ABSTRACTS
Smith JC, Allen PV, Von Burg R. "Hair Methylmercury Levels in U.S. Women." Arch Environ Health. 1997 Nov-
Dec;52(6):476-80.
On Site Therapeutics, Inc., Wayland, Massachusetts 01778, USA.
The scientific community has recently focused its concerns on possible developmental delays in infants exposed to
methylmercury via maternal fish consumption. In this study, the authors reported levels of methylmercury in hair
specimens that corresponded to 2820 monthly seafood consumption diaries recorded by U.S. women of
childbearing age. In this study, the geometric mean hair methylmercury level for diarists who reported some
seafood consumption was 0.36 ppm (one geometric standard deviation [GSD] range = 0.14-0.90 ppm); the
corresponding value for diarists who reported no seafood consumption was 0.24 ppm (one GSD range = 0.09-0.62
ppm). Therefore, the mean hair methylmercury level associated with seafood consumption was 0.12 ppm (one GSD
range = 0.05-0.32 ppm). The results of this study provide evidence that levels of methylmercury in the U.S.
population are quite low. There is a significant contribution to hair methylmercury from sources other than seafood.
It is not likely that maternal hair methylmercury levels in the range found in our study would be associated with
adverse health effects in children.
Von Burg R, Penney DP, Conroy PJ. "Acrylamide neurotoxicity in the mouse: a behavioral,
electrophysiological and morphological study." J Appl Toxicol. 1981 Aug;1(4):227-33.
The development of acrylamide induced neurotoxicity was followed for 3 weeks in the mouse by behavioral testing,
determination of conduction velocities and electron microscopic examination of peripheral nerves. Neurotoxic signs
began to appear during the second week of treatment. A condition of severe intoxication developed within 21 days.
Behavioral assessment for neurological deficits proved to be more sensitive than sensory or motor conduction
velocity determinations either in isolated preparations or in situ. In general, such electrophysiological
determinations did not result in reproducible, statistically significant, differences from control animals until the third
week of acrylamide administration. However, there was a suggestion that temperature reduction may provide a
provocative change to increase the sensitivity of such electrophysiological measurements. Electron microscopic
examination of the nerves of severely poisoned animals revealed myelin corrugation and delamination to be the
most consistent damage. Acrylamide appeared to produce a nonselective attack since degenerating fibers were
found intermingled with almost normal fibers of approximately the same diameter. In general, the production of
neurotoxicity in the mouse closely resembled that seen in the rat but some differences were noted.
Von Burg R, Smith JC. "Biliary mobilization of cadmium by 2,3-dimercaptopropanol and some related
compounds." J Toxicol Environ Health. 1980 Jan;6(1):75-85. Related Articles, Links
No effective therapeutic agent for mobilizing tissue Cd has been reported to date, but the results presented here
demonstrate that 2,3-dimercaptopropanol (BAL) , at doses approaching and surpassing the maximum tolerated,
can produce a rapid transient enhancement of Cd excretion in the rat. When BAL (75 mg/kg) was administered by
a single injection 24 h after a tracer dose of 109Cd, as much as 32% of the administered Cd appeared in the bile.
A correlation between the appearance of radiocadmium and the biliary sulfhydryl concentration was found. There
was indirect evidence for a 1:3 Cd-BAL complex in the bile, which may explain the efficacy of higher doses of BAL.
A comparative study with some selected dithiol compounds suggests that vicinal sulfhydryl groups on an aliphatic
chain are the more effective Cd mobilizing compounds, but BAL was the most effective agent. Although suspending
vehicles alone showed no Cd mobilizing ability, the combination of BAL and oil was far superior to any other BAL-
vehicle combination used. A spectrophotometric method for the determination of sulfhydryl groups in bile and urine
is also presented.
Von Burg R, Northington FK, Shamoo A. "Methylmercury inhibition of rat brain muscarinic receptors."
Toxicol Appl Pharmacol. 1980 Apr;53(2):285-92.
