4.Air pollution: a smoking gun for cancer.
Wei ZHANG ; Chao-Nan QIAN ; Yi-Xin ZENG
Chinese Journal of Cancer 2014;33(4):173-175
Once considered a taboo topic or stigma, cancer is the number one public health enemy in the world. Once a product of an almost untouchable industry, tobacco is indisputably recognized as a major cause of cancer and a target for anticancer efforts. With the emergence of new economic powers in the world, especially in highly populated countries such as China, air pollution has rapidly emerged as a smoking gun for cancer and has become a hot topic for public health debate because of the complex political, economic, scientific, and technologic issues surrounding the air pollution problem. This editorial and the referred articles published in this special issue of the Chinese Journal of Cancer discuss these fundamental questions. Does air pollution cause a wide spectrum of cancers? Should air pollution be considered a necessary evil accompanying economic transformation in developing countries? Is an explosion of cancer incidence coming to China and how soon will it arrive? What must be done to prevent this possible human catastrophe? Finally, the approaches for air pollution control are also discussed.
Air Pollution
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adverse effects
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Carcinogens, Environmental
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toxicity
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China
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Humans
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Neoplasms
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etiology
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Risk Factors
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Smoking
;
adverse effects
5.Impact of intervention on tobacco related knowledge, attitudes and practice of smokers.
Lei WU ; Yao HE ; Bin JIANG ; Fang ZUO ; Qinghui LIU ; Li ZHANG ; Changxi ZHOU ; Miao LIU ; Hongyan CHEN
Chinese Journal of Epidemiology 2015;36(2):119-123
OBJECTIVETo evaluate the impact of intervention on tobacco related knowledge, attitudes and practice of smokers.
METHODSAn observational study was conducted among the smokers seeking counsel at smoking cessation clinic in our hospital from October 2008 to August 2013. First, a face to face counsel and mental intervention for more than 30 minutes was given to smoker, then 4 interventions through telephone call for 15-20 minutes for each time were conducted 1 week later, 1 month later, 3 months later and 6 months later, respectively. The controls were smokers receiving health examination in our hospital. No interventions were conducted among them. The tobacco related knowledge, attitudes and practice at baseline survey and follow up 1 year later were compared between intervention group and control group.
RESULTSThe intervention group included 414 smokers and the control group included 213 smokers. Intentional analysis indicated that the awareness/acceptance rates of 5 items about tobacco related knowledge and attitudes at follow up 1 year later was higher than those at baseline survey in intervention group. The smoking cessation rate was 27.3% in intervention group and 4.7% in control group. Multivariate logistic regression analysis indicated that the smoking cessation rate was positively correlated with intervention, female, highly nicotine dependence and positive change of tobacco related knowledge and attitudes (smoking can cause heart disease, all kinds of tobacco advertisements should be prohibited, smoking waste money and restaurant should be smoking free) with OR (95% CI): 2.85 (2.00-4.07), 3.34 (1.23-9.07), 2.78 (1.64-4.72), 2.30 (1.03-5.15), 5.33 (1.47-19.32), 6.32 (1.56-25.62) and 10.47 (2.25-48.84), respectively.
CONCLUSIONThe awareness rate of tobacco related harm was high among the smokers seeking counsel at smoking cessation clinic. Systematic smoking cessation intervention can improve smokers' tobacco related knowledge and attitudes and increase smoking cessation rate.
Female ; Health Knowledge, Attitudes, Practice ; Humans ; Male ; Smoking ; adverse effects ; Smoking Cessation ; Tobacco ; Tobacco Use Disorder
6.Risk Factors of Acoustic Neuroma: Systematic Review and Meta-Analysis.
Mantao CHEN ; Zuoxu FAN ; Xiujue ZHENG ; Fei CAO ; Liang WANG
Yonsei Medical Journal 2016;57(3):776-783
PURPOSE: Many epidemiological studies have investigated environmental risk factors for the development of acoustic neuroma. However, these results are controversial. We conducted a meta-analysis of case-control studies to identify any potential relationship between history of noise exposure, smoking, allergic diseases, and risk of acoustic neuroma. MATERIALS AND METHODS: We searched PubMed to identify relevant articles. Two researchers evaluated the eligibility and extracted the data independently. RESULTS: Eleven case-control studies were included in our meta-analysis. Acoustic neuroma was found to be associated with leisure noise exposure [odds ratio (OR)=1.33, 95% confidence interval (CI): 1.05-1.68], but not with occupational noise exposure and ever noise exposure (OR=1.20, 95% CI: 0.84-1.72 and OR=1.15, 95% CI: 0.80-1.65). The OR of acoustic neuroma for ever (versus never) smoking was 0.53 (95% CI: 0.30-0.94), while the subgroup analysis indicated ORs of 0.95 (95% CI: 0.81-1.10) and 0.49 (95% CI: 0.41-0.59) for ex-smoker and current smoker respectively. The ORs for asthma, eczema, and seasonal rhinitis were 0.98 (95% CI: 0.80-1.18), 0.91 (95% CI: 0.76-1.09), and 1.52 (95% CI: 0.90-2.54), respectively. CONCLUSION: Our meta-analysis is suggestive of an elevated risk of acoustic neuroma among individuals who were ever exposed to leisure noise, but not to occupational noise. Our study also indicated a lower acoustic neuroma risk among ever and current cigarette smokers than never smokers, while there was no significant relationship for ex-smokers. No significant associations were found between acoustic neuroma and history of any allergic diseases, such as asthma, eczema, and seasonal rhinitis.
