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.
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.
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.
Purpose : This study are the secondary data of Global Youth Tobacco Survey(GYTS) developed by the WHO and United State Center for Disease Control(CDC) and Prevention to trace tobacco use among youth in youth in countries across the world. This study was carried out to serve for a basis for antismoking campaigns and to prevent adolescents from smoking by analyzing the smoking by analyzing the smoking realities factors. Methods : This study is a cross-sectional school-based survey, which employed a two-stage cluster sample design to produce a nationally representative sample of middle school students aged 13 to 15 years olds. Seventy-five schools were selected. All schools containing grade 1, 2 and 3 that contained 40 or students were included in the sampling frame. Results : The results of this study were as follows ; 1. The proportion of smoking students in middle school was 6.4% and the rate of smoking in male students(7.4%) was higher than it of in female students(5.5%). 2. 26.5% of all respondent had a experience to try smoke and the results showed that the rate of trying smoking in male students was increased by grade more than female students. 3. According to test of significance in regression analysis, the independent variables such as sex, school grade, smoking parents, friends distinction, pocket money and others showed statistical significance. 4. There was a statistical significance between smokers and nonsmokers in proportion to the completing the preventive education for nonsmoking(p=0.0023) and the acquirement of knowledge on smoking(p<.0001). 5. Finally there was a statistical significance between the exposure to anti-smoking campaign(p=0.0053) and tobacco advertisement in the mass media and the smoking(p=0.0036). Conclusion : All things considered, the health education for tobacco control in school need to be developed from an elementary school. I suggest that prevent smoking program in school need to be revitalized and be made more accessible for everyone who wish to quit. And the government should develop the regulation on total banning promoting cigarette advertising and smoking scene in the movie for young people.
Oxidative stress by reactive oxygen species (ROS) damages cellular DNA, RNA, proteins, lipids and others causing various diseases such as cancer, arthritis, and heart diseases. 8-Hydroxyguanine (8-OHG) is one of the products formed from DNA or RNA damaged by ROS. Since high amounts of 8-OHG can be excreted in urine, it may serve as a potential biomarker indicating the level of oxidative damage to nucleic acids. Residents in industrial area with severe air pollution are expected to be affected by higher level of oxidative stress from pollutants like polyaromatic hydrocarbons (PAHs), etc. Smokers are also expected to be damaged by higher level of oxidative stress from cigarette smoke components like PAHs than non-smokers. To examine if the determination of the urinary concentration of 8-OHG could be used as exposure biomarker for the oxidative stress caused by air-pollutants, this study was performed to determine and compare the urinary concentrations of 8-OHG in smokers and non-smokers, or non-polluted area residents and polluted area residents. Urine samples were collected and purified by a strong cation exchange and cellulose partition column, then analyzed by HPLC with electrochemical detector at 600 ㎷ potential. Concentrations of urinary 8-OHG in non-smokers and smokers of Seoul area college male students were determined as 15.12$\pm$9.68 (ng/mg creatinine) and 34.72$\pm$11.72 (ng/mg creatinine), respectively, showing significantly higher level of 8-OHG in smokers than in non-smokers. Urine samples of elementary school students were collected from Sokcho area, which is known to be non-polluted, and 3 representative polluted areas; Yocheon industrial area, Ulsan urban and Ulsan industrial area. The concentrations of 8-OHG in these samples were 12.42$\pm$8.27 (ng/ mg creatinine, Sokcho), 22.55$\pm$9.12 (ng/mg creatinine, Yocheon), 17.41$\pm$2.30 (ng/mg creatinine, Ulsan urban), 55.04$\pm$39.73 (ng/mg creatinine, Ulsan industrial). Thus, samples from polluted area tend to have higher level of 8-OHG and the levels of Yocheon and Ulsan industrial area were significantly higher than that of Sokcho area. The results indicate that the residents of polluted industrial area or smokers are more severely exposed to oxidative stress probably caused by air pollutants like PAHs. Thus, the determination of urinary 8-OHG concentration could be used as biomarker for the extent of body exposure to oxidative stress caused by various pollutants.
