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

MERCURY 104
2. HEALTH EFFECTS
Chronic exposure to mercuric chloride resulted in increased mortality in male rats at 1.9 mg Hg/kg/day but
no increase in mortality in female rats at up to 3.7 mg Hg/kg/day or in either male or female mice at up to
7.4 mg Hg/kg/day (NTP 1993). Renal lesions in the male rats were thought to contribute to the early deaths
in these animals.
The highest NOAEL values and all reliable LOAEL values for death for each species and duration category
are recorded in Table 2-2 and plotted in Figure 2-2 for inorganic mercury.
Organic Mercury. The acute lethal dose of organic mercury compounds for humans is difficult to assess
from the available literature. Death resulting from organic mercury ingestion has been amply documented
following outbreaks of poisoning (Minamata disease) after consumption of methylmercury-contaminated
fish in Minamata, Japan (Tsubaki and Takahashi 1986) and after consumption of grains contaminated with
methyl- and ethylmercury in Iraq (Al-Saleem and the Clinical Committee on Mercury Poisoning 1976;
Bakir et al. 1973). Death occurred in two boys who ate meat from a butchered hog that had been fed seed
treated with ethylmercuric chloride (Cinca et al. 1979). However, primarily because of the delay between
mercury consumption and the onset of symptoms, the amount of organic mercury ingested in these cases is
difficult to determine. Fatal doses estimated from tissue concentrations range from 10 to 60 mg/kg (EPA
1985b). A case-control study examining the cause of death for patients with Minamata disease compared to
the cause of death in unexposed persons showed that those patients who died prior to 1970 had significantly
increased noninflammatory diseases of the nervous system; Minamata disease was reported as the
underlying cause of death (Tamashiro et al. 1984). For this group, pneumonia and nonischemic heart
disease were reported as prominent secondary cause of death. For those patients who died between 1970
and 1980, significant increases in Minamata disease were reported as the primary cause of death.
Nonischemic heart disease correlated with the incidence of Minamata disease, and noninflammatory central
nervous system disease was a prominent secondary cause of death in this group.
Methylmercury toxicity is very strain- and sex-specific in mice. A single oral dose of methylmercuric
chloride at 16 mg Hg/kg resulted in the death of 4 of 6 male mice (C57BL/6N Jcl strain) but no deaths in
females (Yasutake et al. 1991b). No increase in mortality was observed in female mice until 40 mg Hg/kg
was administered, at which dosage 4 of 6 females died. Twenty-six weeks of dietary exposure to methylmercuric
chloride resulted in increased mortality in both male and female mice (ICR strain) at
3.1 mg Hg/kg/day (Mitsumori et al. 1981). Chronic (104 weeks) dietary exposure to methylmercuric