PESTICIDE
PROTECTION
a training manual for health personnel
A guide for recognizing, managing, preventing and verifying poisonings
caused by organophosphates, carbamates, and other selected pesticides
By
John E. Davies, M.D., M.P.H.
University of Miami School of Medicine
U.S. Environmental Protection Agency
U.S. DEPARTMENT Office of Pesticide Programs
of HEALTH, EDUCATION, and WELFARE March 1977
The contents of this publication do not necessarily reflect the policies of the
Environmental Protection Agency, nor does mention of trade names or
commercial products constitute endorsement or recommendation for use.
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CONTENTS
Page
Acknowledgments 1
Introduction 2
Chapter I — Pesticides 3
Chapter II'- Pesticide Hazards and How Exposure Occurs 7
Chapter III — Systemic Organophosphate and Carbamate Poisoning 12
Chapter IV - Miscellaneous Poisonings 19
Chapter V - Topical Effects 23
Chapter VI - Pesticide Epidemiology 25
Chapter VII - Methods of Prevention 28
Chapter VIII — Acute Pesticide Poisoning Verification 30
Appendix 1 Pesticide List 32
Appendix 2 Toxicity 39
Appendix 3 Screening Test 42
Appendix 4 Laboratory Methods 43
Appendix 5 Chemtrec 45
Appendix 6 Communications Check List 48
Appendix 7 Notification Locations 49
Appendix 8 Reporting Form 51
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ACKNOWLEDGMENTS
This manual was written by John E. Davies, M.D., M.P.H., University of Miami School of
Medicine, Miami, Florida. It was financed in part by a grant to the University of Miami from
the U.S. Environmental Protection Agency (EPA) and by funds from two EPA offices:
• Health Effects Research Laboratory, Environmental Toxicology Division, Research
Triangle Park, North Carolina, William F. Duram, director, and
• Office of Pesticide Programs, Operations Division, Washington, D.C., William C.
Holmberg, director.
Others who contributed to the project included:
Paul Agnano, Office of Migrant Health, Department of Health, Education, and Welfare
James Boland, EPA, Washington, D.C.
Judy Botana, University of Miami School of Medicine
Don Cook, EPA, Washington, D.C.
Frank Davido, EPA, Washington, D.C.
Erica Koehler, University of Miami School of Medicine
Keith Maddy, California Department of Agriculture
Joel Meltzner, EPA, Washington, D.C.
Dorothy Nayer, Editorial Consultant, New York, N.Y.
Billy Sandlin, Director, Office of Migrant Health, Department of Health, Education and
Welfare
Gerald T. Weekman, North Carolina State University
The ed::o: *-*s M-iy Ann Wiraley. EPA, Washington,D.C. Dlusirations were done by Joan
M. Davies. Miami, Florics.
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INTRODUCTION
This manual is for all health personnel
involved in the prevention, recognition, and
treatment of pesticide poisoning. However,
the information should be of particular
interest to nurses1, especially those working
in rural clinics, hospital emergency rooms,
and departments of public health. They are
the personnel most intimately involved with
the care of patients suffering from pesticide
poisoning.
Nurses are concerned not only with treat-
ment, but also with prevention. If they
understand the nature and use of pesticides,
they can work with their public health
personnel and community health workers
toward the development of safety measures.
They can contribute to improved case
finding and the followup of illness due to
pesticide exposure. They are also ideally
suited to educate agricultural workers and -
their families.
In the primary care setting, nurses in the
clinic are in a strategic position to recognize
cases early and to rapidly implement neces-
sary treatment measures. In this situation,
therefore, they must know the signs and
symptoms of pesticide poisoning, and the
emergency room measures which save lives
and decrease morbidity.
In the intensive care unit, the nurse's
ability to recognize the reappearance of
cholinesterase signs or to detect evidence of
atropine 'excesses can significantly con-
tribute to the successful management of this
medical emergency.
Ambulance attendants and other health
personnel also need this information so they
can begin the rapid treatment which is
necessary for lifesaving before the patient
arrives at the hospital.
There is an urgent need for accurate and
verified data on acute pesticide poisonings.
Present reporting is incomplete, and the
potential of the laboratory to verify possible
pesticide illness is poorly understood. This
book describes the steps necessary to con-
firm suspected pesticide illnesses.
This book deals mainly with two major
types of pesticide illness:
• acute systemic poisoning
—severe
—mild
• topical (local) effects
—eyes
—skin.
Actual case examples of pesticide poison-
ing are used to illustrate:
• the essential diagnostic and manage-
ment needs of the patient, and
• the potential of the laboratory in
verifying the event.
is no intention by the author to stereotype
by sex any health personnel or workers. To avoid a
cumbersome text, the words "he" and "she" have
been used interchangeably.
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CHAPTER I
PESTICIDES
What Are Pesticides?
Pesticides are a diverse group of chemicals
witSiSS've been developed to kill, prevent,
or suppress a wide variety of pests. Six of
the most common types are:
insecticides (insects)
herbicides (weeds)
fungicides (fungi)
molluscicides (snails and slugs)
nematicides (nematodes)
rodenticides (rodents).
Others include miticides (mites), defoliants
(remove unwanted plant growth), repellants
(keep pests away), attractants (lure pests),
and plant growth regulators (stop, speed up,
or otherwise change normal plant processes).
The essential component of a pesticide is
the active ingredient. This is the material
that actually controls the pest. It is pro-
duced in a manufacturing plant.
Following manufacture, the active ingre-
dient usually goes to a formulating plant,
where it is mixed with other chemicals and a
carrier for effective delivery. These are the
inert ingredients. They may include such
materials as talcs, oils, kerosene, and binding
agents (to increase adherence).
These formulated products are sold in
many forms, the most common of which are
liquids, wettable powders, granules, and
dusts. Each form is available in several
concentrations.
From the formulating plant, the products
move to a wide variety of users, including
farmers, commercial pesticide applicators,
and the general public.
Application is by various types of ground
equipment, hand equipment, or aircraft. It is
estimated that aircraft supply about 65
percent of all pesticides used by agriculture.
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Registration
More than 1 billion pounds of pesticides
are produced each year in the.United States.
Before any pesticide product can be sold,
the manufacturer must register it with the
Environmental Protection Agency (EPA).
The manufacturer must provide EPA the
results of many kinds of tests on the product
before it can be registered.
Labeling
EPA requires certain information to be.
on every pesticide label. Much of this
information can be of help to health person-
nel in diagnosis and treatment of pesticide
poisonings. When you know or suspect that
a pesticide is involved in an illness, try to get
the product label or a copy of it as soon as
possible.
Information which must be on a pesticide
label includes:
brand name
common name (simplified chemical
name)
.active ingredients (chemical or
common name, plus percent of the
contents they make up)
inert ingredients (need not be named,
but label must tell what percent of
contents they make up)
net contents
name and address of manufacturer
registration number (shows that the
product has been registered with
EPA)
establishment number (identifies the
factory which made the product)
signal words (one of the following)
fev
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Signal Wards
DANGER
WARNING
CAUTION
Toxicity
Highly toxic
Moderately
toxic
Low.toxicity
or
Comparatively free
from danger
Approximate amount
needed to kill the
average person
a taste to a
teaspoonful
a teaspoonful to a
tablespoonful
an ounce to more
than a pint
All products must bear the statement
"Keep out of reach of children."
• skull and crossbones (must appear,
with the word "poison", on all
highly toxic materials)
• ha/.ards to humans and animals
(includes ways in which the
product may be poisonous and pro-
tective equipment needed)
• environmental hazards
• physical and chemical hazards (special
fire, chemical, or explosion
hazards)
• statement of practical treatment
(emergency first aid measures and
information for physicians on the
treatment of poisoning)
• statement of use classification (tells
whether the pesticide is restricted
to use by certified applicators)
• directions for use (may include reentry
times, storage and disposal instruc-
• tions).
Chemical Groups and.
Mode of Action
Because most pesticides kill unwanted
organisms, they are obviously toxic
materials. Their mode of action depends on
the chemical group to which they belong.
The five major chemical groups are:
• organophosphates and carbamates
• organochlorines
• nitro and chloro phenols
• "anticoagulants
• bipyridyls.
The organophospliate and carbamate
group is the greatest public health problem.
It contains many widely used insecticides. In
the United States, severe organophosphate
poisoning results more often' from ethyl
parathion and phosdrin. Carbamates com-
monly used include carbaryl (Sevin), pro-
poxur (Baygon), and methomyl (Lannate or
Nudrin).
Organophosphates and carbamates inhibit
the enzyme cholinesterase (ChE). This in-
hibition causes a buildup of acetylcholine in
the body. Acetylcholine is the primary
chemical transmitter for:
• the preganglionic neurons of the
sympathetic and parasympathetic
fibers
• the postganglionic parasympathetic
fibers
• the central nervous system.
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These nerve fibers are called cholinergic
fibers. Anticholinesterase poisoning causes
parasympathetic effects in the organs they
supply. Some of these muscarinic effects are
shown in the following table.
Organ
Eyes • Pupil
Ciliary Muscle
Glands - Lacrimal
Salivary
Gastric
Heart • Muscle
Lungs - Bronchi
Intestines - Lumen
Sphincters
Bladder • Detrusor
muscle
Trigone
Effects
Constricted
Stimulated
Stimulated
Stimulated
Stimulated
Slow Rate
Constricted
Stimulated
Relaxation
Stimulated
. Inhibition
Physical Findings
Miosis
Blurred Vision
Tearing
Salivation
Increased Secretions
Bradycardia
Bronchospasm
Increased Peristalsis
Evacuation
Increased Peristalsis
Evacuation
Acetylcholine is also secreted at the
skeletal nerve endings, where, in excess,' it
produces weakness and paralysis. These
neuromuscular effects are called nicotinic
effects. Acetylcholine is also the chemical
mediator between the sympathetic nerve
fibers and the sweat glands. This is the
reason for excessive sweating in poisonings
with these cholinergic chemicals.
Atropine is the specific antidote for
cholinergic poisoning.. It blocks the effects
of acetylcholine. Atropine has no effect on
the neuromuscular nerve endings, however.
Tliis is where the oxinie drugs are beneficial.
They break up the chemical binding between
the pesticide and the cholinesterase
enzymes. This frees cholinesterase to stop
the acetylcholine action at the neuro-
muscular junction and thus end the paralytic
effects. Oximes are contraindicated, how-
ever, in cases of carbamate poisoning.
The effects of this group of chemicals are
both systemic and topical. If there is a
topical eye exposure, the effects are those of
topical effects of acetylcholine on the eye:
• the pupils are constricted
• the ciliary muscles are stimulated,
causing blurring of vision and an eye-
brow headache.
The organochlorine pesticides are power-
ful nervous system stimulators, but their
modes of action are not completely known.
These chemicals are soluble in fat, accumu-
late in the human body, and are very
persistent in the environment. Most uses of
these pesticides (such as DDT, aldrin, diel-
drin) are prohibited in the United States, so
acute poisonings are not frequent. Systemic
poisonings occur most often with endrin,
which is one of the most toxic members of
this group.
The nitro and chloro phenols are strong
metabolic stimulators causing increased
metabolism and hyperthermia. These are
widely used as fungicides and herbicides.
The anticoagulants are rodenticides, such
as Warfarin. They produce their effects by
inhibiting prothrombin and causing capillary
damage.
The bipyridyls include paraquat and
diquat, which are widely used in agriculture
. for weed control and defoliation. These
chemicals produce proliferative changes irt a
variety of tissues.
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CHAPTER II
PESTICIDE HAZARDS AND
HOW EXPOSURE OCCURS
Hazards of Pesticide Use
The hazard of a pesticide-its potential
for producing injury-depends on:
• the inherent toxicity of the active
ingredient (see Appendix 2)
• the dose and/or concentration of the
pesticide
• the physical and chemical properties
of the material
• the route of absorption of the chem-
ical
• the duration of exposure.
The dose (amount) of pesticide taken
into the body is the most important factor
in determining the hazard of a chemical. A
small amount of some pesticides may cause
severe illness; large doses of others may be
fairly harmless. Pesticide concentrates are
tlie most hazardous form. Persons working
with them are at the greatest risk of getting a
harmful dose.
The physical and chemical properties of
some pesticides make them more hazardous
in certain situations. Parathion, for example,
changes to a more toxic chemical (paraoxon)
at high temperatures.
The three possible routes of absorption
are:
• ingestion—the result of accidents or
suicide or homicide attempts; usually
causes the most serious effects.
• inhalation—occurs mainly in confined
spaces (warehouses, pesticide tanks);
usually causes less serious effects than
ingestion.
• dermal absorption—most common
method of occupational exposure;
causes the least severe effects.
The duration of exposure helps determine
the dose absorbed. Brief exposure to a
concentrate could produce effects similar to
longer exposure to the dilute pesticide.
How Exposure Occurs
There is some degree of hazard at each
step of pesticide manufacture and use. Be-
cause they work with pesticide concentrates,
workers in pesticide manufacturing and for-
mulating plants are in positions with a high
potential hazard. Most manufacturing plants,
however, use a closed system which does not
expose the workers to the pesticide. Safe
occupational practices and good industrial
hygiene help to minimize the danger at both
these stages of pesticide production.
Health personnel are most likely to en-
counter . pesticide poisonings in three main
groups of people:
• applicators
• pickers
• children.
Each is clinically different and each must
be recognized at once.
Applicator Poisoning
The hazard to applicators results from the
dilution and application of the pesticide
concentrate. Hazards exist, therefore, in
both mixing and applying the pesticide. The
toxicity and concentration of pesticides
varies in different applicator situations.
Every applicator, however, is at risk of
exposure to varying degrees of pesticide
concentrate, and therefore is in danger of
poisoning. The further down a person is in
the chain of pesticide handling and use, the
less training he usually has and the greater is
his risk of poisoning.
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Workers associated with the aerial appli-
cation of pesticides are especially highly
exposed.
It is unwise for a pilot to mix and load
chemicals. The normal procedure is to em-
ploy aircraft loaders and swampers. They
dilute the material and load the aircraft
before each run. This is done on the airstrip
with fixed wing aircraft. Helicopters are
often loaded from an accompanying trailer
at the scene of application. Loaders are one
of the most highly exposed occupational
groups in the entire application process.
An example of applicator poisoning
was Tony B., who was employed as a
pesticide mixer and loader for a fixed-
wing crop dusting firm. He had started
loading the aircraft at 6 a.m. with a
mixture of parathion 6-3 and toxaphcne.
Rubber gloves were the only protective
clothing worn, and fie was a heavy
smoker. .
He soon began to feel unwell. He was
admitted at 11:35 a.m. to the emergency
room of a local hospital. He complained
of nausea, vomiting, weakness, and
blurring of vision. His pupils were con-
stricted and there was profuse perspira-
tion.
A screening cholinesterase test re-
vealed severe inhibition. After being put
in a shower and scrubbed all over, he was
given a total of 12 mg of atropine
intravenously in the emergency room
over a brief period of time. Tfie oxime
2-PAM was also administered in a one
gram dose in 1,000 cc of D5W. Atropine
therapy was continued after his transfer
to the medical ward and he proceeded to
improve.over the next few days.
Subsequent blood and urine metabo-
lite studies by the laboratory confirmed
that the poisoning was due to an ex-
posure to ethyl and methyl parathion.
The special lessons of this case are:
• the illness was severe
• no protective clothing was worn
• there was no positive history of an
accidental spill
• only one applicator was affected.
