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Mercuric Chloride Toxicity


http://toxnet.nlm.nih.gov

TABLE OF CONTENTS

  • Human Health Effects
  • Emergency Medical Treatment
  • Animal Toxicity Studies
  • Metabolism/Pharmacokinetics
  • Pharmacology
  • Environmental Fate & Exposure
  • Environmental Standards & Regulations
  • Chemical/Physical Properties
  • Chemical Safety & Handling
  • Occupational Exposure Standards
  • Manufacturing/Use Information
  • Laboratory Methods
  • Special References
  • Synonyms and Identifiers
  • Administrative Information

MERCURIC CHLORIDE
CASRN: 7487-94-7
For other data, click on the Table of Contents

Human Health Effects:

Evidence for Carcinogenicity:

Evaluation: There is limited evidence in experimental animals for the carcinogenicity of mercuric chloride. Overall evaluation: Metallic mercury and inorganic mercury compounds are not classifiable as to their carcinogenicity to humans (Group 3).  [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).,p. 58 324 (1993)]**QC REVIEWED**

A4. A4= Not Classifiable as a Human Carcinogen. (1994) /Mercury, inorganic forms including metallic mercury, as Hg (Sin)  [American Conference of Governmental Industrial Hygienists. Threshold Limit Values (TLVs) for Chemical Substances and Physical Agents and BiologicalExposure Indices (BEIs) for 1995-1996. Cincinnati, OH: ACGIH, 1995. 25]**QC REVIEWED**

CLASSIFICATION: C; possible human carcinogen. BASIS FOR CLASSIFICATION: Based on the absence of data in humans and limited evidence of carcinogenicity in rats and mice. Focal papillary hyperplasia and squamous cell papillomas in the forestomach as well as thyroid follicular cell adenomas and carcinomas were observed in male rats gavaged with mercuric chloride for 2 years. The relevance of the forestomach papillomas to assessment of cancer in humans is questionable because no evidence indicated that the papillomas progressed to malignancy. The relevance of the increase in thyroid tumors has also been questioned because these tumors are generally considered to be secondary to hyperplasia; this effect was not observed in the high-dose males. It should also be noted that the authors considered the doses used in the study to exceed the MTD for male rats. In the same study, evidence for increases in squamous cell papillomas in the forestomach of female rats was equivocal.

In a second study, equivocal evidence for renal adenomas and adenocarcinomas was observed in male mice; there was a significant positive trend. This tumor type is rare in mice, and the increase in incidence was statistically significant when compared with historic controls. Two other nonpositive lifetime rodent studies were considered inadequate. Mercuric chloride showed mixed results in a number of genotoxicity assays. HUMAN CARCINOGENICITY DATA: None. ANIMAL CARCINOGENICITY DATA: Limited.  [U.S. Environmental Protection Agency's Integrated Risk Information System (IRIS) on Mercuric Chloride (HgCl2) (7487-94-7) from the National Library of Medicine's TOXNET System, May 3, 1995]**QC REVIEWED**

Human Toxicity Excerpts:

SERIAL MEASUREMENTS OF PLASMA MERCURY WERE MADE IN A PATIENT WITH SEVERE & PROLONGED ACUTE RENAL FAILURE DUE TO POISONING WITH MERCURIC CHLORIDE. INITIAL MERCURY CONCN IN WHOLE BLOOD OF 1200 UG/L (6 UMOL/L) WAS RECORDED, & RECOVERY OF RENAL FUNCTION COINCIDED WITH A FALL IN PLASMA MERCURY CONCN TO BELOW 100 UG/L (0.5 UMOL/L).   [NEWTON JA ET AL; HUM TOXICOL 2 (3): 535 (1983)]**PEER REVIEWED**

ACUTE SYSTEMIC POISONING APPEARS SELDOM TO HAVE CAUSED DISTURBANCES OF THE EYE, BUT IN 3 YOUNG PEOPLE BILATERAL MYDRIASIS, HYPEREMIA OF OPTIC NERVEHEADS & RETINAL VENOUS DISTENSION WITH RAPID DECREASE IN VISUAL ACUITY HAVE BEEN REPORTED.  [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986. 579]**PEER REVIEWED**

... Acute systemic mercurialism may be fatal within a few minutes, but death by uremic poisoning is usually delayed 5-12 days. Acute poisoning has resulted from inhaling dust concn of 1.2-8.5 mg/cu m in air. ... /Mercury compounds/  [U.S. Coast Guard, Department of Transportation. CHRIS -  Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.]**PEER REVIEWED**

Mercuric chloride ... directly affects the human placental syncytiotrophoblast microvillous membrane. ... /Mercuric chloride/ alters the facilitated diffusion of alpha-aminoisobutyric acid into vesicles of this membrane in microM concn. Mercuric chloride abolishes temporal kinetics of alpha-aminoisobutyric acid transport, inducing an initial increase in alpha-aminoisobutyric acid transport (27% at 100 microM) but subsequently lowering equilibrium values when compared to equilibrium time points in control. ... Preincubation was necessary for mercuric chloride-induced perturbation of alpha-aminoisobutyric acid transport. Cysteine protects against mercuric chloride ... effects on alpha-aminoisobutyric acid   transport but did not reverse these pertubations. ...  [Goodman DR et al; Teratogenesis Carcinog Mutagen 3 (1): 89-100 (1983)]**PEER REVIEWED**

Segregational errors of chromosomes were studied in human lymphocytes and in Indian muntjac fibroblasts exposed to ... mercury chloride (HgCl2). The cells were exposed to /mercury chloride/ only during a limited period of the pre-DNA synthetic stage of the cell cycle or from that stage up to mitosis. In the lymphocytes a clear incr of C-mitotic figures for /mercury chloride was observed/. Segregational errors were, however, much more important after the shorter exposure period.  [Verschaeve L et al; Toxicol Lett 21 (3): 247-53 (1984)]**PEER REVIEWED**

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 diffused 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. /Mercury cmpd/  [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984.,p. 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. /Mercury cmpd/  [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984.,p. 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. /Mercury cmpd/  [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984.,p. III-270]**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 accompanied 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 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. 1612]**PEER REVIEWED**

A man believed to have had normal eyes before swallowing a 0.5 g tablet of mercuric chloride, which caused diarrhea and moderate albuminuria for a few days, two years later had vision 20/60 OD 20/200 OS. The media were clear, but in both fundi many discrete white areas were seen deep to the retina in the whole central area and around the disc, with patches of degeneration with glistening crystalline appearance, but no vascular abnormalities or appearances to suggest inflammation.  [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986. 579]**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 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). /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. 413]**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. /Mercury 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**

CHRONIC POISONING WITH INORGANIC MERCURY CAUSES GINGIVITIS, STOMATITIS, & EXCESSIVE SALIVATION. MERCURIALENTIS (A COLORED REFLEX FROM THE LENS) IS ALSO OBSERVED BUT DOES NOT INDICATE INTOXICATION. ... ANOREXIA, WEIGHT LOSS, ANEMIA, AND MUSCULAR WEAKNESS ARE ALSO ASSOC WITH CHRONIC EXPOSURE ... /INORGANIC MERCURY CMPD/  [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 hr. ... /Mercuric compounds/  [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 PATIENT 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. /MERCURY 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**

A 19 yr old girl was treated for a heavy mercuric chloride intoxication (3 g mercuric chloride) with 2,3-dimercaptopropane-1-sulfonate and dialysis. The anuric stage lasted for 10 days. With 2,3-dimercapto- propane-1-sulfonate the mecury clearance by hemodialysis was 3.5-5.0 ml/min, with BAL 0.6 ml/min. 2,3-dimercaptopropane-1-sufonate is an effective water-soluble mercury chelator and is subjectively better tolerated and less toxic than 2,3-dimercaptopropanol.  [Nadig J et al; Schweiz Med Wochenschr 115 (15): 507-11 (1985)]**PEER REVIEWED**

Among mecuric iodide, mercuric chloride, and HGNH2Cl, the acute toxic concn to monolayer cell cultures (Hep-2, Vero and amnion) was the lowest for mercuric iodide (cell degeneration), followed by that of mercuric chloride. The mercury (II) cmpd belonged to class II type materials (highly toxic). The sensitivity of the cell lines to the mercury cmpds was practically similar; only human amnion cells were somewhat more sensitive than the remaining ones. The mercury cmpds inhibited the cell growth and multiplication and the max effect was observed by 48 hr. The investigated cmpds inhibited monoamine oxidase activity in the hepatic mitochondria at 10-2M.  [Ivanova LA, Nizharadze MA; Gig Tr Prof Zabol (14): 43-5 (1987)]**PEER REVIEWED**

AMONG INORG CMPD, ELEMENTAL MERCURY & DIVALENT MERCURY SALT ARE ... 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. /MERCURY/  [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. /MERCURY/  [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**

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**

Soluble salts have violent corrosive effects on skin and mucous membranes.
/Mercury salts/  [The Merck Index. 10th ed. Rahway, New Jersey: Merck Co., Inc., 1983. 842]**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**

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. /Mercury cmpd/  [Hamilton, A., and H. L. Hardy. Industrial Toxicology. 3rd ed. Acton, Mass.: Publishing Sciences Group, Inc., 1974. 132]**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**

Human Toxicity Values:

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%; 0.4-22 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. /MERCURY CMPD/
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984.,p. III-263]**PEER REVIEWED**

Soluble salts have violent corrosive effects on skin and mucous membranes.
/Mercury salts/  [The Merck Index. 10th ed. Rahway, New Jersey: Merck Co., Inc., 1983. 842]**PEER REVIEWED**  Medical Surveillance:

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.,p. 15(81) 167]**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 would be suggestions of possible mercury intoxication. /Mercury cmpds/  [Sittig, M. Handbook of Toxic and Hazardous Chemicals and Carcinogens, 1985. 2nd ed. Park Ridge, NJ: Noyes Data Corporation, 1985. 571]**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. /Inorganic mercury/   [NIOSH/OSHA; Occupational Health Guide for Chemical Hazards: Inorganic Mercury (1981) DHHS Pub. NIOSH 81-123]**PEER REVIEWED**

SINCE MERCURY CMPD IN GENERAL MAY CAUSE INJURY TO THE KIDNEYS IT IS DESIRABLE TO EXCLUDE FROM EMPLOYMENT PERSONS WHO HAVE HAD PREVIOUS KIDNEY DISEASE. ATTENTION TO DENTAL AND ORAL HYGIENE IS IMPORTANT ... /MERCURY CMPD/  [International Labour Office. Encyclopedia of Occupational Health and Safety. Volumes I and II. New York: McGraw-Hill Book Co., 1971. 865]**PEER REVIEWED**

Populations at Special Risk:

Children are more susceptible than adults to mercury poisoning. /Mercury salts/   [Britt DL, Hushon JM; Biological Effects, Criteria and Standards for Hazardous Pollutants Associated with Energy Technologies p.6-38 (1976)]**PEER REVIEWED**

Persons with a history of allergies or known sensitization to mercury, chronic respiratory disease, nervous system disorders, or kidney disorders are at increased risk from exposure. /Mercury cmpd/  [NIOSH/OSHA; Occupational Health Guide for Chemical Hazards: Inorganic Mercury p.1 (1981) DHHS Pub. NIOSH 81-123]**PEER REVIEWED**

Probable Routes of Human Exposure:

The dominant food source of mercury in the human diet is fish and fish products. ... In terms of total mercury (Hg), the diet greatly exceeds other media, including air and water, as a source of human exposure and absorption of Hg. /Mercury/  [USEPA; Mercury Health Effects Update p.2-4 (1984) EPA 600/8-84-019F]**PEER REVIEWED**

Accumulation of mercury in the terrestrial and aquatic food chains results in risks for man mainly through the consumption of: ... fish from contaminated waters; especially predator species, tuna fish, swordfish and other large oceanic fish even if caught considerably off shore; other seafoods including mussels and crayfish, fish-eating birds and mammals; and eggs of fish eating birds. /Mercury/  [WHO; Environ Health Criteria: Mercury p.55 (1976)]**PEER REVIEWED**

Acute poisoning usually results from oral ingestion of highly dissociated inorganic prepn, but it may also be caused by ... mercurial ointments applied topically. /Mercury cmpd/   [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**

Acute poisoning is major threat in home & on farm, but, because mercury is a cumulative poison, subacute & chronic intoxications are recognized, particularly in industry. /Mercruy cmpd/  [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984.,p. III-266]**PEER REVIEWED**

Emergency Medical Treatment:

Emergency Medical Treatment:

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The following Overview, *** MERCURIC CHLORIDE ***, is relevant for this HSDB record chemical. Life Support:   This overview assumes that basic life support measures have been instituted.

Clinical Effects:
SUMMARY OF EXPOSURE
0.2.1.1 ACUTE EXPOSURE
Mercuric chloride is one of the most toxic mercury salts. This review is based on the properties of inorganic mercury compounds in general, except where specific effects have been attributed to mercuric chloride.

Mercuric salts are corrosive and nephrotoxic. Salivation, metallic taste, abdominal pain, seizures, proteinuria, and nephrotic syndrome (oliguria and anuria) may occur. Circulatory collapse, bloody diarrhea, and acute renal failure have been reported following peritoneal lavage with mercuric chloride.

Mercury compounds can be absorbed by inhalation and through the skin. The principal concerns from acute inorganic mercury poisoning are sudden, profound circulatory collapse with tachycardia, hypotension and peripheral vasoconstriction, vomiting, and bloody diarrhea. Renal failure usually develops within 24 hours and may be life-threatening.

The brain is the critical organ for chronic inorganic mercury poisoning. Tremor and psychological changes encompassing increased irritability and sensitivity, xenophobia, insomnia, hallucinations, and mania may occur. Eventually there is spongeous degeneration of the brain with loss of many higher functions.

When mercury poisoning is suspected in critically ill patients, chelation therapy should be started regardless of the form of mercury causing toxicity.

VITAL SIGNS
0.2.3.1 ACUTE EXPOSURE

o Sudden and profound circulatory collapse with tachycardia, weak and shallow pulse, hypotension and peripheral vasoconstriction can occur from ingestion of inorganic mercurials.
HEENT
0.2.4.1 ACUTE EXPOSURE
o Mercuric chloride is corrosive to the eyes and throat. Persistent visual disturbance has been seen from acute systemic poisoning.
0.2.4.2 CHRONIC EXPOSURE
o Brown deposits of mercury in the lens and visual defects can occur.
CARDIOVASCULAR
0.2.5.1 ACUTE EXPOSURE
o Profound circulatory collapse, with tachycardia and hypotension, can occur from acute exposure to inorganic mercurials.
NEUROLOGIC
0.2.7.1 ACUTE EXPOSURE
o Peripheral neuropathy and brain damage can occur even from acute exposures.
0.2.7.2 CHRONIC EXPOSURE
o The brain is the critical target organ for chronic mercury toxicity. Tremor, characteristic psychiatric changes, ataxia, peripheral neuropathy, and degeneration of higher brain functions appear with chronic exposure to inorganic mercurials.
GASTROINTESTINAL
0.2.8.1 ACUTE EXPOSURE
o Hematemesis, nausea, bloody diarrhea, and edema of the upper GI tract have occurred from ingestion.
GENITOURINARY
0.2.10.1 ACUTE EXPOSURE
o Renal failure may occur within 24 hours of an acute exposure.
0.2.10.2 CHRONIC EXPOSURE
o Renal dysfunction has occurred from chronic exposure to mercuric chloride in humans and animals.
FLUID-ELECTROLYTE
0.2.12.1 ACUTE EXPOSURE
o Fluid and electrolyte loss secondary to corrosion of tissues is often the cause of death in acute
poisonings.
HEMATOLOGIC
0.2.13.2 CHRONIC EXPOSURE
o Anemia occurs with chronic poisoning from inorganic mercurials. Inhibition of polymorphonuclear leukocyte function occurred in vitro.
DERMATOLOGIC
0.2.14.1 ACUTE EXPOSURE
o Severe skin irritation has been seen with mercuric chloride.
0.2.14.2 CHRONIC EXPOSURE
o Hypersensitivity reactions may rarely occur.
MUSCULOSKELETAL
0.2.15.1 ACUTE EXPOSURE
o Evidence of rhabdomyolysis was seen in a case of acute mercuric chloride ingestion.
0.2.15.2 CHRONIC EXPOSURE
o Muscular weakness occurs with chronic poisoning from inorganic mercurials.
ENDOCRINE
0.2.16.2 CHRONIC EXPOSURE
o Increased thyroid function was observed in experimental animals.
PSYCHIATRIC
0.2.18.2 CHRONIC EXPOSURE
o Mercurial erethism is a characteristic psychiatric syndrome involving short-term memory loss, increased irritability, xenophobia, apathy, and mania in extreme
cases.
IMMUNOLOGIC
0.2.19.2 CHRONIC EXPOSURE
o Alterations in T-cell function have been seen in mice.
o Autoimmune disorders were induced in mice, but strain
differences occurred (Kosuda et al, 1994).
REPRODUCTIVE HAZARDS
o Mercuric chloride has been linked with spontaneous abortions in humans. It has been embryotoxic, fetotoxic, and teratogenic, and has affected the testes and sperm in rodents.
CARCINOGENICITY
0.2.21.3 ANIMAL OVERVIEW
o Mercury has not been carcinogenic in mice. Mercuric chloride produced equivocal evidence of carcinogenic activity in F-344 rats and in male, but not female,
B6C3F1 mice.
GENOTOXICITY
o DNA damage/repair, mutations, sister chromatid exchanges, chromosome aberrations, and in vitro oncogenic transformation have been induced by mercuric chloride in short-term test systems. It induced dominant lethal mutations in rats.
OTHER
0.2.23.1 ACUTE EXPOSURE
o Mercuric chloride is hazardous by inhalation, skin contact, and ingestion.
0.2.23.2 CHRONIC EXPOSURE
o Persons receiving regular injections of gamma-globulin containing merthioloate as a preservative may be more sensitive to other mercury compounds.

Laboratory:
o Obtain whole blood mercury levels, 24 hour urine collection for mercury, baseline BUN, creatinine, urinalysis and electrolytes.
o NORMAL RANGE - Blood mercury levels rarely exceed 1.5
mcg/dL.
o Normal urine excretion without chelation therapy rarely exceeds 50 mcg/24hrs of mercury.

Treatment Overview:
ORAL EXPOSURE
o Consider gastric emptying in patients presenting soon after ingestion of inorganic mercury compounds. Mercury salts may be corrosive but GI perforation is not common.
o EMESIS: Use is controversial. May be indicated in the prehospital setting if administered soon (within 30 minutes) after substantial ingestion.
CONTRAINDICATIONS: loss of airway protective reflexes; CNS depression; seizures; ingestion of a substance that might impair airway protective reflexes or require advanced life support within 60 minutes; ingestion of a corrosive substance or hydrocarbon with high aspiration potential; debilitated patient. (Dose of Ipecac Syrup: ADULT: 15 - 30 mL; CHILD 1 to 12 years: 15 mL; CHILD 6 to 12 months of age: 5 - 10 mL; CHILD under 6 months of age: Not recommended for prehospital use.).

GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in Trendelenburg and left lateral decubitus position or by endotracheal intubation. Control any seizures first.

1. CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
o ACTIVATED CHARCOAL/CATHARTIC: Administer charcoal slurry, aqueous or mixed with saline cathartic or sorbitol. The FDA suggests 240 mL of diluent/30 g of charcoal. Usual charcoal dose is 25 to 100 grams in adults and adolescents, 25 to 50 grams in children (1 to 12 years old), and 1 gram/kilogram in infants less than 1 year old.
1. Routine use of cathartics is NOT recommended. If used, administer only ONE dose of cathartic. Administer one dose of a cathartic, mixed with charcoal or given separately. See "Treatment: Prevention of Absorption" in the main document.
o Perform chelation in symptomatic patients.
1. SUCCIMER DOSE: INITIAL DOSE: 10 mg/kg every 8 hours orally for 5 days, then increase interval to every 12 hours for next 14 days; repeat course(s) if indicated, minimum of 2 weeks between courses.
2. D-PENICILLAMINE/DOSE: ADULT: 15 to 40 mg/kg/day; maximum 250 to 500 mg QID, before meals. CHILD: 20 to 30 mg/kg/day orally once or twice daily before meals. Avoid in patients with penicillin allergy. Monitor for proteinuria.
3. BAL (Dimercaprol): Is indicated for patients with severe gastrointestinal symptoms or patients in renal failure. Administer 3 to 5 mg/kg/dose every 4 hours IM for the first 48 hours, then 2.5 to 3 mg/kg every 6 hours for the second 48 hours, then every 12 hours for 7 additional days.
4. DMPS: An alternate chelator used especially in Europe. DOSE: 5% solution IM or SC 5 mg/kg three or four times during the first 24 hours, 2 to 3 times on day two, and 1 to 2 times daily thereafter.
o Monitor volume status, hematocrit, urine output and renal function tests.
o HEMODIALYSIS should be considered early in severe cases, with diminishing urine output following chelation. The BAL-mercury complex is dialysable.
INHALATION EXPOSURE
o DECONTAMINATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer 100 percent humidified supplemental oxygen with assisted ventilation as required.

o Treatment should include recommendations listed in the ORAL/PARENTERAL EXPOSURE section when appropriate. EYE EXPOSURE
o DECONTAMINATION: Exposed eyes should be irrigated with copious amounts of tepid water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist, the patient should be seen in a health care facility.
o Take precautions to avoid exposure of health care professionals and other individuals.
o Observe for development of clinical signs and symptoms and follow treatment recommendations in DERMAL EXPOSURE where appropriate.
DERMAL EXPOSURE
o Wash exposed area extremely thoroughly with soap and water. A physician may need to examine the area if irritation or pain persists after washing.
o Take precautions to avoid exposure of health care professionals and other individuals.
o SYSTEMIC EFFECTS
1. Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
2. Administration of chelators may be required. Provide supportive care.

Range of Toxicity:
o Mercuric chloride is one of the most toxic inorganic mercury salts. Fatalities have occurred from exposure to as little as 0.5 gram.



[Rumack BH: POISINDEX(R) Information System. Micromedex, Inc., Englewood, CO, 2001; CCIS Volume 107, edition exp February, 2001. Hall AH & Rumack BH (Eds):TOMES(R) Information System. Micromedex, Inc., Englewood, CO, 2001; CCIS Volume 107, edition exp February, 2001.] **PEER REVIEWED**

Antidote and Emergency Treatment:

In previous studies in rats given mercuric chloride administration of furosemide has been found to either attenuate, exacerbate, or not affect the severity of the acute renal failure otherwise expected to obtain. In the curent study in rats given large doses of furosemide and in which urinary fluid losses were replaced by intravenous infusions of saline, administration of mercury chloride induced less severe acute renal failure than that induced in rats not given furosemide, a diuresis induced by continous reinfusion of urine also conferred protection against the nephrotoxic effect of mercury chloride.   [Kurtz TW, Hsu CH; Nephron 43 (4): 279-82 (1986)]**PEER REVIEWED**

Animal Toxicity Studies:

Evidence for Carcinogenicity:

Evaluation: There is limited evidence in experimental animals for the carcinogenicity of mercuric chloride. Overall evaluation: Metallic mercury and inorganic mercury compounds are not classifiable as to their carcinogenicity to humans (Group 3).  [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).,p. 58 324 (1993)]**QC REVIEWED**

A4. A4= Not Classifiable as a Human Carcinogen. (1994) /Mercury, inorganic
forms including metallic mercury, as Hg (Sin)
[American Conference of Governmental Industrial Hygienists.
Threshold Limit Values (TLVs) for Chemical Substances and
Physical Agents and BiologicalExposure Indices (BEIs) for
1995-1996. Cincinnati, OH: ACGIH, 1995. 25]**QC REVIEWED**

CLASSIFICATION: C; possible human carcinogen. BASIS FOR CLASSIFICATION: Based on the absence of data in humans and limited evidence of carcinogenicity in rats and mice. Focal papillary hyperplasia and squamous cell papillomas in the forestomach as well as thyroid follicular cell adenomas and carcinomas were observed in male rats gavaged with mercuric chloride for 2 years. The relevance of the forestomach papillomas to assessment of cancer in humans is questionable because no evidence indicated that the papillomas progressed to malignancy. The relevance of the increase in thyroid tumors has also been questioned because these tumors are generally considered to be secondary to hyperplasia; this effect was not observed in the high-dose males. It should also be noted that the authors considered the doses used in the study to exceed the MTD for male rats. In the same study, evidence for increases in squamous cell papillomas in the forestomach of female rats was equivocal. In a second study, equivocal evidence for renal adenomas and adenocarcinomas was observed in male mice; there was a significant positive trend. This tumor type is rare in mice, and the increase in incidence was statistically significant when compared with historic controls. Two other nonpositive lifetime rodent studies were considered inadequate. Mercuric chloride showed mixed results in a number of genotoxicity assays. HUMAN CARCINOGENICITY DATA: None. ANIMAL CARCINOGENICITY DATA: Limited.
[U.S. Environmental Protection Agency's Integrated Risk
Information System (IRIS) on Mercuric Chloride (HgCl2)
(7487-94-7) from the National Library of Medicine's TOXNET
System, May 3, 1995]**QC REVIEWED**

Non-Human Toxicity Excerpts:

IN ACUTE LETHAL POISONING BY SC OR IV INJECTION OF MERCURY BICHLORIDE NEPHROTOXIC ACTION IS ESP PROMINENT. WHEN DEATH OCCURS WITHIN 48 HR, KIDNEYS ARE CONGESTED AND CYANOTIC BUT TOXIC ACTION IS EXERTED CHIEFLY ON TUBULAR EPITHELIUM. ...  [Browning, E. Toxicity of Industrial Metals. 2nd ed. New York: Appleton-Century-Crofts, 1969. 230]**PEER REVIEWED**

... INHIBITION OF SPERMATOGENESIS IN MICE GIVEN MERCURIC CHLORIDE, 1 MG/KG BODY WT INTRAPERITONEALLY.  [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. 414]**PEER REVIEWED**

