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.

1) SUCCIMER: INITIAL DOSE: 10 mg/kg or 350 mg/m(2) every 8 hours orally for 5 days, then increase interval to every 12 hours for next 14 days; repeat course(s) if indicated. A minimum of 2 weeks between courses is recommended, unless the patient's symptoms or blood concentrations indicate a need for more prompt treatment.
2) D-PENICILLAMINE: Use only if less toxic agents not available or not tolerated. USUAL DOSE: ADULT: 1 to 1.5 g/day given orally in 4 divided doses. CHILD: 15 to 30 mg/kg/day in 3 to 4 divided doses. Initially, a small dose may be given to minimize side effects and then increased gradually (eg, 25% of the desired dose in week 1, 50% in week 2, and the full dose by week 3). Avoid if penicillin allergic. Monitor for proteinuria, hematuria, rash, leukopenia, thrombocytopenia.
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: A chelating agent, available in Europe, for the treatment of arsenic, bismuth, lead, copper, and mercury toxicity. ADULT DOSE: IV: DAY 1: 250 mg every 3 to 4 hours (1500 to 2000 mg total); DAY 2: 250 mg every 4 to 6 hours (1000 to 1500 mg total); DAY 3: 250 mg every 6 to 8 hours (750 to 1000 mg total); DAY 4: 250 mg every 8 to 12 hours (500 to 750 mg total); SUBSEQUENT DAYS: 250 mg every 8 to 24 hours (250 to 750 mg total). ORAL: ACUTE TOXICITY: 1200 to 2400 mg/day in equally divided doses (100 to 200 mg 12 times daily); CHRONIC TOXICITY: 300 to 400 mg/day orally (in single doses of 100 to 200 mg). The dose may be increased in severe toxicity.

1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
2) Take precautions to avoid exposure of health care professionals and other individuals.
3) SYSTEMIC EFFECTS

1) Severe local reaction, including edema of the tongue and lips within five minutes after contact, occurred in a 23-month-old boy who ingested powdered mercuric chloride (Stack et al, 1983).

1) Circulatory collapse may occur (Sittig, 1991).

1) Mercury crosses the blood-brain barrier (Blum & Manzo, 1985).
2) In a case of acute mercuric chloride ingestion, the victim suffered a grand mal seizure on day 43 after poisoning. Postmortem examination revealed a large cerebellar abscess (Murphy et al, 1979).

1) A neurological syndrome resembling amyotrophic lateral sclerosis (Lou Gehrig disease) can occur even from acute exposure to mercury and its salts (Adams et al, 1983). The peripheral effects involve a dying-back axonopathy, followed by demyelinization. General loss of brain function may also occur (Folkl & Konig, 1983).
2) In mice receiving intraperitoneal mercuric chloride, mercury was shown to accumulate in spinal motor neuron cell bodies and to induce shrinkage of the motor neurons and spinal motor root (Pamphlett & Png, 1998).

1) Hematemesis along with nausea and bloody diarrhea may occur from ingestion or inhalation (Lewis, 1996; Budavari, 1996).

1) Edema of the upper GI tract may occur (Lewis, 1996).

1) Nephrotoxicity is characterized by an initial reduction in renal blood flow accompanied by an early and progressive decline in glomerular filtration rate. Urinary volume may increase early after poisoning, but declines as tubular dysfunction develops (Clayton & Clayton, 1994).

1) Renal failure usually develops within 24 hours and is associated with albuminuria, epithelial cell casts, hematuria, glycosuria, and aminoaciduria.
2) In one case of acute poisoning by mercuric chloride, the patient was oliguric for 12 days, followed by a diuretic phase, and renal function was recovered over the next 10 days (Chugh et al, 1978).
3) Excretion of low molecular weight proteins such as beta2-microglobulin was seen in a case of mercuric chloride ingestion. This implies impairment of tubular function (Pesce et al, 1977).
4) In one case involving ingestion of 0.9 gm mercuric chloride, anuria persisted for 14 days. One month following ingestion, BUN and creatinine were normal but beta-2-microglobulin in urine was increased; this returned to normal at 5 months post-ingestion (Yoshida et al, 1997).

