• Journal of Soil and Groundwater Environment
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• v.12 no.1
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• pp.87-96
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• 2007

Risk assessment was carried out in order to improve the remediation and management strategy on a contaminated gunnery site, where a flood control reservoir is under construction nearby. Six chemicals, including explosive chemicals and heavy metals, which were suspected to possess risk to humans by leaching events from the site were the target pollutants for the assessment. A site-specific conceptual site model was constructed based on effective, reasonable exposure pathways to avoid any overestimation of the risk. Also, conservative default values were adapted to prevent underestimation of the risk when site-specific values were not available. The risks of the six contaminants were calculated by API's Decision Support System for Exposure and Risk Assessment with several assumptions. In the crater-formed-area(Ac), the non-carcinogenic risks(i.e., HI values) of TNT(Tri-Nitro-Toluene) and Cd were slightly larger than 1, and for RDX(Royal Demolition Explosives), over 50. The total non-carcinogenic risk of the whole gunnery range calculated to a significantly high value of 62.5. Carcinogenicity of Cd was estimated to be about $10^{-3}$, while that of Pb was about $5\;{\times}\;10^{-4}$, which greatly exceeded the generally acceptable carcinogenic risk level of $10^{-4}{\sim}10^{-6}$. The risk assessment results suggest that an immediate remediation practice for both carcinogens and non-carcinogens are required before the reservoir construction. However, for more accurate risk assessment, more specific estimations on condition shifts due to the construction of the reservoir are required, and more over, the effects of the pollutants to the ecosystem is also necessary to be evaluated.

• Tuberculosis and Respiratory Diseases
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• v.39 no.4
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• pp.304-309
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• 1992

Background: The alveolar macrophage may metabolize arachidonic acid through cyclooxygenase- and lipoxygenase- catalyzed pathways to produce a variety of metabolites of arachidonic acid. The production of these metabolites of arachidonic acid may enhance the defensive ability of the challenged lung. However, continued stimulation with the consequent production of proinflammtory metabolites of arachidonic acid, may ultimately enhance the disease process by contributing to chronic bronchoconstriction, fibrosis, and the persistent release of toxic oxygen species. Silicosis is an example of a disease process resulting from chronic exposure of the lung to foreign particles. This study was carried out to evaluate the changes of arachidonic acid metabolites from macrophages in experimental silicosis. Methods: We measured $PGE_2$, and $LTB_4$ in cultured macrophages taken from rats by radioimmunoassay at 24 and 48 hours after stimulation by silica dust, natural carbon dust, lipopolysaccharide, calcium ionophore (A23187) and medium (RPMI) as a control. For the experimental silicosis, 50 mg silica in 0.5 ml saline was administered intratracheally into the rat and grown to 20 weeks and measured $PGE_2$, and $LTB_4$ in the cultured macrophages lavaged from that rat. The used stimulants were the same as above. Results: 1) The amount of $PGE_2$ in the cultred macrophages from normal rat was significantly decreased in the group which was stimulated with silica dust for 48 hours compare with control non-stimulated group. 2) In the experimental silicosis group, $PGE_2$, release in cultured macrophages after 48 hours incubation with silica and natural carbon dust tended to be lower than those of non-stimulated group. 3) There were marked changes of $LTB_4$ in the groups of normal rats which were incubated with silica for 24, 48 hours and natural carbon for 48 hours compared with non-stimulated group. 4) In the experimental silicosis group, the release of $LTB_4$ was significantly increased macrophages cultured with silica and natural carbon dust after 24 and 48 hours incubation compared with non-stimulated group. Conclusion: The results of these studies suggest that the in vitro exposure of rat alveolar macrophge to silica and coal dust results in an alteration in alveolar macrophage metabolism of arachidonic acid that may promote an inflammatory reaction in lung tissue.

