• Journal of Environmental Health Sciences
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• v.40 no.6
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• pp.492-501
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• 2014

Objectives: The purpose of this study was to assess the validity of self-reported cigarette smoking status and investigate factors associated with the accuracy self-reported and measured urinary cotinine in Korean adults. Methods: We used data from the $1^{st}$ Korean National Environmental Health Survey (2009-2011) among adults aged ${\geq}19$ years (N=6,246). The survey examined self-reported smoking status, and urinary cotinine was regarded as the biomarker of exposure to tobacco smoke. Urinary cotinine was analyzed using a gas chromatography-mass spectrometry (GC/MS) and data analysis was conducted using IBM SPSS version 20.0, which uses the sample weight and calculates variance estimates to adjust for the unequal probability of selection into the survey. Results: We calculated a cut-off point (53.3 ug/L) by using a ROC (Receiver Operating Characteristic) curve. The smoking prevalence was 24.6% based on self-reported data and 28.2% based on urinary cotinine concentrations. When we assessed the agreement between self-reported and urinary cotinine, we found an average agreement of 97.7% among self-reported smokers and 94.5% among self-reported non-smokers. Among self-reported smokers, factors affected the discrepancy were age, household economic status and average number of cigarettes smoked per day. On the other hand, gender, former smoking experience, and exposure to SHS (second hand smoke) were associated with discrepancies among self-reported non-smokers. Conclusion: These results suggest that self-reported data on smoking status provide a valid estimate of actual smoking status. In future research, we will conduct a continuous monitoring study for reliability verification of the data to reduce potential interpretation errors.

• Molecular & Cellular Toxicology
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• v.2 no.1
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• pp.29-34
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• 2006

Immunoglobulin E (IgE) plays an important role in the development of allergic disorders including asthma. Cigarette smoking was reported to elevate serum IgE level and air pollutants such as $NO_{2}$ have been reported to modulate the immune system including inflammation. Moreover, genetic polymorphisms of glutathione S-transferases (GSTs) were reported to affect inflammatory diseases including asthma. Therefore, in the present study we tried to investigate whether tobacco smoke or $NO_{2}$ exposure increases the level of IgE and the GST gene polymorphisms are associated with change of IgE level due to tobacco smoke or $NO_{2}$ exposure. We measured urinary cotinine, personal $NO_{2}$ exposure, and serum IgE levels in 300 healthy university students without allergic disorders. Allelic loss of the GSTM1 and GSTT1 and the GSTP1 (lle105Val) polymorphism were determined by PCR and RFLP. Total serum IgE levels were significantly different according to urinary cotinine levels (P=0.046), while $NO_{2}$ passive dosimeter level and genetic polymorphisms of three GSTs were not associated with total IgE level. Moreover, subjects with cotinine $500\;{\mu}g/g$ creatinine or more showed the highest level of total IgE when they had null type of GSTM1, null type of GSTT1, or variant type of GSTP1 (P<0.05). When we considered IgE level according to urinary cotinine levels in strata with the combinations of GSTM1, GSTT1, and GSTP1 genetic polymorphisms, the subjects with GSTM1 null, GSTT1 null, and GSTP1 variant types showed the largest difference between IgE levels of subpopulations according to cotinine levels (P=0.030). However, there was no significant difference between IgE levels of subpopulations according to $NO_{2}$ passive dosimeter levels in any group with combinations of GSTM1, GSTT1, and GSTP1 polymorphisms. This result suggests that smoking increases allergic response measured as IgE level and combinations of the GSTM1, GSTT1, and GSTP1 polymorph isms modify the effect of smoking on serum IgE level.

