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

MERCURY 247
2. HEALTH EFFECTS
Myers et al. (1997) evaluated the population of the SCDS for developmental milestones similar to those
determined in Iraq. As part of this ongoing study, cohort children were evaluated at 6.5, 19, 29, and
66 months of age. At 19 months care-givers were asked at what age the child walked (n=720 out of 738)
and talked (n=680). Prenatal mercury exposure was determined by atomic absorption analysis of maternal
hair segments corresponding to hair growth during the pregnancy. The median mercury level in maternal
hair for the cohort in this analysis was 5.8 ppm, with a range of 0.5–26.7 ppm. The mean age (in months) at
walking was 10.7 (SD=1.9) for females and 10.6 (SD=2.0) for males. The mean age for talking (in months)
was 10.5 (SD=2.6) for females, and 11 (SD=2.9) for males. After adjusting for covariates and statistical
outliers, no association was found between the age at which Seychellois children walked or talked and
prenatal exposure to mercury. The ages for achievement of the developmental milestones were normal for
walking and talking in the Seychellois toddlers following prenatal exposure to methylmercury from a
maternal fish diet.
Clarkson (1995) raised some interesting issues concerning whether is it reasonable to apply health effects
data based on an acute exposure to methylmercury fungicide eaten in homemade bread (in the 1971–1972
Iraq incident) to fish-eating populations having chronic exposure to much lower concentrations of methylmercury.
He addressed two specific issues. The first regards the body's "defense mechanisms" that serve to
mitigate the potential damage from mercury. One such mechanism in the case of methylmercury involves
an enterohepatic cycling process in which methylmercury from dietary sources absorbed through the
intestine is carried to the liver, where substantial quantities are secreted back into the bile and returned to
the intestinal tract. During the residence time in the gut, microflora break the carbon-mercury bond,
converting methylmercury into inorganic mercury, which in turn is poorly absorbed and is excreted in the
feces. This creates an effective detoxification pathway for low-dose dietary exposures to methylmercury,
but probably not for acute, high-dose exposures, such as occurred in Iraq. Secondly, the transport of
methylmercury into brain tissue is inhibited by the presence of many amino acids, including leucine,
methionine, and phenylalanine. Thus, it is possible that the rising plasma concentrations of amino acids
from ingestion of fish protein may serve to depress the uptake of methylmercury by the brain.
While both of these issues need further laboratory/clinical investigation, they do raise appropriate questions
concerning the relevance of the relatively short-term (i.e., about 6 weeks), high-level contaminated grain
exposure scenario encountered in Iraq to the dietary methylmercury exposure scenarios encountered in
many fish-eating populations (e.g., the Seychelles Islanders, Faroe Islanders, Peruvian villagers, and Inuit
native people of Greenland). This position is supported by Cicmanec (1996), who reviewed data from the