• Tuberculosis and Respiratory Diseases
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• v.58 no.5
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• pp.515-520
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• 2005

Acute eosinophilic pneumonia (AEP) has been described as an idiopathic febrile illness with a duration of less than seven days with severe hypoxemia, pulmonary infiltrates, and no history of asthma. It has been reported that AEP is associated with smoking. Although the pathogenesis of smoking induced AEP is being actively studied, there is no direct histological evidence that smoking actually induces AEP. Recently, we encountered a case of AEP that may have been caused by smoking. We performed a cigarette smoking challenge test to verify that smoking was indeed the cause of AEP in this patient. Smoking induced an increase the proportion of eosinophils in the bronchoalveolar lavage fluid without any respiratory symptoms or abnormal radiological findings. This result suggests that smoking was the cause of AEP in this patient.

• Journal of agricultural medicine and community health
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• v.33 no.1
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• pp.90-100
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• 2008

=Objectives: The aim of this study was to investigate the smoking rate and the related factors to early smoking of high school students.Methods: A questionnaire was administered to 920 students in 3 high schools in Daegu Metropolitan Results: Of total respondents, 1.8% had experience of smoking. Of those, 20.2% citied curiosity, 9.0% cited upon recommendation of friends, and 6.2% cited stress management as the main reason for their smoking. Separately, 53.1% responded habitually and 26.5% responded stress management as the main reason for continuing smoking. Of total former smokers, 68.4% said 'worry about their health' as the main reason for quitting smoking. Of those who failed to quit smoking, 58.7% cited 'weakness of will' as the main reason for their failure. Of total respondents, 10.8% were smoking currently. 'Smoking of family member'(p<0.01) and 'intent to smoke'(p<0.05) were significantly associated to early smoking of the subjects.In multivariate logistic regression analysis, 'higher levels of stress' and 'smoking of family member' were significant related factors to early smoking.Conclusions: Amid growing number of early smokers, it is imminent to identify the actual state of discourage smoking. In addition, education programs need to be developed to assist early smokers in quitting smoking and prevent smoking among youth.

• Journal of Life Science
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• v.18 no.11
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• pp.1543-1550
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• 2008

We studied the effects of smoking, which is one of indoor-environmental pollutants and related to various cancers, on glycoconjugates of rat sebaceous glands with the lectin histochemistry. To investigate the effects of smoking on glycoconjugates, male Sprague-Dawley rats were exposed to tabacco smoke for 10 minutes per day in an inhalation chamber for 1, 2, 3, and 5 days with active and passive exposure. For the structure of sebaceous glands we used PAS reaction, and for the glycoconjugates binding pattern 9 biotinylated lectins (DBA, SBA, PNA, BSL-1, WGA, RCA-1, UEA-1, Con A, and LCA) were used. Some remarkable changes, such as the decrease in the size of sebaceous glandular acini, the destruction of upper portion of sebaceous glands, vacuolation of central portion of sebocytes, and the immature sebaceous glandular acini were seen in the smoke-exposed rats. In the control rats, basal cells were stained with BSL-1, PNA and WGA, but the stronger reaction was founded in BSL-1 binding. Also, sebocytes were stained with PNA, WGA, Con A, BSL-1 and SBA, but stronger reactions were founded in PNA and Con A stainings. Specific changes in the lectin binding patterns were also observed in the smoke-exposed rats. In the basal cells of exposed rats, PNA binding increased, BSL-1 decreased but returned to control level, and WGA disappeared. Plus, immature glandular acini, which were not found in the control rats, were stained PNA, Con A and BSL-1, but the stronger reaction were founded in PNA and Con A binding. In conclusion, it was assumed that the tabacco smoke seriously effected on the structure and glycoconjugates metabolism of sebaceous glands.

