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Background: The evidence for a role of tobacco smoking, alcohol drinking, and body mass index (BMI) in the etiology of small intestine cancer is based mainly on case-control studies from Europe and United States., Subjects and Methods: We harmonized the data across 12 cohort studies from mainland China, Japan, Korea, Singapore, and Taiwan, comprising over 500,000 subjects followed for an average of 10.6 years. We calculated hazard ratios (HRs) for BMI and (only among men) tobacco smoking and alcohol drinking., Results: A total of 134 incident cases were observed (49 adenocarcinoma, 11 carcinoid, 46 other histologic types, and 28 of unknown histology). There was a statistically non-significant trend toward increased HR in subjects with high BMI [HR for BMI>27.5 kg/m2, compared with 22.6-25.0, 1.50; 95% confidence interval (CI) 0.76-2.96]. No association was suggested for tobacco smoking; men drinking>400 g of ethanol per week had an HR of 1.57 (95% CI 0.66-3.70), compared with abstainers., Conclusions: Our study supports the hypothesis that elevated BMI may be a risk factor for small intestine cancer. An etiologic role of alcohol drinking was suggested. Our results reinforce the existing evidence that the epidemiology of small intestine cancer resembles that of colorectal cancer.

Objective: To assess the mortality risks from injuries for smokers and ex-smokers and to quantify the mortality burden of smoking from injury in Taiwan., Methods: Smokers' (and ex-smokers') mortality risks from injuries were compared with that of non-smokers in a merged cohort from Taiwan. A total of 64,319 male subjects were followed up for 12-18 years. Relative risks (RR) (adjusted for age and alcohol use) and 95% confidence intervals (CI) for cause specific injury deaths were calculated using the Cox proportional hazard model. Relative risks of injury mortality were also calculated to assess the presence of dose-response relations with daily smoking quantity., Results: Alcohol use adjusted relative mortality risks for all injuries (RR 1.69, 95% CI 1.39 to 2.05) including those from motor vehicle accidents (RR 1.88, 95% CI 1.44 to 2.45) and non-motor vehicle accidents (RR 1.48, 95% CI 1.11 to 1.99) were significantly higher for smokers than non-smokers. Mortality was also increased for most subtypes of non-motor vehicle injuries including falls, fires, and job related injuries. Furthermore, these increases were dose dependent, with the heaviest smokers having the highest risk and the lightest smokers the lowest risk, and ex-smokers, no increase. In 2001, over one fifth (23%) of all male injury deaths in Taiwan was associated with smoking., Conclusion: This study demonstrated the significant association between fatal injuries and smoking. This relation adds further weight to smoking cessation campaigns.

Objectives: To estimate smoking attributable mortality (SAM) in Taiwan for the years 2001 through 2020 under scenarios of reductions in smoking rates by 0%, 2%, 4%, and 10% per year., Method: The smoking attributable fraction (SAF) was used to calculate SAM from the risk experience in following up a large cohort (86 580 people) in Taiwan. Smoking rates were based on the 2001 National Health Interview Survey and other national surveys. An average 10 year lag was assumed between smoking rates and subsequent mortality., Results: In 2001, 18 803 deaths, or 1 out of 4 deaths (27%), in middle aged men (35-69 years old) were attributable to smoking. SAM has been increasing and will continue to increase if smoking rates remain constant or even if reduced annually by 2%. SAM would begin to decrease only if rates were to be reduced by at least 4% a year., Conclusions: The projected SAM in this study illustrates the seriousness of smoking caused mortality. Current efforts in tobacco control would lead to a progressive increase in SAM, unless efforts were doubled and smoking rates reduced by more than 4% a year. The urgency in requiring stronger tobacco control programmes to attenuate the staggering death tolls is compelling.

