Respiratory effects of non-tobacco cigarettes.

Data from the Tucson epidemiological study of airways obstructive disease on smoking of non-tobacco cigarettes such as marijuana were analysed to determine the effect of such smoking on respiratory symptoms and pulmonary function. Among adults aged under 40, 14% had smoked non-tobacco cigarettes at some time and 9% were current users. The prevalence of respiratory symptoms was increased in smokers of non-tobacco cigarettes. After tobacco smoking had been controlled for men who smoked non-tobacco cigarettes showed significant decreases in expiratory flow rates at low lung volumes and in the ratio of the forced expiratory volume in one second to the vital capacity. This effect on pulmonary function in male non-tobacco cigarette smokers was greater than the effect of tobacco cigarette smoking. These data suggest that non-tobacco cigarette smoking may be an important risk factor in young adults with respiratory symptoms or evidence of airways obstruction.     

Mortality in relation to tar yield of cigarettes: a prospective study of four cohorts.

OBJECTIVE--To investigate relation between tar yield of manufactured cigarettes and mortality from smoking related diseases. DESIGN--Prospective epidemiological study of four cohorts of men studied between 1967 and 1982. SETTING--Combined data from British United Provident Association (BUPA) study (London), Whitehall study (London), Paisley-Renfrew study (Scotland), and United Kingdom heart disease prevention project (England and Wales). SUBJECTS--Of the 56,255 men aged over 35 who were included in the studies, 2742 deaths occurred among 12,400 smokers. Average follow up was 13 years. MAIN OUTCOME MEASURES--Relative mortality from smoking related diseases according to tar yields of cigarettes smoked. RESULTS--Age adjusted mortality from smoking related diseases in smokers of filter cigarettes was 9% lower (95% confidence interval 1% to 17%) than in smokers related diseases consistently decreased with decreasing tar yield. Relative mortality in cigarette smokers for a 15 mg decrease in tar yield per cigarette was 0.75 (0.52 to 1.09) for lung cancer, 0.77 (0.61 to 0.97) for coronary heart disease, 0.86 (0.50 to 1.50) for stroke, 0.78 (0.40 to 1.48) for chronic obstructive lung diseases, 0.78 (0.65 to 0.93) for these smoking related diseases combined, and 0.77 (0.65 to 0.90) for all smoking related diseases. CONCLUSION--About a quarter of deaths from lung cancer, coronary heart disease, and possibly other smoking related diseases would have been avoided by lowering tar yield from 30 mg per cigarette to 15 mg. Reducing cigarette tar yields in Britain has had a modest effect in reducing smoking related mortality.     

Modifying risk of developing lung cancer by changing habits of cigarette smoking.

Data from a hospital based case-control study of lung cancer in Western Europe were used to examine changes in the risk of developing lung cancer after changes in habits of cigarette smoking. Only data for subjects who had smoked regularly at some time in their lives were included. The large size of the study population (7181 patients and 11 006 controls) permitted precise estimates of the effect of giving up smoking. Risks of developing lung cancer for people who had given up smoking 10 or more years before interview were less than half of those for people who continued to smoke. The reduction in risk was seen in men and women and in former smokers of both filter and non-filter cigarettes but varied by duration of smoking habit before giving up. The protective effect of giving up became progressively greater with shorter duration of smoking habit. The risks after not smoking for 10 years for both men and women who had previously smoked for less than 20 years were roughly the same as those for lifelong non-smokers. Reducing the number of cigarettes smoked a day or switching from non-filter to filter cigarettes also lowered the risk of developing lung cancer but not to the extent associated with giving up smoking.     

Smoking Habits of Men Employed in Industry,and Mortality

A study of the relation between smoking habits and lung cancer in male industrial workers over a period of three years has confirmed the earlier findings in doctors that the death-rate from lung cancer correlates closely with the number of cigarettes smoked. Of 54,460 men studied 68.7% were current cigarette smokers. The annual mortality rate from lung cancer was 0.33 per thousand in non-smokers and ex-smokers, and 1.2 per thousand for all cigarette smokers, and higher in heavy smokers.Heavy cigarette smokers who retained the cigarette in the mouth between puffs (“drooping” cigarette habit) had an annual mortality rate of 4.1 per thousand.The mortality from coronary thrombosis in smokers was nearly three times that in non-smokers. A mortality gradient with rising consumption of cigarettes was observed.Some correlation between smoking and cancer of other sites and from non-neoplastic lung disease was observed in older men, but no correlation was found with other cardiovascular diseases and cerebrovascular diseases.     

