• Journal of the Korean Society of Tobacco Science
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• v.27 no.2
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• pp.212-218
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• 2005

Cigarette smoking has been known to have a few beneficial effects on some neuronal diseases such as Alzheimer's disease(AD), Parkinson's disease(PD) and prion disease by scrapie agent shows many similar properties with AD. In this respect, we investigated what biological effects are exerted by cigarette smoke exposure(CSE) in the brain of mouse infected by 87V scrapie. The scrapie agent was inoculated through stereotaxic microinjection of the homogenates of the scrapie agent infected brain into the intracerebral system in the 1M mice. The inoculation into mice typically exhibits neurochemical, physiological and histopathological characteristics of prion disease: loss of neurotransmitters and induction of astrocytosis and vacuolation in brain as well as reduction of spatial movement and loss of body weight. CSE led to alleviated the loss of body weight and also improved spatial movement of the infected mice. Most interestingly, CSE attenuated astrocytosis and vacuolation caused by scrapie infection in the brain. In addition, decreased levels of dopamine in striatal and hypothalamic regions as well as serotonin level in hippocampus caused by scrapie infection were also attenuated by exposure to cigarette smoke. These findings suggest that cigarette smoke, by its inhibition of astrocytosis and vacuolation followed by its restoration of levels of some neurotransmitters, may partly contribute to suppression in the progress of neurodegeneration caused by scrapie infection.

• Nuclear Engineering and Technology
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• v.40 no.7
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• pp.539-550
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• 2008

Lung cancer is the most prevalent global cancer, ${\sim}90%$ of which is caused by cigarette smoking. The LNT hypothesis has been inappropriately applied to estimate lung cancer risk due to ionizing radiation. A threshold of ${\sim}1\;Gy$ for lung cancer has been observed in never smokers. Lung cancer risk among nuclear workers, radiologists and diagnostically exposed patients was typically reduced by ${\sim}40%$ following exposure to <100 mSv low LET radiation. The consistency and magnitude of reduced lung cancer in nuclear workers and occurrence of reduced lung cancer in exposed non-worker populations could not be explained by the HWE. Ecologic studies of indoor radon showed highly significant reductions in lung cancer risk. A similar reduction in lung cancer was seen in a recent well designed case-control study of indoor radon, indicating that exposure to radon at the EPA action level is associated with a decrease of ${\sim}60%$ in lung cancer. A cumulative whole-body dose of ${\sim}1\;Gy$ gamma rays is associated with a marked decrease in smoking-induced lung cancer in plutonium workers. Low dose, low LET radiation appears to increase apoptosis mediated removal of $\alpha$-particle and cigarette smoke transformed pulmonary cells before they can develop into lung cancer.

• Development and Reproduction
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• v.26 no.4
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• pp.155-163
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• 2022

Human pluripotent stem cells (hPSCs) can give rise to a vast array of differentiated derivatives, which have gained great attention in the field of in vitro toxicity evaluation. We have previously demonstrated that hPSC-derived alveolar epithelial cells (AECs) are phenotypically and functionally similar to primary AECs and could be more biologically relevant alternatives for assessing the potential toxic materials including in fine dust and cigarette smoking. Therefore, in this study, we employed hPSC-AECs to evaluate their responses to exposure of various concentrations of diesel particulate matter (dPM), cigarette smoke extract (CSE) and nicotine for 48 hrs in terms of cell death, inflammation, and oxidative stress. We found that all of these toxic materials significantly upregulated the transcription of pro-inflammatory cytokines such as IL-1α, IL-β, IL-6, and TNF-α. Furthermore, the exposure of dPM (100 ㎍/mL) strongly induced upregulation of genes related with cell death, inflammation, and oxidative stress compared with other concentrations of CSE and nicotine. These results suggest that hPSC-AECs could be a robust in vitro platform to evaluate pulmotoxicity of various air pollutants and harmful chemicals.

