=DA 5/10/077010 Do not remove. This document
-r M'O^rU/ y-//"UiO . • • • . • .. -• T-.TI A
should be retained in the EPA
Region 5 Library Collection.
RECOGNITION AND MANAGEMENT
OF PESTICIDE POISONINGS
Second Edition
U. S. ENVIRONMENTAL PROTECTION AGENCY
OFFICE OF PESTICIDE PROGRAMS
WASHINGTON, D.C. 20460
AUGUST 1977
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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.
U.S. Envlrorai'sr^ v." " ' ' '
Region 5, !•-'.'. .-"
250 S. U'--' " - -
Chicago, IL
Second Edition
For sale by the Superintendent of Documents, U.S. Government
Printing Office, Washington, D.C. 20402
Stock number 055-004-00013-7
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CONTENTS
Page
INTRODUCTION i
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
ORGANONITROGEN HERBICIDES 27
DIMETHYLDITHIOCARBAMATE COMPOUNDS 31
ANTICOAGULANT RODENTICIDES 35
ARSENICAL PESTICIDES 39
VACOR 8 and DLP-787 44
HALOCARBON and SULFURYL FUMIGANTS 47
MISCELLANEOUS FUMIGANTS 53
PESTICIDES INDEX 64
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INTRODUCTION
Sound judgment is as important as ever in the management of poisonings.
But emergency personnel cannot be expected to know instantly the properties
of dozens of modern pesticides and the mechanisms by which they produce
toxic effects. It is equally unrealistic to suppose that professionals who only
occasionally encounter pesticide poisonings can bring together quickly the
accumulated clinical and laboratory experience needed for the best possible
treatment of each case. These considerations inspired preparation of an
excellent manual, Clinical Memoranda of Economic Poisons, in 1956 by
Wayland J. Hayes, Jr., M.D., Ph.D., U.S. Public Health Service. Dr. Hayes
revised the manual in 1963 under the title Clinical Handbook on Economic
Poisons—Emergency Information for Treating Poisoning. The present pub-
lication further updates both these useful handbooks.
Pesticides with similar chemical structures and toxic properties are grouped
into major classes, such as chlorinated hydrocarbons, chlorophenoxy com-
pounds, and arsenicals. Under these major classes are listed chemical struc-
tures, examples of commonly used pesticides, pertinent toxicology and fre-
quent symptoms of poisoning, methods to confirm diagnoses of poisoning,
and the latest information on clinical management of poisonings caused by
the respective classes of chemicals.
A deliberate effort has been made to suggest treatment measures that can
be implemented (or at least initiated) in small hospitals and clinics, where
victims of pesticide poisonings are likely to be received. At the expense of
some repetition, treatment procedures are spelled out sequentially for the
several classes of chemical poisonings included.
The author assumes full responsibility for judgments when alternative
interpretations and recommendations have appeared in the published litera-
ture. Generous assistance has been extended by colleagues and other pro-
fessionals interested in the treatment of poisonings: Dr. Albert L. Picchioni,
Professor of Pharmacology, College of Pharmacy; and Dr. Elmer S. Light-
ner, Professor of Pediatrics, College of Medicine, University of Arizona;
Dr. Robert J. Roberts, Professor of Pediatrics; Dr. John J. Ambre, Asso-
ciate Professor of Internal Medicine; Dr. Raymond F. Sheets, Professor
of Medicine; and Dr. Henry E. Hamilton, Professor of Medicine, University
of Iowa College of Medicine. Dr. Maynard B. Chenoweth, Biomedical
Research, Dow Chemical, U.S.A.; Dr. Jon E. Ford, Chevron Environmental
Health Center; and Dr. Robert H. Lang, Corporate Medical Director of Rohm
and Haas Co. Members of the staff of the Human Effects Monitoring Branch
and Technical Services Division, Office of Pesticide Programs, U.S. Environ-
mental Protection Agency, have patiently edited the manuscript, prepared
the index and attended to the details of publication.
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SOLID ORGANOCHLORINE PESTICIDES
CHEMICAL STRUCTURES
ci
CHLORDANE
CI
S=0
CI
CH30
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
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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 in 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, occasional hypotension, and respiratory
depression.
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 mgtn/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 SYRUIP 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, 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
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.
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ORGANOPHOSPHATE
CHOLINESTERASE-INHIBITING
PESTICIDES
GENERAL CHEMICAL STRUCTURE
C2H5O or CH3O^ ^S (or O)
C2H5O or CH30
COMMON COMMERCIAL PESTICIDE PRODUCTS (approximately in
order of decreasing toxicity)
Highly toxic: TEPP, phorate (Thimet), mevinphos (Phosdrin), fensul-
fothion (Dasanit), demetonf (Systox), disulfotonf (Disyston), sulfotepp
(Bladafume, Dithione), Counter, ethyl parathion (Parathion, Thiophos),
fonofos (Dyfonate), EPN, azinphosmethyl (Guthion), methyl parathion (Dalf),
monocrotophos (Azodrin), dicrotophos (Bidrin), methamidophos (Monitor),
carbophenothion (Trithion), phosphamidon (Dimecron).
Moderately toxic: famphur (Warbex, Bo-Ana, Famfos), ethoprop (mocap),
coumaphos (Co-Ral), demeton-methylt (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).
t Certain of the organophosphates 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
acetylcholine 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 (-oxons) before they are metabolized. All undergo hydrolytic
degradation in liver and other tissues, usually within hours of absorption.
Degradation 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-
firmation of diagnosis by blood analysis.
TABLE 1. Approximate Lower Limits of Normal Plasma and
Red Cell Cholinesterase Activities in Humans *
METHOD PLASMA RBC
ApH (Michel) 0.4 0.5
pH STAT (Nabb-Whitfield) 2.3 8.0
ChE-tel (Pfizer) 40
A ChE-tel (Pfizer) 210
1-Test Cholinesterase
(EM Diagnostics) 3.6
ACHOLEST Test Paper >20
Dupont ACA <8
Garry-Routh Male 7.8
(Micro) Female 5.8
Merckotest 3.0
* Because measurement technique varies among
estimates of minimum normal values are usu
laboratories.
UNITS
ApH per ml per hour
/jM per ml per minute
ChE-tel units
A ChE-tel units
Units per ml
Minutes
Units per ml
/iM-SH per ml per 3 min
Units per ml
laboratories, more accurate
ally provided by individual
-------
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 IV injection is not possible. Atropine protects the end-organs from
excessive concentrations of acetylcholine. It does not reactivate cho-
linesterase, and 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: 0.05 mgm/kg body weight (0.125
ml/kg of usual 0.4 mgm/ml solution) repeated every 15-30 minutes
until atropinization is achieved. Maintain atropinization with repeated
dosage of 0.02-0.05 mgm/kg.
Severely poisoned individuals may exhibit remarkable tolerance to
atropine: twice the doses suggested above may sometimes be needed.
Signs of over-atropinization are: muscle twitching, FEVER anddelirium.
3. Administer PRALIDOXIME (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
6
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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 5-10 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 water.
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. Give adrenergic amines ONLY if there is a specific indication.
-------
9. 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.
10. 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.
11. DO NOT administer atropine or pralidoxime prophylactically to work-
ers exposed to organophosphate pesticides. It is neither practical nor
medically sound to do so.
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CARBAMATE
CHOLINESTERASE-INHIBITING
PESTICIDES
GENERAL CHEMICAL STRUCTURE
O
.N C O—
H3C^
COMMON COMMERCIAL PESTICIDE PRODUCTS (approximately in
order of decreasing toxicity)
Highly toxic: aldicarbf (Temik), oxamyl (Vydate), carbofuran (Furadan),
methomyl (Lannate, Nudrin), Zectran, methiocarb (Mesurol).
Moderately toxic: propoxur (Baygon), Landrin, carbaryl (Sevin), metal-
kamate (Bux).
f 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 PLASMA RBC
ApH (Michel) 0.4 0.5
pH STAT (Nabb-Whitfield) 2.3 8.0
ChE-tel (Pfizer) 40
A ChE-tel (Pfizer) 210
1-Test Cholinesterase
(EM Diagnostics) 3.6
ACHOLEST Test Paper >20
Dupont ACA <8
Garry-Routh Male 7.8
(Micro) Female 5.8
Merckotest 3.0
UNITS
ApH per ml per hour
iuM per ml per minute
ChE-tel units
A ChE-tel units
Units per ml
Minutes
Units per ml
/xM-SH 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: 0.05 mgm/kg body weight (0.125 ml/kg of usual 0.4
mgm/ml solution) repeated every 15-30 minutes until atropinization is
achieved. Maintain atropinization with repeated dosage of 0.02-0.05
mgm/kg.
Severely poisoned individuals may exhibit remarkable tolerance to atropine:
twice the doses suggested above may sometimes be needed. Signs of over-
atropinization are: muscle twitching, FEVER, delirium.
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 emesis, 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
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INTUBATION, ASPIRATION, and LAV AGE, using isotonic saline
or 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. Give adrenergic amines ONLY if there is a specific indication.
9. 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 mgnn/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.
10. 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.
