Radon-222 concentration in groundwater and cancer mortality in North Carolina

Summary In a geographic correlation study, we explored the possibility that residential exposure to radon in groundwater may be related to cancers other than lung cancer. Measurements of radon in groundwater and 1978–1982 cancer mortality data from North Carolina, USA were used to investigate this relationship. Counties were categorized in two levels of radon exposure according to measured radon concentration and geology. In the lower exposure group (unexposed) county mean radon concentrations ranged from 0–228 pCi/1 (0–8436 Bq/m³), and in the upper group (potentially exposed) the range of county average concentrations was 229–10892 pCi/1 (8473–403004 Bq/m³), (median 1375 pCi/1 (50875 Bq/m³)). Adjusted mortality ratios and 95% confidence intervals were calculated for selected cancers, including leukemias, gastro-intestinal tract cancers, and respiratory tract cancers excluding lung cancer. In contrast to other ecologic studies, we found no consistent association between radon level and cancer mortality.     

Testing a BEIR-VI suggestion for explaining the lung cancer vs. radon relationship for U.S. counties

The BEIR-VI Report suggests that the large discrepancy between the observed lung cancer rate vs. radon exposure relationship for U.S. counties, and the predictions of linear no-threshold theory, may be explained by a strong negative correlation between smoking intensity and radon exposure. It proposes a model for testing that suggestion. We apply that model to the detailed data for U.S. counties; analysis shows that even a perfect negative correlation explains little more than half of the discrepancy, and the largest not-implausible correlation can explain less than a quarter of the discrepancy. We then extend the BEIR-VI suggestion to include a strong negative correlation between both the prevalence of smoking and the intensity of smoking. The largest not-implausible correlations can explain no more than 30% of the discrepancy. It is concluded that the previous interpretation of these data, that linear no-threshold theory fails this test, is sustained.     

A test of the linear-no threshold theory of radiation carcinogenesis

It has been pointed out that, while an ecological study cannot determine whether radon causes lung cancer, it can test the validity of a linear-no threshold relationship between them. The linear-no threshold theory predicts a substantial positive correlation between the average radon exposure in various counties and their lung cancer mortality rates. Data on living areas of houses in 411 counties from all parts of the United States exhibit, rather, a substantial negative correlation with the slopes of the lines of regression differing from zero by 10 and 7 standard deviations for males and females, respectively, and from the positive slope predicted by the theory by at least 16 and 12 standard deviations. When the data are segmented into 23 groups of states or into 7 regions of the country, the predominantly negative slopes and correlations persist, applying to 18 of the 23 state groups and 6 of the 7 regions. Five state-sponsored studies are analyzed, and four of these give a strong negative slope (the other gives a weak positive slope, in agreement with our data for that state). A strong negative slope is also obtained in our data on basements in 253 counties. A random selection-no charge study of 39 high and low lung cancer counties (+4 low population states) gives a much stronger negative correlation. When nine potential confounding factors are included in a multiple linear regression analysis, the discrepancy with theory is reduced only to 12 and 8.5 standard deviations for males and females, respectively. When the data are segmented into four groups by population, the multiple regression vs radon level gives a strong negative slope for each of the four groups. Other considerations are introduced to reduce the discrepancy, but it remains very substantial. Since cigarette sales data are available only on a statewide basis, mean radon data for states are analyzed. The linear regression for lung cancer rates vs radon levels is also negative and has a much steeper slope than that for the county data. When cigarette sales per capita is introduced into the regression, the negative slope for dependence on radon level is essentially unchanged.     

The residential radon-lung cancer association in U.S. counties: a commentary

There is little doubt that underground miners exposed to radon and its progeny have increased rates of lung cancer. Residential radon exposures should carry a possibly smaller risk of increased cancer. When it became possible to collect radon data in a large number of U.S. homes and the data were aggregated by counties, the apparent association with lung cancer was a negative one, even when many other variables were taken into account. Residential radon levels are higher in suburban residences leading to a negative association with population density. Population density is strongly positively associated with lung cancer. It follows that aggregate residential radon and lung cancer rates should be negatively associated for reasons having nothing to do with the possibility of radon being carcinogenic to the lung. A second problem presented by the data is the one of sampling bias since the county lung cancer data are from the whole county population, but only a few residences are tested. Examples of other inherent associations in environmental epidemiology are cited. One strategy is to study areas of the same population density but with radon exposure gradients. This is approximated by choice of rural high radon states. Counties in such states have weak and inconsistent associations between radon and lung cancer, some of which are positive. I conclude that counties are generally inappropriate units for study of radon and lung cancer associations.     