Picker Poisoning
Once a pesticide has been diluted to its
final concentration and is applied to the
crop, the pesticide residue remaining on the
fruit and leaves becomes a new source of
exposure. The concentrations of these resi-
dues are high at first. They decline with time
as a result of biodegradation and exposure to
light. The rate of dissipation of foliar resi-
dues varies considerably with different pesti-
cides and with different concentrations of
pesticides. Weather factors also affect the
rate of dissipation. Rain removes pesticides
more rapidly, and high temperatures favor
the changing of some pesticides to more
toxic forms.
«fe|^,^ryFi-
• ^A^'- • j^V^i^ '•SSfe-K 1L->!>:
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Too early a reentry to a treated site
creates a hazard for the worker. The worker
is at risk during the process of thinning and
harvesting the crop.
One type of pesticide worker who is at
special risk of intoxication is called a
"scout." This person goes into the fields
regularly to count the number of pests on
the plants. Since the job often involves going
into the field shortly after application, there
is a special risk of residue intoxication.
This type of human illness is sometimes
called "picker poisoning." It occurs most
frequently with exposures to plants with
large leaf surfaces such as citrus, peaches,
grapes and tobacco.
Cotton is a crop with a large leaf surface,
but it is almost entirely machine-harvested in
the United States, so that—except for scouts
—residue poisoning is not a serious threat
with this crop. This is not the case, however,
for Central America, where hand harvesting
is still practiced and hundreds of cases of
"picker poisoning" have been reported.
Because pesticide poisoning from residues
may be milder, it may be overlooked in the
health clinic. Health personnel should take
special care to be on the lookout for this
syndrome with people working in high-
exposure crops, especially when the weather
is hot.
A nurse may be confronted by a picker
who was picking beans or citrus or working
in a field with high foliar crops and suddenly
became dizzy, developed a headache, and
became progressively weak. He would pro-
bably complain of sweating profusely. She
may soon find that other members of the
crew have developed the same symptoms
and are waiting outside the clinic or have
gone to another doctor.
The clue is that residue poisoning cases:
• are usually multiple
• are mild
• require only small doses of antidotes.
The following outbreak is a typical
example:
An emergency room nurse had three
patients with mild symptoms resembling
•those seen in organophosphate poison-
ings.
Three other patients were in the wait-
ing room with similar symptoms, and
four more were on their way to the
hospital. • All were weak, sweating and
complaining of abdominal cramps,
nausea, and vomiting. Some had dif-
ficulty with breathing. Others had
diarrhea as well as vomiting. Most had
miotic pupils.
Bv the end of the evening, 10 of a
crew of 17 migrant workers who had
been detasseling corn that morning had
been admitted to the hospital. They
received atropine intravenously and were
beginning to respond after decontamina-
tion and intravenous fluids.
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10
The epidemic was clearly due to an
anticholinesterase pesticide, a fact that
was later confirmed when 64 mg of a
carbamate insecticide called methomyl
was identified from a methylene chloride
extraction from the shirt of one of the
exposed victims.
At 7 a.m. they had entered a cornfield
where an airplane had sprayed the field
with methomyl. Their clothes and canvas
shoes had become moistened from the
dew on the ground and from the moisture
on the leaves.
Child Poisonings
Children are the group at the greatest risk
of accidental poisoning from pesticides
which have not been stored or disposed of
properly. Prompt action is especially im-
portant in these poisonings.
The nurse must always be on the lookout
for these dire emergencies. In this type of
case, the nurse is usually confronted with a
very sick child who is semicomatose, vomit-
ing profusely, and has diarrhea and pinpoint
pupils. For example:
A 4-1/2-year-old boy who was playing
in his grandfather's barn spilled some
liquid over his pants at about 1 p.m.
When he returned home at 6 p.m. he was
not feeling well and he looked pale and
listless. He was put to bed. At 9 p.m., his
parents noted that he was drowsy and
that his respirations were labored. His
father rushed him from his home to the
emergency room of a nearby hospital His
mother checked his clothes and noticed
they had an insecticide smell. The grand:
father checked the barn and found a
bottle of ethyl parathion.
By the time the boy reached the
emergency room, he was moribund, in
deep coma with his eyes rolled back, and
barely breathing. His respirations soon
ceased and he had to be kept alive by
artificial respiration and endotracheal in-
tubation. When the mother reported that
parathion had been spilled on the child,
he was stripped, washed all over, and
oxygenated. Atropine was administered
intravenously every JO minutes through
the night, and 2-PAM was given. By 5:30
a.m. he was much improved and con-
tinued to recover over the next 2 days.
Here, the point is that exposure might
not be recognized. Children get extremely ill
very rapidly and treatment must be prompt
and vigorous.
There is a high incidence of pica among
migrant families. This is a situation where
the ingestion of a pesticide might not be
realized. Geophagia is not uncommon.
A 3-year-old child was taken to a local
migrant clinic with extreme miosis, foam-
ing at the mouth and nose, and diffuse
rales throughout both lung fields. An
exposure history revealed that the child
had been playing in a strawberry field
which had been heavily treated within the
last three days with phosdrin, Kelthane,
and parathion. Pesticide analyses showed
total inhibition of cholinesterase. Para-
thion was identified in the gastric con-
tent. It was later determined that the
intoxication was the result of ingestion of
soil containing parathion.
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This case illustrates the point that chil-
dren eat dirt—which is not commonly recog-
nized. It exemplifies the real possibility of
this mechanism of poisoning when a toddler
is playing in the fields where the mother is
working.
Emergency Personnel
In a rural area, the emergency personnel
in the ambulance can expect to encounter
anticholinesterase poisonings. Recognition
and early treatment are of vital importance.
A migrant worker might fall off a ladder
while picking citrus which had been treated
with parathion. His pesticide exposure might
not be recognized while the patient is being
transported to the hospital, particularly if he
appears dazed. The diagnosis may be
clouded by other evidence of trauma which
he may have sustained during his fall. The
questions which should be asked are, "Why
did the worker fall?" and, "Was the fall due
to pesticides?"
Pesticide poisoning might also go un-
recognized in a pilot who has had an aircraft
accident. The possibility of injury is likely to
be of greater concern than the possibility of
chemical intoxication which may have been
the result of a spill before, during, or after
the accident. It is essential to evaluate
whether the pilot has sustained a serious
pesticide exposure. If the exposure is al-
lowed to pass unrecognized, it could cost
him his life.
Emergency personnel who are trans-
porting suspected cases to the hospital
should always be in radio contact with the
hospital. The patient's condition might sud-
denly deteriorate in transit, requiring im-
mediate therapy. If the physician is alerted
ahead of time, he can communicate with the
emergency personnel to prescribe whatever
is necessary.
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CHAPTER III
SYSTEMIC ORGANOPHOSPHATE AND CARBAMATE
POISONING
12
Symptoms and Signs
Symptoms and signs of systemic organo-
phosphate and carbamate poisonings are
almost entirely due to cholinergic manifesta-
tions. They include both muscarinic and
nicotinic effects and are the result of acetyl-
choline accumulation.
Early symptoms depend on the route of
absorption and the severity of the intoxica-
tion.
• Gastric symptoms appear earlier if the
material has been ingested.
• Shortness of breath, salivation, and
excessive bronchial secretions occur if
the material has been inhaled.
• With dermal exposure, gastrointestinal
and respiratory symptoms appear at
the same time.
• In children, a convulsion may be the
first symptom.
• In serious intoxication, both mus-
carinic and nicotinic symptoms and
signs begin shortly after exposure.
Muscarinic effects^ which usually precede
nicotinic effects, include:
• anorexia
• nausea
• vomiting
• abdominal cramps
• diarrhea
• involuntary defecation and urination
• sweating
• salivation
• lacrimation
• pain in the chest
• ' excessive bronchial secretions
• blurring of vision due to miosis.
Nicotinic effects include:
• muscle twitching
• fasciculations
• weakness
• flaccid paralysis.
With involvement of the muscles of res-
piration, further respiratory failure occurs
from bronchial constriction, blockage by
secretions, and depression of the respiratory
center.
Central nervous signs and symptoms in-
clude anxiety, restlessness, giddiness, head-
ache, drowsiness, convulsions, and coma.
In the advanced state, the patient is pale,
sweating, and frothing at the mouth. The
pupils usually are miotic and non-responsive
to light. Pupils will sometimes be dilated if
the patient is in extremis. They will then
become miotic with initial treatment.
The. most important neurological findings
are:
• Fasciculations—localized and general-
ized involuntary twitching may be
elicited by tapping the muscles over
the cheekbone, over the thorax, or on
the arms.
• Sometimes generalized clonic seizures
may be observed. The plantar reflex is
extensor and electroencephalographic
changes may be noted.
• Miosis—the pupil is small, usually less
than 5 mm. The diameter of the pupil
in millimeters should be recorded.
Metabolic signs and symptoms include
the following:
• Blood sugar may be elevated at first,
and glycosuria may be observed. The
level of hyperglycemia is much less
than levels observed with diabetic
coma. Ketoacidosis is not seen.
• Serum electrolytes are usually normal,
though hypokalemia may occur and be
aggravated by diuretic therapy. Serum
K levels should be checked early.
• Fever is not a constant finding. The
patient's temperature usually is normal
or subnormal, though severe dehydra-
tion may occasionally cause fever.
• Polymorphonuclear leukocytosis is
common.
Clinical Diagnosis
In severe poisoning, the initial diagnosis
and institution of appropriate treatment
must be made on clinical grounds alone,
since there is not enough time to wait for
confirmatory laboratory results.
The most important factors in the clinical
diagnosis of organophosphate poisoning are:
• a pesticide exposure history
• symptoms and signs typical of an
anticholinesterase illness
• the presence of atropine refractoriness.
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Pesticide Exposure History
The first prerequisite to diagnosis is to
determine whether the patient has been
exposed to any of the anticholinesterase
pesticides. Symptoms begin shortly after
exposure. They are seen especially early
after ingestion or inhalation.
" With few exceptions the patient will
begin to feel ill within 1 5 minutes to an hour
after ingestion.
If a patient has ingested a pesticide, this is
usually known or admitted, except in the
case of a toddler. Ingestion of a pesticide as
a result of pica might not be realized.
Dermal exposure may be obvious and the
patient may recall spilling the pesticide on
his skin and clothing. On the other hand, he
may not be aware that pesticides can be
absorbed in this way. He may not mention
that his shirt, pants, or shoes were wet from
the pesticide or from moist residue on
leaves. In arid areas, dermal exposure occurs
from dry, dusty residues on the leaves of
the plant and there is no sensation of
wetness. In all suspected cases, however,
diagnosis is materially helped if the attend-
ing health personnel are made aware that the
patient has sustained a pesticide exposure.
Use the exposure history form in Appendix
Symptoms and Signs
Symptoms and signs compatible with
cholinergic excess are the second most im-
portant variables contributing to the clinical
diagnosis of anticholinesterase poisoning.
Although symptoms of cholinergic
poisoning may be easily confused with those
of other conditions, a pesticide cause should
always be considered. Physical signs are less
subject to misinterpretation. Miosis is a rare
condition in the clinic setting. It should
always lead to first consideration of ex-
posure to anticholinesterase pesticides.
Miosis is doubly significant if it is accom-
panied by nicotinic and muscarinic symp-
toms and muscle fasciculations. These signs,
together with the general appearance of the
patient, should prompt the nurse and the
physician io a diagnosis of organophosphate
poisoning.
Atropine Refractoriness
This is the third important clinical ob-
servation which helps substantiate the diag-
nosis of an anticholinesterase illness. When a
physician prescribes a larger than normal
dose of atropine in a person not exposed to
anticholinesterase pesticides, the early signs
of atropine toxicity soon become apparent.
These signs include:
• dry mouth
• flushed skin
• increased heart rate
• dilated pupils.
If the patient has anticholinesterase
poisoning, large doses of atropine are re-
quired to produce these normal reactions.
Differential Diagnosis
Mild anticholinesterase poisoning causes
such symptoms as:
• headache
• fatigue
• dizziness
• blurred vision
• excessive sweating
• nausea and vomiting
• stomach cramps
• diarrhea
« salivation.
These symptoms are shared by many
illnesses not related to pesticides, such as
influenza, heat stroke or heat exhaustion,
and gastroenteritis.
Moderately severe poisoning causes all of
the symptoms found in mild poisoning, but
in addition, the patient:
• is unable to walk
• often complains of chest discomfort
and tightness
• exhibits marked miosis
• exhibits muscle twitching.
These symptoms might be reasonably
mistaken for such conditions as pneumonia,
myocardial infarction, and encephalitis.
Severe poisoning results in:
• unconsciousness
• local or generalized seizures
• the manifestation of a florid choliner-
gic crisis.
In these cases, several alternative causes
of coma enter into the differential diagnosis.
13
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If there is glycosuria, diabetic coma might be
considered. The miosis might lead to con-
sideration of a cerebrovascular accident.
particularly a pontine hemorrhage. '
14
Screening Tests
At all three levels of clinical severity, a
screening cholinesterase test can help con-
firm a cholinergic poisoning diagnosis. These
are colorimetric procedures using filter paper
impregnated with a color reagent which is
sensitive to pH change. The time taken for
the color to change is a crude index of the
degree of cholinesterase inhibition. The
severity of inhibition is categorized as none,
suspicious, or severe.
Although these tests have several limita-
tions, they offer the most immediate con-
firmation which is within the laboratory
expertise in any hospital or clinic. The
Acholest test is the most reliable of the
several available screening methods for
plasma cholinesterase determinations. It can
detect inhibition as low as 20 percent of
plasma cholinesterase. The results correlate
well with more quantitative procedures.
The test should be administered:
• to any patient who claims to have
been exposed to a pesticide
• to any worker having regular and
heavy pesticide exposure, such as
spraying chemicals or loading aircraft
(see Chanter VII-PREVENTION)
• to any patient complaining of three or
more of the previously cited symp-
toms
• to any patient with any one of the
following physical signs:
—miosis (less than 5 mm in size)
—muscle fasciculations
—bronchial exudation
-bradycardia (pulse rate of 50 or less
per minute).
To prepare a blood sample for the
Acholest or other qualitative screening test,
collect 1 cc of blood in a green stoppered
vacutainer tube (heparin-lined) and separate
the plasma by centrifugation.
(See Appendix 3 for complete description
of the test.)
No further laboratory confirmation is
needed in the clinical setting.
Definitive verification and validation of
the poisoning episode, however, calls for:
• quantitative measurements of the
plasma and red cell cholinesterase
• specific analysis of the intact pesticide
and/or urinary pesticide metabolites to
help identify the specific offending
pesticide.
Laboratory Diagnosis
Three types of laboratory investigations
can help confirm a clinical diagnosis of
cholinergic poisoning:
• cholinesterase determination
• ' urinary metabolite studies
• intact pesticide studies.
Cholinesterase Determination
The levels of cholinesterase in the red
blood cells and in the plasma are used to
confirm human poisoning. They correlate
well with nervous system cholinesterase in-
hibition. It is believed that ChE values of 0.5.
or less (Michel method) for either red blood
cell or plasma represent abnormal de-
pressions for most individuals.
The four laboratory techniques most
commonly used for quantitative expressions
of these enzyme activities are the elec-
trometric (Michel), the titrimetric (pH stat),
the colorimetric (Ellman) and gas chromato-
graphic (Cranmer) methods (see Appendix
4).
