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1.
Chinese Journal of Health Management ; (6): 230-236, 2018.
Artículo en Chino | WPRIM | ID: wpr-709004

RESUMEN

Objective To clarify the status of tobacco exposure and identify risk factors of smoking among smear-positive pulmonary tuberculosis patients in Shenzhen,in order to provide a scientific basis for the formulation of tuberculosis-tobacco control strategy in Shenzhen.Methods From January to December 2016,a special survey was carried out in 8 districts in Shenzhen.A unified questionnaire was used to make face to face interviews for 958 smear-positive pulmonary tuberculosis patients registered in 2016.Descriptive statistics was conducted to analyze the status of tobacco exposure.Single factor analysis and multiple logistic regression were used to identify the important risk factors of smoking.Results Among smear-positive pulmonary tuberculosis patients in Shenzhen,the rates of general smoking,current smoking,regular smoking were 40.9%,34.2% and 30%,respectively.All smoking rates were higher among male than female participants (x2=255.226,197.463 and 162.707,respectively,and the P values were all<0.001);164cases of heavy smokers accounted for 50.0% of current smokers.Among 392 smokers,64 had quitted smoking,and the rate of smoking cessation was 16.3%.Among 566 nonsmokers,the rate of passive smoking from cohabiting smokers was 17.8% (101/566),and it was higher in female than male participants (23.1% vs.12.3%,x2=11.219,P=0.001).In single factor analysis,gender,work or living environment,age,education level,marital status,and body mass index were closely related to smoking (x2=255.226,28.375,40.922,29.585,9.117,and 7.052,respectively,and the P values were all<0.05).In multiple logistic regression,the major risk factors for smoking included in the model were gender (x2=120.797,P<0.001),age (x2=5.728,P=0.017),education level (x2=17.159,P<0.001),mode of case-finding (x2=3.670,P=0.055),work or living environment (x2=6.039,P=0.049),and marital status (x2=5.091,P=0.078).Conclusion The smoking status of smear-positive pulmonary tuberculosis patients was serious in Shenzhen.Tuberculosis patients were the key smokers.We should provide accurate intervention and health guidance for patients,such as,macro policy guidance,instillation of knowledge,mental health intervention,and smoke-free environment.

2.
Korean Circulation Journal ; : 510-515, 2006.
Artículo en Inglés | WPRIM | ID: wpr-183599

RESUMEN

BACKGROUND AND OBJECTIVES: Passive smoking increases the risk of cardiovascular disease, but the factors responsible for this association remain largely unknown. We sought to determine whether passive smoke exposure is associated with systemic inflammation in a dose-dependent fashion, which is a known risk factor for cardiovascular events. SUBJECTS AND METHODS: We analyzed the data of self-reported non-smokers, > or =40 years of age, who were from the Third National Health and Nutrition Examination Survey (n=6,595). We quantified the passive nicotine exposure by dividing the non-smokers into quartiles, as based on the serum cotinine values. We used multiple linear and logistic regression models to determine the independent relationship between serum cotinine and the levels of C-reactive protein, fibrinogen and leukocytes, and the platelet expression. RESULTS: After adjustments were done for age, gender, body mass index and race, the participants in the highest serum cotinine quartile (quartile 4) had circulating platelet, fibrinogen and homocysteine levels that were 6,893/microliter higher (95% confidence interval [CI]: 1,886 to 11,900/microliter, p=0.007), 8.74 mg/dL (95% CI: 2.63 to 14.84 mg/dL, p=0.005) and 0.90 micromol/L (95% CI: 0.36 to 1.43 (micromol/L, p=0.001), respectively, than in those in the lowest quartile of serum cotinine (quartile 1). There was a dose-dependent increase in the circulating fibrinogen, homocysteine and platelet levels across the quartiles of cotinine. CONCLUSION: These findings indicate that even among nonsmokers, elevated serum cotinine is an independent risk factor for systemic inflammation. This suggests that passive smoke exposure promotes systemic inflammatory response in a dose-dependent fashion. These observations may explain why passive smoking is a risk factor for atherosclerosis and cardiovascular events.


Asunto(s)
Humanos , Aterosclerosis , Plaquetas , Índice de Masa Corporal , Proteína C-Reactiva , Enfermedades Cardiovasculares , Grupos Raciales , Cotinina , Epidemiología , Fibrinógeno , Homocisteína , Inflamación , Leucocitos , Modelos Logísticos , Nicotina , Encuestas Nutricionales , Estudio Observacional , Factores de Riesgo , Humo , Contaminación por Humo de Tabaco
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