I found numerous examples of exposures to chemicals that are thought
to have contributed to myocarditis in humans or in laboratory animals.
I've presented the results below in summarized form. Where available,
I've included links to the articles in question, although a few of the
sources come from databases that are not routinely available over the
internet, and these do not have links.
I want to echo two things that were mentioned earlier by my research
1. As the disclaimer notes at the bottom of this page, Google Answers
is not a source of medical advice, nor is it a substitute for seeking
input from a medical professional.
2. I found no associations between the specific chemicals you listed,
and myocarditis. However, that certainly does NOT mean that acute
exposures to any of these chemicals could not have caused this
particular pathology. But I did not find examples of this in the
literature search I conducted, despite accessing a wide variety of
general and medical databases.
The information that I did find follows, below. I trust this
information fully answers your question. However, please don't rate
this answer until you have everything you need. If you would like any
additional information, just post a Request for Clarification to let
me know how I can assist you further, and I'm at your service.
All the best,
[This article is not available in full online, but you can see its
abstract at the above link]
Mutation Research 410 1998 123?140 The genetic effects of
environmental lead F.M. Johnson Toxicology Operations Branch National
Institute of En═ironmental Health Sciences PO Box 12233 Research
Triangle Park, NC 27709
...Lead has adverse effects on the heart and vasculature (Kopp et al.,
1988) . These effects include myocarditis, electrocardiographic
abnormalities, altered heart rate activity, slowed ventricular
systole, hypertension and vascular degeneration.
[The Kopp reference cited is this article]
Kopp, S.J., Barron, J.T., Tow, J.P., 1988. Cardiovascular actions of
lead and relationship to hypertension: a review. Environ. Health
Perspect. 78, 91?99.
[This article -- not available online -- relates a harrowing chemical
spill of liquefied methylamine, and details the lethal effects on two
of the people exposed, both who suffered from myocarditis]
Journal of Hazardous Materials 56 (1997) 117-136
A scheme of hazardous chemical identification for transportation
incidents Longmei Chen a, Dahe Jiang, Jiyang Xia
...At a small town named Shaxi in Jiangxi Province,southeast China,
650 people were intoxicated, with 39 deaths, in a severe accidental
release of a toxic chemical. Among the casualties, 8 died right at the
scene. It was in the early morning, 2:30 am on 3 September 1991, when
a truck carrying a tank filled with 2.4 tonnes of liquefied
methylamine under 3 to 4 atm pressure was being driven from Shanghai
to a factory in Jiangxi.
...In the dark, the top of the truck hit a branch of a large tree. The
pressure valve broke and this led to a rapid release of the chemical,
creating a fire and a thick cloud. It was hot and humid, 27?C,
relative humidity 82%, and almost calm. The surface temperature was
26░C so that the air was in a stable condition. The nearby structures
were all one or two story country buildings. People slept with their
door open to get some cool feeling. The release lasted nearly 10 min.
Because of the meteorological conditions, the hazard persisted for 30
min....When the release started, the driver and the technician were so
frightened that they could only break into shouting: ?hurry, escape,
toxic gas out!?, then ran away. The combustion was incomplete, so that
most of the liquid evaporated to form a toxic cloud which dispersed
slowly. The toxic cloud was about 5-6m high, headed first to the
southeast, then turned to the opposite direction after several
...The clinical manifestations of two severe intoxication cases are
provided. (1) A young man, 29, awakened by the suffocating feeling
caused by several minutes? intake of the toxic vapor, managed to get
himself to the hospital. He was found to have a body temperature of
37.4?C, respiration 20min-?, pulse 96 mm?, blood pressure 17/10kPa. He
exhibited violent coughing, dyspnea, stridor, lacrimation,
photophobia, irritating feeling of mouth and lips, palpitation,
depressed consciousness, bums on bare skin, and cornea1 hyperemia.
Wheezing, pneumonisis, pulmonary edema, cardiac arrhythmia and
myocarditis were found three days later. (2) A boy, 15, breathed in
the toxic vapor during sleep, experienced tachypnea and upper airway
obstruction, then fell into a coma. After being rescued and taken to
hospital, he was found to have body temperature 39░C respiration 38
min-?, pulse 124min- ?, blood pressure 16/l 1 kPa, bums on bare skin,
hyperemia and edema on eyelids, cornea1 and mouth membranes, and &es
in his airway. Pneumonisis and pulmonary edema, cardiac arrhythmia and
myocarditis were diagnosed 24 h later.