Objective: To describe the characteristics of betel quid chewers and to investigate the behavioural and mortality relations between betel quid chewing and cigarette smoking., Method: Prevalence and mortality risks of betel quid chewers by smoking status were calculated, based on the National Health Interview Survey in 2001 and a community based cohort, respectively. Cox's proportional hazards model was used to adjust mortality risks for age, alcohol use, and education., Results: Almost all betel quid chewers were smokers, and most started chewing after smoking. Chewers were predominantly male, mostly in their 30s and 40s, more likely being among the lowest educational or income group, and residing in the eastern regions of Taiwan. On average, betel quid chewers who smoked consumed 18 pieces of betel quid a day, and smoked more cigarettes per day. Far more smokers use betel quid than non-smokers (27.5% v 2.5%), but ex-smokers quit betel quid more than smokers (15.1% v 6.8%). The significantly increased mortality of betel quid users who also smoked, for all causes, all cancer, oral cancer, and cancer of the nasopharynx, lung, and liver, was the result of the combined effects of chewing and smoking. Smokers who chewed betel quid nearly tripled their oral cancer risks from a relative risk of 2.1 to 5.9. Increasing the number of cigarettes smoked among betel quid chewers was associated with a synergistic effect, reflective of the significant interaction between the two., Conclusion: To a large extent, the serious health consequences suffered by betel quid chewers were the result of the combined effects of smoking and chewing. Betel quid chewing should not be considered as an isolated issue, but should be viewed conjointly with cigarette smoking. Reducing cigarette smoking serves as an important first step in reducing betel quid chewing, and incorporating betel quid control into tobacco control may provide a new paradigm to attenuate the explosive increase in betel quid use in Taiwan.

Objectives: This study determined the prevalence of and risk factors for substance use among rural Taiwanese., Methods: We used a survey of a representative sample of 6318 participants aged 13 to 35 years in I-Lan, Taiwan, in 1996 through 1997., Results: Perceived use of illicit drugs by peers, tobacco smoking, betel quid chewing, and male gender were the strongest predictors of illicit drug use. The prevalence of illicit drug use ranged from 0.3% among those who did not use any other substance to 7.1% among those using tobacco, betel quid, and alcohol., Conclusions: Preventive measures should address substance use in general rather than aiming at single substances.

Background: Persistent infection with hepatitis B virus (HBV) causes chronic phasic necroinflammation and regenerative proliferation in the liver. The sustained hepatocellular proliferation may render chronic HBV carriers more susceptible to the effects of environmental carcinogens. Aromatic amines are potential hepatocarcinogens in humans. N-acetyltransferase (NAT) is involved in the metabolic activation and detoxification of these compounds., Aims: To investigate if genetic polymorphisms in N-acetylation are related to hepatocellular carcinoma (HCC) among chronic HBV carriers., Methods: Genotyping of NAT1 and NAT2 was performed using polymerase chain reaction-restriction fragment length polymorphism on peripheral leucocyte DNA from 151 incident cases of HCC and 211 controls. All subjects were male, and were chronic HBV surface antigen carriers., Results: A significant association between NAT2 genetic polymorphism and HCC was observed among chronic HBV carriers who were smokers but not among those who were non-smokers. For smoking HBV carriers, the odds ratios of developing HCC for those heterozygous and homozygous for the NAT2*4 functional allele compared with those without any copies of the functional allele (reference group) were 2.67 (95% confidence interval 1.15-6.22) and 2.58 (95% confidence interval 1.04-6.43), respectively. The interaction between cigarette smoking and the presence of the NAT2*4 allele just failed to reach statistical significance (p=0.06). No association between NAT1 genotype and HCC was evident overall or within the smoking stratified subgroups., Conclusions: Our results suggest that NAT2 activity may be particularly critical in smoking related hepatocarcinogenesis among chronic HBV carriers. Our data also indirectly support a role for tobacco smoke derived aromatic amines in the aetiology of HCC.

