header: environmental hazards

photo Historic lake mercury plant

This section will discuss the target organs, and subsequent toxic health effects according to the form of mercury absorbed along with its route of ingestion, as well as review data available on the toxic effects of mercury on other organs.

Elemental or Metallic Mercury & Methylmercury

Target Organ: Brain

The critical target organ for both ionic and organic mercury is the brain. When elemental mercury is inhaled, due to high lipid solubility 75-85% is rapidly absorbed across the lungs and into the blood stream. A portion is transformed into divalent mercury in the red blood cells, while another portion is directly transported to the brain unchanged. The substance readily crosses the blood-brain barrier, is oxidized to mercuric Hg and becomes bound to macromolecules (NAS, 2000. p.54).

MeHg from fish consumption is the most common source of exposure to the general population from the environment. MeHg is slowly metabolized to ionic mercury in the brain.

Several hypothesis have been suggested for the cause of neurotoxicity of MeHg. Research by Yoshino et al., discuss biochemical and ultrastructural changes occur in the mitochondria after exposed to MeHg (Yoshino, Mozai , & Nakao, 1966). Sugano et al., 1975 found that both elemental and MeHg disrupts protein synthesis, with ionic mercury in the rat 10 times more potent as an inhibitor of cell-free protein synthesis as compared to MeHg (Nas, 2000, p. 55). Serrafin & Verity, discovered MeHg also causes membrane peroxidation in nerve cells(1991) . Research by Chang et al, revealed antioxidants such as, selenium and vitamin E offered protection in vivo against MeHg toxicity in rats ( Chang, Gilbert, & Sprecher, 1978). From these studies, a theory has been proposed that free radical induced lipid peroxidation could play a role in the cellular damaged caused by MeHg. According to research by Mira & Clarkson, 1993, oxidative stress may be a factor in MeHg toxicity, since concentrations of glutathione, (the major antoxidant of the cell) declines and then increases after exposure to MeHg. In addition, resistent cells to MeHg toxicity had an increased rate of efflux from the cells and had four times greater glutathione concentrations than normal cells (NAS, 2000, p.55). Another mechanism reported involves binding of MeHg to protein molecules that form the micro-tubules of the neuron causing nerve cell disruption of cellular processes, including cell division and migration (Clarkson, 1992). Although all of these observed effects have been discussed, no single theory has provided convincing evidence to be accepted as “the primary” mechanism of MeHg toxicity (NAS, 2000, p.55). Neuropathologic studies have shown cerebral edema with destruction of gray matter and cerebral atrophy. However, the mechanism of damage to the mature brain is unknown (Goyer & Clarkson, 2001, p.836).

Symptoms of neurotoxicity from both elemental mercury and MeHg include the following sensory, motor function, cognitive, and personality impairments:

  • remors affecting the hands that may progress to other parts of the body
  • neuromuscular weakness, muscle twitching, and muscle atrophy
  • polyneuropathy-- parathesias (numbness in fingers and toes), hyperactive tendon reflexes, slowed sensory and motor nerve conduction velocities with gait ataxia
  • slurred speech
  • memory loss and decreased performance in cognitive functioning
  • emotional lability known as “erethism” : irritability, extreme nervousness, shyness, and loss of confidence
  • fatigue
  • headaches
  • insomnia
  • visual loss – constriction of visual fields
  • hallucinations
  • hearing loss

In the fishing village of Minamata, Japan (1953-1960) where a plastics factory had been discharging mercury wastes into Minamata Bay, 700 people died and 9,000 were left with degrees of paralysis and brain damage (Nadakavukaren, 2000, p.266). In Iraq (1971-72), where mass poisonings occurred from the consumption of rice treated with mercurial fungicide, over 6000 people were hospitalized and over 500 deaths occurred, largely due to CNS failure. In both episodes, neurotoxicity was the most common adverse health effect noted (Nadakavukaren, 2000).
Return to top of page