11. 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
PARAQUAT
2cr
DIQUAT
-CH
2\
CH
CH
MORFAMQUAT
-CH.,
2CP
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 hurnans
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, OPT, 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 kidnev 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
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 toxicity, 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 st'" ,ach 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 the gut. 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, in
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. In one case, a regimen
16
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of AZATHIOPRINE and POTASSIUM AMINOBENZOATE appears
to have been effective. Laithwaite, J.A., Brit. J. Clin. Pract. 30(3): 71-73
March 1976)
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
OH
N
or
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 Killer, Dande-
lion Killer, Vegetation Killer, Chickweed and Clover Killer. Several hundred
herbicide preparations include one or more chlorophenoxy compounds. 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 in 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
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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
MUSCLJE TWITCHING, SKELETAL MUSCLE TENDERNESS, and
MYOTONIA (stiffness of muscles of extremities). Respiratory insufficiency
from muscle weakness apparently occurred in one victim of accidental poison-
ing, 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 absofption.
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
state health departments, universities, agricultural research facilities, com-
mercial 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
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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, trachea! 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 ]2,
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
NO,
O—H(or ESTER)
(ALKYL) (ALKYL)
COMMON COMMERCIAL 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
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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 (deep), or slowly TV. 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 LAV AGE 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 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 atropine, aspirin or other antipyretics to con-
trol 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
\ //
\ _ /J
°
(or Na)
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 POISONINGS:
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 in 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 atropine, 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.
-------
ORGANONITROGEN HERBICIDES
CLASSES OF ORGANONITROGEN HERBICIDES AND
COMMON COMMERCIAL PRODUCTS
X = HALOGEN
UREA DERIVITIVES
R = ALKYL
o = c
monuron (Monurex, Telvar)
diuron (Di-on, diurex, Karmex, Von-
duron)
linuron (HOE-2810, Afalon, Lorox. Sarc-
lex)
URACIL DERIVITIVES
H
H,C — C
X — C
\
C
II
0
C = 0
I /CH3
N-C^-H
' \C2H5
bromacil (Borea, Hyvar X, Hyvar X-L,
Borocil IV, Urox HX or B, Isocil)
terbacil (Sinbar)
ACETANILIDE DERIVITIVES
' MR)
Isopropyl or
Methoxymethyl
\ "
NC —C—Cl
II H
propachlor (Ramrod),
alachlor (Lasso)
propanil (DPA, Propanex, Stam F-34)
ACETAMIDE COMPOUNDS
Allyl —N
/
\
Allyl
H
C —C—Cl
II H
0
alhdochlor (Randox, CDAA)
27
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s-TRIAZINE COMPOUNDS
^
N
H I
N— C
fOR
X or ISR
1
>\
N
II H
C — N
PICOLINIC ACID DERIVITIVES
atrazine (Aatrex. Atranex, Gesaprim, Pri-
matol A)
simazine (Princep, Primatol S, Simanex,
Gesatop)
propazine (Milogard, Gesamil, Primatol
P)
prometone (Pramitol, Gesafram, prome-
ton)
atraton (Atratone)
prometryn (Caparol, Gesagard, Primatol
Q, Prometrex)
ametryn (Evik, Ametrex, Gesapax)
desmetrjn (Semeron)
terbutryn (Igran, Shortstop E)
cyanazine (Bladex, Scogal)
cyprazine (Outfox)
Cl
—OH
U Cl
NH,
picloram (Tordon, Borolin)
CARBAMATE COMPOUNDS
o
— N—C —0-
CH,
r
-CH
I
CH,
chlorpropham (Chloro IPC, CIPC, Fur-
loe)
Liquid technical formulations of these products are usually dissolved
in petroleum distillates.
TOXICOLOGY
Adverse effects have occurred only rarely as a result of human or animal
contact with these herbicides. LD50 values for most compounds are in the
thousands of mgm per kg. A few are in the range of several hundred mgm
per kg; the lowest LDM value listed is 180 mgm per kg for cyanazine.
28
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Certain of these chemicals, however, irritate the skin and mucous mem-
branes (uracil, acetanilide, acetamide and picolinic acid compounds), and
particular classes can cause sensitization (acetanilides and acetamides).
When administered to experimental animals at extreme dosage levels
some of these chemicals can injure the nervous system, liver, kidney, and
capillary membranes. Large doses of triazines have caused anemia and
impaired adrenal function. No such effects have been observed in persons
exposed to the herbicides occupationally, or by accidental ingestion. Absorbed
herbicide is not stored in the body; the native chemical and metabolites are
excreted primarily through the urine. Ingestion of large quantities of any
of these materials is likely to cause gastrointestinal irritation. In such cases,
the hazard of the petroleum distillate solvent may equal or exceed hazards
presented by the active herbicidal ingredients.
SYMPTOMS AND SIGNS OF UNDUE EXPOSURE
IRRITANT EFFECTS on skin and mucous membranes are the most
common reactions to these chemicals. Large ingestions can cause nausea,
vomiting, abdominal distress, and diarrhea. SENSITIZATION to acetanilides
or acetamides can result in protracted DERMATITIS.
CONFIRMATION OF ABSORPTION
Particular industrial, university, and government laboratories can detect
some compounds or metabolites in the urine of persons who have absorbed
significant amounts. The laboratories can be reached through health depart-
ments or poison control centers.
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 with soap and water.
Severe irritation may require medical attention. Persons who become
sensitized may require specialized medical management with anti-
inflammatory agents. Thereafter they will need to take stringent pre-
cautions to avoid contact with the chemical.
3. Considering the low inherent toxicities of these herbicides, and the
risk of hydrocarbon pneumonitis when the stomach is intubated or
emesis is induced, INGESTIONS of these chemicals KNOWN TO IN-
VOLVE LESS THAN 10 MGM PER KG body weight are probably
treated best by administering 30-60 gm of activated charcoal in 5-10
ounces of water. If diarrhea has not already developed, follow the
charcoal administration in 4 hours with SODIUM SULFATE catharsis:
adult dose (over 12 years of age), 15 gm in 6-8 ounces of water; for
children under 12, 0.2 gm per kg in 1-6 ounces of water.
29
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4. Ingestions of more than 10 mgm per kg body weight, especially when
ingestion occurred less than an hour before treatment, should be
managed by EVACUATING the STOMACH:
A. If victim is alert and respiration is not depressed give SYRUP of
IPECAC: 30 ml for adults; 15 ml for children under 12 years.
CAUTION: OBSERVE the victim closely after administering ipecac.
If consciousness level declines, or if vomiting has not
occurred in 15 minutes, proceed immediately to 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
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 available)
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 end of table tipped downward).
Keep the 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 by
way of stomach tube to limit absorption of remaining toxicant. Do
NOT instill milk, cream or other substances containing vegetable or
animal fats, as they may enhance toxicant absorption. If bowel
movement has not occurred in 4 hours, and if patient is fully
conscious, give SODIUM SULFATE as a cathartic.
30
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DIMETHYLDITHIOCARBAMATE
COMPOUNDS*
GENERAL CHEMICAL STRUCTURE
(CH,)2-N-C-S
II
COMMON COMMERCIAL PESTICIDE PRODUCTS
Tetramethyl thiuram disulfide:
Thiram (Arasan, Thiramad, Thirasan, Thylate, Tirampa, Pomasol forte,
TMTDS, Thiotex, Fernasan, Nomersan, Tersan, TUADS)
Metallodimethyldithiocarbamates:
Ziram, Pomasol Z forte (zinc), Ferbatn (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, demyelinization 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.
31
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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, circulatory 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
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.
32
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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:
15ml).
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.
33
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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 artificially 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 LAV AGE, 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.
34
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ANTICOAGULANT RODENTICIDES
STRUCTURES OF PRINCIPAL CLASSES
OH
ALKYL, PHENYL.
DIPHENYLACETYLor
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,
IX, 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
35
-------
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: 0.6 mgm/kg body weight
IM.
Note: PHYTONADIONE (Vitamin K,, Mephyton, Aquamephyton,
Konakion) specifically is required- Vitamin K., (menadione,
Hykinone) and vitamin K, (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
36
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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: 0.6 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 in 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 0.6 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
37
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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).
38
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ARSENICAL PESTICIDES
CHEMICAL STRUCTURES
EXTREMELY TOXIC: (TRIVALENT INORGANIC ARSENICALS)
O^As — O—As^O K—O—As = O
ARSENIC TRIOXIDE POTASSIUM ARSENITE
O
II H
Cu—(O—C—CH3)2
As—H
Cu3—
-------
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-forming 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.
40
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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 NEPHROSIS, HEPATITIS (hepatomegaly and
jaundice), and NEUROLOGIC INJURY (delirium, paralysis, respiratory de-
pression) may progress to a fatal outcome.
SUBACUTE 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 /tgm/day, but diets rich in seafood may generate as much
as 200 jugm/day. Excretions above 100 /tgm/day should be viewed with sus-
picion and tests should be repeated. Excretions above 200 jugm/day reflect
41
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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:
42
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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, lachrymation, 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.