Aromatic amines from cigarette smoking or occupational exposure, recognized risk factors for bladder cancer, are metabolized by N-acetyltransferases (NAT). This study examined the association of (NAT) 1 and 2 genotypes with the risk of smoking-related bladder cancer. A total of 74 pathologically confirmed bladder cancer patients and 184 controls were serially recruited from the National Taiwan University Hospital. History of cigarette smoking and other risk factors for bladder cancer was obtained through standardized questionnaire interview. Peripheral blood lymphocytes were collected from each subject and genotyped for NAT1 and NAT2 by DNA sequencing and polymerase chain reaction-restriction fragment length polymorphism methods. Allele frequency distributions of NAT1 and NAT2 were similar between cases and controls. There was a significant dose-response relationship between the risk of bladder cancer and the quantity and duration of cigarette smoking. The biological gradients were significant among subjects carrying NAT1*10 allele or NAT2 slow acetylators, but not among NAT2 rapid acetylators without NAT1*10 allele. The results are consistent with the hypothesis that NAT1 and NAT2 might modulate the susceptibility to bladder cancer associated with cigarette smoking.

Objectives: Nasopharyngeal carcinoma (NPC) is rare in most countries but occurs with relatively high frequency among southern Chinese populations throughout the world. A case-control study of NPC was conducted in Taiwan to investigate the importance of active and passive cigarette exposure and alcohol consumption as risk factors for this disease., Methods: 375 histologically confirmed incident NPC cases (99% response rate) were prospectively identified from two hospitals in Taipei between July 1991 and December 1994 and administered a detailed questionnaire. 327 healthy community controls individually matched to cases on sex, age and residence were selected (88% response rate)., Results: After multivariate adjustment, the odds ratio (OR) and 95% confidence interval (CI) was 1.7 (1.1-2.9 with p = 0.03 for increasing dose-response) for those who smoked for > or = 25 years compared with non-smokers. Passive smoking during childhood or adult life was not associated with an increased risk of disease. Alcohol consumption was not associated with NPC risk. The OR for subjects with > or = 15 grams of ethanol per day compared to non-drinkers was 1.1 (95% CI = 0.7-1.7)., Conclusions: Our results suggest that long term cigarette smoking is associated with NPC but that low level exposure to cigarette smoke via passive exposure and alcohol consumption are not associated with disease risk.

Background: Assessment of the impact of cigarette smoking on mortality helps to indicate the importance of tobacco control in a given country., Objectives: To examine the relative risk of dying from various diseases for cigarette smoking and to estimate annual mortality attributable to cigarette smoking in Taiwan., Design: Prospective cohort study., Subjects and Setting: A cohort of 14,397 male and female residents aged 40 years or older recruited from 12 townships and precincts in Taiwan from 1982 to 1986. Information on cigarette smoking was collected from each subject at local health centres through a standardised personal interview based on a structured questionnaire. They were followed up regularly to determine their vital status until 1994., Main Outcome Measures: Cox's proportional hazards regression models were used to derive relative risks of cause-specific mortality for current cigarette smokers compared with never-smokers, and to examine dose-response relationships between mortality from various causes and several measures of cigarette smoking (daily consumption, duration, age of initiation, and cumulative smoking in pack-years)., Results: A total of 2552 persons died during the study period. Among men, cigarette smoking was significantly associated with an increased risk of dying from all causes combined (relative risk (RR) = 1.3); cancer of all sites combined (RR = 1.5); cancers of the stomach (RR = 1.9), liver (RR = 2.2), and lung (RR = 3.7); ischaemic heart disease (RR = 1.8); other heart diseases (RR = 1.4); and chronic obstructive pulmonary disease (RR = 1.9). Among women, cigarette smoking was significantly associated with an increased risk of dying from all causes combined (RR = 1.8), cancer of the lung (RR = 3.6), and peptic ulcer (RR = 17.8). The estimated number of deaths attributable to cigarette smoking in Taiwan in 1994 was 8161 (13.9% of total deaths) for men and 1216 (3.3% of total deaths) for women. In the same year cigarette smoking caused 21.3% and 2.9% of cancer deaths in men and women, respectively, in Taiwan., Conclusions: Cigarette smoking has a striking impact on overall mortality and deaths from various causes in the Taiwanese population. Tobacco control should be established as the top priority in public health programmes in Taiwan.

