Risks of premature death from smoking in 15-year-old Australians

Abstract: This cross-sectional actuarial analysis of 1990 mortality data aimed to estimate absolute risk of premature death from all causes, and from lung cancer, ischaemic heart disease and chronic bronchitis/emphysema due to tobacco smoking in the Australian population, and to estimate the number of current 15-year-old smokers in the 1990 Australian population who will die prematurely due to smoking. Competing risks were allowed for in the calculations. In males, conditional life expectancy for 15-year-olds was 78.0 years in nonsmokers, 73.3 years in ever-smokers, and 71.5 years in smokers of more than one packet a day. For 15-year-old females, life expectancy was 82.0 years in nonsmokers, 78.4 years in eversmokers, and 76.9 years in smokers of more than one packet a day. The risk of premature death due to smoking in ever-smokers was estimated as 14.6 per cent in males (before 75 years) and 11.9 per cent in females (before 80 years), with lung cancer (male: 4.2 per cent; female: 3.4 per cent), ischaemic heart disease (male: 3.7 per cent; female: 1.7 per cent) and chronic bronchitis/emphysema (male: 2.4 per cent; female: 2.5 per cent) as the major contributors. From one year of 15-year-old male smokers (26 713), 3 916 premature deaths due to tobacco can be expected; this includes 1 106 lung cancer deaths, 991 ischaemic heart disease deaths and 641 chronic bronchitis/emphysema deaths. From one year of 15-year-old female smokers (32 355), 3 861 premature deaths can be expected; this includes 1 086 lung cancer deaths, 559 ischaemic heart disease deaths and 798 chronic bronchitis/emphysema deaths.     

南充市居民吸烟归因早死分析

本文调查了南充市居民１９９０年的死因和生前吸烟情况，并应用ＰＹＬＬ和ＰＹＬＬＲ来衡量吸烟对居民的早死影响。结果表明，吸烟人群与非吸烟人群死亡率有极显著性差异（χ２＝５９．２９，Ｐ＜０．００１），ＲＲ１．６８，吸烟特异死亡数（ＳＡＭ）２９２例，归因危险比分（ＳＡＦ）０．５０３。性别率比（ＲＲ）２．３８，肺癌和ＣＯＰＤ的ＳＡＦ分别０．７２和０．６６。吸烟超肺癌死亡０．８３。     

Cohort analysis of cigarette smoking and lung cancer incidence among Norwegian women

BACKGROUND: Cancer registries have for decades surveyed the development of cancer diseases. Data on incident cases includes demographic variables. Knowledge of the temporal distribution of risk factors on the same variables makes it possible to model the relationship between disease and risk factor. The results of such analyses might be difficult to interpret since they are based on aggregated data. But the availability of these data sources should encourage further exploration of its possibilities and limitations. METHODS: The temporal pattern of smoking habits in 5-year birth cohorts from 1890-1949 was established, with data on the proportions of current smokers, former smokers and non-smokers and estimated average daily consumption of tobacco and average duration of smoking. The lung cancer incidence among the cohorts in 1953-1992 was analysed by a model which included an additive excess risk for smokers that depended on daily dose and duration of smoking. RESULTS: The lung cancer incidence in later decades was adequately described by the model, which showed a simple relationship with smoking behaviour in the cohorts. For both current smokers and former smokers, the excess risk was about proportional to the daily amount smoked and the 4.5 power of duration of smoking. The age-specific rates for non-smokers were close to a fifth-power curve of age. CONCLUSIONS: Even if lung cancer incidence is not determined separately for groups with known smoking habits, plausible estimates of the effect of smoking can be derived if appropriate information is available on temporal smoking habits in the population.     

Marriage to a smoker and lung cancer risk.

As part of a population-based case-control study of lung cancer in New Mexico, we have collected data on spouses' tobacco smoking habits and on-the-job exposure to asbestos. The present analyses include 609 cases and 781 controls with known passive and personal smoking status, of whom 28 were lifelong nonsmokers with lung cancer. While no effect of spouse cigarette smoking was found among current or former smokers, never smokers married to smokers had about a two-fold increased risk of lung cancer. Lung cancer risk in never smokers also increased with duration of exposure to a smoking spouse, but not with increasing number of cigarettes smoked per day by the spouse. Our findings are consistent with previous reports of elevated risk for lung cancer among never smokers living with a spouse who smokes cigarettes.     

