Prospective study of cigarette smoking and amyotrophic lateral sclerosis

Cigarette smoking has been proposed as a risk factor for amyotrophic lateral sclerosis (ALS), but because of the low incidence of ALS this association has been examined only with case-control methods. The authors prospectively assessed the relation between cigarette smoking and ALS mortality among participants in the Cancer Prevention Study II cohort of the American Cancer Society, a cohort of over 1 million people enrolled in 1982 who completed a lifestyle questionnaire including a detailed smoking history at baseline. Causes of deaths were ascertained through death certificates; ALS was not identified separately until 1989. From January 1, 1989, through 1998, 291 women and 330 men died from ALS. The relative risk of ALS among current smokers compared with never smokers was 1.67 (95% confidence interval: 1.24, 2.24; p = 0.002) in women and 0.69 (95% confidence interval: 0.49, 0.99; p = 0.04) in men. The difference in the relative risk estimates between the sexes was statistically significant (p < 0.0003). This large prospective study provides limited evidence that current cigarette smoking may be associated with increased death rates from ALS in women but not in men.     

The temporal relation between cigarette smoking and pancreatic cancer

Temporal trends in US cigarette smoking prevalence rates 1920 to 1978, were related to temporal trends in US pancreatic cancer mortality rates in both sexes. In males, the rise and fall in smoking prevalence was followed by a rise and recent fall in cancer rates. In females, the later rise in smoking prevalence has been accompanied by a rise in cancer rate, and a recent slight decline in smoking rate has been associated with a slowing of the rise in cancer rate.     

A prospective cohort study of bladder cancer risk in relation to active cigarette smoking and household exposure to secondhand cigarette smoke

Active cigarette smoking is a major risk factor for bladder cancer. Secondhand exposure to cigarette smoke may also contribute to bladder carcinogenesis. The authors conducted a prospective cohort study to examine the influence of both active smoking and household exposure to secondhand smoke (SHS) on subsequent bladder cancer risk. The study population included persons from two cohorts established from private censuses conducted in Washington County, Maryland, in 1963 (n = 45,749; 93 cases) and 1975 (n = 48,172; 172 cases). Poisson regression models were fitted to estimate the relative risk of bladder cancer associated with active and passive smoke exposure in the two cohorts (referent category: never smokers who did not live with any smokers). Current smokers had an elevated risk of bladder cancer in both the 1963 cohort (relative risk (RR) = 2.7, 95% confidence limits (CL): 1.6, 4.7) and the 1975 cohort (RR = 2.6, 95% CL: 1.7, 3.9) after adjustment for age, education, and marital status. Among nonsmoking women, current household SHS exposure was associated with bladder cancer risk in the 1963 cohort (RR = 2.3, 95% CL: 1.0, 5.4) but not in the 1975 cohort (RR = 0.9, 95% CL: 0.4, 2.3). This study further solidifies the evidence that active smoking is causally associated with bladder cancer. Additional studies are needed to determine whether passive smoking is a risk factor for bladder cancer.     

Prospective study of educational background and stomach cancer in Japan

BACKGROUND: Different lifestyle choices are commonly regarded as a reflection of socioeconomic status, and the latter is inversely correlated with the risk of developing stomach cancer. However, the details of this association are still unclear in terms of the degree to which lifestyle factors are having impact. To explain the correlation between socioeconomic status and stomach cancer, we therefore examined the roles played by different lifestyle factors. METHODS: A prospective cohort study of diet and cancer was initiated in Japan during 1988. Data were collected by means of a self-administered questionnaire. A follow-up survey was conducted annually, and the cause of death was recorded from the death certificate. The total of 127,477 study participants resided in 45 areas of Japan, and we retrieved data for 18,746 men and 26,184 women for the present analysis. After 328,030 person-years of follow-up, 379 deaths from stomach cancer were detected: 261 in men and 118 in women. RESULTS: For men, the age-adjusted relative risk was lowest in the highly educated group (relative risk = 0.72, 95% CI: 0.50-1.04). Relative risk after adjustment for age and dietary choices (including pickles, vegetables, fruit, green tea, and preference for salty foods) was the same as the age-adjusted relative risk (relative risk = 0.72, 95% CI: 0.50-1.04). CONCLUSION: The expected inverse correlation between education level and death from stomach cancer was observed in men. However, this association could not be explained by differences in dietary habits, smoking, or alcohol consumption associated with socioeconomic status.     