• Laboraroty Animal Research
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• v.33 no.2
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• pp.76-83
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• 2017

Chronic obstructive pulmonary diseases (COPD) is an important disease featured as intense inflammation, protease imbalance, and air flow limitation and mainly induced by cigarette smoke (CS). In present study, we explored the effects of $Pycnogenol^{(R)}$ (PYC, pine bark extract) on pulmonary fibrosis caused by CS+lipopolysaccharide (LPS) exposure. Mice were treated with LPS intranasally on day 12 and 26, followed by CS exposure for 1 h/day (8 cigarettes per day) for 4 weeks. One hour before CS exposure, 10 and 20 mg/kg of PYC were administered by oral gavage for 4 weeks. PYC effectively reduced the number of inflammatory cells and proinflammatory mediators caused by CS+LPS exposure in bronchoalveolar lavage fluid. PYC inhibited the collagen deposition on lung tissue caused by CS+LPS exposure, as evidenced by Masson's trichrome stain. Furthermore, transforming growth $factor-{\beta}1$ ($TGF-{\beta}1$) expression and Smad family member 2/3 (Smad 2/3) phosphorylation were effectively suppressed by PYC treatment. PYC markedly reduced the collagen deposition caused by CS+LPS exposure, which was closely involved in $TGF-{\beta}1$/Smad 2/3 signaling, which is associated with pulmonary fibrotic change. These findings suggest that treatment with PYC could be a therapeutic strategy for controlling COPD progression.

• Tuberculosis and Respiratory Diseases
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• v.85 no.3
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• pp.237-248
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• 2022

Background: We evaluated the effect of particulate matter (PM) and cigarette smoke extract (CSE) on bronchial epithelial cell survival, as well as oxidative stress and autophagy levels. Moreover, we aimed to assess the effect of the antioxidant N-acetylcysteine (NAC) on the adverse effects of PM and CSE exposure. Methods: Normal human bronchial epithelial cells (BEAS-2B cells) were exposed to urban PM with or without CSE, after which cytotoxic effects, including oxidative stress and autophagy levels, were measured. After identifying the toxic effects of urban PM and CSE exposure, the effects of NAC treatment on cell damage were evaluated. Results: Urban PM significantly decreased cell viability in a concentration-dependent manner, which was further aggravated by simultaneous treatment with CSE. Notably, pretreatment with NAC at 10 mM for 1 hour reversed the cytotoxic effects of PM and CSE co-exposure. Treatment with 1, 5, and 10 mM NAC was shown to decrease reactive oxygen species levels induced by exposure to both PM and CSE. Additionally, the autophagy response assessed via LC3B expression was increased by PM and CSE exposure, and this also attenuated by NAC treatment. Conclusion: The toxic effects of PM and CSE co-exposure on human bronchial epithelial cells, including decreased cell viability and increased oxidative stress and autophagy levels, could be partly prevented by NAC treatment.

• Toxicological Research
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• v.33 no.1
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• pp.31-41
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• 2017

Side stream cigarette smoke (SSCS) is known to be as harmful and hazardous to human health as is active smoking. In this study, we investigated the relationship between the exposure to SSCS and its stimulatory and subacute effects on the progression of non-alcoholic steatohepatitis (NASH). A methionine and choline-deficient plus high fat (MCDHF) diet was administered to C57BL/6 mice for 6 weeks. During the first three weeks of MCDHF diet feeding, each diet group was exposed to SSCS (0, 20, $40{\mu}g/L$) or fresh air for 2 hrs per day and 5 days per week. Additional experiments were performed by increasing the concentration (0, 30, $60{\mu}g/L$) and exposure time (6 hours per day) of SSCS. According to histopathologic analysis and serum levels of Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST), there were no differences in hepatic fat deposition, fibrosis, apoptosis or liver damage in MCDHF-fed mice based on SSCS exposure. There were also no differences in the expression of inflammation-, oxidative stress- or fibrosis-related genes between MCDHF-fed mice with or without SSCS exposure. Therefore, it is concluded that SSCS with current exposure amounts does not have additive detrimental effects on the early stage of NASH.

• Korean Journal of Oriental Medicine
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• v.3 no.1
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• pp.261-278
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• 1997

