Toxicological
Profile for Mercury
March 1999
The ATSDR (Agency for Toxic Substances and Disease Registry)
toxicologic profile succinctly characterizes the toxicological and
adverse health effects information for the hazardous substance,
mercury . Each peer-reviewed profile identifies and and reviews the
key literature that describes a hazardous substance's toxicological
properties. Other pertinent literature is also presented, but is
described in less detail than the key studies. The profile is not
intended to be an exhaustive document; however, more comprehensive
sources of specialty information are referenced.
MERCURY COMPOUNDS
“Methyl, ethyl, n-propyl & perhaps n-butyl mercury derivatives are
virulent neurotoxins on either acute or chronic exposure. They are especially hazardous because of their volatility, their
ability to penetrate epithelial & blood-brain barriers & their persistence in vivo."
[Gosselin,
R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial
Products. 5th ed. Baltimore: Williams and Wilkins,
1984.III-267]**PEER REVIEWED**
CASRN: NO CAS RN
This record contains general information for the mercury ion and
compounds, including statements referenced in the literature to
organic mercury compounds, inorganic mercury salts, etc. For
compound-specific information, refer to the appropriate individual
records as listed in the RELATED HSDB RECORDS (RELT) field; for
information on the metal itself, to the MERCURY, ELEMENTAL record.
For other data, click on the
Table of Contents
Human Health Effects:
Toxicity Summary:
IDENTIFICATION: In its elemental form,
mercury is a heavy silvery liquid at room temperature and has a very
high vapour pressure. Mercury vapor is more soluble in plasma, whole
blood, and hemoglobin than in distilled water, where it dissolves
only slightly. The major natural sources of mercury are degassing of
the earth's crust, emissions from volcanoes, and evaporation from
natural bodies of water. (The world-wide mining of mercury is
estimated to yield about 10,000 tons per year. The activities lead
to some losses of mercury and direct discharges to the atmosphere).
Other important sources are fossil fuel combustion, metal sulfide
ore smelting, gold refining, cement production, refuse incineration,
and industrial applications of metals. A major use of mercury is as
a cathode in the electrolysis of sodium chloride. Mercury is used in
the electrical industry, in control instruments in the home and
industry, and in laboratory and medical instruments. A very large
amount of mercury is used for the extraction of gold. Dental silver
amalgam for tooth filling contains large amounts of mercury. Use of
skin-lightening soap and creams can give rise to substantial mercury
exposure. Occupational exposure to inorganic mercury has been
investigated in chloralkali plants, mercury mines, thermometer
factories, refineries, and in dental clinics. High mercury levels
have been reported for all these occupational exposure situations,
although levels vary according to work environment conditions.
HUMAN EXPOSURE: The general population
is primarily exposed to mercury through the diet and dental amalgam.
Acute inhalation exposure to mercury vapor may be followed by chest
pains, dyspnea, coughing, hemoptysis, and sometimes interstitial
pneumonitis leading to death. (The ingestion of mercuric compounds,
in particular mercuric chloride, has caused ulcerative
gastroenteritis and acute tubular necrosis causing death from anuria
where dialysis was not available). The central nervous system is the
critical organ for mercury vapor exposure. Subacute exposure has
given rise to psychotic reactions characterized by delerium,
hallucinations, and suicidal tendency. Occupational exposure has
resulted in erethism as the principal feature of a broad ranging
functional disturbance. The kidney is the critical organ following
the ingestion of inorganic divalent mercury salts. Occupational
exposure to metallic mercury has long been associated with the
development of proteinuria. Both metallic mercury vapor and mercury
compounds have given rise to contact dermatitis. Mercurial
pharmaceuticals have been responsible for Pink disease (acrodynia)
in children, and mercury vapor exposure may be a cause of "Kawasaki"
disease. Results of both human and animal studies indicate that
about 80% of inhaled metallic mercury vapour is retained by the
body, whereas liquid metallic mercury is poorly absorbed via the
gastrointestinal tract.
ANIMAL STUDIES: Evidence of damage to brain, kidney, heart, and
lungs have been reported in rabbits exposed acutely to metallic
mercury vapor at certain concentrations. Both reversible and
irreversible toxic effects may be caused by mercury and its
compounds. In two studies, tremor and behavioural effects were
observed in rabbits and rats after several weeks of exposure to
metallic mercury vapour. Depending upon the animal strain tested,
either auto-immunity or immunosuppression is observed. The most
sensitive adverse effect caused by mercuric mercury is the formation
of mercuric-mercury-induced auto-immune glomerulonephritis. Mercuric
chloride was found to induce gene mutations in mouse lymphoma cells
and DNA damage in rat and mouse fibroblasts. The World Health
Organization reported no evidence that inorganic mercury is
carcinogenic. The neurotoxic effect seen after exposure to metallic
mercury vapour is attributable to the divalent mercury ion formed
through oxidation in the brain tissue. Significantly more mercury is
transported to the brain of mice and monkeys after the inhalation of
elemental mercury than after the intravenous injection of equivalent
doses of the mercuric form.
[World Health
Organization/International Programme on Chemical Safety.
Environmental Health Criteria 118 Inorganic Mercury. pp. 13-21,
68-83 (1991)]**PEER REVIEWED**
Evidence for
Carcinogenicity:
Evaluation: There is inadequate evidence in humans for the
carcinogenicity of mercury and mercury compounds. There is
inadequate evidence in experimental animals for the carcinogenicity
of metallic mercury. There is limited evidence in experimental
animals for the carcinogenicity of mercuric chloride. There is
sufficient evidence in experimental animals for the carcinogenicity
of methylmercury chloride. In making the overall evaluation, the
Working Group took into account evidence that methylmercury
compounds are similar with regard to absorption, distribution,
metabolism, excretion, genotoxicity and other forms of toxicity.
Overall evaluation: Methylmercury compounds are possibly
carcinogenic to humans (Group 2B). Metallic mercury and inorganic
mercury compounds are not classifiable as to their carcinogenicity
to humans. (Group 3). /Mercury and mercury compounds/
[IARC. Monographs on the
Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva:
World Health Organization, International Agency for Research on
Cancer, 1972-PRESENT. (Multivolume work).V58 324 (1993)]**PEER
REVIEWED**
Human Toxicity
Excerpts:
SYMPTOMATOLOGY: A. First phase after ingestion of inorganic mercury
salts. 1) Burning pain, sense of constriction, and ashen
discoloration of the mucous membrane in mouth and pharynx, occurring
immediately after the ingestion of corrosive mercury salts. 2)
Within a few minutes intense epigastric pain, followed by diffuse
abdominal pain and associated with almost continuous vomiting of
mucoid material, which frequently contains blood and shreds of
mucous membrane. 3) Severe purging, with liquid, bloody feces and
considerable tenesmus. 4) Metallic taste, excessive salivation and
thirst. 5) A rapid, weak pulse; Shallow breathing; Pallor;
Prostration, collapse, and death. 6) Signs and symptoms listed above
are not encountered with mercury compounds of low irritancy or with
portals of entry other than the mouth. In these cases the first
clinical evidence of poisoning may be phase 2.
[Gosselin, R.E., R.P.
Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th
ed. Baltimore: Williams and Wilkins, 1984.III-270]**PEER REVIEWED**
SYMPTOMATOLOGY: Second phase. If death does not intervene, phase 2
begins in 1-3 days in untreated cases (unless vomiting so
effectively removed the poison that absorption was negligible). 1)
The gastroenteritis described above tends to subside in about 36 hr
under the influence of local treatment. 2) Mercurial stomatitis may
or may not appear within 24-36 hr. It is characterized by a
glossitis and ulcerative gingivitis. Salivation is marked. In
chronic neglected cases severe infections, loosening of teeth, and
necrosis of the jaw are major complications. 3) Necrosis of the
renal tubules is evident within 2-3 days. In sequence, the results
are transient polyuria, albuminuria, cylindruria, hematuria, anuria,
and eventual death associated with azotemia and renal acidosis or
recovery within 10-14 days.
[Gosselin, R.E., R.P.
Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th
ed. Baltimore: Williams and Wilkins, 1984.III-270]**PEER REVIEWED**
SYMPTOMATOLOGY: 4) Especially in untreated cases, a membranous
colitis may first appear many days after the original exposure. It
is evidenced by dysentery, tenesmus, ulceration of the colonic
mucosa, and hemorrhage. Liver necrosis sometimes develops. In
neglected cases collapse and death may occur weeks after the start
of the illness. 5) Rarely neurologic signs and symptoms may appear
late in the course of a slow convalescence after an acute exposure.
[Gosselin, R.E., R.P.
Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th
ed. Baltimore: Williams and Wilkins, 1984.III-270]**PEER REVIEWED**
Nervous symptoms are prominent & severe, though sometimes
transitory; they include headache, vertigo, ataxia, decrease in the
visual fields, delirium, & paresis. /Ethyl mercury phosphate/
[Gosselin, R.E., R.P.
Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th
ed. Baltimore: Williams and Wilkins, 1984.II-136]**PEER REVIEWED**
Methyl, ethyl, n-propyl & perhaps n-butyl mercury derivatives are
virulent neurotoxins on either acute or chronic exposure. They are
especially hazardous because of their volatility, their ability to
penetrate epithelial & blood-brain barriers & their persistence in
vivo. /Alkyl mercury/
[Gosselin, R.E., R.P.
Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th
ed. Baltimore: Williams and Wilkins, 1984.III-267]**PEER REVIEWED**
Signs & symptoms in acutely poisoned men ... /from exposure to aryl
or alkoxyalkyl mercury compounds/ have not been adequately
described. Local irritant effects are well established, such as
dermatitis & burns from skin exposures to phenylmercuric salts.
Blistering has occurred when methoxyethyl mercury acetate was
applied to the skin in high concn, & pulmonary symptoms have arisen
when methoxyethyl mercury oxalate or silicate was inhaled. /Aryl and
alkoxyalkyl mercury compounds/
[Gosselin, R.E., R.P.
Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th
ed. Baltimore: Williams and Wilkins, 1984.III-266]**PEER REVIEWED**
In terms of systemic effects /from exposure to aryl or alkoxyalkyl
mercury compounds/ the only well documented acute reaction is sudden
death during intravenous mercurial diuretic therapy. Most of these
deaths were ascribed to cardiac arrest or ventricular fibrillation,
but rarely respiratory failure was observed without cardiac
manifestations. Hypersensitivity reactions have also been reported.
/Aryl and alkoxyalkyl mercury/
[Gosselin, R.E., R.P.
Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th
ed. Baltimore: Williams and Wilkins, 1984.III-266]**PEER REVIEWED**
No unequivocal central neural effects have been recognized in acute
exposures. Even an attempted suicide with phenyl mercury is said to
have elicited no significant neurological signs. The same was true
of a suicidal ingestion of 5.7 g of methoxyethyl mercury chloride,
which elicited vomiting & chemical burns of the mouth & throat but
little else. Most intoxications by aryl & alkoxyalkyl mercury,
however, have not been detected until after repeated or continuous
exposures of long duration. Even then, the number of reported
poisonings, aside from skin rashes, is remarkably low. /Aryl and
alkoxyalkyl mercury/
[Gosselin, R.E., R.P.
Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th
ed. Baltimore: Williams and Wilkins, 1984.III-266]**PEER REVIEWED**
In subacute & chronic poisonings & probably sometimes in the late
stages of acute poisonings, these organomercurials /aryl &
alkoxyalkyl mercury/ appear to produce intoxication syndromes that
are in practice indistinguishable from those induced by inorganic
mercury. ... Death in renal failure, as well as the production of a
nephrotic syndrome, has been ascribed to mercurial diuretics.
Nephrosis ... appeared in a 60 yr old man who for 5 years had
handled grain treated with methoxyethyl mercury silicate. A 5 yr old
boy exposed to a methoxyethyl mercury seed disinfectant developed
acrodynia. As in chronic inorganic mercury poisoning, neurological
signs (tremor, motor & sensory nerve disorders) have been detected
in a few individuals chronically exposed to these forms of organic
mercury. A 39 yr old farmer who had used no precautions in dusting
oat seeds with phenylmercuric acetate over a period of 5 to 6 years
& who excreted large amounts of mercury in the urine died of an
apparently progressive neurologic disease resembling amyotrophic
lateral sclerosis. Five other farmers similarly exposed were said to
have various motor disabilities. /Aryl and alkoxyalkyl mercury/
[Gosselin, R.E., R.P.
Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th
ed. Baltimore: Williams and Wilkins, 1984.III-266]**PEER REVIEWED**
These two classes of organomercurials /aryl & alkoxyalkyl mercury/
are rather similar in terms of toxicity, instability in vivo, tissue
distribution, retention & excretion; they differ markedly from alkyl
mercury compounds ... /Aryl and alkoxyalkyl mercury/
[Gosselin, R.E., R.P.
Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th
ed. Baltimore: Williams and Wilkins, 1984.III-265]**PEER REVIEWED**
Available data point to great similarities in symptoms & signs of
poisoning due to ethylmercury & methylmercury. Most detailed
information deals with methylmercury. There is no sharp difference
between acute & chronic poisoning from exposure to methylmercury
compounds. Once a toxic dose has been absorbed in the body, it is
retained for a long time, causing functional disturbances & damage.
On the other hand, a single toxic dose does not produce signs or
symptoms until after a latency period, which may vary from 1 to
several weeks. Two clinical types of intoxication may be discerned,
a prenatal & a postnatal type. These give rise to different kinds of
signs & symptoms. /Alkylmercury compounds/
[Friberg, L., Nordberg,
G.F., Kessler, E. and Vouk, V.B. (eds). Handbook of the Toxicology
of Metals. 2nd ed. Vols I, II.: Amsterdam: Elsevier Science
Publishers B.V., 1986.V2 426]**PEER REVIEWED**
The clinical picture in prenatal methylmercury poisoning is that of
an unspecific infantile cerebral palsy, involving ataxic motor
disturbances & mental symptoms. Upon autopsy, the brain is found to
be hypoplastic with a symmetrical atrophy of cerebrum & cerebellum.
Decreased numbers of neurons & distortion of the cytoarchitecture in
the cortical areas are histological features. The changes coincide
with those of cerebral palsy of unknown etiology. Similar findings
have been reported in cases of ethylmercury poisoning. In less
severe cases, psychomotor retardation has been observed, as revealed
by a delayed debut of walking & talking by more than 12 months, & an
increased incidence of seizures. In-fish consuming populations, a
moderate increase in hair-mercury levels during pregnancy has been
assoc with impaired psychomotor test performance of the child at 4-5
years of age. /Alkylmercury compounds/
[Friberg, L., Nordberg,
G.F., Kessler, E. and Vouk, V.B. (eds). Handbook of the Toxicology
of Metals. 2nd ed. Vols I, II.: Amsterdam: Elsevier Science
Publishers B.V., 1986.V2 427]**PEER REVIEWED**
The clinical signs of postnatal intoxication due to methylmercury
are characterized by sensitivity disturbances with paresthesia in
the distal extremities, in the tongue & around the lips. These are
early signs occurring after slight intoxication. In more severe
intoxication, ataxia, concentric constriction of the visual field,
impairment of hearing, & extrapyramidal symptoms may appear. In
severe cases, clonic seizures have been observed. The pathological
changes in the CNS are characterized by general neuron degeneration
in the cerebral cortex with gliosis, most pronounced in the
calcarine, the precentral & postcentral areas. These changes are
accompanied by atrophy of the cerebral cortex. In the cerebellar
cortex, less pronounced changes, involving a loss of granular cells
in the neocerebellum, may be encountered. /Alkylmercury compounds/
[Friberg, L., Nordberg,
G.F., Kessler, E. and Vouk, V.B. (eds). Handbook of the Toxicology
of Metals. 2nd ed. Vols I, II.: Amsterdam: Elsevier Science
Publishers B.V., 1986.V2 427]**PEER REVIEWED**
Considering that methylmercury is excreted by breast milk, postnatal
poisoning of the nursed child can easily arise. Symptoms for this
type of poisoning are similar to those of the adult. It is, however,
unclear to what extent poisoning during this period may, except for
neuron damage, give rise to inhibition of the development &
maturation of the brain. Some reports seem to indicate that
regeneration & compensatory adaptation during this period are better
than during childhood. When neurological signs due to methylmercury
poisoning appear, the duration of exposure is of importance for
recovery & rehabilitation. The outlook for recovery & for
rehabilitation seems to be better in case of acute exposure compared
to prolonged exposure. /Alkylmercury compounds/
[Friberg, L., Nordberg,
G.F., Kessler, E. and Vouk, V.B. (eds). Handbook of the Toxicology
of Metals. 2nd ed. Vols I, II.: Amsterdam: Elsevier Science
Publishers B.V., 1986.V2 427]**PEER REVIEWED**
Possible distinctions between poisoning by methyl mercury & ethyl
mercury. There is some indication that, compared to methyl
compounds, the illness produced by ethylmercuric compounds involves
relatively greater injury to the GI system (aphthous stomatitis,
catarrahal gingivitis, nausea, liquid stool, pain, & laboratory
evidence of liver disorder) & the cardiovascular & hematopoietic
systems & less disorder of sensation & coordination. The contrast
between the two has been pointed out on the basis of outbreaks /of
poisoning/ in Iraq, the one in 1960 caused by ethyl mercury & the
one in 1972 caused by methyl mercury. However, poisoning by ethyl
mercury may be fatal, & those who survive may have residual
symptoms. A description of poisoning by ethyl mercury in children
makes it appear impossible to distinguish poisoning by ethyl &
methyl mercury. At present it is unclear whether an important,
clinical distinction is justified between poisoning by ethyl &
methyl mercury either in adults or in children. /Alkyl mercury
compounds/
[Hayes, Wayland J., Jr.
