Cigar smoking in men and risk of death from tobacco-related cancers

BACKGROUND: Cigar consumption in the United States has increased dramatically since 1993, yet there are limited prospective data on the risk of cancer associated with cigar smoking. We examined the association between cigar smoking and death from tobacco-related cancers in a large, prospective cohort of U. S. men. METHODS: We used Cox proportional hazards models to analyze the relationship between cigar smoking at baseline in 1982 and mortality from cancers of the lung, oral cavity/pharynx, larynx, esophagus, bladder, and pancreas over 12 years of follow-up of the American Cancer Society's Cancer Prevention Study II cohort. A total of 137 243 men were included in the final analysis. Women were not included because we had no data on their cigar use. We excluded men who ever smoked cigarettes or pipes and adjusted all rate ratio (RR) estimates for age, alcohol use, and use of snuff or chewing tobacco. RESULTS: Current cigar smoking at baseline, as compared with never smoking, was associated with an increased risk of death from cancers of the lung (RR = 5.1; 95% confidence interval [CI] = 4.0-6.6), oral cavity/pharynx (RR = 4.0 [95% CI = 1.5-10.3]), larynx (RR = 10.3 [95% CI = 2.6-41.0]), and esophagus (RR = 1.8; 95% CI = 0.9-3.7). Although current cigar smokers overall did not appear to be at an increased risk of death from cancer of the pancreas (RR = 1.3; 95% CI = 0.9-1.9) or bladder (RR = 1.0; 95% CI = 0.4-2.3), there was an increased risk for current cigar smokers who reported that they inhaled the smoke (for pancreas, RR = 2.7; 95% CI = 1.5-4.8; for bladder, RR = 3.6; 95% CI = 1.3-9.9). CONCLUSIONS: Results from this large prospective study support a strong association between cigar smoking and mortality from several types of cancer.     

Lung cancer and women: results of a French case-control study

Ninety-six women with histologically confirmed lung cancer and 192 matched controls were involved in an international case-control study conducted from 1976 to 1980. The aim of this study was an examination of the effects of different smoking habits, especially the type of cigarettes smoked (light or dark tobacco and filter or nonfilter use) on the occurrence of lung cancer in French females. All these patients were either nonsmokers or lifetime cigarette smokers. Matched relative risk (RR) of smokers compared to nonsmokers was found to be increased for both Kreyberg I (RR = 6.6) and Kreyberg II (RR = 2.1) categories; however, this increase was significant (P less than 0.0001) only for Kreyberg I lung cancer. A significant increase (P less than 0.0001) in matched RR was found with early age at first cigarette smoked, daily consumption, duration of smoking, frequency of inhalation, use of dark tobacco and use of nonfilter cigarettes. Matched RR associated with smokers not always using dark tobacco and those smoking only dark tobacco as compared to nonsmokers were significantly increased (trend test P less than 0.0001). On the contrary, the increase of RR was not significant when either daily consumption, or duration of smoking, or age at first cigarette was taken into account. Lung cancer appeared to be associated with daily consumption and use of nonfilter cigarettes in a matched logistic regression.     

Cigarette smoking,use of other tobacco products and stomach cancer mortality in US adults: The Cancer Prevention Study II