In two instances, laboratory tests may
not show low levels of cholinesterase
enzymes, even though cholinergic poisoning
is present. These are:
• overexposure to carbamate pesticides—
With this group of chemicals, cholin-
esterase reactivation is rapid. In vitro
reactivation often occurs before the
blood reaches the laboratory. Normal
red cell and plasma levels may be
reported even in the presence of ob-
v'ous cholinergic illness.
• reu cell cholinesterase determinations
made after the administration of 2-
PAM—if this oxime is given early in
the case, red cell cholinesterase re-
activates rapidly, even in the presence
of continued cholinergic symptoms.
-------
Low plasma cholinesterase levels may
sometimes be due to other causes including:
• liver diseases, malnutrition, hyper-
pyrexia, myocardial infarction, der-
matomyositis
• after certain drugs
• as a result of genetically determined
low plasma cholinesterase. This con-
dition may lead to respiratory arrest
after being anesthetized with succinyl-
choline. The defect occurs in about 3
percent of the population. Recog-
nition of this defect is primarily of
medico-legal importance. Special
laboratory procedures permit dif-
ferentiation of pesticide exposure
from this phenoty.pic mechanism.
Low red blood cell cholinesterase is
found:
• in paroxysmal hemoglobinuria
• in the newborn after complicated
delivery
• with disseminated sclerosis
Urinary Metabolite Studies
These breakdown products are excellent
measures of exposure. Qualitatively they
often provide valuable information on the
exact type of pesticide which has caused the
illness. Quantitatively, their concentrations
in urine can be used as a measure of:
• the severity of the poisoning
• its probable duration.
The analysis of these breakdown products,
therefore, is the second laboratory technique
which will assist in the confirmation of the
illness. (See Appendix 4)
Intact Pesticide Studies
The identification of the intact pesticide
is the third way in which the laboratory can
confirm an anticholinesterase pesticide
poisoning. In the case of ingestion of the
material, the intact-pesticide can be identi-
fied by gas chromatographic studies of the
gastric contents. In severe exposures, the
intact pesticides may even be identified in
the blood and other tissues. (See Appendix
4)
Collecting Specimens
Confirmatory tests must be done by a
special pesticide analytical laboratory. When
confirmatory tests are required, specimens
should be handled in specific ways:
Blood-If the Acholest test is positive,
collect an additional 8 cc of blood for
definitive red blood cell and plasma cholin-
esterase determination. A 10 ml green
stoppered vacutainer tube (heparin-lined) is
the best method of collection. Invert the
tube gently once or twice to insure proper
mixing. Take care to avoid hemolysis. Label
the tube to show:
• the name of the patient
• the time and.date of collection
• whether a sample was obtained before
or after 2-PAM administration.
Cover the label with transparent tape.
Refrigerate (do not freeze) the tube
before transferring it to the laboratory. If
the specimen must be sent to another
laboratory, it should be airshipped. Pack it
with crushed ice in a styrofoam container.
Urine and other tissues—In cases of sus-
pected organophosphate and carbamate
poisonings, collect 20 ml of urine as soon as
possible. Place the urine in a hexane-washed
glass bottle with an aluminum foil lined
metal screw top. The label should contain:
• patient identification
• the time and date of voiding.
C'jvfT tie iabiJ vitb .V i-.wi^ir.v.v..' '.iC'j- m^
close the lid securely. Freeze the bottle and
its contents and airship it with the blood as
soon as possible.
In special circumstances, other tissues
may be collected for laboratory analysis.
Handle them the same way as urine.
Gastric contents-Gastric washings should
be labeled and frozen before sending to the
laboratory. Collect the first washing for
lexicological studies.
15
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Treatment
The five basic steps in emergency treat-
ment are:
• airway clearance
• oxygenation
• antidotal therapy
• decontamination, including gastric
lavage
• collection of appropriate biological
materials.
Time is of the utmost importance. The
prompt action required in a serious intoxica-
tion, particularly with a child, is similar to
that required by a patient with ventricular
fibrillation with cardiac arrest.
What a nurse may or may not do in such
circumstances depends on:
• her previous training and experience in
the necessary resuscitative procedures
• whether there is a written protocol.
In both the rural health clinic and the
emergency room, standing orders should be
drawn up ahead of time to cover pesticide
emergency situations. The nurse and
physician should agree on procedures in-
volved in all five of the steps of emergency
treatment.
Airway Clearance and
Oxygenation
Remove dentures and use a finger or,
preferably, suction to clean mucus and
debris from the mouth and pharynx. In-
troduce an orOpharyngeal or nasopharyngeal
airway, and administer 50 percent oxygen
by mask or nasal catheter. Draw serial blood
gases to monitor respiratory and metabolic
dynamics.
Antidotal Therapy
Atropine-Atropine sulphate is lifesaving
and should be given as soon as possible. It
should not be withheld while efforts are
being made to overcome any respiratory
embarrassment.
The nurse should be instructed by pro-
tocol to administer atropine when the
patient is first seen. Under no circumstances
should such a patient be transferred to the
emergency room without having had atro-
.pine therapy.
For an adult, the physician will order 2 to
4 mg of atropine sulphate intramuscularly or
intravenously every 10 minutes during the
early phase of treatment. Doses for children
should be proportionate to weight-0.05 mg
per kg of body weight.
The pulse rate, pupil size, and amount of
bronchial exudate are important variables
which influence the frequency of atropine
administration. Large doses may be required.
In a severe poisoning case, a man was
unconscious for 14 days and required atro-
pine continuously for 18 days. The thera-
peutic goals are to reach and maintain
atropinization during the period of poison-
ing. Dilation of the pupils and a pulse rate of
140 per minute are the indications that
atropinization has been reached.
With certain types of organophosphate
pesticides, the intoxication period may be
prolonged. The signs of cholinesterase in-
hibition reappear as the effects of atropine
wear off. These periods may be followed by
periods of atropine excesses with the pulse
rate exceeding .140/min and the pupils be-
coming fully dilated. It is thus very im-
portant for the nurse to continuously moni-
tor:
• the pulse rate
• the degree of bronchial secretions
• rate of respiration
• changes in pupil size.
This information helps the physician de-
cide when it is necessary to readminister
atropine or when there are signs of atropine
toxicity. As recovery occurs, the intervals
between atropine administration get longer
until there is no further need to continue
this treatment. When no further treatment is
necessary, the patient should be observed in
the hospital for another 24 hours.
Even if the poisoning appears mild and
atropinization is reached after only a single
dose, observe the patient for 24 hours. The
atropine may have produced only temporary
relief of symptoms in what may prove to be
a serious case of poisoning.
Oxime-The only oxime available in the
United States is N-Methyl 2 formyl-
pyridinium oxime, used as the chloride (2
PAM-C1) or Protopam Chloride. This should
be available in any health clinic or emer-
gency room likely to have to treat choliner-
gic poisonings. Give 2-PAM as early as
possible and always in conjunction with
atropine. The two drugs are complementary
in their action.
-------
The oximes are not recommended for use
in cases of carbamate poisoning—in fact,
they are contraindicated—but more research
is needed in this area. Therefore, the
physician faces a dilemma when it is not
known whether the poisoning has been
caused by an organophosphate or a car-
bamate. Make every possible effort immedi-
ately to find out the specific pesticide
involved.
The oximes are not active against all of
the organophosphates. Depending upon the
particular organophosphate, "aging" of the
phosphorylated enzyme occurs, at which
time the inhibited enzyme can no longer be
reactivated by 2-PAM.
With parathion, aging does not occur for
2 days after exposure, so 2-PAM may be
used up to that time. With malathion, aging
is early. Effects of oxime therapy in this
intoxication are generally disappointing.
The usual adult dose is 1 gm intraven-
ously, preferably as an infusion in 250 ml of
saline given over 30 minutes. If this is not
practicable, give it in not less than 2
minutes. A second dose of 1 gm can be given
in 1 hour. In children, 20 to 50 mg per kg is
given intravenously in 250 ml of saline over
30 minutes.
If convulsions are troublesome, tri-
methadione or thiopental may be used. Res-
piratory embarrassment is usually due to
excessive bronchial secretions rather than
pulmonary edema. For this reason, opiates,
aminophylline, reserpine, phenothiazine,
tranquilizers, succinylcholine, and
furosemide are contraindicated.
Decontamination
The first step should be to remove the
patient from further exposure. Bring him
out of the exposure area and try to limit
further absorption of the pesticide.
The attendant should strip the patient
and place all clothing in a plastic bag. The
patient must be thoroughly washed. If he is
conscious, place him in a shower and wash
him all over with large amounts of soap and
water. Be sure to rinse the hair thoroughly
and remove any residue from under the
nails.
Decontamination also includes the re-
moval of the ingested pesticide. Vomiting
should not be induced:
• in stuporous or unconscious patients,
or
• if petroleum distillates .are part of the
pesticide formulation.
In these instances, or if there is doubt
about what pesticide is involved, gastric
lavage is preferable to the use of an emetic.
Place the patient head down and on his side
to avoid aspiration of vomitus. V/ash out the
stomach with large amounts of water.
The use of an esophageal obturator is the
best way to avoid aspiration of stomach
contents, if the nurse has had previous
training in inserting the obturator.
Collection of Biological Materials
(See instructions in previous section,
"Laboratory Diagnosis.")
Carbamate Poisoning
Carbamate pesticides, like the organo-
phosphates, are powerful cholinesterase in-
hibitors. Special considerations in the
diagnosis and treatment of carbamate
poisonings include the following:
• Cholinesterase reactivates rapidly after
carbamate poisoning. Laboratory
cholinesterase determination tests may
be misleading.
• Since blood tests may not be reliable,
identification of the nonhalogenated
phenols-the urinary metabolites of
carbamates-becomes more significant.
• The oxime 2-PAM should not be used
to treat carbamate intoxications.
Interprofessional
Communication
A systemic pesticide poisoning involves a
wide variety of health professionals. Good
communication among these professionals is
essential.
If the clinic nurse is the first point of
patient contact, she should contact the -
attending physician as soon as possible, as
well as the patient's next of kin and his
employer.
If the physician is not immediately avail-
able, the nurse will have to communicate
with an ambulance service and the nearest
hospital emergency room to arrange for the
transfer of the patient. Meanwhile, she must
begin emergency treatment to stabilize the
patient's condition.
If there is an epidemic of poisonings, the
17
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health department must be informed. These
are usually "picker poisoning" incidents. If
there is a massive chemical spill with a
potential community hazard, the nurse
should communicate with CHEMTREC (See
Appendix 5).
If a sick child has been brought in from
the home and the source of the pesticide has
not been identified or removed, other
children in the home may be at immediate
risk of poisoning. The police should be
contacted. The nurse should also contact the
regional pesticide analytical laboratory for
poisoning verification.
The implementation of these com-
munication needs are best insured by work-
ing through a checklist of persons who
should be contacted. This is shown in
Appendix 6.
stfe^^Hfr^^^r
f*£*fst~l~'tX~'5$^ S* '-fJf> .
tgg&si
If the patient comes straight from the
field or the home to the hospital, the
emergency room nurse is primarily con-
cerned with reporting significant changes in
her patient's condition to the attending
physician. She should contact the immediate
family, employer, police, or health depart-
ment if this has not already been done.
EMT personnel should be in constant
radio contact with the emergency room
while transporting the poisoned patient to
the hospital. If the patient suddenly
collapses, the attendant can apply the appro-
priate treatment while in transit.
The public health nurse or the com-
munity health worker will encounter special
risk factors when investigating the scene of
the accident. These must be reported to the
employer or landowner and local health and
environmental resources so that further
poisonings can be prevented.
-------
CHAPTER IV
MISCELLANEOUS POISONINGS
Orgahochlorine Insecticides
These pesticides:
• are soluble in fat
• build up in the human body
• are persistent (break down slowly and
remain unchanged in the environment
for a long time)
• are powerful nervous system stimu-
lators. Organochlorine poisoning
causes excitation. Convulsions are the
most important symptom.
Applicator poisonings and residue in-
toxication are not common with these pesti-
cides, since most of their uses are prohibited.
Most systemic poisonings are caused by
accidental oral ingestion of endrin.
Acute poisonings may be caused by the
organochlorine pesticides which are no
longer sold but still remain in some homes.
A. 2-year-old boy was brought to the
emergency room of a local hospital. On
arrival, he had a convulsive seizure. The
parents reported that the- child had in-
gested an unknown amount of an in-
secticide. The child was hyperactive,
atoxic, and unsteady. He fell down when
he tried to walk. Pupils were 2 to 3 mm
in size. There was no vomiting, sweating,
or increased bronchial secretions. The
chest was clear. He was given diphenylhy-
dantoin and a large intravenous dose of
phenobarbitaL He was admitted to the
Pediatric Intensive Care Unit for observa-
tion. Both heparinized and whole blood
were collected. By the Michel method the
RBC ChE was 0.69 &ph/hr, and the
plasma ChE was 0.90 Aph/hr which are
normal enzyme levels with this method.
Blood tests for intact pesticide, however,
identified dieldrin in a concentration of
407 ppb. This confirmed an organo-
chlorine pesticide poisoning due to
dieldrin.
Nursing care for organochlorine poisoning
is the same as that for other convulsive
disorders. There are no specific antidotes.
Sodium phenobarbital and diphenylhy-
dantoin are the drugs most often used to
control the convulsive seizures. Tri-
methadione or thiopental may also be used.
Diagnosis can be confirmed by identi-
fying the intact pesticide in the serum. In a
case of suspected organochlorine pesticide
poisoning, draw 10 cc into a red stoppered
vacutainer tube. Label the sample and allow
it to clot. Separate the serum and freeze it.
If the specimen must be sent to another
laboratory, it should be airshipped. Pack it
with crushed ice in a styrofoam container.
Dieldrin seldom causes convulsions when
blood levels are less than 200 ppb. With
blood levels greater than 200 ppb, convulsive
seizures may be seen. The worker should be
taken off his work with levels of this
magnitude.
Bipyridyls
Paraquat is more toxic than diquat. and
produces proliferative changes in the lung,
cornea, lens, nasal mucosa, skin, and finger-
nails. Diquat affects the lens and gastro-
intestinal mucosa. It does not produce the
lung changes characteristic of paraquat.
Except for eye lesion, illness due to
occupational exposure is usually mild and is
the result of topical exposure. Epistaxis
occurs in workers following droplet inhala-
tion. Conjunctival changes occur with ac-
cidental spills.
The clinical picture following accidental
or suicidal ingestion is very different. Para-
quat ingestions are frequently fatal. Their
management is unsatisfactory and largely
symptomatic. Three clinical stages follow
ingestion of as little as an ounce of paraquat:
• The first is a gastrointestinal phase
with burning in the mouth and throat,
nausea, vomiting, and abdominal pain
with diarrhea.
• Several days after exposure, signs of
hepatic and renal toxicity appear.
These are due to central zone necrosis
in the liver and acute tubular necrosis
of the kidney.
• Ten to 20 days after ingestion, pro-
gressive proliferative changes develop
in the lungs. Hyperplastic changes in
the terminal bronchioles occur with
alveolar fibroblastic proliferation. Loss
of lung surfactant has been demon-
19
-------
20
strated. Within a few days, death from
respiratory failure occurs.
Urine studies have indicated that 90
percent of the ingested paraquat is excreted
in the first 24 hours. Delayed pulmonary
effects appear to be the result of an irrever-
sible process that develops long after the
initial stimuli has gone.