Pesticides Studied in Man. Baltimore/London: Williams and Wilkins,
1982.22]**PEER REVIEWED**
Acute poisoning by organic mercury has been reported infrequently in
man, although cases of such poisoning by methyl & other alkyl
compounds have occurred. There have been many cases of chronic
poisoning involving organic mercury. The classical description of
poisoning by an alkyl mercury compound is that of ... headache;
paresthesia of the tongue, lips, fingers, & toes; & other
nonspecific dysfunction. In mild cases, the symptoms do not develop
beyond this point, & in such instances they usually disappear
gradually. /Alkyl mercury compounds/
[Hayes, Wayland J., Jr.
Pesticides Studied in Man. Baltimore/London: Williams and Wilkins,
1982.21]**PEER REVIEWED**
Some but not all workers equally exposed to alkyl mercury compounds
complain of a metallic taste in the mouth & slight gastrointestinal
disturbances, such as excessive flatus & diarrhea. However, the
acute symptoms assoc with irritation of the GI system & renal
failure caused by inorganic mercury compounds are seldom observed in
poisoning by alkyl mercury compounds & then almost exclusively in
acute poisoning. Even the mild digestive disturbances & sore mouth
seen in moderate, chronic, occupational poisoning by inorganic
mercury are relatively rare. Instead, the nervous symptoms appear
1st, sometimes after relatively slight exposure & after weeks or
months of latency. /Alkyl mercury compounds/
[Hayes, Wayland J., Jr.
Pesticides Studied in Man. Baltimore/London: Williams and Wilkins,
1982.21]**PEER REVIEWED**
Early signs of more severe poisoning include fine tremors of the
extended hands, loss of side vision, & slight loss of coordination,
esp with the eyes closed as in the finger-to-nose test.
Incoordination is esp noticeable in speech, writing, & gait.
Incoordination may progress to the point of inability to stand or
carry out other voluntary movements. Occasionally there is muscle
atrophy & flexure contractures. In other cases, there are
generalized myoclonic movements. There may be difficulty in
understanding ordinary speech, although hearing & the understanding
of slow deliberate speech often remain unaffected. Irritability &
bad temper are frequently present & may progress to mania.
Occasionally the mental picture deteriorates to stupor or coma.
Especially in children, mental retardation may be added to the
symptoms of poisoning already mentioned. /Alkyl mercury compounds/
[Hayes, Wayland J., Jr.
Pesticides Studied in Man. Baltimore/London: Williams and Wilkins,
1982.21]**PEER REVIEWED**
... /Chromosome/ aberration & aneuploidy in ethylmercury-exposed
workers /have been reported/. /Alkylmercury compounds/
[Friberg, L., Nordberg,
G.F., Kessler, E. and Vouk, V.B. (eds). Handbook of the Toxicology
of Metals. 2nd ed. Vols I, II.: Amsterdam: Elsevier Science
Publishers B.V., 1986.V2 428]**PEER REVIEWED**
Secondary poisoning can arise from the ingestion of the flesh of
animals which have been fed on mercurial fungicides; a farming
family has been poisoned in this way. /Organic mercury compounds/
[Clarke, M. L., D. G.
Harvey and D. J. Humphreys. Veterinary Toxicology. 2nd ed. London:
Bailliere Tindall, 1981.62]**PEER REVIEWED**
Alkyl mercury salts are more toxic than are elemental Hg (liquid or
vapor) & inorganic Hg+2 salts. /Alkyl mercury salts/
[Venugopal, B. and T.D.
Luckey. Metal Toxicity in Mammals, 2. New York: Plenum Press,
1978.92]**PEER REVIEWED**
Inorganic, ionic mercury can produce severe acute toxicity.
Precipitation of mucous membrane proteins by mercuric salts results
in an ashen-gray appearance of the mucosa of the mouth, pharynx and
intestine and also causes intense pain, which may be accompained by
vomiting. ... Systemic toxicity may begin within a few hours after
exposure to mercury and last for days. A strong metallic taste is
followed by stomatitis with gingival irritation, foul breath and
loosening of the teeth. The most serious and, unfortunately, the
most frequently encountered systemic effect of inorganic mercury is
renal toxicity. Renal tubular necrosis occurs after acute exposure,
leading to oliguria or anuria. /Inorganic mercury/
[Gilman, A.G.,
L.S.Goodman, and A. Gilman. (eds.). Goodman and Gilman's The
Pharmacological Basis of Therapeutics. 7th ed. New York: Macmillan
Publishing Co., Inc., 1985.1612]**PEER REVIEWED**
DISTURBANCES OF EYES IN MERCURY POISONING CONSISTS OF DISCOLORATION
OF CORNEA & LENS, TREMOR OF EYELIDS, & POSSIBLY ... DISTURBANCES OF
VISION & EXTRAOCULAR MUSCLES. ... IN VERY YOUNG CHILDREN ACRODYNIA.
... CHARACTERTISTIC BY OCULAR SYMPTOMS ... PHOTOPHOBIA ...
CONJUNCTIVITIS, ITCHING ... KERATITIS ... /INORGANIC MERCURY/
[Grant, W.M. Toxicology
of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher,
1986.583]**PEER REVIEWED**
Lethal Blood Level: The concn of organic mercury present in the
blood (serum or plasma) that has been reported to cause death in
humans is: >0.06%; >0.6 ug/ml. /Organic mercury/
[Winek, C.L. Drug and
Chemical Blood-Level Data 1985. Pittsburgh, PA: Allied Fischer
Scientific, 1985.]**PEER REVIEWED**
The two most widely known epidemics of methyl mercury poisoning
occurred in Minamata Bay and Niigata, Japan in 1953 to the early
sixties. These episodes were caused by the industrial release of
methyl and other mercury (Hg) compounds into the neighboring waters,
followed by accumulation of the Hg by edible fish. The median level
of total Hg in fish caught was estimated between 10-11 mg/kg fresh
weight. By 1974, a total of 1200 cases of methyl mercury poisoning
were identified, of which 55 proved fatal. Highest concentration of
Hg were found in the blood and hair.
[WHO; Environ Health
Criteria: Mercury p.90-107 (1976)]**PEER REVIEWED**
Idiosyncratic reactions to mercury and mercury cmpd on local contact
have been seen in connection with mercury applied locally to skin
and mucous membranes. Typical manifestations are erythemas and
contact dermatitis. ... A special form of hypersensitivity was found
in children between 4 months and 4 years of age. This syndrome,
called acrodynia or pink disease, is characterized by a general rash
over the body. Other symptoms are chills, swelling & irritation of
hands, feet cheeks & nose, usually followed by desquamation, loss of
hair & ulceration. In addition to skin symptoms, the disease
features irritability, photophobia, sleeplessness & profuse
perspiration, which may lead to dehydration. Perspiration is
accompanied by dilated & enlarged sweat glands & desquamation of
soles & palms. Hyperplasia & hyperkeratosis of skin in peripheral
parts of extremities are seen. ... Acrodynia cases ... usually show
increased levels of mercury in urine (above 50 ug/l).
[Friberg, L., Nordberg,
G.F., Kessler, E. and Vouk, V.B. (eds). Handbook of the Toxicology
of Metals. 2nd ed. Vols I, II.: Amsterdam: Elsevier Science
Publishers B.V., 1986.413]**PEER REVIEWED**
The most extensive episodes of mercury poisoning have resulted from
contamination of bread made from cereal grains treated with
alkyl-mercury fungicides. These incidents have occurred in Iraq,
Pakistan, Guatemala, and on limited scale in other countries. The
largest of these episodes occurred in Iraq, 1971-72. It involved
some 6,000 cases and 500 deaths. The mean methyl-mercury content of
wheat was found to be 7.9 mg/kg (3.7-14.9 mg/kg). In the most
severely affected group of the population, the highest daily intake
of Hg was about 130 ug/kg; The average period of consumption ranged
from 43-68 days. /Alkyl mercury fungicide/
[WHO; Environ Health
Criteria: Mercury p.90-107 (1976)]**PEER REVIEWED**
THERE ... IS A DISEASE OF INFANTS KNOWN AS ACRODYNIA OR "PINK
DISEASE" IN WHICH INORGANIC MERCURY SEEMS TO PLAY A ROLE. IT IS
CHARACTERIZED BY NEUROPSYCHIATRIC DISTURBANCES, PERIPHERAL VASCULAR
EFFECTS, DISTURBANCES OF SENSATION OF THE EXTREMITIES, STOMATITIS, &
OTHER VAGUE, NONSPECIFIC SIGNS. /INORGANIC MERCURY/
[Doull, J., C.D.Klassen,
and M.D. Amdur (eds.). Casarett and Doull's Toxicology. 3rd ed., New
York: Macmillan Co., Inc., 1986.426]**PEER REVIEWED**
MERCURIALS EVEN IN LOW CONCENTRATIONS ARE CAPABLE OF INACTIVATING
SULFHYDRYL ENZYMES AND THUS OF INTERFERING WITH CELLULAR METABOLISM
AND FUNCTION. /MERCURIALS/
[Gilman, A.G.,
L.S.Goodman, and A. Gilman. (eds.). Goodman and Gilman's The
Pharmacological Basis of Therapeutics. 7th ed. New York: Macmillan
Publishing Co., Inc., 1985.1611]**PEER REVIEWED**
Oral ingestion ... causing severe abdominal cramps, bloody diarrhea,
and suppression of urine ... corrosive ulceration, bleeding, and
necrosis of the gastrointestinal tract ... shock and circulatory
collapse ... renal failure occurs within 24 hrs ...