2013年中国居民吸烟对归因死亡和期望寿命的影响

目的 分析2013年我国吸烟的归因死亡和对期望寿命的影响。方法 利用2013年死因监测数据和慢性病及其危险因素监测数据,针对不同疾病特点,将以现在吸烟率作为暴露水平的直接法和以吸烟影响比作为暴露水平的间接法相结合,计算吸烟导致不同疾病死亡的人群归因分值,从而估计吸烟对于死亡和期望寿命的影响。结果 2013年中国人群由于吸烟导致约159.33万人死亡,占总死亡人数的17.38%,其中男性吸烟导致的死亡占比（23.66%）远远高于女性（8.30%）,城市人群吸烟导致的死亡占比（17.24%）略低于农村人群（17.51%）,东部地区人群吸烟导致的死亡占比最低（16.81%）,西部地区最高（17.91%）。2013年中国人群吸烟导致死亡人数在前三位的疾病是肺癌、COPD和缺血性心脏病,吸烟导致死亡归因分值最大的前三位疾病是肺癌、COPD和鼻咽癌。2013年中国人群吸烟导致期望寿命损失2.04岁,其中最高的为西部地区男性,共损失3.05岁。结论 吸烟仍是我国重要的公共卫生问题,针对重点地区人群开展控烟工作,可以降低吸烟相关疾病的死亡,有效地提高我国人群健康水平。     

Temporal changes and determinants of smoking habits with respect to prevention

Smoking habits are seen as one of the most important risk factors in developed countries for the incidence of cardiovascular diseases and as the major single cause of premature death. The present study analysed smoking habits in participants of the MONICA-Surveys S1 (1984/85), S2 (1989/90) and S3 (1994/95) concerning prevalence, associated factors, time trends and preventive consequences. An essential aim of these studies was to identify risk groups, that should be addressed in prevention campaigns leading to a reduction of the high mortality due to cardiovascular diseases. The participants of the MONICA-Survey S3 (1994/95) had lower proportions of smokers (31.2 % for men and 22.0 % for women) as compared to estimated proportions of the entire German population (National health survey 1998: 37.4 % und 29.9 %). Women had always a lower proportion of smokers than men in each age group or sociodemographic factor. Strong associations of smoking habits with educational levels, family status and occupational position were observed for men and women. A positive time trend with decreasing smoking prevalence was determined for men. In contrast, an increase in the prevalence of female smokers was observed. The intention to change smoking habits was associated with different factors in men and women. For men, mainly "external" factors like social status or physical activity were important. Women seemed to be more influenced by "internal" matters (somatic complaints, negative self-rated health). Sex-, age- and educational status-specific activities and recommendations are considered to be essential for targeting different person groups in a more focused way.     

A case-control study of lung cancer in relation to silica exposure and silicosis in a rural area in Japan

PURPOSE: In southeast Okayama Prefecture, Japan, there have been reports of a high prevalence of silicosis among refractory brick production workers. Recently, a high mortality rate of lung cancer among the local residents has been observed. Therefore, a population based case-control study was conducted concerning the relationship between silica, silicosis, and lung cancer using multiple cancer controls. METHODS: Cases and controls were restricted to male subjects and information was obtained from death certificates from 1986 to 1993 in the area. Three categories of deceased control groups were selected: a series of deaths from liver cancer, colon cancer, and cancers of other organs, which was assumed not to be related to silica exposure. Age and smoking habits were adjusted by stratified analysis using the Mantel-Haenszel odds ratio estimates. Unconditional logistic regression analysis was also conducted to control potential confounding factors; such as age and smoking habits. RESULTS: The age-, smoking-adjusted odds ratios were 1.94 (0.94-4.43) for the colon cancer control group, 2.13 (1.19-3.85) for the other cancer control group related to silica exposure, and 2.94 (1.30-8.90) and 2.69 (1.43-5.37) related to silicosis, respectively. The direct weighted average using the estimates for colon and the other cancer controls was 2.06 (1.29-3.29) for silica exposure, and 2.77 (1.60-4.77) for silicosis. Histological or cytological types of lung cancer cases were obtained from 64.1% of the subjects (118/184). As for the histologic type of lung cancer, small cell carcinoma was higher among those who had been silica-exposed workers than the unexposed lung cancer cases and the data from the general Japanese population. On chest x-ray findings, elevated lung cancer mortality compared with cancers other than lung cancer was demonstrated among patients without large opacities. CONCLUSIONS: Silica exposure increased the lung cancer mortality in the area. A high lung cancer mortality rate in the area could be explained by silica exposure and silicosis prevalence in this area.     