Paraquat is poorly absorbed from the gut.
Excretion data suggest that only 1 to 5
percent of the ingested material is absorbed
in man. Maximal blood concentrations are
reached within 4 to 6 hours after ingestion.
Treatment, therefore, is primarily concerned
with:
• decreasing the amount of paraquat
absorbed
• perfusion of the circulating blood
through charcoal columns.
Steps to decrease the amount of the
paraquat absorbed include:
• gastric lavage with every precaution to
avoid aspiration of gastric contents
• repeated administration of large
amounts of adsorbents together with
the administration of purgatives.
The ability of Bentonite, Fuller's earth
and other clays to absorb bipyridyls has
been studied. Fuller's earth was more ef-
fective than Bentonite. 500 ml. of a 30
percent suspension of Fuller's earth together
with 5 percent magnesium sulphate should
be administered after lavage,
Perfusion of the blood through charcoal
columns has been advocated.2 In addition to
hemoperfusion, forced diuresis with
Mannitol, hemodialysis, and corticosteroid
and immunosuppresant therapy have also
been recommended.•*
Although steroids and alkaloids are given
for pulmonary complications, no treatment
has shown to be effective at this stage of the
intoxication.
There is a simple urine test for paraquat
that can provide presumptive evidence of
paraquat poisonings in suspected cases ex-
hibiting early symptomatology.4
2Smith, L.L., Wright, A., Wyatt, I., Rose, M.S.
Brit. Med. J. 1974, (4):569.
3The Lancet Editorial, 1976, (1):1057.
4Goulding, R., Volans, G.N., Crome, P., Widdop,
B.Brit. Med. J. 1976, (1):42.
Rodenticides
These are not particularly hazardous, but
they are widely used. Children often ac-
cidentally ingest rodent tablets or baits-an
event which leads to much anxiety, ques-
tions, and the need for reassurance.
Fumigants
Fumigants can present serious health
hazards resulting in human illnesses and,
occasionally, death. Methyl bromide,
acrylonitrile, calcium cyanide, and carbon
tetrachloride are the fumigants most likely
to cause death if overexposure occurs.
Others which can cause skin and eye injury
and systemic illness include:
• sulfuryl fluoride (Vikane)
• 1,3 dichloropropene (Telone)
• 1,2 dibromo 3 chloropropane
(Nemagon)
• ethylene dibromide
• formaldehyde
• chloropicrin
• phosphine
• sodium .methyl dithiocarbamate
(Vapam).
Methyl bromide is sold as a liquid under
pressure. At atmospheric' pressure, it
vaporizes at 40°F to a colorless and odorless
gas. Because of this property, methyl
bromide should always be used in formula-
tions which contain chloropicrin (tear gas),
which serves as a warning agent. A worker
who is exposed to enough of this mixture to
cause tearing has also been exposed to
dangerous quantities of methyl bromide.
Methyl bromide is absorbed through the
lungs, skin, and mucous membranes. It can
cause:
• acute poisoning, either topical or
systemic, and
• chronic effects.
Acute Poisoning
" Topical effects-Skin contact with the
liquid or high concentrations of the vapor
produces itching and prickling of the skin.
This is followed by reddening and formation
of vesicles and slow-healing blisters. Getting
the liquid in the eyes may cause corneal
ulceration.
Systemic poisoning-Symptoms usually
develop 3 to 12 hours after inhalation of the
vapor. Early symptoms include nausea,
vomiting, dizziness, headache, blurring of
-------
vision, and changing taste of food. These are
followed by listlessness, weakness, staggering
gait, and slurring of speech. In addition, the
patient may complain of double vision and
even temporary blindness.
In severe poisoning, the victim becomes
comatose and has a high fever and respira-
tory embarrassment. Death is usually the
result of either respiratory failure or cardio-
vascular collapse. Death is preceded by
cyanosis, pulmonary edema, and renal
failure. Muscle'twitching and convulsion are
not uncommon.
Chronic Effects
A papular pustular rash, not unlike acne,
may develop on the face, arms, back, and
chest. This is the result of repeated dermal
exposures. All the symptoms and signs listed
under acute effects may also appear as a
result of chronic exposure. Fatigability and
loss of appetite are frequent complaints.
More severe chronic manifestations include a
change of personality, a chronic central
nervous system effect which may persist for
years. Visual disturbances and locomotor
impairment are common.
Treatment
First, quickly get the patient out of the
contaminated atmosphere and remove all
contaminated clothing. Methyl bromide can
penetrate rubber gloves. Wash skin burns
carefully withvwater. Administer a thera-
peutic trial with dimercaprol (BAL). If there
is severe respiratory depression, give oxygen
under positive pressure. Artificial respiration
may be necessary. Keep the patient under
observation for at least 48 hours after
symptoms have subsided.
No simple laboratory tests are available
for confirmation, but blood levels of
bromine correlate well with the severity of
the exposure.
Prevention
Methyl bromide mus't be applied by a
closed-delivery system. All State and local
requirements concerning the use of plastic
sheets or tarpaulins must be followed.
Guards and warning signs should be posted.
The application should be done at a safe
distance from inhabited structures, and
under appropriate weather conditions.
Animals and humans must be removed from
the area to be treated.
Methyl bromide must be kept under lock
except when the applicator or other respon-
sible persons are present. The material
should be stored in a cool, dry, well-.
ventilated building in order to avoid an
explosion hazard and the possible buildup of
toxic concentrations of vapors caused by
leaking containers. The storage sites should
be at a safe distance from populated areas
and inhabited buildings.
Dinitrqphenol and
Pentachlorophenol
These materials are used as insecticide
sprays, fungicides, and wood preservatives.
They are rapidly absorbed by the gastro-
intestinal and respiratory tracts and the skin.
They are profound stimulators, stimulating
all the cells of the body by blocking
oxidative phosphorylation. Body fat is the
major, if not exclusive, fuel for this extra
metabolism.5 The body temperature be-
comes elevated and the breathing and heart
rate increase rapidly. Because respiratory
and cardiac stimulation do not accelerate in
proportion to the increased metabolism,
anoxia and acidosis develop rapidly.
Acute and Subacute Poisoning
The patient complains of marked fatiga-
bility, excessive thirst, and profuse sweating.
His face is flushed. These are the result of
the higher metabolic state, as is the ex-
ceptionally high fever, which may reach
110°F. The higher the fever, the more
serious is the intoxication.
In such cases, tachycardia, hyperpnea,
cyanosis, and muscle cramps will occur.
Death, which is usually the result of respira-
tory or circulatory collapse, occurs within
24 hours.
In mild or subacute cases, most workers
will complain of lassitude, headache, and
malaise. Some, however, may have an alarm-
ing sense of excessive energy, drive, and
hyperactivity. They should be warned of the
dangers of overheating, because the meta-
bolic activities of these compounds are
exaggerated by heat.
5Shils, M.E. and Gpldwater, L.I. Effect of diet on
the susceptibility of the rat to poisoning by 2,4-
dinitrotoluene. Arch Environ Health 8:262, 1953.
21
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Treatment
The essential goals of treatment are:
• prompt elimination of the material
and curtailment of all possible further
sources of exposure,
• symptomatic treatment designed to
control the high fever and its second-
ary consequences, such as anoxia,
dehydration, and acidosis.
Gastric lavage with large amounts of
sodium bicarbonate solution should be fol-
lowed by saline catharsis using 15 to 30
grams of sodium or magnesium sulphate in
water. To control the fever, use cold packs
and alcohol sponges. Cold water enemas may
be needed.
Supportive measures include:
• intravenous fluids to control dehydra-
tion and acidosis,
• oxygen and artificial respiration as
required.
Following the acute phase of the intoxica-
tion, liver and renal complications may
develop. These are the result of the toxic
action of these materials on the renal tubules
and on the liver cells.
22
Laboratory Confirmation
Laboratory confirmation of the intoxica-
tion is provided by the detection of high
levels of dinitrophenols or pentachlorophe-
nol in the urine and blood of the victim.
-------
CHAPTER V
TOPICAL EFFECTS
Skin Problems Among
Agricultural Workers
Skin problems accounted for 62 percent
of all occupational diseases reported in the
United States in 1973. The agricultural
worker who is exposed to pesticides is four
times more likely to develop a skin rash than
the average industrial worker.
Diagnosis
Because the agricultural worker is ex-
posed to a wide variety of agents besides
pesticides, determining the cause of der-
matitis is highly complex.
Dermatitis from pesticides can result
from:
• exposure to primary irritants, or
• contact with contact sensitizers (aller-
gens).
The first diagnostic consideration is to
differentiate between these two types of
skin rash.
Primary Irritants-Primary irritants are
either absolute or relative.
Absolute 'irritants are usually chemicals
which can cause a chemical burn or severe
irritation on almost anyone's skin. The
reaction occurs immediately or within an
hour or so. It usually does not present a
diagnostic problem.
Relative irritants are agents which can
cause varying degrees of dermatitis (inflam-
mation of the skin) according to environ-
mental conditions. Some, like kerosene or
turpentine, are more likely to cause pro-
blems on sweating skin, or under occlusive
clothing and boots. All are more damaging
to skin which is already abnormal (sunburn,
eczema, and atopic dermatitis).
Some areas of the body are more sus-
ceptible than others. The genitalia, scrotum,
and eyelids are particularly vulnerable. Thus,
a worker might have dermatitis on the penis
and eyelids due to contamination by ma-
terials on the hands.
The primary irritants usually produce a
short term dermatitis which goes away and
can be related to a known definite exposure.
The rash caused by primary irritants is
more likely to be confined to the areas of
the skin actually exposed to the chemical.
Irritants in solution often are confined to
the hands and the forearms, but relative
irritants may be absorbed in clothing and
boots. The rash will appear where the
clothing is in closest contact with the skin-
buttocks, knees, and dorsum of the feet..
Irritants dispersed in sprays or aerosols
more often affect the face and neck.
Powders tend to accumulate at the waistline,
the collar, and tops of boots.
A primary irritant is likely to be the cause
if several workers experience a rash on
exposed surfaces at the same time, especially
if burning or itching occurs soon after
exposure. It is useful to ask the patient if he
knows whether any other workers in the
same area have the same problem.
When multiple cases of dermatitis follow
the application of an agricultural chemical,
the material or its carrier is clearly too
irritating for continued use. The nurse
should notify the physician as soon as
possible.
Treatment—When the person is removed
from further exposure, this type of der-
matitis usually clears up, especially if a
topical steroid cream is applied to the
affected areas. '
23
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24
Contact Sensitizers—Substances which
cause allergic contact dermatitis may affect
only a few individuals who have become
"sensitized" or "allergic" to the material.
Even then, there may be marked differences
between individuals in the degree of cutane-
ous reaction or seventy of the clinical
dermatitis.
A new product occasionally has a high
potential for producing allergic skin condi-
tions. These usually are soon recognized and
taken off the market, but it is still worth-
while to ask whether a new product has been
used. First reports of a hazardous substance
often come from nurses or other medical
personnel who are closest to actual field
conditions.
Depending on the patient's sensitization,
the reaction may occur within a few hours
of contact to as long as a week. Most occur
within 48 hours. Redness, itching, swelling
(especially around the eyes), and "water
blisters" are the clues to this type of
dermatitis.
Having a basic knowledge of the principal
sensitizers, reading the ingredients on the
labels, or checking the Physicians' Desk
Reference will often help in diagnosis. Plant
dermatitis is common and must be con-
sidered as a cause of allergic contact der-
matitis.
Some chemicals may be both primary
irritants and contact sensitizers. In addition,
many agricultural compounds are dissolved
in solvents such as kerosene or xylene. This
creates a perfect mechanism for both pri-
mary skin damage and an allergic reaction.
Treatment—The treatment of allergic con-
tact dermatitis includes:
• using cool compresses
• treating infections
• identifying the offending agent.
It may be necessary to refer the patient to a
facility which performs patch testing.
Topical steroid creams, gels, or lotions are
beneficial. Severe or extensive cases may
require a short course of systemic steroids.
Systemic steroid therapy should always be
under the direction of a physician. It should
never be given to patients who may have
undetected tuberculosis or are at risk of
tuberculosis.
Apart from the highly specialized area of
patch testing, the laboratory has no place in
the verification of topical skin effects from
pesticides.
The illnesses are often a sensitivity
phenomenon and are therefore not strictly
dose related. Cholinesterase determinations
and urinary metabolite studies are not neces-
sary.
Effects of Pesticides
on the Eyes
Eye injuries are common in agricultural
workers. Topical effects can occur as the
result of exposure to any of the pesticides in
common use today. In addition, xylene and
petroleum distillates in common use as
pesticide carriers are very irritating ma-
terials. They produce a severe inflammatory
response when they get into the eyes.
Eye injuries can result from:
• accidentally splashing or spilling the
material into the eye
• exposure to pesticide drift
• rubbing the eyes with contaminated
hands.
Sulphur, paraquat, Omite, parathion, and
dieldrin are some of the most common
causes of eye injuries.
Eye injuries are most common in pesti-
cide mixers, loaders, and applicators because
of their risk of exposure to the pesticide
concentrate.
Damage is the result of:
• a direct irritating effect of the chemi-
cal or the vehicle
• an allergic reaction
• direct phamiacologic action on the
eye, as is the case with anticholin-
esterase pesticides.
Conjunctivitis, corneal ulceration, uveitis
and lenticular opacities are some of the
lesions which occur. These chemicals have a
delayed effect on visual accommodation and
diminish the peripheral fields of vision.
Treatment
If there is a conjunctival infection, ir-
rigate the eyes from the inside to the outside
with large amounts of water or sterile
normal saline solution. After the eyes have
been thoroughly irrigated, evert first the
upper and then the lower lid and clean them
with a moist cotton tip to remove any
debris. Then irrigate the eyes once more.
Apply an eye shield and make an appoint-
ment for the patient to see the attending
physician for definitive diagnosis and treat-
ment.
-------
CHAPTER VI
PESTICIDE EPIDEMIOLOGY
The possible effects of pesticide exposure
can be divided into three categories:
• acute exposure, which produces acute
poisoning and topical injuries
• chronic high exposure, which is con-
cerned with long term effects of pesti-
cides
• chronic low exposure or incidental
exposure, which is concerned with
human pesticide residue and the pub-
lic's concern for the possible risks of
carcinogenesis.
Those at risk in the first category are:
• pesticide workers
• members of the general public who
become accidentally poisoned in the
home or garden.
In the second category is the occupa-
tionally exposed worker. The third category
includes the general public, who are exposed
to small amounts of pesticides in water, air,
food, and clothing. (.
The nurse is primarily concerned with the
first and second categories. She is most
likely to encounter acute pesticide poisoning
in the clinic and hospital. She has an
important role in preventing both acute and
unnecessary chronic exposure to the workers
in the second category.
As an individual she is probably also
concerned with the third level of exposure
for her own and her community's sake.
Acute Poisonings
Acute pesticide poisonings are a serious
health problem in many areas of the world.
The World Health Organization estimates
that there are approximately 500,000 cases
annually, with about a 1 percent fatality
rate.
No accurate statistics exist for the United
States as a whole, but reports from selected
populations suggest the size of the problem.
In California in 1975, there were 503
systemic pesticide poisonings in persons em-
ployed in agriculture. Some authors, how-
ever, believe that these reported statistics
represent no more than 1 percent of the
number.
