RECOGNITION AND MANAGEMENT
OF PESTICIDE POISONINGS
U. S. ENVIRONMENTAL PROTECTION AGENCY
OFFICE OF PESTICIDE PROGRAMS
WASHINGTON, D.C. 20460
AUGUST 1976
-------
EPA-540/9-011
RECOGNITION AND MANAGEMENT OF
PESTICIDE POISONINGS
Donald P. Morgan, M.D., Ph.D.*
Support for this publication was provided by the Epidemiologic
Studies Program, Human Effects Monitoring Branch, Technical
Services Division, Office of Pesticide Programs, U.S. Environ-
mental Protection Agency, Washington, D.C. 20460.
* Director, Iowa Epidemiologic Studies Program, located at University of
Iowa Medical School, Iowa City, Iowa 52240.
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CONTENTS
Page
SOLID ORGANOCHLORINE PESTICIDES 1
ORGANOPHOSPHATE CHOLINESTERASE-
INHIBITING PESTICIDES 4
CARBAMATE CHOLINESTERASE-INHIBITING
PESTICIDES 9
PARAQUAT, DIQUAT, AND MORFAMQUAT
(Dipyridyls) 13
CHLOROPHENOXY COMPOUNDS 18
NITROPHENOLIC HERBICIDES 21
PENTACHLOROPHENOL OR SODIUM
PENTACHLOROPHENATE 24
UREA-, URACIL- AND TRIAZINE- BASED
HERBICIDES 27
ACETANILIDE-, ACETAMIDE-, CARBANILATE-,
AND ANILIDE-, BASED HERBICIDES 30
DIMETHYLDITHIOCARBAMATE COMPOUNDS 33
ANTICOAGULANT RODENTICIDES 37
ARSENICAL PESTICIDES 41
PESTICIDES INDEX 46
-------
SOLID ORGANOCHLORINE PESTICIDES
CHEMICAL STRUCTURES
ci
Cl
LINDANE
Cl
CHLORDANE
Cl
DIELDRIN
S=O
Cl
OCH,
METHOXYCHLOR
COMMON COMMERCIAL PESTICIDE PRODUCTS (approximately in
order of toxicity)
Highly toxic: endrin (Hexadrin), a stereoisomer of dieldrin.
Moderately toxic: aldrin (Aldrite, Drinox), endosulfan (Thiodan), dieldrin
(Dieldrite), toxaphene (Toxakil, Strobane-T), lindane (Isotox, Gammexane),
benzene hexachloride (BHC, HCH), DDT (Chlorophenothane), heptachlor,
kepone, terpene polychlorinates (Strobane), chlordane (Chlordan), dicofol
(kelthane), chlorobenzilate (Acaraben), mirex, methoxychlor (Marlate).
TOXICOLOGY
In adequate dosage, these chemicals interfere with axonic transmission of
nerve impulses and therefore disrupt the function of the nervous system,
principally that of the brain. This results in behavioral changes, sensory
and equilibrium disturbances, involuntary muscle activity, and depression of
vital centers, particularly that controlling respiration. Adequate doses in-
crease the irritability of the myocardium and cause degenerative changes in
the liver.
FREQUENT SYMPTOMS AND SIGNS OF POISONING
APPREHENSION, excitability, dizziness, HEADACHE, DISORIENTA-
TION, weakness, PARESTHESIAE, muscle twitching, tremor, tonic and
clonic CONVULSIONS (often epileptiform), coma. Soon after ingestion,
nausea and vomiting are often prominent. When chemicals are absorbed
by parenteral routes, apprehension, twitching, tremors, and convulsions may
be the first symptoms. Respiratory depression is caused by the pesticide and
by the petroleum solvents in which these pesticides are usually dissolved.
Pallor occurs in moderate to severe poisoning. Cyanosis may result as con-
vulsive activity interferes with respiration.
1
-------
CONFIRMATION OF DIAGNOSIS
Pesticide and/or metabolites can usually be identified in blood or urine
by gas-liquid chromatographic examination of samples taken within 72 hours
of poisoning. Some chlorinated hydrocarbon pesticides persist in the serum
for weeks or months after absorption. DO NOT DELAY TREATMENT
of acute poisoning pending confirmatory blood analysis. Presence of chlori-
nated hydrocarbon residues in blood or tissues does not, of itself, indicate
poisoning; actual concentrations are critical to a diagnosis of poisoning.
TREATMENT
1. Establish CLEAR AIRWAY and TISSUE OXYGENATION by aspira-
tion of secretions, and if necessary, by assisted pulmonary ventilation
with oxygen.
2. CONTROL CONVULSIONS. The anticonvulsant of choice is DI-
AZEPAM (VALIUM). Adult dosage, including children over 6 years
of age or 23 kg in weight: inject 5-10 mgm (1-2 ml) slowly intra-
venously (no faster than one ml per minute), or give total dose intra-
muscularly (deep). Repeat in 2-4 hours if needed.
Dosage for children under 6 years or 23 kg hi weight: inject 0.1-0.2
mgm/kg (0.02-0.04 ml/kg) slowly intravenously (no faster than one-
half total dose/minute), or give total dose intramuscularly (deep). Re-
peat in 2-4 hours if needed.
CAUTION: Administer intravenous injection slowly to avoid irrita-
tion of the vein and occasional hypotension.
Because of a greater tendency to cause respiratory depression, BAR-
BITURATES are probably of less value than DIAZEPAM. One used
successfully in the past is PENTOBARBITAL (NEMBUTAL). Maxi-
mum safe dose: 5 mgm/kg body weight, or 0.20 ml/kg body weight,
using the usual 2.5% solution.
If possible, inject solution intravenously, at a rate not exceeding one
ml/minute until convulsions are controlled. If intravenous administra-
tion is not possible, give total dose rectally, not exceeding 5 mgm/kg
body weight (0.2 ml/kg of 2.5% solution).
CAUTION: Be prepared to assist pulmonary ventilation mechanically
if respiration is depressed.
3. If pesticide has been INGESTED in quantity sufficient to cause poison-
ing, the stomach must be emptied.
If victim is ALERT and respiration is not depressed, give SYRUP OF
IPECAC to induce vomiting (adults and children 12 years and older:
30 ml; children under 12 years: 15 ml).
CAUTION: OBSERVE THE VICTIM closely after administering
IPECAC. If consciousness level declines, or if vomiting
has not occurred in 15 minutes, proceed immediately to
INTUBATE the stomach.
-------
Following emesis, have victim drink a suspension of 30 gm ACTI-
VATED CHARCOAL in 3-4 ounces of water to limit absorption of
toxicant remaining in the gut.
If the victim is NOT FULLY ALERT, empty the stomach immediately
by INTUBATION, ASPIRATION, and LAVAGE, using isotonic
saline or 5% sodium bicarbonate. Because many pesticides are dis-
solved in petroleum distillates, emes,is and intubation of the stomach
involve a serious risk that solvent will be aspirated, leading to chemical
pneumonitis.
For this reason:
A. If the victim is unconscious or obtunded, and if facilities are at
hand, insert an ENDOTRACHEAL TUBE (cuffed, if available)
prior to gastric intubation.
B. Keep the victim's HEAD BELOW THE LEVEL OF THE STOM-
ACH during intubation and lavage (Trendelenburg, or left lateral
decubitus, with: head of table tipped downward). Keep the victim's
head turned to the left.
C. ASPIRATE PHARYNX as regularly as possible to remove gagged
or vomited stomach contents.
After aspiration of gastric contents and washing of stomach, instill 30
gm of ACTIVATED CHARCOAL in 3-4 ounces of water through
stomach tube to limit absorption of remaining toxicant. Do NOT instill
milk, cream, or other substances containing vegetable or animal fats
which enhance absorption of chlorinated hydrocarbons.
If bowel movement has not occurred in 4 hours and if patient is fully
conscious, give SODIUM SULFATE (Glauber's Salts) as a cathartic.
(Adults, 12 years and older: 15 gm in 6-8 ounces of water; children
under 12: 0.2 gm/kg body weight in 1-6 ounces of water).
4. BATHE and SHAMPOO the victim vigorously with soap and water
if SKIN and HAIR are contaminated.
5. DO NOT give epinephrine or other adrenergic amines, because of the
myocardial irritability produced by chlorinated hydrocarbons.
6. During convalescence, enhance CARBOHYDRATE, PROTEIN, and
VITAMIN intake by diet or parenteral therapy to minimize toxic in-
jury to the liver.
7. The chemical ENDRIN is much more HEPATOTOXIC than are other
chlorinated hydrocarbons in common use. Bilirubinemia and elevated
blood enzyme activities occur commonly in poisoning. Special measures
should be taken to minimize injury by supplying ample nutrients.
8. With the exception of endrin poisoning, the likelihood of recovery from
poisoning by most chlorinated hydrocarbon pesticides is generally good,
even when convulsions occur. Fatalities occur as a result of massive
doses. The prognosis in endrin poisoning is more guarded.
-------
ORGANOPHOSPHATE
CHOLINESTERASE-INHIBITING
PESTICIDES
GENERAL CHEMICAL STRUCTURE
C2H5O or CH3O ^ .. S (or O)
C2H5O or CH3O
LEAVING
GROUP
COMMON COMMERCIAL PESTICIDE PRODUCTS (approximately in
order of decreasing toxicity)
Highly toxic: TEPP, phorate (Thimet), mevinphos (Phosdrin), fensul-
fothion (Dasanit), demeton (Systox), disulfoton (Disyston), sulfotepp (Blada-
fume, Dithione), Counter, ethyl parathion (Parathion, Thiophos), fonofos
(Dyfonate), EPN, azinphosmethyl (Guthion), methyl parathion (Dalf), mono-
crotophos (Azodrin), dicrotophos (Bidrin), methamidophos (Monitor), car-
bophenothion (Trithion), phosphamidon (Dimecron).
Moderately toxic: famphur (Warbex, Bo-Ana, Famfos), ethoprop (mocap),
coumaphos (Co-Ral), demeton-methyl (Metasystox), dichlorvos (DDVP,
Vapona) dioxathion (Delnav), crotoxyphos (Ciodrin), chlorpyrifos (Dursban),
ethion, fenthion (Baytex, Entex), diazinon (Spectracide), dimethoate (Cygon),
naled (Dibrom), trichlorfon (Dylox, Dipterex, Neguvon), crufomate (Rue-
lene), ronnel (Korlan), malathion (Cythion). Certain of the organophos-
phates are systemic, i.e., they are taken up by the plant and translocated into
foliage and sometimes into the fruit.
TOXICOLOGY
Toxicants of this class phosphorylate almost irreversibly varying amounts
of the acetylcholinesterase enzyme of tissues, allowing accumulation of
acetylchloline at cholinergic neuro-effector junctions (muscarinic effects), and
at skeletal muscle myoneural junctions and in autonomic ganglia (nicotinic
effects). Poison also impairs CNS function. Toxicants can be absorbed by
inhalation, ingestion, and skin penetration. Some are converted to more toxic
intermediates before they are metabolized. All undergo hydrolytic degrada-
tion in liver and other tissues, usually within hours of absorption. Degrada-
tion products are of low toxicity, and are excreted in urine and feces.
FREQUENT SYMPTOMS AND SIGNS OF POISONING
Symptoms of acute poisoning develop during exposure or within 12 hours
of contact. HEADACHE, DIZZINESS, EXTREME WEAKNESS,
ATAXIA, TINY PUPILS, blurred or dark vision, muscle TWITCHING,
-------
TREMOR, sometimes convulsions, mental confusion, incontinence, uncon-
sciousness. NAUSEA, vomiting, abdominal cramps, diarrhea. Tightness in
chest, SLOW HEARTBEAT, wheezing, productive cough, sometimes PUL-
MONARY EDEMA (up to 12 hours after poisoning). SWEATING, rhi-
norrhea, tearing, salivation. Severe poisoning may cause sudden uncon-
sciousness or TOXIC PSYCHOSIS resembling acute alcoholism. Extreme
BRADYCARDIA and heart block have been observed. RESPIRATORY
DEPRESSION is caused by toxicant and also by hydrocarbon solvent. Con-
tinuing absorption at intermediate dosage may cause an INFLUENZA-LIKE
ILLNESS characterized by weakness, anorexia, and malaise.
CONFIRMATION OF DIAGNOSIS
Depression of plasma and/or RBC cholinesterase activity is the most
satisfactory and generally available evidence of excessive absorption of this
class of toxicants. Depression of plasma cholinesterase often persists from
1 to 3 weeks; depression of RBC acetylcholinesterase persists up to 12
weeks. Organophosphates yield metabolites that are commonly detectable in
the urine of poisoning victims 12 to 48 hours after absorption of significant
quantities. The table below lists approximate LOWER LIMITS OF NOR-
MAL of plasma and red cell CHOLINESTERASE ACTIVITIES of human
blood, measured by generally available methods. Test values BELOW these
levels usually indicate excessive absorption of a cholinesterase-inhibiting
chemical. (About 3% of individuals have a genetically determined low
plasma cholinesterase activity due to generation of an atypical enzyme by
the liver.) Whenever possible, comparison of the test sample with a pre-
exposure value offers the best confirmation of organophosphate absorption:
a depression of 25% or more is strong evidence of excessive absorption.
CAUTION: If diagnosis is probable, do not delay treatment pending con-
nrmation of diagnosis by blood analysis.
TABLE 1. Approximate Lower Limits of Normal Plasma and
Red Cell Cholinesterase Activities in Humans *
METHOD
ApH (Michel)
pH STAT (Nabb-Whitfield)
ChE-tel (Pfizer)
A ChE-tel (Pfizer)
1-Test Cholinesterase
(EM Diagnostics)
ACHOLEST Test Paper
Dupont ACA
Garry-Routh Male
(Micro) Female
Merckotest
PLASMA RBC
0.4
2.3
40
3.6
>20
<8
0.5
8.0
210
7.8
5.8
3.0
UNITS
ApH per ml per hour
fjM per ml per hour
ChE-tel units
A ChE-tel units
Units per ml
Minutes
Units per ml
/tM-SH per ml per 3
Units per ml
mm
* Because measurement technique varies among laboratories, more accurate
estimates of minimum normal values are usually provided by individual
laboratories.