Summary Report: NA/920 1,1,1,3,3-Pentafluoropropane
...Honeywell Polymers of 71 Queens Rd, Melbourne, VIC, together with
Huntsmen Polyurethanes of Gate 3 Ballarat Rd, Deer Park, VIC. and
Ariel Industries of 26 Kembla St. Cheltenham, VIC., have submitted a
standard notification statement in support of their application for an
assessment certificate for HFC-245fa. The notified chemical is
intended to be used as a blowing agent for production of polyurethane,
polyisocyanurate, polystyrene, polyolefin and other polymeric foams;
also as a refrigerant and as an industrial aerosol solvent.
...Several repeated dose inhalation studies were conducted in
rats...In the subsequent 13-week study at concentrations up to 50 555
ppm, a dose-related incidence in myocarditis was observed in addition
to the clinical chemistry changes noted in the preliminary studies.
Focal myocarditis was taken to be spontaneous as it was seen in
control and treated rats, however, diffuse myocarditis was observed in
animals at the 10 000 and 50 000 nominal doses and in one animal at
2069 ppm, with the NOAEL taken to be 508 ppm (2.78 mg/L).
Occupational Health and Safety
The critical health effect for acute exposure is cardiac
sensitisation, with the lowest NOAEL being 34 100 ppm, established in
a dog inhalation study. For chronic effects, the critical health
effect is diffuse myocarditis, observed in a 90-day rat inhalation
study. For the purposes of the risk assessment, the NOAEL from this
study, 508 ppm, will be used for chronic exposure.
...Chronic exposure via gavage has resulted in myocarditis
(inflammation of the muscular tissue of the heart wall) and mortality
due to myocardial failure in rats and hepatic vacuolar degeneration in
...An intermediate in nickel refining and used as a catalyst in the
petroleum, plastic and rubber industries.
...Substantial inhalation...A chemical pneumonitis may develop in
severe cases, sometimes after a latent period of a few days.
Anorexia, abdominal pain, jaundice and diarrhoea are also reported and
rarely myocarditis, delirium, convulsions or coma. Death may occur
due to pulmonary haemorrhage, pulmonary or cerebral oedema or toxic
...Paraquat is a non-selective foliage applied contact herbicide which
is inactivated on contact with soil, so that replanting can be
performed almost immediately after spraying.
...Ingestion of moderate amounts of paraquat causes the sequence of 3
stages of morbid course...Stage II: lasting 2 to 8 days. Signs of
liver, kidney, cardiac damage Jaundice, fever, tachycardia,
myocarditis, respiratory distress, cyanosis, elevated BUN, creatinine,
serum alkaline phosphatase, serum bilirubin, serum transaminases, low
[Paraquat] Case reports from the literature
...Death following subcutaneous injection...A 24 year old woman
injected paraquat liquid concentrated subcutaneously into her left
arm. Next morning she injected herself again then went to
hospital...She developed widespread muscle pain, oedema, jaundice,
hypoxia and myocarditis with widespread T wave inversion. Treatment
was supportive with buprenorphine then diamorphine to control pain.
She became comatose 6 days after admission and died 2 days later.
Methyl ethyl ketone peroxide
...MEKP is a commonly used curing agent for thermosetting polyester
resins, a cross-linking agent and catalyst used in the production of
other polymers and polyester resins. It is used in the automobile,
airline, boating, fabric, and paint industries (
...The toxic oral dose of MEPK (in dimethyl phthalate) has been
reported to be 50 to 100 mL. Case reports showed that ingestion of
MEKP resulted in acute toxic symptoms such as gastrointestinal
bleeding, abdominal burns, necrosis, stomach perforation, oesophageal
stricture, severe metabolic acidosis, rapid hepatic failure,
rhabdomyolysis, and respiratory failure while temporary cardiac arrest
and toxic myocarditis were observed as well.
http://www.emedicine.com/emerg/topic42.htm Arsenic Toxicity
Hall JC, Harruff R: Fatal cardiac arrhythmia in a patient with
interstitial myocarditis related to chronic arsenic poisoning.
Southern Medical Journal 1989; 82: 1557-60.
[The above title clearly indicates that arsenic poisoning can lead to
myocarditis. However, I was not able to review the text of this
Deaths Associated with Exposure to Fumigants in Railroad Cars -- United States
...Fumigants, such as aluminum phosphide, can liberate toxic gases
that are rapidly absorbed through the respiratory tract (6). Symptoms
may begin immediately and can include fatigue, headache, nausea,
vomiting, abdominal pain, cough, and shortness of breath. Acute
poisoning, such as occurs after inhalation of phosphine, can lead to
pulmonary edema, central nervous system depression, toxic myocarditis,
and circulatory collapse
...Organophosphate (OP) compounds are the most widely used group of
insecticides in the world. Their acute toxicity causes a hazard both
to professional and amateur users. In the UK, this has led to concern
over OP use in sheep-dips, in agriculture generally and in the home.