• The Korean Nurse
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• v.36 no.5
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• pp.91-100
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• 1998

This study aims to investigate smoking patterns in high school student and to give student smoker effective information. The sample of 250 male highschool students out of two different schools in Tae-Jon was questioned from July 10th to 15th. 1995. In analyzing these date. the statistics shows the realities by means of number of students. The results are summarized into 17 items as follows. Regarding the level of smoking. 140 students out of 250 admit that they have ever smoked. 52.1% of smoking students say that the motivation of beginning smoking is mainly curiosity. The survey shows that 22.9% of smoking students feel very good when smoking. It also shows that 30.0% of smoking students began smoking in the first grade of high school. With regard to the volume of smoking per day. 41.4% of smoking students smoke variably. 42.1% drink when smoking. 15.0% spend more than W 70.000 a month. About the question who knows the fact of their smoking. 51.5% answer that their friends know the fact of their smoking. In regard to the resaltionship between smoking and school per-formance. 18.2% of non smoking students make poor grades as compared with 40% of smoking students. 9.3% of smoking students say that they are satisfied with the school life. but 35.7% of them are not satisfied. Regarding the attitude to smoking teachers. 35% of smoking students state that they are affected by them. 69.3% of smoking students say that they will stop smoking. while the remaining 30.7% say that they will keep smoking. The reason of 63.9% to stop smoking is that smoking is bad for the health. The reason of 46. 5% to keep smoking is the acquired habit of smoking. 97.2% know the fact that the major element of cigarettes is nicotine and it is very harmful to the health. 40.8% recognize the harmful effect of smoking by TV and radio programs. 97.2% know that smoking could cause lung cancer. From the above results. I propose as follows We should make specific plan to keep smoking by simple curiosity from being developed into habitual smoking. We should teach them how harmful smoking is and make them stop smoking by themselves. It is very essential for family members and teachers to give continuous interest since childhood. As the teacher affect the students very much, they should give up smoking first. The incidence of smoking should be identified in each of the middle and high schools. smoking prohibition programs relevant to each school should be developed and implemented. The local community should ban cigarette vending machines. Cigarettes should not be sold to adolescents. By setting every place where adolescents gather including schools nonsmoking area. we should decrease their impulse to smoke. then smoking opportunities. and harmful effects to them caused by passive smoking.

• Journal of Periodontal and Implant Science
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• v.43 no.5
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• pp.215-220
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• 2013

Purpose: Cigarette smoking is a major risk factor in periodontal diseases. The pathogenesis of periodontal diseases may be affected by alterations of the inflammatory response by smoke. Nitric oxide (NO) is a gaseous, colorless, highly reactive, short-lived free radical with a pivotal role in the regulation of various physiological and pathological mechanisms in the body. It is important in host defense and homeostasis, on the one hand, whereas, on the other hand, it modulates the inflammatory response in periodontitis, leading to harmful effects. The aim of this study was to assess the levels of NO in both the serum and saliva of smokers and nonsmokers having chronic periodontitis and to compare them with periodontally healthy controls. Methods: Sixty subjects participated in the study and were divided into three groups: group I, healthy nonsmoking subjects; group II, nonsmoking patients with chronic periodontitis; group III, smoking patients with chronic periodontitis. Each group consisted of twenty subjects. The biochemical estimation of NO in the collected serum and in the saliva was performed using the Griess colorimetric reaction. Results: The results showed that the mean value of the salivary and serum NO was greater in group II than in group I, and also greater in group III than in group II. Conclusions: NO appears to play an important and rather complex role in the immuno-inflammatory process and in the remodeling and maintenance of osseous structures. It is therefore logical that modulation of this mediator has potential for the treatment of a number of inflammatory conditions including periodontal disease.

• Journal of Preventive Medicine and Public Health
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• v.34 no.3
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• pp.183-190
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• 2001