-------
TREATMENT
CAUTION: Persons attending the victim must avoid contamination
with vomitus and other sources of toxicant. Wear rubber
gloves while decontaminating the victim.
1. Establish CLEAR AIRWAY and TISSUE OXYGENATION by aspira-
tion of secretions, and if necessary, by assisted pulmonary ventilation
with oxygen. Do not administer atropine until a satisfactory level of
oxygenation has been achieved. Atropine may induce ventricular fibril-
lation if victim is severely asphyxic.
2. Administer ATROPINE SULFATE intravenously, or intramuscularly
if TV injection is not possible. Atropine protects the end-organs from
excessive concentrations of acetylcholine. It does not reactivate cho-
linesterase, arid the effects of unmetabolized toxicant may appear as
atropinization wears off.
In MODERATELY SEVERE poisoning:
Adult dosage, including children over 12 years: 0.4-2.0 mgm (1.0 to 5.0
ml of usual 0.4 mgm/ml solution) repeated every 15-30 minutes until
atropinization is achieved (tachycardia, flushing, dry mouth, mydriasis).
Maintain atropinization by repeated doses for 2-12 hours, depending
on severity of poisoning. Watch the patient closely for relapse as atro-
pinization wears off.
Dosage for children under 12 years: 0.02 mgm/kg body weight (0.05
ml/kg of usual 0.4 mgm/ml solution) repeated every 15-30 minutes
until atropinization is achieved.
In SEVERE poisoning, use TWICE the dosage of atropine recom-
mended above.
3. Administer PRALBDOXIME (Protopam-Ayerst, 2-PAM) in those
cases of severe poisoning by organophosphate (specifically) pesticides
in which muscle weakness and twitchings persist despite atropine ther-
apy. When administered early (less than 36 hours after poisoning)
protopam is of value in relieving the nicotinic effects of severe poison-
ing that are not reversed by atropine.
Note: Protopam is of no value in poisonings by cholinesterase-inhibit-
ing carbamate compounds.
Adult dose (including children over 12 years): give 1.0 gm intravenously,
at no more than 0.5 gm per minute, repeating dose in one hour if
muscle weakness has not been relieved.
Child's dose (under 12 years): give 20-50 mgm per kg (depending on
severity) intravenously, injecting no more than half the total dose per
minute. This dosage amounts to 0.4 ml-1.0 ml per kg of the recom-
mended 5% solution. Repeat every 10-12 hours as needed, up to 3
times.
In very severe poisonings, dosage rates may be doubled. Slow adminis-
tration may be achieved by administering pralidoxime in 250 ml normal
saline over a 30-60 minute interval. If intravenous injection is not
-------
possible, pralidoxime may be given by deep intramuscular injection.
CAUTION: Be prepared to assist pulmonary ventilation if respiration
is depressed.
4. Observe patient closely at least 24 hours to insure that symptoms
(sometimes pulmonary edema) do not occur as atropinization wears off.
In very severe poisonings, metabolic disposition of toxicant may require
as long as 3 days.
5. BATHE and SHAMPOO victim with soap and water if there is any
chance that SKIN and HAIR are contaminated.
6. If pesticide has been INGESTED in quantity sufficient to cause poison-
ing, the stomach must be emptied. If victim is alert and respiration is
not depressed, give SYRUP OF IPECAC to induce vomiting:
Adults (12 years and over): 30 ml; children under 12 years: 15 ml.
CAUTION: OBSERVE the victim closely after administering
IPECAC. If consciousness level declines, or if vomiting
has not occurred in 15 minutes, proceed immediately to
INTUBATE the stomach.
Following emesis, have victim drink a suspension of 30 gm ACTI-
VATED CHARCOAL in 3-4 ounces of water to limit absorption of
toxicant remaining in the gut.
If victim is obtunded or respiration is depressed, empty the stomach
by INTUBATION, ASPIRATION, and LAVAGE, using isotonic
saline or 5% sodium bicarbonate. Because many pesticides are dis-
solved in petroleum distillates, emesis and intubation of the stomach
involve a serious risk that solvent will be aspirated, leading to chemical
pneumonitis. For this reason:
A. If the victim is unconscious or obtunded, and if facilities are at
hand, insert an ENDOTRACHEAL TUBE (cuffed, if available)
prior to gastric intubation.
B. Keep the victim's HEAD BELOW THE LEVEL OF THE STOM-
ACH during intubation and lavage (Trendelenburg, or left lateral
decubitus, with head of table tipped downward). Keep the victim's
head turned to the left.
C. ASPIRATE PHARYNX as regularly as possible to remove gagged
or vomited stomach contents.
After aspiration of gastric contents and washing of stomach, instill 30
gm of ACTIVATED CHARCOAL in 3-4 ounces of water through a
stomach tube to limit absorption of remaining toxicant.
If bowel movement has not occurred in 4 hours, and if patient is fully
conscious, give SODIUM SULFATE (Glauber's Salts) as a cathartic:
Adults (12 years and older): 15 gm in 6-8 ounces of watei^.
Children under 12: 0.2 gm/kg body weight in 1-6 ounces of water.
7. DO NOT give morphine, aminophylline, phenothiazines, or reserpine.
8. If 'intractable CONVULSIONS (unresponsive to antidotes) occur in
severe poisoning, causes unrelated to direct organophosphate action may
-------
be responsible: head trauma, cerebral anoxia, mixed poisoning.
Although not thoroughly tested in these circumstances, DIAZEPAM
(Valium) (5-10 mgm for adults, 0.1-0.2 mgm/kg for children under 6
years or 23 kg) is probably the safest and most reliable anticonvulsant
CAUTION: Be prepared to assist pulmonary ventilation mechanically
if respiration is depressed, and to counteract hypotensive
reactions.
9. Persons who have been clinically poisoned by organophosphate pesti-
cides should not be re-exposed to cholinesterase-inhibiting chemicals
until symptoms and signs have resolved completely and blood cholines-
terase activities have returned to at least 80% of pre-poisoning values.
If blood cholinesterase was not measured prior to poisoning, blood
enzyme activities should reach at least minimum normal levels (Table 1)
before the victim is returned to a pesticide-contaminated environment.
10. DO NOT administer atropine or pralidoxime prophylactically to work-
ers exposed to organophosphate pesticides. It is neither practical nor
medically sound to do so.
8
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CARBAMATE
CHOLINESTERASE-INHIBITING
PESTICIDES
GENERAL CHEMICAL STRUCTURE
O
n
N - C - O
H3C
LEAVING
GROUP
COMMON COMMERCIAL PESTICIDE PRODUCTS (approximately in
order of toxicity)
Highly toxic: aldicarb (Temik), oxamyl (Vydate), carbofuran (Furadan),
methyomyl (lannate, Nudrin), Zectran, methiocarb (Mesurol).
Moderately toxic: propoxur (Baygon), Landrin, carbaryl (Sevin), metal-
kamate (Dux).
Some chemicals of this class are "systemic," i.e., they are taken up by
the plant and translocated into foliage and sometimes into the fruit.
TOXICOLOGY
Toxicants of this class cause reversible carbamylation of the acetylcho-
linesterase enzyme of tissues, allowing accumulation of acetylcholine at
cholinergic neuroeffector junctions (muscarinic effects), and at skeletal muscle
myoneural junctions and in autonomic ganglia (nicotinic effects). Poison
also impairs CNS function. The carbamyl-enzyme combination dissociates
more readily than the phosphorylated enzyme produced by organophosphate
insecticides. The lability tends to mitigate the toxicity of carbamates, but
also limits the usefulness of blood enzyme measurements in diagnosis of
poisoning. Carbamates are absorbed by inhalation, ingestion, and dermal
penetration. They are actively metabolized by the liver, and the degradation
products are excreted by the liver and kidneys.
A few of the carbamate insecticides are formulated in methyl (wood) alco-
hol. In cases of ingestion of these formulations, the toxicology of the metha-
nol must be taken fully into consideration: severe gastroenteric irritation,
acidosis, and CNS injury.
FREQUENT SYMPTOMS AND SIGNS OF POISONING
Symptoms of acute poisoning develop during exposure or within 12 hours
of contact. HEADACHE, DIZZINESS, WEAKNESS, ATAXIA, TINY
PUPILS, blurred or "dark" vision, muscle TWITCHING, TREMOR, some-
times convulsions, mental confusion, incontinence, unconsciousness.
-------
NAUSEA, vomiting, abdominal cramps, diarrhea. Tightness in chest, SLOW
HEARTBEAT, wheezing, productive cough, occasionally pulmonary edema.
Sweating, rhinorrhea, tearing, SALIVATION. Severe poisoning may cause
sudden unconsciousness, or a toxic psychosis. RESPIRATORY DEPRES-
SION may result from actions of the toxicant and solvent. Continuing ab-
sorption at intermediate dosage may cause protracted weakness, anorexia,
and malaise.
CONFIRMATION OF DIAGNOSIS
Depression of plasma and/or RBC cholinesterase activity is sometimes
useful in detecting excessive absorption of carbamates. However, enzyme activ-
ities commonly revert to normal within a few hours. They are not, therefore,
reliable detectors of carbamate poisoning; i.e., intoxication may exist when
blood cholinesterase activities are normal. The rapid methods for cholines-
terase estimation (ACHOLEST, ChE-TEL, MERCKOTEST) are more likely
to detect depressions. Some carbamates yield metabolites that are meas-
urable in the urine of poisoning victims up to 48 hours after absorption of
significant quantities.
The table below lists the approximate LOWER LIMITS OF NORMAL
plasma and red cell CHOLINESTERASE ACTIVITIES of human blood,
measured by generally available methods. When test values are BELOW
these levels, excessive absorption of a cholinesterase-inhibiting carbamate
may be suspected. Whenever possible, comparison of the "test" sample with
a "pre-exposure" value offers the best confirmation of excessive carbamate
absorption: a depression of 25% or more is strong evidence of excessive
exposure. (About 3"% of individuals have a genetically determined low
plasma cholinesterase activity, due to generation of an atypical enzyme by
the liver. The red cell acetylcholinesterase is normal in these cases.)
TABLE 1. Approximate Lower Limits of Normal Plasma and
Red Cell Cholinesterase Activities in Humans *
METHOD
ApH (Michel)
pH STAT (Nabb-Whitfield)
ChE-tel (Pfizer)
A ChE-tel (Pfizer)
1-Test Cholinesterase
(EM Diagnostics)
ACHOLEST Test Paper
Dupont ACA
Garry-Routh Male
(Micro) Female
Merckotest
PLASMA RBC
UNITS
0.4
2.3
40
3.6
>20
<8
0.5 ApH per ml per hour
8.0 pM per ml per hour
ChE-tel units
210 A ChE-tel units
Units per ml
Minutes
Units per ml
7.8
5.8
3.0
per ml per 3 min
Units per ml
* Because measurement technique varies among laboratories, more accurate
estimates of minimum normal values are usually provided by individual
laboratories.
10
-------
CAUTION: If diagnosis is probable, do not delay treatment pending con-
firmation of diagnosis by blood analysis.
TREATMENT
CAUTION: Persons attending the victim must avoid contamination
with vomitus and other sources of toxicant. Wear rubber
gloves while decontaminating the victim.
1. Establish CLEAR AIRWAY and TISSUE OXYGENATION by aspira-
tion of secretions, and if necessary, by assisted pulmonary ventilation
with oxygen. Do not administer atropine until a satisfactory level of
oxygenation has been achieved. Atropine may induce ventricular fibril-
lation if the victim is severely asphyxic.
2. Administer ATROPINE SULFATE intravenously, or intramuscularly
if IV injection is not possible. Atropine protects the end-organs from
excessive concentrations of acetylcholine. It does not reactivate cholin-
esterase, and effects of unmetabolized toxicant may appear as atropiniza-
tion wears off.
In MODERATELY SEVERE poisoning.
Adult dose (including children over 12 years): 0.4-2.0 mg/kg body
weight (1.0-5.0 ml of usual 0.4 mgm/ml solution) repeated every 15-30
minutes until atropinization is achieved (tachycardia, flushing, dry
mouth, mydriasis). Maintain atropinization by repeated doses for 2-12
hours, depending on severity of poisoning.
Child's dose: 0.01 mgm/kg body weight (0.05 ml/kg of usual 0.4 mgm/
ml solution) repeated every 15-30 minutes until atropinization is
achieved. In SEVERE poisoning: use TWICE the dosage of atropine rec-
ommended above.
3. Do NOT give pralidoxime Protopam-Ayerst, 2-PAM). It is of no
value in carbamate poisonings.
4. OBSERVE patient closely at least 24 HOURS to insure that symp-
toms (possibly pulmonary edema) do not occur as atropinization wears
off.
5. BATHE and SHAMPOO victim with soap and water if there is any
chance that SKIN and HAIR are contaminated.
6. If pesticide has been INGESTED, the stomach must be emptied. If
victim is alert and respiration is not depressed, give SYRUP OF
IPECAC to induce vomiting: adults (including children over 12), 30
ml; children under 12, 15 ml.
CAUTION: OBSERVE the victim closely after administering
IPECAC. If consciousness level declines, or if vomiting
has not occurred in 15 minutes, proceed immediately to
INTUBATE the stomach.
Following emesjis, have victim drink a suspension of 30 gm ACTI-
VATED CHARCOAL in 3-4 ounces of water to bind toxicant remain-
ing in the gastrointestinal tract.