Chronic Low Level Exposure to Ionic Mercury

Target Organ: Brain & CNS

Chronic low-level exposure to mercury vapor results in “ asthenic-vegetative syndrome or micromecurialism -- a non-specific condition of the CNS consisting of three or more of the following symptoms: tremor, enlarged thyroid, increased radio-iodine uptake by the thyroid, labile pulse, tachycardia, dermographism, gingivitis, hematologic changes, or increased mercury excretion in urine. With increased exposure, symptoms of peripheral nervous system toxicity become more pronounced—“tremors in muscles that perform fine motor tremors, such as fingers, eyelids, and lips progress to generalized trembling of the entire body and violent, chronic spasms of the extremities” (Goyer & Thomas, 2001, p.835). Other accompanying symptoms are due to central nervous system effects and include: changes in behavior and personality, with memory loss, increased emotional excitability known as “erethism”, severe depression, delirium, and hallucination. Severe salivation can also occur (Goyer & Thomas, 2001, p.835).
Return to top of page

Toxicity to Fetuses of Mothers Exposed to Methylmercury in Pregnancy

Target organ: Brain & CNS

The effects of exposure to MeHg in the developing fetuses of pregnant women has been studied extensively in Minimata, Japan, Iraq, and in populations with high fish consumption. In Minimata, 22 babies were born with brain damage while their mothers were largely asymptomatic for MeHg toxicity except for a few women with slight numbness in their fingers (Nadakavukaren, 2000, p. 266). Archived umbilical cord blood from 151 placentas (saved by women due to Japanese tradition) were correlated with the MeHg exposures and showed a dose-response effect between the concentration of MeHg and the degree of neurologic damage diagnosed in offspring ( Harada, Akagi, Tsuda, Kizaki, & Ohno, 1999). MeHg crosses the placental barrier and enters the brain of the developing fetus. Exposure to the fetus results in pathological changes in neuronal migration patterns including, abnormal organization of clusters of neurons and layering of neurons in the cortex. “Mercury binds to thiols in the tubulin [which are] the protein molecules that form microtubules in the neurons, and blocks depolorization and repolarization of the microtublules”. Since the breakdown and production of microtubules are essential for cell division and migration, it is hypothesized that the fetus is especially vulnerable to MeHg due to developing fetal brain processes such as, cellular division, differentiation, and migration (NAS, 2000, p.56). Another factor thought to increase sensitivity to MeHg is the incomplete blood-brain barrier of the fetus (Clarkson).
Return to top of page

Chronic Low Exposure to Fetuses: Effects in Infants & Children

Neurophysiological Development

Several studies have been conducted on infants and children who were chronically exposed to low doses of MeHg in utero, two of which will be discussed here. Steuerwald et al. evaluated the neurological function of 182 singleton, full-term infants in the Faroe Islands representing 64% of all births in the area. The babies were examined at the age of two weeks by a single pediatrician who was blinded to the parameters of the study. The neurological optimality score (NOS) assesses reflexes, responsiveness and stability of state as a reflection of an infant’s functional abilities. A significant inverse relationship existed between the NOS scores and the level of Hg measured in cord whole-blood. A three-week reduction in gestational age based on the NOS score was correlated with a 10-fold increase in cord blood Hg. PCB’s and essential fatty acids were also collected as potential confounding factors, and after adjustments were made neither substance affected the results (Steuerwald et al., 1999).

In New Zealand, Kjellstrom et al. (1989) reports that 237 children were followed up to six years of age consisting of 57 matched groups of 4 children to control for factors such as, ethnicity, gender, maternal age, maternal smoking, area, and duration of maternal residence. To assess general intelligence, language development, fine and gross motor coordination, social adjustment, and academic attainment, 26 psychological and scholastic tests were administered. Several potential confounding factors were adjusted in analyses including: maternal age, maternal ethnic group, smoking and alcohol during pregnancy, apgar scores, birth weight, fetal maturity, duration of breast feeding, social class, primary language and siblings. Poorer scores on full-scale IQ, language development, visual-spatial skills and gross motor- skills were associated with maternal hair Hg concentrations above 10 ppm, which were considered to fall into the high-Hg group range of this study (NAS, 2000, p. 201-2).