... REPRODUCTIVE DYSFUNCTION IN JAPANESE QUAIL WHEN ... FED HgCl2 (125 PPM HG) IN DRINKING WATER; FERTILITY & HATCHABILITY OF THEIR EGGS WERE REDUCED. THINNING OF EGG SHELLS OF MIGRATORY BIRDS & HEAVY MORTALITY IN THEIR YOUNG ...  [Venugopal, B. and T.D. Luckey. Metal Toxicity in Mammals, 2. New York: Plenum Press, 1978. 96]**PEER REVIEWED**

ADULT B6C3F1 MALE MICE WERE GIVEN WATER CONTAINING 3, 15 & 75 PPM MERCURY (AS MERCURIC CHLORIDE) FOR 7 WK. NONSPECIFIC TOXICITY OCCURRED AT 75 PPM, CONSISTING OF SMALL DIFFERENCES IN BODY & ORGAN WEIGHTS, HEMATOLOGICAL CHANGES & GENERAL ENZYME INHIBITION IN BONE MARROW & SPLEEN. HOWEVER, THERE WERE SPECIFIC IMMUNOTOXIC & BIOCHEMICAL ALTERATIONS IN LYMPHOID ORGANS OF MICE TREATED AT LOWER DOSES. IMMUNOLOGICAL DEFECTS WERE CONSISTENT WITH ALTERED T-CELL FUNCTION.  [DIETER MP ET AL; TOXICOL APPL PHARMACOL 68 (2): 218 (1983)]**PEER REVIEWED**

EFFECTS OF MERCURIC CHLORIDE ON RENAL FUNCTION DURING POSTNATAL MATURATION WERE STUDIED. SPRAGUE-DAWLEY RATS WERE TREATED WITH SINGLE INJECTION OF 5 MG/KG MERCURIC CHLORIDE ON DAY 1, 8, 15, 22 OR 29 AFTER BIRTH. RENAL SENSITIVITY INCR THROUGHOUT MATURATION FOR EVERY PARAMETER MEASURED. NO PUPS TREATED ON DAY 1 DIED, BUT MORTALITY INCR TO ALMOST 20% IN THOSE TREATED 22 & 29 DAYS AFTER BIRTH. NEONATAL KIDNEY WAS LARGELY INSENSITIVE; HOWEVER, A TREND TOWARD INCR SENSITIVITY WITH INCR AGE WAS DEMONSTRATED.  [DASTON GP ET AL; TOXICOL APPL PHARMACOL 71 (1): 24 (1983)]**PEER REVIEWED**

Mercuric salts in vitro enhanced the viral transformations of hamster cells and reduced the molecular weight of DNA in Chinese hamster ovary cells, but did not produce mutagenesis in non-mammalian cells. /Mercury salts/
[USEPA; Mercury Health Effects Update p.5-14 (1984) EPA 600/8-84-019F]**PEER REVIEWED**

Mercuric iodide, and mercuric chloride ... were administered via stomach to male and female rats (1-20 days of pregnancy) to study the toxic effects on the male gonads and embryogenesis, respectively. In the second series, Hg salts were given to male rats daily for 2 mo. All the cmpd were markedly embryotoxic and the  severity depended on the dose and the intake schedule. ... Mercuric iodide was more toxic than mercuric chloride. These materials characteristically decreased the size of the placenta. They showed no teratogenic activity. The embryolethal effect of mercuric iodide (1/8 LD50) was most pronounced when it was administered during 1-4 days of pregnancy. The embryo deaths were not practically any different from the control if mercuric iodide was administered on other days. Thus, these Hg cmpd are sufficiently effective with reference to intrauterine development (cause embryo death but show no teratogenicity), whereas the embryolethal effect is most evident during the initial stage of embryogenesis.  [Barilyak IR et al; Gig Sanit 10: 65-7 (1984)]**PEER  REVIEWED**

Uca pugilator (fiddler crab, adult) exposed to 180 ug/l of mercuric chloride over a 24 hr 6 day period exhibited a 20-25% reduction in percent survival and an increase in oxygen consumption.  [Vernberg WB, Vernberg J; Fish Bull 70: 415 (1972) as cited in USEPA; Ambient Water Quality Criteria Doc: Mercury p.69 (1984) EPA 440/5-84-026]**PEER REVIEWED**

Five seaweed species, Ascophyllum nodosum, Fucus spiralis, Fucus versiculosus, Fucus serratus, and Pelvetia canaliculata exposed to 10 ug/l of mercuric chloride over a 10 day period, caused a 10-30% reduction in growth.  [Stromgren T; J Exp Mar Biol Ecol 43: 107 (1980) as cited in USEPA; Ambient Water Quality Criteria Doc: Mercury p.64 (1984) EPA 440/5-84-026]**PEER REVIEWED**

50% inhibition of the Hill reaction occurred when isolated spinach chloroplasts were exposed at pH 7.8 to 3.6 µM solutions of mercuric chloride ... .  [Lee SS et al; Pest Biochem Physiol 3: 225-9 (1973) as cited in Nat'l Research Council Canada; Effects of Mercury in the Canadian Environment p.105 (1979) NRCC No. 16739]**PEER REVIEWED**

Chromosome anomalies were increased after exposure of dry seeds (Hordeum
sativum, Vicia faba or Nigella damascera) to 1x10-5 M mercuric chloride
(inorganic mercury). This effect was strongly synergistic with previous treatment
using the carcinogens ethylmethane sulfonate or N-nitroso-N-methyl urea. ...
Mercuric chloride interfered with DNA repair.  [Nat'l Research Council Canada; Effects of Mercury in the Canadian Environment p.115 (1979) NRCC No. 16739]**PEER REVIEWED**

Exposure to a mercury (Hg)-equilibrated algal suspension containing 0.25, 0.42, and 1 µg mercury/l as mercuric chloride (HgCl2) in solution reduced the growth and condition of pairs of adult slipper limpet mollusk, Crepidula foricata, in a 16 wk period. Reproduction rates and larval survival to settlement were also reduced over the first 3 spawnings when the exposed pairs reached sexual maturity. The adult and larval 96 hr median lethal concn (LC50s) were 330 and 60 µg Hg/l respectively, as HgCl2 in solution, indicating that a safety factor of 10-1 needs to be applied to adult data to protect the most sensitive stage in the life cycle. However, the chronic exposure of the maturing adults showed that levels of Hg below the safe concn derived from the adult 96 hr LC50 affected growth and reproductive success.  [Thain JE; Mar Environ Res 12 (4): 285-309 (1984)]**PEER REVIEWED**

Five groups of four wk old male chickens were exposed to 0 or 500 mg/l (ppm) of Hg(2+) as mercuric chloride in their drinking water for 3, 6, 9, 12 and 15 days. Rates of growth and feed and water consumption decreased within 3 days of Hg(2+) treatment. Mortality increased in the groups receiving Hg(2+). Red blood cell numbers, hematocrit, mean corpuscular volume, and Hg level increased within 3 days of treatment with Hg(2+). While mean corpuscular Hb concn decreased within the same treatment period. Mean corpuscular Hb level was not influenced by Hg(2+) treatment.
[Grissom RE Jr, Thaxton JP; Arch Environ Contam Toxicol 14 (2): 193-6 (1985)]**PEER REVIEWED**

Mice were exposed to 0.02, 0.23, or 2.1 mg mercuric chloride/cu m fumes for 4 hr/day for 4 days, starting from day 9 of pregnancy. The 0.23 and 2.1 mg/cu m dose caused fetal mortality. The surviving fetuses showed retarded growth, disturbances of the bone system and chromosome aberrations in the liver.  [Selypes A et al; Munkavedelem, Munka-Uzemegeszsegugy 29 (7-9): 152-4 (1983)]**PEER REVIEWED**

The effects of mercuric compounds on the proliferation and protein synthesis of mouse blastocysts were examined in vitro by treating the embryos with ... mercuric chloride. Late blastocysts were exposed to various concentrations of mercuric compounds for 24 hr and incubated for another 24 hr in a mercury-free medium. The protein synthesis of the mercury-treated blastocysts was measured by counting the incorporation of L-(35)S-methionine into the acid-insoluble protein fraction of a cell; 0.1 µM of methyl mercury (MMC) was equivalent to 20 µM of MC with regard to the inhibitory effect on proliferation, and equivalent to 2 to 5 µM of MC after 24 hr culture, and 10-20 muM after 48 hr culture with regard to the inhibitory effect on protein synthesis of the blastocysts. Methyl mercury was more toxic than mercuric chloride with regard to cell number proliferation, and
20-50 times so with regard to protein synthesis capability.  [Katayama S et al; Acta Obstet Gynaecol 36 (10): 1957-62
(1984)]**PEER REVIEWED**

The influence of inorganic mercury (Hg) on the erythrocytes and leukocytes was
studied in pregnant female rats injected with labeled and unlabeled mercuric
chloride (635 ug/rat, im). On day 20 of pregnancy the formed blood elements
were counted in the blood of mothers and fetuses. The number of erythrocytes
decreased slightly in mothers and fetuses. Leukocyte counts, especially
lymphocytes, eosinophils, and monocytes, increased slightly as a reflection of
toxicity of Hg. Slight change in the hematocrit index accompanied the change in
numbers of formed blood elements.
[Marszalek K; Acta Biol Cracov Ser Zool 25: 1-14 (1984)]**PEER
REVIEWED**

The freshwater murrel, Channa punctatus, was exposed to a sublethal concn of
mercuric chloride (3 micrograms/liter) for 120 days. ... Mercury-treated fish were
hypoglycemic and hypolactemic. The glycogen content of liver and muscles
remained unaltered but the muscle lactic acid level decreased significantly. The rate
of intestinal absorption of glucose was reduced significantly by exposure to
mercury. G-6-Pase activity was decreased in all the tissues. Hexokinase activity
also decreased in mercury-exposed fish but it was significant only in intestine,
kidney, and liver. The activities of lactate dehydrogenase (LDH), pyruvate
dehydrogenase (PDH), succinate dehydrogenase (SDH), and malate
dehydrogenase (MDH) also were decreased significantly except LDH in brain and
MDH in kidney where an insignificant decrease and an insignificant increase,
respectively, were recorded. Glutamate dehydrogenase (GDH) and L-amino acid
oxidase (AO) activities were elevated in most of the tissues except GDH in gills,
and AO in gills and muscles where a decrease was observed. Xanthine oxidase
(XO) activity in brain, gills, and kidneys was significantly elevated, but no marked
alteration was noted in other tissues.
[Sastry KV, Rao DR; Environ Res 34 (2): 343-50 (1984)]**PEER
REVIEWED**

Bilateral ligation of the ureter in Nubian goats caused arching of the back, pica,
convulsions, anuria, and cystic dilation of the kidneys and degeneration of the renal
tubules and death within 4-6 days. Kidney damage was accompanied by an
increase in the concn of creatinine, NH3 and K, and a decr in the levels of calcium
in the serum. Mercuric chloride caused necrosis of the renal tubules, hemorrhagic
enteritis and congestion and or minimal fatty changes in the liver when given
intraruminally at 60 mg/kg once or 5 times at weekly intervals. Mercuric chloride
to a great extent potentiated the mentioned effects of bilateral ligation of the ureter.
This was shown by the short survival times of goats with ligated ureters following
the administration of mercuric chloride, the degree of damage to the kidneys and
further pathologic changes in serum constituents.
[Mohamed FHA et al; Acta Vet 33 (4): 209-14 (1983)]**PEER
REVIEWED**

The effects of mercuric chloride intoxication on the activities of acid and alkaline
phosphatases and glucose-6-phosphatase in the hepatopancreas of a freshwater
prawn Macrobrachium lamarrei were determined after 24, 48, 72, and 96 hr.
Mercuric chloride intoxication resulted in elevation of acid phosphatase and
inhibition of alkaline phosphatase activities, but glucose-6-phosphatase activity was
elevated up to 72 hr after which (ie, after 96 hr of exposure) inhibition in the
enzyme activity was noted at two higher concn. Alterations in the activities of these
enzymes after mercuric chloride intoxication have been shown to adversely affect
the general metabolism of the freshwater prawn.
[Murti R et al; Ecotoxicol Environ Safety 8 (6): 581-6
(1984)]**PEER REVIEWED**

Mercuric chloride (HgCl2) is extremely cytotoxic to Chinese hamster ovary cells in
culture since a 1 hr exposure to a 75 µM concn of this compound reduced cell
plating efficiency to 0 and cell growth was completely inhibited at 7.5 uM. The
level of HgCl2 toxicity depended upon the culture incubation medium and has
previously been shown to be inversely proportional to the extracellular concn of
metal chelating amino acids such as cysteine. Thus, HgCl2 toxicity in a minimal
salts/ glucose maintenance medium was about ten-fold greater than the toxicity in
McCoy's culture medium. The HgCl2 toxicity in the latter medium was three-fold
greater than that in alpha-MEM /alpha-minimum essential medium/ which contains
more of the metal chelating amino acids. When cells were exposed to HgCl2 there
was a rapid and pronouced induction of single strand breaks in the DNA at time
intervals and concn that paralleled the cellular toxicity. The DNA damage was
shown to be true single strand breaks and not alkaline sensitive sites or double
strand breaks by a variety of techniques. Consistent with the toxicity of HgCl2, the
DNA damage under an equivalent exposure situation was more pronounced in the
salts/glucose than in the McCoy's medium and more striking in the latter medium
than in alpha-MEM. Most of the single strands breaks occurred within 1 hr
exposure to the metal.
[Cantoni O et al; Chem Biol Interact 49 (1-2): 209-24
(1984)]**PEER REVIEWED**

Two groups of male Sprague-Dawley rats received from weaning 50 ug/ml of
mercuric chloride (HgCl2) in drinking water for 320 and 350 days. Mercury (Hg)
exposure increased cardiac inotropism, without chronotropic changes, in both
groups, and induced arterial hypertension in the rats exposed for 350 days. In the
exposed rats, cardiovascular responses to the stimulation of peripheral alpha and
beta adenoceptors were decreased and increased, respectively, possibly through
an intracellular availability of calcium ions for contractile mechanisms. Hg exposure
did not affect either vagal or sympathetic activity or cardiovascular reactivity to
several physiological agonists. On the other hand, Hg exposure induced baroreflex
hyposensitivity and produced a drastic alteration of the levels of copper and zinc in
brain and kidney.
[Carmignani M, Boscolo P; Arch Toxicol 7: 338-83 (1984)]**PEER
REVIEWED**

In Brown-Norway (BN) rats, oral administration of mercuric chloride (HgCl2)
induced morphological lesions of the ileum and, in lesser degree, of the colon, with
abnormal deposits of IgA in the basement membranes of the intestinal glands and
of IgG in the basement membranes and in the lamina propria. IgG is reactive with
renal and intestinal basement membranes and in the lamina propia. IgG reactive
with renal and intestinal basement membranes and with the lamina propia of a
normal BN rat was found in the serum and IgG deposits were present in renal
glomeruli of Brown-Norway rats receiving HgCl2. Thus, it is conceivable that the
deposits of the IgG present in the intestine resulted from local fixation of circulating
autoantibodies. In contrast, IgA with basement membrane reactivity was not
detected in the sera nor in the renal glomeruli, suggesting that the intestinal deposits
of IgA were formed in situ. This IgA-IgG intestinal disease inducible in
Brown-Norway rats may provide a model for the study of alterations of the
secretory IgA system, as well as for testing the possiblity that abnormal deposits
IgA-IgG in the intestinal structures are associated with local functional changes.
[Andres P; Clin Immunol Immunopathol 30 (3): 488-94
(1984)]**PEER REVIEWED**

Administration of inorg and org mercury (Hg) (0.6 Hg/kg as mercuric chloride
and phenylmercury acetate for 10 days affected reduced glutathione (GSH)
reductase and glucose 6-phosphate dehydrogenase of the bone marrow and
erythrocytes. The activity of the enzymes of the bone marrow and GSH reductase
in the erythrocyte increased. Bone marrow was more resistant to the action of Hg
cmpd and org Hg was much more toxic.
[Miszta H; Folia Haematol (Leipzig) 3 (5): 638-44
(1985)]**PEER REVIEWED**

The toxic effects of various mercury cmpd (eg, mercurous chloride, mercuric
chloride, mercuric acetate, and phenylmercury acetate) on percentage germination,
pigment concn, root-shoot lengths, and fresh wt & dry wt of 7 day old seedlings of
barley were investigated. Phenylmercury acetate was the most toxic, followed by
mercuric acetate, while mercurous chloride was the least toxic.
[Mukhiya YK et al; Int J Environ Stud 20 (3-4): 323-7
(1983)]**PEER REVIEWED**

Studies were carried out on male Wistar rats, where the activity of
acetylcholinesterase was determined in red blood cells and bone marrow after
exposure to organic and inorganic mercury cmpd. A marked decline in the activity
of the enzyme was noted, along with a more pronounced effect of the organic
mercury cmpd. /Mercury cmpd/
[Miszta H; Folia Haematol 111 (5): 632-7 (1984)]**PEER
REVIEWED**

THE INSECTICIDAL ACTION OF MERCURY SALTS WAS RELATED
TO THEIR DECOMPOSITION BY SOIL ORGANISMS AND RELEASE OF
MERCURY VAPORS. THIS REACTION REQUIRED MOISTURE AND
PROCEEDED MORE RAPIDLY AS SOIL PH AND TEMPERATURE WAS
INCREASED. /MERCURY SALTS/
[Menzie, C.M. Metabolism of Pesticides. U.S. Department of the
Interior, Bureau of Sport Fisheries and Wildlife, Publication
127. Washington, DC: U.S. Government Printing Office, 1969.
240]**PEER REVIEWED**

DISCOLORATION OF CORNEA ... PRODUCED EXPTL IN ANIMALS
BY REPEATED SYSTEMIC ADMIN OF MERCURY. ... IT CONSISTS OF
GRAYISH RING IN CORNEA JUST ANTERIOR TO ENDOTHELIUM
EXTENDING APPROX 2 MM FROM LIMBUS. /INORG MERCURY/
[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL:
Charles C. Thomas Publisher, 1986. 583]**PEER REVIEWED**

Toxicity data from various inorg salts and oxides of mercury after their admin via
stomach or a single inhalation indicated that irrespective of the solubility the
functional changes caused by these compd were similar. The toxicity depended on
the valence state of the metal. Hg2+ cmpd exerted stronger biological effects at
low concn than the Hg+ cmpd. In the case of salts and oxides of mercury (Hg),
the major role was played by the cation; anions affected the threshold concn only a
little. /Mercury salts/
[Ermachenko AB; Gig Sanit 9: 67-8 (1983)]**PEER REVIEWED**

... Long term exposure to inorganic mercury (II) indicates that concn above 0.23
ug/l caused significant effects on the fathead minnow and caused the concn of total
mercury in the whole body to exceed 1.0 mg/kg. /Mercuric salts/
[USEPA; Ambient Water Quality Criteria Doc: Mercury p.22
(1984) EPA 440/5-84-026]**PEER REVIEWED**

Mercuric chloride in both a life-cycle test and an early life-stage test on mercuric
chloride with the fathead minnow, the chronic value was less than 0.26 mg/l and
the acute-chronic ratio was over 600.
[USEPA/OWRS; Quality Criteria for Water 1986 (1986) EPA
440/5-86-001]**PEER REVIEWED**

Serum and urinary biochemical changes were recorded in 5 ponies in which acute
tubular nephrosis had been induced over 5 days with mercuric chloride and
potassium dichromate. Serum osmolality, the serum concentrations of urea
nitrogen, creatinine, sodium, potassium, and chloride, and blood pH and blood
gases were measured daily for 14 days or until humane euthanasia was performed.
Levels of the same substances were quantitated daily in urine. In addition, routine
urinalyses and determination of urinary gamma glutamyl transferase activity were
performed on each sample. Changes in the values of the urinary variables
preceded alterations in the serum value of the same substance by at least one day.
The first notable abnormality detected was in urinary gamma glutamyl transferase
activities. These changes occurred up to 6 days before the detection of azotemia.
[Bayly WM et al; Cornell Vet 76 (3): 306-16 (1986)]**PEER
REVIEWED**

Histopathological changes induced by mixture of pollutants were studied at 2, 15,
30 and 45 days of exposure in fish to a concentration of 0.033 ppm mercuric
chloride, 33.3 ppm cadmium chloride, 3.33 ppm phenol and 9 ppm ammonia
where no mortality was recorded. Marked abnormalities in the renal histology and
interrenal tissues could be discerned. In the case of trunk kidney, the epithelial cells
of the renal tubules were desquamated and vacuolated. Irregular orientation of the
nuclei, shrinkage of the glomerular tuft and capsule were noted. After 45 days,
glomerular cells developed vacuolations as observed in tubular cells. The interrenal
tissues lost their regular arrangement, rupturing the blood sinusoids, blood cells
remaining intermingled with hemopoietic cells. This degeneration was more severe
at 15 days of exposure but on 30 and 45 days, the histopathological condition of
the head kidney was found to improve giving place to normalization of the
histological picture.
[Bhattacharya T et al; Z Mikrosk-Anat Forsch 99 (2): 327-34
(1985)]**PEER REVIEWED**

Glomerular dynamicas tubular integrity, and whole kidney function were examined
at 24 hr in rats given either mercuric chloride, 3.5 mg/kg, or a similar vol of 0.9%
saline soln im. Arterial blood pressure was elevated in mercuric chloride injected
rats, but renal blood flow and its distribution were similar to those of controls.
Inulin clearance, however, was reduced by 89% in mercuric chloride injected
animals. Glomerular dynamics expts demonstrated similar glomrular plasma flows
(QA) and glomerular capillary an tubular pressures in control and mercuric
chloride injected animals but a higher net afferent ultrafiltration pressure and lower
ultrafiltration coeff (Kf) in the mercuric chloride injected group. Single- nephron
glomerular filtration rate, when measured from Bowman's space in mercuric
chloride rats, was similar to that measured from late proximal tubules in controls.
However, single-nephron glomerular filtration rate determined from the late
proximal tubules in mercuric chloride injected rats was only one third of that
measured from Bowman's space.
[Conger JD, Falk LSA; J Lab Clin Med 107 (4): 281-9
(1986)]**PEER REVIEWED**

Isolated rat nephron segments were used for the evaluation of nephrotoxicity by
chemical glomerular specificity of metabolic changes was demonstrated in rats
following puromycin aminonucleoside (80 mg/kg) treatment. Intraproximal
nephrotoxic sites of mercury chloride and gentamicin were identified via urinalysis
and detection of enzyme activities along single nephrons form untreated rats.
[Endou H et al; Dev Toxicol Environ Sci 14: 207-16
(1986)]**PEER REVIEWED**

... Mercury chloride was administered subcutaneously in gradually increasing amt
over a period of 21 wk. The dose ranged from 1.125 mg/kg once a week to 2.0
mg/kg twice a week. Measured parameters of renal function included plasma urea
nitrogen, plasma creatinine, 24 hr urine output vol, and 24 hr urinary protein
excretion. When compared to pretreatment values and the age/wt matched control
animals, the mercury chloride treated rats exhibited no abnormalities in these
parameters with the exception of a mild proteinuria at 21 wk. Light microscopic
exam of the kidneys of the mercury treated rats revealed mild tubular, interstitial,
and glomerular lesions which were worse than in the kidneys of the controls.
[Hall RL et al; Vet Hum Toxicol 28 (4): 305-7 (1986)]**PEER
REVIEWED**

The relationship between coelomic injections of mercuric chloride doses and
osmoregulatory responses was measured. Response parameters were weight
increases and blood osmolarity decreases 72 hr after dose administration. Edema
and large decreases in blood osmolarity could be completely prevented by
subcutaneous injections of equimolar sodium selenite. Mercury induced damage
did not involve alterations of either selenium dependent or non-selenium dependent
glutathione peroxidase activities.
[Heisinger JF, Scott L; Comp Biochem Physiol Comp Pharmacol
Toxicol 80 (2): 295-8 (1985)]**PEER REVIEWED**

Studies have been carried out on the ability of calcium
disodium-ethylenediaminetetraacetate to offset the acute toxicity of mercuric
chloride. The lethality of mercury was tested in female Bufo regularis species
(amphibia) which were given calcium disodium-ethylenediaminetetracetate
immediately after the Hg2+ injection. The results show that the inherent toxicity of
the calcium disodium-ethylenediaminetetraacetate mercury complex is sufficiently
high for it to be ineffective as an antidote.
[Hilmy AM et al; Comp Biochem Physiol Comp Pharmacol Toxicol
85 (1): 253-4 (1986)]**PEER REVIEWED**

The 20 min median lethal concn (LC50) of mercuric chloride in killifish (Fundulus
heteroclitus) eggs from Pile Creek (1.0 ppm) was significantly lower than in those
from Long Island (1.6 ppm). Exposure of both Pile Creek and Long Island eggs
prior to insemination to 0.5 ppm mercuric chloride did not effect the mean percent
fertilization success or embryonic development. However, exposure of both Pile
Creek and Long Island eggs to 1.0 ppm before insemination caused a significant
reduction in mean percent fertilization success, but Pile Creek eggs showed only
45% fertilization success. Pile Creek eggs also showed higher (38%)
malformations in the craniofacial, cardiovascular, and skeletal systems than Long
Island killifish eggs (16%) after exposure to 2.5 ppm prior to fertilization. The 96
hr LC50 values were 0.7 ppm for Pile Creek and 0.6 ppm on a Long Island
juvenile fish.
[Khan AT, Weis JS; Mar Pollut Bull 18 (9): 504-5 (1987)]**PEER
REVIEWED**

Oral LD50 values (at 24 and 168 hr) for 8 metal salts were determined in female
mice pretreated orally with small doses (1/10 of the challenge doses) of the same
metal ions or with deionized water at 24 hr prior to the challenge doses. The LD50
values for Cd2+ or Mn2+ increased with pretreatment by the same ion, but those
for Hg2+ decreased. ... Pretreatment with Cu2+, Hg2+, or Zn2+ protected mice
against the toxic action of Cd2+.
[Morita S; Seikatsu E 29 (5): 274-8 (1985)]**PEER REVIEWED**