43
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VACOR® and DLP-787
CHEMICAL STRUCTURE
H
-C-N-C-N-// YV
i i n i \ /
N02
I II I
H H O H
RH-787
COMMON COMMERCIAL PESTICIDE PRODUCTS
Vacor® Rat Killer (2% RH-787 in vehicle resembling corn meal); DLP-
787 Bait (2% RH-787 in vehicle resembling corn meal); DLP-787 House
Mouse Tracking Powder (10% RH-787 in a light green powder vehicle).
Compound RH-787 is the active ingredient of both formulations.
TOXICOLOGY
Acute oral LD50 values for RH-787 in the dog and Rhesus monkey are
2000-4000 mgm/kg. LD50 ratings of the diluted formulations ingested by
rodents are quoted as follows:
Rats Mice
Vacor® Rat Killer or Bait 580 mgm/kg 4,120 mgm/kg
DLP-787, 10% Tracking Powder 1,050 mgm/kg
The minimum lethal dose in humans is not known.
The exact mechanism of RH-787 toxicity is not known. It has no anti-
coagulant action, and is therefore entirely different from the coumarin-
indandione rodenticides. One established effect in rats is interference with
nicotinamide metabolism. Symptoms and signs in poisoned animals suggest
toxic actions on the brain, the peripheral nerves, myoneural junctions, the
pancreas (including islet tissues), the autonomic nervous system, and the
conducting tissues of the heart. Abnormalities of renal and vascular function
may be due to direct toxic effects, or may reflect metabolic and autonomic
nervous system disturbances (hypotension).
If absorbed in adequate dosage by rats or by humans, RH-787 can induce
persistent diabetes mellitus, manifest as hyperglycemia, glycosuria, and
ketoacidosis. This has occurred in humans following ingestion of one 30 gm
package of Vacor®.
FREQUENT SYMPTOMS AND SIGNS OF POISONING
Human poisonings of a significant nature have occurred only after de-
liberate ingestions of RH-787. Symptoms vary, depending on dose and indi-
vidual susceptibility.
Symptoms may not appear until 4-48 hours after ingestion of the formu-
lated rodenticide. EARLY symptoms include NAUSEA, VOMITING, AB-
DOMINAL CRAMPS, CHILLS, and MENTAL CONFUSION.
44
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LATER clinical manifestations have included: ACHING and FINE
TREMORS of the extremities, DILATED PUPILS, PERIPHERAL NEU-
ROPATHY (plantar hyperesthesia), MUSCLE WEAKNESS, DYSPHAGIA,
CHEST PAIN, POSTURAL HYPOTENSION, ANOREXIA, CONSTI-
PATION or DIARRHEA, URINARY BLADDER DYSTONIA (urinary
retention), HYPOTHERMIA and the consequences of diabetes mellitus:
GLYCOSURIA, POLYURIA, KETOACIDOSIS, and DEHYDRATION.
Abnormal laboratory findings include hyperglycemia, glycosuria, ketosis
(acidosis and electrolyte disturbances), and elevation of serum amylase and
lipase activities.
Temporary blindness has occurred in dogs.
Death may result from respiratory failure, cardiovascular collapse, or keto-
acidosis.
LATE and PERSISTENT manifestations of poisoning are POSTURAL
HYPOTENSION and DIABETES MELLITUS.
CONFIRMATION OF DIAGNOSIS
Analysis of blood, urine, and tissues for RH-787 is difficult, and cannot
yet be done on a routine basis. In particular cases of poisoning that require
chemical confirmation, contact the Office of Pesticide Programs, U.S. En-
vironmental Protection Agency.
TREATMENT
1. If no more than 12 hours have elapsed since toxicant ingestion,
EVACUATE THE STOMACH by INDUCED EMESIS and LAV-
AGE.
A. INDUCE EMESIS with SYRUP OF IPECAC (30 ml for adults and
children over 12 years; 15 ml for children under 12) ONLY if
copious vomiting has not already occurred and if the victim is fully
alert. If consciousness declines after ipecac administration, proceed
immediately with gastric intubation.
B. Following emesis, INTUBATE the STOMACH, ASPIRATE CON-
TENTS, and LAVAGE with 2-3 liters of isotonic saline or 5%
sodium bicarbonate solution. To avoid aspiration of stomach con-
tents, put the victim in left lateral Trendelenburg position, aspirate
the pharynx frequently, and, in unconscious patients, intubate the
trachea with a cuffed tube prior to gastric intubation.
C. After gastric lavage, instill 30 gm of ACTIVATED CHARCOAL
in 3-4 ounces of water through the stomach tube to limit absorption
of the toxicant.
45
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2. Administer NIACINAMIDE (nicotinamide) intravenously (slowly) or
intramuscularly. In adults and in children over 12 years or 30 kg body
weight, give 500 mg immediately, then repeat injections of 200-400 mgm
every 4 hours for 10-12 doses. Select the proper dosage on the basis
of body weight and estimated quantity of Vacor® or DLP 787 in-
gested. If symptoms and signs of rodenticide toxicity appear, adminis-
ter nicotinamide by continuous IV infusion at a rate of 400 mgm every
4 hours. Avoid total dosage of nicotinamide above 3000 mgm/day.
Dosage for children under 12 years, or less than 30 kg body weighl,
is approximately half that needed for adults.
When the patient is able to take medication by mouth, give 100
mgm nicotinamide orally four times daily for two weeks.
3. MONITOR blood and urine sugar concentrations, serum alkaline
phosphatase, amylase, LDH, and GOT activities, urine ketone concen-
trations, blood electrolytes and BUN. Examine the electrocardiogram
for arrhythmias.
4. Unless the patient is able to void easily, put in place a RETENTION
CATHETER to monitor urine flow and urinary glucose excretion.
5. Infuse ELECTROLYTE SOLUTIONS intravenously to accelerate toxi-
cant excretion and correct errors in specific ion concentrations. If keto-
acidosis appears, use bicarbonate or Ringer's-lactate to control acidosis.
6. If DIABETIC KETOACIDOSIS appears (ketonuria, metabolic acidosis,
hyperglycemia) administer enough regular insulin to control the acido-
sis and hyperglycemia, as in naturally occurring diabetic ketosis. The
diabetes resulting from RH-787 tends to be brittle and correspondingly
difficult to control.
7. In all cases of ingestion of Vacor® or DLP-787 (whether or not acute
poisoning occurs), follow the patient's clinical status carefully for at
least 6 months. Look for indications of diabetes mellitus, and for con-
sequences of autonomic nervous system disorders: orthostatic hypo-
tension, urinary retention, constipation, diarrhea, or abdominal
cramping.
46
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HALOCARBON and SULFURYL
FUMIGAIMTS
COMMON COMMERCIAL PESTICIDE PRODUCTS
H
I
Cl — C —Cl
I
H
METHYLENE
CHLORIDE
Cl
I
Cl— C — H
I
Cl
CHLOROFORM
Cl Cl
I I
H — C — C — H
I I
H H
ETHYLENE
DICHLORIDE
Br Br
I I
H — C — C — H
I I
H H
ETHYLENE
DIBROMIDE
J Cl H Cl
I I '
H— C — C s= C
I I
H H
1.3.DICHLORO-
PROPENE
Cl
I
H— C— C — C — H
I I I
H H H
1,2-DICHLORO-
PROPANE
Cl
I
Cl — c —Cl
I
Cl
CARBON
TETRACHLORIDE
BR
I
H — C— H
METHYL
BROMIDE
Cl
I
Cl — C — N02
Cl
CHLOROPICRIN
Cl H
I I
Cl- C — C — H
I I
Cl H
1.1.1 -TRICHLORO
ETHANE
PARADICHLOROBENZENE
SULFURYL
FLUORIDE
ALIPHATIC
Chloroform, carbon tetrachloride, methyl bromide (Brom-O-Gas, Fumi-
gant-1, Kayafume, Me Br, Meth-O-Gas, Pestmaster, Profume); chloropicrin
(Acquinite, Chlor-O-Pic, Pic-Clor, Picfume; Trichlor); ethylene dichloride
(EDC); ethylene dibromide (EDB, Bromofume, Celmide, Dowfume W-85,
Kop-Fume, Nephis, Pestmaster EDB-85, Soilbrom); dichloroprop-ene and
-ane (Telone, D-D). The Dowfume fumigants manufactured by the Dow
Chemical Company are mixtures of halocarbons, mainly EDC, EDB, carbon
tetrachloride, Me Br, and chloropicrin, formulated to meet specific needs.
4/
-------
AROMATIC
Paradichlorobenzene (PDB, Paracide, Paradow)
SULFURYL
Sulfuryl fluoride (Vikane)
TOXICOLOGY
Except for the solid paradichlorobenzene moth crystals, these chemicals
are gases or highly volatile liquids at room temperature. As fumigants, they
have a remarkable capacity for penetration. Some, especially the bromine
compounds, pass readily through human skin and rubber protective gear,
thus complicating the protection of exposed workers. In varying degrees they
irritate the skin, eyes, and respiratory tract. When held on the skin by an
occluding cover, such as contaminated gloves, these chemicals not only
irritate, but cause acute dermatitis and vesiculation. Repeated contact with
the liquid halocarbons defats the skin, leading to chronic dermatitis. All are
capable of producing pulmonary edema and/or hemorrhage in persons
heavily exposed by inhalation, ingestion, or dermal absorption. Death follow-
ing exposure to the halocarbon fumigants is usually due either to pulmonary
edema or to respiratory depression.
