• KDI Journal of Economic Policy
• /
• v.31 no.2
• /
• pp.127-153
• /
• 2009

There is a growing concern about potential harmful effect of second-hand or environmental tobacco smoking. As a result, smoking bans in workplace become more prevalent worldwide. In Korea, workplace smoking ban policy become more restrictive in 2003 when National health enhancing law was amended. The new law requires all office buildings larger than 3,000 square meters (multi-purpose buildings larger than 2,000 square meters) should be smoke free. Therefore, a lot of indoor office became non smoking area. Previous studies in other counties often found contradicting answers for the effects of workplace smoking ban on smoking behavior. In addition, there was no study in Korea yet that examines the causal impacts of smoking ban on smoking behavior. The situation in Korea might be different from other countries. Using 2001 and 2005 Korea National Health and Nutrition surveys which are representative for population in Korea we try to examine the impacts of law change on current smoker and cigarettes smoked per day. The amended law impacted the whole country at the same time and there was a declining trend in smoking rate even before the legislation update. So, the challenge here is to tease out the true impact only. We compare indoor working occupations which are constrained by the law change with outdoor working occupations which are less impacted. Since the data has been collected before (2001) and after (2005) the law change for treated (indoor working occupations) and control (outdoor working occupations) groups we will use difference in difference method. We restrict our sample to working age (between 20 and 65) since these are the relevant population by the workplace smoking ban policy. We also restrict the sample to indoor occupations (executive or administrative and administrative support) and outdoor occupations (sales and low skilled worker) after dropping unemployed and someone working for military since it is not clear whether these occupations are treated group or control group. This classification was supported when we examined the answers for workplace smoking ban policy existing only in 2005 survey. Sixty eight percent of indoor occupations reported having an office smoking ban policy compared to forty percent of outdoor occupation answering workplace smoking ban policy. The estimated impacts on current smoker are 4.1 percentage point decline and cigarettes per day show statistically significant decline of 2.5 cigarettes per day. Taking into account consumption of average sixteen cigarettes per day among smokers it is sixteen percent decline in smoking rate which is substantial. We tested robustness using the same sample across two surveys and also using tobit model. Our results are robust against both concerns. It is possible that our measure of treated and control group have measurement error which will lead to attenuation bias. However, we are finding statistically significant impacts which might be a lower bound of the true estimates. The magnitude of our finding is not much different from previous finding of significant impacts. For cigarettes per day previous estimates varied from 1.37 to 3.9 and for current smoker it showed between 1%p and 7.8%p.

• Analytical Science and Technology
• /
• v.16 no.4
• /
• pp.299-308
• /
• 2003

The purpose of this study is to investigate cadmium concentrations among metals in ETS (Environmental Tobacco Smoke) of indoor environments and to evaluate the cadmium as a marker of ETS. The correlations of cadmium concentrations and nicotine, 3-EP, RSP, SD (Smoking Density), and SI (Smoking Index). Air samples of metals, nicotine, 3-EP, and RSP were taken in smoking room, smoking allowed office, corridor outside smoking room, and non-smoking office respectively. The SD, ACH, and SI were investigated during sampling. Airborne concentration of cadmium known as human carcinogen were qualified and quantified. The SD was 0.2 to $2.6cig/m^2{\cdot}hr$, and the mean value of SD in smoking rooms was $1.2cig/m^2{\cdot}hr$ that is higher than other researches. The mean of ACH in smoking rooms was 11.1. The concentrations of cadmium showed log-normal distributions and the geometric mean concentrations of cadmium in smoking rooms, corridor outside smoking rooms, smoking allowed offices, and non-smoking offices were $0.045{\mu}g/m^3$, $0.018{\mu}g/m^3$, $0.021{\mu}g/m^3$, and $0.017{\mu}g/m^3$ respectively. The concentrations of cadmium in smoking room showed significant difference according to category of indoor office environments (p<0.05) and showed compliance with occupational exposure limits. The correlation coefficients between cadmium and nicotine, 3-EP, and RSP were 0.53, 0.41, 0.43 respectively. The cadmium among metals showed the highest correlations (r=0.63) with SI. It was recommended cadmium among metals is a good indicator for ETS.

• Tuberculosis and Respiratory Diseases
• /
• v.55 no.1
• /
• pp.88-97
• /
• 2003

Background : Although smoking is a major cause of chronic obstructive pulmonary disease (COPD), only 10-20% of cigarette smokers develop symptomatic COPD, which suggests the presence of genetic susceptibility. This genetic susceptibility to COPD might depend on variations in the activities of the enzyme that detoxify hazardous chemical products, such as microsomal epoxide hydrolase (mEPHX) and glutathione-S transferase M1 subunit (GSTM1) genes. Methods : The genotypes of 58 patients with COPD, and 79 age matched control subjects, were determined by a polymerase chain reaction, followed by restriction fragment length polymorphism (PCR-RFLP) for the mEPHX, and multiplex PCR for the GSTM1. Results : GSTM1 was deleted in 53.3% of the subjects. There was no difference in GSTM1 deletion rates between the COPD patients (32/58, 55.2%) and the control subjects (41/79, 51.9%). The combination patterns of two polymorphisms of mEPHX showed slow enzyme activity in 29(21.2%), normal in 73(53.3%) and fast in 32(23.4%). The COPD group (7/57, 12.3%) showed a significantly lower incidence of slow enzyme activity compared to the control subjects (22/77, 28.6%, p<0.05). However, when the COPD and control groups were compared with smokers only, there were no significant differences in the genotypes of GSTM1 and mEPHX. Conclusion : The genotypes of GSTM1 and mEPHX were not significant risk factors of COPD in this cohort of study.