Incidence data is equally incomplete in
Florida, a state second only to California in
the amount of pesticides used. Between
1970 and 1975, pesticides were listed as a
PESTICIDE EXPOSURES, HEALTH CONCERNS AND NURSING GOALS
Pesticide Dose
High
Intermediate
Low
Types of Exposure
Acute
Overexposure
Occupational
Incidental
Health Concerns
Pesticide Poisonings
Topical Injuries
(Skin and Eyes)
Occupational Safety
Human and Environmental
Pesticide Residues
Nursing Goals
Prevention
Early Diagnosis
Industrial Hygiene
Occupational Health
Health Education
Surveillance
Safety Standards
Monitoring
25
-------
26
cause "of death in 26 persons in Florida.
• Ten deaths (35 percent) were children
under the age of 10.
• Males accounted for 19 cases (73
percent).
• Fifteen ingested the toxicants (57 per-
cent).
• Three inhaled the agent (11 percent).
• Two persons died from dermal con-
tact.
These statistics, however, tell nothing of
the occupational hazards of pesticides or
why these materials were in the home. The
total picture is still incomplete. Information
on the acute morbidity of pesticides is of
extreme importance, for it is only with this
knowledge that decisions can be made on
future pesticide management, policies, and
regulations.
Applicator and Picker Poisoning
These two syndromes have distinct
clinical, epidemiologic, and public health
features.
Clinically, because residues are much less
toxic than pesticide concentrates, picker
poisoning is of shorter duration. Cases are
often multiple and the case fatality rate is
low.
Illness which is the result of exposure to
the concentrate is usually more severe and
protracted. The case fatality rate is high.
Epidemiologically, too, there are dif-
. ferences. Residue intoxications occur pri-
marily in the agricultural worker and the
migrant worker through dermal exposure to
the foliar residues. In this situation, the
worker is not aware of the potential hazard,
because he does not know that the residues
are there. Occasionally, exposure may occur
when workers are accidentally sprayed or
come in contact with pesticide drift.
The applicator, on the other hand, should
be aware of the potential hazard of the
chemical which he is applying or mixing.
Such persons should be acquainted with the
hazards of spills and should have been taught
to wear protective clothing. They are gen-
erally more informed and better trained.
•Applicator poisonings occur wherever ap-
plication is done. Residue poisonings occur
mainly in hot, arid areas.
Preventive strategies also • differ. With
residue poisoning the preventive goal is to
make the place of work safe. The federal
government has established reentry times for
different pesticides. These are the time
intervals which must elapse after a crop has
been treated before it is safe for an agricul-
tural worker to enter the field. The pre-
ventive approach is very different for appli-
cators. It focuses on the preventive potential
of worker education, personal hygiene, and
the wearing of protective clothing. These are
skills for which the nurse is ideally suited.
Child Poisoning
Children are the group at greatest risk of
accidental poisoning from pesticides which
have not been securely stored or correctly
J 0
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r~FTT|
\I\IJ. ,!,
i— —
-------
disposed of, although adults, too, are at risk
if chemicals are stored in improper bottles.
The home, the garden, and the local refuse
dump are often the scene for the other
category • of acute accidental pesticide
poisoning. The toddler is the person at
greatest risk.
When water is added to a pesticide, the
liquid often becomes milky. If this is stored
in a bottle, there is a real danger that the
poison will be inadvertently given to a baby.
Incorrect disposal of pesticide containers
causes many fatal cases.
A 2/6-year-old Mexican child died after
being sprayed with what seemed to be a
harmless fluid in a simple spray gun. Her
father, who could speak no English, could
not understand the label on the container
which he brought home from the field
where he had been working. There were
remnants of the pesticide concentrate at
the bottom of the drum. He knew that
the liquid was effective against the pests
in the fields, so he told his 14-year-old
daughter to spray the home because of
heavy roach infestation. She did this, but
tragically also sprayed her younger sister
who was asleep in the crib.
Transportation and storage also can be
hazardous. If there is a large spill, such as
might occur with a tanker collision or train
crash, a highly dangerous situation can arise.
In this event, a telephone call (collect) can
be made to CHEMTREC, which is a special
service to assist in such cases. A description
of CHEMTREC service is in Appendix 5.
Careless unloading of pesticides can cause
leaking containers. If these are stored in
warehouses close to food, accidental con-
tamination of food may occur. This is
especially true during storms and floods. The
general upkeep and waste disposal practices
of the pesticide storehouse should be in-
spected regularly.
It is apparent that pesticide poisonings
are a problem area for several agencies and
institutions. A cooperative effort is needed
to insure human safety through improved
pesticide management.
27
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CHAPTER VII
METHODS OF PREVENTION
28
The rural health clinic nurse and the
public health nurse are in key positions to
prevent pesticide poisoning.
These nurses are often the first to learn
about a case. They are usually the first
contact of the patient and his family. This
gives them the opportunity to follow up the
case.
The nurse can go to the site of the
poisoning to try to retrace how the episode
came about. She can visit the home to
discuss safety and explain to the worker and
his family how poisonings happen. Since
other members of the camp will be in-
terested, the nurse can use the incident as a
teaching point.
She should also meet with crew chiefs
and employers to promote pesticide safety.
The nurse can meet with workers, em-
ployers, and even local government groups,
civic clubs, and labor groups to explain how
the occupational health hazards of the
worker can be minimized with sound pesti-
cide management. Her visibility at the place
of work and in the home will facilitate her
acceptance greatly. It also will allow her to
see for herself the whole chain of pesticide
formulation, application, and exposure.
Applicator Safety
The nurse should check for the correct
use of protective clothing. She should find
out whether goggles, masks, coveralls, rubber
gloves and boots are provided and if they are
in good repair. She should also watch for
skin conditions in the workers. When
abrasions in the skin occur through cuts or
dermatitis, the skin loses its natural pro-
tective barrier and chemical- absorption is
greatly increased.
She should discuss with the operator such
issues as the availability to the worker of
showers at the end of the day and the
opportunities for a wash and change of
clothing.
She also should discuss procedures for
rinsing and disposing of empty pesticide
containers. Too often, they are left in the
fields or are picked up and dumped into an
empty lot or garbage pit, where they con-
tinue to present a poisoning potential.
She should make sure the employer
knows the name of the nearest physician and
hospital. She might leave her own card and
tell'him about the pesticide poisoning pro-
gram at the clinic.
Routine cholinesterase testing is neces-
sary for highly exposed workers such as
formulators, spray rig operators, pilots, and
aircraft mixers and loaders. The nurse and
the employer should explore ways in which
a program can be organized. Pre-employ-
-------
ment cholinesterase determination can be
built into the pre-employment physical
examination.
It is customary to advise the withdrawal
of the worker from continued anticholin-
esterase exposure if there is a 20 percent
decline in these enzymes.
If a baseline level is not available, the
worker should be temporarily changed to a
job away from anticholinesterase pesticides
if the red blood cell cholinesterase is less
than 0.4 Aph/hr (Michel method).
Picker Safety
In the education of the agricultural
laborer whose pesticide risk is from plant
residues, field reentry regulations are most
important. In addition, the nurse can help
the migrant worker understand the need for:
• changing clothing
• showering after work
• laundering the clothes correctly
• keeping contaminated clothes away
from living areas
• washing hands and face before
smoking or eating while working in
treated fields.
Parathion has been identified in the house
dust of workers' homes. This is probably due
to the dusty residues dropping off the
workers' clothing or shoes.
One worker was hospitalized with
parathion poisoning. When he went back
to work-a few days later, he became sick
a second time after putting the same
clothes on again. High concentrations of
parathion were detected in the clothing.
ESfflH
The nurse can discuss laundering with the
worker's wife. The worker's clothing should
be laundered separately and subjected to
several washes. Laundering of contaminated
fabric three times is not effective in re-
moving all of the residues of some pesticides
(such as parathion and toxaphene).
29
Child Safety
The nurse should inform families about
correct storage of chemicals in the home.
She also should warn them about taking the
child into the fields. Often it is impossible to
leave the child at home, because there are no
day nurseries nearby. If one is available and
the mother agrees to use it, the risk that
occurs from a child playing in the field while
her father and mother are working would be
removed.
One 5-year-old girl, for example, was.
hospitalized for organophosphate poison-
ing which she sustained while playing in
the fields where her parents worked. She
was poisoned as a result of eating
tomatoes which had been treated earlier
with phosdrin, me thorny I, dimethioate
and monocrotophos. The mother recog-
nized the condition because five of her
eight children had been hospitalized for
parathion poisoning several years earlier.
-------
CHAPTER VIII
ACUTE PESTICIDE POISONING VERIFICATION
30
Verification of acute pesticide poisonings
has two aspects:
• the confirmation of diagnosis, using
clinical and laboratory procedures, and
• collecting and tabulating data on con-
firmed pesticide poisonings to gain a
fuller understanding of the problem.
Diagnosing a full-blown organophosphate
illness usually poses no real problem. It
appears, however, that many milder intoxi-
cations of agricultural laborers and migrant
workers pass unrecognized or are not re-
ported or satisfactorily investigated in the
field. Even in the more obvious cases,
laboratory confirmation is insufficiently
practiced. The specific pesticide involved is
rarely identified.
The verification and chemical confirma-
tion of an acute pesticide poisoning is
important to many people:
• The agricultural worker is interested,
for within the process rests his as-
surance for just consideration and com-
pensation for any job-related poisoning.
• Farmers are vitally interested in having
safe products to use.
• Chemical manufacturers and formula-
tors want to make a safe product and
to insure that an alleged pesticide
illness attributed to their product is
correctly investigated and verified.
Jurisdictions, legislators, law enforcers,
and insurance organizations are also served
by verification of pesticide-related illnesses.
The attending physician also has a profes-
sional interest, having often proceeded with
vigorous treatment measures without initial
laboratory confirmation.
Steps in Poisoning Verification
The four ingredients of poisoning verifica-
tion are:
• a pesticide exposure history in which
the symptoms complained of are com-
patible in time and with a known
toxicity of a pesticide
• physical signs which reflect the known
toxicity of the pesticide
• demonstration of significant red blood
cell and plasma cholinesterase in-
hibition in acute organophosphate
poisoning
• identification of the specific urinary
pesticide metabolites and/or the intact
pesticides in certain tissues of the body.
(See Chapter III. for information on
clinical and laboratory tests and instructions
for collecting laboratory specimens.)
Many of the symptoms of acute pesticide
poisoning are common to a wide variety of
more frequently occurring illnesses not re-
lated to pesticides. Some of the diseases
included in this list are influenza, gastro-
enteritis, heat exhaustion, diseases of the.
heart and lung, and central nervous system
disorders. To distinguish mild or subacute
cases of pesticide illnesses from these other
conditions, an arbitrary and reasonable selec-
tion process is necessary. The following
guidelines are suggested.
Apply a simple cholinesterase screening
test such as the Acholest:
• to any patient who complains of having
sustained a pesticide exposure '
• to any worker having regular and heavy
pesticide exposure
• to any patient who has three or more
of the following symptoms: weakness,
sweating, headache, nausea and vomit-
ing, diarrhea, abdominal cramps, ex-
cessive tearing, salivation, bronchial
secretions, shortness of breath, pains in
the chest, blurring of vision, and con-
vulsions
• to any patient with either miosis (less
than 5 mm in size), muscle twitching or
fasciculations, or clinical evidence of
bronchial spasm or bronchial exudation
• to any patient with a pulse rate of 50
or less.
In the event of a convulsion, serum should
not only be analyzed for cholinesterase
inhibition but it should also be sent to a
special pesticide analytical laboratory for
electron capture and mass spectrometry gas
chromatographic studies for organochlorine
poisonings.
If the screening test is positive, the
nursing and medical staff should be in-
formed at once. The following additional
steps are necessary:
• Collect 8 cc of blood in a heparinized
tube for quantitation of red cell and
plasma cholinesterase determinations.
-------
• Collect 20 cc of urine for urinary
pesticide studies.
• Ship both as soon as possible to a
specialized pesticide analytical labora-
tory for more specific and precise
analyses.
• Send a resume of the pertinent clinical
findings and exposure history with the
specimens. (Use form in Appendix 8.)
• Inform the local community health
worker and public health nurse so that
a field visit can be made as soon as
possible.
Shipping and Notification
Even in the verification process, speed is
of the utmost importance. Inform the
special pesticide laboratory by telephone of
the time of shipment and the expected time
of arrival of the specimens and enclosures.
The laboratory should complete the analyses
quickly. Results should be communicated to
the referral center first by telephone and
then by written confirmation.
Farm worker clinics may send specimens,
together with background information, to
the appropriate laboratory as listed in Ap-
pendix 7.
Notice:Clinics forwarding specimens via
air shipment should notify the
laboratory via telephone so the
shipment can be met at the air-
port. Flight number and date
should be provided (if known)
together with names . and tele-
phone numbers to be used in
calling back results.
County hospitals, private clinics, industry
health units and emergency rooms wishing
to have samples analyzed may do so, if cost
reimbursement conditions are acceptable.
If suspected cases of poisoning are being
treated in rural areas distant 'from possible
air connections to the verification labora-
tory, consult state departments of health or
agriculture for nearby laboratory facilities
which can provide blood and urine analyses.
- Collection of Data
For administrative purposes, reports on
pesticide poisoning should contain the fol-
lowing information:
1. Name of patient or patient identi-
fication number (Patient identi-
fication is needed so that followup
studies can be done. Because this
form is a medical record, the infor-
mation will remain confidential.)
2. Sex and age of patient
3. Time and date of occurrence
4. Location of occurrence
5. Route of exposure
6. Symptoms and signs
7. Type of pesticide used:
a) name (copy or original of label,
if possible)
b) active ingredients
c) EPA registration number
8. Crop pesticide was applied to and
target pest
9. Means by which pesticide was
applied-plane, spray rig, etc.
10. Immediate first aid measures taken,
medical attention provided
11. Any other facts which could be
useful in analyzing the causes and
effects of the poisoning.
To provide this information, duplicate
the form in Appendix 8, fill it in, and
furnish it with medical specimens to be
analyzed. Locally used forms providing the
above data may be substituted.