[Doull, J., C.D.Klassen,
and M.D. Amdur (eds.). Casarett and Doull's Toxicology. 3rd ed., New
York: Macmillan Co., Inc., 1986.607]**PEER REVIEWED**
UPON ACCIDENTAL OR SUICIDAL INGESTION OF SUBLIMATE OR OTHER MERCURIC
SALTS THE CRITICAL ORGANS ARE KIDNEY & INTESTINAL TRACT. ... IF PT
SURVIVES GI DAMAGE, CRITICAL ORGAN WILL BE KIDNEY. WITHIN 24 HR,
RENAL FAILURE DUE TO NECROSIS OF PROXIMAL TUBULAR EPITHELIUM, WHICH
DEVELOPS INTO ANURIA & UREMIA, OCCURS. /MERCURIC SALTS/
[Friberg, L., Nordberg,
G.F., Kessler, E. and Vouk, V.B. (eds). Handbook of the Toxicology
of Metals. 2nd ed. Vols I, II.: Amsterdam: Elsevier Science
Publishers B.V., 1986.412]**PEER REVIEWED**
Following exposure to mercuric Hg(2+) salts ... by inhalation of
dusts ... kidney is critical organ of injury. Although site of
diuretic action of Hg(2+) salts has not been demonstrated, it is
suspected to be the proximal tubules. /Mercuric salts/
[Clayton, G. D. and F. E.
Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume
2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons,
1981-1982.1777]**PEER REVIEWED**
Systemic - The central nervous system, including the brain, is the
principal target tissue for this group of toxic compounds. Severe
poisoning may produce irreversible brain damage resulting in loss of
higher functions. The effects of chronic poisoning with alkyl
mercury compounds are progressive. In the early stages, there are
fine tremors of the hands, and in some cases, of the face and arms.
With continued exposure, tremors may become coarse and convulsive;
scanning speech with moderate slurring and difficulty in
pronunciation may also occur. The worker may then develop an
unsteady gait of a spastic nature which can progress to severe
ataxia of the arms and legs. Sensory disturbances including tunnel
vision, blindness, and deafness are also common. A later symptom,
constriction of the visual fields, is rarely reversible and may be
associated with loss of understanding and reason which makes the
victim completely out of touch with his environment. Severe cerebral
effects have been seen in infants born to mothers who had eaten
large amounts of methyl mercury-contaminated fish. /Methyl mercury
compounds/
[Sittig M; Handbook of
Toxic and Hazardous Chemicals p.421 (1981)]**PEER REVIEWED**
Phenylmercury absorbed through the skin from contaminated diapers
affected urinary excretion in infants in Buenos Aires. The effects
were reversible and quantitatively related to the concn of urinary
Hg. /Phenylmercury cmpd/
[Gotelli CA et al;
Science 227 (4687): 638-640 (1985)]**PEER REVIEWED**
RENAL FUNCTION MAY BE DISTURBED WITHIN A FEW MINUTES AFTER POISON
REACHES CIRCULATION. IF CIRCULATION IS ADEQUATE, 1ST RESPONSE OF
KIDNEY MAY BE A DIURESIS CAUSED BY INHIBITION OF TUBULAR
REABSORPTIVE FUNCTION. SOON, RENAL DAMAGE IS SO EXTENSIVE THAT
OLIGURIA ... RESULTS. /MERCURIC SALTS/
[Gilman, A. G., L. S.
Goodman, and A. Gilman. (eds.). Goodman and Gilman's The
Pharmacological Basis of Therapeutics. 6th ed. New York: Macmillan
Publishing Co., Inc. 1980.1624]**PEER REVIEWED**
... /A disease/ prevalent among hatters ... manifested all the
characteristics of mercurial poisoning: Swelling & ulceration of
gums, loosening of teeth, fetid breath, abnormal flow of saliva &
shaking palsy of limbs. ... Outstanding findings in these reports
incl irritability, timidity, apprehension & restlessness; Vasomotor
disorders ... incr reflexes, gingivitis & slight abnormalities in
speech. Psychic disturbances were detected. ... Incr of systolic
blood pressure, albuminuria, & hematuria were also noted.
[Hamilton, A., and H. L.
Hardy. Industrial Toxicology. 3rd ed. Acton, Mass.: Publishing
Sciences Group, Inc., 1974.132]**PEER REVIEWED**
ACUTE POISONING ... /MAY RESULT FROM/ INHALATION OF VAPORS OF ...
ORGANIC MERCURIALS ... IF POISONING OCCURS BY INHALATION OF FUMES OF
... ORGANIC MERCURIALS, THE SYNDROME IS CHARACTERIZED BY PNEUMONITIS,
LETHARGY OR RESTLESSNESS, FEVER, TACHYPNEA, COUGH, CHEST PAIN,
CYANOSIS, DIARRHEA & VOMITING; ATELECTASIS, EMPHYSEMA, HEMORRHAGE &
PNEUMOTHORAX OFTEN FOLLOW. SYSTEMIC EFFECTS OF THE POISON START
WITHIN FEW HOURS & MAY LAST FOR DAYS; DEATH MAY ENSUE. ... SYSTEMIC
SIGNS OF ACUTE POISONING BY ... METHYLMERCURIC COMPOUNDS INCL THOSE
REFERABLE TO CNS ... /ORGANIC MERCURIALS/
[Gilman, A. G., L. S.
Goodman, and A. Gilman. (eds.). Goodman and Gilman's The
Pharmacological Basis of Therapeutics. 6th ed. New York: Macmillan
Publishing Co., Inc. 1980.1624]**PEER REVIEWED**
THE MOST CONSISTENT & PRONOUNCED EFFECTS OF /CHRONIC/ EXPOSURE TO
... SHORT-CHAIN ALKYLMERCURY COMPOUNDS SUCH AS METHYLMERCURY ARE ON
CNS. EFFECTS ... ARE NEUROLOGICAL & PSYCHIATRIC. COMMON SYMPTOMS
INCL DEPRESSION, IRRITABILITY, EXAGGERATED RESPONSE TO STIMULATION (ERETHISM),
EXCESSIVE SHYNESS, INSOMNIA, EMOTIONAL INSTABILITY, FORGETFULNESS,
CONFUSION, & VASOMOTOR DISTURBANCES SUCH AS EXCESSIVE PERSPIRATION &
UNCONTROLLED BLUSHING. TREMORS ARE ALSO COMMON ... ... SENSORY
EFFECTS ... OCCUR MORE CONSISTENTLY & AT LOWER LEVELS OF EXPOSURE.
EARLIEST SIGN IS PARESTHESIA. AT ... HIGHER LEVELS OF EXPOSURE OTHER
EFFECTS OCCUR, SUCH AS ATAXIA, CONSTRICTION OF VISUAL FIELD,
DYSARTHRIA, & HEARING DEFECTS. THESE ALTERATIONS ARE IRREVERSIBLE
WHEN POISONING IS SEVERE. NEUROPSYCHIATRIC EFFECTS ... ARE LIKELY TO
INVOLVE SPONTANEOUS FITS OF LAUGHING & CRYING & INTELLECTUAL
DETERIORATION. /ALKYLMERCURY COMPOUNDS/
[Gilman, A. G., L. S.
Goodman, and A. Gilman. (eds.). Goodman and Gilman's The
Pharmacological Basis of Therapeutics. 6th ed. New York: Macmillan
Publishing Co., Inc. 1980.1624]**PEER REVIEWED**
The alkyl mercury compounds are strong irritants of the skin & may
cause blisters or other dermatitis with or without assoc systemic
illness. /Alkyl mercury compounds/
[Hayes, Wayland J., Jr.
