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

MERCURY 328
2. HEALTH EFFECTS
Probably the most widely recognized form of hypersensitivity to mercury is the occurrence of acrodynia,
or pink disease, in persons exposed to mercury. Acrodynia is characterized by itching, flushing, swelling,
and/or desquamation of the palms of the hands or soles of the feet, morbilliform rashes, excessive
sweating and/or salivation, tachycardia, elevated blood pressure, insomnia, weakness, irritability,
fretfulness, and peripheral sensory disturbances (Warkany and Hubbard 1953). The occurrence of
acrodynia was determined to be an idiosyncratic reaction to mercury exposure. Despite widespread
exposure of children to mercury-containing laxatives, antiascariasis medications, and teething powders in
the 1940s and 1950s, only a few children developed acrodynia. The affected population was not the most
highly exposed; numerous reports identified higher exposures in others with no evidence of the disease.
The physiological basis for this hypersensitivity is unknown, but patch testing indicated that it is not an
allergic response to mercury exposure.
Animal studies (Aten et al. 1992; Druet et al. 1978; Hirszel et al. 1985; Hultman and Enestrom 1992;
Matsuo et al. 1989; Michaelson et al. 1985; Pelletier et al. 1990; Pusey et al. 1990; Roman-Franco et al.
1978; van der Meide et al. 1993) and limited human data (Lindqvist et al. 1974; Tubbs et al. 1982) also
indicate that there may be persons with a genetic predisposition to develop an autoimmune glomerulonephritis
upon exposure to mercury. In this form of renal toxicity, proteinuria is observed following the
reaction of autoantibodies with renal tissues and deposition of immune material (i.e., IgG and complement
C3) in the renal mesangium and glomerular blood vessels. Both susceptible and resistant mouse and rat
strains have been identified, and susceptibility appears to be governed by both MHC genes and nonMHC
genes (Aten et al. 1991; Druet et al. 1978; Hultman and Enestrom 1992; Hultman et al. 1992; Michaelson
et al. 1985; Sapin et al. 1984).
Unborn children are another known susceptible population to the toxic effects of mercury (see Section
2.2.2.4). Data from large-scale poisonings in Japan (Harada 1978) and Iraq (Marsh et al. 1987) indicate
that infants exposed in utero to alkyl mercury compounds developed severe neurological toxicity whereas
their mothers may have experienced no or only mild toxicity. This difference may be due to
methylmercury binding to tubulin (Vogel et al. 1985, 1989) and the role of microtubules in neuronal cell
division and migration in the developing nervous system (Sager et al. 1982). There is evidence indicating
that the developing male fetus may be more susceptible to methylmercury exposure than the female fetus
(Buelke-Sam et al. 1985; Grant-Webster et al. 1992; Sager et al. 1984).