Does asbestosis increase the risk of lung cancer?

Summary The question of whether asbestos workers with or without asbestosis have the same risk of lung cancer has not been adequately addressed in the literature. Studies of asbestos workers indicate that clinical symptoms and abnormal lung X-rays are more frequent among smokers than non-smokers, and some studies show that workers with asbestosis compared to those without asbestosis are more likely to be smokers or ex-smokers. Since smoking has a large affect on the risks of lung cancer, smoking habits should be considered when evaluating the risk of lung cancer among persons with and without asbestosis. Some studies show that the risk of lung cancer is higher for persons with asbestosis compared to persons without asbestosis, but none of these studies also considered the combined effects of smoking and asbestos exposure on the risk of lung cancer. It is unlikely that the higher risk of lung cancer to persons with asbestosis is only due to their higher prevalence of smoking. Some studies have suggested that asbestos workers with asbestosis may have a higher risk of lung cancer, but no definite conclusions can be drawn since dose-response relations were not evaluated. Further studies are needed to evaluate the interrelationships of smoking, asbestosis and the risk of lung cancer.     

Do adolescents appreciate the risks of smoking? Evidence from a national survey.

PURPOSE: To evaluate whether adolescents understand the risks of smoking when they decide to start. Estimates of objective risks that can be compared with epidemiologic evidence suggest that adolescents overstate the risks. Ratings of personal risk suggest the opposite. METHODS: A nationally representative telephone survey of 300 14- to 22-year-old nonsmokers and 300 14- to 22-year-old smokers was conducted. Respondents estimated both objective and personal risks of smoking, and smokers reported their plans to quit. Objective estimates were compared with both epidemiologic evidence and personal ratings of risk. Regression procedures were used to assess relationships between different estimates of risk and between risk estimates and plans to quit. RESULTS: Two of the three objective estimates of risk revealed high proportions of misunderstanding. Over 40% of smokers and 25% of nonsmokers underestimated, or did not know, the likelihood of smoking-related death, and over 40% did not know, or underestimated, the number of years of life lost owing to smoking. Although young people overestimated lung cancer risk relative to objective data, these estimates are inflated by underestimation of the fatality of lung cancer and by overlap with other illnesses not included in objective risk measures. Young smokers exhibited optimism about personal risks of smoking regardless of their perceptions of objective risk. Both objective and personal measures of risk predicted plans to quit. CONCLUSIONS: Because perceptions of both personal and objective risks are related to plans to quit, antismoking messages should include evidence about risk, particularly to the individual smoker.     

The risk of lung cancer with increasing time since ceasing exposure to asbestos and quitting smoking

Objectives

To examine if the risk of lung cancer declines with increasing time since ceasing exposure to asbestos and quitting smoking, and to determine the relative asbestos effect between non‐smokers and current smokers.

Methods

A cohort study of 2935 former workers of the crocidolite mine and mill at Wittenoom, who responded to a questionnaire on smoking first issued in 1979 and on whom quantitative estimates of asbestos exposure are known. Conditional logistic regression was used to relate asbestos exposure, smoking category, and risk of lung cancer.

