a training  manual for  health  personnel

A guide for recognizing, managing, preventing and verifying poisonings
caused by organophosphates, carbamates, and other selected pesticides
                                   John E. Davies, M.D., M.P.H.
                                   University of Miami School of Medicine
                                    U.S. Environmental Protection Agency
           U.S. DEPARTMENT                Office of Pesticide Programs
   of HEALTH, EDUCATION, and WELFARE             March 1977
                   The contents of this publication do not necessarily reflect the policies of the
                   Environmental Protection Agency, nor does mention of trade names or
                   commercial products constitute endorsement or recommendation for use.


Acknowledgments   	1
Introduction	2
Chapter I — Pesticides   	3
Chapter II'- Pesticide Hazards and How Exposure Occurs   	7
Chapter III — Systemic Organophosphate and Carbamate Poisoning  	12
Chapter IV - Miscellaneous Poisonings   	19
Chapter V - Topical Effects	23
Chapter VI - Pesticide Epidemiology   	25
Chapter VII - Methods of Prevention   	28
Chapter VIII — Acute Pesticide Poisoning Verification	30
   Appendix 1 Pesticide  List   	32
   Appendix 2 Toxicity   	39
   Appendix 3 Screening Test  	42
   Appendix 4 Laboratory Methods   	43
   Appendix 5 Chemtrec	45
   Appendix 6 Communications Check List  	48
   Appendix 7 Notification Locations	49
   Appendix 8 Reporting Form	51

   This manual was written by John E. Davies, M.D., M.P.H., University of Miami School of
Medicine, Miami, Florida. It was financed in part by a grant to the University of Miami from
the U.S. Environmental Protection Agency (EPA) and by funds from two EPA offices:

   •  Health Effects  Research Laboratory,  Environmental  Toxicology Division,  Research
     Triangle Park, North Carolina, William F. Duram, director, and
   •  Office  of  Pesticide  Programs,  Operations  Division,  Washington, D.C., William  C.
     Holmberg, director.

   Others who contributed to the project included:

   Paul Agnano, Office of Migrant Health, Department of Health, Education, and Welfare

   James Boland, EPA, Washington, D.C.

   Judy Botana, University of Miami School of Medicine

   Don Cook, EPA, Washington, D.C.

   Frank Davido, EPA, Washington, D.C.

   Erica Koehler, University of Miami School of Medicine

   Keith Maddy, California Department of Agriculture

   Joel Meltzner, EPA, Washington, D.C.

   Dorothy Nayer, Editorial Consultant, New York, N.Y.

   Billy Sandlin, Director,  Office of Migrant Health,  Department of Health, Education and

   Gerald T. Weekman, North Carolina State University

   The ed::o: *-*s M-iy Ann Wiraley.  EPA,  Washington,D.C. Dlusirations were done by Joan
 M. Davies. Miami, Florics.

   This manual  is for all  health personnel
involved in the prevention, recognition, and
treatment of pesticide poisoning. However,
the  information  should  be  of particular
interest to nurses1, especially those working
in rural  clinics, hospital emergency rooms,
and  departments of public health. They are
the personnel most intimately involved with
the care of patients suffering from pesticide
   Nurses are concerned not only with treat-
ment,  but  also  with prevention.  If they
understand the nature and use of pesticides,
they  can work  with their public  health
personnel and  community health  workers
toward the development  of safety measures.
They  can  contribute  to  improved  case
finding and the  followup of illness due  to
pesticide  exposure. They are   also ideally
suited  to educate agricultural  workers and -
their families.
   In the primary care setting, nurses in the
clinic are in a strategic position  to recognize
cases early and  to rapidly implement neces-
sary treatment  measures.  In this  situation,
therefore, they must know the signs and
symptoms  of pesticide poisoning,  and  the
emergency room measures which  save  lives
and decrease morbidity.
   In  the intensive care unit,  the nurse's
ability  to  recognize  the  reappearance  of
cholinesterase signs or to detect evidence of
atropine 'excesses   can  significantly   con-
tribute to the successful management of this
medical emergency.
   Ambulance attendants and  other health
personnel also need this information so they
can  begin the  rapid  treatment  which  is
necessary for lifesaving  before  the patient
arrives at the  hospital.
   There is an urgent need for accurate and
verified data  on acute pesticide poisonings.
Present  reporting  is  incomplete,  and the
potential of the laboratory to verify possible
pesticide illness  is poorly understood. This
book describes the steps necessary to con-
firm suspected pesticide illnesses.

   This book deals mainly with two major
types of pesticide illness:

   •  acute systemic poisoning

   •  topical  (local) effects

   Actual case examples  of pesticide poison-
ing are used to illustrate:

   •  the essential  diagnostic and manage-
      ment needs of the patient, and
   •  the potential  of  the  laboratory  in
      verifying the  event.
       is no intention by the author to stereotype
 by sex any health personnel or workers. To avoid a
 cumbersome text, the words "he" and "she" have
 been used interchangeably.

                                     CHAPTER I
What Are  Pesticides?

   Pesticides are a diverse group of chemicals
witSiSS've been developed to  kill, prevent,
or suppress a wide variety  of pests. Six of
the most common types are:
     insecticides (insects)
     herbicides (weeds)
     fungicides (fungi)
     molluscicides (snails and slugs)
     nematicides (nematodes)
     rodenticides (rodents).
Others include miticides (mites), defoliants
(remove unwanted plant growth), repellants
(keep pests away), attractants (lure pests),
and plant  growth regulators (stop, speed up,
or otherwise change normal plant processes).
   The essential component of a  pesticide is
the active ingredient.  This is the  material
that actually  controls  the pest. It is  pro-
duced in a manufacturing plant.
   Following manufacture, the active ingre-
dient  usually  goes to a formulating plant,
where it is mixed with other chemicals and a
carrier for effective delivery. These  are the
inert  ingredients.  They  may  include  such
materials as talcs, oils, kerosene, and  binding
agents (to increase adherence).
                                                    These formulated products  are  sold in
                                                 many forms, the most common of which are
                                                 liquids,  wettable  powders,  granules,  and
                                                 dusts.  Each  form  is  available  in  several
                                                    From the formulating plant, the products
                                                 move to a wide variety of users, including
                                                 farmers,  commercial pesticide  applicators,
                                                 and the general public.
                                                    Application is by various types of ground
                                                 equipment, hand equipment, or aircraft. It is
                                                 estimated  that  aircraft  supply about  65
                                                 percent  of all pesticides used by agriculture.


   More than 1 billion pounds of pesticides
are produced each year in the.United States.
Before any  pesticide product  can  be  sold,
the manufacturer must register it with the
Environmental  Protection  Agency  (EPA).
The  manufacturer  must  provide  EPA the
results of many kinds of tests on the product
before it can be registered.

   EPA  requires certain  information to be.
on  every pesticide  label.   Much  of  this
information  can be of help to health person-
nel in diagnosis and  treatment of pesticide
poisonings. When you know or suspect that
a pesticide is involved in an illness, try to get
the product  label or a copy of it as soon as
   Information which must be on a pesticide
label includes:
brand name
common  name  (simplified  chemical
.active   ingredients  (chemical  or
   common name, plus percent of the
   contents they make up)
inert  ingredients (need not be named,
   but label must tell what percent of
   contents they make up)
net contents
name and address of manufacturer
registration number (shows that the
   product  has  been registered  with
establishment  number  (identifies the
   factory which made the product)
signal words (one of the following)

Signal Wards
Highly toxic
Comparatively free
from danger
Approximate amount
needed to kill the
average person
a taste to a
a teaspoonful to a
an ounce to more
than a pint
All products must bear the statement
"Keep out of reach of children."
   • skull  and  crossbones  (must appear,
         with the  word  "poison",  on  all
         highly toxic materials)
   • ha/.ards  to  humans   and  animals
         (includes  ways  in  which   the
         product may be poisonous and pro-
         tective equipment needed)
   • environmental hazards
   • physical and chemical hazards (special
         fire,   chemical,   or  explosion
   • statement   of  practical  treatment
         (emergency first aid measures and
         information  for  physicians on  the
         treatment of poisoning)
   • statement  of  use  classification (tells
         whether the pesticide is restricted
         to use by certified applicators)
   • directions for use (may include reentry
         times, storage and disposal instruc-
       •  tions).

Chemical  Groups  and.
 Mode  of   Action
   Because  most pesticides  kill  unwanted
 organisms,   they   are   obviously   toxic
 materials. Their mode of action depends on
 the  chemical group to which they belong.
 The  five major chemical groups are:
     • organophosphates and carbamates
     • organochlorines
     • nitro and chloro phenols
     • "anticoagulants
     • bipyridyls.
   The  organophospliate  and   carbamate
group is the greatest public health problem.
It contains many widely used insecticides. In
the United States, severe  organophosphate
poisoning  results more  often'  from ethyl
parathion  and  phosdrin. Carbamates com-
monly  used include  carbaryl (Sevin), pro-
poxur (Baygon), and methomyl  (Lannate or
   Organophosphates  and carbamates inhibit
the enzyme cholinesterase (ChE).  This  in-
hibition causes a buildup of acetylcholine in
the  body.   Acetylcholine  is the  primary
chemical transmitter for:

   • the  preganglionic  neurons  of  the
     sympathetic   and  parasympathetic
   • the  postganglionic  parasympathetic
   • the central nervous system.

   These nerve fibers are called cholinergic
fibers. Anticholinesterase poisoning  causes
parasympathetic effects  in the organs they
supply. Some of these muscarinic effects are
shown in the following table.
Eyes • Pupil
Ciliary Muscle
Glands - Lacrimal
Heart • Muscle
Lungs - Bronchi
Intestines - Lumen
Bladder • Detrusor
Slow Rate
. Inhibition
Physical Findings
Blurred Vision
Increased Secretions
Increased Peristalsis
Increased Peristalsis
   Acetylcholine  is  also  secreted  at  the
skeletal nerve endings, where, in excess,' it
produces   weakness  and  paralysis.  These
neuromuscular effects  are  called nicotinic
effects. Acetylcholine is  also the chemical
mediator  between the  sympathetic  nerve
fibers  and  the  sweat  glands. This  is  the
reason for excessive  sweating in poisonings
with these cholinergic chemicals.
   Atropine  is  the  specific antidote  for
cholinergic  poisoning.. It  blocks  the effects
of acetylcholine. Atropine has no effect on
the neuromuscular nerve  endings, however.
Tliis is where the oxinie drugs are beneficial.
They break up the chemical binding between
the   pesticide   and  the   cholinesterase
enzymes.  This frees  cholinesterase  to  stop
the  acetylcholine  action  at  the   neuro-
muscular  junction and thus end the paralytic
effects. Oximes  are  contraindicated, how-
ever, in cases of carbamate poisoning.
   The effects of this group of chemicals are
both  systemic  and  topical. If  there  is  a
topical eye exposure, the effects are those of
topical effects of acetylcholine on the eye:

   •  the pupils are constricted
   •  the  ciliary  muscles  are  stimulated,
      causing blurring of vision and an eye-
      brow headache.
   The organochlorine pesticides are power-
 ful  nervous system  stimulators, but  their
 modes of action are not completely known.
 These chemicals are  soluble in fat,  accumu-
 late  in  the  human  body,  and  are  very
 persistent in the environment. Most uses of
 these  pesticides (such  as DDT, aldrin, diel-
 drin) are prohibited in the  United States, so
 acute  poisonings are  not frequent. Systemic
 poisonings  occur most often  with endrin,
 which is one of the most toxic members of
 this group.
    The nitro and chloro phenols are strong
 metabolic   stimulators  causing  increased
 metabolism and  hyperthermia. These are
 widely used as fungicides and herbicides.
    The anticoagulants are rodenticides, such
 as Warfarin. They produce their effects by
 inhibiting prothrombin and causing capillary
    The  bipyridyls   include   paraquat  and
 diquat,  which are widely used in agriculture
. for weed  control  and  defoliation. These
 chemicals produce proliferative changes irt a
 variety of tissues.

                                  CHAPTER  II
                       PESTICIDE HAZARDS AND
                       HOW  EXPOSURE OCCURS
Hazards of Pesticide  Use
   The hazard of a pesticide-its potential
for producing injury-depends on:
   •  the inherent toxicity  of  the active
     ingredient (see Appendix 2)
   •  the dose and/or  concentration of the
   •  the physical  and chemical properties
     of the material
   •  the route of absorption of the chem-
   •  the duration of exposure.
   The  dose  (amount) of  pesticide taken
into  the body is the most important factor
in determining the hazard of a chemical. A
small amount of some pesticides may cause
severe illness; large doses  of others may be
fairly harmless. Pesticide  concentrates  are
tlie most hazardous form. Persons  working
with them are at the greatest risk of getting a
harmful dose.
   The physical and chemical properties of
some pesticides make  them more hazardous
in certain situations. Parathion, for example,
changes to a more toxic chemical (paraoxon)
at high temperatures.
   The three  possible  routes  of absorption
   •  ingestion—the result of accidents or
     suicide  or homicide attempts; usually
     causes the most serious effects.
   •  inhalation—occurs mainly in  confined
     spaces (warehouses,  pesticide  tanks);
     usually causes less serious effects than
   •  dermal  absorption—most   common
     method  of  occupational  exposure;
     causes the least severe effects.
   The duration of exposure helps determine
the  dose  absorbed.  Brief  exposure to a
concentrate could produce effects similar to
longer exposure to the  dilute pesticide.

How  Exposure Occurs

   There is some degree of hazard at each
step  of pesticide  manufacture and  use.  Be-
cause they work with pesticide concentrates,
workers in  pesticide manufacturing  and for-
mulating plants are in positions with a high
potential hazard. Most  manufacturing plants,
however, use  a closed system which does not
expose the workers to the pesticide. Safe
occupational  practices and good  industrial
hygiene help to minimize the danger at both
these stages of pesticide production.
   Health  personnel are  most likely to en-
counter . pesticide  poisonings  in three main
groups of people:
   • applicators
   • pickers
   • children.
   Each is clinically different and  each must
be recognized at once.

   Applicator  Poisoning

   The hazard to applicators results from the
dilution  and application  of  the  pesticide
concentrate.  Hazards  exist,  therefore,  in
both mixing and applying the pesticide. The
toxicity  and  concentration   of  pesticides
varies  in  different  applicator   situations.
Every  applicator,  however,  is at  risk  of
exposure  to  varying  degrees of pesticide
concentrate,  and  therefore is in  danger  of
poisoning. The further down a person is in
the chain of pesticide  handling and use, the
less training he usually has and the greater is
his risk of poisoning.

   Workers associated with the aerial appli-
cation  of  pesticides  are especially highly
   It is unwise for a pilot to  mix and load
chemicals. The normal procedure is to em-
ploy aircraft loaders and swampers. They
dilute  the material  and load the aircraft
before each run. This is done on the airstrip
with fixed  wing  aircraft. Helicopters are
often loaded from an accompanying  trailer
at the scene of application. Loaders are one
of the most highly exposed  occupational
groups in the entire application process.
  An example of applicator poisoning
was Tony  B., who was employed as a
pesticide mixer and loader for a fixed-
wing crop  dusting firm. He had started
loading the aircraft at 6 a.m.  with a
mixture of parathion 6-3 and toxaphcne.
Rubber gloves were the only  protective
clothing  worn, and  fie  was a  heavy
smoker. .
  He soon began to feel unwell.  He was
admitted at 11:35 a.m. to the emergency
room of a  local hospital. He complained
of  nausea,  vomiting,  weakness,  and
blurring of vision. His pupils were con-
stricted and there was profuse perspira-
       A  screening cholinesterase  test re-
     vealed severe inhibition. After being put
     in a shower and scrubbed all over, he was
     given  a  total  of 12  mg of  atropine
     intravenously  in  the emergency  room
     over a brief period of time.  Tfie oxime
     2-PAM was also administered in a one
     gram  dose in 1,000 cc of D5W. Atropine
     therapy  was continued after his transfer
     to the medical ward and he proceeded to
     improve.over the next few days.
       Subsequent blood and urine metabo-
     lite studies by the laboratory confirmed
     that the poisoning was due  to an ex-
     posure to ethyl and methyl parathion.
       The special lessons of this case are:
       •  the illness was severe
       •  no protective clothing was worn
       •  there was no  positive  history of an
          accidental spill
       •  only one applicator was  affected.

