• Journal of Environmental Health Sciences
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• v.36 no.2
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• pp.77-81
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• 2010

Tobacco smoking and secondhand smoke exposure are linked to a number of adverse health outcomes. There is a new concept of thirdhand smoke that is residual tobacco smoke contamination remained after the cigarette is extinguished. This paper reviews published studies examining the residual tobacco smoke. Tobacco smoke can be attached to various surfaces and reemitted to air for long period of time. The dynamic process can allow thirdhand smoke exposure to tobacco smoke without direct exposure to secondhand smoke. One critical evidence of the thirdhand smoke exposure was significantly high urinary cotinine level of infant who did not have direct secondhand smoke exposure. Potential exposure to new and more potent chemicals generated from chemical reactions between residual tobacco smoke and ambient air pollutants can get more attention. Considering toxicity and exposure route, children are uniquely susceptible to thirdhand smoke exposure. The review provides strong background information for thirdhand smoke but warrant more researches on this issue.

• Journal of the Korean Society of Tobacco Science
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• v.18 no.2
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• pp.160-169
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• 1996

Effect of cigarette smoke exposure on 1-methyl-4-phpnyl-1,2,3,6-tetrahydro-pyidine (Mm)-induced neurotoxicity was investigated in C57BL6 mice. Cigarette smoke exposure of mice to the mainstream smoke generated from 15 cigarettes for 10 mins per day, 5 days per week, for fi weeks, effectively attenuated the decline both in the level of striatal dopamine and the number of brrosine hydros:ylase-positive ceils in the brain caused by MPTP treahent. Exposure to cigarette smoke significantly decreased monoamine oxidate B activity in the cerebral cortex and cerebellum. The activity of brain antioxidant enzymes such as catalase, glutathione peroxidase, and Cu, Zn-superoxide dismutase, was not changed by cigarette smoke exposure or MPTP treatment. Sulfhydryl compounds content in all brain regions except for the striatum was uniquely increased by MPTP treatment, however, such an effect of MPTP was not observed in mice exposed to cigarette smoke. These results suggest that cigarette smoke exposure inhibits MPTP-induced neurotoxicity without influencing free radical metabolism in the brain of mice. This protective effect of cigarette smoke seems to be closely related with the decreased activity of brain monoamine oxidase H. Key words : cigarette smoke exposure, dopamine, monoamine oxidase B, antioxidant enzywles, MPTP.

• Korean Journal of Child Studies
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• v.26 no.4
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• pp.101-112
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• 2005

Subjects were 279 parents of 4- and 5-year-old day care children. Statistical techniques were factor analysis, t-test, ANOVA, Pearson's correlation, and multiple regression. Major findings were that parents with higher levels of education and income showed a higher level of attitudes and coping behavior toward preschoolers' exposure to secondhand smoke. Parents who were smokers had a higher level than non-smokers of knowledge and coping with preschoolers' secondhand smoke. Parents with higher levels of knowledge and more negative attitudes about secondhand smoke were more active in dealing with secondhand smoke. Parents' knowledge and attitudes were significant predictors of their coping behavior with preschoolers' secondhand smoke. Parents' knowledge was more predictive of parents' coping behavior than their attitudes.

• Journal of the Korean Society of Tobacco Science
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• v.36 no.1
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• pp.20-25
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• 2014

As part of a balanced testing battery, subchronic inhalation studies on rats are performed to ensure that proposed cigarette modifications do not increase the toxicity of smoke and to demonstrate any instances where a modification may actually contribute to harm reduction. For subchronic inhalation studies with aerosols, the OECD suggests an exposure regimen of 6 hours/day (OECD Guideline 413, 1981), but alternative regimens have also been published: 1 hour/day and $2{\times}1$ hour/day. The aim of this study was to validate a rodent nose-only exposure system for the assessment of inhalation toxicity of cigarette smoke. In this study, cigarette smoke exposure system is consisted of cigarette smoke generator, smoke concentration adjusting system, and 20-port nose-only exposure system. Male SD rats were exposed for 35 days ($2{\times}1$ hour/day) to 3R4F Reference cigarette smoke and analysed major monitoring items of OECD Gudeline 413. WTPM, was measured in the test atmosphere, respiratory function (Buxco Biosystems) during exposure, postexposure urinary exposure biomarkers and alveolar neutrophiles in BAL fluid (Day 35) were evaluated. Validation demonstrated steady WTPM ($257{\pm}20ug/L$, $502{\pm}27ug/L$) and spatial uniformity (<10%). Nose port temperature ($22{\sim}26^{\circ}C$ and RH (45~75%) were acceptable over 35 days. Reductions in respiratory rate and minute volume and increase in the neutrophiles in BALF and the urinary exposure biomarkers were observed cigarette smoke dose dependently. This validation and 35-day inhalation study has shown that the rodent nose-only exposure system may be useful in the inhalation toxicity assessment of cigarette smoke.

