Report of the Scientific Committee on Tobacco and HealthPart 6


 
Part Six
 
Miscellaneous Topics
 
Introduction
 
In addition to considering the major tobacco-associated illnesses such as chronic obstructive pulmonary disease, arterial disease and lung cancer, the Committee has also assessed a number of other tobacco-associated effects and conditions which are brought together in this section.
 
6.1  The Effect of Smoking on Cognitive Performance and Mood
 
6.1.1  Many smokers claim that they smoke to alleviate boredom and fatigue, reduce tension, increase concentration and aid relaxation. Furthermore, it has been suggested that smoking confers psychological benefits and that a major motivation for many smokers is the use of smoking as a means of obtaining desired psychological effects, primarily enhancement of cognitive performance or reduction of negative influences such as anxiety, impulsive anger or other adverse situations.98
 
6.1.2  In order to explore some aspects of this widely held belief, the Committee received a presentation on the effect of smoking on cognitive performance and mood.
 
Cognitive Performance
 
6.1.3  Data from the Health and Lifestyle Survey99 were presented. Results of a simple reaction time test showed that cigarette smokers have shorter reaction times than non-smokers or ex-smokers. No dose response effect among smokers was demonstrated. More sophisticated tests assessing choice reaction time, verbal memory and spatial processing showed no difference between smokers, non-smokers and ex-smokers. These results contrast markedly with the results of studies on caffeine intake, where a clear dose response is demonstrated. From these data it can be concluded, therefore, that nicotine has no clear performance enhancing effect.
 
Mood
 
6.1.4  Further data from the Health and Lifestyle Survey were considered in which adults completed the General Health Questionnaire, which is a measure of current psychological well being. Results showed that smokers felt worse than never- or ex-smokers and a clear dose response effect was demonstrated, with heavy smokers feeling worst of all.
 
6.1.5  A malaise questionnaire was completed by subjects in the National Child Development Cohort Study100 at ages 23 and 33 years. The malaise questionnaire is scored on a continuum from 0-24, with 24 being the most unhappy. Results showed progressive unhappiness with the number of cigarettes smoked and that the risk of current psychiatric disorder increased with increasing cigarette consumption. The results were most striking in women. When confounding factors such as unemployment were eliminated, the relationship between a high malaise score and smoking persisted. Between the two phases of the study malaise scores fell among those who had given up smoking but remained high in those who continued to smoke. Malaise scores were highest of all in those taking up smoking in the period between the two phases of the study.
 
6.1.6  The conclusion, that smokers do not do better in performance tests nor do they score more favourably on measures of well being, runs counter to commonly held views. Giving up smoking is associated with a reduction in malaise score. It appears that tolerance develops to the mood and performance enhancing effects of cigarettes, with habitual smokers maintaining their habit in order to avert negative mood and performance states. The evidence that smoking relieves stress is weak; rather the reverse is true.101
 
Conclusions
 
6.1.7  In habitual smokers, nicotine does not appear to enhance performance above non-smoker levels.
 
6.1.8  In spite of widespread perceptions to the contrary, stress and anxiety are reduced rather than increased after giving up smoking.
 
6.1.9  The evidence that smoking relieves stress is weak; rather the reverse is true.
 
Recommendation
 
6.1.10  The public should be made aware of the association between smoking and negative mood states.
 
6.2  Smoking and Cancers of the Mouth and Pharynx
 
6.2.1  Each year in the UK there are more than 2500 new cases of cancers of the mouth and pharynx and, annually, about 1400 people die as a result of developing these tumours.102 The incidence of oral and pharyngeal cancers was reasonably static in the 1980s but recent reports from several western countries suggest that oral cancers are becoming more common among women and younger patients.103 The 5- and 10- year survival rates from the time of diagnosis are poor, particularly for large tumours, and early recognition and treatment are critical.
 