       Picker Poisoning
       Once  a  pesticide has been  diluted to its
     final concentration and is applied  to  the
     crop, the pesticide residue remaining on  the
     fruit and leaves becomes a new source of
     exposure. The concentrations  of these resi-
     dues are high at first. They decline with time
     as a result of biodegradation and exposure to
     light.  The  rate of dissipation  of foliar resi-
     dues varies considerably with different pesti-
     cides and  with  different concentrations of
     pesticides.  Weather factors also affect  the
     rate of dissipation. Rain removes pesticides
     more  rapidly, and  high temperatures favor
     the changing of some  pesticides to more
     toxic forms.
• ^A^'- • j^V^i^ '•SSfe-K 1L->!>:
   Too  early  a reentry to a  treated  site
creates a hazard for the worker. The worker
is at risk during the process of thinning and
harvesting the crop.
   One  type of pesticide worker who is at
special  risk  of  intoxication   is  called  a
"scout." This  person  goes  into  the  fields
regularly to count the number of pests on
the plants. Since the job often involves going
into the field shortly after application, there
is a special risk of residue intoxication.
   This  type of human illness is sometimes
called "picker  poisoning."  It occurs  most
frequently with exposures  to  plants  with
large  leaf surfaces such as citrus, peaches,
grapes and tobacco.
   Cotton is a crop with a large leaf surface,
 but it is almost entirely machine-harvested in
 the United States, so that—except for scouts
 —residue  poisoning  is not  a  serious threat
 with  this  crop. This is not the case, however,
 for Central America, where hand  harvesting
 is still  practiced and hundreds of cases  of
 "picker poisoning" have been reported.
   Because pesticide poisoning from  residues
 may  be milder,  it may be overlooked in the
 health  clinic. Health personnel  should  take
 special  care  to  be on  the  lookout  for this
 syndrome with people  working  in  high-
 exposure  crops, especially when the  weather
 is hot.
   A nurse may be confronted by a picker
who was picking beans or citrus or working
in a field with high foliar crops and suddenly
became dizzy,  developed a headache, and
became progressively  weak. He  would pro-
bably complain  of sweating profusely. She
may soon  find  that other members of the
crew have  developed the  same symptoms
and are waiting outside  the  clinic  or have
gone to another doctor.
   The clue is that residue poisoning cases:
   • are usually multiple
   • are mild
   • require only  small doses of antidotes.
   The  following   outbreak   is  a   typical
     An emergency room nurse had three
   patients  with mild symptoms resembling
  •those  seen in organophosphate  poison-
     Three other patients were in the wait-
   ing  room with  similar symptoms, and
   four more were on  their  way  to  the
   hospital. • All were  weak,  sweating and
   complaining  of  abdominal  cramps,
   nausea,  and  vomiting.  Some  had  dif-
   ficulty   with  breathing.   Others had
   diarrhea  as  well as vomiting. Most  had
   miotic pupils.
     Bv the end  of the evening,  10 of a
   crew  of 17  migrant  workers who  had
   been detasseling corn  that morning had
   been  admitted  to  the  hospital.  They
   received  atropine intravenously and were
   beginning to  respond after decontamina-
   tion and intravenous fluids.

                     The epidemic was clearly  due to an
                  anticholinesterase  pesticide, a fact  that
                  was later  confirmed when 64 mg of a
                  carbamate insecticide called  methomyl
                  was identified from a methylene chloride
                  extraction from  the shirt  of  one of the
                  exposed victims.
                     At  7 a.m.  they had entered a cornfield
                  where an airplane had sprayed the field
                  with methomyl. Their clothes  and canvas
                  shoes  had become moistened from  the
                  dew on the ground and from the moisture
                  on the leaves.

                  Child Poisonings
                  Children are  the group at the greatest risk
                of  accidental  poisoning  from   pesticides
                which  have not been stored  or disposed of
                properly.  Prompt action  is  especially  im-
                portant in these poisonings.
                  The nurse must always be  on the lookout
                for  these  dire emergencies. In this  type of
                case, the nurse is usually confronted with  a
                very sick child who is semicomatose, vomit-
                ing  profusely, and has diarrhea and pinpoint
                pupils. For example:
                      A  4-1/2-year-old boy who was playing
                   in  his  grandfather's  barn  spilled  some
                   liquid over his pants  at about 1 p.m.
                    When he returned home at 6 p.m. he was
                   not feeling well and  he looked pale and
                   listless. He was put to bed. At 9 p.m., his
                   parents noted that  he was drowsy and
                    that  his respirations were  labored.  His
                   father rushed him from his home to  the
                    emergency room of a nearby hospital  His
                    mother checked his clothes and noticed
                    they had an insecticide smell. The grand:
                    father  checked  the  barn and found  a
                    bottle of ethyl parathion.
     By  the  time  the  boy  reached the
   emergency  room, he  was moribund,  in
   deep coma  with his eyes rolled back, and
   barely  breathing. His respirations soon
   ceased  and  he had to  be kept alive by
   artificial respiration and endotracheal in-
   tubation. When the mother reported that
   parathion had been spilled on the child,
   he was stripped, washed all over,  and
   oxygenated. Atropine was administered
   intravenously every  JO minutes through
   the night, and 2-PAM was given. By 5:30
   a.m.  he was  much  improved and con-
   tinued to recover over the next 2 days.
   Here, the point  is that exposure might
not be recognized. Children get extremely ill
very rapidly and treatment must be prompt
and vigorous.
   There is a high incidence  of  pica among
migrant families. This is a situation where
the  ingestion  of a  pesticide might not  be
realized. Geophagia is not uncommon.
     A 3-year-old child was taken to a local
   migrant clinic with extreme miosis, foam-
   ing  at  the  mouth and nose, and diffuse
   rales throughout both  lung fields.  An
   exposure history revealed that the child
   had  been playing in  a strawberry field
   which had been heavily treated within the
   last three days with phosdrin, Kelthane,
   and parathion. Pesticide analyses showed
   total inhibition  of cholinesterase. Para-
   thion was  identified  in the gastric  con-
   tent. It was later determined  that  the
   intoxication was the result of ingestion of
   soil containing parathion.

   This case  illustrates  the  point that chil-
dren eat dirt—which  is not commonly recog-
nized.  It exemplifies the real  possibility of
this mechanism of poisoning when a toddler
is playing in  the  fields where  the mother is

   Emergency Personnel
   In a rural area, the emergency personnel
in the ambulance can expect to encounter
anticholinesterase  poisonings.  Recognition
and early treatment  are of vital importance.
   A migrant worker might  fall off a ladder
while picking citrus  which had been treated
with parathion. His pesticide exposure might
not be recognized while the patient is being
transported to the hospital, particularly if he
appears  dazed.  The  diagnosis  may  be
clouded by other evidence of trauma which
he  may have sustained during his fall.  The
questions which should be asked are, "Why
did the worker fall?" and, "Was the fall due
to pesticides?"
   Pesticide  poisoning might  also  go  un-
 recognized in a  pilot who has had an aircraft
 accident. The possibility of injury is likely to
 be of greater concern  than the possibility of
 chemical intoxication  which may have been
 the  result  of a  spill before,  during,  or after
 the   accident.  It  is  essential  to  evaluate
 whether the pilot  has sustained a serious
 pesticide exposure. If the  exposure  is  al-
 lowed to  pass  unrecognized, it  could  cost
 him his life.
   Emergency  personnel   who  are  trans-
porting   suspected  cases   to  the  hospital
should always be in radio  contact with the
hospital. The patient's condition might sud-
denly deteriorate  in  transit,  requiring im-
mediate therapy. If the physician is alerted
ahead of time, he can communicate with the
emergency personnel  to prescribe whatever
is necessary.

                                                   CHAPTER III

Symptoms  and  Signs
   Symptoms and signs of systemic organo-
phosphate  and  carbamate  poisonings  are
almost entirely due to cholinergic manifesta-
tions. They include  both muscarinic and
nicotinic effects and are the result of acetyl-
choline accumulation.
   Early symptoms depend on the route of
absorption and the severity of the  intoxica-
   • Gastric symptoms appear earlier  if the
     material has been ingested.
   • Shortness of breath,  salivation, and
     excessive bronchial secretions occur if
     the material has been inhaled.
   • With dermal exposure, gastrointestinal
     and  respiratory symptoms appear at
     the same time.
   • In children, a convulsion  may be  the
     first symptom.
   • In  serious  intoxication,  both  mus-
     carinic and nicotinic  symptoms and
     signs begin shortly after exposure.
   Muscarinic effects^ which usually precede
nicotinic effects, include:
   • anorexia
   • nausea
   • vomiting
   • abdominal cramps
   • diarrhea
   • involuntary  defecation and  urination
   • sweating
   • salivation
   • lacrimation
   • pain in the chest
   • ' excessive bronchial secretions
   • blurring of vision due to miosis.
   Nicotinic effects include:
   • muscle twitching
   • fasciculations
   • weakness
   • flaccid paralysis.
   With  involvement of the muscles of  res-
piration,  further  respiratory failure occurs
from  bronchial  constriction, blockage  by
secretions, and depression of the respiratory
   Central nervous signs and symptoms in-
clude anxiety, restlessness, giddiness,  head-
ache, drowsiness, convulsions, and coma.
   In the advanced state, the patient is pale,
sweating, and  frothing  at  the mouth.  The
pupils usually are miotic and non-responsive
to light. Pupils will sometimes be dilated if
the patient is  in extremis.  They will then
become miotic with initial treatment.
   The. most important neurological findings
   • Fasciculations—localized and  general-
     ized  involuntary  twitching  may  be
     elicited  by tapping the muscles over
     the cheekbone, over the thorax, or on
     the arms.
   • Sometimes generalized clonic seizures
     may be  observed.  The plantar reflex is
     extensor and electroencephalographic
     changes may be noted.
   • Miosis—the pupil  is small,  usually less
     than 5 mm. The diameter of the pupil
     in millimeters should be recorded.
   Metabolic  signs and  symptoms include
the following:
   • Blood sugar may  be  elevated at first,
     and glycosuria may be observed. The
     level  of  hyperglycemia is much less
     than  levels  observed  with   diabetic
     coma. Ketoacidosis is not seen.
   • Serum electrolytes are usually normal,
     though hypokalemia may occur and be
     aggravated by diuretic therapy. Serum
     K levels should be checked early.
   • Fever is  not a constant finding. The
     patient's temperature usually  is normal
     or subnormal, though severe  dehydra-
     tion may occasionally cause fever.
   • Polymorphonuclear  leukocytosis  is

Clinical Diagnosis
   In  severe poisoning,  the initial  diagnosis
and  institution  of appropriate treatment
must  be made on clinical grounds alone,
since  there is  not  enough  time  to wait  for
confirmatory laboratory results.
   The most important factors in the clinical
diagnosis of organophosphate poisoning are:
   • a pesticide exposure history
   • symptoms  and  signs  typical of an
     anticholinesterase  illness
   • the presence of atropine refractoriness.

   Pesticide Exposure History
   The  first prerequisite to diagnosis  is to
determine  whether  the patient  has  been
exposed to any  of  the  anticholinesterase
pesticides.  Symptoms  begin  shortly  after
exposure.  They  are  seen especially  early
after ingestion or inhalation.
  " With  few  exceptions  the  patient  will
begin to feel ill within 1 5 minutes to an hour
after ingestion.
   If a patient has ingested a pesticide, this is
usually  known or admitted, except in the
case of a toddler. Ingestion of a pesticide as
a result of pica might not be realized.
   Dermal  exposure may be obvious and the
patient  may recall spilling the pesticide on
his skin and clothing. On the other hand, he
may  not  be  aware  that  pesticides  can be
absorbed in this way. He may not  mention
that his shirt,  pants,  or  shoes were wet from
the  pesticide   or  from moist residue  on
leaves. In arid areas,  dermal exposure occurs
from  dry,  dusty  residues  on the  leaves of
the  plant  and there  is   no  sensation of
wetness. In  all suspected cases,  however,
diagnosis is materially helped if the attend-
ing health personnel are made aware that the
patient has sustained a pesticide exposure.
Use the exposure history form in Appendix
   Symptoms  and Signs
   Symptoms  and  signs  compatible  with
cholinergic excess are the second most im-
portant variables contributing to the clinical
diagnosis of anticholinesterase poisoning.
   Although   symptoms   of  cholinergic
poisoning may be easily confused with those
of other  conditions, a pesticide cause should
always be considered. Physical signs are less
subject to misinterpretation. Miosis  is a rare
condition  in the  clinic setting. It should
always  lead  to first consideration of ex-
posure   to  anticholinesterase  pesticides.
Miosis is doubly  significant if it is accom-
panied by nicotinic and  muscarinic symp-
toms and muscle  fasciculations. These signs,
together with the general  appearance of the
patient,  should prompt the nurse  and the
physician io a diagnosis of organophosphate
   Atropine Refractoriness
   This is  the third important clinical  ob-
servation which  helps substantiate the diag-
nosis  of an anticholinesterase illness. When a
physician  prescribes a  larger than normal
dose of atropine in a person not exposed to
anticholinesterase pesticides,  the early signs
of atropine toxicity soon become apparent.
These signs include:
   •  dry mouth
   •  flushed skin
   •  increased heart rate
   •  dilated pupils.
   If   the   patient  has  anticholinesterase
poisoning,  large doses  of atropine are  re-
quired to produce these normal reactions.

Differential Diagnosis

   Mild anticholinesterase poisoning causes
such symptoms as:
   •  headache
   •  fatigue
   •  dizziness
   •  blurred vision
   •  excessive sweating
   •  nausea and vomiting
   •  stomach cramps
   •  diarrhea
   «  salivation.
   These  symptoms are  shared  by many
illnesses not related to  pesticides, such as
influenza,  heat stroke or heat exhaustion,
and gastroenteritis.
   Moderately severe  poisoning causes all of
the symptoms found  in  mild poisoning, but
in addition, the patient:
   •  is unable to walk
   •  often complains of chest discomfort
      and tightness
   •  exhibits marked miosis
   •  exhibits muscle twitching.
   These  symptoms  might  be reasonably
mistaken for such  conditions as pneumonia,
myocardial infarction, and encephalitis.
   Severe poisoning results in:
   •  unconsciousness
   •  local or generalized seizures
   •  the manifestation of a  florid choliner-
      gic crisis.
In  these  cases,  several  alternative causes
of coma enter into the differential diagnosis.

                 If there is glycosuria, diabetic coma might be
                 considered. The miosis might  lead to con-
                 sideration  of  a  cerebrovascular  accident.
                 particularly a pontine hemorrhage.          '
Screening Tests
   At  all  three levels of clinical  severity, a
screening  cholinesterase  test can help con-
firm a cholinergic poisoning diagnosis. These
are colorimetric procedures using filter paper
impregnated with a color reagent which is
sensitive to pH change. The time taken  for
the color  to change is a crude index of  the
degree  of  cholinesterase   inhibition. The
severity of inhibition is categorized as none,
suspicious, or severe.
   Although these tests have several limita-
tions,  they offer the most immediate con-
firmation  which is within  the  laboratory
expertise   in  any hospital or  clinic. The
Acholest  test  is the most reliable of  the
several available screening  methods   for
plasma cholinesterase determinations. It  can
detect inhibition as low as 20  percent of
plasma cholinesterase. The results correlate
well with  more quantitative procedures.
   The test should be administered:
   •  to  any patient who claims  to have
      been exposed to a pesticide
   •  to  any  worker  having regular  and
      heavy  pesticide  exposure,  such   as
      spraying  chemicals or loading aircraft
      (see Chanter VII-PREVENTION)
    •  to any patient complaining of three or
       more  of the  previously cited symp-
    •  to  any patient with any  one of  the
       following physical signs:
       —miosis  (less than 5 mm in  size)
       —muscle fasciculations
       —bronchial exudation
       -bradycardia  (pulse rate of 50 or  less
       per minute).
    To  prepare  a   blood  sample   for  the
 Acholest or other qualitative screening test,
 collect 1  cc of blood in a green stoppered
 vacutainer  tube (heparin-lined) and separate
 the plasma by  centrifugation.
    (See Appendix 3 for complete description
 of the test.)
    No further laboratory confirmation  is
 needed in the clinical setting.
   Definitive  verification and validation of
the poisoning episode, however, calls for:
   •  quantitative  measurements   of  the
     plasma and red  cell cholinesterase
   •  specific analysis of the intact pesticide
     and/or urinary pesticide metabolites to
     help  identify  the specific  offending

Laboratory  Diagnosis
   Three types of laboratory investigations
can  help  confirm a clinical diagnosis of
cholinergic poisoning:
   •  cholinesterase determination
   • ' urinary metabolite studies
   • intact pesticide studies.