31
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APPENDIX I
SELECTED CHOLINESTERASE-INHIBITING ORGANIC PHOSPHORUS
PESTICIDES
Common or
Trade Name Chemical Name
Acephate 0,S-Dimethyl acetyl phosphoramidothioate
Acethion 0,0-Diethyl S-carboethoxymethyl phosphorodithioate
Acetoxon 0,0-Diethyl 0-carboethoxymethyl phosphorothioate
Akton* or Axiom* O,0-Diethyl 0-(2-chloro-l-(2,5-dichlorophenyl) (vinyl)
phosphorothioate
Alamos* or Azothoate* or Slam* . O-(p-chloro'phenylazo) 0,0-dimethyl phosphorothioate
Amidithion 0,0-Dimethyl-S-[[2-methoxyethyl) carbamoyl]
methyl] phosphorodithioate
Amiton 0,0-Diethyl-S-(2-diethylamino) ethyl phosphoro-
dithioate
Aphidan* 0,0-Diisopropyl-S-ethylsulfinyl methyl dithiophos-
phate
Aspon* 0,0,0,0-Tetra-n-propyl dithiopyrophosphate
Azethion 0,0-Diethyl S-(carbomethoxymethyl) phosphoro-
thioate
Azinphosmethyl 0,O-Dimethyl S-[(4-oxo-l,2,3-benzotriazin-3(4H)-yl>
methyl] phosphorodithioate
Bensulide S-(0,0-Diisopropyl phosphorodithioate) ester of
N-(2-mercaptoethyl)benzenesulfonamide
Bomyl* •. . Dimethyl 3-hydroxyglutaconate dimethylphosphate
Bromophos ethyl 0,0-Diethyl-0(4-bromo-2,5-dichlorophenyl) phospho-
rothioate
Butonate 0,0-Dimethyl-(2,2,2-trichloro-l-n-butyryloxyethyl
phosphonate
Carbophenothion -0,0-Diethyl-S-[[(p-chlorophenyl)thio] methyl] phos-
phorodithioate
Chlorfenvinphos 2-Chloro-l-(2,4-dichlorophenyl) vinyl diethyl phos-
phate
Chlormephos S-Chlqrmethyl-0,0-diethyl phosphorothiolothionate
Chlorthion 0,O-Dimethyl 0-(3-chloro-4-nitrophenyl) phosphoro-
thioate
Conen* 0-Butyl-S-benzyl-S-ethyl phosphorodithioate
Coroxon 6,0-Diethyl-0-(3-chloro-4-methylcoumarin-7-yl) phos-
phate
Coumaphos .- 0,0-Diethyl 0-(3-chloro-4-methyl-2 oxo (2H)-l-benzo-
pyran-7-yl) phosphorothioate
Crufomate 4-tert-Butyl-2-chlorophenyl methyl methyl-phos-
phoramidate
Cyanthoate S-[[(l-Cyano-l-methylethyl)carbamoyl]methyl] 0,0-
diethyl phosphorothioate
Cythioate O,O-Dimethyl 0-p-sulfanoylphenyl phosphorothioate
DAEP 0,0-Dimethyl-S-2-(acetylamino)ethyl dithiophosphate
DEF* S,S,S,-Tributyl phosphorotrithioate
Demeton 0,0-Diethyl O-(and S)-[2-(ethylthio)ethyl] phosphoro-
thioate
Demeton methyl 0,0-Dimethyl-S-[2(ethylthio)ethyl] phosphorothioate
Diazinon 0,0-Diethyl-O-(2-isopropyl-6-methyl-4-pyrimidinyl)
phosphorothioate
*Trade name.
-------
Common or
Trade Name Chemical Name
Dicapthon 0-(2-Chloro-4-nitrophenyl) 0,0-dimethyl phosphoro-
thioate
Dichlorvos 2,2-Dichlorovinyl 0,0-dimethyl phosphate
Dicrotophos Dimethyl phosphate of 3-hydroxy-N,N-dimethyl-cis-
crotonamide
Diethquinalphione O,0-Diethyl-0-(2-chinoralyl)-phosphorothioate
Dimethoate 0,0-Dimethyl S-(N-methyl carbamoyl methyl) phos-
phorodithioate
Dioxathion 2,3-p-Dioxanedithiol S,S-bis(0,0-diethyl phosphoro-
dithioate)
Disulfoton O,0-Diethyl S-[2-(ethylthio)ethyl] phosphorodithioate
DMCP S-(p-Chlorophenyl) 0,0-dimethyl phosphorothioate
Dursban* 0,0-Diethyl 0-(3,5,6-trichloro-2-pyridyl) phosphoro-
thioate
Dyfonate* 0-Ethyl-S-phenylethylphosphonodithioate
EPN 0-Ethyl O-(p-nitrophenyl) phenylphosphonothioate
Ethion 0,0,O',0'-Tetraethyl S,S'-methylene bisphosphorodi-
thioate
Fenitrothion . . .." •. .. 0,0-Dimethyl 0-(4-nitro-m-tolyl) phosphorothioate
Fensulfothion 0,0-Diethyl 0-[p-(methylsulfmyl)phenyl] phosphoro-
thioate
Fenthion 0,0-Dimethyl 0-[4-(methylthio(-m-toly] phosphoro-
thioate
Folex* Tributyl] phosphorotrithioite
Formothion O,O-Dimethyl S-(N-formyl-N-methylcarbomylmethyl)
phosphorodithioate
Forstenon Diethyl carbethoxydichloromethyl-phosphonate 33
Fostion* O,0-Diethyl-S-(N-isopropylcarbamolymethyl) phos-
phorodithioate
Gardona* 2-Chloro-l-(2,4,5-trichlorophenyl) vinyl dimethyl
phosphate
Hosdon* 0,0-Dimethyl-S-2(isopropylthio) ethyl phosphorodi-
thioate
Imidan* N-(Mercaptomethyl) phthalimide S-(0,0-dimethyl
phosphorodithioate)
Inezin* O-Ethyl-S-benzylphenylphosphonothiolate
lodofenphos 0,0-Dimethyl-0-(2,5-dichloro-4-iodophenyl) thiophos-
phate
Ketothion O,0-Diethyl S-acetonyl phosphorodithioate
Lepto'phos O-(4-Bromo-2,5-dichlorophenyl) 0-methyl phenylphos-
phonothioate
Malathion O,0-Dimethyl dithiophosphate of diethyl mercaptosuc-
cinate
Mecarbam O,0-Diethyl S-[[(ethoxycarbonyl)methylcarbamoyl]-
methyl] phosphorodithioate
Mecarpon : S-(N-Methoxycarbonyl-N-methylcarbamonylmethyl)
dimethyl phosphonothiolothionate
Metasystox-S*+ 0,0-Dimethyl S-[(2-ethylsulfinyl> isopropyl] phos-
phorothioate
Methyl mercaptophos O-Methyl-O-et.hyl-2-ethylmercaptoethyl thiophosphate
Methyl parathion 0,O-Dimethyl 0-p-nitrophenyl phosphorothioate
Methyl phencapton 0,O-Dimethyl S-(2,5-dichlorophenylthio) methyl phos-
phorodithioate
Methyl potasan* '... 0,0-Dime.thyl 0-(4-methylumbelliferone) phosphoro-
thioate
*Trade name.
-------
('om/non or
Trade Name Chemical Name
Methyl trithion S-(((p-Chlorpphenyl)thio)methyl) 0,0-dimethyl phos-
phorodithioate
Mevinphos 2-Carbomethoxy-l-methylvinyl dimethyl phosphate
Monitor* O,S-Dimethylphosphoramidothioate
Monocrotophos Dimethyl phosphate of 3-hydroxy-N-methyl-cis-
crotonamide
Morphothion 0,0-Dimethyl S-(morpholinocarbonylmethyl) phos-
phorodithioate
Naled 1,2-Dibromo-2,2-dichloroethyl dimethyl phosphate
Naphthalaphos N-Hydroxynaphthalimide diethylphosphate
Orthene* 0,S-Dimethyl N-acetyl phosphoramidothioate
Oxydemetonmethyl 0,0-Dimethyl S[2-(ethylsulfinyl)ethyl] phosphoro-
thioate
Oxydisulfoton 0,O-Diethyl S-(2-(ethylsulfinyl)ethyl) phosphorodi-
thioate
Paraoxon 0,0-Diethyl 0-p-nitrophenyl phosphate
Parathion 0,0-Diethyl 0-p-nitrophenyl phosphorothioate
Phencapton 0,0-Diethyl S-[[(2,5 dichlorophenyl)thio] methyl]
phosphorodithioate
Phenthoate 0,0-Dimethyl S-(a-ethoxycarbonylbenzyl) phosphoro-
dithioate
Phorate 0,0-Diethyl S-(ethylthio)methyl phosphorodithioate
Phosalone 0,0-Diethyl S-[(6-chloro-3(mercaptomethyl)-2-benz-
oxazolinone] phosphorodithioate
Phosphamidon 2-Chloro-2-diethylcarbamoyl-l-methylvinyl dimethyl
phosphate
Phosphinon 0,0-Diethyl O-(l-(2-chloroethoxy)-2,2-dichlorovinyl)
phosphate
Phosvel* 0-(2,5-Dichloro-4-bromophenyl) 0-methyl phenylthio-
phosphate
Phoxim Phenylglyoxyonitrile oxime 0,0-diethyl phosphoro-
thioate
Pirazinon* 0,0-Diethyl 0-(6-methyl-2-propyl-4-pyrimidyl) phos-
phorothioate
Potasan 0,0-Diethyl 0-(4-methylumbelliferone) phosphoro-
thioate
Prophos 0-Ethyl S,S-dipropyl phosphorodithioate
Propoxon 0,0-Diethyl-S-carboethoxyethyl-phosphorothioate
Prothion O,0-Diethyl S-carboethoxyethyl phosphorodithioate
Pyrazoxon* 0,0-Diethyl 0-(3-methylpyrazol-5-yl) phosphate
Pyrazothion* 0,0-Diethyl 0-(3-methylpyrazol-5-yl) phosphoro-
thioate
Ronnel 0,0-Dimethyl 0-(2,4,5-trichlorophenyl) phosphoro-
thioate .
Schradan Octamethylphpsphoramide
S-Seven* 0-Ethyl-0-(2,4-dichlorophenyl)-pliosphonothionate
Sulfotepp 0,0,0,0-Tetraethyl dithiopyrophosphate
TEPP Tetraethyl pyrophosphate
Thiometon 0,0-Dimethyl-S-[2-(ethylthio)ethyl] phosphorodi-
thioate
Trichlorfon Dimethyl (2,2,2-trichloro-l-hydroxyethyl) phos-
phonate
Trichloronate 0-Ethyl 0-(2,4,5-trichlorophenyl) ethylphosphono-
thioate
VC-13 Nemacide 0-2,4-Dichlorophenyl 0, 0-diethyl phosphorothioate
Zytron O-(2,4-Dichlorophenyl) 0-methyl N-isopropylophos-
phoroamidothioate
*Trade name.
-------
CROSS REFERENCE FOR SOME OF THE CHOLINESTERASE-INHIBITING
ORGANIC PHOSPHORUS PESTICIDE TRADE NAMES
Aflix* see
Afos* see
Agrisil* see
Agritox* see
Agrothion* see
Alkron* see
Aileron* see
Amiphos* see
Anthio* see
Anthon* see
Appex* see
Asuntol* see
Azodrin* see
Basudin* .see
Baymix* see
Bayrusil* see
Baytex* see
Baythion* see
Betasan* see
Bidrin* see
Bilobran* see
Birlane* see
Bladafume* see
Bladen* see
Borinox* ....... see
Bromex* see
Carbicron* see
Carfene* see
Cidial* see
Citram* see
Co-Ral* see
Corothion* 'see
Cygon* see
Cythion* see
Dagadip* . see
Dalf* :. see
Dasanit* see
Daphene* see
Dazzel* see
Dedevap* see
De-Fend* see
De-Green* see
Delnav* .*. see
Diazajet* . see
Diazide* see
Diazol* see
Dibrom* see
Di-Captan* ....... see
Dimecron* see
formothion
mecarbam
trichloronate
trichloronate
fenitrothion
parathion
parathion
DAEP
formothion
trichlorfon
Gardona+
coumaphos
monocrotophos
diazinon
coumaphos
diethquinalphione
fenthion
phoxim
bensulide
dicrotophos
monocrotophos
chlorfenvinphos
sulfotepp
parathion
trichlorfon
naled
dicrotophos
azinphos-methyl
phenthoate
amiton
coumaphos
parathion
dimethoate
malathion
carbophenothion
methyl parathion
fensulfothion
dimethoate
diazinon
dichlorvos
dimethoate
DEF*
dioxathion
diazinon
diazinon
diazinon
naled
dicapthon
phosphamidon
Dimethogen* .... see dimethoate
Dipterex* see trichlorfon
Di-Syston* see disulfoton
Disyston S* see oxydisulfoton
Dithione* see sulfotepp
Dylox* see trichlorfon
E-605* see parathion
Easy Off-D* see Folex*
Ectoral* see ronnel
Ekatin* see thiometon
Ekatin M* see morphothion
Ektafos* see dicrotophos
Els'an* see phenthoate
Emmatos* see malathion
Entex* see fenthion
Equino-Aid* see trichlorfon
Ethyl Parathion* . see parathion
Etilon* see parathion
Etrolene* see ronnel
Exothion* see endothion
Filariol* see bromophos ethyl
Folidol E—605* .. see parathion
Folidol M* see methyl parathion
Folithion* see fenitrpthion
Fostion MM* .... see dimethoate
Frumin Al* .see disulfoton
Fujithion* see DMCP
Fyfanon* ....... see malathion
Gardentox* see diazinon
Garrathion* see carbophenothion
Gusathion M* .... see azinphos-methyl
Guthion* see azinphos-methyl
Hercules AC527* . see dioxathion
Karbofos* see malathion
Klimite 40* see TEPP
Korlan* see ronnel
Lebaycide* see fenthion
Malamar* see malathion
Malaspray* see malathion
Maretin* see naphthalaphos
Meldane* see coumaphos
Menite* see mevinphos
Metasystox* see demeton methyl
Metasystox-R* ... see oxydemeton-methyl
Metron* see methyl parathion
Mintacol* see paraoxon
MLT* see malathion
Mocap* see prophos
Morphotox* see morphothion
35
*Trade name.
-------
36
Murfotox*
Muscatox*
N-2790*
Nankor*
Neragan*
Neguvon*
Nialate*
Niram*
Nitrox*
No Pest*
Novathion*
Nuvacron*
Nuvanol*
Orthophos*
Ortho Phosphate
Defoliant* ....
Panthion*
Parathene*
Parawet*
Partron M*
Perfekthion* ......
Pestan*
Pestox III*
Phosdrin*
Phosfene*
Phoskit*
Phospliopyran* . . .
Phosvit*
Phytosol*
Prolate*
Rabon*
Rampart*
Rawetin*
Resistox*
Rhodiatox*
Rogor*
Roxion*
Ruelene*
Ruphos*
Sapecron*
see mecarbam
see coumaphos
see dyfonate
see ronnel
see bromophos ethyl
see trichlorfon
see ethion
see parathion
see methyl parathion
see dichlorvos
see fenitrothion
see monocrotophos
see fenitrothion
see parathion
see DBF*
see parathion
see parathion
see parathion
see methyl parathion
see dimethoate
see mecarbam
see schradan
see mevinphos
see mevinphos
see parathion
see endothion
see dichlorvos
see trichloronate
see imidan
see Gardona+
see phorate
see naphthalaphos
see coumaphos
see parathion
see dimethoate
see dimethoate
see crufomate
see dioxathion
see chlorfenv.inphos
Solverex*
Soprathion*
Spectracide*
Stathion*
Sumithion*
Supona*
Systox*
Sytam*
Tamaron
Tanone*
Tartan*
Task*
Tekwaisa*
Terracur P*
Tetrachlorvinphos.
Tetraethyl
Pyrophosphate .
Tetram*
Tetron*
Thimet*
Thiocron*
Thiodemeton
Thiophos
Thiotepp
Tiguvon*
Timet
Trichlorphon
Trimetion*
Trinox*
Trithion*
Trolene*
Tugon
Valexon*
Vapona*
Vaponite*
Vapotone*
Viozene*
Volaton*
Zithiol*
Zolone*
see disulfoton
see parathion
see diazinon
see parathion
see fenitrothion
see chlorfenvinphos
see demeton
see schradan
see Monitor*
see phenthoate
see cyanthoate
see dichlorvos
see methyl parathion
see fensulfothion
see Gardona*
see TEPP
see amiton
see TEPP
see phorate
see amidthion
see disulfoton
see parathion
see sulfotepp
see fenthion
see phorate
see trichlorfon
see dimethoate
see trichlorfon
see carbophenothion
see ronnel
see trichlorfon
see phoxim
see dichlorvos
see dichlorvos
see TEPP
see ronnel
see phoxim
see malathion
see phosalone
*Trade name.