Inhalation of pyrolysis products of these fumigants has caused massive
necrosis of respiratory tract linings in exposed firemen.
Toxic action on the central nervous system is generally depressant,
causing unconsciousness, seizures, and general muscle weakness, including
weakened respiratory effort. The neurotoxic action of methyl bromide ap-
parently includes the basal ganglia as well as the cerebrum, causing not only
sensory and motor impairments but also behavioral and emotional dis-
turbances. These may or may not progress to epileptiform seizures and coma.
In some cases, behavioral and neurologic manifestations have first appeared
several hours or even days after exposure, then they have persisted for days
to months.
The chlorocarbons, notably chloroform, increase myocardial irritability
and impair contractile strength. Large inhalation dosages may cause death
by inducing ventricular fibrillation.
In varying degree, these fumigants damage the liver and kidneys. In
laboratory animals, and in autopsy specimens from fatal human cases, this
is commonly manifest as fatty degeneration. More severe poisoning causes
centrilobular necrosis of the liver and acute tubular necrosis of the kidney.
Fatty degeneration of the myocardium and corneal opacities have been
observed in dogs following systemic absorption of ethylene dichloride.
Methyl bromide and ethylene dichloride (and possibly other chemicals of
this series, by analogy) are alkylating agents in mammalian tissues; they can
inhibit multiple enzyme systems, including the sulfhydryl enzymes and hexo-
kinases in multiple tissues. This may be a major mechanism of toxicity of
this series of chemicals.
48
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Paradichlorobenzene is substantially less toxic to humans than are the
gaseous and liquid fumigants. It has neither the hemolytic nor the cataracto-
genic properties of naphthalene fumigant, which it has largely displaced.
Given at extreme dosage to laboratory animals, it causes liver injury and
neurologic disturbances.
FREQUENT SYMPTOMS AND SIGNS OF POISONING
HEADACHE, DIZZINESS, NAUSEA, and VOMITING are prominent
early symptoms of the poisonings produced by these fumigants. Irritants,
especially METHYL BROMIDE and the 3-carbon CHLOROCARBONS
often produce TEARING, RHINORRHEA, PHARYNGITIS, COUGH, and
DYSPNEA. These symptoms may progress to PULMONARY EDEMA,
with coughing of frothy sputum.
DROWSINESS, TREMORS, ATAXIA, DIPLOPIA, MUSCLE TWITCH-
INGS and WEAKNESS, and JACKSONIAN SEIZURES are the major
early manifestations of central nervous system injury. Twitching and regional
myoclonic movements may progress to general and severe EPILEPTIFORM
SEIZURES, coma, and death in respiratory failure.
DELAYED MANIFESTATIONS have characterized some poisonings by
METHYL BROMIDE. Convulsions and/or pulmonary edema may appear
up to 48 hours after exposure. Bizarre myotonic states, behavioral and
emotional disturbances, impaired speech, and awkward gait have developed
after repeated, relatively low-level occupational exposures, persisting there-
after for weeks or months.
Following heavy accidental exposures to the CHLOROPROPANES -
ENES, a few victims have complained of protracted neurologic sympto-
matology: headache, irritability, poor memory and personality changes.
INGESTION of acutely toxic amounts of liquid HALOCARBONS is
likely to be followed by PULMONARY EDEMA, SEIZURES, and SHOCK.
Because toxic dosages and individual susceptibilities vary widely, cases of
ingestion should be treated vigorously, regardless of estimated dosage.
PARADICHLOROBENZENE has occasionally caused dermal sensitiza-
tion. Tremors and liver injury produced by extreme doses in laboratory
animals have occurred rarely, if ever, in humans.
SULFURYL FLUORIDE may cause MUSCLE TWITCHINGS, then
CONVULSIONS, on acute exposure. Because pulmonary and renal damage
may develop on repeated contact, every attempt should be made to minimize
exposure.
CONFIRMATION OF POISONING
Although there are methods available for measuring gaseous halocarbons
in expired air, these facilities are found only in anesthesiology research units
or industrial plants. Paradichlorobenzene concentrations can be measured
in the blood.
49
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Blood bromide concentrations* have some value in identifying poisonings
by methyl bromide, and possibly ethylene dibromide, provided it can be es-
tablished that the person exposed to the fumigant has not recently taken
inorganic bromide medication. A level of organic bromide of more than 5
mgm/100 ml indicates excessive absorption of fumigant. A blood con-
centration of more than 10 mgm/100 ml of organic bromide represents a
serious threat to health. A blood level of more than 15 mgm/100 ml
endangers life.
TREATMENT
1. FLUSH contaminating fumigant FROM the EYES with copious
amounts of water, for at least 10 minutes.
2. WASH liquid fumigant FROM the SKIN with soap and water. Severe
inflammation and vesiculation will require continuing medical manage-
ment.
3. REMOVE VICTIMS of FUMIGANT INHALATION to FRESH AIR.
Even though initial symptoms and signs are mild, put victim in a
comfortable sitting or reclining position so as to REDUCE PHYSICAL
ACTIVITY to an absolute minimum. If respiration is depressed,
RESUSCITATE by mechanical intermittent positive pressure breath-
ing (IPPB), if available. Use whatever concentrations of oxygen are
necessary to overcome hypoxemia. Mouth-to-mouth or mouth-to-nose
resuscitation may be necessary.
4. PULMONARY EDEMA must be treated initially by vigorous inter-
mittent (sometimes continuous) positive pressure breathing, using
sufficient oxygen to overcome hypoxemia. Administer with the victim
in a sitting or semi-reclining position.
CAUTION: Whenever possible, avoid prolonged use of high concen-
trations of oxygen (80%-100%), as these may aggravate
existing injury to lung tissue.
5. CONTROL CONVULSIONS. Although there is no published ex-
perience to document its value in these poisonings, DIAZEPAM is
probably the drug of choice to control seizures caused by the halo-
carbon fumigants. Give 5-10 mgm by slow intravenous injection, stop-
ping with the lowest effective dose. Deep intramuscular injection can be
used if seizures preclude intravenous administration.
CAUTION: Inject diazepam slowly IV to avoid irritation of the vein,
hypotension, and respiratory depression.
Severe seizures caused by methyl bromide have been controlled with
barbiturates. A maximum dosage of PENTOBARBITAL (NEM-
BUTAL) of 5 mgm/kg body weight may be given slowly IV until
convulsions are controlled, and repeated in 4-6 hours if necessary. If
t Conway, E. J. Microdiffusion Analysis and Volumetric Error. 3rd Edition.
Crosby Lockwood, London 1950.
50
-------
IV administration is not possible, the total 5 mgm/kg dose can be
administered rectally.
CAUTION: Be prepared to assist pulmonary ventilation mechanically,
if respiration is depressed.
In methyl bromide poisoning, it may be necessary to give diazepam
or pentobarbital orally for some time after the acute convulsive episode
to control involuntary motor activity.
6. INGESTED FUMIGANT liquids MUST BE REMOVED from the gut.
Because of the strong likelihood of respiratory depression shortly
after ingestion, it is probably best to AVOID use of IPECAC, and to
undertake GASTRIC INTUBATION, ASPIRATION, and LAVAGE
immediately. To avoid aspiration of gastric contents: a) place the
victim in left lateral Trendelenburg; b) if the victim is unconscious,
insert a cuffed endotracheal tube prior to gastric intubation; c) if
victim is conscious, or if it is not possible to accomplish tracheal
intubation for other reasons, aspirate the pharynx as regularly as
possible during gastric intubation.
ASPIRATE the stomach as completely as possible. Then LAVAGE
with 2-3 liters of 0.9% sodium chloride, or 5% sodium bicarbonate,
containing a slurry of 60-90 gms ACTIVATED CHARCOAL. After
lavage, instill 30 gnr activated charcoal into the stomach before with-
drawing the tube, to adsorb remaining toxicant.
7. In poisonings by METHYL BROMIDE and ETHYLENE DI-
CHLORIDE (and possibly by other chemicals of this series, by infer-
ence) there may be some therapeutic value in the administration of
DIMERCAPROL (BAL, dimercaptopropanol), especially if it can be
given within a few minutes of absorption of the toxicant. Administered
in vegetable oil intramuscularly, the usually recommended dosage is 3
mgm/kg body weight q 6h for 8 doses in first 2 days; then 3 mgm/kg
q 12h for 2 doses during day 3; then 3 mgm/kg q 24h for 10 doses
during succeeding 10 days.
CAUTION: DIMERCAPROL may cause troublesome side effects
(hypertension, tachycardia, nausea, headache, paresthesiae,
pain, lachrymation, sweating, anxiety and restlessness).
Although usually not so severe as to handicap treatment,
these manifestations may require antihistamine therapy
for adequate control.
8. MONITOR poisoning victims closely FOR RECURRENT PULMO-
NARY EDEMA and secondary BRONCHOPNEUMONIA. Fluid
balance should be charted, and the urine sediment examined regu-
larly, to detect incipient TUBULAR NECROSIS. Measure serum
alkaline phosphatase, GOT, GPT, LDH and bilirubin to assess LIVER
INJURY. Administer intravenous fluids cautiously to avoid exacerbat-
ing the pulmonary edema.