If victim is obtunded or respiration is depressed, empty the stomach by
11
-------
INTUBATION, ASPIRATION, and LAVAGE, using isotonic saline
of 5% sodium bicarbonate. Because many pesticides are dissolved in
petroleum distillates, emesis and intubation of the stomach involve a
serious risk that solvent will be aspirated, leading to chemical pneu-
monitis. For this reason:
A. If the victim is unconscious or obtunded, and if facilities are at
hand, insert an ENDOTRACHEAL TUBE (cuffed, if available)
prior to gastric intubation.
B. Keep the victim's HEAD BELOW THE LEVEL OF THE
STOMACH during intubation and lavage (Trendelenburg, or left
lateral decubitus, with head of table tipped downward). Keep the
victim's head turned to the left.
C. ASPIRATE PHARYNX as regularly as possible to remove gagged
or vomited stomach contents.
After aspiration of gastric contents and washing of stomach, instill 30
gm of ACTIVATED CHARCOAL in 3-4 ounces of water through a
tube to limit absorption of remaining toxicant.
If bowel movement has not occurred in 4 hours, and if patient is fully
conscious, give SODIUM SULFATE as a cathartic. Adult dose, includ-
ing children over 12: 15 gm in 6-8 ounces of water. For children under
12, give 0.2 gm/kg body weight in 1-6 ounces of water.
7. DO NOT give morphine, aminophylline, phenothiazines, or reserpine.
8. CONVULSIONS are uncommon manifestations of poisoning by car-
bamates. If they occur, causes other than direct carbamate action
should be considered: cerebral anoxia, head trauma, mixed poisoning.
Although not tested in these circumstances, DIAZEPAM (Valium) is
probably the anticonvulsant of choice. Dosage for adults and children
over 6 years or 23 kg body weight is 5-10 mgm given slowly IV (no
more than half total dose per minute, or intramuscularly, (deep). Dosage
for children under 6 years, or 23 kg body weight, is 0.1-0.2 mgm/kg.
Repeat this dosage every 2-4 hours if needed to control convulsions.
Be prepared to intubate and to assist pulmonary ventilation mechani-
cally if respiration is depressed. Hypotensive reactions may also occur.
9. Persons who have been clinically poisoned by carbamate pesticides
should not be re-exposed to cholinesterase-inhibiting chemicals until
symptoms and signs have resolved completely and blood cholinesterase
activities have returned to at least 80% of pre-poisoned values. If blood
cholinesterase was not measured prior to poisoning, blood enzyme
activities should reach at least minimum normal levels (Table 1) before
the victim is returned to a pesticide-contaminated environment.
10. Do NOT administer atropine prophylactically to workers exposed to
carbamate insecticides. It is neither practical nor medically sound to
do so.
12
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PARAQUAT, DIQUAT, AND
MORFAMQUAT (Dipyridyls)
CHEMICAL STRUCTURES
CH3-N
2cr
PARAQUAT
2Br
CH.
I *
CH
N
C CH2N
CH.
CH
I
CH.
CH.
I *
.CH
JCH0CN
\
MORFAMQUAT
CH
I
CH.
CH.
-CH.
!\
2CI
COMMON COMMERCIAL PESTICIDE PRODUCTS
The highly polar dipyridyl compounds are available commercially as
halide and dimethyl sulfate salt solutions. Both are used as contact herbi-
cides; diquat is particularly effective against water weeds. Plant tissues and
soil particles adsorb dipyridyl compounds strongly. Concentrates are more
likely to cause poisoning than are the more dilute agents sold over the
counter.
Paraquat products: Paraquat Cl, Dual Paraquat, EM-7217, Gramoxone S,
Weedol and Dextrone X are all concentrates containing 20% paraquat ion.
Preeglone extra and Gramonol are concentrate mixtures with other herbi-
cides. Ortho Spot Weed and Grass Killer contains 0.2% paraquat ion.
Diquat products: Aquakill, Aquacide, Heavy Duty Weed Control, Aqua-
tate, Aquatic Weed Killer, Reglone, Vegetrole, Watrol, and Di-Kill Vegeta-
tion Killer are all packaged as concentrates. Preeglone extra is a concentrate
mixture with paraquat.
Morfamquat products: Morfoxone, PP-745.
TOXICOLOGY
The dipyridyl compounds bind to, and injure, the epithelial tissues of the
skin, nails, eyes, nose, mouth, and respiratory and gastrointestinal tracts.
Concentrated solutions cause inflammation and sometimes necrosis and
ulceration of mucosal linings.
The toxicology of paraquat has been more thoroughly investigated than
13
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that of the other dipyridyls. Diquat appears to be substantially less toxic
than paraquat. Little is known of the effects of morfamquat.
The consequences of ingestion of paraquat concentrate (which accounts
for nearly all of the mortality and serious morbidity from these compounds)
are unique. Because dosages necessary to produce poisoning in humans
vary widely, all cases of ingestion should be treated vigorously, regardless
of estimated intake.
For 24-72 hours, there is often very little indication of systemic toxicity.
Evidence of poisoning may be limited to pain, vomiting, and diarrhea from
irritation of the gastrointestinal linings. At 48 to 72 hours, kidney damage
may be apparent from proteinuria, hematuria, and rising BUN and creatinine
levels. Liver damage is reflected in hyperbilirubinemia, often associated with
increased serum GOT, GPT, alkaline phosphatase, and LDH enzyme activi-
ties. From 72 hours to as long as 14 days after ingestion, indications of a
diffuse toxic pneumonitis often appear.
Histopathology of the pulmonary lesion is complex, commencing with
intra-alveolar edema and hemorrhage, then rapid proliferation of bron-
chiolar epithelium and fibrous connective tissue. Focal atelectasis occurs,
possibly as a result of impaired synthesis of pulmonary surfactant. The func-
tional consequence is impaired gas exchange, due to patchy consolidation,
alveolar collapse and increased airway resistance. The proliferation of fibrous
connective tissue is often progressive, and so generalized as to cause death
in 1-3 weeks. Surviving patients should be examined for evidence of residual
fibrosis up to 6 months after poisoning. Injuries to liver and kidney are
commonly reversible, ameliorating even as the pulmonary lesion worsens.
Electrocardiographic evidence of toxic myocarditis is commonly observed,
and cranial nerve palsies have been reported as toxic manifestations.
Lens cataracts have been reported in laboratory animals given diquat
by mouth.
FREQUENT SYMPTOMS AND SIGNS OF POISONING
Skin IRRITATION, drying, and cracking follow untreated skin contact
with paraquat. DISCOLORATION and IRREGULARITY of FINGER-
NAILS commonly occur in workers regularly exposed to paraquat concen-
trates. Delayed CONJUNCTIVITIS and KERATITIS develop 12-48 hours
after contact with the eye. Inhalation of spray droplets irritates the nose
and throat, and sometimes causes NOSEBLEED.
FOLLOWING INGESTION of paraquat concentrate, the earliest symp-
toms and signs are due to mucosal irritation and ulceration of the gastro-
intestinal tract. PAIN (oral, substernal, abdominal), VOMITING, and
DIARRHEA (sometimes melena) occur. Generalized MUSCLE ACHING
is reported. Early symptoms are sometimes so mild that vigorous treatment
is improperly delayed.
From 48-72 hours, indications of renal and hepatic insult appear. Albu-
minuria, hematuria, pyuria, and elevated BUN and creatinine occur. OLI-
GURIA may develop, and this signals severe poisoning. JAUNDICE and
i
14
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elevations of serum GOT, GPT, alkaline phosphatase and LDH reflect
hepatocellular injury. The effects on liver and kidney are generally reversible.
Indications of lung injury usually appear 72-96 hours after exposure, but
may be delayed as long as 14 days. COUGH, DYSPNEA, and TACHYPNEA
often progress in the manner of a diffuse pneumonitis. In some cases, severe
PULMONARY EDEMA occurs and persists for several days. The lung dis-
ease usually progresses to death.
CONFIRMATION OF DIAGNOSIS
Qualitative and quantitative methods for paraquat and diquat in urine
are available at some toxicology laboratories and at the Chevron Environ-
mental Health Center, 225 Bush Street, San Francisco, California 94104,
telephone (415) 233-3737.
TREATMENT
1. Contaminated SKIN must be FLUSHED with copious amounts of
water. Material splashed in the EYES must be removed by PRO-
LONGED IRRIGATION with clean water. Eye contamination should
thereafter be treated by an ophthalmologist.
2. INGESTION of ANY DIPYRIDYL should be treated promptly and
vigorously to LIMIT ABSORPTION from the gastrointestinal tract
and ACCELERATE EXCRETION of material already absorbed. Be-
cause the absorption of dipyridyls from the gut is relatively slow,
measures to MINIMIZE ABSORPTION offer the most promising op-
portunity to save the victim. These measures must be undertaken even
though the patient is essentially free of signs of systemic toricity, and
even when, by all accounts, the ingested dose was probably small and
was taken as long as 72 hours before treatment.
A. LAVAGE THE STOMACH with at least 2 liters normal saline or
5% sodium bicarbonate solution. With stomach tube still in place,
introduce a slurry of 8-10 ounces of ADSORBENT, allowing as
much time as necessary for the material to be accommodated with-
out overdistension of the stomach. Suitable adsorbents are, in order
of effectiveness: Fuller's Earth *, 30% suspension, and bentonite
(or Montmorillonite), 7% suspension. These agents effectively bind
* Optimal mesh 100-200. Sources of adsorbents are as follows:
Sigma Chemical Company, 3500 Dekalb Street, St. Louis, Missouri
63178
Robinson's Bentonite U.S.P., Cat. No. 1138, Robinson Laboratories,
Inc., San Francisco, California 94104
Robinson's Fuller's Earth U.S.P., Cat. No. 1343, Robinson Labora-
tories, Inc., San Francisco, California 94104
U.S.P. Volclay Bentonite, American Colloid Company, Skokie, Illinois
Emathlite VMP 600, Mid-Florida Mining Co., Lowell, Florida 32663
15
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dipyridyls with which they come in contact in vivo. Activated char-
coal is less effective, but should be used if other agents are not
immediately available. Allow about one hour for the adsorbent to
contact the toxicant before administering SODIUM SULFATE as
a cathartic (adults, 12 years and older: 15 gm in 6-8 ounces of
water; children under 12: 0.2 gm/kg body weight in 1-6 ounces of
water). Repeat dosage of Fuller's Earth (or other adsorbent if
Fuller's Earth is not available) by mouth every 4 hours for at least
12 complete doses. Repeat saline catharsis if continuing bowel
movements do not occur.
B. Institute a regimen of FORCED DIURESIS. Put a retention cath-
eter in place to insure accurate monitoring of urine output. Inquire
into possible medical limitations to the victim's ability to tolerate
high fluid loads. Examine the urine sediment to assess likelihood
that dipyridyl injury to the kidneys has already reduced tolerance
to fluid infusion by severe tubular injury.
In the absence of contraindications, INFUSE intravenously, hi
rotation, solutions of either glucose, electrolyte or mannitol. As
time progresses, particular electrolyte solutions will be required to
maintain normal extracellular fluid composition.
Give parenteral FUROSEMIDE (Lasix) by slow intravenous injec-
tion to sustain diuresis. Adult dose: 20-40 mgm every 2-6 hours.
MONITOR FLUID BALANCE AND BLOOD ELECTROLYTE
CONCENTRATIONS regularly, and look for signs of fluid overload
(basilar rales, venous distension, high central venous pressure) that
would warn of excessive fluid accumulation.
If circumstances do not permit vigorous forced diuresis undertake
PERITONEAL DIALYSIS or EXTRACORPOREAL HEMO-
DIALYSIS. These measures appear to offer little advantage over
forced diuresis in victims able to tolerate high rates of intravenous
fluid infusion. Hemodialysis with ultrafiltration is reported to offer
effective removal of paraquat from the circulating blood.
Measure dipyridyl in urine to estimate levels of remaining toxicant.
3. DO NOT ADMINISTER SUPPLEMENTAL OXYGEN, unless arterial
pO2 drops below 60-70 mm Hg. Increased levels of alveolar oxygen
accelerate the pathologic process caused by dipyridyls.
4. SUPEROXIDE DISMUTASE (Truett Laboratories) is an enzyme from
bovine erythrocytes which, by virtue of its free radical scavenging prop-
erty, represents a rational antidote for dipyridyl poisoning. Tests of
antidotal power in rats have yielded very promising results. The value of
the material in treating human poisonings has not yet been reported. It
can be given both by aerosol and intravenously, and appears to be
nontoxic.
5. Corticosteroids have usually been administered in human poisoning
cases. While they have not influenced the outcome adversely, neither
have they proven definitely beneficial. Immunosuppressive drugs have
been tried in a few cases without apparent benefit.
16
-------
6. There is some evidence that expectorants (especially ammonium chloride
and potassium iodide) may be of therapeutic value in minimizing the
reduction in lung surfactant activity that is characteristic of paraquat
poisoning.
17
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CHLOROPHENOXY COMPOUNDS
GENERAL CHEMICAL STRUCTURE
H
C
H
H
ESTER
GROUP
or
N
METAL
ION
COMMON COMMERCIAL PESTICIDE PRODUCTS
2,4-D (Weedone), 2,4,5-T 2,4,5-TP, Silvex (Kuron), 2,4-DB (Butyrac,
Butoxone), erbon, Fenac, 2,4-DEP, MCPA, MCPB, MCPP (Mecoprop),
Weedestron, Esteron, Estone, Dacamine, Weed-B-Gon, Weed-No-More,
Weed-Out, Ded-Weed, Weed or Brush-Rhap, Broadleaf Weed KiUer, Dande-
lion Killer, Vegetation Killer, Chickweed and Clover Killer. Several hundred
herbicide preparations include one or more CHLOROPHENOXY COM-
POUND. They can usually be identified in the active ingredient description
on the product label.
