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Ci-dessous l’un des résultats trouvé en moins de 30 secondes, à partir du Guide de recherche en toxicologie d’UVMT. METHYLMERCURY CASRN: 22967-92-6 For other data, click on the Table of Contents Human Health Effects: Toxicity Summary: The general population is primarily exposed to methymercury through the diet. However, air and water, depending upon the level of contamination, can contribute significantly to the daily intake of total mercury. … Fish and fish products are the dominant source of methylmercury in the diet … Methylmercury in the human diet is almost completely absorbed into the bloodstream and distributed to all tissues within about 4 days. … Methylmercury is converted to inorganic mercury in experimental animals and humans. … The rate of excretion of mercury in both laboratory animals and humans is directly proportional to the simultaneous body burden and can be described by a single-compartment model with a biological half-time, in fish-eating humans, of 39-70 days … In every animal species studied, the nervous system is a target of methylmercury, fetuses appearing to be at higher risk than adults. … Methylmercury is fetotoxic in mice (single dose of 2.5-7.5 mg/kg); teratogenic in rats, and adversely affects the behavior of monkey offspring (mercury doses of 50-70 ug/kg per day before and during pregnancy). It also affects spermatogenesis in mice …. The clinical and epidemiological evidence indicates that prenatal life is more sensitive to the toxic effects of methylmercury than in adult life. The inhibition of protein synthesis is one of the earliest detectable biochemical effects in the adult brain … Methylmercury can also react directly with important receptors in the nervous system, as shown by its effect on acetylcholine receptors in the peripheral nerves. In the case of prenatal exposure … it affects normal neuronal development, leading to altered brain architecture, heterotopic cells and decreased brain size. Methylmercury may also be exerting an effect, perhaps through inhibition of the microtubular system, on cell division during critical stages in the formation of the central nervous system. … No adverse effects /in adults/ have been detected with long-term daily methylmercury intakes of 3-7 ug/kg body weight (hair mercury concentrations of approximately 50-125 ug/g). Pregnant women may suffer effects at lower methylmercury exposure levels than non-pregnant adults, suggesting a greater risk for pregnant women. Severe derangement of the developing central nervous system can be caused by prenatal exposure to methylmercury. … Evidence of pyschomotor retardation (delayed achievement of developmental milestones, a history of seizures, abnormal reflexes) was seen … at maternal hair levels below those associated with severe effects. … CONCLUSIONS: The general population does not face a significant health risk from methylmercury. Certain groups with a high fish consumption may attain a blood methylmercury level … associated with a low (5%) risk of neurological damage to adults. The fetus is at particular risk. … There is a need for epidemiological studies on children exposed in utero to levels of methylmercury that result in peak maternal hair mercury levels below 20 ug/g, in order to screen for those effects only detectable by available psychological and behavioral tests. [Environmental Health Criteria 101: Methylmercury pp. 13-17 (1990) by the International Programme on Chemical Safety (IPCS) under the joint sponsorship of the United Nations Environment Programme, the International Labor Organisation and the World Health Organization.]**PEER REVIEWED** Evidence for Carcinogenicity: CLASSIFICATION: C; possible human carcinogen. BASIS FOR CLASSIFICATION: Based on inadequate data in humans and limited evidence of carcinogenicity in animals. Male ICR and B6C3F1 mice exposed to methylmercuric chloride in the diet had an increased incidence of renal adenomas, adenocarcinomas and carcinomas. The tumors were observed at a single site and in a single species and single sex. The renal epithelial cell hyperplasia and tumors were observed only in the presence of profound nephrotoxicity and were suggested to be a consequence of reparative changes in the cells. Several nonpositive cancer bioasays were also reported. Although genotoxicity test data suggest that methylmercury is capable of producing chromosomal and nuclear damage, there are also nonpositive genotoxicity data. HUMAN CARCINOGENICITY DATA: Inadequate. ANIMAL CARCINOGENICITY DATA: Limited.