• Journal of Yeungnam Medical Science
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• v.28 no.1
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• pp.45-53
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• 2011

Background: Increasing numbers of young people go to clubs. In Korea, however, no studies have been conducted regarding the exposure of club patrons to secondhand smoke. The present study was conducted to evaluate the degree of club customers' exposure to secondhand smoke. Methods: The study subjects included 10 male and 12 female non-smokers. The investigational site was a club located in Daegu. Urine samples were collected before exposure to secondhand smoke in the club and 6 hours after a 3-hour exposure. The urine cotinine levels were measured via the LC -MS/MS method. A survey was conducted to collect data regarding the subjects' smoking experiences and the degree of exposure to secondhand smoke in their daily lives. Results: The average urine cotinine level increased from 1.09 ${\mu}g/L$ to 5.55 ${\mu}g/L$ ($p$<0.05). No significant difference existed in the change in urine cotinine level between the male and female subjects. In addition, there was no significant difference in the change in urine cotinine level by the degree of exposure to secondhand smoke in daily life. Conclusions: The average urine cotinine level in all the subjects significantly increased after exposure to secondhand smoke. This is the first study on exposure to secondhand smoke in clubs; these results can be used to craft measures that reduce exposure to secondhand smoke in public places, such as clubs.

• Environmental Analysis Health and Toxicology
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• v.19 no.2
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• pp.169-176
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• 2004

ETS (environmental tobacco smoke) is composed of exhaled mainstream smoke (MS) from the smoker, sidestream smoke (SS) emitted from the smoldering tobacco between puffs and contaminants that diffuse through the cigarette paper and mouth between puffs. These emissions contain both vapor phase and particulate contaminants. ETS is a complex mix of over 4,000 compounds. This mix contains many known or suspected human carcinogens and other toxic agents. More of these toxic compounds are found in SS than in MS. Workplace exposure to ETS can result in significant smoke intake, and passive smoke exposure may be related to impair respiratory function and an increase risk of lung cancer in nonsmokers. For nonsmokers sharing a work environment with cigarette smokers, the workplace must be considered hazardous independently of any specific industrial toxic exposure. The risk is particularly important when a high percentage of the workers smoke or where smokers and nonsmokers work in poorly ventilated areas. Nicotine is converted in the body to cotinine; cotinine therefore can be used as an indirect measure of a person's recent exposure to tobacco smoke. Levels of nicotine in hair and levels of cotinine in body fluids (saliva and urine) have been shown to increase with increasing environmental nicotine levels and with self-reported ETS exposure. The measurement of nicotine or cotinine in hair may be more appropriate for longer-term exposure to tobacco. The purpose of this study is to comparing airborne nicotine levels and hair cotinine level in restaurant workers. Concentration of airborne nicotine and hair nicotine (and cotinine) is closely related to exposed frequency of sidestream smoke in the workplace. Nicotine in hair is a better predictor of airborne nicotine than hair cotinine. Hair nicotine can be a useful tool to assess ETS exposure interventions. It may have limiting levels of ETS exposure by placing regulatory restrictions on smoking in workplaces and in public spaces.

• Journal of the Korean Society of Tobacco Science
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• v.20 no.1
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• pp.99-107
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• 1998

Numerous studies have demonstrated a negative association between cigarette smoking and Parkinson's disease. The present study was undertaken to investigate whether chronic exposure of mice to cigarette smoke a(footed the metabolism of 1-methyl-1113,6-tetrahydro-pyridine (MPTP) by cytochrome P4SO (P-450) or flavin-containing monooxygenase (FMO) in the hepatic microsomes of C57BL6/J mice. Adult male C57BL6/J mice were exposed to mainstream smoke generated from 15 cigarettes for 10 min a day and 5 day per week for 6 weeks. MPTP (10 mg/kg body weight) was administered to mice by subcutaneous injection for 6 consecutive days. Microsolnal P-450 content was increased by MPTP, smoke exposure, or both, but NADPH cytochrome P-450 reductase activity was rather decreased by the same treatments. The activities of benzo(a)pyrene hydroxylase, 7-ethoxycoumarin O-deethylase and ethoxyresorufin O-deethylase were significantly increased by the exposure of cigarette smoke, but were not or little affected by MPTP treatment. Benzphetamine N-demethylase activity was not affected either by MPTP treatment or by cigarette smoke exposure, but it was significantly increased by the combined MPTP treatment with cigarette smoke exposure, showing their synergic effect for the induction of the enzyme activity. Interestingly, in vitro studies of hepatic FMO and P-450 system both O-oxygenation and N-demethylation of MPTP were increased in the smoke-exposed or in the MPTP-treated mice. These results suggest that the enhancement in the N-demethylation as well as O-deethylation of P-450 system and in the N-oxygenation of FMO activity by cigarette smoke exposure in mouse liver may contribute to attenuating the neurotoxic effects of MPTP on the nigrostriatal dopaminergic neurons.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.17
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• pp.7407-7411
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• 2014