Rates of feeding and feed absorption, and conversion of Cyprinus carpio reared in
media containing sublethal concn of mecury chloride significantly decreased.
Efficiencies of absorption and conversion of the ingested food decreased with
increasing concn of mercury chloride in the medium. At the highest tested
sublethal concn (0.304 ppm), the gross production efficiency of the fish was
approximately 8-fold less than that reared in tap water. Energy, protein, and lipid
contents of the fish reared in mercury chloride media were below controls. At the
highest sublethal concn, the fish displayed a neg nitrogen balance. With increasing
concn of mercury chloride, rate of oxygen consumption by the fish decreased,
while NH3 quotient increased.
[Muthukrishnan J et al; Environ Ecol 4 (4): 526-32
(1986)]**PEER REVIEWED**

An injection of 0.01% mercuric chloride into fully adult male grasshopers,
Spathosternum prasiniferum, induced chromosomal abnormalities which included
stretching and elongation of bivalents, dispiralization of chromatids, sticky bridge,
and elongation of X-chromosome, pulverizaton etc. There was a preponderance of
chromosome breaks over chromatid breaks. Mercuric chloride induced
spermatocytic chromosome aberrations may be caused by its reactin with the -SH
groups of nucleoproteins or due to inhibition of enzyme system responsible or
chromosome reduplication or break repair.
[Saha AK et al; Environ Ecol 4 (2): 320-3 (1986)]**PEER
REVIEWED**

The pharmacological effects of methyl mercury chloride and mercuric chloride
(2-16 mg/kg per day subcutaneously, for 6 days) upon the growth were studied in
the incisors and proximal tibiae of immature rats histologically. Lead acetate was
used as a time marker. Mercury compounds slightly affected the body weight
gains of the rats but apparently inhibited the longitudinal growth of proximal tibia
and the effect increased with higher dosages. Mercury compounds definitely
inhibited not only the longitudinal growth (incisor growth) but also the appositional
growth (dentin formation) of incisal dentin. The inhabitory efect on the growth was
ranked as follows: bone growth > dentine formation > incisor growth. In mercuric
chloride groups, the inhibitory effect on the growth appeared rapidly. The effect
increased with higher dosages and became stronger as the injections were
repeated. However, this effect was weakened promptly after the injection was
discontinued. The repeated injections of mercury compounds hardly affected the
level of serum calcium but disturbed the calcification of incisal dentin.
[Yonaga T et al; Anat Anz 159 (1-5): 373-83 (1985)]**PEER
REVIEWED**

Exposure of plaice (Pleuronectes platessa) a marine teleost, to 0.3 ppm mercury (as mercuric chloride) resulted in a reduction in blood hematocrit values over seven days due to erythrocyte lysis. The decrease was significant within four days of exposure and by seven days there was a 72% reduction in prebleed hematocrit values. There was also a steady decline in serum lysozyme but not in serum protein concentration. The spleen is actively phagocytic for affected erythrocytes and although not erythropoietic, splenomegaly occurred by day 6. Urine analysis showed significant proteinuria by day 3, but although kidney proximal tubule damage was severe, the onset of lysozymuria was not observed until the seventh day of exposure, presumably only occurring when tubular damage extended to the absorptive area of the first proximal segment.  [Fletcher TC, White A; Aquat Toxicol 8 (2): 77-84 (1986)]**PEER REVIEWED**

Species of Acrididae (Acrotylus patuelis, Acrotylus halassinus, and Oedipoda caerulescens) were used as test animals, which deposit their eggs in the soil. The chem tested wer mercuric chloride, urea, phenol, perylene, methanol and ETOAc. The insect number decreased in concn of > 0.001% mercuric chloride/kg dry sand in the lab tests and of > 0.0001% under field conditions; mercury mainly affected the embryonic development taking place in the soil. Urea at > 0.055 g nitrogen/kg dry sand decreased the number of deposited egg pods and the number of eggs laid; increasing am+ of urea also decreased the hatching of the larvae.  [Schmidt GH; Agric Ecosys Environ 16 (3-4): 175-88 (1986)]**PEER REVIEWED**

The effect of mercuric chloride on akinete germination and sporulation with respect to time lapse and extent was studied in Pithophora oedogonia. At mercuric chloride concn from 1.25 to 45 mg/l akinetes showed progressive delay in the initiation and reduction in the extent of germination. Mercuric chloride concn of greater than or equal to 60 mg/l were lethal to the spores as they failed to germinate. The time necessary for the initiation of akinete formation and the percentage sporulation also decreased with an increase in the concn of mercuric chloride from 1.25 to 45 mg/l where spore germination was encountered.   [Chaudhary BR, Singh HV; J Basic Microbiol 26 (1): 3-7 (1986)]**PEER REVIEWED**

Juvenile rainbow trout (Salmo gairdner) were exposed to 100 ppb mercury (as mercuric chloride in the water for 14 days. Concn of mercury(Hg) in water and fish organs were monitored using radiolabeled mercury. Tissues from kidney and liver were fixed, and sections were developed by autometallogy, a method whereby accumulations of mercury sulfides and/or mercury selenides are silver amplified. In the kidney, mercury was found within lysosomes and extracellularly in the basal lamina of proximal tubules. In the liver, mercury was found in lysosomes of the hepatocytes. Additional groups of mercury exposed trout were subjected to selenium (as Na2SeO3), administered ip 2 hr before fixation. Following this treatment, mercury could be visualized in the kidney circulatory system, including glomeruli, and in the nucleus and endoplasmic reticulum of liver cells. Hg visualized prior to selenium treatment may represent inorg Hg, whereas additional Hg visualized after selenium administration may represent an organic form.  [Baatrup E et al; Ecotoxicol Environ Saf 12 (3): 267-82 (1986)]**PEER REVIEWED**

The lethal toxicity of inorg (mercuric chloride) and org (methyl mercury chloride) mercury was compared for Coturnix coturnix japonica of different ages from hatch through adulthood by single-dose acute and intramuscularly injection and by a 5 day dietary trial. Sublethal mercury toxicity was studied by evaluation of plasma and brain cholinesterase activity. Methyl mercury chloride was more toxic than mercuric chloride in all tests at each age tested. LD50s consistently increased over the 1st 4 wk for both acute methods and both mercurials and then stabilized. The striking difference between single-dose acute and 5 day tests was that methyl mercury chloride averaged about twice as toxic as mercury chloride by both acute methods, compared to 100 times as toxic by the dietary method. For example, at 2 wk of age, the oral LD50s for methyl mercury chloride and mercuric chloride were 18 and 42 mg/kg and the dietary LC50s were 47 and 5086 ppm. When birds were fed mercuric chloride and developed clinical signs of intoxication, they could recover once treatment was withdrawn.  [Hill EF, Soares JH; J Toxicol Environ Health 20 (1-2): 105-16 (1987)]**PEER REVIEWED**

Mercuric salts in vitro enhanced viral transformations of hamster cells and reduced the molecular weight of DNA in Chinese hamster ovary cells, but did not produce   mutagenesis in non-mammalian cells. /Mercury salts/  [USEPA; Mercury Health Effects Update p.5-14 (1984) EPA 600/8-84-019F]**PEER REVIEWED**

EXPTL EVIDENCE FROM ANIMAL STUDIES /ON PATHOGENETIC MECHANISM OF ANURIA & POLYURIA/ SUGGESTS THAT SEVERAL FACTORS ARE INVOLVED. THESE ARE TUBULAR OBSTRUCTION, INCR BACK DIFFUSION OF TUBULAR FILTRATE, & PREGLOMERULAR VASOCONSTRICTION. /MERCURIC SALTS/   [Doull, J., C.D. Klaassen, and M. D. Amdur (eds.). Casarett and Doull's Toxicology. 2nd ed. New York: Macmillan Publishing  Co., 1980. 426]**PEER REVIEWED**

/IN ANIMALS/ MERCURY IS A POTENT NEPHROTOXIN & PRODUCES NEPHROSIS & EVENTUALLY UREMIA ... AT NECROPSY THE FIRM SHRUNKEN KIDNEYS ARE OBVIOUS. /MERCURY CMPD/   [Casarett, L.J., and J. Doull. Toxicology: The Basic Science of Poisons. New York: MacMillan Publishing Co., 1975. 717]**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. /Mercury cmpd/  [Trakhtenberg IM et al; Gig Tr Prof Zabol (7): 27-30 (1981)]**PEER REVIEWED**

Baseline data on Hg accumulation in organs and tissues, and their variations with age, sex, and habitat in Japanese serows (Capricornus crispus) were determined. The animals were killed during the winter 1981-82 in the Gifu and Nagano Prefectures, Japan. The Hg concentrations were measured by flame absorption spectrometry. On a wet wt basis, the mean Hg concentration in muscle, liver, kidney, and whole body of fetuses (gestation age 0.3-0.7 yr, N= 13) were 1.9, 2.3, 2.0, and 2.2 ng/g, respectively; in fawns (age 0.0-0.5 yr, N= 12), 1.4, 9.1, 44.6, and 24.3 ng/g, respectively; in yearlings (age 0.5-2.5 yr, N= 6), 2.5, 11.2, 97.2, and 35.3 ng/g, respectively; in adults (age 2.5 to 10 yr, N= 42), 2.1, 13.2, 94.5, and 36.3 ng/g, respectively; and in adults (age 10 to 17.5 yr, N= 17), 2.0, 11.0, 87.9, and 33.3 ng/g, respectively. The mean Hg concentration in fleece of fawns, yearlings, and adults (age 2.5 to 10 yr) was 372, 377, and 350 ng/g. Bone samples of two adult serows contained 5.3 to 17.1 ug/g. The Hg burden of fetuses was very low ( < 1%) compared with those of their mothers. Although the Hg accumulation in muscle, liver, and kidney varied during the developmental stage, the age-related accumulation was similar to that in the whole body. In fleece, however, the Hg concentration remained constant throughout life. Fleece contained about 40% of the body burden, indicating that Hg is excreted by molting. The Hg uptake agreed well with the concentration found in food plants. There was no significant difference in Hg concentration between collection locations.  [Honda K et al; Arch Environ Contam Toxicol 16: 551-61 (1987)]**PEER REVIEWED**

Dunaliella tertiolecta (alga) exposed to 100-200 ug/l/8 days of mercuric chloride exhibited about a 10-45% incr in maximum chlorophyll-a concn.  [Betz M; Mar Biol 41:89 (1977) as cited in USEPA; Ambient Water Quality Criteria Doc: Mercury p.63 (1984) EPA 440/5-84-026]**PEER REVIEWED**

Mytilus edulis (blue mussel larva) exposed to 32 ug/l/24 hr of mercuric chloride exhibited abnormal development.  [Okubo K, Okubo T; Bull Tokai Reg Fish Res Lab 32: 131 (1962) as cited in USEPA; Ambient Water Quality Criteria Doc: Mercury p.66 (1984) EPA 440/5-84-026]**PEER REVIEWED**

Skeletonema costatum (diatom) exposed to 0.08 ug/l/15 days of mercuric chloride
exhibited reduced cell density.
[Cloutier-Mantha L, Harrison PJ; Mar Biol 56: 219 (1980) as
cited in USEPA; Ambient Water Quality Criteria Doc: Mercury
p.63 (1984) EPA 440/5-84-026]**PEER REVIEWED**

Dunaliella tertiolecta (alga) exposed to 10 ug/l/3 days of mercuric chloride
exhibited about 15% reduction in growth.
[Davies AG; J Mar Biol Assoc 56: 39 (1976) as cited in USEPA;
Ambient Water Quality Criteria Doc: Mercury p.63 (1984) EPA
440/5-84-026]**PEER REVIEWED**

Dunaliella tertioloecta (alga) exposed to 2 ug/l/8 days of mercuric chloride
exhibited no effect on growth.
[Davies AG; J Mar Biol Assoc 56: 39 (1976) as cited in USEPA;
Ambient Water Quality Criteria Doc: Mercury p.63 (1984) EPA
440/5-84-026]**PEER REVIEWED**

Laminaria hyperborea (kelp), zoospores, gametophytes and sporophytes exposed
to 10 ug/l/28 days of mercuric chloride. This was the lowest concn causing growth
inhibition.
[Hopkins R, Kain JM; Mar Pollut Bull 2: 75 (1971) as cited in
USEPA; Ambient Water Quality Criteria Doc: Mercury p.63 (1984)
EPA 440/5-84-026]**PEER REVIEWED**

Scenedesmus quadricauda (green algae) exposed to 30 ug/l/96 hr of mercury
chloride exhibited incipient inhibition.
[USEPA; Ambient Water Quality Criteria Doc: Mercury p.48
(1984) EPA 440/5-84-026]**PEER REVIEWED**

Daphnia magna (cladoceran) exposed to 34 ug/l/3 wk of mercuric chloride
exhibited reproductive impairment.
[Biesinger KE, Christensen GM; Jour Fish Res Board Can 29:
1691 (1972) as cited in USEPA; Ambient Water Quality Criteria
Doc: Mercury p.49 (1984) EPA 440/5-84-026]**PEER REVIEWED**

Cyprinus carpio (common carp) exposed to 13,000 ug/l/60-72 hr mercuric
chloride exhibited reduced hatching success.
[Huckabee JW, Griffin NA; Trans Am Fish Soc 103:822 (1974) as
cited in USEPA; Ambient Water Quality Criteria Doc: Mercury
p.52 (1984) EPA 440/5-84-026]**PEER REVIEWED**

Adult B6C3F1 male mice were given water containing 3, 15, and 75 ppm
mercury (Hg) (as mercuric chloride (HgCl2)) for 7 wk. There were dose-related
increases in blood and kidney Hg levels, but only the former showed a
time-dependent change. Hg was not detected in any of the lymphoid organs except
for the spleen. There was no mortality, and only minimal histological changes
occurred in kidneys of dosed mice. Non-specific toxicity occurred at the 75 ppm
dose level, consisting of small differences in body and organ weights, hematological
changes, and general enzyme inhibition in the bone marrow and spleen. There were
specific immunotoxic and biochemical alterations in lymphoid organs of mice
treated at the lower doses of Hg. The immunological defects were consistent with
altered T-cell function, as evidenced by decreases in both T-cell mitogen and
mixed leukocyte responses. There was a particular association between the T-cell
defects and inhibition of thymic pyruvate kinase, the rate-limiting enzyme for
glycolysis. The differences in the pattern of enzyme responses among lymphoid
organs implied that 2 mechanisms of Hg physiochemical enzyme inhibiton and
another at low concentrations that caused indirect enzyme inhibition.
[Dieter MP et al; Toxicol Appl Pharmacol 68 (2): 218-28
(1983)]**PEER REVIEWED**

... CONCLUSIONS Under the conditions of these 2 year gavage studies, there
was some evidence of carcinogenic activity of mercuric chloride in male F344 rats
based on the increased incidence of squamous cell papillomas of the forestomach.
Marginally increased incidences of thyroid follicular cell adenomas and carcinomas
may have been related to mercuric chloride exposure. There was equivocal
evidence of carcinogenic activity of mercuric chloride in female F344 rats based on
two squamous cell papillomas of the forestomach. There was equivocal evidence
of carcinogenic activity of mercuric chloride in male B6C3F1 mice based on the
occurrences of two renal tubule adenomas and one renal tubule adenocarcinoma.
There was no evidence of carcinogenic activity of mercuric chloride in female
B6C3F1 mice receiving 5 or 10 mg/kg.
[Toxicology & Carcinogenesis Studies of Mercuric Chloride in
F344/N Rats and B6C3F1 Mice (Gavage Studies). Technical Report
Series No. 408 (1993) NIH Publication No. 93-3139 U.S.
Department of Health and Human Services, National Toxicology
Program, National Institute of Environmental Health Sciences,
Research Triangle Park, NC 27709]**QC REVIEWED**

National Toxicology Program Studies:

Toxicology and carcinogenesis studies were conducted by administering mercuric
chloride (greater than 99% pure) in deionized water by gavage to groups of F344
rats or B6C3F1 mice for ... 2 years. ... 2 YEAR STUDIES: Groups of 60 rats of
each sex received 0, 2.5, or 5 mg mercuric chloride/kg body weight and groups of
60 mice of each sex received 0, 5, or 10 mg/kg in deionized water by gavage 5
days/wk for 2 years. ... CONCLUSIONS Under the conditions of these 2 year
gavage studies, there was some evidence of carcinogenic activity of mercuric
chloride in male F344 rats based on the increased incidence of squamous cell
papillomas of the forestomach. Marginally increased incidences of thyroid follicular
cell adenomas and carcinomas may have been related to mercuric chloride
exposure. There was equivocal evidence of carcinogenic activity of mercuric
chloride in female F344 rats based on two squamous cell papillomas of the
forestomach. There was equivocal evidence of carcinogenic activity of mercuric
chloride in male B6C3F1 mice based on the occurrences of two renal tubule
adenomas and one renal tubule adenocarcinoma. There was no evidence of
carcinogenic activity of mercuric chloride in female B6C3F1 mice receiving 5 or
10 mg/kg.
[Toxicology & Carcinogenesis Studies of Mercuric Chloride in
F344/N Rats and B6C3F1 Mice (Gavage Studies). Technical Report
Series No. 408 (1993) NIH Publication No. 93-3139 U.S.
Department of Health and Human Services, National Toxicology
Program, National Institute of Environmental Health Sciences,
Research Triangle Park, NC 27709]**QC REVIEWED**

Ecotoxicity Values:

LC50 PHASIANUS COLCHICHUS (RING-NECKED PHEASANTS) ORAL
3790 PPM (95% CONFIDENCE LIMIT 2768-5541 PPM)
[U.S. Department of the Interior, Fish and Wildlife Service,
Bureau of Sports Fisheries and Wildlife. Lethal Dietary
Toxicities of Environmental Pollutants to Birds. Special
ScientificReport - Wildlife No. 191. Washington, DC: U.S.
Government Printing Office, 1975. 25]**PEER REVIEWED**

LC50 ANAS PLATYRHYNCHOS (MALLARDS) ORAL MORE THAN
5000 PPM (NO MORTALITY TO 5000 PPM)
[U.S. Department of the Interior, Fish and Wildlife Service,
Bureau of Sports Fisheries and Wildlife. Lethal Dietary
Toxicities of Environmental Pollutants to Birds. Special
ScientificReport - Wildlife No. 191. Washington, DC: U.S.
Government Printing Office, 1975. 25]**PEER REVIEWED**

TLm Carassius auratus (goldfish) 0.82 ppm/7 days (fresh water) /Conditions of
bioassay not specified/
[U.S. Coast Guard, Department of Transportation. CHRIS -
Hazardous Chemical Data. Volume II. Washington, D.C.: U.S.
Government Printing Office, 1984-5.]**PEER REVIEWED**

TLm Penaeus duorarum (pink shrimp) 0.075 ppm/48 hr (salt water) /Conditions of
bioassay not specified/
[U.S. Coast Guard, Department of Transportation. CHRIS -
Hazardous Chemical Data. Volume II. Washington, D.C.: U.S.
Government Printing Office, 1984-5.]**PEER REVIEWED**

TLm Crassostreaa gigas (oyster) 4.2 ppm/48 hr (sea water) /Conditions of
bioassay not specified/
[U.S. Coast Guard, Department of Transportation. CHRIS -
Hazardous Chemical Data. Volume II. Washington, D.C.: U.S.
Government Printing Office, 1984-5.]**PEER REVIEWED**

LC50 Balanus balanoides (barnacle, cyprid) 90 ug/l/6 hr /Conditions of bioassay
not specified/
[Pyefinch KA, Mott JC; J Exp Biol 25: 296 (1948) as cited in
USEPA; Ambient Water Quality Criteria Doc: Mercury p.67 (1984)
EPA 440/5-84-026]**PEER REVIEWED**

LC50 Balanus crenatus (barnacle, nauplius) 60 ug/l/6 hr /Conditions of bioassay
not specified/
[Pyefinch KA, Mott JC; J Exp Biol 25: 296 (1948) as cited in
USEPA; Ambient Water Quality Criteria Doc: Mercury p.67 (1984)
EPA 440/5-84-026]**PEER REVIEWED**

LC50 Palaemonetes pugio (grass shrimp) 148 ug/l/120 hr /Conditions of bioassay
not specified/
[Barthalmus GT; Mar Pollut Bull 8: 87 (1977) as cited in
USEPA; Ambient Water Quality Criteria Doc: Mercury p.67 (1984)
EPA 440/5-84-026]**PEER REVIEWED**

LC50 Asterias forbesi (starfish, adult) 20 ug/l/168 hr /Conditions of bioassay not
specified/
[Eisler R, Hennekey RJ; Arch Environ Contam Toxicol 6: 315
(1977) as cited in USEPA; Ambient Water Quality Criteria Doc:
Mercury p.69 (1984) EPA 440/5-84-026]**PEER REVIEWED**

EC50 Ambystoma opacum (marbled salamander, embryo, larva) 107.5-108
ug/l/7-8 day toxic effect: death and deformity /Conditions of bioassay not
specified/
[USEPA; Ambient Water Quality Criteria Doc: Mercury p.55
(1984) EPA 440/5-84-026]**PEER REVIEWED**

EC50 Laminaria hyperborea (kelp) 450 ug/l/22 hr toxic effect: on respiration
/Conditions of bioassay not specified/
[Hopkins R, Kain JM; Mar Pollut Bull 2: 75 (1971) as cited in
USEPA; Ambient Water Quality Criteria Doc: Mercury p.63 (1984)
EPA 440/5-84-026]**PEER REVIEWED**

LC50 Mercenaria mercenaria (quahog clam, larva) 14 ug/l/8-10 days /Conditions
of bioassay not specified/
[USEPA; Ambient Water Quality Criteria Doc: Mercury p.66
(1984) EPA 440/5-84-026]**PEER REVIEWED**

LC50 Crassostrea virginica (eastern oyster embryo) 12 ug/l/12 days /Conditions
of bioassay not specified/
[USEPA; Ambient Water Quality Criteria Doc: Mercury p.66
(1984) EPA 440/5-84-026]**PEER REVIEWED**

LC50 Lymnaea stagnalia (snail) 443 ug/l/48 hr /Conditions of bioassay not
specified/
[USEPA; Ambient Water Quality Criteria Doc: Mercury p.49
(1984) EPA 440/5-84-026]**PEER REVIEWED**

EC50 Daphnia magna (cladoceran) 30 ug/l/48 hr /Conditions of bioassay not
specified/
[USEPA; Ambient Water Quality Criteria Doc: Mercury p.47
(1984) EPA 440/5-84-026]**PEER REVIEWED**

LC50 Daphnia magna (cladoceran) 13 ug/l/24 hr /Conditions of bioassay not
specified/
[Bringmann G, Kuhn R; Z Wasser Abwasser Forsch 10: 161 (1977)
as cited in USEPA; Ambient Water Quality Criteria Doc: Mercury
p.49 (1984) EPA 440/5-84-026]**PEER REVIEWED**

EC50 Hyla squirella (squirrel treefrog, embryo, larva) 2.4 ug/l/7 days toxic effect:
death and deformity /Conditions of bioassay not specified/
[USEPA; Ambient Water Quality Criteria Doc: Mercury p.54
(1984) EPA 440/5-84-026]**PEER REVIEWED**

LC50 Gambusia affinis (mosquito fish) 500 ug/l/ > 10 days /Conditions of
bioassay not specified/
[Bondou A et al; Bull Environ Contam Toxicol 22:813 (1979) as
cited in USEPA; Ambient Water Quality Criteria Doc: Mercury
p.53 (1984) EPA 440/5-84-026]**PEER REVIEWED**

LC50 Poecilla reticulta (guppy) 13-303 ug/l/24-48 hr (respectively) /Conditions of
bioassay not specified/
[USEPA; Ambient Water Quality Criteria Doc: Mercury p.53
(1984) EPA 440/5-84-026]**PEER REVIEWED**

EC50 Lepomis macrochirus (bluegill, embryo, larva) 88.7 ug/l/7-8 days toxic
effect: death and deformity /Conditions of bioassay not specified/
[USEPA; Ambient Water Quality Criteria Doc: Mercury p.53
(1984) EPA 440/5-84- 026]**PEER REVIEWED**

EC50 Micropterus salmoides (largemouth bass, embryo, larva) 5.3-140 ug/l/8
days toxic effect: death and deformity /Conditions of bioassay not specified/
[USEPA; Ambient Water Quality Criteria Doc: Mercury p.53
(1984) EPA 440/5-84-026]**PEER REVIEWED**

EC50 Rana pipiens (leopard frog, embryo, larva) 7.3 ug/l/7 days toxic effect:
death and deformity /Conditions of bioassay not specified/
[USEPA; Ambient Water Quality Criteria Doc: Mercury p.53
(1984) EPA 440/5-84-026]**PEER REVIEWED**

EC50 Bufo punctatus (red-spotted toad, embryo, larva) 36.8 ug/l/7 days toxic
effect: death and deformity /Conditions of bioassay not specified/
[USEPA; Ambient Water Quality Criteria Doc: Mercury p.54
(1984) EPA 440/5-84-026]**PEER REVIEWED**

LC50 Salmo gairdneri (rainbow trout, juvenile) 903 ug/l/24 hr /Conditions of
bioassay not specified/
[Wobeser GA; PhD Thesis University of Saskatchewan, Canada as
cited in USEPA; Ambient Water Quality Criteria Doc: Mercury
p.51 (1984) EPA 440/5-84-026]**PEER REVIEWED**

EC50 Salmo gairdneri (rainbow trout, embryo, larva) 4.7-5.0 ug/l/28 days toxic
effect: death and deformity /Conditions of bioassay not specified/
[USEPA; Ambient Water Quality Criteria Doc: Mercury p.51
(1984) EPA 440/5-84-026]**PEER REVIEWED**

EC50 Carassius auratus (goldfish, embryo, larva) 0.7-121.9 ug/l/7 days toxic
effect: death and deformity /Conditions of bioassay not specified/
[USEPA; Ambient Water Quality Criteria Doc: Mercury p.52
(1984) EPA 440/5-84-026]**PEER REVIEWED**

LC50 Pimephales promelas (fathead minnow) 37 ug/l/48 hr /Conditions of
bioassay not specified/
[Slooff W et al; Aquat Toxicol 4: 113 (1983) as cited in
USEPA; Ambient Water Quality Criteria Doc: Mercury p.52 (1984)
EPA 440/5-84-026]**PEER REVIEWED**

