1) In one study, 8 of 38 brands of cosmetic cream purchased from Hong Kong and China had mercury contents exceeding 1 mcg/g, the recommended limit of the US Food and Drug Administration. In one case, the mercury content of an antifreckle cosmetic cream was 6.5% w/w (Chan et al, 2001).
2) A woman developed nephrotic syndrome secondary to membranous nephropathy after using a skin-whitening cream containing mercury (mercury concentration 1,762 ppm, almost 2000 times above the allowable limit) for 5 years (Soo et al, 2003).
3) A woman developed nephrotic syndrome after using a mercury-containing facial cream (mercury concentrations of 30,000 ppm, reference level, less than 1 ppm) once daily for the past 4 month (Tang et al, 2006).
4) Four patients developed minimal change disease after chronic exposure to mercury-containing skin lightening cream. Analysis of the facial creams revealed mercury content of 7420 to 30,000 ppm (Tang et al, 2013).

a) No baseline eye or visual acuity examination results were reported in the citation. The individual's vision was assumed to be normal before ingestion of the tablet.

a) Tachycardia has been reported with inorganic mercury intoxication (Erkek et al, 2010; Verma et al, 2010).

a) Hypertension has been reported with inorganic mercury intoxication (Koh et al, 2009; Erkek et al, 2010).
b) CASE REPORT: An 11-month-old boy presented with failure to thrive and developmental regression, irritability, painful, swollen, erythematous extremities, swollen fingers and toes, and hypertension (BP 140/100 mmHg). Laboratory results revealed a blood mercury concentration of 13.8 mcg/L (adult reference, less than 15.4 mcg/L), a urine mercury of 61.6 mcg/L (adult reference, less than 20 mcg/L), and urine mercury/creatinine ratio of 150 mcg/g creatinine (adult reference, less than 5 mcg/g creatinine). His pediatrician later reported a blood mercury concentration of 18 mcg/L and urine mercury/creatinine after a succimer challenge of 340 mcg/g. It was found that he was given a Chinese medicinal powder (mercury content, 1228 ppm) for 4 months (from 6 months to 10 months of age). Following treatment with one course of succimer 100 mg every 8 hours for 10 days and amlodipine 1.5 mg daily, his symptoms gradually resolved (Koh et al, 2009).

a) Tremor has also been reported after inorganic mercury exposure (Erkek et al, 2010; Cordeiro et al, 2003; Garza-Ocanas et al, 1997).
b) CASE REPORT: Tremor and loss of coordination developed 24 hours after mercuric chloride ingestion in one case (Giunta et al, 1983).
c) Tremor developed in 2 of 12 patients following the use of a facial cream containing mercuric chloride (5.9%) from 2 to 10 years. Despite chelation therapy with DMPS, tremor persisted in one of the patients (Garza-Ocanas et al, 1997).

a) Hyperreflexia and CNS excitation may occur (Winship, 1985). Nervousness, irritability, anxiety, insomnia and personality changes can occur (Erkek et al, 2010; CDC, 1996; Kang-Yum & Oransky, 1992).
b) CASE REPORT: A 5-year-old boy with recurrent oral ulceration developed motor and vocal tics after using a Chinese medicinal herb mouth spray (Watermelon Frost; mercury content, 878 ppm; 98% inorganic mercury and 2% methylmercury) up to 20 times a day for 4 weeks instead of the recommended dose of one spray twice daily. His blood mercury concentration was 83 nmol/L (normal for adults less than 50 nmol/L). Following the discontinuation of the mouth spray, his ticks resolved completely (Li et al, 2000).
c) CASE REPORT: Emotional instability, insomnia, coarse tremors of hands, seizures, and a stroke developed in a 10-year-old girl approximately 2 weeks after swimming in a creek containing inorganic mercury. She also developed gastrointestinal hemorrhage, renal dysfunction, elevated liver enzymes, hemolytic anemia, tachycardia, hypertension, and decreased left ventricular function. Following chelation therapy with succimer and BAL, she gradually recovered and was discharged after 67 days of hospitalization (Erkek et al, 2010).

a) CASE REPORT: Peripheral neuropathy has been reported following long term dermal application of a 5% to 10% ammoniated mercury ointment for the treatment of psoriasis. The neurological symptoms included burning sensations on the soles of the feet, loss of sensation in the extremities, aching of the legs and feet, weakness and difficulty in raising one foot. Clinical observations included diffuse muscle weakness with bilateral sensory loss within the median nerve distribution, decreased vibration, absent joint proprioception sense, muscle wasting, unilateral foot drop, and weight loss. Sensorimotor defects were chiefly limited to one leg. There were no apparent central nervous system effects. Blood mercury levels were 128 mcg/L. The comparable dose of elemental mercury which was administered in the ointment over the 40 year period of application was approximately 1.5 to 2 kg. The neuropathy gradually improved after treatment with D-penicillamine (Kern et al, 1991).
b) Paresthesias of the hands and feet, progressive weakness of the extremities, and/or delayed nerve conduction velocities were reported in 3 individuals who applied "Crema de Belleza-Manning" to the skin for 5 months to 10 years. Urine mercury levels confirmed mercury poisoning. Samples of Crema de Belleza contained 6% to 8% (by weight) mercury, as mercurous chloride or "calomel" (CDC, 1996).
c) A neurological syndrome resembling amyotrophic lateral sclerosis (Lou Gehrig disease) reportedly can occur 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).
d) CASE REPORT: A 45-year-old man, with a history of schizophrenia, presented with numbness of the distal limbs, generalized weakness and muscle wasting, which progressed to quadriparesis after drinking a traditional Chinese herb mixture (Huei Chen Shai) every day for 3 months. The mixture was prepared by mixing 200 gram of the herb with mercurial droplets from 10 broken thermometers in boiled water. Neurological examinations revealed diffuse muscle weakness and wasting in all limbs and sensory impairment including pin-prick, temperature, touch, vibration and position sensation in a glove and stocking pattern. In addition, tendon reflexes were absent in all limbs. Nerve conduction studies indicated a severe axonal polyneuropathy affecting both sensory and motor fibers. Sural nerve biopsy showed axonal degeneration with demyelination and a predominant loss of large myelinated fibers. The laboratory analysis of the herb drug showed mercury concentration of 10,000 ppm, lead 116 ppm, arsenic 18.9 ppm, and cadmium 0.97 ppm. Blood and urine mercury concentrations were not measured in acute stage until 2 months later; however, the concentrations of mercury in the scalp hair (14.2 mcg/g; reference, less than 5.5 mcg/g) and pubic hair (9.1 mcg/g; reference, less than 1.6 mcg/g) were high even 6 months later. Following supportive therapy, his muscle weakness improved slowly; however, at the 2-year follow-up examination, he still had sensory and motor impairment (Chu et al, 1998).