Background : With the increase of cigarette consumption by women and the young, the incidence of lung cancer is expected to increase during the next three or four decades in Korea. The purpose of this study was to analyze the smoking habits in patients with lung cancer and to identify the gender differences in terms of their susceptibility to cigarette related carcinogens. Method : This investigation was a hospital-based case control study, which included the data of 178 case subjects (72 females, 106 males) with lung cancer and 218 control subjects (97 females, 121 males) with diseases unrelated to smoking. The information was obtained through a direct personal interview and a questionnaire related to personal smoking history. Results : The relative frequency of the squamous cell carcinoma was substantially higher in males than in females (61.3% in males, and 29.2% in females), while adenocarcinoma including bronchoalveolar cell carcinoma was higher in females(31.9% in females, 18.9% in males). Kreyberg I lung cancer was of relatively higher frequencies in males and smokers, while Kreyberg II lung cancer was higher in females and never smokers. The odds ratios (ORs) at each exposure level were consistently higher in females than males. For all cell types, the risk of lung cancer was increased with the quantity of smoked cigarettes, duration of smoking, and depth of inhalation. Odds ratio was distinctly higher in Kreyberg I lung cancer than in total lung cancer and a steeper gradient of risk with increased smoking was observed in females. Conclusion : The relative risk for lung cancer was consistently higher in females than in males at every level of exposure to cigarette smoke. This is believed to be due to the higher susceptibility of females to tobacco carcinogens, such as gender associated differences of carcinogen activation and/or the elimination of smoking related metabolites.
This study has done to investigate the relationship between the icreased lipid oncentration caused by smoking and plama levels of vitamin A and vitamin E, antiodative enzyme activity, and lipid peroxidation , in 52 male smokers and 32 non-smokers, Dietary vitamin A and vitamin E intake was imilar in both smokers and non-smokers. Absolute plasma concentrations of vitamin A and vitamin E were not significantly different between two groups, whereas vitamin E/cholesterol ration in plasma was low or in smokers than in that of non-smokers(p<0.05). It was considered that this lowered effect was due to the elevated plasma lipid concentration rather than oxidant stress derived from smoking, in view of the fact that smokers had higher cholesterol (15.2%) adn LDL-C(26.6%) levels than non-smokers. In non-smokers, plasma thiobarbiturin acid reactive substances(TBARS) conrrelated positively with total cholesterol(r=0.63466, p<0.001), LDL-C level(r=0.57166, p<0.01) , and LDL-C/HDL-C ratio(r=0.45926, p<0.05) . Activities of glutathione perosidase(GSH-Px) , superoside dismutase(SOD), and catalse made no difference in both groups. However, it was observed in non-smokers that GSH-Px activity had negative correlations with total cholesterol(r=-0.67293, p<0.001), LDL-C level(r=-0.62878, p<0.001), and LDL-C/HDL-C ratio (r=-0.58824, p<0.01), indicating that there was a dependent relationship between lipid perosidation and plasma lipid level. The smokers also showed negative correlations for GSH-Px activity with total cholesterol (r=-0.29946, p<0.05) and LDL-c level (r=0.45914, p<0.001), and LDL-C/HDL-c ratio(r=-0.35438, p<0.05). It seemed that the lipid that the lipid level elevated by sustaines smoking resulted in reducing vitamin E/cholesterol ratio and proportion of antioxidant to oxidant load, and then GSH-Px activity, with insufficient removal of free radicals(TBARS 2.43$\pm$0.51 and 1.81$\pm$0.15nmol/ml in smokers and non-smokers, respectively). These findings suggest that higher plasma lipid levels may play a more important role in perturbing the antioxidant defense system including vitamin E status and GSH-Px activity, at least in circumstances that increase lipid concentration . In addition, in exposure to free radicals like those in cigarette smoke. In those cases the ratio of vitamin E/lipid in plasma can be a more indicator of vitamin E status than plasma levels of vitamin E alone.