The results of these studies showing subtle neuro-developmental delays and impairment are also reflected in animal research. Subtle behavior differences were observed in the offspring of 129 SvSt mice who were injected with 1/3--1/4 of the LD (50) for MeHg at days seven and nine of gestation. At one month of age, 12 out of 20 offspring displayed one or more signs of neuromuscular impairment while swimming in an open water tank, as compared to none from the control group. In an open field test, mice in the experimental group took a significantly longer time to begin exploring compared to the control group. “Walking backward” was displayed by 10 out of 20 mice in the experimental group, vs. 1 out of 19 in the control group. Even though the exposed mice appeared normal, and showed no difference in brain weight, protein, and acetylcholine enzymes when compared to the unexposed mice-- subtle behavior differences were seen in performance (Spyker, J.M., 1972).
Return to top of page

Ionic Mercury

Target Organ: Kidneys

The kidneys are also a primary target organ for ionic elemental or mercuric mercury, where it is accumulated with a half-life of two months due to bio-transformation of ionic ions to mercuric ions (Wedeen, R.P., 200, p.646). Mercury has a strong affinity for sulfhedryl molecules, which are widely distributed in proteins. Both “ionic and organic mercurials bind avidly to sulfhydryl groups and amino acids in circulating proteins as well as to glutathione, cysteine, and metallothionein” (Wedeen, R.P., 2000, p. 647). Even though the precise mechanism of toxicity is not known, it is thought to be caused by the binding of mercury to key enzymes and structural proteins (NAS, 2000, p.54).

Renal accumulation of mercuric chloride (Hg chloride) is caused by the bio-transformation of ionic mercury to mercuric ions, where Divalent mercury binds to metallothionein and sulfhydryl groups in the kidney. Elemental mercury or the mercurous salt, “colomel” results in renal tubular proteinuria after 100 micrograms of mercury appears in the urine, however, it does not cause permanent tubular injury. Acute tubular necrosis results when mercuric chloride is injected at parenteral doses greater than 1 mg/kg of body weight. Incomplete recovery may result in persistent tubular-interstitial nephritis, chronic renal insufficiency and tubular calcifications (Wedeen, R. P., 2000, p.646-7).

Kazantzis et al, (1962) reports exposure to metallic mercury through inhalation has induced the following symptoms: mild transient proteinuria, gross proteinuria, hematuria, and oliguria. Proximal tubular damage with glomerular changes have been detected on biopsy in workers with proteinuria. (NAS, p. 165).
The following early renal changes in workers with chronic low level exposure to elementary mercury vapor have been detected: urinary excretions indicating tubular cytotoxicity, such as, increased tubular antigens and enzymes; altered levels of biochemical enzymes such as decreased urinary output of eicosanoids and glycosaminoglycans; and a more acidic pH. However since urinary function was normal, the clinical significance of these findings is yet to be determined (Cardenas et al., 1993).

Autoimmune glomeruler nephritis

Autoimmune glomeruler nephritis has been induced in genetically susceptible strains of rats and mice. When rodents are injected with Hg chloride, they produce antibodies which attack the kidneys causing an autoimmune glomeruler nephritis (NAS,2000, p.160). Evidence exists that human exposure to metallic mercury can trigger an autoimmune response. Tubs et al., 1982, reported deposits of IgG and complement C3 were found in the glomeruli of two workers exposed to metallic Hg (NAS, 2000, p.160). Cardenas et al, reports high anti-DNA antibody titers were seen in 8 of 44 workers exposed to mercury vapor from a chloralkali plant at urinary excretions of Hg more than 50 micrograms/liter (1993).
Return to top of page

