• 한국발생생물학회지:발생과생식
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• 제26권4호
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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.

• Journal of Preventive Medicine and Public Health
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• 제40권6호
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• pp.467-474
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• 2007

Objectives : Gastric cancer is the most common incident cancer in Korea. Although Helicobacter pylori infection is the most important risk factor for the development of gastric cancer, cigarette smoking has also been suggested to play an important role in the development of gastric cancer. The objective of this study is to evaluate the relationship between cigarette smoking and gastric cancer risk in a Korean population. Methods : The study population consisted of 13,785 subjects who had been enrolled in the Korean Multi-Center Career Cohort between 1993 and 2002. As of December 2002, 139 incident gastric cancer cases were ascertained through the Korea Central Cancer Registry and the National Death Certificate Database. Relative risks (RR) and 95% confidence intervals (CI) for gastric cancer were estimated using Cox#s proportional hazard model adjusted for age, education, alcohol drinking status and history of gastritis or ulcer. Results : Significant dose-response relationships were observed between the duration of smoking and the risk of gastric cancer among the male subjects in comparison to non-smokers: men who smoked for 20-39 years had a 2.09-fold (95% CI 1.00-4.38) increase, and those who smoked for more than 40 years had a 3.13-fold (95% CI 1.59-6.17) increase in the risk of gastric cancer ($P_{trend}<0.01$). Conclusions : This study suggests that a longer duration of cigarette smoking may increase the risk of gastric cancer development in a dose-response manner in Korean men. The association between smoking and gastric cancer risk in women should be verified in future studies with a larger number of cases.

• Asian Pacific Journal of Cancer Prevention
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• 제13권11호
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• pp.5539-5543
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• 2012

Objective: The smoking prevalence in Malaysia is high, especially among men and adolescents. This study aimed to determine the prevalence and associated factors towards cigarette smoking among school teachers in Malaysia. Methodology: This study was a school-based cross-sectional study conducted among 495 secondary school teachers. The questionnaire used in this study consisted of 29 questions categorized into two sections: socio-demographic characteristics and smoking behaviour. Data were analyzed using the Statistical Package for the Social Sciences (SPSS) program 13.0. ANOVA; t-tests were used in univariate analysis; multiple linear regression was applied for multivariate analysis. Results: The majority of the participants were female (81.6%), in the age group ranged between 30-39 years (44%), Malay (90.1%), married (89.7%), degree holders (85.1%), with monthly income ranged between 3000-3999 Ringgit Malaysia (33.5%), from urban areas (94.7%), their specialty is social studies (33.9%) and with no family history of cancer (83.6%). The prevalence of smoking among school teachers in Malaysia was found to be 7.8%. Regarding reasons to start smoking among school teachers: the major reason was found to be relaxation (33.3%), followed by stress-relief (28.2%). Univariate analysis showed that sex, educational status, monthly income and residency were significantly associated with smoking among school teachers (p<0.001, p=0.004, p=0.031, p=0.010; respectively). Multivariate analysis showed that gender and marital status were significantly associated with smoking among school teachers (p<0.001, p=0.033; respectively). Conclusion: The prevalence of smoking among school teachers in Malaysia was found to be relatively low. Sex, marital status, educational status, monthly income and residency were significantly associated with smoking among school teachers.

• Tuberculosis and Respiratory Diseases
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• 제58권5호
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• pp.515-520
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• 2005

최근 일본 연구자들을 중심으로 새로 시작한 흡연에 의해 발생한 급성 호산구성 폐렴의 증례 보고가 증가하고 있고 또 발병기전에 대한 연구도 점차 증가하고 있는 추세이다. 본 저자들도 흡연에 의해 발생한 급성 호산구성 페렴환자를 경험하고 이 환자에서 흡연유발검사를 통해 새로 시작한 흡연이 급성 호산구성폐렴의 원인임을 확인하여 이 환자의 임상적인 특징과 경과를 문헌고찰과 함께 보고하는 바이다.