A prospective cohort study of rectal cancer risk in relation to active cigarette smoking and passive smoke exposure

PURPOSE: The present investigation prospectively examined active cigarette smoking and household passive smoke exposure and the risk of developing rectal cancer. METHODS: Cigarette smoking data were collected on all household members during two private censuses in Washington County, Maryland. These two cohorts were followed up, one cohort from 1963-1978 and the other from 1975-1994 for first-time diagnoses of rectal cancer. We identified 148 and 169 rectal cancer cases in the 1963 and 1975 cohorts, respectively. Relative risks were estimated by means of Poisson regression models. RESULTS: In men, the adjusted relative risks (aRR) and 95% confidence intervals (CI) for the association between current smoking and rectal cancer were 3.1 (1.2-7.8) in the 1963 cohort and 1.8 (0.9-3.7) in the 1975 cohort; the corresponding aRRs in women were 0.9 (0.5-1.8) and 1.6 (0.9-3.8) in the 1963 and 1975 cohorts, respectively. In nonsmokers, household passive smoke exposure was strongly associated with rectal cancer among men in the 1963 cohort (aRR = 5.8; 1.8-18.4) but not the 1975 cohort (aRR = 1.1; 0.2-5.0). In women, household passive exposure was not strongly associated with rectal cancer in either cohort. CONCLUSIONS: The results of our study suggest that active cigarette smoking may contribute to rectal cancer risk, but inconsistencies in the findings preclude drawing strong, clear-cut inferences.     

Bladder cancer mortality in England and Wales in relation to cigarette smoking and saccharin consumption

Cohort analyses of bladder cancer mortality rates in men and women in England and Wales have been compared with figures for the per caput consumption of saccharin and cigarette tobacco and with similar analyses of cigarette smoking habits. The increase in bladder cancer mortality rates in male cohorts born since 1870 can be attributed to cigarette smoking, and there is no evidence of any break in the continuity of the trends in either men or women which corresponds to the introduction of saccharin.     

Trends in lung cancer mortality in Scotland and their relation to cigarette smoking and social class.

This paper describes the trends in lung cancer rates in Scottish men and women during 1959-85, the relationship between lung cancer and cigarette consumption, and between lung cancer and social class, and the urban-rural gradient of lung cancer. Lung cancer rates in Scottish men have declined in all age groups under the age of 74 for at least the past two decades; the most notable decrease was in men aged 40-44 years, whose rates halved between 1970 and 1980. In women, who began smoking in large numbers only after World War II, lung cancer mortality declined slightly in those between 40-54 years and rose in those over 54 years. Trends in cigarette consumption did not fully explain the decline in lung cancer. Marked urban-rural gradients in the SMRs for lung cancer were evident in all periods, and these strengthened over time. Correlations between lung cancer and social class differed markedly from those found in previous studies, except for those with social classes II and V.     

吸烟与饮酒对肺癌发病的影响及交互作用

目的探讨吸烟与饮酒及其交互作用对肺癌发病的影响。方法在肿瘤高发地区开展以人群为基础的病例对照研究,通过调查问卷收集主要人口学、吸烟和饮酒等相关信息,采用非条件logistic回归分析计算比值比(OR)及95%CI,并分析吸烟与饮酒在肺癌发病中的交互作用。结果调整相关因素(包括饮酒)后,与不吸烟者相比,吸烟者患肺癌的风险增加(P0.05),吸烟≥40年者患肺癌的风险是不吸烟者的4.79倍,每日吸烟≥20支者患肺癌的风险是不吸烟者的4.44倍,吸烟至肺部者患肺癌风险是不吸烟者的4.44倍(P值均0.001)。调整变量(包括吸烟)后,饮酒和饮酒年限与肺癌发病之间无统计学关联(P0.05)。吸烟和饮酒相乘交互作用的OR值(95%CI)为0.90(0.47~1.70)。吸烟和饮酒相加交互作用的超额相对危险度(RERI)值及其95%CI为0.36(-0.92~1.64),交互作用归因比(AP)值及95%CI为0.09(-0.22~0.40),交互作用指数(SI)值及95%CI为1.13(0.71~1.80)。结论吸烟是肺癌发病的主要危险因素,且该风险随吸烟年限、吸烟量、吸烟深度的增加而显著增加,现有证据并不支持饮酒与肺癌发病之间存在关联,吸烟和饮酒在肺癌发病中也未见交互作用。     

Pulmonary function in relation to cigarette smoking and smoking cessation. MRFIT Research Group.