Organic Mercury

Target Organ: Kidneys

Renal toxicity from exposure to organic forms of mercury has only been reported in cases of severe poisoning accompanied by symptoms of neurologic toxicity. Cinca et al., 1979, reports that two children who died of complications from severe poisoning after consuming pork contaminated by ethyl-Hg were found to have high urinary protein, urinary sediment, and blood urea at the onset of their symptoms, and severe nephritis on autopsy (NAS, 2000, p.165). In addition 62 out of 86 cases of ethyl mercury poisoning from Iraqi grain seed exhibited clinical symptoms of kidney damage such as, oliguria, polydipsia, polyuria, and albuminuria (Jalili & Abasi, 1961).
Return to top of page

Toxicity to Other Organs and Systems in the Body

Cardiovascular Toxicity

Both organic and ionic mercury accumulates in the heart and has been associated with elevated blood pressure and abnormal heart rhythms such as, tachycardia and ventricular heart rhythmns (NAS, 2000, p.168). It is unknown whether cardiovascular effects of mercury are due to direct cardiac toxicity or to indirect toxicity caused by effects on the neural control of cardiac function (U.S. EPA, 1997, p.3-20).

Numerous studies have reported tachycardia, high blood pressure and heart palpitations after acute exposure to elemental mercury vapor. A positive correlation was found between heart palpitations and urinary Hg concentrations in workers from a chlor-alkali plant by Piikivi (1989) (U.S. EPA, 1997). In addition, tachycardia and elevated blood pressure have been reported in numerous instances after children were treated with medicines containing mercurous chloride, such as calomel containing teething powder, worm medicine, or ammoniated mercury ointments used for diaper rash (Warkeny & Hubbard, 1953). Adverse cardivascular effects have been associated with exposure to MeHg. A retrospective study of cord-blood levels on 1000 children in the Faroe Islands at age seven who had been exposed prenatally to MeHg was conducted. After body weight adjustments, as the cord-blood levels of MeHg increased from 1-10 micrograms/ liter, the diastolic and systolic pressures increased by 13.9 and 14.6 mm Hg. In boys, as cord-blood levels increased from 1-10 micrograms/liter their heart rate variability decreased by 47%. Heart rate variablility is a reflection of cardiac autonomic control (Sorensen, Murata, Butz-Jorgensen, Weihe, & Grandjean, 1999).

A cohort of 1833 Finnish men were followed over 7 years by Salonen et al. (1995), to compare dietary intake of fish, and MeHg concentrations in hair and urine with the incidence of cardiovascular disease. All participants were free of clinical heart disease, stroke, claudication, and cancer at the onset of the study. Fish intake correlated with hair Hg and daily urinary Hg excretions. Men who consumed at least 30 grams of fish per day had a 2.1 fold greater risk of acute myocardial infarction. For each additional 10 grams of fish consumed there was an incremental 5% increase in the five-year risk of acute myocardial infarction. As a qualifier, mercury content in Finnish lakes is high. Mean daily intake of MeHg was 7.6 micrograms/liter—double the average mean concentration of MeHg intake of the average U.S. citizen (Salonen, et al., 1994).

Reproductive Toxicity

A study evaluated the reproductive effects of MeHg on sperm production, motility and morphology at sub-neurotoxic levels in male Macaca fascicularis monkeys. Primates were randomly placed in three groups consisting of a control, a low dose group who received 50 micrograms of MeHg/kg/day, and a high dose group who were fed 70 micrograms of MeHg/kg/day. Baseline sperm analysis was performed and testosterone levels obtained. Oral administration of mercury occurred each day for 20 days while a schedule of blood samples were collected for mercury and testosterone. At the end of the treatment, a testicular biopsy was performed for histologic and microscopic evaluation, and mercury assay. Although no overt signs of neuro-toxicity was displayed by the monkeys, all exhibited decreased sperm motility, lower scores for sperm speed and forward progression, and a higher percent of abnormal sperm tail forms marked by bent, kinked, and coiled tails. The total amount of MeHg intake was positively correlated with Mercury levels in testicular biopsies. No changes were observed in serum testosterone levels. While sperm motility did show a good pattern of recovery, sperm morphology remained unchanged.