TOXICOLOGY
The chlorophenoxy acids, salts, and esters are mildly to severely irritating
to skin, eyes, and respiratory and gastrointestinal linings. They are absorbed
across the gut wall, the lung, and the skin. They are not significantly fat
storable: excretion occurs within hours, or at most days, primarily in the
urine.
These compounds apparently have very low toxic potential for most indi-
viduals. Human subjects have tolerated 0.5 gm ingested doses daily for 2-4
weeks without adverse effects. Paradoxically, several cases of peripheral
neuropathy have been reported in workers after seemingly minor exposures
to 2,4-D. Whether these individuals were peculiarly predisposed, or were
exposed concurrently to other unidentified neurotoxic materials, is not known.
In a few individuals, local depigmentation has apparently resulted from pro-
longed and repeated dermal contact with chlorophenoxy materials.
Given hi large doses to experimental animals, 2,4-D causes vomiting,
diarrhea, anorexia, weight loss, ulcers of the mouth and pharynx, and toxic
injury to the liver, kidneys, and central nervous system. Myotonia (stiffness
and incoordination of hind extremities) develops in some species and is ap-
parently due to CNS damage: demyelination has been observed in the dorsal
columns of the cord, and EEG changes have indicated functional disturbances
in the brains of heavily dosed experimental animals. A single victim of acci-
18
-------
dental ingestion of over 7 gm of 2,4-D exhibited direct toxic damage to
skeletal muscle, manifest as myoglobinuria and creatinuria. Other chemicals
in the ingested formulation may have contributed to the unusual pathology
in this case. In another isolated instance of extreme dosage, convulsions
apparently occurred before death.
FREQUENT SYMPTOMS AND SIGNS OF INJURY AND POISONING
IRRITATION of the skin follows excessive contact with many chloro-
phenoxy compounds. Protracted inhalation of spray is likely to irritate the
nose, eyes, throat and bronchi, causing disagreeable local BURNING SEN-
SATIONS and COUGH. Prolonged inhalation has also caused DIZZINESS
and ATAXIA, usually of a transient nature. WHEN INGESTED, these
compounds IRRITATE the MOUTH and THROAT, and usually cause
enough gastrointestinal irritation to induce prompt EMESIS. CHEST PAIN
from esophagitis is common. ABDOMINAL PAIN and TENDERNESS and
DIARRHEA usually ensue. Absorption of large quantities of chlorophenoxy
herbicide may produce FIBRILLARY MUSCLE TWITCHING, SKELE-
TAL MUSCLE TENDERNESS, and MYOTONIA (stiffness of muscles of
extremities). Respiratory insufficiency from muscle weakness apparently oc-
curred in one victim of accidental poisoning, although poisoning in this case
may have involved additional toxicants.
CONFIRMATION OF DIAGNOSIS
Gas-liquid chromatographic methods are available for detecting and meas-
uring many of the chlorophenoxy compounds in urine. These analyses are
useful in confirming and assessing the magnitude of toxicant absorption.
Urine samples should be collected as soon as possible after exposure because
the herbicides may be almost completely excreted in 24-72 hours, depending
on the dose. Analyses can be performed at special laboratories operated by
States, agricultural research facilities, commercial chemical companies, and
the U.S. Environmental Protection Agency.
Treatment should not be delayed pending confirmation of the causative
agent, if there is a strong circumstantial basis for the diagnosis.
TREATMENT
1. BATHE and SHAMPOO with soap and water to remove chemicals
from the skin and hair. Individuals with chronic skin disease or known
sensitivity to chemicals should either avoid using these herbicides or
should take extraordinary measures to avoid direct contact.
2. FLUSH contaminating chemicals from the eyes with copious amounts of
clean water for 10-15 minutes.
3. If symptoms of illness occur during or following inhalation of spray,
REMOVE the victim FROM CONTACT with the material for at least
2 days. Allow subsequent use of chlorophenoxy compounds only if
effective respiratory protection is practiced.
19
-------
4. When chemicals of this class have been INGESTED, spontaneous
emesis usually occurs, and may empty the stomach as effectively as
intubation and lavage. If vigorous emesis has not occurred, and IF
VICTIM IS FULLY ALERT, induce EMESIS with SYRUP of IPECAC
(adults 12 years and older, 30 ml; children under 12 years, 15 ml).
A. If consciousness level is depressed, an effect of the solvent petroleum
distillates and/or other pesticides should be suspected. In this case,
empty the stomach by INTUBATION, ASPIRATION, AND
LAVAGE, using all available means to avoid aspiration of vomitus:
Trendelenberg or left lateral decubitus position, frequent aspiration
of the pharynx, and in unconscious victims, tracheal intubation
(using a cuffed tube), prior to gastric intubation.
B. After emesis or aspiration of the stomach and washing with isotonic
saline or sodium bicarbonate, administer or instill 30 gm of ACTI-
VATED CHARCOAL in 3-4 ounces of water to limit absorption
of remaining toxicant.
C. If the irritant properties of the toxicant fail to produce a bowel
movement in 4 hours, and if the patient is fully conscious, give
SODIUM SULFATE (Glauber's Salts) as a cathartic (adults 12
years and older, 15 gm in 6-8 ounces of water; children under 12,
0.2 gm/kg of body weight in 1-6 ounces of water).
D. If absorption of as much as 0.5 gm may have occurred in an adult
(or about 0.02 gm/kg in children under 12 years), administer glu-
cose and electrolyte solution intravenously to accelerate excretion
of toxicant. Observe the patient for renal irritation (albuminuria,
hematuria); liver injury (serum bilirubin, alkaline phosphatase,
serum LDH, GOT and GPT); gastrointestinal ulceration (melena);
leukopenia (WBC and differential); myalgia and myotonia (manifest
as stiffness and incoordination); and peripheral neuropathy (par-
esthesiae, pain, hypesthesia and paresis of the extremities).
20
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NITROPHENOLIC HERBICIDES
GENERAL CHEMICAL STRUCTURE
OH(or ESTER)
(ALKYL) (ALKYL)
COMMON COMMERICIAL PESTICIDE PRODUCTS
Dinitrophenol (Chemox PE), dinitroorthocresol (DNOC, DNC, Sinox),
Dinoseb (DNBP, DN-289), dinosam (DNAP), DN-111 (DNOCHP), dinoprop,
dinoterbon, dinoterb, dinosulfon, binapacryl (Morocide, Endosan, Ambox,
Mildex), dinobuton, dinopenton.
TOXICOLOGY
These materials should be regarded as highly toxic to humans and ani-
mals. Most nitrophenols and nitrocresols are well absorbed from the gas-
trointestinal tract, across the skin, and by the lung when very fine droplets
are inhaled. Except in a few sensitive individuals, they are only moderately
irritating to the skin. They usually produce a yellow stain wherever contact
occurs. Like other phenols, they are toxic to the liver, kidney, and nervous
system. Basic mechanism of toxicity is a stimulation of oxidative metabolism
in cell mitochondria, by interference with the normal coupling of carbo-
hydrate oxidation to phosphorylation reactions. Increased oxidative metab-
olism depletes body carbohydrate and fat stores and leads to pyrexia,
tachycardia, and dehydration. Most severe poisonings from absorption of
these compounds have occurred in workers who were concurrently exposed
to hot environments. Direct action on the brain causes cerebral edema, mani-
fest clinically as a toxic psychosis and sometimes as convulsions. Liver
parenchyma and renal tubules show degenerative changes. Albuminuria,
pyuria, hematuria, and increased BUN are often prominent signs of renal
injury. Agranulocytosis has occurred following large doses of dinitrophenol.
Cataracts have occurred in some chronically poisoned laboratory species.
This is a possible, but as yet unconfirmed, hazard in humans.
Death in nitrophenol poisoning is followed promptly by intense rigor
mortis.
FREQUENT SYMPTOMS AND SIGNS OF POISONING
YELLOW STAINING of skin and hair signify contact with a nitrophenolic
chemical. Staining of the sclerae and urine indicate absorption of potentially
21
-------
toxic amounts. PROFUSE SWEATING, HEADACHE, THIRST, MAL-
AISE, and LASSITUDE are the common early symptoms of poisoning.
WARM, FLUSHED, SKIN, TACHYCARDIA, and FEVER characterize
a serious degree of poisoning. APPREHENSION, restlessness, anxiety, manic
behavior, or unconsciousness reflect severe cerebral injury. Cyanosis, tachy-
pnea and dyspnea occur as a consequence of extreme stimulation of metab-
olism, pyrexia, and tissue anoxia. Weight loss occurs in persons chronically
poisoned at low dosages.
CONFIRMATION OF DIAGNOSIS
Unmetabolized nitrophenols and nitrocresols can be identified spectro-
photometrically in the serum and urine at concentrations well below those
necessary to cause poisoning. Many laboratories can also analyze for these
compounds by gas-liquid chromatography. If poisoning is probable, do not
await confirmation before commencing treatment.
TREATMENT
1. WASH contaminated SKIN and HAIR promptly with soap and water.
2. FLUSH chemical from EYES with copious amounts of clean water.
3. IN EVENT OF SYSTEMIC POISONING:
A. REDUCE BODY TEMPERATURE BY PHYSICAL MEANS.
Sponge baths and low-temperature blankets probably offer the best
opportunity for survival of poisonings by these agents. In fully con-
scious patients, administer cold, sugar-containing liquids by mouth,
as tolerated.
B. Administer OXYGEN continuously by mask to minimize tissue
anoxia.
C. Administer INTRAVENOUS FLUIDS at maximum tolerated rates
,to enhance urinary excretion of toxicant and to support physiologic
mechanisms for heat loss. Monitor blood electrolytes and sugar, ad-
justing IV infusions to stabilize electrolyte concentrations.
D. Administer SEDATIVES if necessary to control apprehension and
excitement. Amobarbital or PENTOBARBITAL, 100-200 mgm IM
or slowly IV, every 4-6 hours, may be needed in adults (child's dose:
up 5 mgm/kg body weight). Although not previously used in this
type of poisoning, DIAZEPAM (Valium) should be of value: adult
dose 5-10 mgm intramuscularly, or slowly IV, dosage for children
under 6 years or 23 kg: 0.1-0.2 mgm/kg. Repeat every 2-4 hours as
needed.
CAUTION: Be prepared to counteract respiratory depression and
hypotension, which may occur following administra-
tion of anticonvulsants.
E. If toxicant has been INGESTED, the stomach must be emptied.
If victim is alert and respiration is not depressed, give SYRUP OF
IPECAC to induce vomiting (adults 12 years and older: 30 ml;
22
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children under 12: 15 ml).
CAUTION: OBSERVE the victim closely AFTER administering
IPECAC. If consciousness level declines, or if vomit-
ing has not occurred in 15 minutes, proceed immedi-
ately to INTUBATE and LAVAGE the stomach.
Following emesis, have victim drink a suspension of 30 gm ACTI-
VATED CHARCOAL in 3-4 ounces of water to bind toxicant re-
maining in the gastrointestinal tract.
IF VICTIM IS NOT FULLY ALERT, empty the stomach immedi-
ately by INTUBATION, ASPIRATION, and LAVAGE, using
isotonic saline or 5% sodium bicarbonate. Because these pesticides
are usually dissolved in petroleum distillates, emesis and intubation
of the stomach involve a serious risk that solvent will be aspirated,
leading to chemical pneumonitis. For this reason:
(1) If the victim is unconscious or obtunded, and if facilities are
at hand, insert an ENDOTRACHEAL TUBE (cuffed, if avail-
able) prior to gastric intubation.
(2) Keep the victim's HEAD BELOW THE LEVEL OF THE
STOMACH during intubation and lavage (Trendelenburg, or
left lateral decubitus, with head of table tipped downward).
Keep the victim's head turned to the left.
(3) ASPIRATE PHARYNX as regularly as possible to remove
gagged or vomited stomach contents.
After aspiration of gastric contents and washing of stomach, instill
30 gm of ACTIVATED CHARCOAL in 3-4 ounces of water
through the stomach tube to limit absorption of remaining toxicant.
Do NOT instill milk, cream or other materials containing vegetable
or animal fats, as these are likely to enhance absorption.
If bowel movement has not occurred in 4 hours, and if patient is
fully conscious, give SODIUM SULFATE (Glauber's Salts) as a
cathartic (adults 12 years and older: 15 gm hi 6-8 ounces of water;
children under 12: 0.2 gm/kg body weight in 1-6 ounces of water).
F. DO NOT administer aspirin or other antipyretics to control fever.
Animal tests indicate that aspirin enhances, rather than reduces,
the toxicity of nitrophenolic and nitrocresolic compounds.
G. During convalescence, administer high-calorie, high-vitamin diet
to facilitate repletion of body fat and carbohydrate stores.
H. Discourage subsequent contact with the toxicant for at least 4
weeks, to allow full restoration of normal metabolic processes.
23
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PENTACHLOROPHENOL OR SODIUM
PENTACHLOROPHENATE
CHEMICAL STRUCTURE
Cl Cl
Cl
COMMON COMMERCIAL PESTICIDE PRODUCTS
PCP, Dowicide-7, Penchlorol, Pentacon, Penwar, Weedone, Veg-I-Kill,
Wood Preserver, Wood Tox 140, Purina Insect Oil Concentrate, Gordon
Termi Tox, Usol Cabin Oil, Certified Kiltrol-74 Weed Killer, Ciba-Geigy
Ontrack OS 3, 4 or 5, Ortho Triox Liquid Vegetation Killer, Black Leaf
Grass. Weed and Vegetation Killer Spray.
Pentachlorophenol has many uses as a weed killer, defoliant, wood pre-
servative, germicide, fungicide, and molluscicide. It is an ingredient of many
other formulated mixtures sold for one or more of these purposes.
TOXICOLOGY
Pentachlorophenol irritates the skin, eyes, and upper respiratory mucous
membranes. It is efficiently absorbed across the skin, the lung, and the gastro-
intestinal lining. Like the nitrophenolic compounds, it stimulates oxidative
metabolism of tissue cells by uncoupling oxidative processes from the normal
stepwise phosphorylation reactions. In common with other phenols, it is toxic
to the liver, kidney, and central nervous system. Impurities in the technical
formulation may well be responsible for chloracne.