1) Mercuric chloride is a severe skin irritant (Lewis, 1996).
2) Severe irritation was observed in the Standard Draize Test in the rabbit by skin and eye exposure (RTECS , 2000).

1) Rhabdomyolysis, as evidenced by elevated serum CPK, myoglobinuria, and pigment granular casts in the urine, was seen in a case of ingestion of approximately 2 grams of mercuric chloride (Chugh et al, 1978).

1) Lauwerys et al (1987) reported the case of a 3 month old with cataracts, anemia, and renal dysfunction resulting from mercury exposure during fetal life and the 1 month lactation period due to the mother's extensive use of soap containing inorganic mercury.
2) A series of 81 infant-mother pairs were evaluated for identification of a dose-response relationship between methylmercury concentrations in single strands of maternal hair and observed effects in the child following an incident where methyl-mercury-treated seed grain was used in daily preparation of home baked bread and then consumed by the pregnant woman. Children of women with higher exposures to methylmercury during gestation were at greater risk for the development of neurologic findings and developmental delays (Marsh et al, 1987). No mercury concentrations were done in the children.
3) ORGANIC mercury compounds are human teratogens. Serious or fatal neurological defects were seen in children born to mothers exposed to methyl mercury-contaminated fish in Minimata, Japan, to phenylmercuric acetate-contaminated pork consumed by Native Americans, and to methyl mercury-treated grain in Iraq (Baranski, 1981).

1) Pre- and post-implantation mortality, extra embryonic structures, fetotoxicity, cytological changes in the embryo, fetal death, changes in weaning/lactation index and growth statistics, and specific developmental abnormalities in the musculoskeletal, blood, lymphatic and central nervous systems have been observed in the rat (RTECS , 2000).
2) In the mouse, pre- and post-implantation mortality, fetotoxicity, cytological changes, fetal death, and specific developmental abnormalities including the musculoskeletal system and cytological changes have been observed. Toxic maternal effects on oogenesis and the uterus, cervix and vagina have been reported in the hamster (RTECS , 2000).
3) Abnormal embryos, in proportion to the dose of mercuric chloride given in a single IV injection on day 0 of gestation, were seen in mice (Kajiwara & Inouye, 1986).
4) Retarded fetal growth, chromosome aberrations, and abnormalities in the skeletal system were seen in fetal mice when the dams were exposed to mercuric chloride fumes at 0.02 to 2.1 mg/m(3) for 4H/D for 4 days, beginning at day 9 of gestation (HSDB , 2000).
5) Exposure of 6-8 somite cultured mouse embryos to mercuric chloride resulted in abnormal development of the cranial nerves and nerve nuclei (van Maele- Fabry et al, 1996).
6) Mercury is available to the fetus (Lauwerys, 1978; Tsuchiya et al, 1984; Lien et al, 1983; pp 505-509).
7) When injected at doses of 2 or 4 mg/kg during the last 9 days of pregnancy in rats, mercuric chloride did not produce fetal kidney damage (24). In mice, mercuric chloride was available to the fetus (Dencker, 1976). Fetal rats had lower levels than dams injected with radioactive mercuric chloride (Marszalek, 1981). Mercuric chloride may act indirectly to cause malformations in rats by interfering with uptake of nutrients (Holt & Webb, 1986).

1) All forms of mercury move freely across the placenta, and fetal concentrations are at least as high as those in the mother (HSDB , 2000).
2) Mercuric chloride affected the placental syncytiotrophoblast microvillous membrane in humans (HSDB , 2000).
3) CASE REPORT - Lien et al (1983) reported a case of acute mercury inhalation toxicity in a pregnant woman. Twenty-six days after the exposure the child was born without clinical abnormalities, but with serum blood levels comparable with the mother's.
4) Mercuric chloride induced aryl hydrocarbon hydroxylase, quinone reductase, and catechol-amine-O-methyltransferase in explants of human placenta in vitro. The placental explants accumulated mercury in proportion to its concentration in the culture medium (Boadi et al, 1992).

