• Asian Journal of Atmospheric Environment
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• v.5 no.4
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• pp.247-262
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• 2011

This study assessed the health risks of childhood exposure to PBDEs via different possible pathways in children's facilities and indoor playgrounds. When PBDE contamination was measured, it was determined through multiple routes, including inhalation of indoor dust, dermal contact with product surfaces and children's hands, and incidental dust ingestion. Samples were collected from various children's facilities (playrooms, daycare centers, kindergartens, and indoor playgrounds) during summer (Jul-Sep, 2007) and winter (Jan-Feb, 2008). The hazard index (HI) was estimated for non-carcinogens, and PBDEs, such as TeBDE, PeBDE, HxBDE, and DeBDE, were examined. The sensitivity to the compounds did not exceed 1.0 (HI) for any of the subjects in any facility. However, current data about toxicity does not reflect effects that were fully sensitive in children, so there is uncertainty in the dose-response data. The contribution rates of PBDEs were 71.4 to 96.1% and 3.7 to 28.2% for intake and inhalation exposure, respectively, indicating that intake of floor dust and inhalation are the primary routes.

• Fire Science and Engineering
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• v.30 no.6
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• pp.57-63
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• 2016

In this study, the toxicity of combustion products of wood-based materials (MDF, OSB) were analyzed using experimental animal techniques. The average deed stopping time of MDF was shorter than that of OSB. This means that the toxicity of the combustion products of MDF is higher than that of OSB. To analyze the cause of the result quantitatively, Fourier transform infrared spectroscopy (FT-IR) of the gas phase materials was performed. Qualitative analysis result, CO and $CO_2$ were detected. Quantitative analysis results, the gas generation rate was higher in OSB than in MDF. Blood analysis of mice revealed, COHb to be higher in OSB than MDF. A correlation between the gas generation rate and COHb was found. Currently, the toxicity of the combustion products of the materials is being examined using the toxicity index, such as Fractional Effective Dose (FED). The FED is based on the gas emissions. The average deed stopping time decreased with increasing toxicity of exposed material. On the other hand, the result of this study showed that, the CO emissions of OBS were 186.5% that of MDF. The COHb of OSB was > 129.6% that of MDF. Nevertheless, the average deed stopping time of the OSB is 51 seconds longer than that of MDF. Therefore, more toxicity studies on factors other than the gas phase materials in the combustion products will be needed.

• Toxicological Research
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• v.21 no.2
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• pp.179-186
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• 2005

Dimethylamine (DMA) is a widely used commodity chemical with few toxicity data. Groups of 10 male and female F-344 rats were exposed by inhalation to 0, 5, 10, 20, 40 and 80 ppm of DMA for 6 hrs/day, 5 days/week for 90 days. The changes of body weight, organ weight, hematology, clinical chemistry, and histopathological changes were evaluated after the exposure. As the results, the body weight was significantly decreased at 80 ppm in male and female rats (p<0.05). The absolute lung weight showed no statistically significant changes in any group. In contrast, the relative lung weight significantly increased at 80 ppm in male and female rats (p<0.05). Erythrocytes, mean cell hemoglobin, leukocytes, neutrophil, and platelet numbers were significantly increased in male and female at 40 or 80 ppm of DMA (p<0.05, p<0.01). In addition, the serum values of total protein, urea nitrogen were increased in male and creatine kinase, total protein were increased in female rats at 40 or 80 ppm (p<0.05, p<0.01). Histopathological examinations of the male and female lung samples showed slight hyperplasia and congestion at 80 ppm. Taken together, our study revealed that maximum tolerated dose of DMA would be over 40 ppm.

• Journal of the Korean Institute of Gas
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• v.18 no.2
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• pp.55-61
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• 2014

In this study, we evaluated the measurement of working environment, the amount of exposure, the hazards and risks of biphenyl, that was registered as 2A in IARC. Based on the exposure scenario, it was calculated that the exposure amounts are $1.0{\times}10^{-2}$, $4.2{\times}10^{-4}$, $7.0{\times}10^{-6}mg/m^3$, respectively, and the $RfC_{work}$ is 0.21, 2.13, 0.53 $0.31mg/m^3$ as carcinogenicity, target toxicity (oral), target toxicity (inhalation), developmental toxicity, respectively. According to these hazards evaluation and risk assessments, it was estimated that 0.57, 0.39 as carcinogenicity and non-carcinogenicity (developmental toxicity), respectively. It was also estimated relatively lower risks below 1. But since biphenyl is hazardous used much amounts, and could be exposed to workers directly, it was determined to require exposure monitoring to protect workers' health.

