• Journal of Korean Society of Occupational and Environmental Hygiene
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• v.22 no.4
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• pp.316-328
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• 2012

Objectives: This study was designed to provide the information regarding chemicals classification and health hazard by evaluating the toxicological effect through repeated inhalation exposure of methyl acrylate(MA) in Sprague-Dawley(SD) rat for 13 weeks. Methods: According to the notification with Ministry of Labor(No. 2009-68) and OECD Test Guideline 413, the rats were exposed to MA at concentration of 0, 56, 168, 280 ppm via whole body inhalation for 6 hours per day, 5 days per week, for 13 weeks. All animals were observed for mortality, morbidity and the change of body weight and food consumption were determined during the exposure period. Necropsy finding, organ weight, hematology, clinical biochemistry and histopathological examination following exposure were also performed. Results: There were no death and abnormal clinical signs relate to exposure MA. However, At 160 ppm and 280 ppm exposure groups, body weight and food consumption showed statistically significant decrease and histopathological changes in lung, trachea, nasal cavity, larynx were observed. Conclusions: MA was mainly affected respiratory tract. It is consequently provided to be classified as category 2(0.2 mg/L/6h < category 2 ${\leq}$ 1.0 mg/L/6h) for specific target organ toxicity following repeated exposure according to Standard for Classification and Labeling of Chemical Substance and Material Safety Data Sheet. The NOAEL(no observable adverse effect level) of MA was also determined to be lower than 56 ppm.

• Toxicological Research
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• v.27 no.1
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• pp.19-23
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• 2011

It has been proposed that acute phase response can be a mechanism by which inhaled particles exert adverse effects on the cardiovascular system. Although some of the human acute phase proteins have been widely studied as biomarkers of systemic inflammation or cardiovascular diseases, there are only a few studies that investigated the role of serum amyloid P (SAP), a major acute phase protein in mice. In this study, we investigated the changes in SAP, following inhalation exposure to nickel hydroxide nanoparticles (nano-NH). We conducted 1) acute (4 h) exposure to nano-NH at 100, 500, and $1000\;{\mu}g/m^3$ and 2) sub-acute (4h/d for 3d) exposure at $1000\;{\mu}g/m^3$, then measured serum SAP protein levels along with hepatic Sap mRNA levels. The results show that inhaled nano-NH can induce systemic acute phase response indicated by increased serum SAP levels and hepatic Sap mRNA levels. To the best of our knowledge, this is the first study showing induction of SAP in response to repeated particle exposure, and the results suggest that SAP can be used as a biomarker for systemic inflammation induced by inhaled particles.

• Environmental Analysis Health and Toxicology
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• v.25 no.2
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• pp.131-143
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• 2010

We performed the tests of acute and subchronic inhalation toxicity of methyl formate, which has limited toxicological data in spite of its widespread use and enhanced hazard consequent on its high volatility. The median lethal concentration ($LC_{50}$) was evaluated to be above 5,000ppm(12.27 mg/L). In the test with subchronic inhalation, there are no deaths, but with reduction of body weight, food intake, organ weight by exposure to 400 (0.98 mg/L) and 1,600 (3.92 mg/L) ppm, dose-dependently. There were statistical differences in some hematological and blood biochemical parameters as compared to control (e.g. neutrophile and lymphocyte in the 1,600 ppm group, calcium and A/G in 1,600 ppm group). Methyl formate under the exposure of 1,600 ppm showed the respiratory findings with nasal, it was confirmed that the chemical has respiratory hazard with 1,600 ppm inhalation exposure, induces nasal epithelial atrophy, olfactory cell degeneration/regeneration and the contraction of olfactory cells, etc. According to the notification with Ministry of Labor (No. 2009-68) for classification, labeling and MSDS of chemicals, it is suggested for methyl formate to be classified as category 4 in acute (10.0$4\leq20.0$ mg/L), category 2 (0.2$\leq$1.0 mg/L/6h, 90 days) in specific target organ-repeated exposure.