EC50 Ictalurus punctatus (channel catfish, embryo, larva) 0.3 ug/l/10 days toxic
effect: death and deformity /Conditions of bioassay not specified/
[USEPA; Ambient Water Quality Criteria Doc: Mercury p.52
(1984) EPA 440/5-84-026]**PEER REVIEWED**

LC50 Orconectes limosus (crayfish, juvenile) (unfed/fed) 2 ug/l/30 day /Conditions
of bioassay not specified/
[Boulet C, Chaisemartin C; CR Soc Biol 167 :1933 (1973) as
cited in USEPA; Ambient Water Quality Criteria Doc: Mercury
p.50 (1984) EPA 440/5-84-026]**PEER REVIEWED**

LC50 Aedes aegypti (mosquito) 776-4,100 ug/l/48 hr /Conditions of bioassay not
specified/
[Slooff W et al; Aquat Toxicol 4: 113 (1983) as in cited in
USEPA; Ambient Water Quality Criteria Doc: Mercury p.50 (1984)
EPA 440/5-84-026]**PEER REVIEWED**

LC50 Guppy 0.03-0.054 mg/l/26 hr /Conditions of bioassay not specified/
[Deshmukh SS, Morothe VB; Indian J Exp Biol 18: 421-423 (1980)
as cited in Environment Canada; Tech Info for Problem Spills:
Mercury (Draft) p.35 (1982)]**PEER REVIEWED**

EC50 Fundulus heteroclitus (mummichog, embryo) 67.4 ug/l/32 day /Conditions
of bioassay not specified/
[Sharp JR, Neff JM; Mar Environ Res 3:195 (1980) as cited in
USEPA; Ambient Water Quality Criteria Doc: Mercury p.70 (1984)
EPA 440/5-84-026]**PEER REVIEWED**

LC50 Paramecium caudatum 0.21 ppm/1 hr; 0.16 ppm/2 hr /Conditions of
bioassay not specified/
[Chen T; Dongwuxue Zachi 3:15-17 (1984)]**PEER REVIEWED**

LC50 Lepomis macrochirus (bluegill sunfish) 280 (220-370) ug/l 24 hr, wt 0.6 g,
static bioassay, dissolved oxygen 4.1 (2.9-6.4) mg/l, water hardness 45.6
(45.6-45.6) mg/l as CaCO3, pH 7.1-7.3, alkalinity 46.5 (42.0-51.0) mg/l as
CaCO3, temp: 24.8 (23.5-26.2) deg C, Purity 99%
[Holcombe GW et al; Ecotoxicol Environ Safety 7 (4): 400-9
(1983)]**QC REVIEWED**

LC50 Lepomis macrochirus (bluegill sunfish) 250 (210-300) ug/l 48 hr, wt 0.6 g,
static bioassay, dissolved oxygen 4.1 (2.9-6.4) mg/l, water hardness 45.6
(45.6-45.6) mg/l as CaCO3, pH 7.1-7.3, alkalinity 46.5 (42.0-51.0) mg/l as
CaCO3, temp: 24.8 (23.5-26.2) deg C, Purity 99%
[Holcombe GW et al; Ecotoxicol Environ Safety 7 (4): 400-9
(1983)]**QC REVIEWED**

LC50 Lepomis macrochirus (bluegill sunfish) 160 (140-190) ug/l 72 hr, size 0.6 g,
static bioassay, dissolved oxygen 4.1 (2.9-6.4) mg/l, water hardness 45.6
(45.6-45.6) mg/l as CaCO3, pH 7.1-7.3, alkalinity 46.5 (42.0-51.0) mg/l as
CaCO3, temp: 24.8 (23.5-26.2) deg C, Purity 99%
[Holcombe GW et al; Ecotoxicol Environ Safety 7 (4): 400-9
(1983)]**QC REVIEWED**

LC50 Lepomis macrochirus (bluegill sunfish) 160 (130-180) ug/l 96 hr, size 0.6 g,
static bioassay, dissolved oxygen 4.1 (2.9-6.4) mg/l, water hardness 45.6
(45.6-45.6) mg/l as CaCO3, pH 7.1-7.3, alkalinity 46.5 (42.0-51.0) mg/l as
CaCO3, temp: 24.8 (23.5-26.2) deg C, Purity 99%
[Holcombe GW et al; Ecotoxicol Environ Safety 7 (4): 400-9
(1983)]**QC REVIEWED**

TSCA Test Submissions:

The frequency of forward mutations was determined at the thymidine kinase (TK)
locus of the mouse lymphoma L5178Y cell line exposed in vitro to zinc chloride in
the presence of metabolic activation provided by Aroclor-induced rat liver S9
fraction. Mutagenic effects were observed in cultures after exposure to test article
at concentrations ranging from 4.2 to 56 ug/plate, as indicated by 2 to 19.2 fold
increases in mean mutant frequency compared to controls. The percent growth
ranged from 95% to 10%, while in a preliminary cytotoxicity assay, all cells were
killed at 50 ug/ml.
[ Microbiological Associates; L5178Y TK +/- Mouse Lymphoma
Mutagenesis Assay: Nine Zinc Dialkyl Dithiophosphates and
Calcium Dialkyl Dithiophosphate, Zinc Oleate, Lot No. 34495-10
and Zinc Chloride, Lot No. KTJY (1984), EPA Document No.
FYI-AX-1084-0324, Fiche No. OTS0000324-0 ] **UNREVIEWED**

Metabolism/Pharmacokinetics:

Metabolism/Metabolites:

STUDIES INDICATED THAT LIVERS OF YELLOWFIN TUNA AND
ALBACORE HAVE HIGH ACTIVITY IN FORMATION OF
METHYLMERCURY FROM HGCL2. THIS ACTIVITY ... NOT FOUND IN
THE MEAT. WHEN LIVER-HgCl2 MIXTURES WERE EXPOSED TO
VISIBLE LIGHT DURING INCUBATION, FORMATION OF METHYL
MERCURY WAS REDUCED BY ABOUT 75%.
[Menzie, C. M. Metabolism of Pesticides, An Update. U.S.
Department of the Interior, Fish, Wild-life Service, Special
Scientific Report - Wildlife No. 184, Washington, DC: U.S.
GovernmentPrinting Office, l974. 241]**PEER REVIEWED**

FROM A CELL-FREE EXTRACT OF MERCURY-RESISTANT
PSEUDOMONAS, AN ENZYME WAS OBTAINED WHICH CATALYZED
REDUCTION OF MERCURY IN ... INORG MERCURIALS TO
METALLIC MERCURY. A PROSTETIC GROUP OF THE ENZYME WAS
IDENTIFIED AS FAD (FLAVINE ADENINE DINUCLEOTIDE).
/MERCURY/
[Menzie, C. M. Metabolism of Pesticides, An Update. U.S.
Department of the Interior, Fish, Wild-life Service, Special
Scientific Report - Wildlife No. 184, Washington, DC: U.S.
GovernmentPrinting Office, l974. 239]**PEER REVIEWED**

Mercuric ion Hg(2+) can be methylated by both aerobic and anaerobic bacteria.
/Mercuric ion/
[Nat'l Research Council Canada; Effects of Mercury in the
Canadian Environment p.33 (1976) NRCC No. 16739]**PEER
REVIEWED**

Absorption, Distribution & Excretion:

A COMPARATIVE STUDY OF THE LOCALIZATION OF HG FROM
HgCl2 ... FOLLOWING SC ADMIN IN RABBIT SHOWED HG TO
ACCUMULATE IN ... COLLECTING TUBULES, THE DISTAL PORTIONS
OF PROXIMAL CONVOLUTED TUBULES & THE WIDE PARTS OF
HENLE'S LOOP. NO HG ... IN GLOMERULI ...
[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. 1783]**PEER REVIEWED**

KINETIC STUDIES OF MERCURIC CHLORIDE INDICATED THAT
MERCURY WAS CONTAINED IN 3 COMPARTMENTS OF SHORT,
MEDIUM & LONG RETENTION TIME WITHIN RAT. KIDNEYS WERE
LARGEST COMPARTMENT FOR MERCURY & KIDNEY RETENTION
PROBABLY ACCOUNTED FOR LONG-TERM COMPARTMENT.
[Menzie, C.M. Metabolism of Pesticides, Update II. U.S.
Department of the Interior, Fish Wildlife Service, Special
Scientific Report - Wildlife No. 2l2.Washington, DC: U.S.
Government Printing Office, 1978. 175]**PEER REVIEWED**

WHEN GOAT WAS GIVEN (203)HGCL2, LESS THAN 30% OF DOSE WAS ABSORBED. EXCRETION OF (203)HG IN MILK ACCOUNTED FOR 0.22% OF DOSE.  [Menzie, C.M. Metabolism of Pesticides, Update II. U.S. Department of the Interior, Fish Wildlife Service, Special Scientific Report - Wildlife No. 2l2.Washington, DC: U.S. Government Printing Office, 1978. 175]**PEER REVIEWED**

DATA ... INDICATE THAT LESS THAN 10% OF INGESTED MERCURIC CHLORIDE IS ABSORBED. UPON HIGH INTAKE CORROSIVE ACTION ... MAY ALTER PERMEABILITY OF GASTROINTESTINAL TRACT ENHANCING ABSORPTION.  [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. 409]**PEER REVIEWED**

In the case of inorganic divalent mercury, approx 15% of an oral, non-toxic dose is absorbed from the gastrointestinal tract in adults and retained in body tissues. /Inorganic mercury/  [USEPA; Mercury Health Effects Update p.4-32 (1984) EPA-600/8-84-019F]**PEER REVIEWED**

MERCURY MOVES READILY ACROSS THE PLACENTA INTO FETAL TISSUE. REGARDLESS OF THE CHEMICAL FORM ADMIN, FETAL TISSUES ATTAIN CONCN OF MERCURY AT LEAST EQUAL TO THOSE OF THE MOTHER. /INORGANIC MERCURY SALTS/  [Doull, J., C.D.Klassen, and M.D. Amdur (eds.). Casarett and Doull's Toxicology. 3rd ed., New York: Macmillan Co., Inc., 1986. 606]**PEER REVIEWED**

... IF SUBJECT IS EXPOSED TO HG2+ SALTS FOR A LONG TIME ... THE SKIN READILY ABSORBS MERCURY SALTS ... INORG MERCURY HAS ... AFFINITY TOWARD THIOL GROUPS OF SOFT TISSUE PROTEINS ... /MERCURIC CMPD/  [Venugopal, B. and T.D. Luckey. Metal Toxicity in Mammals, 2. New York: Plenum Press, 1978. 90]**PEER REVIEWED**

... Inorganic mercury has a markedly nonuniform distribution after absorption. The highest concentration of mercury is found in the kidneys, where the metal is  retained longer than in other tissues. Concn of inorganic mercury are similar in whole blood and plasma. Inorganic mercurials do not readily pass the blood-brain barrier or the placenta. The metal is excreted in the urine and feces. /Inorganic mercury cmpd/  [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**

CHEM ANALYSES SHOWING ACCUMULATION OF MERCURY IN LENS /OF EYE/ IN MERCURIALENTIS HAVE BEEN REPORTED ... /MERCURY SALTS/  [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986. 583]**PEER REVIEWED**

ABSORPTION FROM INTESTINAL TRACT IS GREATER WITH INORG THAN ORG FORM OF MERCURY. BY INHALATION OF INORG MERCURY ... CONCN RANGING FROM 2.91 TO 26.18 MG/CU M, AN AVG OF 24.16% OF THAT INHALED WAS ABSORBED. /MERCURY CMPD/  [Browning, E. Toxicity of Industrial Metals. 2nd ed. New York: Appleton-Century-Crofts, 1969. 227]**PEER REVIEWED**

SLOW ELIMINATION OF /MERCURY/ ... IS ... CHARACTERISTIC OF NUCLEUS DENTATUS. INORG MERCURY IS SELECTIVELY ACCUMULATED BY LYSOSOMAL SYSTEM. ... STEADILY ACCUMULATES IN KIDNEYS WHERE IT IS BOUND IN PART TO SULFHYDRYL GROUPS. /MERCURY/  [Doull, J., C.D.Klassen, and M.D. Amdur (eds.). Casarett and Doull's Toxicology. 3rd ed., New York: Macmillan Co., Inc., 1986. 485]**PEER REVIEWED**

The experimental study of the trophic mercury contamination of Salmo gairdneri shows very specific patterns of bioaccumulation and transfer of the two compounds studied, mercuric chloride and methyl mercury chloride. Analyses of the participation of the principal organs in these processes reveals the fundamental importance of the intestinal barrier. ... Mercuric chloride has a preferential site of accumulation, substantially reducing its transfer to th other organs in the fish.  [Boudou A, Ribeyre F; Water Air Soil Pollut 26 (2): 137-48 (1985)]**PEER REVIEWED**

The distribution of (203)Hg was studied in toadfish (Opsanus tau) 1-48 hr after the injection of mercuric chloride or methyl mercury chloride into a close intestinal sac. Both mercury compd were initially (1 hr after the injection) predominantly bound to the luminal surface of the gut tissue (72 and 78%, respectively). After 24 hr, mercuric chloride was found mainly in luminal fluid plus mucus, whereas methyl mercury chloride was transferred into blood. Mucus secretion by the intestine was larger after mercuric chloride tha after methyl mercury chloride injection. Leucine intestinal uptake was inhibited by 50% immediately after mercuric chloride
injection (when mucus secrtion was low); the absorption was normal 24 hr after mercuric chloride injection (when mucus secretion was greatly increased).  [Farmanfarmaian A; Mar Environ Res 17 (2-4): 176-80 (1985)]**PEER REVIEWED**

IN VIEW OF ANIMAL DATA, OTHER ORGANS OR CELLS /BESIDES KIDNEY/ WHERE MERCURY IS LIKELY TO ACCUMULATE ARE LIVER, MUCOUS MEMBRANE OF INTESTINAL TRACT, & EPITHELIUM OF SKIN, SPLEEN, INTERSTITIAL CELLS OF TESTICLES, & SOME PARTS OF BRAIN. IN ANIMAL EXPT, PLACENTA & FETAL MEMBRANE ... ACCUMULATE & RETAIN MERCURY. /Mercuric cmpd/   [Friberg, L., G.R. Nordberg, and V.B. Vouk. Handbook on the Toxicology of Metals. New York: Elsevier North Holland, 1979. 517]**PEER REVIEWED**

... MERCURIC MERCURY IS EXCRETED BY ... SWEAT GLANDS, LACRIMAL GLANDS, MAMMARY GLANDS, & SALIVARY GLANDS. MAJOR PART ... IS EXCRETED IN URINE & FECES. PARTITION BETWEEN THESE TWO ROUTES IS DOSE-DEPENDENT & DATA INDICATE A LARGER FRACTION EXCRETED BY URINE UPON ADMIN OF LARGER DOSES. /Mercury cmpd/  [Friberg, L., G.R. Nordberg, and V.B. Vouk. Handbook on the Toxicology of Metals. New York: Elsevier North Holland, 1979. 517]**PEER REVIEWED**

Biological Half-Life:

The average biological half-time of a tracer dose of divalent inorganic mercury compounds in man is 42 days for the whole body and 26 days for blood. /Mercury cmpd/  [USEPA; Mercury Health Effects Update p.2-5 (1984) EPA  600/8-84-019F]**PEER REVIEWED**

SOLUBLE INORG MERCURIALS (HG2+) READILY GAIN ACCESS TO CIRCULATION WHEN TAKEN BY MOUTH, ALTHOUGH CONSIDERABLE PORTION OF INGESTED HG2+ MAY REMAIN FIXED TO ALIMENTARY MUCOSA & INTESTINAL CONTENTS. ... HG2+ IS FIRST FIXED TO ALPHA-GLOBULINS & ERYTHROCYTES ... LATER... TO ALBUMIN ... TO TISSUES ... HALF-LIFE ... 15 DAYS. /INORGANIC MERCURIC CMPD/   [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**

In general, body burden of mercury in man has a half-life of about 60 days.
/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**

EXCEPT FOR EXCRETION BY SALIVA, MERCURY IS EXCRETED BY LIVER THROUGH BILE & ALSO BY MUCOUS MEMBRANES OF SMALL INTESTINES & COLON. ... IN RATS ... ELIMINATION CURVE IS ... A MULTI-PHASIC EXPONENTIAL CURVE, HAVING A RAPID PHASE WITH HALF- LIFE ABOUT 5 DAYS, ANOTHER PHASE WITH HALF-LIFE OF 1 MO, & STILL ANOTHER ... OF ABOUT 3 MO. /MERCURIC ION/  [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**

Mechanism of Action:

Mercury readily forms covalent bonds with sulfur, & it is this property that accounts for most of the biological properties of the metal. When sulfur is in form of sulfhydryl groups, divalent mercury replaces the hydrogen atom to form mercaptides. ... Mercurials even in low concn are capable of inactivating sulfhydryl enzymes and ... interfering with cellular metabolism & function. ... Mercury also combines with other ligands of physiological importance, such as phosphoryl, carboxyl, amide & amine groups. /Mercury cmpd/  [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**

... They cause agglutination and hemolysis of erythrocytes; Hg2+ ions enter into ... coordination or chelation complexes with erythrocytes, causing clumping of cells. At low concn Hg2+ ions initially block glucose entry by complexing with phosphate ligands and by incr passive alkali-ion permeability, and then enter the cell & accumulate. In vitro studies on erythrocytes show presence of Hg2+ binding sites on erythrocyte membranes; cellular membrane permeability is affected by binding of mercury ions to thiol & phosphate ligands. /Mercury salts/  [Venugopal, B. and T.D. Luckey. Metal Toxicity in Mammals, 2. New York: Plenum Press, 1978. 95]**PEER REVIEWED**

At low concn Hg2+ ions accumulate in liver lysosomes, & at high concn Hg2+ ions rupture the lysosomes & release destructive acid hydrolases. Studies on Hg2+ induced kidney necrosis revealed decreased lysosomal enzyme activity and mitochondrial cytochrome-C activity. The nephrotoxic effect of Hg2+ in female is more prominent than in male. ... Studies with isolated cells indicate changes in cell membrane permeability, decr electric potential across cell membrane, loss of cellular potassium, reduced cellular uptake of glucose, & a strong inhibition of cellular respiratory enzymes. ... It induces formation of metallothionein. ... Mercury ions induce diuresis by increasing permeability of renal proximal tubules to Na+ ions. /Mercury ions/  [Venugopal, B. and T.D. Luckey. Metal Toxicity in Mammals, 2. New York: Plenum Press, 1978. 96]**PEER REVIEWED**

Unilateral nephrectomy induces a dramatic change in single-kidney structure and function. Therefore, the effects of nephrotoxins may be altered. To evaluate this possibility, mercuric chloride (2 mg/kg, subcutaneous was given to male, Sprague-Dawley rats 2 days following either unilateral nephrectomy or sham surgery. Nonoliguric acute renal failure developed and was qualitatively similar in both groups. Glomerular filtration rate reached a nadir on day 2 and was reduced to a greater extent in the unilateral nephrectomy group. Furthermore, recovery of glomerular filtration was slower and occurred to lesser extent by day 10 in the animals subjected to unilateral nephrectomy. Evidence of significant tubular dysfunction was present during the acute phase in both groups, as reflected by changes in the fractional excretion of sodium or lysozyme. Persistent tubular dysfunction was noted on day 10 in both the sham and unilateral nephrectomy groups, but the degree of dysfunction was greater in the unilateral nephrectomy animals. The in vitro uptake of organic ions by renal cortical slices was reduced 24 hr following the injection of mercuric chloride although no difference was seen between the experimental groups. Merury content within renal cortex was not increased in the unilateral nephrectomy group at 1 or 3 hr but was higher 24 hr postinjection. Total urinary mercury excretion during the first day was not altered by unilateral nephrectomy although single-kidney excretion was increased dramatically.  [Houser MT, Berndt WO; Toxicol Appl Pharmacol 83 (3): 506-15 (1986)]**PEER REVIEWED**

Six day old rats were treated subcutaneously with the proximal tubule toxicant mercuric chloride (1 or 3.2 mg/kg) or saline. Twenty four hours later, when evidence of mercury nephrotoxicity is detectable, creatinine clearance, and the fractonal excretion of water and various components of the filtrate were determined using a 2 hr clearance priod immediately after injection of a diuretic. The effects of mercury (3.2 mg/kg) were consistent with its ability to cause acute renal failure and proximal tubular necrosis and also indicated an apparent disruption of the cycling of urea in the nephron. A decrease in the fractional excretion of water, combined sodium and potassium and total osmotic solutes indicated that the diuretic response tho acetazolamide was markedly attenuated in the mercuric chloride-treated pups whereas the responses to furosemide, chlorothiazide and amiloride were not altered by mercury treatment.  [Gray JA, Kavlock RJ; J Pharmacol Exp Ther 242 (1): 212-16 (1987)]**PEER REVIEWED**

Cultures of some aerobically grown strains of Salmonella typhimurium and
Escherichia coli contain up to 24 µM extracellular glutathione ... in addition to
having intracellular glutathione concentrations in the millimolar range. The addition
of 26 µM glutathione to cultures of S typhimurium strain TA1534 partially
protected the bacteria from the toxic effects causing growth delay by 54 µM
N-methyl-N'-nitro-N-nitrosoguanidine. ... The addition of micromolar glutathione
to cultures of an Escherichia coli glutathione strain protected the cells from growth
inhibition by micromolar concentrations of mercuric chloride, methyl mercuric
chloride, silver nitrate, cisplatin, cadmium chloride, cadmium sulfate, and
iodoacetamide. In the cases of mercuric chloride, cisplatin,
N-methyl-N'nitro-nitorsoguanidine, silver nitrate, and iodoacetamide, reaction
products with glutathione were detected by paper chromatography.
[Owens RA, Hartman PE; Environ Mutagen 8 (5): 659-74
(1986)]**PEER REVIEWED**

As manifest by tubular collapse and the virtual absence of flow into the
glomerulotubular junction, filtration in most nephrons (SNGFR) of rats poisoned
with 9 mg/kg body wt mercuric chloride 16 to 28 hours earlier was virtually
absent. Arterial colloid osmotic pressure and Bowman's space pressure were
modestly depressed (p < 0.05) and mean blood pressure was reduced from 115
+/- mm mercury (SEM) to 97 +/- 1 mm mercury (p < 0.001). Glomerular
capillary hydraulic pressure (Pg), 25.6 +/- 1.3 mm mercury was some 24 mm
mercury lower than control (p < 0.001) and yielded a net afferent effective
filtration pressure (Pnet) of 4.1 +/- 1.2 mm mercury. Excluding three rats with
values greater than 10 mm mercury net afferent effective filtration pressure
averaged 2.0 +/- 0.9 mm mercury (n= 7 rats) versus 20.0 +/- 1.8 mm mercury
in controls (n= 10, p < 0.001), the former being statistically almost
indistinguishable from 0 mm mercury and barely able to support any filtration. This
decrease in Hg was caused by a major increase in preglomerular resistance and a
reciprocal fall in efferent arteriolar resistance, the preglomerular resistance/efferent
arteriolar resistance ratio of 7.2 +/- 0.8 being four fold higher than control (p <
0.001). Renocortical blood flow was not different from control (p > 0.2).
[Wolfert AI et al; Kidney Int 32 (2): 246-55 (1987)]**PEER
REVIEWED**

... Using an in vivo technique /in fish/, the effects of mercuric chloride, mercurous
chloride, and cadmium chloride on the absorption of the essential amino acid
L-leucine absorption /were studied/. Among the heavy metal cmpd tested,
mercuric chloride appears to act on the active transport and facilitated diffusion
components of uptake. ...
[Farmanfarmanian A, Socci R; Aquat Toxicol 7 (1-2): 107-18
(1985)]**PEER REVIEWED**

Partially hepatectomized rats were exposed to an acute dose of mercury (5 mg
Hg+2/kg ip as mercuric chloride and its influence on renal glutathione redox
system, 24 hr later was studied. Significant loss of glutathione reductase,
glutathione peroxidase and G-6-P-dehydrogenase occurred in mercury exposed
non-hepatectomized (sham) and hepatectomized rats. Mercury intoxicated
hepatectomized rats had a considerable decrease in total shame and glutathione
levels. Further, the process of lipid peroxidation was significantly enhanced.
[Dwivedi RS, Kaur G; J Environ Sci Health Part A 21 (8):
759-68 (1987)]**PEER REVIEWED**

Administration of mercuric chloride at a dose of 5 mg/kg body weight/day for 15
days to male albino rats brought about a marked depression of the scavenging
enzymes via glutathione peroxidase and glutathione S-transferase, in the kidney.
There was an adaptive rise in the levels of catalase and no incr in lipid peroxidation
was observed. The levels of both glutathione and glutathione reductase were
decreased, whereas total thiol increased. In the intoxicated rats, vitamin E was
effective in glutathione levels returning to normal. The adaptation in this group of
animals is reflected by increased superoxide dimutase activities.
[Addya S et al; Acta Vitaminol Enzymol 6 (2): 103-7
(1984)]**PEER REVIEWED**

The effects of 1.5 ppm of mercuric chloride (LC50/48 hr) on some enzymes and
organic substances of liver tissue of Sarotherodon mossambicus were studied.
Significant decreases in the activities of succinate dehydrogenase, lactate
dehydrogenase, glucose-6-phosphate dehydrogenases, alkaline phosphatase, and
acid phosphatase and in the levels of organic substances like total anthrine-positive
substances, glycogen, and total ninhydrin-positive substances were observed. The
results indicate impaired oxidative and transphosphorylative activities and utilization
of carbohydrates during acute mercury toxicosis in fish.
[Naidu KA et al; Ecotoxicol Environ Safety 8 (3): 215-8
(1984)]**PEER REVIEWED**