Results

Eighteen per cent of the cohort reported never smoking; 66% of cases and 50% of non‐cases were current smokers. Past smokers who ceased smoking within six years of the survey (OR = 22.1, 95% CI 5.6 to 87.0), those who ceased smoking 20 or more years before the survey (OR = 1.9, 95% CI 0.50 to 7.2), and current smokers (<20 cigarettes per day (OR = 6.8, 95% CI 2.0 to 22.7) or >20 cigarettes per day (OR = 13.2, 95% CI 4.1 to 42.5)) had higher risks of lung cancer compared to never smokers after adjusting for asbestos exposure and age. The asbestos effect between non‐smokers and current smokers was 1.23 (95% CI 0.35 to 4.32).

Conclusion

Persons exposed to asbestos and tobacco but who subsequently quit, remain at an increased risk for lung cancer up to 20 years after smoking cessation, compared to never smokers. Although the relative risk of lung cancer appears higher in never and ex‐smokers than in current smokers, those who both smoke and have been exposed to asbestos have the highest risk; this study emphasises the importance of smoking prevention and smoking cessation programmes within this high risk cohort.     

A review of residential radon case-control epidemiologic studies performed in the United States.

Lung cancer is the leading cause of cancer death in the United States for both men and women. Although most lung cancer deaths are attributable to tobacco usage, even secondary causes of lung cancer are important because of the magnitude of lung cancer incidence and its poor survival rate. This review summarizes the basic features and major findings from the published U.S. large-scale residential radon case-control studies performed in New Jersey, Iowa, and Missouri (two studies). The methodology from an unpublished study covering Connecticut, Utah, and Southern Idaho is also presented. Overall, the higher categorical risk estimates for these published studies produced a positive association between prolonged radon exposure and lung cancer. Two studies (Missouri-II and Iowa) that incorporated enhanced dose estimates produced the most compelling evidence suggesting an association between prolonged residential radon exposure and lung cancer. The prevailing evidence suggests that the statistically significant findings may be related to improved retrospective radon exposure estimates. The general findings from the U.S. studies, along with extrapolations from radon-exposed underground miners, support the conclusion that after cigarette smoking, prolonged residential radon exposure is the second leading cause of lung cancer in the general population.     

Lung function predicts survival in a cohort of asbestos cement workers

Purpose  To study the predictive power of respiratory screening examinations a cohort of asbestos workers was followed from active work in an asbestos cement plant until death. Methods  From a cohort with data on individual exposure since first employment 309 workers who had a preventive medical examination in 1989/1990 were observed until death or the end of 2006. The impact of asbestos exposure (fibre years) and of smoking history on lung function was examined by linear regression, on specific causes of death and total mortality by Cox regression. The prognostic value of lung function, chest X-ray, and various clinical findings regarding total mortality was also examined by Cox regression. Results  Lung function proved to be the best predictor of survival apart from current smoking. Depending on the lung function variable an impairment by the interquartile range resulted in a hazard ratio of 1.5–1.6 while for current smokers it was 2.3. An increase of 70 fibre years (interquartile range) led to a hazard ratio of only 1.1. Lung function was influenced by asbestos exposure, current (but not former) smoking, and by pathological X-ray findings. The risk for pleural mesothelioma was dominated by time since first exposure to crocydolite in the pipe factory while the risk for bronchial cancer increased with smoking and total fibre years. An unexpected finding was an increase of gastric cancer in asbestos cement workers. Conclusion  Lung function decrease predicts risk of premature death better than exposure history and regular spirometry should therefore be offered as primary screening to all former asbestos workers. In workers with a history of high cumulative exposure or rapid lung function decrease or radiological signs (diffuse pleural thickening or small irregular opacities) more sensitive techniques (high resolution computer tomography) need to be applied. All smokers with a history of asbestos exposure should be given free smoking cessation therapy to prevent premature death and lung cancer in particular.     

