We are offering CME for
this topic. Click on the GetCME button to take CME (Your first test is
Free!)
AUTHOR INFORMATION
Section 1 of 11
Authored by Barry Diner, MD,
Clinical Instructor, Division of Emergency Medicine, University of Alberta
Coauthored by Barry Brenner, MD, PhD, Chairman, Department
of Emergency of Medicine, Professor, Departments of Emergency Medicine and
Internal Medicine,
University of Arkansas for Medical Sciences
Edited by Michelle Ervin, MD, Chair, Department of Emergency
Medicine, Howard University Hospital; John T VanDeVoort, PharmD, DABAT,
Manager, Clinical Assistant Professor, Pharmacy Department, Regions Hospital;
Fred Harchelroad, MD, FACMT, Chair, Department of Emergency
Medicine, Director of Medical Toxicology, Associate Professor, Department of
Emergency Medicine, Allegheny General Hospital; John Halamka, MD,
Chief Information Officer, CareGroup Healthcare System, Assistant Professor of
Medicine, Department of Emergency Medicine, Beth Israel Deaconess Medical
Center; Assistant Professor of Medicine, Harvard Medical School; and
Raymond J Roberge, MD, MPH, FAAEM, FACMT, Research Director, Department
of Emergency Medicine, Ohio Valley Medical Center; Clinical Associate Professor,
Department of Emergency Medicine, University of Pittsburgh
eMedicine Journal, May 25 2001, Volume 2, Number 5
INTRODUCTION
Section 2 of 11
Background: Throughout the
centuries, several incidents of mercury toxicity have been reported. Mercury has
been found in Egyptian tombs, indicating it was used as early as 1500 BC. In the
late 18th century, antisyphilitic agents contained mercury. It was during the
1800s that the phrase "mad as a hatter" was coined because of the chronic
mercury exposure that the felters faced because mercury was used in hat making.
In the 1940s and 1950s, mercury became known as the product that caused
acrodynia, also known as Pink Disease. Manifestations of acrodynia include pain
and erythema of the palms and soles, irritability, insomnia, anorexia,
diaphoresis, photophobia, and rash.
Some of the more recent exposures include Minamata Bay in Japan (1960),
mercury contaminated fish in Canada, methylmercury-treated grain in Iraq (1960,
1970), and, in the US (1996), a beauty cream product from Mexico called "Crèma
de Belleza-Manning."
For centuries, mercury was an essential part of many different medicines,
such as diuretics, antibacterial agents, antiseptics, and laxatives. More
recently, these drugs have been substituted and drug-induced signs of mercury
toxicity are rare. Mercury toxicity in environmental pollution is a major
concern because of increased usage of fossil fuels and agricultural products,
both of which contain mercury.
Mercury poisoning usually is misdiagnosed because of the insidious onset,
nonspecific signs and symptoms, and lack of knowledge within the medical
profession. Mercury is found in many industries such as battery, thermometer,
and barometer manufacturing. Mercury can be found in fungicides used in the
agricultural industry. Before 1990, paints contained mercury as an antimildew
agent. In medicine, mercury is used in dental amalgams and various antiseptic
agents.
On July 7, 1999, a joint statement by the American Academy of Pediatrics (AAP)
and the US Public Health Service (USPHS) was issued alerting clinicians and the
public of thimerosal, a mercury-containing preservative used in some vaccines.
Pathophysiology: Mercury is the only metal that is liquid at
room temperature. Its elemental symbol is Hg, which is derived from the Greek
word hydrargyrias, meaning "water silver." Mercury is found in organic
and inorganic forms. The inorganic form can be further divided into elemental
mercury and mercuric salts. Organic mercury can be found in long and short alkyl
and aryl compounds.
Mercury in any form is toxic. The difference lies in how it is absorbed, the
clinical signs and symptoms, and the response to treatment modalities. Mercury
poisoning can result from vapor inhalation, ingestion, injection, or absorption
through the skin.