Since MeHg inhibits micro-tubule assembly through the interaction with sulfhydral groups on micro-tubules it is hypothesized that the mechanism of toxicity on sperm morphology might be caused by an interference with microtubule assembly during spermiogenesis. Sperm production may be decreased due to the established inhibitory effects of MeHg on cellular mitosis (Mohammed et al., 1987).

Popescu reports following patients with long term occupational exposure over 6-8 years to methyl and ethyl Hg. Ambient air levels frequently exceeded the Swiss maximum allowable ambient air concentrations of 0.005mg/ m(3). Urinary excretion levels of Hg with no exposure for 2-6 months ranged between 340-480 micrograms/liter. Clinical symptoms included: (1) decreased sperm count, (2) increased abnormal morphology, (3) C/O impotence, and (4) C/O decreased libido. Mild symptoms of neuro-toxicity were also displayed by the men (Popescu, 1978).

In a study conducted to determine the effects of paternal exposure on pregnancy outcomes, the rate of miscarriage on the wives of 152 workers exposed to mercury was compared to a control of 374 non-exposed plant employees. The rate of miscarriage doubled at urine mercury concentrations above 50 micrograms/liter (95% confidence interval). Retrospective questionnaires determined the rate of miscarriage, which was defined as a “confirmed” pregnancy ending spontaneously before 28 weeks gestation. The two groups were similar in ages of workers and their wives, number of years spent in the plant, number of pregnancies, number of births and percentage of smokers. Maternal age, gravidy, tobacco or alcohol use did not explain the relationship found in the study.

The authors hypothesize the following mechanisms of toxicity: “mutagenesis or male germ cell damage, paternal reproductive toxicity leading to problems of fertililty but without genetic damage, germ cell damage from the mother, and maternal toxicity or embryo toxicity through indirect exposure to mercury from the father” (Cordier et al., 1991).

Rowland et al, conducted a study using retrospective questionnaires on 418 female dental assistants ages 18-39—correlating exposure to amalgams with poor handling practices and fertility. Fertility was determined by the number of menstrual cycles to pregnancy. Women who prepared more than 30 amalgams per day and reported five or more poor hygiene practices handling practices (as per industrial hygiene guidelines) had only a 63% probability of conception in each cycle as compared to those dental assistants not preparing amalgams. Confounding factors that were accounted for include: pertinent gynecological & obstetrical history variables, smoking , alcohol use, drug use, fish consumption, personal number of amalgam surfaces. In addition, other occupational exposures were considered such as: nitrous oxide, ethylene oxide, formaldehyde, x-ray exposure and methyl methacrylate (Rowland et al. 1994) (Rowland et al., 1994).

Gastrointestinal Tract

Liquid metallic mercury is a liquid at room temperatures. This form of mercury is very poorly absorbed from the gastrointestinal tract. The mercury reacts with sulfur to form mercuric sulfide, which coats the ingested metallic mercury and prevents the release of its vapor (U.S. EPA, 1997. P.2-1). If the amount of mercury in a thermometer is swallowed, it is slowly absorbed into the gastrointestinal tract and is not considered to pose a significant toxicologic risk (Klassen, C., D., 2001).

Human case studies show mercuric chloride when ingested by the oral route creates the following range of acute gastrointestinal effects: Nausea, vomiting, severe abdominal cramps and diarrhea, to corrosive ulceration, bleeding and necrosis of the gastrointestinal tract, causing shock and circulatory collapse. Inflammation and necrosis of the stomach tissue in mice have been found on histopathologic exam (EPA, 1997, p.3-50).