• Tuberculosis and Respiratory Diseases
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• v.74 no.3
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• pp.120-123
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• 2013

Inhalation of toxic gases can lead to pneumonitis. It has been known that methane gas intoxication causes loss of consciousness or asphyxia. There is, however, a paucity of information about acute pulmonary toxicity from methane gas inhalation. A 21-year-old man was presented with respiratory distress after an accidental exposure to methane gas for one minute. He came in with a drowsy mentality and hypoxemia. Mechanical ventilation was applied immediately. The patient's symptoms and chest radiographic findings were consistent with acute pneumonitis. He recovered spontaneously and was discharged after 5 days without other specific treatment. His pulmonary function test, 4 days after methane gas exposure, revealed a restrictive ventilatory defect. In conclusion, acute pulmonary injury can occur with a restrictive ventilator defect after a short exposure to methane gas. The lung injury was spontaneously resolved without any significant sequela.

• Environmental Analysis Health and Toxicology
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• v.10 no.1_2
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• pp.15-20
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• 1995

The effects of volatile substances inhalation on lactate dehydrogenase and cholinesterase in rats were investigated. Male Sprague-Dawley rats were exposed to marketed odorant, ethyl acetate and ethyl ether for 15 days. Enzyme activities were measured in serum and several tissues such as liver, lung, brain, heart, kidney and muscle to find differences of effects according to the organ. Cholinesterase activity in serum and most of tissues revealed time-dependent decrease in the case of marketed odorant inhalation. Especially in heart and kidney significant decrease was observed. Ethyl acetate exposure to rats revealed also decrease in serum and all tissues by 40% to 60%. Ethyl ether inhalation showed significant decrease by 30% to 50%. Lactate dehydrogenase activity was markedly increased in serum and similarly in heart, brain and kidney by exposure to marketed odorant. No changes were observed in liver. Ethyl acetate exposure to rats revealed increase in serum by about 200%, compared to normal group and in other tissues by 40% to 70% except in liver and muscle. Ethyl ether inhalation showed significant increase in serum by about 100%. There was no change in 'liver and slight increase in muscle.

• Safety and Health at Work
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• v.2 no.1
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• pp.34-38
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• 2011

Objectives: The antimicrobial activity of silver nanoparticles has resulted in their widespread use in many consumer products. Yet, despite their many advantages, it is also important to determine whether silver nanoparticles may represent a hazard to the environment and human health. Methods: Thus, to evaluate the genotoxic potential of silver nanoparticles, in vivo genotoxicity testing (OECD 474, in vivo micronuclei test) was conducted after exposing male and female Sprague-Dawley rats to silver nanoparticles by inhalation for 90 days according to OECD test guideline 413 (Subchronic Inhalation Toxicity: 90 Day Study) with a good laboratory practice system. The rats were exposed to silver nanoparticles (18 nm diameter) at concentrations of $0.7\;{\times}\;10^6$ particles/$cm^3$ (low dose), $1.4\;{\times}\;10^6$ particles/$cm^3$ (middle dose), and $2.9\;{\times}\;10^6$ particles/$cm^3$ (high dose) for 6 hr/day in an inhalation chamber for 90 days. The rats were killed 24 hr after the last administration, then the femurs were removed and the bone marrow collected and evaluated for micronucleus induction. Results: There were no statistically significant differences in the micronucleated polychromatic erythrocytes or in the ratio of polychromatic erythrocytes among the total erythrocytes after silver nanoparticle exposure when compared with the control. Conclusion: The present results suggest that exposure to silver nanoparticles by inhalation for 90 days does not induce genetic toxicity in male and female rat bone marrow in vivo.