Elemental mercury (Hg) is found in liquid form, which easily vaporizes at
room temperature and is well absorbed (80%) through inhalation. Its
lipid-soluble property allows for easy passage through the alveoli into the
bloodstream and red blood cells (RBCs). Once inhaled, elemental mercury is
mostly converted to an inorganic divalent or mercuric form by catalase in the
erythrocytes. This inorganic form has similar properties to inorganic mercury (eg,
poor lipid solubility, limited permeability to the blood brain barrier, and
excretion in feces). Small amounts of nonoxidized elemental mercury continue to
persist and account for central nervous system toxicity.
Elemental mercury as a vapor has the ability to penetrate the CNS, where it
is ionized and trapped, attributing to its significant toxic effects. Elemental
mercury is not well absorbed by the GI tract and, therefore, when ingested (eg,
thermometers), is only mildly toxic.
Inorganic mercury, found mostly in the mercuric salt form (eg, batteries), is
highly toxic and corrosive. It gains access to the body orally or dermally and
is absorbed at a rate of 10% of that ingested. It has a nonuniform mode of
distribution secondary to poor lipid solubility and accumulates mostly in the
kidney, causing significant renal damage. Although poor lipid solubility
characteristics limit CNS penetration, slow elimination and chronic exposure
allow for significant CNS accumulation of mercuric ions and subsequent toxicity.
Chronic dermal exposure to inorganic mercury also may lead to toxicity.
Excretion of inorganic mercury, as with organic mercury, is mostly through
feces. Renal excretion of mercury is considered insufficient and attributes to
its chronic exposure and accumulation within the brain, causing CNS effects.
Organic mercury can be found in 3 forms, aryl and short and long chain alkyl
compounds. Organic mercurials are absorbed more completely from the GI tract
than inorganic salts are; this is because of intrinsic properties, such as lipid
solubility and mild corrosiveness (although much less corrosive than inorganic
mercury). Once absorbed, the aryl and long chain alkyl compounds are converted
to their inorganic forms and possess similar toxic properties to inorganic
mercury. The short chain alkyl mercurials are readily absorbed in the GI tract
(90-95%) and remain stable in their initial forms. Alkyl organic mercury has
high lipid solubility and is distributed uniformly throughout the body,
accumulating in the brain, kidney, liver, hair, and skin. Organic mercurials
also cross the blood brain barrier and placenta and penetrate erythrocytes,
attributing to neurological symptoms, teratogenic effects, and high blood to
plasma ratio, respectively.
Methylmercury has a high affinity for sulfhydryl groups, which attributes to
its effect on enzyme dysfunction. One enzyme that is inhibited is choline acetyl
transferase, which is involved in the final step of acetylcholine production.
This inhibition may lead to acetylcholine deficiency, contributing to the signs
and symptoms of motor dysfunction.
Excretion of alkyl mercury occurs mostly in the form of feces (90%),
secondary to significant enterohepatic circulation. The biological half-life of
methyl mercury is approximately 65 days. Organic mercury is found most commonly
in antiseptics, fungicides, and industrial run-off.
Frequency:
In the US: The 1998 annual report of the American
Association of Poison Control Centers' Toxic Exposure Surveillance System
documented 4039 exposures to mercury. Of these, 1039 were in children younger
than 6 years and 1385 were in persons older than 19 years. Overall, 68
individuals were reported to have moderate effects, 12 had major effects, and
3 died as a result of mercury exposure.
Race: No scientific evidence has demonstrated any difference
in outcome of mercury exposure that is attributable to race.
Sex: No scientific evidence has demonstrated any difference
in outcome of mercury exposure that is attributable to sex.
CLINICAL
Section 3 of 11
History: The diagnostic approach
for patients with suspected mercury toxicity begins with a thorough history that
includes occupations, hobbies, and levels of seafood intake. All toxic
presentations, whether acute, chronic, or subacute, are difficult diagnoses
because multiple organ systems are affected (eg, CNS, kidney, mucous membranes)
and can mimic a variety of other diseases. If no such history exists, clinical
suspicion can be confirmed by laboratory analysis.
