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 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.
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 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.
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 clinical characteristics, short-term therapy outcome and survival in patients of lung cancer with different smoking status. Methods 3751 cases were enrolled and the differences in age, sex, pathological type, stage, treatment modality, efficiency and survival were compared according patients′smoking status. Results 1206 ( 32. 2% ) patients were never smokers and 2545 ( 67. 8% ) were smokers. 80. 3% male patients and 10. 5% female patients were smokers. Among never smoking lung cancer patients, proportion of female gender, adenocarcinoma, second primary neoplasm,advanced stages and non-operative treatment were high. In the smokers, much more COPD and pulmonary tuberculosis, squamous cancer and operative treatmentwere found. No statistical differences were detected in overall outcome and survival. Conclusions The clinical characters and treatmentmodalities of patients with lung cancer of different smoking status were significant different, but had the same survival. Patients’smoking status should be accountted into the diagnosis and treatment of lung cancer.
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.
Objective To study the correlation between smoking and obstructive sleep apnea (OSA). Methods A total of 454 patients from October 2015 to July 2021 were retrospectively collected for nocturnal polysomnography monitoring (no less than 7 hours). The patients were divided into an OSA group (n=405) and a control group (n=49, patients with primary snoring) according to the results of polysomnography monitoring. According to the apnea hypopnea index (AHI) and the lowest oxygen saturation during sleep, the severity of OSA was classified into a mild to moderate group (5 times/h ≤ AHI<30 times/h) and a severe group (AHI ≥30 times/h). The patients were inquired about their smoking history, then the patients diagnosed with OSA were further divided into a smoking group, a smoking cessation group, and a non-smoking group based on their smoking history. Results The smoking rate of the patients in the OSA group was higher than that in the control group (50.9% vs. 32.7%, P<0.05), while the smoking rate in the severe OSA group was higher than that in the mild to moderate group (55.7% vs. 39.8%, P<0.05). Smoking was positively correlated with AHI, cumulative percentages of time spent at oxygen saturation below 90% (Ts90%), and total apnea time (r value was 0.196, 0.197, 0.163, P<0.05), while negatively correlated with the lowest and average SpO2 during sleep (r value was –0.202, –0.214, P<0.05). The logistic regression analysis with severe OSA as the outcome variable showed that smoking (OR=1.781) and obesity (OR=1.930) were independent risk factors of severe OSA (P<0.05). The comparison between groups of the OSA patients with different smoking states showed that the proportion of severe OSA, AHI, Ts90%, and total apnea time (77.8%, 53.55 times/h, 18.35%, and 111.70 minutes, respectively) of the smoking group were higher than those of the non-smoking group (62.8%, 40.20 times/h, 8.40%, and 76.20 minutes, respectively, P<0.05). The lowest SpO2 and average SpO2 during sleep (69.50%, 93.00%, respectively) of the smoking group were lower than those of the non-smoking group (75.00%, 94.00%, respectively, both P<0.05). The average SpO2 of the smoking cessation group was higher than that of the smoking group (94.00% vs. 93.00%, P<0.05), and the Ts90% of the smoking cessation group was lower than that of the smoking group (6.75% vs. 18.35%, P<0.05). Conclusions Smoking significantly affects the degree of sleep-disordered breathing and may be an independent risk factor for severe OSA. Smoking can exacerbate the severity of OSA and the degree of hypoxia, while smoking cessation can improve the degree of hypoxia in OSA patients.
Objective To investigate the expression of dipeptidyl peptidase 4 (DPP4) and angiotensin-converting enzyme 2 (ACE2) in lung tissues of patients with four different diseases including coronavirus disease 2019 (COVID-19), chronic obstructive pulmonary disease (COPD), pulmonary sarcoidosis and pulmonary bullae, and to find out the potential risk factors affecting COVID-19. Methods This study retrospectively analyzed the clinical data of 40 patients admitted to Renmin Hospital of Wuhan University with COVID-19 (COVID-19 group), COPD (COPD group), pulmonary sarcoidosis (pulmonary sarcoidosis group) and pulmonary bullae (pulmonary bullae group) and surgically resected paraffin-embedded pathological lung tissues were obtained from their lung tissue pathological specimens after surgery and paraffin embedding. The GEO database (https://www.ncbi.nlm.nih.gov/geo/) was used for bioinformatics analysis to explore the expression difference of DPP4 and ACE2 mRNA in COVID-19, COPD, pulmonary sarcoidosis and normal lung tissues. Immunohistochemistry method was used to detect the expression of DPP4 and ACE2 protein in lung tissues of each group and the average optical density was measured by image analysis software. Results The results of GEO database analysis showed that compared with pulmonary bullae group, the expression level of DPP4 mRNA had no significant difference in the COPD group and pulmonary sarcoidosis group (both P>0.05), but it was increased in the COVID-19 group (P<0.05); There was no significant difference in the expression level of ACE mRNA in the pulmonary sarcoidosis group (P>0.05), but it was increased in the lung tissue of COVID-19 group and COPD group (both P<0.05). The results of immunohistochemistry showed that DPP4 and ACE2 proteins were lowly expressed in the pulmonary sarcoidosis group and pulmonary bullae group, while their expression level was high in COVID-19 and COPD groups without significant difference (P>0.05). The expression of DPP4 and ACE2 proteins in COVID-19 group was not related to the patient’s gender and age (P>0.05), but was related to smoking and long smoking duration (P<0.05), and there was a positive correlation between DPP4 and ACE2 expression (P<0.05). Conclusions DPP4 and ACE2 proteins are lowly expressed in the pulmonary sarcoidosis group and pulmonary bullae group, while their expression level is high in COVID-19 and COPD groups. There is no significant difference in the expression level of DPP4 and ACE2 protein in the COVID-19 and COPD lung tissues. There may be a positive correlation between DPP4 and ACE2 proteins expression in lung tissue, and smoking may be a potential risk factor for COVID-19.