• Proceedings of the Korean Environmental Health Society Conference
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• 2005.12a
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• pp.4-15
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• 2005

Methylmercury (MeHg) is an environmental pollutant with neurotoxic effects on the central nervous system. The major exposure route of MeHg to humans is via consumption of fish and shellfish which accumulate the chemical through the food web in an aquatic environment. Hair mercury level is an excellent marker for MeHg exposure. We have been conducting a survey on hair mercury contents among general populations from 14 districts to estimate the current Japanese MeHg exposure level. Total mercury levels of all hair samples collected (12923 in total) were analyzed by the oxygen combustion-gold amalgamation method using an atomic absorption mercury detector. Multiple regression analysis revealed that mercury levels were significantly correlated with several covariates, such as sex, age, the amount of daily intake of total fish/shellfish, a preference for certain fish such as tuna or bonito, and artificial waving. The geometric means for the population without artificial waving were 2.47 and 1.65 ${\mu}g/g$ for males (n = 5623) and females (n = 3470), respectively. Hair mercury levels varied with age, and the variations were more significant in males. Since the difference between sexes was not evident at younger ages, some hormonal control might also be involved in the mercury uptake by human hair. The average mercury levels in our hair samples varied among the sampling districts. Tuna is a major carnivorous fish with high mercury accumulations that is often consumed in Japan. The amount of fish consumption and the preference rate far tuna would appear to be responsible far the regional variation in hair mercury levels in Japan. Recently, a provisional tolerable weekly intake (PTWI) of MeHg was revised by 61st JECFA to 1.6 ${\mu}g/kg/week$, which was about half that of the Japanese standard, and corresponded to a hair level of 2.2 ppm. The distribution of hair mercury levels in Japanese populations in the present study indicated that 25% of the Japanese females of child-bearing age were estimated to be exposed to MeHg over the PTWI level. This would reflect the high Japanese consumption of marine products. However, not only mercury contamination, but also the nutritional benefit may have to be considered when discussing the risk involved in the current level of fish and shellfish consumption in Japan.

• Proceedings of the Korea Society of Environmental Toocicology Conference
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• 2004.05a
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• pp.74-74
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• 2004

• Molecular & Cellular Toxicology
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• v.4 no.2
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• pp.164-169
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• 2008

Methylmercury (MeHg) is known to have devastating effects on the mammalian nervous system. In order to characterize the mechanism of MeHg-induced neurotoxicity, we investigated the analysis of transcriptional profiles on human 8k cDNA microarray by treatment of $1.4{\mu}M$ MeHg at 3, 12, 24 and 48h in human neuroblastoma SH-SY5Y cell line. Some of the identified genes by MeHg treatment were significant at early time points (3h), while that of others was at late time points (48h). The early response genes that may represent those involved directly in the MeHg response included pantothenate kinase 3, a kinase (PRKA) anchor protein (yotiao) 9, neurotrophic tyrosine kinase, receptor, type 2 gene, associated with NMDA receptor activity regulation or perturbations of central nervous system homeostasis. Also, when SH-SY5Y cells were subjected to a longer exposure (48h), a relative increase was noted in a gene, glutamine-fructose-6-phosphate transaminase 1, reported that overexpression of this gene may lead to the increased resistance to MeHg. To confirm the alteration of these genes in cultured neurons, we then applied real time-RT PCR with SYBR green. Thus, this result suggests that a neurotoxic effect of the MeHg might be ascribed that MeHg alters neuronal receptor regulation or homeostasis of neuronal cells in the early phase. However, in the late phase, it protects cells from neurotoxic effects of MeHg.

• Korean Journal of Food Science and Technology
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• v.45 no.3
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• pp.376-381
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• 2013

In this study, we monitored total mercury and methylmercury concentrations in tuna, billfish, and deep-sea fish distributed in Seoul city. With the acquired data, we carried out statistical analysis and an exposure assessment for intake. The mean concentrations (mg/kg) of total mercury and methylmercury were $0.32{\pm}0.31/0.20{\pm}0.20$ for tuna, $0.43{\pm}0.48/0.20{\pm}0.17$ for patagonian toothfish, $0.99{\pm}0.72/0.51{\pm}0.40$ for billfish and $1.20{\pm}0.70/0.95{\pm}0.51$ for sharks, respectively. We found that sharks, billfish, patagonian toothfish, and tuna were more contaminated with total mercury and methylmercury, in sequence, and that 66% of the total mercury concentration consisted of methylmercury, on average. Although the estimated weekly intakes of methylmercury from commercial deep-sea fish were lower than the weekly intakes recommended by the Joint FAO/WHO Expert Committee on Food Additives (JECFA), we identified that the total mercury and methylmercury concentrations in tuna, billfish, and deep-sea fish continued to increase with the passage of time. Therefore, we confirmed the necessity of continuous monitoring and comprehensive analysis for general safety.

• Journal of Environmental Health Sciences
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• v.33 no.3
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• pp.180-183
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• 2007

Over the last century the mercury (Hg) concentration in the environment has been increased by human activities with inputs from sources such as atmospheric deposition, urban runoff, and industrial effluents. Mercury can be transformed to methylmercury (MeHg) in anaerobic conditions by sulfate reducing bacteria (SRB) and sediments are the principal location for MeHg production in aquatic environments. Interest in bioaccumulation of Hg and MeHg into lower trophic levels of benthic and pelagic organisms stems from public health concerns as these organisms provide essential links for higher trophic levels of food chains such as fish and larger invertebrates. Fish consumption is the major exposure route of MeHg to humans. Recently, it was reported that blood samples in Korea showed much higher Hg levels (5-8 times) than those in USA and Germany. Although this brings much attention to Hg research in Korea, there are very few studies on Hg biogeochemical cycling and bioaccumulation in aquatic environments. Given the importance of Hg methylation and MeHg transfer through food chains in aquatic environments, it is imperative that studies should be done in much detail looking at the fate, transport, and bioaccumulation of Hg and MeHg in the environment. Moreover, there should be long-term monitoring plans in Korea to evaluate the environmental and health effects of Hg and MeHg.