The majority of severe poisonings have occurred in workers exposed to
hot environments. However, a major epidemic of poisoning occurred in
newborn infants who absorbed PCP from treated diapers. Dehydration and
metabolic acidosis are important features of poisoning in children.
Albuminuria, glycosuria, and elevated BUN reflect renal injury. Liver
enlargement has been observed in some cases. Anemia and leukopenia have
been found in chronically exposed workers, but leucocytosis is more com-
monly found in acute poisoning.
FREQUENT SYMPTOMS AND SIGNS OF POISONING
IRRITATION of nose, throat, eyes, and skin is the most common symp-
tom of exposure to PCP. Severe or protracted exposure may result in a
CONTACT DERMATITIS. Intensive occupational exposure has resulted in
chloracne.
24-
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PROFUSE SWEATING, HEADACHE, WEAKNESS, and NAUSEA are
the most consistent presenting symptoms of systemic poisoning by absorbed
PCP. FEVER is usually present but may be minimal or absent. TACHY-
CARDIA, TACHYPNEA, and PAIN in the CHEST and ABDOMEN are
often prominent. THIRST is usually intense, but may be masked by nausea
and vomiting. DECLINING MENTAL ALERTNESS may progress to stupor
and/or convulsions. Protracted exposure results in WEIGHT LOSS from
increased basal metabolic rate.
CONFIRMATION OF DIAGNOSIS
PCP can be measured in blood, urine, and adipose tissue by gas-liquid
chromatography. A few parts per billion can usually be found in the blood
and urine of persons having no known exposure. Based on studies of persons
occupationally exposed to PCP, symptoms of systemic toxicity probably do
not appear in adults until blood and urine concentrations reach at least one
part per million (0.1 mgm %, or 1,000 parts per billion).
If poisoning is strongly suspected on grounds of exposure history, symptoms
and signs, do not postpone treatment until diagnosis is confirmed.
TREATMENT
1. BATHE and SHAMPOO contaminated SKIN and HAIR promptly
with soap and water.
2. FLUSH chemical from EYES with copious amounts of clean water.
3. IN EVENT OF SYSTEMIC POISONING
A. REDUCE BODY TEMPERATURE BY PHYSICAL MEANS.
Sponge baths and low-temperature blankets probably offer the best
opportunity for survival of poisonings by these agents. In fully
conscious patients, administer cold, sugar-containing liquids by
mouth, as tolerated.
B. Administer OXYGEN continuously by mask to minimize tissue
anoxia.
C. Administer INTRAVENOUS FLUIDS at maximum tolerated rates
to enhance urinary excretion of toxicant and to support physiologic
mechanisms for heat loss. Monitor blood electrolytes and sugar,
adjusting IV infusions to stabilize electrolyte concentrations.
D. Administer SEDATIVES if necessary to control apprehension and
excitement. Amobarbital or pentobarbital, 100-200 mgm IM or
slowly IV, every 4-6 hours may be needed. (Children's dosage: 5
mgm/kg.) Diazepam, 10 mgm intramuscularly, should be valuable,
although its use has not been reported in this type of poisoning.
(Children's dosage: 0.1-0.2 mgm/kg.)
CAUTION: Be prepared to assist pulmonary ventilation mechani-
cally in event of respiratory depression, and to coun-
teract any hypotensive reaction.
25
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E. If toxicant has been INGESTED, the stomach must be emptied. If
victim is alert and respiration is not depressed, give SYRUP OF
IPECAC to induce vomiting. (Adults, 12 years and older: 30 ml;
children under 12: 15 ml.)
CAUTION: OBSERVE the victim closely AFTER administering
IPECAC. If consciousness level declines, or if vomit-
ing has not occurred in 15 minutes, proceed immedi-
ately to INTUBATE the stomach.
Following emesis, have victim drink a suspension of 30 gm ACTI-
VATED CHARCOAL in 3-4 ounces of water to bind toxicant re-
maining in the gastrointestinal tract.
If victim is not fully alert, empty the stomach immediately by
INTUBATION, ASPIRATION, and LAVAGE, using isotonic
saline or 5% sodium bicarbonate. Because these pesticides are usu-
ally dissolved in petroleum distillates, emesis and intubation of the
stomach involve a serious risk that solvent will be aspirated, leading
to chemical pneumonitis. For this reason:
(1) If the victim is unconscious or obtunded, and if facilities are
at hand, insert an ENDOTRACHEAL TUBE (cuffed, if avail-
able) prior to gastric intubation.
(2) Keep the victim's HEAD BELOW THE LEVEL OF THE
STOMACH during intubation and lavage (Trendelenburg, or
left lateral decubitus, with head of table tipped downward).
Keep the victim's head turned to the left.
(3) ASPIRATE PHARYNX as regularly as possible to remove
gagged or vomited stomach contents.
After aspiration of gastric contents and washing of stomach, instill
30 gm of ACTIVATED CHARCOAL hi 3-4 ounces of water
through a stomach tube to limit absorption of remaining toxicant.
Do NOT instill milk, cream, or other materials containing vegetable
or animal fats which are likely to enhance absorption.
If bowel movement has not occurred in 4 hours, and if patient is
fully conscious, give SODIUM SULFATE (Glauber's Salts) as a
cathartic (adults 12 years and older: 15 gm in 6-8 ounces of water;
children under 12: 0.2 gm/kg body weight in 1-6 ounces of water).
F. DO NOT administer aspirin or other antipyretics to control fever.
G. During convalescence, administer high-calorie, high-vitamin diet
to facilitate repletion of body fat and carbohydrate stores.
H. Discourage subsequent contact with the toxicant for at least 4 weeks,
to allow full restoration of normal metabolic processes.
26
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UREA-, URACIL- AND TRIAZJNE- BASED
HERBICIDES
GENERAL CHEMICAL STRUCTURES
H
,N
H,C C
II I CH.
II
o
C2H5
UREA URACIL s-TRIAZINE
DERIVATIVES DERIVATIVES DERIVATIVES
X=HALOGEN R=ALKYL
COMMON COMMERCIAL PESTICIDE PRODUCTS
Urea derivatives: monuron (Monurex, Telvar), diuron (Di-on, Diurex, Kar-
mex, Vonduron), linuron (HOE 2810, Afalon, Lorox, Sarclex).
Uracil derivatives: bromacil (Borea, Hyvar X, Hyvar X-L, Borocil IV,
Urox HX or B, Isocil), terbacil (Sinbar).
Triazine derivatives: atrazine (Aatrex, Atranex, Gesaprin, Primatol A),
simazine (Princep, Primatol S, Simanex, Gesatop), propazine (Milogard,
Gesamil, Primatol P), prometone (Pramitol, Gesafram, prometon), atraton
(Atratone), prometryn (Caparol, Gesagard, Primatol Q, Prometrex), ametryn
(Evik, Ametrex, Gesapax), desmetryne (Semeron), terbutryn (Igran, Short-
stop E), cyanazine (Bladex, Scogal), cyprazine (Outfox).
TOXICOLOGY
Adverse effects have occurred only rarely as a result of human contact
with these herbicides. Most injuries reported have been skin irritation after
prolonged contact. Improbability of severe systemic poisoning is indicated
by LD50 values over 180 for all of the compounds listed under COMMON
COMMERCIAL PESTICIDE PRODUCTS. In fact, LD50's for all but one
herbicide are over 1,000; that for cyanazine is 182 mgm/kg.
Administered at very high dosage levels to laboratory animals and to sheep
and cattle, some of these chemicals have been found to injure the nervous
system, liver, and kidneys, and to cause increased permeability of capillaries.
Anemia and altered adrenal function have also been detected in animals
given extreme doses of certain triazine compounds. These effects have not
been observed in persons exposed occupationally or by accidental ingestion.
27
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In varying degree these herbicides are likely to produce irritation of the gut
if ingested in substantial quantity. They are efficiently absorbed from the
intestine, and presumably there is some absorption across the skin and lung.
Following absorption, they are partially metabolized: native chemicals and
metabolities are promptly excreted by the kidney and liver. In cases of
accidental ingestion in humans, the hazards of petroleum distillate solvents
may equal or exceed hazards presented by the active herbicidal ingredients.
POSSIBLE PRESENTING SYMPTOMS AND SIGNS OF INJURY
Some compounds of these classes cause IRRITATION of the eyes and
mucous membranes, particularly if direct contact is protracted. NAUSEA,
VOMITING, and DIARRHEA can be expected to result from ingestion
of large quantities.
CONFIRMATION OF ABSORPTION
Certain industrial, university, and government laboratories can detect these
compounds or their metabolites in the urine of persons who have absorbed
significant amounts. These laboratories can be reached through health de-
partments, poison control centers, or the U.S. Environmental Protection
Agency.
TREATMENT
1. FLUSH contaminant from the eyes with copious amounts of clean
water.
2. WASH chemical from the skin and hair with soap and water.
3. If one of these compounds has been INGESTED, optimal treatment will
depend on dosage:
A. Ingestions known to involve less than 10 mgm/kg body weight of
the compounds having LD50 values over 1,000 (all except cyanazine)
are probably managed best without induced emesis or gastric lav-
age, particularly if the ingestion occurred more than an hour prior
to treatment. In these cases, administer 30 gm ACTIVATED
CHARCOAL in 3-4 ounces of water to limit absorption. If a bowel
movement does not occur in 4 hours, give SODIUM SULFATE as
a cathartic (adults, 12 years and older: 15 gm in 6-8 ounces of
water; children under 12: 0.2 gm/kg body weight in 1-6 ounces of
water).
B. In all other cases (unknown dosage, dosage over 10 mgm/kg body
weight, and all cyanazine ingestions), EMPTY THE STOMACH
either by induced EMESIS or by gastric LAVAGE:
(1) If victim is alert and respiration is not depressed, give SYRUP
OF IPECAC (adults, 12 years and older: 30 ml; children un-
der 12: 15 ml).
28
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CAUTION: OBSERVE the victim closely after administering
IPECAC. If consciousness level declines, or if
vomiting has not occurred in 15 minutes, proceed
immediately to EVTUBATE, ASPIRATE, and
LAV AGE the stomach with isotonic saline or
sodium bicarbonate solution.
Following emesis, have victim drink a suspension of 30 gm
ACTIVATED CHARCOAL in 3-4 ounces of water to limit
toxicant absorption.
(2) If victim is not fully alert or if respiration is depressed, empty
the stomach immediately by INTUBATION, ASPIRATION,
and LAV AGE, using isotonic saline or 5% sodium bicarbon-
ate. Because these herbicides are usually dissolved in petroleum
distillates, emesis and intubation of the stomach involve a
serious RISK of chemical pneumonitis if solvent is aspirated.
For this reason:
(a) If the victim is unconscious or obtunded, and if facilities
are at hand, insert an ENDOTRACHEAL TUBE (cuffed,
if available) prior to gastric intubation.
(b) Keep the victim's HEAD BELOW THE LEVEL OF
THE STOMACH during intubation and lavage (Tren-
delenburg, or left lateral decubitus, with head end of
table tipped downward). Keep the victim's head turned
to the left.
(c) ASPIRATE PHARYNX as regularly as possible to re-
move gagged or vomited stomach contents.
After aspiration of gastric contents and washing of stomach,
instill 30 gm of ACTIVATED CHARCOAL in 3-4 ounces of
water through a stomach tube to limit absorption of remaining
toxicant. Do NOT instill milk, cream, or other substances con-
taining vegetable or animal fats which may enhance toxicant
absorption.
(3) If bowel movement has not occurred in 4 hours and if patient
is fully conscious, give SODIUM SULFATE (Glauber's Salts)
as a cathartic (adults, 12 years and older: 15 gm in 6-8 ounces
of water; children under 12: 0.2 gm/kg body weight in 1-6
ounces of water).
29
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ACETANILIDE-, ACETAMIDE-,
CAR BAN I LATE-, AND ANILIDE-,
BASED HERBICIDES
CHEMICAL STRUCTURES
PROPACHLOR
H
H2C=C H2C
H
\ H
NCCCl
N Cl
ALLIDOCHLOR
O CH.
ALACHLOR
0
o
PROPANIL
O
CHLORPROPHAM
CH.
I '
CH
I
CH-
COMMON COMMERCIAL PESTICIDE PRODUCTS
Propachlor (Ramrod), allidochlor (Randox, CDAA), alachlor (Lasso),
chlorpropham (Chloro IPC, CIPC, Furloe), propanil (DPA, Stam,Propanex).
Most technical formulations of these materials are in petroleum distillates.
TOXICOLOGY
These newer herbicides exhibit low systemic toxicity in laboratory rats
(lowest oral LD50 of those listed is 700 mgm/kg). They are, however, irri-
tating to skin, eyes, and mucous membranes. Propachlor and alachlor appear
to have sensitizing properties. Severe skin reactions have occurred in sen-
sitive individuals.
Any systemic toxicity of these compounds appears only at high dosage
levels. Adverse effects from accidental ingestion by humans have not been
reported. In all likelihood, substantial doses would cause gastrointestinal
irritation.
30
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SYMPTOMS AND SIGNS OF UNDUE EXPOSURE
IRRITATION of the skin and membranes of the upper respiratory tract
is the principal adverse effect of contact with these compounds. Exaggerated
reactions on repeated contact (SENSITIZATION) occur in some individuals.
Propachlor has been the principal offender. Sensitization can result in
ACUTE and CHRONIC SKIN INJURY, and in protracted irritation of the
nose, eyes, and throat.
Nausea, abdominal distress, and diarrhea may be expected to result from
ingestion of these compounds.
TREATMENT
1. FLUSH the chemical from the eyes with copious amounts of clean
water. Severe contamination may require specialized ophthalmologic
attention.
