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

MERCURY 140
2. HEALTH EFFECTS
Testicular effects were also observed after chronic-duration exposure to methylmercuric chloride. Tubular
atrophy of the testes was observed in mice ingesting 0.69 mg Hg/kg/day in their feed for up to 2 years
(Mitsumori et al. 1990). Decreased spermatogenesis was observed in mice receiving 0.73 mg Hg/kg/day in
the diet (Hirano et al. 1986). No adverse effects on the testes were observed in these studies at
0.14–0.15 mg Hg/kg/day. Similarly, no adverse effects were observed in the testes, prostate, ovaries, or
uterus of rats exposed through the diet to 0.1 mg Hg/kg/day as methylmercuric chloride for 2 years
(Verschuuren et al. 1976).
The highest NOAEL values and all reliable LOAEL values for reproductive effects in each species and
duration category are recorded in Table 2-3 and plotted in Figure 2-3 for organic mercury.
2.2.2.6 Developmental Effects
Inorganic Mercury. No studies were located regarding developmental effects in humans or animals
following oral exposure to inorganic mercury.
Organic Mercury. When grains treated with fungicides containing mercury have been accidentally
consumed or when fish with high levels of methylmercury have been eaten, epidemics of human mercury
poisonings have occurred with high incidences of developmental toxicity. These episodes, as well as case
reports from isolated incidences of maternal consumption of organic forms of mercury during pregnancy,
have provided evidence that the developing nervous system of the fetus is highly sensitive to mercury
toxicity. The first such incident was reported in Sweden in 1952 when flour from grain treated with an
unspecified alkyl mercury compound ingested by a pregnant woman was associated with developmental
toxicity. An apparently normal infant was born, but the infant later displayed brain damage manifested by
mental retardation, incoordination, and inability to move (Engleson and Herner 1952). A 40-year-old
woman, 3 months pregnant, consumed methylmercury-contaminated meat for an unspecified duration and
subsequently delivered a male infant with elevated urinary mercury levels (Snyder and Seelinger 1976). At
3 months, the infant was hypotonic, irritable, and exhibited myoclonic seizures. At 6 years of age, the child
displayed severe neurological impairment (e.g., blindness, myoclonic seizures, neuromuscular weakness,
inability to speak) (Snyder and Seelinger 1976). In the 1955 mercury poisoning outbreak in Minamata,
Japan, severe brain damage was described in 22 infants whose mothers had ingested fish contaminated with
methylmercury during pregnancy (Harada 1978). The types of nervous system effects described in the
Minamata outbreak included mental retardation; retention of primitive reflexes; cerebellar symptoms;