• Journal of the Korea Convergence Society
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• v.9 no.12
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• pp.295-299
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• 2018

The aim of this study was to evaluate the association between the level urine cotinine and periodontal diseases in Korea adults. The date from the 2014, 2015 Korean National Health and Nutrition Survey were used, and 5,146 subjects over 30 years were included in the analysis. Periodontal disease was assessed using the Community Periodontal Index. Binary logistic regression model was used to estimate the odds ratio with 95% confidence intervals. There was a 2.08-fold (95% CI; 1.73-2.05) increased in the odds of periodontal disease for those with any ETS exposure compared with those with non-smokers following adjustment for sex, age, education, and income. The level of urine cotinine also showed a dose-dependent increase in extent of periodontal disease. Among persons in the Korea who had never used tobacco, those exposed to ETS were more likely to have periodontal disease than were those not exposed to ETS. In the future, voluntary compliance of smokers to measures to reduce ETS exposure should be encouraged.

• Tuberculosis and Respiratory Diseases
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• v.58 no.5
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• pp.490-497
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• 2005

Background : The paraoxonase enzyme plays a significant role in the detoxification of various organophosphorous compounds in mammals, and paraoxonase (PON) 1 is one of the endogenous free-radical scavenging systems in the human body. In this study, we investigated the interaction between cigarette smoking and the genetic polymorphism of PON1 with lung cancer in Korean males. Methods : Three hundred thirty five patients with lung cancer and an equal number of age-matched controls were enrolled in this study. Every subject was asked to complete a questionnaire concerning their smoking habits and alcohol drinking habits. A 5' exonuclease assay (TaqMan) was used to genotype the PON1 Q192R polymorphism. The effects of smoking habits and drinking habits, the PON1 Q192R polymorphism and their interactions were statistically analyzed. Results : Cigarette smoking and the Q/Q genotype of PON1 were significant risk factors for lung cancer. Individuals carrying the Q/Q genotype of PON1 were at a higher risk for lung cancer as compared with those individuals carrying the Q/R or R/R genotype (odds ratio, 2.84; 95% confidence interval, 1.69 - 4.79). When the groups were further stratified by the smoking status, the Q/Q PON1 was associated with lung cancer among the current or ex-smokers (odds ratio, 2.56; 95% confidence interval, 1.52 - 4.31). Current smokers or ex-smokers who had the Q/Q genotype showed an elevated risk for lung cancer (odds ratio: 15.50, 95% confidence interval: 6.76 - 35.54) as compared with the group of subjects who never smoked, and had the Q/R or R/R genotype. The odds ratios (95% confidence interval) of smokers with the PON1 Q/Q type compared to the nonsmokers with the PON1 Q/R or R/R type were 53.77 (6.55 - 441.14) for squamous cell carcinoma, 6.25 (1.38 - 28.32) for adenocarcinoma, and 59.94 (4.66 - 770.39) for small cell carcinoma, and these results were statistically significant. Conclusion : These results suggest that cigarette smoking and the PON1 Q/Q genotype are risk factors for lung cancer. The combination of cigarette smoking and the PON1 Q/Q genotype significantly increased the lung cancer risk irrespective of the histologic type of cancer.

• Journal of the Korean Society of Food Science and Nutrition
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• v.33 no.3
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• pp.523-532
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• 2004

The spontaneous frequency of genetic damage and the possible relationship of this damage to dietary and nutritional variables were investigated in peripheral blood lymphocytes from 45 elderly people using sister chromatid exchange (SCE). The relationship of dietary and nutritional factors on SCE was assessed by different degrees of smoking status such as smokers (n=14), ex-smokers (n=16) and non-smokers (n=15). Significant relationship of the SCE frequency to nutrient intake of the combined subjects (n=45) was found. When cigarette smoking status was taken into account, there were negative linear relationships between SCE and fat, phosphorus or vitamin A intakes of the non-smokers as well as SCE and the dietary quality scores. There was a positive linear relationship between SCE and food frequency of meat and fish among the smokers. Use of artificial sweetners in ex-smokers of the elderly people produced a significant increase of SCE in comparison with the mean SCE for those not using sweetners. Other dietary parameters, including intake of coffee, green tea and ginseng tea, alcohol consumption, use of processed foods, and administration of vitamin pills did not show any correlation with SCE. These results suggested that dietary fat, phosphorus or vitamin A status are the major determinants of spontaneous DNA damage in lymphocytes of the elderly people.