BACKGROUND. More than half of the subjects in the MRFIT smoked at baseline and 10% of the subjects stopped smoking permanently during the first year of the trial. In this report, rates of decline in forced expiratory volume in 1 sec (FEV1) are compared for early permanent quitters and smokers who continued to smoke throughout the trial. METHODS. Since pulmonary function testing was not standardized across all centers until the third annual visit cycle, change in FEV1 is examined over the latter half of the trial; the level of FEV1 is analyzed cross-sectionally at the midpoint of the trial. Analyses are limited to 4,926 subjects who never used beta-blockers or smoked cigars, cigarillos, or pipes during the trial and who had annual FEV1s measured over 2-4 years in the latter half of the trial. RESULTS. Quitters during the first 12 months experienced smaller declines in FEV1 over the latter half of the trial than continuing smokers, with -50.7 ml/year versus -59.0 ml/year, respectively, adjusted for the level of FEV1 (P = 0.05). Cross-sectionally, those who had never smoked, former smokers, quitters, and continuing smokers showed a gradient of decreasing FEV1, and all four smoking groups were significantly different from each other (P less than 0.05). CONCLUSIONS. These data suggest that if a middle-aged, healthy smoker stopped smoking permanently, he could expect his FEV1 to deteriorate at a more gradual rate 3-4 years after stopping smoking than a similar smoker who continued to smoke. No information was available for the complete MRFIT cohort on the pulmonary function effects immediately following smoking cessation.     

Prospective study of smoking and tuberculosis in India

OBJECTIVE: Although tuberculosis has already become uncommon in industrialised countries, is a major burden in many developing countries, including India. This paper examines the association between smoking (mainly bidi smoking) and tuberculosis in Mumbai, India. METHOD: To study the possible association between smoking and tuberculosis, recruitment of a cohort of 81,443 men > or =35 years began in 1991 and was followed up to the end of 2003 in Mumbai. RESULTS: The adjusted risk of tuberculosis deaths among bidi smokers was 2.60 (95% confidence interval (CI): 2.02, 3.33) times higher than never-smokers, with a significant trend for daily frequency of bidi smoking. Also the risk of prevalence of self reported tuberculosis among bidi smokers was 5.23 (95% CI: 4.01, 6.82) times higher than never-smokers. CONCLUSION: In India around 32% of tuberculosis deaths can be attributable to bidi smoking. Thus, bidi smoking seems to be an important cause of manifestation and death from tuberculosis.     

Impact of smoking and smoking cessation on lung cancer mortality in the Asia-Pacific region

Cigarette smoking is becoming increasingly common in Asia while quitting remains rare, in part because of a lack of knowledge about the risks of smoking. This study compared the risk of death from lung cancer associated with smoking habits in Australia and New Zealand and in Asia by using data from the Asia Pacific Cohort Studies Collaboration: 31 studies involving 480,125 individuals. Cox regression models were used. The hazard ratios for lung cancer mortality associated with current smoking were, for men, 2.48 (95% confidence interval (CI): 1.99, 3.11) in Asia versus 9.87 (95% CI: 6.04, 16.12) in Australia and New Zealand; p for homogeneity <0.0001. For women, the corresponding estimates were 2.35 (95% CI: 1.29, 4.28) in Asia versus 19.33 (95% CI: 10.0, 37.3) in Australia and New Zealand; p for homogeneity <0.0001. Quitting was beneficial in both regions; the hazard ratios for former compared with current smokers were 0.69 (95% CI: 0.53, 0.92) in Asia and 0.30 (95% CI: 0.22, 0.41) in Australia and New Zealand. The lesser effect in Asia was partly explained by the fewer number of cigarettes smoked and the shorter duration of follow-up in Asian studies. These results suggest that tobacco control policies in Asia should not solely concentrate on preventing the uptake of smoking but also attend to cessation.     

A prospective study of the attributable risk of cancer due to cigarette smoking.

BACKGROUND. The goals of this study were to measure the impact of cigarette smoking on cancer incidence and to determine the attributable risk of cancer due to smoking. METHODS. A cigarette smoking history was obtained from 8006 Japanese-American men examined from 1965 through 1968. After 22 years, 1389 incident cases of cancer were identified. There were 212 men with lung cancer; 202 with oral, esophageal, laryngeal, pancreatic, renal, ureteral, or bladder (oral-bladder) cancer; and 975 with cancer at other sites. RESULTS. Current smokers at time of examination had a higher incidence than nonsmokers for each of the three cancer site categories. Eighty-five percent of lung cancer cases diagnosed among current and never smokers can be attributed to cigarette smoking. The attributable risks were 46%, 16%, and 29%, respectively, for oral-bladder cancers, other cancers, and all cancers combined. In turn, the corresponding attributable risks were 60%, 26%, 13%, and 21% in comparing current smokers with past smokers. CONCLUSIONS. Current smokers can greatly reduce their risk of cancer, especially lung cancer, if they quit smoking.     