Cigarette smoking is associated with increased risk of stomach cancer in many studies but there are limited data on this relationship in women and on risk associated with use of tobacco products other than cigarettes. We examined stomach cancer death rates in relation to cigarette smoking in women and use of cigarette, cigar, pipe, or smokeless tobacco in men in a nationwide prospective mortality study in the United States (US). Cohort follow-up from 1982-96 identified 996 and 509 stomach cancer deaths among 467,788 men and 588,053 women, respectively. Cox proportional hazards models were fitted to estimate rate ratios (RR) and 95% confidence intervals (CI) using non-users of tobacco as the referent group. Multivariate-adjusted RRs were the highest for men who currently smoked cigars (RR = 2.29, 95% CI = 1.49-3.51) or cigarettes (RR = 2.16, 95% CI = 1.75-2.67) and both increased with smoking duration. Women who currently (RR = 1.49, 95% CI = 1.18-1.88) or formerly (RR = 1.36, 95% CI = 1.08-1.71) smoked cigarettes were at significantly increased risk, as were men who formerly smoked cigarettes (RR = 1.55, 95% CI = 1.28-1.88), or currently (RR = 1.81, 95% CI = 1.40-2.35) or formerly (RR: 1.57, 95% CI = 1.22-2.03) used more than one type of tobacco. Men who reported a history of chronic indigestion or gastroduodenal ulcer had substantially higher mortality rates associated with current cigarette (RR = 3.45, 95% CI = 2.05-5.80) or cigar (RR = 8.93, 95% CI = 4.02-19.90) smoking, as did men who were current aspirin users. If causal, the estimated proportion of stomach cancer deaths attributable to tobacco use would be 28% in US men and 14% in women. We conclude that prolonged use of tobacco products is associated with increased stomach cancer mortality in men and women. The accumulated evidence from this and other studies support reconsidering stomach cancer as a tobacco-related cancer.     

Smokeless and other noncigarette tobacco use and pancreatic cancer: a case-control study based on direct interviews.

Cigarette smoking is an important and well-established cause of pancreatic cancer. In contrast, little is known about the effects of smoking cigars, pipes, and use of smokeless tobacco on pancreatic cancer risk. The objective of the present study was to examine the association between noncigarette tobacco use (i.e., cigars, pipes, smokeless tobacco) and pancreatic cancer risk among nonsmokers of cigarettes. A population-based case-control study of pancreatic cancer was conducted during 1986-1989 among residents of Atlanta, Georgia, Detroit, Michigan, and 10 counties in New Jersey. Direct interviews were successfully completed with 526 newly diagnosed pancreatic cancer patients and 2153 controls ages 30-79 years. This analysis was restricted to lifelong nonsmokers of cigarettes and based on interviews with 154 cases newly diagnosed with carcinoma of the exocrine pancreas and 844 population controls who reported no history of cigarette smoking. We observed a consistent pattern of increased risk associated with cigar smoking, although these elevations were not statistically significant. Participants who smoked cigars regularly (i.e., at least one cigar/week for >/=6 months) experienced a 70% increased risk [95% confidence interval (CI): 0.9-3.3], and those who never used other form of tobacco had a 90% increased risk (95% CI: 0.8-4.3). Risk was elevated among those who smoked more than one cigar/day [odds ratio (OR) = 1.8; 95% CI: 0.8-4.2) and among those who smoked cigars > 20 years (OR = 1.9; 95% CI: 0.9-3.9). Trends in risk with increasing amount and duration smoked were consistent but not statistically significant (P = 0.17 and P = 0.16, respectively). Subjects who used smokeless tobacco regularly had a 40% increased risk of pancreatic cancer (95% CI: 0.5-3.6) compared with nonusers of tobacco. We observed a marginally significant increasing risk with increased use of smokeless tobacco (P = 0.04); participants who used >2.5 oz of smokeless tobacco a week had an OR of 3.5 (95% CI: 1.1-11). Long-term use of smokeless tobacco (i.e., >20 years) was also associated with a nonsignificant increased risk (OR = 1.5; 95% CI: 0.6-4.0). In contrast, pipe smokers experienced no increased risk (OR = 0.6; 95% CI: 0.1-2.8). Our results suggest that heavy use of smokeless tobacco, and to a lesser extent, cigar smoking may increase the risk of pancreatic cancer among nonsmokers of cigarettes.     