2. WASH contaminating herbicide from the skin and hair with soap and
water. Severe irritation may require medical attention. Persons who
become sensitized may need to take stringent precautions to avoid
subsequent contact with these chemicals.
3. Ingestions known to involve less than 10 mgm/kg body weight are
probably managed best without induced emesis or lavage, particularly
if the ingestion occurred more than an hour before treatment. Admin-
ister 30 gm ACTIVATED CHARCOAL in 3-4 ounces of water to limit
absorption. If a bowel movement has not occurred in 4 hours, give
SODIUM SULFATE as a cathartic (adults, 12 years and older: 15 gm
in 6-8 ounces of water; children under 12: 0.2 gm/kg body weight in
1-6 ounces of water).
4. Ingestions of more than 10 mgm/kg body weight, especially when
ingestion occurred less than an hour before treatment, should be man-
aged by prompt EVACUATION of the STOMACH:
A. If victim is alert and respiration is not depressed, give SYRUP of
IPECAC (adults, 12 years and older: 30 ml; children under 12:
15ml).
CAUTION: OBSERVE the victim closely after administering
ipecac. If consciousness level declines or if vomiting
has not occurred in 15 minutes, immediately IN-
TUBATE, ASPIRATE, and LAVAGE the stomach
with isotonic saline or sodium bicarbonate solution.
Following emesis, have victim drink a suspension of 30 gm ACTI-
VATED CHARCOAL in 3-4 ounces of water to limit toxicant
absorption.
B. If victim is not fully alert, or if respiration is depressed, empty the
stomach immediately by INTUBATION, ASPIRATION, and
LAVAGE, using isotonic saline or 5% sodium bicarbonate. Be-
cause these herbicides are usually dissolved in petroleum distillates,
emesis and intubation of the stomach involve a serious risk of
31
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chemical pneumonitis if solvent is aspirated. For this reason:
(1) If the victim is unconscious or obtunded, and if facilities are
at hand, insert an ENDOTRACHEAL TUBE (cuffed, if avail-
able) prior to gastric intubation.
(2) Keep the victim's HEAD BELOW THE LEVEL OF THE
STOMACH during intubation and lavage (Trendelenburg, or
left lateral decubitus; with head of table tipped downward).
Keep the victim's head turned to the left.
(3) ASPIRATE PHARYNX as regularly as possible to remove
gagged or vomited stomach contents.
After aspiration of gastric contents and washing of stomach,
instill 30 gm of ACTIVATED CHARCOAL in 3-4 ounces of
water through the stomach tube to limit absorption of remain-
ing toxicant. Do not instill milk, cream, or other substances
containing vegetable or animal fats which may enhance toxi-
cant absorption.
C. If bowel movement has not occurred in 4 hours, and if patient is
fully conscious, give SODIUM SULFATE (Glauber's Salts) as a
cathartic (adult, 12 years and older: 15 gm in 6-8 ounces of water;
children under 12: 0.2 gm/kg body weight in 1-6 ounces of water).
Severe sensitization reactions may require specialized medical manage-
ment to control inflammatory responses that threaten to impair breath-
ing or compromise circulation to the distal extremities. Reactions of
this severity are rare.
32
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DIMETHYLDITHIOCARBAMATE
COMPOUNDS*
GENERAL CHEMICAL STRUCTURE
C-S--- -S-C-N-(CH3)2
COMMON COMMERCIAL PESTICIDE PRODUCTS
Tetramethyl thiuram disulfide:
Thiram (Arasan, Thiramad, Thirasan, Thylate, Tirampa, Pomasol forte,
TMTDS, Thiotex, Feraasan, Nomersan, Tersan, TUADS)
Metallodimethyldithiocarbamates:
Ziram, Pomasol Z forte (zinc), Ferbam (iron), Vapam (sodium).
TOXICOLOGY
Many compounds of this class are irritants and sensitizers. They may
exacerbate allergic skin and respiratory disease, and sensitize otherwise
normal individuals to subsequent contact with similar chemicals.
The two types of fungicide listed above are metabolized in a manner
similar to disulfiram (tetraethyl thiuram disulfide) that is used to condition
individuals against beverage alcohol. The molecule is first cleaved to yield
two of alkyl dithiocarbamate, then- further degraded to dialkyl amine and
carbon disulfide. The metabolites are powerful inhibitors of multiple sulf-
hydryl enzymes in the liver and CNS. CS2 is neurotoxic in its own right. To
this extent, the toxicology of these fungicides probably resembles that of
disulfiram, whose effects have been most thoroughly explored. Animal ex-
periments indicate that thiram is more toxic than the medicinal disulfiram.
Even so, systemic reactions (excluding irritation and sensitization) to the
fungicides themselves have been rare.
The systemic toxicologic effects of these compounds fall into two cate-
gories: those following absorption of toxicant alone, and those resulting
from ingestion of alcohol following absorption of a dithiocarbamate com-
pound.
Given to laboratory animals in extreme doses, disulfiram itself causes
gastrointestinal irritation, demyelmization of the central nervous system,
and necrosis of the liver, spleen, and kidney parenchyma. Functional and
anatomical CNS damage has been demonstrated in rats on high chronic
dietary intakes of the iron and zinc dimethyldithiocarbamates. Peripheral
* The ethylene bisdithiocarbamate fungicidal compounds are chemically
similar to those considered here, but are metabolized in different ways
and have somewhat different toxicologic properties.
33
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neuropathy and psychotic reactions have occurred in alcohol-abstinent in-
dividuals on disulfiram regimens (ingestion of several hundred mgm daily).
A possible role of the metabolite carbon disulfide has been suspected in these
neurotoxic reactions.
Illness following combined intake of disulfiram and alcohol is due pri-
marily to inhibition of liver enzymes necessary for oxidation of acetaldehyde
to acetic acid. Peripheral vasodilation is the main pathophysiologic feature
of the disulfiram-alcohol reaction, presumably due to high tissue levels of
acetaldehyde. This may occasionally lead to shock, and even more rarely,
to myocardial ischemia, cardiac arrhythmias, failure, and death. Animal
experimentation has supported certain other biochemical mechanisms of
toxicity involving reaction products of ethanol and disulfiram.
FREQUENT SYMPTOMS AND SIGNS OF INJURY AND POISONING
BY DIALKYLDITHIOCARBAMATES
ITCHING, REDNESS, and ECZEMATOID DERMATITIS have resulted
when sensitive or predisposed individuals come in contact with these com-
pounds. Persons excessively exposed to air-borne fungicides have suffered
UPPER RESPIRATORY CONGESTION, HOARSENESS, COUGH, and
even PNEUMONITIS. When large amounts have been ingested, NAUSEA,
EMESIS, and DIARRHEA ensue. HYPOTHERMIA and ATAXIA are
characteristic. MUSCLE WEAKNESS, progressing to a condition of
ASCENDING PARALYSIS, and finally RESPIRATORY PARALYSIS,
can be anticipated from animal toxicologic studies based on extreme dosage.
The reaction to ethanol which follows absorption of disulfiram is char-
acterized by FLUSHING, SWEATING, POUNDING HEADACHE, SEN-
SATION OF WARMTH, WEAKNESS, CONGESTION OF UPPER RES-
PIRATORY and CONJUNCTIVAL MEMBRANES, DYSPNEA, HYPER-
PNEA, CHEST PAIN, TACHYCARDIA, PALPITATION, and HYPO-
TENSION.
Respiratory distress may resemble ASTHMA, and, in some instances,
RESPIRATORY DEPRESSION has been life-threatening. EMESIS com-
monly occurs. Severe reactions may result in SHOCK, UNCONSCIOUS-
NESS and/or CONVULSIONS, and, therefore, threaten coronary insuf-
ficiency in predisposed individuals. Only under exceptional occupational cir-
cumstances can a person absorb enough of these fungicidal compounds to
suffer a severe reaction to ethanol.
CONFIRMATION OF DIAGNOSIS
i
The native pesticides are so rapidly metabolized in the body that detec-
tion in blood or urine is rarely possible. There are biochemical methods for
measuring blood acetaldehyde to confirm an ethanol-dithiocarbamate re-
action.
34
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TREATMENT
1. WASH contaminating fungicide from the skin and hair with soap and
water. Atopic individuals and persons specifically sensitive to thiuram
disulfide compounds (individuals recognized as "rubber-sensitive")
should be permanently REMOVED FROM CONTACT with chemi-
cals of this nature.
2. FLUSH contaminant from the eyes with fresh water for 10-15 minutes.
3. Treatment for INGESTION OF DIMETHYLDITHIOCARBAMATE
COMPOUNDS, NOT COMPLICATED BY ALCOHOL INGESTION:
A. If fungicidal compounds of this type have been INGESTED, it is
first essential that the individual NOT TAKE ANY FORM OF
ALCOHOLIC BEVERAGE for at least 3 weeks. (Gastrointestinal
absorption of dialkyldithiocarbamates is protracted, and effects on
critical enzymes are slowly reversible.)
B. If vigorous emesis has not already occurred, and if victim is fully
alert and respiration is normal, give SYRUP OF IPECAC to in-
duce vomiting (adults, 12 years and older: 30 ml; children under 12:
15 ml).
CAUTION: OBSERVE the victim closely AFTER administering
IPECAC. If consciousness level declines, or if vomit-
ing has not occurred in 15 minutes, proceed to empty
the stomach by INTUBATION, ASPIRATION and
LAVAGE.
Following emesis, administer 30 gm ACTIVATED CHARCOAL
in 3-4 ounces of water to bind toxicant remaining in the gut.
C. If consciousness level or respiration is depressed, empty the stomach
by INTUBATION, ASPIRATION, and LAVAGE, using all avail-
able means to avoid aspiration of vomitus: left lateral Trendelenburg
position, frequent aspiration of the pharynx, and, in unconscious
victims, tracheal intubation (using a cuffed tube) prior to gastric
intubation.
, After aspiration of the stomach and washing with isotonic saline
or sodium bicarbonate, instill 30 gm of ACTIVATED CHARCOAL
in 3-4 ounces of water through the stomach tube to limit absorption
of remaining toxicant.
D. If the irritant properties of the toxicant fail to produce a bowel
movement in 4 hours, and if the patient is fully conscious, give
SODIUM SULFATE (Glauber's Salts) as a cathartic (adults, 12
years and older: 15 gm in 6-8 ounces of water; children under 12:
0.2 gm/kg of body weight in 1-6 ounces of water). '
4. Treatment for a reaction to ETHANOL INGESTION following absorp-
tion of a DIALKYLDITHIOCARBAMATE COMPOUND:
A. Administer 100% OXYGEN as long as the reaction continues.
Oxygen usually gives substantial relief from the distressing symp-
toms and hypotension.
35
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CAUTION: If respiration is depressed, administer oxygen by an
intermittent positive pressure breathing device and
observe the victim closely to maintain pulmonary ven-
tilation artifically in case of apnea.
B. If the fungicide was INGESTED no more than 4 hours prior to
treatment and vigorous emesis has not occurred, evacuate the
stomach by INTUBATION, ASPIRATION, and LAVAGE, ob-
serving precautions cited in 3C, above.
C. Regardless of time interval since ingestion of fungicide, ADMIN-
ISTER 30 gm ACTIVATED CHARCOAL in 3-4 ounces of water
to limit absorption of toxicant remaining in the gut. Absorption of
the dithiocarbamate compounds is slow.
D. For adults and children over 12 years, inject 1.0 gm ASCORBIC
ACID (Vitamin C) intravenously at a rate not exceeding 0.2 gm/
minute. For children under 12, give 10-20 mgm per kg body weight.
As a hydrogen-donor, ascorbic acid may have significant antidotal
action against absorbed, but unreacted, dithiocarbamate compound.
E. For severe or protracted reactions, INFUSE 5% GLUCOSE in
D/W, or alternative glucose-containing fluids, to accelerate dis-
position of absorbed toxicants and metabolites.
F. Use sodium sulfate catharsis (3D above) only if no bowel movement
occurs within 4 hours of the beginning of the reaction.
G. If the victim has suffered from arteriosclerosis, myocardial insuffi-
ciency, diabetes, neuropathy, cirrhosis, or other severe chronic dis-
ease, OBSERVE him CAREFULLY for 48 hours to insure that
complications (especially myocardial infarction, toxic psychosis,
and neuropathy) are treated promptly.
36
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ANTICOAGULANT RODENTICIDES
STRUCTURES OF PRINCIPAL CLASSES
ALKYL. PHENYL.
DIPHENYLACETYL or
CHLORODIPHENYLACETYL
WARFARIN (COUMARIN-TYPE)
1.3-INDANDIONE TYPE
COMMON COMMERCIAL PESTICIDE PRODUCTS
Coumarin type: warfarin (Kypfarin, Warf-42, D-Con, Warficide, Prolin),
coumafuryl (Fumarin), Dethmor, Rax.
1,3-indandione type: diphacinone, or diphenadione (Ramik), chlorophaci-
none (Drat, Caid, Liphadione, Microzul, Ramucide, Rotomet, Raviac, Topi-
tox), pindone (Pivalyn, Pivacin, Tri-ban, Pival), valone, (PMP).
These materials are commonly added to baits or dissolved in small amounts
of water for pest rodents to drink. One hundred grams of the prepared com-
mercial baits must be ingested to yield 25 mgm of anticoagulant. Rodenti-
cide "drinks" are made by adding dry concentrate (0.54 gm of active in-
gredient per 100 gm of powder) to specified volumes of water. The poison in
the concentrate is coated on sugar or sand to facilitate measurement and
handling.
TOXICOLOGY
Gastrointestinal absorption of these toxicants is efficient, beginning with-
in minutes of ingestion and continuing for 2-3 days. Apparently, warfarin can
also be absorbed across the skin, although the circumstances under which
this has occurred are extraordinary.