Epidemiological associations among lung cancer,radon exposure and elevation above sea level--a reassessment of Cohen''s county level radon study

Inhalation of radon (222Rn) decay products by persons living in homes has been associated with increased risk of lung cancer. Some epidemiological studies have shown a positive association between radon exposure and lung cancer rates. However, a large U.S.-wide ecological study (Cohen 1995) has shown a clear inverse association between average county radon concentration in homes and average lung cancer rates in the county. Cohen's strong inverse association between radon and lung cancer is surprising since there is no plausible biological reason for an inverse causal relationship between the two. We plot the county average lung cancer rate vs. the elevation above sea level (altitude) and show an inverse association between county average lung cancer rate and elevation. The elevation used for each county is the altitude of the most populous place in the county. We postulate that the decrease in lung cancer rates with higher elevations is caused by the carcinogenic effect of higher absolute oxygen concentration in the inspired air at lower elevations. Stratifying Cohen's lung cancer vs. radon data into ten groups of counties with similar elevations removes some, but not all, of his inverse association between radon and lung cancer.     

Cancer rates by county: how well does mortality relate to incidence?

The extent to which excess cancer mortality in a county is indicative of excess cancer incidence in the same county in the same time period was studied in white Iowa residents using routinely available 1973-1977 data. Evaluation consisted of population-weighted correlation analysis. The best correlations were obtained for cancers of the lung, pancreas, liver, stomach, brain (males), and kidney (males). These are the cancers for which excess mortality best indicates excess incidence. Correlations were low for prostate, female breast, and corpus uteri. The best indications of excess incidence are made for cancers with five year relative survival rates of 37.0 percent or less for males and 33.4 percent or less for females. Studies relating cancer mortality rates to occupational, environmental, or other demographic variables may be very misleading as to risk factors if the cancers selected have low correlations of incidence with mortality. Further development of the correlation model is recommended using data from all Surveillance, Epidemiology, and End Results Program counties for a ten-year period.     

Canadian individual risks of radon-induced lung cancer for different exposure profiles

BACKGROUND: Indoor radon has been determined to be the second leading cause of lung cancer after tobacco smoking. There is an increasing need among radiation practitioners to have numerical values of lung cancer risks for men and women, ever-smokers and never-smokers exposed to radon in homes. This study evaluates individual risks for the Canadian population exposed to radon in homes at different radon concentrations and for different periods of their lives. METHODS: Based on the risk model developed recently by U.S. Environmental Protection Agency (EPA), individual risks of radon-induced lung cancers are calculated with Canadian age-specific rates for overall and lung cancer mortalities (1996-2000) as well as the Canadian smoking prevalence data in 2002. RESULTS: Convenient tables of lifetime relative risks are constructed for lifetime exposures and short exposures between any two age intervals from 0 to 110, and for various radon concentrations found in homes from 50 to 1000 Bq/m3. CONCLUSIONS: The risk of developing lung cancer from residential radon exposure increases with radon concentration and exposure duration. For short exposure periods, such as 10 or 20 years, risks are higher in middle age groups (30-50) compared especially to the later years. Individuals could lower their risks significantly by reducing radon levels earlier in life. The tables could help radiation protection practitioners to better communicate indoor radon risk to members of the public.     

Radon and lung cancer risk: an extension of the mortality follow-up of the Newfoundland fluorspar cohort