Active and passive smoking and breast cancer risk in middle-aged Japanese women

To examine the hypothesis that tobacco smoke is associated with the risk of female breast cancer, we estimated the relative risks of active and passive smoke in middle-aged Japanese women in a population-based prospective study. The cohort consisted of residents in 4 public health center areas, aged 40 to 59 years. A self-administered questionnaire survey was conducted in 1990. This analysis included 21,805 subjects, 180 of whom had developed breast cancer by December 31, 1999. When the reference was defined as never-active smokers without passive smoking, adjusted relative risks (RRs) were 1.9 (95% confidence interval [CI] = 1.0-3.6) in current active smokers, 1.2 (95% CI = 0.4-4.0) in ex-active smokers and 1.2 (95% CI = 0.8-1.6) in never-active smokers with passive smoking. The elevated risk for ever-smokers was clearly observed in premenopausal women at baseline (RR = 3.9, 95% CI = 1.5-9.9) but not in postmenopausal women (RR = 1.1, 95% CI = 0.5-2.5). In never-active smokers, the adjusted RR for passive smoking, residential or occupational/public tobacco smoke exposure was 1.1 (95% CI = 0.8-1.6). In premenopausal women, passive smoking increased the risk (RR = 2.6; 95% CI = 1.3-5.2) but not in postmenopausal women (RR = 0.7; 95% CI = 0.4-1.0). We conclude that tobacco smoking increases the risk of female breast cancer in premenopausal women.     

Invasive cervical cancer and smoking in Latin America

A case-control study of 667 patients with invasive squamous cell carcinoma of the cervix and 1,430 controls from four Latin American countries showed an age-adjusted relative risk (RR) of 1.2 [95% confidence interval (CI) = 1.0-1.4] for women who had ever smoked, with risk rising to 1.7 (95% CI, 0.8-3.6) for women who smoked greater than or equal to 30 cigarettes per day. The associations were practically eliminated after adjustment for the number of sexual partners and alcohol consumption, probably a surrogate for an unidentified life-style risk factor. Some excess risk persisted among women who smoked for extended periods (RR = 1.5 for greater than or equal to 40 yr), as well as those who began smoking at older ages (RR = 1.7 for greater than 30 yr), which suggests a late-stage effect. In addition, among women who tested positive for human papillomavirus (HPV) type 16 or 18 by filter in situ hybridization, there was an increased risk for women who had ever smoked and a dose-response relationship with the number of cigarettes smoked (adjusted RRs compared with HPV-negative nonsmokers = 5.0 for HPV-positive nonsmokers, 5.5 for less than 10 cigarettes/day, and 8.4 for greater than or equal to 10 cigarettes/day). In contrast, HPV-negative women had no increased risk associated with smoking. These results, from a high-incidence area where intensive smoking among women is still relatively rare, suggest that smoking has a limited effect on cervical cancer risk, possibly only among women with specific types of HPV.     

The Copenhagen case-control study of renal pelvis and ureter cancer: role of smoking and occupational exposures

Smoking habits and occupational exposures were investigated for 96 patients with cancer of the renal pelvis and ureter (including papilloma) and 294 hospital controls. In comparison with persons who never smoked, significantly increased relative risks were seen for smokers of cigarettes alone (RR = 2.6; 95% CI: 1.0-6.7) and in combination with other types of tobacco (RR = 3.8; 95% CI: 1.3-11.5). Non-significantly increased relative risks were observed for pipe smokers (RR = 2.2; 95% CI: 0.1-97) and for mixed pipe, cigar, and cigarillo smokers (RR = 6.5; 95% CI: 0.4-21.2). A strong dose-effect (p less than 0.001) relationship was seen between the lifetime total amount of tobacco smoked and the risk of pelvis-ureter tumors, with the heaviest smokers having an 8-fold risk. Comparison with the dose-effect relationship for a parallel study of bladder cancer indicated that the relationship with tobacco was stronger for pelvis-ureter tumors. Deep inhalation of cigarette smoke increased the risk (RR = 3.4; 95% CI: 1.9-6.1), while stopping smoking (RR = 0.6; 95% CI: 0.3-1.1) and use of filter cigarettes (RR = 0.5; 95% CI: 0.3-0.9) decreased the risk. Significantly increased risks emerged for employment in the chemical, petrochemical and plastics industries (RR = 4.0; 95% CI: 1.6-9.8), and for exposure to coal and coke (RR = 4.0; 95% CI: 1.2-13.6), asphalt and tar (RR = 5.5; 95% CI: 1.6-19.6). Cigarette smoking accounted for 56% of male and 40% of female pelvis and ureter tumors in eastern Denmark.     