51
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Protracted neurologic manifestations of poisoning may require sever-
al days or weeks of sedative therapy. Pulmonary function tests should
be done after resolution of acute symptoms to evaluate the degree of
permanent lung damage, if any.
52
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MISCELLANEOUS FUMIGANTS
CHEMICAL FORMULAE OF COMMON FUMIGANTS:
ORGANIC OXIDES
CH,
ETHYLENE
OXIDE
ALDEHYDES
CH,
CH2"
PROPYLENE
OXIDE
' CH,
JC»
H
C= O
1
H
FORMALDEHYDE
H
1
C =O
•
O
1
H— C — H
H
METHYL
FORMATE
H
1
C =0
1
1
H — C — H
1
H-C — H
1
H
H
C= 0
I
H-C
1
H-C — H
ACROLEIN
FORMATE
SULFUR-CONTAINING
O = S = O
SULFUR DIOXIDE
CYANIDE AND NITRILE
H — C H N
HYDROGEN CYANIDE
S = C = S
CARBON DISULFIDE
H
H2C = C — C s. N
ACRYLONITRILE
PHOSPHINE
V
H
PHOSPHINE
FROM
H2O
AROMATIC HYDROCARBON
AL = P
METAL PHOSPHIDE
COMMON COMMERCIAL PESTICIDE PRODUCTS
Many fumigants are identified by generic chemical names.
Published common and commercial names are identified below:
Ethylene oxide: ETO, oxirane
Propylene oxide: epoxy propane
Formaldehyde: Formalin (40% soln); Paraformaldehyde (solid
polymer) Methyl and ethyl formates: Areginal
53
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Propenal: Acrolein, Aqualin, Acrylaldehyde
Carbon disulfide (carbon bisulfide): an ingredient of many grain fumigant
mixtures
Hydrogen cyanide: hydrocyanic acid, prussic acid (Cyclon)
Acrylonitrile: ingredient of Acrylofume, Acritet, Carbacryl. These are
fumigant mixtures with halocarbons
Phosphine: generated by contact of moisture in air with aluminum
phosphide; Phostoxin
Naphthalene: ingredient of many domestic moth repellent balls and flakes
TOXICOLOGY
The primary toxic actions of the organic oxides, aldehydes, and sulfur
dioxide are irritant effects on the skin, mucous membranes, and lung. Dermal
contact with the oxide and aldehyde gases may cause reactions varying from
mild irritation to vesiculation and deep necrosis of the skin. Inhaled fumigant
may induce edema of the larynx or lung.
Like other fumigants, these substances are rapidly absorbed by the lung.
Also, the oxides and aldehydes may penetrate the skin in sufficient dosage to
cause poisoning by this route of absorption alone.
Deep dermal necrosis has resulted from severe skin exposures to ethylene
oxide. Liquid forms of ethylene and propylene oxide are the most damaging
on contact. Material splashed in the eyes may result in permanent corneal
scarring. Propylene oxide is somewhat less tissue-damaging than ethylene
oxide. Excessive absorption of these oxides results in systemic illness due
mainly to toxic effects on the central nervous system. The oxides also damage
the liver and kidneys. They are usually formulated with carbon dioxide to
reduce explosion hazard.
The aldehydes also produce systemic illness when absorbed. This is mani-
fest primarily as CNS depression. Systemic toxicity may result from degrada-
tion products in the cases of ethyl formate (formic acid) and methyl formate
(methyl alcohol). Although pulmonary edema can result from excessive
exposure, formaldehyde and acrolein are more likely to embarrass respiration
by inducing laryngeal edema.
The primary toxic actions of carbon disulfide, hydrogen cyanide, acrylonit-
rile, phosphine, and naphthalene are systemic rather than irritative.
Carbon disulfide (CSu), or thiocarbamates formed metabolically from
CSL>, impair the activities of multiple enzymes essential to normal function
of the brain and the peripheral nerves. In acute exposure, this neurotoxic
action is much more prominent than are effects on the liver and kidneys. The
ability of thiocarbamates to chelate the copper components of certain cerebral
enzymes has been cited as a major mechanism of neurotoxicity. Protracted
occupational exposure to carbon disulfide has caused a great variety of
disabling neuropsychiatric disorders, due, apparently, to irreversible effects
of the toxicant on brain tissue itself, or on the cerebral vasculature. Peripheral
54
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neuropathy is another common sequel of long-term carbon disulfide exposure.
Hydrogen cyanide (HCN) and its salts poison by inactivating the cyto-
chrome oxidase of cells in critical tissues, primarily the heart and brain.
Acrylonitrile degrades slowly to HCN in the body, and therefore acts by
the same mechanism, although the slow release of free cyanide renders it
less toxic than HCN itself. Both HCN and acrylonitrile are sufficiently
absorbable across the skin to cause poisoning in the absence of inhalation
exposure. Manifestations of poisoning are due mainly to intracellular anoxia
of brain tissue (leading to respiratory failure), and to the circulatory in-
sufficiency that results from myocardial weakness. The liver has substantial
capacity for conversion of cyanide to the less toxic thiocyanate, a metabolic
conversion that is accelerated by therapeutically administered thiosulfate.
Inhaled phosphine gas (PH3) and ingested metal phosphides cause pul-
monary edema, CNS depression, toxic myocarditis, and circulatory collapse.
Victims who survive these immediate actions suffer liver injury (fatty de-
generation and necrosis), and acute renal tubular necrosis. Phosphine is not
hemolytic, like its analogue arsine. Enzymatic mechanisms of toxicity are
not known. Ingested metal phosphide causes intense gastrointestinal irrita-
tion, followed by degenerative and necroti/ing lesions of the liver, kidney
and heart. Death is often due either to cardiogenic shock or pulmonary
edema.
Naphthalene is metabolized to naphthols, which are chemical hemolysins.
Some members of dark-skinned races are genetically more vulnerable to
these metabolites because of red cell deficiency of glucose-6-phosphate dehy-
drogenase. Severe anemia and/or acute renal tubular necrosis result from
the hemolysis. A few individuals develop dermal hypersensitivity to naphtha-
lene. Corneal ulcers and cataracts have occurred in laboratory animals, and
rarely in humans as a result of occupational exposure to vapor and dust.
FREQUENT SYMPTOMS AND SIGNS OF POISONING
The ORGANIC OXIDES, ALDEHYDES, and SULFUR DIOXIDE
irritate skin and mucous membranes, causing BURNING, REDNESS and
SWELLING on contact. LARGE BLISTERS, and sometimes deep tissue
BURNS, result when an area of contact has been occluded by gloves or other
clothing. CONJUNCTIVAL REDNESS and LACHRYMATION result from
eye exposure. HOARSENESS reflects laryngeal irritation, and may portend
life-threatening laryngeal edema. DYSPNEA, SUBSTERNAL PRESSURE,
HACKING COUGH, and FROTHY SPUTUM are signs of pulmonary
edema, which may progress to cause CYANOSIS and UNCONSCIOUS-
NESS. Although irritant effects are usually severe enough that exposed indi-
viduals leave contaminated atmospheres promptly, rapid absorption of oxides
and aldehydes has resulted in severe systemic toxicity: HEADACHE,
NAUSEA, VOMITING, DIARRHEA, PAIN IN CHEST AND ABDOMEN,
and DEPRESSED RESPIRATION.
CARBON DISULFIDE has moderate irritative effects on the skin and
mucous membranes, but the major symptoms of poisoning are those of a
55
-------
toxic encephalopathy: HEADACHE, NAUSEA, DIZZINESS, WEAKNESS,
DELIRIUM, PARESTHESIAE, HALLUCINATIONS of hearing, vision,
and smell, CONVULSIONS and RESPIRATORY DEPRESSION.
Excessive absorption of HCN or ACRYLONITRILE may produce sud-
den UNCONSCIOUSNESS and RESPIRATORY ARREST, without warn-
ing symptoms. Lesser exposures cause HEADACHE, NAUSEA, and a
sense of CONSTRICTION in the THROAT, followed by APPREHENSION,
DIZZINESS, and HYPERPNEA. Deepening toxicosis is manifest as IR-
REGULAR RESPIRATION, BRADYCARDIA, THREADY PULSE and
UNCONSCIOUSNESS. CONVULSIONS may be either EPILEPTIFORM
or TONIC, with OPISTHOTONUS, TRISMUS, and loss of sphincter con-
trol. RESPIRATORY PARALYSIS follows the seizures. Heart action often
continues after breathing has stopped: vigorous treatment at this critical
stage has saved some victims of cyanide poisoning. The SKIN generally
remains PINK in color, rather than becoming cyanotic, due to failure
of poisoned tissue cells to remove oxygen from the capillary blood.
PHOSPHINE GAS poisoning is usually heralded by WEAKNESS,
TREMORS, VOMITING, SENSE OF PRESSURE in the CHEST, COUGH
and DYSPNEA, the latter sometimes progressing to PULMONARY EDEMA.