a) Exposure to mercury at an early age is suggested as a possible factor in the reported increased rates of autism in the United States and the United Kingdom.

a) CASE REPORT: A 45-year-old previously healthy male developed severe depression, along with loss of recent memory and insomnia following 6 months of daily contact with a metal containing mercury. Urine mercury level was 105 mg/L (normal 25 mg/L) at the time of exam (more than a year after ongoing exposure). Shortly after that level was obtained the patient was dismissed from work and had no healthcare benefits. Three years after exposure (mercury urine levels were normal) the patient continued to be depressed and improved with antidepressant therapy, but recent memory impairment and insomnia persisted. The authors suggested that neuropsychiatric symptoms associated with mercury poisoning may persist and are not limited to the immediate acute toxicity stage of exposure (Cordeiro et al, 2003).

a) CASE REPORT/ALTERNATIVE THERAPY: Irritability, weakness, anorexia, along with developmental regression occurred in previously healthy 20-month-old female twins who had been given a mercury containing "teething powder" (calomel) from India once or twice a week over a four month period. Both had reduced muscle strength and diminished reflexes. Before admission they had regressed developmentally and were no longer able to feed orally, sit or walk. Blood mercury levels were 176 and 209 mcmol/L (normally less than 18 mcmol/L), respectively. The toddlers were treated with succimer (DMSA) with only minor neurocognitive improvements; long term recovery was uncertain (Weinstein & Bernstein, 2003).
b) CASE REPORT: An 11-month-old boy presented with failure to thrive and developmental regression, irritability, painful, swollen, erythematous extremities, swollen fingers and toes, and hypertension. Laboratory results revealed a blood mercury concentration of 13.8 mcg/L (adult reference, less than 15.4 mcg/L), a urine mercury of 61.6 mcg/L (adult reference, less than 20 mcg/L), and urine mercury/creatinine ratio of 150 mcg/g creatinine (adult reference, less than 5 mcg/g creatinine). His pediatrician later reported a blood mercury concentration of 18 mcg/L and urine mercury/creatinine after a succimer challenge of 340 mcg/g. It was found that he was given a Chinese medicinal powder (mercury content, 1228 ppm) for 4 months (from 6 months to 10 months of age). Following treatment with one course of succimer 100 mg every 8 hours for 10 days and amlodipine 1.5 mg daily, his symptoms gradually resolved (Koh et al, 2009).

a) CASE REPORT: Generalized tonic-clonic seizures and a stroke developed in a 10-year-old girl approximately 2 weeks after swimming in a creek containing inorganic mercury. An EEG revealed diffused slowing and an epileptogenic focus in the right parieto-occipital regin. A brain computerized tomography (CT) revealed bilateral fronto-parietal infarction and leukoencephalomalasia involving subcortical white matter tracts from left nucleus lentiformis to vertex. She also experienced hearing difficulty and her audiogram revealed bilateral, mild sensorineural hearing loss. Her hospital course was complicated by gastrointestinal hemorrhage, renal dysfunction, elevated liver enzymes, hemolytic anemia, tachycardia, hypertension, and decreased left ventricular function. Following chelation therapy with succimer and BAL, she gradually recovered and was discharged after 67 days of hospitalization (Erkek et al, 2010).

a) CASE REPORT: Generalized tonic-clonic seizures and a stroke developed in a 10-year-old girl approximately 2 weeks after swimming in a creek containing inorganic mercury. An EEG revealed diffused slowing and an epileptogenic focus in the right parieto-occipital regin. A brain computerized tomography (CT) revealed bilateral fronto-parietal infarction and leukoencephalomalasia involving subcortical white matter tracts from left nucleus lentiformis to vertex. She also experienced hearing difficulty and her audiogram revealed bilateral, mild sensorineural hearing loss. Her hospital course was complicated by gastrointestinal hemorrhage, renal dysfunction, elevated liver enzymes, hemolytic anemia, tachycardia, hypertension, and decreased left ventricular function. Following chelation therapy with succimer and BAL, she gradually recovered and was discharged after 67 days of hospitalization (Erkek et al, 2010).

a) While inorganic mercury does not easily cross the blood brain barrier, long-term exposure may lead to conversion to organic mercury compounds which deposit into the CNS. Neurologic symptoms include tremor, neurasthenia, and withdrawn behavior (erethism). However, inorganic mercury exposure is unlikely to cause significant neurotoxicity.