Smoking and infectious agents and risk of in situ cervical cancer in Sydney, Australia

In a study of 116 in situ cervical cancer patients and 193 matched community controls in Sydney, Australia, smoking was found to be a major risk factor. Current smokers had a adjusted relative risk [RR] of 4.5 compared to nonsmokers [95% confidence interval (CI) 2.2-9.1] and exsmokers a RR of 1.3 [95% CI 0.6-3.0]. There was a stepwise dose-response relationship between risk and number of cigarettes smoked (30+ cigarettes/day, RR = 5.1, 95% CI 1.5-17.3); this dose-response relationship was more marked among current smokers. Years of cigarette smoking was not consistently related to risk. Exposures to herpes simplex virus type 2 and cytomegalovirus as measured by antibody prevalence were unrelated to risk (RR = 1.1 for both measures). However, cases appeared to have more exposure than controls to herpes simplex virus type 1 (RR = 2.3, 95% CI 1.1-4.4).     

Oral cavity cancer risk in relation to tobacco chewing and bidi smoking among men in Karunagappally, Kerala, India: Karunagappally cohort study

The Karunagapally cohort in Kerala, India was established in the 1990s. The present study examined oral cancer risk among 66,277 men aged 30-84 years in the cohort, using Poisson regression analysis of grouped data, stratified on attained age, calendar time, education, and family income. By the end of 2005, 160 oral cancer cases were identified by the Karunagapally Cancer Registry. Tobacco chewing increased oral cancer risk (P < 0.001). Particularly increased was the risk of cancers of the gum and mouth (relative risk [RR] = 4.7; 95% confidence interval [CI] = 2.8-7.9), which increased with higher daily frequencies (P < 0.001) and longer duration (P < 0.001) of tobacco chewing. Alcohol drinking was not significantly related to oral cancer risk regardless of tobacco chewing. Bidi smoking significantly increased oral cancer risk (RR = 2.6; 95%CI = 1.4-4.9) only among men without tobacco chewing habits. The risk increased with higher daily consumption (P < 0.001), longer duration (P = 0.001), and younger age at start of bidi smoking (P = 0.007). In location-specific analysis, bidi smoking was significantly associated with cancer of the gum and mouth (RR = 3.6; 95%CI = 1.1-12.1), and its risk significantly increased with larger daily consumption of bidis (P = 0.013) and younger age at the start of smoking (P = 0.044). Tongue cancer risk was significantly increased among men who smoked bidis for 30 years or longer, and men started bidi smoking at 18 years old or younger. The present study is the first cohort study showing that tobacco chewing increases cancers of the gum and mouth among men keeping chewing tobacco in the cheek, and that bidi smoking strongly increased oral cancer risk among men without a tobacco chewing habit.     

The role of alcohol, tobacco, and dietary factors in upper aerogastric tract cancers: a prospective study of 10,900 Norwegian men

Previous knowledge on risk factors for oral, pharyngeal, laryngeal, and esophageal cancer has been based mainly on case-control studies. In the present study, the impact of alcohol consumption, tobacco smoking, and dietary factors on upper aerogastric tract cancer risk was studied in a cohort of 10,960 Norwegian men followed from 1968 through 1992, in which period a total of 71 upper aerogastric tract cancers occurred. The relative risk (RR) of cancer was 3.9 (95 percent confidence interval [CI] = 2.1-7.1) for the highest consumption group of alcohol and 4.7 (CI = 1.7-13.2) for the highest smoking level, compared with the respective reference groups. Among the dietary items, high consumption of oranges was associated with reduced cancer risk (RR = 0.5, CI = 0.3-1.0), as was high consumption of bread (RR = 0.2, CI = 0.1-0.5). Frequent consumption of beef and bacon increased relative cancer risk bordering on significance. The present results are largely in accordance with previous studies. The decreased risk associated with a high intake of bread deserves further investigation.     