...Cardiac effects: A number of studies have drawn attention to
cardiac effects associated with occupational exposure to OPs...In a
Health and Safety Executive publication (MS 17 December 1980) there is
mention of "slowing of the heart with decreased cardiac output."
Professor William McKenna of St George's Hospital, London, believes
that myocarditis (akin to a heart attack) can be caused after exposure
to propetamphos, an OP sheep dip...
Antimony poisoning has resulted from accidental occupational
inhalation, ingestion of food contaminated by storage containers and
therapeutic treatment with tartar emetic (potassium antimony
tartrate)...Antimony compounds have been used for a long time as
therapeutic agents for parasitic diseases such as schistosomiasis,
leishmaniasis, trypanosomiasis and ulcerative granu-loma. Side effects
of antimony therapy (the average dose is up to 1 g/d for 10 days)
include myocarditis, hepatitis and nephritis
Type of product...Fungicide, herbicide, commercial chemical and found
in some chemistry and crystal growing sets. The anhydrous form is
white, the pentahydrate is blue.
...Muthusethupathi et al (1988) reported toxic myocarditis as a cause
of death following copper sulphate poisoning although this information
is poorly referenced....Copper deposits have been noted in the heart
at autopsy following ingestion of some 280 mL copper sulphate solution
(Agarwal et al, 1975).
...Yellow phosphorus (also known as white phosphorus) is a corrosive
agent and damages all tissues it comes in contact with, including skin
and the gut lining. Initial symptoms usually reflect mucosal injury
and occur a few minutes to 24 hours following ingestion. The first
symptoms include severe vomiting and burning pain in the throat,
chest, and abdomen. The emesis may be bloody (either red, brown, or
black)and on occasion may have a garlic smell. In some cases, central
nervous system signs such as lethargy, restlessness, and irritability
are the earliest symptoms, followed by symptoms of gastrointestinal
injury. Shock and cardiopulmonary arrest leading to death may occur
early in severe ingestions. If the patient survives, a relatively
symptom-free period of a few hours or days may occur, although this is
not always the case. The third stage of toxicity then ensues with
systemic signs indicating severe injury to the liver, myocardium, and
brain. This is due to phosphine gas (PH3) formed in and absorbed from
the gut. Nausea and vomiting recur. Hemorrhage occurs at various sites
reflecting a depression of clotting factor synthesis in the damaged
liver. Also, thrombocytopenia may contribute. Hepatomegaly and
jaundice appear. Hypovolemic shock and toxic myocarditis may develop.
Brain injury is manifested by convulsions, delirium, and coma. Anuric
renal failure commonly develops due to shock and to the toxic effects
of phosphorus products and accumulating bilirubin on renal tubules.
The mortality rate of phosphorus poisonings may be as high as 50
INHALATION: ACUTE EXPOSURE
Pneumonia, bronchitis, bradycardia, myocarditis, cardiac dilation, and
gastrointestinal disturbances may follow acute exposures.
The above citations struck me as the main instances of chemical
exposures that have been associated with myocarditis.
As I said earlier, please let me know if you need any additional
information. Just post a follow-up request to let me know what you
need, and I'm at your service.
search strategy -- Google searches on:
[ myocarditis (toxic OR chemical OR exposure OR occupational) ]
[ "toxic myocarditis" and (occupational OR exposure OR acute) ]
Similar searches were also conducted in a number of health and medical databases.
Clarification of Answer by
06 Apr 2005 08:30 PDT
Thanks for the additional information you provided...it was quite helpful.
I was surprised that the accident is considered "confidential" as my
understanding is that all occupationally-related deaths are
investigated -- usually by OSHA -- and that there is a case file
report on each one. At least, that's generally the case in the U.S.
It's also hard to imagine exposures to the chemicals you listed NOT
resulting in evident burns, although obviously, this would depend on
the particular details of the actual incident in question.
I've compiled additional information about "toxic myocarditis", which
is the phrase use to refer to myocarditis caused by chemical exposure.
Once again, a very comprehensive review has not turned up any
information linking the particular chemicals you listed with
myocarditis, although I did uncover one result for the general
category of "aluminum compounds". This is probably the closest direct
connection you're likely to get, and the information on this is
Another thing to note is that exposure to fluorosilic acid (more
commonly known as fluorosilicic acid) -- while not associated directly
with myocarditis -- has strong and well documented detrimental effects
on the heart, and (to my mind) can certainly be construed as
contributing to chemical-induced heart failure.