a) CASE REPORT: Elevated liver enzymes and abnormal renal function developed in a 10-year-old girl approximately 2 weeks after swimming in a creek containing inorganic mercury. An abdominal ultrasound revealed diffuse hyperechogenic hepatomegaly with ascites and renal enlargement. She also developed gastrointestinal hemorrhage, emotional instability, sleeplessness, coarse tremors of hands, tachycardia, hypertension, hemolytic anemia, seizures, stroke, and decreased left ventricular function. Following chelation therapy with succimer and BAL, she gradually recovered and was discharged after 67 days of hospitalization (Erkek et al, 2010).

a) Clinical findings have included albuminuria, beta2 microglobulinuria, epithelial cell casts, hematuria, glycosuria, oliguria or anuria, and aminoaciduria (US DHHS, 1994). The onset is often within 24 hours of ingestion, but may be delayed.

a) Non-oliguric renal failure developed in a 2-year-old boy 3 days after ingesting an unknown quantity of mercury chloride powder. Following supportive care, including IV BAL, he recovered gradually and was discharged after 2 weeks of hospitalization. His renal function was normal 2 months postingestion (Verma et al, 2010).
b) Transient anuria and renal failure developed after intravenous injection of mercuric chloride (Will et al, 1991).
c) In one case of acute mercuric chloride poisoning, the patient was oliguric for 12 days, followed by a diuretic phase, with recovery of renal function over the next 10 days (Chugh et al, 1978).
d) Numerous cases of acute renal failure and other nephrotoxic effects of inorganic mercury compounds are reviewed by the US DHHS (1994) (US DHHS, 1994).
e) A 39-year-old man developed two consecutive episodes of acute renal failure after ingesting 400 mg of mercuric salt, corrosive sublimate, in a suicide attempt. Initially, he presented with nausea, hematemesis, severe abdominal pain, and rash. He developed progressive oliguria and renal insufficiency within the first 2 days of ingestion. Following treatment with BAL and 10 hemodialysis sessions, he was discharged 22 days after admission with normal renal function. Approximately 7 days later, he presented with a temperature of 38 degrees C, a generalized morbilliform rash, pruritus and progressive oliguria. He underwent hemodialysis 6 days after admission. Following renal biopsy on day 35, histological findings confirmed the diagnosis of allergic granulomatous interstitial nephritis. Following treatment with prednisone, a marked improvement in his symptoms and renal function was observed. He was discharged on day 48 (Franco et al, 1997).

a) Membranous glomerulonephropathy with nephrotic syndrome has been associated with the chronic use of mercury-containing skin creams (Chakera et al, 2011; Soo et al, 2003; Oliveira et al, 1987; Jeddeloh et al, 1985).
b) Nephrotic syndrome of minimal change disease following exposure to mercury-containing skin-lightening cream has been reported (Zhang et al, 2014; Tang et al, 2013; Tang et al, 2006).
c) CASE SERIES: Four patients developed minimal change disease after chronic exposure (2 to 6 months) to mercury-containing skin lightening cream. All patients presented with nephrotic syndrome and heavy proteinuria. Laboratory analysis revealed blood and urine mercury concentrations of 26 to 129 nmol/L and 316 to 2521 nmol/day, respectively. Analysis of the facial creams revealed mercury content of 7420 to 30,000 ppm. Following chelation therapy with D-penicillamine, all patients recovered gradually, with blood mercury concentration normalizing 1 to 7 months later and urine mercury concentration normalizing 9 to 16 months later (Tang et al, 2013).
d) CASE REPORT: A 34-year-old woman developed nephrotic syndrome secondary to membranous nephropathy (serum creatinine, 0.63 mg/dL (56 mcmol/L), serum albumin 16 g/L, proteinuria 4.9 g/day) after using a skin-whitening cream containing mercury for 5 years. Mercury concentration in a cream sample was 1762 ppm, almost 2000 times above the allowable limit. Renal biopsy revealed minor glomerular abnormality under light microscopy, granular deposition of IgG and C3 along capillary wall under immunofluorescence examination, and small scattered subepithelial electron deposits under electron microscopy. Her blood mercury and 24-hour urinary mercury excretion concentrations were 163 nmol/L (normal, less than 50 nmol/L) and 754.6 nmol/d (normal, below 10 nmol/d), respectively. Following supportive therapy, her symptoms resolved gradually (Soo et al, 2003).
e) CASE REPORT: A 34-year-old woman developed nephrotic syndrome after using a mercury-containing facial cream (mercury concentrations of 30,000 ppm, reference level, less than 1 ppm) once daily for the past 4 month. Laboratory results revealed serum creatinine of 52 mcmol/L (creatinine clearance of 114 mL/min), urea 3.9 mmol/L, 24-hour urine protein excretion of 8.35 g, blood mercury level of 124 nmol/L (reference level, less than 50 nmol/L), and urine mercury of 287 nmol/L (reference level, less than 50 nmol/L). The pathological diagnosis of minimal change disease was confirmed by light microscopy, immunofluorescence, and electron microscopy findings (Tang et al, 2006).
f) CASE REPORTS: Two patients developed membranous glomerulonephritis (MGN) after using mercury-containing facial creams. The first patient, a 44-year-old woman, presented with peripheral edema, an albumin of 32 g/L, a plasma creatinine of 95 mcmol/L, and a urine protein-creatinine ratio of 1419 mg/mmol (normal, less than 30). Elevated serum (150 nmol/L; normal less than 30) and urine (16.5 nmol/mmol; normal, less than 5.5) mercury concentrations were observed. Although her blood and urine mercury concentrations decreased after the discontinuation of the cream, her renal function deteriorated and remained impaired (serum creatinine of 136 mcmol/L). The second patient, a 26-year-old woman, presented with peripheral and periorbital edema and heavy proteinuria. Laboratory results revealed albumin 28 g/L, proteinuria of greater than 9 g/day, and normal renal function (creatinine 62 mcmol/L). A renal biopsy showed MGN. Blood mercury concentration was 233 nmol/L (normal less than 30) and urinary mercury-creatinine ratio was 77.5 nmol/mmol (normal, less than 5.5). Although her nephrotic syndrome improved after the discontinuation of the cream, she continued to have proteinuria (urinary protein: creatinine ratio 238 mg/mmol). Although an antibody with specificity for the M-type phospholipase A2 receptor (PLA2R) has been identified in greater than 70% of patients with idiopathic MGN, these antibodies were not present in these patients (Chakera et al, 2011).

