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

MERCURY 269
2. HEALTH EFFECTS
died following acute-duration, high-level exposure to elemental mercury vapor (Kanluen and Gottlieb 1991;
Rowens et al. 1991). A lethal oral dose of mercuric chloride in a 35-year-old man also resulted in jaundice,
an enlarged liver, and elevated aspartate aminotransferase, alkaline phosphatase, lactate dehydrogenase, and
bilirubin (Murphy et al. 1979).
Inhalation of 6–28.8 mg/m 3 mercury vapor for 6 hours to 11 weeks by rabbits produced effects ranging from
mild pathological changes to severe necrosis in the liver, including necrosis and degeneration; effects were
less severe at the shorter durations (Ashe et al. 1953). Intermediate-duration oral exposure to inorganic
mercury has also been associated with increases in hepatic lipid peroxidation (Rana and Boora 1992) and in
serum alkaline phosphatase (Jonker et al. 1993a). It is unclear to what extent these effects were due to the
direct toxic effects of mercury on the liver or were secondary to shock in the exposed animals. Reliable
information regarding hepatic effects following organic mercury exposure was not located. These limited
data suggest the potential hepatic toxicity of short-term inhalation of high concentrations of mercury vapor to
humans. It is unlikely that persons at hazardous waste sites would ingest sufficiently large amounts of
mercuric chloride to cause hepatic toxicity.
Renal Effects. The kidney is one of the major target organs of mercury-induced toxicity. Adverse
renal effects have been reported following exposure to metallic, inorganic, and organic forms of
mercury in both humans and experimental animals. The nephrotic syndrome in humans associated
with the ingestion, inhalation, or dermal application of mercury is primarily identified as an
increase in excretion of urinary protein, although depending on the severity of the renal toxicity,
hematuria, oliguria, urinary casts, edema, inability to concentrate the urine, and
hypercholesterolemia may also be observed (Agner and Jans 1978; Afonso and deAlvarez 1960;
Anneroth et al. 1992; Barr et al. 1972; Buchet et al. 1980; Campbell 1948; Cinca et al. 1979;
Danziger and Possick 1973; Dyall-Smith and Scurry 1990; Engleson and Herner 1952; Friberg et
al. 1953; Hallee 1969; Jaffe et al. 1983; Jalili and Abbasi 1961; Kang-Yum and Oransky 1992;
Kanluen and Gottlieb 1991; Kazantzis et al. 1962; Langworth et al. 1992b; Murphy et al. 1979;
Pesce et al. 1977; Piikivi and Ruokonen 1989; Roels et al. 1982; Rowens et al. 1991; Samuels et al.
1982; Snodgrass et al. 1981; Soni et al. 1992; Stewart et al. 1977; Tubbs et al. 1982). These effects
are usually reversible. However, in the most severe cases, acute renal failure has been observed
(Afonso and deAlvarez 1960; Davis et al. 1974; Jaffe et al. 1983; Kang-Yum and Oransky 1992;
Murphy et al. 1979; Samuels et al. 1982). Renal biopsies and/or autopsy results have primarily