A cohort study of tobacco use,diet, occupation,and lung cancer mortality

In 1966, a cohort of White males aged 35 or over, who were policy-holders with the Lutheran Brotherhood Insurance Society (United States), completed a mail questionnaire on tobacco use, diet, and demographic characteristics. During the 20 years of follow-up, 219 lung cancer deaths occurred. Besides the strong relationship with cigarette smoking, we observed an effect on lung cancer risk among current users of cigars or pipes who were nonsmokers of cigarettes (relative risk [RR]=3.5, 95 percent confidence interval[CI]=1.0–12.6) or who were past/occasional users of cigarettes (RR=2.7, CI=1.4–5.3). In addition, elevated risks (from 1.5 to 2.6) of lung cancer were found among craftsmen and laborers, with the highest risks among subjects who worked in the mining or manufacturing industry. No association between current (as of 1966) use of beer or hard liquor and lung cancer was observed, although past users were at elevated risk. An inverse association between lung cancer and intake of fruits was observed, and risks of lung cancer were lower among persons in the highest dietary intake quintiles of vitamins A and C. Except for oranges, however, none of the inverse associations with fruits or dietary nutrients had statistically significant trends. The findings from this cohort study add to the evidence of an adverse effect of cigar/pipe smoking and possibly protective effect of dietary factors on lung cancer risk.     

A prospective study of tobacco use and multiple myeloma: evidence against an association

The relationship between the use of cigarettes and other tobacco products and the risk of multiple myeloma was examined in a cohort of nearly 250,000 American veterans followed prospectively for 26 years. Compared with men who had never used tobacco, the risk of death from myeloma was not increased among current (relative risk [RR]=0.9, 95 percent confidence interval [CI]=0.8–1.2) or former (RR=1.0, CI=0.8–1.3) cigarette smokers, nor among users of chewing tobacco or snuff (RR=1.0, CI=0.4–2.3). Risk was only slightly and nonsignificantly increased among pipe or cigar smokers (RR=1.2, CI=0.9–1.5). There was no indication of increasing risk with amount of tobacco used or earlier age at first use. With over 90 percent power to detect a 30 percent increased risk of this tumor occuring among current cigarette smokers, this study provides the strongest evidence to date against an association of cigarette smoking with multiple myeloma.Epidemiology and Biometry Program, Division of Cancer Etiology, National Cancer Institute. Westat, Inc. Rockville, MD. National Cancer Institute, 6130 Executive Blvd, Room 418, Rockville, MD 20892, USA.     

Lung cancer and use of cigarettes: a French case-control study

A case-control study of 1,625 cases and 3,091 controls was conducted in France from 1976 to 1980 to compare the effects of different smoking habits, especially the use of filter cigarettes, tobacco types (light or dark), and the use of hand-rolled or manufactured cigarettes on the occurrence of lung cancer. All cases had histologically confirmed lung cancer; the controls were matched by sex, age, hospital of admission, and interviewer. The reported results concern only male nonsmokers and males who smoked (or had smoked) cigarettes exclusively, i.e., a total of 1,217 Kreyberg I and Kreyberg II cancer cases and 1,915 controls. Cigarette smoking was associated with both Kreyberg I and Kreyberg II cell categories although with different relative risks (RR) (17.2 and 3.6, resp.). Within the Kreyberg I category, RR were significantly increased (P less than .0001) with certain indices of duration and intensity of cigarette exposure, such as early age at first cigarette smoked, daily consumption, depth of inhalation, and duration of smoking. A significant difference in risk was found within the Kreyberg I category for nonfilter versus filter cigarette smokers (RR = 18.1 and 10.9, resp.) and dark versus light tobacco smokers (RR = 18.1 and 4.9, resp.) but not for hand-rolled versus manufactured cigarette smokers (RR = 19.8 and 16.0, resp.). When all the covariates were taken into account in a matched logistic regression, lung cancer risks for nonfilter versus filter cigarette smokers was RR = 1.23, for hand-rolled versus manufactured cigarette users RR = 1.22, and for dark versus light tobacco users RR = 1.94.     

