revised final - Agency for Toxic Substances and Disease Registry ...

MERCURY 120
2. HEALTH EFFECTS
admission, the patient developed a progressive deterioration in balance, gait, and speech. During the
previous 2 months, she had experienced brief episodes (spaced weeks apart) of nausea, diarrhea, and
abdominal discomfort; and had lost 6.8 kg (15 lb). Medical examination revealed moderate upper-
extremity dysmetria, dystaxic handwriting, a widely based gait, and “mild scanning speech.” Routine
laboratory test results were normal. Computed tomography (CT) and magnetic resonance imaging (MRI) of
the head were normal except for the incidental finding of a probable meningioma, 1 cm in diameter. The
cerebrospinal fluid was clear, with a protein concentration of 42 mg/dL and no cells. A preliminary
laboratory report indicated that the whole-blood mercury concentration was more than 1,000 µg/L (normal
range, 1–8 µg/L; toxic level, >200 µg/L). Chelation therapy with oral succimer (10 mg/kg orally every
8 hours) was begun on day 168 after exposure. Whole blood concentrations rose to 4,000 µg/L after one
day of chelation, and urinary mercury levels were 234 µg/L (normal range, 1–5 µg/L; toxic level,
>50 µg/L). Despite the initial success of chelation therapy, administration of vitamin E, and a blood
exchange transfusion, at 176 days postexposure, the patient became comatose. Further aggressive general
support and chelation therapy failed, life support ws removed (following the patient’s advance directive),
and the patient died 298 days post exposure. Autopsy results revealed diffusely thin cortex of the cerebral
hemispheres (to 3 mm), and extensive gliosis of the visual cortex around the calcarine fissure and the
superior surface of the superior temporal gyri. The cerebellum showed diffuse atrophy of both vermal and
hemispheric folia. Microscope evaluation revealed extensive neuronal loss and gliosis bilaterally within the
primary visual and auditory cortices, with milder loss of neurons and gliosis in the motor and sensory
cortices. There was widespread loss of cerebellar granular-cell neurons, Purkinje cells, and basket-cell
neurons, with evidence of loss of parallel fibers in the molecular layer. Bergmann’s gliosis was well
developed and widespread.
In the only other organic mercury studies identified for dermal exposures, a study of a large group of people
who consumed methylmercury-contaminated bread over a 1- to 3-month period showed a dose-related
history of rashes (Al-Mufti et al. 1976). These may also have been allergic responses. A 13-month-old
child who ingested porridge made from flour that had been treated with an alkyl mercury compound
(specific mercury compound not reported) developed a measles-like rash, fever, and facial flushing
(Engleson and Herner 1952). Also, Iraqis who consumed flour made from grain treated with ethylmercury
p-toluene sulfonanilide exhibited skin lesions consisting of pruritus on the palms, soles, and genitalia (Jalili
and Abbasi 1961). In severe cases, exfoliative dermatitis of the hands and feet was also observed.