Changes in smoking behavior and subsequent mortality risk during a 35-year follow-up of a cohort in Xi'an, China.

Prospective evidence of the associations of smoking cessation with chronic obstructive pulmonary disease (COPD) and other causes of death in Asia is scarce. Previous studies, which were mostly based on baseline smoking behavior only, were subject to sick-quitter bias and misclassification resulting from changes in smoking behavior during follow-up. We followed up a cohort for 18 years (1976-1994) to assess changes in smoking behavior and then for an additional 17 years (1994-2011) to examine the relationships of continuing to smoke and new quitting with mortality risk in 1,494 Chinese people (961 men, 533 women). Of the baseline current smokers, 38.7% quit between 1976 and 1994. From 1994 to 2011, a total of 488 persons (359 men, 129 women) died. Ever smokers had increased risks of lung cancer, coronary heart disease, thrombotic stroke, and COPD, with dose-response relationships. For all tobacco-related mortality, the relative risk for new quitters compared with continuing smokers was 0.68 (95% confidence interval: 0.46, 0.99) for those who had quit 2-7 years previously and 0.56 (95% confidence interval: 0.37, 0.85) for those who had quit 8 years or more previously. The corresponding relative risks were 0.69 and 0.45 for lung cancer, 0.78 and 0.51 for coronary heart disease, 0.76 and 0.84 for thrombotic stroke, and 0.89 and 0.61 for COPD, respectively. Smoking increased tobacco-related deaths, and particularly deaths from COPD, in China, whereas quitting at middle age (at approximately 50 years of age) substantially reduced the risks of death from these causes. The benefits of smoking cessation were underestimated in previous studies that did not use repeated measures.

Metabolic syndrome vs. its components for prediction of cardiovascular mortality: A cohort study in Chinese elderly adults.

OBJECTIVE: The predictive value of the metabolic syndrome (MetS) for mortality from all-cause and cardiovascular disease (CVD) in the Chinese population is unclear. The aim of this present study was to compare MetS with its individual components as predictors of mortality in Chinese elderly adults. METHODS: A cohort of 1,535 subjects (994 men and 541 women) aged 50 years or older was selected from employees of a machinery factory in 1994 and followed until 2009. Cox models were used to estimate the hazard ratios (HRs) predicted by MetS according to the harmonized definition and by its individual components. RESULTS: The baseline prevalence of MetS was 28.0% in men and 48.4% in women. During a median follow-up of 15 years, 414 deaths occurred, of these, 153 participants died from CVD. Adjusted for age and gender, the HRs of mortality from all-cause and CVD in participants with MetS were 1.47 (95% confidence interval (CI): 1.20-1.80) and 1.96 (95%CI: 1.42-2.72), respectively, compared with those without MetS. Non-significant higher risk of CVD mortality was seen in those with one or two individual components (HR = 1.22, 95%CI: 0.59-2.50; HR = 1.82, 95%CI: 0.91-3.64, respectively), while a substantially higher risk of CVD mortality only appeared in those with 3, 4, or 5 components (HR = 2.81-3.72), compared with those with no components. On evaluating the MetS components individually, we found that, independent of MetS, only hypertension and impaired glucose predicted higher mortality. CONCLUSIONS: The number of positive MetS components seems no more informative than classifying (dichotomous) MetS for CVD risks assessment in this Chinese cohort.

Secondhand smoke exposure predicted COPD and other tobacco-related mortality in a 17-year cohort study in China.

BACKGROUND: Prospective evidence on the association between secondhand smoke (SHS) and COPD and ischemic stroke is scarce. METHODS: We prospectively examined the relationship between SHS and major tobacco-related deaths, particularly COPD and stroke, in 910 Chinese (439 men, 471 women) who never smoked from a 17-year follow-up study in Xi'an, China. SHS exposure was defi ned as exposure to another person's tobacco smoke at home or in the workplace. RESULTS: At baseline among the 910 subjects, 44.2% were exposed to SHS at home, 52.9% in the workplace, and 67.1% at home, work, or both. From March 1, 1994, to July 1, 2011, 249 (150 men,99 women) died within 14,016 person-years. Those who were exposed to SHS had increased mortality due to coronary heart disease (adjusted relative risk [RR], 2.15; 95% CI, 1.00-4.61), ischemic stroke (RR, 2.88; 95% CI, 1.10-7.55), lung cancer (RR, 2.00; 95% CI, 0.62-6.40), COPD (RR, 2.30;95% CI, 1.06-5.00), and all causes (RR, 1.72; 95% CI, 1.29-2.20), with significant dose-response relationships between cumulative SHS exposure at home and work and the increased risk of cause-specific and total mortality (P for linear trend ranged from .045 to , .001). CONCLUSIONS: This study shows dose-response relationships between SHS and major tobacco-related mortality and provides new evidence to support causation for COPD and ischemic stroke.