The clinical presentation of mercury toxicity can manifest in a variety of
ways, depending on the nature of the exposure, the intensity of the exposure,
and the chemical form. Acute toxicity usually is related to the inhalation of
elemental mercury or ingestion of inorganic mercury. Exposure to organic mercury
leads to chronic toxicity and, occasionally, acute toxicity.
Acute exposure caused by inhaled elemental mercury can lead to pulmonary
symptoms. Initial signs and symptoms, such as fever, chills, shortness of
breath, metallic taste, and pleuritic chest pain, may be confused with metal
fume fever. Other possible symptoms could include stomatitis, lethargy,
confusion, and vomiting.
Recovery is usually without sequela, but pulmonary complications of
inhaled toxicity may include interstitial emphysema, pneumatocele,
pneumothorax, pneumomediastinum, and interstitial fibrosis. Fatal ARDS has
been reported following elemental mercury inhalation.
Chronic and intense acute exposure causes cutaneous and neurological
symptoms. The classic triad found in chronic toxicity is tremors, gingivitis,
and erethism (ie, a constellation of neuropsychiatric findings that includes
insomnia, shyness, memory loss, emotional instability, depression, anorexia,
vasomotor disturbance, uncontrolled perspiration, and blushing).
Additional findings may include headache, visual disturbance (eg, tunnel
vision), peripheral neuropathy, salivation, insomnia, and ataxia.
Without a complete history, mercury toxicity, especially in elderly
individuals, can be misdiagnosed as Parkinson disease, senile dementia,
metabolic encephalopathy, depression, or Alzheimer disease.
Elemental mercury has poor GI absorption and, therefore, oral or rectal
exposure to elemental mercury from a thermometer should have no toxic effect.
Dental amalgams also contain elemental mercury. Dental professionals who are
in contact with amalgam must follow specific guidelines to avoid exposure to
toxic amounts of aerosolized elemental mercury. Patients with dental amalgam
fillings have slightly elevated levels in their urine, but these findings have
not correlated with any systemic disease.
Inorganic mercury or mercuric salt exposure mainly occurs through the oral
and GI tract. Its corrosive properties account for most of the acute signs and
symptoms of inorganic mercury or mercuric salt toxicity. The acute
presentation can include ashen-gray mucous membranes secondary to
precipitation of mercuric salts, hematochezia, vomiting, severe abdominal
pain, and hypovolemic shock. Systemic effects usually begin several hours
postingestion and may last several days. These effects include metallic taste,
stomatitis, gingival irritation, foul breath, loosening of teeth, and renal
tubular necrosis leading to oliguria or anuria.
Batteries contain inorganic mercury but are rarely the cause of systemic
symptoms. Ingestion of batteries by pediatric patients is a common problem,
and its complications are related to local corrosive complications.
Administer chelation therapy to patients who ingest mercury-containing
batteries if symptoms of mercury toxicity are present.
Use of cathartics and water-soluble enemas is useful for increasing
transit time of released mercury, but these treatments are not indicated for
intact batteries.
Chronic exposure usually results from prolonged occupational exposure to
elemental mercury that is converted into the inorganic form, topical
application of mercurial salves, and the chronic use of diuretics or
cathartics.
Chronic exposure results in renal failure, dementia, and acrodynia.
Acrodynia, known as Pink disease and considered to be a mercury allergy,
presents with erythema of the palms and soles, edema of the hands and feet,
desquamating rash, hair loss, pruritus, diaphoresis, tachycardia,
hypertension, photophobia, irritability, anorexia, insomnia, poor muscle
tone, and constipation or diarrhea.
Acrodynia does not present in everyone who is exposed to inorganic
mercury, but it is an indicator of widespread disease.
Organic mercury poisoning usually results from ingestion of contaminated
food. The long chain and aryl forms of organic mercury have similar
characteristics of inorganic mercury toxicity.
The onset of symptoms usually is delayed (days to weeks) after exposure.
