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 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 explore the effect of smoking on pulmonary function parameters of male patients with chronic obstructive pulmonary disease (COPD) and to analyze the correlation between smoking and pulmonary function parameters. Methods From January 2014 to October 2015, the pulmonary function parameters of 223 male outpatients or hospitalized patients with COPD in the Department of Respiratory Medicine were retrospectively analyzed by using SPSS 17.0 software. The patients were randomly divided into smoking group (n=98), smoking cessation group (n=82) and non-smoking group (n=43). Results Various degrees of damage or abnormality of lung capacity, ventilatory function, gas exchange function and airway resistance (Raw) existed in the patients with COPD. Compared with smoking cessation group and non-smoking group, residual volume/ total lung capacity (RV/TLC) and Raw were significantly higher (P< 0.05), maximum ventilatory volume, ventilation reserve percent, forced vital capacity, the percent of first second forced expiratory volume compared its predicted value (FEV1%pred), maximum mid-expiratory flow (MMEF), forced expiratory flow 50%, forced expiratory flow 75% and diffusing capacity of carbon monoxide were significantly lower (P<0.05) in the smoking group. There was a negative relationship between MMEF, FEV1%pred and smoking index (r=–0.352, –0.381, P<0.05), and a positive relationship between Raw, RV/TLC and smoking index (r=0.403, 0.378, P<0.05). Conclusions Most of the male COPD patients smoke or used to smoke. Smoking leads to ventilation and gas exchange function decrease, small airway limitation aggravation, airway resistance and emphysema degree increase in COPD patients. Smoking index has a negative relationship with MMEF, FEV1%pred and a positive relationship with Raw and RV/TLC.
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.
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.
Objective This study aims to investigate the changes of inflammatory markers of oropharynx and its correlation with prognosis in the stable phase of chronic obstructive pulmonary disease (COPD). Methods Sixty-two patients with COPD in stable stage were divided into smoking and non-smoking groups, and 31 healthy persons were selected as controls. The pharyngeal swabs were collected to determine tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8), collagen type Ⅳ (COL-4), and fibronectin (FN) by an enzyme-linked immunosorbent assay. Meanwhile, eosinophil count and C-reactive protein (CRP) in peripheral blood were measured. The correlations between the above metrics and COPD and the prognosis of the patients were analyzed. Results TNF-α, IL-8, COL-4, FN and CRP levels in patients with COPD were significantly higher compared with control groups (P<0.05), and there were significant differences between smoking and non-smoking groups in inflammatory markers such as TNF-α, IL-8, FN, CRP (P<0.05). The forced expiratory volume in one second (FEV1) and FEV1%pred of patients with COPD were significantly lower than the control group (P<0.05). The smoking index of patients with COPD in smoking group was significantly higher than that in smoking control group (P<0.05). TNF- α and IL-8 were positively associated with blood CRP in patients with COPD. Conclusion The inflammatory markers of oropharynx in patients with COPD are different from those in healthy persons and smoking may promote the increase of inflammatory markers of oropharynx in patients with COPD; the non-invasive detection of paired pharyngeal inflammatory markers may be helpful in determining acute onset and prognosis.
Objective The Global Burden of Diseases (GBD) data were used to analyze the trend of the burden of disease of tracheal, bronchial, and lung cancer (TBL Cancer) caused by tobacco in China and globally from 1990 to 2021, and to predict the future development trend. Methods We performed descriptive analysis of the indicators of death and disability-adjusted life years (DALY) in the GBD 2021 database; The Joinpoint regression model was used to calculate the average annual percent change (APCC); The age-period-cohort (APC) model was used to estimate the effect of three independent factors, age, period and cohort, on disease mortality; and the BAPC model was used to project the burden of disease for TBL Cancer from 2022 to 2036. Results From 1990 to 2021, the disease burden of TBL Cancer attributable to tobacco showed an increasing trend in both China and globally, with a much higher burden of disease in men than in women, and a much higher burden of disease attributable to smoking than to secondhand smoke. The APC model showed that the net drift values of mortality in China and globally were −0.1982% and −1.5921%, respectively, from 1992 to 2021; the age effect showed that the mortality rate of both China and the world increased with age; the period effect model showed that the mortality rate of China increased and then decreased, and the global mortality rate generally decreased; the cohort model showed that the mortality rate of China and the world increased and then decreased; the BAPC model showed that the mortality rate of China declined slowly in the period of 2022-2036, and the global mortality rate declined even more dramatically. Conclusion The burden of TBL Cancer attributable to tobacco was higher in China than in the world from 1990 to 2021. Tobacco control measures in China have begun to bear fruit in recent years, and we should continue to strengthen our tobacco control initiatives and popularize health knowledge in order to make progress towards the goal of the "Healthy China 2030" plan.