Mercuric chloride (HgCl2) was administered at 3 dosage levels (0.5, 1, and 2.5
mg/kg sc) daily to newborn rats beginning at 1 day and continuing through
weaning. HgCl2 produced a dose-dependent inhibition of body growth which was
apparent only after weaning and which worsened as the animals approached
adulthood; brain growth was also adversely affected, but less so than was body
weight. Growth of other tissues (heart, kidney, liver) was influenced in a different
manner, with initial increases over control organ weights and a subsequent decline
toward normal (kidney) or to subnormal levels (heart, liver). Examination of
ornithine decarboxylase (ODC) activity, an index of cellular maturation, confirmed
that HgCl2 produced separable types of effects in different organ systems.
Although the patterns of growth alterations caused by HgCl2 resembled those seen
with methylmercury, the effects on ODC were dissimilar, suggesting that there
were some differences in the underlying biochemical mechanisms. In addition to
causing generalized alterations of cellular development, HgCl2 produced specific
effects on catecholamine neurotransmitter systems, with increases in brain
norepinephrine levels and turnover as well as elevations in synaptosomal uptake
capabilities for norepinephrine. Dopamine levels and turnover were slightly
reduced or unchanged, but synaptosomal uptake was still elevated. Target-specific
effects were also apparent in the peripheral sympathetic nervous system, where
renal but not cardiac norepinephrine was elevated in the HgCl2 group. Again,
some but not all of these changes can be produced by comparable exposure to
methyl mercury; many of the neuronal effects in the animals exposed to HgCl2
were in the opposite direction from those seen with the organomercurial.
[Bartolome J et al; Toxicol Lett 22 (1): 101-11 (1984)]**PEER
REVIEWED**

Mercuric chloride was administered once intraperitoneally to female fischer 344
rats at doses of 0, 0.2, 0.6 and 1.8 mg/kg. Although there were no alterations in
the urinary excretion of lactate dehydrogenase, significant elevations in the activities
of urinary alkaline phosphatase, glutamic-pyruvic transaminase and glutamic-
oxalacetic transaminase indicated that mercuric chloride was nephrotoxic. There
was no evidence of hepatotoxicity as hepatic glucose-6-phosphatase and serum
sorbitol dehydrogenase were esentially unaffected by mercuric chloride
administration. Of the four phase-II reactions measured, only the glucuronidation
of chloramphenicol was diminished by treatment with mercuric chloride.
[Trela BA et al; Toxicol Lett 32 (1-2): 133-40 (1986)]**PEER
REVIEWED**

Specimens of Notopterus notopterus were exposed to 0.088, 0.044, 0.029,
0.022 and 0.018 mg/l of mercuric chloride for 30 and 60 days, and their effects on
metabolic enzymes succinic dehydrogenase (SDH) < pyruvate dehydrogenase
(PDH) and lactic dehydrogenase (LDH) in liver and gills were evaluated. SDH and
PDH inhibited significantly in both the tissues, while LDH elevated significantly (p <
0.01; p < 0.05) in liver and insignificantly in gills of Notopterus notoptrus.
[Verma SR, Chand R; Indian J Environ Health 18 (1): 1-7
(1986)]**PEER REVIEWED**

Interactions:

EXPLANTS OF RAT CEREBRUM IN CULTURE WERE TREATED WITH
TOXIC CONCN OF HgCl2 AND VARYING CONCN OF SODIUM
SELENITE, RESULTING IN REDUCED NEUROTOXICITY OF HGCL2.
[AOSHIMA K, KASUYA M; TOXICOL LETT (AMST) 6 (3): 181
(1980)]**PEER REVIEWED**

TOXICITIES OF COMBINATIONS OF
PENTACHLORONITROBENZENE WITH MERCURIC CHLORIDE AND
HEXACHLOROBENZENE WITH MERCURIC CHLORIDE ADMIN
ORALLY TO RATS WAS HIGHER THAN THE SUM OF THE TOXICITIES
PRODUCED BY THE INDIVIDUAL DOSES.
[RENNER G; XENOBIOTICA 10: (7-8) 551 (1980)]**PEER REVIEWED**

ALPHA-MERCAPTO-BETA-(2-FURYL)ACRYLIC ACID (MFA)
SIGNIFICANTLY REDUCED LETHALITY OF MERCURIC CHLORIDE IN
RATS (2.2 MG HG/KG, IP) WHEN ADMIN (25 MG/KG, ORALLY) AT 1,
24, 48 & 72 HR. DAILY ADMIN OF MFA (25 MG/KG, ORALLY)
REDUCED LETHALITY OF DAILY INJECTION OF INCR AMT OF
MERCURIC CHLORIDE (1 MG HG/KG X 7 DAYS, 2 MG HG/KG X 7
DAYS, 4 MG HG/KG X 14 DAYS, IP). MERCURY CONCN IN KIDNEYS
OF MFA-TREATED RATS WAS HIGHER THAN IN CONTROLS,
WHEREAS CONCN IN LIVER WAS (NONSIGNIFICANTLY) LOWER.
ENHANCED MERCURY DEPOSITION IN KIDNEY AS
MANIFESTATION OF ANTIDOTAL EFFECT IS NOT CHARACTERISTIC
OF THIOL CHELATORS USED IN PRACTICE FOR MERCURY
POISONING.
[GIROUX E, LACHMANN PJ; TOXICOL APPL PHARMACOL 67 (2): 178
(1983)]**PEER REVIEWED**

IN ANIMALS INJECTED WITH 31 MG/KG BODY WT DITHIOTHREITOL
60 MIN AFTER 3 MG/KG MERCURIC CHLORIDE INJECTION, URINE
FLOW RATE & FRACTIONAL EXCRETION OF SOLUTES WERE
REDUCED WITHIN 30 MIN TO VALUES INTERMEDIATE BETWEEN
CONTROL & MERCURIC CHLORIDE-TREATED RATS. INJECTION OF
MERCURIC CHLORIDE ALONE OR FOLLOWED BY DITHIOTHREITOL
RESULTED IN CHANGES IN MEAN ARTERIAL BLOOD PRESSURE OR
GLOMERULAR FILTRATION RATE. THERE WERE NO ALTERATIONS
IN MERCURY DISTRIBUTION IN ORGANS OF RATS INJECTED WITH
MERCURIC CHLORIDE ALONE OR PRIOR TO DITHIOTHREITOL.
THESE STUDIES DEMONSTRATE THAT DITHIOTHREITOL CAN
AMELIORATE RENAL TOXICITY OF MERCURY & SUGGEST THAT
THIS EFFECT IS MEDIATED THROUGH INTRARENAL SITE OF
ACTION.
[KLONNE DR, JOHNSON DR; TOXICOL APPL PHARMACOL 70 (3): 459
(1983)]**PEER REVIEWED**

Interaction of zinc with mercuric chloride and sodium selenite was studied in the rat
at the organ and subcellular levels (liver and kidneys). Zinc chloride was
administered subcutaneously at dose of 5 mg zinc/kg, mercury chloride into the
tail vein at a dose of 0.5 mg mercury/kg (both metals every other day during 2
weeks) and sodium selenite intragastrically, at doses of 0.1 mg Selenium/kg, every
day. Zinc retention in the rat did not exceed 20% and was unchanged in the
presence of mercury. ... In the presence of selenium no peak of metallothione-like
proteins stimulated by zinc or mercury was found in the soluble fraction of the
kidneys. The metallothionein level did not differ from that typical for control group
animals. A significant incr in the level of endogenous copper was found only in the
kidneys of rats exposed to zinc in the presence of mercury and selenium.
[Chimielnicka J et al; Arch Toxicol 53 (2): 165-75
(1983)]**PEER REVIEWED**

When male Spraque- Dawley rats were treated with 1 mg mercuric chloride/kg
subcutaneous 6 hr prior to or simultaneously with a single 2.5 mmole/kg ip dose of
bromobenzene and sacrificed 48 hr after the bromobenzene dose, the activities of
serum transaminases (SGOT and SGPT) were found to be significantly reduced
when compared with those obtained in bromobenzene alone treated rats. Similar
phenomena were observed when rats were treated simultaneously with 1 or 2 mg
mercury chloride/kg and 1 mmole bromobenzene/kg, but not when
bromobenzene was given 6 hr prior to mecury chloride injection. When 5 mmole
bromobenzene/kg and 1 mg mercury chloride/kg were given simultaneously to the
animals, an apparent reduction in bromobenzene toxicity was again observed. In
each case mercury chloride alone had no effect on the transaminase activities.
Mercury chloride (1 mg/kg, subcotaneous) treatment reduced the hepatic
microsomal cytochrome p.450 content. Treatment with 1 mg mercury chloride/kg
6 hr prior to bromobenzene injection (2.5 mmole/kg) significantly reduced the
urinary excretion of para- and meta-bromophenols, and para-bromocatechol
during 0 to 24 hr period without affecting the urinary thioethers.
[Chakrabarti S, Brodeur J; Environ Res 39 (1): 50-9
(1986)]**PEER REVIEWED**

To investigate the mechanism by which zinc suppresses mercury toxicity, the
effects of zinc and mercury on glutahione metabolism in the rat kidney were
studied. When the time course of glutathione level in the rat kidney was examined
at 2, 6, and 12 hr after treatment of rats with both metals, an increase of
glutathione was found and was apparently related to the activation of some
glutathione associated enzymes. In the kidney of rats treated with both metals, the
response of protective function involving glutathione and glutathione associated
enzymes depended on the magnitude of mercury toxicity but appeared to be
independent in the zinc dosage. The administration of diethyl maleate, which
depletes glutathione, increased lipid peroxidation and mercury toxicity
concomitantly with a decrease of glutathione level in the kidney of rats treated with
zinc and mercury.
[Fukino H et al; J Toxicol Environ Health 19 (1): 75-90
(1986)]**PEER REVIEWED**

Five metal compounds, zinc chloride, mercury chloride, chromium chloride
hexahydrate, cadmium chloride hemidihydrate, and nickel chloride hexahydrate,
were selected and tested for potential modifying influence on renal tumorigenesis.
Six groups, each consisting of 15 male F344 rats, were given
N-ethyl-N-hydroxyethylnitrosamine at a concentration of 500 ppm in their drinking
water for the first 2 weeks as the initiation of carcinogenesis. Thereafter, the rats
were treated orally for 25 weeks with zinc chloride, mercuric chloride, chromium
chloride, cadmium chloride, and nickel chloride, respectively, at concentrations of
450, 40, 600, 100, and 600 ppm in the drinking water. The control group was
given unsupplemented distilled water after N-ethyl-N-hydroxyetylnitrosamine
initiation. Renal neoplatic lesions were classified histologically into dysplastic foci
and renal cell tumors. As a result, statistically significant increases were found in the
mean numbers of dysplastic foci per sq cm in rats treated with the five metal
compounds. On the other hand the incidence of renal cell tumors was significantly
higher only in rats treated with nickel chloride.
[Kurokawa Y et al; J Am Coll Toxicol 4 (6): 321-30
(1986)]**PEER REVIEWED**

Various combinations of mercuric chloride and sodium selenite were administered
orally to rats and mice in vivo for both chronic and acute treatment. The
antagonistic interaction and the optimum combination at which the action of
mercuric chloride could be neutralized by sodium selenite was investigated. Of the
concentrations employed in rats when sodium selenite was fed after 1 hr treatment
with mercuric chloride, the percentage of chromosomal abnormalities significantly
decreased as compared to animals treated with mercuric chloride alone. All other
experiments with different combinations of mercuric chloride and sodium selenite
gave higher frequencies of chromosomal abnormalities as compared to sodium
selenite alone. ...
[Das SK et al; Cytobios 42 (169): 271-8 (1985)]**PEER
REVIEWED**

The effects of many combinations of toxic concn of heavy metal pollutants,
mercuric chloride, lead acetate, cadium chloride and cupric sulfate, on the
senescence of isolated mature leaves of submerged aquatic plants, Potamogeton
pectinatus, Vallisneria spiralis, and Hydrilla verticillata were studied. All of the
combinations of heavy metal pollutants caused senescence in all 3 species by
decreasing chlorophyll, DNA, RNA, protein, and dry wt, and increasing free
amino acids, tissue permeability, the activities of protease and RNAse, and the
ratio of acid to alkaline pyrophosphatase activity over control values. The effects
were highest in Potamogeton and lowest in Hydrilla. The degree of senescence in
the three submerged plants by combination of toxic concn of heavy metal
pollutants is much higher due to synergism than that by individual heavy metal
pollutants.
[Jana S, Choudhuri MA; Water Air Soil Pollut 21 (1-4): 351-8
(1983)]**PEER REVIEWED**

Male Porton-Wistar rats (4/ group) were used to study the effects of selenite
against the renotoxicity of mercury (Hg) when Hg and selenium (Se) were given
simultaneously at equimolar concentrations. Mercury as (203)HgCl2 (0.5 uCi/ml)
was given sc at doses of 2.5, 5.0, or 7.5 umol/kg/4.0 ml saline. The rats were
maintained in metabolism cages to obtain 48 hr urine samples for assay of alkaline
phosphatase (AP) and urinary Hg. After 48 hr the animals were killed, the kidneys
removed for histologic examination, and cervical blood samples collected for assay
of plasma urea nitrogen (PUN). Selenite, given simultaneously with Hg, significantly
(p < 0.05) decreased renal disposition of Hg at all doses. The renal Hg in % of
dose was: 17.4, 12.8, 10.9, and 9.3 for doses of 2.5 oral, 2.5 sc, 5.0 sc, and 7.5
sc umole Hg/kg. Urinary excretion of Hg declined in the order of controls >
biological selenium > selenomethionine > selenite. Excretion of alkaline
phosphatase (AP) and plasma urea nitrogen declined (p < 0.05) in the same order;
AP at 2.5 and 5.0 umol Hg/kg; and, plasma urea nitrogen at 5.0 and 7.5 umol
Hg/kg. Examination of kidney tissue indicated that selenite protected the pars recta
and distal part of the proximal convoluted tubules.
[Magos L et al; Arch Toxicol 60 (6): 422-6 (1987)]**QC
REVIEWED**

The effect of unfractionated heparin and a low molecular weight heparin fragment
on the DNA synthesis response of human peripheral blood T lymphocytes from
nickel-allergic patients, activated by mercuric chloride and nickel sulfate was
tested. Inhibition was found with 1.1 mg/ml unfractionated heparin added 1 hr after
mercuric chloride and nickel sulfate and with the same concentration of the heparin
fragment, added 1 hr after nickel sulfate; no effect was seen after at 72 hr. Both
heparin preparations in concentrations of 0.0001-0.11 mg/ml stimulated the
response to nickel sulfate andd in concentrations of 0.001-0.11 mg/ml stimulated
the response to mercuric chloride. Heparin preparations seem to have modulating
effects on both nickel and mercury activation of lymphocytes. The effect was
dependent on both heparin concentration and the time of addition to the activation
process.
[Nordlind K; Int Arch Allergy appl Imunol 84 (2): 156-8
(1987)]**PEER REVIEWED**

Pharmacology:

Therapeutic Uses:

Anti-Infective Agents, Local; Disinfectants
[National Library of Medicine's Medical Subject Headings
online file (MeSH, 1999)]**QC REVIEWED**

TOPICAL ANTISEPTIC, DISINFECTANT; MEDICATION (VET):
CAUSTIC, ANTISEPTIC, DISINFECTANT
[The Merck Index. 10th ed. Rahway, New Jersey: Merck Co.,  ., 1983. 839]**QC REVIEWED**

Interactions:

EXPLANTS OF RAT CEREBRUM IN CULTURE WERE TREATED WITH
TOXIC CONCN OF HgCl2 AND VARYING CONCN OF SODIUM
SELENITE, RESULTING IN REDUCED NEUROTOXICITY OF HGCL2.
[AOSHIMA K, KASUYA M; TOXICOL LETT (AMST) 6 (3): 181
(1980)]**PEER REVIEWED**

TOXICITIES OF COMBINATIONS OF
PENTACHLORONITROBENZENE WITH MERCURIC CHLORIDE AND
HEXACHLOROBENZENE WITH MERCURIC CHLORIDE ADMIN
ORALLY TO RATS WAS HIGHER THAN THE SUM OF THE TOXICITIES
PRODUCED BY THE INDIVIDUAL DOSES.
[RENNER G; XENOBIOTICA 10: (7-8) 551 (1980)]**PEER REVIEWED**

ALPHA-MERCAPTO-BETA-(2-FURYL)ACRYLIC ACID (MFA)
SIGNIFICANTLY REDUCED LETHALITY OF MERCURIC CHLORIDE IN
RATS (2.2 MG HG/KG, IP) WHEN ADMIN (25 MG/KG, ORALLY) AT 1,
24, 48 & 72 HR. DAILY ADMIN OF MFA (25 MG/KG, ORALLY)
REDUCED LETHALITY OF DAILY INJECTION OF INCR AMT OF
MERCURIC CHLORIDE (1 MG HG/KG X 7 DAYS, 2 MG HG/KG X 7
DAYS, 4 MG HG/KG X 14 DAYS, IP). MERCURY CONCN IN KIDNEYS
OF MFA-TREATED RATS WAS HIGHER THAN IN CONTROLS,
WHEREAS CONCN IN LIVER WAS (NONSIGNIFICANTLY) LOWER.
ENHANCED MERCURY DEPOSITION IN KIDNEY AS
MANIFESTATION OF ANTIDOTAL EFFECT IS NOT CHARACTERISTIC
OF THIOL CHELATORS USED IN PRACTICE FOR MERCURY
POISONING.
[GIROUX E, LACHMANN PJ; TOXICOL APPL PHARMACOL 67 (2): 178
(1983)]**PEER REVIEWED**

IN ANIMALS INJECTED WITH 31 MG/KG BODY WT DITHIOTHREITOL
60 MIN AFTER 3 MG/KG MERCURIC CHLORIDE INJECTION, URINE
FLOW RATE & FRACTIONAL EXCRETION OF SOLUTES WERE
REDUCED WITHIN 30 MIN TO VALUES INTERMEDIATE BETWEEN
CONTROL & MERCURIC CHLORIDE-TREATED RATS. INJECTION OF
MERCURIC CHLORIDE ALONE OR FOLLOWED BY DITHIOTHREITOL
RESULTED IN CHANGES IN MEAN ARTERIAL BLOOD PRESSURE OR
GLOMERULAR FILTRATION RATE. THERE WERE NO ALTERATIONS
IN MERCURY DISTRIBUTION IN ORGANS OF RATS INJECTED WITH
MERCURIC CHLORIDE ALONE OR PRIOR TO DITHIOTHREITOL.
THESE STUDIES DEMONSTRATE THAT DITHIOTHREITOL CAN
AMELIORATE RENAL TOXICITY OF MERCURY & SUGGEST THAT
THIS EFFECT IS MEDIATED THROUGH INTRARENAL SITE OF
ACTION.
[KLONNE DR, JOHNSON DR; TOXICOL APPL PHARMACOL 70 (3): 459
(1983)]**PEER REVIEWED**

Interaction of zinc with mercuric chloride and sodium selenite was studied in the rat
at the organ and subcellular levels (liver and kidneys). Zinc chloride was
administered subcutaneously at dose of 5 mg zinc/kg, mercury chloride into the
tail vein at a dose of 0.5 mg mercury/kg (both metals every other day during 2
weeks) and sodium selenite intragastrically, at doses of 0.1 mg Selenium/kg, every
day. Zinc retention in the rat did not exceed 20% and was unchanged in the
presence of mercury. ... In the presence of selenium no peak of metallothione-like
proteins stimulated by zinc or mercury was found in the soluble fraction of the
kidneys. The metallothionein level did not differ from that typical for control group
animals. A significant incr in the level of endogenous copper was found only in the
kidneys of rats exposed to zinc in the presence of mercury and selenium.
[Chimielnicka J et al; Arch Toxicol 53 (2): 165-75
(1983)]**PEER REVIEWED**

When male Spraque- Dawley rats were treated with 1 mg mercuric chloride/kg
subcutaneous 6 hr prior to or simultaneously with a single 2.5 mmole/kg ip dose of
bromobenzene and sacrificed 48 hr after the bromobenzene dose, the activities of
serum transaminases (SGOT and SGPT) were found to be significantly reduced
when compared with those obtained in bromobenzene alone treated rats. Similar
phenomena were observed when rats were treated simultaneously with 1 or 2 mg
mercury chloride/kg and 1 mmole bromobenzene/kg, but not when
bromobenzene was given 6 hr prior to mecury chloride injection. When 5 mmole
bromobenzene/kg and 1 mg mercury chloride/kg were given simultaneously to the
animals, an apparent reduction in bromobenzene toxicity was again observed. In
each case mercury chloride alone had no effect on the transaminase activities.
Mercury chloride (1 mg/kg, subcotaneous) treatment reduced the hepatic
microsomal cytochrome p.450 content. Treatment with 1 mg mercury chloride/kg
6 hr prior to bromobenzene injection (2.5 mmole/kg) significantly reduced the
urinary excretion of para- and meta-bromophenols, and para-bromocatechol
during 0 to 24 hr period without affecting the urinary thioethers.
[Chakrabarti S, Brodeur J; Environ Res 39 (1): 50-9
(1986)]**PEER REVIEWED**

To investigate the mechanism by which zinc suppresses mercury toxicity, the
effects of zinc and mercury on glutahione metabolism in the rat kidney were
studied. When the time course of glutathione level in the rat kidney was examined
at 2, 6, and 12 hr after treatment of rats with both metals, an increase of
glutathione was found and was apparently related to the activation of some
glutathione associated enzymes. In the kidney of rats treated with both metals, the
response of protective function involving glutathione and glutathione associated
enzymes depended on the magnitude of mercury toxicity but appeared to be
independent in the zinc dosage. The administration of diethyl maleate, which
depletes glutathione, increased lipid peroxidation and mercury toxicity
concomitantly with a decrease of glutathione level in the kidney of rats treated with
zinc and mercury.
[Fukino H et al; J Toxicol Environ Health 19 (1): 75-90
(1986)]**PEER REVIEWED**

Five metal compounds, zinc chloride, mercury chloride, chromium chloride
hexahydrate, cadmium chloride hemidihydrate, and nickel chloride hexahydrate,
were selected and tested for potential modifying influence on renal tumorigenesis.
Six groups, each consisting of 15 male F344 rats, were given
N-ethyl-N-hydroxyethylnitrosamine at a concentration of 500 ppm in their drinking
water for the first 2 weeks as the initiation of carcinogenesis. Thereafter, the rats
were treated orally for 25 weeks with zinc chloride, mercuric chloride, chromium
chloride, cadmium chloride, and nickel chloride, respectively, at concentrations of
450, 40, 600, 100, and 600 ppm in the drinking water. The control group was
given unsupplemented distilled water after N-ethyl-N-hydroxyetylnitrosamine
initiation. Renal neoplatic lesions were classified histologically into dysplastic foci
and renal cell tumors. As a result, statistically significant increases were found in the
mean numbers of dysplastic foci per sq cm in rats treated with the five metal
compounds. On the other hand the incidence of renal cell tumors was significantly
higher only in rats treated with nickel chloride.
[Kurokawa Y et al; J Am Coll Toxicol 4 (6): 321-30
(1986)]**PEER REVIEWED**

Various combinations of mercuric chloride and sodium selenite were administered
orally to rats and mice in vivo for both chronic and acute treatment. The
antagonistic interaction and the optimum combination at which the action of
mercuric chloride could be neutralized by sodium selenite was investigated. Of the
concentrations employed in rats when sodium selenite was fed after 1 hr treatment
with mercuric chloride, the percentage of chromosomal abnormalities significantly
decreased as compared to animals treated with mercuric chloride alone. All other
experiments with different combinations of mercuric chloride and sodium selenite
gave higher frequencies of chromosomal abnormalities as compared to sodium
selenite alone. ...
[Das SK et al; Cytobios 42 (169): 271-8 (1985)]**PEER
REVIEWED**

The effects of many combinations of toxic concn of heavy metal pollutants,
mercuric chloride, lead acetate, cadium chloride and cupric sulfate, on the
senescence of isolated mature leaves of submerged aquatic plants, Potamogeton
pectinatus, Vallisneria spiralis, and Hydrilla verticillata were studied. All of the
combinations of heavy metal pollutants caused senescence in all 3 species by
decreasing chlorophyll, DNA, RNA, protein, and dry wt, and increasing free
amino acids, tissue permeability, the activities of protease and RNAse, and the
ratio of acid to alkaline pyrophosphatase activity over control values. The effects
were highest in Potamogeton and lowest in Hydrilla. The degree of senescence in
the three submerged plants by combination of toxic concn of heavy metal
pollutants is much higher due to synergism than that by individual heavy metal
pollutants.
[Jana S, Choudhuri MA; Water Air Soil Pollut 21 (1-4): 351-8
(1983)]**PEER REVIEWED**

Male Porton-Wistar rats (4/ group) were used to study the effects of selenite
against the renotoxicity of mercury (Hg) when Hg and selenium (Se) were given
simultaneously at equimolar concentrations. Mercury as (203)HgCl2 (0.5 uCi/ml)
was given sc at doses of 2.5, 5.0, or 7.5 umol/kg/4.0 ml saline. The rats were
maintained in metabolism cages to obtain 48 hr urine samples for assay of alkaline
phosphatase (AP) and urinary Hg. After 48 hr the animals were killed, the kidneys
removed for histologic examination, and cervical blood samples collected for assay
of plasma urea nitrogen (PUN). Selenite, given simultaneously with Hg, significantly
(p < 0.05) decreased renal disposition of Hg at all doses. The renal Hg in % of
dose was: 17.4, 12.8, 10.9, and 9.3 for doses of 2.5 oral, 2.5 sc, 5.0 sc, and 7.5
sc umole Hg/kg. Urinary excretion of Hg declined in the order of controls >
biological selenium > selenomethionine > selenite. Excretion of alkaline
phosphatase (AP) and plasma urea nitrogen declined (p < 0.05) in the same order;
AP at 2.5 and 5.0 umol Hg/kg; and, plasma urea nitrogen at 5.0 and 7.5 umol
Hg/kg. Examination of kidney tissue indicated that selenite protected the pars recta
and distal part of the proximal convoluted tubules.
[Magos L et al; Arch Toxicol 60 (6): 422-6 (1987)]**QC
REVIEWED**