INTENSE THIRST is probably a result of HYPOTENSION and dehydrating
DIARRHEA. Severe poisonings produce CONVULSIONS, COMA, and
RESPIRATORY DEPRESSION, leading to death. Liver injury in those
who survive the initial phases is indicated by elevations of serum activities
of alkaline phosphatase, GOT, GPT and LDH, and sometimes by reduced
prothrombin concentration, hemorrhage, and jaundice. Renal toxicity causes
ALBUMINURIA, HEMATURIA and, in the most severe poisonings,
ANURIA. Chronic exposures to lesser concentrations of phosphine have
caused PAIN in the EYES and NOSE, NOSEBLEEDS', and chronic
ABDOMINAL DISTRESS.
INGESTED METAL PHOSPHIDE produces intense NAUSEA and
(usually) VOMITING, followed by manifestations of liver, kidney, lung,
heart and CNS injury that are characteristic of phosphine poisoning. Hypo-
calcemic TETANY (probably from hyperphosphatemia), and METABOLIC
ACIDOSIS typically develop several hours after metal phosphide ingestion.
Most poisonings by NAPHTHALENE have resulted from occupational
exposures in the petrochemical industry, although one infant victim absorbed
the agent from mothball-treated diapers. Extreme exposures by inhalation
cause HEADACHE, NAUSEA, VOMITING, CONFUSION and TREM-
ORS. Ingestion causes ABDOMINAL PAIN and DIARRHEA. Poisoning by
either route may progress to CONVULSIONS, COMA, and death by RES-
PIRATORY FAILURE. Acute hemolytic action may cause ANURIA
from the tubular damage induced by HEMOGLOBINEMIA and HEMO-
GLOBINURIA. Slow hemolysis may be tolerated by the kidney, but WEAK-
NESS and INANITION result from the ANEMIA. Hemolytic JAUNDICE
may develop from normal degradation of the heavy load of unconjugated
56
-------
hemoglobin. DERMATITIS has appeared where skin was covered by
naphthalene-impregnated fabric. Photosensitization has also occurred.
BLINDNESS from lens cataracts and optic neuritis have resulted from pro-
tracted industrial exposures to naphthalene.
CONFIRMATION OF DIAGNOSIS
Methods for detecting the organic oxides, aldehydes, and sulfur dioxide
are not generally available, but they are rarely needed. A simple method is
available for detecting carbon disulfide in urine (Djuric et al. Brit. J. Indust.
Med. 22:321-323. 1965). Cyanide can be detected and measured in blood
and tissues, as can the thiocyanate metabolite in urine and saliva. There are
no practical analytical methods for phosphine. Exposure to naphthalene can
be assessed by measuring urinary naphthols (although some other toxic
substances yield the same metabolite), and should be suspected in all cases
exhibiting hemoglobinuria. Odor of gases on the victim's breath are some-
times helpful diagnostic clues: cyanide smells like bitter almonds, carbon
disulfide like rotten cabbage, and phosphine somewhat like garlic or acety-
lene.
TREATMENT
1. The following measures are appropriate in treating all injuries and
illnesses caused by FUMIGANTS:
A. REMOVE VICTIM from contaminated atmosphere to FRESH
AIR.
B. If respiration is depressed, RESUSCITATE with intermittent posi-
tive pressure breathing (IPPB) apparatus, if available; if not avail-
able, administer artificial respiration by periodic mouth-to-mouth
or mouth-to-nose inflation of the chest.
C. If SKIN or EYES have been contaminated, FLUSH COPIOUSLY
with water. Leave skin exposed to air until victim can be delivered
to a hospital. EYE INJURIES should always receive PROMPT
MEDICAL ATTENTION.
2. The following treatment measures apply to poisonings by the
ORGANIC OXIDES, ALDEHYDES, and SULFUR DIOXIDE:
A. Insist that the recently exposed individual REDUCE PHYSICAL
ACTIVITY to an absolute minimum. Transport victim to an
emergency vehicle with minimum disturbance and then on to a
hospital, even though early symptoms may not seem serious. Keep
patient comfortably warm. Place him in a comfortable sitting or
semireclining position.
B. COMBAT PULMONARY EDEMA by having the victim sit up-
right, and by administering OXYGEN by IPPB in sufficient
concentration to overcome hypoxemia. Avoid unnecessary use of
high (50-100%) oxygen concentrations, as this may exaggerate the
injury to lung tissue. A slight positive expiratory mask pressure
57
-------
(4 cm) may be advantageous. Once IPPB has been instituted suc-
cessfully, small doses of morphine (8-10 mgm) may be given to
allay anxiety, reduce physical exertion, and promote deeper
respiratory excursions. ROTATING TOURNIQUETS on the
extremities may be of some value; venoclysis should be considered
only if blood pressure is well maintained. AMINOPHYLLINE
(0.25-0.50 gm, slowly IV) may be beneficial, and, occasionally,
rapid digitalization by intravenous digoxin may be considered,
even though the pulmonary edema is not basically cardiac in
origin.
CAUTION: serious arrhythmias can result when the myocardium
is anoxic.
Intravenous 50% glucose or sucrose has only transient benefit.
Epinephrine, atropine, and expectorants are generally not helpful,
and may have harmful side effects: arrhythmias from adreiiergic
agents, thickened sputum from atropine, nausea from expectorants.
ASPIRATE sputum from the upper respiratory passages regularly.
TRACHEOSTOMY may be necessary in some cases to cope with
large flows of edema fluid, and to rescue victims from respiratory
obstruction due to laryngeal edema.
C. COMBAT SHOCK by placing victim in Trendelenburg position.
Administer electrolyte and sugar solutions intravenously with great
care, to avoid precipitating or aggravating pulmonary edema. Use
vasopressor amines with caution, in view of the irritable state of the
myocardium.
D. LIMIT INFLAMMATORY REACTION by administering steroids
on a tapered dosage schedule.
E. CONTROL SECONDARY INFECTION with antibiotics.
F. WATCH for RECURRENT PULMONARY EDEMA, even up to
2 weeks after the initial episode, particularly if the victim becomes
active too soon. Severe physical weakness usually indicates per-
sistent pulmonary injury.
G. Observe the clinical progress of the victim for at least 6 weeks.
Serial pulmonary function testing may be important in assessing
degree of recovery.
3. The following treatment measures apply to poisonings by CARBON
DISULFIDE (CS2):
A. Mild poisonings from brief respiratory and dermal exposure to
CS2 are managed best by CAREFUL OBSERVATION to forestall
serious consequences: respiratory depression, delirium, convulsions,
coma.
58
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B. CAFFEINE and sodium benzoate (0.5 gm subcutaneously) may
help to relieve CNS depression.
C. Do NOT use catecholamine-releasing agents such as reserpine and
amphetamines.
D. CONVULSIONS may be due to anoxia from respiratory depres-
sion. Administer 100% OXYGEN by face mask or IPPB, if
available. If not effective, continue oxygen and administer DIAZE-
PAM (Valium) slowly IV in dose sufficient to control convulsions,
but no more than 10 mgm. Although not tested in this type of
poisoning, diazepam has proven to be a satisfactory anticonvulsant
in many other circumstances.
CAUTION: diazepam may cause hypotension, or may exaggerate
respiratory depression. Extravasation at site of in-
jection may cause severe local irritation.
E. Delirium may require only careful observation and restraint of the
victim until it resolves. If activity threatens safety of the victim,
cautious use of diazepam or another tranquilizer as in (D) may be
necessary.
F. An intravenous infusion containing 0.5-1.5 gm/kg UREA has
been used with apparent benefit. Urea, which must be added to
5 % glucose or normal saline to avoid osmotic hemolysis, inactivates
free CS2 in the tissues.
G. If CARBON BISULFIDE has been INGESTED, empty the stom-
ach by INTUBATION, ASPIRATION and LAV AGE. Do NOT
use IPECAC, because of probable CNS depression by €82.
If victim is already unconscious, insert a cuffed ENDO-
TRACHEAL TUBE prior to gastric intubation.
If conscious, place the victim in Trendelenburg position, or left
lateral decubitus, and prepare to aspirate material from the
pharynx promptly if vomiting occurs during INTUBATION of
the stomach. When tube is in place, ASPIRATE as thoroughly as
possible before LAV AGING the stomach with 2-3 liters of saline
or 5% sodium bicarbonate. Before removing the tube, instill a
slurry of 30 gm ACTIVATED CHARCOAL to limit absorption
of remaining toxicant.
If bowel movement has not occurred within one hour of
ingestion, administer 15 gm SODIUM SULFATE in 6-8 ounces of
water by ingestion (if victim conscious) or by gastric tube (if victim
unconscious) to speed elimination of CS2.
Do NOT give vegetables oils, which may enhance gut absorption
of CS2.
59
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H. Parenteral pyridoxine injections have been recommended for
chronic CS2 poisoning.
I. OBSERVE victims of CS2 poisoning for several weeks or months
for evidence of neurologic disease, psychiatric illness, peripheral
neuropathy, hypertension, and chronic gastrointestinal symptoms.
Every effort should be made to eliminate, or at least minimize,
subsequent exposure to CS2.
The following treatment measures apply to poisoning by HYDROGEN
CYANIDE gas.
A. RESUSCITATE unconscious, apneic individuals. Clear secretions
from airway. Administer 100% OXYGEN by IPPB, if available.
