Current Trends Acute and Chronic Poisoning from Residential Exposures to Elemental Mercury --- Michigan, 1989 - 1990

From May 1989 through November 1990, eight episodes of elemental mercury exposure in private residences or schools in the United States were reported to the Agency for Toxic Substances and Disease Registry (ATSDR). The case studies in this report document two of these episodes (both in Michigan) of residential mercury poisoning---one involving acute mercury exposure, and the other, chronic exposure to elemental mercury. These episodes illustrate the differing clinical and toxicologic manifestations of acute and chronic mercury poisoning.

Episode 1. On August 7, 1989, four adult occupants (two men and two women ranging in age from 40 to 88 years) of a private home were hospitalized for evaluation of nausea, diarrhea, shortness of breath, and nonspecific chest pain. During hospitalization, the patients experienced progressive dyspnea and pulmonary insufficiency. On August 11, investigators learned that one of the patients had been smelting dental amalgam in a casting furnace in the basement of the home in an attempt to recover silver from the amalgam. Mercury fumes released during the operation apparently had entered air ducts in the basement and had circulated throughout the house.

Because of this mercury vapor exposure, chelation therapy with dimercaprol was initiated in the patients. On August 12, urine mercury concentrations from three of the patients ranged from 94 to 423 ug/L; serum mercury concentrations from two patients were 127 and 161 ug/L.

Despite chelation therapy and vigorous ventilatory support treatment, the condition of the patients continued to deteriorate. All of the patients died within 11-24 days after exposure to the mercury vapor. The cause of death was considered to be mercury poisoning, which resulted in adult respiratory distress syndrome and subsequent respiratory failure. Postmortem mercury concentrations in organs from the four patients were 300-2100 ug/g (kidney), 3-2400 ug/g (liver), less than 1-100 ug/g (brain), and 1-150 ug/g (lung); concentrations in blood ranged from 58 ug/L to 369 ug/L.

Measurements of ambient indoor air concentrations of mercury taken 11-18 days after the exposure were as high as 786 ug/m3 in the basement and 912 ug/m3 on the first floor. The house was extensively cleaned to reduce the mercury contamination; however, decontamination efforts did not reduce indoor air mercury concentrations to an acceptable level, and the house was subsequently demolished.

Episode 2. On August 21, 1989, a young girl was admitted to the hospital because of impaired gait. She was diagnosed as having a postinfectious viral syndrome and was discharged on August 23. On September 11, she was readmitted to the hospital when she could no longer walk. On September 19, an older sister of the patient was admitted to the hospital with similar symptoms. Clinical evaluation of both girls revealed numbness in the fingers and toes, absence of deep tendon reflexes, elevated blood pressure, and an elevated level of protein in the cerebrospinal fluid. Mercury poisoning was diagnosed, and chelation therapy was started in the two children. Subsequently, on October 3, their asymptomatic brother was hospitalized for a chelation challenge, which detected a substantial mercury load.

After chelation therapy, the brother remained asymptomatic, and the older sister improved and was discharged from rehabilitation therapy. The index patient had numerous residual neurologic abnormalities, including visual field defects, mild upper and lower extremity weakness, and some emotional lability.

Subsequent investigations revealed that earlier that summer about 20 cm3 of liquid mercury had been spilled in the boy's bedroom. Examination of the house using a mercury vapor analyzer detected indoor air mercury concentrations of 10-40 ug/m3. Clean-up efforts included removing carpet from several areas in the house, replacing the carpet and wooden subfloor in the bedroom where the spill occurred, and commercially cleaning all other carpet and furniture. Reported by: C Taueg, MPH, Wayne County Health Dept; DJ Sanfilippo, MD, Grand Rapids; B Rowens, MD, Detroit; J Szejda, Ottawa County Human Svcs, Holland; JL Hesse, MS, Michigan Dept of Public Health. Div of Health Assessment and Consultation, Agency for Toxic Substances and Disease Registry.