[Study on the relationship between passive smoking and blood lipids, fibrinogen and viscosity among women who never smoke].

OBJECTIVE: To determine whether blood lipids profile, fibrinogen and viscosity were associated with passive smoking (i. e. environmental tobacco smoke, ETS) in Chinese women who never smoke. METHODS: In Xi'an, China, a case-control study was carried out on 115 cases of coronary heart disease (CHD) defined by coronary arteriography (CAG) and 208 non-CHD controls confirmed by CAG and/or exercise electrocardiography. Data on exposure to ETS, defined as exposure from cigarettes smoking husband or co-workers or both for at least 5 years, was obtained through standardized interviews. Standard laboratory methods were used and the lipid measurements were under US CDC quality control programs. RESULTS: In the subjects defined by CAG, the levels of high density lipoprotein cholesterol (HDL-C), HDL2C, apolipoprotein (apo) A1 among passive smokers appeared lower than those in non-passive smokers,but the low density lipoprotein cholesterol (LDL-C), apoB, apoB/A1, fibrinogen, plasma and whole blood viscosity were higher than that in non-passive smokers. There were positive associations of the numbers of coronary arteriosclerosis with the levels of blood lipids,fibrinogen and viscosity. In the non-CHD controls, 81 subjects were not exposed and 127 were exposed to ETS. The P values of t-test for the adjusted (for age, body mass index, present diseases history) means between two groups were listed below: 0.06 (total cholesterol), 0.30 (triglyceride), 0.004 (HDL-C), <0.001 (HDL2-C), < 0.001 (apoA1), 0.009 (apoB), <0.001 (apoB/apoA1), <0.001 (fibrinogen), <0.001 (plasma viscosity), <0.001 and 0.004 [two measures (5.75/s and 230/s) of whole blood viscosity]. The correlation coefficients between cumulative exposure of passive smoking and HDL-C,HDL2-C,apoA1, apoB, apoB/apoA1, fibrinogen, plasma viscosity, and two measures of whole blood viscosity were -0.25, -0.27, -0.30, 0.24, 0.31, 0.32, 0.43, 0.51 and 0.36 (all P<0.01), respectively. CONCLUSION: Passive smoking could affect blood lipid metabolism, fibrinogen and viscosity in the never smoking women which might contribute to the causation of coronary heart disease.

[Meta-analysis on the relationship between tobacco smoking, alcohol drinking and p53 alteration in cases with esophageal carcinoma].

OBJECTIVE: To investigate the relationship between tobacco smoking, drinking and p53 alteration in esophageal carcinoma. METHODS: Literature on the relationship between p53 alteration in esophageal carcinoma and tobacco smoking, drinking through Meta-analysis were reviewed. RESULTS: In 14 selected papers related to tobacco smoking, pooled odds ratio (OR) of tobacco smoking with P53 overexpression and p53 alteration were 1.99 (95% CI: 1.30- 3.06) and 1.64 (95% CI: 1.13 - 2.37), respectively (P < 0.05). Pooled OR of tobacco smoking with p53 mutation was 1.11 (95% CI: 0.47 - 2.76) (P > 0.05). In 11 selected papers on alcohol drinking, pooled OR of drinking with P53 overexpression, p53 mutation and p53 alteration were 1.30 (95% CI: 0.83 - 2.04), 1.13 (95% CI: 0.67 - 1.90) and 1.22 (95% CI: 0.87 - 1.72) respectively (P > 0.05). CONCLUSION: There were significant relations between tobacco smoking and p53 alteration while there were no significant relations between alcohol drinking and p53 alteration.

[Study on the application of the Chinese version of SF-36 scales and selection of interceptive cents for its grade range].

OBJECTIVE: To study the possibility of measuring quality of life by Medical Outcomes Study 36-Item Short-Form Health Survey scale and to subdivide grade range of Medical Outcomes Study 36-Item Short-From Health Survey (SF-36) total cents through a Quality of Life questionnaire among the elderly Chinese. METHODS: The quality of life of the 167 elderly Chinese in Suzhou was measured simultaneously by SF-36 and the Quality of Life questionnaire developed by Epidemiology Group of Geriatric Medicine Committee of China for the elderly. Validity and reliability were analyzed and subdivided the grade range of SF-36 total scores by Quality of Life questionnaire for the Chinese elderly. RESULTS: Eight common factors from factorial analysis were in accordance with their theoretical structure, and the cumulative contribution rates of the Quality of Life questionnaire for the elderly and SF-36 were 74.244% and 72.081%. The split-half reliability of the Quality of Life questionnaire for the elderly was 0.6676. The split-half reliability of SF-36 was 0.9384. In SF-36, the Cronbach's alpha coefficient of internal consistency reliability ranged from 0.81 to 0.89, which was satisfactory for group comparison except 0.63 for the social functioning and 0.42 for mental health scale and 0.69 for vitality scale. The Quality of Life questionnaire for old people seemed to have good validity and reliability but the SF-36 was better. The cent of the furthest truncation between the good quality of life and the medium one in the SF-36 was 117 with a Kappa value of 0.58. CONCLUSION: The SF-36 scale could be used for measuring and evaluating the quality of life for the Chinese elderly. The cent of the furthest truncation could provide reference to judge the level of the quality of life of the elderly.