• Environmental Analysis Health and Toxicology
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• v.18 no.4
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• pp.255-269
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• 2003

The objective of this study was to estimate human exposure to benzo (a)pyrene through multimedia/multi-pathway exposure scenario. The human exposure scenario for benzo(a)pyrene was consisted of 12 multiple exposure pathways, and the multipathway human exposure model based on this scenario constituted. In this study, the multipathway human exposure model was used to estimate the concentrations in the exposure contact media, human intake factors and lifetime average daily dose (LAD $D_{model}$) of benzo(a)pyrene in the environment. Sensitivity analysis was performed to identify the important parameters and Monte-Carlo simulation was undertaken to examine the uncertainty of the model. The total LAD $D_{model}$ was estimated to be 5.52${\times}$10$^{-7}$ mg/kg-day (2.06${\times}$10$^{-7}$ -8.65${\times}$10$^{-7}$ mg/kg-day) using the multipathway human exposure model. The inhalation dose accounted for 78% of the total LADD, whereas ingestion and dermal contact intake accounted for 20.2% and 1.8% of the total exposure, respectively. Based on the sensitivity analysis, the most significant contributing input parameter was benzo (a)pyrene concentration of ambient air. Consequently, exposure via inhalation in outdoor/indoor air was the highest compared with the exposure via other medium/pathways.

• Environmental Analysis Health and Toxicology
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• v.14 no.4
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• pp.203-216
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• 1999

This paper describes a set of multi-pathway models for estimating health risk to lead. The models link concentrations of an environmental contaminant (lead) in air, water and food to human exposure through inhalation, ingestion, and dietary routes. Exposure is used as the foundation for predicting risk of health detriment within the population. The process of estimating exposure using often limited data and extrapolating to a large diverse population requires many assumption, inferences, and simplification. This paper is divided into four section. The first section provides lead contaminant levels on obtaining environmental concentration of air, tap water, and foods. The second section provides a discussion of exposure parameters and uncertainty associated predicting human health risk of contaminants. The third and fourth section illustrate lifetime average daily exposure (LADE) and excess cancer risk (ECR) based on exposure parameters. The relationship between concentration of lead in an environmental medium and human exposure is determined with pathway exposure factors (PEFs). The calculation of LADE and ECR is carried out using Monte-Carlo simulation with probability density function of exposure parameters. Examination of the result reveals that, for lead exposure, ingestion (food) is the dominant route of exposure rather than inhalation (air), and ingestion (tap eater).

• Journal of Environmental Impact Assessment
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• v.18 no.1
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• pp.11-19
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• 2009

We conducted human risk assessment due to inhalation exposure to heavy metals emitted from incinerator. The process of health impact assessment(HIA) on incinerator is as follows: The first step is to presume and calculate the amount of heavy metals emitted using emission factor. The second step is to conduct an exposure assessment using the K-SCREEN model which is used for predicting the concentration in a conservative method. The last step is to carry out a risk assessment on carcinogenic and non-carcinogenic substances. This study revealed that rank of carcinogenic human risk was $Cr^{+6}$ > As > Ni > Cd, and values of human risk assessment on carcinogenic and non-carcinogenic substances is lower than the US criteria for risk assessment except $Cr^{+6}$. It is expected that the technique of HIA, especially human risk assessment on heavy metals, would be applied to the incinerator construction project. In addition, more systematic studies are needed to overcome some weak points and limits found in this study.

• Journal of Korean Society for Atmospheric Environment
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• v.17 no.E2
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• pp.43-51
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• 2001

A report by the national research council in the United States suggested that many lung cancer deaths each year be associated with breathing radon in indoor air. Most of the indoor radon comes directly from soil beneath the basement of foundations. Recently, radon released from groundwater is found to contribute to the total inhalation risk from indoor air. This study presents the quantitative assessment of human exposures to radon released from the groundwater into indoor air. At first, a three-compartment model is developed to describe the transfer and distribution of radon released from groundwater in a house through showering, washing clothes, and flushing toilets. Then, to estimate a daily human exposure through inhalation of such radon for an adult. a physiologically-based pharmacokinetic(PBPK) model is developed. The use of a PBPK model for the inhaled radon could provide useful information regarding the distribution of radon among the organs of the human body. Indoor exposure patterns as input to the PBPK model are a more realistic situation associated with indoor radon pollution generated from a three-compartment model describing volatilization of radon from domestic water into household air. Combining the two models for inhaled radon in indoor air can be used to estimate a quantitative human exposure through the inhalation of indoor radon for adults based on two sets of exposure scenarios. The results obtained from the present study would help increase the quantitative understanding of risk assessment issues associated with the indoor radon released from groundwater.