Editorial Note

Editorial Note:

Although the toxic properties of elemental mercury have been recognized since at least the 1500s, occupational and residential exposures to mercury remain a source of poisoning.

Although death is an infrequent outcome of acute exposure to mercury, the first episode described in this report illustrates the clinical progression following exposure. Patients are usually asymptomatic during the first 1-4 hours following acute exposure to high air concentrations of mercury vapor. Symptoms start abruptly and may include fever, chills, nausea, general malaise, and respiratory difficulties (shortness of breath, pain and tightness in the chest, and paroxysmal coughing). In severe cases, pulmonary edema may cause death within a few days (1,2).

After inhalation, elemental mercury is readily absorbed through the alveolar membranes and transported by blood to the brain and other tissues of the nervous system. Mercury is rapidly converted by the blood to mercuric ions, which are then excreted in the urine and feces. Diagnosis of mercury toxicity is aided by the detection of elevated concentrations of mercury in blood or urine samples. Background urine concentrations of mercury in persons with no unusual exposure to mercury range from 1 to 25 ug/L; 95% of such urine samples contain less than 20 ug/L (1). Although urine mercury concentrations correlate poorly with manifestations of mercury poisoning, symptoms may appear when the urine mercury concentrations exceed 300 ug/L (3). In unexposed persons, blood mercury concentrations are usually less than 3 ug/L, but may be substantially higher in persons with a high dietary intake of fish (1).

Residential and occupational cases of mercury poisoning more commonly result from chronic exposures, as illustrated by the second episode described in this report. Spilled mercury gravitates to cracks in the floor and into the pile of carpets. Even though it may not be visible, the mercury can slowly volatilize indoors and may lead to chronic mercury poisoning through inhalation exposure. Vacuuming a contaminated area may facilitate the spread of mercury vapor throughout the house.

The potential for indoor mercury exposure is increased when indoor air exchange is reduced (e.g., when doors and windows are kept closed). Warm air from heating ducts and vents may enhance volatilization when circulated over spilled mercury. Mercury vapor concentration is likely to be higher near the floor, and children may be exposed to higher concentrations of mercury than adults.

The vagueness of the early clinical signs of central nervous system (CNS) toxicity characteristic of mercury poisoning often result in misdiagnosis. If exposure to mercury continues, the severity of symptoms may progress as a function of mercury concentration, length of exposure, and individual sensitivity. The CNS toxicity of mercury is both neurologic and psychologic. Fine tremors in the fingers, eyelids, and lips are early signs of mercury toxicity. Tremors in the hands and arms may interfere with precision movements and impair skills such as handwriting. Common psychopathologic symptoms include depression, irritability, exaggerated response to stimuli, excessive shyness, insomnia, and emotional instability (1,2).

Potential sources of elemental mercury in the home include mercury switches and mercury-containing devices such as thermostats, thermometers, and barometers. Family members may also bring into the home elemental mercury obtained from laboratories, dental offices, or other industrial sources.

In the ATSDR Toxicological Profile for Mercury, the minimal risk level (MRL) for chronic inhalation exposure to elemental mercury was determined to be 0.3 ug/m3 (1). An MRL is an estimate of the daily human exposure to a chemical that is likely to be without an appreciable risk of deleterious (noncarcinogenic) effects during a specified period of exposure. Chronic inhalation exposure to elemental mercury concentrations below the MRL would not be expected to result in adverse health effects (1).

References

1. Agency for Toxic Substances and Disease Registry. Toxicological profile for mercury. Atlanta: US Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry, 1989; publication no. ATSDR/TP-89/16.

2. Gerstner HB, Huff JE. Clinical toxicology of mercury. J Toxicol Environ Health 1977;2:491--526.

3. Knight AL. Mercury and its compounds. In: Zenz C, ed. Occupational medicine: principles and practices. 2nd ed. Chicago: Year Book Medical Publishers, 1988:590--6.

4. Occupational Safety and Health Administration. Air contaminants: final rule. Federal Register 1989;54:2415--6.

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