Cigarette smoking and risk of prostate cancer in the physicians' health study (United States)

To assess whether cigarette smoking is associated with prostate cancer incidence or mortality, we analyzed a large cohort of 22,071 men, aged 40-84 at baseline, in the Physicians' Health Study. During an average of 12.5 years of follow-up, we documented 996 cases of prostate cancer, including 113 fatal cases. Men were categorized according to smoking status, total pack-years smoked, and duration of smoking. We used Cox proportional hazard models to estimate the relative risks associated with smoking. Compared to never smokers, the age-adjusted relative risks (RR) of total prostate cancer were 1. 14 (95% confidence interval [CI] = 1.00-1.30) for past smokers, 1.10 (95% CI = 0.78-1.55) for current smokers of less than 20 cigarettes per day, and 1.10 (95% CI = 0.84-1.44) for current smokers of 20 or more cigarettes per day. Adjustment for body mass index, height, alcohol intake, and physical activity did not materially alter these findings. No significant association was observed in analyses of total pack-years smoked or duration of smoking. The results were similar for non-fatal and fatal prostate cancer. These data indicate no material association between cigarette smoking and prostate cancer incidence or mortality.     

Smoking and liver cancer in China: case-control comparison of 36,000 liver cancer deaths vs. 17,000 cirrhosis deaths

Liver cancer and liver cirrhosis are common causes of death in China, where chronic lifelong hepatitis B infection is a major cause of both diseases. To help determine whether smoking is a cofactor for the development of liver cancer, we ascertained retrospectively the smoking habits of 36,000 adults who had died from liver cancer (cases) and 17,000 who had died from cirrhosis (controls) in 24 Chinese cities and 74 rural counties. Calculations of the smoker vs. nonsmoker risk ratios (RR) for liver cancer mortality were standardised for age and locality. Among adult men (aged 35+) there was a 36% excess risk of death from liver cancer among smokers (smoker vs. nonsmoker standardised risk ratio [RR] =1.36, with 95% confidence interval [CI] 1.29-1.43, 2p<0.00001; attributable fraction 18%). In the general male population this indicates absolute risks of death from liver cancer before age 70 of about 4% in smokers and 3% in nonsmokers (in the absence of other causes). Most liver cancer, however, occurs among the 10-12% of men with haematological evidence of chronic hepatitis B infection, so among them the corresponding risks would be about 33% in smokers and 25% in nonsmokers. The RR was approximately independent of age, was similar in urban and rural areas, was not significantly related to the age when smoking started but was significantly (p<0.001) greater for cigarette smokers than for smokers of other forms of tobacco. Among men who smoked only cigarettes, the RR was significantly (p<0.001 for trend) related to daily consumption, with a greater hazard among those who smoked 20/day (RR 1.50, 95% CI 1.39-1.62) than among those who smoked fewer (mean 10/day: RR=1.32, 95% CI 1.23-1.41). Smoking was also associated with a significant excess of liver cancer death in women (RR 1.17, 95% CI 1.06-1.29, 2p=0.003; attributable fraction 3%), but fewer women (17%) than men (62%) were smokers, and their cigarette consumption per smoker was lower. Among women who smoked only cigarettes, there was a significantly greater hazard among those who smoked at least 20/day (mean 22/day: RR=1.45, 95% CI 1.18-1.79) than among those who smoked fewer (mean 8/day: RR=1.09, 95% CI 0.94-1.25). These associations indicate that tobacco is currently responsible for about 50,000 liver cancer deaths each year in China, chiefly among men with chronic HBV infection.     