   Cholinesterase  Determination
   The  levels  of cholinesterase  in the red
blood cells and in the  plasma are used to
confirm human poisoning.  They  correlate
well  with  nervous system cholinesterase in-
hibition. It is believed that ChE values of 0.5.
or less (Michel method) for either red blood
cell  or  plasma   represent   abnormal   de-
pressions for most individuals.
   The  four  laboratory  techniques  most
commonly used for quantitative expressions
of  these  enzyme activities  are   the  elec-
trometric  (Michel), the  titrimetric (pH stat),
the colorimetric (Ellman) and gas chromato-
graphic  (Cranmer) methods  (see  Appendix

   In two instances, laboratory tests  may
not   show   low  levels  of  cholinesterase
enzymes,  even though cholinergic  poisoning
is present. These are:
   • overexposure to carbamate pesticides—
      With this group of chemicals, cholin-
      esterase reactivation is rapid. In vitro
      reactivation often occurs before  the
      blood reaches  the laboratory. Normal
      red  cell  and  plasma  levels  may be
      reported  even  in  the presence  of ob-
      v'ous cholinergic illness.
   • reu  cell cholinesterase  determinations
      made after  the administration  of 2-
      PAM—if this oxime is given early in
      the  case,  red   cell  cholinesterase re-
      activates rapidly,  even  in the presence
      of continued cholinergic symptoms.

   Low  plasma cholinesterase levels  may
sometimes be due to other causes including:
   • liver  diseases,  malnutrition,  hyper-
     pyrexia,  myocardial infarction,  der-
   • after certain drugs
   • as  a result  of genetically determined
     low plasma cholinesterase.  This  con-
     dition  may lead to respiratory arrest
     after being anesthetized with succinyl-
     choline. The defect occurs in about 3
     percent  of  the population.  Recog-
     nition  of  this defect  is primarily  of
     medico-legal  importance.   Special
     laboratory  procedures  permit  dif-
     ferentiation   of pesticide   exposure
     from this  phenoty.pic mechanism.
   Low  red  blood  cell  cholinesterase   is
   • in paroxysmal hemoglobinuria
   • in  the  newborn  after  complicated
   • with disseminated sclerosis

   Urinary  Metabolite  Studies
   These breakdown products are  excellent
measures of exposure.  Qualitatively  they
often provide valuable information on the
exact type of pesticide which has caused the
illness. Quantitatively, their concentrations
in urine can be used as a measure of:
   • the severity of the poisoning
   • its probable duration.
The analysis of these breakdown  products,
therefore, is the second laboratory technique
which  will  assist in the confirmation of the
illness. (See Appendix 4)
   Intact Pesticide  Studies
   The identification of the intact pesticide
is the third way in which the laboratory can
confirm   an  anticholinesterase   pesticide
poisoning.  In  the  case of ingestion of the
material, the intact-pesticide can be identi-
fied by gas chromatographic studies of the
gastric contents.  In severe exposures, the
intact  pesticides may even be identified in
the blood and other tissues. (See Appendix
   Collecting Specimens
   Confirmatory  tests must  be done  by a
special pesticide analytical laboratory. When
confirmatory tests  are  required,  specimens
should be handled in specific ways:
   Blood-If the  Acholest test is positive,
collect  an  additional 8  cc   of  blood  for
definitive red blood cell and plasma cholin-
esterase   determination. A  10  ml  green
stoppered vacutainer  tube (heparin-lined) is
the  best  method of collection.  Invert the
tube gently once or twice to insure proper
mixing. Take care to  avoid hemolysis. Label
the tube to show:
   •  the name of the patient
   •  the time of collection
   •  whether a sample  was obtained before
      or after 2-PAM administration.
   Cover the label with transparent tape.
   Refrigerate  (do  not  freeze)   the  tube
before transferring it to  the  laboratory. If
the  specimen  must  be  sent to  another
laboratory,  it should  be airshipped. Pack it
with crushed ice in a styrofoam container.
   Urine and other tissues—In  cases  of sus-
pected   organophosphate  and  carbamate
poisonings, collect 20 ml of urine as soon as
possible. Place the urine in a hexane-washed
glass  bottle  with an aluminum  foil  lined
metal screw  top. The label should contain:
   •  patient identification
   •  the time and date of voiding.
   C'jvfT tie iabiJ vitb .V i-.wi^ir.v.v..' '.iC'j- m^
close the lid securely. Freeze the bottle and
its contents  and airship it with  the blood as
soon as possible.
   In special  circumstances,  other  tissues
may be  collected for laboratory analysis.
Handle them the same way as urine.
   Gastric contents-Gastric washings should
be labeled and  frozen before  sending to the
laboratory.  Collect  the  first  washing for
lexicological studies.

   The five  basic steps in emergency  treat-
ment are:
   • airway clearance
   • oxygenation
   • antidotal therapy
   • decontamination,  including  gastric
   • collection  of  appropriate  biological
   Time is of the utmost importance. The
prompt action required in a serious intoxica-
tion, particularly with a  child,  is similar to
that required by a  patient with ventricular
fibrillation with cardiac arrest.
   What a nurse  may or may not do in such
circumstances depends on:
   • her previous training and experience in
     the  necessary  resuscitative procedures
   • whether there is a written protocol.
   In both the  rural  health clinic  and  the
emergency room, standing orders should be
drawn  up ahead of time to cover pesticide
emergency   situations.  The   nurse    and
physician  should agree  on procedures in-
volved  in  all five of the steps of emergency

   Airway Clearance and
   Remove dentures and use  a finger  or,
preferably,  suction  to   clean  mucus  and
debris  from the mouth  and pharynx.  In-
troduce an orOpharyngeal or nasopharyngeal
airway, and  administer  50 percent  oxygen
by mask or nasal catheter. Draw serial blood
gases to monitor respiratory and metabolic

   Antidotal  Therapy
   Atropine-Atropine sulphate  is lifesaving
and should be given as soon as possible. It
should not  be  withheld  while  efforts  are
being  made  to overcome any  respiratory
   The nurse should  be  instructed  by pro-
tocol  to  administer  atropine  when  the
patient is  first seen. Under no circumstances
should such a patient be transferred to the
emergency room without having had atro-
.pine therapy.
   For an adult, the physician will order 2 to
4 mg of atropine sulphate intramuscularly or
intravenously every  10 minutes during the
early phase of treatment. Doses for children
should be proportionate to weight-0.05 mg
per kg of body weight.
   The pulse  rate, pupil size, and amount of
bronchial  exudate are  important  variables
which  influence the frequency of atropine
administration.  Large doses may be required.
In  a   severe  poisoning  case, a man  was
unconscious for 14 days and required atro-
pine continuously for  18 days. The thera-
peutic  goals  are  to  reach  and maintain
atropinization during the  period of poison-
ing. Dilation of the pupils and a pulse rate of
140  per  minute are  the  indications  that
atropinization has been reached.
   With certain types  of organophosphate
pesticides, the  intoxication  period  may  be
prolonged. The signs  of cholinesterase  in-
hibition reappear as  the effects of atropine
wear off.  These periods may be followed  by
periods of atropine excesses with the pulse
rate exceeding .140/min and  the pupils be-
coming fully dilated.  It  is thus very  im-
portant for the nurse to continuously moni-
   • the pulse rate
   • the degree of bronchial secretions
   • rate of respiration
   • changes in pupil size.
   This information helps the physician de-
cide  when it  is  necessary to readminister
atropine or when there are signs of atropine
toxicity.  As  recovery  occurs, the  intervals
between  atropine administration get longer
until there is no further  need to continue
this treatment. When no further treatment is
necessary, the patient should be observed in
the hospital for another 24 hours.
   Even if the  poisoning appears mild and
atropinization is reached after only  a single
dose, observe the patient for  24 hours. The
atropine may have produced only temporary
relief of symptoms in what may prove to  be
a serious case  of poisoning.
   Oxime-The  only  oxime available in  the
United  States   is   N-Methyl  2   formyl-
pyridinium oxime, used as the chloride  (2
PAM-C1) or Protopam Chloride. This should
be available in any  health clinic or emer-
gency room likely to have to  treat choliner-
gic poisonings.  Give  2-PAM as early  as
possible and  always  in conjunction with
atropine. The two drugs are complementary
in their action.

   The oximes are not recommended for use
in  cases  of carbamate  poisoning—in  fact,
they are contraindicated—but more research
is  needed  in  this  area.  Therefore,  the
physician  faces a dilemma when  it is not
known  whether  the  poisoning has  been
caused by  an  organophosphate or a  car-
bamate. Make every possible effort immedi-
ately  to  find  out the  specific  pesticide
   The oximes are not active against all of
the organophosphates. Depending  upon the
particular  organophosphate, "aging" of the
phosphorylated enzyme  occurs,  at  which
time the inhibited enzyme can no  longer be
reactivated by 2-PAM.
   With parathion, aging does not  occur for
2  days  after exposure,  so 2-PAM may be
used up to that time. With malathion, aging
is  early.  Effects of oxime therapy in this
intoxication are generally disappointing.
   The usual adult  dose is  1 gm intraven-
ously, preferably as an infusion in 250 ml of
saline given  over 30 minutes. If this is not
practicable,  give  it in  not less  than  2
minutes. A second dose of 1 gm can be given
in 1  hour. In children, 20 to 50  mg per kg is
given intravenously in  250 ml of saline over
30 minutes.
   If convulsions  are   troublesome,  tri-
methadione  or thiopental may be used. Res-
piratory embarrassment is usually  due to
excessive  bronchial secretions  rather than
pulmonary edema. For this reason, opiates,
aminophylline,  reserpine,  phenothiazine,
tranquilizers,   succinylcholine,   and
furosemide are contraindicated.

   The first step  should be to  remove the
patient  from further  exposure. Bring him
out  of the exposure area and  try to limit
further absorption of the pesticide.
   The attendant should  strip  the  patient
and  place  all clothing in a plastic bag. The
patient must be thoroughly washed. If he is
conscious, place him in a  shower  and wash
him  all over with large amounts of soap and
water.  Be  sure to rinse  the hair thoroughly
and  remove  any residue  from under the
   Decontamination  also  includes  the  re-
moval  of  the ingested pesticide.  Vomiting
should not be induced:
  •  in stuporous or unconscious patients,
  •  if petroleum distillates .are part of the
     pesticide formulation.
  In  these instances, or if there is doubt
about  what  pesticide  is involved,  gastric
lavage is preferable to the use of an emetic.
Place the patient head down and on his side
to avoid aspiration of vomitus. V/ash out the
stomach with large amounts of water.
  The use  of an esophageal obturator is the
best  way  to avoid  aspiration of stomach
contents,  if  the  nurse has  had previous
training in inserting the obturator.

  Collection of Biological Materials
  (See instructions  in  previous  section,
"Laboratory Diagnosis.")

Carbamate Poisoning
  Carbamate pesticides, like the organo-
phosphates, are powerful cholinesterase in-
hibitors.  Special  considerations  in   the
diagnosis   and   treatment   of  carbamate
poisonings include the following:
  •  Cholinesterase reactivates rapidly after
     carbamate  poisoning.  Laboratory
     cholinesterase determination tests may
     be misleading.
  •  Since blood tests may not be reliable,
     identification  of the nonhalogenated
     phenols-the  urinary  metabolites  of
     carbamates-becomes more significant.
  •  The oxime 2-PAM should not be used
     to treat carbamate intoxications.
   A systemic pesticide poisoning involves a
wide variety  of health professionals. Good
communication among these professionals is
   If  the clinic nurse is the  first point of
patient contact,  she  should contact the -
attending physician as soon  as possible, as
well  as the  patient's next of kin and his
   If the physician  is not immediately  avail-
able,  the nurse will have to communicate
with an ambulance service  and the  nearest
hospital emergency room to  arrange for the
transfer of the patient. Meanwhile, she must
begin emergency treatment to stabilize the
patient's condition.
   If there  is an epidemic of poisonings, the

health department must be informed. These
are usually "picker poisoning" incidents. If
there is  a  massive  chemical  spill  with  a
potential  community  hazard,  the  nurse
should communicate  with CHEMTREC (See
Appendix 5).
   If a sick child has been brought in from
the home and the source of the pesticide has
not   been  identified or  removed, other
children  in the home may be at immediate
risk  of  poisoning.  The  police should  be
contacted. The nurse  should also contact the
regional  pesticide analytical  laboratory for
poisoning verification.
  The  implementation  of   these  com-
munication needs are best insured by work-
ing  through  a  checklist of  persons  who
should be contacted.  This  is  shown  in
Appendix 6.

                               f*£*fst~l~'tX~'5$^ S* '-fJf> .
   If  the  patient comes  straight from  the
field  or   the  home  to  the  hospital,  the
emergency room nurse  is primarily  con-
cerned with reporting significant changes in
her patient's  condition  to  the  attending
physician. She should contact the immediate
family, employer, police, or health depart-
ment if this has not already been done.
   EMT  personnel should  be in  constant
radio  contact with  the  emergency  room
while  transporting the  poisoned patient to
the  hospital.  If the   patient  suddenly
collapses, the attendant can apply the appro-
priate treatment while in transit.
   The public health  nurse  or  the com-
munity health worker will encounter special
risk factors when investigating the scene of
the accident.  These must be reported to the
employer  or landowner and local health and
environmental resources   so  that  further
poisonings can be prevented.

