Delayed cerebellar disease and death after accidental exposure to dimethylmercury

Delayed cerebellar disease and death after accidental exposure to dimethylmercury
Ingestion of fish or grains contaminated with methylmercury led to epidemics of severe neurotoxicity and death in Japan in the 1950s and 1960s and in Iraq in 1972. The World Health Organization and other organizations have warned of the dangers of methylmercury compounds to the environment and scientific researchers .1,3-6 Dimethylmercury may be more dangerous than methylmercury compounds. The physical properties of dimethylmercury allow transdermal absorption, and the volatility of the liquid allows intoxication by inhalation. Because a dose of approximately 400 milligrams of mercury (the equivalent of a few drops, or approximately 5 milligrams per kilogram of body weight) is fatal, dimethylmercury is classified as hypertoxic according to classic toxicology textbook ratings. 7
We report the case of accidental dimethylmercury poisoning in a chemist whose research focused on the biological toxicity of heavy metals. 8,9 Records show she handled dimethylmercury on just one day, while wearing latex gloves and working under a ventilation hood designed to prevent exposure to chemical dimethylmercury fumes. She had delayed but ultimately fatal neurotoxic effects similar to those caused by methylmercury compounds. This case illustrates the potent toxicity of dimethylmercury and the need for additional safety precautions if it is used in any scientific research

On January 20, 1997, a 48-year-old chemistry professor was admitted to Dartmouth-Hitchcock Medical Center in Lebanon, New Hampshire, with a five-day history of progressive deterioration in balance, gait, and speech. She lost 6.8 kilograms (15 pounds) in two months and experienced several brief bouts of nausea, diarrhea, and abdominal discomfort.
The patient recalled that in August 1996, while she was transferring liquid dimethylmercury from a container to a capillary tube, she spilled a few drops from the pipette tip onto the back of her gloved hand. (Subsequent review of her dated laboratory notebooks, historical records provided by colleagues, and examination of dated materials used in the experiment later determined the date to be August 14, 1996.) She reported that she had The spill was cleaned up and removed. Her protective gloves.
The patient is thin but appears healthy and is appropriately concerned about her neurological problems. Examination revealed moderate upper limb dysmetria, dysgraphia, a broad gait, and mild “saccadic speech.” Routine laboratory test results were normal. Computed tomography (CT) and magnetic resonance imaging (MRI) of the head were normal except for the incidental discovery of a possible meningioma, 1 cm in diameter. The cerebrospinal fluid was clear, with a protein concentration of 42 mg/dl and no cells.
Because methylmercury can be neurotoxic, blood and urine samples were sent for emergency measurement of mercury levels. Given the long interval between the date of mercury exposure and the onset of neurological symptoms (154 days) and the rapid progression of symptoms, other causes of acute cerebellar dysfunction were considered.
Over the next few days, the patient experienced symptoms such as tingling in the fingers, brief flashes of light in the eyes, faint background noise in both ears, and progressive difficulty with speech, walking, hearing, and vision (narrow field of vision). Preliminary laboratory reports show whole blood mercury levels exceeding 1,000 micrograms per liter. Oral succinic acid chelation therapy (10 mg/kg PO every 8 hours) was initiated on day 168 after exposure. The next day, the following laboratory values were reported: whole blood mercury, 4000 micrograms per liter (normal range, 1 to 8; toxic level, >200); urine mercury, 234 micrograms per liter (normal range, 1 to 5; toxic level) level, >50).

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