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 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.
ObjectiveTo systematically review the efficacy of exercise intervention on smoking cessation. MethodsCNKI, WanFang Data, VIP, Web of Science, PubMed and EMbase databases were electronically searched to collect randomized controlled trials (RCTs) and randomized cross controlled trials (RCDs) on exercise intervention for smoking cessation from inception to September 2021. Two reviewers independently screened literature, extracted data and assessed the risk of bias of the included studies. Then, meta-analysis was performed using Stata 12.0 software. ResultsA total of 47 studies (35 RCTs and 12 RCDs) involving 5 130 subjects were included. The results of meta-analysis showed that acute exercise could significantly reduce the quitters’ desire to smoke (P<0.05), alleviate most of the withdrawal symptoms, and the effect of acute exercise was maintained for at least 30 minutes. Periodic exercise significantly reduced 7-day point abstinence and sustained abstinence rates in ex-smokers (P<0.05), and the effect of periodic exercise was maintained for at least 12 weeks, however, depression and stress were not found to be effectively relieved, and mood was not found to be significantly improved (P>0.05). ConclusionExercise intervention to quit smoking has a positive effect, however, more high-quality studies are needed to verify the above conclusion.
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.
ObjectiveTo observe the asynchrony patterns between left and right lungs in smokers and non-smokers,to assess the role of vibration response imaging(VRI) in the early detection and evaluation of smoking-related lung abnormalities. MethodsData were collected as follows:(1)past history and smoking history were collected;(2)exhaled CO test to confirm smoking status was performed;(3)VRI test was performed and the curve of Breath Energy Unit(BEU)was drawn,which is an energy versus time graph of the breath energy.The asynchrony between left and right lungs was derived from this graph;(4)pulmonary function test was performed.In the end,26 villagers with normal spirometry findings were included in the study.The subjects were divided into an ever-smoking group and a never-smoking group. ResultsThe BEU lung asynchrony was 2.0(3.0) frame in the never-smoking group,and 2.0(3.0) frame too in the ever-smoking group.Rank sum test showed that there was no significant difference(Z=-0.29,P=0.77) between the never-smokers and the ever-smokers in the lung asynchrony.Rank correlation analysis suggested that in the ever-smoking group,smoking index and BEU asynchrony had significant correlation(r=0.61,P=0.03).In the never-smoking group,the coefficient of passive smoking index and lung asynchrony was 0.52(P=0.07).The P value of the coefficient between passive smoking index and lung asynchrony was nearly 0.05,scatter between them could be seen a presence of a certain trend. ConclusionThe lung asynchrony in VRI has dose-effect relationship with ever-smokers' smoking level(smoking index).Thus,the lung abnormalities in VRI caused by the exposure to passive smoking is maybe the same as the abnormalities caused by direct smoking.
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.
Lung cancer in never-smokers has been identified as a separate disease entity. Notably, the proportion of this distinct disease has been reported to increase in recent decades. Due to its occult onset and lack of clinical specificity, patients with this disease are always diagnosed with advanced stage. This review summarizes the current literatures about the risk factors, clinicopathological characteristics, molecular features, and prognosis of lung cancer in never-smokers, which will enhance our understanding and facilitate the precise management of this distinct disease.
ObjectiveTo investigate the effects of smoking combined with intermittent hypoxia on the pathophysiology of lung tissue and thoracic aorta, and the endothelial injury.MethodsTwenty-four rats (SPF, female, six weeks old) were divided randomly into 4 groups (n=6). The control group was given false smoking and normal oxygen exposure, the smoking-exposed group was exposed in smoking, the intermittent hypoxia group was exposed in intermittent hypoxia environment, and the overlap group was exposed to smoking and intermittent hypoxia. After 8 weeks, body weight, right ventricular hypertrophy index (RVHI), the pathological changes of lung tissue and thoracic aorta were measured, and the level of endothelin-1 (ET-1), endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF) and stromal cell-derived factor-1α (SDF-1α) in serum of rats were evaluated.ResultsRVHI of rats in the smoking-exposed group, intermittent hypoxia group, overlap group were higher than that in the control group. In addition, RVHI in the overlap group was higher than that in the smoking-exposed group, intermittent hypoxia group (all P<0.05). The levels of ET-1, VEGF and SDF-1α in the serum of the smoking-exposed group, intermittent hypoxia group and overlap group were higher than those in the control group, while the level of eNOS was lower than that in the control group, (all P<0.05), the most significant difference was between control group and the overlap group. Pathological observation of lung tissue and thoracic aorta showed obvious emphysema in the smoking-exposed group and overlap group, which was more obvious in the overlap group than that in the smoking-exposed group (all P<0.05). Lung interstitial inflammatory infiltration, bronchial wall lymphocyte hyperplasia and pulmonary fibrosis were shown in different degrees in the smoking-exposed group, intermittent hypoxia group and overlap group, and the pulmonary arteriole wall showed thickening, fibrosis and peripheral inflammatory infiltration also were found in these groups. Thoracic aorta in the smoking-exposed group, intermittent hypoxia group and overlap group showed different degrees of endothelial cell injury, middle membrane thickening, and collagen fiber hyperplasia. The pathological features of the overlap group were most obvious compared to the other two groups.ConclusionsSmoking and intermittent hypoxia exposure can lead to different degrees of lung tissue and vascular endothelial injury and decrease of vascular endothelial protective factors in rats, resulting in dysfunction of vascular endothelial cells, which leads to the structural remodeling of pulmonary arterioles and aorta, such as thickening, fibrosis, etc. Combined smoking and intermittent hypoxia exposure can lead to more serious pathological damage.
Objective To analyze the characteristic and temporal trend in mortality and disease burden of Alzheimer’s disease (AD) and other forms of dementia in Guangzhou from 2008 to 2019, and estimate the disease burden attributable to smoking to provide evidence for promoting local health policy of prevention and intervention of dementia. Methods Based on the data of Guangzhou surveillance point of the National Mortality Surveillance System (NMSS), the crude mortality, standardized mortality, years of life lost (YLL) of AD and other dementia were calculated. The indirect method was used to estimate years lived with disability (YLD) and disability-adjusted life years (DALY).The distribution and changing trends of the index rates were compared from 2008 to 2019 using Joinpoint Regression Program. Based on the data of Guangzhou Chronic Disease and Risk Factors Monitoring System in 2013, the indexes of disease burden of AD and other forms of dementia attributable to smoking in 2018 was calculated. Results The standardized mortality rate, YLL rate, YLD rate and DALY rate of AD and other forms of dementia in Guangzhou increased from 0.45/100 000, 0.05‰, 0.02‰ and 0.07 ‰ in 2008 to 1.28/100 000, 0.15‰, 0.07‰ and 0.22‰ in 2019, respectively. The average annual changing trend was statistically significant (AAPC=11.30%, 13.09%, 13.09%, 13.09%, P<0.001）. In most years, the mortality and disease burden of women were higher than those of men, but men had higher growing trend than women in standardized mortality rate, YLL rate, YLD rate and DALY rate from 2008 to 2019, with a slower growing speed after the year 2012.The disease burden of dementia attributable to smoking in men was significantly higher than that in women. Conclusion The mortality and disease burden of AD and other forms of dementia in Guangzhou have dramatically increased over the past twelve years. Intervention against modifiable factors such as smoking, and prevention and screening for dementia in key populations should be strengthened. Support policies for dementia care management should be adopted to reduce the disease burden caused by premature death and disability.