Tobacco use and prostate cancer in Blacks and Whites in the United States

Prostate cancer occurs more frequently in Blacks than Whites in the United States. A population-based case-control study which investigated the association between tobacco use and prostate cancer risk was carried out among 981 pathologically confirmed cases (479 Blacks, 502 Whites) of prostate cancer, diagnosed between 1 August 1986 and 30 April 1989, and 1,315 controls (594 Blacks, 721 Whites). Study subjects, aged 40 to 79 years, resided in Atlanta (GA), Detroit (MI), and 10 counties in New Jersey, geographic areas covered by three, population-based, cancer registries. No excesses in risk for prostate cancer were seen for former cigarette smokers, in Blacks (odds ratio [OR]=1.1, 95 percent confidence interval [CI]=0.7–1.5) and in Whites (OR=1.2, CI=0.9–1.6), or for current cigarette smokers, in Blacks (OR=1.0, CI=0.7–1.4) and in Whites (OR=1.2, CI=0.8–1.7). Increases in risk were noted for smokers of 40 or more cigarettes per day, among former (OR=1.4, CI=1.0–1.5) and current (OR=1.5, CI=1.0–2.4) smokers. Duration of cigarette use and cumulative amount of cigarette use (pack-years) were not associated with prostate cancer risk for Blacks or Whites. By age, only the youngest subjects, aged 40 to 59 years, showed excess risk associated with current (OR=1.5, CI=1.0–2.3) and former (OR=1.7, CI=1.1–2.6) use of cigarettes, but there were no consistent patterns in this group according to amount or duration of smoking. Risks also were not elevated for former or current users of pipes, cigars, or chewing tobacco, but the risk associated with current snuff use was OR=5.5 (CI=1.2–26.2). This subgroup finding may have been due to chance. The results of the present study may be consistent with a small excess risk for prostate cancer associated with tobacco use, but the lack of consistent findings in population subgroups and the lack of a clear dose-response relationship argue more strongly that no causal association exists. The data do not indicate that the Black-White difference in prostate cancer risk is related to tobacco use.This research was performed under contracts: NO1-CP-51090, NO1-CN-0522, NO1-CP-51089, NO1-CN-31022, NO1-CP-51092, and NO1-CN-5227.     

Cigarette smoking and liver cancer among US veterans

The relationship of tobacco use with risk of primary liver cancer was investigated using data from a 26-year mortality follow-up of nearly 250,000 US veterans, mostly from World War I. Significantly increased risks for liver cancer (289 deaths) were associated with most forms of tobacco use, including pipe and cigar smoking. Elevated relative tisks (RRs) were seen for current cigarette smokers (RR=2.4; 95 percent confidence interval [CI] 1.6–3.5) and former cigarette smokers (RR=1.9, 1.2–2.9). A strong dose-response relationship (P<0.001) was found for cigarette smoking, with smokers of 40 or more cigarettes per day having almost a fourfold risk (RR=3.8, 1.9–8.0). Risks were also found to increase significantly with years of cigarette use and with earlier age at the start of cigarette smoking. These results are consistent with those of other cohort and case-control studies, suggesting that cigarette smoking may be related to the risk of liver cancer.All authors are in the Epidemiology and Biostatistics Program, Division of Cancer Etiology, National Cancer Institute. Address correspondence to Dr Hsing at Executive Plaza North, Room 415, Bethesda, MD 20892, USA.     

