No abstract available.
Tobacco Smoke Pollution*

No abstract available.
Tobacco Smoke Pollution

No abstract available.
Tobacco Smoke Pollution

No abstract available.
Tobacco Smoke Pollution

BACKGROUND: Cotinine, a nicotine metabolite detected in urine, has been recommended as the best quantitative marker of smoking and environmental tobacco smoke (ETS) exposure. The aim of this study was to analyze the relationship between indoor ETS and urinary cotinine level of the passive smokers. METHODS: We selected 42 nonsmokers who lived in Seoul and were not exposed to passive smoking at least 5 days before test. Urinary cotinine levels were measured by Smokescreen Colorimeter (Surescreen Diagnostics LTD, U.K.). We measured urinary cotinine levels twice (before and after smoking exposure). RESULTS: The mean urinary cotinine level was 0.33microgram/mL before smoking exposure, and 0.46microgram/mL after smoking exposure. There was statistically significant difference (P-value=0.003). There was no significant difference between exposure time and increase of urinary cotinine level(P=0.138, r=-0.233). There was also no significant difference between measuring time taking after exposure and increase of urinary cotinine level (P=0.671, r=0.067). CONCLUSION: One experience of indoor exposure to ETS caused significant elevation of urinary cotinine level.
Cotinine ; Nicotine ; Seoul ; Smoke ; Smoking ; Tobacco ; Tobacco Smoke Pollution

Many studies have linked cigarette smoke (CS) exposure and tuberculosis (TB) infection and disease although much fewer have studied second-hand smoke (SHS) exposure. Our goal is to review the epidemiologic link between SHS and TB as well as to summarize the effects SHS and direct CS on various immune cells relevant for TB. PubMed searches were performed using the key words “tuberculosis” with “cigarette,”“tobacco,” or “second-hand smoke.” The bibliography of relevant papers were examined for additional relevant publications. Relatively few studies associate SHS exposure with TB infection and active disease. Both SHS and direct CS can alter various components of host immunity resulting in increased vulnerability to TB. While the epidemiologic link of these 2 health maladies is robust, more definitive, mechanistic studies are required to prove that SHS and direct CS actually cause increased susceptibility to TB.
Mycobacterium tuberculosis ; Smoke* ; Smoking ; Tobacco Products ; Tobacco Smoke Pollution ; Tuberculosis*

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 microg/L to 5.55 microg/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.
Cotinine ; Female ; Humans ; Korea ; Male ; Smoke ; Smoking ; Tobacco Smoke Pollution

No abstract available.
Asthma* ; Child* ; Humans ; Lung* ; Tobacco Smoke Pollution*

No abstract available.
Asthma* ; Child* ; Humans ; Lung* ; Tobacco Smoke Pollution*

Acute eosinophilic pneumonia (AEP) is characterized by eosinophilic infiltration in the lungs, respiratory distress, a rapid therapeutic response to corticosteroids, and the absence of relapse. Some cases of AEP are caused by infections, drugs, and inhaled antigens. Cigarette smoking is considered a probable cause of AEP, as AEP has developed soon after starting to smoke in some patients and a challenge with cigarette smoking was positive in some patients. All reported patients with cigarette smoking.induced AEP were active smokers, while no case of AEP caused by passive smoking has been reported. We present a case of AEP presumed to have been caused by passive cigarette smoking.
Adrenal Cortex Hormones ; Eosinophils ; Humans ; Lung ; Pulmonary Eosinophilia ; Recurrence ; Smoke ; Smoking ; Tobacco Products ; Tobacco Smoke Pollution