                                        CHAPTER IV
                       MISCELLANEOUS   POISONINGS
Orgahochlorine Insecticides

  These pesticides:
  • are soluble in fat
  • build up in the human body
  • are persistent (break down slowly and
     remain unchanged in the environment
     for a long time)
  • are  powerful  nervous system stimu-
     lators.  Organochlorine  poisoning
     causes excitation.  Convulsions are the
     most important symptom.
  Applicator  poisonings  and  residue  in-
toxication are not common with these  pesti-
cides, since most of their uses are prohibited.
Most  systemic poisonings are caused  by
accidental oral ingestion of endrin.
  Acute  poisonings may be caused by the
organochlorine  pesticides  which  are  no
longer sold but still remain in some homes.
     A. 2-year-old boy  was brought to the
  emergency room  of a local hospital. On
  arrival,  he had a  convulsive seizure. The
  parents reported  that the- child had in-
  gested  an unknown  amount  of an  in-
  secticide.  The  child was  hyperactive,
  atoxic, and unsteady. He fell down  when
  he tried to walk.  Pupils were 2 to 3 mm
  in size.  There was no vomiting, sweating,
  or  increased  bronchial  secretions.   The
  chest was clear. He was given diphenylhy-
  dantoin  and a  large intravenous dose of
  phenobarbitaL  He was admitted to the
  Pediatric Intensive Care Unit for observa-
  tion. Both heparinized and whole blood
  were collected.  By the Michel method the
  RBC ChE  was  0.69 &ph/hr,  and the
  plasma  ChE was  0.90 Aph/hr which are
  normal enzyme levels with  this  method.
  Blood tests for intact pesticide, however,
  identified dieldrin in a concentration of
  407 ppb.  This  confirmed an organo-
  chlorine  pesticide  poisoning   due  to
  Nursing care for organochlorine poisoning
is the  same as  that  for  other  convulsive
disorders.  There  are no  specific antidotes.
Sodium   phenobarbital   and  diphenylhy-
dantoin  are the  drugs  most often used to
control   the  convulsive  seizures.   Tri-
methadione or thiopental may also be  used.
   Diagnosis  can  be confirmed  by identi-
fying the intact pesticide in the serum. In a
case of suspected organochlorine pesticide
poisoning, draw  10 cc  into a red stoppered
vacutainer tube. Label the sample and allow
it  to clot. Separate the serum and freeze it.
If the specimen  must be sent to another
laboratory, it should be airshipped. Pack it
with crushed ice in a styrofoam container.
   Dieldrin seldom causes convulsions when
blood  levels  are  less than 200 ppb.  With
blood levels greater than 200 ppb, convulsive
seizures may  be seen. The worker should be
taken  off his  work  with  levels  of  this

   Paraquat  is more toxic than diquat. and
produces proliferative  changes in the  lung,
cornea, lens,  nasal mucosa, skin, and finger-
nails. Diquat affects the  lens  and gastro-
intestinal  mucosa. It does not produce the
lung changes characteristic of paraquat.
   Except  for  eye  lesion,  illness  due   to
occupational  exposure is usually  mild and is
the  result of topical  exposure.  Epistaxis
occurs in  workers following droplet inhala-
tion. Conjunctival  changes  occur  with  ac-
cidental spills.
   The  clinical picture following accidental
or suicidal ingestion is very different. Para-
quat  ingestions  are  frequently fatal.  Their
management  is  unsatisfactory and largely
symptomatic. Three clinical  stages follow
ingestion of as little as an ounce of paraquat:
   •  The  first  is  a gastrointestinal phase
      with burning in the mouth and throat,
      nausea, vomiting, and abdominal pain
      with diarrhea.
   •  Several days  after exposure, signs  of
      hepatic  and renal  toxicity  appear.
      These are due to central zone necrosis
      in the liver and acute tubular necrosis
      of the kidney.
   •  Ten to 20 days  after ingestion, pro-
      gressive proliferative  changes develop
      in the  lungs. Hyperplastic changes in
      the  terminal bronchioles  occur with
      alveolar fibroblastic proliferation. Loss
      of lung surfactant  has  been demon-

       strated. Within a few days, death from
       respiratory failure occurs.
    Urine  studies   have  indicated  that  90
 percent of the ingested paraquat is excreted
 in the first 24 hours. Delayed  pulmonary
 effects appear to be the result of an irrever-
 sible  process  that develops long after  the
 initial stimuli has gone.
    Paraquat is poorly absorbed from the gut.
 Excretion data suggest that only 1  to 5
 percent of the ingested material is absorbed
 in man.  Maximal  blood concentrations  are
 reached within 4 to 6 hours after ingestion.
 Treatment, therefore, is primarily concerned
    •  decreasing  the  amount  of paraquat
    •  perfusion of  the  circulating  blood
       through charcoal columns.
    Steps  to  decrease  the  amount  of  the
 paraquat absorbed include:
    • gastric lavage with every precaution to
      avoid aspiration of gastric contents
    • repeated  administration  of   large
      amounts of adsorbents together with
      the administration of purgatives.
   The  ability  of  Bentonite, Fuller's earth
and other clays  to absorb  bipyridyls has
been  studied.  Fuller's earth was more  ef-
fective  than  Bentonite.  500  ml. of  a  30
percent suspension of Fuller's earth together
with 5 percent magnesium sulphate should
be administered after lavage,
   Perfusion of the blood through charcoal
columns has been advocated.2 In addition to
hemoperfusion,   forced   diuresis  with
Mannitol, hemodialysis,  and corticosteroid
and  immunosuppresant therapy  have  also
been recommended.•*
   Although steroids and alkaloids are given
for pulmonary complications,  no treatment
has shown to be effective at this stage of the
   There is a simple urine test for paraquat
that can  provide presumptive evidence  of
paraquat poisonings in  suspected cases ex-
hibiting early symptomatology.4
                 2Smith, L.L., Wright, A., Wyatt,  I., Rose, M.S.
                  Brit. Med. J. 1974, (4):569.
                 3The Lancet  Editorial, 1976, (1):1057.
                 4Goulding, R., Volans, G.N., Crome, P., Widdop,
                  B.Brit. Med. J.  1976, (1):42.
    These are not particularly hazardous, but
 they are widely  used.  Children  often ac-
 cidentally ingest rodent tablets or baits-an
 event which leads to much anxiety,  ques-
 tions, and the need for reassurance.

    Fumigants  can  present  serious health
 hazards resulting  in human  illnesses  and,
 occasionally,   death.   Methyl  bromide,
 acrylonitrile,  calcium  cyanide,  and carbon
 tetrachloride are the fumigants most likely
 to  cause  death  if overexposure  occurs.
 Others  which can cause skin and eye injury
 and systemic illness include:
    • sulfuryl fluoride (Vikane)
    • 1,3 dichloropropene (Telone)
    • 1,2   dibromo    3   chloropropane
    • ethylene dibromide
    • formaldehyde
   • chloropicrin
   •  phosphine
   •  sodium  .methyl  dithiocarbamate
    Methyl bromide is sold as a liquid under
 pressure.   At  atmospheric'   pressure,  it
 vaporizes at 40°F to a colorless and odorless
 gas.  Because  of  this  property,  methyl
 bromide should always  be used in formula-
 tions which contain chloropicrin (tear gas),
 which serves as a warning agent. A  worker
 who is  exposed to enough of this mixture to
 cause  tearing  has  also  been  exposed to
 dangerous quantities of methyl bromide.
    Methyl bromide is absorbed through the
 lungs, skin, and mucous membranes. It can
    • acute  poisoning,  either  topical  or
      systemic, and
   • chronic effects.

    Acute Poisoning
 " Topical  effects-Skin  contact  with  the
 liquid or  high  concentrations of the vapor
 produces itching  and prickling  of  the skin.
 This is followed by reddening and formation
 of vesicles and slow-healing blisters. Getting
 the  liquid  in  the eyes  may cause corneal
   Systemic  poisoning-Symptoms  usually
develop 3 to 12 hours after inhalation of the
vapor.   Early  symptoms include  nausea,
vomiting,  dizziness,  headache,  blurring of

vision, and changing taste of food. These are
followed by listlessness, weakness, staggering
gait, and slurring of speech. In addition, the
patient may complain of double vision and
even temporary blindness.
   In severe poisoning, the victim becomes
comatose and has  a high fever and respira-
tory embarrassment.  Death is usually  the
result of either respiratory failure or cardio-
vascular  collapse.   Death  is  preceded  by
cyanosis,   pulmonary  edema,  and  renal
failure. Muscle'twitching and convulsion are
not uncommon.

   Chronic  Effects
   A papular  pustular rash, not unlike acne,
may develop on the  face, arms,  back, and
chest. This is  the  result of repeated dermal
exposures. All the  symptoms and signs listed
under  acute  effects may  also appear as  a
result of chronic exposure. Fatigability and
loss  of  appetite  are  frequent complaints.
More severe chronic manifestations include a
change  of personality, a chronic central
nervous system effect which may persist for
years.  Visual  disturbances  and locomotor
impairment are common.

   First, quickly get the  patient out of the
contaminated  atmosphere  and  remove  all
contaminated clothing. Methyl bromide can
penetrate  rubber  gloves.  Wash skin  burns
carefully  withvwater. Administer a  thera-
peutic trial with dimercaprol (BAL). If there
is severe respiratory depression, give oxygen
under positive pressure. Artificial respiration
may be  necessary. Keep  the  patient  under
observation  for  at   least  48 hours after
symptoms have subsided.
   No simple  laboratory  tests are available
for  confirmation, but   blood  levels  of
bromine correlate  well with the severity of
the exposure.

   Methyl  bromide mus't be  applied by  a
closed-delivery system. All  State and local
requirements concerning  the  use of plastic
sheets  or tarpaulins  must  be  followed.
Guards  and warning signs  should be posted.
The application should be  done at a safe
distance   from  inhabited  structures,  and
under   appropriate  weather  conditions.
Animals and humans must be removed from
the area to be treated.
   Methyl bromide must be kept under lock
except when the applicator or other respon-
sible  persons   are  present.  The  material
should  be stored  in  a  cool,  dry,  well-.
ventilated building in order  to avoid  an
explosion hazard and the possible buildup of
toxic  concentrations  of  vapors  caused  by
leaking containers. The storage sites should
be at a safe distance  from populated areas
and inhabited buildings.

Dinitrqphenol and
   These  materials  are used as insecticide
sprays, fungicides, and wood preservatives.
They  are rapidly  absorbed by  the gastro-
intestinal and respiratory tracts and the skin.
They  are profound stimulators,  stimulating
all  the  cells   of  the body  by  blocking
oxidative  phosphorylation. Body fat  is  the
major, if not  exclusive,  fuel for this extra
metabolism.5  The  body temperature  be-
comes elevated and the breathing and heart
rate  increase  rapidly.  Because  respiratory
and cardiac stimulation do not accelerate in
proportion  to the  increased metabolism,
anoxia and acidosis develop rapidly.

   Acute and  Subacute Poisoning
   The patient complains  of marked fatiga-
bility, excessive thirst, and profuse sweating.
His face  is flushed. These are  the result of
the higher metabolic state,  as  is  the  ex-
ceptionally high  fever,  which  may  reach
110°F.  The   higher the  fever,  the  more
serious is the intoxication.
   In  such  cases, tachycardia,  hyperpnea,
cyanosis,  and  muscle  cramps  will  occur.
Death, which is usually the result of respira-
tory or circulatory collapse, occurs within
24 hours.
   In  mild or  subacute cases, most  workers
will complain of  lassitude, headache, and
malaise. Some, however, may have an alarm-
ing sense of  excessive  energy,  drive, and
hyperactivity.  They should be warned of the
dangers of overheating, because  the  meta-
bolic  activities  of these  compounds  are
exaggerated by heat.
 5Shils, M.E. and Gpldwater, L.I. Effect of diet on
  the susceptibility of the rat to poisoning by 2,4-
  dinitrotoluene. Arch Environ Health 8:262, 1953.

                  The essential goals of treatment are:
                  •  prompt elimination  of the  material
                     and curtailment of all possible further
                     sources of exposure,
                  •  symptomatic  treatment  designed  to
                     control the  high fever and  its second-
                     ary  consequences,  such  as   anoxia,
                     dehydration, and acidosis.
                  Gastric  lavage with  large  amounts  of
                sodium bicarbonate  solution should be fol-
                lowed by saline  catharsis  using 15 to  30
                grams of sodium  or magnesium sulphate in
                water. To control the fever, use  cold packs
                and alcohol sponges. Cold water enemas may
                be needed.
                  Supportive measures include:
                  •  intravenous  fluids to control dehydra-
                     tion and acidosis,
                  •  oxygen and artificial respiration  as
                Following the acute phase  of the intoxica-
                tion,  liver  and   renal complications  may
                develop.  These are  the  result  of the  toxic
                action of these materials on the renal tubules
                and on the liver cells.
                   Laboratory Confirmation
                   Laboratory confirmation of the intoxica-
                tion is provided  by the  detection  of high
                levels of dinitrophenols or pentachlorophe-
                nol in the urine and blood of the victim.

                                       CHAPTER V
                                 TOPICAL  EFFECTS
 Skin   Problems   Among
 Agricultural Workers

   Skin  problems  accounted for 62 percent
of all occupational diseases reported in the
United  States  in  1973.  The  agricultural
worker who is exposed to pesticides is four
times more likely to develop a skin rash than
the average industrial worker.
   Because  the agricultural worker is  ex-
 posed to a wide variety of agents besides
 pesticides,  determining the cause  of  der-
 matitis is highly complex.
   Dermatitis   from pesticides  can result
   •  exposure to primary irritants, or
   •  contact  with contact  sensitizers (aller-
   The first  diagnostic consideration is to
 differentiate  between  these two  types of
 skin rash.
   Primary  Irritants-Primary  irritants  are
 either absolute or relative.
   Absolute 'irritants  are usually chemicals
 which can cause  a  chemical burn  or severe
 irritation on   almost  anyone's skin.  The
 reaction occurs immediately  or within an
 hour or so.  It usually does not present a
 diagnostic problem.
   Relative  irritants are agents which  can
 cause varying degrees  of dermatitis (inflam-
 mation  of the skin) according to environ-
mental conditions. Some, like kerosene or
turpentine, are more likely to cause pro-
blems on sweating skin, or under occlusive
clothing and boots. All are more  damaging
to skin which is already abnormal (sunburn,
eczema, and atopic dermatitis).
   Some  areas of the body are  more  sus-
ceptible than others. The  genitalia, scrotum,
and eyelids are particularly vulnerable. Thus,
a worker might have dermatitis on the penis
and  eyelids due to contamination by  ma-
terials on the hands.
   The primary  irritants  usually produce a
 short term dermatitis which goes away and
 can  be related to a known definite exposure.
   The rash caused  by primary  irritants is
 more likely to be confined to the areas of
 the  skin actually exposed to the chemical.
 Irritants in solution often are confined to
 the  hands and  the  forearms, but  relative
 irritants may  be  absorbed in  clothing and
 boots. The  rash  will  appear  where the
 clothing is in closest contact with the skin-
 buttocks,  knees, and dorsum of the feet..
   Irritants dispersed in  sprays or aerosols
 more  often   affect  the face  and  neck.
 Powders tend to accumulate at the waistline,
 the collar, and tops of boots.
   A primary irritant is likely to be the cause
 if several  workers  experience a  rash  on
 exposed surfaces at the same time, especially
 if burning or  itching   occurs soon  after
 exposure.  It is useful to ask the patient if he
 knows whether  any  other workers  in the
 same area have the same problem.
   When multiple cases of dermatitis follow
 the  application of an agricultural chemical,
 the  material  or  its  carrier is clearly too
 irritating   for continued use. The  nurse
 should  notify the  physician as  soon as
   Treatment—When the  person is removed
 from further  exposure,  this type  of der-
 matitis  usually  clears up, especially  if a
 topical  steroid  cream  is  applied  to the
 affected areas.  '

    Contact   Sensitizers—Substances  which
 cause allergic contact dermatitis may affect
 only  a few individuals who have  become
 "sensitized" or "allergic" to the  material.
 Even then, there may be marked differences
 between individuals in the degree of cutane-
 ous  reaction or  seventy  of  the  clinical
   A  new  product occasionally  has a  high
 potential  for producing allergic skin condi-
 tions. These usually are soon recognized and
 taken off the market, but it is still worth-
 while to ask whether a new product has been
 used. First reports of a hazardous substance
 often come  from nurses or other medical
 personnel who  are  closest  to  actual  field
   Depending on the patient's sensitization,
the reaction  may occur within a few hours
of contact to as long as a week. Most occur
within 48 hours. Redness, itching, swelling
(especially  around  the eyes), and  "water
blisters" are  the  clues  to  this  type of
   Having a  basic knowledge of the principal
sensitizers,  reading the ingredients  on the
labels,   or  checking  the  Physicians'  Desk
Reference will often help  in diagnosis. Plant
 dermatitis  is common and  must  be  con-
sidered  as a cause  of allergic contact  der-
   Some chemicals  may  be both  primary
irritants and  contact sensitizers.  In addition,
many agricultural compounds are dissolved
in solvents such as kerosene or xylene.  This
creates  a  perfect mechanism for  both pri-
mary  skin damage and an allergic reaction.
   Treatment—The treatment of allergic con-
tact dermatitis includes:
   •  using cool compresses
   •  treating infections
   •  identifying the offending agent.
It may be necessary to refer  the patient to a
facility which performs patch testing.
   Topical steroid creams, gels, or lotions are
beneficial.  Severe or  extensive  cases  may
require  a short course of systemic steroids.
Systemic steroid therapy should always be
 under the direction of a physician. It should
never be given  to  patients who may have
undetected  tuberculosis  or  are  at  risk of
   Apart from the highly  specialized area of
 patch testing, the laboratory has no place in
the verification of topical skin effects from
   The  illnesses   are  often  a  sensitivity
phenomenon and are therefore  not strictly
dose related. Cholinesterase determinations
and urinary metabolite studies are not neces-
 Effects of Pesticides
 on  the  Eyes
    Eye injuries are common  in agricultural
 workers.  Topical effects can occur as the
 result of exposure to any of the pesticides in
 common  use today. In addition, xylene and
 petroleum  distillates  in  common  use as
 pesticide   carriers  are  very  irritating  ma-
 terials. They produce a severe inflammatory
 response when they get into the eyes.
    Eye injuries can result from:
    •  accidentally  splashing  or spilling the
      material into the eye
    •  exposure to pesticide drift
    •  rubbing  the  eyes with contaminated
    Sulphur, paraquat, Omite, parathion, and
 dieldrin  are  some  of  the   most  common
 causes of eye injuries.
    Eye injuries are most common in pesti-
 cide mixers, loaders, and applicators because
 of their  risk of exposure to the  pesticide
    Damage is the result of:
    •   a direct  irritating  effect of the chemi-
      cal or the vehicle
    •  an allergic reaction
    •   direct phamiacologic   action  on the
       eye,  as  is the  case  with anticholin-
      esterase pesticides.
    Conjunctivitis, corneal ulceration, uveitis
 and lenticular opacities are some  of the
 lesions which occur. These chemicals have a
 delayed effect  on visual accommodation and
 diminish the peripheral fields of vision.
    If  there is a  conjunctival infection, ir-
 rigate the eyes from the  inside to the outside
 with   large  amounts  of  water  or  sterile
 normal saline solution.  After the eyes have
 been  thoroughly irrigated,  evert  first the
 upper and then the lower lid and clean them
 with   a  moist cotton  tip to  remove  any
 debris. Then irrigate  the eyes once  more.
 Apply  an  eye  shield and make an appoint-
 ment  for  the  patient to see the  attending
 physician for definitive diagnosis and treat-

