This study was conducted to determine the effects of processed tobacco leaves on the development, adult emergence and body weight of the cigarette beetle, Lasioderma serricorne Fabricius) (Coleoptera: Anobiidae) is serious insect pest of tobacco leaves and cigarette during storage. Developmental time, adult emergence rate and adult weight of the cigarette beetle, were evaluated on the cured tobacco and burley tobacco leaves at $30{\pm}1^{\circ}C$ with $70{\pm}5$ % RH under 12L:12D. The developmental time on all of the flue-cured tobacco leaves was about 61 days, but in the only CD3W and CD4TR grade burley tobacco, the developmental times ranged from 70 days to 74 days. Among the flue-cured tobacco leaves, the highest beetle emergence rate was 123 % on the CD3L grade, and the lowest was on the AB4OR grade. Adult body weights of the cigarette beetle reared on flue-cured tobacco were about 2.11~2.46 mg, and on the only CD3W and CD4TR grade burley tobacco were about 1.86~1.96 mg. Among the flue-cured tobacco leaves, the highest adult body weight(2.46 mg) of cigarette beetle was observed on the B1O grade flue-cured tobacco, whereas the lowest adult weight(2.11 mg) was observed on the CD4L grade flue-cured tobacco. The adult weight of cigarette beetle reared on whole meal was 2.04mg.

Activated carbon fiber (ACF) was surface modified by nitric acid to improve the adsorption efficiency of the propylamine. Functional groups and textural properties of modified ACF were investigated. The total surface acidity increased about 7 times to that of as-received ACF by modification with 1 M nitric acid solution, carboxylic and phenolic groups mainly increased. However, the specific surface areas and the total pore volumes of the modified ACFs were decreased by 5-8% due to the increased blocking (or demolition) of micropores in the presence of newly introduced complexes. Despite the decrease of textural properties, it was found that the amount of propylamine adsorbed by the modified ACFs was increased by approximately 17%. The oxygen and nitrogen contents on the modified ACF increased by 1.5 and 3 times compared with the as-received ACF. From the XPS results, it was observed that propylamine reacted with strong or weak acidic groups, such as -COOH or -OH on the ACF surfaces, resulting in the formation of pyrrolic-, pyridonic- or pyridine-like structures.

This study describes the manufacturing method of antioxidant filter and evaluate the reduction of free radical and biological activity from mainstream smoke. When we used spray-brush for the application of antioxidant solution to the filter, cv(coefficient of variation) levels of antioxidant added to filter ranged within 3 %, which means stable and constant feeding process. 0.3~0.5mg per cigarette of antioxidant were sprayed to acetate and active carbon part in the filter plug, respectively. It was considered that the use of antioxidant added filter resulted in the reduction of the gaseous compounds of free radicals from 17 % to 19 % in the mainstream smoke. Variation for removal efficiency of free radical in antioxidant filter added to acetate part was more pronounced than that of filter added to active carbon part. Smoking deliveries of tar, nicotine for the antioxidant added filters were similar when comparing to the non-antioxidant added filter, but the delivering amounts of isoprene were significantly reduced. The estimation of consumed GSH(glutathion) showed that the gaseous toxicity of the antioxidant added filter was 14 % ~ 23 % lower than that of non-antioxidant added filter. No significant differences were observed for the total taste quality in sensory evaluation.

