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Epidemiologic Notes and Reports Elemental Mercury Poisoning in a Household -- Ohio, 1989

On November 22, 1989, a 15-year-old male who had been hospitalized in Columbus, Ohio, was diagnosed with acrodynia, a form of mercury poisoning. This report describes the investigation by the Columbus Health Department (CHD) to determine the source of the patient's exposure to mercury.

In early November, following an acute illness, the patient was diagnosed with measles. He was subsequently referred for psychiatric evaluation because of his declining performance in school and nonspecific complaints (e.g., aches, irritability, and inability to think clearly) that were presumed to be psychosomatic. On November 17, he was admitted to the hospital after his blood pressure measured 142 mm Hg systolic and 106 mm Hg diastolic. Additional manifestations noted at that time included rash, sweating, cold intolerance, tremor, irritability, insomnia, and anorexia. When analysis of a 24-hour urine collection detected a mercury level of 840 ug/L (reference: less than 20 ug/L (1)), acrodynia was diagnosed. On December 1, the patient's 11-year-old sister was hospitalized with hypertension, mild acrodynia, irritability, and mild generalized muscle weakness. Her 24-hour urine mercury level was 1500 ug/L. Although both parents were asymptomatic, their 24-hour urine mercury levels were 820 ug/L and 1250 ug/L.

On November 29, the CHD investigated the apartment where the family had lived since August 26, 1989. Neighbors reported that the previous tenant had spilled a large jar of elemental mercury within the apartment. Although this tenant could not be located for confirmation, mercury vapor concentrations in seven rooms ranged from 50-400 ug/m3 (the Agency for Toxic Substances and Disease Registry's acceptable residential indoor air mercury concentration is less than or equal to 0.5 ug/m3 (2)). The apartment was sealed, pending decontamination efforts which are ongoing. In three other apartments in the same building, air mercury concentrations were less than the measuring instrument's detection limit of 10 ug/m3. The CHD did not detect evidence of mercury cross-contamination in a mobile home where the patients' family had relocated in November 1989.

After both patients were diagnosed as having acrodynia with neuropsychiatric impairment, they were treated with oral 2,3-dimercaptosuccinic acid (DMSA). From December 1, 1989, to April 4, 1990, the male patient's 24-hour urine mercury values declined from 1540 ug/L to 101 ug/L. Except for a persistent mild tremor, acrodynia and other neurologic symptoms resolved following two 21-day courses of DMSA therapy. The female patient's course was complicated by a progressive sensorimotor peripheral neuropathy that caused profound upper and lower extremity weakness. During DMSA treatment, she gradually improved; within 3 months, she was able to walk short distances without assistance. By February 6, 1990, her 24-hour urine mercury excretion was 352 ug/L; DMSA therapy was continued. Reported by: ME Mortensen, MD, S Powell, TJ Sferra, MD, Dept of Pediatrics, The Ohio State Univ, Central Ohio Poison Center, Children's Hospital, Columbus, Ohio; R Lautzenheiser, I Sobeih, M Pompili, TC Long, MD, Columbus Health Dept, Columbus, Ohio. TW Clarkson, PhD, Environmental Health Sciences Center, Univ of Rochester School of Medicine, Rochester, New York. B Semple, MD, Johnson & Johnson Consumer Products, Inc, Skillman, New Jersey. Div of Environmental Hazards and Health Effects, Center for Environmental Health and Injury Control, CDC.edEditorial Note:

Although nonoccupational elemental mercury poisoning occurs less frequently than occupational mercury poisoning (3), cases of elemental mercury exposure and toxicity in children have been reported (3-9). Because mercury vapors are dense and tend to settle, children playing near the floor may be exposed to mercury if it is present (8). Moreover, children may be physiologically more susceptible to the health hazards of mercury exposure than adults.

Elemental mercury (also termed metallic mercury or quicksilver) is volatile at room temperature, and its rate of vaporization is a function of both temperature and surface area (10). Mercury enters the bloodstream after it is inhaled; because of its lipid solubility, mercury crosses both the blood brain barrier and the placenta (1,11,12). Elemental mercury is excreted in the urine and has an elimination half-life of approximately 60 days (11).

Because of mild symptomotology and the potential for misdiagnosis, cases of mercury poisoning may not be readily recognized. Individual susceptibility to mercury poisoning varies considerably, and not all persons exposed will develop symptoms (5). Manifestations of mercury poisoning include intention tremor, memory loss, insomnia, timidity, gingivitis, diarrhea, anorexia, weight loss, and, in severe cases, delirium. Acrodynia may be misdiagnosed as measles, other viral exanthems, or Kawasaki disease. Manifestations of acrodynia include a generalized rash; irritability; photophobia; profuse perspiration; and redness, swelling, and peeling of the skin on hands and feet (11,12). Although acrodynia is more common in infants and young children, it has been reported in adolescents and a 41-year-old male (5).

Mercury is used in some school laboratories; in such settings, its ambient concentrations (and the safeguarding of mercury supplies) should be carefully monitored. Additionally, mercury is added into many household products, such as latex paints, adhesives, joint compounds, acoustical plates, and cleaning solutions. Because not all products that contain mercury are labeled as such, adequate ventilation must be ensured when using potentially toxic household chemicals.


  1. Friberg L, Vostal J, eds. Mercury in the environment: an

epidemiological and toxicological appraisal. Cleveland, Ohio: CRC Press, 1972.

2. Agency for Toxic Substances and Disease Registry. Preliminary health assessment, Olin Chemical Co. Atlanta: US Department of Health and Human Services, Public Health Service, 1988.

3. CDC. Elemental mercury vapor poisoning--North Carolina, 1988. MMWR 1989;38:770-2, 777.

4. CDC. Mercury exposure in a high school laboratory--Connecticut. MMWR 1988;37:153-5.

5. McNeil NI, Oliver RE, Issler HC, Wrong OM. Domestic metallic mercury poisoning. Lancet 1984;1:269-71.

6. Sexton DJ, Powell KE, Liddle J, Smrek A, Smith JC, Clarkson TW. A nonoccupational outbreak of inorganic mercury vapor poisoning. Arch Environ Health 1978;33:186-91.

7. Tunnessen WW, McMahon KJ, Baser M. Acrodynia: exposure to mercury from fluorescent light bulbs. Pediatrics 1987;79:786-9.

8. Curtis HA, Ferguson SD, Kell RL, Damuel AH. Mercury as a health hazard. Arch Dis Child 1987;62:293-5.

9. Alexander JF, Rosario R. A case of mercury poisoning: acrodynia in a child of 8. Can Med Assoc J 1971;104:929-30. 10. Goldwater LJ. The toxicology of inorganic mercury. Ann N Y Acad Sci 1957;65:498-503. 11. Braunwald E, Isselbacher KJ, Petersdorf RG, Wilson JD, Martin JB, Fauci AS, eds. Harrison's principles of internal medicine. 11th ed. New York: McGraw-Hill, 1987. 12. Last JM. Public health and preventive medicine. 12th ed. Norwalk, Connecticut: Appleton-Century Crofts, 1986.

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