a) CASE REPORT: Approximately a week after swimming in a creek containing inorganic mercury, hemolytic anemia occurred in a 10-year-old girl who also developed gastrointestinal hemorrhage, renal dysfunction, elevated liver enzymes, tachycardia, hypertension, seizures, stroke, and decreased left ventricular function. Following chelation therapy with succimer and BAL, she gradually recovered and was discharged after 67 days of hospitalization (Erkek et al, 2010).

a) Chronic exposure to mercurial powders has led to acrodynia (Pink Disease), characterized by a morbilliform rash and erythematous edematous hyperkeratotic induration of the palms and soles associated with excessive sweating, tachycardia, photophobia, paraesthesias, and decreased reflexes (Sue, 1994).
b) Symptoms of acrodynia, including fever, redness of the palms of the hands and soles of the feet, itching, dermal swelling and desquamation, rashes and limb pain, have been reported in children who received mercurous chloride for constipation, worms or teething discomfort. Patch tests were negative in several of the children (US DHHS, 1994).
c) CASE REPORT/ALTERNATIVE THERAPY: Acrodynia (papular rash along with swollen, red, desquamated and painful hands and feet) along with recent developmental regression occurred in healthy 20-month-old female twins who had been given a mercury containing "teething powder" (calomel) from India once or twice a week over a four month period. Blood mercury levels were 176 and 209 mcmol/L (normally less than 18 mcmol/L), respectively. The toddlers were treated with succimer (DMSA) with only minor neurocognitive improvements; long term recovery was uncertain (Weinstein & Bernstein, 2003).
d) CASE REPORT: An 11-month-old boy presented with failure to thrive and developmental regression, irritability, painful, swollen, erythematous extremities, swollen fingers and toes, and hypertension (BP 140/100 mmHg). Laboratory results revealed a blood mercury concentration of 13.8 mcg/L (adult reference, less than 15.4 mcg/L), a urine mercury of 61.6 mcg/L (adult reference, less than 20 mcg/L), and urine mercury/creatinine ratio of 150 mcg/g creatinine (adult reference, less than 5 mcg/g creatinine). His pediatrician later reported a blood mercury concentration of 18 mcg/L and urine mercury/creatinine after a succimer challenge of 340 mcg/g. It was found that he was given a Chinese medicinal powder (mercury content, 1228 ppm) for 4 months (from 6 months to 10 months of age). Following treatment with one course of succimer 100 mg every 8 hours for 10 days and amlodipine 1.5 mg daily, his symptoms gradually resolved (Koh et al, 2009).

a) Exanthem developed in 2 of 12 patients following the use of a facial cream containing mercuric chloride (5.9%) from 2 to 10 years. Following chelation therapy with DMPS, exanthem resolved completely (Garza-Ocanas et al, 1997).
b) Rash developed in a 39-year-old man after ingesting 400 mg of mercuric salt, corrosive sublimate (Franco et al, 1997).
c) CASE REPORT: Evanescent erythematous rash on extremities, dryness, and peeling of skin developed in a 10-year-old girl approximately 2 weeks after swimming in a creek containing inorganic mercury. Her hospital course was complicated by gastrointestinal hemorrhage, abnormal renal function, hemolytic anemia, elevated liver enzymes, emotional instability, sleeplessness, coarse tremors of hands, tachycardia, hypertension, seizures, stroke, and decreased left ventricular function. Following chelation therapy with succimer and BAL, she gradually recovered and was discharged after 67 days of hospitalization (Erkek et al, 2010).

a) Severe irritation was observed in the Standard Draize Test in the rabbit by skin and eye exposure to mercuric chloride (RTECS, 1990).

a) Muscular weakness occurs with chronic exposure to inorganic mercurials (HSDB, 1990).
b) CASE REPORT/ALTERNATIVE THERAPY: Weakness, anorexia and symptoms of acrodynia, along with developmental regression occurred in healthy 20-month-old female twins who had been given a mercury containing "teething powder" (calomel) from India once or twice a week over a four month period. Both had reduced muscle strength and diminished reflexes. Before admission they had regressed developmentally and were no longer able to feed orally, sit or walk. Blood mercury levels were 176 and 209 mcmol/L (normally less than 18 mcmol/L), respectively. The toddlers were treated with succimer (DMSA) with only minor neurocognitive improvements; long term recovery was uncertain (Weinstein & Bernstein, 2003).

a) Increased release of iodine, decreased serum levels of thyroid hormones, increased thyroid weight and increased or decreased iodine uptake have been reported following administration of mercuric chloride or mercuric sulfide by gavage to rats or mice over a period of 6 days to 40 days (US DHHS, 1994).
b) Increased thyroid function, as measured by an increase in (131)I-release rate, was seen in rats given 3 mg of mercuric chloride orally for 6 days. A 40-day regimen of 2.5 mg increased (125)I uptake. Irreversible decrease in (131)I release rate was seen after administration of 100 ppm in the diet for 3 months (Goldman & Blackburn, 1979).

a) Administration of mercuric chloride in drinking water in concentrations of 0, 9, 18 or 36 mg/kg/day for 60 to 180 days resulted in increased adrenal and plasma cortisone levels in rats (US DHHS, 1994).