I have also come across some information that is quite suggestive of a
relationship between myocarditis and exposure to the other acid
chemicals that you listed. Myocarditis can occur as a result of
serious burns...apparently substances produced by the burns
themselves, by secondary infections, or as a result of the body's
attempt to heal itself, can lead to myocarditis in burn victims.
This is an important link, because the chemicals you listed are by and
large a very caustic group of materials, and can lead to extensive
chemical burns upon exposure. It could very well be that the burns
then resulted in a case of myocarditis. Again, this link wouldn't be
relevant if burning was not a factor in the particular case, but I
wanted to make sure you were aware of the literature, just in case.
There is no way of confirming a link between chemical burns from the
chemicals you listed and myocarditis...it is just suggested here as a
I've listed below the additional information I found for all
chemicals...hopefully not overkill.
If you are in need of any further clarification, just let me know.
[Here are some articles linking burns to myocarditis]
J Trauma. 1979 May;19(5):358-69
A review of the complications of burns, their origin and importance
for illness and death.
--Complications are the major causes of illness and death after
burning and most of them stem from the burn wound.
--Bacterial infection and invasion of the burn are usually responsible
for septicemia, bronchopneumonia, and pyelonephritis although other
sources also contribute. Indirect manifestations of septicemia include
paralytic ileus, acute gastric dilatation, toxic myocarditis, and some
cases of renal failure.
Br Med J. 1979 Mar 17;1(6165):718-9.
Survival after major burn complicated by gas gangrene, acute renal
failure, and toxic myocarditis.
Davies DM, Brown JM, Bennett JP, Rainford DJ, Pusey CD, Chesshire A, Maw DS.
[This appears to be a case of myocarditis induced by a chemical burn,
though it would be necessary to review the full article to be sure]
Angiology. 1962 Jul;13:297-302.
Toxic myocarditis. Report of a case arising from ingestion of liquid
Dines De, Shipman K.
[Here is a link to detailed reports of the health effects of
fluorosilic acid. Myocarditis is NOT mentioned as a specific health
risk. However, the write-up does indicate serious cardiac impacts,
and also emphasizes the ability of the chemical to cause serious
--Corrosive to skin
--High inhalation exposure may cause pulmonary edema
--The substance is corrosive to the eyes, the skin and the respiratory
tract. Corrosive on ingestion. Inhalation of the vapor of this
substance may cause lung edema. ...The symptoms of lung edema often do
not become manifest until a few hours have passed and they are
aggravated by physical effort.
--On the morning of September 6, 1994, a tanker truck spilling 4500
gallons of fluorosilicic acid on Interstate 4 near Deltona, Florida,
covering an area 600 feet long and 60 feet wide, resulted in the
evacuation of approximately 2300 people form their homes into
shelters. Later in the day, fumes were detected in the Deltona Woods
neighborhood; because the acid could by carried by the wind, everyone
within a mile radius was evacuated. ...More than 50 people went to
hospitals, complaining of skin and respiratory irritation, including
burning in the throat, and headaches. An individual riding in a truck
with his arm out the window experienced burning on his forearm.
0.2.5.1 ACUTE EXPOSURE
A) Cardiac dysrhythmias consistent with hyperkalemia may
be noted. Fatal cardiac arrest occurred in several
patients with renal failure exposed to fluoride during
hemodialysis. QT prolongation secondary to hypocalcemia
can occur following fluoride toxicity.
[The health effects summary for hydrochloric acid also emphasizes its
nature as a caustic substance, but does not offer any direct links to
--The major effects of hydrogen chloride are those of local irritation
. It is generally believed that exposure to hydrogen chloride does not
result in effects on organs some distance from the portal of entry.
--Caution: Corrosive burns may result from the inhalation of acid
fumes and from skin contact with or the ingestion of strong acid.
Symptoms after ingestion or skin contact include immediate pain and
ulceration of all membranes and tissues which come in contact with the
acid. Ingestion may be assoc with nausea, vomiting and intense thirst;
corrosion of the stomach may lead within a few hours or a few days to
gastric perforation and peritonitis. Late esophageal, gastric and
pyloric strictures and stenoses should be anticipated. Contact of conc
acid with the eye can cause extensive necrosis of the conjunctiva and
corneal epithelium, resulting in perforation or opaque scarring.
Chemical pneumonitis can be expected after respiratory exposure to
acid vapors or after tracheobronchial aspiration of ingested acid.
