual grounds of safety and efficacy. Not long afterwards the Advisory Committee on Borderline Substances ruled against its use on National Health Service prescriptions, one of the reasons being their doubts about its efficacy, a matter on which they were not competent to judge. The chewing gum (’Nicorette’) was thus the only prescription-only medicine not available on the NHS. From May 1, the 2 mg dose of Nicorette but not the 4 mg dose has been available over the counter. Meanwhile, other less pure and untested nicotine-containing lozenges based on tobacco extracts were allowed to be promoted and sold without medical prescription or evidence of clinical
efficacy Y These examples of regulatory decisions in two countries do not augur well for the initiation of any strategy to replace smoking with a purer source of nicotine. For such a strategy to succeed, it would need to be radical. Suitable nicotine replacement products would have to be made as acceptable and palatable as possible, advertised, actively promoted with health authority endorsement, and given tax advantages over tobacco. Support from the antismoking movement, coupled with progressive restrictions on tobacco might ultimately lead to an effective ban on smoking in public places, which is feasible only if an alternative is available. As tobacco is phased out the emphasis could shift to avoidance of nicotine, if by then it proves to be an unacceptable burden to health. What are the risks of nicotine itself? It has no known role in tobacco-related cancers, neither is it implicated in chronic obstructive lung disease. The possibility of endogenous formation of carcinogenic nitrosamines from nicotine metabolites has been suggested.13 However, this has not been documented and, if it occurs, the amounts would be negligible compared with those present in tobacco and formed when tobacco is burned. While the negligible cardiovascular risks in primary pipe and cigar smokers who have never smoked cigarettes14 may be reassuring as far as slow buccal absorption is concerned, there are various mechanisms through which rapid nicotine absorption from cigarettes might interact with carbon monoxide to exacerbate cardiovascular disease. For example, propranolol largely abolishes the deleterious effects of smoking on mortality following a first heart attack,
indicating that adrenergic mechanisms are involved.15 This observation strongly implicates nicotine, which is the only major smoke component with effects on adrenergic systems. Thus the view of the Chairman and a member of the UK Independent Scientific Committee on Smoking and Health may be oversanguine. They state "That nicotine has a role in the cause of cardiovascular disease has its adherents, but the evidence is not compelling". 16 There is no good reason why a switch from tobacco products to less harmful nicotine delivery systems should not be encouraged. Smoking-related deaths after the year 2000 would fall steadily and substantially if this can be achieved. There is no compelling objection to the recreational and even addictive use of nicotine provided it is not shown to be physically, psychologically, or socially harmful to the user or to
others.
1. Nicotine addiction:
a report of the Surgeon General. Washington, DC: US Department of Health and Human Services, 1988. 2. Abelin T, Buehler A, Muller P, et al. Controlled trial of transdermal nicotine patch in tobacco withdrawal. Lancet 1989; i: 7-10. 3. Feyerabend C, Russell MAH. A rapid gas-liquid chromatographic method for the determination of cotinine and nicotine in biological fluids. J Pharm Pharmacol 1990; 42: 450-52. 4. Russell MAH, Jarvis MJ, Sutherland G, Feyerabend C. Nicotine replacement in smoking cessation: absorption of nicotine vapor from smoke-free cigarettes. JAMA 1987; 257: 3262-65. 5. Office of Population Censuses and Surveys. General Household Survey 1988. London: HM Stationery Office, 1990. 6. Peto R. 7th World Conference on Tobacco and Health, Perth, Western
Australia, 1-5 April, 1990. 7. Fourth Report of the Independent Scientific Committee on Smoking
and
Health. London: HM Stationery Office, 1988. 8. Wald N, Froggatt P, eds. Nicotine, smoking and the low tar programme. Oxford: Oxford University Press, 1989. 9. RJ Reynolds Tobacco Company. Chemical and biological studies on new cigarette prototypes that heat instead of bum tobacco. Winston-Salem, NC: RJ Reynolds Tobacco Co, 1988. 10. DeBethizy JD, Borgerding MF, Doolittle DJ, et al. Chemical and biological studies of a cigarette that heats rather than burns tobacco. J Clin Pharmacol 1990; 30: 755-63. 11. US House of Representatives. Subcommittee on Health and Environment Hearing. Serial no 100-68, July 29, 1988. Washington, DC: US Government Printing Office, 1988. 12. Belcher M, Jarvis MJ, Sutherland G. Nicotine absorption and dependence on an over-the-counter aid to stop smoking. Br Med J
1989; 289: 570. Nicotine, a tobacco-specific precursor for carcinogens. In. Wald N, Froggatt P, eds. Nicotine, smoking and the low tar programme. Oxford: Oxford University Press, 1989: 29-40. 14. Doll R. Prospects for prevention. Br Med J 1983; 286: 445-53. 15. Jafri SM, Tilley BC, Peters R, Schultz LR, Goldstein S. Effects of
13. Hoffman D.
cigarette smoking and propanolol in survivors of acute myocardial infarction. Am J Cardiol 1990; 65: 271-76. 16. Froggatt P, Wald N. The role of nicotine in the tar reduction programme. In: Wald N, Froggatt P, eds. Nicotine, smoking and the low tar programme. Oxford: Oxford University Press, 1989: 229-35.
The autistic dimension A child usually begins to speak at about twelve months. During that first year an internal map of the world is constructed from a mass of incoming sensory data. Once a certain degree of thought, based on this experience, is achieved, the child goes on to acquire a range of communication skills of which language is the most important. Cognitive development therefore depends on the evolution of thought processes that are
![[Sialadenosis of the parotid gland after chronic nicotine use].](/assets/img/hold.png)
