• Proceedings of the Korean Society of Toxicology Conference
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• 2003.05a
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• pp.29-30
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• 2003

The heavy metal cadmium is a xenobiotic toxicant of environmental and occupational concern and it has been classified as a human carcinogen. Inhalation of cadmiumhas been implicated in the development of emphysema and pulmonary fibrosis, but, the detailed mechanism by which cadmium induces adverse biological effects is not yet known.(omitted)

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.5
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• pp.1257-1263
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• 2003

The modified engineering methodology and the modified electronic circuit in classical ultrasonic principles were applied to ultrasonic aerosol nebulizer for inhalation toxicology study of cadmium aerosol. 1532.96ppm Cd nebulizing solution was used to generate cadmium aerosol for particle size analysis with the modifying source and inlet temperatures. The results of particle size analysis for cadmium aerosol were as following. The highest particle counting for source temperature 20℃ was 399.75 × 10² in inlet temperature 100℃ and particle diameter 0.75㎛. The highest particle counting for source temperature 50℃ was 399.70 × 10² in inlet temperature 50℃ and particle diameter 0.75㎛. The highest particle counting for source temperature 70℃ was 411.14 × 10² in inlet temperature 100℃ and particle diameter 0.75㎛. The ranges of geometric mean diameter were 0.74-0.79㎛ in source temperature 20℃, 0.65-0.72㎛ in source temperature 50℃, and 0.65-0.80㎛ in source temperature 70℃. The smallest geometric mean diameter was 0.65㎛ in source temperature 50, 70℃ and inlet temperature 20, 50℃, and the largest geometric mean diameter was 0.80㎛ in source temperature 70℃ and inlet temperature 100℃. The ranges of geometric standard deviation were 1.71-1.80 in source temperature 20℃, 1.27-1.61 in source temperature 50℃, and 1.27-2.29 in source temperature 70℃. The lowest geometric standard deviation was 1.27 in source temperature 50, 70℃ and inlet temperature 20, 50℃, and the highest geometric standard deviation was 2.29 in source temperature 70℃ and inlet temperature 100℃. Generated aerosol for cadmium inhalation toxicology study was polydisperse aerosol with the above geometric standard deviation 1.2. The ranges of mass median diameter(MMD) were 1.75-2.25㎛ in source temperature 20℃, 1.27-1.61㎛ in source temperature 50℃, and 1.27-2.29㎛ in source temperature 70℃. The smallest MMD was 1.27㎛ in source temperature 50, 70℃ and inlet temperature 20, 50℃, and the largest MMD was 2.29㎛ in source temperature 70℃ and inlet temperature 100℃. Cadmium chloride concentration in nebulizing solution affected the particle size and distribution of cadium aerosol in air. MMO for inhalation toxicology testing in OECD and EU is less than 3㎛ and EPA guidance is less than 4㎛. In our results, in source temperatures of 20, 50, 70℃, and inlet temperatures of 20, 50, 100, 150, 200, 250℃ were conformed to the those guidance.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.6
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• pp.1243-1252
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• 2002

To experiment the effects between cadmium inhalation toxicity and extracts of Folium Mori, rat inhalation exposure groups were exposed to cadmium aerosol in air by whole-body inhalation exposure for 6 hours/day, 5 days/week, and 4 weeks. Cadmium concentration in the air of cadmium aerosol was 1.02㎎/㎥ and mass median diameter(MMD) was 1.40μm. Intraperitoneal injection of extracts of Folium Mori to inhalation exposure groups was done for 4 weeks and the results were as follows: The highest body weight gain for 4 weeks and food intake per day were 126.39g/4 weeks and 19.18g/day from inhalation exposure group III, respectively. The highest lung and liver weight were 1.27g and 8.19g from inhalation exposure group II, respectively. The highest kidney weight was 1.805g from inhalation exposure control. The lowest cadmium content in lung was 86.39μg/g from inhalation exposure group III. The lowest cadmium concentration in blood was 7.12㎍/㎗ from inhalation exposure group III. Cadmium concentrations of 40.02㎍/g in liver and 69.18㎍/g in kidney were the lowest from inhalation exposure group I and III, respectively. For weekly cadmium concentration in urine, the value of the fourth week from inhalation exposure group III was the highest, 3.12㎍/㎖. For weekly cadmium concentration in feces, the value of the fourth week from inhalation exposure group III was the highest, 2.67 ㎍/g. The highest metallothionein concentration in lung was 74.65㎍/g from inhalation exposure group III and the highest metallothionein concentration in liver was 386.84㎍/g from inhalation exposure group II. The highest metallothionein concentration in kidney was 236.17 ㎍/g from inhalation exposure group II.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.3
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• pp.464-471
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• 2002