Journal of the Korean Association of Oral and Maxillofacial Surgeons
/
v.34
no.5
/
pp.509-517
/
2008
DNA damage accumulates in cells as a result of exposure to exogenous agents such as benzopyrene, cigarette smoke, ultraviolet light, X-ray, and endogenous chemicals including reactive oxygen species produced from normal metabolic byproducts. DNA damage can also occur during aberrant DNA processing reactions such as DNA replication, recombination, and repair. The major of DNA damage affects the primary structure of the double helix; that is, the bases are chemically modified. These modification can disrupt the molecules'regular helical structure by introducing non-native chemical bonds or bulky adducts that do not fit in the standard double helix. DNA repair genes and proteins scan the global genome to detect and remove DNA damage and damage to single nucleotides. Direct reversal of DNA damage, base excision repair, double strand break. DNA repair are known relevant DNA repair mechanisms. Four different mechanisms are distinguished within excision repair: direct reversal, base excision repair, nucleotide excision repair, and mismatch repair. Genetic variation in DNA repair genes can modulate DNA repair capacity and alter cancer risk. The instability of a cell to properly regulate its proliferation in the presence of DNA damage increase risk of gene mutation and carcinogenesis. This article aimed to review mechanism of excision repair and to understand the relationship between genetic variation of excision repair genes and head and neck cancer.
Journal of the Korean Applied Science and Technology
/
v.31
no.1
/
pp.120-129
/
2014
The structure and physiological function of human skin continuously weaken due to growing older. The reasons of aging from external conditions are long term exposure to sun, wind, heat, cigarette smoke, and etc. This also palmitoyl oligopeptide or ceramide oligopeptide are known asc ingredient stimulating collagens and have the effect of reproducing the upper level of skin. Acetyl hexapeptide is an ingredient that makes the skin and muscle suppler and reduces wrinkles. It is a major high function beauty ingredient that substitutes botox. After dividing 7%, 14%, and 20% Acetyl hexapeptide experimental groups as groups A, B, and C the control group and experiment groups' change of wrinkles, hair follicles, moisture content, and dead skin cells was analyzed. According to the results, Acetyl hexapeptide seems to affect wrinkles, hair follicles and moisture content contrasting to the control group. Experimental groups and control group showed similar change in dead skin cells. In contrast to the control group satisfaction of examines was affected in wrinkles, hair follicles and moisture but removing dead skin cells had similar result in experimental groups and control group.
Acrolein is a highly toxic, reactive mutagenic aldehyde. Humans are exposed to acrolein vapors from overheated cooking oil, cigarette smoke, and combustion of organic products. In this study, we investigated elementary and middle school students' consumption of foods cooked at high heat, such as fried, direct fire, and indirect fire cooked foods. The subjects of this survey study were 265 fifth grade students and 396 middle school students nationwide. According to the results of the frequency test, broiled fish was the most frequently consumed, followed by fried fish, indirect cooked samgyebsal, and other fried foods, which were eaten more than three times per month. The total intake of foods cooked at high heat per child over 1 year was in the following order: Fried chicken(7.50 kg) > Samgeybsal(6.57 kg) > Broiled pork ribs(4.18 kg) > Broiled fish(4.12 kg) > Bulgogi(3.31 kg) > Fried dish(3.18 kg) > Pork cuttlet(3.17 kg) > Jeyukbockeum(3.13 kg) > Charcoal-broiled beef ribs(2.74 kg) > Roasted whole chicken(2.05 kg) > Dackochi(1.87 kg) > Tangsuyuk(1.87 kg) > Fried fish(1.83 kg) > Hamburger patties(1.21 kg) > Fried potato(1.01 kg) > Barbecue(0.95 kg) > Doughnut(0.80 kg) > Corn dog(0.66 kg) > Croquette(0.51 kg). The favorite cooking method was indirect fire cooking for beef, pork, and fish, whereas frying was preferred for chicken. The results of this study provide important data for assessment of acrolein exposure via foods cooked at high heat temperature. The results also indicate that children might be exposed to acrolein through consumption of foods cooked at high heat temperature, suggesting the need to promote education of proper food consumption behavior.
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