-------
SELECTED CHOLINESTERASE-INHIBITNG
CARBAMATE PESTICIDES
Common or Trade Name Chemical Name
Aldicarb 2-Methyl-2-(methylthio) propionaldehyde 0-(methyl-
carbamoyl) oxime
Banol 6-Chloro-3,4-xylyl methylcarbamate
Baygon 0-Isopropoxyphenyl methylcarbamate
Bufencarb 3-(l-Methylbutyl) phenyl methylcarbamate and
3-(l-Ethylpropyl) phenyl methylcarbamate (3:1)
Butacarb 3,5 Di-tert-butylphenyl methylcarbamate
Carbaryl 1-Naphthyl N-methylcarbamate
Carbofuran , 2,3-dihydro-2,2-dimethyl-7-benzofuranyl methyl-
carbamate
Dichlormate . .. 3,4-and 2,3-Dichlorobenzyl methylcarbamate
Dimetilan 3,-Hyrdroxy-N,N, 5-trimethylpyrazole-l-carboxamide
dimethylcarbamate
Dioxacarb 0-l,3-Dioxolan-2-ylphenyl methylcarbamate
Ficam 2,2-Dimethyl-l,3-benzodioxol-4-yl-methykarbamate
Formetanate.(hydrochloride) M-[((Dimethylamino)methylene) amino phenyl meth-
ylcarbamate] (hydrochloride)
Landrin : 3,4,5-Trimethylphenyl methylcarbamate and 2,3,5-Tri-
• methylphenyl methylcarbamate
Matacil 4-(Dimethylamino)-m-tolyl methylcarbamate
Mesurol 4-(Methylthio)-3,5-xylyl methylcarbamate 37
Methomyl 5-Methyl N-[(methylcarbamoyl) OXyl] thioacetimidate
Mexacarbate 4-(Dimethylamino)-3,5-xylyl methylcarbamate
Mobam 4-Benzothienyl methylcarbamate
Oxamyl Methyl N',N'-dimethyl-N-[(methylcarbamoyl)oxy] -1-
thiooxamidate
Pirimicarb 2-(Dimethylamino)-5, 6-dimethyl4-pyrimidinyl
dimethylcarbamate
Promecarb 3-methyl-5-isopropylphenyl methylcarbamate
Thiofanox 3,3-Dimethyl-l-(methylthio)-2-butanone 0-[(meth-
ylamino)carbonyl] oxime
-------
38
CROSS REFERENCE FOR SOME OF THE
CHOLINESTERASE-INHIBITING
CARBAMATE PESTICIDE TRADE NAMES
A 363 see Matacil
Ambush see Aldicarb
Aminocarb see Matacil
Aphox see Pirimicarb
Arprocarb see Baygon
Bay 9010 see Baygon
B-37344 see Mesurol
Bay 39007 .. see Baygon
Bay 44646 see Matacil
Bay 70142 see Carbofuran
Bendiocarb see Ficam
Blattenex see Baygon
Bux see Bufencarb
Carbamult see Promecarb
Cafbanolate see Banol
Carpolin see Carbaryl
Carzol see Formetanate
(Hydrochloride)
CIBA 8353 see Dioxacarbe
Curaterr see Carbofuran
D-1221 see Formetanate
(Hydrochloride)
D-1410 seeOxamyl
Dicarol see Formetanate
(Hydrochloride)
Dowco 139 see Mexacarbate
Draza see Mesurol
Elocron see Dioxacarb
ENT 27164 see Carbofuran
ENT 27300 see Promecarb
EP 316 see Promecarb
EP 332 see Formetanate
(Hydrochloride)
Famid see Dioxacarb
FMC 10242 see Carbofuran
Furadan see Carbofuran
G-22870 . see Dimetilan
G-13332 see Dimetilan
Hexavin see Carbaryl
IPMC see Baygon
Karbaspray see Carbaryl
Lannate see Methomyl
Maz
MCA-600
Mercaptodimethur
Metalkamate ....
Methiocarb
Metmercaptron . .
Minacide
Mos 78
MXMC
NC 6897
NIA10242
Nudrin
QMS 716
Ortho 5353
PHC
Pirimor
PP062
Propoxur
Ravyon
Romate
Rowmate
Schering34615 . .
Schering 36056 ..
Sendran .
Septene . .
Sevin ....
Sirmate . .
Snip ....
Sok .
Suncide . .
Temik :..
Tendex ..
Tricarnam
UC 9880 .
UC21149
UC 22463
UC 7744 .
Unden . ..
Vydate . .
Yaltox . .
Zectron ..
see Mexacarbate
see Mobam
see Mesurol
see Bufencarb
see Mesurol
see Mesurol
see Promecarb
see Mobam
see Mesurol
see Ficam
see Carbofuran
see Methomyl
see Promecarb .
see Bufencarb
see Baygon
see Pirimicarb
see Pirimicarb
see Baygon
see Carbaryl
see Dichlormate
see Dichlormate
see Promecarb
see Formetanate
(Hydrochloride)
see Baygon
see Carbaryl
see Carbaryl
see Dichlormate
see Dimetilan
see Banol
see 'Baygon
see Aldicarb
see Baygon
see Carbaryl
see Promecarb
see Aldicarb
see Dichlormate
see Carbaryl
see Baygon
see Oxamyl
see Carbofuran
see Mexacarbate
-------
APPENDIX 2
PESTICIDE TOXICITY
Because most pesticides destroy unwant-
ed organisms, they obviously are toxic ma-
terials. Some pesticides are much more toxic
than others. Severe illness may result when
only a small amount of one type of pesticide
has been ingested; with another type, a large
amount may be ingested with no serious
effects.
Toxicologists use a simple animal toxicity
test to rank pesticides according to their
inherent toxicity. Before any pesticide can
be registered, the manufacturer must provide
the results of these tests to EPA. The 11)50
(the dosage level of a toxic chemical which is
lethal to 50 percent of a population of test
animals) is measured in terms of:
• oral toxicity (material is fed to rats)
• dermal toxicity (material is applied to
the skin of rats)
• respiratory toxicity (material is in-
haled).
In this way an arbitrary toxicologic ranking
has been obtained for the organophosphate
and organochlorine pesticides. The materials
on the top of the list are the most toxic, and
those at the bottom are the least toxic. The
size of the dose is the most important single
item in determining the safety of a given
chemical. Actual statistics of human poison-
ings correlate reasonably well with these
toxicity ratings. Health personnel will be
able to get some idea of the probable
severity of the poisoning being treated by
referring to these figures.
The amount of pesticide required to kill
an adult male can be correlated with
Oral ingestions are more toxic than res-
piratory inhalations and these are more toxic
than dermal absorptions. In addition, there
are individual physical and chemical dif-
ferences in a chemical which render the
material more likely to produce poisoning.
Thus, parathion changes to the more toxic
"paraoxon" with high temperatures. Ethyl
parathion is more toxic than methyl para-
thion, yet there is no great difference in
their oral toxicity. Work exposure is usually
dermal and that is why many more illnesses
are seen 'in workers exposed to ethyl para-
thion than those exposed to methyl para-
thion.
39
Acute Oral LD5Q
5
5-50
50 - 500
500 - 5,000
5,000-15,000
Material which will kill
an adult male
a few drops
a pinch to a teaspoonful
a teaspoonful to a tablespoonful
a I ounce to 1 pint
1 pint to 1 quart
-------
40
BTEPP (Oral L0so=1, Dermal 1050=2.4)^
8 THIMET (OuM.1, Dermal-2.5)
iDI-SYSTON (Oral=2.3, Dermal 6]
IDEMETON (Systox] (Oral=2.5, DermaN.2]
iPARATHION (Oral=3.6, Dermal=6.8]
IPHOSDRIN (Oral=3.7, Dermal 4.2!
UTRITHION (OraNO, Dermal^])
IlGUTHION (OraNI, Dermah220)
EH METHYL PARATHION (Oral=14, Dermah-67)
l^CO-RAL (Oral=15.5, Dermal-860]
BIDRIN (Oral=22, Dermal=225)
IOELNAV iOfal 23, Dermal 63|
IPHOSPHAMIOON (Oral 23.5, Dermal 10))
11DDVP (Oral=56, Dermal--75)
(Oral=76, Dermal-455)
gjDIPTEREX (Oral=560, Dermal-2000]
, Dermal-4100)
1 MALATHION (OraMOOO,
Dermah-4444)
RONNEL (Oral=1250)
10 20 30 40 50 60 70 80 600 700 800 900 1000 1100 1200
ACUTE LD5Q IN MG/KG
Acute Oral and Dermal Toxicity Values for Some Organophosphate Pesticides.
(Prepared by the Bureau of Occupational Health, State of California Department of Public
Health. Copied with permission.)
-------
ENDRIN (Oral LD50=7.5 MG/KG, Dermal 1050=15 M6/KG)
! THIODAH (OraHS, Deunal=74)
U ALDRIN (Oral=39, Dermal=98)
H DIELDRIN (OraMB, DermaHO)
^^TOXAPHENE(Oral=80, Dermal=780)
LINDANE (Oral=88, Dermal=900)
HEPTACHLOR (Oral-100, DermaNSS)
DDT (Orah113, DermaN2510]
CHLOROANE (Oral=335, Dermal=690]
KELTHANE (Oral=1000, Dermal=1000)
CHLOROBENZILATE (Oral=1040, Dermal^)
ODD (Oral=3400)
PERTHANE (OralMOOO)
41
METHOXYCHLBR (Orai=Sltfi]
100 200 303 490 1000 2000
LD50 IN MG/Kfi
4088
sew
Acute Oral and Dermal Toxicity Values for Some Chlorinated Hydrocarbon Pesticides.
(Prepared by the Bureau of Occupational Health, State of California Department of Public Health.
Copied with permission.)
-------
APPENDIX 3
I.M.
42
ACHOLEST
(Cholinesteroie Test-Poper)
METHOD FOR USING ACHOLEST TEST PAPER
Equipment
I. ACHOLEST Cholinesterose Test-Paper, Bottle I.
Test Strip
2. Four slides.
3. 0.} ml. pipette (0.01 ml. graduations)
A. Comparative color strips. Bottle II.
Comparative Strip
5. Watch or stop-watch.
Procedure: Place 0.05 ml. of non-hemolyzed plasma* on
each of two thoroughly cleaned slides (avoid traces of
acid or alkali). The plasma is to be quickly separated
from the blood sample inasmuch as blood cells present
in the plasma interfere with the reaction. With a pair
of clean, dry scissors, cut one-half of a strip (2x1 cm.)
of Acholest Test Paper from Bottle I, and one-half of a
strip of control paper from Bottle II. Using tweezers,
place the untouched half of each strip on each slide
containing the plasma and cover with a second thorough-
ly cleaned slide, using gentle, even pressure several
times in order to ensure complete saturation of the test
and control papers and prevent mottling. To prevent
evaporation of fluid, do not separate the slides until the
test has been completed. Record the moment of contact
of the test and control papers with the plasma as th<
beginning of the test.
* Heparinized, not citrated or oxalated tubes may be
used for collection.
The Acholest Test Paper and the control paper, when
dry, are similarly egg yolk colored. When exposed to the
plasma, the Acholest Test Paper turns green, gradually
developing into o yellowish color, after passing through
various tones of green-yellow. The control paper, how-
ever, upon contort with the blood plasma, turns im-
mediately yellowish with no further change in color.
The plasma cholinesterase activity is measured by the
time required for the Acholest Test Paper to reach
the color of the control paper. For accurate comparison
of the color, it is recommended that the test be performed
on a white background with diffused light.
From the moment of contact of the plasma and Acholest
Test Paper to the point when the comparative tone of
color has been reached, the following time values have
been established:
Minutes
Below 5
5 -20
20-30
30 and longer
Activity of Plasma
Cholinesterase
"increased"
"normal"
"suspicious"
"decreased,"
Precaution: Acholest Test Paper should be stored away
from light in tightly closed containers to protect it from
moisture and chemical vapors. Avoid contact with fingers.
Plasma to be used should bo free of cellular component*.
Always place Acholest Test Paper on the platma, never
drip plasma on the Test Paper; this similarly applies to
the control strip.
Readings should always be carried out under the some
light conditions and room temperature. (Room tempera-
ture differences in the range from 68° F (19° C) to
75° F (25° Ci do not influence the reliability and ac-
curacy of Acholest Test Paper). Also hemolysis of a minor
degree does not affect the accuracy of Acholest Test
Paper. It is important, however, to note that pH changes
of the plasma might interfere with the accuracy of
Acholest Test Paper independent of the plasma choli-
nesterase activity. Such pH changes might be the result
of alkali or acid cleansing materials on test equipment
or of undue storage of plasma which might have led to
degradation or decoy (e.g. protein fractions). However,
as o rule, storage of the plasma up to seven days at a
temperature of 20° C or below (refrigeration of plasma
is desirable), does not interfere with the accuracy of
Acholest Test Paper.
DISTRIBUTED BY
E. FOUGERA & CO., INC.
HICKSVILLE, NEW YORK 11802
-------
APPENDIX 4
LABORATORY METHODS
Cholinesterase Determination
The four laboratory techniques most
commonly used for quantitative expressions
of these enzyme activities are the electro-
metric (Michel), the titrimetric (pHstat), the
colorimetric (Ellman) and gas chromato-
graphic (Cranmer) methods.
1. Michel method (pH meter)-Plasma
and red cells are incubated with acetyl-
choline for one hour. The drop of the pH is
due to the formation of acetic acid and is
directly proportional to the cholinesterase
activity. Normal values: Plasma 0.53 - 1.24
ApH units and Red Blood Cells 0.57 - 0.98
ApH units.
2. pH Stat (titrimetric)—The plasma and
red cells are incubated with acetylcholine for
3 minutes and the acid formed is titrated
with a base. The amount of base used is
directly proportional to the cholinesterase
activity in the blood sample. Normal values:
Plasma 3.6 - 6.8 AiM/ml/min and Red Blood
Cells 11.1 - 16.0juM/ml/min.
3. Ellman method (colorimetric)—Plasma
and red cells are incubated for 10 minutes
with acetyl thiocholine and the resultant
thiocholine produces a yellow color in the
presence of 5:5-dithiobis-(2-nitrobenzoic
acid). The concentration of the yellow com-
plex is directly proportional to the amount
of cholinesterase present. Normal values:
Plasma 5.8-16.6 M-SH/ml/3 min.
4. GLC method (cluomatographic)-
Plasma and red cells are reacted for 30
minutes with a compound that is similar to
acetylcholine. The product formed,
dimethyl butanol, is quantitated using a gas
chromatograph. Normal values: Plasma 2.1 -
4.6 /iM/ml/min and Red Blood Cells 8.2 -
Urinary Pesticide
Metabolite Data
The organophosphates are metabolized in
man to produce two major types of pesticide
metabolites in urine. These are the phenolic
metabolites (e.g. nitrophenols and halo-
genated phenols) and the alkyl phosphate
metabolites (namely, diethyl thiophosphate
(DETP), diethyl phosphate (DEP), dimethyl
thiophosphate. (DMTP) and dimethyl phos-
phate (DMP). The carbamates, the other
major group of anticholinesterase pesticides,
are metabolized to non-halogenated phenols
which are excreted in urine.