Changes of smoking habits and cough in men smoking cigarettes with 30% NSM tobacco substitute.

The effects of smoking cigarettes with 30% of the tobacco replaced by NSM tobacco substitute, which lowered their tar and nicotine delivery, were studied by comparing them with the effects of conventional cigarettes in a controlled crossover trial lasting 20 months. Chest symptoms, cigarette consumption, and forced expiratory volume in one second (FEV1) were measured each month. Two-hundred men began the trial and 159 completed it. The test cigarettes were acceptable to all but one of the men. In a subsample of 35 men estimates of nicotine intake were obtained from monthly analyses of cigarette stubs. On changing from NSM to control cigarettes six of the 17 men, who were accustomed to low nicotine, kept their nicotine intake down by some change in smoking habit. Before the crossover and this change in smoking habit the men smoking NSM cigarettes had a small but significant reduction of cough. Cigarettes containing 30% NSM and delivering only 1 mg of nicotine are likely to be acceptable to smokers and may reduce coughing. Further trials are needed to confirm these findings and establish what long-term effects such cigarettes may have on smokers'' health.     

Trends in mortality among California physicians after giving up smoking: 1950-79.

A study was conducted to assess how lung cancer and other mortality trends among California physicians had been influenced by the high proportion who had given up smoking since 1950. Several sample surveys indicated that the proportion of California physicians who currently smoked cigarettes had declined dramatically from about 53% in 1950 to about 10% in 1980. During the same period the proportion of other American men who smoked cigarettes had declined only modestly, from about 53% to 38%. Using the 1950 American Medical Directory a cohort of 10 130 California male physicians was established and followed up for mortality till the end of 1979, during which time 5090 died. The information from follow up and death certification was exceptionally good. The standardised mortality ratio for lung cancer among California male physicians relative to American white men declined from 62 in 1950-9 to 30 in 1970-9. The corresponding decline in standardised mortality ratio was from 100 to 63 for other smoking related cancer, from 106 to 71 for ischaemic heart disease, and from 62 to 35 for bronchitis, emphysema, and asthma. The standardised mortality ratio remained relatively constant for other causes of death not strongly related to smoking. The overall ratio declined in all age groups at a rate of about 1% a year. The total death rate among all physicians converged towards the rate among non-smoking physicians. By the end of the study period physicians had a cancer rate and total death rate similar to or less than those among typical United States non-smokers. This "natural experiment" shows that lung cancer became relatively less common on substantial elimination of the primary causal factor, cigarette smoking. Other smoking related diseases also became relatively less common, though factors other than cigarette smoking may have contributed to this change.     

Prospective study of effect of switching from cigarettes to pipes or cigars on mortality from three smoking related diseases.

OBJECTIVE: To estimate the extent to which cigarette smokers who switch to cigars or pipes alter their risk of dying of three-smoking related diseases-lung cancer, ischaemic heart disease, and chronic obstructive lung disease. DESIGN: A prospective study of 21520 men aged 35-64 years when recruited in 1975-82 with detailed history of smoking and measurement of carboxyhaemoglobin. MAIN OUTCOME MEASURES: Notification of deaths (to 1993) classified by cause. RESULTS: Pipe and cigar smokers who had switched from cigarettes over 20 years before entry to the study smoked less tobacco than cigarette smokers (8.1 g/day v 20 g/day), but they had the same consumption as pipe and cigar smokers who had never smoked cigarettes (8.1 g) and had higher carboxyhaemoglobin saturations (1.2% v 1.0%, P < 0.001), indicating that they inhaled tobacco smoke to a greater extent. They had a 51% higher risk of dying of the three smoking related diseases than pipe or cigar smokers who had never smoked cigarettes (relative risk 1.51; 95% confidence interval 0.96 to 2.38), a 68% higher risk than lifelong non-smokers (1.68; 1.16 to 2.45), a 57% higher risk than former cigarette smokers who gave up smoking over 20 years before entry (1.57; 1.04 to 2.38), and a 46% lower risk than continuing cigarette smokers (0.54; 0.38 to 0.77). CONCLUSION: Cigarette smokers who have difficulty in giving up smoking altogether are better off changing to cigars or pipes than continuing to smoke cigarettes. Much of the effect is due to the reduction in the quantity of tobacco smoked, and some is due to inhaling less. Men who switch do not, however, achieve the lower risk of pipe and cigar smokers who have never smoked cigarettes. All pipe and cigar smokers have a greater risk of lung cancer than lifelong non-smokers or former smokers.     