The effect of unfractionated heparin and a low molecular weight heparin fragment
on the DNA synthesis response of human peripheral blood T lymphocytes from
nickel-allergic patients, activated by mercuric chloride and nickel sulfate was
tested. Inhibition was found with 1.1 mg/ml unfractionated heparin added 1 hr after
mercuric chloride and nickel sulfate and with the same concentration of the heparin
fragment, added 1 hr after nickel sulfate; no effect was seen after at 72 hr. Both
heparin preparations in concentrations of 0.0001-0.11 mg/ml stimulated the
response to nickel sulfate andd in concentrations of 0.001-0.11 mg/ml stimulated
the response to mercuric chloride. Heparin preparations seem to have modulating
effects on both nickel and mercury activation of lymphocytes. The effect was
dependent on both heparin concentration and the time of addition to the activation
process.
[Nordlind K; Int Arch Allergy appl Imunol 84 (2): 156-8
(1987)]**PEER REVIEWED**

Environmental Fate & Exposure:

Probable Routes of Human Exposure:

The dominant food source of mercury in the human diet is fish and fish products.
... In terms of total mercury (Hg), the diet greatly exceeds other media, including
air and water, as a source of human exposure and absorption of Hg. /Mercury/
[USEPA; Mercury Health Effects Update p.2-4 (1984) EPA
600/8-84-019F]**PEER REVIEWED**

Accumulation of mercury in the terrestrial and aquatic food chains results in risks
for man mainly through the consumption of: ... fish from contaminated waters;
especially predator species, tuna fish, swordfish and other large oceanic fish even if
caught considerably off shore; other seafoods including mussels and crayfish,
fish-eating birds and mammals; and eggs of fish eating birds. /Mercury/
[WHO; Environ Health Criteria: Mercury p.55 (1976)]**PEER
REVIEWED**

Acute poisoning usually results from oral ingestion of highly dissociated inorganic
prepn, but it may also be caused by ... mercurial ointments applied topically.
/Mercury cmpd/
[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**

Acute poisoning is major threat in home & on farm, but, because mercury is a
cumulative poison, subacute & chronic intoxications are recognized, particularly in
industry. /Mercruy cmpd/
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology
of Commercial Products. 5th ed. Baltimore: Williams and
Wilkins, 1984.,p. III-266]**PEER REVIEWED**

Artificial Pollution Sources:

ENVIRONMENTAL ACCUMULATION: MONOMERIC VINYL
CHLORIDE IS PRODUCED BY ... THE ADDITION OF HYDROGEN
CHLORIDE TO ACETYLENE IN THE PRESENCE OF HGCL2. THIS
PROCESS HAS BEEN RESPONSIBLE FOR THE INTRODUCTION OF
MERCURY CMPD INTO NATURAL BODIES OF WATER FROM
WHICH HG ... EVENTUALLY ABSORBED BY FISH ...
[Hamilton, A., and H. L. Hardy. Industrial Toxicology. 3rd ed.
Acton, Mass.: Publishing Sciences Group, Inc., 1974.
341]**PEER REVIEWED**

Concentrated local discharges associated with industrial activities and waste
disposal. Diffuse discharges generally associated with combustion of fuels
containing mercury impurities. Mercury is released in various chemical forms.
/Mercury compounds/
[Miller DR, Buchanan JM; MARC Report: Atmos Trans of Mercury:
Exposure Commitment and Uncertainty Calculations #14 p.1
(1979)]**PEER REVIEWED**

Environmental Fate:

MERCURIC SALTS ARE STILL WIDELY EMPLOYED IN INDUSTRY, &
INDUSTRIAL DISCHARGE ... INTO RIVERS HAS POLLUTED MANY
PARTS OF WORLD. ... MICROORGANISMS CONVERT INORG
MERCURY TO METHYLMERCURY ... /WHICH/ IS ... TAKEN UP
RAPIDLY BY PLANKTON ALGAE & IS CONCN IN FISH BY WAY OF
FOOD CHAIN. /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**

Atmospheric Fate: 50% of volatile form is Hg vapor with sizeable portion of
remainder being Hg(II) and methyl mercury, 25 to 50% of mercury (Hg) in
water is organic. Hg in the environment is deposited and revolatilized many times,
with a residence time in the atmosphere of at least a few days. In the volatile phase
it can be transported hundreds of kilometers. /Mercury compounds/
[Miller DR, Buchanan JM; Atmospheric Transport of Mercury:
Exposure Commitmen and Uncertainty Calculations. MARC Report
#14 p.3-6 (1979)]**PEER REVIEWED**

Aquatic Fate: The conversion, in aquatic environments, of inorganic mercury
cmpd to methyl mercury implies that recycling of mercury from sediment to
water to air and back could be a rapid process. /Mercury cmpd/
[Callahan, M.A., M.W. Slimak, N.W. Gabel, et al. Water-Related
Environmental Fate of 129 Priority Pollutants. Volume I.
EPA-440/4 79-029a. Washington, DC: U.S.Environmental
Protection Agency, December 1979.,p. 14-11]**PEER REVIEWED**

Mercury adsorbed from mercuric chloride and 2-methoxy-ethylmercury chloride
(Aretan) solutions by three contrasting soils showed a dependence on soil:solution
ratio and initial mercury (Hg) concentration in soil solution. Changing the soil
solution ratio from 1:10 to 1:100 but keeping the intitial concentration constant
resulted in an increase in initial concentration on other hand, resulted in decrease in
Hg adsorption. Upon manipulating of the pH of the surface soils, adsorption of
mercuric chloride (HgCl2) at 100 mg Hg/l concentration increased from about 70
to over 95 mg Hg/kg when pH was raised from 5.0 to 8.0. Precipitation of Hg
may also have contributed to this trend. Removal of organic matter from soil
resulted in large reductions of Hg adsorbed, as much as 95% from the HgC12
solutions.
[Semu E et al; Water Air Soil Pollut 32 (1-2): 1-10
(1987)]**PEER REVIEWED**

The rate and extent of the methylation of inorganic mercury (Hg) depends
markedly on the chemical speciation of the Hg and the methylating agent. The
presence of Hg(II)-C1 covalent bonding has an inhibitory effect on methylation by
methyl cobalamin and in natural sediments. The role of radical and carbonium ion
methylation mechanisms was also investigated. Methylation occurs by attack of a
methyl carbanion (CH3-) on inorganic Hg (II) ions derived by microbial
breakdown of the orginial Hg compounds added.
[Craig PJ, Moreton PA; Environ Pollut Ser B Chem Phys 10 (2):
141-58 (1985)]**PEER REVIEWED**

Environmental Biodegradation:

Inorganic forms of mercury (Hg) can be converted to organic forms by microbial
action in the biosphere. /Inorganic mercury/
[Schroeder WH; Envir Sci Tech 16 (7): 394A-400A (1982) as
cited in Environment Canada; Tech Info for Problem Spills:
Mercury (Draft) p.41 (1982)]**PEER REVIEWED**

... Certain bacteria are capable of transforming mercuric ion to volatile elemental
mercury. /Mercuric ion/
[Callahan, M.A., M.W. Slimak, N.W. Gabel, et al. Water-Related
Environmental Fate of 129 Priority Pollutants. Volume I.
EPA-440/4 79-029a. Washington, DC: U.S.Environmental
Protection Agency, December 1979.,p. 14-9]**PEER REVIEWED**

THE INSECTICIDAL ACTION OF MERCURY SALTS WAS RELATED
TO THEIR DECOMPOSITION BY SOIL ORGANISMS AND RELEASE OF
MERCURY VAPORS. THIS REACTION REQUIRED MOISTURE AND
PROCEEDED MORE RAPIDLY AS SOIL PH AND TEMPERATURE WAS
INCREASED. /MERCURY SALTS/
[Menzie, C.M. Metabolism of Pesticides. U.S. Department of the
Interior, Bureau of Sport Fisheries and Wildlife, Publication
127. Washington, DC: U.S. Government Printing Office, 1969.
240]**PEER REVIEWED**

Upon entering an aqueous system, virtually any mercurial cmpd may be microbially
converted to methyl mercury. /Mercurial cmpd/
[Callahan, M.A., M.W. Slimak, N.W. Gabel, et al. Water-Related
Environmental Fate of 129 Priority Pollutants. Volume I.
EPA-440/4 79-029a. Washington, DC: U.S.Environmental
Protection Agency, December 1979.,p. 14-9]**PEER REVIEWED**

Environmental Bioconcentration:

Many organisms are capable of accumulating mercury from water.
Bioconcentrating up to 10,000 fold. /Mercury/
[U.S. Coast Guard, Department of Transportation. CHRIS -
Hazardous Chemical Data. Volume II. Washington, D.C.: U.S.
Government Printing Office, 1984-5.]**PEER REVIEWED**

Bioconcentration factors of 10,000 and 40,000 have been obtained for mercuric
chloride and methylmercury with an oyster.
[USEPA/OWRS; Quality Criteria for Water 1986 (1986) EPA
440/5-86-001]**PEER REVIEWED**

Mercuric salts are still widely employed in industry, & industrial discharge ... into
rivers has polluted many parts of the world. ... Microorganisms convert inorg
mercury to methyl mercury ... /which/ is ... taken up rapidly by planktonic algae
& is concentrated in fish by way of food chain. /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**

Volatilization from Water/Soil:

Volatilization of mercury from land and lakes was estimated to enhance the
atmosphere concn over continental land masses by a factor of 45. /Mercury/
[Miller DR, Buchanan JM; Atmospheic Transport of Mercury:
Exposure Commitment and Uncertainty Calculations. MARC Report
#14 p.67 (1979)]**PEER REVIEWED**

... Certain bacteria are capable of transforming mercuric ion to volatile elemental
mercury. /Mercuric ion/
[Callahan, M.A., M.W. Slimak, N.W. Gabel, et al. Water-Related
Environmental Fate of 129 Priority Pollutants. Volume I.
EPA-440/4 79-029a. Washington, DC: U.S.Environmental
Protection Agency, December 1979.,p. 14-9]**PEER REVIEWED**

Sediment/Soil Concentrations:

Approximate concn of all forms of mercury in the earth's crust is 80 ppb.
/Mercury/
[Jonasson IR; Mercury in the Natural Environment: A Review of
Recent Work: Geological Survey of Canada p.13-14 (1970)]**PEER
REVIEWED**

Atmospheric Concentrations:

Over low soil concn areas, atmospheric concn= 5 ug/cu m. Over soil containing
greater than 10 ppm atmospheric concn= 200 ug/cu m. /Mercury compounds/
[Casarett, L.J., and J. Doull. Toxicology: The Basic Science
of Poisons. New York: MacMillan Publishing Co., 1975.
484]**PEER REVIEWED**

Food Survey Values:

Tuna, 0.2 mg/kg (natural), 10.6 mg/kg (abnormal); eggs, 0.009 mg/kg (natural),
0.029 mg/kg (abnormal); cabbage, 0.09 mg/kg (natural), 0.57 mg/kg (abnormal).
/Mercury Compounds/
[OECD; Mercury and the Environment p.135-141 (1974)]**PEER
REVIEWED**

Plant Concentrations:

Mercury and its compounds occur naturally in trace amounts in plants growing in
soils with low mercury concentrations ( < 500 ppb). /Mercury cmpd/
[OECD; Mercury and the Environment p.135-147 (1974)]**PEER
REVIEWED**

Environmental Standards & Regulations:

FIFRA Requirements:

All uses of mercury are cancelled except the following: 1) as a fungicide in the
treatment of textiles and fabrics intended for continuous outdoor use; 2) as a
fungicide to control brown mold on freshly sawn lumber; 3) as a fungicide
treatment to control Dutch elm disease; 4) as an in-can preservative in water based
paints and coatings; 5) as a fungicide in water-based paints and coatings used for
exterior application; 6) as a fungicide to control "winter turf diseases" such as
Sclerotinia boreales, and gray and pink snow mold subject to the following: a. the
use of these products shall be prohibited within 25 feet of any water body where
fish are taken for human consumption. b. these products can be applied only by or
under the direct supervision of golf course superintendents. c. the products will be
classified as restricted use pesticides when they are reregistered and classified in
accordance with section 4(c) of FEPCA. /Mercury/
[Environmental Protection Agency/OPTS. Suspended, Cancelled
and Restricted Pesticides. 3rd Revision. Washington, D.C.:
Environmental Protection Agency, January 1985. 16]**PEER
REVIEWED**

RCRA Requirements:

A solid waste containing mercuric chloride may become characterized as a
hazardous waste when subjected to the Toxicant Extraction Procedure listed in 40
CFR 261.24, and if so characterized, must be managed as a hazardous waste.
[40 CFR 261.24 (7/1/87)]**PEER REVIEWED**

Atmospheric Standards:

Emissions to the atmosphere from sludge incineration plants, sludge drying plants,
or a combination of these sludge wastewater treatment plant processes shall not
exceed 3200 grams of mercury per 24-hour period. /Total mercury/
[40 CFR 61.52(b) (7/1/87)]**PEER REVIEWED**

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause
serious health problems. The Clean Air Act, as amended in 1990, directs EPA to
set standards requiring major sources to sharply reduce routine emissions of toxic
pollutants. EPA is required to establish and phase in specific performance based
standards for all air emission sources that emit one or more of the listed pollutants.
Mercuric chloride is included on this list.
[Clean Air Act as amended in 1990, Sect. 112 (b) (1) Public
Law 101-549 Nov. 15, 1990]**QC REVIEWED**

Clean Water Act Requirements:

Toxic pollutant designated pursuant to section 307(a)(1) of the Clean Water Act
and is subject to effluent limitations. /Mercury and cmpds/
[40 CFR 401.15 (7/1/87)] **QC REVIEWED**

Federal Drinking Water Standards:

EPA 2 ug/l /Mercury/
[USEPA/Office of Water; Federal-State Toxicology and Risk
Analysis Committee (FSTRAC). Summary of State and Federal
Drinking Water Standards and Guidelines (11/93)] **QC
REVIEWED**

Federal Drinking Water Guidelines:

EPA 2 ug/l /Mercury/
[USEPA/Office of Water; Federal-State Toxicology and Risk
Analysis Committee (FSTRAC). Summary of State and Federal
Drinking Water Standards and Guidelines (11/93)] **QC
REVIEWED**

State Drinking Water Guidelines:

(AZ) ARIZONA 3 ug/l /Mercury/
[USEPA/Office of Water; Federal-State Toxicology and Risk
Analysis Committee (FSTRAC). Summary of State and Federal
Drinking Water Standards and Guidelines (11/93)] **QC
REVIEWED**

(ME) MAINE 2 ug/l /Mercury/
[USEPA/Office of Water; Federal-State Toxicology and Risk
Analysis Committee (FSTRAC). Summary of State and Federal
Drinking Water Standards and Guidelines (11/93)] **QC
REVIEWED**

FDA Requirements:

Bottled water shall, when a composite of analytical units of equal volume from a
sample is examined by the methods described in paragraph (d)(1)(ii) of this
section, meet the standards of chemical quality and shall not contain mercury in
excess of 0.002 mg/l. /Total mercury/
[21 CFR 103.35 (4/1/88)]**PEER REVIEWED**

The color additive FD&C Blue Number 2 shall conform to the specifications in the
CFR 74.102 and shall be free from impurities other than those named; including
mercury (as Hg) in not more than 1 part per million, to the extent that such other
impurities may be avoided by current good manufacturing practice. /Total
mercury/
[21 CFR 74.102 (4/1/88)]**PEER REVIEWED**

The color additive FD&C Green Number 3 shall conform to the specifications in
the CFR 74.203 and shall be free from impurities other than those named;
including mercury (as Hg) in not more than 1 part per million, to the extent that
such other impurities may be avoided by current good manufacturing practice.
/Total mercury/
[21 CFR 74.203 (4/1/88)]**PEER REVIEWED**

The color additive FD&C Yellow Number 5 shall conform to the specifications in
the CFR 74.705 and shall be free from impurities other than those named;
including mercury (as Hg) in not more than 1 part per million, to the extent that
such other impurities may be avoided by current good manufacturing practice.
/Total mercury/
[21 CFR 74.705 (4/1/88)]**PEER REVIEWED**

Chemical/Physical Properties:

Molecular Formula:

Cl2-Hg
**PEER REVIEWED**

Molecular Weight:

271.52
[The Merck Index. 10th ed. Rahway, New Jersey: Merck Co.,
Inc., 1983. 839]**PEER REVIEWED**

Color/Form:

COLORLESS RHOMBIC CRYSTALS OR WHITE POWDER
[Weast, R.C. (ed.) Handbook of Chemistry and Physics, 68th ed.
Boca Raton, Florida: CRC Press Inc., 1987-1988.,p.
B-107]**PEER REVIEWED**

White crystalline solid
[Association of American Railroads. Emergency Handling of
Hazardous Materials in Surface Transportation. Washington,
D.C.: Assoc. of American Railroads,Hazardous Materials Systems
(BOE), 1987. 433]**PEER REVIEWED**

Odor:

None
[U.S. Coast Guard, Department of Transportation. CHRIS -
Hazardous Chemical Data. Volume II. Washington, D.C.: U.S.
Government Printing Office, 1984-5.]**PEER REVIEWED**

Boiling Point:

302 DEG C
[Weast, R.C. (ed.) Handbook of Chemistry and Physics, 68th ed.
Boca Raton, Florida: CRC Press Inc., 1987-1988.,p.
B-107]**PEER REVIEWED**

Melting Point:

276 DEG C
[Weast, R.C. (ed.) Handbook of Chemistry and Physics, 68th ed.
Boca Raton, Florida: CRC Press Inc., 1987-1988.,p.
B-107]**PEER REVIEWED**

Corrosivity:

Corrosion rate: 0.0003 mm/yr (1% concn) at 100 deg C
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed.,
Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984.,p.
23(83) 111]**PEER REVIEWED**

Corrosion rate: 0.01 mm/yr (5% concn) at 100 deg C
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed.,
Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984.,p.
23(83) 111]**PEER REVIEWED**

Corrosion rate: 0.001 mm/yr (10% concn) at 100 deg C
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed.,
Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984.,p.
23(83) 111]**PEER REVIEWED**

Density/Specific Gravity:

5.44 @ 25 DEG C
[Weast, R.C. (ed.) Handbook of Chemistry and Physics, 68th ed.
Boca Raton, Florida: CRC Press Inc., 1987-1988.,p.
B-107]**PEER REVIEWED**

pH:

ABOUT 4.7 ALSO REPORTED AS 3.2 FOR 0.2 MOLAR AQ SOLN
[The Merck Index. 10th ed. Rahway, New Jersey: Merck Co.,
Inc., 1983. 839]**PEER REVIEWED**

Solubilities:

6.9 G/100 CC WATER @ 20 DEG C
[Shiu WY et al; Rev Environ Contam Toxicol 116: 15-187
(1990)]**QC REVIEWED**

48 G/100 CC WATER @ 100 DEG C
[Weast, R.C. (ed.) Handbook of Chemistry and Physics, 68th ed.
Boca Raton, Florida: CRC Press Inc., 1987-1988.,p.
B-107]**PEER REVIEWED**

33 G/100 CC ALCOHOL @ 25 DEG C
[Weast, R.C. (ed.) Handbook of Chemistry and Physics, 68th ed.
Boca Raton, Florida: CRC Press Inc., 1987-1988.,p.
B-107]**PEER REVIEWED**

4 G/100 CC ETHER
[Weast, R.C. (ed.) Handbook of Chemistry and Physics, 68th ed.
Boca Raton, Florida: CRC Press Inc., 1987-1988.,p.
B-107]**PEER REVIEWED**

SOL IN ACETIC ACID
[Weast, R.C. (ed.) Handbook of Chemistry and Physics, 68th ed.
Boca Raton, Florida: CRC Press Inc., 1987-1988.,p.
B-107]**PEER REVIEWED**

36 G/L WATER @ 0 DEG C
[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. 1772]**PEER REVIEWED**

SLIGHTLY SOL IN CARBON DISULFIDE, PYRIDINE; SOL IN
METHANOL, ACETONE, ETHYL ACETATE
[The Merck Index. 10th ed. Rahway, New Jersey: Merck Co.,
Inc., 1983. 839]**PEER REVIEWED**

1G/200 ML BENZENE
[The Merck Index. 10th ed. Rahway, New Jersey: Merck Co.,
Inc., 1983. 839]**PEER REVIEWED**

1G/200 ML GLYCEROL
[The Merck Index. 10th ed. Rahway, New Jersey: Merck Co.,
Inc., 1983. 839]**PEER REVIEWED**

Spectral Properties:

INDEX OF REFRACTION: 1.859
[Weast, R.C. (ed.) Handbook of Chemistry and Physics, 68th ed.
Boca Raton, Florida: CRC Press Inc., 1987-1988.,p.
B-107]**PEER REVIEWED**

Intense mass spectral peaks: 202 m/z, 272 m/z
[Pfleger, K., H. Maurer and A. Weber. Mass Spectral and GC
Data of Drugs, Poisons and their Metabolites. Parts I and II.
Mass Spectra Indexes. Weinheim, FederalRepublic of Germany.
1985. 462]**QC REVIEWED**

Vapor Pressure:

1 MM HG @ 136.2 DEG C
[Sax, N.I. Dangerous Properties of Industrial Materials. 5th
ed. New York: Van Nostrand Rheinhold, 1979. 793]**PEER
REVIEWED**

Other Chemical/Physical Properties:

COAGULATES ALBUMIN; PRODUCES YELLOW PRECIPITATE WITH
SODIUM HYDROXIDE
[The Merck Index. 10th ed. Rahway, New Jersey: Merck Co.,
Inc., 1983. 839]**PEER REVIEWED**

Heat of fusion: 15.3 cal/g
[U.S. Coast Guard, Department of Transportation. CHRIS -
Hazardous Chemical Data. Volume II. Washington, D.C.: U.S.
Government Printing Office, 1984-5.]**PEER REVIEWED**

Mercury salts, when heated with Na2CO3, yield metallic mercury and are
reduced to metal by H2O2 in the presence of alkali hydroxide. Copper, iron, zinc,
and many other metals ppt metallic mercury from neutral or slightly acid soln of
mercury salts. /Mercury salts/
[The Merck Index. 10th ed. Rahway, New Jersey: Merck Co.,
Inc., 1983. 842]**PEER REVIEWED**

Soluble ionized mercuric salts give a yellow precipitate of HgO with NaOH and a
red precipitate of HgI2 with alkali iodide. /Soluble mercuric salts/
[The Merck Index. 10th ed. Rahway, New Jersey: Merck Co.,
Inc., 1983. 842]**PEER REVIEWED**

Chemical Safety & Handling:

DOT Emergency Guidelines:

Health: TOXIC, inhalation, ingestion, or skin contact with material may cause
severe injury or death. Contact with molten substance may cause severe burns to
skin and eyes. Avoid any skin contact. Effects of contact or inhalation may be
delayed. Fire may produce irritating, corrosive and/or toxic gases. Runoff from fire
control or dilution water may be corrosive and/or toxic and cause pollution.
[U.S. Department of Transportation. 1996 North American
Emergency Response Guidebook. A Guidebook for First Responders
During the Initial Phase of aHazardous Materials/Dangerous
Goods Incident. U.S. Department of Transportation (U.S. DOT)
Research and Special Programs Administration, Office of
HazardousMaterials Initiatives and Training (DHM-50),
Washington, D.C. (1996).,p. G-154]**QC REVIEWED**

Fire or explosion: Non-combustible, substance itself does not burn but may
decompose upon heating to produce corrosive and/or toxic fumes. Some are
oxidizers and may ignite combustibles (wood, paper, oil, clothing, etc.). Contact
with metals may evolve flammable hydrogen gas. Containers may explode when
heated.
[U.S. Department of Transportation. 1996 North American
Emergency Response Guidebook. A Guidebook for First Responders
During the Initial Phase of aHazardous Materials/Dangerous
Goods Incident. U.S. Department of Transportation (U.S. DOT)
Research and Special Programs Administration, Office of
HazardousMaterials Initiatives and Training (DHM-50),
Washington, D.C. (1996).,p. G-154]**QC REVIEWED**

Public safety: CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number listed on the inside back cover. Isolate spill or leak area immediately for at least 25 to 50 meters (80 to 160 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate enclosed areas.  [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-154]**QC REVIEWED**

Protective clothing: Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing which is specifically recommended by the manufacturer. Structural firefighters' protective clothing is recommended for fire situations ONLY, it is not effective in spill situations.  [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of   HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-154]**QC REVIEWED**

Evacuation: Spill: See the Table of Initial Isolation and Protective Action Distances for highlighted substances. For non-highlighted substances, increase, in the downwind direction, as necessary, the isolation distance shown under "PUBLIC SAFETY". Fire: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.  [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-154]**QC REVIEWED**

Fire: Small fires: Dry chemical, CO2 or water spray. Large fires: Dry chemical, CO2, alcohol-resistant foam or water spray. Move containers from fire area if you can do it without risk. Dike fire control water for later disposal; do not scatter the material. Fire involving tanks or car/trailer loads: Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Do not get water inside containers. Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from the ends of tanks.  [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-154]**QC REVIEWED**

Spill or leak: ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area). Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. DO NOT GET WATER INSIDE CONTAINERS.  [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-154]**QC REVIEWED**

First aid: Move victim to fresh air. Call emergency medical care. Apply artificial respiration if victim is not breathing. Do not use mouth-to-mouth method if victim ingested or inhaled the substance; induce artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. For minor skin contact, avoid spreading material on unaffected skin. Keep victim warm and quiet. Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed. Ensure that medical personnel are aware of the material(s) involved, and take precautions to protect themselves.  [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-154]**QC 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. /MERCURY CMPD/   [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984.,p. III-263]**PEER REVIEWED**

Soluble salts have violent corrosive effects on skin and mucous membranes.
/Mercury salts/  [The Merck Index. 10th ed. Rahway, New Jersey: Merck Co., Inc., 1983. 842]**PEER REVIEWED**

Fire Fighting Procedures:

If material involved in fire: Extinguish fire using agent suitable for type of surrounding fire (Material itself does not burn or burns with difficulty). Use water in flooding quantities as fog. Use "alcohol" foam, dry chemical, or carbon dioxide.   [Association of American Railroads. Emergency Handling of Hazardous Materials in Surface Transportation. Washington, D.C.: Assoc. of American Railroads,Hazardous Materials Systems (BOE), 1987. 433]**PEER REVIEWED**

Hazardous Reactivities & Incompatibilities:

MIXTURE OF POTASSIUM & ANY OF FOLLOWING METALLIC HALIDES PRODUCES STRONG EXPLOSION ON IMPACT: ... MERCURIC CHLORIDE ...  [National Fire Protection Association. Fire Protection Guide on Hazardous Materials. 9th ed. Boston, MA: National Fire Protection Association, 1986.,p. 491M-167]**PEER REVIEWED**

MIXTURE OF SODIUM & ANY OF FOLLOWING HALIDE CMPD PRODUCES STRONG EXPLOSION ON IMPACT: ... MERCURIC CHLORIDE ...  [National Fire Protection Association. Fire Protection Guide on Hazardous Materials. 9th ed. Boston, MA: National Fire Protection Association, 1986.,p. 491M-187]**PEER REVIEWED**

INCOMPATIBILITIES: FORMATES, SULFITES, HYPOPHOSPHITES, PHOSPHATES, SULFIDES, ALBUMIN, GELATIN, ALKALIES, ALKALOID SALTS, AMMONIA, LIME WATER, ANTIMONY AND ARSENIC, BROMIDES, BORAX, CARBONATES, REDUCED IRON, COPPER, IRON, LEAD, SILVER SALTS, INFUSIONS OF CINCHONA, COLUMBO, OAK BARK OR SENNA; TANNIC ACID; VEGETABLE ASTRINGENTS.  [The Merck Index. 10th ed. Rahway, New Jersey: Merck Co., Inc., 1983. 839]**PEER REVIEWED**

Aluminum foil is unsuitable as a packing material in contact with mercury(II)salts in presence of moisture, when vigorous amalgamation ensues. /Mercuric salts/   [Bretherick, L. Handbook of Reactive Chemical Hazards. 3rd ed. Boston, MA: Butterworths, 1985. 282]**PEER REVIEWED**

Acetylene, ammonia, chlorine dioxide, azides, calcium (amalgam formation), sodium carbide, lithium, rubidium, copper. /Mercury compounds [except (organo) alkyls] (as Hg)/   [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 192]**QC REVIEWED**

Hazardous Decomposition:

When heated to decomp, emits toxic fumes of /mercury/. /Mercury compounds, inorganic/   [Sax, N.I. Dangerous Properties of Industrial Materials. 6th ed. New York, NY: Van Nostrand Reinhold, 1984. 1751]**QC REVIEWED**

Immediately Dangerous to Life or Health:

10 mg/cu m (as Hg) /Mercury compounds [except (organo) alkyls] (as Hg)/
[NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 192]**QC REVIEWED**

Protective Equipment & Clothing:

/SRP: IN THE LABORATORY:/ USE SKIN & RESP PROTECTION WHEN DRY MERCURIC SALTS ARE TO BE USED. USE SKIN PROTECTION WHEN CONCN AQUEOUS SOLN OF MERCURIC SALTS ARE USED. /MERCURIC SALTS/  [Association of Official Analytical Chemists. Official Methods of Analysis. 10th ed. and supplements. Washington, DC: Association of Official Analytical Chemists, 1965. New editions through13th ed. plus supplements, 1982.,p. 13/883 51.079]**PEER REVIEWED**

BUREAU OF MINES APPROVED AIRLINE RESPIRATOR; IMPERVIOUS SUIT; APPROPRIATE EYE PROTECTION.   [U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.]**PEER REVIEWED**

In areas where the exposures are excessive, respiratory protection shall be provided either by full-face canister-type mask or supplied air respirator, depending on the concentration of mercury fumes. Above 50 mg mercury/cu m requires supplied-air positive-pressure full-face respirators. Full-body work clothes including shoes or shoe covers and hats should be supplied and clean work clothes should be supplied daily. ... Work clothes should not be stored with street clothes in the same locker. /Mercury inorganic/  [Sittig, M. Handbook of Toxic and Hazardous Chemicals and Carcinogens, 1985. 2nd ed. Park Ridge, NJ: Noyes Data Corporation, 1985. 571]**PEER REVIEWED**

Wear appropriate chemical protective gloves, boots, and goggles. Wear positive pressure self-contained breathing apparatus when fighting fires involving this material.   [Association of American Railroads. Emergency Handling of Hazardous Materials in Surface Transportation. Washington, D.C.: Assoc. of American Railroads,Hazardous Materials Systems (BOE), 1987. 433]**PEER REVIEWED**

Wear appropriate personal protective clothing to prevent skin contact. /Mercury compounds [except (organo) alkyls] (as Hg)/  [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 193]**QC REVIEWED**

Recommendations for respirator selection. Max. concn for use: 0.5 mg/cu m. Respirator Class(es): Any chemical cartridge respirator with cartridge(s) providing protection against the compound of concern. End of service life indicator (ESLI) required. Any supplied-air respirator. /Mercury compounds [except (organo) alkyls] (as Hg), mercury vapor/  [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 193]**QC REVIEWED**

Recommendations for respirator selection. Max. concn for use: 1.25 mg/cu m. Respirator Class(es): Any supplied-air respirator operated in a continuous-flow mode. Any powered, air-purifying respirator with cartridge(s) providing protection against the compound of concern. End of service life indicator (ESLI) required. (Canister) /Mercury compounds [except (organo) alkyls] (as Hg), mercury vapor/  [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 193]**QC REVIEWED**

Recommendations for respirator selection. Max. concn for use: 2.5 mg/cu m. Respirator Class(es): Any chemical cartridge respirator with a full facepiece and cartridge(s) providing protection against the compound of concern. End of service life indicator (ESLI) required. Any air-purifying, full-facepiece respirator (gas mask) with a chin-style, front- or back-mounted canister providing protection against the compound of concern. End of service life indicator (ESLI) required. Any supplied-air respirator that has a tight-fitting facepiece and is operated in a continuous-flow mode. Any powered, air-purifying respirator with a tight-fitting facepiece and cartridge(s) providing protection against the compound of concern. End of service life indicator (ESLI) required. (Canister) Any self-contained breathing apparatus with a full facepiece. Any supplied-air respirator with a full facepiece. /Mercury compounds [except (organo) alkyls] (as Hg), mercury vapor/  [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 193]**QC REVIEWED**

Recommendations for respirator selection. Max. concn for use: 10 mg/cu m. Respirator Class(es): Any supplied-air respirator operated in a pressure-demand or other positive-pressure mode. /Mercury compounds [except (organo) alkyls] (as Hg), mercury vapor/  [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 193]**QC REVIEWED**

Recommendations for respirator selection. Condition: Emergency of planned entry into unknown concentrations or IDLH conditions: Respirator Class(es): Any self-contained breathing apparatus that has a full facepiece and is operated in a pressure-demand or other positive pressure-mode. Any supplied-air respirator that has a full facepiece and is operated in a pressure-demand or other positive-pressure mode in combination with an auxiliary self-contained breathing apparatus operated in pressure-demand or other positive-pressure mode. /Mercury compounds [except (organo) alkyls] (as Hg), mercury vapor/  [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 193]**QC REVIEWED**

Recommendations for respirator selection. Condition: Escape from suddenly occurring respiratory hazards: Respirator Class(es): Any air-purifying, full-facepiece respirator (gas mask) with a chin-style, front- or back-mounted canister providing protection against the compound of concern. End of service life indicator (ESLI) required. Any appropriate escape-type, self-contained breathing apparatus. /Mercury compounds [except (organo) alkyls] (as Hg), mercury vapor/  [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 193]**QC REVIEWED**

Recommendations for respirator selection. Max. concn for use: 1 mg/cu m.
Respirator Class(es): Any chemical cartridge respirator with cartridge(s) providing protection against the compound of concern. End of service life indicator (ESLI) required. Any supplied-air respirator. /Mercury compounds [except (organo) alkyls] (as Hg), other non (organo) alkyl mercury compounds/  [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 193]**QC REVIEWED**

Recommendations for respirator selection. Max. concn for use: 2.5 mg/cu m. Respirator Class(es): Any supplied-air respirator operated in a continuous-flow mode. Any powered, air-purifying respirator with cartridge(s) providing protection against the compound of concern. End of service life indicator (ESLI) required. (Canister) /Mercury compounds [except (organo) alkyls] (as Hg), other non (organo) alkyl mercury compounds/   [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 193]**QC REVIEWED**

Recommendations for respirator selection. Max. concn for use: 5 mg/cu m.
Respirator Class(es): Any chemical cartridge respirator with a full facepiece and cartridge(s) providing protection against the compound of concern. End of service life indicator (ESLI) required. Any air-purifying, full-facepiece respirator (gas mask) with a chin-style, front- or back-mounted canister providing protection against the compound of concern. End of service life indicator (ESLI) required. Any supplied-air respirator that has a tight-fitting facepiece and is operated in a continuous-flow mode. Any powered, air-purifying respirator with a tight-fitting facepiece and cartridge(s) providing protection against the compound of concern. End of service life indicator (ESLI) required. (Canister) Any self-contained breathing apparatus with a full facepiece. Any supplied-air respirator with a full facepiece. /Mercury compounds [except (organo) alkyls] (as Hg), other non (organo) alkyl mercury compounds/   [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 193]**QC REVIEWED**

Recommendations for respirator selection. Max. concn for use: 10 mg/cu m. Respirator Class(es): Any supplied-air respirator operated in a pressure-demand or other positive-pressure mode. /Mercury compounds [except (organo) alkyls] (as Hg), other non (organo) alkyl mercury compounds/  [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 193]**QC REVIEWED**

Recommendations for respirator selection. Condition: Emergency of planned entry into unknown concentrations or IDLH conditions: Respirator Class(es): Any self-contained breathing apparatus that has a full facepiece and is operated in a pressure-demand or other positive pressure-mode. Any supplied-air respirator that has a full facepiece and is operated in a pressure-demand or other positive-pressure mode in combination with an auxiliary self-contained breathing apparatus operated in pressure-demand or other positive-pressure mode. /Mercury compounds [except (organo) alkyls] (as Hg), other non (organo) alkyl mercury compounds/  [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 193]**QC REVIEWED**

Recommendations for respirator selection. Condition: Escape from suddenly occurring respiratory hazards: Respirator Class(es): Any air-purifying, full-facepiece respirator (gas mask) with a chin-style, front- or back-mounted canister providing protection against the compound of concern. End of service life indicator (ESLI) required. Any appropriate escape-type, self-contained breathing apparatus. /Mercury compounds [except (organo) alkyls] (as Hg), other non (organo) alkyl mercury compounds/  [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 193]**QC REVIEWED**

Preventive Measures:

If material not involved in fire: Keep material out of water sources and sewers.   [Association of American Railroads. Emergency Handling of  Hazardous Materials in Surface Transportation. Washington, D.C.: Assoc. of American Railroads,Hazardous Materials Systems (BOE), 1987. 433]**PEER REVIEWED**

Use disposable uniforms, so that a contaminated uniform is not a source of
absorption through the skin: use of disposable mercury-vapor-absorbing masks; Preventative measure: adequate ventilation; careful attention to good housekeeping, eg, avoidance of spills, and prompt and proper cleaning if a spill occurs; all containers of mercury and its cmpd should be kept tightly closed; floors should be washed on a regular basis with dilute calcium sulfide solution or other suitable reactant; floors should be nonporous; all workers directly involved in the plant operation should shower thoroughly each day before leaving. /Mercury cmpd/  [Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984.,p. 15(81) 167]**PEER REVIEWED**

If material not on fire and not involved in fire: Keep sparks, flames, and other sources of ignition away. Keep material out of water sources and sewers.  [Association of American Railroads. Emergency Handling of Hazardous Materials in Surface Transportation. Washington, D.C.: Assoc. of American Railroads,Hazardous Materials Systems (BOE), 1987. 433]**PEER REVIEWED**

Avoid breathing dusts, and fumes from burning material. Keep upwind. Avoid bodily contact with the material. Do not handle broken packages unless wearing appropriate personal protective equipment. Wash away any material which may have contacted the body with copious amounts of water or soap and water. If contact with the material anticipated, wear appropriate chemical protective clothing.  [Association of American Railroads. Emergency Handling of Hazardous Materials in Surface Transportation. Washington, D.C.: Assoc. of American Railroads,Hazardous Materials Systems (BOE), 1987. 433]**PEER REVIEWED**

The worker should immediately wash the skin when it becomes contaminated. /Mercury compounds [except (organo) alkyls] (as Hg)/  [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 193]**QC REVIEWED**

Work clothing that becomes wet or significantly contaminated should be removed and replaced. /Mercury compounds [except (organo) alkyls] (as Hg)/  [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 193]**QC REVIEWED**

Workers whose clothing may have become contaminated should change into uncontaminated clothing before leaving the work premises. /Mercury compounds [except (organo) alkyls] (as Hg)/  [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 193]**QC REVIEWED**

Contact lenses should not be worn when working with this chemical. /Mercury compounds [except (organo) alkyls] (as Hg)/  [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 193]**QC REVIEWED**

Stability/Shelf Life:

SLIGHTLY VOLATILE AT ORDINARY TEMP; APPRECIABLY SO AT 100 DEG C; VOLATILIZES UNCHANGED @ ABOUT 300 DEG C  [The Merck Index. 10th ed. Rahway, New Jersey: Merck Co., Inc., 1983. 839]**PEER REVIEWED**

DECOMP IN PRESENCE OF ORG MATTER BY SUNLIGHT TO METALLIC MERCURY, VIA MERCUROUS CHLORIDE   [Spencer, E. Y. Guide to the Chemicals Used in Crop Protection. 7th ed. Publication 1093. Research Institute, Agriculture Canada, Ottawa, Canada: Information Canada, 1982. 368]**PEER REVIEWED**

Shipment Methods and Regulations:

No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./   [49 CFR 171.2 (7/1/96)]**QC REVIEWED**

The International Air Transport Association (IATA) Dangerous Goods Regulations are published by the IATA Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry carrier regulations to be followed by all IATA Member airlines when transporting hazardous materials.  [IATA. Dangerous Goods Regulations. 38th ed. Montreal, Canada and Geneva, Switzerland: International Air Transport Association, Dangerous Goods Board, January, 1997. 173]**QC  REVIEWED**

The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article.  [IMDG; International Maritime Dangerous Goods Code; International Maritime Organization p.6158 (1988)]**QC REVIEWED**

Cleanup Methods:

Mercury removal from waste water can be accomplished by these processes:
BMS process; Chlorine is added to the waste water, oxidizing any mercury present to the ionic state. The BMS adsorbent (an activated carbon concentrated of sulfur cmpd on its surface) is used to collect ionic mercury. The spent adsorbent is then distilled to recover the mercury, leaving a carbon residue for reuse or disposal. TMR IMAC Process; Waste water is fed into a reactor, whereby a slight excess of chlorine is maintained, oxidizing any mercury present to ionic mercury. The liquid is then passed through the TMR IMAC ion-exchange resin where mercury ions are adsorbed. The mercury is then stripped from the spent resin with hydrochloric acid solution. /Mercury cmpds/  [Environment Canada; Tech Info for Problem Spills: Mercury (Draft) p.59 (1982)]**PEER REVIEWED**

Disposal Methods:

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.  **PEER REVIEWED**

Chemical Treatability of Mercury; Concentration Process: Biological treatment; Chemical Classification: Metals; Scale of Study: Respirometer study; Type of Wastewater Used: Synthetic wastewater; Influent concentration: 0-200 ppm; Results of Study: O2 uptake inhibited. /Mercury cmpd/  [Lamb JC III et al; J Water Pollut Control Fed 36 (10): 1263-84 (1964) as cited in USEPA; Management of Hazardous Waste Leachate, EPA Contract No. 68-03-2766 p. E-53 (1982)]**PEER REVIEWED**

Chemical Treatability of Mercury; Concentration Process: Biological treatment; Chemical Classification: Metals; Scale of Study: Laboratory scale; Type of Wastewater Used: Synthetic wastewater; Influent concentration: 5-10 ppm; Results of Study: 51-58% reduction. /Mercury cmpd/  [Ghosh MM, Zugger PD; J Water Pollut Control Fed 45 (3): 424-33 (1973) as cited in USEPA; Management of Hazardous Waste Leachate, EPA Contract No. 68-03-2766 p. E-53 (1982)]**PEER REVIEWED**

Chemical Treatability of Mercury; Concentration Process: Chemical Precipitation; Chemical Classification: Metals; Scale of Study: Pilot scale; Type of Wastewater Used: Domestic wastewater and pure compound; Influent concentration: 0.5 ppm at 4 gpm at pH= 7.0; Results of Study: High lime system- 70% reduction. /Mercury cmpd/  [Maruyama T et al; J Water Pollut Control Fed 47 (5): 962-75 (1975) as cited in USEPA; Management of Hazardous Waste Leachate, EPA Contract No. 68-03-2766 p. E-72 (1982)]**PEER REVIEWED**

Chemical Treatability of Mercury; Concentration Process: Chemical Precipitation; Chemical Classification: Metals; Scale of Study: Full scale, continuous flow; Type of Wastewater Used: Domestic wastewater; Results of Study: 9 ppb: 71% reduction with lime; 1.2 ppb: 25% reduction with lime. /Mercury cmpd/  [McCarty PL et al; Water Factory 21: Reclaimed Water, Volatile Organics, Virus, and Treatment Performance EPA-600/2-78-076 (1978) as cited in USEPA; Management of Hazardous Waste Leachate, EPA Contract No. 68-03-2766 p. E-72 (1982)]**PEER REVIEWED**

Chemical Treatability of Mercury; Concentration Process: Chemical Precipitation; Chemical Classification: Metals; Scale of Study: Pilot scale; Type of Wastewater Used: Synthetic wastewater; Results of Study: 500 ppb: 70% reduction with lime; 60 ppb: 94% reduction with alum; 50 ppb: 98% reduction with ferric chloride. /Mercury cmpd/  [Hannah SA et al; J Water Pollut Control Fed 49 (11): 2297-309 (1977) as cited in USEPA; Management of Hazardous Waste Leachate, EPA Contract No. 68-03-2766 p. E-72 (1982)]**PEER REVIEWED**

Chemical Treatability of Mercury; Concentration Process: Solvent extraction; Chemical Classification: Metals; Scale of Study: Literature review; Type of Wastewater Used: Unknown; Influent concentration: 2 ppm; Results of Study:  99% reduction with high molecular weight amines and quartenary salts. /Mercury cmpd/  [Dryden FE et al; Priority Pollutant Treatability Review EPA Contract No. 68-03-2579 (1978) as cited in USEPA; Management of Hazardous Waste Leachate, EPA Contract No. 68-03-2766 p. E-119 (1982)]**PEER REVIEWED**

Chemical Treatability of Mercury; Concentration Process: Activated carbon;
Chemical Classification: Metals; Scale of Study: Laboratory scale, Isotherm test; Type of Wastewater Used: Pure compound; Influent concentration: 100 ppm; Results of Study: Carbon dose; % removal: 0 ppm 0%; 500 ppm 99%; 1,000 ppm 99%; 5,000 ppm 99%; 10,000 ppm 99%. /Mercury cmpd/  [Pilie RJ et al; Methods to Treat, Control, and Monitor Spilled Hazardous Materials EPA-670/2-75-042 (1975) as cited in USEPA; Management of Hazardous Waste Leachate, EPA Contract No. 68-03-2766 p. E-165 (1982)]**PEER REVIEWED**

Chemical Treatability of Mercury; Concentration Process: Activated carbon;
Chemical Classification: Metals; Scale of Study: Unknown; Type of Wastewater Used: Unknown; Influent concentration: 10 ppb; Results of Study: 80% reduction  acheived with carbon dose of 100 mg/l. PAC plus chelating agent. /Mercury cmpd/  [Thiem L et al; J Amer Water Works Assoc 68 (8): 447-51 (1976) as cited in USEPA; Management of Hazardous Waste Leachate, EPA Contract No. 68-03-2766 p. E-165 (1982)]**PEER REVIEWED**

Chemical Treatability of Mercury; Concentration Process: Activated carbon;
Chemical Classification: Metals; Scale of Study: Literature review; Type of Wastewater Used: Unknown; Results of Study: 80% reduction by PAC and Alum coagulation. /Mercury cmpd/   [Dryden FE et al; Priority Pollutant Treatability Review EPA Contract No. 68-03-2579 (1978) as cited in USEPA; Management of Hazardous Waste Leachate, EPA Contract No. 68-03-2766 p. E-165 (1982)]**PEER REVIEWED**

Recycling: Dissolve in water after converting soluble nitrate if the cmpd is not water-soluble. Adjust the pH and precipitate mercury as mercury sulfide. Wash and dry the precipitate and return to the suppliers. Recommendable methods: Solidification & landfill. Not recommendable methods: Thermal destruction, discharge to sewer, evaporation.   [United Nations. Treatment and Disposal Methods for Waste Chemicals (IRPTC File). Data Profile Series No. 5. Geneva, Switzerland: United Nations Environmental Programme, Dec. 1985. 203]**QC REVIEWED**

Occupational Exposure Standards:

OSHA Standards:

Permissible Exposure Limit: Table Z-2 Acceptable Ceiling Concentration: 1 mg/10 cu m). /Mercury/  [29 CFR 1910.1000 (7/1/98)]**QC REVIEWED**

Vacated 1989 OSHA PEL Ceiling limit: 0.1 mg/cu m, skin designation, is still enforced in some states. /Non-alkyl mercury compounds, as Hg/  [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 367]**QC REVIEWED**

Threshold Limit Values:

8 hr Time Weighted Avg (TWA) 0.025 mg/cu m, skin /Mercury, inorganic forms including metallic mercury/  [American Conference of Governmental Industrial Hygienists. Threshold Limit Values (TLVs) for Chemical Substances and Physical Agents Biological Exposure Indices for 1998. Cincinnati, OH: ACGIH, 1998. 46]**QC REVIEWED**

BEI (Biological Exposure Index): Total inorganic mercury in urine (preshift): 35 ug/g creatinine. The determinant is usually present in a significant amt in biological specimens collected from subjects who have not been occupationally exposed. Such background levels are incl in the BEI value. /Mercury/  [American Conference of Governmental Industrial Hygienists. Threshold Limit Values (TLVs) for Chemical Substances and Physical Agents Biological Exposure Indices for 1998. Cincinnati, OH: ACGIH, 1998. 101]**QC REVIEWED**

BEI (Biological Exposure Index): Total inorganic mercury in blood (end of shift at end of workweek): 15 µg/l. The determinant is usually present in a significant amt in biological specimens collected from subjects who have not been occupationally exposed. Such background levels are incl in the BEI value./Mercury/  [American Conference of Governmental Industrial Hygienists. Threshold Limit Values (TLVs) for Chemical Substances and Physical Agents Biological Exposure Indices for 1998. Cincinnati, OH: ACGIH, 1998. 101]**QC REVIEWED**

Excursion Limit Recommendation: Excursions in worker exposure levels may exceed three times the TLV-TWA for no more than a total of 30 min during a work day, and under no circumstances should they exceed five times the TLV-TWA, provided that the TLV-TWA is not exceeded. /Mercury, inorganic forms including metallic mercury/  [American Conference of Governmental Industrial Hygienists. Threshold Limit Values (TLVs) for Chemical Substances and Physical Agents Biological Exposure Indices for 1998. Cincinnati, OH: ACGIH, 1998. 6]**QC REVIEWED**

A4. A4= Not Classifiable as a Human Carcinogen.  [American Conference of Governmental Industrial Hygienists. Threshold Limit Values (TLVs) for Chemical Substances and Physical Agents Biological Exposure Indices for 1998. Cincinnati, OH: ACGIH, 1998. 46]**QC REVIEWED**

NIOSH Recommendations:

Recommended Exposure Limit: 10 Hr Time-Weighted Avg: 0.05 mg/cu m, skin. /Mercury compounds [except (organo) alkyls] (as Hg), mercury vapor/  [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 192]**QC REVIEWED**

Recommended Exposure Limit: Ceiling Value: 0.1 mg/cu m. /Mercury compounds [except (organo) alkyls] (as Hg), other/  [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 192]**QC REVIEWED**

Immediately Dangerous to Life or Health:

10 mg/cu m (as Hg) /Mercury compounds [except (organo) alkyls] (as Hg)/
[NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 192]**QC REVIEWED**

Manufacturing/Use Information:

Major Uses:

PRESERVING WOOD AND ANATOMICAL SPECIMENS; EMBALMING; BROWNING & ETCHING STEEL & IRON; INTENSIFIER IN PHOTOGRAPHY; WHITE RESERVE IN FABRIC PRINTING; TANNING LEATHER; DEPOLARIZER FOR DRY BATTERIES; ELECTROPLATING ALUMINUM; MORDANT FOR RABBIT AND BEAVER FURS; MFR INK FOR MERCUROGRAPHY; REAGENT IN ANALYTICAL CHEMISTRY; MFR OF OTHER HG COMPOUNDS; FOR FREEING GOLD FROM LEAD; IN MAGIC PHOTOGRAMS; STAINING WOOD & VEGETABLE IVORY PINK; MEDICATION: TOPICAL ANTISEPTIC, DISINFECTANT; MEDICATIONS (VET): CAUSTIC, ANTISEPTIC, DISINFECTANT  [The Merck Index. 10th ed. Rahway, New Jersey: Merck Co., Inc., 1983. 839]**PEER REVIEWED**

SOLUTIONS USED AS DIP FOR BULBS & TUBERS, INCLUDING SEED POTATOES, ON GREENHOUSE BEDS FOR EARTHWORM CONTROL, & ON FIRE BLIGHT CANKERS OF QUINCE TREES. ALSO USED AS REPELLENT TO ANTS, ROACHES, & TERMITES.  [Farm Chemicals Handbook 87. Willoughby, Ohio: Meister Publishing Co., 1987.,p. C-70]**PEER REVIEWED**

CATALYST-EG, FOR POLYMERIZATION OF POLYVINYL CHLORIDE
[SRI]**PEER REVIEWED**

CHEM INT FOR ORGANIC CHEMS-EG, ETHYL MERCURIC CHLORIDE

[SRI]**PEER REVIEWED**

INSECTICIDE, FUNGICIDE
[SRI]**PEER REVIEWED**

AGENT IN REMOVAL OF MERCURY FROM ZINC BY-PRODUCT
GASES
[SRI]**PEER REVIEWED**

CHEM INT FOR INORGANIC CHEMS, EG, MERCURIC IODIDE &
OXIDE
[SRI]**PEER REVIEWED**

... Used in the past century as a disinfectant.
[WHO; Environ Health Criteria: Mercury p.29 (1976)]**PEER
REVIEWED**