• Toxicological Research
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• 제30권3호
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• pp.149-157
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• 2014

Smoking is one of the most serious but preventable causes of cardiovascular disease (CVD). Key aspects of pathological process associated with smoking include endothelial dysfunction, a prothrombotic state, inflammation, altered lipid metabolism, and hypoxia. Multiple molecular events are involved in smoking-induced CVD. However, the dysregulations of reactive oxygen species (ROS) generation and metabolism mainly contribute to the development of diverse CVDs, and NADPH oxidase (NOX) has been established as a source of ROS responsible for the pathogenesis of CVD. NOX activation and resultant ROS production by cigarette smoke (CS) treatment have been widely observed in isolated blood vessels and cultured vascular cells, including endothelial and smooth muscle cells. NOX-mediated oxidative stress has also been demonstrated in animal studies. Of the various NOX isoforms, NOX2 has been reported to mediate ROS generation by CS, but other isoforms were not tested thoroughly. Of the many CS constituents, nicotine, methyl vinyl ketone, and ${\alpha}$,${\beta}$-unsaturated aldehydes, such as, acrolein and crotonaldehyde, appear to be primarily responsible for NOX-mediated cytotoxicity, but additional validation will be needed. Human epidemiological studies have reported relationships between polymorphisms in the CYBA gene encoding p22phox, a catalytic subunit of NOX and susceptibility to smoking-related CVDs. In particular, G allele carriers of A640G and $-930^{A/G}$ polymorphisms were found to be vulnerable to smoking-induced cardiovascular toxicity, but results for C242T studies are conflicting. On the whole, evidence implicates the etiological role of NOX in smoking-induced CVD, but the clinical relevance of NOX activation by smoking and its contribution to CVD require further validation in human studies. A detailed understanding of the role of NOX would be helpful to assess the risk of smoking to human health, to define high-risk subgroups, and to develop strategies to prevent or treat smoking-induced CVD.

• 한국연초학회:학술대회논문집
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• 한국연초학회 2000년도 24회 정기총회 및 43회 학술발표회
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• pp.12-21
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• 2000

The smoke from a burning cigarette is classified as mainstream, which is the smoke inhaled by the smoker during a puff, and sidestream, which is defined by ISO 10185 as all smoke which leaves a cigarette during the smoking process other than from the butt end. Most of the sidestream smoke is generated during static burn, that is, in between puffs. The amount of sidestream smoke generated by a cigarette depends on the cigarette construction, tobacco blend, and properties of the cigarette paper, The main paper properties affecting sidestream smoke generation are: porosity, basis weight, type and amount of filler, type and amount of burn additive.Sidestream smoke is composed of a visible phase (small liquid droplets) and an invisible phase (gaseous molecules). This paper focuses on the visible portion of the sidestream smoke. Optical methods, which are based on the relationship between light scattering and density of the rising plume of smoke, have been used successfully by the industry. However, the present trend is to use gravimetric methods where the particulate matter is captured on a Cambridge(R) filter pad and weighed. The gaseous portion of the sidestream smoke, which does not contribute to the visible sidestream smoke, passes through the Cambridge filter pad.Sidestream smoke reduction is achieved by modifying certain mass transport processes occurring in a smoldering cigarette. There are four main pathways for reducing sidestream smoke: A) less tobacco burned, B) slower rate of tobacco combustion, C) more efficient trapping of smoke by the cigarette paper, and D) more complete combustion of tobacco. This paper discusses how the physical properties of paper and cigarette construction affect sidestream smoke reduction via the above four mechanisms.

• 한국연초학회지
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• 제12권1호
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• pp.19-27
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• 1990

지금까지 연기중의 Nicotine, CO등 몇몇 화합물의 함량 측정과 관능 검사등을 통하여 담배의 품질을 평가해 왔다. 그러나 담배 연기중의 수 많은 화학 성분들을 고려할 때 전연기 성분이 생체에 미치는 영향을 측정함으로써 그 품질을 평가할수 있는 새로운 방범이 요구된다. 담배연기에 의한 생체 손상 쿵 가장 일차적이고 영향이 큰 것으로 알려진 활성 산소종(H2O2, O2-, ·OH)은 그 반응성이 크고 life time이 짧기 때문에 측정이 어렵다. 저자들은 이들을 분해하는 효소를 이용하여 연기중에서 생성되는 이들 산소 자유 라디칼을 측정하였으며 그 결과 담배의 종류에 따라 이들의 생성이 현저한 차이를 보여 일반적으로 고급 담배로 알려진 것들은 낮았고 저급 담배일 수록 높았다. 따라서 이들 산소 자유 라디칼의 측정은 흡연과 건강이라는 측면에서 매우 유용한 담배의 품질 평가 방법으로 이용될수 있을 것으로 생각된다.