Pesticides Studied in Man. Baltimore/London: Williams and Wilkins,
1982.22]**PEER REVIEWED**
AMONG INORG CMPD, ELEMENTAL MERCURY & DIVALENT MERCURY SALT ARE THE
CMPD OF TOXICOLOGICAL INTEREST. IT IS DOUBTFUL WHETHER MERCUROUS
MERCURY HAS ANY SURVIVAL IN THE ORGANISM, ALTHOUGH AT PRESENT
POSSIBILITY ... THAT MERCUROUS MERCURY MAY BE INTERMEDIATE IN REDOX
TRANSFORMATION OF ELEMENTAL & MERCURIC MERCURY OR VICE VERSA IN
BODY. /INORGANIC MERCURY CMPD/
[Friberg, L., Nordberg,
G.F., Kessler, E. and Vouk, V.B. (eds). Handbook of the Toxicology
of Metals. 2nd ed. Vols I, II.: Amsterdam: Elsevier Science
Publishers B.V., 1986.389]**PEER REVIEWED**
MOLECULAR STRUCTURE OF THE MERCURY CMPD, ITS STABILITY IN THE
ORGANISM & ITS ROUTES OF BIOTRANSFORMATION & EXCRETION WILL GOVERN
TOXICOLOGICAL PROPERTIES FOR THE HIGHER ORGANISMS. THUS EACH MERCURY
CMPD HAS ITS OWN TOXICOLOGY IN RELATION TO DOSE-EFFECT &
DOSE-RESPONSE RELATIONSHIPS.
[Friberg, L., Nordberg,
G.F., Kessler, E. and Vouk, V.B. (eds). Handbook of the Toxicology
of Metals. 2nd ed. Vols I, II.: Amsterdam: Elsevier Science
Publishers B.V., 1986.389]**PEER REVIEWED**
Mercury(2+) compounds are more toxic than the mercury(1+) compounds
by all routes of admin (except mercuric nitrate by way of ip route);
no species resistance to oral LD was observed; the order of toxicity
by ip admin practically repeated oral admin. Toxicity of mercury(2+)
compounds was less uniform than of mercury(1+) compounds; and
solubility of the compounds had no effect on the toxicity. Water sol
mercurous nitrate was 7 fold less toxic than mercuric nitrate, while
being less toxic than the insol mercurous chloride.
[Trakhtenberg
IM et al; Gig Tr Prof Zabol (7): 27-30 (1981)]**PEER REVIEWED**
Mercuric salts are the most toxic form of mercury. /Mercuric salts/
[Gilman, A.G.,
L.S.Goodman, and A. Gilman. (eds.). Goodman and Gilman's The
Pharmacological Basis of Therapeutics. 7th ed. New York: Macmillan
Publishing Co., Inc., 1985.1611]**PEER REVIEWED**
IN GENERAL, TOXICITY DEPENDS UPON RELEASE OF MERCURIC ION. /MERCURY/
[Gosselin, R.E., R.P.
Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th
ed. Baltimore: Williams and Wilkins, 1984.II-134]**PEER REVIEWED**
Soluble salts have violent corrosive effects on skin and mucous
membranes. /Soluble mercury salts/
[The Merck Index. 10th
ed. Rahway, New Jersey: Merck Co., Inc., 1983.842]**PEER REVIEWED**
When deposited on the skin, they give no warning, and if contact is
maintained, can cause second-degree burns. Sensitization may occur.
/Methyl mercury compounds/
[Sittig M; Handbook of
Toxic and Hazardous Chemicals p.421 (1981)]**PEER REVIEWED**
MERCURIC SALTS ARE THE MORE IRRITATING & ACUTELY TOXIC FORM OF THE
METAL. /MERCURIC SALTS/
[Hardman, J.G., L.E.
Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman
and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New
York, NY: McGraw-Hill, 1996.1655]**PEER REVIEWED**
Either acute or chronic exposure may produce permanent changes to
affected organs and organ systems. Acute poisoning due to mercury
vapors affects the lung primarily, in the form of acute interstitial
pnuemonitis, bronchitis, and bronchiolitis. ... In general, chronic
exposure produces four classical signs: gingivitis, sialorrhea,
increased irritability, and muscular tremors. Rarely are all four
seen in together in an individual case. /Mercury vapors/
[Sittig, M. Handbook of
Toxic And Hazardous Chemicals. Park Ridge, NJ: Noyes Data
Corporation, 1981.424]**PEER REVIEWED**
SECONDARY POISONING CAN ARISE FROM INGESTION OF FLESH OF ANIMALS
WHICH HAVE BEEN FED ON MERCURIAL FUNGICIDES; A FARMING FAMILY HAS
BEEN POISONED IN THIS WAY... /MERCURIAL FUNGICIDES/
[Clarke, M. L., D. G.
Harvey and D. J. Humphreys. Veterinary Toxicology. 2nd ed. London:
Bailliere Tindall, 1981.62]**PEER REVIEWED**
IN HUMANS THE NEUROTOXIC SYMPTOMS OF METHYL MERCURY SALTS, THE
HUNTER-RUSSEL SYNDROME, INVOLVE FOCAL CEREBRAL & CEREBELLAR ATROPHY.
THE GRANULAR CELL LAYER OF NEOCEREBELLUM IS AFFECTED FOLLOWED BY
CORTICAL ATROPHY OF AREA STRIATA, WHICH LEADS TO BLINDNESS. /METHYL
MERCURY SALTS/
[Venugopal, B. and T.D.
Luckey. Metal Toxicity in Mammals, 2. New York: Plenum Press,
1978.95]**PEER REVIEWED**
Phenylmercury absorbed through the skin from contaminated diapers
affected urinary excretion in infants in Buenos Aires. The effects
were reversible and quantitatively related to the concn of urinary
mercury. /Phenylmercury cmpd/
[Gotelli CA et al;
Science 227 (4687): 638-40 (1985)]**PEER REVIEWED**
Exposure of the skin to a concentrated solution of phenylmercury
cmpd may cause chemical burns with blistering. /Organo-mercurials/
[International Labour
Office. Encyclopedia of Occupational Health and Safety. Vols. I&II.
Geneva, Switzerland: International Labour Office, 1983.1336]**PEER
REVIEWED**
Chronic poisoning with inorganic mercury causes ... mercurialentis
(a colored reflex from lens) ... but does not indicate intoxication.
... Nonspecific symptoms such as anorexia, wt loss, anemia &
muscular weakness are also assoc with chronic exposure ...
/Inorganic mercury salts/
[Gilman, A. G., L. S.
Goodman, and A. Gilman. (eds.). Goodman and Gilman's The
Pharmacological Basis of Therapeutics. 6th ed. New York: Macmillan
Publishing Co., Inc. 1980.1625]**PEER REVIEWED**
Corrosive ulceration, bleeding, and necrosis of the gastrointestinal
tract are usually accompanied by shock and circulatory collapse. If
the patient survives the gastrointestinal damage, renal failure
occurs within 24 hours owing to necrosis ... followed by oliguria,
anuria, and uremia. /Mercuric salts/
[Klaassen, C.D., M.O.
Amdur, Doull J. (eds.). Casarett and Doull's Toxicology. The Basic
Science of Poisons. 5th ed. New York, NY: McGraw-Hill,
1995.711]**PEER REVIEWED**
Inorganic forms of mercury ... produce symptoms of metallic taste,
burning, irritation, salivation, vomiting, diarrhea, upper
gstrointestinal tract edema, abdominal pain, and hemorrhage.
/Inorganic mercury/
[Amdur, M.O., J. Doull,
C.D. Klaasen (eds). Casarett and Doull's Toxicology. 4th ed. New
York, NY: Pergamon Press, 1991.938]**PEER REVIEWED**
Mercuric ... compounds locally applied to skin may cause
idiosyncratic skin symptoms like erythema & more severe exfoliative
dermatitis, involving whole body. A specific form of
hypersensitivity is seen in children between 4 months & 4 years of
age. This syndrome, called acrodynia or pink disease, is
characterized by a general rash over body. Other symptoms are
chills, swelling & irritation of hands, feet, cheeks & nose, usually
followed by desquamation, loss of hair & ulceration. In addn to skin
symptoms, the disease features irritability, photophobia,
sleeplessness, & profuse perspiration, which may lead to
dehydration. Perspiration is accompanied by dilated & enlarged sweat
glands & desquamation of soles & palms. Hyperplasia & hyperkeratosis
of skin in peripheral parts of extremities are seen. ... Acrodynia
cases ... usually show incr levels of mercury in urine (above 50 ug/L).
[Friberg, L., G.R.
Nordberg, and V.B. Vouk. Handbook on the Toxicology of Metals. New
York: Elsevier North Holland, 1979.518]**PEER REVIEWED**
Lethal Blood Level: The concn of inorganic mercury present in blood
(serum or plasma) that has been reported to cause death in humans
is: 0.04-2.2 mg%; 0.4-2.2 ug/ml. /Inorganic mercury/
[Winek CL; Drug &
Chemical Blood Level Data Inorganic Mercury (1985)]**PEER REVIEWED**
A 54 year old man who experienced a 2 day exposure to high levels of
mercury vapor resulting in a urine concentration of 100 ug Hg/l
developed a syndrome resembling amyotrophic lateral sclerosis. The
syndrome disappeared when the urinary mercury concentration returned
to normal. /Mercury/
[Clayton, G.D., F.E.
Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes
2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley
& Sons Inc., 1993-1994.2132]**PEER REVIEWED**
Chloro-alkali plant workers exposed to mercury (probably inorganic)
concentrations of <0.1 to 0.2.7 mg/cu m had significant exposure
related effects that included weight loss, tremors, insomnia, and
abnormal reflexes. At 0.1 mg/cu m there was a slight increase in
insomnia and loss of appetite. There was no evidence of kidney
damage in these workers. Additionally, based on blood and urine
analyses from the workers, ... /it was/ estimated that a 0.1 mg
Hg/cu m TWA exposure was correlated with 6 ug Hg/100 ml of blood and
with 250 ug/l of urine. /Inorganic mercury/
[Clayton, G.D., F.E.
Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes
2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley
& Sons Inc., 1993-1994.2133]**PEER REVIEWED**
Six of 75 workers exposed to 0.05 to 0.1 mg Hg/cu m of mercury vapor
in a glass manufacturing plant reported insomnia, and one had
tremors. Hyperexcitability was observed in 33 percent of the workers
exposed to mercury vapor at concentrations above 0.05 mg Hg/cu m,
whereas only 8 percent of the workers exposed below this
concentration were hyperexcitable. Tremors were observed in 20
percent of the workers in both groups. Occupational mercury
exposures resulting in tremors are associated with urinary mercury
concentrations ranging from 50 to 200 ug/g creatinine. /Mercury
vapor/
[Clayton, G.D., F.E.
Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes
2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley
& Sons Inc., 1993-1994.2133]**PEER REVIEWED**
Mercury urinary concentrations of 87 control workers (mean urinary
mercury in the range of 3.3 to 4.6 mg Hg/g creatinine, based upon
three separate visits) were compared to those of 105 exposed workers
(mean urinary mercury in the range of 63 to 71 ug Hg/g creatinine,
based upon three separate visits). The range of individual values
was 0.4 to 275 ug Hg/g creatinine. The corresponding mean blood
mercury values were 5 and 17.5 ug Hg/l, respectively. Highly
significant correlations were found between blood and urinary
mercury concentrations. Urinary gamma-glutamyl transferase
correlated with urinary mercury levels in the exposed group. The
prevalence of greater than normal activities of the enzymes
N-acetyl-glucosaminidase (NAG) and gamma-glutamyl transferase
appeared to increase when the mercury concentration in urine
exceeded 100 ug Hg/g creatinine; but there was no evidence of a dose
response relationship over the full range of mercury concentration.
/Mercury/
[Clayton, G.D., F.E.
Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes
2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley
& Sons Inc., 1993-1994.2133]**PEER REVIEWED**
When 84 mercury exposed workers in a thermometer factory were
compared to 79 workers not exposed to mercury, the exposed workers
were found to have a higher prevalence of static tremor, abnormal
Romberg test, and dysdiadochokinesia. There was a correlation
between urinary mercury Hg and NAG suggestive of recent mercury
toxicity, whereas the CNS signs and symptoms were considered a
result of chronic toxicity. No differences existed between the
groups of workers with regard to beta-microglobulin and
retinol-binding protein, which are considered markers of proximal
renal tubule function. /Mercury/
[Clayton, G.D., F.E.
Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes
2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley
& Sons Inc., 1993-1994.2133]**PEER REVIEWED**
Forty one male mercury exposed workers were examined for serum
concentration levels of immunoglobulins (IgG, IgA, IgM),
alpha-1-antitrypsin (AIAT), alpha-2-macroglobulin (A2M),
ceruloplasmin (CPL), and orosomucoid (ORO). In the period preceding
this investigation the mercury concentrations in workplace air
ranged from 0.106 to 0.783 mg/cu m; the range of urinary mercury
concentrations was from 0.029 to 0.545 mg/l. All but two (IgG and
AIAT) of the immune parameters tested were at levels much higher
than those found in a control group of 55 workers matched by age to
the exposed workers and who lived in a relatively clean area. Almost
80% of the workers in the control group demonstrated no value out of
the range of normal physiological limits, but only 36.6% of the
exposed workers showed normal values. /Mercury/
[Clayton, G.D., F.E.
Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes
2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley
& Sons Inc., 1993-1994.2136]**PEER REVIEWED**
The most extensive episodes of mercury (Hg) poisoning have resulted
from contamination of bread made from cereal grains treated with
alkyl-mercury fungicides. These incidents have occurred in Iraq,
Pakistan, Guatemala, and on a limited scale in other countries. The
largest of these episodes occurred in Iraq, 1971-72. It involved
some 6,000 hospital admissions and 500 deaths. The mean methyl
mercury content of wheat was found to be 7.9 mg/kg (3.7-14.9 mg/kg).
In the most severely affected group of the population, the highest
daily intake of Hg was about 130 ug/kg; The average period of
consumption ranged from 43-68 days. /Alkyl-mercury fungicides/
[WHO; Environ Health
Criteria: Mercury p.90-107 (1976)]**PEER REVIEWED**
THE MOST CONSISTENT & PRONOUNCED EFFECTS OF /CHRONIC/ EXPOSURE TO
... SHORT-CHAIN ALKYLMERCURY COMPOUNDS SUCH AS METHYLMERCURY ARE ON
CNS. EFFECTS ... ARE NEUROLOGICAL & PSYCHIATRIC. COMMON SYMPTOMS
INCL DEPRESSION, IRRITABILITY, EXAGGERATED RESPONSE TO STIMULATION (ERETHISM),
EXCESSIVE SHYNESS, INSOMNIA, EMOTIONAL INSTABILITY, FORGETFULNESS,
CONFUSION, & VASOMOTOR DISTURBANCES SUCH AS EXCESSIVE PERSPIRATION &
UNCONTROLLED BLUSHING. TREMORS ARE ALSO COMMON ... ... SENSORY
EFFECTS ... OCCUR MORE CONSISTENTLY & AT LOWER LEVELS OF EXPOSURE.
EARLIEST SIGN IS PARESTHESIA. AT ... HIGHER LEVELS OF EXPOSURE OTHER
EFFECTS OCCUR, SUCH AS ATAXIA, CONSTRICTION OF VISUAL FIELD,
DYSARTHRIA, & HEARING DEFECTS. THESE ALTERATIONS ARE IRREVERSIBLE
WHEN POISONING IS SEVERE. NEUROPSYCHIATRIC EFFECTS ... ARE LIKELY TO
INVOLVE SPONTANEOUS FITS OF LAUGHING & CRYING & INTELLECTUAL
DETERIORATION. /ALKYLMERCURY COMPOUNDS/
[Hardman, J.G., L.E.
Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman
and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New
York, NY: McGraw-Hill, 1996.1657]**PEER REVIEWED**
Of 60 adult African women using skin-lightening creams containing
inorganic mercury, 26 developed the nephrotic syndrome ... Reported
one case of membranous nephropathy, due to the use of
skin-lightening cream, where immunofluorescence showed finely
granular IgG, IgM, and C3 complement deposits. /Inorganic mercury/
[WHO; Environmental
Health Criteria 118: Inorganic Mercury p. 93 (1991)]**PEER
REVIEWED**
... Thiomersal (sodium ethylmercurithiosalicilate) and ammoniated
mercury have been found to be common sensitizers in a survey on the
epidemiology of contact dermatitis ... Both aryl- and alkylmercurial
seed dressings have also been shown to be potent skin sensitizers.
Mercury compounds give rise to a type IV cell-mediated delayed
hypersensitivity reaction ... .
[WHO; Environmental
Health Criteria 118: Inorganic Mercury p. 97 (1991)]**PEER
REVIEWED**
Acute poisoning is major threat in home & on farm, but, because
mercury is a cumulative poison, subacute & chronic intoxications are
recognized, particularly in industry.
[Gosselin, R.E., R.P.
Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th
ed. Baltimore: Williams and Wilkins, 1984.III-266]**PEER REVIEWED**
Human Toxicity
Values:
Lethal Blood Level: The concn of inorganic mercury present in the
blood (serum or plasma) that has been reported to cause death in
humans is: 0.04-2.2 mg%; 0.4-22 ug/ml. /Inorganic mercury/
[Winek, C.L. Drug and
Chemical Blood-Level Data 1985. Pittsburgh, PA: Allied Fischer
Scientific, 1985.]**PEER REVIEWED**
Skin, Eye and
Respiratory Irritations:
MANY MERCURY CMPD ARE IRRITATING TO SKIN & MAY PRODUCE DERMATITIS
WITH OR WITHOUT VESICATION. ... CONTACT WITH EYES CAUSES ULCERATION
OF CONJUNCTIVA & CORNEA.