Objective : To estimate the annual economic costs attributable to cigarette smoking in Korea. Methods : The costs were classified as being direct medical and non-medical costs, indirect costs and others. We focused on those costs related that are incurred in the treatment of selected diseases (cardiovascular diseases, respiratory diseases, and cancers), which have been proven to be caused by smoking. In addition to the basic costs of treatment, the additional amount of costs occurred due to smoking was obtained by computing the population attributable risk (PAR%) caused by smoking. To compute the PAR%, relative risks of smoking to the number of outpatient visits, hospitalizations, and the death were estimated using the Cox proportional hazard model, respectively. Our major data source was the 'Korea Medical Insurance Corporation (KMIC) cohort study,' which was composed of a total of 115,682 male and 67,932 female beneficiaries who had complete records of their smoking histories in the year of 1992. Results : The annual costs that could be attributable to smoking were estimated to be in the range of 2,847,500 million Won to 3,959,100 million Won. The maximum estimate of 3,959,100 million Won includes 233,100 million Won for medical costs, 5,100 million Won for transportation costs, 27,600 million Won for care giver's economic costs, 69,100 million Won in productivity loss, 3,435,000 million Won lost because of premature death, 172,100 million Won in costs resulting from passive smoke inhalation and 17,100 million Won for costs that resulted from fires that were caused by careless smoking. Conclusion : Our study confirms that the magnitude of the economic burden of smoking to Korean society is substantial. Therefore, this study provides strong evidence that there is a strong need for a national policy of tobacco control in Korea.

• Tuberculosis and Respiratory Diseases
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• v.83 no.1
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• pp.1-13
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• 2020

For the past three decades, more than a thousand of genetic studies have been performed to find out the genetic variants responsible for the risk of asthma. Until now, all of the discovered single nucleotide polymorphisms have explained genetic effects less than initially expected. Thus, clarification of environmental factors has been brought up to overcome the 'missing' heritability. The most exciting solution is epigenesis because it intervenes at the junction between the genome and the environment. Epigenesis is an alteration of genetic expression without changes of DNA sequence caused by environmental factors such as nutrients, allergens, cigarette smoke, air pollutants, use of drugs and infectious agents during pre- and post-natal periods and even in adulthood. Three major forms of epigenesis are composed of DNA methylation, histone modifications, and specific microRNA. Recently, several studies have been published on epigenesis in asthma and allergy as a powerful tool for research of genetic heritability in asthma albeit epigenetic changes are at the starting point to obtain the data on specific phenotypes of asthma. In this presentation, we mainly review the potential role of DNA CpG methylation in the risk of asthma and its sub-phenotypes including nonsteroidal anti-inflammatory exacerbated respiratory diseases.

• BMB Reports
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• v.36 no.1
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• pp.95-109
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• 2003

Inflammatory lung diseases are characterized by chronic inflammation and oxidant/antioxidant imbalance. The sources of the increased oxidative stress in patients with chronic inflammatory lung diseases such as asthma and chronic obstructive pulmonary disease (COPD) derive from the increased burden of inhaled oxidants, and from the increased amounts of reactive oxygen species (ROS) generated by several inflammatory, immune and various structural cells of the airways. Increased levels of ROS produced in the airways is reflected by increased markers of oxidative stress in the airspaces, sputum, breath, lungs and blood in patients with lung diseases. ROS, either directly or via the formation of lipid peroxidation products such as 4-hydroxy-2-nonenal may play a role in enhancing the inflammation through the activation of stress kinases (JNK, MAPK, p38) and redox sensitive transcription factors such as NF-${\kappa}B$ and AP-1. Recent evidences have indicated that oxidative stress and pro-inflammatory mediators can alter nuclear histone acetylation/deacetylation allowing access for transcription factor DNA binding leading to enhanced pro-inflammatory gene expression in various lung cells. Understanding of the mechanisms of redox signaling, NF-${\kappa}B$/AP-1 regulation, the balance between histone acetylation and deacetylation and the release and expression of pro- and anti-inflammatory mediators may lead to the development of novel therapies based on the pharmacological manipulation of antioxidants in lung inflammation and injury. Antioxidants that have effective wide spectrum activity and good bioavailability, thiols or molecules which have dual antioxidant and anti-inflammatory activity, may be potential therapeutic agents which not only protect against the direct injurious effects of oxidants, but may fundamentally alter the underlying inflammatory processes which play an important role in the pathogenesis of chronic inflammatory lung diseases.

