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

BACKGROUND: We aimed to examine the association of exposure to environmental tobacco smoke with dental caries among preschool children. Exposure to environmental tobacco smoke was assessed in terms of urinary cotinine concentrations and pack-years of exposure to smoking by parents and other family members at home. METHODS: This cross-sectional study included 405 preschool children aged 3-6 years from two preschools in Japan in 2006. Information on the smoking habits of family members living with the child was obtained from parent-administered questionnaires. Dental examination was conducted to assess dental caries, that is, decayed and/or filled teeth. Urinary cotinine levels were measured using first-void morning urine samples. RESULTS: Overall, 31.1% of the children had dental caries, and 29.5% had decayed teeth. Exposure to current maternal and paternal smoking was positively associated with the presence of dental caries after controlling for covariates. More than three pack-years of exposure to maternal smoking and more than five pack-years of exposure to smoking by all family members were significantly associated with the presence of dental caries as compared with no exposure (odds ratio [OR] = 5.55, 95% confidence interval [CI] = 2.17-14.22, P for trend < 0.001 and OR = 2.00, 95% CI = 1.12-3.58, P for trend = 0.004, respectively). These exposure variables were similarly associated with the presence of decayed teeth (OR = 2.92, 95% CI = 1.23-6.96, P for trend = 0.01 and OR = 1.75, 95% CI = 0.96-3.20, P for trend = 0.03, respectively). As compared with lowest tertile of the urinary cotinine level, the highest tertile of the urinary cotinine level was significantly associated with the presence of dental caries as well as decayed teeth; the ORs for the highest vs. lowest tertile of urinary cotinine levels were 3.10 (95% CI = 1.71-5.63, P for trend = 0.012) and 2.02 (95% CI = 1.10-3.70, P for trend = 0.10), respectively. CONCLUSIONS These data suggest that exposure to tobacco smoke may have a dose-dependent influence on the development of caries.
Child ; Child, Preschool ; Cotinine ; urine ; Cross-Sectional Studies ; Dental Caries ; epidemiology ; etiology ; Female ; Humans ; Japan ; epidemiology ; Logistic Models ; Male ; Maternal Exposure ; adverse effects ; Parents ; Paternal Exposure ; adverse effects ; Risk Factors ; Surveys and Questionnaires ; Tobacco Smoke Pollution ; adverse effects ; Tobacco Smoking ; adverse effects ; epidemiology

BACKGROUND: There have been inconsistent findings reported on maternal passive smoking during pregnancy and child risk of ADHD. In this study, ADHD symptoms at pre-school age children in association with prenatal passive and active tobacco smoke exposure determined by maternal plasma cotinine levels in the third trimester were investigated. METHODS: This was a follow-up study of the birth cohort: the Hokkaido Study on Environment and Children's Health. Children whose parents answered Strengths and Difficulties Questionnaire (SDQ) to identify child ADHD symptoms (hyperactivity/inattention and conduct problems) and total difficulties at age 5 years with available maternal plasma cotinine level at the third trimester were included (n = 3216). Cotinine levels were categorized into 4 groups; ≦ 0.21 ng/ml (non-smoker), 0.22-0.51 ng/ml (low-passive smoker), 0.52-11.48 ng/ml (high-passive smoker), and ≧ 11.49 ng/ml (active smoker). RESULTS: Maternal cotinine levels of active smokers were significantly associated with an increased risk of total difficulties (OR = 1.67) and maternal low- and high-passive smoking also increased the risk (OR = 1.11, 1.25, respectively) without statistical significance. Similarly, maternal cotinine levels of active smokers were associated with an increased risk of hyperactivity/inattention (OR = 1.49). Maternal low- and high-passive smoking and active smoking increased the risk of hyperactivity/inattention (OR = 1.45, 1.43, and OR = 1.59, respectively) only in boys. CONCLUSION Our findings suggested that maternal active smoking during pregnancy may contribute to the increased risk of child total difficulties and hyperactivity/inattention at pre-school age. Pregnant women should be encouraged to quit smoking and avoid exposure to tobacco smoke.
Adult ; Attention Deficit Disorder with Hyperactivity ; epidemiology ; etiology ; physiopathology ; psychology ; Child, Preschool ; Cotinine ; blood ; Female ; Follow-Up Studies ; Humans ; Japan ; epidemiology ; Male ; Maternal Exposure ; adverse effects ; Mothers ; Pregnancy ; Pregnancy Trimester, Third ; Prenatal Exposure Delayed Effects ; epidemiology ; etiology ; Risk ; Sex Factors ; Tobacco Smoking ; adverse effects ; epidemiology