Genetic susceptibility and environmental factors of esophageal cancer in Xi'an.

AIM: To analyse the role of genetic susceptibility and environmental factors in the process of esophageal cancer (EC) formation in Xi'an, China. METHODS: A hospital based case-control study, combined with molecular epidemiological method, was carried out. A total of 127 EC cases and 101 controls were interviewed with questionnaires containing demographic items, habit of tobacco smoking, alcohol drinking, and family history of EC. Polymorphism of CYP1A1 and GSTM1 of 127 EC cases and 101 controls were detected by PCR method. The interactions between genetic susceptibility and environmental factors were also discussed. RESULTS: Tobacco smoking, alcohol drinking and a family history of EC were risk factors for EC with an OR of 2.04(95% CI 1.15-3.60), 3.45(95% CI 1.74-6.91), 3.14 (95% CI 1.28-7.94), respectively. Individuals carrying CYP1A1 Val/Val genotype compared to those with CYP1A1 Ile/Ile genotype had an increased risk for EC (OR 3.35, 95% CI 1.49-7.61). GSTM1 deletion genotype was a risk factor for EC (OR1.81, 95% CI 1.03-3.18). Gene-environment interaction analysis showed that CYP1A1 Val/Val genotype, GSTM1 deletion genotype had synergetic interactions with tobacco smoking, alcohol drinking and family history of EC. CONCLUSION: Tobacco smoking, alcohol drinking and a family history of EC are risk factors for EC. CYP1A1 Val/Val and GSTM1 deletion genotypes are genetic susceptibility biomarkers for EC. There are synergic interactions between genetic susceptibility and environmental factors.

Triglyceride and coronary heart disease mortality in a 24-year follow-up study in Xi'an, China.

PURPOSE: To study whether serum triglyceride (TG) was associated with coronary heart disease (CHD) mortality. METHODS: A cohort analytic study carried out in a machinery factory in Xi'an, China on 1696 subjects aged 35 years or above (1124 men and 572 women) examined in 1976 and followed up till 2000. RESULTS: At baseline, the mean serum total cholesterol (TC) and triglyceride (TG) was 4.64 and 1.16 mmol/L in men, 4.62 and 1.10 mmol/L in women, respectively. Three hundred six (239 men, 67 women) had died within 37,781 person-years of follow-up, with 49 CHD deaths (36 male, 13 female). The relative risk (95% confidence interval) of CHD mortality per mmol/L increase in TG was 2.13 (1.46-3.17) after adjusting for age, marital status, occupation, education, systolic blood pressure and TC. Dose-response relationship between TG levels by tertiles and CHD risk was found. Stratified analyses showed TG was an independent predictor for CHD mortality in subjects with lower or higher TC. CONCLUSIONS: Chinese had lower levels of TC and TG than Western populations. This study provides new evidence that TG is an independent risk factor of CHD in subjects with lower or higher TC levels, and supports the lowering of cut-off value for elevated triglyceride.

[Application of "time series analysis" in the prediction of schistosomiasis prevalence in areas of "breaking dikes or opening sluice for waterstore" in Dongting Lake areas, China].

OBJECTIVE: To provide the fittest model for forecasting schistosomiasis prevalence in Haokou village of "breaking dikes or opening sluice for waterstore" in Dongting Lake areas by comparing the results of Moving Average, Exponential Smoothing, Autoregressive Model and Autoregressive integrated moving average model (ARIMA model) from 1990 to 2002. METHODS: Error sum of square of four statistical methods was compared and the fittest model was chosen. RESULTS: Error sum of square of predicted schistosomiasis prevalence rates in Haokou village from 1994 to 2002 were 39.40, 39.86, 26.63, 22.54 respectively. CONCLUSION: ARIMA model seemed to be the fittest one in the prediction of schistosomiasis prevalence in Haokou village of "breaking dikes or opening sluice for waterstore" in Dongting Lake from 1990 to 2002.