Otherwise use mouth-to-mouth or mouth-to-nose resuscitation.
B. Administer AMYL NITRITE (perles) by inhalation for 15-30
seconds of every minute, while a fresh solution of 3% sodium
nitrite is being prepared.
C. As soon as solution is available, INJECT intravenously 10 ml of
3% SODIUM NITRITE solution over 2-4 minute interval, keeping
the NEEDLE IN PLACE.
CAUTION: Monitor PULSE and BLOOD PRESSURE during
administration of amyl nitrite and sodium nitrite. If
systolic blood pressure falls below 80 mm Hg, slow
or stop nitrite administration until blood pressure
recovers.
D. FOLLOW sodium nitrite injection with an infusion of 50 ml of
25% aqueous solution of SODIUM THIOSULFATE administered
over 10-minute period. Total adult dose should not exceed 12.5
gm.
E. If symptoms persist or recur, treatment by sodium nitrite and
sodium thiosulfate should be REPEATED at HALF THE DOS-
AGES listed in paragraphs C and D.
F. Measure HEMOGLOBIN and METHEMOGLOBIN in blood. If
more than 50% of total hemoglobin has been converted to methe-
moglobin, BLOOD TRANSFUSION or EXCHANGE TRANS-
FUSION should be considered, because conversion back to normal
hemoglobin proceeds slowly.
G. Dosage of ANTIDOTES in CHILDREN:
C. M. Berlin (Pediatrics 46: 793-796. 1970) has recommended
the following procedures in case of cyanide poisoning in children.
(1) Children over 25 kg body weight should receive adult dosages
of sodium nitrite and sodium thiosulfate.
60
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(2) Children less than 25 kg body weight should first have a 3-4 ml
sample of blood drawn, then, through the same needle, receive
10 mgm/kg (0.33 ml/kg of 3% solution) of SODIUM NI-
TRITE injected over a 2-4 minute interval. Following sodium
nitrite, administer an infusion of 1.65 ml/kg of 25% SODIUM
THIOSULFATE at rate of 3-5 ml per minute.
(3) At this point, determine the hemoglobin content of the original
blood sample. If symptoms and signs of poisoning persist, or
return, give supplemental infusions of sodium nitrite and
sodium thiosulfate based on hemoglobin level, as presented in
TABLE 2. (These recommended quantities are calculated to
avoid life-threatening methemoglobinemia in anemic children.)
TABLE 2. Recommended dosages of supplemental sodium nitrite and
sodium thiosulfate based on hemoglobin level.
Initial Supplemental Supplemental
Hemoglobin Volume of 3% Volume of 25%
Concentration, Sodium Nitrite. Sodium Thiosulfate,
gm/100 ml ml/kg ml/kg
14.0 0.26 1.28
13.0 0.21 1.05
12.0 0.17 0.83
11.0 0.12 0.60
10.0 0.07 0.38
9.0 0.04 0.23
8.0 0 0
7.0 0 0
(4) When methodology is available, monitor BLOOD levels of
METHEMOGLOBIN to achieve approximtely 40% conver-
sion of hemoglobin to methemoglobin.
H. Alternative antidoes, notably cobalt EDTA, are under investigation
in Europe, but are not available for use in the U.S.
5. The following measures apply to poisonings by PHOSPHINE GAS
and INGESTED METAL PHOSPHIDES:
A. Advise person recently exposed to PHOSPHINE to LIMIT PHYSI-
CAL ACTIVITY STRICTLY, even though early symptoms do not
seem serious. Put victim in comfortable sitting or semi-reclining
position during removal to a treatment facility. Provide comfortable
warmth. WATCH closely for PULMONARY EDEMA and
SHOCK, also for subsequent LIVER DAMAGE and ACUTE
TUBULAR NECROSIS.
B. Combat PULMONARY EDEMA and SHOCK as outlined under
treatment for poisonings by ORGANIC OXIDES, section 2, para-
graphs B and C.(p. 57-58).
61
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C. Treat CONVULSIONS as outlined under treatment for CARBON
BISULFIDE poisonings, section 3, paragraph D. (pg. 59)
D. Intravenous INFUSIONS of electrolyte and glucose solutions may
accelerate excretion of toxicant and protect the liver from to»cic
injury. However, it is essential to MONITOR FLUID BALANCE
and to take other precautions to avoid an excessive fluid load. Many
factors—lung tissue injury, toxic myocarditis, renal tubular damage
—predispose to pulmonary edema.
E. MONITOR urine albumin and sediment to assess renal injury.
Observe serum bilirubin, and serum activities of alkaline phos-
phatase, GOT, GPT and LDH to evaluate effects on liver. Examine
EKG tracings for indications of toxic myocarditis.
F. For INGESTIONS of METAL PHOSPHIDES, promptly EVACU-
ATE the stomach. If victim is fully alert and is not already vomit-
ing copiously, INDUCE EMESIS with SYRUP of IPECAC: adult
dose 30 ml; child's dose 15 ml.
If victim is unconscious, evacuate stomach by INTUBATION,
ASPIRATION and LAVAGE while observing precautions cited
in treatment of poisonings by CARBON DISULFIDE, paragraph
G. Follow by CATHARSIS as described in the same paragraph.
(Pg- 59)
6. The following measures apply to poisonings by NAPHTHALENE:
A. Careful OBSERVATION and tranquilization may be the only
necessary treatment of mild poisoning when no hemolytic reaction
occurs.
B. If naphthalene has been INGESTED, evacuate stomach by
INTUBATION, ASPIRATION, and LAVAGE, observing pre-
cautions cited in the treatment of poisonings by CARBON DISUL-
FIDE, paragraph G. Follow by CATHARSIS, as described in the
same paragraph. (Children's dosage of sodium sulfate is 0.2 gm per
kg body weight.) Do NOT give vegetable oils, which may accelerate
absorption of naphthalene.
C. For HEMOLYTIC REACTION, give intravenous INFUSIONS of
electrolytes and glucose to accelerate excretion of unconjugated
hemoglobin. Administer enough sodium bicarbonate to keep urine
mildly alkaline.
CAUTION: MONITOR fluid balance and urine sediment regular-
ly to forestall excessive hydration should anuria occur
from acute tubular necrosis. In this event, maintain
fluid and electrolyte balance by extracorporeal hemo-
dialysis.
Corticosteroids may limit the hemolytic reaction. Monitor serum
BILIRUBIN. Severe hyperbilirubinemia may have to be treated
62
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by exchange transfusion or hemodialysis. ANEMIA may require
multiple small TRANSFUSIONS of cells, preferably those not
deficient in glucose-6-phosphate dehydrogenase.
D. WARN sensitive individuals to avoid all future contact—domestic
and occupational—with naphthalene.
63
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PESTICIDES INDEX
T. *
Page
Aatrex ............................... 27
Acaraben ............................. 1
Acetamide based herbicides .............. 27
Acetanilide based herbicides .............. 27
Acme Weed Killer ...................... 40
Acquinite ............................ 48
Acritet ............................ 48, 54
Acrolein .............................. 54
Acrylaldehyde ......................... 54
Acrylofume ......................... 48, 54
Acrylonitrile .......................... 54
Af alon .................... ........... 27
alachlor .............................. 27
aldicarb .............................. 9
aldrin ................................ I
Aldrite ............................... 1
allidochlor ............................ 27
AMA ............................... 40
Ambox .............................. 21
Ametrex ............................. 27
ametryn ............................. 27
ammonium methane arsenate ............ 40
Anilide based herbicides ................ 27
Ansar 157 ............................ 40
Ansar 170 .......................... 40
Ansar 529 ............................ 40
Ansar 8100 ........................... 40
Anticoagulant Rodenticides .............. 35
Antrol Crabgrass Killer .................. 40
Aquacide ............................. 13
Aquakill .............................. 13
Aqualin .............................. 54
Aquatate ............................. 13
Aquatic Weed Killer .................... 13
Arasan ............................... 31
Areginal ............................. 54
Arsanilic Acid ......................... 40
Arsenical Pesticides ..................... 40
arsenic acid ........................... 40
arsenic trioxide ........................ 40
Arsine gas ............................ 40
As-655 Weed Killer ..................... 40
*Page number refers to chapter in which pesticide is covered
rather than the specific page number it appears on.