a) No apparent effects on the serum concentrations of IgA, IgG, IgM, and IgE were detected as a result of low level exposure to mercury among workers in the chloralkali industry, fluorescent light bulb industry and dentistry (Langworth et al, 1992).
b) No apparent differences in serum immunoglobulin levels among individuals who exhibited skin hypersensitivity to inorganic mercury as compared to controls were detected.

a) Expression of the low affinity IgE and transferrin receptors was decreased, but expression of CD69 was unaffected. Exposure to the mercury compounds for 24 hours significantly decreased B lymphocyte viability. Increased intracellular levels of calcium were detected. B cells were refractory to immunological effects with exposure to mercury beyond 48 hours.

a) Evidence of immunosuppression, immunostimulation, and the development of antibodies to renal antigens has been reported in animals. There are strain related differences in some of these immunotoxic responses, with some strains being sensitive to the effects of mercury, and other strains being resistant (Ellingsen et al, 1993) 1994; (Kosuda et al, 1993; Kosuda & Hosseinzadeh, 1994; Hultman & Johansson, 1991; US DHHS, 1994).
b) PMN LEUKOCYTES: In vitro models have demonstrated that inorganic and organic mercury may hamper the bacteriotoxic capacity of polymorphonuclear leukocytes (Obel et al, 1993).

a) Mercury is available to the fetus (Lauwerys, 1978; Tsuchiya et al, 1984; Lien et al, 1983; pp 505-509).
b) 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).
c) 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).
d) 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).
e) 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).

a) Mercuric iodide has caused post-implantation mortality, fetal death, weakened the placenta, and been fetotoxic, but did not cause birth defects in rats exposed by inhalation (RTECS; (Barilyak, 1984; Govorunova, 1981; Ermachenko, 1982; Shtenberg & Safronova, 1979).

a) Listed as: Mercury and inorganic mercury compounds
b) Carcinogen Rating: 3

a) CONCLUSIONS (Mercuric chloride) - 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.
b) 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.
c) 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.
d) Reference: US DHHS, 1993

a) Mercury at 5 ppm in the drinking water was not carcinogenic in mice (Schroeder & Mitchener, 1975), and mercury is generally not regarded as a carcinogen.

a) Blood analysis is useful only for detecting acute exposure immediately after it has occurred, since blood mercury levels rapidly decline after exposure. Whole blood mercury concentrations are most useful in cases of acute high dose exposure.
b) Plasma mercury concentrations may be more useful for monitoring low level exposure (US DHHS, 1992).

a) 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).

a) Monitoring of spot urine mercury levels did correlate with occurrence of neuropsychological toxicity and motor nerve conduction velocity in 42 chronically exposed workers (Rosenmann et al, 1986).

a) TREMOR ANALYSIS: Clinically apparent tremors often occur with chronic mercury poisoning (Knight, 1988). One study described methods of measuring tremor frequency and other tremor characteristics which may enable identification of subtle neurological effects before clinical signs of poisoning are evident (Chapman et al, 1990).

a) Nerve conduction velocity studies have been used to evaluate mercury toxicity in workers chronically exposed to inorganic mercury (Singer et al, 1987).

a) Psychometric tests have been used to detect early toxic effects of organic and inorganic mercury exposure. Application of these test batteries in mercury exposures are described (Yeates & Mortensen, 1994; Liang et al, 1993; Langworth et al, 1992; Soleo et al, 1990).

a) Longitudinal analysis of sections of hair from a patient who ingested mercuric chloride revealed a peak in inorganic mercury which corresponded with the time of ingestion (Suzuki et al, 1992).

a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.

a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
b) ADVERSE EFFECTS/CONTRAINDICATIONS

a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.

a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.

a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.

a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).

a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.

a) WHOLE BOWEL IRRIGATION/INDICATIONS: Whole bowel irrigation with a polyethylene glycol balanced electrolyte solution appears to be a safe means of gastrointestinal decontamination. It is particularly useful when sustained release or enteric coated formulations, substances not adsorbed by activated charcoal, or substances known to form concretions or bezoars are involved in the overdose.
b) CONTRAINDICATIONS: This procedure should not be used in patients who are currently or are at risk for rapidly becoming obtunded, comatose, or seizing until the airway is secured by endotracheal intubation. Whole bowel irrigation should not be used in patients with bowel obstruction, bowel perforation, megacolon, ileus, uncontrolled vomiting, significant gastrointestinal bleeding, hemodynamic instability or inability to protect the airway (Tenenbein et al, 1987).
c) ADMINISTRATION: Polyethylene glycol balanced electrolyte solution (e.g. Colyte(R), Golytely(R)) is taken orally or by nasogastric tube. The patient should be seated and/or the head of the bed elevated to at least a 45 degree angle (Tenenbein et al, 1987). Optimum dose not established. ADULT: 2 liters initially followed by 1.5 to 2 liters per hour. CHILDREN 6 to 12 years: 1000 milliliters/hour. CHILDREN 9 months to 6 years: 500 milliliters/hour. Continue until rectal effluent is clear and there is no radiographic evidence of toxin in the gastrointestinal tract.
d) ADVERSE EFFECTS: Include nausea, vomiting, abdominal cramping, and bloating. Fluid and electrolyte status should be monitored, although severe fluid and electrolyte abnormalities have not been reported, minor electrolyte abnormalities may develop. Prolonged periods of irrigation may produce a mild metabolic acidosis. Patients with compromised airway protection are at risk for aspiration.