• Journal of Environmental Health Sciences
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• v.45 no.5
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• pp.443-456
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• 2019

Objectives: Children are exposed to various environmental pollutants through contact with children's products. We investigated the KC mark, certification number, and contained substances labeled on children's products through market research and collected the toxicological data on these substances. Methods: The environmentally hazardous substances labeled on children's products (n=6576), including toys (n=2812), personal care products (n=2212), stationary/books (n=1333), and playground equipment (n=219) were examined. For the components that could be identified by CAS number, toxicological data on oral, inhalation, and dermal routes, cancer slope factor, and reference dose were collected. Results: Among the investigated products, KC marks or certification numbers were found for 4557 products (69.3%). Except for cosmetics and cleansers, the material information was labeled on most of the products. The frequency of labeling substance information in toys and stationary/books was low since this information could be omitted if KC certification was obtained. In the target products, 617 substances were identified by CAS number, and polypropylene, acrylonitrile butadiene styrene, and polyester were the most frequently displayed. Chronic toxicity data was found for only 32.4% of individual components, and information on toxicity through the dermal route was also highly limited. Conclusion: Our study suggested that labeling guidelines should be required to identify the environmentally hazardous substances contained in children's products. In addition, the toxicological data on many ingredients in children's products were insufficient. The data gap for toxicity data should be filled for future risk assessment.

• Journal of Korean Society of Occupational and Environmental Hygiene
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• v.10 no.2
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• pp.109-123
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• 2000

Inhaled halogen compound was examined through micronucleus tests and toxicity tests using SD (Sprague-Dawley) rats with repeated dosages for six hours a day, five days a week, during four weeks. In four-week repeated exposure, no specific sign caused by the $CF_3I$ compound was observed on the clinical symptoms, body weight variation, feed consumption, and urinalysis data in the testing groups with reference to the control group. In hematological and biochemical blood tests of the testing groups, the significant, but in their normal ranges, value dependencies of glucose, aspartate aminotransferase, alanine aminotransferase and etc., on the halogen carbohydride concentration was observed. In histo-pathological tests, no specific lesion or concentration dependent change due to the $CF_3I$ compound dosage was observed in both sexes of the female and male in the tested animals. But, micronucleus tests on marrow cells extracted from the tested animals which were repeatedly exposed in the $CF_3I$ compound during four weeks, the frequencies of micronuclei were significantly increased dose-dependently compared to the control groups.

• Development and Reproduction
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• v.13 no.4
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• pp.321-327
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• 2009

This study aimed to examine the testis toxicities of metal compound, manganese (Mn), which may be generated as mist or fume in the industrial sites. As well as serum prolactin (PRL) concentration was analyzed because Mn accumulation in basal ganglia up-regulates serum PRL and hyperprolactinemia consecutively induces the testis toxicity. Male F344 rats were divided into the 4 groups (2 controls and 2 Mn treated groups, n=10) on the basis of the test condition (inhalation, Mn $1.5mg/m^3$ or not) and treatment period (for 4-weeks and 13-weeks). The treatment time was 6 hr. a day, 5 days a week for the whole body. Basic tests including changes in body weight, feed rate were observed. Blood and testis Mn concentration, and testis toxicity test such as the number and deformity test of sperm were also observed. Serum PRL level was analyzed by ELISA to certify the relationship between the Mn induced increase of the serum PRL level and sperm production. Blood and testis Mn concentrations were significantly and dose-dependently increased. Sperm count was decreased in Mn-treatment groups than control in a treatment time dependent manner. Morphological analysis of cauda epidydimal sperm showed that the frequencies of morphologically abnormal sperms such as bent tail and small head were increased in the both Mn-treatment groups than control. A significant increase in serum PRL levels was found in response to Mn treatment but it was not hyperprolactinemia range. These results suggest that treatment of Mn up-regulates the serum PRL concentration and induces the testis toxicity. The No Aversed Effect Level (NOAEL) of inhaled Mn on the male rat testis may be under the $1.5mg/m^3$.