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 systematically evaluate the association between passive smoking during pregnancy and adverse birth outcomes in Chinese, as well as to provide evidence for the prevention of adverse birth outcomes. MethodsWe electronically searched the CNKI, VIP, WanFang Data, PubMed and EMbase databases to collected cohort studies about the association between passive smoking during pregnancy and adverse birth outcomes in Chinese. The search date was from January 1st 1980 to 30th August, 2014. Two reviewers independently screened literature according to the inclusion and exclusion criteria, extracted data and assessed the risk bias of included studies. Then meta-analysis was performed using RevMan 5.1 software. ResultsA total of 24 studies were included in the meta-analysis. The results of meta-analysis showed that, the passive smoking during pregnancy was associated with increased risks of preterm (RR=1.97, 95%CI 1.38 to 2.80), low birth weight (RR=1.94, 95%CI 1.37 to 2.76), birth defects (RR=2.01, 95%CI 1.58 to 2.56), neonatal asphyxia (RR=3.34, 95%CI 1.76 to 6.33), small-for-gestational age (RR=2.62, 95%CI 1.49 to 4.63), stillbirth (RR=3.10, 95%CI 2.00 to 4.80) and spontaneous abortion (RR=1.37, 95%CI 1.19 to 1.59). ConclusionPassive smoking during pregnancy is associated with increased risks of adverse birth outcomes.
Objective To investigate the effects of smoking on β-defensin-2 ( BD-2) expression in induced sputumand lung tissue, and its role in chronic obstructive pulmonary disease ( COPD) . Methods Patients suffering with early peripheral squamous celled lung cancer and underwent lobectomy were divided into a smoking COPD group ( COPD group) , a non-COPD smoking group ( smoker group) , and a nonsmoking group ( control group) . Preoperative induced sputumsamples were collected after hypertonic saline induction. Lung tissue samples were intraoperatively collected far from the tumor site. The sputum samples were prepared for total and differential cell count, while the lung tissue samples for pathology examination. The BD-2 concentration in sputumand lung homogenate were measured by ELISA. Correlation were analyzed between BD-2 concentration and smoking index, airway inflammation, and lung function. Results The lung pathology were highly consistent with the experimental grouping. The total cell count and neutrophils proportion in sputum and BD-2 concentration in lung homogenate were ( 2. 32 ±0. 51) ×106 / g, ( 35. 7 ±9. 8) % , and ( 14. 5 ±5. 7) ng/L in the control group respectively, while increased in the smoker group [ ( 4. 57 ±0. 87) ×106 / g, ( 52. 5 ±10. 9) % , and ( 78. 3 ±13. 1) ng/L, P lt;0. 05] , and further increased in the COPD group [ ( 6. 61 ±1. 03) ×106 / g, ( 65. 5 ±12. 3) % , and ( 127. 0 ±35. 0) ng/L, P lt; 0. 05] . The lymphocytes proportion and BD-2 concentration in sputum increased in the COPD group [ ( 3. 2 ±1. 7) % and ( 298. 0 ±135. 0) ng/L] as well as in the smoker group [ ( 2. 5 ±1. 2) % and ( 315. 0 ±124. 0) ng/L] ,as compared with the control group [ ( 1. 1 ±0. 3) % and ( 132. 0 ±48. 0) ng/L] ( P lt; 0. 05) . Linear correlation analysis revealed that BD-2 concentration in sputumwas positively correlated with smoking index,sputum total cell count and neutrophils proportion, whereas BD-2 concentration in lung homogenate wasreversely correlated with pulmonary ventilation function ( P lt; 0. 05) . Conclusions Smoking up-regulates the BD-2 level in sputum and lung tissues. Further more, the BD-2 expression status in lung tissue of smoking individuals might be associated with COPD susceptibility.