Death may occur due to complications such as circulatory shock,
asphyxia due to glottic or laryngeal edema, perforation of the stomach
with peritonitis, gastric hemorrhage, infection or anition due to
[no effects for myocarditis or heart-related effects were noted for
aluminum sulfate, though there were effects noted for the more general
category of "aluminum compounds"]
[No link was available for this record -- instead, go to:
http://toxnet.nlm.nih.gov and search for "aluminum compounds" ]
Histological alterations of the heart consisted of interstitial
hyperplasia, muscle cell necrosis, and myocarditis all involving both
ventricles. Increased eosinophilia, nuclear picnosis, and
homogeneous-appearing cytoplasm were observed in myocardial cells.
Cells exhibiting microvacuolation or contraction bands were noted.
Multifocal myocarditis associated with interstitial hyperplasia, and
myocardial necrosis were also observed. Myocardial aluminum
accumulation (1.3-2.1 ug aluminum/g lyophilized tissue) representing a
3-4 fold increase over controls was found for aluminum acetylacetonate
A complete search of the Hazardous Substance Database at [
http://toxnet.nlm.nih.gov ] for any mention of the term "myocarditis"
resulted in a list of 180 chemicals. This is probably as
comprehensive a list as you are likely to find of chemicals that have
been associated -- in one way or another -- with myocarditis. The
list of chemicals, along with their CAS (chemical identification)
numbers is here:
HSDB Search Results
2 NICKEL CARBONYL
4 POTASSIUM BROMATE
5 PENICILLIN V
7 ALUMINUM COMPOUNDS
NO CAS RN
8 DIISOPROPYL FLUOROPHOSPHATE
9 ZINC PHOSPHIDE
13 ARSENIC TRIIODIDE
14 ARSENIC TRIFLUORIDE
15 CALCIUM ARSENITE
17 TETRAETHYL PYROPHOSPHATE
18 ARSENIC TRIBROMIDE
19 CYCLOHEXANONE PEROXIDE
20 ARSENIC TRISULFIDE
21 ETHYLENE GLYCOL DIACETATE
23 ARSENIC ACID
25 ARSANILIC ACID
26 DIMETHYLARSENIC ACID
30 FERRIC ARSENATE
31 MAGNESIUM ARSENATE
34 S,S,S-TRIBUTYL PHOSPHOROTRITHIOATE
35 SODIUM METHANEARSONATE
36 SODIUM SELENITE
39 TETRAETHYLENE GLYCOL
40 METHANEARSONIC ACID
42 TRIETHYL PHOSPHITE
48 MALEIC HYDRAZIDE
49 FERROUS ARSENATE
51 METHYL PARATHION
53 DIAMMONIUM SULFIDE
55 POTASSIUM ARSENATE
60 POLYPROPYLENE GLYCOL
61 ARSENIC, ELEMENTAL
79 LEAD ARSENATE
82 DISODIUM METHANEARSONATE
97 STRONTIUM ARSENITE TETRAHYDRATE
101 IRON CACODYLATE
102 SODIUM BROMATE
103 TRI(2-BUTOXYETHYL) PHOSPHATE
104 DI-N-PROPYLPHOSPHORODITHIOIC ACID
107 PHENYLTHIONOPHOSPHONIC DICHLORIDE
119 PENICILLIN G
120 PHENETHICILLIN POTASSIUM
125 METHYL TRITHION
130 COPPER(II) ARSENITE
132 2-BUTANONE PEROXIDE
133 3-NITRO-4-HYDROXYPHENYLARSONIC ACID
134 ETHYLENE GLYCOL
135 POLYPROPYLENE GLYCOL MONOMETHYL ETHER
136 SODIUM ARSANILATE
137 TRIETHYLENE GLYCOL BIS(2-ETHYLBUTYRATE)
139 TRIGLYCOL DIACETATE
140 O,O-DIMETHYL DITHIOPHOSPHATE
141 O-ETHYL ETHYLTHIOPHOSPHONYL CHLORIDE
142 ALUMINUM PHOSPHIDE
145 O,O-DIETHYL S-METHYL DITHIOPHOSPHATE
147 PENICILLIN VK
150 DIETHYL CHLOROPHOSPHATE
162 LONDON PURPLE
173 ISOPROPYLPHENYL DIPHENYL PHOSPHATE
174 BIS(ISOPROPYLPHENYL) PHENYL PHOSPHATE
175 ISODECYL DIPHENYL PHOSPHATE
176 BIS(T-BUTYLPHENYL) PHENYL PHOSPHATE
177 LITHIUM COMPOUNDS
NO CAS RN
178 ARSENIC COMPOUNDS
NO CAS RN
I hope this new information provides you with a comprehensive
perspective on the relation between chemical exposures and myocarditis
-- for your specific chemicals and for chemical exposures in general.
However, the question is not answered until you say it is! If you
need anything else, just ask.
Thanks...and all the best.