• Tuberculosis and Respiratory Diseases
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• v.50 no.4
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• pp.426-436
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• 2001

Background : Chronic obstructive pulmonary disease(COPD) is one of the major contributors to morbidity and mortality among the adult population. Cigarette smoking(CS) is undoubtedly the single most important factor in the pathogenesis of COPD. However, its mechanism is unclear. The current hypothesis regarding the pathogenesis of COPD postulates that an imbalance between proteases and antiproteases leads to the destructive changes in the lung parenchyma. This study had two aims. First, to evaluate the effect of CS exposure on histologic changes of the lung parenchyme, and second, to evaluate the effect of CS exposure on the expression of the gelatinolytic enzymes in BAL fluid cells in guinea pigs. Methods : Two groups of five guinea pigs were exposed to the whole smoke of 20 commercial cigarettes per day, 5 hours/day, 5 days/week, for 6weeks, and 12 weeks, respectively, using a smoking apparatus. Five age-matched guinea pigs exposed to room air were used as controls. Five or more sections were microscopically extamined(${\times}400$) and the number of cellular infiltration of the alveolar wall was measured in order to evaluate the effect of CS exposure on the histologic changes of lung parenchyme. The statistical significance was analyzed by a linear regression method. To evaluate the expression of the gelatinolytic enzymes in intraalveolar cells, BAL fluid was obtained and the intraalveolar cells were separated by centrifugation (500 g for 10 min at $4^{\circ}C$). Two sets of culture plates were loaded with $1{\times}10^6$ intraalveolar cells. One plate, contained O.1mM EDTA, a inhibitor of matrix metalloproteases(MMPs), and the other plate had no EDTA. Both plates were incubated for 48 hours at $37^{\circ}C$. After incubation, gelatinolytic protease expression in the supernatants was analyzed by gelatin zymography. Results : At the end of CS exposure, the level of blood carboxy Hb had increased significantly(4.1g/dl in control group, 24g/dl immediately after CS exposure, 18g/dl 30 min after CS exposure, 15g/dl 1 hour after CS exposure). Alveolar inflammatory cells were identified in the CS exposed guinea pigs. The number of alveolar cellular cells observed in a microscopic field ($400{\times}$) was $121.4{\pm}7.2$, $158.0{\pm}20.2$, $196.8{\pm}32.8$, in the control, the 6 weeks, and the 12 weeks group, respectively. The increased extent of inflammatory cellular infiltration of the lung parenchema showed a statistically significant linear relationship with the duration of CS exposure(p=0.001, $r^2=0.675$). Several types of gelatinolytic enzymes in the intraalveolar cells of CS exposed guinea pigs were expressed, of which some were inhibited by EDT A. However, the gelatinolytic enzymes were not expressed in the control groups. Conclusion : CS exposure increases inflammatory cellular infiltration of the alveolar wall and the expression of gelatinolytic proteases in guinea pigs. EDTA inhibits some of the gelatinolytic proteases. These findings suggest a possibility that CS exposure may increase MMP expression in the lungs of guinea pigs.

• Proceedings of the Korean Institute of Information and Commucation Sciences Conference
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• 2016.10a
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• pp.274-276
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• 2016

Recently due to increase of tobacco users, many problems have been issued. Not only smoking in public places, smoking indoors as well causes harm to non-smoking people. Smoking booths that are installed but the quality is considerably less and purification devices are not correctly installed, which leads to harm the people around the smoking booth. In this paper, we introduce the "Augmented Reality Billboard" in order for smokers to effectively recognize the non-smoking warning image and healthy warning messages, Kinect Camera Sensor and Augmented Reality (AR) functions are used to recognize the motion of a person to coordinate the corresponding coordinate values.