a) BAL has been shown to increase mercury excretion in the urine, bile and feces, decrease the body burden of mercury, and decrease mortality in animal models of inorganic mercury poisoning (Neilsen & Andersen, 1991; Kojima et al, 1989; Aaseth et al, 1982; Yonaga & Morita, 1981; Magos, 1968). BAL increased distribution of mercury to the brain in some animal models of inorganic mercury poisoning (Neilsen & Andersen, 1991; Aaseth et al, 1982).
b) BAL therapy in patients with acute inorganic mercury ingestion has been associated with clinical improvement or the failure to develop severe toxicity (Ly et al, 2002; Singer et al, 1994; Pesce et al, 1977; Longcope et al, 1946; Stack et al, 1983; Suzuki et al, 1992; Wang et al, 1992). Changes in mercury excretion were not evaluated in these cases.
c) CASE REPORT: A 10-year-old girl with severe inorganic mercury poisoning (gastrointestinal hemorrhage, renal, hepatic, neurologic, hematologic, and cardiovascular dysfunctions) and a blood mercury concentration of 5,380 mcg/L and urine mercury of 91 mcg/L, was treated with succimer 17 days after swimming in a creek containing inorganic mercury. A week after succimer was discontinued, her blood mercury level increased again and urine mercury level decreased. At this time, she was treated with BAL 3 mg/kg/dose IM every 6 hours for the first 2 days, 3 mg/kg/dose IM every 4 hours for the next 2 days, and then 3 mg/kg/dose IM every 12 hours for 7 days. Her symptoms improved gradually, and she was discharged after 67 days of hospitalization (Erkek et al, 2010).
d) HEMODIALYSIS: The BAL mercury complex is cleared by hemodialysis (Guinta et al, 1983).
e) PERITONEAL DIALYSIS: BAL therapy and peritoneal dialysis was associated with mercury clearance rates of 0.57 to 2.38 mL/minute in an adult who developed acute renal failure after ingesting mercury bichloride (Lowenthal et al, 1974).

a) Monitor urine mercury excretion during chelation therapy to assess the effects of therapy.

a) PEDIATRIC: Initial dose is 10 mg/kg or 350 mg/m(2) orally every 8 hours for 5 days (Prod Info CHEMET(R) oral capsules, 2011).
b) ADULT: Succimer is not FDA approved for use in adults, however it has been shown to be safe and effective when used to treat adults with poisoning from a variety of heavy metals (Fournier et al, 1988). Initial dose is 10 mg/kg or 350 mg/m(2) orally every 8 hours for 5 days (Prod Info CHEMET(R) oral capsules, 2011).

a) The manufacturer recommends monitoring liver enzymes and complete blood count with differential and platelet count prior to the start of therapy and at least weekly during therapy (Prod Info CHEMET(R) oral capsules, 2011).
b) Succimer therapy did not worsen preexisting borderline abnormal liver enzyme levels in a prospective evaluation of 15 children with lead poisoning (Kuntzelman & Angle, 1992).

a) 1 to 1.5 g/day given orally in 4 divided doses (Nelson, 2011).

a) 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) (Caravati, 2004; Prod Info DEPEN(R) titratable oral tablets, 2009).

a) COMMON SIDE EFFECTS/CHRONIC DOSING: Fever, anorexia, nausea, vomiting, diarrhea, abdominal pain, proteinuria, and myalgia(Prod Info DEPEN(R) titratable oral tablets, 2009).

a) Administer d-penicillamine for 3 to 10 days with daily monitoring of urinary excretion of mercury. If urine mercury falls rapidly, body burden is probably small. Wait 10 days and repeat after a baseline collection to determine if there is a rise on re-chelation therapy indicating further body burden.
b) Repeated courses of D-penicillamine may be required. Regular follow-up of blood and urine mercury levels will establish need for treatment.

a) Patients allergic to penicillin products may have cross-sensitivity to penicillamine (Prod Info DEPEN(R) titratable oral tablets, 2009).
b) Monitor for proteinuria and hematuria; heavy metals may also cause renal toxicity (Prod Info DEPEN(R) titratable oral tablets, 2009).
c) Monitor CBC with differential, platelet count, and hepatic enzymes (Prod Info DEPEN(R) titratable oral tablets, 2009).
d) CROSS-REACTIVITY: The use of penicillamine in a patient with penicillin allergy is controversial.

a) Penicillamine is considered FDA pregnancy category D(Prod Info CUPRIMINE(R) oral capsules, 2004); it should be avoided if possible in pregnant patients.
b) Use of penicillamine throughout pregnancy has been associated with connective tissue abnormalities, hydrocephalus, cerebral palsy, cardiac and great vessel anomalies, webbing of fingers and toes, and arthrogryposis multipex (Linares et al, 1979; Solomon et al, 1977; Anon, 1981; Beck et al, 1981; Rosa, 1986). However, the teratogenic effect when used in low doses or for short periods of time, as in metal chelation, has yet to be determined.

a) Anuria or other evidence of renal dysfunction makes therapy with d-penicillamine dangerous since the main route of elimination of this complex is renal.

a) ACUTE TOXICITY
b) CHRONIC TOXICITY
c) DMPS/ADVERSE REACTIONS

a) DMPS is not FDA-approved, but is available outside of the US from Heyl Chem-pharm Fabrik in Germany (Prod Info Dimaval(R) intravenous intramuscular injection solution, 2013; Prod Info DIMAVAL(R) oral capsules, 2004). In the US it may be obtained from some compounding pharmacies.