                                  CHAPTER VI
                       PESTICIDE EPIDEMIOLOGY
  The possible effects of pesticide exposure
can be divided into three categories:
  •  acute exposure, which produces acute
     poisoning and topical injuries
   • chronic high exposure, which  is con-
      cerned with long term effects of pesti-
   • chronic low exposure or  incidental
     exposure,   which is concerned  with
     human pesticide residue and the pub-
     lic's concern for  the possible risks of
   Those at risk in the first category are:
   • pesticide workers
   • members  of the general public who
     become accidentally poisoned in the
     home or garden.
   In the second  category is  the occupa-
tionally exposed worker.  The third category
includes the general public, who are exposed
to small amounts of pesticides in water, air,
food, and clothing.   (.
   The nurse is primarily concerned with the
first and second  categories.  She  is most
likely to encounter acute pesticide poisoning
in  the  clinic  and  hospital.  She  has  an
important role in preventing both acute and
unnecessary chronic exposure to the workers
in the second category.
   As  an individual  she is  probably  also
concerned with the third level of exposure
for her own and her community's sake.

  Acute Poisonings
    Acute pesticide  poisonings are a serious
  health  problem in many areas of the world.
  The  World   Health Organization estimates
  that there are approximately 500,000 cases
  annually, with about  a  1  percent fatality
    No accurate statistics exist for the United
  States as a whole, but reports from selected
  populations suggest  the size of the problem.
    In  California  in  1975,  there were 503
  systemic pesticide poisonings in persons em-
  ployed in  agriculture.  Some authors, how-
  ever,  believe that  these reported  statistics
  represent no more than  1 percent of  the
    Incidence data is equally incomplete in
  Florida, a state second only to California in
  the  amount of  pesticides  used. Between
  1970  and 1975,  pesticides were listed as a
Pesticide Dose



Types of Exposure


Health Concerns
Pesticide Poisonings
Topical Injuries
(Skin and Eyes)

Occupational Safety

Human and Environmental
Pesticide Residues
Nursing Goals
Early Diagnosis
Industrial Hygiene
Occupational Health
Health Education
Safety Standards


                  cause "of death in 26 persons in Florida.
                     • Ten deaths (35 percent) were children
                       under the age of 10.
                     • Males accounted   for  19  cases  (73
                     • Fifteen ingested the toxicants (57 per-
                     • Three inhaled the agent (11 percent).
                     • Two persons died from dermal  con-
                     These statistics, however,  tell nothing of
                  the occupational  hazards  of pesticides or
                  why these materials were in  the home.  The
                  total picture is still incomplete. Information
                  on the acute  morbidity of pesticides is of
                  extreme importance, for it is only with  this
                  knowledge that decisions can be  made on
                  future  pesticide management, policies,  and
                    Applicator and Picker Poisoning
                    These  two   syndromes   have  distinct
                  clinical, epidemiologic,  and  public health
                    Clinically, because residues are much less
                  toxic  than  pesticide concentrates, picker
                  poisoning  is of  shorter duration. Cases are
                  often  multiple and the  case  fatality rate  is
                    Illness which  is the result  of exposure to
                  the  concentrate  is usually more severe and
                  protracted. The case fatality rate is high.
                    Epidemiologically,  too,  there   are  dif-
                 . ferences.  Residue intoxications  occur pri-
                  marily in the agricultural  worker  and the
                  migrant worker through dermal exposure to
                  the  foliar  residues.  In this situation, the
                  worker  is not aware of the potential hazard,
because he does not know that the residues
are there. Occasionally, exposure  may occur
when workers  are accidentally  sprayed or
come in contact with pesticide drift.
   The applicator, on the other hand, should
be  aware of the potential  hazard  of the
chemical  which  he  is applying or mixing.
Such persons should be acquainted with the
hazards of spills and should have been taught
to wear protective clothing. They are  gen-
erally more informed and better trained.
   •Applicator poisonings occur wherever ap-
plication is  done. Residue poisonings occur
mainly in hot, arid areas.
   Preventive  strategies  also • differ.  With
residue  poisoning the  preventive goal is to
make the place  of work safe. The federal
government has established reentry times for
different  pesticides.  These  are   the  time
intervals which must elapse after  a crop has
been treated before it  is safe for  an agricul-
tural worker to  enter the field. The  pre-
ventive  approach is very different for appli-
cators. It focuses on the preventive potential
of worker education, personal hygiene, and
the wearing of  protective clothing. These are
skills for which the nurse is ideally suited.

   Child Poisoning
   Children are the group at greatest risk of
accidental poisoning from pesticides which
have not been securely  stored or correctly
  J  0
          \I\IJ.  ,!,
                   i—  —

disposed of, although adults, too, are at risk
if chemicals are stored in improper bottles.
The home, the garden, and the local refuse
dump  are often  the  scene  for the  other
category • of  acute   accidental   pesticide
poisoning. The  toddler is  the  person  at
greatest risk.
   When water is  added to a pesticide, the
liquid often becomes milky. If this  is stored
in a bottle, there is a real danger  that the
poison will be inadvertently given to a baby.
   Incorrect disposal of pesticide containers
causes many fatal cases.
     A 2/6-year-old Mexican child died after
   being sprayed  with  what seemed to be a
   harmless fluid in a simple  spray gun. Her
   father, who could speak no English, could
   not understand the label on the container
   which  he  brought home from the field
   where he had  been working. There were
   remnants of the pesticide concentrate at
   the  bottom of the  drum.  He knew  that
   the  liquid  was  effective against the pests
   in  the fields, so he told his 14-year-old
   daughter to spray the home because of
   heavy roach infestation.  She did this, but
   tragically also  sprayed her younger sister
   who was asleep  in the crib.
   Transportation and storage  also  can  be
hazardous. If there is a large  spill, such as
might  occur  with a tanker collision or train
crash,  a highly dangerous situation can arise.
In this event, a telephone call (collect) can
be made  to CHEMTREC, which is a special
service  to assist in such cases. A description
 of CHEMTREC service is in Appendix 5.
   Careless unloading of pesticides can cause
leaking containers. If  these  are  stored  in
warehouses  close  to  food, accidental  con-
tamination  of  food  may  occur.  This  is
especially true during storms  and floods. The
general upkeep and waste disposal  practices
of the  pesticide  storehouse  should be in-
spected regularly.
   It  is apparent  that pesticide  poisonings
are a  problem area for several agencies and
institutions. A cooperative effort is needed
to insure human  safety through improved
pesticide management.

                                                   CHAPTER VII
                                        METHODS OF  PREVENTION
                    The  rural health clinic nurse and  the
                 public health nurse  are in key positions to
                 prevent pesticide poisoning.
                    These nurses are  often the first  to learn
                 about a case.  They are usually  the  first
                 contact  of the patient and his family. This
                 gives them the opportunity to follow up the
   The  nurse  can go  to the site  of the
poisoning  to try to retrace how the episode
came  about.  She can  visit  the  home  to
discuss safety and explain to the worker and
his family how poisonings  happen. Since
other  members  of the  camp will  be  in-
terested, the nurse can use the incident as a
teaching point.
   She  should also  meet with crew chiefs
and employers to promote pesticide safety.
The  nurse can  meet  with   workers, em-
ployers, and even local government  groups,
civic clubs, and labor groups  to explain how
the occupational  health  hazards  of  the
worker  can be minimized with sound pesti-
cide management. Her visibility at the place
of work and in the home will facilitate her
acceptance greatly. It  also will allow her to
see for  herself the whole chain of pesticide
formulation, application, and  exposure.

Applicator Safety
   The  nurse  should check for the  correct
use of protective  clothing. She should find
out whether goggles, masks, coveralls, rubber
gloves and boots are provided and  if they are
in good repair. She should also  watch for
skin   conditions  in   the  workers.   When
                                                abrasions in the skin  occur through cuts or
                                                dermatitis, the  skin  loses  its natural  pro-
                                                tective  barrier and chemical- absorption  is
                                                greatly increased.
                                                  She should discuss with the operator such
                                                issues as  the  availability to the worker of
                                                showers  at the end  of the day  and the
                                                opportunities  for  a  wash  and  change of
                                                                    She  also should  discuss  procedures for
                                                                  rinsing  and disposing of empty pesticide
                                                                  containers. Too often, they are left in the
                                                                  fields or are picked up and dumped into an
                                                                  empty  lot or garbage pit, where they con-
                                                                  tinue to present a poisoning potential.
                                                                    She  should  make sure  the employer
                                                                  knows the name of the nearest physician and
                                                                  hospital. She might  leave her own card and
                                                                  tell'him about  the pesticide poisoning pro-
                                                                  gram at the clinic.
                                                                    Routine cholinesterase  testing is neces-
                                                                  sary  for highly exposed workers such  as
                                                                  formulators, spray rig operators, pilots, and
                                                                  aircraft  mixers  and loaders.  The nurse and
                                                                  the employer should explore ways in which
                                                                  a  program can be  organized.  Pre-employ-

ment cholinesterase determination can  be
built into  the  pre-employment  physical
   It is customary to advise the withdrawal
of the worker from continued  anticholin-
esterase exposure  if there  is a 20 percent
decline in these enzymes.
   If a  baseline level is not available,  the
worker should  be  temporarily changed to a
job away  from anticholinesterase pesticides
if the red blood cell cholinesterase  is  less
than 0.4 Aph/hr (Michel method).
Picker  Safety
   In  the   education  of  the  agricultural
laborer whose  pesticide  risk is  from plant
residues, field  reentry regulations are most
important.  In  addition, the nurse can help
the migrant worker understand the need for:
   •  changing  clothing
   •  showering after work
   •  laundering the clothes correctly
   •  keeping   contaminated  clothes  away
      from  living areas
   •  washing   hands  and   face   before
      smoking  or  eating while  working in
      treated fields.
   Parathion has been identified in the house
dust of workers' homes. This is probably due
to  the  dusty  residues  dropping  off  the
workers' clothing or shoes.
    One  worker was hospitalized  with
 parathion poisoning. When he went back
 to work-a few days later, he became sick
 a  second time after putting the  same
 clothes on again. High concentrations of
 parathion were detected in the clothing.
                                                     The nurse can discuss laundering with the
                                                  worker's wife. The worker's clothing should
                                                  be laundered  separately  and  subjected to
                                                  several washes. Laundering of contaminated
                                                  fabric three  times is not effective  in  re-
                                                  moving all of the residues of some pesticides
                                                  (such as parathion and toxaphene).
                                                  Child Safety
   The nurse should inform families about
correct storage of chemicals in  the  home.
She also should warn them about taking the
child into the fields. Often it is impossible to
leave the child at home, because there are no
day nurseries nearby. If one is available and
the mother  agrees to use  it, the  risk that
occurs from a child playing in the field while
her father and mother are working would be
      One 5-year-old girl, for example, was.
   hospitalized for organophosphate poison-
   ing which she  sustained while playing in
   the fields where her parents worked. She
   was  poisoned as a  result  of  eating
   tomatoes which had been treated earlier
   with  phosdrin, me thorny I, dimethioate
   and monocrotophos.  The mother recog-
   nized  the condition because five  of her
   eight children  had been hospitalized for
   parathion poisoning several years earlier.

                                                   CHAPTER  VIII
  Verification of acute pesticide poisonings
has two aspects:
  •  the  confirmation of  diagnosis,  using
     clinical and laboratory procedures, and
  •  collecting and  tabulating data on con-
     firmed pesticide poisonings  to  gain  a
     fuller understanding of the problem.
  Diagnosing a full-blown organophosphate
illness  usually  poses no  real problem.  It
appears, however, that many milder  intoxi-
cations of  agricultural laborers and migrant
workers pass  unrecognized  or are not re-
ported or  satisfactorily investigated  in  the
field. Even  in  the  more  obvious  cases,
laboratory   confirmation  is  insufficiently
practiced. The specific pesticide involved is
rarely identified.
  The verification  and  chemical confirma-
tion   of  an  acute  pesticide poisoning is
important to many people:
  •  The  agricultural worker is interested,
     for  within the  process  rests  his as-
     surance for just consideration and com-
     pensation for any job-related poisoning.
  •  Farmers are vitally interested in having
     safe products to use.
  •  Chemical manufacturers  and formula-
     tors want to make a safe product and
     to insure  that  an  alleged  pesticide
     illness  attributed to their  product is
     correctly investigated and verified.
  Jurisdictions,  legislators,  law  enforcers,
and  insurance organizations are  also served
by verification of pesticide-related illnesses.
The  attending physician also  has a  profes-
sional interest, having often proceeded with
vigorous  treatment  measures without initial
laboratory  confirmation.

Steps  in Poisoning  Verification
  The four ingredients of poisoning verifica-
tion  are:
  •  a pesticide exposure history in  which
     the  symptoms complained of are com-
     patible  in  time  and  with  a  known
     toxicity of a pesticide
   •  physical signs  which reflect the known
     toxicity of the pesticide
   • demonstration of significant red blood
     cell   and  plasma  cholinesterase   in-
     hibition   in   acute   organophosphate
   • identification  of the specific urinary
     pesticide metabolites and/or the intact
     pesticides in certain tissues of the body.
   (See   Chapter  III.  for  information  on
clinical  and laboratory tests and instructions
for collecting laboratory specimens.)
   Many of the symptoms of acute pesticide
poisoning are common to a wide variety of
more frequently occurring illnesses  not re-
lated to  pesticides. Some of  the  diseases
included  in  this list are  influenza,  gastro-
enteritis,  heat exhaustion,  diseases  of the.
heart and  lung, and central nervous system
disorders.  To distinguish  mild or subacute
cases of pesticide illnesses from these other
conditions, an arbitrary and reasonable selec-
tion  process  is  necessary.  The following
guidelines are suggested.
   Apply  a simple cholinesterase  screening
test such as the Acholest:
   • to any patient who complains of having
     sustained a pesticide exposure '
   • to any worker having regular and heavy
     pesticide exposure
   • to any patient who has three or more
     of the following  symptoms: weakness,
     sweating, headache, nausea and vomit-
     ing,  diarrhea, abdominal  cramps, ex-
     cessive  tearing,  salivation, bronchial
     secretions, shortness of breath, pains in
     the chest, blurring of vision, and con-
   • to any patient with either miosis (less
     than 5 mm in size), muscle twitching or
     fasciculations, or clinical evidence of
     bronchial spasm or bronchial exudation
   • to any patient with a pulse rate of 50
     or less.
   In the event of a convulsion, serum should
not only  be  analyzed  for cholinesterase
inhibition  but it should also be sent to a
special  pesticide  analytical  laboratory for
electron capture  and mass  spectrometry gas
chromatographic studies  for  organochlorine
   If  the   screening test  is  positive,  the
nursing  and  medical  staff should  be  in-
formed  at once. The following additional
steps are necessary:
   • Collect 8 cc of blood in a heparinized
     tube for  quantitation of red cell and
     plasma cholinesterase determinations.