[U.S. Environmental Protection Agency’s Integrated Risk Information System (IRIS) on Methylmercury (MeHg) (22967-92-6) Available from: http://www.epa.gov/ngispgm3/iris on the Substance File List as of March 15, 2000]**PEER REVIEWED**

Human Toxicity Excerpts: THE MOST CONSISTENT & PRONOUNCED EFFECTS OF /CHRONIC/ EXPOSURE TO … SHORT-CHAIN ALKYLMERCURY COMPOUNDS SUCH AS METHYLMERCURY ARE ON CNS. EFFECTS … ARE NEUROLOGICAL & PSYCHIATRIC. COMMON SYMPTOMS INCL DEPRESSION, IRRITABILITY, EXAGGERATED RESPONSE TO STIMULATION (ERETHISM), EXCESSIVE SHYNESS, INSOMNIA, EMOTIONAL INSTABILITY, FORGETFULNESS, CONFUSION, & VASOMOTOR DISTURBANCES SUCH AS EXCESSIVE PERSPIRATION & UNCONTROLLED BLUSHING. TREMORS ARE ALSO COMMON … … SENSORY EFFECTS … OCCUR MORE CONSISTENTLY & AT LOWER LEVELS OF EXPOSURE. EARLIEST SIGN IS PARESTHESIA. AT … HIGHER LEVELS OF EXPOSURE OTHER EFFECTS OCCUR, SUCH AS ATAXIA, CONSTRICTION OF VISUAL FIELD, DYSARTHRIA, & HEARING DEFECTS. THESE ALTERATIONS ARE IRREVERSIBLE WHEN POISONING IS SEVERE. NEUROPSYCHIATRIC EFFECTS … ARE LIKELY TO INVOLVE SPONTANEOUS FITS OF LAUGHING & CRYING & INTELLECTUAL DETERIORATION. [Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman’s The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996. 1657]**PEER REVIEWED** IN HUMANS THE NEUROTOXIC SYMPTOMS OF METHYL MERCURY SALTS, THE HUNTER-RUSSEL SYNDROME, INVOLVE FOCAL CEREBRAL & CEREBELLAR ATROPHY. THE GRANULAR CELL LAYER OF NEOCEREBELLUM IS AFFECTED FOLLOWED BY CORTICAL ATROPHY OF AREA STRIATA, WHICH LEADS TO BLINDNESS. [Venugopal, B. and T.D. Luckey. Metal Toxicity in Mammals, 2. New York: Plenum Press, 1978. 95]**PEER REVIEWED** MOTHERS & THEIR INFANTS WERE EXPOSED TO METHYLMERCURY AS WHEAT FUNGICIDE DURING PREGNANCY. PEAK MATERNAL HAIR LEVELS WERE RELATED TO FREQUENCY OF MATERNAL SYMPTOMS & NEUROLOGICAL EFFECTS IN INFANTS EXPOSED IN UTERO. SEVERE NEUROLOGICAL DEFICITS WERE OBSERVED IN 5 CHILDREN WHOSE MATERNAL HAIR MERCURY LEVELS WERE 165-320 PPM. MINIMAL SYMPTOMS WERE REPORTED FOR MOTHERS & CHILDREN WHEN PEAK MATERNAL LEVELS WERE BELOW 68 PPM. GREATER FETAL RISK APPEARS TO BE ASSOC WITH EXPOSURE DURING SECOND TRIMESTER. [MARSH DO ET AL; CLIN TOXICOL 18 (NOV): 1311-8 (1981)]**PEER REVIEWED** … DOSE-RELATED CHROMOSOME ABERRATION /HAVE BEEN REPORTED/ IN LYMPHOCYTES OF CONSUMERS OF METHYL MERCURY CONTAMINATED FISH. … ABERRATIONS /WERE FOUND/ AT BLOOD METHYLMERCURY LEVELS OF … 100 UG/L. [Friberg, L., G.R. Nordberg, and V.B. Vouk. Handbook on the Toxicology of Metals. New York: Elsevier North Holland, 1979. 523]**PEER REVIEWED** Chromatid or chromosome aberrations and aneuploidy were measured in cultured leukocytes from human subjects exposed to methylmercury contaminated fish and from controls. Mean RBC (red blood cell) Hg levels varied greatly among subjects; overall average values were 182 ppb (exposed) and 9 ppb (controls). The frequencies of both breaks and aneuploidy were higher in the exposed group, although no significant correlation with blood-Hg was observed. [Nat’l Research Council Canada; Effects of Mercury in the Canadian Environment p.115 (1979) NRCC No. 16739]**PEER REVIEWED** The two most widely known epidemics of methyl mercury poisoning occurred in Minamata Bay and Niigata, Japan in 1953 to the early sixties. These episodes were caused by the industrial release of methyl and other mercury (Hg) compounds into the neighboring waters, followed by accumulation of the Hg by edible fish. The median level of total Hg in fish was estimated between 10-11 mg/kg fresh weight. By 1974, a total of 1200 cases of methyl mercury poisoning were identified, of which 55 proved fatal. Highest concentrations of Hg were found in the blood and hair. [WHO; Environ Health Criteria: Mercury p.90-107 (1976)]**PEER REVIEWED** Methylmercury poisoning has a pronounced toxic