Radon is a well-recognized cause of lung cancer, and studies of underground miners have provided invaluable insights on the mechanisms of radon carcinogenesis. Given the dramatic decreases in occupational exposures and the latent interval between the time of exposure and the development of lung cancer, continued follow-up of these cohorts is needed to address uncertainties in risk estimates. Here, we report on the relationship between radon and lung cancer mortality in a cohort of 1,742 Newfoundland fluorspar miners between 1950 and 2001; follow-up has been extended 11 y from previous analyses. The standardized mortality ratio (SMR) was used to compare the mortality experience of the cohort to similarly aged Newfoundland males. Poisson regression methods were used to characterize the radon-lung cancer relationship with respect to: age at first exposure, attained age, time since last exposure, interactions with cigarette smoking, and exposure rate. In total, 191 lung cancers were observed among underground miners (SMR = 3.09; 95% CI = 2.66, 3.56). ERR/WLMs decreased with attained age and time since last exposure. An inverse dose-rate effect was observed, while age at first exposure was not associated with lung cancer risk. An important strength of this study is that the effects of gamma radiation, thoron, and radioactive dust, common exposures in other miner studies, can be ruled out because the source of radon was from water running through the mine. However, the results should be interpreted cautiously due to uncertainties associated with the estimation of radon exposure levels before ventilation was introduced into the mine, and the relatively small number of lung cancer deaths that precluded joint modeling of multiple risk factors.     

Exposure to residential radon and lung cancer in Spain: a population-based case-control study

Although high radon concentrations have been linked to increased risk of lung cancer by both experimental studies and investigations of underground miners, epidemiologic studies of residential radon exposure display inconsistencies. The authors therefore decided to conduct a population-based case-control study in northwest Spain to determine the risk of lung cancer associated with exposure to residential radon. The study covered a total of 163 subjects with incident lung cancer and a population sample of 241 cancer-free subjects since 1992-1994. Odds ratios for radon were estimated using logistic regression adjusted for sex, age, lifetime tobacco use, family history, and habitat. The adjusted odds ratios for the second, third, and fourth quartiles of radon (breakpoints: 37.0, 55.2, and 148.0 Bq/m(3)) were 2.73 (95% confidence interval (CI): 1.12, 5.48), 2.48 (95% CI: 1.29, 6.79), and 2.96 (95% CI: 1.29, 6.79), respectively. An additive synergic effect between radon and tobacco was found. The results from this study suggest that, even at concentrations far below official guideline levels, radon may lead to a 2.5-fold rise in the risk of lung cancer. Furthermore, the synergy found between smoking and radon may prove useful when it comes to drafting public health recommendations.     

Residential radon exposure and lung cancer risk: commentary on Cohen's county-based study

The large United States county-based study () in which an inverse relationship has been suggested between residential low-dose radon levels and lung cancer mortality has been reviewed. While this study has been used to evaluate the validity of the linear nonthreshold theory, the grouped nature of its data limits the usefulness of this application. Our assessment of the study's approach, including a reanalysis of its data, also indicates that the likelihood of strong, undetected confounding effects by cigarette smoking, coupled with approximations of data values and uncertainties in accuracy of data sources regarding levels of radon exposure and intensity of smoking, compromises the study's analytic power. The most clear data for estimating lung cancer risk from low levels of radon exposure continue to rest with higher-dose studies of miner populations in which projections to zero dose are consistent with estimates arising from most case-control studies regarding residential exposure.     

The potential for bias in Cohen's ecological analysis of lung cancer and residential radon.

Cohen's ecological analysis of US lung cancer mortality rates and mean county radon concentration shows decreasing mortality rates with increasing radon concentration (Cohen 1995 Health Phys. 68 157-74). The results prompted his rejection of the linear-no-threshold (LNT) model for radon and lung cancer. Although several authors have demonstrated that risk patterns in ecological analyses provide no inferential value for assessment of risk to individuals, Cohen advances two arguments in a recent response to Darby and Doll (2000 J. Radiol. Prot. 20 221-2) who suggest Cohen's results are and will always be burdened by the ecological fallacy. Cohen asserts that the ecological fallacy does not apply when testing the LNT model, for which average exposure determines average risk, and that the influence of confounding factors is obviated by the use of large numbers of stratification variables. These assertions are erroneous. Average dose determines average risk only for models which are linear in all covariates, in which case ecological analyses are valid. However, lung cancer risk and radon exposure, while linear in the relative risk, are not linearly related to the scale of absolute risk, and thus Cohen's rejection of the LNT model is based on a false premise of linearity. In addition, it is demonstrated that the deleterious association for radon and lung cancer observed in residential and miner studies is consistent with negative trends from ecological studies, of the type described by Cohen.     