The incidence of urban female breast cancer has been continuously increasing over the past decade with unknown etiology. One hypothesis for this increase is carcinogen exposure from tobacco. Therefore, the objective of this study was to investigate the risk of urban female breast cancer from tobacco smoke exposure. The matched case control study was conducted among Thai females, aged 17-76 years and living in Bangkok or its surrounding areas. A total of 444 pairs of cases and controls were recruited from the Thai National Cancer Institute. Cases were newly diagnosed and histologically confirmed as breast cancer while controls were selected from healthy women who visited a patient, matched by age ${\pm}5$ years. After obtaining informed consent, tobacco smoke exposure data and information on other potential risk factors were collected by interview. The analysis was performed by conditional logistic regression, and presented with odds ratio (ORs) and 95% confidence intervals(CI). From all subjects, 3.8% of cases and 3.4% of controls were active smokers while 11.0% of cases and 6.1% of controls were passive smokers. The highest to lowest sources of passive tobacco smoke were from spouses (40.8%), the workplace (36.8%) and public areas (26.3%), respectively. After adjusting for other potential risk factors or confounders, females with frequent low-dose passive smoke exposure (${\leq}7$ hours per week) from a spouse or workplace had adjusted odds ratio 3.77 (95%CI=1.11-12.82) and 4.02 (95%CI=1.04-15.50) higher risk of breast cancer compared with non-smokers, respectively. However, this study did not find any association of breast cancer risk in high dose passive tobacco smoke exposure, or a dose response relationship in cumulative passive tobacco smoke exposure per week, or in the active smoker group. In conclusion, passive smoke exposure may be one important risk factor of urban female breast cancer, particularly, from a spouse or workplace. This risk factor highlights the importance of avoiding tobacco smoke exposure as a key measure for breast cancer prevention and control.

• Clinical and Experimental Pediatrics
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• v.55 no.2
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• pp.35-41
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• 2012

Passive exposure to tobacco smoke significantly contributes to morbidity and mortality in children. Children, in particular, seem to be the most susceptible population to the harmful effects of environmental tobacco smoke (ETS). Paternal smoking inside the home leads to significant maternal and fetal exposure to ETS and may subsequently affect fetal health. ETS has been associated with adverse effects on pediatric health, including preterm birth, intrauterine growth retardation, perinatal mortality, respiratory illness, neurobehavioral problems, and decreased performance in school. A valid estimation of the risks associated with tobacco exposure depends on accurate measurement. Nicotine and its major metabolite, cotinine, are commonly used as smoking biomarkers, and their levels can be determined in various biological specimens such as blood, saliva, and urine. Recently, hair analysis was found to be a convenient, noninvasive technique for detecting the presence of nicotine exposure. Because nicotine/cotinine accumulates in hair during hair growth, it is a unique measure of longterm, cumulative exposure to tobacco smoke. Although smoking ban policies result in considerable reductions in ETS exposure, children are still exposed significantly to tobacco smoke not only in their homes but also in schools, restaurants, child-care settings, cars, buses, and other public places. Therefore, more effective strategies and public policies to protect preschool children from ETS should be consolidated.

• Toxicological Research
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• v.22 no.3
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• pp.245-251
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• 2006

Nitric oxide(nitrogen monoxide, NO) plays important physiological roles, but excessive generation can be toxic. NO is present in cigarette smoke at up to 1,000 ppm, and probably represents one of the greatest exogenous sources of NO to which humans are exposed. We investigated whether cigarette smoking reduces the production of endogenous NO and whether it influences the action of lipopolysaccharide(LPS) to induce nitric oxide synthase activity in mouse brain. Mice(C57BL6/J) were exposed to cigarette smoke for 8 weeks. LPS was injected intraperitoneally in single or combination with the exposure to cigarette smoke. Six hours after the injection of LPS, mice were sacrificed and sera and brains were collected. Serum concentrations of nitrate and nitrite were not charged by 4-week smoke exposure, but were significantly increased by 6 and 8 weeks of smoke exposure. Interestingly, cigarette smoke reduced the elevation in serum nitrate and nitrite concentrations produced by LPS after 4-week smoking exposure. NO synthase(NOS) activity in brain was upregulated by LPS-administration. However, cigarette smoke exposure remarkably and consistently decreased the LPS-induced activity in mouse brain. This result suggests that cigarette smoking may affect against overproduction of the endogenous NO by LPS through the inhibition of NOS activity induced by LPS in brain or by modulation of the LPS action for the induction of NOS activity. We also suggest the possibility that the exogenous NO evolved in cigarette smoke enables feedback inhibition of NOS activity or other possibility that it attenuates the toxicity of endotoxin LPS in vivo by unknown mechanisms, which should be further studied.