The impact of declining smoking on radon-related lung cancer in the United States

Objectives. We examined the effect of current patterns of smoking rates on future radon-related lung cancer.Methods. We combined the model developed by the National Academy of Science''s Committee on Health Risks of Exposure to Radon (the BEIR VI committee) for radon risk assessment with a forecasting model of US adult smoking prevalence to estimate proportional decline in radon-related deaths during the present century with and without mitigation of high-radon houses.Results. By 2025, the reduction in radon mortality from smoking reduction (15 percentage points) will surpass the maximum expected reduction from remediation (12 percentage points).Conclusions. Although still a genuine source of public health concern, radon-induced lung cancer is likely to decline substantially, driven by reductions in smoking rates. Smoking decline will reduce radon deaths more that remediation of high-radon houses, a fact that policymakers should consider as they contemplate the future of cancer control.The Environmental Protection Agency (EPA) estimates that radon in the home is responsible for over 21 000 lung cancer deaths annually among Americans, making radon the major cause of lung cancer after tobacco use. The agency considers radon a major public health problem and, since 1986, has mounted an aggressive campaign urging the public to test their homes for radon and take remedial actions when airborne concentrations of radon exceed 4 picocuries per liter of air (4 pCi/L).¹For its most current risk assessment, the EPA employed the BEIR VI model, developed by the Committee on Health Risks of Exposure to Radon (the BEIR VI committee) of the National Academy of Sciences (NAS).² The BEIR VI model''s calculation of radon-related risk (as was the case for its predecessor, BEIR IV) was estimated from data on miners, who are subject to much higher levels of radon than is the average population and have shown a significant correlation between lung cancer risk and radon exposure. Although the extrapolation of the results from miners to the much less exposed general public initially caused controversy, the BEIR VI implications of risk have been validated by recent case–control studies at the population level.^3–5 The BEIR VI model is thus broadly accepted as a valid predictor of the radon-related risk for typical individuals.The available data suggest a strong interaction effect between radon exposure and smoking status in the determination of lung cancer risk, which means that smokers are at a much higher risk of dying from radon-induced lung cancer than are nonsmokers. This interaction is recognized in the BEIR VI model, which postulates a superadditive (but less than multiplicative) interaction between smoking and radon. To appreciate the magnitude of this interaction, consider the fact that the background lung cancer risk ratio between ever and never smokers is 13 to 1.⁶ A multiplicative interaction between radon and smoking would imply that, at the same level of radon exposure, the ratio of radon-induced excess risk between ever and never smokers would be the same as the ratio of background lung cancer risks between those 2 groups (i.e., 13 to 1). On the other hand, an additive relationship between radon and smoking would imply that radon would add the same extra risk to ever and never smokers exposed to the same dosage, making the excess risks ratio between the 2 groups equal 1 to 1. Using the BEIR VI model, the EPA calculates that, at a radon level of 4 pCi/L, the lifetime risk of radon-induced lung cancer death is 62 per 1000 for ever smokers and 7 per 1000 for never smokers, yielding an excess risk ratio of 8.86 to 1 between the 2 groups.¹ As 8.86 falls between 1 and 13, the BEIR VI model implies that radon adds more risk to ever smokers than to never smokers, but that excess risk is less than proportional to the lung cancer background risk of those 2 groups, suggesting a submultiplicative (but superadditive) relationship between smoking and radon. The BEIR VI model does not distinguish between current and former smokers.Given this implied superadditive interaction, the number of future radon deaths will heavily depend on population smoking rates. As smoking rates in the United States have been falling for several decades and are expected to continue declining, the overall magnitude of the radon death toll is likely to decline as well. The question we try to address is what is the magnitude of this expected decline?We extend the EPA''s analysis by examining the sensitivity of radon-related lung cancer in the United States to future smoking rates. We estimate the proportional decline in the number of lung cancer deaths caused by radon for the period 2006 through 2100, assuming a likely scenario for smoking rates. We do not forecast specific numbers of radon-induced lung cancer deaths because these numbers will depend on many factors likely to change over such a long period of time. Instead, we concentrate on the relative impact of the smoking decline on the overall radon death toll and also examine the benefits of remediating houses with high radon levels given the results of our analysis. Following the EPA''s approach, in our computations, we employ the BEIR VI model, thereby assuming a submultiplicative relationship between smoking and radon. In the remaining sections of the report, we discuss the assumptions, models, and data employed in our analysis, our findings, and the implications of the results for both the magnitude of radon-related risk to the population and the effectiveness of housing remediation in reducing such risk.     