MEDICATION
**QC REVIEWED**

MEDICATION (VET)
**QC REVIEWED**

Manufacturers:

Alfa Products, Morton Thiokol Inc, Hq, 152 Andover St, Danvers, MA 01923
(617) 777-1970
[McCurdy P.P. (ed.) Chemical Week Buyer's Guide 87. New York,
NY: McGraw Hill, In c. 1987. 377]**PEER REVIEWED**

Atomergic Chemetals Corp, Hq, 100 Fairchild Ave, Plainview, NY 11803 (516)
349-8800
[McCurdy P.P. (ed.) Chemical Week Buyer's Guide 87. New York,
NY: McGraw Hill, In c. 1987. 377]**PEER REVIEWED**

EM Chemicals, A Division of EM Ind, Inc, Hq, 5 Skyline Dr, Hawthorne, NY
10532 (914) 592-4660  [McCurdy P.P. (ed.) Chemical Week Buyer's Guide 87. New York, NY: McGraw Hill, In c. 1987. 377]**PEER REVIEWED**

Goldsmith, DF Chem & Metal Co, Hq, 909 Pitner Ave, Evanston, IL 60202 (312) 869-7800   [McCurdy P.P. (ed.) Chemical Week Buyer's Guide 87. New York, NY: McGraw Hill, In c. 1987. 377]**PEER REVIEWED**

Rhone-Poulenc Inc, Hq, PO Box 125, Black Horse Ln, Monmouth Junction, NJ  08852 (201) 297-0100  [McCurdy P.P. (ed.) Chemical Week Buyer's Guide 87. New York, NY: McGraw Hill, In c. 1987. 377]**PEER REVIEWED**

Noah Chemical Div Noah Ind Corp, Hq, 87 Gazza Blvd, Farmingdale, NY 11735 (516) 293-3336   [McCurdy P.P. (ed.) Chemical Week Buyer's Guide 87. New York, NY: McGraw Hill, In c. 1987. 377]**PEER REVIEWED**

Spectrum Chemical MFG Corp, Hq, 14422 S San Pedro St, Gardena, CA 90248 (213) 516-8000   [McCurdy P.P. (ed.) Chemical Week Buyer's Guide 87. New York, NY: McGraw Hill, In c. 1987. 377]**PEER REVIEWED**

Cerac, Inc, Hq, PO Box 1178 (407 N 13 St), Milwaukee, WI (414) 289-9800  [McCurdy P.P. (ed.) Chemical Week Buyer's Guide 87. New York, NY: McGraw Hill, In c. 1987. 377]**PEER REVIEWED**

Award Corp, Hq, 1011 Hudson Ave, PO Box 725, Ridgefield, NJ 07657 (201)
941-8020  [McCurdy P.P. (ed.) Chemical Week Buyer's Guide 87. New York, NY: McGraw Hill, In c. 1987. 377]**PEER REVIEWED**

AC Industries Inc, Sattva Chemical Co, Div, 26 Sixth St, Suite 603A, Stanford, CT 06905 (203) 348-8002, TLX 6819048  [Van, H. and C.A. Deyrufs (eds.). OPD Chemical Buyer's Directory 1987. 74th ed. New York, NY: Schnell Publishing Co., Inc., 1987. 252]**PEER REVIEWED**

AAKASH Chemicals & Dyestuffs, Inc, 1707 S First Ave, 306 Maywood, IL 60153 (312) 344-4855, TLXTWX 901-206-0440  [Van, H. and C.A. Deyrufs (eds.). OPD Chemical Buyer's Directory 1987. 74th ed. New York, NY: Schnell Publishing Co., Inc., 1987. 252]**PEER REVIEWED**

Anderson Laboratories, Inc, 5901 Fitzhugh, Fort Worth, TX 76119 (817) 457-4474  [OPD Chemical Buyer's Directory 1988 p. 413]**PEER REVIEWED**

GFS Chemicals Inc, PO Box 23214, Columbus, OH 43223 (614) 881-5501  [OPD Chemical Buyer's Directory 1988 p. 413]**PEER REVIEWED**

Thor Chemicals, Inc, Brook House, 37 North Ave, Norwalk, CT 06851 (203) 846-8613   [Kuney, J.H. and J.N. Nullican (eds.) Chemcyclopedia. Washington, DC: American Chemical Society, 1988. 196]**PEER REVIEWED**

Methods of Manufacturing:

REACTION OF MERCURY WITH EXCESS CHLORINE GAS FOLLOWED BY CONDENSATION; REACTION OF MERCURIC SULFATE & SODIUM CHLORIDE FOLLOWED BY PURIFICATION, IF NECESSARY   [SRI]**QC REVIEWED**

Formulations/Preparations:

BLENDED WITH CALOMEL AS TURF FUNGICIDE (AS IN CALO-CLOR, CALOCURE, FUNGCHEX).  [Farm Chemicals Handbook 87. Willoughby, Ohio: Meister Publishing Co., 1987.,p. C-70]**PEER REVIEWED**

... WETTABLE POWDER (MIXTURE WITH MERCUROUS CHLORIDE); DUST (MIXTURE WITH MERCUROUS CHLORIDE & MALACHITE GREEN).  [Worthing, C. R. (ed.). Pesticide Manual. 6th ed. Worcestershire, England: British Crop Protection Council, l979. 333]**PEER REVIEWED**

TECHNICAL; CRYSTALS; GRANULAR; POWDER; CP; NF  [Sax, N.I. and R.J. Lewis, Sr. (eds.). Hawley's Condensed Chemical Dictionary. 11th ed. New York: Van Nostrand Reinhold Co., 1987. 742]**PEER REVIEWED**

Grade or Purity: Reagent; Analytical  [U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.]**PEER REVIEWED**

U. S. Imports:

(1977) 5.06X10+5 G
[SRI]**PEER REVIEWED**

(1982) 8.18X10+6 G
[SRI]**PEER REVIEWED**

Laboratory Methods:

Clinical Laboratory Methods:

Urine samples analyzed for mercury by flameless atomic absorption. Range: 0.003 to above 0.3 mg/l. /Total mercury/  [U.S. Department of Health, Education Welfare, Public Health Service. Center for Disease Control, National Institute for Occupational Safety Health. NIOSH Manual ofAnalytical Methods. 2nd ed. Volumes 1-7. Washington, DC: U.S. Government Printing Office, 1977-present.,p. V1 165-1]**PEER REVIEWED**

Blood samples analyzed for mercury by flameless atomic absorption. Range:  0.005 to 4.5 ug/ml. /Total mercury/  [U.S. Department of Health, Education Welfare, Public Health Service. Center for Disease Control, National Institute for Occupational Safety Health. NIOSH Manual ofAnalytical Methods. 2nd ed. Volumes 1-7. Washington, DC: U.S. Government Printing Office, 1977-present.,p. V1 167-1]**PEER REVIEWED**

Radiochemical method for neutron activation analysis of mercury in biological materials was developed based on combination of 2 precipitation steps. Applications to analysis of hair & foodstuff samples are presented. Quantities as low as 0.001 µg were detected in hair samples. /Total mercury/  [Biso JN et al; Radiochem Radioanal Lett 58 (3): 175 (1983)]**PEER REVIEWED**

A dual-stage atomization atomic absorption spectroscopy technique was developed to allow speciation of 11 mercury containing compounds in aqueous soln & biological fluids. The temp control used was not adequate for mercury salts extremely volatile below 200 deg C. Absorption traces of whole blood, blood serum, sweat & urine spiked with mercuric chloride indicated that the technique is useful for their detection. /Total mercury/   [Robinson JW, Skelly EM; J Environ Sci Health, Part A A17 (3): 391-425 (1982)]**PEER REVIEWED**

NAA (Neutron Activation Analysis) was used to detect protein-bound mercury in fractions of human liver separated by gel-filtration chromatography. /Total mercury/  [Norheim G, Steinnes E; Anal Chem 47 (9): 1688-90 (1975) as cited in Nat'l Research Council Canada; Effects of Mercury in the Canadian Environment p.195 (1979) NRCC No. 16739]**PEER REVIEWED**

The analysis of mercury in stomach content, vomitus, urine, or homogenized kidney is determined when a clean, copper wire, which has been dropped in an acidified test solution, is covered with a silver gray deposit. This wire can then be removed from the solution and the mercury thereon characterized by suitable reactions which produce characteristic colors. Quantitation can be realized by oxidizing away the organic matter in the sample and determining the mercury remaining in the aqueous digest. The test is sensitive to 30 µg of mercury, and estimates may be made at 25 µg intervals up to about 100 µg. /Total mercury/  [Sunshine, Irving (ed.) Methodology for Analytical Toxicology. Cleveland: CRC Press, Inc., 1975. 224]**PEER REVIEWED**

The analysis of mercury in urine is done colorimetrically using dithizone as a chelating agent. The absorbance of mercury dithizone is determined with a spectrophotometer at a wavelength of 490 nm. Samples of vomitus or gastric lavage can also be analyzed by this method. /Total mercury/  [Sunshine, Irving (ed.) Methodology for Analytical Toxicology. Cleveland: CRC Press, Inc., 1975. 226]**PEER REVIEWED**

Mercury in urine is easily analyzed using a flameless atomic absorption spectrophotometer, with a special mercury detector assembly. A commercial unit (Model MAS-50 Mercury Analyzer System from Coleman Instruments Division) designed to facilitate the analysis of various samples for their mercury content is available. The unit contains a circulating pump, a mercury light source, an absorption cell, a photodetector, and a five and a half inch meter calibrated to read directly to read from 0 to 9 µg of mercury. A scale expansion unit provides reading to 28 µg, if required. Response time is less than one minute over the full concentration range. /Total mercury/  [Sunshine, Irving (ed.) Methodology for Analytical Toxicology. Cleveland: CRC Press, Inc., 1975. 225]**PEER REVIEWED**

Analytic Laboratory Methods:

FLAMELESS ATOMIC ABSORPTION METHOD FOR DETERMINATION OF HG IN WATERS, MINERAL, & SALT. /TOTAL MERCURY/  [Association of Official Analytical Chemists. Official Methods of Analysis. 10th ed. and supplements. Washington, DC: Association of Official Analytical Chemists, 1965. New editions through13th ed. plus supplements, 1982.,p. 12/469-33.C01]**PEER REVIEWED**

Flameless atomic absorption method for dissolved & suspended mercury applicable to detection of 0.2-10 µg Hg/l of drinking, surface, & saline waters & domestic & industrial wastes. /Total mercury/  [Association of Official Analytical Chemists. Official Methods of Analysis. 10th ed. and supplements. Washington, DC: Association of Official Analytical Chemists, 1965. New editions through13th ed. plus supplements, 1982.,p. 13/559 33.095]**PEER REVIEWED**

MERCURY WAS DETECTED IN WATER BY SELECTIVE ION EXCHANGE CHROMATOGRAPHY. /TOTAL MERCURY/   [CLECHET P, ESCHALIER G; ANAL CHIM ACTA 156: 295-9 (1984)]**PEER REVIEWED**

EPA (1979) Method 245.1 states that the analysis of mercury in water and wastewater can be performed by cold vapor techniques, manual or automated. This method is also listed as Standard Methods 303F, ASTM D3223-80, and USGS I-3462-84. /Total mercury/  [51 FR 23696 (6/30/86)]**PEER REVIEWED**

The analysis of mercury in fish can be performed with flameless atomic
absorption. A digestion of the sample with hydrochloric and nitric acid occurs in a special apparatus which is connected to the spectrophotometer. /Total mercury/   [Association of Official Analytical Chemists. Official Methods of Analysis. 10th ed. and supplements. Washington, DC: Association of Official Analytical Chemists, 1965. New editions through13th ed. plus supplements, 1982.,p. 14/469 25.134]**PEER REVIEWED**

The following method is applicable for the examination of ground and surface waters, domestic and industrial waste effluents, and treatment process samples. Method 245.1 for the determination of mercury employs manual cold vapor technique. The detection limit is 0.2 µg Hg/l. Standard deviation at 0.35 level was + or - 0.16. Percent recoveries at the three levels were 89, 87, and 87% respectively. /Total mercury/  [USEPA; Methods for Chemical Analysis of Water and Wastes p.245.1-1 (1983) EPA-600/4-79-020]**PEER REVIEWED**

The following method is applicable for the examination of ground and surface waters, domestic and industrial waste effluents, and treatment process samples. Method 245.5 for the determination of mercury employs manual cold vapor technique. The optimum concentration range is 0.2 to 5 ug/g. Recovery of mercury at these levels added as methyl mercuric chloride, was 97% and 94% respectively. /Total mercury/  [USEPA; Methods for Chemical Analysis of Water and Wastes p.245.5-1 (1983) EPA-600/4-79-020]**PEER REVIEWED**

The following method is applicable for the examination of ground and surface waters, domestic and industrial waste effluents, and treatment process samples. Method 245.2 for the determination of mercury employs automated cold vapor technique. The optimum concentration range is 0.2 to 20.0 µg Hg/l. Recoveries of the same ten organic mercurials in distilled water at 10 ug/l level, ranged from 92% to 125%. /Total mercury/    [USEPA; Methods for Chemical Analysis of Water and Wastes p.245.2-1 (1983) EPA-600/4-79-020]**PEER REVIEWED**

Mercury in Solid or Semisolid Waste (Manual Cold Vapor Technique). Method  7471, a cold vapor atomic absorption method is based on the absorption of radiation at 243.7 nm wavelengths by mercury vapor. Aqueous samples must be acidified to a pH of less than 2 with nitric acid. /Total mercury/  [USEPA; Test Methods for Evaluating Solid Waste. Physical/Chemical Methods 3rd Ed (1986) EPA 955-001-00000-1]**PEER REVIEWED**

Mercury in Liquid Waste (Manual Cold Vapor Technique) Method 7470 is a
cold vapor atomic absorption procedure approved for determining the concentration of mercury in mobility- procedure extracts, aqueous wastes, and ground waters. Based on the absorption of radiation at 253.7 nm by mercury vapor. Typical detection limit is 0.0002 mg/l. /Total mercury/  [USEPA; Test Methods for Evaluating Solid Waste. Physical/Chemical Methods 3rd Ed (1986) EPA 955-001-00000-1]**PEER REVIEWED**

DETECTION OF HG IN FISH MUSCLE SAMPLES CAN BE MADE BY AN ANODIC STRIPPING VOLTAMMETRIC TECHNIQUE (ASV) USING A AU DISK AS WORKING ELECTRODE. GOOD AGREEMENT IS ACHIEVED WHEN COMPARED WITH RESULTS OBTAINED FROM NEUTRON ACTIVATION ANALYSIS. /TOTAL MERCURY/   [GOLIMOWSKI J, GUSTAVASSON I; SCI TOTAL ENVIRON 31 (1): 89 (1983)]**PEER REVIEWED**

Sampling Procedures:

The sampling/preserving method of choice appears to be in pyrex glass containers using 5% HNO3 + 0.01% K2Cr2O7 preservative to prevent losses due to volatilization and adsorption on the glass. Samples treated in this manner have remained stable for more than 5 mo. /Mercury and mercury cmpd/  [Feldman C; Anal Chem 46 (1): 99-102 (1974) as cited in Nat'l Research Council Canada; Effects of Mercury in the Canadian Environment p.193 (1979) NRCC No. 16739]**PEER REVIEWED**

The collection of sample prior to analysis requires particular attention. The sample bottle whether borosilicate glass, polyethylene polypropylene or Teflon should be thoroughly washed with detergent and tap water; rinsed with 1:1 nitric acid, tap water, 1:1 hydrochloric acid, tap water and finally deionized distilled water in that order. /Metals/  [USEPA; Methods for Chemical Analysis of Water and Wastes p. METALS-4-5 (1983) EPA-600/4-79-020]**PEER REVIEWED**

A simple method to isolate both organic and inorganic mercury in natural waters is described. The mercuric compounds were quantitatively extracted with dithizone from six different kinds of water spiked at nanogram levels with radioactive mercuric chloride and methylmercuric chloride. After the separation from the inorganic mercury with sodium nitrite, methyl mercury was transferred to aqueous medium with sodium thiosulfate. The method provides a high recovery of organic as well as inorganic mercruy to an aqueous medium, prior to their determination by gold-trap cold vapor atomic absorption spectrophotometry. This method is easy, rapid, and inexpensive. furthermore, the limited number of analytical steps should reduce loss and contamination.  [Schintu M et al; Ecotoxicol Environ Safety 14 (3): 208-14 (1987)]**PEER REVIEWED**

Air samples containing mercury are taken with a glass tube, 2 cm x 4 mm ID, with unsealed ends containing one section of 30 mg of silvered Chromosorb P held in place with quartz wool plugs. A sampling pump is connected to this tube and accurately calibrated at a flow rate of 0.01 to 2.0 l/min for a total sample size of 0.5 to 7.0 liters. Elution is performed with a thermal desorption unit. This NIOSH approved technique has an overall precision of 0.061, over a studied range of 0.046 to 0.18 mg/cu m using 3.0 liter samples. /Mercury and mercury cmpd/  [U.S. Department of Health, Education Welfare, Public Health Service. Center for Disease Control, National Institute for Occupational Safety Health. NIOSH Manual ofAnalytical Methods. 2nd ed. Volumes 1-7. Washington, DC: U.S. Government Printing Office, 1977-present.,p. 6000-1-3]**PEER REVIEWED**

Special References:

Special Reports:

Nat'l Research Council Canada; Effects of Mercury in the Canadian Environment (1979) NRCC No. 16739

USEPA; Ambient Water Quality Criteria Doc: Mercury (1984) EPA 440/5-84-026

Environment Canada; Tech Info for Problem Spills: Mercury (Draft) (1982)

USEPA; Mercury Health Effects Update (1984) EPA 600/8-84-019F

Wren CD; Environ Res 40 (1): 210-44 (1986). A review of the available literature on mercury levels and toxicity in wild mammals (excluding marine mammals).

Miller DR, Buchanan JM; Atmospheric Transport of Mercury: Exposure Commitment and Uncertainty Calculations, MARC Report # 14 (1979)

WHO; Environ Health Criteria: Mercury (1976)

DHHS/NTP; Toxicology & Carcinogenesis Studies of Mercuric chloride in F344/N Rats and B6C3F1 Mice (Gavage Studies) Technical Report Series No. 408 (1993) NIH Publication No. 93-3139

DHHS/ATSDR; Toxicological Profile for Mercury (Update) (1994) ATSDR/TP-93/10

De Flora S, Bennicelli C, and Bagnesco, M. Genotoxicity of mercury compounds. A review. Mutat Res 375(1):57-79 (1994).

Ratcliffe HE, Swanson GM, and Fischer LJ. Human exposure to mercury: a
critical assessment of the adverse health effects. J Toxicol Enviro Health 49(3):221-70 (1996).

Brune D, et al. A review of normal concentrations of mercury in total blood. Sci Total Environ: 100 Spec No: 235-82 (1991).

Synonyms and Identifiers:

Related HSDB Records:

1208 [MERCURY]

829 [MERCURIC BROMIDE] (Analog)

Synonyms:

ABAVIT B
**PEER REVIEWED**

BICHLORIDE OF MERCURY
**PEER REVIEWED**

BICHLORURE DE MERCURE (FRENCH)
**PEER REVIEWED**

CALOCHLOR
**PEER REVIEWED**

Caswell No 544
**PEER REVIEWED**

CHLORID RTUTNATY (CZECH)
**PEER REVIEWED**

CHLORURE MERCURIQUE (FRENCH)
**PEER REVIEWED**

CORROSIVE MERCURY CHLORIDE
**PEER REVIEWED**

Corrosive sublimate
**PEER REVIEWED**

DICHLOROMERCURY
**PEER REVIEWED**

EPA pesticide chemical code 052001
**PEER REVIEWED**

MERCURIC BICHLORIDE
**PEER REVIEWED**

MERCURY BICHLORIDE
**PEER REVIEWED**

MERCURY CHLORIDE (HGCL2)
**PEER REVIEWED**

MERCURY DICHLORIDE
**PEER REVIEWED**

MERCURY(II) CHLORIDE
**PEER REVIEWED**

MERCURY PERCHLORIDE
**PEER REVIEWED**

NCI-C60173
**PEER REVIEWED**

PERCHLORIDE OF MERCURY
**PEER REVIEWED**

QUECKSILBER CHLORID (GERMAN)
**PEER REVIEWED**

SUBLIMAT (CZECH)
**PEER REVIEWED**

SUBLIMATE
**PEER REVIEWED**

SULEM
**PEER REVIEWED**

Formulations/Preparations:

BLENDED WITH CALOMEL AS TURF FUNGICIDE (AS IN CALO-CLOR, CALOCURE, FUNGCHEX).  [Farm Chemicals Handbook 87. Willoughby, Ohio: Meister Publishing Co., 1987.,p. C-70]**PEER REVIEWED**

... WETTABLE POWDER (MIXTURE WITH MERCUROUS CHLORIDE);
DUST (MIXTURE WITH MERCUROUS CHLORIDE & MALACHITE
GREEN).  [Worthing, C. R. (ed.). Pesticide Manual. 6th ed. Worcestershire, England: British Crop Protection Council, l979. 333]**PEER REVIEWED**

TECHNICAL; CRYSTALS; GRANULAR; POWDER; CP; NF  [Sax, N.I. and R.J. Lewis, Sr. (eds.). Hawley's Condensed Chemical Dictionary. 11th ed. New York: Van Nostrand Reinhold Co., 1987. 742]**PEER REVIEWED**

Grade or Purity: Reagent; Analytical  [U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.]**PEER REVIEWED**

Shipping Name/ Number DOT/UN/NA/IMO:

IMO 6.1; Mercuric chloride

UN 1624; Mercuric chloride

Standard Transportation Number:

49 232 45; Mercuric chloride

49 232 71; Mercuric chloride, solid (mercuric chloride and charcoal catalyst
spent)

EPA Hazardous Waste Number:

D009; A waste containing mercuric chloride may (or may not) be characterized a hazardous waste following testing by the Toxicant Extraction Procedure as prescribed by the Resource Conservation and Recovery Act (RCRA) regulations.

RTECS Number:

NIOSH/OV9100000

Administrative Information:

Hazardous Substances Databank Number: 33

Last Revision Date: 20000912

Last Review Date: Reviewed by SRP on 05/20/1988

Update History:

Field Update on 09/12/2000, 1 field added/edited/deleted.
Field Update on 03/28/2000, 1 field added/edited/deleted.
Complete Update on 02/08/2000, 1 field added/edited/deleted.
Complete Update on 02/02/2000, 1 field added/edited/deleted.
Complete Update on 01/11/2000, 6 fields added/edited/deleted.
Field Update on 11/18/1999, 1 field added/edited/deleted.
Field Update on 09/21/1999, 1 field added/edited/deleted.
Complete Update on 06/03/1999, 2 fields added/edited/deleted.
Field Update on 05/17/1999, 5 fields added/edited/deleted.
Complete Update on 04/02/1999, 1 field added/edited/deleted.
Complete Update on 01/20/1999, 1 field added/edited/deleted.
Complete Update on 11/23/1998, 1 field added/edited/deleted.
Complete Update on 11/12/1998, 1 field added/edited/deleted.
Complete Update on 06/02/1998, 1 field added/edited/deleted.
Complete Update on 02/25/1998, 1 field added/edited/deleted.
Complete Update on 01/15/1998, 3 fields added/edited/deleted.
Complete Update on 08/13/1997, 1 field added/edited/deleted.
Complete Update on 03/27/1997, 2 fields added/edited/deleted.
Complete Update on 03/11/1997, 3 fields added/edited/deleted.
Complete Update on 02/04/1997, 1 field added/edited/deleted.
Complete Update on 12/11/1996, 1 field added/edited/deleted.
Complete Update on 06/21/1996, 2 fields added/edited/deleted.
Complete Update on 06/07/1996, 1 field added/edited/deleted.
Complete Update on 01/18/1996, 1 field added/edited/deleted.
Complete Update on 08/21/1995, 1 field added/edited/deleted.
Complete Update on 05/26/1995, 1 field added/edited/deleted.
Complete Update on 05/17/1995, 1 field added/edited/deleted.
Complete Update on 02/13/1995, 1 field added/edited/deleted.
Complete Update on 01/26/1995, 1 field added/edited/deleted.
Complete Update on 12/19/1994, 1 field added/edited/deleted.
Complete Update on 11/18/1994, 1 field added/edited/deleted.
Complete Update on 10/12/1994, 2 fields added/edited/deleted.
Complete Update on 08/17/1994, 1 field added/edited/deleted.
Complete Update on 05/05/1994, 1 field added/edited/deleted.
Complete Update on 03/25/1994, 1 field added/edited/deleted.
Complete Update on 01/26/1994, 2 fields added/edited/deleted.
Complete Update on 09/15/1993, 1 field added/edited/deleted.
Complete Update on 08/07/1993, 1 field added/edited/deleted.
Complete Update on 04/27/1993, 1 field added/edited/deleted.
Field update on 12/10/1992, 1 field added/edited/deleted.
Complete Update on 12/08/1992, 1 field added/edited/deleted.
Complete Update on 12/03/1992, 1 field added/edited/deleted.
Complete Update on 11/25/1992, 1 field added/edited/deleted.
Complete Update on 11/05/1992, 1 field added/edited/deleted.
Complete Update on 09/18/1992, 1 field added/edited/deleted.
Complete Update on 09/03/1992, 1 field added/edited/deleted.
Complete Update on 04/27/1992, 1 field added/edited/deleted.
Complete Update on 01/23/1992, 1 field added/edited/deleted.
Complete Update on 09/26/1991, 1 field added/edited/deleted.
Complete Update on 01/07/1991, 6 fields added/edited/deleted.
Field Update on 05/14/1990, 1 field added/edited/deleted.
Complete Update on 04/17/1989, 91 fields added/edited/deleted.
Complete Update on 04/28/1986

Record Length: 215510

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