[Study on mortality, incidence and risk factors of stroke in a cohort of elderly in Xi'an, China].

OBJECTIVE: To prospectively study the relationship between risk factors and stroke incidence and mortality in the Chinese elderly. METHODS: An analytic study in a cohort population of 1,268 male retired cadres in a military setting. A health-screening program was carried out for all cadres aged 55 years or older in Xi'an in February 1987. Baseline data on smoking, cholesterol, triglyceride, blood pressure, body mass index (BMI), histories of hypertension, hyperlipidemia and coronary heart disease (CHD), stroke, diabetes and family histories of cardiovascular disease were investigated. Main outcome measures were stroke incidence, stroke and all-cause mortality. RESULTS: The cohort was followed up until June 30, 2001 and a total number of follow-up person-year was 15,546. During the follow-up period, there were 113 new stroke cases identified and the adjusted incidence was 727 per 100,000 person-year. Forty-five deaths were due to stroke and the adjusted mortality was 289 per 100,000 person-year. Using Cox model analysis, after adjustment on age, total cholesterol, triglyceride, smoking, drinking and physical exercise, we noticed that the systolic pressure, BMI, history of CHD and hyperlipidemia were independent risk factors for stroke incidence and morality. CONCLUSION: The incidence and mortality of stroke in this cohort were lower than those in the same age group of general population. Monitoring and controlling body mass index and blood pressure level seemed to be important factors for the prevention of stroke in the elderly.

Smoking, quitting, and mortality in a Chinese cohort of retired men.

PURPOSE: To examine the relationship between smoking, quitting, and mortality in older Chinese men. DESIGN AND METHODS: A cohort analytic study was carried out in Xi'an, China. A total of 1268 retired male military cadres aged 60 or older were examined in 1987 and followed for 12 years. RESULTS: At baseline, 388 men were never-smokers, 461 were former smokers, and 419 were current smokers. Through May 1999, a total of 299 had died. The relative risks [95% confidence intervals (CI)] for ever-smoking, after adjusting for age, blood pressure, body mass index, total cholesterol, triglycerides, alcohol drinking, exercise and existing diseases, for deaths resulting from all causes, chronic obstructive pulmonary disease (COPD), lung cancer, and coronary heart disease (CHD) were, respectively, 1.34 (1.02-1.76), 3.23 (0.95-10.91), 2.31 (0.95-5.61), and 1.60 (0.81-3.19). The risks increased significantly with increasing amount and duration of smoking. Compared with current smokers, former smokers had lower risks of total mortality (excess risk reduction of 56%) and from CHD death, but had higher risks for COPD death. CONCLUSIONS: Smoking is a major cause of death in older Chinese and quitting can save lives. Early recognition of the significance of COPD symptoms followed by prompt quitting should be emphasized in the control of the growing tobacco epidemic.

Relationship of tobacco smoking CYP1A1 GSTM1 gene polymorphism and esophageal cancer in Xi'an.

AIM: To analyze the association of tobacco smoking polymorphism of CYP1A1 (7th exon) and GSTM1 genotype and esophageal cancer(EC) in Xi'an. METHODS: A hospital based case-control study, with molecular epidemiological method, was carried out. Polymorphism of CYP1A1 and GSTM1 of samples from 127 EC cases and 101 controls were detected by PCR method. RESULTS: There were no significant difference of age and gender between cases and controls. Tobacco smoking was the main risk factor OR=1.97;95% CI=1.12-3.48 for EC in Xi'an. The proportions of CYP1A1 Ile/Ile, Ile/Val and Val/Val gene types in cases and controls was 19.7% 45.7% 34.6% and 30.7%,47.5%, 21.8% respectively(P=0.049). Individuals with CYP1A1 Val/Val genotype compared to those with CYP1A1 Ile/Ile genotype had higher risk for EC increased (OR=2.48, 95%CI=1.12-5.54). The proportions of GSTM1 deletion genotype in cases and controls were 58.3% and 43.6%(OR=1.81, 95%CI=1.03-3.18, P=0.028). Analysis of gene-environment interaction showed that tobacco smoking and CYP1A1 Val/Val genotype; tobacco smoking and GSTM1 deletion genotype had synergism interaction respectively. Analysis of gene-gene interaction did not find synergistic interaction between these two genes. But in GSTM1 deletion group there was significant difference of distribution of CYP1A1 genotype between cases and controls (P=0.011). CONCLUSION: CYP1A1 Val/Val and GSTM1 deletion genotypes are genetic susceptibility biomarkers for EC. The risk increases, when person with CYP1A1 Val/Val and/or GSTM1 deletion genotype. And these two-metabolic enzymes seem to have interactions with tobacco smoking, in which the mechanism still needs further study.