1) Abortions have been linked with a dose of 50 mcg/kg mercuric chloride given to women in the 10th week of pregnancy (RTECS , 2000). Increased spontaneous abortions, and menstrual dysfunction, have been reported in women exposed to mercury (Goncharuk, 1971; Panova & Ivanova, 1976; Goncharuk, 1977; Marinova, 1973).

1) Mercury is found in human breast milk (Mattison, 1983). Oral absorption of mercury is greater in infants than in adults (Barlow & Sullivan, 1982). A level of 4 mcg/L in breast milk is considered dangerous for infants (Mattison, 1983).
2) Gonzalez et al (1985) report a correlation between total mercury concentrations measured in the hair of nursing neonates and their mothers to be significant.

1) Mercuric chloride was transferred to the breast milk of guinea pigs and dogs after a single maternal injection of 1 mg Hg/kg. Mercury levels were somewhat lower in breast milk than in maternal plasma, but there was good correlation (r = 0.934) (Yoshida et al, 1994).

1) IARC Classification

1) LACK OF EFFECT

1) Normal whole blood mercury levels rarely exceed 1.5 mcg/dL in unexposed individuals. Normal levels are approximately 0.5 mcg/dL (Skerfving, 1972). Levels of 0.4 to 22 mcg/mL have been lethal (HSDB , 2000).
2) Most commonly used analytical methods do not distinguish between inorganic and organic mercury in the blood (Zenz, 1988). The use of blood mercury levels after acute exposure should be considered with the knowledge that a single seafood meal will elevate levels for 20 to 30 hours (Kershaw et al, 1980; Sherlock et al, 1984). Specific analysis of inorganic mercury in the blood did correlate with the level of exposure in workers exposed chronically (Yoshida, 1985).
3) In acute exposures, elevation of blood-mercury level to ranges of 25 to 50 mcg/dL (1246.2 to 2492.5 nmol/L) precede elevations in urinary excretion because of the body's capacity to store mercury (Cherian et al, 1978).
4) Blood mercury levels did not correlate with indicators of toxicity in chronically exposed workers (Rosenman et al, 1986).

1) Normal urine excretion rarely exceeds 15 mcg/L (74.7 nmol/L) in unexposed individuals. Normal levels are approximately 0.5 mcg/L, with the upper limit of normality being 20 mcg/L (Clayton & Clayton, 1981). Levels of 0.1 to 0.5 mg Hg/L (100 to 500 mcg/L) are considered significantly elevated (Sittig, 1985).
2) Spot urine levels are inconsistent due to diurnal variation. The interpretation of these levels is most accurate when samples are taken at the same time of day and corrected for creatinine. Because proteinuria and glycosuria cause specific gravity changes, correction using this method is less accurate than the creatinine method. Patients with kidney damage should be excluded (Calder et al, 1984).
3) Monitoring of spot urine mercury levels did correlate with occurrence of neuropsychological toxicity and motor nerve conduction velocity in 42 chronically exposed workers (Rosenman et al, 1986).
4) Urine 24-hour delta ALA levels are invariably elevated to the ranges of 3 to 10 mg/liter in chronic poisoning cases. Although urinary levels as high as 2000 mcg/L have been seen without symptoms, levels greater than 100 mcg/L may need careful behavioral and neurological evaluation (Adams et al, 1983).
5) Workers chronically exposed to mercury vapor exhibited preclinical renal toxicity at spot urine mercury levels of greater than 50 mcg/g creatinine (Roels et al, 1985).
6) Collection of a 24-hour urine sample, followed by challenge with D-penicillamine for 4 days, has been used to document mercury body burden (Ishihara et al, 1974).
7) Normal parameters of kidney function--plasma urea nitrogen, plasma creatinine, urine volume, and urinary protein--failed to identify renal toxicity which was evident upon microscopic examination of the kidneys of rats treated with increasing amounts of mercuric chloride over a period of 21 weeks (Hall et al, 1986).

