ObjectiveTo analyze the burden of digestive diseases attributed to smoking in China from 1990 to 2019 and forecast its change in the next 10 years. MethodsThe Global Burden of Disease database 2019 was used to analyze the burden of digestive diseases attributed to smoking in China from 1990 to 2019. Joinpoint regression model was used to analyze the time variation trend. A time series model was used to predict the burden of digestive diseases attributable to smoking over the next 10 years. ResultsIn 2019, there were 12 900 deaths from digestive diseases attributed to smoking in China, with a DALY of 398 600 years, a crude death rate of 0.91/100 000 and a crude DALY rate of 28.02/100 000. The attributed standardized mortality rate was 0.69 per 100 000, and the standardized DALY rate was 19.79 per 100 000, which was higher than the global level. In 2019, the standardized mortality rate and DALY rate of males were higher than those of females (1.48/ 100 000 vs. 0.11/ 100 000, 38.42/ 100 000 vs. 293/100 000), and the standardized rates of males and females showed a downward trend over time. In 2019, both mortality and DALY rates from digestive diseases attributed to smoking increased with age. ARIMA predicts that over the next 10 years, the burden of disease in the digestive system caused by smoking will decrease significantly. ConclusionFrom 1990 to 2019, the burden of digestive diseases attributed to smoking showed a decreasing trend in China, and the problem of disease burden is more serious in men and the elderly population. A series of effective measures should be taken to reduce the smoking rate in key groups. The burden of digestive diseases caused by smoking will be significantly reduced in the next 10 years.
Objective To systematically assess the correlation between smoking and the risk of endometriosis, so as to offer scientific basis to health education and preventing decision. Methods A literature search was performed in The Cochrane Library, Pubmed, Embase, CBM, CNKI and Wanfang database to collect the case control studies on the correlation between smoking and endometriosis. Two reviewers independently screened the literatures according to the inclusion and exclusion criteria, extracted the data, assessed the quality, and then conducted Meta-analyses on the 13 included RCTs by using RevMan 5.0 software, with calculation of the OR value and 95%CI. Results A total of 13 case control studies involving 14260 cases were included, of which 1900 ones were endometriosis. The quality assessment indicated that 2 studies were in quality of Level A, 4 were Level B, 7 were Level C, totally meant low quality. Meta-analyses showed that compared with non-smokers, there was no increasing possibility of endometriosis in smokers (OR= 0.91, 95%CI 0.82 to 1.02). The geographical subgroup analyses showed there was no significant difference in the incidence of endometriosis between the non-smokers and smokers in North America (OR=0.96, 95%CI 0.84 to 1.08), but a significant difference was found between non-smokers and smokers in Europe (OR=0.72, 95%CI 0.54 to 0.97). Conclusion There is no causative relationship between smoking and incidence of endometriosis. However, more high-quality trials are expected for further study because of the heterogeneity and poor quality of the current included studies.
Objective To investigate the role of endogenous Hydrogen Sulfide ( H2S) in airway inflammation and responsiveness in a rat model of chronic passive-smoking. Methods Male SD rats were randomly divided into a control group ( breathing fresh air) and a passive smoking group [ cigarette smoking( CS) passively] , with 18 rats in each group. Six rats in each group were randomly intraperitoneally injected with normal saline, sodium hydrosulfide ( NaHS) or propargylglycine ( PPG, an irreversible inhibitor of cystathionine- γ-lyase) . The animals were divided into six subgroups, ie. Con group, NaHS group, and PPG group, CS group, CS+ NaHS group, and CS + PPG group. After 4 months, lung histological change and airway tension were measured. The H2S levels of plasma and lung tissue were analyzed by the sensitive sulphur electrode assay. The expression of cystathionine-γ-lyase ( CSE) was measured by western blot. Results Compared with the Con group, CSE protein expression in lung tissues was increased in CS group( P lt;0. 05) ; the H2 S levels of plasma were significantly higher in CS group, NaHS group and CS + NaHS group, and much lower in PPG group ( P lt; 0. 05, respectively) . Compared with CS group, the H2S levels of plasma were significantly higher in CS + NaHS group, and much lower in CS + PPG group( P lt; 0. 05, respectively) . The H2S level of lung tissue in each group had no significant difference ( P gt; 0. 05) . Compared with Con group,score of lung pathology was significant elevated, and the responsiveness of airway smooth muscles to ACh and KCl was significant augmented in CS group. Compared with CS group, the score of lung pathology was decreased, and the responsiveness of airway smooth muscles was decreased in CS +NaHS group( P lt;0. 05) , and vise versa in CS + PPG group( P lt; 0. 01) . Conclusion H2S can alleviate airway inflammation and hyperresponsiveness induced by CS, and administration of H2S might be of clinical benefit in airwayinflammation and airway responsiveness.