Histological types of lung cancer among smelter workers exposed to arsenic.

The histological distribution of lung cancer was investigated in 93 men who had worked at a Swedish smelter with high levels of arsenic. A comparison was made with a group of 136 patients with lung cancer from the county where the smelter was located. Company records provided information on occupational exposure and data on smoking habits were obtained from a next of kin of each subject. No pronounced differences in the histological types of lung carcinomas between smelter workers and the reference group could be seen for smokers. Some analyses indicated an increased proportion of adenocarcinomas among the smelter workers, which confirmed earlier data, but these findings were difficult to interpret. Cases among smelter workers who had never smoked showed a histological distribution resembling that in smokers, indicating that the work environment at the smelter and smoking had a similar influence on the risk for different types of lung cancer.     

Relative importance of cigarette smoking in occupational lung disease.

Since 1900 respiratory disease has remained a constant serious cause of chronic ill health and premature death in Britain. The falling importance of tuberculosis and pneumonia has been off-set by the rise in lung cancer. Bronchitis morbidity and mortality have fallen only slightly since 1935. To produce any real improvement in the future existing information as to cause must be studied. The relative contribution of occupational exposure is compared with the importance of cigarette smoking. Relevant information is scanty and has been produced to emphasise the existence of occupational diseases rather than assess their importance to the community as whole. In Britain the evidence is that within the coal mining and iron and steel industries conditions are now such that dust exposure contributes little to the morbidity or mortality compared with the workers' smoking habits. Similar results have been shown by a cross-sectional survey of many dusty occupations in Western Germany. Only in the disappearing Welsh slate industry has dust disease been at least as important as smoking. Until the current regulations were introduced conditions existed among asbestos workers such that the combined effect of cigarette smoking and dust exposure led to a loss of life expectation of over 10 years in moderate smokers. Since the new regulations were introduced the risk for asbestos workers should approximate to that for other industrial workers. While control of occupational exposure to respiratory hazards remains important, a far greater improvement to respiratory health would be produced by controlling tobacco smoking.     

Lung cancer risk in white and black Americans

PURPOSE: To test whether differences in smoking-related lung cancer risks in blacks and whites can explain why lung cancer incidence is greater in black males than in white males but about equal in black and white females, given that a greater proportion of blacks are smokers, but smoke far fewer cigarettes per day than do whites. METHODS: A hospital-based case-control study was conducted between 1984 and 1998 that included interviews with 1,710 white male and 1,321 white female cases of histologically confirmed lung cancer, 254 black male and 163 black female cases, and 8,151 controls. Relative risks were estimated via odds ratios using logistic regression, adjusted for age, education, and body mass index. RESULTS. We confirmed prior reports that smoking prevalence is higher but overall dosage is lower among blacks. Overall ORs were similar for blacks and whites, except among the heaviest smoking males (21+ cigarettes per day or 37.5 pack-years), in whom ORs for blacks were considerably greater than for whites. Long-term benefits of cessation were similar for white and black ex-smokers. Smokers of menthol flavored cigarettes were at no greater risk for lung cancer than were smokers of unflavored brands. CONCLUSIONS. Lung cancer risks were similar for whites and blacks with similar smoking habits, except possibly for blacks who were very heavy smokers; this sub-group is unusual in the general population of African American smokers. Explanations of racial disparities in lung cancer risk may need to account for modifying factors including type of cigarette (yield, mentholation), diet, occupation, and host factors such as ability to metabolize mainstream smoke carcinogens.     

Histological types of lung cancer among smelter workers exposed to arsenic

The histological distribution of lung cancer was investigated in 93 men who had worked at a Swedish smelter with high levels of arsenic. A comparison was made with a group of 136 patients with lung cancer from the county where the smelter was located. Company records provided information on occupational exposure and data on smoking habits were obtained from a next of kin of each subject. No pronounced differences in the histological types of lung carcinomas between smelter workers and the reference group could be seen for smokers. Some analyses indicated an increased proportion of adenocarcinomas among the smelter workers, which confirmed earlier data, but these findings were difficult to interpret. Cases among smelter workers who had never smoked showed a histological distribution resembling that in smokers, indicating that the work environment at the smelter and smoking had a similar influence on the risk for different types of lung cancer.     