6.2.2  The principal risk factors for this group of tumours in the UK are smoking tobacco and drinking large amounts of alcohol.9,51,104,105 Chewed tobaccos, which vary widely in form and composition in different parts of the world, are sources of potent carcinogens in the mouth but these and similar materials - notably betel quid - are rarely used in this country except by certain ethnic minority groups. Smoked tobacco and alcohol exert their carcinogenic effects interactively, although it is uncertain whether the interactive effects are additive or multiplicative. It is difficult to evaluate the contribution made by each factor alone as most epidemiological studies are based on patients who both smoke tobacco and drink alcohol, often in large amounts. Relatively few patients with oral and pharyngeal cancers only smoke or only drink alcohol.
 
6.2.3  For cancers of the mouth and pharynx (and also larynx and oesophagus), alcohol appears to play the dominant role in the alcohol-tobacco synergy. The additional carcinogenic effects of tobacco are, however, consistent and show a dose response effect: the risks of alcohol-related cancers in the head and neck rising in proportion to the amount of tobacco smoked. Cancers of the lip, which are now rare in the UK are something of an anomaly. Traditionally associated with pipe smoking,10 this tumour develops almost invariably on the lower lip where the hot pipe stem is habitually held between the teeth. Cigarette smoking is also associated with an increased risk of cancers of the lip, and an additional important factor is chronic exposure to UV light. There is no clear association with alcohol consumption.
 
6.2.4  When deaths from cancers of the oral cavity and cancers of the uterine cervix are compared, the totals for both are similar. In England and Wales in 1996 the figures were 1142 (oral cavity) and 1329 (cervix).107 There has been intensive screening for cervical cancer for several years but much less attention has been paid to the need to screen for cancers of the oral cavity and pharynx, most of which can be detected by simple inspection.
 
Conclusions
 
6.2.5  Many cancers of the mouth and pharynx are caused by smoking tobacco and drinking excessive amounts of alcohol, the effect of the two factors together being greater than the sum of each alone.
 
6.2.6  Oral cancer, in particular, can be easily detected and early treatment is successful.
 
Recommendations
 
6.2.7  The National Screening Committee should consider screening programmes for early detection of cancers in the mouth.
 
6.2.8  Mandatory training and updating courses, in the detection of oral cancers, should be organised for dental surgeons and dental hygienists.
 
6.2.9  Consideration should be given to the re-introduction of dental health checks.
 
6.2.10  Health education should include information about the increased risk in smokers of these cancers
 
6.3  The Effect of Smoking on Tooth Loss.
 
6.3.1  The association between smoking and gum disease is an issue of increasing interest and importance, not only to dental practitioners, but to other health professionals and members of the public. In some parts of the world dental practitioners are already very active in raising awareness of the contribution smoking makes to gum disease.108
 
6.3.2  Gum disease starts with gingivitis (inflammation where the gum meets the tooth) which is in turn related to plaque formation. Gingivitis may lead to periodontitis, a condition where the gum comes away from the tooth due to destruction of the underlying bony support. Gum disease is a common cause of tooth loss in later life.
 
6.3.3  Whilst the development of gingivitis is, to some extent, an inevitable consequence of poor dental hygiene, progression to periodontitis is less predictable. Certain diseases such as diabetes increase the likelihood of serious gum disease, and periodontitis becomes more severe with increasing age. It is now widely accepted that smoking plays a major part in the development of periodontitis and a large study carried out in the United States in 1983109 showed smoking as an independent risk factor for the development of this disease.
 
6.3.4  Smoking is important in the evolution of gum disease because it masks the early warning signs of the disease. A comparison of smokers and non-smokers with the same amount of plaque shows smokers to have less inflammation and bleeding than non-smokers. Under normal circumstances bleeding from the gums is an early warning sign that something is wrong, but this is reduced in smokers due to the effect of nicotine, which reduces bleeding. By diminishing this early sign of gingivitis, smoking may delay its recognition to the point where periodontitis sets in and the likelihood of returning to a healthy state is reduced.
 
Conclusions
 
6.3.5  Smoking plays a major part in the development of periodontitis, which is the major cause of tooth loss.
 
6.3.6  Smoking masks the early warning signs of the disease.
 
6.3.7  Dental surgeons and dental hygienists can play an important role in providing information to the general public on the known health risks of smoking including those associated with dental disease.
 