Respiratory Tract

Elemental mercury can enter the body through inhalation of vapor. Inhalation is the most common form of occupational exposure to mercury in America. Due to high lipid solubility, when inhaled, 75-85% is rapidly absorbed across the lungs and into the blood stream. From the blood stream it diffuses to all bodily tissues. Inhalation at high concentrations (acute exposure) causes acute respiratory symptoms including : coughing, congestion, dyspnea, bronchitis, pneumonitis, chest pain, reduced vital capacity, pulmonary edema, respiratory failure, and death (U.S. EPA, 1997, p.3-18). Central nervous system (CNS) symptoms of toxic effects may be present along with these respiratory manifestations (Goyer, R.A. & Clarkson, T.W., 2001, p.835).


MeHg has been classified by the EPA as a Class C, “possible” human carcinogen (NAS, 2000, p.149). In animal studies, MeHg increases the incidence of renal tumors only in male mice with pre-existing tumors. (The increase was not noted in female mice.) Since the phenomenon was only seen at levels of MeHg that were toxic to the kidneys, the tumorigenic effects was presumed to be “secondary” to cell damage and repair. Therefore, it has been concluded that “ in the absence of a tumor initiator, long term exposure to sub-toxic doses of MeHg does not appear to increase tumor formation” (NAS, 2000, p.149).

A cohort study by Tamishiro et al. (1984) evaluated the causes of death of 334 survivors of Minimata Disease (M.D.) who died between 1970-1980. Control cases were matched for age, gender, and year of deaths in the same municipality as the M.D. cases. No significant differences in cancer rates between the two groups were found, indicating MeHg poisoning does not increase the risk for dying from cancer (NAS, 2000, p.150). No data is available about the evidence of carcinogenic effects from ionic mercury on humans, and animal studies show mixed results with limitations in interpretation (U.S. EPA, 1997, p. 3-39).

Immune Toxicity

Autoimmune glomeruler-nephritis, as discussed in the section on nephrotoxicity, can be induced in humans from exposure to ionic mercury. Studies indicate MeHg can affect the immune system, although no data is available concerning immune system effects on human function.

The peripheral blood of a group of 81 men occupationally exposed men to metalic Hg vapors was analyzed for T-cells, T-helper, and T-suppressor cells and compared to a control group of 36 unexposed men by Moszczynski et al., (1995). Mercury concentrations of the subjects were measured in blood and in urine, along with mercury concentrations in the workplace air. An increased number of T-cells, T-helper cells, and T-suppressor cells was noted indicating stimulation of T-lymphocyte production (NAS, 2000, p.156).

A hypersensitivity reaction to mercury salts in the skin called “Pink Disease” has occurred in children when using medications containing mercurous chloride used in teething powder and ointments for skin rashes. Symptoms of Pink Disease or “Acrodynia” consists of these symptoms: fever, a pink colored rash, swelling of the spleen and lymph nodes, and hyperkeratosis and swelling of the fingers (Goyer, R. A. & Clarkson, T.W., 2001, p.836).

In animal studies, Koller (1975) reports that mice exposed to sub-toxic doses of MeHg for 84 days had an increased susceptibility to viral infections, as seen by a significantly higher mortality rate in the exposed mice as compared to unexposed mice after they were innoculated with encephalomyocarditis virus (NAS, 2000, p.158).


Dose-related aberrations in chromosomes and bone marrow cells were noted when Hg chloride was administered to mice by gavage. The effects of Hg chloride on genetic material is thought to be caused by the ability of Hg to “inhibit the formation of the mitotic spindle which can result in C-mitotic figures” (U.S. EPA, 1997, p. 3-58).
Return to top of page