• Journal of Environmental Health Sciences
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• v.31 no.3
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• pp.179-186
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• 2005

The purpose of this paper was to concisely review the practical changes in MeHg concentrations in fetus and offspring throughout gestation and suckling from our recent animal and human studies. In the animal study, adult female rats were given a diet containing 5ug/g Hg (as MeHg) for 8 weeks. Then they were mated and subsequently given the same diet throughout gestation and suckling. On embryonic days 18, 20, 22 and at parturition, the concentrations of Hg in the brains of fetus were approximately 1.5-2.0 times higher than those in the mothers. However, during the suckling period Hg concentrations in the brain rapidly declined to about 1/10 of that during late pregnancy. Hg concentrations in blood also decreased rapidly after birth. In human study, Hg concentrations in red blood cells (RBC-Hg) in 16 pairs of maternal and umbilical cord blood samples were compared at birth and 3 months of age after parturition. RBC-Hg in the umbilical cords was about 1.6 times higher than those in the mothers at parturition. However, all the infants showed declines in Hg concentrations throughout the breast-feeding period. RBC-Hg at 3 months of age was about half that at birth. Both the animal and human studies indicated that MeHg exposure to the fetus might be especially high but it dramatically decreases during the suckling period. Therefore, close attention should be paid to the gestation rather than the breast-feeding period to avoid the risk of MeHg to human infants.

• Journal of Yeungnam Medical Science
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• v.28 no.2
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• pp.105-115
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• 2011

Mercury is a toxic, persistent pollutant that bioaccumulates and biomagnifies through food webs. People are exposed to methyhnercruy mainly through their diet, especially through the consumption of freshwater and marine fish and of other animals that consume fish (e.g., marine mammals). All humans are exposed to low levels of mercury. Dietary patterns can increase exposure to a fish-eating population where the fish and seafood are contaminated with mercury. The primary toxicity targets of mercury and mercury compounds are the nervous system, kidneys, and cardiovascular system. It is generally accepted that developing organ systems are most sensitive to the toxic effects of mercury. The fetal-brain mercury levels appear to be significantly higher than the maternal-blood mercury levels, and the developing central nervous system of the fetus is currently regarded as the main system of concern as it demonstrates the greatest sensitivity. The subpopulation that may be at greater risk for mercury toxicity are those exposed to higher levels of methylmercury due to carnivorous fish, including sharks.

• Journal of Preventive Medicine and Public Health
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• v.47 no.2
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• pp.74-83
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• 2014

Mercury exists naturally and as a man-made contaminant. The release of processed mercury can lead to a progressive increase in the amount of atmospheric mercury, which enters the atmospheric-soil-water distribution cycles where it can remain in circulation for years. Mercury poisoning is the result of exposure to mercury or mercury compounds resulting in various toxic effects depend on its chemical form and route of exposure. The major route of human exposure to methylmercury (MeHg) is largely through eating contaminated fish, seafood, and wildlife which have been exposed to mercury through ingestion of contaminated lower organisms. MeHg toxicity is associated with nervous system damage in adults and impaired neurological development in infants and children. Ingested mercury may undergo bioaccumulation leading to progressive increases in body burdens. This review addresses the systemic pathophysiology of individual organ systems associated with mercury poisoning. Mercury has profound cellular, cardiovascular, hematological, pulmonary, renal, immunological, neurological, endocrine, reproductive, and embryonic toxicological effects.

• Journal of Food Hygiene and Safety
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• v.23 no.3
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• pp.276-283
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• 2008

To provide the research strategy for protection of children's health from hazardous chemical, we reviewed the hazardous chemicals can be exposed through maternity, children's life style and living environment. Recently, diseases related with children's living condition were focused as asthma, atopy, childhood developmental disability, congenital malformations and obesity. Children can be exposed to hazardous chemicals through an ambient air, water, soil, food, toys and other factors such as floor dust. Also children's health was deeply related with a wrong life style and neglectful caring by a lack of knowledge and information of harmful ones at parents and child care center's nursers. According to the previous study, the chemical risk factor of children's health were identified as inorganic arsenic, bisphenol A, 2,4-D, dichlorvos, methylmercury, PCBs, pesticide, phthalates, PFOA/PFOS, vinyl chloride, et al. Domestic studies for identification of causality between children exposure to chemicals and resulted hazardous effects were not implemented. The confirmation of chemical risk factors through simultaneously performing toxicological analysis, human effect study, environmental/human monitoring, and risk assessment is needed for good risk management. And also, inter-agency collaboration and sharing information can support confirming scientific evidence and good decision making.

• Safety and Health at Work
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• v.4 no.1
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• pp.1-11
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• 2013

This review surveys the recent literature on the neurodevelopmental impacts of chemical exposures during pregnancy. The review focuses primarily on chemicals of recent concern, including phthalates, bisphenol-A, polybrominated diphenyl ethers, and perfluorinated compounds, but also addresses chemicals with longer histories of investigation, including air pollutants, lead, methylmercury, manganese, arsenic, and organophosphate pesticides. For some chemicals of more recent concern, the available literature does not yet afford strong conclusions about neurodevelopment toxicity. In such cases, points of disagreement among studies are identified and suggestions provided for approaches to resolution of the inconsistencies, including greater standardization of methods for expressing exposure and assessing outcomes.