ObjectiveTo evaluate the effect of smoking and drinking status on the prognosis of patients with esophageal squamous cell carcinoma (ESCC).MethodsThe clinical data of 483 patients with ESCC who underwent surgical treatment in Shannxi Provincial People's Hospital from 2007 to 2016 were retrospectively analyzed. Among them, 352 patients were male and 131 were female, with a median age of 64 (37-80) years. There were 311 smokers and 172 drinkers. The relationship between preoperative drinking or smoking status and the clinicopathological characteristics of patients with ESCC was analyzed. Log-rank method and Cox risk regression were used to conduct univariate and multivariate survival analysis, respectively.ResultsThe preoperative smoking status was related to the patient's tumor location (P=0.030). Drinking status was associated with tumor location (P=0.001), degree of differentiation (P=0.030), pathological T stage (P=0.024) and pathological N stage (P=0.029). Univariate survival analysis showed that smoking status did not affect the disease-free survival (DFS) (P=0.188) and overall survival (OS) (P=0.127) of patients with ESCC. However, patients who drank alcohol had worse PFS than non-drinking patients (29.37 months vs. 42.87 months, P=0.009). It was further proved that alcohol consumption was an independent risk factor affecting patients' recurrence and metastasis by using multivariate analysis (RR=1.28, P=0.040). Alcohol consumption also reduced the OS of patients by 21.47 months (P=0.014), however, multivariate analysis did not yield significant results.ConclusionPreoperative drinking status is related to the stage and differentiation of patients with ESCC. It is an independent risk factor affecting the recurrence and metastasis of ESCC.
Objective To observe the levels of malonaldehyde (MDA) , interleukin-8 (IL-8) and tumor necrosis factor-α(TNF-α) in lung tissues of subjects with or without chronic obstructive pulmonary disease (COPD) , and investigate their roles in the the pathogenesis of COPD. Methods The content of MDA, IL-8 and TNF-αin lung tissues of smokers with COPD (n=9) , ex-smokers with COPD (n=8) , non-smokers with COPD (n=7) , healthy smokers (n=9) , healthy ex-smokers (n=8) and healthy nonsmokers (n=6) was measured with enzyme-linked immunosorbent assay ( ELISA) and corrected by creatinine. Results The levels of MDA, IL-8 and TNF-α in lung tissues of the COPD patients were significantly higher than those in the healthy subjects (Plt;0.05) , which were also significantly higher in the smokers when compared with the non-smokers (Plt;0.05) , whether suffering from COPD or not. In the COPD patients, not the levels of IL-8 but MDA and TNF-αin lung tissues of the smokers were significantly higher than those in the ex-smokers (Plt;0.05) ; whereas in the healthy cases, no statistical significance was revealed between the smokers and the ex-smokers on the levels of MDA and IL-8 in lung tissues except TNF-α( Pgt;0.05) . Conclusion The abnormal increase of MDA, IL-8 and TNF-αin lung tissues caused by chronic smoking may play an important role in the the pathogenesis of COPD.