• Proceedings of the Korean Environmental Health Society Conference
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• 2003.06a
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• pp.24-25
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• 2003

Lead is ubiquitous in the human environment as a result of industrialization. China's rapid industrialization and traffic growth have increased the potential for lead emissions. Lead poisoning in children is one of the most common public health problems today, and it is entirely preventable. Children are more vulnerable to lead pollution and lead in their bodies can affect their nervous, circulatory, and digestive systems. Children are exposed to lead from different sources (such as paint, gasoline, and solder) and through different pathways (such as air, food, water, dust, and soil). Although all children are exposed to some lead from food, air, dust, and soil, some children are exposed to high dose sources of lead. Significant sources of lead for China's children include industrial emissions (often close to housing and schools), leaded gasoline, and occupational exposure that occurs when parents wear lead-contaminated clothing home from work, burning of coal for home heat and cooking, contaminated food, and some traditional medicines. To assess the blood lead level in children in China, a large-scale study was conducted in 19 cities among 9 provinces during 1997 to 2000. There were 6502 children, aged 3-5 years, were recruited in the study The result indicates that the mean blood lead level was 8.83ug/dl 3-5 year old living in city area. The mean blood lead level of boys was higher than that of girls (9.1l ug/dl vs 8.73ug/dl). Almost 30 percent childrens blood lead level exceeded 10ug/dl. The average blood lead level was higher than that of in 1985 (8.83ug/dl vs 8.lug/dl). An epidemiological study was carried on the children living around the cottage industries recycling the lead from battery. Nine hundreds fifty nine children, aged 5-12 years, living in lead polluted villages where the lead smelters located near the residential area and 207 control children live in unpolluted area were recruited in the study. The lead levels in air, soil, drinking water and crops were measured. The blood lead and ZnPP level were tested for all subjects. The results show that the local environment was polluted. The lead levels both in the air and crops were much higher than that of in control area. In the polluted area, the average blood level was 49.6ug/dl (rang 19.5-89.3ug/dl). Whereas, in the unpolluted area, the average blood level was 12.4ug/dl (rang 4.6-24.8ug/dl). This study indicates that in some countryside area, some cottage industries induce seriously lead pollution and cause children health problem. For the introducing of unleaded gasoline in some large cities, such as Beijing and Shanghai, the blood lead level showed a declined trend since 1997. By 2000, the use of leaded gasoline in motor vehicles has been prohibited in China. The most recent data available show that levels of lead in blood among children in Shanghai decreased from 8.3ug/dl in 1997 to 7.6ug/dl in 1999. The prevalence rate of children lead poisoning (blood lead >10ug/dl) was also decreased from 37.8% to 24.8%. In children living in downtown area, the blood lead level reduced dramatically. To explore the relationship between gene polymorphisms and individual susceptibility of lead poisoning, a molecular epidemiological study was conducted among children living in lead polluted environment. The result showed that the subjects with ALAD2 allele has higher ZPP level, and the subjects with VDR B allele has larger head circumference than only with b allele. In the present study, we demonstrated that ALAD genotypes modify lead effects on heme metabolism and VDR gene variants influence the skull development in highly exposed children. The polymorphism of ALAD and VDR genes might be the molecular inherited factor modifying the susceptibility of lead poisoning. Recently, Chinese government pays more attention to lead pollution and lead poisoning in children problem. The leaded gasoline was prohibited used in motor vehicles since 2000. The government has decided to have a clampdown on the high-polluted lead smelters for recycling the lead from battery in countryside. It is hopeful that the risk of lead poisoning in children will be decreased in the further

• Journal of Life Science
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• v.15 no.2 s.69
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• pp.169-175
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• 2005

Resveratrol (3,4',5-trihydroxy-trans-stilbene), a phytoalexin found in grape skins, peanuts, and red wine, has been reported to have a wide range of biological and pharmacological properties. $Amyloid-\beta$ deposition and senile plaque-associated astrocytes are common neuropathological features of Alzheimer's disease. In this study, we have explored the effects of resveratrol on $amyloid-\beta-peptide-mediated$ cytotoxicity in vitro and modulation of cell growth-regulatory gene products in astroglioma C6 cells to elucidate its possible mechanism for anti-cytotoxicity. Exposure of C6 cells to $Amyloid-\beta$ resulted in dose-dependent growth inhibition and morphological changes of C6 cells, which were recovered by pre-treatment with resveratrol. The anti-proliferative effect of $amyloid-\beta$ was associated with the induction of tumor suppressor p53 and cyclin-dependent kinase (Cdk) inhibitor p21 (WAF1/CIP1) expression assessed by RT-PCR and Western blot analysis in time-dependent manner in C6 cells. In addition, the pro-apoptotic Bax expression was also up-regulated in $amyloid-\beta-treated$ C6 cells without alteration of anti-apoptotic Bcl-2 and $Bcl-X_L$ expression. However, pre-treatment of resveratrol significantly inhibited $amyloid-\beta-induced$ p53, p21 and Bax levels, suggesting that the modulation of p53, p21 and Bax levels could be one of the possible pathways by which resveratrol functions as anti-cytotoxic agent. Our results demonstrate that resveratrol may enhance the protection against $amyloid-\beta-induced$ cytotoxicity by promoting the survival of glial cells.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2007.11a
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• pp.79-92
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• 2007