Both types of anticoagulant depress the hepatic synthesis of substances
essential to normal blood clotting: prothrombin (factor II), and factors VII,
DC, and X. The anti-prothrombin effect is best known and provides the basis
for detection and assessment of clinical poisoning. Direct damage to capil-
lary permeability occurs concurrently. In rare instances, coumarin-type anti-
coagulants have caused ecchymosis and extensive skin necrosis in humans
for reasons not related to excessive dosage.
Unlike the coumarin anticoagulants, the indandiones cause symptoms and
signs of neurologic and cardiopulmonary injury in laboratory rats; these
often lead to death before hemorrhage occurs. These actions may account for
the somewhat greater toxicity of this class of anticoagulants. Cardiopulmo-
nary and neurologic symptoms and signs have not been reported in human
poisonings.
Lengthened prothrombin time from a toxic dose usually appears within 24
37
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hours of toxicant ingestion and reaches a maximum in 36 to 72 hours. With-
out intervention, hypoprothrombinemia may persist 10-15 days, depending
on the agent and dosage. Prothrombin depression will occur in response to
doses that are much lower than those necessary to cause hemorrhage.
FREQUENT SYMPTOMS AND SIGNS OF POISONING
In most instances of accidental ingestion of anticoagulant baits, victims
have remained asymptomatic, due to the small dosage taken. Even in cases
involving ingestion of substantial doses, hypoprothrombinemia occurs with-
out symptoms of poisoning. Hemorrhage appears only when extraordinary
amounts have been absorbed. In these cases, the anticoagulants were either
taken deliberately, were absorbed over long periods out of neglect of ele-
mentary hygienic standards, or were ingested by starving indigents who
used quantities of rodent bait for food.
Victims of large doses exhibit HEMATURIA, NOSEBLEED, HEMATO-
MATA, BLEEDING GUMS, and MELENA. ABDOMINAL PAIN and
BACK PAIN probably reflect hemorrhage in the abdominal and retroperi-
toneal tissues. WEAKNESS occurs as a result of ANEMIA. RENAL COLIC
often complicates severe hematuria. Nasal and gastrointestinal hemorrhages
have caused death from exsanguination.
CONFIRMATION OF DIAGNOSIS
Increase of the prothrombin time (Quick) reflects a reduction in serum
prothrombin concentration, and occurs in response to physiologically sig-
nificant absorption of these toxicants. This widely available clinical test offers
a sensitive and reliable diagnostic method for detecting a toxic effect of these
compounds. Readily detectable change in prothrombin time appears within
24-48 hours of ingesting the anticoagulant.
A few laboratories can measure warfarin and its metabolites in human
urine, but it is rarely practical to use these determinations for diagnostic
purposes.
TREATMENT
1. If it is known or suspected that anticoagulant rodenticide has been
ingested recently, but that the total amount ingested was LESS THAN
0.25 MGM/KG body weight, administer a single dose of the specific
antidote, PHYTONADIONE, INTRAMUSCULARLY: adults 12 years
and older: 25 mgm IM; children under 12: 0.4 mgm/kg body weight
IM.
Note: PHYTONADIONE (Vitamin Kv Mephyton, Aquamephyton,
Konakion) specifically is required. Vitamin K3 (menadione,
Hykinone) and vitamin K4 (menadiol) have little or no anti-
dotal effect.
This treatment is adequate when the total amount of toxicant ingested
is known not to have exceeded the limits stated above, and in which no
38
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pre-existing liver injury or blood clotting disease is present.
2. If the victim ingested anticoagulant rodenticide WITHIN the PRECED-
ING 2-3 HOURS in a quantity that may have exceeded 0.25 mgm/kg,
INDUCE VOMITING with SYRUP of IPECAC (adults 12 years and
older: 30 ml; children under 12: 15 ml). After emesis, give 30 gm
ACTIVATED CHARCOAL in 4-6 ounces of water to limit absorp-
tion of rodenticide still in the gut.
3. If the victim may have ingested anticoagulant rodenticide any time
within the preceding 15 days IN AMOUNTS EXCEEDING 0.25 mgm/
kg, or if the victim may have a pre-existing liver or bleeding disease,
determine the PROTHROMBIN TIME. Then administer PHYTO-
NADIONE INTRAMUSCULARLY (adults, 12 years and older: 25
mgm; children under 12: 0.4 mgm/kg). Subsequent treatment will de-
pend on the degree of prothrombin time lengthening, and on the esti-
mated dosage and time of toxicant ingestion. High dosage or lengthen-
ing of the prothrombin time by more than 10 seconds over the control
may dictate administration of a second dose of phytonadione (as above)
and another measurement of prothrombin time 24 hours after the
first. Reversal of prothrombin time usually occurs in 12-24 hours, but
may require as long as three days.
CAUTION: Doses of phytonadione in excess of 25 mgm are some-
times hepatotoxic, and should be given only when lower
doses have not been effective. Doses hi excess of 50 mgm
involve significant hazard and are of doubtful benefit.
4. If the victim shows SYMPTOMS or SIGNS of POISONING (bleeding,
anemia, hematomata) in addition to hypoprothrombinemia, it may be
necessary to give PHYTONADIONE INTRAVENOUSLY. Aquame-
phyton may be administered by this route in doses of 25 mgm for adults,
12 years and older; or 0.4 mgm/kg for children under 12, repeating
this amount once in 24 hours if bleeding continues. Inject at rates not
exceeding 1 mgm/minute for adults, but proportionately slower in
children. To achieve slow intravenous injection, dilute the phytonadione
in either 0.9% saline or 5% glucose solution. Bleeding is usually con-
trolled within 3-6 hours of intravenous infusion.
CAUTION: Adverse reactions, some fatal, have occurred from
intravenous phytonadione injections, even when rec-
ommended dosage limits and injection rates were
observed. For this reason, the INTRAVENOUS
route should be used ONLY IN cases of SEVERE
POISONING. Flushing, dizziness, hypotension, dy-
spnea and cyanosis have characterized adverse re-
actions.
5. A. Antidotal therapy in cases of severe poisoning should be supple-
mented with TRANSFUSIONS of FRESH BLOOD or FRESH
FROZEN PLASMA. Use of fresh blood or plasma represents the
most rapidly effective method for stopping hemorrhage due to these
39
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anticoagulants.
B. Determine PROTHROMBIN TIMES (and hemoglobin concentra-
tions, if appropriate) every 6-12 hours to assess effectiveness of
antidotal and antihemorrhagic measures.
C. When normal blood coagulability is restored, it may be advisable to
drain large hematomata.
D. Ferrous sulfate therapy may be appropriate in the recuperative
period to rebuild lost erythrocyte mass.
6. Give ASCORBIC ACID (vitamin C) orally or intramuscularly in mild
and severe poisoning to limit capillary injury caused by the anticoagu-
lants (adults, 12 years and older: 100 mgm; children under 12: 50-100
mgm).
40
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ARSENICAL PESTICIDES
CHEMICAL STRUCTURES
EXTREMELY TOXIC: (TRIVALENT INORGANIC ARSENICALS)
O=A$ O As s=O
ARSENIC TRIOXIDE
O
II
Cu (O C
KOAs=O
POTASSIUMARSENITE
Cu3_
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COMMON COMMERCIAL PESTICIDE PRODUCTS
Inorganic arsenicals: arsenic trioxide (white arsenic), sodium arsenite
(Acme Weed Killer, Atlas A, Penite, As-655 Weed Killer, Kill All), copper
arsenite (Paris Green), copper ammonium arsenite (Chemonite), arsenic
acid (Zotox Crabgrass Killer, Dessicant L-10, Lincks Liquid Di-met, Pax
Total, Purina Top Grass and Weed Killer).
Organic arsenicals: MSMA (Ansar 170, Bueno, Weed-E-Rad, Ansar 529,
Broadside, Crabgrass Dallis Grass Killer, Daconate, Fertilome Nutgrass and
Weed Killer, Mad, Nutgrass Spray, Selector #1, Spot Grassy Weed Killer);
DSMA (Ansar 8100, Biochecks, Burpee Crabgrass Killer, Chipco Crab
Kleen, Clout, D Krab R + Prills, DMA, E Krab R, Greenfield Crabgrass
and Dandelion Killer, Sears Liquid Crabgrass Killer, Lawn Weed Killer, Pro-
turf Monocot Weed Control); cacodylic acid (Silvisar 510); sodium cacody-
late (sodium dimethyl arsinate, Phytar 560, Acme Weed Killer); ammonium
methane arsenate (AMA, Ansar 157, Super Crab E-Rad, C-4000, Antrol
Crabgrass Killer, Crabgrass Broadleaf Killer, Systemic Crabgrass and Broad-
leaf Killer); methane arsonic acid (MAA, Ortho Crabgrass Killer).
TOXICOLOGY
Although the pentavalent arsenicals are generally less toxic than the in-
organic trivalent chemicals, all poisonings by arsenic-containing substances
should be regarded as serious threats to life and health. To some degree, the
pentavalent compounds undergo reduction in the gut and/or body tissues to
trivalent forms. Some absorption of solid arsenical compounds may occur
by dermal or pulmonary routes, but the great majority of poisonings result
from ingestion. Intestinal absorption is generally efficient. Most absorbed
arsenic is excreted by way of the kidneys; a lesser proportion is excreted by
the liver and gut. Arsine gas in absorbed rapidly by the lung; an arsenic
metabolite is excreted in the urine.
Toxicology of arsine gas (absorbed by inhalation) is unique in that it
causes hemolysis and secondary acute renal tubular necrosis. Arsine is not
used as a pesticide, but is involved in the manufacture of organic arsenicals.
Trivalent arsenicals bind critical sulfhydryl-containing enzymes in tissues.
When taken up from the gut, they injure the splanchnic vasculature, causing
colic and diarrhea. Once absorbed, they produce toxic injury to the liver,
kidney, bone marrow, brain and peripheral nerves. Liver injury is manifest
as hepatomegaly, jaundice, and an increase in circulating hepatocellular
enzymes LDH and GOT. Renal damage is reflected in albuminuria, hema-
turia, pyuria, cylindruria, then azotemia. Acute tubular necrosis may occur
in severe poisoning. Injury to blood-fonnhig tissues can take the form of
agranulocytosis, aplastic anemia, thrombocytopenia, or pancytopenia. Toxic
encephalopathy may become manifest as speech and behavioral distur-
bances. Peripheral neuropathy occurs in both acute and chronic forms. In-
halation of arsenic dusts may cause bronchitis or pneumonitis.
Sequelae of arsenic poisoning include cirrhosis, hypoplastic bone marrow,
renal insufficiency, and peripheral neuropathy. Excessive exposures to arseni-
cals have caused cancers of skin and various epithelial tissues.
42
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FREQUENT SYMPTOMS AND SIGNS OF POISONING
ACUTE arsenic poisoning (solid compounds):
COLIC, BURNING ABDOMINAL PAIN, VOMITING, and WATERY
or BLOODY DIARRHEA are the primary manifestations of ingestion of
solid arsenical poisons. Symptoms following ingestion of inorganic arsenicals
are more severe than those resulting from ingestion of pentavalent organic
arsenicals. Symptoms sometimes do not appear for minutes or even hours
after ingestion. HEADACHE, DIZZINESS, MUSCLE SPASMS, DELIR-
IUM, and sometimes CONVULSIONS reflect direct injury to the central
nervous system, as well as extracellular electrolyte disturbances and shock.
A GARLIC ODOR to the breath and feces helps to identify the responsible
toxicant. SHOCK, TOXIC NE^HROSIS, HEPATITIS (hepatomegaly and
jaundice), and NEUROLOGIC INJURY (delirium, paralysis, respiratory de-
pression) may progress to a fatal outcome.
SUB ACUTE arsenic poisoning (solid compounds):
Dosages less than those necessary to produce severe acute symptoms are
known to cause CHRONIC HEADACHE, ABDOMINAL DISTRESS,
SALIVATION, LOW-GRADE FEVER, AND PERSISTENT symptoms of
UPPER RESPIRATORY IRRITATION. Stomatitis and garlicky breath are
characteristic.
CHRONIC arsenic poisoning (solid compounds):
Prolonged low intakes of arsenic cause PERIPHERAL NEUROPATHY
(paresthesiae, pain, anesthesia, paresis, ataxia); ENCEPHALOPATHY
(apathy); varied DERMATOLOGIC DISORDERS (keratoses, pigmentation,
eczemas, brittle nails, loss of hair); and TOXIC HEPATITIS (hepatomegaly,
sometimes progressing to cirrhosis with ascites). WEAKNESS and vulner-
ability to infections may result from bone marrow depression. Local EDEMA,
frequently of the eyelids, characterizes some chronic poisoning cases.
ACUTE arsine poisoning (gas):
The gas causes HEMOLYSIS of red blood cells in addition to inhibition
of cellular sulfhydryl respiratory enzymes. Hemolysis causes HEMOGLO-
BINEMIA AND HEMOGLOBINURIA. This in turn, causes ACUTE
TUBULAR NECROSIS. Early symptoms of poisoning (chills, weakness, burn-
ing sensations) are followed by abdominal cramps, vomiting, and prostration,
as renal function deteriorates to ANURIA.
CONFIRMATION OF DIAGNOSIS
Measurement of 24-hour urinary excretion of arsenic is probably the best
way to confirm excessive arsenic absorption, although methods for blood
arsenic concentration are available. Persons on ordinary diets usually ex-
crete less than 20 /Agm/day, but diets rich in seafood may generate as much
as 200 /igm/day. Excretions above 100 /xgm/day should be viewed with sus-
picion and tests should be repeated. Excretions above 200 /Agm/day reflect
43
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a potentially toxic intake.
The qualitative Gutzeit test for arsenic in the urine is available in most
hospital laboratories, and is useful in identifying acute poisonings promptly.
Chronic storage of arsenic can be detected by analysis of hair or finger-
nails.