The present community-based study was performed to provide predictive equations and lower boundaries of normal values for forced expiratory volume in one second (FEVI), forced vital capacity (FVC), and their percent ratio (FEV1%) in non-smoking, healthy adult men and women residing in communities, using ATS-recommended techniques and equipment. Use was made of data collected cross-sectionally from Nov. 1990 to Dec. 1993 in an ongoing longitudinal study on evolution of cardiovascular disease risk factors in Chinese. The spirometric values in our population reached their peak at around age 20. After age 20, a downward age trend was observed for FVC, FEV1, and FEV1%. Linear and negative relations were found in adults for each of the three spirometric values with age. Linear and positive relations were found between height and FVC or FEV1, but not between height and FEV1%. The age trends of FVC and FEV1 in Chinese adults were similar to those in Caucasians. Mean FVC and FEV1 levels of Chinese in Taiwan were systematically lower than those of Caucasians for a given height and a given age. Age and height specific percentile values of FVC and FEV1 and the age-specific percentile value of FEV1% are provided for adult men and women in this community study.

To investigate the potential role of neu oncogene expression in hepatocarcinogenesis, a nested case-control study was conducted within a cohort of 9691 male adults in Taiwan. Blood samples of study subjects were collected during 1984-1986 and frozen at -30 degrees C until subsequent analysis. The neu oncoprotein level in the stored serum was measured by an enzyme-linked immunosorbent assay for 27 cases of newly developed hepatocellular carcinoma (HCC), 12 liver cirrhosis cases, and 40 healthy controls. The mean level of neu oncoprotein was significantly higher in HCC and liver cirrhosis cases than in controls. The risk of HCC increased significantly with increasing serum level of neu oncoprotein (trend test, P = 0.02). The proportion of subjects having an elevated serum level of neu oncoprotein, defined as a level greater than the mean level of all controls, was significantly higher among asymptomatic HBsAg carriers than noncarriers (P = 0.05), showing a multivariate-adjusted odds ratio of 4.0. Among HCC cases, a strong association was observed between cigarette smoking and elevated prediagnostic serum level of neu oncoprotein. The association remained highly significant (P = 0.017) even when adjustment was made for potential confounders. The multivariate-adjusted odds ratio of having an elevated serum level of neu oncoprotein, defined as a level greater than the mean plus 1 SD of control levels, for HCC cases who smoked more than 10 cigarettes a day was as high as 386.5 compared with the cases who smoked less than 10 cigarettes a day or nonsmoking cases. The results suggest that both HBsAg carrier status and cigarette smoking are related to the increased expression of neu oncogene, and cigarette smoking seems to play a significant role in the latter stages of hepatocarcinogenesis. There was no association between alcohol drinking and serum neu oncoprotein level.

The effect of smoking habits on Graves' disease with or without ophthalmopathy and nontoxic nodular goiter has been discussed for more than 10 years in Western countries, but there are no published reports from Oriental countries, where the prevalence of cigarette smoking among women is lower than in Western women. The purpose of this study was to determine the relationship between smoking and Graves' ophthalmopathy, Graves' disease without ophthalmopathy, and nontoxic nodular goiter in Taiwan. The study included 349 patients with thyroid disease from endocrinologic clinics, including 116 patients with Graves' ophthalmopathy (92 women, 24 men), 108 patients with Graves' disease but without ophthalmopathy (96 women, 12 men), and 125 patients with nontoxic nodular goiter (114 women, 11 men). Information on smoking habits at the time of onset of the disease was obtained by a self-administered structured questionnaire. Since women generally smoke less than men, female and male smoking habits were compared separately with those of controls matched with patients on the basis of age. There was a significantly higher prevalence of cigarette smoking in women with Graves' ophthalmopathy and nontoxic nodular goiter than for healthy female controls, showing an odds ratio of 8.15 and 6.48, respectively, despite a lower prevalence of cigarette smoking in Taiwan (7.6% in women with Graves' ophthalmopathy, 6.1% in women with nontoxic nodular goiter) than in the West (64.2% in women with Graves' ophthalmopathy, 30% in women with nontoxic nodular goiter). Men in these three disease groups and women with Graves' disease without ophthalmopathy showed no significant association with cigarette smoking.(ABSTRACT TRUNCATED AT 250 WORDS)