Oxidative stress have known to be a risk factor for the degenerative processes and closely related to a lot of diseases. It is well established that antioxidants are good in protection and therapeutic means against oxidative damage. There is increasing interest in natural antioxidants and many natural antioxidants have been found and utilized as the possible protection for various diseases and skin aging. We have screened natural antioxidant agents for cosmeceuticals, nutraceuticals, and drugs as therapeutic and preventive means against oxidative stress, and have developed a number of novel antioxidants from various natural sources. A novel melanin synthesis inhibitor, Melanocin A, isolated from the metabolite of a fungal strain Eupenicillium shearii F80695 inhibited mushroom tyrosinase and melanin biosynthesis of B16 melanoma cells with $IC_{50}$ value of 9.0 nM and MIC value of $0.9\;{\mu}M$, respectively. Melanocin A also exhibited potent antioxidant activity by scavenging of DPPH and superoxide anion radicals. UV was found to increase the level of hydrogen peroxides and other reactive oxygen species (ROS) in skin tissues. This increase in ROS may not only alter the structure and function of many genes and proteins directly but may also modulate their expressions through signal transduction pathways and, ultimately, lead to skin damage. We investigated the effect of Melanocin A on UV-induced premature skin aging. Firstly, the effect of Melanocin A on UV-induced matrix metalloproteinase (MMP)-9 expression in an immortalized human keratinocyte cell line, HaCaT in vitro was investigated. Acute UV irradiation induced MMP-9 expression at both the mRNA and protein levels and Melanocin A suppressed this expression in a dose-dependent manner. We then investigated UV-induced skin changes in hairless mice in vivo by Melanocin A. Chronic exposure of hairless mouse dorsal skin to UV increased skin thickness and induced wrinkle formation and the gelatinase activities of MMP-2 and MMP-9. Moreover, Melanocin A significantly suppressed UV-induced morphologic skin changes and MMP-2 and MMP-9 expression. These results show that Melanocin A can prevent the harmful effects of UV that lead to skin aging. Therefore, we suggest that Melanocin A should be viewed as a potential therapeutic agent for preventing and/or treating premature skin aging. Terrein is a bioactive fungal metabolite isolated from Penicillium species. Terrein has a relatively simple structure and can be easily synthesized. However, the biologic effects of terrein are comparatively unknown. We found for the first time that terrein potently inhibit melanin production in melanocytes and has a strong hypopigmentary effect in a spontaneously immortalized mouse melanocyte cell line, Mel-Ab. Treatment of Mel-Ab cells with terrein (10-100 mM) for 4 days significantly reduced melanin levels in a dose-dependent manner. In addition, terrein at the same concentration also reduced tyrosinase activity. We then investigated whether terrein influences the extracellular signal-regulated protein kinase (ERK) pathway and the expression of microphthalmia-associated transcription factor (MITF), which is required for tyrosinase expression. Terrein was found to induce sustained ERK activation and MITF down-regulation, and luciferase assays showed that terrein inhibits MITF promoter activity in a dose-dependent manner. To elucidate the correlation between ERK pathway activation and a decreased MITF transcriptional level, PD98059, a specific inhibitor of the ERK pathway, was applied before terrain treatment and found to abrogate the terrein-induced MITF attenuation. Terrein also reduced the tyrosinase protein level for at least 72 h. These results suggest that terrain reduces melanin synthesis by reducing tyrosinase production via ERK activation, and that this is followed by MITF down-regulation.