The present review summarizes the results of several follow-up studies assessing an asbestos product manufacturing plant in Chongqing, China, and discusses three controversial issues related to the carcinogenicity of asbestos. The first issue is the amphibole hypothesis, which asserts that the carcinogenicity of asbestos is limited to amphiboles, such as crocidolite, but not serpentines, such as chrysotile. However, considering the possible multiple component of asbestos carcinogenicity in the presence of tobacco smoke or other carcinogens, chrysotile cannot be regarded as non-carcinogenic. Additionally, in a practical sense, it is not possible to assume "pure" chrysotile due to its ubiquitous contamination with tremolite, which is a type of amphibole. Thus, as the International Agency for Research on Cancer (IARC) assessed, all forms of asbestos including chrysotile should be regarded carcinogenic to humans (Group 1). The second issue is the chrysotile/tremolite paradox, which is a phenomenon involving predominant levels of tremolite in the lung tissues of individuals who worked in locations with negligible levels of tremolite due to the exclusive use of chrysotile. Four possible mechanisms to explain this paradox have been proposed but this phenomenon does not support the claim that amphibole is inert. The final issue discussed is the textile mystery, i.e., the higher incidence of cancer in asbestos textile plants compared to asbestos mines where the same asbestos was produced and the exposure levels were comparable. This phenomenon was first reported in North America followed by UK and then in the present observations from China. Previously, levels of fiber exposure were calculated using a universal converting coefficient to estimate the mass concentration versus fiber concentration. However, parallel measurements of fiber and mass concentrations in the workplace and exposed air indicated that there are wide variations in the fiber/mass ratio, which unjustifies the universal conversion. It is possible that contamination by airborne non-fibrous particles in mines with mass fiber conversion led to the overestimation of fiber concentrations and resulted in the textile mystery. Although the use and manufacturing of asbestos has been banned in Japan, more than 10 million tons of asbestos had been imported and the majority remains in existing buildings. Thus, efforts to control asbestos exposure should be continued.
Asbestos ; classification ; toxicity ; Asbestos, Amphibole ; toxicity ; Asbestos, Serpentine ; toxicity ; Carcinogens ; China ; Follow-Up Studies ; Humans ; Lung Neoplasms ; chemically induced ; epidemiology ; Manufacturing and Industrial Facilities ; statistics & numerical data ; Mining ; statistics & numerical data ; Occupational Diseases ; epidemiology ; Occupational Exposure ; adverse effects ; Textiles ; Tobacco Smoking ; epidemiology

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

Objective: To examine the sex-specific associations between tobacco smoking and risk of cardiovascular diseases in Chinese adults. Methods: The present analysis included 487 373 participants from the China Kadoorie Biobank after excluding those with cancer, heart diseases, stroke at baseline survey. The baseline survey was conducted from June 2004 to July 2008. The number of follow-up years was calculated from the time that the participants completed baseline survey to the time of any event: CVD incidence, death, loss of follow-up, or December 31, 2015, whichever occurred first. We used Cox proportional hazards regression models to estimate the HRs and 95%CI of incident cardiovascular diseases with tobacco smoking. Results: During a median follow-up of 8.9 years(a total of 4.1 million person years), we documented 33 947 cases of ischemic heart diseases, 6 048 cases of major coronary diseases, 7 794 cases of intracerebral hemorrhage, and 31 722 cases of cerebral infarction. The prevalence of smoking was much higher in men (67.9%) than in women (2.7%). Smoking increased risk of all subtypes of cardiovascular diseases. Compared with nonsmokers, the multivariable-adjusted HRs (95% CI) for current smokers were 1.54 (1.43-1.66) for major coronary event, 1.28 (1.24-1.32) for ischemic heart disease, 1.18 (1.14-1.22) for cerebral infarction, and 1.07 (1.00-1.15) for intracerebral hemorrhage, respectively. Female smokers tended to have greater risk of developing major coronary event associated with amount of tobacco smoked daily (interaction P=0.006) and age when smoking started (interaction P=0.011). There was no sex difference in these two effects for ischemic heart diseases, intracerebral hemorrhage and cerebral infarction (all interaction P>0.05). Conclusions: This prospective study confirmed increased risk of all subtypes of cardiovascular diseases in current smokers. Smoking was more harmful to women than to men for major coronary event.
Adult ; Asian People/statistics & numerical data* ; Cardiovascular Diseases/epidemiology* ; China/epidemiology* ; Female ; Humans ; Incidence ; Male ; Neoplasms/epidemiology* ; Prevalence ; Prospective Studies ; Risk Factors ; Smoking/ethnology* ; Smoking Cessation ; Stroke/epidemiology* ; Tobacco Smoking/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: The number of children with polydactyly is increasing. In addition to genetic factors, an influence of maternal behavior or environmental effects during pregnancy is becoming increasingly apparent. However, epidemiological data on these effects are lacking. Methods: This hospital-based, case-control study enrolled 143 infants with polydactyly and 286 controls without genetic diseases to evaluate the association between active and passive maternal smoking during pregnancy and the likelihood of giving birth to a child with polydactyly. Results: Active and passive maternal smoking during pregnancy was associated with an increased risk of giving birth to a child with polydactyly (active smoking: OR=4.74, 95%CI: 1.43-15.65, P=0.011; passive smoking: OR=2.42, 95%CI: 1.32-4.44, P=0.004). After adjusting for confounders, smoking during pregnancy remained significant influence on polydactyly (active smoking: aOR=7.27, 95%CI: 1.72-30.72, P=0.007; passive smoking: aOR=2.41, 95%CI: 1.11-5.23, P=0.026). Conclusion: Active and passive maternal smoking during pregnancy appears to be a risk factor for polydactyly in newborns.
Case-Control Studies ; Child ; Female ; Fingers/abnormalities* ; Humans ; Infant ; Infant, Newborn ; Inhalation Exposure/statistics & numerical data* ; Maternal Exposure/statistics & numerical data* ; Polydactyly/epidemiology* ; Pregnancy ; Pregnancy Complications/etiology* ; Risk Factors ; Smoking/adverse effects* ; Tobacco Smoke Pollution/statistics & numerical data*