Recommendations
 
6.3.8  The public should be made aware of the role of smoking in the development of gum disease and subsequent tooth loss.
 
6.3.9  Dentists and dental hygienists should be trained in smoking cessation techniques and encouraged to play an active part in smoking cessation and health education on known health risks of smoking including those associated with dental disease.
 
6.4  Smoking and Congenital Defects
 
Orofacial clefts
 
6.4.1  The role of maternal smoking during pregnancy and a possible association with orofacial clefts has been investigated in studies such as that by Kallen110 who found a statistically significant association (OR 1.29, 95% CI: 1.08-1.54) with maternal smoking and cleft palate alone and an OR of 1.16 (95% CI: 1.02-1.32) for cleft lip with or without cleft palate. A meta-analysis was carried out by Wyszynski et al111 which gave a combined OR from 11 studies of 1.29 (95% CI: 1.18-1.42) for cleft lip and palate, and for cleft palate alone gave an OR of 1.32 (95% CI: 1.10-1.62). The authors concluded that their analyses suggest a small but statistically significant association between maternal cigarette smoking in the first trimester of gestation and increased risk of having a child with cleft lip and/or cleft palate.
 
Congenital Limb Defects
 
6.4.2  In July 1994 the Committee considered a paper112 setting out the results of a case control study which examined genetic and environmental factors in the origin of isolated congenital limb deficiencies. The paper concluded that maternal smoking during the first trimester of pregnancy may raise the relative odds for terminal transverse limb deficiencies. (Relative odds 1.48; 95% CI: 0.98-2.23). A recent study from Sweden113 identified a similar modest increase in the odds ratio for limb-reduction in the babies of women who smoke in pregnancy. (OR 1.26, 95% CI: 1.06-1.50)
 
6.4.3  Members concluded that there may be an increased risk of congenital limb abnormalities associated with smoking during pregnancy but more research is needed.
 
Craniosynostosis
 
6.4.4  Members noted a paper114 analysing data from a population based case control study to determine whether maternal prenatal smoking or alcohol drinking might increase the risk of craniosynostosis. This paper concluded that maternal prenatal smoking may increase the risk of craniosynostosis in the study population.
 
Conclusion
 
6.4.5  Maternal smoking in pregnancy may increase the risk of congenital defects. Prevention may require smoking cessation before conception.
 
Recommendations
 
6.4.6  The public should be kept aware of the known hazards of smoking in pregnancy.
 
6.4.7  Further work on smoking in pregnancy and congenital defects is needed.
 
6.5  Diseases with a Lower Risk in Smokers
 
6.5.1  There is evidence that smoking reduces the risk of a few diseases and these findings need to be weighed against the substantial harm.
 
6.5.2  Members reviewed the current evidence on the effects of smoking in relation to Parkinson's Disease, endometrial cancer, ulcerative colitis and Alzheimer's Disease. A paper was prepared for the Committee by Sir Richard Doll and is attached at Annex J.
 
6.5.3  With respect to Parkinson's disease, endometrial cancer and ulcerative colitis smoking exerts a protective effect which appears to relate to nicotine.
 
6.5.4  The effect of smoking on Alzheimer's disease is more complicated and studies linking a reduced risk of the disease with smoking habits may demonstrate statistical bias because, for example, younger sufferers may have already been screened out of case control studies by smoking related mortality. Consequently it cannot be concluded that smoking reduces the risk of acquiring Alzheimer's disease.
 
6.5.5  It is important to recognise that any “beneficial health effects” derived from smoking are far out-weighed by the detrimental effects on health. There are likely to be more than one hundred times as many deaths due to smoking than prevented by smoking. Any beneficial effects are likely to be attributable to nicotine rather than to smoking.
 
Conclusion
 
6.5.6  The health benefits of active smoking in a few conditions are far outweighed by the substantial risks.
 
Recommendation
 
6.5.7  The apparent beneficial effects of smoking on a few aspects of health offer an opportunity for research on the precise mechanisms involved, and the possibility for developing new pharmaceutical approaches to treatment.
 

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Prepared 20 March 1998