Predicted reduction in lung cancer risk following cessation of smoking and radon exposure

Recently there has been considerable public and regulatory concern that radon, produced by the decay of naturally occurring uranium, can accumulate in homes, offices, and schools at levels that may substantially increase the risk of lung cancer. The major cause of lung cancer is smoking, and radon appears to interact multiplicatively with smoking in causing lung cancer. Thus, the most effective way to reduce the increased risk of lung cancer resulting from radon exposure is to cease smoking. In this paper, a model for the risks associated with radon exposure that was developed by a committee of the National Academy of Sciences is used to calculate the benefits, in terms of reduction in lifetime risk of lung cancer, of ceasing to smoke, ceasing radon exposure, or ceasing both. Ceasing to smoke is considerably more beneficial than ceasing radon exposure, and thus policymakers addressing the health effects of radon should place priority on encouraging individuals to stop smoking.     

Residential radon and risk of lung cancer in an Italian alpine area

To evaluate whether residential radon exposure explains the excess mortality for lung cancer in an Italian alpine valley with high natural radioactivity, the authors conducted a population-based case-control study on 138 deceased cases and 291 sex- and year-of-birth-matched controls. Year-long alpha-track measurements of radon were performed in the most recent residence, and information about occupational history and lifetime smoking habits was obtained. The authors adjusted for smoking, and radon was associated with lung cancer risk among men: compared with a radon level of < 40 becquerels (Bq) per cubic meter (m3), the odds ratios for 40-76 Bq/m3, 77-139 Bq/m3, 140-199 Bq/m3, and 200+ Bq/m3 were 2.1, 2.0, 2.7, and 1.4, respectively. The association between radon and lung cancer, as determined with a multiplicative model, was found only among male smokers.     

Clinical measures, smoking, radon exposure, and risk of lung cancer in uranium miners.

OBJECTIVES: Exposure to the radioactive daughters of radon is associated with increased risk of lung cancer in mining populations. An investigation of incidence of lung cancer following a clinical survey of Ontario uranium miners was undertaken to explore whether risk associated with radon is modified by factors including smoking, radiographic silicosis, clinical symptoms, the results of lung function testing, and the temporal pattern of radon exposure. METHODS: Miners were examined in 1974 by a respiratory questionnaire, tests of lung function, and chest radiography. A random selection of 733 (75%) of the original 973 participants was followed up by linkage to the Ontario Mortality and Cancer Registries. RESULTS: Incidence of lung cancer was increased threefold. Risk of lung cancer among miners who had stopped smoking was half that of men who continued to smoke. There was no interaction between smoking and radon exposure. Men with lung function test results consistent with airways obstruction had an increased risk of lung cancer, even after adjustment for cigarette smoking. There was no association between radiographic silicosis and risk of lung cancer. Lung cancer was associated with exposures to radon daughters accumulated in a time window four to 14 years before diagnosis, but there was little association with exposures incurred earlier than 14 years before diagnosis. Among the men diagnosed with lung cancer, the mean and median dose rates were 2.6 working level months (WLM) a year and 1.8 WLM/year in the four to 14 year exposure window. CONCLUSIONS: Risk of lung cancer associated with radon is modified by dose and time from exposure. Risk can be substantially decreased by stopping smoking.     

Examining the relationship between lung cancer and radon in small areas across Scotland

Numerous studies have suggested that long-term exposure to radon gas may be an important cause of lung cancer, yet the precise effects are still not fully understood, especially in residential settings. This paper considers whether there is a relationship between the distribution of naturally occurring radon gas and lung cancer incidence in Scotland, for the period 1988-1991. We use regression analysis to test whether exposure to radon was a significant cause of lung cancer in Scotland, once smoking and other possible confounding factors were controlled for. The results demonstrate that for the population aged over 54, there was no significant relationship between radon exposure and lung cancer incidence. However, for those aged less than 55, lung cancer rates were significantly higher in places expected to have the highest levels of radon. These results suggest that more research is needed into the relationship between exposure to naturally occurring radon gas and lung cancer in Scotland, particularly among younger age groups.     

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.     

Study of occupational lung cancer in asbestos factories in China.