In poisoning cases the information from
both types of metabolites is informative.
Take ethyl parathion as an example. This is a
diethyl thiophosphate pesticide and the ex-
cretion of the diethyl phosphate moiety in
the urine is related to the parent compound.
Parathion is oxidized to the more toxic pro-
duct paraoxon, and it is this which is largely
responsible for illness. Paraoxon is reflected
by the excretion of diethyl phosphate (DEP)
so that high concentrations of the oxon
derivative are seen in the urine in poisoned
victims. Paranitrophenol is the phenolic
moiety and the identification of this in urine
facilitates the specific diagnosis of the pesti-
cide involved in the exposure, for para-
nitrophenol is only found in the urine
following exposure to parathion and two
other pesticides being used today (EPN and
chlorthion).
43
-------
Both the alkyl phosphate and phenolic
metabolites have been found to be excellent
indices of exposure if this exposure is a
significant one, such as occurs in occupa-
tional and accidental exposure. The follow-
ing chart illustrates the sequential excretion
of these metabolites expressed as concentra-
tions of the metabolites per milliliter in a
parathion poisoning case.
44
.8
.4
0
2.0
1.0
:
RNP
6
PM
6
AM
6
PM
6
AM
6
PM
6
AM
6
PM
6
AM
10-9
10-10
10-11-74
Intact Pesticide Studies
The intact pesticide may be identified in
blood, in other body tissues, and in gastric
washing by electron capture gas chromato-
graphy using a flame photometric detector.
-------
APPENDIX 5
CHEMTREC
CHEMICAL
TRANSPORTATION
EMERGENCY
CENTER
For assistance in any transportation emer-
gency involving chemicals (in the continental 45
U.S.)
PHONE: Day or Night—Toll-Free
*800- 424-9300
'Add long-distance access number if required
483-7616 in District of Columbia
For calls originating outside the continental
U.S.: 202—483-7616—Washington, D. C.
-------
CHEMTREC
46
WHAT IT IS
CHEMTREC stands for Chemical Transportation
Emergency Center, a public service of the Manu-
facturing Chemists Association at its offices in
Washington, D. C.
CHEMTREC provides immediate advice for
those at the scene of emergencies, then promptly
contacts the shipper of the chemicals involved
for more detailed assistance and appropriate
follow-up.
CHEMTREC operates around the clock—24
hours a day, seven days a week—to receive
direct-dial toll-free calls from any point in the
continental United States through a wide area
telephone service (WATS) number, 800-424-9300
(483-7616 for calls originating within the District
of Columbia; 202-483-7616 for calls originating
outside the continental U.S.).
Shippers, including MCA members and non-
members, are notified through pre-established
phone contacts providing 24-hour accessibility,
via information operators, or through cooperation
of fire and police services.
As circumstances warrant, the National Trans-
portation Safety Board or appropriate offices of
other agencies may be notified.
CHEMTREC's capabilities have been recognized
by the Department of Transportation, and a close
and continuing relationship is maintained between
CHEMTREC and the Department.
WHAT IT IS NOT
Because chemicals find so many uses and have
such a wide range of characteristics, there is
much need for information abput them—composi-
tion and purity, physical and chemical properties,
effects on people and the environment, sources
of supply, etc. It is important to understand that
CHEMTREC is not intended and is not equipped
to function as a general information source, but
by design is confined to dealing with chemical
transportation emergencies. Drivers should not
call CHEMTREC on problems other than chemical
cargo emergencies.
MODE OF OPERATION
CHEMTREC's number has been widely circu-
lated in professional literature distributed to
emergency service personnel, carriers, and the
chemical industry, and has been further circu-
lated in bulletins of governmental agencies, trade
associations, etc.
Shipping documents of participating companies
are requested to include the following: "For help
in chemical emergencies involving spill, leak, fire
or exposure, call toll-free 800-424-9300 day or
night."
An emergency reported to CHEMTREC is re-
ceived by the Communicator on duty, who records
details in writing and by tape recorder. The Com-
municator then attempts to determine the essen-
tials of the problem (as detailed on the left column
of this page under "USER GUIDANCE"). This is
to enable him to provide the best available infor-
mation on the chemical(s) reported to be involved,
thereby giving specific indication of the hazards
and what to do (as well as what not to do) in case
of spills, fire, or exposure as the immediate first
steps in controlling the emergency. Information
on the various chemicals, as furnished by the
producers, is within easy reach. Trade names
and synonyms of chemical names are cross-
referenced for ready identification by whatever
name is given.
CHEMTREC's Communicators are not scientists.
They are chosen for their ability to remain calm
under emergency stresses. To preclude unfounded
personal speculation regarding a reported emer-
gency, they are under instructions to abide strictly
by the information prepared by technical experts
for their use.
Having advised the caller, the Communicator
proceeds immediately to notify the shipper by
phone. The known particulars of the emergency
thus relayed, responsibility for further guidance—
including dispatching personnel to the scene or
whatever seems warranted—passes to the shippei.
Although proceeding to the second stage of
assistance becomes more difficult where the
shipper is unknown, the Communicator is armed
with other resources to fall back on. For example:
Concerning radioactive materials, CHEMTREC can
call on the Energy Research and Development
Administration (ERDA). (Formerly Atomic Energy
Commission).
Identification of product and shipper is impor-
tant. Shipping papers are carried by truck drivers,
and in engine or caboose of trains. Car and truck
numbers and carrier names can be useful in trac-
ing unknown cargoes.
Mutual aid programs exist for some products,
whereby one producer will service field emergen-
cies involving another producer's product. In such
cases, initial referral may be in accord with the
applicable mutual aid plan rather than direct to
the shipper. Arrangements of this sort are estab-
lished on chlorine through the Chlorine Institutr
and on pesticides through the National Agricul-
tural Chemicals Association.
The former has CHLOREP, the Chlorine Emer-
gency Plan, in which the nearest producer re-
sponds to a problem. NACA has a Pesticide
Safety Team Network of some 40 emergency
teams distributed throughout the country. CHEM-
TREC serves as the communication link for both
programs.
-------
In Canada, the Canadian Chemical Producers'
Association operates a Transportation Emergency
Assistance . Program (TEAP) through regional
teams prepared to give phone and field response.
Many individual companies have well organized
response capabilities, for their own products,
some of which preceded CHEMTREC by several
years. This program does not seek to displace
these, but rather collaborates with them and en-
hances their effectiveness. CHEMTREC's single
telephone number affords this opportunity.
BACKGROUND
MCA is a trade association of chemical manu-
facturers, large and small, representing more than
90% of the production capacity tor basic indus-
trial chemicals in the United States and Canada.
It has long been active in programs to improve
the safety of chemical shipping containers, both
package and bulk units, and their reliability in
handling and shipment, thereby minimizing fail-
ures and leakage of contents under extraordinary
stress. Such efforts continue unabated.
Nevertheless, despite, precautions taken, train
derailments, truck upsets and collisions, and
barge accidents, do occur. Such emergencies
deserve to be handled as well as possible to
minimize the consequences to life and properly.
Emergency services—fire and police—ate nor-
mally well prepared to cope with common mate-
rials, including certain flammables such as fuel
oil and gasoline. Too often they are at a disad-
vantage when chemicals are encountered, espe-
pecially since "what should be done"—and of
equal importance, "what should not be done"—in
the early stages may bear so heavily on the out-
come. They need accurate and clearly under-
standable information to help them evaluate the
situation and act with proper precautions for their
own safety, as well as for the protection of the
general public.
Realizing that personnel of chemical producers
possessed the necessary expertise, officials of
concerned Federal departments approached MCA.
A study was undertaken by industry safety, pack-
aging, and transportation specialists. After thor-
ough consideration, it was concluded that a single
center, nationwide in coverage and accessible to
all through a single telephone number, would be
the most expeditious arrangement—for contact
with it and for feedback from it. Following review
and confirmation by the industrial specialists of
MCA's technical committees, CHEMTREC as now
in operation was a&thorized.
CHEMTREC was established and continues as
a voluntary project of the chemical manufacturing
industry, wholly supported through the Manufac-
turing Chemists Association. It became opera-
tional on September 5, 1971.
USER GUIDANCE
CHEMTREC can usually provide hazard infor-
mation warnings and guidance when given only
the NAME OF THE PRODUCT and the NATURE
OF THE PROBLEM. For more detailed informa-
tion and/or assistance, or if product is unknown,
attempt to provide as much of the following infor-
mation as possible:
Name of caller and call back number
Location of problem
Shipper or manufacturer
Container type
Rail car or truck number
Carrier name
Consignee
Local conditions
FOR MORE INFORMATION
Questions regarding the operation of CHEM-
TREC should be directed to: Manager, Chemical
Transportation Emergency Center, 1825 Connec-
ticut Avenue, N.W., Washington, D. C. 20009.
Phone: 202—483-6126.
47
-------
APPENDIX 6
COMMUNICATIONS CHECKLIST FOR
HEALTH PROFESSIONALS
V Attending Physician
\/ Family Members
V Employers
V Hospital Emergency Room
V Ambulance Service
V Health Department
V Local, County or State Police
\/ Landowner
\/ Pesticide Analytical Resource Laboratory
>/ EPA Resource (if necessary)
\' Chemirec (.n necessary)
-------
APPENDIX?
LABORATORY AND EPA REGIONAL OFFICE LOCATIONS
Pesticide Verification
Laboratory
Robert Alt'man M.D., M.P.H.
Project Director
Epidemiologic Studies Program
New Jersey State Dept. of Health
\John Fitch Plaza
P. 0. Box 1 540
Trenton, New Jersey 08625
(609) 292-7608
Off-hour number: (609) 392-2020
Dr. Ana Barquet
Dept. of Epidemiology and
Public Health
University of Miami School
of Medicine
P. 0. Box 520875
Miami, Florida 33152
(305) 547-6972
Off-hour
number:
(305) 235-6280
E. Gomes
152E. Stenger
San Benito, Texas 78586
(512)399-5352
Off-hour number:
(512)399:3455
State
Service
Area
ME
VT
NH
MA
Rl
CT
NJ
NY
PR
VI
DE
DC
MD
PA
VA
WV
AL
FL
GA
KY
MS
NC
SC
TN
AR
LA
NM
OK
TX
EPA
EPA Regional Pesticide
Region Branch Chief
A. Charles Lincoln, Chief
EPA, Pesticide Branch
I John F. Kennedy Bldg.
Boston, Massachusetts 02203
(617)223-5126
Stanley Fenidiel, Chief
EPA, Pesticide Branch
II 26 Federal Plaza, Room 1005
New York, New York 10007
(212)264-8356
Nelson Davis, Chief
EPA, Pesticide Branch
Curtis Building
III 6th and Walnut Streets
Philadelphia, Pa 19106
(215)597-9869
Roy Clark, Chief
EPA, Pesticide Branch
IV
345 Courtland Street, N.E. Ro
Atlanta, Georgia 30308
(404) 257-3222
Norman E. Dyer, Chief
EPA, Pesticide Branch
.VI 1201 Elm Street
1st International Bldg.
Dallas, TX 75270
(214)749-7126
49
-------
50
Donald P. Morgan, M.D., Ph.D.
Project Director
Epidemiologic Studies Program
University of Iowa
Oakdale Campus, AMRF
Oakdale, I A 523 19
(319)353-5558
Off-hour number:
(319)338-8474
Dr. Darrell Brock
Acting Project Director
Epidemiologic Studies Program
Bureau of Laboratories
Department of Health & Welfare
Statehouse
Boise, Idaho 83707
(208) 384-2233
1L
IN
Ml'
•MN
OH
WI
IA
KS
MO
NE
CO
MT
ND
SD
UT
WY
AZ
CA
GU
HI
NV
AK
ID
OR
WA
. Mitchell Wrich, Chief
EPA, Pesticide Branch
V 230 S. Dearborn St.
Chicago, IL. 60604
(312)353-2192
John Wicklund, Chief
EPA, Pesticide Branch
VII 1735 Baltimore Ave.
Room 249
Kansas City, MO 64 108
(816)374-3036
Ivan Dodson, Chief
EPA, Pesticide Branch
VIII Lincoln Tower Building
1860 Lincoln Street
Suite 900
Denver, CO 80203
(303) 837-3926
Jake McKenzie, Chief
EPA, Pesticide Branch
IX 100 California Street
Room 340
San Francisco, CA. 94111
(415)556-3352
Robert Poss, Chief
X EPA, Pesticide Branch
12006th Avenue
Room 1 1 -C
Seattle, WA 98101
(206)442-1090
-------
APPENDIX 8
PESTICIDE POISONING EXPOSURE HISTORY
(MEDICAL RECORD)
Name of Patient
Age Race Sex _
Address
Date of incident Location of incident
Taken to Hospital or Clinic
Date of Admission •_
Address .
Person to contact with results Telephone No..
EXPOSURE HISTORY: (Circle Appropriate Information)
Type of pesticide exposure: Ingestion Dermal Inhalation
Was this episode due to: Accidental Exposure Suicide Occupational Exposure
Name of pesticide involved :
EPA Registration No.
Active ingredients.
Crop pesticide was applied to and target pest
Time of last pesticide exposure of patient: Hour Date.
If Occupational Exposure patient was: (Circle)
Applying Pesticides: g-j
Aerially Ground spray (hand) Spray rig (mechanical)
Or:
Loading Picking crops Mixing . Thinning crops
Other
SYMPTOMATOLOGY DATA (Please Circle Appropriate Information if Present)
Weakness Sweating Nausea Vomiting Diarrhea
Abdominal Cramps Excessive Tearing Excessive Salivation
Excessive Bronchial Secretions Shortness of Lieath Pains in Chest
Blurring of Vision Convulsions "her
SIGNS (Please circle appropriate information if present)
Miosis (less than 5 mm) Muscle twitching Muscle fasciculations
Bronchial spasms Bronchial exudation
Cholinesterase Screening Test: Positive Negative
' Other
SPECIMEN COLLECTION
Date Time
1. Heparinized blood Collected before 2-PAM Administration?
YES NO
Atropine Administration?
YES NO
2. Urine
3. Other
(over)
-------
ADDITIONAL COMMENTS:
Such as—
• important details relating to victim's pesticide exposure
• others affected and how
• other damage caused by occurrence.
52
SHIPPING
Send specimens and this form to one of the following laboratories:
Robert Altman. M.D., M.P.H.
Project Director
Epidemiologic Studies Program
New Jersey State Dept. of Health
John Fitch Plaza
P. O. Box 1540
Trenton, New Jersey 08625
(609) 292-7608
Donald P. Morgan, M.D., Ph.D.
Project Director
Epidemiologic Studies Program
University of Iowa
Oakdale Campus, AMRF
Oakdale, Iowa 52319
(319) 353-5558
Dr. Ana Barquet
Dept. of Epidemiology and Public Health
University of Miami School of Medicine
P.O. Box 520875
Miami, Florida 33152
(305) 547-6972
E. Gomes .
152 E. Stenger
San Benito, Texas 78586
(512) 399-5352
D. Darrell Brock
Acting Project Director
Epidemiologic Studies Program
Bureau of Laboratories
Dept. of Health and Welfare
Statehouse
Boise, Idaho 83707
(208)384-2233
•U.S. GOVERNMENT PRINTING OFFICE I 1976 0-720-335/6035
------- |