Objective To investigate the effects of smoking intensity, duration and cessation on mRNA and protein expressions of matrix metalloproteinase-9 ( MMP-9) in tracheal epitheliumof rats, and the relationship between smoking or smoking cessation and airway remodeling in chronic obstructive pulmonary disease ( COPD) . Methods Forty Wistar rats were randomly divided into 5 groups, ie. a normal control group, a long termheavy smoking group, a short termheavy smoking group, a long termlight smoking group,and a smoking cessation group which was exposed to room air for 10 weeks after long term heavy smoking.The expressions of MMP-9 mRNA and protein in tracheal epithelium of rats were detected by in situ hybridization and munohistochemistry respectively. Results ( 1) The pathological changes of emphysema were observed in the lung tissue of every smoking rat, and were most sever in the long term heavy smoking group. ( 2) Compared with the normal control group [ ( 0. 88 ±0. 88) PU, ( 2. 80 ±1. 66) PU] , the expressions of MMP-9 mRNA and proteins in tracheal epithelium were remarkable elevated in the long term heavy smoking group [ ( 22. 01 ±2. 86) PU, ( 20. 81 ±2. 46) PU] , the short term heavy smoking group [ ( 14. 94 ±3. 46) PU, ( 13. 68 ±2. 00) PU] , the long term light smoking group [ ( 6. 92 ±2. 71) PU,( 8. 84 ±1. 80) PU] and the smoking cessation group [ ( 19. 00 ±3. 36) PU, ( 14. 82 ±1. 74) PU] ( P lt;0. 01) . Compared with the long term heavy smoking group, the expressions of MMP-9 in tracheal epithelium were decreased in other three smoking groups ( P lt; 0. 05) . Conclusions Smoking could increase the expression of MMP-9 in tracheal epithelium and cause trachea damage and remodeling with intensity and duration in rats. Smoking cessation could decrease the MMP-9 expression and alleviate trachea remodeling,suggesting its role in the prevention of COPD.
Objective To make an evidence-based treatment plan for a smoker with periimplantitis. Methods Based on the clinical problems raised from the case, we searched The Cochrane Library (Issue 2, 2009), ACP Journal Club (1991 to July 2009), MEDLINE (1950 to July 2009), EMbase (1980 to July 2009) and Chinese Journal Fulltext Database (1994 to July 2009) for guidelines, systematic reviews, meta-analyses and randomized controlled trials (RCTs). The quality of the included studies was assessed. Results A total of 4 systematic reviews, 8 RCTs were included. The following methods were supported by Level A evidence: (1) Scaling combined with local antibiotics; (2) Guided bone regeneration; (3) Non-surgical debridement with titanium hand-instruments or with an ultrasonic device. Based on the available evidence, we proposed a three-stage therapy plan for the patient: In the first stage, full mouth ultrasonic scaling was performed. The peri-implant pocket was debrided with plastic curettes, and then minocycline gel was applied once a week for four times. The patient was persuaded to maintain oral hygiene and quit smoking. In the second stage, four weeks later, open flap debridement and guided bone regeneration were conducted. In the third stage, long-term care of oral hygiene and dental implants were performed. After 6 months of follow-up, the peri-implant tissues were healthy with no evidence of inflammation, bleeding or suppuration. Conclusion Based on the approach of evidence-based medicine, we accomplished the treatment of the case with reliable outcomes.
Objective To study the prevalence and risk factors of chronic obstructive pulmonary disease ( COPD) and provide reliable data for COPD prevention and management. Methods By cluster-random-sampling survey, the residents aged 40 yrs or older in a community in South Bank District of Chongqing were investigated.The post-bronchodilator FEV1 /FVC lt; 0. 7 was defined as COPD. Those individuals with FEV1 /FVC lower than 0. 7 would received history inquiry, X-ray of chest and ECG to exclude other disease that could impair pulmonary function. Results 1518 residents were enrolled( 517 male and 1001 female) . The prevalence of COPD was 12. 78% ( male 23. 02% and female 7. 49% ) . The major risk factors were cigarettes smoke( OR: 2. 88, 95% CI:2. 118-3. 928) and indoor cooking smoke( OR: 1. 98, 95% CI: 1. 685-3. 317) . There were 22.06% smokers were diagnosed as COPD. Only 9. 30% patients had known themselves disease condition about chronic bronchitis,emphysema or COPD. Conclusion The prevalence of COPD in Chongqing city is significant higher than average level of the whole country and the patients have poor knowledge about the disease.