effect on developing fetuses; the fetal brain appears to be the most sensitive organ. [National Academy of Sciences; An Assessment of Mercury in the Environment p.12 (1978)]**PEER REVIEWED** Methylmercury affects the central nervous system in man–especially the sensory, visual, and auditory areas concerned with coordination; the most severe effects lead to widespread brain damage, resulting in metal derangement, coma, and death. [US Department of the Interior; Mercury Hazards to Fish, Wildlife, and Invertebrates: A Synoptic Review (1987)]**PEER REVIEWED** A review of strengths and weaknesses of evoked potentials as an index of toxic insult to the nervous system. Evoked potentials are obtained by averaging successive samples of EEG time-locked to the presentation of stimuli. Components of the resulting waveform can be measured for amplitude, latency, and distribution. Normal ranges of these parameters have been characterized for auditory, visual and somatosensory stimuli. Methyl mercury, n-hexane, and carbon monoxide cause complex changes in the waveshape of flash and patterned visual evoked potentials. [Arezzo JC et al; Neurobehav Toxicol Teratol 7 (4): 299-304 (1985)]**PEER REVIEWED** Available chronic data indicate that methylmercury is the most chronically toxic of the tested mercury compounds. [USEPA/OWRS; Quality Criteria for Water 1986 (1986) EPA 440/5-86-001]**PEER REVIEWED** Methylmercury is the most hazardous mercury species due to its high stability, its lipid solubility, and its possession of ionic properties that lead to a high ability to penetrate membranes in living organisms. [U.S. Department of the Interior; Mercury Hazards to Fish Wildlife, and Invertebrates: A synoptic Review (1987)]**PEER REVIEWED** /It was/ estimated that lowest level of MeHg in the brain capable of inducing onset of symptoms of intoxication to be 6 ug/g. Twelve victims of the Minimata disaster were reported to have brain concentrations ranging from 2.6 to 24 ug Hg/g … . “Normal” brain Hg levels (neutron activation analysis) in the Eastern US, based on autopsy samples from 7 individuals (age range: 33 to 79 years) ranged from 0.02 to 2.0 ug/g wet weight … . The range for a full term stillborn was 0.04 to 0.05 ng/g. Analysis of similar brain areas … from a larger sampling (30 to 100 individuals ranging in age from neonates to 91 years) from the same study area revealed a range 0.02 to 2.59 ug Hg/g … . A similar range has been reported more recently … . [Chang, L.W. (ed.). Toxicology of Metals. Boca Raton, FL: Lewis Publishers, 1996 1054]**PEER REVIEWED** MeHg is a potent developmental toxicant. It crosses the placental barrier and accumulates in the conceptus … . Thus, human neonates born to mothers exposed to MeHg through consumption of contaminated fish or grain were found to have higher RBC Hg levels than their mothers … . Furthermore, numerous reports indicate developmental toxicity in the absence of apparent maternal effects … . [Chang, L.W. (ed.). Toxicology of Metals. Boca Raton, FL: Lewis Publishers, 1996 1054]**PEER REVIEWED** The case of a woman who experienced dizziness, mispronounced words, and manifested tremor of the hands and tongue and loss of memory and reading comprehension was described. Originally, the illness was diagnosed as psychoneurosis. However, it was learned eventually that she had consumed 0.35 kg of swordfish (approximately 1 mg Hg/kg) per day for a 21 month period prior to the onset of symptomology and had repeated the diet for periods of 3 to 6 weeks, 2 to 3 times per year for 5 years. Apparently, she had suffered MeHg intoxication. [Chang, L.W. (ed.). Toxicology of Metals. Boca Raton, FL: Lewis Publishers, 1996 1058]**PEER REVIEWED** It is has been observed that offspring of pregnant women exposed to MeHg through consumption of