Adult
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Asthma/complications
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Environmental Exposure/*adverse effects
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Female
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Humans
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Hypersensitivity
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*Leisure Activities
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Neuroma, Acoustic/epidemiology/*etiology
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Noise/*adverse effects
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Occupational Exposure/adverse effects
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Risk Factors
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Smoking/adverse effects
7.Association of prenatal and childhood environment smoking exposure with puberty timing: a systematic review and meta-analysis.
Yiwen CHEN ; Qin LIU ; Wenyan LI ; Xu DENG ; Bo YANG ; Xin HUANG
Environmental Health and Preventive Medicine 2018;23(1):33-33
OBJECTIVES:
Mothers who smoke during pregnancy or while their children are small were common in some populations. Epidemiological studies have tried to detect the effect of prenatal tobacco smoke (PTS), and childhood environmental tobacco smoke (ETS) on puberty timing have not shown a consensus results. We aimed to examine current evidence and estimate the associations between PTS or/and ETS and puberty timing.
METHODS:
Seven databases were searched from inception to May 2017. All the cohort studies examining the associations between PTS and/or ETS and puberty timing were identified. Two reviewers independently screened all studies, evaluated the quality of eligible studies, and extracted the data. The quality assessment of the eligible cohort studies was based on the Newcastle-Ottawa Scale. Risk ratio (RR), standard mean difference (SMD), and 95% confidence intervals (CIs) were calculated and pooled by CMA (Version 2.0, Biostat, Inc., USA).
RESULTS:
Compared with controls, girls with PTS and ETS exposure have an earlier age at menarche (SMD - 0.087, 95% CI 0.174 to - 0.000), and similar results were found in both PTS subgroup (SMD - 0.097, 95% CI - 0.192 to - 0.002) and prospective cohort subgroup (SMD - 0.171, 95% CI - 0.253 to - 0.090). And number of boys with early voice break in PTS group was significantly increasing than non-exposed boys (RR 1.34, 95% CI 1.29 to 1.40).
CONCLUSIONS
PTS exposure possibly decrease age of menarche of girls, and studies on boys were urgent needed. Appropriate and comprehensive outcome measures using unified criteria to classify puberty should be reported in future studies.
Aging
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physiology
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Environmental Exposure
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adverse effects
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Female
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Humans
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Menarche
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physiology
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Pregnancy
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Prenatal Exposure Delayed Effects
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etiology
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Puberty
;
physiology
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Smoking
;
adverse effects
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Tobacco Smoke Pollution
;
adverse effects
8.Evaluation on a cohort based population intervention project regarding risk factors for cerebrovascular diseases.
Yun-hai LIU ; Qi-dong YANG ; Zun-jing LIU ; Le ZHANG ; Yan-hong ZHOU ; Hong-wei XU
Chinese Journal of Epidemiology 2003;24(2):102-105
OBJECTIVETo analyze the changes of risk factors in cerebrovascular diseases in cohort-based population after intervention and evaluating the intervention effect.
METHODSIn 1987, an intervention cohort and a control cohort were selected randomly in urban areas of Changsha. Risk factors in cerebrovascular diseases were investigated in two cohort populations aged over 35 years as baseline indication. Then comprehensive prevention of cerebrovascular diseases was carried out in intervention cohort during 1987 - 2000. After intervention for 14 years, a reexamination was taken in the two groups noted above.
RESULTSAfter 14 years, the prevalence of diabetes mellitus, hypertension, mean systolic and diastolic pressure, weight increased from 33.8% to 35.7%, 30 to 129 per 10,000, 128.41 mm Hg to 134.49 mm Hg, 77.78 mm Hg to 78.54 mm Hg, 54.80 kg to 57.78 kg in the intervention group, respectively while the baseline indication increased from 35.9% to 56.8%, 30 to 228 per 10,000, 127.70 mm Hg to 141.80 mm Hg, 78.27 mm Hg to 82.89 mm Hg, 54.92 kg to 59.69 kg in the control one. The changes were of statistical significance in each group except diastolic pressure and the prevalence of hypertension in intervention group, but all the parameters increased significantly in the control group; rate of alcohol intake decreased significantly in two groups, but rate of cigarette smoking decreased with no significance. The changes between two groups were not significant either; the cumulative incidence of stroke was significantly lower in intervention cohort (3.4%) than in control cohort (4.7%).