Author applied several engineering methodologies to classical ultrasonic nebulizer to cope with it's demerits. After several trials and errors, we got the several meaningful results. To evaluate the modified ultrasonic nebulizer for inhalation toxicology of cadmium, author used light-scattering photometer. This paper is the one part of inhalation exposure systems for inhalation toxicology study of cadmium. According to the testing conditions, source temperature 50℃ and inlet-duct band temperature 150℃, aerosol generation results for sodium chloride and cadmium chloride were as followings: Coefficients of variation(CV) of sodium chloride and cadmium chloride for repeated trials were 3.38 and 4.77 for 10g, 2.47 and 5.02 for 5g, and 4.70 and 2.98 for 2.5g. All the CVs were within 10% of acceptance variability. Count Per Minute(CPM) changes of NaCl and CdCl₂ for 5 repeated trials were similar. CPM ratios of CdCl₂/NaCl were 1.13 for 10g, 0.76 for 5g, and 1.06 for 2.5g. Relative aerosol generation of cadmium chloride to sodium chloride was the highest in 10g. Efficiency increases of 24.50% for 5g NaCl, 14.91 % for 2.5g NaCl, and 16.48% for 2.5g CdCl₂ with respect to theoretical efficiency were observed but 0.04% efficiency decrease was observed in 5g CdC₂. According to the modifications of source temperature(20, 50, 70℃) and inlet-duct band temperature(20, 50, 100, 150, 200℃), aerosol generation results for NaCl and CdCl₂ were as followings: CPM trends for each quantity excepting 10g NaCl in inlet-duct band temperature 200℃ were similar, and the highest CPM was observed in source temperature 70℃ to each inlet-duct band temperature. The highest CPMs to 10, 5, and 2.5g NaCl were observed in source temperature 70℃ and inlet-duct band temperature 20℃. Aerosol generation of cadmium chloride was increased with the higher source temperature, excepting inlet-duct band temperature 200℃. The highest CPMs for 10, 5, and 2.5g CdCl₂ were observed in source temperature 70℃ and inlet-duct band temperature 20℃, and this trend was similar to NaCl aerosol generation The highest CPMs for 10, 5, and 2.5g CdCl₂ were observed in source temperature 70℃ and inlet-duct band temperature 20℃, and this result was similar to NaCl aerosol generation. Observed efficiencies of 5 and 2.5g NaCl were similar to ifs theoretical efficiency but -3.08% efficiency decrease of 5g CdCl₂, 17.47% efficiency increase of 2.5g CdCl₂ were observed. CPM ratio of CdCl₂/NaCl of 10g was different to 5 and 2.5g, and 2.5g ratio was higher than 5g ratio. In conclusion, to get maximum aerosol generation for NaCl and CdCl₂ will be the conditions that set the appropriate inlet-duct band temperature for each materials and increase the source temperature. Sodium chloride can be used to evaluate the performance and predict the concentration for cadmium aerosol in aerosol generator and inhalation exposure system.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.5
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• pp.1035-1041
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• 2002