contaminated seafood exhibited mental retardation and cerebral palsy-like symptoms in the apparent absence of maternal effects. [Chang, L.W. (ed.). Toxicology of Metals. Boca Raton, FL: Lewis Publishers, 1996 1058]**PEER REVIEWED** Food and Environmental Agents: Effect on Breast-Feeding: Methyl mercury, mercury: May affect neurodevelopment. /from Table 7/ [Report of the American Academy of Pediatrics Committee on Drugs in Pediatrics 93 (1): 142 (1994)]**PEER REVIEWED** Gold mining and deforestation in the Brazilian Amazon are increasing mercury pollution of the extensive water system, exposing riverine populations to organic mercury through fish-eating. The aim of the present study was to evaluate the effect of such exposure on motor performance. This cross-sectional study was carried out in May 1996, in a village located on the banks of the Tapajos river in the Amazonian Basin, Brazil. Information concerning sociodemographics, health, smoking habits, alcohol drinking, dietary habits and work history were collected using an interview-administered questionnaire. Mercury concentrations were measured by cold vapor atomic absorption in blood and hair of each participant, of whom those aged between 15 and 79 years were assessed for motor performance (n = 84). Psychomotor performance was evaluated using the Santa Ana manual dexterity test, the Grooved Pegboard Fine motor test and the fingertapping motor speed test. Motor strength was measured by dynamometry for grip and pinch strength. Following the exclusion of 16 persons for previous head injury, working with mercury in the goldmining sites, or for diabetes, the relationship between performance and bioindicators of mercury was examined using multivariate statistical analyses, taking into account covariables. All participants in the study reported eating fish, which comprised 61.8% of the total meals eaten during the preceding week. The median hair total mercury concentration was 9 microg/g. Organic mercury accounted for 94.4 = 1.9% of the total mercury levels. Multivariate analysis of variance indicated that hair mercury was inversely associated with overall performance on the psychomotor tests, while a tendency was observed with blood mercury. Semipartial regression analyses showed that hair total mercury accounted for 8% to 16% of the variance of psychomotor performance. Neither hair nor blood total mercury was associated with the results of the strength tests in women and men. Although dose-effect relationships were observed in this cross-sectional study, they may reflect higher exposure levels in the past. The findings of this study demonstrated neurobehavioral manifestations of subtle neurotoxic effects on motor functions, associated with low-level methylmercury exposure. [Dolbec J et al; Int Arch Occup Environ Health 73 (3): 195-203 (2000)]**PEER REVIEWED** Differences in pathology were found between acute and chronic exposure to methylmercury, mercury vapor, and inorganic mercury. Characteristic pathologic changes produced by organic mercury in the brain have previously been described in patients with Minamata disease. The brains of patients who presented with acute onset of symptoms and died within 2-mo showed loss of neurons with reactive proliferation of glial cells, microcavitation, vascular congestion, petechial hemorrhage, and edema in the cerebral cortices, predominantly in the calcarine, pre- and postcentral, and transverse temporal cortices and in the cerebellar cortex. The neuropathologic changes in the patients with acute onset of symptoms who survived for a long period (>10 yr) were also included neuronal loss with reactive proliferation of glial cells in similar anatomic locations. The neuropathologic changes in patients with inorganic mercury poisoning are quite different. Autopsies