ObjectiveTo evaluate the smoking environment, its related knowledge and difference between urban and rural areas in Chengdu. MethodsIn December 2010, we randomly sampled and investigated 60 dwellers aged from 35 to 70 from urban and rural communities, who were 1:1 paired by the age and sex. Questionnaires survey was used. ResultsThere were 48.3% (29/60) dwellers thought that smoking should be allowed freely at home, of which 30.0% (9/30)rural homes had no rules about smoking prohibited. There were 93.3% (28/30) urban dwellers supported male smoking. About 86.7%-98.3% urban dwellers realized that many diseases such as heart disease, stroke, and lung cancer may be due to smoking. And 16.7% urban dwellers also realized that cigarettes can result in diabetes mellitus, but none of rural dwellers did. The publicity of smoking cessation among urban dwellers (91.7%) by mass media was better than rural ones (0.0%). There were 95.0% dwellers denied any institution or organization for smoking control. ConclusionThe dwellers were short of cognition about restrictions of smoking environment and non-smoking knowledge. It's different between urban and rural area in tobacco advertisement and publicity of smoking cessation. We should continue enhancing public education, forbiding tobacco advertisement and providing institutions for smoking control.
Objective To investigate the relationship between smoking and lung cancer by evidence-based evaluation. Methods Using Meta-analysis method, the results of 29 case-control studies involving the relationship between smoking and lung cancer in recent decade were analyzed by Review Manager 4. 2 software. Results The association between smoking and lung cancer was significant ( Z =12. 16, P lt; 0. 000 01) , and the pooled OR value was 5. 75( 4. 34, 7. 62) . The population attributable risk percentage( PARP) of smoking was 69. 16% . The pooled OR of 1-10 cpd( cigarettes per day) , 10-20 cpd, 20-40 cpd and more than 40 cpd were 1. 97( 1. 69, 2. 30) , 5. 20( 3. 54, 7. 62) , 7. 46( 5. 22, 10. 67) and 15. 14 ( 5. 27, 43. 44) respectively. The pooled OR of less than 20 years of smoking duration, 20-40 years and more than 40 years were 1. 25( 1. 01, 1. 53) , 5. 10( 3. 03, 8. 57) and 10. 77( 7. 30, 15. 89) respectively. While the pooled ORof less than 10 pack-years, 10-20 pack-years, 20-40 pack-years and more than 40 pack-years were 1. 73( 1. 01, 2. 96) , 3. 73 ( 3. 02, 4. 61) , 5. 69 ( 3. 79, 8. 54) and 8. 41 ( 4. 56, 15. 51) respectively. The pooled OR of initial smoking age less than 15 years old, 15-20 years old and more than 20 years old were 13. 31( 7. 09, 24. 97) , 7. 21( 4. 51, 11. 52) and 4. 74( 3. 47, 6. 47) respectively. The pooled OR of quitting smoking for 1-10 years, 10-20 years and more than 20 years were 7. 16( 4. 70, 10. 91) , 2. 12( 1. 16, 3. 86)and 1. 47 ( 0. 67, 3. 20 ) respectively, and more than 20 years of quitting smoking had no significant difference. The pooled OR of light smoking and deep smoking were 3. 26( 1. 24, 8. 58) and 8. 07( 4. 67, 13. 94) respectively. Conclusions Smoking is an important risk factor of lung cancer. Meta-anlalysis revealed cigarettes comsuption per day, smoking duration, total amount of cigarettes ( pack-years) , smoking behaviour( depth) , initial age of smoking and duration of quitting smoking can increase the risk of lung cancer.