Cardenas, A., Roels, H., Bernard, A. M., Barbon, R., Buchet, J. P., Lauwerys, R. R., et al. (1993). Markers of early renal changes induced by industrial pollutants. I Application to workers eposed to mercury vapour. Journal of Industrial Medicine, 50, 17-27.
Chang, L. W., Gilbert, M., & Sprecher, J. (1978). Modification of methylmercury neorotoxicity by vitamin E. Environmental Research, 17, 356-366.
Clarkson, T. (1992). Mercury: Major issues in environmental health. Environmental Health Perspectives, 100, 31-38.
Cordier, S., Deplan, F., Mandereau, L., & Hemon, D. (1991). Paternal exposure to mercury and spontaneous abortions. British Journal of Industrial Medicine, 48(6), 375-381.
Goyer, R.A. & Clarkson, T.W. (2001). Toxic Effects of Metals. In Klassen, C.D. (Ed.), Casarett & Doull's toxicology: The basic science of poisons (6th ed., pp. 811-837). New York: McGraw-Hill Medical Publishing Division .
Harada, M., Akagi, H., Tsuda, T., Kizaki, T., & Ohno, H. (1999). Methylmercury level in umbilical cords from patients with congenital Minamata disease . The Science of Total Environment, 234, 59-62.
Jalili, M. A., & Abbassi, A. H. (1961). Poisoning by ethyl mercury toluene sulphonanilide. British Journal of industrial Medicine, 18, 303-308.
Levy,B.S., & Wegman, D.H. (Eds.). (2000). Occupational health: Recognizing and preventing work-related disease and injury (4th ed.). Philadelphia: Lippincott Williams & Wilkins.
Mohamed, K. M., Burbacher, T. M., & Mottet, N. K. (1987). Effects of methyl mercury on testicular functions in macaca fascicularis monkeys. Pharmacology & Toxicology, 60, 29-36.
Nadakavukaren, A. (2000). Our global environment (5th ed., Rev.). Prospect Heights, Illinois: Waveland Press, Inc..
Office of Air Quality Planning & Standards and Office of Research and Development. (1997, December). Mercury study report to congress volume V: Health effects of mercury and mercury compounds. Retrieved October 27, 02, from U.S. Environmental Protection Agency Web Site: http://www.epa.gov
Popescu, H. I. (1978). Poisoning with alkylmercury compounds. British Medical Journal, 1, 1347.
Rowland, A. S., Baird, D. D., Weinberg, C. R., Shore, D. L., Shy, C. M., & Wilcox, A. J. (1994). The effect of occupational exposure to mercury vapour on the fertility of female dental assistants. Occupational & Environmental Medicine, 51, 28-34.
Salonen, J. T., Seppanen, K., Korpela, H., Kauhanen, J., & Kantola, M., et al. (1994). Intake of mercury from fish, lipid, peroxidation, and the risk of myocardial infarction and coronary, cardiovascular, and any death in Eastern Finnish Men. Circulation, 91, 3.
Serafin, T., & Verity, A. (1991). Oxidative mechanisms underlying methyl mercury neurotoxicity. International Journal of Developmental Neuroscience, 9(2), 147-153.
Sorensen, N., Murata, K., Butz-Jorgensen, E., Weihe, P., & Grandjean, P. (1999). Prenatal methymercury expposure as a cordiovscular risk factor at seven years of age. Epidemiology, 10(4), 370-375.
Spyker, J. M. (1972). Subtle consequences of methylmercury exposure: Behavioral deviations in offspring of treated mothers. Science: New Series, 177(4049), 621-623. Retrieved November 27, 2002, http://www.jstor.org
Steuerwald , U., Weibe, P., Jorgensen, P., Bjerve, K., Brock, J., Heinzow, B., et al. (1999). Maternal seafood diet, methymercury exposure, and neonatal neurologic function. The Journal of Pediatrics, 136(5),599-605.
Warkeny, J., & Hubbard, CH. E. (1953). Acrodynia and mercury. Journal of Pediatrics, 42(3), 365-386.
Yoshino, Y., Mozai , T., & Nakao (1966). Distribution of mercury in the brain and its subcellular unnits in experimental organic mercury poisonings, Journal of Neurochemistry. Neurochemistry, 13, 397-406.

Return to top of page

Return to Hazards Home Page