Organic mercury targets enzymes, and the depletion of these enzymes must
occur before the onset of symptoms.
Symptoms related to toxicity are typically neurological, such as visual
disturbance (eg, scotomata, visual field constriction), ataxia, paresthesias
(early signs), hearing loss, dysarthria, mental deterioration, muscle
tremor, movement disorders, and, with severe exposure, paralysis, and death.
Organic mercury targets specific sites in the brain, including the
cerebral cortex (especially visual cortex), motor and sensory centers (precentral
and postcentral cortex), auditory center (temporal cortex), and cerebellum.
All forms of mercury are toxic to the fetus, but methylmercury most
readily passes through the placenta. Even with an asymptomatic patient,
maternal exposure can lead to spontaneous abortion or retardation.
Physical: Focus the physical examination on the areas most
commonly affected.
Perform a complete neurological examination, including a detailed
cerebellar examination. Perform a full visual field evaluation.
Perform abdominal and rectal examinations, with stool guaiac testing, and
include documentation of a skin examination.
Causes:
Causes of elemental mercury toxicity include barometers, batteries,
bronzing, calibration instruments, chlor-alki production, dental amalgams,
electroplating, fingerprinting products, fluorescent and mercury lamps,
infrared detectors, the jewelry industry, manometers, neon lamps, paints,
paper pulp production, photography, silver and gold production, semiconductor
cells, and thermometers.
The causes of inorganic mercury toxicity include antisyphilitic agents,
acetaldehyde production, chemical laboratory work, cosmetics, disinfectants,
explosives, embalming, fur hat processing, ink manufacturing, mercury vapor
lamps, mirror silvering, the perfume industry, photography, spermicidal
jellies, tattooing inks, taxidermy production, vinyl chloride production, and
wood preservation.
The causes of organic mercury toxicity include antiseptics, bactericidals,
embalming agents, the farming industry, fungicides, germicidal agents,
insecticidal products, laundry products, diaper products, paper manufacturing,
pathology products, histology products, seed preservation, and wood
preservatives.
Another cause of organic mercury toxicity is thimerosal, an additive
preservative used in vaccines to prevent bacterial contamination. The most
commonly used vaccines that contain Thimerosal are for
diphtheria-tetanus-whole cell pertussis (DTP), Haemophilus influenzae
(HIB), and hepatitis B.
Adverse effects of therapeutic medication (eg, lithium, theophylline, phenytoin)
Alzheimer disease
Cerebellar degenerative disease or tumor
Delayed neuropsychiatric sequela of carbon monoxide poisoning
Ethanol or sedative hypnotic drug withdrawal
Lacunar infarction
Metabolic encephalopathy
Parkinson disease
Senile dementia
Inorganic mercury toxicity (mercury salts)
Acid ingestion
Alkali ingestion
Arsenic toxicity
Iron toxicity
Phosphorus toxicity
Similar to the causes of acute gastroenteritis
Organic mercury toxicity
Cerebral palsy
Intrauterine hypoxia
Teratogenic effects in the embryo
WORKUP
Section 5 of 11
Lab Studies:
Obtain a complete blood count and serum chemistries to assess possible
anemia secondary to GI hemorrhage, determine the onset of acute and chronic
renal failure, and rule out the possibility of electrolyte abnormality.
Consider pregnancy tests in women of childbearing age.
Whole blood mercury levels are usually less than 2 mcg/dL in unexposed
individuals (exceptions may be individuals with a high dietary intake of
fish).
Methylmercury concentrates in erythrocytes; therefore, mercury levels
in blood remain high in acute toxicity. The blood level correlation with
chronic methylmercury toxicity is more variable. Methylmercury exhibits a
blood-to-plasma ratio of 20:1, a characteristic of inorganic mercury. This
higher ratio may be useful in determining if the patient was exposed to
organic or inorganic mercurials. Aryl mercury compounds accumulate in RBCs
but are metabolized to inorganic mercury more rapidly, thus, demonstrating
lower blood-to-plasma ratios than those observed with methyl mercury
exposures. Following high exposure to inorganic mercury salts, the
blood-to-plasma ratio ranges from a high of 2:1, to 1:1. Paraesthesias are
expected if blood mercury levels are higher than 20 mcg/dL.