1) POSTMORTEM
2) ELECTROPHYSIOLOGICAL TESTING
3) MONITORING
4) PULMONARY FUNCTION TESTS

1) Inorganic mercury salts may produce severe gastric erosion requiring gastrectomy (Sauder et al, 1988). but no cases of perforation have been described following spontaneous vomiting or gastric lavage. The role of gastric decontamination is unclear.
2) Abdominal x-ray may be useful in evaluating the need for gastric lavage.

1) CHARCOAL ADMINISTRATION
2) CHARCOAL DOSE

1) CAUTION: Progressive pulmonary distress, leading to fatal cardiopulmonary arrest, was attributed to aspiration of mercury during unprotected gastric lavage following a large overdose of mercuric chloride. Elective tracheal intubation should be considered prior to performance of gastric lavage (McLauchlan, 1991).
2) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
3) PRECAUTIONS:
4) LAVAGE FLUID:
5) COMPLICATIONS:
6) CONTRAINDICATIONS:

1) Chelation should be performed with one of the following drugs in severe poisonings.
2) All of the effective complexing agents administered to facilitate removal of mercury from the body contain sulfhydryl groups (Clarkson, 1990).

1) INDICATION
2) DOSE
3) EFFICACY
4) LABORATORY
5) ADVERSE EFFECTS

1) USUAL ADULT DOSE
2) USUAL PEDIATRIC DOSE
3) ADVERSE REACTIONS
4) DURATION OF THERAPY
5) CAUTIONS
6) PREGNANCY
7) IMPAIRED RENAL FUNCTION
8) EFFICACY

1) SUCCIMER/DMSA/EFFICACY
2) SUCCIMER/DOSE/ADMINISTRATION
3) MONITORING PARAMETERS
4) SUCCIMER/ADVERSE EFFECTS: The following adverse events have occurred in children and adults during clinical trials: nausea, vomiting and diarrhea; transient liver enzyme elevations; rash, pruritus; drowsiness and paresthesia. Events reported infrequently include: sore throat, rhinorrhea, mucosal vesicular eruption, thrombocytosis, eosinophilia, and mild to moderate neutropenia (Prod Info CHEMET(R) oral capsules, 2011).
5) ODOR: Succimer has a sulfurous odor that may be evident in the patient's breath or urine (Prod Info CHEMET(R) oral capsules, 2005).
6) HYPERTHERMIA: One adult developed acute severe hyperthermia associated with hypotension; rechallenge resulted in hyperthermia with shaking chills and hypertension (Marcus et al, 1991).
7) AVAILABLE FORMS: Succimer (Chemet (R)), 100 mg capsules (Prod Info CHEMET(R) oral capsules, 2011).
8) Succimer has a sulfurous odor that may be evident in the patients' breath and urine (Prod Info, 1991a).

1) DOSE
2) EFFICACY
3) AVAILABILITY

1) DMPS/INDICATIONS: Chelating agent for heavy metal toxicities associated with arsenic, bismuth, copper, lead and mercury (Blanusa et al, 2005).
2) DMPS/DOSING
3) SOURCES
4) EFFICACY
5) ADVERSE REACTIONS

1) N-acetyl cysteine has been shown to protect against mercury-induced nephrotoxicity in animal models of inorganic mercury poisoning (Girardi & Elias, 1991).