  •  Collect 20 cc   of urine  for  urinary
     pesticide studies.
  •  Ship  both  as soon  as  possible to a
     specialized pesticide  analytical labora-
     tory  for   more  specific  and  precise
  •  Send a resume of the pertinent clinical
     findings and exposure history with the
     specimens. (Use  form in Appendix 8.)
  •  Inform the  local  community  health
     worker and public health nurse so that
     a  field visit  can be  made  as soon as

  Shipping and Notification
  Even in  the verification process, speed is
of  the utmost  importance.  Inform  the
special pesticide laboratory by telephone of
the  time of shipment and  the expected time
of arrival  of the specimens and enclosures.
The  laboratory should complete the analyses
quickly. Results should be communicated to
the   referral center first by telephone and
then by written confirmation.
  Farm worker clinics may send specimens,
together with  background information, to
the   appropriate  laboratory as listed  in Ap-
pendix 7.
  Notice:Clinics  forwarding  specimens via
         air shipment  should  notify  the
         laboratory via telephone  so  the
         shipment can be met at  the air-
         port.   Flight  number  and  date
         should  be  provided  (if known)
         together  with  names . and  tele-
         phone  numbers to  be used  in
         calling back results.
  County hospitals,  private clinics, industry
health  units and emergency rooms wishing
to have samples analyzed may do so, if cost
reimbursement conditions  are acceptable.
  If suspected cases of poisoning are being
treated  in rural areas distant 'from possible
air  connections  to the verification labora-
tory, consult state departments of health or
agriculture  for  nearby  laboratory facilities
which can provide blood and urine analyses.

 - Collection of Data
  For  administrative purposes, reports on
pesticide poisoning should contain the  fol-
lowing information:
     1. Name  of patient  or patient identi-
        fication  number   (Patient  identi-
        fication is needed so that followup
        studies can  be  done. Because this
         form is a medical record, the infor-
         mation will remain confidential.)
      2. Sex and age of patient
      3. Time and date of occurrence
      4. Location of occurrence
      5. Route of exposure
      6. Symptoms and signs
      7. Type of pesticide used:
         a)   name (copy or original of label,
             if possible)
         b)   active ingredients
         c)   EPA registration number
      8. Crop pesticide was applied to and
         target pest
      9. Means  by  which  pesticide  was
         applied-plane, spray rig, etc.
     10.  Immediate first aid measures taken,
         medical attention provided
     11.  Any  other  facts which  could  be
         useful  in analyzing the causes  and
         effects of the poisoning.
   To  provide  this  information,  duplicate
the  form in  Appendix  8, fill it in,  and
furnish  it  with  medical  specimens to  be
analyzed. Locally used  forms providing the
above data may be substituted.

                                        APPENDIX  I



         Common or
         Trade Name                                             Chemical Name

         Acephate  	 0,S-Dimethyl acetyl phosphoramidothioate
         Acethion	 0,0-Diethyl  S-carboethoxymethyl phosphorodithioate
         Acetoxon	 0,0-Diethyl  0-carboethoxymethyl  phosphorothioate
         Akton* or Axiom*	 O,0-Diethyl  0-(2-chloro-l-(2,5-dichlorophenyl) (vinyl)
         Alamos* or Azothoate* or Slam*  . O-(p-chloro'phenylazo) 0,0-dimethyl phosphorothioate
         Amidithion	 0,0-Dimethyl-S-[[2-methoxyethyl)   carbamoyl]
                                        methyl] phosphorodithioate
         Amiton	 0,0-Diethyl-S-(2-diethylamino)   ethyl  phosphoro-
         Aphidan*	 0,0-Diisopropyl-S-ethylsulfinyl  methyl  dithiophos-
         Aspon*	 0,0,0,0-Tetra-n-propyl dithiopyrophosphate
         Azethion  	 0,0-Diethyl   S-(carbomethoxymethyl)  phosphoro-
         Azinphosmethyl	 0,O-Dimethyl  S-[(4-oxo-l,2,3-benzotriazin-3(4H)-yl>
                                        methyl] phosphorodithioate
         Bensulide 	 S-(0,0-Diisopropyl   phosphorodithioate)  ester  of
         Bomyl*  	•. .	 Dimethyl 3-hydroxyglutaconate dimethylphosphate
         Bromophos ethyl	 0,0-Diethyl-0(4-bromo-2,5-dichlorophenyl)  phospho-
         Butonate	 0,0-Dimethyl-(2,2,2-trichloro-l-n-butyryloxyethyl
         Carbophenothion	-0,0-Diethyl-S-[[(p-chlorophenyl)thio] methyl] phos-
         Chlorfenvinphos	 2-Chloro-l-(2,4-dichlorophenyl)  vinyl  diethyl   phos-
         Chlormephos  	 S-Chlqrmethyl-0,0-diethyl phosphorothiolothionate
         Chlorthion 	 0,O-Dimethyl  0-(3-chloro-4-nitrophenyl) phosphoro-
         Conen*	 0-Butyl-S-benzyl-S-ethyl phosphorodithioate
         Coroxon	 6,0-Diethyl-0-(3-chloro-4-methylcoumarin-7-yl)  phos-
         Coumaphos  	.-	 0,0-Diethyl  0-(3-chloro-4-methyl-2 oxo (2H)-l-benzo-
                                        pyran-7-yl) phosphorothioate
         Crufomate 	 4-tert-Butyl-2-chlorophenyl  methyl   methyl-phos-
         Cyanthoate	 S-[[(l-Cyano-l-methylethyl)carbamoyl]methyl]  0,0-
                                        diethyl phosphorothioate
         Cythioate	 O,O-Dimethyl  0-p-sulfanoylphenyl phosphorothioate
         DAEP	 0,0-Dimethyl-S-2-(acetylamino)ethyl dithiophosphate
         DEF*	 S,S,S,-Tributyl phosphorotrithioate
         Demeton  	 0,0-Diethyl  O-(and S)-[2-(ethylthio)ethyl] phosphoro-
         Demeton methyl  	 0,0-Dimethyl-S-[2(ethylthio)ethyl]  phosphorothioate
         Diazinon	 0,0-Diethyl-O-(2-isopropyl-6-methyl-4-pyrimidinyl)

            *Trade name.

Common or
Trade Name                                  Chemical Name
Dicapthon  	 0-(2-Chloro-4-nitrophenyl)  0,0-dimethyl  phosphoro-
Dichlorvos  	 2,2-Dichlorovinyl 0,0-dimethyl phosphate
Dicrotophos	 Dimethyl  phosphate of  3-hydroxy-N,N-dimethyl-cis-
Diethquinalphione	 O,0-Diethyl-0-(2-chinoralyl)-phosphorothioate
Dimethoate	0,0-Dimethyl S-(N-methyl carbamoyl methyl)  phos-
Dioxathion	 2,3-p-Dioxanedithiol S,S-bis(0,0-diethyl  phosphoro-
Disulfoton  	 O,0-Diethyl S-[2-(ethylthio)ethyl] phosphorodithioate
DMCP	 S-(p-Chlorophenyl) 0,0-dimethyl phosphorothioate
Dursban*	0,0-Diethyl  0-(3,5,6-trichloro-2-pyridyl)  phosphoro-
Dyfonate*  	 0-Ethyl-S-phenylethylphosphonodithioate
EPN	 0-Ethyl O-(p-nitrophenyl) phenylphosphonothioate
Ethion  	 0,0,O',0'-Tetraethyl S,S'-methylene bisphosphorodi-
Fenitrothion . . .."	•. .. 0,0-Dimethyl 0-(4-nitro-m-tolyl) phosphorothioate
Fensulfothion	 0,0-Diethyl 0-[p-(methylsulfmyl)phenyl]  phosphoro-
Fenthion  	 0,0-Dimethyl 0-[4-(methylthio(-m-toly]  phosphoro-
Folex*	 Tributyl] phosphorotrithioite
Formothion	 O,O-Dimethyl S-(N-formyl-N-methylcarbomylmethyl)
Forstenon	 Diethyl carbethoxydichloromethyl-phosphonate                          33
Fostion*	 O,0-Diethyl-S-(N-isopropylcarbamolymethyl)   phos-
Gardona*	 2-Chloro-l-(2,4,5-trichlorophenyl)   vinyl   dimethyl
Hosdon*	 0,0-Dimethyl-S-2(isopropylthio)  ethyl phosphorodi-
Imidan*	 N-(Mercaptomethyl)  phthalimide   S-(0,0-dimethyl
Inezin*	 O-Ethyl-S-benzylphenylphosphonothiolate
lodofenphos	 0,0-Dimethyl-0-(2,5-dichloro-4-iodophenyl) thiophos-
Ketothion	 O,0-Diethyl S-acetonyl phosphorodithioate
Lepto'phos  	 O-(4-Bromo-2,5-dichlorophenyl) 0-methyl phenylphos-
Malathion	O,0-Dimethyl dithiophosphate of diethyl mercaptosuc-
Mecarbam	O,0-Diethyl  S-[[(ethoxycarbonyl)methylcarbamoyl]-
                                 methyl] phosphorodithioate
Mecarpon	:	 S-(N-Methoxycarbonyl-N-methylcarbamonylmethyl)
                                 dimethyl phosphonothiolothionate
Metasystox-S*+  	 0,0-Dimethyl S-[(2-ethylsulfinyl>  isopropyl]   phos-
Methyl mercaptophos	 O-Methyl-O-et.hyl-2-ethylmercaptoethyl  thiophosphate
Methyl parathion	 0,O-Dimethyl 0-p-nitrophenyl phosphorothioate
Methyl phencapton  	0,O-Dimethyl S-(2,5-dichlorophenylthio) methyl phos-
Methyl potasan*	'... 0,0-Dime.thyl 0-(4-methylumbelliferone) phosphoro-

   *Trade name.

('om/non or
Trade Name                                    Chemical Name
Methyl trithion	 S-(((p-Chlorpphenyl)thio)methyl) 0,0-dimethyl  phos-
Mevinphos  	2-Carbomethoxy-l-methylvinyl dimethyl phosphate
Monitor*  	O,S-Dimethylphosphoramidothioate
Monocrotophos	 Dimethyl  phosphate   of  3-hydroxy-N-methyl-cis-
Morphothion 	 0,0-Dimethyl   S-(morpholinocarbonylmethyl)  phos-
Naled	 1,2-Dibromo-2,2-dichloroethyl dimethyl phosphate
Naphthalaphos	N-Hydroxynaphthalimide diethylphosphate
Orthene*  	 0,S-Dimethyl N-acetyl phosphoramidothioate
Oxydemetonmethyl	0,0-Dimethyl   S[2-(ethylsulfinyl)ethyl]  phosphoro-
Oxydisulfoton 	0,O-Diethyl   S-(2-(ethylsulfinyl)ethyl)  phosphorodi-
Paraoxon	 0,0-Diethyl 0-p-nitrophenyl phosphate
Parathion	 0,0-Diethyl 0-p-nitrophenyl phosphorothioate
Phencapton 	 0,0-Diethyl  S-[[(2,5  dichlorophenyl)thio]  methyl]
Phenthoate	 0,0-Dimethyl S-(a-ethoxycarbonylbenzyl) phosphoro-
Phorate	 0,0-Diethyl  S-(ethylthio)methyl  phosphorodithioate
Phosalone	 0,0-Diethyl   S-[(6-chloro-3(mercaptomethyl)-2-benz-
                                 oxazolinone] phosphorodithioate
Phosphamidon	2-Chloro-2-diethylcarbamoyl-l-methylvinyl   dimethyl
Phosphinon 	 0,0-Diethyl   O-(l-(2-chloroethoxy)-2,2-dichlorovinyl)
Phosvel*	 0-(2,5-Dichloro-4-bromophenyl) 0-methyl phenylthio-
Phoxim	Phenylglyoxyonitrile oxime 0,0-diethyl phosphoro-
Pirazinon*  	 0,0-Diethyl  0-(6-methyl-2-propyl-4-pyrimidyl)  phos-
Potasan	 0,0-Diethyl   0-(4-methylumbelliferone) phosphoro-
Prophos  	 0-Ethyl S,S-dipropyl phosphorodithioate
Propoxon	 0,0-Diethyl-S-carboethoxyethyl-phosphorothioate
Prothion	 O,0-Diethyl  S-carboethoxyethyl  phosphorodithioate
Pyrazoxon* 	 0,0-Diethyl 0-(3-methylpyrazol-5-yl) phosphate
Pyrazothion* 	 0,0-Diethyl   0-(3-methylpyrazol-5-yl)  phosphoro-
Ronnel	 0,0-Dimethyl  0-(2,4,5-trichlorophenyl) phosphoro-
                                 thioate .
Schradan  	 Octamethylphpsphoramide
S-Seven*	 0-Ethyl-0-(2,4-dichlorophenyl)-pliosphonothionate
Sulfotepp	 0,0,0,0-Tetraethyl dithiopyrophosphate
TEPP 	 Tetraethyl pyrophosphate
Thiometon	 0,0-Dimethyl-S-[2-(ethylthio)ethyl]   phosphorodi-
Trichlorfon	 Dimethyl  (2,2,2-trichloro-l-hydroxyethyl)  phos-
Trichloronate	 0-Ethyl   0-(2,4,5-trichlorophenyl)   ethylphosphono-
VC-13 Nemacide  	 0-2,4-Dichlorophenyl 0, 0-diethyl  phosphorothioate
Zytron	 O-(2,4-Dichlorophenyl)   0-methyl  N-isopropylophos-
   *Trade name.

Aflix*	see
Afos*	  see
Agrisil*	  see
Agritox*	  see
Agrothion*	  see
Alkron*  	see
Aileron*	  see
Amiphos*	  see
Anthio*  	see
Anthon*	  see
Appex*	see
Asuntol*	  see
Azodrin*  	  see
Basudin*	.see
Baymix*	  see
Bayrusil*  	  see
Baytex*  	  see
Baythion*	  see
Betasan*	see
Bidrin*	  see
Bilobran*	see
Birlane*	  see
Bladafume*  	see
Bladen*   	  see
Borinox*  .......  see
Bromex*	see
Carbicron*	  see
Carfene*	  see
Cidial*  	see
Citram*   	see
Co-Ral*   	see
Corothion*	'see
Cygon*	  see
Cythion*  	  see
Dagadip*	 .  see
Dalf* 	:.  see
Dasanit*	  see
Daphene*	  see
Dazzel*	  see
Dedevap*	  see
De-Fend*	see
De-Green*  	  see
Delnav*   .*.	see
Diazajet*	 .  see
Diazide*	see
Diazol*	see
Dibrom*	  see
Di-Captan* .......  see
Dimecron*	  see
methyl parathion
Dimethogen*  .... see dimethoate
Dipterex*	 see trichlorfon
Di-Syston*	see disulfoton
Disyston S* 	see oxydisulfoton
Dithione*	 see sulfotepp
Dylox*	see trichlorfon
E-605*	 see parathion
Easy Off-D* 	see Folex*
Ectoral*	 see ronnel
Ekatin*	 see thiometon
Ekatin M*	see morphothion
Ektafos*	see dicrotophos
Els'an*	 see phenthoate
Emmatos*  	see malathion
Entex*	see fenthion
Equino-Aid*	see trichlorfon
Ethyl Parathion*  . see parathion
Etilon*	see parathion
Etrolene*	 see ronnel
Exothion*  	 see endothion
Filariol* 	see bromophos ethyl
Folidol E—605*  .. see parathion
Folidol M*	see methyl parathion
Folithion*  	 see fenitrpthion
Fostion MM*  .... see dimethoate
Frumin Al*	.see disulfoton
Fujithion*  	see DMCP
Fyfanon* ....... see malathion
Gardentox* 	see diazinon
Garrathion* 	see carbophenothion
Gusathion M*  .... see azinphos-methyl
Guthion* 	see azinphos-methyl
Hercules AC527* . see dioxathion
Karbofos*	see malathion
Klimite 40* 	see TEPP
Korlan*  	see ronnel
Lebaycide*	see fenthion
Malamar*	see malathion
Malaspray*	 see malathion
Maretin*	 see naphthalaphos
Meldane* 	see coumaphos
Menite*  	 see mevinphos
Metasystox*	see demeton methyl
Metasystox-R* ... see oxydemeton-methyl
Metron*	see methyl parathion
Mintacol*	see paraoxon
MLT*	see malathion
Mocap*	see prophos
Morphotox*	see morphothion
   *Trade name.