performed on 3 individuals with fatal cases of acute inorganic mercury poisoning who were exposed to mercury vapor for about 2 wk revealed diffuse organized pneumonia, renal cortical necrosis, disseminated intravascular coagulopathy, and infarctions in the brain and kidneys. In 2 other patients who worked in mercury mines for about 10 yr and who suffered from chronic inorganic poisoning, no specific lesions were demonstrated in the brain. However, the assay and the histochemistry of mercury revealed that inorganic mercury was present in the brain in all 3 groups irrespective of the brain lesions and the duration of clinical signs. [Eto K et al; Toxicol Pathol 27 (6): 664-71 (1999)]**PEER REVIEWED** Prenatal methylmercury exposure is associated with neuropsychological deficits in Faroese children at age 7 years. Lower confidence bounds of benchmark doses (BMDLs) have now been calculated. With the cord-blood mercury concentration as the dose parameter, a logarithmic dose-response model tended to show a better fit than a linear dose model for the attention, language and verbal memory tests. The lowest BMDLs averaged approximately 5 ug/l cord blood, which corresponds to a maternal hair concentration of approximately 1 ug/g. However, most BMDLs for hair mercury concentrations were higher. Thus, the results of the benchmark calculations depend on the assumed dose-response model. [Budtz-Jorgensen E et al; Toxicol Lett 112-113: 193-9 (2000)]**PEER REVIEWED** The two most widely known epidemics of methyl mercury poisoning occurred in Minamata Bay and Niigata, Japan in 1953 to the early sixties. These episodes were caused by the industrial release of methyl and other mercury (Hg) compounds into the neighboring waters, followed by accumulation of the Hg by edible fish. The median level of total Hg in fish caught was estimated between 10-11 mg/kg fresh weight. By 1974, a total of 1200 cases of methyl mercury poisoning were identified, of which 55 proved fatal. Highest concentration of Hg were found in the blood and hair. /Mercury cmpd/ [WHO; Environ Health Criteria: Mercury p.90-107 (1976)]**PEER REVIEWED** Systemic – The central nervous system, including the brain, is the principal target tissue for this group of toxic compounds. Severe poisoning may produce irreversible brain damage resulting in loss of higher functions. The effects of chronic poisoning with alkyl mercury compounds are progressive. In the early stages, there are fine tremors of the hands, and in some cases, of the face and arms. With continued exposure, tremors may become coarse and convulsive; scanning speech with moderate slurring and difficulty in pronunciation may also occur. The worker may then develop an unsteady gait of a spastic nature which can progress to severe ataxia of the arms and legs. Sensory disturbances including tunnel vision, blindness, and deafness are also common. A later symptom, constriction of the visual fields, is rarely reversible and may be associated with loss of understanding and reason which makes the victim completely out of touch with his environment. Severe cerebral effects have been seen in infants born to mothers who had eaten large amounts of methyl mercury-contaminated fish. /Methyl mercury compounds/ [Sittig M; Handbook of Toxic and Hazardous Chemicals p.421 (1981)]**PEER REVIEWED** When deposited on the skin, they give no warning, and if contact is maintained, can cause second-degree burns. Sensitization may occur. /Methyl mercury compounds/ [Sittig M; Handbook of Toxic and Hazardous Chemicals p.421 (1981)]**PEER REVIEWED** IN HUMANS THE NEUROTOXIC SYMPTOMS OF METHYL MERCURY SALTS, THE HUNTER-RUSSEL SYNDROME, INVOLVE FOCAL CEREBRAL & CEREBELLAR ATROPHY. THE GRANULAR CELL LAYER OF NEOCEREBELLUM IS AFFECTED FOLLOWED BY CORTICAL ATROPHY OF AREA STRIATA, WHICH LEADS TO BLINDNESS. /METHYL MERCURY SALTS/ [Venugopal, B. and T.D. Luckey. Metal Toxicity in Mammals, 2. New York: Plenum Press, 1978. 95]**PEER REVIEWED** Skin, Eye and Respiratory Irritations: Alkyl mercury compounds are primary skin irritants and may cause dermatitis. /Methyl mercury compounds/ [Sittig M; Handbook of Toxic and Hazardous Chemicals p.421 (1981)]**PEER REVIEWED** Medical Surveillance: As urinary excretion of methylmercury is very small, methylmercury concn in urine is easily masked by the presence of inorganic mercury. Thus, urine concn of mercury is not a good index of methylmercury body burden or of methylmercury concn in the critical organ. /Methylmercury compounds/ [Friberg, L., Nordberg, G.F., Kessler, E. and Vouk, V.B. (eds). Handbook of the Toxicology of Metals. 2nd ed. Vols I, II.: Amsterdam: Elsevier Science Publishers B.V., 1986.,p. V2 429]**PEER REVIEWED** Populations at Special Risk: Females of child bearing age should not be occupationally exposed to methylmercury cmpd. Prenatal life may be the stage of the life-cycle most sensitive to methylmercury cmpd. [WHO; Environ Health Criteria: Mercury p.119 (1976)]**PEER REVIEWED** Females of child bearing age should not be occupationally exposed to methyl mercury cmpd. Prenatal life may be the stage of the life-cycle most sensitive to methyl mercury cmpd. /Methyl mercury cmpd/ [WHO; Environ Health Criteria: Mercury p.119 (1976)]**PEER REVIEWED** Probable Routes of Human Exposure: EXPOSURE TO METHYL- AND ETHYLMERCURY HAS BEEN DESCRIBED IN CONNECTION WITH MFR AND USE OF THESE SALTS IN CHEMICAL INDUSTRIAL WORKERS AND IN PERSONNEL CARRYING OUT SEED TREATMENT. DUE TO RESTRICTIONS ON AGRICULTURAL APPLICATIONS OF ALKYLMERCURY COMPOUNDS, OCCUPATIONAL EXPOSURE IS LIKELY TO BE RARE AT PRESENT IN MOST INDUSTRIALIZED COUNTRIES. [Friberg, L., G.R. Nordberg, and V.B. Vouk. Handbook on the Toxicology of Metals. New York: Elsevier North Holland, 1979. 510]**PEER REVIEWED** Accumulation of methylmercury in aquatic and terrestrial food chains represents a potential hazard to man by consumption of certain species of oceanic fish, of fish or shellfish from contaminated waters, and of game birds in areas where methylmercury fungicides are used. [WHO; Environ Health Criteria: Mercury p. 20 (1976)]**PEER REVIEWED** Methylmercury can react with free S-H groups of biologically important molecules, leading to diseases that have been caused by mercury and its derivatives(1). Consumption of fish and shellfish is the main source of methylmercury exposure in the general population(2-5). Fish and shellfish generally contain two orders of magnitude more mercury than other food items(2). In the goldmining regions of the Amazon Basin, the critical exposure population is inhabitants of riverside villages that routinely eat fish and not the goldminers, with better economic conditions and diversified food options(5). [(1) Simon M et al; Ullmann’s Encycl Indust Chem. 5th ed. Weinheim, Germany: VCH A16: 290 (1990) (2) Dermelj M et al; Chemosphere 16: 877-86 (1987) (3) Tollefson L, Cordle F; Environ H Pers 68: 203-8 (1986) (4) Inskip MJ, Piotrowski JK; J Appl Tox 5: 113-33 (1985) (5) Malm O et al; Sci Total Environ 175: 127-40 (1995)]**PEER REVIEWED** Methylmercury is of major toxicological significance. Methylmercury exposure occurs primarily through the consumption of fish(1) and shellfish(2) as the main source of exposure in the general population. Sources of past exposure to methylmercury include fungicide-treated grains and meat from animals fed this treated grain(1). However, fungicides containing mercury are now banned in the US, and therefore, this source of exposure is now negligible(1). It may diffuse into the atmosphere and return to the earth’s crust or to bodies of water as methylmercury in rainfall(3).

