Mutagenicity Tests ; methods ; Tobacco Smoke Pollution ; adverse effects

Humans ; Male ; Middle Aged ; Occupational Exposure ; adverse effects ; Pneumoconiosis ; diagnosis ; etiology ; Tobacco ; Tobacco Industry

Humans ; Pulmonary Disease, Chronic Obstructive ; Smoke/adverse effects* ; Tobacco ; Tobacco Smoke Pollution

OBJECTIVETo reduce tobacco consumption and exposure to passive smoking in China.

METHODSDiscussion consisting of 80 focus groups and 35 interviews were held in three rural intervention counties of Jiangxi, Henan, and Sichuan Provinces. Participants came from hospitals, schools, rural areas, and urban areas.

RESULTSTobacco use and exposure to passive smoking were widely prevalent in the investigated schools, hospitals, county towns, and rural areas. Knowledge of the risks for passive smoking on health is lacking, especially in rural areas. Barriers to the control of tobacco use in public places include reluctance of administrators to implement tobacco control policies, lack of consistent policies, difficulties with regulations and enforcement, and reluctance of non-smokers to exercise their right to clean air.

CONCLUSIONTo curb the current tobacco epidemic in China, tobacco control efforts must focus on reducing exposure to passive smoking. A strategy should be formulated to reduce the factors that contribute to tobacco use and exposure to passive smoking.

China ; epidemiology ; Data Collection ; Health Knowledge, Attitudes, Practice ; Hospitals ; Humans ; Schools ; Smoking ; psychology ; Social Responsibility ; Tobacco ; adverse effects ; Tobacco Smoke Pollution ; adverse effects ; prevention & control ; statistics & numerical data

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 ; physiology ; Environmental Exposure ; adverse effects ; Female ; Humans ; Menarche ; physiology ; Pregnancy ; Prenatal Exposure Delayed Effects ; etiology ; Puberty ; physiology ; Smoking ; adverse effects ; Tobacco Smoke Pollution ; adverse effects

Nicotine is the main addictive component in cigarettes that motivates dependence on tobacco use for smokers and makes it difficult to quit through regulating a variety of neurotransmitter release and receptor activations in the brain. Even though nicotine has an analgesic effect, clinical studies demonstrated that nicotine abstinence reduces pain threshold and increases pain sensitivity in smoking individuals. The demand for opioid analgesics in nicotine abstinent patients undergoing surgery has greatly increased, which results in many side effects, such as nausea, vomiting, and respiratory depression, etc. In addition, these side effects would hinder patients' physical and psychological recovery. Therefore, identifying the neural mechanism of the increase of pain sensitivity induced by nicotine abstinence and deriving a way to cope with the increased demand for postoperative analgesics would have enormous basic and clinical implications. In this review, we first discussed different experimental pain stimuli (e.g., cold, heat, and mechanical pain)-induced pain sensitivity changes after a period of nicotine dependence/abstinence from both animal and human studies. Then, we summarized the effects of the brain neurotransmitter release (e.g., serotonin, norepinephrine, endogenous opioids, dopamine, and γ-aminobutyric acid) and their corresponding receptor activation changes after nicotine abstinence on pain sensitivity. Finally, we discussed the limits in recent studies. We proposed that more attention should be paid to human studies, especially studies among chronic pain patients, and functional magnetic resonance imaging might be a useful tool to reveal the mechanisms of abstinence-induced pain sensitivity changes. Besides, considering the influence of duration of nicotine dependence/abstinence and gender on pain sensitivity, we proposed that the effects of nicotine abstinence and individual differences (e.g., duration of abstinence from smoking, chronic/acute abstinence, and gender) on abstinence-induced pain sensitivity should be fully considered in formulating pain treatment protocols. In summary, this paper could deepen our understanding of nicotine abstinence-induced pain sensitivity changes and its underlying neural mechanism, and could also provide effective scientific theories to guide clinical pain diagnosis and treatment, which has important clinical significance.
Animals ; Humans ; Nicotine/adverse effects* ; Pain ; Pain Threshold ; Smoking Cessation ; Tobacco Use Disorder

Objective: To understand the relationship between secondhand smoke exposure and dyslipidemia among adults in Beijing and to provide a scientific basis for relevant intervention. Methods: Data were from Beijing Adult Non-communicable and Chronic Diseases and Risk Factors Surveillance Program in 2017. A total of 13 240 respondents were selected by multistage cluster stratified sampling method. The monitoring contents include a questionnaire survey, physical measurement, collection of fasting venous blood, and determination of related biochemical indicators. SPSS 20.0 software was used for the chi-square test and multivariate logistic regression analysis. Results: The prevalence of total dyslipidemia (39.27%), hypertriglyceridemia (22.61%), and high LDL-C (6.03%) were the highest among those exposed to daily secondhand smoke. Among the male respondents, the prevalence of total dyslipidemia (44.42%) and hypertriglyceridemia (26.12%) were the highest among those exposed to secondhand smoke daily. Multivariate logistic regression analysis after adjustment for confounding factors showed that compared with no exposure to secondhand smoke, the population with an average exposure frequency of 1-3 days per week had the highest risk of total dyslipidemia (OR=1.276, 95%CI: 1.023-1.591). Among the patients with hypertriglyceridemia, those exposed to secondhand smoke daily had the highest risk (OR=1.356, 95%CI: 1.107-1.661). Among the male respondents, those exposed to secondhand smoke for 1-3 days per week had a higher risk of total dyslipidemia (OR=1.366, 95%CI: 1.019-1.831), and the highest risk of hypertriglyceridemia (OR=1.377, 95%CI: 1.058-1.793). There was no significant correlation between the frequency of secondhand smoke exposure and the risk of dyslipidemia among female respondents. Conclusions: Secondhand smoke exposure in Beijing adults, especially men, will increase the risk of total dyslipidemia, especially hyperlipidemia. Improving personal health awareness and minimizing or avoiding exposure to secondhand smoke is necessary.
Adult ; Humans ; Female ; Male ; Tobacco Smoke Pollution/adverse effects* ; Beijing ; Dyslipidemias/epidemiology* ; Hypertriglyceridemia/epidemiology* ; Fasting

OBJECTIVETo study the in vitro effect of herb components on scavenging harmful components of cigarette smoke such as radicals, polycyclic aromatic hydrocarbons, nitrosamines in vitro, and its reducing effect on cytotoxicity of cigarette smoke.

METHODspectrophotometry was used to examine the scavenging effect of herb components on DPPH free radicals, superoxide anion radical, and hydroxyl radical, and the results were compared with the anti-oxidation of ascorbic acid. Fluorescence spectroscopy was used to examine the scavenging effect of herb components on polycyclic aromatic hydrocarbons. UV spectrophotometry was used to examine the scavenging effect of herb components on volatile nitrosamines. MTT assay was used to examine cytotoxicity of cigarette smoke.

RESULTAll the herb components showed a certain scavenging effect on DPPH free radicals, superoxide anion radical, hydroxyl radical, polycyclic aromatic hydrocarbons and volatile nitrosamines, espacially the ginkgo biloba extract (GBE), flavonoids of glycyrrhiza, procyanidine, total saponins in ophiopogonin, total saponins of astragalus and epimediun flavonoids. After these six herb components were added to cigarette, the cytotoxicity of cigarette smoke on BEP2D cells was remarkably reduced, by increasing cell survival fraction (SF, %) and mean lethal dose (DML).

CONCLUSIONThe herb components can scavenge harmful components of cigarette smoke such as radicals, polycyclic aromatic hydrocarbons and nitrosamines, which reduce the damage of cigarette smoke on human being.

Cell Survival ; drug effects ; Cells, Cultured ; Drugs, Chinese Herbal ; pharmacology ; Free Radical Scavengers ; pharmacology ; Humans ; Smoke ; adverse effects ; Tobacco ; adverse effects

Objective: To understand the rate on tobacco use and associated factors in junior middle school students in Shaanxi province. Methods: We used a multi-stage stratified random sampling method to select students from 30 junior middle schools in 10 areas of Shaanxi province in 2013. All the participants completed a self-administered questionnaire. Results: A total of 4 633 questionnaires were dispatched and 4 298 were qualified for further analysis. The current smoking rate of junior middle school students in Shaanxi was 6.5%, with rate in male (11.1%) higher than that of female students (1.7%). The current smoking rate of students in grade three (9.3%) was higher than those of students in grade one (3.5%) or in grade two (7.0%). The smoking rate of students with pocket money more than 31 Yuan per week was (10.0%) higher than those of students with pocket money less than 10 Yuan (4.6%) or 10-30 Yuan (6.3%) per week. Results from the logistic regression analysis showed that factors as: male, school located in the city, older age, with more pocket money, having smokers in the family and exposure to second hand smoking were high risk factors for current smoking. Conclusion: Rate on current smoking was high in junior middle schools students in Shaanxi, suggesting that comprehensive intervention programs be developed to reduce the rate of tobacco use in junior middle school students.
China/epidemiology* ; Cities ; Cross-Sectional Studies ; Female ; Humans ; Male ; Prevalence ; Schools ; Smoking/epidemiology* ; Students/statistics & numerical data* ; Surveys and Questionnaires ; Tobacco Smoke Pollution/adverse effects* ; Tobacco Use/epidemiology*

OBJECTIVE: To investigate the mechanism of activator protein-1 (AP-1) on cigarette smoke-induced airway mucous hypersecretion and to explore the possible signal transduction pathway that activates AP-1. METHODS: The airway epithelial cell line (BEAS-2B) was cultured in vivo and treated with cigarette smoke extract (CSE). The DNA binding activity of AP-1 was blocked by the transfection of c-Jun dominant negative mutant TAM67 into the cells. SP600125 and PD98059 were used to block the activation of c-Jun terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) respectively. MUC5AC protein was detected by enzyme-linked immunosorbent assay, MUC5AC mRNA level was analyzed by RT-PCR, while the protein contents of p-JNK, p-ERK and p-P38 were detected by Western blot, and the DNA binding activity of AP-1 was determined by electrophoretic mobility shift assay. RESULTS: The MUC5AC protein production and mRNA expression in the CSE group were significantly higher than those in the control group, and the DNA binding activity of AP-1 was also higher than that in the control group (P<0.01). The protein contents of p-ERK and p-JNK in the CSE group were higher than those in the control group (P<0.01), but the p-P38 level was not significantly different from that in the control group (P>0.05). After the transfection of TAM67 into the cells, the expression levels of MUC5AC protein and mRNA and the binding activity of AP-1 decreased significantly (P<0.01). The DNA binding activity of AP-1 and the expression levels of MUC5AC protein and mRNA were lower in the SP600125 group and in the PD98059 group than those in the CSE group (P<0.05). CONCLUSION After being activated by JNK and ERK which are phosphorylated by cigarette smoke, AP-1 binds to its DNA binding elements on the promoter of MUC5AC gene and up-regulates the MUC5AC expression at the transcriptional level.
Bronchi ; cytology ; Cells, Cultured ; Epithelial Cells ; cytology ; metabolism ; Humans ; Mucin 5AC ; genetics ; metabolism ; Smoke ; adverse effects ; Smoking ; adverse effects ; Tobacco ; chemistry ; Transcription Factor AP-1 ; pharmacology