Ultrasonic nebulizer with the application of new engineering methodology and the design of electronic circuit and 766ppm Cd nebulizing solution were used to generate cadmium aerosol for inhalation toxicology study. The results of particle size analysis for cadmium aerosol were as following. The highest particle counting for source temperature 20℃ was 43.449 x 10³ in inlet temperature 250℃ and particle diameter 0.75㎛. The highest particle counting for source temperature 50℃ was 43.211 x 10³ in inlet temperature 100 ℃ and particle diameter 0.75㎛. The highest particle counting for source temperature 70℃ was 41.917x10³ in inlet temperature 250℃ and particle diameter 0.75㎛. The ranges of geometric mean diameter(GMD) were 0.677-1.009㎛ in source temperature 20℃, 0.716-0.963㎛ in source temperature 50℃, and 0.724-0.957㎛ in source temperature 70℃. The smallest GMD was 0.677㎛ in source temperature 20℃ and inlet temperature 20℃. and the largest GMD was 1.009㎛ in source temperature 20℃ and inlet temperature 20℃. The ranges of geometric standard deviation(GSD) were 1.635-2.101 in source temperature 20℃. 1.676-2.073 in source temperature 50℃, and 1.687-2.051 in source temperature 70℃. The lowest GSD was 1.635 in source temperature 20℃ and inlet temperature 20℃, and the highest GSD was 2.101 in source temperature 20℃ and inlet temperature 200℃. Aerosol generated for cadmium inhalation toxicology study was polydisperse aerosol. The ranges of mass median diameter(MMD) were 1.399-5.270㎛ in source temperature 20℃. 1.593-4.742㎛ in source temperature 50℃, and 1.644-4.504㎛ in source temperature 70℃. The smallest MMD was 1.399㎛ in source temperature 20℃ and inlet temperature 20℃, and the largest MMD was 5.270㎛ in source temperature 20℃ and inlet temperature 200℃. Increasing trends for GMD, GSD, and MMD were observed with same source temperature and increase of inlet temperature. MMD for inhalation toxicology testing in EPA guidance is less than 4㎛. In our results. inlet temperature 20 and 50℃ in source temperature 20℃, and inlet temperature 20 to 150℃ in source temperature 50 and 70℃ were conformed to the EPA guidance. MMD for inhalation toxicology testing in OECD and EU is less than 3㎛. In our results, inlet temperature 20 and 50℃ in source temperature 20, 50, and 70℃ were conformed to the OECD and EU guidance.

• Proceedings of the Korea Society of Environmental Toocicology Conference
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• 2003.05a
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• pp.107-107
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• 2003

The heavy metal cadmium is a xenobiotic toxicant of environmental and occupational concern and it has been classified as a human carcinogen. Inhalation of cadmium has been implicated in the development of emphysema and pulmonary fibrosis, but, the detailed mechanism by which cadmium induces adverse biological effects is not yet known. Therefore, we undertook the investigation of genes that are induced after cadmium exposure to illustrate the mechanism of cadmium toxicity For this purpose, we employed the polymerase chain reaction-based suppression subtractive hybridization technique. We identified 29 different cadmium-inducible genes in human peripheral mononuclear cells, such as macrophage migration inhibitory factor, lysophosphatidic acid acyltransferase-${\alpha}$, enolase-1${\alpha}$, VEGF, Bax, neuron-derived orphan receptor-1, and Nur77, which are known to be associated with inflammation, cell survival, and apoptosis. Induction of these genes by cadmium treatment was further confirmed by semi-quantitative reverse-transcription polymerase chain reaction. Further, we found that these genes were also induced after cadmium exposure in normal human lung fibroblast cell line, WI-38, suggesting potential use of this induction profile to monitor cadmium toxicity in the lung. Next, Nur77, one of cadmium-inducible genes, was further studied since the products of Nur77 are known to be involved in the apoptotic process of lung cells. Following cadmium treatment, Nur77 gene expression was increased at protein-level in A549 cells. Consistently, the reporter containing Nur77 binding sequence was activated by 2.5-fold after exposure to cadmium in reporter gene analysis by transient transfection experiments. When the plasmid encoding dominant negative Nur77 that represses the transcriptional function of wild-type Nur77 was transfected into A549 cells, the expression of Bax was significantly reduced, suggesting that induction of Nur77 was an important process in cadmium-induced apoptosis in the cells. Cadmium induced the expression of Nur77 in vivo, confirming the relevance of the data obtained in viro. Together our results suggest that Nur77 gene expression in exposure to cadmium leads apoptosis of lung cells which may cause pathological changes in lung.