a) Oral unithiol (a 5-day cycle, 200 mg/day) increased urinary mercury excretion in 12 women with mercury poisoning from using mercury-containing facial cream (mercuric chloride 5.9%) for 2 to 10 years (Garza-Ocanas et al, 1997).
b) Intravenous unithiol (250 milligrams every 6 hours for 7 days, then every 8 hours for 1 day, then every 12 hours for 8 days, then once daily for 7 days) and continuous venovenous hemofiltration were successfully used to reduce blood mercury levels in a patient with inorganic mercury salt poisoning and renal failure (Pai et al, 2000).
c) One source reported one patient who ingested over 10 grams of mercury. He developed 10 days of renal failure, but survived (Ashton et al, 1992).
d) One study reported the use of DMPS in a case of mercury chloride ingestion. Initial blood and urine levels were 14,300 and 36,000 micrograms per liter, respectively. Intravenous DMPS was used initially, but followed by oral use for 4 weeks. The patient recovered without sequelae. Hemodialysis performed with the patient was receiving DMPS, and mercury could not be detected in the dialysate (dialysis clearance less than 1 milliliter/minute) (Toet et al, 1994).
e) Intravenous DMPS, 250 mg every 4 to 12 hours for 14 days, followed by oral DMPS (Dimaval), 100 mg 3 times per day for 5 weeks and then reduced to 100 mg daily, were successfully used to treat an adolescent who had ingested 2 grams of mercury chloride and developed acute renal failure during BAL treatment (Gricar et al, 1994).
f) ANIMAL STUDIES: In animal models of inorganic mercury poisoning, DMPS has been shown to increase survival, reduce nephrotoxicity, increase urinary and fecal mercury elimination, and decrease tissue mercury levels, particularly in brain and kidney (Zalups et al, 1991; Neilsen & Andersen, 1991; Gale et al, 1993).

a) SKIN REACTIONS: Urticaria, maculopapular rash, and erythema multiforme (Hla et al, 1992).

a) These recommendations apply to patients with MINOR chemical burns (FIRST DEGREE; SECOND DEGREE: less than 15% body surface area in adults; less than 10% body surface area in children; THIRD DEGREE: less than 2% body surface area). Consultation with a clinician experienced in burn therapy or a burn unit should be obtained if larger area or more severe burns are present. Neutralizing agents should NOT be used.

a) After initial flushing with large volumes of water to remove any residual chemical material, clean wounds with a mild disinfectant soap and water.
b) DEVITALIZED SKIN: Loose, nonviable tissue should be removed by gentle cleansing with surgical soap or formal skin debridement (Moylan, 1980; Haynes, 1981). Intravenous analgesia may be required (Roberts, 1988).
c) BLISTERS: Removal and debridement of closed blisters is controversial. Current consensus is that intact blisters prevent pain and dehydration, promote healing, and allow motion; therefore, blisters should be left intact until they rupture spontaneously or healing is well underway, unless they are extremely large or inhibit motion (Roberts, 1988; Carvajal & Stewart, 1987).

a) TOPICAL ANTIBIOTICS: Prophylactic topical antibiotic therapy with silver sulfadiazine is recommended for all burns except superficial partial thickness (first-degree) burns (Roberts, 1988). For first-degree burns bacitracin may be used, but effectiveness is not documented (Roberts, 1988).
b) SYSTEMIC ANTIBIOTICS: Systemic antibiotics are generally not indicated unless infection is present or the burn involves the hands, feet, or perineum.
c) WOUND DRESSING:
d) DRESSING CHANGES:
e) Analgesics such as acetaminophen with codeine may be used for pain relief if needed.

a) The patient's tetanus immunization status should be determined. Tetanus toxoid 0.5 milliliter intramuscularly or other indicated tetanus prophylaxis should be administered if required.

1) An adult woman survived ingestion of 900 milligrams (13.8 milligrams/kilogram) of mercuric chloride. The woman vomited several times immediately after the ingestion and was treated with BAL, hemodialysis, peritoneal dialysis, and plasma exchange by 3 hours postingestion (Suzuki et al, 1992).

a) The following mercury levels were obtained from a woman with mercury poisoning after using a cosmetic cream twice daily for several months: Hair, 22.5 mcg/g (normal, 11.6 mcg/g or less); blood 94 nmol/L (normal, 45 nmol/L or less), urine excretion 345 nmol/day (normal, 50 nmol/day or less). The mercury content of the cosmetic cream was 6.5% w/w (Chan et al, 2001).
b) A woman developed nephrotic syndrome secondary to membranous nephropathy after using a skin-whitening cream containing mercury (concentration, almost 2000 times above the allowable limit) for 5 years. Her blood mercury and 24-hour urinary mercury excretion concentrations were 163 nmol/L and 754.6 nmol/d, respectively (Soo et al, 2003)
c) A man developed acute lung injury (progressive dyspnea and acute respiratory failure) after mercury vapor inhalation from heating Chinese red (Cinnabar, mercury sulfide). His initial serum and urine mercury concentrations were 33 mcg/dL (normal less than 6 mcg/dL) and 0.87 mcg/dL (normal less than 5 mcg/dL), respectively. Despite supportive therapy and treatment with DMPS and penicillamine, he eventually died from profound hypoxemia 39 days after Inhalation of the vapor (Ho et al, 2003).
d) A man, with a history of schizophrenia, developed severe axonal sensorimotor polyneuropathy, which progressed to quadriparesis after drinking a traditional Chinese herb mixture (Huei Chen Shai) daily for 3 months. The mixture was prepared by mixing 200 grams of the herb with mercurial droplets from 10 broken thermometers in boiled water. The laboratory analysis of the herb drug showed mercury concentration of 10,000 ppm, lead 116 ppm, arsenic 18.9 ppm, and cadmium 0.97 ppm. Blood and urine mercury concentrations were not measured in acute stage until 2 months later; however, the concentrations of mercury in the scalp hair (14.2 mcg/g; reference, less than 5.5 mcg/g) and pubic hair (9.1 mcg/g; reference, less than 1.6 mcg/g) were high even 6 months later. Following supportive therapy, his muscle weakness improved slowly; however, at the 2-year follow-up examination, he still had sensory and motor impairment (Chu et al, 1998) .
e) Urinary mercury excretion in 12 women after using a mercury-containing facial cream (mercuric chloride, 5.9%) ranged from 180 to 1876 mcg/g creatinine (Garza-Ocanas et al, 1997).
f) In one study, mercury concentrations in urine specimens from 22 patients in 5 households with potential mercury exposure were obtained. Ten patients (age range, 16 to 62 years) used mercury-containing skin-lightening creams (mercury content range, 2% to 5.7% by weight) from Mexico intermittently to twice daily (duration range, several months to 5 years). Elevated urinary mercury concentrations were observed in 15 patients, 9 cream users (range, 26 to 317 mcg/g creatinine) and 6 nonusers (range, 20 to 276 mcg/g creatinine). One cream user had a mercury concentration of only 4 mcg/g. Mercury concentrations of 17 to 50 mcg/m(3) were obtained from areas close to where creams were stored (eg, near cleaning supplies, clothing, and furniture), and near items frequently touched by cream users (Centers for Disease Control and Prevention, 2012).
g) Two hours post-ingestion, a woman with mercury poisoning (ingested one 15 mL vial of a stool fixative (Para-Pak) containing 4.5% mercuric chloride (675 mg)) had the following serum and urinary mercury levels, respectively: 710 ng/mL and 276 mcg/L (Singer et al, 1994).