Inorganic mercury redistributes to other body tissue; thus, its levels
in the blood only are accurate after an acute ingestion. In general, blood
levels of mercury are helpful for recent exposures and for determining if
the toxicity is secondary to organic or inorganic mercury, but they are
not useful for a guide to therapy.
Urine mercury levels are typically less than 10-20 mcg/L. Excretion of
mercury in urine is a good indicator of inorganic and elemental mercury
exposure but is unreliable for organic mercury (methylmercury) because
elimination occurs mostly in the feces. No absolute correlation exists between
the urine mercury levels and the onset of symptoms; however, levels higher
than 300 mcg/L are associated with overt symptoms. Mercury levels in the urine
also can be used to gauge the efficacy of chelation therapy. For workers
chronically exposed to mercury compounds, urinary excretion with mercury
levels higher than 50 mcg/L is associated with an increased frequency of
tremor.
Hair has high sulfhydryl content. Mercury forms covalent bonds with sulfur
and, therefore, can be found in abundance in hair samples. However, the rate
of false-positive results is high with hair analysis secondary to
environmental exposure. Do not use hair analysis solely as a means to confirm
mercury toxicity or exposure.
Imaging Studies:
Obtain a flat plate radiograph of the abdomen to visualize ingested
elemental mercury, which appears radiopaque.
TREATMENT
Section 6 of 11
Prehospital Care: Prehospital
management includes gathering information on the time, type, and mode of mercury
exposure.
Initial assessment (ABCs)
Oxygen
IV access
Emergency Department Care: Supportive care begins with the
ABCs, especially when managing the inhalation of elemental mercury and the
ingestion of caustic inorganic mercury, both of which may cause the onset of
airway obstruction and failure. The next step in supportive care is the removal
of contaminated clothing and copious irrigation of exposed skin. Aggressive
hydration may be required for acute inorganic mercury poisoning because of its
caustic properties.
Do not induce emesis if the compound ingested is of the caustic inorganic
form.
Gastric lavage is recommended for organic ingestion, especially if the
compound is observed on the abdominal x-ray series. Gastric lavage with
protein-containing solutions (eg, milk, egg whites, salt-poor albumin) or 5%
sodium formaldehyde sulfoxylate solution may bind gastric mercury and limit
its absorption.
Activated charcoal is indicated for GI decontamination because it binds
inorganic and organic mercury compounds to some extent.
Whole bowel irrigation may be used until rectal effluent is clear and
void of any radiopaque material. However, effectiveness in decreasing the GI
transit time of elemental mercury is doubtful because of the high density of
elemental mercury and the low density of the whole bowel irrigant solutions.
Likewise, whole bowel irrigation has no adsorptive effect on any type of
mercury within the GI tract.
Use chelating agents if the patient is symptomatic, if systemic absorption
is anticipated, or if increased blood or urine levels are present. Chelating
agents contain thiol groups, which compete with endogenous sulfhydryl groups.
Hemodialysis is used in severe cases of toxicity when renal function has
declined. The ability of regular hemodialysis to filter out mercury is limited
because of mercury's mode of distribution among erythrocytes and plasma.
However, hemodialysis, with L-cysteine compound as a chelator, has been
successful.
Neostigmine may help motor function in methylmercury toxicity. This
toxicity often leads to acetylcholine deficiency.
Polythiol is a nonabsorbable resin that can help in facilitating the
removal of methylmercury (short chain alkyl organic mercury), which is then
excreted in the bile after enterohepatic circulation.
Consultations: Consult with the regional poison control
center or a medical toxicologist (certified through the American Board of
Medical Toxicology and/or the American Board of Emergency Medicine) for
additional information and patient care recommendations.
