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

MERCURY 320
2. HEALTH EFFECTS
dysfunction was evident in 62 mercury workers with average blood mercury levels of 1.6 µg/100 mL
(range, 0.25–7.56 µg/100 mL) and average urine mercury levels of 56 µg/g creatinine (range, 3–272 µg/g
creatinine) (Lauwerys et al. 1983). Another renal parameter evaluated is β-microglobulin, which has a
normal range of 0.004–0.37 mg/L (Naleway et al. 1991). No statistically significant relationship was
found between urinary β-microglobulin levels and elevated urinary mercury concentrations (Ehrenberg et
al. 1991; Naleway et al. 1991). Examination of a wide range of biomarkers for renal toxicity in a group of
chloralkali workers identified several other changes at low urinary mercury levels (Cardenas et al. 1993).
Workers with urinary mercury levels in the range of 5–50 µg/g creatinine showed statistically significant
increases in urinary Tamm-Horsfall glycoprotein (localized in the epithelial cells of the convoluted
tubules) and decreases in urinary prostaglandins E2 and F2α. In workers with >50 µg/g creatinine,
increased NAG, tubular brush border antigens, alkaline phosphatase, thromboxane B2, and
glycosaminoglycans were also observed. Urinary porphyrins, which are intermediates in the biosynthesis
of heme, may be another potential biomarker of effect for mercury exposure. A correlation was observed
between urinary mercury and urinary coproporphyrin (Wada et al. 1969). Correlations were also observed
for decreases in δ-aminolevulinic acid-dehydratase and cholinesterase activity with increases in urinary
mercury. Porphyrins are considered a nonspecific measure of effect because they are influenced by other
metal exposures. Woods et al. (1991) present data suggesting that there is a specific urinary porphyrin
profile that may serve as a biomarker of mercury accumulation in the kidneys during prolonged inorganic
and organic mercury exposure. A urinary porphyrin pattern, characterized by elevated coproporphyrin,
pentacarboxyl porphyrin, and precoproporphyrin, for methylmercury hydroxide exposure was observed in
mice for up to 30 weeks. This profile is observed at variable dose levels, as well as up to at least 40 weeks
after cessation of exposure. The time course of the profile during prolonged treatment is closely associated
with divalent inorganic mercury (Hg +2 ), suggesting that the effects are mediated by this cation because it
inhibits the heme pathway (Woods et al. 1991). Specificity may be a problem unless the porphyrin levels
are analyzed at the same time as urinary mercury measurements.
The neurophysiological and neuropsychological health effects of mercury have been extensively studied in
occupationally exposed individuals in an effort to monitor body levels and to determine a threshold value
below which these effects are unlikely to occur. As with other biomarkers of effect, neurological changes
induced by mercury may resemble exposure to other chemicals that can cause damage to the brain.
Case studies have associated exposure to mercury vapor with neurological effects (e.g., tremors, insomnia,
shyness, emotional instability, decreased motor function and muscle reflexes, headaches, and abnormal