64
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Atlas A 40
Atranex 27
atraton 27
Atratone 27
atrazine 27
azinphos-methyl 4
Azodrin 4
Baygon 9
Baytex 4
benzene hexachloride 1
BHC 1
Bidrin 4
binapacryl 21
Biochecks 40
Black Leaf Grass Weed and Vegetation
Killer Spray 24
Bladafume 4
Bladex 27
Bo-Ana 4
Borea 27
Borocil IV 27
Borolin 27
Broadleaf Weed Killer 18
Broadside 40
bromacil 27
Bromofume 48
Brom-O-Gas 48
Bueno 40
Burpee Crabgrass Killer 40
Butoxone 18
Butyrac 18
Bux 9
cacodylic acid 40
Caid 35
Caparol 27
Carbanilate based herbicides 27
Carbamates 9
Carbacryl 48, 54
carbaryl 9
carbofuran 9
carbon bisulfide 54
65
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Carbon disulfide 54
carbon tetrachloride 48
carbophenothion 4
CDAA 27
Celmide 48
Certified Kiltrol-74 Weed Killer 24
C-4000 40
Chemonite 40
Chemox PE 21
Chickweed and Clover Killer 18
Chipco Crab Kleen 40
Chlordan 1
chlordane 1
chlorobenzilate 1
Chloroform 48
Chloro IPC 27
chlorophacinone 35
Chlorophenothane 1
Chlorophenoxy compounds 18
Chlor-O-Pic 48
chloropicrin 48
chlorpropham 27
chlorpyrifos 4
Ciba-Geigy Ontrack OS 3, 4 or 5 24
Ciodrin 4
CIPC 27
Clout 40
Copper acetoarsenite 40
copper arsenite 40
Co-Ral 4
coumafuryl 35
Coumarin 35
coumophos 4
Counter 4
Crabgrass Broadleaf Killer 40
Crabgrass Dallis Grass Killer 40
crotoxyphos 4
crufomate 4
cyanazine 27
Cyanide 54
Cyclon 54
Cygon 4
cyprazine 27
Cythion 4
66
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—D—
Dacamine 18
Daconate 40
Dalf 4
Dandelion Killer 18
Dasanit 4
D-Con 35
D-D 48
DDT 1
DDVP 4
Ded-Weed 18
Delnav 4
demeton 4
demeton-metnyl 4
desmetryn 27
Dessicant L-10 40
Dethmor 35
Dextrone X 13
diazinon 4
Dibrom 4
dichloropropane 48
dichloropropene 48
dichlorvos 4
dicofol 1
dicrotophos 4
dieldrin 1
Dieldrite 1
Di-Kill Vegetation Killer 13
Dimecron 4
dimethoate 4
Dimethyldithiocarbamate compounds 31
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 35
diphenadione 35
Dipterex 4
67
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Diquat 13
Di Sodium Methyl Arsonate 40
disulfoton 4
Disyston 4
Dithione 4
Diurex 27
diuron 27
D Krab R + Prills 40
DLP-787 44
DMA 40
DNAP 21
DNBP 21
DNC 21
DNOC 21
DNOCHP 21
DN-111 21
DN 289 21
Dowfume W-85 48
Dowicide-7 24
DPA 27
Drat 35
Drinox 1
DSMA 40
Dual Paraquat 13
Dursban 4
Dyfonate 4
Dylox 4
—E—
EDB 48
EDC 48
E Krab R 40
EM-7217 13
Endosan 21
endosulfan 1
endrin 1
Entex 4
EPN 4
epoxy propane 54
erbon 18
Esteron 18
Estone 18
ethylene dibromide 48
ethylene dichloride 48
Ethylene oxide 54
68
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ethyl formate 54
ETO 54
Evik 27
—F—
Famfos 4
famphur 4
Fenac 18
fensulfothion 4
fenthion 4
Ferbam 31
Fernasan 31
Fertilome Nutgrass and Weed Killer 40
fonofos 4
Formaldehyde 54
Formalin 54
forte 31
Fumarin 35
Fumigant-1 48
Furadan 9
Furloe 27
Gammexane 1
Gesafram 27
Gesagard 27
Gesamil 27
Gesapax 27
Gesaprim 27
Gesatop 27
Gordon Termi Tox 24
Gramonol 13
Gramoxone S 13
Greenfield Crabgrass and Dandelion Killer ... 40
Guthion 4
—H—
Heavy Duty Weed Control 13
HCH 1
heptachlor 1
Hexadrin 1
HOE 2810 27
hydrocyanic acid 54
Hydrogen cyanide 54
69
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Hyvar X ............................. 27
Hyvar X-L ........................... 27
—I—
Igran ................................ 27
Isocil ................................ 27
Isotox ............................... 1
Karmex .............................. 27
Kayafume ............................ 48
Kelthane ............................. 1
Kepone .............................. 1
Kill All .............................. 40
Kop-Fume ............................ 48
Korlan ............................... 4
Kuron ............................... 18
Kypfarin ............................. 35
Landrin 9
Lannate 9
Lasso 27
Lawn Weed Killer 40
Lincks Liquid Di-met 40
lindane 1
linuron 27
Liphadione 35
Lorox 27
—M—
MAA 40
Mad 40
malathion 4
Marlate 1
MCPA 18
MCPB 18
MCPP 18
Me Br 48
Mecoprop 18
Mesurol 9
metalkamate 9
Metallodimethyldithiocarbamates 31
Metasystox 4
70
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methamidophos 4
methane arsonic acid 40
methiocarb 9
Meth-O-Gas 48
methomyl 9
methoxychlor 1
methyl bromide 48
methylene chloride 47
methyl formate 54
methyl parathion 4
mevinphos 4
Microzul 35
Mildex 21
Milogard 27
mirex 1
Mocap 4
Monitor 4
monocrotophos 4
Mono Sodium Methyl Arsonate 40
Monurex 27
monuron 27
Morfamquat 13
Morfoxone 13
Morocide 21
MSMA 40
—N—
naled 4
Naphthalene 54
Neguvon 4
Nephis 48
Nitrophenolic Herbicides 21
Nomersan 31
Nudrin 9
Nutgrass Spray 40
Organochlorine Pesticides 1
Organophosphate Pesticides 4
Ortho Crabgrass Killer 40
Ortho Spot Weed and Grass Killer 13
Ortho Triox Liquid Vegetation Killer 24
Outfox 27
oxamyl 9
oxirane 54
71
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—p—
Paracide 48
Paradichlorobenzene 48
Paradow 48
Paraformaldehyde 54
Paraquat Cl 13
Parathion 4
Paris Green 39
Pax Total 40
PCP 24
PDB 48
Penchlorol 24
Penite 40
Pentachlorophenol 24
Pentacon 24
Penwar 24
Pestmaster 48
Pestmaster EDB-85 48
phorate 4
Phosdrin 4
phosphamidon 4
Phosphine 54
Phostoxin 54
Phytar 560 40
Pic-Clor 48
Picfume 48
picloram 27
pindone 35
Pivacin 35
Pival 35
Pivalyn 35
PMP 35
Pomasol 31
Pomasol Z forte 31
Potassium Arsenite 39
PP-745 13
Pramitol 27
Preeglone extra 13
Primatol A 27
Primatol P 27
Primatol Q 27
Primatol S 27
Princep 27
Profume 48
Prolin 35
prometon 27
prometone 27
72
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Prometrex 27
prometryn 27
Propachlor 27
Propanex 27
propanil 27
propazine 27
Propenal 54
propoxur 9
Propylene oxide 54
Proturf Monocot Weed Control 40
prussic acid 54
Purina Insect Oil Concentrate 24
Purina Top Grass and Weed Killer 40
—R—
Ramik 35
Ramrod 27
Ramucide 35
Randox 27
Raviac 35
Rax 35
Reglone 13
RH-787 44
ronnel 4
Rotomet 35
Ruelene 4
§
Sarclex 27
Scogal 27
Sears Liquid Crabgrass Killer 40
Selector #1 40
Semeron 27
Sevin 9
Shortstop E 27
Silvex 18
Silvisar 510 40
Simanex 27
simazine 27
Sinbar 27
Sinox 21
sodium arsenite 40
sodium cacodylate 40
sodium dimethyl arsinate 40
Sodium pentachlorophenate 24
73
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Soilbrom 48
Spectracide 4
Spot Grassy Weed Killer 40
Stam 27
Strobane 1
Strobane-T 1
sulfotepp 4
Sulfuryl fluoride 48
Super Crab E-Rad 40
Systemic Crabgrass and Broadleaf Killer 40
Systox 4
—T—
Telone 48
Telvar 27
Temik 9
TEPP 4
terbacil 27
terbutryn 27
terpenepolychlorinates 1
Tersan 31
Tetramethyl thiuram disulfide 31
Thimet 4
Thiodan 1
Thiophos 4
Thiotex 31
Thiram 31
Thiramad 31
Thirasan 31
Thylate 31
Tirampa 31
TMTDS 31
Topitox 35
Tordon 27
Toxakil 1
toxaphene 1
Triazine based herbicides 27
Tri-ban 35
Trichlor 48
trichlorfon 4
Trithion 4
TUADS 31
2,4-D 18
2-4-DB 18
2,4-DEP 18
2,4,5-T 18
74
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2,4,5-TP 18
—U—
Uracil based herbicides 27
Urea based herbicides 27
Urox HX or B 27
Usol Cabin Oil 24
—V—
Vacor® Rat Killer 44
valone 35
vapam 31
Vapona 4
Vegetation Killer 18
Vegetrole 13
Veg-I-Kill 24
Vikane 48
Vonduron 27
Vydate 9
—W—
warfarin 35
Warf-42 35
Warficide 35
Watrol 13
Weed-B-Gon 18
Weed-E-Rad 40
Weedestron 18
Weed-No-More 18
Weedol 13
Weedone 18, 24
Weed or Brush-Rhap 18
Weed-Out 18
white arsenic 40
Wood Preserver 24
Wood Tox 140 24
Zectran 9
Ziram 31
Zotox Crabgrass Killer 40
75
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