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

MERCURY 106
2. HEALTH EFFECTS
difficulties in Long-Evans rats after dietary exposure to 2.2 mg Hg/kg/day as mercuric chloride for
3 months (Goldman and Blackburn 1979).
Organic Mercury. Limited information was located regarding respiratory effects in humans after oral
exposure to organic mercury. Two boys who died after eating meat from a hog that had eaten seed treated
with ethylmercuric chloride developed bronchopneumonia and edematous alveolitis, and required artificial
ventilation (Cinca et al. 1979). Bronchopneumonia was also identified as the cause of death in four adults
and one infant who died as the result of methylmercury poisoning in Iraq during 1972 (Al-Saleem and the
Clinical Committee on Mercury Poisoning 1976). It is unclear whether these respiratory effects were the
result of direct effects on the respiratory system or were secondary to other effects.
The only information located regarding respiratory effects in animals after oral exposure to organic mercury
comes from a study in which rats were exposed to methylmercuric chloride in the diet for 2 years
(Verschuuren et al. 1976). This study showed no treatment-related histopathological lesions in the lungs of
exposed rats at 0.1 mg Hg/kg/day.
Cardiovascular Effects
Inorganic Mercury. Cardiovascular toxicity has been observed following ingestion of mercuric chloride
and mercurous chloride in humans. The majority of the information regarding cardiovascular effects comes
from reports of children who were treated with mercurous chloride tablets for worms or mercurous
chloride-containing powders for teething discomfort (Warkany and Hubbard 1953). These authors
described multiple cases in which tachycardia and elevated blood pressure were observed in the affected
children. The only information located regarding cardiovascular effects in humans after ingestion of
mercuric chloride comes from a case study of a 22-year-old who attempted suicide by ingesting
approximately 20 mg Hg/kg as mercuric chloride (Chugh et al. 1978). An electrocardiogram showed no
P wave, prolongation of the QRS segment, and a high T wave. The authors suggested that these
cardiovascular effects were secondary to severe hyperkalemia.
Exposure of rats to 28 mg Hg/kg/day as mercuric chloride for 180 days in drinking water resulted in an
increase in blood pressure, a decrease in cardiac contractility, and no effect on heart rate (Carmignani et al.
1992). The increase in blood pressure was attributed to a vasoconstrictor effect, and the decrease in
contractility was attributed to the direct toxic effect of the mercury on the cardiac muscle. Slightly