A retrospective cohort study (1972-81) of occupational cancers in asbestos (chrysotile) factories has been previously published. In this paper the results of continued tracing and interviewing of members of this cohort from 1982 to 1986 is reported. The cohort included 5893 persons (45,974 person-years for men and 39,445 person-years for women). Malignant tumours played a large part in causes of death (36.9%). There were 183 cancers and 67 lung cancers among 496 deaths. The mortality due to lung cancer had a tendency to increase. By comparison with a control group, the RR of lung cancer was 5.32 (p < 0.01), and the SRR of lung cancer was 4.2 (p < 0.01), significantly higher than those of a control group. Among 148 cases of death from asbestosis there were 33 cases complicated with lung cancer (22.3%). The dose-response relations between exposure to asbestos and incidence of asbestosis and lung cancer were also studied in one asbestos factory. There was a positive correlation. A synergistic effect was found between cigarette smoking and lung cancer. Preventive and control measures and exposure limits for asbestos dust in the air of workplaces were recommended.     

Is residual confounding a reasonable explanation for the apparent protective effects of beta-carotene found in epidemiologic studies of lung cancer in smokers?

The results of three randomized trials of beta-carotene supplementation for the prevention of lung cancer among smokers are in contradiction to a large body of epidemiologic evidence for the reduction of risk of lung cancer among smokers with higher intake and/or higher serum levels of beta-carotene. Complicating this issue are widely noted negative associations between tobacco use and intake or serum levels of beta-carotene. Although observational studies attempt to control for reported smoking histories, the accuracy of self-reported smoking is uncertain; correlations as low as 0.5 between reported and true smoking exposure are not inconsistent with studies of biomarkers of cigarette exposure. The authors developed a simple statistical model for random errors in reported smoking (relative to true tobacco exposure) and assumed a modest (inverse) relation between true tobacco exposure and serum beta-carotene. Calculations from this model, combined with a model for lung cancer contemplated by Doll and Peto (J Epidemiol Community Health 1978;78:303-13), suggest that biases in assessment of smoking exposure between smokers with low versus high beta-carotene intake may plausibly explain much or all of the observed protective effect of high beta-carotene levels. Appropriate cohort studies of lung cancer in smokers, utilizing biomarkers of smoking, are needed and are presently ongoing.     

Impacts of land use on spatial distribution of mortality rates of cancers caused by naturally occurring asbestos

This study investigated the spatial distributions of mortality rates of six cancers: mesothelioma, lung cancer, intestinal cancer, nasopharyngeal and laryngeal cancer, liver cancer, and stomach cancer in Dayao using Geographic Information Systems. Relationships between the mortality rates of the six cancers and land use patterns were investigated by Pearson Correlation Coefficients. The results indicated that the mortality rates of nasopharyngeal and laryngeal cancer, lung cancer, intestinal cancer, and mesothelioma were significantly associated with outcropped asbestos. Both the proportions of farmland and urban area were positively related to the mortality rates of nasopharyngeal and laryngeal cancer, lung cancer, intestinal cancer, and mesothelioma, and significant negative correlations were found between the proportion of forestland and nasopharyngeal and laryngeal cancer and intestinal cancer. It can be concluded that naturally occurring asbestos may significantly elevate the mortality rates of nasopharyngeal and laryngeal cancer, intestinal cancer, lung cancer, and mesothelioma. Moreover, higher proportions of farmland, urban area, and lower proportions of forested land may elevate the mortality rate of the four cancers.     

Cigarette smoking and mortality. MRFIT Research Group.

METHODS. The relationship of cigarette smoking and smoking cessation to mortality was investigated among men screened for and also among those randomized to the Multiple Risk Factor Intervention Trial (MRFIT). RESULTS. Among the 361,662 men screened for the MRFIT, cigarette smoking was an important risk factor for all-cause, coronary heart disease (CHD), stroke, and cancer mortality. These risks, on the log relative scale, were strongest for cancers of the lung, mouth, and larynx. The excess risk associated with cigarette smoking was greatest for death from CHD. Overall, approximately one-half of all deaths were associated with cigarette smoking. Among the 12,866 randomized participants, weak positive associations with duration of cigarette smoking habit and tar and nicotine levels were found with all-cause mortality. For both SI and UC men, substantial differences in subsequent CHD (34-49%) and all-cause (35-47%) mortality were evident for men who reported cigarette smoking cessation by the end of the trial compared with those continuing to smoke. There was no evidence that lung cancer death rates were lower among cigarette smokers who quite compared with those who continued to smoke in this 10-year follow-up period. CONCLUSION. The data are consistent with results of previous epidemiologic studies indicating that the benefits of smoking cessation on CHD are rapid, while for lung cancer, the benefit is not evident in a 10-year follow-up period.