• Toxicological Research
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• v.32 no.4
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• pp.353-358
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• 2016

The generation and collection of cigarette smoke (CS) is a prerequisite for any toxicology study on smoking, especially an in vitro CS exposure study. In this study, the effects on blood and vascular function were tested with two widely used CS preparations to compare the biological effects of CS with respect to the CS preparation used. CS was prepared in the form of total particulate matter (TPM), which is CS trapped in a Cambridge filter pad, and cigarette smoke extract (CSE), which is CS trapped in phosphate-buffered saline. TPM potentiated platelet reactivity to thrombin and thus increased aggregation at a concentration of $25{\sim}100{\mu}g/mL$, whereas 2.5~10% CSE decreased platelet aggregation by thrombin. Both TPM and CSE inhibited vascular contraction by phenylephrine at $50{\sim}100{\mu}g/mL$ and 10%, respectively. TPM inhibited acetylcholine-induced vasorelaxation at $10{\sim}100{\mu}g/mL$, but CSE exhibited a minimal effect on relaxation at the concentration that affects vasoconstriction. Neither TPM nor CSE induced hemolysis of erythrocytes or influenced plasma coagulation, as assessed by prothrombin time (PT) and activated partial thromboplastin time (aPTT). Taken together, CS affects platelet activity and deteriorates vasomotor functions in vitro. However, the effect on blood and blood vessels may vary depending on the CS preparation. Therefore, the results of experiments conducted with CS preparations should be interpreted with caution.

• Proceedings of the Korea Society of Environmental Toocicology Conference
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• 2002.05a
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• pp.37-38
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• 2002

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.1
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• pp.78-88
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• 2002

Experimental animals were divided into 5 groups; normal, cadmium control, and 3 experimental groups. Cadmium control and experimental groups were exposed to 1 mg/㎥ of cadmium aerosol in air by inhalation exposure for 6 hours/day, 5 days/week during 4 weeks. Dosages of 20, 40, and 80mg/kg of extracts of persimmon leaves were intraperitoneally injected to experimental groups respectively and several toxicological parameters and induction of metallothionein were measured from the rats that inhaled cadmium aerosol in air. The results of this study were as follows. Cadmium concentration that cadmium control and experimental groups were inhaled was 0.980±0.061 mg/㎥. Mass median diameter of cadmium aerosol for inhalation exposure was 4.93±0.483㎛. Cadmium content of normal group in lung was 0.088㎍/g and the highest cadmium content in lung, 55.492㎍/g was from 80mg/kg dose group. Cadmium concentration of normal group in blood was 0.348㎍/100㎖ and the highest cadmium concentration in blood, 2.642㎍/100㎖ was from cadmium control. Cadmium concentration of normal group in liver was 0.010㎍/g and the highest cadmium concentration in liver, 31.100㎍/g was from 20mg/kg dose group. Cadmium concentration of normal group in kidney was 0.030㎍/g and the highest cadmium concentration in kidney, 2.526㎍/g was from cadmium control. Cadmium concentration of normal group in intestine was O.064㎍/g and the highest cadmium concentration in intestine, 0.300㎍/g was from 80mg/kg dose group. The highest cadmium concentration in urine by week was 6.080㎍/day from 20mg/kg dose group in the fouth week and the highest cadmium concentration in feces by week was 341.731㎍/day from 20mg/kg dose group in the fouth week. Metallothionein concentration of normal group in lung was 5.769㎍/g and the highest in lung, 30.986㎍/g was from 80mg/kg dose group. Metallothionein concentration of normal group in liver was 38.856㎍/g and the highest in liver, 169.378㎍/g was from 40mg/kg dose group. Metallothionein concentration of normal group in kidney was 22.228㎍/g and the highest in kidney, 47.898㎍/g was from 80mg/kg dose group. Metallothionein concentration of normal group in intestine was 2.170㎍/g and the highest in intestine, 13.642㎍/g was from 80mg dose group.