Recommendation: The American Academy of Pediatric and US Public Health
Service states that the use of products containing thimerosal is preferable to
withholding vaccinations, which protect against diseases that represent
immediate threats to infants (ie, pertussis, H influenzae). For the
hepatitis B vaccine, adjustments in timing within the ranges proposed in the
immunization schedule provide additional opportunities to minimize thimerosal
exposure to infants. If thimerosal-free vaccine is not available, the
hepatitis B virus vaccination should be initiated in infants aged 6 months.
MEDICATION
Section 7 of 11
Use chelating agents if the patient is
symptomatic, systemic absorption is anticipated, or increased blood or urine
levels are present.
Drug Category: Chelating agents -- Thiol
groups in the chelating agent compete with endogenous sulfhydryl groups.
Drug Name
Dimercaprol (BAL) -- DOC for treatment
of acute mercury toxicity.
Administered IM q4h, mixed in a peanut oil base. Excreted in urine and bile.
May be given to patients with renal failure. Used only in acute ingestion.
Adult Dose
3-5 mg/kg IM q4h for 2 d, followed by
2.5-3 mg/kg IM q6h for 2 d, followed by 2.5-3 mg/kg IM q12h for 7 d
Pediatric Dose
Administer as in adults
Contraindications
Documented hypersensitivity; concurrent
iron supplementation therapy; methylmercury toxicity
Interactions
Toxicity may increase when
coadministered with selenium, uranium, iron, or cadmium
Pregnancy
C - Safety for use during pregnancy has
not been established.
Precautions
May be nephrotoxic and may cause
hypertension; caution in oliguria or G-6-PD deficiency; may induce hemolysis
in G-6-PD deficiency; adverse effects include abdominal pain, nausea,
vomiting, headache, elevated blood pressure, tachycardia, burning sensation
to the lips and throat, constricting feeling of the throat, conjunctivitis,
blepharospasm, lacrimation, rhinorrhea, salivation, burning sensation to the
penis, and urticaria (some adverse effects are responsive to diphenhydramine
cotherapy)
Drug Name
Penicillamine (Cuprimine, Depen) --
Forms a complex with mercury and is excreted in urine; therefore, do not use
in renal failure. Cannot be considered as first-line agent because of the
safer and more efficacious agent, dimercaptosuccinic acid.
Adult Dose
15-40 mg/kg/d; not to exceed 250-500 mg
PO q6h ac (continue 1 wk until decline in urine mercury levels)
Increases effects of immunosuppressants,
phenylbutazone, and antimalarials; decreases digoxin effects; effects may
decrease with coadministration of zinc salts, antacids, and iron
Pregnancy
D - Unsafe in pregnancy
Precautions
Thrombocytopenia, agranulocytosis, and
aplastic anemia may occur; adverse effects include GI disturbances, rash,
leukopenia, thrombocytopenia, and proteinuria; caution in renal
insufficiency
Drug Name
Succimer (Chemet) -- DMSA
(2,3-dimercaptosuccinic acid) is used in inorganic and organic mercurials.
Considered superior to penicillamine because PO and with fewer adverse
effects. Because of ease of use, good efficacy, and safety, initiate
treatment if good evidence indicates that significant absorption can occur
(mercury levels may not be readily available).
Adult Dose
10 mg/kg PO tid for 5 d, followed by 10
mg/kg PO bid for 14 d
Pediatric Dose
10 mg/kg or 350 mg/m2 PO q8h
for 5 d, followed by 10 mg/kg PO bid for 14 d
Contraindications
Documented hypersensitivity
Interactions
Do not administer concomitantly with
edetate calcium disodium, or penicillamine
Pregnancy
C - Safety for use during pregnancy has
not been established.