To investigate the effects of cigarette smoking in different manners on acute lung injury in rats.The commercially available cigarettes with tar of 1,5, 11 mg were smoked in Canada depth smoking (health canada method, HCM) manner, and those with tar of 11 mg were also smoked in international standard (ISO) smoking manner. Rats were fixed and exposed to mainstream in a manner of nose-mouth exposure. After 28 days, the bronchoalveolar lavage fluids from left lung were collected for counting and classification of inflammatory cells and determination of pro-inflammatory cytokines IL-1β and TNF-α. The right lungs were subjected to histological examination and determination of myeloperoxidase (MPO) and superoxide dismutase (SOD) activities and glutathione, reactive oxygen species (ROS) and malondialdehyde (MDA) levels.In both HCM and ISO manners, the degree of lung injury was closely related to the tar content of cigarettes, and significant decrease in the body weight of rats was observed after smoking for one week. In a HCM manner, smoking with cigarette of 11 mg tar resulted in robust infiltration of macrophages, lymphocytes and neutrophils into lungs, significant increase in IL-1β and TNF-α levels and MPO activities, and significant decrease in GSH levels and SOD activities and increase in ROS and MDA levels (all<0.05). Smoking with cigarette of 5 mg tar led to moderate increase in IL-1β and TNF-α levels, and MPO activities (all<0.05), and moderate decrease in GSH levels and SOD activities and increase of ROS and MDA levels (all<0.05). However, smoking with cigarette of 1 mg tar affected neither inflammatory cell infiltration nor IL-1β and TNF-α levels.Cigarette smoking in nose-mouth exposure manner can induce acute lung injury in rats; and the degree of lung injury is closely related to the content of tar and other hazards in cigarettes.
Acute Lung Injury ; etiology ; pathology ; physiopathology ; Animals ; Bronchoalveolar Lavage Fluid ; chemistry ; cytology ; Chemotaxis, Leukocyte ; drug effects ; Glutathione ; analysis ; drug effects ; Interleukin-1beta ; analysis ; drug effects ; Lung ; chemistry ; pathology ; Lymphocytes ; drug effects ; pathology ; Macrophages ; drug effects ; pathology ; Male ; Malondialdehyde ; analysis ; Neutrophil Infiltration ; drug effects ; Neutrophils ; drug effects ; pathology ; Peroxidase ; analysis ; drug effects ; Rats ; Reactive Oxygen Species ; analysis ; Smoking ; adverse effects ; Superoxide Dismutase ; analysis ; drug effects ; Tobacco Products ; adverse effects ; classification ; Tumor Necrosis Factor-alpha ; analysis ; drug effects ; Weight Loss ; drug effects

The aim of this study was to investigate the inhibitory effect of Cnidium monnieri fruit (CM) extracts on pulmonary inflammation induced in mice by cigarette smoke condensate (CSC) and lipopolysaccharide (LPS). Pulmonary inflammation was induced by intratracheal instillation of LPS and CSC five times within 12 days. CM extract was administered orally at a dose of 50 or 200 mg·kg(-1). The number of inflammatory cells in the bronchoalveolar lavage fluid was counted using a fluorescence activated cell sorter. Inflammatory mediator levels were determined by enzyme-linked immunosorbent assay. The administration of LPS and CSC exacerbated airway hyper-responsiveness (AHR) and induced an accumulation of inflammatory cells and mediators, and led to histological changes. However, these responses are modulated by treatment with CM, and the treatment with CM extract produces similar or more extensive results than the treatment with cyclosporin A (CSA). CM extract may have an inhibitory effect on pulmonary inflammation related with chronic obstructive pulmonary disease.
Animals ; Anti-Inflammatory Agents ; pharmacology ; therapeutic use ; Bronchoalveolar Lavage Fluid ; Cnidium ; Female ; Fruit ; Lipopolysaccharides ; Mice, Inbred BALB C ; Phytotherapy ; Plant Extracts ; pharmacology ; therapeutic use ; Pneumonia ; chemically induced ; drug therapy ; Pulmonary Disease, Chronic Obstructive ; drug therapy ; pathology ; Smoke ; adverse effects ; Smoking ; adverse effects ; Tobacco Products ; adverse effects