a) An 11-month-old boy presented with failure to thrive and developmental regression, irritability, painful, swollen, erythematous extremities, swollen fingers and toes, and hypertension. Laboratory results revealed a blood mercury concentration of 13.8 mcg/L (adult reference, less than 15.4 mcg/L), a urine mercury of 61.6 mcg/L (adult reference, less than 20 mcg/L), and urine mercury/creatinine ratio of 150 mcg/g creatinine (adult reference, less than 5 mcg/g creatinine). His pediatrician later reported a blood mercury concentration of 18 mcg/L and urine mercury/creatinine after a succimer challenge of 340 mcg/g. It was found that he was given a Chinese medicinal powder (mercury content, 1228 ppm) for 4 months (from 6 months to 10 months of age). Following treatment with one course of succimer 100 mg every 8 hours for 10 days and amlodipine 1.5 mg daily, his symptoms gradually resolved (Koh et al, 2009).
b) A 5-year-old boy with recurrent oral ulceration developed motor and vocal tics after using a Chinese medicinal herb mouth spray (Watermelon Frost; mercury content, 878 ppm; 98% inorganic mercury and 2% methylmercury) up to 20 times a day for 4 weeks instead the recommended dose of one spray twice daily. His blood mercury concentration was 83 nmol/L (normal for adults less than 50 nmol/L). Following the discontinuation of the mouth spray, his ticks resolved completely (Li et al, 2000).
c) A 10-year-old girl with severe inorganic mercury poisoning (gastrointestinal hemorrhage, renal, hepatic, neurologic, hematologic, and cardiovascular dysfunctions) and a blood mercury concentration of 5,380 mcg/L and urine mercury of 91 mcg/L, was treated with succimer and BAL. Her symptoms improved gradually, and she was discharged after 67 days of hospitalization (Erkek et al, 2010).
d) A 2-year-old boy developed corrosive trauma to the gastrointestinal tract mucosa and acute non-oliguric renal failure after ingesting an unknown quantity of mercury chloride. His blood and urinary mercury concentrations were 35 mcg/dL and 24 mcg/dL, respectively (Verma et al, 2010).

1) Mercury, elemental and inorganic forms, as Hg
b) Adopted Value

a) ASPCA Animal Poison Control Center, An Allied Agency of the University of Illinois, 1717 S. Philo Rd, Suite 36, Urbana, IL 61802, website www.aspca.org/apcc
b) It is an emergency telephone service which provides toxicology information to veterinarians, animal owners, universities, extension personnel and poison center staff for a fee. A veterinary toxicologist is available for consultation.
c) The following 24-hour phone number is available: (888) 426-4435. A fee may apply. Please inquire with the poison center. The agency will make follow-up calls as needed in critical cases at no extra charge.

a) Induce emesis with syrup of ipecac, 10 to 30 mL orally or hydrogen peroxide 5 to 25 mL orally repeated in 5 to 10 minutes if there is no response. DOGS ONLY may receive apomorphine 0.05 to 0.10 mg/kg IV, IM, or subcutaneously.
b) Gastric lavage may be performed using tap water or normal saline.
c) Administer activated charcoal, 5 to 50 g, orally, as a slurry in water.
d) Then administer Milk of Magnesia 1 to 15 mL orally, mineral oil 2 to 15 mL orally, sodium sulfate 20%, 2 to 25 g orally or magnesium sulfate 20% 2 to 25 g orally, for catharsis.

a) Give 250 to 500 g of activated charcoal in a water slurry, orally. Administer an oral cathartic: mineral oil (1 to 3 liter), 20% sodium sulfate (25 to 10,000 g), 20% magnesium sulfate (25 to 1,000 g), or Milk of Magnesia (20 to 30 mL).
b) Ruminants (cattle and sheep) cannot be made to vomit. Horses should not be made to vomit.

1) The following recommendations are principally intended for inorganic or organic mercury exposure.
2) Begin treatment immediately.
3) Keep animal warm.
4) Sample vomitus, blood, urine, and feces for analysis.
5) If skin exposure has occurred, wash animal thoroughly with a mild detergent and flush with copious amounts of water.
6) ANIMAL POISON CONTROL CENTERS

1) SMALL ANIMALS
2) LARGE ANIMALS