BACKGROUND: Epidermal growth factor receptor (EGFR) gene mutations are the most common driver mutations in non-small cell lung cancer (NSCLC). To prolong the survival of the patients, EGFR tyrosine kinase inhibitors (TKIs) resistance in NSCLC is a major challenge that needs to be addressed urgently, and this study focuses on investigating the mechanism of cigarette smoke (CS) induced Gefitinib resistance in NSCLC. METHODS: PC-9 and A549 cells were cultured in vitro and treated with 1 µmol/L Gefitinib for 4 h and 10% cigarette smoke extract (CSE) for 48 h. Western blot was used to detect Sirtuin 3 (Sirt3) and superoxide dismutase 2 (SOD2) protein expressions; DCFH-DA probe was used to detect intracellular reactive oxygen species (ROS); CCK-8 kit was used to detect cell activity, and EdU was used to detect cell proliferation ability. Sirt3 overexpression plasmid (OV-Sirt3) was transfected in PC-9 and A549 cells and treated with 1 µmol/L Gefitinib for 4 h and 10% CSE for 48 h after N-acetylcysteine (NAC) action. The expressions of Sirt3 and SOD2 were detected by Western blot; the ROS level in the cells was detected by DCFH-DA probe, and the cell activity was detected by CCK-8. RESULTS: CSE induced an increase in the 50% inhibitory concentration (IC50) of both PC-9 and A549 cells to Gefitinib (P<0.01) and enhanced the proliferation of PC-9 and A549 cells, suggesting that CS induced Gefitinib resistance in NSCLC. ROS was involved in CSE-induced Gefitinib resistance (P<0.05). CSE induced low expressions of Sirt3 and SOD2 (P<0.01), and Sirt3/SOD2 was associated with poor prognosis in lung cancer patients (P<0.05). OV-Sirt3 in PC-9 and A549 cells reversed CSE-induced Gefitinib resistance (P<0.05) and significantly reduced ROS production. NAC reversed CSE-induced Gefitinib resistance in PC-9 and A549 cells (P<0.05). CONCLUSIONS The ROS/Sirt3/SOD2 pathway is involved in CS-induced Gefitinib resistance in NSCLC.
Humans ; Gefitinib/therapeutic use* ; Carcinoma, Non-Small-Cell Lung/metabolism* ; Sirtuin 3/therapeutic use* ; Lung Neoplasms/metabolism* ; Reactive Oxygen Species/therapeutic use* ; Antineoplastic Agents/therapeutic use* ; Cigarette Smoking ; Sincalide/therapeutic use* ; ErbB Receptors/metabolism* ; Drug Resistance, Neoplasm/genetics* ; Cell Line, Tumor

OBJECTIVE: To explore the mechanism of Yifei Jianpi recipe for improving cigarette smoke- induced inflammatory injury and mucus hypersecretion in cultured human bronchial epithelial cells. METHODS: Serum samples were collected from 40 SD rats treated with Yifei Jianpi recipe (n=20) or normal saline (n=20) by gavage. Cultured human bronchial epithelial 16HBE cells were stimulated with an aqueous cigarette smoke extract (CSE), followed by treatment with the collected serum at different dilutions. The optimal concentration and treatment time of CSE and the medicated serum for cell treatment were determined with CCK-8 assay. The expressions of TLR4, NF-κB, MUC5AC, MUC7, and muc8 at both the mRNA and protein levels in the treated cells were examined with RT- qPCR and Western blotting, and the effects of TLR4 gene silencing and overexpression on their expressions were assessed. The expressions of TNF-α, IL-1 β, IL-6 and IL-8 in the cells were detected using ELISA. RESULTS: At the optimal concentration of 20%, treatment with the medicated serum for 24 h significantly lowered the mRNA and protein expressions of TLR4, NF- κB, MUC5AC, MUC7, and MUC8 in CSE- exposed 16HBE cells, and these effects were further enhanced by TLR4 silencing in the cells. In 16HBE cells with TLR4 overexpression, the expressions of TLR4, NF-κB, MUC5AC, MUC7, and MUC8 were significantly increased after CSE exposure and were lowered following treatment with the medicated serum (P < 0.05). The medicated serum also significantly lowered the levels of TNF-α, IL-1β, IL-6 and IL-8 in CSE-exposed 16HBE cells (P < 0.05). CONCLUSIONS In the 16HBE cell model of chronic obstructive pulmonary disease (COPD), treatment with Yifei Jianpi recipe-medicated serum improves inflammation and mucus hypersecretion possibly by reducing MUC secretion and inhibiting the TLR4/NF-κB signaling pathway.
Humans ; Rats ; Animals ; NF-kappa B/metabolism* ; Toll-Like Receptor 4/metabolism* ; Interleukin-8/metabolism* ; Tumor Necrosis Factor-alpha/metabolism* ; Cigarette Smoking/adverse effects* ; Interleukin-6/metabolism* ; Rats, Sprague-Dawley ; Pulmonary Disease, Chronic Obstructive/drug therapy* ; Signal Transduction ; Epithelial Cells/metabolism* ; Mucus/metabolism* ; RNA, Messenger/metabolism*

BACKGROUND: Heated tobacco product (HTP) use has increased substantially between 2016 and 2017 in Japan. This study aims to clarify how HTP use (IQOS, Ploom, and glo) spread across the different combustible cigarette smoking statuses during 2015-16 and 2017-18 in Japan. METHODS: We compared the two periods of (i) 2015 to 2016 (N = 5,366) and (ii) 2017 to 2018 (N = 3,422) from a longitudinal study randomly sampling members from the Japan "Society and New Tobacco" Internet Survey (JASTIS). Multivariable logistic regression models for current HTP use in the previous 30 days by combustible cigarette smoking status in the previous year were used adjusting for socio-demographic factors. RESULTS: HTP use increased by 10 times in the 2017-18 cohort compared with the 2015-16 cohort according to the adjusted odds ratio (95% confidence interval) for current HTP use as 10.2 (7.03-14.8). According to smoking status, significantly higher adjusted ORs (95% CIs) of current HTP use for the after period were observed: 2.60 (1.37-4.94) for never smokers, 7.82 (3.64-16.8) for former smokers, 21.1 (5.73-77.9) for current smokers with intention to quit, and 17.0 (9.58-30.3) for current smokers without intention to quit. CONCLUSION During 2015 to 2018 in Japan, HTP use dramatically increased in all subgroups except for never smokers.
Humans ; Japan/epidemiology* ; Longitudinal Studies ; Tobacco Products ; Tobacco ; Cigarette Smoking ; Surveys and Questionnaires

Humans ; Adult ; Cigarette Smoking/epidemiology* ; Prevalence ; Electronic Nicotine Delivery Systems ; Tobacco Products ; Republic of Korea/epidemiology*

BACKGROUND: This systematic and meta-analysis review aimed to provide an updated estimate of the prevalence of ever and current cigarette smoking in women, in geographic areas worldwide, and demonstrate a trend of the prevalence of smoking over time by using a cumulative meta-analysis. METHODS: Following PRISMA guidelines, we conducted a systematic review and meta-analysis of studies published on the prevalence of ever and current cigarette smoking in women. We searched PubMed, Web of Science (ISI), Scopus, and Ovid from January 2010 to April 2020. The reference lists of the studies included in this review were also screened. Data were reviewed and extracted independently by two authors. A random effects model was used to estimate the pooled prevalence of ever and current cigarette smoking in women. Sources of heterogeneity among the studies were determined using subgroup analysis and meta-regression. RESULTS: The pooled prevalence of ever and current cigarette smoking in women was 28% and 17%, respectively. The pooled prevalence of ever cigarette smoking in adolescent girls/students of the school, adult women, pregnant women, and women with the disease was 23%, 27%, 32%, and 38%, respectively. The pooled prevalence of ever cigarette smoking in the continents of Oceania, Asia, Europe, America, and Africa was 36%, 14%, 38%, 31%, and 32%, respectively. CONCLUSIONS The prevalence of cigarette smoking among women is very high, which is significant in all subgroups of adolescents, adults, and pregnant women. Therefore, it is necessary to design and implement appropriate educational programs for them, especially in schools, to reduce the side effects and prevalence of smoking among women.
Cigarette Smoking/trends* ; Female ; Humans ; Prevalence

Animals ; Bronchoalveolar Lavage Fluid ; Cigarette Smoking ; Interleukin-17/genetics* ; Lung ; MAP Kinase Signaling System ; Mice ; Mice, Inbred C57BL ; Pulmonary Disease, Chronic Obstructive

OBJECTIVE: To survey the cigarette smoking status and periodontal status, and to study the correlation between cigarette smoking and periodontal status. METHODS: Questionnaires were distributed (including self-assessed periodontal status, such as bleeding while brushing teeth, oral odor, tooth loosening, gum swelling, etc.) and clinical periodontal examinations performed for parameters including probing depth (PD), bleeding index (BI), attachment loss (AL), plaque index (PLI) and amount of teeth loss, which was recorded in the population above 35 years of a community in Beijing. A total of 974 subjects were recruited in the study. The population was divided into current smokers and non-smokers, and the differences of self-assessed periodontal status and periodontal parameters between the groups analyzed. RESULTS: The smokers had significantly less bleeding during toothbrushing, and in the meantime, had significantly more self-reported tooth loosening compared with the non-smokers. The smokers brushed their teeth less than the non-smokers (P<0.05). The self-reported gum swelling and oral odor had no significant difference between the smokers and non-smokers. The smokers had 0.565 times and 1.572 times the risk of bleeding during toothbrushing, self-reported tooth loosening and from Logistic regression analyses, respectively (P<0.05). The mean PD, AL, PLI and the amount of tooth loss of the smokers were significant higher than the non-smokers (P<0.05). However, the mean BI of the smokers was slightly less than the non-smokers' (1.93±0.540 vs. 1.94±0.512, P=0.707). The smokers had 2.129 times, 1.698 times and 1.933 times the risk of the mean PD>3 mm, the mean AL>3 mm, and the amount of tooth loss above 8, respectively compared with the non-smokers (P<0.05) from Logistic regression analyses. CONCLUSION The self-assessed periodontal status is different between smokers and non-smokers in the population of a community in Beijing. Smokers have less bleeding during toothbrushing but no significant difference with BI. Smokers also have more self-reported tooth loosening. Compared with non-smokers, smokers have more severe periodontal destruction.
Adult ; Beijing ; Cigarette Smoking ; Dental Plaque Index ; Humans ; Periodontal Attachment Loss ; Surveys and Questionnaires

We assessed the concomitant impact of cigarette smoking and alcohol consumption in men presenting for primary couple's infertility. Data from 189 infertile men were analyzed. Semen analysis, serum hormones, and sperm DNA fragmentation (SDF) were obtained. Smoking status was categorized as follows: current nonsmoker (-S), moderate smoker (+MS), and heavy smoker (+HS). Alcohol consumption was categorized as follows: abstainer (-D), moderate drinker (+MD), and heavy drinker (+HD). Descriptive statistics and logistic regression models were applied. Among all the participants, 132 (69.8%), 30 (15.9%), and 27 (14.3%) patients were -S, +MS, and +HS, respectively. In addition, 67 (35.4%), 77 (40.7%) and 45 (23.8%) men were -D, +MD and +HD, respectively. Regarding concomitant habits, 52 (27.5%) patients were nonsmokers and abstainers (-S/-D: Group 1), 91 (48.1%) had at least one recreational habit (-S/+D or +S/-D: Group 2), and 46 (24.3%) were both smokers and drinkers (+S/+D: Group 3). Sperm concentration and progressive motility were lower in +HS and +HD, compared with -S and -D (all P < 0.05), respectively. Similarly, both parameters were significantly lower in Group 3 than Groups 1 and 2 (all P < 0.05). SDF values were higher in Group 3 than Groups 1 and 2 (both P < 0.05). In multivariate analysis, follicle-stimulating hormone (FSH) levels and concomitant +S/+D status were independent predictors of impaired sperm concentration and progressive motility (all P < 0.05). Heavy smoking and heavy drinking were associated with worse seminal parameters than moderate smoking/drinking and nonsmoking/abstaining. When concomitant, +S/+D status has an even greater detrimental effect on semen parameters.
Adult ; Alcohol Drinking/adverse effects* ; Alcoholism/complications* ; Cigarette Smoking/adverse effects* ; Cohort Studies ; Female ; Follicle Stimulating Hormone/blood* ; Humans ; Infertility, Male/pathology* ; Male ; Middle Aged ; Semen Analysis ; Sperm Count ; Sperm Motility ; Spermatozoa/ultrastructure*

Objective: To explore the relations between the prevalence of multiple chronic diseases and cigarette smoking behavior in the Chinese adults. Methods: Based on the results: from the 2013 Chronic Disease Risk Factor Surveillance (NCD Surveillance), 176 534 Chinese residents aged 18 years and above, covering 298 counties (districts) in 31 provinces, was randomly recruited, using the multi-stage stratified clustering sampling method. Information on demographics, cigarette smoking (status, quantity and period) was obtained through face-to-face interviews and questionnaires. Anthropometric data and blood samples were collected and properly stored for analysis. Results In total, 175 386 adults were included for statistical analyses, with 42.7% as males and 57.3% as females. The prevalence rates of hypertension, high total cholesterol and high triglycerides were 30.4%, 7.2% and 18.0% in male smokers, 35.6%, 14.0%, 10.3% and 15.9% in female smokers respectively, which were all higher than those in the respective non-smokers. Male smokers were found under lower risk on hypertension, but 19% higher on total glycerides when compared with non-smokers of the same sex(OR=1.19, 95%CI:1.10-1.30), when multiple risk factors were under control. Male current smokers with more than 20 cigarettes per day have 41% (OR=1.41, 95%CI: 1.28-1.55) higher risk of high TG than non-smokers. Female smokers presented 40% (OR=1.40, 95%CI: 1.15-1.70) higher risk in high glycerides than the non-smokers. Specifically, women smoking longer than 20 years have 60% (OR=1.60, 95%CI: 1.31-1.95) higher risk of high TG than women smoking less than 20 years. Conclusions: Prevalence rates of certain chronic diseases were seen higher in smokers of both genders. People with longer history of smoking or being heavier smokers, appeared at advanced risk on developing chronic diseases.
Adult ; Aged ; Asian People ; Chronic Disease/ethnology* ; Cigarette Smoking/ethnology* ; Female ; Humans ; Hypertension/epidemiology* ; Male ; Prevalence ; Risk Factors ; Sex Distribution ; Sex Factors ; Smoking Cessation ; Surveys and Questionnaires

INTRODUCTION: In the Philippines, lung, breast, colon-rectum, and oral cavity cancers are among the top 10 most common cancers. This study evaluates the risk factors for these cancers among Filipinos.

METHODS: This age-matched case-control study included incident primary cancers (histologically-diagnosed) of the lung, breast (also matched for sex), colon-rectum and oral cavity. Controls (clinically free and no history of cancer) were obtained from the same tertiary hospitals as the cases. Target sample size was 283 cases and 283 controls per cancer type. Conditional logistic regression was done.

RESULTS: Exposure to cigarette/tobacco was a significant risk factor for lung (OR of current smoker compared to non-smoker [95% Confidence Interval]: 3.6 [1.6-7.9]) and oral cavity cancers (2.0 [1.2-3.3]); family history (1st degree) for lung (4.3 [1.314.2]) and breast cancers (3.0 [1.2-7.5]); every year increase in age at first pregnancy for breast cancer (1.06 [1.02-1.11]). Other risk factors for oral cavity were passive smoking (2.8 [1.6-5.1]), chewing tobacco (5.2[1.4-19.5]) and inverted cigarette smoking (3.2[1.3-8.1]). Fish sauce (patis) was found to be a protective factor for breast cancer (0.34 [0.22-0.51]) and oral cavity (0.44 [0.25-0.78]) and use of shrimp paste (bagoong) (0.48 [0.27-0.84]) for oral cavity.

CONCLUSION AND RECOMMENDATIONS: Except for family history of cancer, the identified risk factors for lung, colon-rectum, and oral cavity cancers are preventable. Proper diet and lifestyle, avoidance of cigarettes and tobacco, and environmental safety in the workplace are key cancer prevention measures. Public awareness campaign and continuing healthcare provider education must always be part of a cancer prevention program.

Pregnancy ; Tobacco ; Tobacco, Smokeless ; Tobacco Smoke Pollution ; Cigarette Smoking ; Rectum ; Smokers ; Smoking ; Breast Cancer 3 ; Breast Neoplasms ; Mouth Neoplasms ; Health Personnel ; Colon