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

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

In this study, two proposed scales of nicotine dependence were compared: self-administered nicotine intake and acute heart rate sensitivity to smoking. Our aim was to determine if these nicotine dependence scales would rank relative dependence the same in a sample of 15 male chronic smokers who smoked their first cigarette in the morning after overnight abstinence. Heart rate and plasma nicotine levels were measured before and 5, 10, 15, and 30 min after smoking. The results of this pilot study suggest that heart rate sensitivity and nicotine intake do not have a direct linear relationship, but rather a curvilinear relationship. A marked increase in heart rate sensitivity was observed at approximately the 70th percentile of nicotine intake.
Heart Rate ; Humans ; Male ; Nicotine ; administration & dosage ; Pilot Projects ; Sensitivity and Specificity ; Smoking ; adverse effects ; Tobacco Use Disorder ; physiopathology

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*

OBJECTIVETo study the effects of different doses of cigarette smoke extract (CSE) on the erectile function of male rats and the mechanism of smoking-induced erectile dysfunction (ED).

METHODSA total of 75 healthy male SD rats were randomly divided into Groups A (control), B (dimethyl sulphoxide [DMSO]), C (low-dose CSE), D (medium-dose CSE) and E (high-dose CSE). CSE models were established in male SD rats by hypodermic injection, and 60 days later observed for penile erection following subcutaneous injection of apomorphine. Then the rats were killed and the penile cavernous body obtained for the examination of NOS activity by chromatometry and the determination of Cx43 expression by laser scanning confocal fluorescence microscopy (LCSM).

RESULTSCompared with the control and DMSO groups, penile erection frequency, NOS activity and Cx43 expression in the penile cavernous tissue were significantly decreased in the CSE groups (P < 0.05), and the decrease was proportional to the increase of the doses of CSE. No statistically significant differences were observed between the control and DMSO groups (P > 0.05).

CONCLUSIONCigarette smoke obviously reduces NOS activity and Cx43 expression in the penile cavernous tissue and seriously affects penile erection. The higher the dose, the more serious the influence. The decreases of NOS activity and Cx43 expression may be an important mechanism of ED.

Animals ; Connexin 43 ; metabolism ; Male ; Nitric Oxide Synthase ; metabolism ; Penile Erection ; Penis ; metabolism ; Rats ; Rats, Sprague-Dawley ; Smoke ; Smoking ; adverse effects ; Tobacco ; adverse effects

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

OBJECTIVETo determine the level of awareness of the hazards of tobacco smoking and secondhand smoke inhalation among adults in China.

METHODSHousehold surveys were conducted with a total of 13,354 respondents aged 15 years or over from 100 counties of 28 Chinese provinces using a stratified multi-stage geographically clustered sample design.

RESULTSThe findings revealed that 81.8% of the population was aware that smoking causes serious diseases, and 27.2% and 38.7% were aware that smoking causes stroke and heart attack, respectively. Only 64.3% of respondents were aware that secondhand smoke can cause serious diseases, and 27.5%, 51.0%, and 52.6% were aware that secondhand smoke causes heart disease in adults, lung disease in children and lung cancer in adults, respectively. Awareness regarding smoking-related hazards across all participants was significantly associated with several factors, including gender, smoking status, urban/rural residency, education level and exposure to tobacco control publicity in the last 30 days. Awareness regarding tobacco-related hazards in smokers was significantly associated with urban/rural residency, education level, exposure to tobacco control publicity in the last 30 days, and physician's advice. Awareness relating to the hazards of inhaling secondhand smoke was associated with smoking status, urban/rural residency, age, education level, and exposure to tobacco control publicity in the last 30 days. Medical professionals were found to know more about the health hazards of tobacco compared with people in other types of employment.

CONCLUSIONSOverall awareness of the health hazards of tobacco has improved in the last 15 years in China, but is still relatively poor. Improved means of communicating information and more effective warning labels on cigarette packaging are necessary for increasing public awareness of tobacco hazards, particularly among rural residents and people with less education.

Adolescent ; Adult ; Aged ; Child ; China ; epidemiology ; Health Knowledge, Attitudes, Practice ; Health Surveys ; Heart Diseases ; etiology ; Humans ; Lung Diseases ; Middle Aged ; Smoking ; adverse effects ; Tobacco Smoke Pollution ; adverse effects ; Tobacco Use Disorder ; epidemiology ; Young Adult

OBJECTIVETo review the current evidence that links smoking to obstructive sleep apnea (OSA) and to discuss some potential mechanisms proposed for these links.

DATA SOURCESWe searched PubMed and Medline to identify studies investigating the interaction between smoking and OSA.

STUDY SELECTIONArticles regarding the relationship between smoking and OSA were selected. Studies considered smoking as a confounding factor were excluded.

RESULTSThe association of smoking and OSA has been confirmed in several studies. The effects of smoking on the pathophysiology of OSA may include smoking-induced upper airway inflammation, stimulant effects of nicotine on upper airway muscles, and a "rebound effect" due to nightly short-term nicotine withdrawal, or all of the above. In addition, the coexistence of OSA and smoking may have more widespread implications for cardiovascular dysfunction in patients with OSA. Finally, OSA might be responsible for the addiction to nicotine.

CONCLUSIONSSmoking may act as a risk factor for OSA and join with OSA in a common pathway to increase the risk of systematic injury. OSA, in turn, may be a predisposing factor for smoking. Thus, smoking cessation is recommended when considering treatment for OSA, and treating OSA may be a necessary precondition for successful smoking cessation.

Asthma ; epidemiology ; etiology ; Bronchi ; drug effects ; Humans ; Nicotine ; pharmacology ; Risk Factors ; Sleep ; physiology ; Sleep Apnea, Obstructive ; epidemiology ; etiology ; Smoking ; adverse effects ; Tobacco Use Disorder ; epidemiology ; etiology

Tobacco use is the single most preventable cause of death, disability and disease in the world and is projected to be the leading cause of death and disability across all developed and developing countries by 2020. Nicotine, the primary active ingredient of cigarettes that contributes to physical dependence, acts on nicotine receptors in the central nervous system and leads to the release of neurotransmitters (such as dopamine). Like other drugs of abuse, nicotine is thought to produce reinforcing effect by activating the mesocorticolimbic dopamine system. A wide variety of cessation treatments of nicotine dependence is commercially available, yet only 2 general approaches have received empirical validation: behavioral intervention (including 5 As brief intervention) and pharmacotherapy. The evidences show that 5 As brief intervention is one of the most cost-effective treatments in clinical work for busy physicians. Three types of medications have been available in market for smoking cessation treatment: nicotine replacement treatment (NRT, i.e., transdermal patch, gum, inhaler, nasal spray, and lozenge), sustained release bupropion and varenicline. Varenicline, a novel alpha4beta2 nicotinic receptor partial agonist, is effective for tobacco dependence. Phase III trials suggest that it is more effective than NRT and bupropion SR. The safety profile of varenicline is excellent, with the most commonly occurring adverse events, nausea, typically mild and well tolerated. However, new safety warnings are added to the varenicline label because of post-marketing report including agitation, depression and suicidality. A causal connection between varenicline use and these symptoms has not been established.
Benzazepines ; adverse effects ; therapeutic use ; Bupropion ; therapeutic use ; Dopamine Uptake Inhibitors ; therapeutic use ; Humans ; Nicotinic Agonists ; adverse effects ; therapeutic use ; Quinoxalines ; adverse effects ; therapeutic use ; Smoking Cessation ; methods ; psychology ; Tobacco Use Disorder ; therapy ; Varenicline