Tobacco smoking, harm reduction, and nicotine product regulation

Abstract

Cigarette smoking is highly addictive, widely prevalent, and very hazardous. Smoking killed 100 million people in the 20th century, and is predicted to kill 1 billion in the 21st century. Worldwide, there are about 1·1 billion smokers, and there are expected to be 1·6 billion by 2025. Half of all smokers will die prematurely, unless they stop smoking. In the 50 years since the health risks of smoking fi rst became widely recognised, the political and public health responses to smoking at national and international levels have been grossly inade quate. Although the main components of current recommended tobacco control policy (panel 1) have changed little from those fi rst proposed in 1962, they have still not been widely applied and, in any case, achieve a reduction in smoking prevalence of typically about 0·5, and at best 1·0, percentage point per year. Full implementation of these policies might be suffi cient to prevent smoking in countries in which the smoking epidemic has yet to take hold, but this is only part of the necessary solution for countries with an estab lished smoking population. In the UK, for example, where 24% of adults still smoke, at a reduction rate of 0·5 percentage point per year it would take more than 20 years to reduce the prevalence of smoking by half. Even then, there will be more than 5 million smokers in the UK alone, predominantly from the most socioeconomically disadvantaged sectors of society, bearing a vast burden of avoidable morbidity and mortality. In fact most of the 150 million deaths from smoking that are expected over the next 20 years will occur in current smokers who are alive today. Since millions of these are unlikely to stop smoking in the near future, we argue, on the basis of a new report from the Royal College of Physicians, that in addition to conventional tobacco control policies, the application of harm reduction principles to nicotine and tobacco use could deliver substantial reductions in the morbidity and mortality currently caused by tobacco consumption. However, achievement of these reductions will require radical structural reform of the way in which nicotine and tobacco products are regulated and used. Most people continue to smoke because they are addicted to nicotine. Inhaled tobacco smoke is especially addictive because it delivers high doses of nicotine to the brain very rapidly, and because nicotine confers rewarding properties on other stimuli associated with smoking. Exposure to high nicotine concentrations at an early age might also determine the intensity of addiction through eff ects on nicotinic receptor numbers in the brain. Nicotine is available from a wide range of products: smoked tobacco, of which the cigarette is pre-eminent; medicinal nicotine, currently available as nicotine replacement therapy; and smokeless tobacco products, of which oral tobacco is the most widely used. Cigarettes and other smoked tobacco products, such as cigars and pipes, are by far the most harmful because they deliver nicotine in conjunction with hundreds of other toxins and carcinogens. It is these toxins and carcinogens that are mainly responsible for the major adverse health eff ects of smoking—particularly lung cancer, chronic obstructive pulmonary disease (COPD), heart disease, and stroke. By contrast, the safety record of medicinal nicotine products is very good. Nicotine is not a recognised carcinogen and does not cause COPD. It has eff ects on blood pressure and heart rate that might be expected to increase risk of cardiovascular disease, but these eff ects are not seen in practice. Nicotine reduces placental blood fl ow, but medicinal nicotine does not reduce birthweight as much as smoking does. Therefore, although medicinal nicotine is not wholly safe, for practical purposes, and certainly when compared with smoking, the hazard associated with medicinal nicotine use is very low. The risk profi le of smokeless tobacco products is more wide ranging and includes oral cancer, other gastrointestinal cancers, and heart disease. These risks vary substantially between diff erent smokeless products, but are low for products low in nitrosamine, such as Swedish snus. Snus use increases the risk of pancreatic cancer, but not of lung and oral cancers, or COPD. Use of other smokeless products has been linked to an increased risk of cardiovascular disease, but snus has little, if any, eff ect. The risk of adverse eff ects associated with snus use is lower than that associated with smoking, overall by an estimated 90%. Whatever the true overall hazard, use of low nitrosamine smokeless products is clearly substantially less harmful than tobacco smoking. The rationale behind harm reduction is that although the best option would be to avoid the harmful behaviour Lancet 2008; 371: 441–45