The hemoglobinuria caused by arsine is identified by finding the pigment
in fresh urine from which intact red cells are absent.
TREATMENT FOR POISONING BY SOLID ARSENICALS
1. Flush contaminated EYES, HAIR and SKIN with copious amounts of
fresh water.
2. In cases of poisoning by RECENTLY INGESTED (up to 6 hours)
ARSENICALS:
A. INTUBATE the stomach, ASPIRATE, and LAVAGE with 3 liters
of isotonic saline or 5% sodium bicarbonate. Use all available pre-
cautions to avoid aspiration of vomitus:
(1) If the victim is unconscious or obtunded, it is helpful to insert
an ENDOTRACHEAL TUBE (cuffed, if available) prior to
intubation.
(2) Keep the victim's HEAD BELOW THE LEVEL OF THE
STOMACH during intubation (Trendelenburg, or left lateral
decubitus, with head of table tipped downward). Keep the vic-
tim's head turned toward the left.
(3) ASPIRATE the pharynx as regularly as possible to remove
gagged or vomited stomach contents.
B. After lavage, INSTILL 60 gm ACTIVATED CHARCOAL in
water: 6-8 ounces, or the smallest amount necessary to deliver the
charcoal.
C. If diarrhea or colic have not ensued within an hour of gastric lavage
and charcoal administration, give SODIUM SULFATE as a cathar-
tic (adults, 12 years and older: 15 gm in 6-8 ounces of water;
children under 12: 0.2 gm/kg body weight in 1-6 ounces of water.
D. Administer INTRAVENOUS ELECTROLYTE and GLUCOSE
solutions to maintain hydration and to accelerate toxicant excretion.
COMBAT SHOCK with TRANSFUSIONS of WHOLE BLOOD,
and by inhalation of 100% OXYGEN.
CAUTION: Monitor urine flow via catheter. Monitor fluid balance,
body weight, and/or central venous pressure to guard
against fluid overload resulting from acute tubular
necrosis (anuria).
E. PROMPTLY administer DIMERCAPROL (BAL, British antile-
wisite, dimercaptopropanol) INTRAMUSCULARLY, as the 10%
solution in vegetable oil, to neutralize the toxic action of arsenicals.
Recommended dosage schedule is:
44
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Mild Poisoning Severe Poisoning
Days 1&2 2.5 mgm/kg q6h X 8 doses 3.0 mgm/kg q4h X 12 doses
Day 3 2.5 mgm/kg q!2h X 2 doses 3.0 mgm/kg q6h X 4 doses
Succeeding
10 days 2.5 mgm/kg q24h X 10 doses 3.0 mgm/kg q!2h X 20 doses
CAUTION: DIMERCAPROL can cause troublesome side effects
(hypertension, tachycardia, nausea, headache, pares-
thesiae and pain, lachrimation, sweating, anxiety, and
restlessness). Although usually not so severe as to
handicap treatment, these manifestations may require
antihistaminic therapy for adequate control.
F. Intense abdominal pain may require morphine (adults, 12 years and
older: 4-15 mgm; children under 12: 0.1-0.2 mgm/kg.)
G. Severe poisoning (especially when renal function is impaired) may
require hemodialysis to remove arsenic combined with dimercaprol
from the blood.
3. If arsenical was ingested more than 48 hours prior to treatment, or if
excessive absorption has occurred over an extended period, treatment
should probably be limited to administration of dimercaprol as pre-
scribed in 2E plus nutritional supplements to restore metabolic func-
tions as promptly as possible.
TREATMENT FOR POISONING BY ARSINE GAS
1. REMOVE the victim to FRESH AIR.
2. MAINTAIN RESPIRATION and CIRCULATION by resuscitation
and cardiac massage, if necessary.
3. Administer INTRAVENOUS FLUIDS as promptly as possible to dilute
hemoglobin in the glomerular filtrate and minimize tubular injury. Use
enough sodium bicarbonate to keep the urine alkaline.
CAUTION: Monitor urine flow via catheter. Monitor fluid balance,
body weight, and/or central venous pressure to guard
against fluid overload resulting from acute tubular necrosis.
4. Administer DIMERCAPROL as recommended in 2E even though it
has only limited effect in arsine poisoning.
5. EXCHANGE BLOOD TRANSFUSIONS and PERITONEAL DIAL-
YSIS have saved the lives of victims of arsine poisoning suffering acute
tubular necrosis.
45
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PESTICIDES INDEX
Page
A
Aatrex 27
Acaraben 1
Acetamide based herbicides 30
Acetanilide based herbicides 30
Acme Weed Killer 42
Afalon 27
alachlor 30
aldicarb 9
aldrin 1
Aldrite 1
allidochlor 30
AMA 42
Ambox 21
Ametrex 27
ametryn 27
ammonium methane arsenate 42
Anilide based herbicides 30
Ansar 157 42
Ansar 170 42
Ansar 529 42
Ansar 8100 42
Anticoagulant Rodenticides 37
Antrol Crabgrass Killer 42
Aquacide 13
Aquakill 13
Aquatate 13
Aquatic Weed Killer 13
Arasan 33
Arsanilic Acid 42
Arsenical Pesticides 42
arsenic acid 42
arsenic trioxide 42
Arsine gas 42
As-655 Weed Killer 42
Atlas A 42
Atranex 27
atraton 27
Atratone 27
atrazine 27
azinphos-methyl 4
Azodrin 4
46
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Baygon 9
Baytex 4
benzene hexachloride 1
BHC 1
Bidrin 4
binapacryl 21
Biochecks 42
Black Leaf Grass Weed and Vegetation
Killer Spray 24
Bladafume 4
Bladex 27
Bo-Ana 4
Borea 27
Borocil IV 27
Broadleaf Weed Killer 18
Broadside 42
bromacil 27
Bueno 42
Burpee Crabgrass Killer 42
Butoxone 18
Butyrac 18
Bux 9
cacodylic acid 42
Caid 37
Caparol 27
Carbanilate based herbicides 30
Carbamates 9
carbaryl 9
carbofuran 9
carbophenothion 4
CDAA 30
Certified Kiltrol-74 Weed Killer 24
C-4000 42
Chemonite 42
Chemox PE 21
Chickweed and Clover Killer 18
Chipco Crab Kleen 42
Chlordan 1
chlordane 1
chlorobenzilate 1
Chloro IPC 30
chlorophacinone 37
Chlorophenothane 1
47
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Chlorophenoxy compounds 18
chlorpropham 30
chlorpyrifos 4
Ciba-Geigy Ontrack OS 3, 4 or 5 24
Ciodrin 4
CIPC 30
Clout 42
Copper acetoarsenite 42
copper arsenite 42
Co-Ral 4
coumafuryl 37
Coumarin 37
coumophos 4
Counter 4
Crabgrass Broadleaf Killer 42
Crabgrass Dallis Grass Killer 42
crotoxyphos 4
cmfomate 4
cyanazine 27
Cygon 4
cyprazine 27
Cythion 4
Dacamine 18
Daconate 42
Dalf 4
Dandelion Killer 18
Dasanit 4
D-Con 37
DDT 1
DDVP 4
Ded-Weed 18
Delnav 4
demeton 4
demeton-methyl 4
desmetryne 27
Dessicant L-10 42
Dethmor 37
Dextrone X 13
diazinon 4
Dibrom 4
dichlorvos 4
dicofol 1
dicrotophos 4
dieldrin 1
48
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Dieldrite 1
Di-Kill Vegetation Killer 13
Dimecron 4
dimethoate 4
Dimethyldithiocarbamate compounds 33
dinitroorthocresol 21
Dinitrophenol 21
dinobuton 21
dinopenton 21
dinoprop 21
dinosam 21
Dinoseb 21
dinosulfon 21
dinoterb 21
dinoterbon 21
Di-on 27
dioxathion 4
diphacinone 37
diphenadione 37
Dipterex 4
Diquat 13
Di Sodium Methyl Arsonate 42
disulfoton 4
Disyston 4
Dithione 4
Diurex 27
diuron 27
D Krab R + Prills 42
DMA 42
DNAP 21
DNBP 21
DNC 21
DNOC 21
DNOCHP 21
DN-111 21
DN 289 21
Dowicide-7 24
DPA 30
Drat 37
Drinox 1
DSMA 42
Dual Paraquat 13
Dursban 4
Dyfonate" 4
Dylox 4
49
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E Krab R 42
EM-7217 13
Endosan 21
endosulfan 1
endrin 1
Entex 4
EPN 4
erbon 18
Esteron 18
Estone 18
F
Famfos , 4
famphur 4
Fenac 18
fensulfothion 4
fenthion 4
Ferbam 33
Fernasan 33
Fertilome Nutgrass and Weed Killer 42
fonofos 4
forte 33
Fumarin 37
Furadan 9
Furloe 30
G
Gammexane 1
Gesafram 27
Gesagard 27
Gesamil 27
Gesapax 27
Gesaprin 27
Gesatop 27
Gordon Termi Tox 24
Gramonol 13
Gramoxone S 13
Greenfield Crabgrass and Dandelion Killer ... 42
Guthion 4
H
Heavy Duty Weed Control 13
HCH 1
50
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heptachlor 1
Hexadrin 1
HOE 2810 27
Hyvar X 27
Hyvar X-L 27
I
Igran 27
Isocil 27
Isotox 1
K
Karmex 27
Kelthane 1
Kepone 1
Kill All 42
Korlan 4
Kuron 18
Kypfarin 37
Landrin 9
Lannate 9
Lasso 30
Lawn Weed Killer 42
Lincks Liquid Di-met 42
lindane 1
linuron 27
Liphadione 37
Lorox 27
M
MAA 42
Mad 42
malathion 4
Marlate 1
MCPA 18
MCPB 18
MCPP 18
Mecoprop 18
Mesurol 9
metalkamate 9
Metallodimethyldithiocarbamates 33
Metasystox it
51
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methamidophos 4
methane arsonic acid 42
methiocarb 9
methomyl 9
methoxychlor 1
methyl parathion 4
mevinphos 4
Microzul 37
Mildex 21
Milogard 27
mirex 1
Mocap 4
Monitor 4
monocrotophos 4
Mono Sodium Methyl Arsonate 42
Monurex 27
monuron 27
Morfamquat 13
Morfoxone 13
Morocide 21
MSMA 42
N
naled 4
Neguvon 4
Nitrophenolic Herbicides 21
Nomersan 33
Nudrin 9
Nutgrass Spray 42
Organochlorine Pesticides ................ 1
Organophosphate Pesticides .............. 4
Ortho Crabgrass KiUer .................. 42
Ortho Spot Weed and Grass Killer ......... 13
Ortho Triox Liquid Vegetation Killer ....... 24
Outfox ............................... 27
oxamyl ............................... 9
Paraquat Cl ........................... 13
Parathion ............................. 4
Paris Green ........................... 41
Pax Total ............................ 42
PCP ......................... . ....... 24
52
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Penchlorol 24
Penite 42
Pentachlorophenol 24
Pentacon 24
Penwar 24
phorate 4
Phosdrin 4
phosphamidon 4
Phytar 560 42
pindone 37
Pivacin , 37
Pival 37
Pivalyn 37
PMP 37
Pomasol 33
Pomasol Z forte 33
Potassium Arsenite 41
PP-745 13
Pramitol 27
Preeglone extra 13
Primatol A 27
Primatol P 27
Primatol Q 27
Primatol S 27
Princep 27
Prolin 37
prometon 27
prometone 27
Prometrex 27
prometryn 27
Propachlor 30
Propanex 30
propanil 30
propazine 27
propoxur 9
Proturf Monocot Weed Control 42
Purina Insect Oil Concentrate 24
Purina Top Grass and Weed Killer 42
R
Ramik 37
Ramrod 30
Ramucide 37
Randox 30
Raviac 37
Rax 37
53
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Reglone 13
ronnel 4
Rotomet 37
Ruelene 4
Sarclex 27
Scogal 27
Sears Liquid Crabgrass Killer 42
Selector #1 42
Semeron 27
Sevin 9
Shortstop E 27
Silvex 18
Silvisar 510 42
Simanex 27
simazine 27
Sinbar 27
Sinox 21
sodium arsenite 42
sodium cacodylate 42
sodium dimethyl arsinate 42
Sodium pentachlorophenate 24
Spectracide 4
Spot Grassy Weed Killer 42
Stam 30
Strobane 1
Storbane-T 1
sulfotepp 4
Super Crab E-Rad 42
Systemic Crabgrass and Broadleaf Killer .... 42
Systox 4
X
Telvar 27
Temik 9
TEPP 4
terbacil 27
terbutryn 27
terpenepolychlorinates 1
Tersan 33
Tetramethyl thiuram disulfide 33
Thimet 4
Thiodan 1
Thiophos 4
54
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Thiotex 33
Thiram 33
Thiramad 30
Thirasan 30
Thylate 30
Tirampa 30
TMTDS 30
Topitox , 37
Toxakil 1
toxaphene 1
Triazine based herbicides 27
Tri-ban 37
trichlorfon 4
Trithion 4
TUADS 33
2,4-D 18
2-4-DB 18
2,4-DEP 18
2,4,5-T 18
2,4,5-TP 18
U
Uracil based herbicides 27
Urea based herbicides 27
Urox HX or B 27
Usol Cabin Oil 24
y
valone 37
vapam 33
Vapona 4
Vegetation Killer 18
Vegetrole 13
Veg-I-Kill 24
Vonduron 27
Vydate 9
W
warfarin 37
Warf-42 37
Warficide 37
Watrol 13
Weed-B-Gon 18
Weed-E-Rad 42
Weedestron 18
55
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Weed-No-More 18
Weedol 13
Weedone 18,24
Weed or Brush-Rhap 18
Weed-Out 18
white arsenic 42
Wood Preserver 24
Wood Tox 140 24
Zectran 9
Ziram 33
Zotox Crabgrass Killer 42
56
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