Precautions
Caution in renal or hepatic impairment;
patient should be well hydrated to prevent toxicity; adverse effects include
mild GI disturbances and a transient rise in liver enzymes; product has a
strong sulfur smell; thrombocytosis, eosinophilia, and neutropenia reported
with use and are reported to resolve when therapy ends
FOLLOW-UP
Section 8 of 11
Prognosis:
Outcome depends on the form of the mercury compound and severity of
exposure. Mild exposure to inorganic (ie, elemental, mercuric salt) and
organic compounds can result in a complete recovery. Fatality is usually the
result of severe exposure to mercuric salt. Most organic mercury exposures
leave a neurological sequela. Very minimal dermal exposure to dimethyl mercury
has resulted in progressive neurologic deterioration and death, with initial
symptoms delayed for several months.
Individuals who need to be admitted to the hospital include the following:
Individuals who ingested (or are thought to have ingested) mercury salts
Individuals thought to have elemental mercury inhalation and have
pulmonary injury
Individuals who require intensive chelating therapy
MISCELLANEOUS
Section 9 of 11
Medical/Legal Pitfalls:
Failure to obtain a history of exposure to mercury compounds in patients
with significant historical features of the signs and symptoms of mercury
exposure
Failure to initiate treatment in a patient with significant exposure and
symptoms before obtaining the confirmatory laboratory analysis, which may be
delayed for a week.
Failure to consult a medical toxicologist or regional poison control
center for updated information on this rare type of poisoning.
Special Concerns:
Significant oral ingestion of elemental mercury may lead to significant
environmental contamination as the mercury is passed, essentially unabsorbed,
through the GI tract and expelled in the feces.
PICTURES
Section 10 of 11
Caption: Picture 1. This
is a one view, abdominal, upright radiograph in a male patient who
intentionally ingested 8 ounces of elemental mercury. Notice how the mercury
outlines the large intestine from ascending to descending. (Image courtesy
of Fred P. Harchelroad, MD, and Ferdinando L. Mirarchi, DO)
Abramson, JS: Thimerosal in vaccines--An interim report to clinicians.
American Academy of Pediatrics. Committee on Infectious Diseases and Committee
on Environmental Health. Pediatrics 1999 Sep; 104(3 Pt 1): 570-4[Medline].
Bates B: Heavy metals and inorganic agents. In: Clinical Management of
Poisoning and Drug Overdose. Vol 55. WB Saunders; 1998:750-6.
Ford M: Heavy metals. In: Tintinalli JE, ed. Emergency Medicine: A
Comprehensive Study Guide. 4th ed. Vol 158. McGraw-Hill; 1996:839-41.
Goyer RA: Toxic effects of metals. In: Casarett LJ, ed. Casarett and
Doull's Toxicology: The Basic Science of Poisons. 5th ed. New York:
McGraw-Hill; 1996:709-713.
Graeme KA, Pollack CV Jr: Heavy metal toxicity, Part I: arsenic and
mercury. J Emerg Med 1998 Jan-Feb; 16(1): 45-56[Medline].
Kershaw TG, Clarkson TW, Dhahir PH: The relationship between blood levels
and dose of methylmercury in man. Arch Environ Health 1980 Jan-Feb; 35(1):
28-36[Medline].
Klaassen C: Heavy metals and heavy metal antagonists. In: Hardman JG,
Limbird LE, ed. Goodman and Gilman's The Pharmacological Basis of
Therapeutics. 9th ed. New York: McGraw-Hill; 1996:1654-1659.
Norseth T, Clarkson TW: Studies on the biotransformation of 203Hg-labeled
methyl mercury chloride in rats. Arch Environ Health 1970 Dec; 21(6): 717-27[Medline].
Poddar AS, Kim JG, Gill KP, et al: Generation and characterization of a
polyclonal antipeptide antibody to human glycodelin. Fertil Steril 1998 Mar;
69(3): 543-8[Medline].
Taueg C, Sanfilippo DJ, Rowens B, et al: Acute and chronic poisoning from
residential exposures to elemental mercury--Michigan, 1989-1990. J Toxicol
Clin Toxicol 1992; 30(1): 63-7[Medline].