γH2AX: A potential DNA damage response biomarker for assessing toxicological risk of tobacco products

Differentiation among American cigarettes relies primarily on the use of proprietary tobacco blends, menthol, tobacco substitutes, paper porosity, paper additives, and filter ventilation. These characteristics substantially alter per cigarette yields of tar and nicotine in standardized protocols promulgated by government agencies. However, due to compensatory alterations in smoking behavior to sustain a preferred nicotine dose (e.g., by increasing puff frequency, inhaling more deeply, smoking more cigarettes per day, or blocking filter ventilation holes), smokers actually inhale similar amounts of tar and nicotine regardless of any cigarette variable, supporting epidemiological evidence that all brands have comparable disease risk. Consequently, it would be advantageous to develop assays that realistically compare cigarette smoke (CS)-induced genotoxicity regardless of differences in cigarette construction or smoking behavior. One significant indicator of potentially carcinogenic DNA damage is double strand breaks (DSBs), which can be monitored by measuring Ser 139 phosphorylation on histone H2AX. Previously we showed that phosphorylation of H2AX (defined as γH2AX) in exposed lung cells is proportional to CS dose. Thus, we proposed that γH2AX may be a viable biomarker for evaluating genotoxic risk of cigarettes in relation to actual nicotine/tar delivery. Here we tested this hypothesis by measuring γH2AX levels in A549 human lung cells exposed to CS from a range of commercial cigarettes using various smoking regimens. Results show that γH2AX induction, a critical event of the mammalian DNA damage response, provides an assessment of CS-induced DNA damage independent of smoking topography or cigarette type. We conclude that γH2AX induction shows promise as a genotoxic bioassay offering specific advantages over the traditional assays for the evaluation of conventional and nonconventional tobacco products.     

Smoking habits of men and women.

The smoking habits of 1501 cigarette smokers attending 28 general practitioners in five group practices in London were assessed. Prevalence of smoking, daily cigarette consumption, and the use of cigars, untipped cigarettes, and hand-rolled cigarettes were lower in the women. After controlling for consumption the proportions of men and women who smoked every day were similar. Women who smoked 20 or more a day were similar to men in their self-reported inhaling habits and use of low-nicotine cigarettes. The results suggest that women differ from men in those aspects of smoking that are determined predominantly by social factors but that their smoking habits become similar when pharmacological motivation takes over. This apparently occurs when consumption reaches about 20 cigarettes a day, when smoking almost inevitably becomes a regular event and the sex differences disappear.     

Cigarette smoking by socioeconomic group,sex, and age: effects of price,income, and health publicity.

OBJECTIVE--To assess effects of price, income, and health publicity on cigarette smoking by age, sex, and socioeconomic group. DESIGN--Econometric multiple regression analysis of data on cigarette smoking from the British general household survey. SUBJECTS--Random sample of adult population in Britain interviewed for biennial general household surveys 1972-90. MAIN OUTCOME MEASURES--Changes in cigarette consumption and prevalence of smoking. RESULTS--Price elasticities of demand for cigarettes (percentage change in cigarette consumption for a 1% change in price) were significant at -0.5 (95% confidence interval -0.8 to -0.1) for men and -0.6 (-0.9 to -0.3) for women, were highest in socioeconomic group V (-1.0 for men and -0.9 for women), and lowest (not significantly different from zero) in socioeconomic groups I and II. The gradient in price elasticities by socioeconomic group was significant for men (F = 5.6, P = 0.02) and for women (F = 6.1, P = 0.02). Price was a significant factor in cigarette consumption by age for women in every age group and for men aged 25-34. Cigarette consumption by young men aged 16-34 increased with income. There was a significant decrease in smoking over time by women in socioeconomic groups I and II and by men in all age and social groups except socioeconomic group V attributable to health publicity. Price significantly affected smoking prevalence in socioeconomic group V (-0.6 for men and -0.5 for women) and for all women (-0.2). CONCLUSIONS--Men and women in lower socioeconomic groups are more responsive than are those in higher socioeconomic groups to changes in the price of cigarettes and less to health publicity. Women of all ages, including teenagers, appear to have been less responsive to health publicity than have men but more responsive to price. Response to health publicity decreased linearly with age. Real price increases in cigarettes could narrow differences between socioeconomic groups in smoking and the related inequalities in health, but specific measures would be necessary to ameliorate effects on the most deprived families that may include members who continue to smoke. The use of a policy to steadily increase cigarette tax is likely to help achieve the government''s targets for smoking and smoking related diseases.     

Effect of cigarette smoking on gastric emptying.