1) There is little information regarding the use of endoscopy, corticosteroids or surgery in the setting of concentrated mercuric chloride ingestion. The following information is derived from experience with other corrosives.
2) SUMMARY: Obtain consultation concerning endoscopy as soon as possible, and perform endoscopy within the first 24 hours when indicated.
3) INDICATIONS: Endoscopy should be performed in adults with a history of deliberate ingestion, adults with any signs or symptoms attributable to inadvertent ingestion, and in children with stridor, vomiting, or drooling after unintentional ingestion (Crain et al, 1984). Endoscopy should also be performed in children with dysphagia or refusal to swallow, significant oral burns, or abdominal pain after unintentional ingestion (Gaudreault et al, 1983; Nuutinen et al, 1994). Children and adults who are asymptomatic after accidental ingestion do not require endoscopy (Gupta et al, 2001; Lamireau et al, 2001; Gorman et al, 1992).
4) RISKS: Numerous large case series attest to the relative safety and utility of early endoscopy in the management of caustic ingestion.
5) The risk of perforation during endoscopy is minimized by (Zargar et al, 1991):
6) GRADING
7) FOLLOW UP - If burns are found, follow 10 to 20 days later with barium swallow or esophagram.
8) SCINTIGRAPHY - Scans utilizing radioisotope labelled sucralfate (technetium 99m) were performed in 22 patients with caustic ingestion and compared with endoscopy for the detection of esophageal burns. Two patients had minimal residual isotope activity on scanning but normal endoscopy and two patients had normal activity on scan but very mild erythema on endoscopy. Overall the radiolabeled sucralfate scan had a sensitivity of 100%, specificity of 81%, positive predictive value of 84% and negative predictive value of 100% for detecting clinically significant burns in this population (Millar et al, 2001). This may represent an alternative to endoscopy, particularly in young children, as no sedation is required for this procedure. Further study is required.
9) MINIPROBE ULTRASONOGRAPHY - was performed in 11 patients with corrosive ingestion . Findings were categorized as grade 0 (distinct muscular layers without thickening, grade I (distinct muscular layers with thickening), grade II (obscured muscular layers with indistinct margins) and grade III (muscular layers that could not be differentiated). Findings were further categorized as to whether the worst appearing image involved part of the circumference (type a) or the whole circumference (type b). Strictures did not develop in patients with grade 0 (5 patients) or grade I (4 patients) lesions. Transient stricture formation developed in the only patient with grade IIa lesions, and stricture requiring repeated dilatation developed in the only patient with grade IIIb lesions (Kamijo et al, 2004).

1) CORROSIVE INGESTION/SUMMARY: The use of corticosteroids for the treatment of caustic ingestion is controversial. Most animal studies have involved alkali-induced injury (Haller & Bachman, 1964; Saedi et al, 1973). Most human studies have been retrospective and generally involve more alkali than acid-induced injury and small numbers of patients with documented second or third degree mucosal injury.
2) FIRST DEGREE BURNS: These burns generally heal well and rarely result in stricture formation (Zargar et al, 1989; Howell et al, 1992). Corticosteroids are generally not beneficial in these patients (Howell et al, 1992).
3) SECOND DEGREE BURNS: Some authors recommend corticosteroid treatment to prevent stricture formation in patients with a second degree, deep-partial thickness burn (Howell et al, 1992). However, no well controlled human study has documented efficacy. Corticosteroids are generally not beneficial in patients with a second degree, superficial-partial thickness burn (Caravati, 2004; Howell et al, 1992).
4) THIRD DEGREE BURNS: Some authors have recommended steroids in this group as well (Howell et al, 1992). A high percentage of patients with third degree burns go on to develop strictures with or without corticosteroid therapy and the risk of infection and perforation may be increased by corticosteroid use. Most authors feel that the risk outweighs any potential benefit and routine use is not recommended (Boukthir et al, 2004; Oakes et al, 1982; Pelclova & Navratil, 2005).
5) CONTRAINDICATIONS: Include active gastrointestinal bleeding and evidence of gastric or esophageal perforation. Corticosteroids are thought to be ineffective if initiated more than 48 hours after a burn (Howell, 1987).
6) DOSE: Administer daily oral doses of 0.1 milligram/kilogram of dexamethasone or 1 to 2 milligrams/kilogram of prednisone. Continue therapy for a total of 3 weeks and then taper (Haller et al, 1971; Marshall, 1979). An alternative regimen in children is intravenous prednisolone 2 milligrams/kilogram/day followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks then tapered (Anderson et al, 1990).
7) ANTIBIOTICS: Animal studies suggest that the addition of antibiotics can prevent the infectious complications associated with corticosteroid use in the setting of caustic burns. Antibiotics are recommended if corticosteroids are used or if perforation or infection is suspected. Agents that cover anaerobes and oral flora such as penicillin, ampicillin, or clindamycin are appropriate (Rosenberg et al, 1953).
8) STUDIES

