Methylmercury is a potent neurotoxic chemical compound and is known as the causal agent of Minamata Disease. Mercury naturally occurs in the environment and is methylated. Methylmercury thus generated is bioconcentrated through food chain to be accumulated in large carnivorous fish and sea mammals at high concentrations. Populations consuming such seafood may be exposed to an excess amount of methylmercury. Since fetuses are more susceptible than their mothers, possible neurodevelopmental effects have been concerned among these populations. Therefore, risk assessment of fetal methylmercury exposure is needed. The Food Safety Committee in Japan made the risk assessment based on large-scale cohort studies, the Faroe and the Seychelles studies. The reported TWI(tolerable weekly intake)of methylmercury is 2.0 μg/kg b.w. of pregnant women, since the fetuses are considered to be a high risk subpopulation and TWI should be applied to pregnant women and women possibley pregnant.

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The toxicity and carcinogenicity of arsenic depend on its species. Individuals living in Japan consume much seafood that contains high levels of organoarsenics. Speciation analysis of urinary arsenic was performed for 210 Japanese male subjects without occupational exposure using HPLC-ICP-MS. The median values of dimethylarsinic acid(DMA)and arsenobetaine(AsBe)were 42.6 and 61.3 μgAs/L, respectively. These findings indicate that DMA and AsBe levels in Japan are much higher than those found in Italian and American studies. It appears that the high levels of DMA and AsBe observed in Japanese may be due in part to seafood intake. Hijiki(hizikia fusiforme)is a traditional food and used as a part of a balanced diet in Japan for centuries. In 2004 the UK Food Standards Agency advised not to eat Hijiki seaweed. To clarify the risks of Hijiki ingestion, a 42-year-old male volunteer ingested 825 μg of inorganic arsenic compounds contained in eight servings of commercial Hijiki food, after refraining from eating seafood for 3 months. The total amounts of sodium arsenate, sodium arsenite, monomethylarsonic acid and DMA excreted in urine over 50 h were 11.2, 31.8, 40.9 and 104.0 μgAs, respectively. Long-term ingestion of Hijiki might elevate the risk of carcinogenicity.

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The major source of exposure to cadmium among Japanese is rice. A half of total dietary cadmium intake comes from rice. Since 2001, we have been investigated in relationship between dietary cadmium exposure and health effects such as renal tubular among 1310 farm housewives in 5 districts in Japan, who have been consumed their rice harvested in their paddy. The geometric means of Cd in the rice(R-Cd)were 0.022, 0.061, 0.054, 0.113, and 0.154 µg/g in district A, B, C, D, and E, respectively. The estimates of total dietary Cd exposure revealed that 0.5 - 2.5% of the participants in district A were exposed to a higher Cd dose than the current Provisional Tolerable Weekly Intake(PTWI),i.e. 4.5 - 20.3% in district B, 6.9 - 22.2% in district C, 24.0 -52.5% in district D, and 35.6 - 66.8% in district E. Creatinin-adjusted urinary Cd(U-Cd)increased age-dependently, and correlated with the degree of Cd contamination in the districts. Renal biomarkers showed statistically significant increases in an age-dependent manner in all the districts, but were correlated with neither U-Cd nor B-Cd, nor R-Cd. Multiple regression analysis depicted no significant increase in the prevalence of renal biomarkers in each district after adjustment for age. In conclusion, this study showed that the prevalence of renal tubular dysfunction remains the same among female farmers exposed to life-long dietary Cd close to or above the current PTWI.

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Boron is a bioactive element of low molecular weight. Since discovery of the first boron biomolecule, boromycin, in 1967, several other similar biomolecules are now well-characterized. Most recently described was a bacterial cell-to-cell communication signal that requires boron. Boron is a natural constituent of the diet and human consumption is not trivial: ∼1.00 mg/d for males aged 51 to 70 y. Boron may be under homeostatic control in humans and other mammals through regulatory mechanisms that remain undefined. Evidence for such control is enhanced by discovery of a specific mammalian borate transporter, NaBC1, expressed in the basolateral membranes of epithelial cells in tissues with excretory functions including kidney. Gastrointestinal absorption of boron approaches 100% but, even so, boron has a low order of toxicity. For adults, the Tolerable Upper Intake Level(UL)for boron is 20 mg/d, i.e ∼20-fold typical intakes. The Institute of Medicine has not set an Estimated Average Requirement(EAR),Recommended Dietary Allowance(RDA),or Adequate Intake(AI)for boron because the collective body of evidence has yet to establish a clear biological function for boron in humans. The evidence to date suggests that humans and higher animals(frog, zebrafish, chick, rat, and pig)may use boron to support normal biological functions. These findings suggest that boron has a role in bone structure and function, inflammation and immune processes, insulin metabolism, and completion of the life cycle. Development of animal models that lack boron transporters may help in identification of mechanisms of action responsible for the beneficial effects of dietary boron.

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The content of fluoride, calcium and magnesium was determined by means of a fluoride ion selective electrode and inductively coupled plasma atomic emission spectroscopy in thirty-three brands of bottled mineral waters sold in the Japanese market. The geometric means of fluoride, calcium and magnesium were 79.8 μg/l, 19.1 μg/l and 2.8 μg/l, respectively. The fluoride content of Japanese and European brands was significantly higher than that of other brands. The calcium and magnesium concentrations were higher in the European brands than in all other brands. Simple linear regression and multiple linear regression analysis show that calcium and fluoride reach mineral water simultaneously. Our results show that only two brands imported from France and Italy exceed the World Health Organization's guideline value of 1.5 mg/l. All of the other samples analyzed contain less than 10% of that value. We also found that the fluoride intake of Japanese adults from mineral water is only 0.018-2.14% of the National Research Council upper recommended intake of 1.5-4.0 mg/day. Bottled mineral water can be considered as a source of fluoride but most brands are not a risk for fluorosis. However, sensitivity to fluoride depends on the subject's general health and age. To minimize the potential risk of exposure posed by mineral water the fluoride content should be fully disclosed on the label.

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A relation between serum zinc level and susceptibility to infection in older inpatients has not been studied well. A relation between serum zinc level and susceptibility to infection in older adults with long-term hospitalizations was studied. Forty-four(13 men, 31 women)hospitalized patients aged 45 years and older(mean, 81.4 years; range, 45-98 years with 38 patients(86%)aged 65 years and older)were divided into two groups. Retrospectively, 22 were assigned to the "no-infection group," with 22 assigned to the "infection group." Patients in the "no-infection group" did not receive any intravenous antibiotic treatment for bacterial infection for six months, whereas the others received at least one such treatment in the past six months. Serum concentrations of zinc, copper, albumin, total cholesterol, glucose, hemoglobin, and c-reactive protein were measured by general methods after six months observation. Mean serum Zn level was 56.9 μg/dL(SD, 14.4)in the "no-infection group" and 47.7 μg/dl(SD,14.9)in the "infection group." Difference in levels was significant(P=.043). Serum levels of albumin, total cholesterol, and hemoglobin in the "no-infection group" were also significantly higher than those in the "infection group." Deficiency in serum zinc appears to be associated with susceptibility to infection among older patients with long-term hospitalizations.

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We investigated genetic polymorphism of 287Met>Thr(Met-to-Thr substitution at amino acid base 287)in arsenic(+3 oxidation state)methyltransferase(AS3MT),which is an S-adenosyl-L-methionine-dependent enzyme that catalyzes the methylation of arsenite(As^III)and methylated As, and its relation to urinary arsenic profile in 100 individuals from the Red River Delta, Vietnam. Allele mutation frequency(2%)in this population was similar to that in other Asian populations, but relatively lower than those in Caucasians and Africans. Dimethylarsinic acid was the predominant compound in urine, followed by arsenobetaine. Low levels of inorganic arsenic(IA)and monomethylarsonic acid(MMA)were also detected. Concentration ratio of urinary MMA/IA for TC heterozygote was significantly higher than that for TT homozygote, suggesting higher methylation capacity from IA to MMA in individuals with TC.

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Cadmium nitrate(CdN)and cadmium fluoride(CdF)have been recently used for battery and electronics device in industrial fields. In previous study, we investigated the dose-effect relationships of acute toxicities of these substances from the standpoint of occupational health. From these results, it was strongly suggested that CdF have more hepatotoxicity than CdN, even if the contained cadmium was the same dose. Therefore, this study was designed to investigate the differences by biochemical and pathohistological comparison. Rats were received a single intravenous injection of saline, CdN(2.1, 4.2, 6.3 mg/kg),or CdF(1.34, 2.67, or 4.01 mg/kg). Both group contained Cadmium 1, 2, 3 mg/kg, respectively. Serum hepatic enzymes and liver samples stained H&E were examined 5 hours later. There were dose-dependent degenerative changes of hepatocytes such as necrosis, vascular degeneration, fatty droplet, inflammatory neutrophil infiltration in sinusoids. The chaneges of sinusoids caused prior to the other findings. It was suggested that sinusoid change be involved the early stage of hepatotoxic mechanism, because endothelial cell injury has been considered an essential component in the initial phase of acute Cd toxicity. They were accompanied by increase in the activities of ASL, ALT, m-AST and LDH. Biochemical evidence paralleled those morphorogical changes. Both findings confirmed the more severe damages in CdF group compared with CdN group that contained the same dose of Cd.

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Our previous study reported the lethal dose of cadmium fluoride(CdF₂, CdF for short)24 hours after intravenous injection in rats, the dose-effect relationships and the metabolism of cadmium(Cd)and fluoride(F)in bile and urine for investigating the acute toxicities from the standpoint of occupational health. This study was designed to determine the early dynamics of the absorption, systemic distribution, and metabolism of CdF. The kinetics of Cd and F were investigated in the blood in rats as a model of accidental occupational exposure to CdF. Rats were received a single intravenous injection of saline or CdF(1.34, 2.67, or 4.01(LD₈₈)mg/kg)which were the same doses of the previous study. Because this study investigates the dose-effect relationships of serum kinetic changes of Cd and F. Blood samples were obtained from each individual animal 0, 5, 10, 30, 60, 120, and 300 min after the CdF administration. The serum concentration-time profiles were analyzed by compartmental modeling using the WinNonlin program. These kinetic profiles indicated that the clearance of Cd was diminished in the 2.67 and 4.01 mg/kg groups. The abnormal kinetics of Cd was attributable to caused by severe hepatic injury that diminished the capacity for Cd accumulation. The elimination of serum F was delayed in the 4.01 mg/kg group. The abnormal kinetics of F was attributable to caused by nephrotoxicity that diminished its elimination from the kidney.

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