This experiment was performed in order to study the clinical effects of Gyumsuyukgunjun on the pulmonary injury caused by exposure of cigarette smoke in rats. Therefore, a writer reports on present experimental results having significant effects on the level of oxygen consumption, the lungs volume, the leukocyte, the hemoglobin level, and the $PaO_2$, $PaCO_2$ after administration of Gyumsuyukgunjun in order to study the clinical effects of Gyumsuyukgunjun on the pulmonary injury caused by exposure of cigarette smoke in rats. The results were obtained as follows: 1. In comparison with control group, The group of Gyumsuyukgunjun administration was revealed significant effects(P<0.005) of increase on the level of oxygen consumption. 2. In comparison with control group, The group of Gyumsuyukgunjun administration was revealed significant effects(P<0.005) of decrease on the lungs volume. 3. In comparison with control group, The group of Gyumsuyukgunjun administration was revealed significant effects(P<0.05) of decrease on the leukocyte counts. 4. In comparison with control group, The group of Gyumsuyukgunjun administration was revealed significant effects(P<0.05) of decrease on the hemoglobin level. 5. In comparison with control group, The group of Gyumsuyukgunjun administration was revealed significant effects(P<0.01) of increase on the $PaO_2$ level only of $PaO_2$, $PaCO_2$ level. It was concluded from the above results that Gyumsuyukgunjun has a significant effects on the pulmonary injury caused by cigarette smoke.

• Journal of Preventive Medicine and Public Health
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• v.41 no.3
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• pp.136-146
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• 2008

Objectives : The purpose of this study was to estimate the willingness to quit cigarette price among Korean male adults, and to examine the factors affecting the willingness to quit cigarette price. Methods : The data was collected by a random digit dial telephone survey. 702 samples were analyzed by using t-tests, ANOVA and OLS regression analysis. To estimate the willingness to quit cigarette price, smokers were asked dichotomous questions with open-ended follow-up and the starting point of the price was randomized by one of 5 bid prices elicited from a pilot study. Results : The mean of the willingness to quit cigarette price was 4,287 Won per package, which was about 2,000 Won higher than the mean of the actual price the smokers now paid. About 41% of respondents were willing to quit smoking if the price of cigarette would be increased by 3,000 Won, and if the price would be increased by 20,000 Won, all respondents were willing to quit smoking. The factors associated with the willingness to quit cigarette price were the place of residence, the amount of smoking and the degree of exposure to smoking through the mass media. Conclusions : The results showed that to get people to quit smoking, increasing the cigarette price would obviously be effective and much higher prices have a greater effect. Furthermore, to enlarge the effect of increased cigarette prices, providing more cessation programs to small towns, reducing the amount of smoking and decreasing or prohibiting advertisements of cigarettes and smoking in the mass media will be efficient.

• Journal of the Korean Society of Tobacco Science
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• v.20 no.2
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• pp.218-224
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• 1998

Long-term exposure of cigarette smoke or air pollutants to human can induce damages in the airway mucociliary function and can be closely related to the irritation and sputum formation in the respiratory system. This study was undertaken to investigate whether rat trachea can be used as a tool for evaluating the cigarette smoke quality. It was identified that, through the examination with inverted microscope, ciliary beating in 1 mm long cut of nat trachea ring was continued for at least 48 hours in saline solution at $25^{\circ}C$. The ciliostasis time in a KCN solution as a positive control was decreased with increasing the concentration of KCN. There were no significant differences in the ciliostasis time by body weight and individual variation of rats. Ciliotoxicity of whole smoke trapped in saline was not significantly changed by aging for more than 6 hrs. The ciliostasis time was in inverse proportion to the number of sample cigarettes applied. As moisture in the cigarette was increased, ciliostasis time was linearly increased. Therefore, these data indicate that the ciliotoxicity test using rat trachea in vitro can be applied to evaluate the cigarette smoke quality and to search factors for the irritation and sputum formation by cigarette smoke as well as air pollutants.

• Survey Research
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• v.12 no.2
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• pp.159-173
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• 2011

The goal of this study is to identify and compare predictors of smoking initiation, persistence and smoking status among Hispanics and Whites. The sample includes 1,410 Hispanic and non-Hispanic White adults living in El Paso, TX, USA and Do$\tilde{n}$a Ana and Otero counties, NM, USA from the Paso del Norte 2002 BRFSS. Whites reported higher rates of cigarette smoking and became regular smokers earlier than Hispanics. Males were twice more likely to initiate cigarette smoking and progress to regular smoking than females among Hispanics, but this gender difference among Whites was not significant. Childhood exposure to drinkers or alcoholics was an important predictor of smoking initiation and becoming a regular smoker, but only among Hispanics. Few identified ethnic differences in predictors of smoking were found. The findings underscore the importance of Hispanic norms on smoking behaviors. Prevention efforts need to address the culture as one of the important components relevant to smoking.