No Pest*	
Ortho  Phosphate
   Defoliant* ....
Partron M*	
Perfekthion* ......
Pestox III*	
Phospliopyran* . . .
see mecarbam
see coumaphos
see dyfonate
see ronnel
see bromophos ethyl
see trichlorfon
see ethion
see parathion
see methyl parathion
see dichlorvos
see fenitrothion
see monocrotophos
see fenitrothion
see parathion

see DBF*
see parathion
see parathion
see parathion
see methyl parathion
see dimethoate
see mecarbam
see schradan
see mevinphos
see mevinphos
see parathion
see endothion
see dichlorvos
see trichloronate
see imidan
see Gardona+
see phorate
see naphthalaphos
see coumaphos
see parathion
see dimethoate
see dimethoate
see crufomate
see dioxathion
see chlorfenv.inphos
Terracur P*	
   Pyrophosphate .
see disulfoton
see parathion
see diazinon
see parathion
see fenitrothion
see chlorfenvinphos
see demeton
see schradan
see Monitor*
see phenthoate
see cyanthoate
see dichlorvos
see methyl parathion
see fensulfothion
see Gardona*

see TEPP
see amiton
see TEPP
see phorate
see amidthion
see disulfoton
see parathion
see sulfotepp
see fenthion
see phorate
see trichlorfon
see dimethoate
see trichlorfon
see carbophenothion
see ronnel
see trichlorfon
see phoxim
see dichlorvos
see dichlorvos
see TEPP
see ronnel
see phoxim
see malathion
see phosalone
                    *Trade name.


                    CARBAMATE PESTICIDES

Common or Trade Name           Chemical Name

Aldicarb	  2-Methyl-2-(methylthio)  propionaldehyde 0-(methyl-
                               carbamoyl) oxime
Banol	6-Chloro-3,4-xylyl methylcarbamate
Baygon	0-Isopropoxyphenyl methylcarbamate
Bufencarb	  3-(l-Methylbutyl)  phenyl  methylcarbamate  and
                               3-(l-Ethylpropyl) phenyl methylcarbamate (3:1)
Butacarb	  3,5 Di-tert-butylphenyl methylcarbamate
Carbaryl	  1-Naphthyl N-methylcarbamate
Carbofuran	,	2,3-dihydro-2,2-dimethyl-7-benzofuranyl   methyl-
Dichlormate . ..	3,4-and 2,3-Dichlorobenzyl methylcarbamate
Dimetilan	  3,-Hyrdroxy-N,N,  5-trimethylpyrazole-l-carboxamide
Dioxacarb	  0-l,3-Dioxolan-2-ylphenyl methylcarbamate
Ficam	2,2-Dimethyl-l,3-benzodioxol-4-yl-methykarbamate
Formetanate.(hydrochloride)	M-[((Dimethylamino)methylene) amino phenyl meth-
                               ylcarbamate] (hydrochloride)
Landrin  	:	  3,4,5-Trimethylphenyl methylcarbamate and 2,3,5-Tri-
                             •  methylphenyl methylcarbamate
Matacil	4-(Dimethylamino)-m-tolyl methylcarbamate
Mesurol  	4-(Methylthio)-3,5-xylyl methylcarbamate                             37
Methomyl	  5-Methyl N-[(methylcarbamoyl) OXyl]  thioacetimidate
Mexacarbate	4-(Dimethylamino)-3,5-xylyl methylcarbamate
Mobam	  4-Benzothienyl methylcarbamate
Oxamyl  	Methyl  N',N'-dimethyl-N-[(methylcarbamoyl)oxy] -1-
Pirimicarb	  2-(Dimethylamino)-5,   6-dimethyl4-pyrimidinyl
Promecarb 	  3-methyl-5-isopropylphenyl methylcarbamate
Thiofanox 	3,3-Dimethyl-l-(methylthio)-2-butanone  0-[(meth-
                               ylamino)carbonyl]  oxime

                           CROSS REFERENCE FOR SOME OF THE
                           CARBAMATE PESTICIDE TRADE NAMES
A 363	see Matacil
Ambush 	  see Aldicarb
Aminocarb	  see Matacil
Aphox  	see Pirimicarb
Arprocarb	  see Baygon
Bay 9010 	  see Baygon
B-37344	  see Mesurol
Bay 39007 ..	see Baygon
Bay 44646 	  see Matacil
Bay 70142 	  see Carbofuran
Bendiocarb	see Ficam
Blattenex 	  see Baygon
Bux	see Bufencarb
Carbamult	see Promecarb
Cafbanolate  	see Banol
Carpolin	  see Carbaryl
Carzol	  see Formetanate
CIBA 8353	  see Dioxacarbe
Curaterr 	see Carbofuran
D-1221	  see Formetanate
D-1410	  seeOxamyl
Dicarol	see Formetanate
Dowco 139	  see Mexacarbate
Draza  	see Mesurol
Elocron	  see Dioxacarb
ENT 27164	  see Carbofuran
ENT 27300	  see Promecarb
EP 316	  see Promecarb
EP 332	  see Formetanate
Famid	see Dioxacarb
FMC 10242  	see Carbofuran
Furadan 	  see Carbofuran
G-22870	 .  see Dimetilan
G-13332	see Dimetilan
Hexavin 	  see Carbaryl
IPMC  	  see Baygon
Karbaspray	  see Carbaryl
Lannate 	see Methomyl
Metalkamate ....
Metmercaptron . .
Mos 78	
NC 6897 	
QMS 716 	
Ortho  5353	
Schering34615 . .
Schering 36056 ..
                                                      Sendran  .
                                                      Septene . .
                                                      Sevin ....
                                                      Sirmate . .
                                                      Snip  ....
                                                      Sok	.
                                                      Suncide . .
                                                      Temik :..
                                                      Tendex ..
                                                      UC 9880 .
                                                      UC 22463
                                                      UC 7744 .
                                                      Unden . ..
                                                      Vydate . .
                                                      Yaltox  . .
                                                      Zectron ..
see Mexacarbate
see Mobam
see Mesurol
see Bufencarb
see Mesurol
see Mesurol
see Promecarb
see Mobam
see Mesurol
see Ficam
see Carbofuran
see Methomyl
see Promecarb  .
see Bufencarb
see Baygon
see Pirimicarb
see Pirimicarb
see Baygon
see Carbaryl
see Dichlormate
see Dichlormate
see Promecarb
see Formetanate
see Baygon
see Carbaryl
see Carbaryl
see Dichlormate
see Dimetilan
see Banol
see 'Baygon
see Aldicarb
see Baygon
see Carbaryl
see Promecarb
see Aldicarb
see Dichlormate
see Carbaryl
see Baygon
see Oxamyl
see Carbofuran
see Mexacarbate

                                    APPENDIX 2
                             PESTICIDE TOXICITY
   Because most pesticides destroy unwant-
ed organisms,  they  obviously are toxic ma-
terials. Some pesticides are much more toxic
than others. Severe illness may result when
only a small amount of one type of pesticide
has been ingested; with another type, a large
amount  may  be  ingested  with  no serious
   Toxicologists use a simple animal toxicity
test  to rank  pesticides according to their
inherent  toxicity. Before any  pesticide can
be registered, the manufacturer must provide
the results of these  tests to EPA. The  11)50
(the dosage level of a toxic chemical which is
lethal to 50 percent of a population of test
animals) is measured in terms of:
   • oral toxicity (material is fed to rats)
   • dermal toxicity (material is applied to
     the skin of rats)
   • respiratory  toxicity  (material   is  in-
In this way  an arbitrary toxicologic ranking
has been obtained for the organophosphate
and organochlorine  pesticides.  The materials
on the top of the list are the most toxic, and
those at the bottom are the least toxic. The
size of the dose is the most important single
item in determining the safety  of a given
chemical. Actual statistics  of human poison-
ings  correlate   reasonably  well  with  these
toxicity  ratings. Health  personnel  will be
able  to  get  some idea  of the  probable
severity of the poisoning being treated by
referring to these figures.
   The amount of pesticide required to kill
an adult  male  can be correlated with
   Oral  ingestions  are more toxic than res-
piratory inhalations and these are more toxic
than dermal absorptions. In addition, there
are individual  physical and chemical dif-
ferences  in  a  chemical which  render the
material  more likely to produce poisoning.
Thus, parathion changes to the more toxic
"paraoxon"  with high temperatures.  Ethyl
parathion is more toxic than  methyl para-
thion, yet there is no  great  difference  in
their oral toxicity. Work exposure is usually
dermal and that is why many more illnesses
are seen  'in workers exposed to ethyl para-
thion  than those exposed  to  methyl para-
Acute Oral LD5Q
50 - 500
500 - 5,000
Material which will kill
an adult male
a few drops
a pinch to a teaspoonful
a teaspoonful to a tablespoonful
a I ounce to 1 pint
1 pint to 1 quart

BTEPP  (Oral L0so=1,  Dermal  1050=2.4)^
8 THIMET (OuM.1, Dermal-2.5)
iDI-SYSTON (Oral=2.3,  Dermal 6]
IDEMETON (Systox]  (Oral=2.5, DermaN.2]
iPARATHION (Oral=3.6,  Dermal=6.8]
IPHOSDRIN (Oral=3.7,  Dermal 4.2!
UTRITHION (OraNO, Dermal^])
IlGUTHION (OraNI, Dermah220)
EH METHYL  PARATHION (Oral=14, Dermah-67)
l^CO-RAL  (Oral=15.5, Dermal-860]
         BIDRIN  (Oral=22,  Dermal=225)
         IOELNAV  iOfal 23,  Dermal 63|
         IPHOSPHAMIOON (Oral 23.5,  Dermal 10))

                        11DDVP (Oral=56, Dermal--75)
                                              (Oral=76,  Dermal-455)
                                      gjDIPTEREX (Oral=560, Dermal-2000]
                                                                             ,  Dermal-4100)
                                      1                        MALATHION (OraMOOO,
                                                                      RONNEL (Oral=1250)
          10   20  30  40  50  60  70  80   600  700  800  900  1000  1100  1200
                                 ACUTE LD5Q IN MG/KG

                  Acute Oral and Dermal Toxicity Values for Some Organophosphate Pesticides.
              (Prepared by the Bureau of Occupational Health, State of California Department of Public
                                   Health. Copied with permission.)

ENDRIN  (Oral  LD50=7.5 MG/KG, Dermal  1050=15  M6/KG)
! THIODAH  (OraHS, Deunal=74)
U ALDRIN (Oral=39, Dermal=98)
^^TOXAPHENE(Oral=80,  Dermal=780)
       LINDANE (Oral=88,  Dermal=900)
        HEPTACHLOR (Oral-100, DermaNSS)
         DDT (Orah113,  DermaN2510]
                            CHLOROANE (Oral=335,  Dermal=690]
                                            KELTHANE  (Oral=1000, Dermal=1000)
                                            CHLOROBENZILATE  (Oral=1040, Dermal^)
                                                                     ODD (Oral=3400)
                                                                           PERTHANE  (OralMOOO)
                                                                       METHOXYCHLBR (Orai=Sltfi]
       100      200      303      490      1000      2000
                                        LD50 IN MG/Kfi
          Acute Oral and Dermal Toxicity Values for Some Chlorinated Hydrocarbon Pesticides.
     (Prepared by the Bureau of Occupational Health, State of California Department of Public Health.
                                    Copied with permission.)

                                                            APPENDIX 3

                        (Cholinesteroie Test-Poper)
              I.  ACHOLEST Cholinesterose Test-Paper,  Bottle I.
                                                   Test Strip
              2.  Four slides.
              3.  0.}  ml. pipette  (0.01  ml.  graduations)
              A.  Comparative color strips.  Bottle II.
                                              Comparative Strip
5. Watch or stop-watch.
Procedure: Place 0.05 ml. of non-hemolyzed plasma* on
each of two thoroughly cleaned slides  (avoid  traces of
acid or alkali).  The plasma is to be quickly separated
from the blood sample inasmuch as blood cells  present
in the plasma interfere with  the reaction. With a  pair
of clean, dry scissors, cut  one-half of a strip (2x1 cm.)
of Acholest Test Paper from Bottle  I, and one-half of a
strip of  control  paper from Bottle II.  Using  tweezers,
place the untouched  half  of  each strip on each  slide
containing the plasma and cover with a second thorough-
ly cleaned slide,  using  gentle,  even  pressure  several
times in order to ensure  complete saturation of the  test
and  control papers and prevent mottling.  To  prevent
evaporation of fluid, do not separate the slides until  the
test has  been completed. Record the moment of  contact
of the test and  control papers with the plasma as  th<
beginning of the test.

*  Heparinized, not citrated or oxalated tubes may be
   used for collection.
                                                            The Acholest Test Paper and the control paper, when
                                                            dry, are similarly egg yolk colored. When exposed to the
                                                            plasma,  the  Acholest Test Paper turns  green, gradually
                                                            developing into  o yellowish  color, after passing  through
                                                            various tones of green-yellow. The control paper, how-
                                                            ever, upon contort  with the blood plasma,  turns  im-
                                                            mediately  yellowish  with no further change in  color.
                                                            The plasma  cholinesterase activity is measured  by the
                                                            time required for the  Acholest  Test  Paper to  reach
                                                            the color of  the control paper. For accurate  comparison
                                                            of the color,  it is recommended that the test be performed
                                                            on a white background with diffused light.
                                                            From the moment of contact of the plasma and Acholest
                                                            Test Paper to the point when the comparative tone of
                                                            color has  been  reached, the following time values have
                                                            been established:
Below 5
5 -20
30 and longer
Activity of Plasma
Precaution: Acholest Test Paper should be stored away
from light in  tightly closed containers to protect  it from
moisture and chemical vapors. Avoid contact with fingers.
Plasma to  be  used should bo free of cellular component*.
Always place Acholest Test Paper on the platma, never
drip plasma on the  Test  Paper; this similarly applies to
the control strip.