Passive smoking in adulthood and cancer risk

Overall cancer risk from adult passive smoking has been examined using smoking by spouse as the measure of exposure. Information on smoking by spouse was obtained for 518 cancer cases and 518 noncancer controls. Cancer cases were identified from a hospital-based tumor registry in North Carolina. Cases included all sites except basal cell cancer of the skin and were between the ages of 15 and 59 years at the time of diagnosis. Cancer risk among individuals ever married to smokers was 1.6 times that among those never married to smokers (p less than 0.01). This increased risk was not explained by confounding by individual smoking habits, demographic characteristics, or social class. Elevated risks were seen for several specific cancer sites and were not limited to lung cancer or other "smoking-related" tumors. Risks from passive smoking appeared greater among groups generally at lower cancer risk (females, nonsmokers, and individuals younger than age 50 years), but were not limited to these groups.     

Effects of smoking and smoking cessation on life expectancy in an elderly population in Beijing, China, 1992-2000: an 8-year follow-up study

Background

We assessed the effects of smoking and smoking cessation on life expectancy and active life expectancy among persons aged 55 years or older in Beijing.

Methods

This study included 1593 men and 1664 women who participated in the Beijing Longitudinal Study of Aging, which commenced in 1992 and had 4 survey waves up to year 2000. An abridged life table was used to estimate life expectancy, in which age-specific mortality and age-specific disability rates were adjusted by using a discrete-time hazard model to control confounders.

Results

The mean ages (SD) for men and women were 70.1 (9.25) and 70.2 (8.72) years, respectively; mortality and disability rates during follow-up were 34.7% and 8.0%, respectively. In both sexes, never smokers had the highest life expectancy and active life expectancy across ages, as compared with current and former smokers. Current heavy smokers had a shorter life expectancy and a shorter active life expectancy than light smokers. Among former smokers, male long-term quitters had a longer life expectancy and longer active life expectancy than short-term quitters, but this was not the case in women.

Conclusions

Older adults remain at higher risk of mortality and morbidity from smoking and can expect to live a longer and healthier life after smoking cessation.Key words: smoking, smoking cessation, life expectancy, active life expectancy, elderly population, discrete-time hazard model     

Lung cancer and mesothelioma in the pleura and peritoneum among Swedish insulation workers

OBJECTIVES: To estimate the risk of cancer and death in Swedish insulation workers some years after their exposure to asbestos had stopped. One hypothesis was that the risk of lung cancer would tend to decrease some years after the exposure had ended. METHODS: In a cohort study the cancer morbidity and cause of death was investigated in 248 insulation workers and compared with the corresponding morbidity and mortality in the general population. Due to stringent regulations, exposure to asbestos of all types had almost ended in Sweden in the mid- 1970s. Through a questionnaire, surviving insulation workers were asked about their exposure to asbestos and their smoking habits. RESULTS: Between 1970 and 1994 there were 86 deaths compared with the 46.0 expected (standardised incidence ratio (SIR) 1.9; 95% confidence interval (95% CI) 1.5 to 2.3), the increase was mainly due to an increased cancer mortality. The morbidity was increased for lung cancer (11 cases v 2.5 expected (SIR 4.4; 95% CI 2.2 to 7.9)), peritoneal mesothelioma (seven cases; no expected incidence could be calculated as the occurrence is too rare in the general population), cancer in pancreas (five cases v 0.7 expected (SIR 7.1; 95% CI 2.3 to 16.7)). No cases of pleural mesothelioma were found. The risk of lung cancer did not tend to approach that of the general population after the exposure to asbestos decreased. CONCLUSIONS: In the 1980s and the early 1990s, Swedish insulation workers still have a highly increased risk of diseases related to asbestos. The attributable risk for death and cancer was about 50%. The study also confirms the previous finding that mesothelioma in insulation workers seems to be situated in the peritoneum more often than in the pleura.