[(1) USEPA; Technology Transfer Network. Unified Air Toxics Website. Mercury and Compounds. Washington, DC: USEPA. Off Air Qual Plan Standards. Available from: http://www.epa.gov/ttn/uatw/hlthef/mercury.html as of April, 2000 (2) Riisgard HV et al; Marine Biology 86: 55-62 (1985) (5) Pieters H, Geuke V; Wat Sci Tech 30: 213-9 (1994) (3) Klaassen CD et al, eds; Casarett and Doull’s Toxicology. 5th ed. NY, NY: McGraw-Hill, pp. 709-714 (1995)]**PEER REVIEWED**

Body Burden: Mercury (Hg) has been reported in breast milk in women exposed to methylmercury from fish and from bread contaminated with methylmercury fungicides in the 1971-72 outbreak in Iraq. [WHO; Environ Health Criteria: Mercury p.74 (1976)]**PEER REVIEWED** Human hair is accepted as the best indicator for assessment of contamination in populations exposed to methylmercury(5). In 1992, abnormally high levels of mercury (mean range of 7.3-49.8 with an high of 132.6 ppm) were found in human hair from Jacareacanga and Brasilia Legal located near the main goldmining area in the Tapajos river basin, Brazil, as well as from Tres Bocas facing the lake in Amapa state, whereas the levels were much lower in Ponta de Pedras, a long way downstream(6). Hair from people in different Mediterranean areas: 9 contols (negligible to moderate fish consumption), methylmercury concn range 0.01-0.55 ug/g, avg concn 0.16 ug/g; 26 people, residents of a coastal areas, concn range 0.39-36.0 ug/g, avg concn 3.68 ug/g(1). Hair of a Papua New Guinean population, 114 samples, methymercury concn range 3.2-50.5 ug/g, avg concn 15.5 ug/g; a nearby control group who consumed a similiar amount of fish, 51 samples, methylmercury concn range 0.62-25.7 ug/g, avg concn 6.4 ug/g; and a control group who consumed fish much less frequently, 45 samples, methylmercury concn range 0.33-9.0 ug/g, avg concn 2.4 ug/g(2). Peruvian population chronically exposed to methylmercury due to long-term, heavy consumption of fish (70% of dietary protein came from fish), mean methylmercury blood level – 82 ng/ml(3). Human placentae, Italy, 22 samples, mean total organic mercury content 0.076 ug/g dry wt(4). In fishermen from two south Atlantic coastal areas of Spain, mean methylmercury ion content in hair was 8.28 ug/g and 6.72 ug/g(7). The concentration of methylmercury ion in seafood consumed by the fisherman were: Scrobicularia plana, 1.20 ug/g; Tapes decussatus, 0.039 ug/g(7). [(1) Dermelj M et al; Chemosphere 16: 877-86 (1987) (2) Kyle JH, Ghani N; Arch Environ H 37: 266-71 (1984) (3) Turner MD et al; Arch Environ H 35: 367-78 (1980) (4) Capelli R et al; Science Total Environ 48: 69-79 (1986) (5) Malm O et al; Sci Total Environ 175: 127-40 (1995) (6) Akagi H et al; Sci Total Environ 175: 85-95 (1995) (7) Lopez-Artiguez et al; Arch Environ Contam Toxicol 27: 415-9 (1994)]**PEER REVIEWED** In humans, after high oral intake of methylmercury for 2 months, the following values were reported (percentage of total mercury in tissues as inorganic mercury): whole blood, 7%; plasma, 22%; breast milk, 39%; urine, 73%; liver 16-40%(1). [(1) WHO; Environmental Health Criteria 101. Methylmercury. Geneva, Switzerland: World Health Organization. International Programme on Chemical Safety (1990)]**PEER REVIEWED** Average Daily Intake: ATMOSPHERIC INTAKE: 0.14 ug/day total mercury (elemental and methyl mercury) (assuming an avg ambient concn 7 ng/cu m)(1). FOOD INTAKE: 16.3 ug/day total mercury (assuming avg mercury concn in fish, 0.4 ug/g and an avg concn in other foods, 0.004 ug/g(1)). [(1) Bennett BG; IARC 71: 115-28 (1986)]**PEER REVIEWED** AIR INTAKE: 0.008 ug/day; FOOD INTAKE: 2.4 ug/day (fish); 0 ug/day (non-fish); WATER INTAKE: 0 ug/day(1). [(1) WHO; Environmental Health Criteria 101. Methylmercury. Geneva, Switzerland: World Health Organization. International Programme on Chemical Safety (1990)]**PEER REVIEWED**