Young J: Mercury. In: Goldfrank LR, ed. Goldfrank's Toxicology
Emergencies. Vol 74. New York: McGraw-Hill; 1994:1051-62.
NOTE:
Medicine is a constantly changing
science and not all therapies are clearly established. New research changes
drug and treatment therapies daily. The authors, editors, and publisher of
this journal have used their best efforts to provide information that is
up-to-date and accurate and is generally accepted within medical standards
at the time of publication. However, as medical science is constantly
changing and human error is always possible, the authors, editors,
and publisher or any other party involved with the publication of this
article do not warrant the information in this article is accurate or
complete, nor are they responsible for omissions or errors in the article or
for the results of using this information. The reader should confirm the
information in this article from other sources prior to use. In particular,
all drug doses, indications, and contraindications should be confirmed in
the package insert. FULL
DISCLAIMER
eMedicine Journal, May 25 2001, Volume 2, Number 5
ALL INFORMATION, DATA, AND
MATERIAL CONTAINED, PRESENTED, OR PROVIDED HERE IS FOR GENERAL INFORMATION
PURPOSES ONLY AND IS NOT TO BE CONSTRUED AS REFLECTING THE KNOWLEDGE OR OPINIONS
OF THE PUBLISHER, AND IS NOT TO BE CONSTRUED OR INTENDED AS PROVIDING MEDICAL OR
LEGAL ADVICE. THE DECISION WHETHER OR NOT TO VACCINATE IS AN IMPORTANT AND
COMPLEX ISSUE AND SHOULD BE MADE BY YOU, AND YOU ALONE, IN CONSULTATION WITH
YOUR HEALTH CARE PROVIDER.
"A foolish faith in authority is the worst enemy of truth."
-- Albert Einstein, letter to a friend, 1901
"I know of no safe depository of the ultimate powers of the society but the people themselves, and if we think them not enlightened enough to exercise control with a wholesome discretion, the remedy is not to take it from them, but to inform their discretion by education."
-- Thomas Jefferson, letter to William C. Jarvis, September 28, 1820
Sandy's Scandals Column
Past and current Scandals
- columns by Sandy Gottstein (aka Mintz)*
* ►March
18, 2010 - Probe
ordered into tainted vaccines - Report: Nearly 100 children died or
fell ill in Shanxi after shots - China Daily - "The four who died after
being administered tainted vaccines were 9-month-old Wang Xiao'er and
8-month-old Liu Ziyang from Luliang city; and 3-year-old Wang Shichao
and Liu Yi from Yangquan city, the report said. Children from 74
families were crippled or developed serious diseases such as
encephalitis after being vaccinated against hepatitis B, rabies, and
type-B encephalitis, it said."
* ►March 18, 2010
- The
Autism-Vaccine Controversy Continues - Age of Autism -
"There is no doubt that vaccines do injure some babies. Encephalitis
(inflammation of the brain) is a known effect of some vaccines for some
children (even listed on some of the vaccine labels, and in the
government's list of accepted adverse reactions HERE). Studies have found inflammation in
the brains of people with autism (HERE).
But the vaccine court routinely turns down cases where autism is
alleged to be caused by vaccines."
* ►March
17, 2010 - No More
Fear by Dawn Richardson - PROVE via VaccineInfo.net - "Those trying
to discredit parents who have legitimate vaccine safety concerns
mischaracterize parents as “being afraid” of vaccines. They use the
term "fear" to try and mislead the public into thinking that these
parental concerns are somehow irrational, trivial, or not based on
credible information."
* ►March 17, 2010
- Are
we liable if we can't give a vaccine to a child whose parent can't
physically restrain that child? - Nurse.com - "A consent form
developed and used by staff that is clear and inclusive of what is
needed for the immunization to take place is a good tool that can be
used by all staff to ensure compliance with the legal requirements of
informed consent by the parent or other legally authorized consent
giver and to avoid battery allegations. Sharing your concerns with the
clinic CNO, medical director and risk manager would be a start in
helping staff feel more comfortable with their role in the
administration of immunizations."