Gastric emptying after a test meal was studied in 17 normal volunteers--10 habitual smokers and seven non-smokers. The solid component of the test meal was labelled with technetium and the liquid component with indium. After one meal the habitual smokers smoked two cigarettes. Emptying curves were produced for both technetium and indium, and the differences between curves for meals with and without cigarettes were analysed. Cigarette smoking accelerated the rate at which the liquid component of a meal left the stomach. This may be important in the pathogenesis of duodneal ulcer and the delay in healing caused by cigarette smoking.     

Systematic review of the epidemiological evidence comparing lung cancer risk in smokers of mentholated and unmentholated cigarettes

Background

US mentholated cigarette sales have increased considerably over 50 years. Preference for mentholated cigarettes is markedly higher in Black people. While menthol itself is not genotoxic or carcinogenic, its acute respiratory effects might affect inhalation of cigarette smoke. This possibility seems consistent with the higher lung cancer risk in Black men, despite Black people smoking less and starting smoking later than White people. Despite experimental data suggesting similar carcinogenicity of mentholated and non-mentholated cigarettes, the lack of convincing evidence that mentholation increases puffing, inhalation or smoke uptake, and the similarity of lung cancer rates in Black and White females, a review of cigarette mentholation and lung cancer is timely given current regulatory interest in the topic.

Methods

Epidemiological studies comparing lung cancer risk in mentholated and non-mentholated cigarette smokers were identified from MedLine and other sources. Study details were extracted and strengths and weaknesses assessed. Relative risk estimates were extracted, or derived, for ever mentholated use and for long-term use, overall and by gender, race, and current/ever smoking, and meta-analyses conducted.

Results

Eight generally good quality studies were identified, with valid cases and controls, and appropriate adjustment for age, gender, race and smoking. The studies afforded good power to detect possible effects. However, only one study presented results by histological type, none adjusted for occupation or diet, and some provided no results by length of mentholated cigarette use. The data do not suggest any effect of mentholation on lung cancer risk. Adjusted relative risk estimates for ever use vary from 0.81 to 1.12, giving a combined estimate of 0.93 (95% confidence interval 0.84-1.02, n = 8), with no increase in males (1.01, 0.84-1.22, n = 5), females (0.80, 0.67-0.95, n = 5), White people (0.87, 0.75-1.03, n = 4) or Black people (0.90, 0.73-1.10, n = 4). Estimates for current and ever smokers are similar. The combined estimate for long-term use (0.95, 0.80-1.13, n = 4) again suggests no effect of mentholation.

Conclusion

Higher lung cancer rates in Black males cannot be due to their greater preference for mentholated cigarettes. While some study weaknesses exist, the epidemiological evidence is consistent with mentholation having no effect on the lung carcinogenicity of cigarettes.     

Influence of escalating alternative reinforcer values on cigarette choice

The availability of alternative reinforcers reduces drug taking. Escalating alternative reinforcer values have been used to initiate and maintain abstinence from drug use. A reset in reinforcer value has been added to the schedule of alternative reinforcer presentation to discourage relapse. The purpose of this preliminary study was to test the influence of escalating and escalating and resetting alternative reinforcer value on cigarette choice in the human laboratory. Fourteen daily cigarette smokers completed this experiment, which required one practice and three experimental sessions. During each experimental session, subjects made six choices between smoking a cigarette and receiving money, available under Constant, Escalating or Escalating and Resetting conditions. The total number of cigarettes chosen and puffs taken, but not the maximum consecutive number of cigarettes choices, was decreased in the Escalating condition relative to the Constant condition. The maximum number of consecutive cigarettes chosen was decreased in the Escalating and Resetting condition relative to the Constant condition. The proportion of money earned was increased in the Escalating condition relative to the Constant and Escalating and Resetting conditions. These initial findings indicate that whereas an escalating alternative reinforcer schedule reduces cigarette smoking overall, an escalating and resetting alternative reinforcer schedule may reduce repeated cigarette smoking (i.e., relapse).     

Evidence for cigarette smoke-induced calcitonin secretion from lungs of man and hamster

In hamsters, acute cigarette smoke inhalation increased serum levels of the hormone calcitonin; and, in humans, smoking of two high-nicotine content cigarettes increased serum and urine levels of this hormone. The source of this immunoreactive calcitonin (iCT) does not appear to be the thyroid gland, since previously thyroidectomized patients demonstrated a similar response. In the hamster, the increased serum iCT levels were accompanied by a decreased lung tissue iCT content and hypocalcemia. It is suggested that the source of the cigarette smoke-induced hypercalcitonemia is the lung, possibly from the iCT-containing pulmonary neuroendocrine (PNE) cells. Moreover, this response appears to be dependent on the nicotine content of the cigarettes.     

A laryngologist looks at cigarettes

The relationship between cancer of the lung and cigarette consumption is far from proved. It would appear from observations and experiments cited that some form of filtration of smoke is better than none. It is important that physicians be sufficiently acquainted with the subject to enable them to advise their patients concerning cigarettes and cigarette smoking.     

The Chilliwack Respiratory Survey, 1963: Part IV. The Effect of Tobacco Smoking on the Prevalence of Respiratory Disease

Chronic non-specific respiratory disease was found by a survey at Chilliwack, B.C., to affect 29.3% of men and 18.0% of women between the ages of 25 and 74. The habit of current cigarette smoking was found to be the most important single factor associated with respiratory disease, and was found to be related to changes in simple measures of lung function. The authors were unable to confirm the existence of a threshold in lifetime cigarette smoking before respiratory disease occurred.Comparisons were made with a population previously studied at Berlin, New Hampshire, U.S.A., in 1961. At Berlin, where pollution by SO₂ and dust-fall had been thoroughly documented, the comparable prevalence rates for respiratory disease were 40.0% for men and 21.6% for women. When differences between the two populations as to age and number of cigarettes smoked daily were taken into account, the disease rates in these two communities were found to be quite similar. The Chilliwack sample did, however, have significantly higher values for the lung function tests.     

Blood carboxyhaemoglobin,plasma thiocyanate,and cigarette consumption: implications for epidemiological studies in smokers.

Carboxyhaemoglobin and plasma thiocyanate concentrations were found to be significantly correlated with self-reported daily cigarette consumption in 360 smokers (r = 0.416 and 0.412 respectively; p less than 0.001). The extent to which inhalation patterns affected the intake of cigarette smoke constituents was determined from the partial correlation between carboxyhaemoglobin and plasma thiocyanate concentrations after the number of cigarettes smoke per day had been allowed for (r = 0.48). Thus 23% of the variation in carboxyhaemoglobin and thiocyanate concentrations was accounted for by the was a cigarette was smoked and a further 21% by the number smoked a day. Furthermore, the relation between carboxyhaemoglobin or plasma thiocyanate and daily cigarette consumption was not linear but reached an asymptote at consumption rates above 25 cigarettes a day. These results suggest that by itself daily cigarette consumption will not identify those smokers most at risk and will also underestimate and dose-response relationship between smoking and selected diseases.     

'Normal' cigarette smoking increases free cortisol in habitual smokers.

In habitual smokers salivary cortisol responses to cigarette smoking were investigated. In the first study, 31 adults assigned to two experimental groups smoked either one or two cigarettes of their preferred brand. Mean salivary cortisol levels were significantly elevated after smoking of two cigarettes. In the second study, 10 smokers and 10 nonsmokers provided saliva samples at 20 min intervals over a 12-hr period. While environmental stimuli were paralleled in both groups overall cortisol output was significantly elevated in the smokers. These data suggest that 'normal' cigarette smoking can increase free cortisol levels.     

Passive exposure to tobacco smoke: saliva cotinine concentrations in a representative population sample of non-smoking schoolchildren.

Saliva cotinine concentrations in 569 non-smoking schoolchildren were strongly related to the smoking habits of their parents. When neither parent smoked the mean concentration was 0.44 ng/ml, rising to 3.38 ng/ml when both parents were cigarette smokers. Mothers'' smoking had a stronger influence than did fathers'' (p less than 0.01). In addition, there was a small independent effect of number of siblings who smoked (p less than 0.01). The dose of nicotine received from fathers'' smoking was estimated as equivalent to the active smoking of 30 cigarettes a year, that from mothers'' smoking as equivalent to smoking 50 cigarettes a year, and that from both parents smoking as equivalent to smoking 80 cigarettes a year. This unsolicited burden may be prolonged throughout childhood and poses a definite risk to health.     

Carcinoma of Bronchus and the Smoking Habit in Rhodesian Africans

Comparison of the smoking habits of 32 adult male Africans with carcinoma of the bronchus and 32 controls showed that 87.5% of the patients with lung cancer were cigarette smokers compared with only 22% of the controls. The distribution of histological types of growth confirmed findings by other workers.The absence of atmospheric pollution in Rhodesia makes it likely that cigarette-smoking is the most important causative factor in the aetiology of lung cancer among Rhodesian Africans. Further work is needed to determine the level of consumption of cigarettes and type of smoking habits which lead to a serious risk of cancer.