Environmental tobacco smoke and lung cancer mortality in the American Cancer Society's Cancer Prevention Study II

Environmental tobacco smoke (ETS) has been classified as a human lung carcinogen by the United States Environmental Protection Agency (EPA), based both on the chemical similarity of sidestream and mainstream smoke and on slightly higher lung cancer risk in never-smokers whose spouses smoke compared with those married to nonsmokers. We evaluated the relation between ETS and lung cancer prospectively in the US, among 114,286 female and 19,549 male never-smokers, married to smokers, compared with about 77,000 female and 77,000 male never-smokers whose spouses did not smoke. Multivariate analyses, based on 247 lung cancer deaths, controlled for age, race, diet, and occupation. Dose-response analyses were restricted to 92,222 women whose husbands provided complete information on cigarette smoking and date of marriage. Lung cancer death rates, adjusted for other factors, were 20 percent higher among women whose husbands ever smoked during the current marriage than among those married to never-smokers (relative risk [RR]=1.2, 95 percent confidence interval [CI]=0.8-1.6). For never-smoking men whose wives smoked, the RR was 1.1 (CI=0.6-1.8). Risk among women was similar or higher when the husband continued to smoke (RR=1.2, CI=0.8-1.8), or smoked 40 or more cigarettes per day (RR=1.9, CI=1.0-3.6), but did not increase with years of marriage to a smoker. Most CIs included the null. Although generally not statistically significant, these results agree with the EPA summary estimate that spousal smoking increases lung cancer risk by about 20 percent in never-smoking women. Even large prospective studies have limited statistical power to measure precisely the risk from ETS.     

Is cigarette smoking a risk factor for non-Hodgkin's lymphoma or multiple myeloma? Results from the Lutheran Brotherhood Cohort Study.

Among 17,633 U.S. white male insurance policy holders whose use of tobacco was characterized in a 1966 self-administered questionnaire, there were 49 deaths from non-Hodgkin's lymphoma (NHL) and 21 from multiple myeloma (MM) during a 20-year follow-up. Men who had ever smoked cigarettes had an elevated mortality from NHL (RR = 2.1; CI = 0.9-4.9), with risk almost four-fold greater among the heaviest smokers (RR = 3.8; CI = 1.4-10.1) compared with those who used no tobacco. In contrast, risk of MM was only slightly elevated among those who had ever smoked cigarettes (RR = 1.3; CI = 0.4-3.9) and without evidence of a dose-response trend. Since this is the first cohort study suggesting a link between cigarette smoking and NHL and findings from case-control studies have been inconsistent, additional clarification should be sought from larger incidence-based cohort investigations.     

Cigarette smoking, elevated fasting serum glucose, and risk of pancreatic cancer in Korean men

Pancreatic cancer is one of the most fatal human cancers and continues to be a major unsolved health problem. The goal of this study was to estimate the independent effects and interactions between cigarette smoking and diabetes on the risk of pancreatic cancer in Korean male population. Cigarette smoking and the risk of incidence and death from pancreatic cancer were examined in a 10-year prospective cohort study of 446,407 Korean men aged 40 to 65 years who received health insurance from the National Health Insurance Corporation and who had a medical evaluation in 1992. Relative risks (RR) and 95% confidence intervals (CI) were calculated using a Cox proportional hazards model after adjusting for age, body mass index, exercise and alcohol use. Current smoking was associated with an increased risk of incidence (RR = 1.7, 95% CI = 1.6-1.9) and mortality (RR = 1.6, 95% CI = 1.4-1.7) from pancreatic cancer. The RR for pancreatic cancer increased with both duration and amount of smoking. Diabetes was also associated with an increased risk of both incidence (RR = 1.8, 95% CI = 1.5-2.2) and mortality (RR = 1.7, 95% CI = 1.4-2.1) from pancreatic cancer. There was no interaction between smoking and fasting serum glucose in terms of pancreatic cancer risk. Thus, our prospective study has demonstrated that cigarette smoking and elevated fasting serum glucose are independently associated with an increased risk of pancreatic cancer in a large cohort of Korean males.