• 한국연초학회지
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• 제19권2호
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• pp.136-144
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• 1997

Cigarette smoking is known to suppress both 1-methy14-phenyl-155,Ltetrahydropy-ridine (MPTP)-induced parkinsonism and idiopathic Parkinson's disease (PD). However, the precise mechanism underlying its protective action against PD is not clearly elucidated yet. In order to find possible clue on the mechanism of protective action of smoking, we investigated the inhibitory effect of cigarette smoke components on rat brain mitochondria1 monoamine oxidase B (MAO-B), responsible enzyme for the activation of MPTP to its toxic metabolitesr and identified the components having an inhibitory potency on this enzyme from cigarette smoke. Total 31 eligible constituents including nicotine were selected from cigarette smoke condensates via solvents partitioning and silica gel chromatographic separation, and inhibitory potencies of 19 components on MAO-B were determined. Hydroquinone and methylcatechol, the phenolic components, showed the strongest inhibitory potencies on MAO-B activity in the components tested. 3,4-Dihydroxybenzylamino, myosmine and indole in basic fracton, eugenol in phenolic fraction, and farnesol in neutral fraction also inhibited the enzyme activity dose-dependently. Among tobacco alkaloids tested only myosmine was effective for the inhibition of this enzyme. These results suggest that the decrease in MAO-B activity by such components derived from cigarette smoke seems to be related to the suppression of MPTP-induced neurotoxicity and to the less incidence of Parkinson's disease in smokers than in nonsmokers.

• Toxicological Research
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• 제32권4호
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• pp.353-358
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• 2016

The generation and collection of cigarette smoke (CS) is a prerequisite for any toxicology study on smoking, especially an in vitro CS exposure study. In this study, the effects on blood and vascular function were tested with two widely used CS preparations to compare the biological effects of CS with respect to the CS preparation used. CS was prepared in the form of total particulate matter (TPM), which is CS trapped in a Cambridge filter pad, and cigarette smoke extract (CSE), which is CS trapped in phosphate-buffered saline. TPM potentiated platelet reactivity to thrombin and thus increased aggregation at a concentration of $25{\sim}100{\mu}g/mL$, whereas 2.5~10% CSE decreased platelet aggregation by thrombin. Both TPM and CSE inhibited vascular contraction by phenylephrine at $50{\sim}100{\mu}g/mL$ and 10%, respectively. TPM inhibited acetylcholine-induced vasorelaxation at $10{\sim}100{\mu}g/mL$, but CSE exhibited a minimal effect on relaxation at the concentration that affects vasoconstriction. Neither TPM nor CSE induced hemolysis of erythrocytes or influenced plasma coagulation, as assessed by prothrombin time (PT) and activated partial thromboplastin time (aPTT). Taken together, CS affects platelet activity and deteriorates vasomotor functions in vitro. However, the effect on blood and blood vessels may vary depending on the CS preparation. Therefore, the results of experiments conducted with CS preparations should be interpreted with caution.

• 한국연초학회지
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• 제31권1호
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• pp.29-38
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• 2009

Although prion diseases, a group of fatal neurodegenerative diseases of human and animals, are presumed to be caused by several mechanisms including abnormal change of prion protein, oxidative stress is still believed to play a central role in development of the diseases. Cigarette smoking has a few beneficial effects on neuronal diseases such as Alzheimer's disease and Parkinson's disease despite of many detrimental effects. In this study, we investigated how chronic cigarette smoking could exert such beneficial effect against oxidative damage. For this study, homogenates of 87V scrapie-infected brain was inoculated on intracerebral system of IM mice through stereotaxic microinjection and biochemical properties concerning with oxidative stress were examined. The scrapie infection decreased the activity of mitochondrial Mn-containing superoxide dismutase by 50% of the control, meanwhile the effects on other antioxidant enzymes including Cu or Zn-containing superoxide dismutase were not significant. Additionally, the infection elevated superoxide level as well as monoamine oxide-B (MAO-B) in the infected brain. Interestingly, many of the detrimental effects were improved in partial or significantly by long-term cigarette smoke exposure (CSE). CSE not only completely prevented the generation of mitochondrial superoxide but also significantly (p<0.05) decreased the elevated mitochondrial MAO-B activity in the infected brain. Concomitantly, CSE prevented subsequent protein oxidation and lipid peroxidation caused by scrapie infection; however, it did not affect the activities of antioxidant enzymes. These results suggest that chronic exposure of cigarette smoke contribute to in part preventing the progress of neurodegeneration caused by scrapie infection.