Independent and interactive effects related to the development of hepatocellular carcinoma were assessed using a community-based case-control study for hepatitis B virus, habitual alcohol drinking, cigarette smoking, peanut consumption and history of hepatocellular carcinoma among the immediate family. All 200 male newly diagnosed hepatocellular carcinoma patients were recruited consecutively through the period of study as the case group from two teaching medical centers in northern and southern Taiwan. Healthy community residents matched one-to-one with cases on age, sex, ethnic group and residential area were selected as the control group. The carrier status of HBsAg and HBeAg was determined by blind radioimmunoassays, and other risk factors were obtained through standardized interviews according to a structured questionnaire. Conditional logistic regression analysis showed a significant association between hepatocellular carcinoma and the carrier status of HBsAg and HBeAg with an odds ratio of 16.7 and 56.5, respectively, for carriers of HBsAg alone and for carriers of both HBsAg and HBeAg. There was a dose-response relationship between cigarette smoking and hepatocellular carcinoma with an odds ratio of 1.1, 1.5 and 2.6, respectively, for those who smoked 1 to 10, 11 to 20 and more than 20 cigarettes a day. A significant association with hepatocellular carcinoma was also observed for the habitual alcohol consumer with an odds ratio of 3.4. Those whose immediate family had a history of hepatocellular carcinoma were more likely to have the disease develop, with an odds ratio of 4.6. However, the frequency of peanut consumption was not significantly associated with hepatocellular carcinoma.(ABSTRACT TRUNCATED AT 250 WORDS)

A community-based case-control study was carried out to assess multiple risk factors and familial aggregation of nasopharyngeal carcinoma (NPC). All of the 347 pathologically-confirmed NPC new cases were serially recruited from the National Taiwan University Hospital, and healthy community controls one-to-one matched with cases on age, sex and residence were selected from household registration offices. NPC risk factors were obtained from the study subjects through standardized interviews according to a structured questionnaire. Levels of antibody to EBV-specific DNase (anti-EBV DNase) and IgA antibody to EBV viral capsid antigen (anti-EBV VCA) were determined by standard methods blindly. Multiple logistic regression analysis for matched data showed significant associations of NPC with high levels of anti-EBV DNase and anti-EBV VCA independently. The effect of cigarette smoking on NPC was modified by age. The older the age, the more striking the dose-response relation between cigarette smoking and NPC. There was no significant association between alcohol consumption and NPC. Malarial infection history was associated with NPC with an odds ratio of 2.2, but the association was significant in males only. First-degree relatives of NPC cases had a greater NPC-affected rate than those of matched healthy controls with a relative risk of 19.2, and the heritability of NPC was estimated as 0.60 (95% confidence interval = 0.55-0.64) based on the multifactorial inheritance model. Familial NPC cases were younger than sporadic cases, but environmental risk factors were similar in the two groups.

Among 104 cases of squamous-cell oesophageal carcinoma patients and 277 controls in Taiwan, after adjusting for cigarette smoking, alcohol consumption, and other confounders, we found that subjects who chewed from 1 to 495 betel-year and more than 495 betel-years (about 20 betel quid per day for 20 years) had 3.6-fold (95% Cl = 1.3-10.1) and 9.2-fold risk (95% Cl = 1.8-46.7), respectively, of developing oesophageal cancer, compared to those who did not chew betel. [ABSTRACT FROM AUTHOR]