• Journal of the Korean Society of Tobacco Science
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• v.13 no.1
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• pp.19-26
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• 1991

Ames test using special strains which are histidine requiring mutant of Salmonella typhimufium , is widely utilized as short-term bioassay to evaluate the genotoxicity of chemicals. This method requires the liver microsome(5-9 fraction) to provide mammalian metabolism of the compounds, Therefore, the mutagenic potency of the chemicals is affected by not only the intrinsic properties of them but also the efficiency of the in vitro microsomal activation system. For this reason, the complex mixtures such as environmental pollutants from occupational sources, natural products or cigarette smoke condensates(CSC) , might be often appeared the false results. Induction of sister chromatid exchange(SCE) in cultured cells is known as another sensitive and powerful tool for the measurement of genotoxicity and the method has also an advantage which is able to apply to the in vitro and in vivo systems. In the present study, the inducibilities of revertant colonies in tester strain TA98 and SCE in human Iymphocytes by positive controls and total particulated materials(TPM) obtained from various brand(domastic and imported) cigarettes were compared in order to investigate whether the results in Ames test are in agreement with those in SCE analysis. The mutagenic activities of well known mutagens such as B(a)P showed excellent dose-response in the both methods although the induction mechanism was different each other, but cyclophosphamide resulted such effect only in SCE analysis. Most TPM tested showed a similar pattern in the mutagenic activities in those methods. However, only two(one imported brand and one domestic sample cigarettes) among the TMP obtained from various cigarettes appeared the higher induction in SCE than Ames test.

• Journal of Microbiology and Biotechnology
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• v.28 no.3
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• pp.425-431
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• 2018

Benzo[a]pyrene (B[a]P), a polycyclic aromatic hydrocarbon, is a principal component of cigarette smoke. B[a]P can cause lung carcinogenesis and plays a key role in lung cancer progression. The role of B[a]P has been reported in lung cancer, but its effects on lung cancer stem cells (CSCs) have not been investigated. Emerging evidence indicates that CSCs are associated with carcinogenesis, tumor initiation, relapse, and metastasis. Therefore, targeting CSCs to defeat cancer is a challenging issue in the clinic. This study explored whether B[a]P alters gene expression in lung cancer cells and CSCs. The lung adenocarcinoma A549 cell line was used to investigate the role of B[a]P on lung cancer cells and lung CSCs using microarray and quantitative PCR. B[a]P ($1{\mu}M$) provoked gene expression changes in A549 cancer cells and CSCs by deregulating numerous genes. Gene pathway analysis was performed using GeneMANIA and GIANT. We identified genes that were coexpressed and showed physical interactions. These findings improve our understanding of the mechanism of B[a]P in lung cancer and cancer stem cells and can be an attractive therapeutic target.

• Journal of environmental and Sanitary engineering
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• v.14 no.4
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• pp.85-92
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• 1999

Indoor air quality tends to be the dominant contributor to personal exposure because most people spend over 90% of their time indoors. For some contaminants, exposure to indoor air poses a potentially greater health threat than outdoor air exposures. Indoor nitrogen dioxide ($NO_2$) levels are mainly affected gas range, flue gas spillage, kerosene heaters, wood-burning appliances and cigarette smoke. In addition, indoor $NO_2$ levels are influenced by such house characterization as surface reaction and air exchange rate. In this study, the measurements of indoor and outdoor $NO_2$ concentrations were taken using identical protocols, and information was collected on housing characteristics using identical questionnaires in 14 houses out of 15 houses for daily 30 daily 30 days in Brisbane, Australia.The usage of gas range was the most contributing factor in indoor $NO_2$ concentration in relation to house characteristics. Average indoor and outdoor ratios of NO2 concentration in electronic and gas cooking houses were $0.6{\pm}0.1$ and $0.9{\pm}0.2$, respectively. The frequency distributions of $NO_2$ concentration in each house were approximately log-normal Geometric mean of indoor $NO_2$ concentrations of electronic and gas cooking houses for daily 30 days ranged from 2.5 ppm to 11.5 ppm with a mean 6.8 and from 4.7 ppm to 28.6 ppm with a mean 15.6 ppm, respectively. The $NO_2$ concentrations between electronic and gas cooking houses were significantly different (p<0.05). Since each house has different life-style and house characteristics, sampling interval to measure the $NO_2$ levels was recommended above 7 days.