[Gosselin, R.E., R.P.
Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th
ed. Baltimore: Williams and Wilkins, 1984.III-263]**PEER REVIEWED**
Alkyl mercury compounds are primary skin irritants and may cause
dermatitis. /Methyl mercury compounds/
[Sittig M; Handbook of
Toxic and Hazardous Chemicals p.421 (1981)]**PEER REVIEWED**
THE ALKYLMERCURY COMPOUNDS ARE STRONG IRRITANTS OF THE SKIN & MAY
CAUSE BLISTERS OR OTHER DERMATITIS WITH OR WITHOUT ASSOC SYSTEMIC
ILLNESS. /ALKYLMERCURY COMPOUNDS/
[Hayes, Wayland J., Jr.
Pesticides Studied in Man. Baltimore/London: Williams and Wilkins,
1982.22]**PEER REVIEWED**
Exposure of the skin to a concentrated solution of phenylmercury
cmpd may cause chemical burns with blistering. /Aryl mercury cmpd/
[International Labour
Office. Encyclopedia of Occupational Health and Safety. Vols. I&II.
Geneva, Switzerland: International Labour Office, 1983.1336]**PEER
REVIEWED**
Soluble salts have violent corrosive effects on skin and mucous
membranes. /Mercury/
[Budavari, S. (ed.). The
Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals.
Whitehouse Station, NJ: Merck and Co., Inc., 1996.1006]**PEER
REVIEWED**
Irritation levels: The American National Standards Institute (ANSI)
states that "the organomercurials are severe skin, eye & mucous
membrane irritants. /Organo (alkyl) mercury/
[Mackison, F. W., R. S.
Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational
Health Guidelines for Chemical Hazards. DHHS(NIOSH) Publication No.
81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office,
Jan. 1981.3]**PEER REVIEWED**
PROLONGED ABSORPTION OF IODIDES MAY PRODUCE IODISM WHICH IS
MANIFESTED BY SKIN RASH, RUNNING NOSE, HEADACHE, AND IRRITATION OF
MUCOUS MEMBRANES. /IODIDES/
[Sax, N.I. Dangerous
Properties of Industrial Materials. 6th ed. New York, NY: Van
Nostrand Reinhold, 1984.1616]**PEER REVIEWED**
Medical
Surveillance:
The assessment of mercury exposure can be accomplished through
measurement of mercury, which is useful for assessment of recent
exposure to any of the three forms of mercury. ... Whole Blood
Reference Ranges: Normal - mean level in the general population <8
ug/l; Exposed - BEI (sampling time at end of shift at end of
workweek, measured as total inorganic mercury) 15.0 ug/l. BAT
(biological tolerance value for a working material) for metallic and
inorganic compounds (sampling time not fixed) 50 ug/l; BAT for
organic compounds (sampling time not fixed) 100 ug/l. /Mercury/
[Ryan, R.P., C.E. Terry
(eds.). Toxicology Desk Reference 4th ed. Volumes 1-3. Taylor &
Francis, washington, D.C. 1997.1577]**PEER REVIEWED**
The assessment of mercury exposure can be accomplished through
measurement of mercury, which is useful for assessment of recent
exposure to any of the three forms of mercury. ... Whole Blood
Reference Ranges: Toxic - 0.3 ug/100 ml, memory disturbances,
impaired eye-hand coordination; 0.5-3 ug/100 ml, altered
electroencephalograms (EEGs); <1 - >10 ug/deciliter, increased
tremors; 1.4 ug/ ml, decreased immunoglogin G (IgG) and immunoglobin
A (IgA) levels; >1.5 ug/100 ml, disturbances in tests on verbal
intelligence and memory; 1-2 ug/100 ml, increased prevalence of
abnormal psychomotor scores; 1-2 ug/ 100 ml, increased tremors,
impaired eye-hand coordination; >3 ug/100 ml, (estimated threshold
level): increased urinary excretion of beta-galactosidase and high
molecular weight proteins. /Mercury/
[Ryan, R.P., C.E. Terry
(eds.). Toxicology Desk Reference 4th ed. Volumes 1-3. Taylor &
Francis, washington, D.C. 1997.1577]**PEER REVIEWED**
The assessment of mercury exposure can be accomplished through
measurement of mercury. However, measurement of mercury in ...
/serum or plasma/ is insensitive because mercury is found primarily
in the red blood cells. Serum or Plasma Reference Ranges: Normal -
not established; Exposed - not established; Toxic - not established.
/Mercury/
[Ryan, R.P., C.E. Terry
(eds.). Toxicology Desk Reference 4th ed. Volumes 1-3. Taylor &
Francis, washington, D.C. 1997.1578]**PEER REVIEWED**
The assessment of mercury exposure can be accomplished through
measurement of mercury ... Urine Reference Ranges: Normal - <20.0 ug/l;
Exposed - BEI (sampling time is preshift, measured as total
inorganic mercury) 35.0 ug/g creatinine; Toxic - 3-53 ug/g
creatinine, memory disturbances, impaired eye-hand coordination;
4-53 ug/g creatinine, altered EEGs; 3-272 ug/g creatinine, increased
anti-laminin antibodies (implicated in the etiology of autoimmune
glomerulo-nephritis); 44 ug/g creatinine, decreased Iga and IgG
levels; 73 ug/g creatinine, increased static tremors, difficulty
with heel-to-toe gait; 50-100 ug/g creatinine, increased tremors,
impaired eye-hand coordination; >50 ug/g creatinine (estimated
threshold level), increased urinary excretion of beta-galactosidase
and high molecular weight proteins; 7-1,101 ug/24 hr, abnormal
memory tests, decreased tibial nerve velocity, increased median
nerve latency in both motor and sensory nerves; 0-510 ug/l, short
term memory loss; 5-1,000 ug/l, increased tremor frequency and
reaction time, impaired eye-hand coordination; <10->1,000 ug/l,
increased tremors; 20-450 ug/l, increased motor and sensory nerve
latency; >56 ug/l, disturbances in tests on verbal intelligence and
memory; 100-250 ug/l, increased acetyl beta-d-glucosaminidase (NAG)
enzyme levels in urine; >200 ug/l, increased tremors, impaired
eye-hand coordination; 300-1,400 ug/l, nephrotic syndrome,
albuminuria, hypercholesterolemia; 56 ug/g creatinine, no effect
level for proteinuria. /Mercury/
[Ryan, R.P., C.E. Terry
(eds.). Toxicology Desk Reference 4th ed. Volumes 1-3. Taylor &
Francis, washington, D.C. 1997.1578]**PEER REVIEWED**
Urine Albumin: Albuminuria has been shown to be a specific marker of
glomerular dysfunction. Tubular damage, however, can also result in
increased levels of albumin in the urine. /Metallic, inorganic and
organic mercury/
[Ryan, R.P., C.E. Terry
(eds.). Toxicology Desk Reference 4th ed. Volumes 1-3. Taylor &
Francis, washington, D.C. 1997.1580]**PEER REVIEWED**
Urinary Beta-2-Microglobulin and/or Retinal Binding Protein:
Measurements for the presence of either of these low molecular
weight proteins are useful in detection of early impairment of
proximal tubular function. However, beta-2-microglobulin is unstable
at urinary pH less than 6, and may degrade in the bladder prior to
collection and subsequent neutralization of the urine sample.