The distribution of methylmercury (MeHg) in subcellular organelles of the rat brain varied slightly in relation to the
in vivo or the in vitro mode of labeling with Me203HgCl. The differences may be explained by disruption of the
normal diffusion path into the brain cells and the amount of MeHg that is bound along this diffusion path. When
Me203Hg and [3H]QNB (quinuclidinyl benzilate) were added directly to brain homogenates, the subcellular fractions
demonstrated a molar rmQNB/MeHg binding ratio greater than 1:100. This suggests that MeHg binding sites are in
considerable excess over QNB binding sites and represent a relatively large sink for decreasing effective MeHg
concentration. HgCl2 was 100 times as potent as MeHg for blocking specific QNB binding sites. (MeHg, ID50 =
10−5 ; HgCl2, ID50 = 10−7 ) On the basis of the respective ID50 points, a 1% conversion of MeHg to the inorganic
form would produce a separate but equivalent block of muscarinic binding sites. Therefore, it is suggested that the
early theory involving organic to inorganic Hg conversion be reexamined as a possibility for producing the selective
toxicity to the central nervous system observed in cases of MeHg poisoning.
Rustam H, Von Burg R, Amin-Zaki L, El Hassani S. "Evidence for a neuromuscular disorder in methylmercury
poisoning." Arch Environ Health. 1975 Apr;30(4):190-5.
Data suggestive of a neuromuscular disorder responsive to neostigmine was uncovered in the course of
electrophysiological testing of Iraqi patients poisoned by methylmercury. Subsequent neostigmine therapy
produced a remarkable clinical improvement of the patients. Placebo substitution resulted in a substantial loss of
testable strength that was restored when drug therapy was resumed.
Conroy PJ, Von Burg R, Penney DP, Passalacqua W, Sutherland RM. "Effect of acute and chronic
misonidazole administration on peripheral-nerve electrophysiology in mice." Br J Cancer. 1980 Apr;41(4):
523-8.
I.p. administration at several dose levels over periods of up to 12 weeks, or continuous i.v. infusion of high doses of
misonidazole (MISO) for 15 h, produced no significant change in peripheral nerve conduction velocity (NCV) and
did not prevent the normal increase in NCV as the animals matured from 12 to 24 weeks of age. Peripheral NCV
(sural nerve) was reduced in both MISO-treated and control mice with hind-limb tumour implants, presumably owing
to physical pressure due to tumour growth. In addition, neither the medial nerves nor the tibial nerve in the normal
limbs of the tumour-implanted, drug-treated animals showed any change. Consequently our earlier and present
studies do not confirm the recent reports of changes in NCV following either acute or chronic MISO administration
to mice.
Von Burg R, Landry T. "Methylmercury and the skeletal muscle receptor." J Pharm Pharmacol. 1976 Jul;28
(7):548-51.
Methylmercury at bath concentration of 2 X 10(-5) M was capable of inhibiting muscular contractions of the isolated
rat phrenic-nerve hemidiaphragm preparation. At the height of inhibition, nerve action potential could still be
recorded and the muscles continued to respond to direct stimulation. The inhibition was not reversible with L-
cysteine or D-penicillamine but limited protection was possible by prior treatment with (+)-tubocurarine. Treatment
of frog rectus muscles with methylmercury (0-2 mM for 15 min) resulted in a shift to the right of 1 log unit in the
dose response curve to acetylcholine and a reduction in the maximum response of the tissue. The observed
inhibitory action of methylmercury on neuromuscular transmission may be explained by an action on the disulphide
bond believed to be present on a cholinergic receptor.
Whipple, CG; Von Burg, R. "Analytical issues in the exposure assessment of mercury emissions from coal-
fired power plants." Air and Waste Management Association 89. Annual Meeting. [np].
Work done in anticipation of EPA's Mercury Study Report to Congress and a Utility Air Toxics Report to Congress
indicates that the relation between mercury emissions from utility boilers and human exposure to mercury is highly
uncertain and highly variable. Two key issues are (1) the degree to which exposures of the U.S. population to
methylmercury from fish consumption can be characterized and (2) the determination of the degree to which
exposures from fish consumption are due to utility emissions; these issues are explored in this paper.