CONCLUSIONThe risk factors for cerebrovascular diseases (such as hypertension, diabetes mellitus etc.) were increasing along with by aging. Intervention programs can delay the increase of risk factors and down-regulate the incidence of stroke.
Alcohol Drinking ; adverse effects ; Cerebrovascular Disorders ; etiology ; Cohort Studies ; Female ; Humans ; Hypertension ; complications ; Male ; Risk Factors ; Smoking ; adverse effects
9.A study on lymphocyte DNA damage in traffic policemen in Guangzhou.
Chang-qi ZHU ; Th LAM ; Chao-qiang JIANG ; Ba-xiong WEI ; Yue-hua CHEN ; Qi-rong XU
Chinese Journal of Industrial Hygiene and Occupational Diseases 2003;21(1):41-44
OBJECTIVETo study the effect of occupational exposure to traffic exhaust and smoking on DNA damage in traffic policemen.
METHODS812 traffic policemen (741 men and 71 women, 130 of office-work and 682 of outside work) from 8 districts in Guangzhou were investigated. Blood samples were taken by venipuncture and lymphocytes were collected by using lymphocyte separation medium and centrifugation. The comet assay was used to measure DNA damage.
RESULTSThe office-work policemen [(37.7 +/- 9.5) years] were older than the outside-work ones [(32.3 +/- 8.1) years, P < 0.001]. No significant difference was observed in sex (P = 0.08) and age (P = 0.45). Comet assay showed that occupational exposure to traffic exhaust significantly increased tail length [4.20 micro m, 95% CI: (3.98 - 4.42) micro m vs 3.23 micro m, 95% CI: (2.82 - 3.7) micro m, P < 0.001]. Smokers had longer tail length [4.66 micro m, 95% CI: (4.37 - 4.97) micro m] than ex-smokers [3.28 micro m, 95% CI: (2.57 - 4.17) micro m] and nonsmokers [3.47 micro m, 95% CI: (3.21 - 3.75) micro m, P < 0.001]. In nonsmokers, significant increase in tail length was observed by passive smoking at home (P = 0.004) but not at work (P = 0.22). When out-door nonsmokers were excluded, passive smoking at work also significantly increased tail length (P = 0.007). Analysis of covariance showed that occupational exposure to traffic exhaust, tobacco smoking, and female had independent effect on lymphocyte DNA damage (P < 0.001) after these factors were adjusted. Passive smoking and age had no effect on lymphocyte DNA damage.
CONCLUSIONSOccupational exposure to traffic exhaust and tobacco smoking respectively increase lymphocyte DNA damage. Female traffic policemen may have more severe DNA damage than male.
Adult ; DNA Damage ; Female ; Humans ; Lymphocytes ; metabolism ; Male ; Occupational Exposure ; Oxidation-Reduction ; Police ; Smoking ; adverse effects ; Vehicle Emissions ; adverse effects
10.Household air pollution and lung cancer in China: a review of studies in Xuanwei.
Wei Jie SEOW ; Wei HU ; Roel VERMEULEN ; H Dean Hosgood III ; George S DOWNWARD ; Robert S CHAPMAN ; Xingzhou HE ; Bryan A BASSIG ; Christopher KIM ; Cuiju WEN ; Nathaniel ROTHMAN ; Qing LAN
Chinese Journal of Cancer 2014;33(10):471-475
Over half of the world's population is exposed to household air pollution from the burning of solid fuels at home. Household air pollution from solid fuel use is a leading risk factor for global disease and remains a major public health problem, especially in low- and mid-income countries. This is a particularly serious problem in China, where many people in rural areas still use coal for household heating and cooking. This review focuses on several decades of research carried out in Xuanwei County, Yunnan Province, where household coal use is a major source of household air pollution and where studies have linked household air pollution exposure to high rates of lung cancer. We conducted a series of case-control and cohort studies in Xuanwei to characterize the lung cancer risk in this population and the factors associated with it. We found lung cancer risk to vary substantially between different coal types, with a higher risk associated with smoky (i.e., bituminous) coal use compared to smokeless (i.e., anthracite) coal use. The installation of a chimney in homes resulted in a substantial reduction in lung cancer incidence and mortality. Overall, our research underscores the need among existing coal users to improve ventilation, use the least toxic fuel, and eventually move toward the use of cleaner fuels, such as gas and electricity.
Air Pollution, Indoor
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adverse effects
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China
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Coal
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adverse effects
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classification
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Cohort Studies
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Cooking
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Fossil Fuels
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Heating
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Humans
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Incidence
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Lung Neoplasms
;
etiology
;
mortality
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Risk Factors
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Smoke
;
adverse effects
;
Smoking