Measurement of retinal binding protein appears to be a better marker
for early tubular dysfunction due to its stability in the urine
subsequent to collection and analysis. However, retinal binding
protein is produced in the liver and not a constitutive protein of
the kidney, so that its presence in the kidney provides only
indirect evidence of tubular damage. /Metallic, inorganic and
organic mercury/
[Ryan, R.P., C.E. Terry
(eds.). Toxicology Desk Reference 4th ed. Volumes 1-3. Taylor &
Francis, washington, D.C. 1997.1580]**PEER REVIEWED**
Urinary Alpha () and Pi () Isoenzymes of Glutathione S-Transferase:
Radio-immunological and Elisa techniques have been developed for
quantitation of and isoenzymes of glutathione S-transferase, which
are constitutive proteins in the kidney." The isoenzyme is located
only in the proximal tubule, while the isoenzyme is located in the
distal convoluted tubule, the loop of Henle, and the collecting
ducts of the kidney. Damage to epithelial cell membranes can result
in the increased excretion of these isoenzymes in the urine. This
test for assessing renal tubular damage appears to have many
advantages over other available tests, such as: (1) the and
isoenzymes are constitutive proteins in the kidney; (2) these
isoenzymes are stable in the urine; (3) the test is simple and
reproducible; and (4) due to selective localization of the
isoenzymes, differential diagnosis of specific tubular damage is
possible. In addition, increased levels of these isoenzymes were
seen in patients previously exposed to nephrotoxicants
where'conventional tests for kidney function were normal, indicating
a high degree of sensitivity. /Metallic, inorganic and organic
mercury/
[Ryan, R.P., C.E. Terry
(eds.). Toxicology Desk Reference 4th ed. Volumes 1-3. Taylor &
Francis, washington, D.C. 1997.1581]**PEER REVIEWED**
Urinary Enzyme N-Acetylglucosaminidase: This lysosomal enzyme has
shown promise in assessment of subclinical nephrotoxic injury. This
enzyme is not normally filtered at the glomerulus due to its high
molecular weight. In the absence of glomerular injury, this enzyme
will be detected in the urine as a result of leakage or exocytosis
from damaged, stimulated, or exfoliated renal cells. The sensitivity
of measurement for this enzyme has not been thoroughly studied, but
it's usefulness has shown some promise. However, this enzyme is
unstable at urinary pH greater than 8, which could diminish the
sensitivity of the measurement due to enzyme degradation. /Metallic,
inorganic and organic mercury/
[Ryan, R.P., C.E. Terry
(eds.). Toxicology Desk Reference 4th ed. Volumes 1-3. Taylor &
Francis, washington, D.C. 1997.1581]**PEER REVIEWED**
Routine Urinalysis: Performing a routine urinalysis including
parameters such as specific gravity, glucose, and microscopic
examination may be useful for assessing renal toxicity. /Metallic,
inorganic and organic mercury/
[Ryan, R.P., C.E. Terry
(eds.). Toxicology Desk Reference 4th ed. Volumes 1-3. Taylor &
Francis, washington, D.C. 1997.1581]**PEER REVIEWED**
Evaluation of Peripheral Neuropathy: Nerve conduction study;
Electromyography; Quantitative sensory testing; Thermography.
/Metallic, inorganic and organic mercury/
[Ryan, R.P., C.E. Terry
(eds.). Toxicology Desk Reference 4th ed. Volumes 1-3. Taylor &
Francis, washington, D.C. 1997.1584]**PEER REVIEWED**
Evaluation of Central Nervous System Effects: Evaluation of CNS
effects can be performed through neuropsychological assessment,
which consists of a clinical interview and administration of
standardized personality and neuropsychological tests. The areas
that the neuropsychology test batteries focus on include the domains
of memory and attention; visuoperceptual, visual scanning,
visuospatial, and visual memory; and motor speed and reaction time.
There is limited data on which components of the test batteries are
best indicators of early CNS effects. /Metallic, inorganic and
organic mercury/
[Ryan, R.P., C.E. Terry
(eds.). Toxicology Desk Reference 4th ed. Volumes 1-3. Taylor &
Francis, washington, D.C. 1997.1584]**PEER REVIEWED**
Evaluation of Cranial Neuropathies: Evaluation of cranial nerve
damage, as evidenced by symptoms such as loss of balance, visual
function, smell, taste, or sensation on the face, can be
accomplished through a physical examination focusing on tests such
as: Smell Assessment ... Visual Assessment ... Facial and Trigeminal
Nerve Assessment ... Vestibular Assessment ... Hearing Assessment.
/Metallic, inorganic and organic mercury/
[Ryan, R.P., C.E. Terry
(eds.). Toxicology Desk Reference 4th ed. Volumes 1-3. Taylor &
Francis, washington, D.C. 1997.1584]**PEER REVIEWED**
A complete history and physical examination should be performed to
detect existing conditions that might place the exposed employee at
increased risk and to establish a baseline for future health
monitoring. This examination should detect any signs or symptoms of
unacceptable mercury absorption such as weight loss, insomnia,
tremors, personality changes, or other evidence of central nervous
system involvement, as well as evidence of kidney damage. The skin
should be examined for evidence of chronic disorders. Urinalysis
should include at a minimum, specific gravity, albumin, glucose, and
a microscopic examination of centrifuged sediment. Determination of
mercury level in the urine may be helpful in assessing extent of
absorption. /Mercury/
[NIOSH/OSHA; Occupational
Health Guide for Chemical Hazards: Inorganic Mercury (1981) DHHS
Pub. NIOSH 81-123]**PEER REVIEWED**
Routine medical surveillance: periodic medical exams including
analysis of blood and urine for amount of mercury present for all
workers directly involved in production of mercurials, or otherwise
exposed to contact with mercury cmpd or mercury vapor. /Mercury cmpd/
[Kirk-Othmer Encyclopedia
of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John
Wiley and Sons, 1978-1984.15(81) 167]**PEER REVIEWED**
/SRP: Protect/ from exposure those individuals with diseases of
liver, kidneys, lung, and nerves. /Mercury cmpd/
[ITII. Toxic and Hazarous
Industrial Chemicals Safety Manual. Tokyo, Japan: The International
Technical Information Institute, 1982.315]**PEER REVIEWED**
Preemployment and periodic examinations should be concerned
especially with the skin, respiratory tract, central nervous system
and kidneys. The urine should be examined and urinary mercury levels
determined periodically. Signs of weight loss, gingivitis, tremors,
personality changes and insomnia should be suggestions of possible
mercury intoxication. /Mercury cmpd/
[Sittig, M. Handbook of
Toxic and Hazardous Chemicals and Carcinogens, 1985. 2nd ed. Park
Ridge, NJ: Noyes Data Corporation, 1985.571]**PEER REVIEWED**
Medical Surveillance: Placement and periodic physical examinations
should be concerned particularly with the skin, vision, central
nervous system, and kidneys. Consideration should be given to the
possible effects on the fetus of alkyl mercury exposure in the
mother. Constriction of visual fields may be a useful diagnostic
sign. Blood and urine levels of mercury have been studied,
especially in the case of methyl mercury. A precise correlation has
not been found between exposure levels and concentrations. They may
be of some value in indicating that exposure has occurred. /Aryl and
alkyl mercury cmpd/
[Sittig M; Handbook of
Toxic and Hazardous Chemicals p.421 (1981)]**PEER REVIEWED**
Recommended medical surveillance: The following medical procedures
should be made available to each employee who is exposed to organo
(alkyl) mercury at potentially hazardous levels: 1) Initial medical
examination: A complete history & physical examination: The purpose
is to detect pre-existing conditions that might place the exposed
employee at increased risk, & to establish a baseline for future
health monitoring. Examination of the CNS, the kidneys, & eyes
should be stressed. The skin should be examined for evidence of
chronic disorders. Blood test: Analysis of the blood for mercury may
be useful in monitoring absorption. Urinalysis: Since kidney damage
has been observed in humans exposed to organo mercury, a urinalysis
should be obtained to include at a minimum specific gravity,
albumin, glucose & a microscopic /examination/ of centrifuged
sediment. 2) Periodic medical examination: The aforementioned
medical examination should be repeated on an annual basis. /Organo
(alkyl) mercury/
[Mackison, F. W., R. S.
Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational
Health Guidelines for Chemical Hazards. DHHS(NIOSH) Publication No.
81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office,
Jan. 1981.2]**PEER REVIEWED**
Indicators of exposure & concentrations in the critical organ:
Experimental studies in man & primates have shown that mercury concn
in blood is, under steady-state conditions, linearly correlated to
intake of methylmercury & to the concn of methylmercury in the
critical organ (the brain), at non-toxic body burdens. As more than
90% of methylmercury in blood is to be found in the erythrocytes,
the mercury concn in red cells is the most reliable index of
methylmercury body burden & brain concn. Methylmercury is deposited
in the hair during the formation of pile. The deposition of the
methylmercury in the pile is proportional to the mercury concn in
blood at the time of pile formation. Thus, the mercury concn in the
hair pile constitutes a calendar of mercury concn in blood, which
occurred during formation of the pile. The methylmercury concn in
the hair can be used as an indicator of mercury concn in blood, & in
the critical organ, or body burden of mercury, provided that
allowance is made for the growth rate of the hair pile (about 1 cm a
month, dependent upon age) & for the time lag between hair formation
& extrusion. ... the quotent between methylmercury concn in blood &
hair is 1 to 250. Under occupational conditions the possibility of
external contamination of hair should be kept in mind. /Methylmercury
compounds/
[Friberg, L., Nordberg,
G.F., Kessler, E. and Vouk, V.B. (eds). Handbook of the Toxicology
of Metals. 2nd ed. Vols I, II.: Amsterdam: Elsevier Science
Publishers B.V., 1986.V2 428]**PEER REVIEWED**
Organic mercury exposure is best monitored by the measurement of
total mercury (or the specific derivative) in whole blood. It has
been recommended that the blood mercury level not be allowed to
exceed 0.10 mg/l in workers exposed to organomercury compounds. /Organomercury
compounds/
[Baselt, R.C. Biological
Monitoring Methods for Industrial Chemicals. 2nd ed. Littleton, MA:
PSG Publishing Co., Inc. 1988.200]**PEER REVIEWED**
Populations at
Special Risk:
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