• Tuberculosis and Respiratory Diseases
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• v.39 no.6
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• pp.511-516
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• 1992

Background: It is well known that cigarette smoking is the risk factor of lung cancer, chronic obstructive pulmonary disease and ischemic heart disease. But there are few reports about the immediate effect of cigarette smoking on the cardiopulmonary functions. The serum level of carbon monoxide increases during cigarette smoking. It is known that carbon monoxide increases respration rate, heart rate and cardiac output, with decrease in maximal oxygen consumption. So we have studied to determine the immediate effects of cigarette smoking on the cardiopulmonary function during exercise. Method: Thirteen healthy smoking male subjects were included in this study. Each subject was undertaken pulmonary function test and incremental exercise test on two separate days, one without smoking (control) and the other after smoking three cigarettes per hour for five hours. The order of the two tests was randomized. Results: 1) The mean age of the subjects was $25{\pm}4.9$ year-old and the mean smoking history was $6{\pm}5$ pack years. 2) The mean blood level of carbon monoxide on the smoking day was higher than that on the nonsmoking day ($5.97{\pm}1.34%$ vs. $1.45{\pm}0.83%$; p<0.01). 3) The mean maximal oxygen consumption on the smoking day was lower than that on the nonsmoking day ($2.09{\pm}0.32$ L/min vs. $2.39{\pm}0.32$ L/min; p<0.05). 4) The mean anaerobic threshold on the smoking day was lower than that on the nonsmoking day ($1.33{\pm}0.24$ L/min vs. $1.53{\pm}0.20$ L/min; p<0.05). 5) The mean heart rate at rest on the smoking day was higher than that on nonsmoking day ($84.38{\pm}11.06$ beats/min vs. $75.46{\pm}5.83$ beats/min; p<0.05). But the means of maximal heart rate on both days were not different. 6) The pulmonary function tests were similar on both days. Conclusion: There was no change in pulmonary function test, but the maximal oxygen consumption and anaerobic threshold were decreased on the smoking day. So it was concluded that cigarette smoking impaired the cardiovascular functions immediately during exercise.

• Journal of the Korean Society of Tobacco Science
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• v.15 no.1
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• pp.3-14
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• 1993

Oxidants in environment or cigarette smoke are known to be implicated in the oxidative damages of pulmonary system. Such cellular damages are prevented by the presence of adequate levels of antioxidants in the tissue. In the present study, we investigated the influences of smoking duration and concentration of smoke on lung antioxidant defense in rats. Subchronic exposure of rats to smoke generated from 6 cigarettes per day for 90 days caused the activities of catalase and superoxide dismutase (SOD) to increase. However, glutathione peroxidase (GP-Xase) was not significantly changed. Total sulfhydryl compounds (Total-SH) in the lung homogenates from the rats inhaled with cigarette smoke for 15 days was decreased by 44% , thereafter it was returned to the level of normal rats. On the contrary, when rats were daily exposed to a different concentration of smoke generated from 1 to 20 cigarettes per day for 15 days, the activity of catalase was increased gradually with dose, but total SOD activity was increased only in the rats of low dose groups less than 5 cigarettes. Three types of SOD (one Cu, Zn-SOD with pI 4.9, and two Zn-SOD with pI 4.7 and 7.9)were detected in the lung homogenates and Zn-SOD with pI 4.7 was the major and cigarette-smoke inducible form. These results indicate that the protection of lung against oxidants from cigarette smoke seems to be accomplished by the induction of catalase and SOD, especially a cyanide resistant Zn-SOD with pI 4.f, following the consumption of antioxidants such as GSH in the beginning of inhalation period.