Oral contraceptives, cigarette smoking and other factors in relation to arthritis

The data on oral contraceptive use and arthritis in the Oxford-Family Planning Association contraceptive study have been analysed. For rheumatoid arthritis, the rate of first referral to hospital was 0.33 per 1000 woman-years in those who never used oral contraceptives (27 cases), 0.33 per 1000 woman-years in ex-users of oral contraceptives (29 cases) and 0.44 per 1000 woman-years in current users of oral contraceptives (22 cases). Likewise, there was no important association between oral contraceptive use and other forms of arthritis. An unexpected finding was a strong association between referral to hospital for rheumatoid arthritis and cigarette smoking; the rate in women never smoking was 0.27 per 1000 woman-years (34 cases) and in those smoking 15 or more cigarettes per day was 0.64 per 1000 woman-years (19 cases).     

吸烟对甲状腺影响的流行病学研究

目的研究不同碘摄入量地区吸烟对甲状腺体积、功能以及甲状腺自身抗体的影响。方法对辽宁省盘山、彰武、河北省黄骅三个农村社区(分别为碘缺乏地区、碘充足地区、碘过量地区) 1999年初访的3761人进行随访,随访率达80.2%。进行问卷调查、甲状腺B超检查、血液及尿液化验。通过logistic回归进行多因素分析。结果吸烟者甲状腺肿的发生率较不吸烟者增高(15.1% us.11.5%,P<0.05),吸烟者甲状腺的平均体积较不吸烟者大(14.92 ml us.13.18 ml,P<0.05)。通过logistic回归可见吸烟是增加甲状腺肿发生率的主要危险因素。吸烟者平均血清促甲状腺激素(TSH)水平和甲状腺球蛋白(Tg)水平与不吸烟者比没有差别。吸烟者甲状腺过氧化物酶抗体(TPOAb)≥100 IU/ml的为10.8%,不吸烟者为9.0%,差异有统计学意义。多元logistic回归发现吸烟是增加TPOAb强阳性的主要危险因素。对三社区人群进行前瞻性研究,发现由不吸烟到吸烟者TPOAb变为≥100 IU/ml的发生率为7.4%,远大于吸烟情况没有变化者的2.9%(P<0.05)。多元logistic回归发现由不吸烟到吸烟是增加TPOAb≥100 IU/ml发生率的主要危险因素。结论吸烟是增加甲状腺肿发生率和增加TPOAb阳性率的主要危险因素;由不吸烟到吸烟是TPOAb变为阳性的主要危险因素。     

Esophageal cancer mortality: Relationship with alcohol intake and cigarette smoking in Italy

This paper examines changes with time in age-adjusted mortality from esophageal cancer for the years 1950–1981, in relation to changes in smoking habits and alcohol consumption. In both sexes the age-adjusted death rates have shown no marked time variation. Instead in the same period there have been marked temporal variations in consumption of alcohol and tobacco which are considered risk factors associated with esophageal cancer.The male cohort variation seems to indicate some fluctuations in mortality before 1921 and a progressive increase after this year. In females the death rates are very low and the cohort variation is pratically constant.The progressive increase of cohort variation in esophageal cancer mortality for men born after 1921 coincides with a progressive increase in hard alcohol consumption. In the same period there has also been a progressive increase in tobacco consumption but this begun at the turn of this century.     

吸烟与缺血性脑卒中关系的病例-对照研究

目的探讨吸烟与缺血性脑卒中的关系。方法采用病例-对照研究的方法,通过调查问卷收集缺血性脑卒中患者及对照者的研究信息。在哈尔滨医科大学附属第二医院神经内科收集的缺血性脑卒中住院患者1037例作为病例组,同期在黑龙江省电力医院体检中心参加健康体检的自愿者1205例作为对照组。统计分析采用Logistic回归,分析吸烟与缺血性脑卒中的关系。结果吸烟与缺血性脑卒中有关联,OR=1.368,95%CI 1.158~1.616。调整年龄、体质指数、腰臀比、血压、血糖、血脂、脑卒中家族史和饮酒因素后,吸烟与缺血性脑卒中仍存在关联,OR=2.158,95%CI 1.293~3.600。随着吸烟量的增加,患缺血性脑卒中的危险性也在增加,与不吸烟者相比,1~9支/天、10~19支/天和20~支/天的OR值分别为1.097、1.168和2.950。结论吸烟是缺血性脑卒中的危险因素。