Readings should always be carried out under  the some
light conditions and room temperature. (Room tempera-
ture  differences in  the  range  from 68° F  (19° C)  to
75° F  (25° Ci  do  not  influence the  reliability and ac-
curacy of Acholest Test Paper). Also hemolysis of a minor
degree does  not affect the accuracy of Acholest Test
Paper. It is important, however, to  note that pH changes
of the plasma  might  interfere with  the  accuracy  of
Acholest  Test Paper independent of the plasma choli-
nesterase activity. Such  pH changes might  be  the result
of alkali  or acid cleansing materials on test  equipment
or of undue storage of plasma which might have led to
degradation or decoy  (e.g. protein fractions).  However,
as o rule, storage of the plasma up  to seven days at a
temperature of 20°  C or below (refrigeration of plasma
is desirable),  does  not interfere  with the accuracy of
Acholest Test  Paper.
                      DISTRIBUTED BY
               E. FOUGERA & CO., INC.
               HICKSVILLE,  NEW YORK 11802

                                  APPENDIX 4
                         LABORATORY  METHODS
Cholinesterase Determination
   The  four  laboratory techniques  most
 commonly used for quantitative expressions
 of these enzyme activities  are  the electro-
 metric (Michel), the titrimetric (pHstat), the
 colorimetric  (Ellman) and  gas  chromato-
 graphic (Cranmer) methods.
    1. Michel  method  (pH  meter)-Plasma
 and  red  cells  are  incubated  with  acetyl-
 choline for one hour.  The drop of the pH is
 due to the  formation of acetic acid and is
 directly proportional  to the cholinesterase
 activity. Normal values: Plasma 0.53 - 1.24
 ApH units and Red Blood Cells 0.57 - 0.98
 ApH units.
    2. pH Stat (titrimetric)—The plasma and
 red cells are incubated with acetylcholine for
 3 minutes and the acid formed is titrated
 with a base.  The  amount  of base used is
 directly proportional  to the cholinesterase
 activity in the blood sample. Normal values:
 Plasma  3.6 - 6.8 AiM/ml/min and Red Blood
 Cells 11.1 - 16.0juM/ml/min.
    3. Ellman method  (colorimetric)—Plasma
 and red cells are incubated  for 10 minutes
 with acetyl thiocholine  and the resultant
 thiocholine  produces  a  yellow color in the
 presence   of   5:5-dithiobis-(2-nitrobenzoic
 acid). The concentration of the yellow com-
 plex  is  directly proportional to the amount
 of cholinesterase  present.  Normal values:
 Plasma  5.8-16.6 M-SH/ml/3 min.
    4.  GLC  method   (cluomatographic)-
 Plasma  and  red cells are  reacted for 30
 minutes with  a compound that is similar to
 acetylcholine.   The   product  formed,
 dimethyl  butanol,  is quantitated  using a gas
 chromatograph. Normal values: Plasma 2.1 -
 4.6 /iM/ml/min  and Red Blood  Cells 8.2 -
 Urinary Pesticide
                 Metabolite Data

   The organophosphates are metabolized in
man to produce two major types of pesticide
metabolites in urine. These are the phenolic
metabolites  (e.g.  nitrophenols  and  halo-
genated phenols)  and the  alkyl phosphate
metabolites (namely,  diethyl thiophosphate
(DETP), diethyl phosphate  (DEP), dimethyl
thiophosphate. (DMTP) and dimethyl phos-
phate  (DMP).  The  carbamates, the other
major group of anticholinesterase pesticides,
are metabolized to non-halogenated phenols
which are excreted in urine.
   In poisoning cases the information from
both types of metabolites is informative.
Take ethyl parathion as an example. This is a
diethyl thiophosphate pesticide and  the ex-
cretion of the  diethyl phosphate moiety in
the urine is related to the parent compound.
Parathion is oxidized to the more toxic pro-
duct paraoxon, and it is this which is largely
responsible  for illness. Paraoxon is reflected
by the  excretion of diethyl phosphate (DEP)
so  that high concentrations  of the oxon
derivative are seen in the urine in poisoned
victims.  Paranitrophenol  is  the phenolic
moiety and the identification of this in urine
facilitates the specific diagnosis of the pesti-
cide involved  in  the  exposure,  for  para-
nitrophenol  is  only  found  in  the urine
following exposure to parathion and two
other pesticides being used  today (EPN and

                                      Both  the alkyl phosphate and phenolic
                                   metabolites have been found to be excellent
                                   indices of exposure if this exposure is a
                                   significant one,  such as occurs in occupa-
                                   tional and accidental exposure. The follow-
                                   ing chart illustrates the sequential  excretion
                                   of these  metabolites expressed as concentra-
                                   tions of the  metabolites per milliliter in a
                                   parathion poisoning case.



                                      Intact Pesticide Studies
                                        The intact pesticide  may be identified in
                                      blood, in other body tissues, and in gastric
                                      washing by electron capture gas chromato-
                                      graphy using a flame photometric detector.

      APPENDIX 5

For assistance in any transportation emer-
gency involving chemicals (in the continental                   45
  PHONE: Day or Night—Toll-Free

    *800- 424-9300
   'Add long-distance access number if required
  483-7616 in District of Columbia
For calls originating outside the continental
U.S.: 202—483-7616—Washington, D. C.


  CHEMTREC stands for Chemical Transportation
Emergency Center, a public service of the Manu-
facturing Chemists Association at its offices in
Washington, D. C.
  CHEMTREC provides immediate  advice for
those at the scene of emergencies, then promptly
contacts  the shipper of the  chemicals  involved
for  more  detailed  assistance  and  appropriate
  CHEMTREC operates around  the clock—24
hours a  day,  seven days a week—to receive
direct-dial toll-free calls from any point in the
continental United States  through a wide  area
telephone  service (WATS)  number, 800-424-9300
(483-7616  for  calls originating within  the District
of Columbia;  202-483-7616 for calls originating
outside  the continental U.S.).
  Shippers, including  MCA  members and  non-
members,  are notified through pre-established
phone contacts  providing  24-hour accessibility,
via information operators, or through  cooperation
of fire and police services.
  As  circumstances warrant,  the National Trans-
portation Safety  Board or  appropriate offices of
other agencies may be notified.
  CHEMTREC's capabilities have been recognized
by the Department of Transportation,  and a close
and continuing relationship is  maintained between
CHEMTREC and  the Department.


  Because chemicals find so  many uses and have
such  a  wide  range of characteristics,  there is
much need for information abput them—composi-
tion and purity, physical and chemical properties,
effects on people and  the environment, sources
of supply, etc. It is important to understand that
CHEMTREC is not intended and is not equipped
to function as a  general information  source, but
 by  design is confined to  dealing with  chemical
 transportation emergencies.  Drivers should  not
 call CHEMTREC on problems other than chemical
 cargo emergencies.


  CHEMTREC's  number has  been widely  circu-
lated  in  professional  literature  distributed  to
emergency service  personnel, carriers,  and the
chemical  industry, and has  been further  circu-
lated  in  bulletins of governmental agencies,  trade
associations, etc.
  Shipping documents of participating companies
are requested to include the  following: "For help
in chemical emergencies involving spill,  leak, fire
or exposure,  call  toll-free 800-424-9300 day or
  An emergency reported to CHEMTREC is re-
ceived by the Communicator on duty, who records
details in writing and by tape recorder. The Com-
municator then attempts to determine the essen-
tials of the problem (as detailed on the left column
of this page under "USER GUIDANCE").  This is
to enable him to provide the best available infor-
mation on the chemical(s) reported to be involved,
thereby  giving specific indication of the hazards
and what to do (as well as what not to do)  in case
of spills, fire, or exposure as the immediate first
steps in controlling  the emergency.  Information
on the  various  chemicals, as furnished  by the
producers,  is within  easy  reach.  Trade names
and  synonyms  of chemical  names are  cross-
referenced  for ready identification by  whatever
name is given.
  CHEMTREC's Communicators are not scientists.
They are chosen for their ability to remain calm
under emergency stresses. To preclude unfounded
personal speculation regarding  a reported emer-
gency, they are under instructions to abide strictly
by the information prepared by technical  experts
for their use.
  Having advised the caller, the  Communicator
proceeds immediately to notify the shipper  by
phone.  The known particulars of the emergency
thus relayed, responsibility for further guidance—
including dispatching personnel to the scene or
whatever seems warranted—passes to the shippei.
  Although proceeding to the second stage of
assistance  becomes more  difficult where the
shipper is unknown, the  Communicator is armed
with other resources to fall  back  on. For example:
Concerning radioactive materials, CHEMTREC can
call on  the Energy  Research and Development
Administration (ERDA). (Formerly Atomic Energy
  Identification of product  and  shipper is impor-
tant. Shipping papers are carried by truck drivers,
and in engine or caboose of trains. Car and truck
numbers and carrier names can be useful in trac-
ing  unknown cargoes.
  Mutual aid  programs exist for some products,
whereby one producer will service field emergen-
cies involving another producer's product. In such
cases,  initial referral may be in accord with the
applicable mutual aid plan rather than direct to
the shipper. Arrangements of this sort are estab-
lished on chlorine through the  Chlorine  Institutr
and on  pesticides through the National  Agricul-
tural Chemicals Association.
  The former has CHLOREP, the Chlorine Emer-
gency  Plan, in  which the nearest producer  re-
sponds  to  a problem. NACA   has  a  Pesticide
Safety   Team  Network  of  some 40 emergency
teams distributed  throughout  the country. CHEM-
TREC serves as the communication link for both

  In  Canada, the Canadian  Chemical  Producers'
Association operates a Transportation Emergency
Assistance . Program   (TEAP)  through  regional
teams prepared to give phone and field response.
  Many individual companies have well organized
response capabilities, for  their  own  products,
some of which preceded CHEMTREC by several
years.  This program  does not seek to displace
these, but rather collaborates  with them and en-
hances their  effectiveness.  CHEMTREC's single
telephone number affords this  opportunity.

  MCA is a trade  association  of chemical manu-
facturers, large and small, representing more than
90% of the production capacity tor basic indus-
trial  chemicals in the United States and Canada.
It has  long been active  in  programs  to improve
the safety of chemical shipping  containers, both
package  and bulk units, and their reliability  in
handling  and shipment,  thereby minimizing fail-
ures and leakage of contents under extraordinary
stress. Such efforts continue unabated.
  Nevertheless, despite, precautions taken, train
derailments,  truck  upsets  and  collisions, and
barge  accidents,  do  occur.  Such emergencies
deserve to  be handled  as well as  possible  to
minimize the consequences to life  and properly.
Emergency services—fire  and police—ate nor-
mally well prepared to cope with common mate-
rials, including certain flammables such as fuel
oil and gasoline.  Too often they are  at a disad-
vantage when chemicals are encountered, espe-
pecially since "what  should  be  done"—and  of
equal importance, "what should not be done"—in
the early stages may bear so  heavily  on the out-
come.  They  need accurate and clearly  under-
standable information to help them evaluate  the
situation and act with proper precautions for their
own safety,  as well as for  the protection of  the
general public.
  Realizing that personnel of chemical producers
possessed  the  necessary  expertise,  officials  of
concerned Federal departments approached MCA.
A study was undertaken  by  industry safety, pack-
aging,  and  transportation specialists.  After thor-
ough consideration, it was concluded that a single
center, nationwide in coverage and  accessible to
all through a single telephone number, would be
the  most expeditious arrangement—for contact
with it and for feedback from it. Following review
and  confirmation by  the industrial specialists  of
MCA's technical committees, CHEMTREC as now
in operation was a&thorized.
  CHEMTREC was established and continues as
a voluntary project of the chemical manufacturing
industry,  wholly supported through the Manufac-
turing  Chemists Association.  It became  opera-
tional on September 5, 1971.
  CHEMTREC can usually provide hazard infor-
mation warnings and guidance when given only
OF THE PROBLEM.  For  more detailed  informa-
tion and/or assistance, or if product  is unknown,
attempt to provide as much of the following infor-
mation as possible:
  Name of caller and call back number
  Location of problem
  Shipper or manufacturer
  Container type
  Rail car or truck number
  Carrier name
  Local conditions
  Questions regarding  the  operation of CHEM-
TREC should  be directed to: Manager, Chemical
Transportation Emergency Center, 1825 Connec-
ticut Avenue,  N.W.,  Washington, D. C.  20009.
Phone: 202—483-6126.

               APPENDIX 6
      V Attending Physician

      \/ Family Members
      V Employers

      V Hospital Emergency Room
      V Ambulance Service
      V Health Department
      V Local, County or State Police
      \/ Landowner

      \/ Pesticide Analytical Resource Laboratory
      >/ EPA Resource (if necessary)
      \' Chemirec (.n necessary)


Pesticide Verification

Robert Alt'man M.D., M.P.H.
Project Director
Epidemiologic Studies Program
New Jersey State Dept. of Health
\John Fitch Plaza
P. 0. Box 1 540
Trenton, New Jersey 08625
(609) 292-7608
Off-hour number: (609) 392-2020

Dr. Ana Barquet
Dept. of Epidemiology and
Public Health
University of Miami School
of Medicine
P. 0. Box 520875
Miami, Florida 33152
(305) 547-6972
(305) 235-6280
E. Gomes
152E. Stenger
San Benito, Texas 78586
Off-hour number:




EPA Regional Pesticide
Region Branch Chief
A. Charles Lincoln, Chief
EPA, Pesticide Branch
I John F. Kennedy Bldg.
Boston, Massachusetts 02203

Stanley Fenidiel, Chief
EPA, Pesticide Branch
II 26 Federal Plaza, Room 1005
New York, New York 10007

Nelson Davis, Chief
EPA, Pesticide Branch
Curtis Building
III 6th and Walnut Streets
Philadelphia, Pa 19106

Roy Clark, Chief
EPA, Pesticide Branch
345 Courtland Street, N.E. Ro
Atlanta, Georgia 30308
(404) 257-3222

Norman E. Dyer, Chief
EPA, Pesticide Branch
.VI 1201 Elm Street
1st International Bldg.
Dallas, TX 75270


Donald P. Morgan, M.D., Ph.D.
Project Director
Epidemiologic Studies Program
University of Iowa
Oakdale Campus, AMRF
Oakdale, I A 523 19
Off-hour number:

Dr. Darrell Brock
Acting Project Director
Epidemiologic Studies Program
Bureau of Laboratories
Department of Health & Welfare
Boise, Idaho 83707
(208) 384-2233




. Mitchell Wrich, Chief
EPA, Pesticide Branch
V 230 S. Dearborn St.
Chicago, IL. 60604

John Wicklund, Chief
EPA, Pesticide Branch
VII 1735 Baltimore Ave.
Room 249
Kansas City, MO 64 108
Ivan Dodson, Chief
EPA, Pesticide Branch
VIII Lincoln Tower Building
1860 Lincoln Street
Suite 900
Denver, CO 80203
(303) 837-3926
Jake McKenzie, Chief
EPA, Pesticide Branch
IX 100 California Street
Room 340
San Francisco, CA. 94111

Robert Poss, Chief
X EPA, Pesticide Branch
12006th Avenue
Room 1 1 -C
                                                                  Seattle, WA 98101

                              APPENDIX 8
                              (MEDICAL RECORD)
Name of Patient	
Age	Race	Sex _
Date of incident	Location of incident	
Taken to	Hospital or Clinic
Date of Admission	•_	
Address  .  	
Person to contact with results	Telephone No..
EXPOSURE HISTORY: (Circle Appropriate Information)
Type of pesticide exposure:       Ingestion             Dermal          Inhalation
Was this episode due to: Accidental Exposure  Suicide  Occupational Exposure
Name of pesticide involved	:	
EPA Registration No.	
Active ingredients.
Crop pesticide was applied to and target pest	
Time of last pesticide exposure of patient:                Hour	Date.
If Occupational Exposure patient was: (Circle)
   Applying Pesticides:                                                                                 g-j
           Aerially              Ground spray (hand)        Spray rig (mechanical)
           Loading            Picking crops       Mixing      .   Thinning crops

SYMPTOMATOLOGY DATA (Please Circle Appropriate Information if Present)
   Weakness    Sweating        Nausea          Vomiting          Diarrhea
   Abdominal Cramps       Excessive Tearing              Excessive Salivation
   Excessive Bronchial Secretions       Shortness of Lieath    Pains in Chest
   Blurring of Vision           Convulsions           "her	
SIGNS (Please circle appropriate information if present)
   Miosis (less than 5 mm)      Muscle twitching           Muscle fasciculations
   Bronchial spasms            Bronchial exudation
   Cholinesterase Screening Test:        Positive       Negative
  ' Other	

                          Date    Time
1. Heparinized blood                           Collected before 2-PAM Administration?
                                                      YES  NO
                                             Atropine Administration?
                                                      YES  NO
2. Urine
3. Other

                  ADDITIONAL COMMENTS:
Such as—
  • important details relating to victim's pesticide exposure
  • others affected and how
  • other damage caused by occurrence.
                      Send specimens and this form to one of the following laboratories:
                   Robert Altman. M.D., M.P.H.
                   Project Director
                   Epidemiologic Studies Program
                   New Jersey State Dept. of Health
                   John Fitch Plaza
                   P. O. Box 1540
                   Trenton, New Jersey 08625
                   (609) 292-7608
                   Donald P. Morgan, M.D., Ph.D.
                   Project Director
                   Epidemiologic Studies Program
                   University of Iowa
                   Oakdale Campus, AMRF
                   Oakdale, Iowa 52319
                   (319) 353-5558
               Dr. Ana Barquet
               Dept. of Epidemiology and Public Health
               University of Miami School of Medicine
               P.O. Box 520875
               Miami, Florida 33152
               (305) 547-6972
                                                                  E. Gomes  .
                                                                  152 E. Stenger
                                                                  San Benito, Texas 78586
                                                                  (512) 399-5352
               D. Darrell Brock
               Acting Project Director
               Epidemiologic Studies Program
               Bureau of Laboratories
               Dept. of Health and Welfare
               Boise, Idaho 83707
                                                                 •U.S. GOVERNMENT PRINTING OFFICE I  1976 0-720-335/6035