Although prion diseases, a group of fatal neurodegenerative diseases of human and animals, are presumed to be caused by several mechanisms including abnormal change of prion protein, oxidative stress is still believed to play a central role in development of the diseases. Cigarette smoking has a few beneficial effects on neuronal diseases such as Alzheimer's disease and Parkinson's disease despite of many detrimental effects. In this study, we investigated how chronic cigarette smoking could exert such beneficial effect against oxidative damage. For this study, homogenates of 87V scrapie-infected brain was inoculated on intracerebral system of IM mice through stereotaxic microinjection and biochemical properties concerning with oxidative stress were examined. The scrapie infection decreased the activity of mitochondrial Mn-containing superoxide dismutase by 50% of the control, meanwhile the effects on other antioxidant enzymes including Cu or Zn-containing superoxide dismutase were not significant. Additionally, the infection elevated superoxide level as well as monoamine oxide-B (MAO-B) in the infected brain. Interestingly, many of the detrimental effects were improved in partial or significantly by long-term cigarette smoke exposure (CSE). CSE not only completely prevented the generation of mitochondrial superoxide but also significantly (p<0.05) decreased the elevated mitochondrial MAO-B activity in the infected brain. Concomitantly, CSE prevented subsequent protein oxidation and lipid peroxidation caused by scrapie infection; however, it did not affect the activities of antioxidant enzymes. These results suggest that chronic exposure of cigarette smoke contribute to in part preventing the progress of neurodegeneration caused by scrapie infection.

Hydrogen cyanide (HCN) is present in both the particulate and vapor phase of cigarette mainstream smoke. It is one of the 44 harmful substances on Hoffmann's list and is known to be a major ciliatoxic agent in cigarette mainstream smoke. Typically the determination of HCN in cigarette mainstream smoke has been done through colorimetric and electrochemical techniques, such as UV-spectrophotometry (UV), continuous flow analyzer (CFA), ion chromatography (IC) and capillary GC-ECD. In particular, CFA commonly has been using analysis hydrogen cyanide in cigarette smoke and the basic principle is pyridine-pyrazolone reaction. In this study, the more optimized analytical method is suggested isonicotinic acid-pyrazolone reaction method than previous pyridine-pyrazolone reaction method, a commonly used method for the determination of cyanide in water and air, by CFA. Sample collection was optimized by trapping particulate and vapor phase of smoke separately. The optimum NaOH concentration of the trapping solution was shown to be 0.2 M. HCN was stable up to 6 hours in this concentration but only 3 hours in 0.1 M solution. The sensitivity of this method was fairly good and it might be used in analysis of HCN in cigarette mainstream smoke.

In this study, a simple gradient RRLC method for rapid determination of carbonyl compounds of cigarette smoke was developed. Within 10 min, 8 carbonyl compounds have been separated and identified on ZORBAX Eclipse XDB-C18 column ($4.6{\times}50\;mm$, $1.8\;{\mu}m$) with gradient elution using water and acetonitrile as a mobile phase. RRLC was used for the quantification of carbonyl compounds in mainstream smoke of 3R4F reference cigarette, and evaluated those efficiencies in the recovery, repeatability and reproducibility. The correlation coefficients ($r^2$) for calibration curves of carbonyl compounds were over 0.9998. The developed RRLC method was successfully applied to the analysis of smoke samples and the recoveries of carbonyl compounds were in the range of 97.5~102.1% with RSD<3.1%.

Biomarkers could be critical and useful tools for assessing the biological effects of smoking and detecting differences between potentially reduced exposure product (PREP) and conventional cigarettes. Smoking-related biomarkers can be classified into three categories as biomarkers of exposure, biomarkers of effects, and biomarkers of potential harm. When compared with the biomarkers of effects or harm, the biomarkers of exposure for chemical constituents of cigarette smoke are well established and characterized. In addition, they could offer the important information in understanding how cigarette smoke interacts with biological molecules and causes the disease to human. Therefore, we provide an overview of 6 biomarkers of exposure (Nicotine and nicotine metabolites, Carboxyhaemoglobin, NNAL (4-(methylnitrosoamino)-1-(3-pyridyl)-1-butanol) and NNAL - glucuronide, 3-Hydroxypropyl-mercapturic acid, and Monohydroxy-butenyl-mercapturic acids, and Urine mutagenicity) which were validated through extensive research and clinical experience. These reliable biomarkers could help identify the efficacy of PREP by predicting early toxicological effects and lead to improve it.