1) SUMMARY: Initially if severe esophageal burns are found a string may be placed in the stomach to facilitate later dilation. Insertion of a specialized nasogastric tube after confirmation of a circumferential burn may prevent strictures. Dilation is indicated after 2 to 4 weeks if strictures are confirmed. If dilation is unsuccessful colonic intraposition or gastric tube placement may be needed. Early laparotomy should be considered in patients with evidence of severe esophageal or gastric burns on endoscopy.
2) STRING - If a second degree or circumferential burn of the esophagus is found a string may be placed in the stomach to avoid false channel and to provide a guide for later dilation procedures (Gandhi et al, 1989).
3) STENT - The insertion of a specialized nasogastric tube or stent immediately after endoscopically proven deep circumferential burns is preferred by some surgeons to prevent stricture formation (Mills et al, 1978; (Wijburg et al, 1985; Coln & Chang, 1986).
4) DILATION - Dilation should be performed at 1 to 4 week intervals when stricture is present(Gundogdu et al, 1992). Repeated dilation may be required over many months to years in some patients. Successful dilation of gastric antral strictures has also been reported (Hogan & Polter, 1986; Treem et al, 1987).
5) COLONIC REPLACEMENT - Intraposition of colon may be necessary if dilation fails to provide an adequate sized esophagus (Chiene et al, 1974; Little et al, 1988; Huy & Celerier, 1988).
6) LAPAROTOMY/LAPAROSCOPY - Several authors advocate laparotomy or laparoscopy in patients with endoscopic evidence of severe esophageal or gastric burns to evaluate for the presence of transmural gastric or esophageal necrosis (Cattan et al, 2000; Estrera et al, 1986; Meredith et al, 1988; Wu & Lai, 1993).

1) Acute inhalation exposure to mercury compounds can produce local effects on the pulmonary system and can produce elevated urine mercury concentrations (Levin et al, 1988). Chelation may be required.
2) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
3) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
4) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.

1) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.

1) Observe for development of clinical signs and symptoms and follow treatment recommendations in DERMAL EXPOSURE where appropriate.

1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

1) In cases of significant exposure prehospital decontamination should occur outside the medical facility if possible since the wash may contaminate medical personnel and cause them to become poisoned.
2) Remove all contaminated clothing, seal into bags, and treat as hazardous waste. The person performing decontamination may be protected by wearing rubber gloves, disposable shoe covers, and a rubber apron.
3) All medical personnel should wear protective clothing, including respirators if significant amounts of dust are present, to prevent secondary contamination.

1) APPLICATION
2) DEBRIDEMENT
3) TREATMENT
4) TETANUS PROPHYLAXIS

1) Carefully observe patients with SKIN exposure for the development of any systemic signs or symptoms.

a) The total amount of mercury removed (1189 mg) was less than 0.1% of the estimated ingested dose (1425 mg) of mercuric chloride, and the patient died 28 days postingestion.

a) C : Possible human carcinogen.

a) 2B : The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.

1) LD50- (INTRAPERITONEAL)MOUSE:
2) LD50- (ORAL)MOUSE:
3) LD50- (SUBCUTANEOUS)MOUSE:
4) LD50- (INTRAPERITONEAL)RAT:
5) LD50- (ORAL)RAT:
6) LD50- (SKIN)RAT:
7) LD50- (SUBCUTANEOUS)RAT: