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UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
REGION 1
J.F. KENNEDY BUILDING, BOSTON, MASSACHUSETTS 02203-2211.
Curren t A wareness
An Introduction, With Technical Explanations, To...
Pesticides and Safety
by
N. A. Beddows
January 1993
This material is presented in support of the
U.S. EPA Safety, Health and Environmental Management Division's
Center of Excellence Program.
PRINTED ON RECYCLED PAPER
ft T n

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Pesticides and Safety
By Norman A. Beddows, CIH, CSP
Abstract
This article is intended to support the U.S. EPA
Safety, Health and Environmental Management
Division's efforts, under its Center of Excellence
program, to promote en awareness of pesticides
and safety in agriculture and industry. It provides
basic training material and some advanced safety
program information. it is intended to be useful to
safety engineers, industrial hygienists, state
inspectors and professionals who work in
pesticide programs or have an interest in
promoting superior safety programs.
A systematic approach is used to explain
pesticide structures, functions, physical-chemical
properties, and human pesticide absorption,
distribution, metabolism and elimination.
Five families of pesticides are used to show
basic principles: 1! Thio- and organo-phosphates.
2) Carbamates. 3) Triazines. 41 Organoch/orines.
5) Chlorophenoxyalkanoic acids. Other families
are referenced for a future leisurely review.
Information is provided on historical-use
patterns of risk and hazards identified with
certain pesticides. The FIFRA toxicity categories
are explained. Limitations in using acute toxicity
data are discussed. Water solubility, persistence
and fate, and soil mobility - factors of public
safety • are explained.
The 1992 EPA Worker Protection Standard (40
CFR Part 170, August 21, 1992 Federal Register)
is described. Personal protection is explained.
This includes selection of protective clothing,
respiratory protection, qualitative respirator fit
testing and checking, controlling personal
exposures, and decontamination.
Medical monitoring and a basic risk-based
monitoring program, pesticide poisoning and first-
aid are discussed. Emergency response actions
and regulatory reporting requirements are
explained. Information sources are identified.
Disclaimer
This presentation is the sole responsibility of the
author. The information is believed to be
accurate, however, no claim is made for accuracy
or official Agency approval.
Introduction
Pesticide is defined in the Federal Insecticide,
Fungicide and Rodenticide Act [FIFRA] as "any
substance or mixture of substances intended for
preventing or destroying, repelling or mitigating any
pest, and any substance or mixture of substances
intended for use as a plant regulator, defoliant or
desiccant." Pesticides can be simple substances
(copper sulphate); complex compounds (dieldrin); or
biological agents (Bacillus thuringiensis, BT-
bacteria). Hundreds of substances are used as
pesticides. They must be registered for domestic use
by the U.S. Environmental Protection Agency. The
agency restricts their use, sale and distribution to
protect public safety and the ecology, while still
allowing for their beneficial and necessary use.
Restricted pesticides can only be used by a certified
pesticide applicators.
For registration purposes, EPA lists pesticides in
four categories: Agricultural Pesticides (List A),
Agricultural Pesticides and Antimicrobials (List B),
Microbials (List C), Low Production Pesticides, and
Microbials (List D). This arrangement is useful in
considering key safety questions: How is a pesticide
toxic? What happens when it enters the body? What
is its environmental fate, persistence and mobility?
What public safeguards are appropriate?
Familiarity with pesticide families, structures,
chemistry and physical properties is necessary to
understand pesticides and safety. Most commercial
pesticides have readily discernible structures,
functional groups and properties. We need to keep
in mind, however, that even when much is known
about a pesticide, in the real world environment it
can act in an unexpected way relative to what
happens in the laboratory. Changing conditions,
competitive processes, ecological complexities and
species toxicity differences are the order of the day.
Also, a slight change to a chemical can cause a
dramatic change in toxicity, and a simple spacial or
optical property change can affect a chemical or
toxicological situation.(1)

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Although much is known already, there are
limitations to looking at chemical arrangements to
predict properties. Structure-property-activity
relations are still being studied, and computer
predictive models are evolving. Data gaps in
information on subchronic toxicity are common-
place. And, most importantly, real world situations
are often different from what is seen in laboratory
settings (nevertheless, laboratory investigations are
very necessary).
For our purpose, we will look at five pesticide
families and some aspects of their compositions,
toxicities, and physical-chemical properties:
*¦ Thiophosphates and Organophosphates
~	Carbamates
~	Triazines (with two major groups)
~	Organochlorines (with three major groups)
~	.Chlorophenoxyalkanoic Compounds.
There are about twenty other commercially
important families and hybrids of families, all with
at least one characteristic or biological feature. Some
of these families (which we will not be considering)
are the acetamides, anil ides, amides (diuron,
methomyl), carbamoyl compounds (quinoamid),
carboxylic acids (dicamba, picloram),
dithiocarbamates (sodam), chrysanthemum
(dimethrin), nitrogen alicyiics (diazinon, a
pyrimidine; nicotine, a pyrrole), nitriles (chlorotha-
lonil), nitrophenolics (dinoseb), organo-metallic
compounds, picolinic acid compounds, phenols
(catechol), sulfonamides (chloramine T), thiazoles
(vancide), sulfones (aldicarbsulphone), uracils, and
ureas (ureabor). The reader can research these families
at leisure (see Sources of Information, at page 231.
The Thio/Organophosphates
The thiophosphates and organophosphates, named
"OPs\ are insecticides which act by inhibiting
choline esterase (choline ester-splitting enzyme).
An enzyme is a protein which speeds up a specific
reaction (a co-enzyme may be necessary}. An enzyme's
name is based generally on the action and the substrate
involved, and it ends generally in "ase."
One ChE-enzyme is acetylcholine esterase (AChE).
AChE causes the spontaneous disruption of the acetyl
choline-muscle cell receptor complex which is formed
immediately following an impulse to the neuro-muscular
synapse. This disruption occurs immediately after the
acetylcholine ester has depolarized the muscle cell
membrane. which it does in response to the impulse.(2)
The generic formula for thio/organophosphates is:
[R10-,Rs0-,R30-]P=X, where Rx and R, are methyl
or ethyl groups; R, is an alkyl, aryl or heterocyclic
structure; and X is a sulphur atom attached to the
central phosphorus atom (...P=S, a thion) in a
thiophosphate, and attached to an oxygen atom
(...P=0, an oxon) in an organophosphate.
Malathion is a leading thiophosphate insecticide.
Trichlorfon is an organophosphate. Structures are
shown in figure 1.
S
(CH30)2-P-S-CHC00C2H5
dHjCOOCjHj Malathion
(CH30)2-P-0^^-N02 Parathion

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In the body (and in the environment, also), these
pesticides are metabolized to simple alkyl phosphates
(and phenols). Metabolites can be found in urine and
blood within hours of pesticide uptake. (5)
Certain OP-pesticides have high acute dermal
toxicity. For example, tepp, phorate and demeton.
Mevinphos has a notably high acute dermal toxicity
(dermal LD-50, male rat: 4.7 mg/kg). Other OP-
pesticides, for example, azinophosmethyl and
malathion, have oral toxicities which are greater than
their dermal toxicities. Yet others, for example,
abate, parathion, methyl parathion and mevinphos,
have high dermal and oral acute toxicities.
The thio-OP pesticides can act synergistically with
members of their own class. Malathion, one of the
least acutely toxic OP-pesticides, is strongly
potentiated by trichlorfon. Numerous other cases of
potentiation are known.(6) This points out how
important it is for the user not to mix pesticides.
Certain Op-pesticides (e.g., leptophos) pose risks
of acute and delayed neurological problems,
especially with poor personal hygiene practices.
OP-pesticides have been used as human and animal
therapeutic agents, and in human volunteer
experiments.(7) This has provided rare, useful
information on metabolic changes, rates of uptake,
and rates of inhibition and restoration of
cholinesterases in plasma and red blood cells.
Trichlorfon, (CH30)2P(=0)0CH(0H)CC13, which
has a low oral toxicity to small rodents, has been
used to treat schistosomiasis: liver fluke disease.
Studies of this therapeutic use show that trichlorfon
metabolizes in the body to dichlorvos (DDVP), a
pesticide itself. This involves de-hydrohalogenation
(in this case, loss of the elements: hydrogen, oxygen
and chlorine) of trichlorfon, with the terminal -CC13
group becoming a ..CC12 end group. DDVP is more
acutely toxic than trichlorfon (LD50, rat, oral: 50
mg/kg, and 250 mg/kg, respectively). In therapeutic
use, trichlorfon, at a single human dose in the range
of 5-20 mg/kg, is absorbed rapidly into the blood
(within 1/4 hour). Rapid and extensive (90%)
inhibition of plasma-ChE occurs. Restoration (by the
liver creating new enzymes) of lost plasma ChE is
relatively fast. RBC cholinesterase is inhibited to a
lesser extent than is plasma cholinesterase. However,
restoration of lost RBC-ChE activity is slow because
new red blood cells have to form, and this occurs
only at about one percent per day. With repeated
therapeutic dosing, proportionally more RBC-ChE
inhibition occurs. Reportedly, a single treatment
with a dose in the stated range may be accompanied
by mild to moderate clinical signs of poisoning
including disturbance of the gastrointestinal tract.
With higher, single-dose regimens, injury to the
peripheral and spinal cord nerves may occur (this is
believed to be a risk with continued low dosages,
also). Elimination of trichlorfon takes several days,
by urine excretion mostly, but also via expired air.
Urine metabolites are monomethyl and dimethyl
phosphates. In a study involving administering
Propoxur intra-muscularly in single doses to adult
males, a 1.5 mg/kg dose caused a 70 percent RBC-
ChE loss, tremors, a drop in blood pressure and
vomiting. These are the signs of OP-poisoning. (7)
Environmental Persistence and Fate
The thio/organophosphates as a class are not
persistent (e.g., the half-life of parathion is about
one week, and for malathion, one day), however,
some members are persistent (e.g., abate). They are
similar in toxicity or more acutely toxic than the
organochlorines, which they have largely supplanted
in use. In soil, they are degraded initially to alkyl
phosphates (with phenols). Degradation involves
hydrolysis, oxidation, reduction and de-alkylation.(8)
Following a spill on soil, an OP-pesticide can be
persistent. Micro-organisms which normally reside
in soil and which catalyze degradation reactions are
destroyed in the resulting high (i.e., 100 ppm or
greater) concentrations of the pesticide in the top
soil. Also, certain members have very low water
solubility (abate: FIFRA toxicity category III, one
part per billion water solubility).
The Carbamates
The carbamates are insecticides, nematicides and
acaricides; they are cholinesterase inhibitors. Well
known examples of the family are aldicarb
(tradename TEMIK) and carbaryl (tradename
SEVIN). Their basic structure is -0-C(0)-NH-R,
where R is hydrogen or an alkyl (e.g, methyl) or an
aryl (e.g., phenyl) radical. When R is methyl (CH3)
the family is known as the N-methyl carbamates - an
important class of insecticides. TTie nucleus of the
carbamates is (the hypothetical) carbamic acid. Loss
of the nucleus, [-0-C(0)N < ], causes any derivative
to lose anticholinesterase activity.

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The essential structural aspect is shown in figure 2.
CH3-S-C[CH3)2CH=N-0-C(0)NHCH, Aldicarb
0-C(0)-NHCH3 Carbaryl
00
Figure 2. Formulas of Common Carbamates
Toxicology of Carbamates
The carbamates are toxic primarily because they
inhibit esterase function in nerve impulse
transmission. In this respect, carbamates are like the
organophosphate insecticides. Inhibition occurs
because a carbamyl-enzyme complex is formed. The
bond strength of the carbamyl-esterase complex,
however, is not strong. The complex can dissociate.
This labile bond feature accounts for esterase
inhibition by carbamates being reversible.
The carbamates have generally lower oral and
dermal toxicities than the thiophosphates and the
organophosphates. However, across the family,
acute toxicity is widely spanned due to differences in
specific anti-ChE activity. Aldicarb and carbaryl
show major differences in toxicity, both orally and
dennally (aldicarb: oral LD-SO. 0.9 mg/kg: dermal
LD-50, 3 mg/kg. Carbaryl: oral LD-50. 255 mg/kg:
dermal LD-50, 2 grams/kg).
Exceptions exist to carbamates being generally less
toxic than the organophosphates. The carbamate
pesticide aldicarb is several orders of magnitude
more acutely toxic than malathion (a thiophosphate).
Aldicarb is extremely toxic (orally and derm ally).
Carbaryl, the leading carbamate, is moderately toxic
to humans. With uptake, it is quickly metabolized to
l-naphthol, via the liver.(9) This (sparingly water
soluble) metabolite is subsequently conjugated (as o-
glucuronide and sulphate derivatives), detoxification
in this case, and eliminated in urine.
Certain metabolites of the carbamates are more
potent anticholinesterase agents than the parent
pesticides. Temik initially metabolizes to temik
sulphoxide, a potent anticholinesterase agent.(10)
The carbamates act fast in inhibiting brain and
plasma cholinesterase. Sweating, headache, nausea,
blurred vision, pulse-quickening and a rapid increase
in systolic and diastolic blood pressure occurs with
overexposure. Recovery is also fast, reportedly
occurring within hours after cessation of exposure.
. The ChE-inhibitory effect of carbamates is
reversible. That is, the binding of the functional part
of the pesticide to the enzyme surface is not
especially strong.(ll) This accounts for the usually
limited duration of a cholinergic episode with
carbamate poisoning, and the generally large span
between an acute dose which produces symptoms of
poisoning and a dose which is life-threatening (such
| a large span is not seen in the case of the
organophosphates). Neural damage, unrelated to
ChE inhibition, has been associated, but only rarely,
with carbamates. (12) Reproductive risks are bet ieved
to be negligible, but carbaryl is teratogenic.(13)
I Environmental Persistence and Fate
This family of pesticides are moderately persistent
| to persistent in soils. Aldicarb, with a summer half-
| life of one month, is persistent (seven half-lives is
j the approximate period to virtual -99%-
] disappearance). In water (solubilities can be a few
I percent), they have limited stability, that is, days or
weeks. Their fate in soil is hydrolysis and
degradation to mineralization; certain degradation
intermediate products are relatively stable, e.g., 1-
naphthol from carbaryl.(14)
Before leaving the carbamates, we should mention
that sulphur analogues, i.e., [R, R'N-C(=SI-S-]-, ex,ist in
two (single or condensed) molecular arrangements. These
analogues have no or only weak anticholinesterase
activity. They are fungicides. The sulphur analogues are
the:
*¦ Thiocarbamates. These have a single arrangement,
e.g, metham-sodium: CH3NHC(=S)S' Na*. 2H20.
* Ethylene bisffithloqarbamates, known as the EBDCs.
The EBDCs have a condensed 1-S-S-] arrangement,
e.g.. zineb: [-S-C(=S}NH-CH2-N-C(=S)-S-Zn-] x.
Certain EBDCs are metabolized to ethylene thiourea
(ETUJ. ETU is fetotoxic, teratogenic and carcinogenic
in rodent tests, and is mutagenic in the Ames bacteriaI
(Salm. Typhi, HJS-T1530) assay.(15)
The Triazines
The triazines are herbicides which are used alone
or in combination with other herbicides (as selective
and non-selective preparations). They exist in two
ring-forms: symmetrical (sym or s) triazine, and
asymmetrical (asym) triazine. The electron resonance
(that is, the singie-double-single bond arrangement
alternating between carbon and nitrogen atoms in the
ring) in the symmetrical triazines gives relatively

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greater chemical stability compared to die
asymmetrical form. Atrazine, propazine and
simazine are common s-triazines. Metribuzine is a
common asymmetrical triazine. The two molecular
forms are shown in figure 3.
Atrazine (s)

o Metribuzin (asym)
rV
9CH,
Rgura 3. Symmetrical and Asymmetrical Triazines
The triazines are solids which are lowly to
sparingly water-soluble (e.g., atrazine, 33 ppm, at
25°C, metribuzine, 1220 ppm). They are moderately
soluble (several percent) in alcohols and esters. The
air volatility of the triazines is low. Also, their
melting points exceed 170°C. These properties
contribute to their avail ability for degradation; they
do not actually cause persistence.
Toxicity of the Triazines
The triazines are generally moderate in acute oral
toxicity (>1000 mg/kg, rat) and in skin effects.
However, atrazine itself is a contact-dermatitis agent,
and simazine is selectively highly toxic to sheep.
Inhalation of dust is a major route of entry. Poor
personal hygiene in handling these materials is likely
to result in chronic eye and skin irritation.
Persistence and Fate
The triazines are moderately persistent to persistent
in soils. Atrazine applied to soil at recommended
levels has a half-life of one to three months,
depending on the circumstances. In spills on soil and
even with normal applications in arid regions, the
triazines tend to be highly persistent(16) Sunlight
(ultraviolet light) causes rapid degradation of the
triazines at the surfaces of plant leaves, and in
shallow waters. Microbial enzymes degrade the
triazines via substitution or elimination of major
groups, that is, by hydroxylation,.de-amination, and
de-alkylation. The nucleuses are relatively stable. A
principle soil metabolite of atrazine is
monohydroxyatrazine (substitution of -CI by -OH).
Elimination of an alky/ group is termed de-alkylation.
Elimination of an amine group is termed de-amination.
Sofl metabolites of the triazines are variable in
their chemistry, physical properties, mobility and
biological activity. Monohydroxyatrazine from
atrazine has a pKa = 5.15. It is only partially
ionized in mildly acid soils (pH, 5 to 6) but it is
completely ionized in alkaline (pH, 8.5 or greater)
soils. Acidity affects leaching of triazine
metabolites.(17) Monohydroxyatrazine is non-
phytotoxic (the chlorine atom on the atrazine ring is
substituted by the hydroxy! group). Reportedly,
other metabolites of atrazine which keep the parent
ring's carbon to chlorine bond intact are phytotoxic
(as expected). Figure 4 shows a scheme of atrazine
metabolism consistent with these reactions.
CI -suasrmjTtOM 01 -a By -oh- Ot4

CI H/*	~
/ATHASNfi H
H HYDROXY O
ATRA2JNS i
\
M- C(CH

OCSSTHYVATRA21NE
—lOSS OF ETHYL-
MSSOFIIOm-ATRAZINI
—loss or tsopflopvu
Figure 4. Mode of Atrazine Fate in Soil
Hie persistence of atrazine has caused a problem in
the past to suppliers of drinking water. Run-off from
treated farm fields has caused contamination of
sources of drinking water in the Mississippi basin.
The solubility of atrazine is 33 parts per million: the
U.S. allowable concentration for atrazine in drinking
water is 3 parts per billion, as an annual average. The
Canadian Water Quality limit is 2 parts per billion, based
on the preservation of water algae and plants necessary
to support aquatic life.
The Organochlorines
The organochlorines started to be used extensively
in the early 1940s. By die 1950s, they were used
world-wide. Today, their availability and use have
been sharply curtailed. In the U.S.A., most members
of the class have been canceled because of their
histories and potential to harm wildlife and habitat
This family deserves review because of its
historical importance and use in other countries.

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There are three groups in the family:
*¦ The chlorinated ethanes (DDT)
* The cyclodienes (chlordane and dieldrin)
~ The chlorinated cyclohexanes (lindane).
The family is virtually insoluble in water. The
groups are shown in Figure 5.
LINDANE
Gamma taomar
-rs.
DOT
aOtrO*a
aeLotvN	w ca,v—'
Figure 5. Groups in the Orgsnochlorine Class
Toxicity of the Organochlorines
The organochlorines are systemic poisons - contact
and neuro-poisons which enter the body via the
gastrointestinal tract but. also via the lung (as
particulate) and the skin. Lindane (gamma), dieldrin,
chlordane and heptachlor are efficiently absorbed
through intact skin.
The main toxic action with this family of pesticides
is interference with ionic processes across nerve cell
membranes (sodium channels). These pesticides do
not significantly inhibit cholinesterase.
The consequence of such interference is motor and
sensory nerve irregularities and early convulsion,
even when no other signs occur. Toxaphene and the
cyclodienes in general cause early convulsion.
Severe poisoning by pesticides in this family is
likely to result in jerking movements, seizures,
tremors, dizziness, and tingling of the tongue, lips
or face. In a severe case, jerking movements are
severe, and convulsion and respiratory depression
occur. This is life-threatening. With chronic
exposures, blood disorders, liver injury and cancer
are believed to be low-level risks.
The lowly water soluble organochlorines in the
body partition between blood and fat, mostly going
to fat where they are stored. Persistence in fatty
tissues is a hallmark of DDT and some others on the
family. Traces of organochlorine pesticides and their
(epoxidized) metabolites may be found in maternal
milk (a primary excretion route). Heptachlor and a
metabolite (heptachlor epoxide) can cross the
placenta. DDE is a DDT metabolite which may still
be detected at trace levels in a high percentage of
fish. [DDE; (ClC^iC=Cy.
Despite their propensity for long term storage in
fat tissue, the organochlorines do metabolize as they
circulate (at low concentrations) in the blood. For
example, DDT and related substances are reductively
dechlorinated and oxidized in steps. The metabolites
include DDE (an ethene) and a carboxyiic acid.
Overall clearance (via feces and urine) is slow
because of the one-sided distribution of these
hydrophobic substances. DDT has been found in fat
tissue of pesticide workers whose last exposures
were many years ago, and in persons who reside
near defunct DDT manufacturing sites. (18)
Currently, there is no evidence that the reported
body burden causes disease; however, little is known
about the biological effects of persistent toxic
chemicals in man or other mammals.
The organochlorines show acute oral toxicities
ranging from (FIFRA toxicity category) low order of
toxicity (e.g., DDT, with an LD-50 oral, rat: 113
mg/kg.) to toxic (e.g., dieldrin, LD-50 oral, rat: 37-
87 mg/kg).
Specific antidotes to the organochlorines do not exist.
Prescribed medical treatment includes decontamination,
stomach lavage, and medication to control convulsions,
seizures, and pulmonary and cardiac irregularities.
Animal or vegetable oils must not be given in poisoning
by these pesticides. To do so, will enhance
gastrointestinal absorption.
Environmental Persistence and Fate
The organochlorines are moderately persistent to
persistent in soil, with a few exceptions (e.g.,
toxaphene, and DDT in strongly alkaline soil). In the
past, the organochlorines and their terminal
(chlorinated) residues in soil have caused major
ecological problems through direct action or
bioaccumulation. These pesticides are degraded via
dechlorination, hydroxylation, and oxidation to a
variety of substances, some of which can have
residual pesticidal properties if chlorine is present in
their structures.
The Chlorophenoxyalkanoic Compounds
These compounds are post-emergent herbicides;
plant growth regulators. Three well known pesticides
are 2,4-D, 2,4,5-T, 2,4,5-TP (canceled by EPA).
2.4-D is 2,4-dichtorophenoxyacetic acid.
2,4,5-T is 2.4,5-trichlorophenoxyacetic acid.
2.4,5-TP is 2,4.5-trichorophenoxypropionlc acid.

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7
The chlorophenoxyalkanoic pesticides are based on
(chlorinated phenoxy) acetic acid and propionic
acids. They are manufactured as acids, salts, esters
and amides which have different water solubilities.
They are applied aerially and on the ground as
granular material, liquids or aerosols.
Figure 6 shows the formulas of two members
based on acetic acid: 2,4-D and 2,4,5-T, and one
based on propionic acid: 2,4,5-TP, Silvex™-
OCH,COOH	OCH,COOH	OCHICHJCCOH
o° .c5° jy
° 2,4-D Q 2,4,5-T ° 2,4,5-TP
Figure 6. Chlorophenoxyalkanoic Acid Types
Toxicity of the Chlorophenoxyalkanoic Acids
All are orally toxic and can injure the kidneys and
the liver. At the cellular level, mitochondrial activity
(oxidative phosphorylation) is affected. They are
dermally toxic. Severe chloracne and peripheral
neuritis are risks with chronic skin contact. Birth
defects and soft tissue cancers are reported to be
hazards with this class. 2,4-D, however, is listed,
by the EPA Office of Pesticide Programs (OPP), as
a Class D oncogen: "not classifiable as to human
carcinogenity." The acid form, the sodium salt, and
the diethanolamine salt of 2,4-D are FIFRA toxicity
category III pesticides (orally and dermally). The
isopropyl ester is toxicity category II (oral, rat).
In past manufacturing of 2,4,5-T and 2,4,5-TP, a
simultaneous side {condensationI reaction' involving
substituted sodium phenoiate intermediate yielded dioxin
(2,3,7,8-TCDDJ in trace amounts (hence the 1979 EPA
cancellations of 2,4,5-T and 2,4,5-TP). Dioxin is highly
toxic (LD50, oral, guinea pig: <0.001 mg/kgI. It is a
carcinogen(19J. Because of its chemical stability, high
temperature incineration is required for destruction.
Solubility of the Chlorophenoxyalkanoic Acids
This family of pesticides has a wide range of water
solubility. This is because it comprises various acids,
salts, amides and esters. The free acids and higher
molecular weight esters are the least soluble; the
potassium and sodium salts, and the lower molecular
weight esters are the soluble members of the family.
The acid forms of-these herbicides are influenced
somewhat by acidity. With a weak organic acid, low pH
suppresses ionization, this tends to decrease solubility;
and high pH increases ionization, this tends to increase
solubility. With a weak base, the converse is true.
Environmental Persistence and Fate
Salts and low molecular weight esters/amides of
the acids are appreciably water soluble and migrate
readily under a water head. In some circumstances,
they may not reside long enough in soil to fully
degrade, despite their reactivity. 2,4-D (acid)
degrades rapidly (aerobically) in silty clay or loam
soils. These pesticides in soil are non-persistent to
moderately persistent, their fate in soil is primarily
chemical and biological hydrolysis, oxidation and
dechlorination. Despite an appreciable reactivity and
a low solubility, some pesticides in the family
(including 2,4-D) may be detected in groundwater.
Pesticides and Historical Patterns Of Risk
Non-occupational as well as occupational exposures
(skin, oral, and G.I.intake) are a concern with
pesticide exposure. Children, older people, and some
otherwise healthy people who are genetically pre-
disposed to be abnormally sensitive to pesticides may
be at risk. Occupational health risks (including
cancer) and ecological risks have been associated
with farming, manufacturing, and agricultural
operations, and the use of certain pesticides.
Historical risks of acute health impairment and
ecological impact with exposures and use involving some
pesticides are described summarily below:
>	Acute oral toxicity risk in handling demeton,
fluoracetamide and strychnine.
>	Acute Inhalation toxicity risk in handling and using
carbofuran, chloropicrin, clonitralid, disulphoton, ethyl
parathion and su/fotepp.
~	Acute dermaf toxicity risk in handling aldicarb,
chiorfenvinphos, clonitralid, phorate, dichrotophos,
dioxathion, and disulfoton {allergic sensitivity with
anilides. benzonitriles, dithio- and thiocarbamates,
carbanilate, thiophthatidomides and benomyl.
~	Adverse effects on mammals, birds and bees with
using demeton, EPN, methamidophos, methomyl,
methyl parathion, mevinphos and phorate.
*¦ Residual non-target adverse effects on plants, aquatic
and avian life with using aldicarb, ethyl and methyl-
parathion, chloropicrin, picloram, and zinc phosphide.
Fenitron, carbofuran and monocrotophos have been
especially harmful to kestrels, owls and songbirds.

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Absorption and Elimination of Pesticides
Animal studies using radioactive carbon-labeled
pesticides, and studies of pesticide handlers and
workers have provided information on pesticide
absorption, distribution, metabolism, and
elimination. Pesticide absorption from the
gastrointestinal (GI) tract can be fast (minutes) or
slow (hours), depending on the pesticide, its
solubility, the stomach contents and other factors.
Fast human absorption occurs with 2,4,5-T,
atrazine, carbaryl, dalapon, diazinon and
metalochlor. Slow absorption is seen with paraquat
and simazine. Absorption of the ionizable pesticides
(e.g., those with a carboxylic acid, a phenolic, an
amino or a quaternary ammonium group) occur at
different rates in the Gl-tract. One reason is that
ionization (and hence transport across epithelium) is
affected by acidity, and the acidity of the Gl-tract
varies. Saliva is variably slightly acid or alkaline;
the stomach and small intestine are strongly acidic
(gastric juice: hydrochloric acid, pH, 1); the large
intestine is slightly alkaline (pH, 8.4).
Pesticides entering the Gl-tract get into the blood
in one form or another through the small intestine
mostly, but also through the large intestine where
bacterial action may convert (reduce) an insoluble
pesticide to a soluble moiety which is absorbed
through the mucosa at this level, as well as
eliminated in the feces. Once in the blood, they enter
the liver in one or two ways (portal vein, hepatic
artery) where they are metabolized. Pesticides and
metabolites distribute to different degrees to various
parts, organs and fluids of the body. Certain highly
chlorinated, ring-type pesticides and some
organophosphates go to adipose tissue where they
may reside for long periods.(20) Certain metabolites, -
formed during circulation of the parent pesticide in
the body, when tested conventionally for acute
toxicity, are more toxic than the parent.(21)
Propoxur is metabolized to (4)-hydroxypropoxur,
which is several times more effective in inhibiting
cholinesterase activity than propoxur.
Elimination of metabolites occurs mostly via urine
but also via breathing (eg, carbaryl eliminated in
exhaled air as carbon dioxide).
The fate of many pesticides in humans, and the
toxicity of the their metabolites, however, is not
completely known. Biotransformations are complex,
processes are dynamic, and research is costly.
Neurotoxicity of Pesticides
Neurotoxicity is the property of a substance to
cause any adverse effect on, or disruption of, the
function of cells throughout the body involved in
transmission of nerve impulses. One aspect of neural
toxicity with several major families of insecticides is
inhibition of cholinesterases in red blood cells and
plasma in some reversible or irreversible way. Such
neurotoxicity occurs, respectively, with the
carbamates and the organophosphates. Another
aspect of human neurotoxicity with pesticides is the
generally rare occurrence of delayed neuropathy,
which is a different kind of neural effect than that
which follows significant cholinesterase inhibition.
This involves damage to the axons of peripheral and
central nerves and possible axon demyelination, a
dying back of the nerve. Delayed neuropathy
manifests as weakness or paralysis of the limbs and
extremities; the effect may be persistent and even
irreversible. It has occurred, but only rarely, in
handling leptophos, some other organophosphates,
and some other pesticides.(22)
The families of pesticides which are known to be
capable of causing significant neurotoxic effects are
the organophosphates, carbamates, pyrethroids and
organochlorines. The EPA requires pesticides in
these families to be tested for neurotoxicity using
sensitive animal tests. The agency has issued
guidelines for neurotoxicity testing.
Mutagenicity of Pesticides
Mutagenicity is the property of causing changes to
living cells, directly or indirectly through DNA.
Mutagenicity from exposure to any chemical is a
concern because detrimental effects may arise in the
host or the progeny: cancer, reproductive hazards,
fetal injury, and impaired immune system. There do
not appear to be any hard evidence for pesticides
causing human mutagenic effects. However,
screening techniques using live animal cells (e.g.,
Chinese hamster ovarian cells), and bacterial cells
(e.g., histidine-dependent salmonella, as employed in
the Ames mutagenicity test), which are in vitro tests,
as well as studies using rodents have demonstrated
the potential of some pesticides to be mutagenic.
Reported to be mutagenic are: dichlorvos, dieldrin
and methyl parathion.(23)

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Carcinogenicity of Pesticides
In regulatory pesticide toxicology, it is a policy
position that the cancer-causing potential of a	j
pesticide is classifiable using a "weight of evidence"	I
consideration of the quality of the data associated	\
with (i) human evidence and (ii) animal evidence.	j
The scheme of classification used is described	j
summarily in the text box below.
REGULATORY TOXICOLOGY SCHEME for
CARCINOGENICITY CLASSIFICATION
» Group A: Human carcinogen, based on a
sufficiency of human evidence.	j
~	Group B: Probable human carcinogen,
based either on limited human evidence
{B1) or inadequate human evidence but
sufficient animal evidence (B2).
~	Group C: Possible human carcinogen,
based on limited animal evidence.
~	Group D: Not classified as to
carcinogenicity, because the human and
the animal data are inadequate or do not
exist.
~	Group E: No evidence in either human or
animal tests, based on well designed :
studies.
Using this classification scheme, amitrole, dieldrin and
sodium acifluorofen are designated probable human
carcinogens. Atrazine, baygon, bromacilandsimazineare
designated possible human carcinogens. Ametryn.
bentazon, carbaryl, dalapon, decamba, dinoseb, :
prometon and 2,4,5-T are classed Group D (for these
particular pesticides, the current data are not adequate to
assess oncogenicity). Diazinon and paraquat are Group E
Ifor these particular pesticides, the current data provide
evidence that they are not carcinogenic).
Reproductive and Fetal Toxicity
i
Reproductive toxicity can involve the male, the
female and the fetus. Several toxic end-points may I
be involved: sperm or egg damage, failure of the
fetus to survive, or abnormal development of
(teratogenicity), or impact on the health of, the |
offspring because of an exposure occurring at some j
critical period of development.
Hard data on human reproductive and fetal toxicity <
risks with pesticides are scant. Present knowledge is j
-.limited. However, some pesticides cause concern.
Tests on mice, rats and rabbits, and reported cases
of inadvertent pesticide uptake and resulting
teratogenic effects with monkeys in captivity (Tokyo
Zoo, Japan) are strong evidence that certain
pesticides present reproductive risks. Carbaryl is
reported to be an animal teratogen (24) and an
immunotoxicant. Pesticides which are suspected to
present human reproductive hazards include lindane,
aldrin, chlordane, dibromochloropropane, DDVP,
DDT, 2,4-D, methoxychlor, paraquat, diquat,
ethylene oxide, ethylene thiurea (from EBDCs),
captan (which is structurally similar to thalidomide,
the infamous human teratogenic drug of the 1960's),
DBCP, maneb and triphenyl tin.
Immunotoxicity of Pesticides
Suppression of activity of the human T-cells, B-
cells and other cytolytic cells (cells involved in the
mechanisms by which the body defends itself against
diseases) is an emerging concern with exposures to
pesticides.(25) Findings from in vitro screening and
animal tests (26) have given weight to the concern.
Mice exposed to sub-lethal doses of certain
pesticides have shown drastically reduced resistance
to bacterial and viral infections. However, at this
time, there does not appear to be hard data on
human immunotoxicity. Pesticides reported to be
immunotoxic to rodents are 2,4,5-T, acephate,
atrazine, captan, carbaryl, carbofuran, chlordane,
cypermethrin, dieldrin, dieldrin, endosulfan,
ethylparathion, fenitrothion, guthion, matacil,
methomyl, methylparathion, pentachlorophenol,
tributyltin salts and zineb.
Use of currently suspected immunotoxic pesticides
has been commonplace. Chlordane used to be the
standard of drug store pesticides. Tributyl tin salts
have been used extensively as a preservative in
marine paints and as a general biocide. Atrazine,
carbaryl, acephate and pentachlorophenol are in use.
FIFRA Toxicity Categories
Pesticide toxicity is categorized under FIFRA on
oral, dermal, eye and inhalation data from
mammalian tests. LD-50 data are central to the
process. Four toxicity categories are defined (at 40
CFR 156.10). The oral basis (only) of the FIFRA
toxicity categorization is given in the following text.

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10
FIFRATOX. CATEGORY. CLASS. LD-50 (Oral)
I	Highly Toxic 0-50 [MG/KG].
II	Mod. Toxic 50-100
III	Low Order 500-1000
IV	Least Toxic > >
In the FIFRA toxicity categorization scheme:
~	LD50 represents the dose which causes death in 50% \
of the test animals in a test. The value is obtained by \
interpolation of data and may be quoted as a range
when multiple tests have been made.
~	HIGHLY TOXIC (toxicity category II in regard to the j
route of entry means:
. Oral Route: a lethal dose to 50 percent of the
animals (LD50) of 50 (or lessI mg/kg.
. Inhalation: an exposure dose producing death in
half of the animals (rat, mouse, rabbit) at a
respirable concentration of 200 parts per million or \
less, with a one hour or less of continuous
administration.
. Skin Absorption: a 50% lethality response with a
dosage of 200 milligram or less per kilogram body
weight, with continuous bare skin contact for 24
hours or less, using 10 or more rabbits per test.
Common FIFRA Toxicity Category / Pesticides are: j
aciflurofen, alachlor, aluminum phosphide, arsenic acid,
azinphosmethyl, bomyl, calcium cyanide, captan, \
chlofenvinphos, chlorothalonil, copper hydroxide, copper I
8-quinolinolate, dichlorvos, dinoseb, endosulfan,
endothall, ethoprop, ethylene dibromide, ethylene oxide, |
fumarin, floroacetamide, magnesium phosphide, \
mecarbam, methyl parathion, mevinphos, naled, I
nemacur, nicotine, paraquat, parathion, |
pentachlorophenol (PCP, penta), phorate, phenyl mercuric
acetate (PMAI, serafume, sodanit, sodium arsenide, ii
sodium chlorate, sodium fluoracetate, temik (aldicarbl,
tenox and ureabor.
Handling FIFRA toxicity category I pesticides calls
for using high levels of personal protection
(respirators and outer clothing) to protect against
high respiratory and/or dermal hazards, and careful
personal hygiene practices. Handling FIFRA toxicity
category II or III pesticides also calls for the use of j
appropriate personal protection (stated in the I
pesticide label and MSDS).
|
Limitations of Acute Toxicity (LD-50) Data
>
i
i
For many pesticides, there are no available human {
data on which one could establish directly acceptable
short or long-term dose or exposure limits.
Certain pesticides which would appear to be safe
based on the acute toxicity data, that is, they have a
high LD-50 value, are designated as possible human
carcinogens, or are known to be neurotoxic, or are
suspected to be immunotoxic or present reproductive
and fetal hazards (based on tests on rodents). Such
possible effects are not indicated in acute toxicity
data. Also, the data do not indicate the potential for
pesticides to cause cholergic or other types of crises,
or to act either quickly or slowly, or to be toxic with
chronic low level exposures. Moreover, not all
reported LD 50 data are based on similar durations
of testing time.
To the last point, in acute inhalational dose-response
studies of certain common toxic gases (in particular,
chlorine, phosgene, and hydrofluoric acid!, response for
a particular adverse end point, such as lethality, is
expressed by a power function: C "T (where, C is
concentration; T, time; n is greater than unity, but less
than 3). That is, the relationship of concentration and
time, for a given response, is not linear. "Half the time,
double the dose" produces more response than does
"twice the time, half the dose".
Concentration-exposure/dose duration relation, for
sublethal endpoints, is an emerging area of study.
Currently, gaps exist in knowledge in this area and in
data relating to both short-term and long-term exposures
and associated effects and severity.
EPA Pesticide Fact Sheets. One should not assume a
pesticide is entirely safe on the basis of a high LD-50.
The entire data base needs to be reviewed before an
assessment is made.For this purpose, the Pesticide Fact
Sheet publications of the U.S. EPA are invaluable. They
provide information on uses; chemical characteristics;
toxicology characteristics; acute and chronic toxicity;
health risks; environmental characteristics; avian, aquatic
and non-target toxicity; health data gags; personal
safeguards, and more. Also, they identify experts and
other knowledgeable people, and where they may be
contacted.
Aquatic Toxicity of Pesticides
Fish and other aquatic organisms are affected by
pesticides and their metabolites.(27) Bioaccumulation
of pesticides and certain metabolites (e.g., DDE
from DDT) in crustaceans and fish is a concern with
the organochlorine pesticides. Fish have enzyme
systems which transform pesticides. This may
involve hydroxylation, de-hydrohalogenation,
oxidation and other steps. Some of the possible
metabolites are directly toxic to the fish.

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. Fish (flounder) cancers have been associated with
uptake of chlorinated bicyclodienes, subsequent
peroxidation by liver mixed functional oxidases, and
long-time retention of the resultant, lipophilic
metabolites. The transformed products themselves
are suspected to present a human health risk with
repeated ingestion of affected fish.
Aquatic toxicity of pesticides is highly variable.
Certain pesticides are specie-specific. Also,
biological activity depends on water temperature and
other factors. A pesticide at a low concentration
which is lethal to fish may be tolerated by water
insects, mollusks and crustaceans. Certain pesticides
which are relatively safe to humans, for example,
malathion, diazinon and pyrethrin-based pesticides
are highly toxic to fish and other aquatic life.
Certain pesticides which are highly toxic to humans,
for example, parathion and methyl parathion, are
relatively well tolerated by some aquatic species.
There are some pesticides which are highly toxic to
aquatic organisms, humans and other species.
Mercury, tin, copper salts, organic compounds of
these metals, nitrates and nitrites are toxic to humans
and all aquatic life.
Pesticides which are commonly thought of as safe
may be highly toxic to aquatic life. Pesticide
management is crucial for the good of aquatic life.
For illustration purposes only, some reported aquatic
toxicity data (LC-50, 96-hour, ug/l) for 01 certain fish
{bluegill or rainbow trout) and Hi) invertebrates are
respectively: Clorpyrifos -81, and0.04; diazinon - 640,
and 0.07; methyl parathion - 5411, and 11.0; ethyl
parathion - 1391, and 24.0; and malathion - 162, and
49.0.
ISource: Johnson D.W. and Finley. M.T.: Handbook
of Acute Toxicity to Fish and invertebrates. U.S. Dept
of the Interior. Fish and Wildlife Section, Publication
137, 1980].
Toxicity and Listed Inert Ingredients
Pesticides are frequently formulated with solvents
(e.g., xylene), emulsifiers and propellants, and they
may contain foreign substances. These materials may
be listed as inert ingredients. However, they may
contribute to health risks, or be toxic to non-target
species. Xylene can contribute to a dermal hazard by
increasing skin penetration through defatting of the
skin. It is highly toxic to water plants, and it can
affect the viability of bacteria - a factor of
persistence.
Important Public Safety Factors
The public is concerned with pesticides getting into
their foods, and pesticides showing up in drinking
water. Discussion of pesticide contamination of
vegetables and other foods is beyond the scope of
this discussion, except to say that the U.S. EPA and
the Food and Drug Administration (FDA) monitors
pesticidal chemicals in and on foods that infants and
adults consume1.
* A comprehensive report on pesticides in total diet
samples is provided in Gartrell, M.J, Craun, J.C,
Podrebarac, D.S, and Gunderson, E.L.: J. Assoc. Off.
Anal. Chem (Vol. 69, No.1, 1986). Also, specific
tolerances are listed in the Code of Federal Regulations,
at 40 CFR, Part 180.
The concern for pesticides and their soil derivatives
showing up in drinking water centers the water
solubility of pesticides, the persistence of pesticides
(and pesticidal metabolites) in soil, the rate of
degradation (to non-toxic products) and the mobility
of the pesticidal chemicals in soil under the influence
of surface and ground waters. Great concern is
shown by the public whenever a designated human
carcinogen poses a risk of contaminating an aquifer
or drinking water well. Important safety questions
are raised whenever pesticides are used near
communities. Safety specialists and others working
in pesticide programs ought to be informed of the
factors which underlie the public's concern. They
need to be aware of pesticide water solubility,
persistence and fate, and mobility in soil. These
matters impact public safety.
Water Solubility of Pesticides
Virtually all pesticides are soluble in water to a
degree which is at least an order of magnitude
greater that any acceptable safety limit for any
pesticide in drinking water. There are no rules to
estimating water solubility. However, pesticides
which are non-ionic or if anionic, are waxy are
lowly or only sparingly soluble. At the other
extreme, pesticides which are highly ionic (anionic
e.g., metam sodium, or cationic, e.g., diquat di-
bromide) tend to be highly water soluble (i.e., 50%
or greater). Stringent rules exist for the prevention
of water contamination. Pesticide handlers and users
need to be especially careful in their practices to
safeguard public health and protect the environment.

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Most of the non-ionic type families of pesticides are
• lowly water-soluble. However, there are exceptions
especially when oxygen or nitrogen atoms are part of the
chemical structure. Most of the ionic pesticides
(pesticides with Na*. K*. or quaternary ammonium salt.
R/J* structure) are highly water soluble.
Within any particular family, exceptions exist to the
genera/ case, especially when the pesticide is in a family
which is generally insoluble and it has an amino, hydroxy,
carboxyl, phosphate, or amide component. Only in the
(structural) extremes, may one assess accurately the
solubility order from the chemical formula. For example,
one would expect, and one finds, dieidrin to be insoluble
in water. And one expects, and finds, metam-sodium to
be very soluble (> 72%). Inside these extremes,
assessment of solubility becomes highly problematic and
a data base needs to be consulted. In the case of a weak
organic acid-type pesticide, that is. many of the
pesticides with a carboxylic acid functional group, one
would expect that in water with a pH which is
numerically two units greater than the pesticide's Pka
value, the pesticide would be at optimal solubility for a
given temperature. This is because at this pH, the
pesticide is virtually all ionized, and ionization optimizes
solubility: R-COOH <-in equilibrium -> R-COO' + H*.
The term pKa is a convenient way of expressing "minus
the log of the equilibrium constant of the appropriate
dissociation equation". PKa is mathematically like pH.
Some pesticides and metabolites which ionize, and which
have functional groups other than carboxylic acid, and
their respective, reported pKa values are: diazinon, 2.5;
prometryn, 4.05; hydroxyprometryn, 5.2; 2,4
dichlorophenol (from 2,4-D), 7.9; 1-naphthol (from
carbaryl), 9.34; and carbofuran phenol. 10.15.
Information on water solubility for a few pesticide
groups is - the quaternary ammonium salts (e.g.,
paraquat!, the carboxylic acids and salts (e.g., dalapon
and its sodium salt form), the sodium salts of phenolic
and thionyl compounds, and a few other pesticide
families are appreciably water soluble. Atrazine,
parathion, diazinon, and prometryn are soluble to
concentrations up to a few percent, depending on the
particular case. The thiophosphates and
organophosphates are lowly water soluble, except for
dimethoate - 2500 ppm, and a few others. The
organochlorines (aldrin, heptachlor, DDT) are soluble to
about 0.1 ppm. Metallic salts of 2,4-D and certain 2,4-D
amides and low molecular weight esters are appreciably
water soluble. However, 2,4-D itself (pKa = 2.97), is
sparingly water soluble (890 ppm, 25°C.). even though
it is virtually all ionized in neutral conditions.(28)
Water solubility is not suitable as a predictor of
pesticide mobility (also, it is not a useful indicator of
persistence). Paranitrophenol, a parathion metabolite,
has a water solubility of 16,000 ppm, and a Rf in
sandy soil of 0.46 (Rf is discussed at page 14). It is
less mobile in sandy soil than carbofuran (solubility:
700 ppm; R£. 0.77). Other similar cases exist.
Reasons why using water solubility as a predictor
of pesticide mobility is not satisfactory are:
~	Electronic polarity of a pesticide or metabolite
can dominate mobility since polarity itself is a
dominant factor.
~	Strong chemical binding may occur in the soil.
[Chelation with iron (III) compounds (ferric
iron), which may be present in oxidizing soils,
is particularly adept a forming strong chelates -
which are relatively unaffected by acidity or
alkalinity - via coordination with oxygen and
nitrogen atoms],
~	The stability of certain pesticide-soil complexes
is influenced by soil acidity.
Pesticide-soil complexes can be intransient.
Soil Partition Coefficient (SPCI. SPC is widely claimed
to be a reliable guide to predicting mobility when the
appropriate type of soil is used in the determination. PC
values are given in the Farm Chemicals Handbook. The
leaching potential of a pesticide is high when the PC
value is low, and vice versa (provided the soil is not
fissured). Information is offered below on pesticide
mobility in soils high in organic matter, day or loam.
~	Pesticides With High PC-Values (=/> 10,000):
Chlorpyrifos, paraquat, heptachlor and chlordane.
~	Pesticides With Low PC-values (=/< 1000):
Aldicarb, atrazine, alachlor, captan, carbaryl,
chlorpropham, cyanazine, diazinon. dicamba,
diuron, propazine, simazine and terbacil.
Environmental Persistence and Fate of Pesticides
Persistence is the time to virtual disappearance.
For a first-order reaction loss, this (99% loss)
corresponds to seven half-lives. Fate is the outcome
of the chemical, physical or biological reactions on
the pesticide in the media. Fate and persistence are
inexorably linked through chemical and biological
processes. For simplicity, we will discuss them
separately, realizing that this linkage exists and that
in the real world unexpected effects are not unusual.
Persistence may be expressed arbitrarily as:
~	Persistent: 100 days or more
~	Moderately Persistent: 31 to 99 days
~	Non-Persistent: 30 days or less.
Persistence in a particular situation depends largely on:
~	Pesticide type and its soil concentration
~	Soil temperature
~	Microflora, substrates, and toxic moieties present
~	Soil aeration, and oxidants or reductants in the soil.
~	The intimacy of contact with the microflora.
~	Soil composition, and integrity [Clay, sand, silt,
shale, etc.. Fissuring. Amounts present of organic
matter, humic acid and water].

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Patterns of loss of pesticide in soil may be
observed depending on the reaction and process rates
in the particular case. One pattern which is seen in
spills, and even with proper applications in arid
regions, is an initial prolonged lag, followed by an
accelerated loss. In the case of a spill, this can be
ascribed to poisoning of the microflora which
degrade the pesticide, and the long time needed for
their re-establishment. Numerous studies on dieldrin
have shown that it can persist for 5 years after a
spill that results in initial concentrations in top soil
of about one hundred parts per million or greater.
Metabolites themselves can affect persistence.
Certain ones are microbial substrate-food and can
enhance biodegradation via promoting enzymatic
destruction {enhanced or induced biodegradation) of a
parent pesticide or pesticidal substance. Certain other
metabolites are biocidal. In some situations, they can
retard biodegradation. The activity of biocidal
metabolites depends in part on their concentration.
Metabolites which retain chlorine atoms from their
parent pesticides are likely to be broad spectrum
biocides. That is, at, or above, a critical
concentration, they are moderately or highly
effective in killing many species of bacteria and
fimgi in soil, some of which degrade pesticides.
Repeated application of N-methyl carbamates has
been reported to hasten pesticide degradation and
lessen effectiveness. 2,4,5-trichlorophenol (m), TCP,
which is itself a well known, broad spectrum
bactericide, can enhance the persistence of 2,4,5-T.
At this point, a detour is needed to discuss half-life.
Half-life is the time involved in a 50% reduction of a prior
concentration. Half-Hfe can be useful in describing the
loss of a pesticide in steady conditions. When the half-
life period is not affected by the initial concentration, and
its value is the same at points along a concentration v.
time curve, a "first order" reaction (lossI exists. With a
first order loss: 75% loss corresponds to 2 half-lives;
90.6% loss, to 5 half-lives; 99+% toss, to 7 half-lives.
In many situations, a pattern other than "first order" loss
is observed. The concept of half-life is useful to estimate
the time to virtual disappearance of a properly applied
pesticide which is non persistent or moderately
persistent, provided the salient conditions are reported.
Weather and soil conditions need to be "steady." Half-life
is essentially season-dependent: For example, atdicarb
applied in June at a recommended rate might have a half-
life of about one month. An application made in March
might have a half-life of three months; reduced reactivity
could be a problem if run-off were to occur near wells or
other sources of drinking water.
Pesticide degradation rates depend on soil moisture
content temperature and other factors. Certain
pesticides are readily hydrotysed in soils which are
alkaline, while some others are not (e.g., dieldrin).
Notwithstanding that the fate of a pesticide may involve
complex chemistry and biology, and that the rates of the
chemical and biological reactions involved are different,
a provisional guide to persistence can be offered.
The persistence of some pesticides, for regular
permitted agricultural applications, are, provisionally:
~	Persistent: Chlordane, dieldrin, heptachlor, lindane,
paraquat dibromide, phorate and picloram.
~	Moderately Persistent: Aclfluorfen, atrazine, atdicarb,
bentazon, carbofuran, chloramben. 2,4,5-T,
chlorpyrifos, chtorpropham, endrin, glyphosate,
linuron, parathion, permethrin, simazine, and DOT and
its chlorinated metabolites.
~	Non-Perststent: Atachlar, acephate, amitrole,
azinophos-methyl, acifluorofen. benfenox, fonofos,
butylate carbaryf, cyanazineb, captan, diazinon,
dicamba, dalapon, 2,4-D, dinoseb, malathion,
metham-sodium, metribuzin, mevinphos, naled,
propachlor, tn'diphane, turbofos, toxaphene and
trichlorfon.
Chemical, biochemical and photochemical
processes involved in pesticide degradation may
occur simultaneously and involve hydrolysis,
reduction, oxidation (chemically, iron [Fe2*7Fe3+I
has a role in reduction and oxidation -redox-
reactions), de-alkylation and dechlorination.
Chemical hydrolysis may be impeded by bridging
chlorinated carbon groups, branching with steric
hindrance, and high halogenation of an organic ring
in the pesticide structure. These structural features
may influence biological degradation rates.
The end-products of chemical degradation may
depend on soil acidity. Soil acidity can influence the
outcome when different mechanisms for
nucleophilic substitution are possible and one is
energetically more appropriate for the particular
pesticide undergoing substitution. Conditions might
not favor the energetically preferred mechanism,
and so substitution would not be significant
compared to some other possible reaction (e.g.,
elimination).
An example of the possible influence of soil
acidity on the break down of pesticides in soil is
seen with trichlorfon. In alkaline soil, trichlorfon is
primarily dehalooenated to dichlorvos. In acid soil,
it is hvdrolvsed to trichloroethanol and a [P3+l acid.
Microbial degradation can occur in the presence of
oxygen (aerobic) and in its absence (anaerobic), in
either soil or water. Micro-organisms - bacteria,
mycobacteria, fungi - cause reduction, hydrolysis,
oxidation, epoxidation and other degradation

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reactions to occur. The rates of the various
reactions depend partly on the organisms,
substrates and bactericidal moieties present. Soil
acidity is also a factor. Enzymes have individual
optimal pH values for maximal, specific reaction
rates. A pH of 5.5 to 8.5 is optimal for bacterial
oxidative degradation, while a pH of less than
about 5.0 favors the growth of fungi, and different
reactions may then occur. When different reactions
proceed simultaneously, their relative rates
determine the preponderance of the various
metabolites.
Photochemical degradation involves sunlight (ultra
violet energy) causing breakage of chemical bonds:
carbon to carbon bonds, and bonds of carbon to
sulphur, nitrogen, or halogen, etc, which are
energetically different. In air and water,
photochemical action can be significant (ultra violet
light can penetrate water to a depth of several
feet). However, in soil, except for the top-most
level, photochemical action is not a factor. Also,
when it is a factor, it is not effective equally
because the strength of bonds in different
pesticides are different.
Accurately predicting the environmental fate of
a pesticide especially difficult if one knows nothing
about the prevailing oxygen concentration, oxygen
transportation rate, moisture content, temperature,
and soil-pesticide-metabolite interactions. Chemical
and microbial reactions act in concert. And, fate
and persistence are intertwined through substances
which are microbial energy-sources or biocides.
Mobility of Pesticides in Soils.
At this juncture we need to make a brief detour to
describe soil thin layer chromatography (STLC). and Hs
use (as one way) to determine quantitatively mobility
under particular conditions. STLC involves making a
slurry of a soil of interest, applying it in a uniform layer
to a thin glass plate, and drying the plate. A small
amount of pesticide is spotted on the prepared plate,
which is then immersed upright in water just below the
spot-position. After a suitable period, the travel of both
the water front and the pesticide front is measured (the
location of the pesticide on the plate at the end of the
run is determined using chemical agents, or x-ray film
with radioactive carbon labelled pesticides!. The travel-
ratio is known as the reference factor (Rfl. A zero Rf
means that the pesticide was immobile under the
conditions of the test. A value of Rf of unity means that
the material was completely mobile. The value of Rf may
change in a major way with changed test conditions.
Pesticide and metabolite mobility has been
extensively investigated by Somasundaram, Coats,
Racke and Shanbhag. They have shown that mobility
can be greatly different in a single soil, and in
different soils.(29) The mobility rating of several
pesticides and metabolites (m), in either sandy or
clay soils, is given below:
~	Pesticides With Significant Mobility: 2,4-D,
carbofuran and hydroxypyrimidine (from
diazinon). Pesticides which are moderately mobile
in sandy and clay soils are parathion, diazinon,
carbaryl, 1-naphthol (m), isophenphos,
prometryn, and 2,4-dichlorophenol (m).
~	Pesticides With Low Mobility: chlorpyrifos;
2,4,5-T, and 2,4,5-trichlorophenol (m),
hydroxyprometryn (m), and hydroxyatrazine (m).
Soil composition (and fissures in the soil) affects
pesticide mobility. Parathion is much less mobile in
uniform clay loam soil than in sandy soil, in which
it is moderately mobile. Soil characteristics which
generally favor retention (reduced mobility) of a
non-ionic or anionic pesticide are:
~	High organic matter and/or clay content
~	Neutrality or slight acidity
~	Cation exchange capacity.
The range for most soils is pH 5.5 to 8.5 (50%
soil & water). Silt-loam, and loamy sand soils tend
to be slightly alkaline (i.e., pH about 8); high clay-
content or humic soils, slightly acidic (pH about 5).
repeated manuring affects acidity because of
increasing, humic acid content. The mobility of
sparingly water soluble pesticides and their
metabolites in neutral or slightly acid conditions is
generally less in clay loam or sandy loam soils than
in sandy or silty soils.(30)
Lowly soluble, short half-life pesticides which had
been applied to retentive soils have been detected in
ground water. Even these types of pesticides should
be considered to have the potential to contaminate
ground water in some situations.
Protective Standards, and Equipment
U.S. EPA standards on pesticide safety are 40
CFR Part 156 Oabelling) and, its companion rule, 40
CFR Part 170 (Worker Protection Standard, WPS,
for Agricultural Pesticides). These EPA rules were
published in the August 21, 1992, Federal Register.

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16
Key sections of the WPS' rules are:
§ 170.150: Decontamination
§ 170.160: Emergency Assistance
§ 170.230: Safety Training
§ 170.240: Personal Protective Equipment.
Employers are required by this standard to:
~	Provide necessary protective equipment
~	Restrict access appropriately to treated areas
~	Provide clean water and soap for
decontamination
~	Provide appropriate warnings to workers
Provide transportation to medical facilities
~	Provide medical care-providers with exposure
and hazard information
~	Ensure that employees are trained in pesticide
safety by a competent person.
The full scope of the standard's rules can not be
described here. However, some aspects of protective
equipment are discussed in the following parts.
Coveralls and gloves: finely woven fabrics and
non-woven spun polymer materials are effective
against penetration by dusts and mists, but not
liquids. Composites of nonwoven materials and
plastics, and coated materials are effective against
penetration by dusts, mists and liquids. However, no
fabric or composite material can be relied upon to
provide protection if it is repeatedly immersed. No
coverall or glove is intended for immersion usage; if
this is the case, with time, penetration by liquids and
permeation by vapors are inevitable. Excessive
contact of protective clothing and gloves with liquid
and solid pesticides must be guarded against. When
surface contamination occurs, decontamination by
washing with a detergent is required. When
permeation occurs (as evidenced by the material
swelling or smelling), the article must be discarded.
When a highly toxic, skin-absorbable pesticide is
handled, a laminated coverall, head covering, rubber
gloves, and a full-face mask should be used.
As a preliminary guide to selecting coveralls and gloves;
sararf/tyvek* material is best for protection against wet,
granular or powdery pesticidal preparations. Neoprene
and vinyl materials have good resistance to many organic
solvent-based pesticides. Materials which have excellent
resistance to water penetration may have poor resistance
to permeation, however. Guidance on penetration,
permeation and comfort of protective apparel for
pesticide applicators has been provided by EPA. (31)
Respirators: the selection and use of respirators are
regulated by the EPA Worker Protection Standard
and also by the OSHA General Industry Respiratory
Protection Standard (at 29 CFR 1910. 134). These
standards provide comprehensive guidance on
establishing respiratory protection programs for
pesticide workers. Also, information on respiratory
protection is contained in the material safety data
sheet, and the pesticide label. Guidance is available
also from EPA Regional Offices, and State pesticide
program offices.
Special Note: Persons should not occupationally use
respirators unless specifically medically authorized.
People with chronic obstructive respiratory disease,
emphysema, bronchial asthma. X-ray evidence of
pneumoconiosis, significant ventilation capacity or rate
(VC, FEV,! loss, coronary artery disease, high blood
pressure, or grand mat should not wear respirators.
Respirators are either:
~	AIR-PURIFYING: Negative pressure, or
positive Pressure, air-purifying respirators.
For pesticide exposure control, apart from the
disposable mask, these types will be fitted with
either an organic-vapor-removing cartridges and
a prefilter approved for pesticides, or dust/mist
cartridges, or a canister; (a positive pressure type
is the powered air-purifying respirator, PAPR, as
a mask or helmet), or
~	AIR-SUPPLYING: Positive pressure
respirators with air supplied by compressors or
portable personal tanks or small cylinders
(escape respirator type*).
Two basic types of Air-Supplying respirators exist
for sustained work: The Hose-Mask (which is
seldom used), and the Self-Contained-Breathing-
Apparatus (SCBA)
* An emergency air-supplied, mask-cylinder type also
exists which is used in conjunction with hose-masks and
air-purifying respirators in some dangerous situations
(various types of respirators are discussed on page 17).
Respirator Selection & Technical Committee
Specifications (TC Numbersl: Ordinarily, the respirator
required to be used will be specified on the Pesticide
label and also in the pesticide material safety data sheet
(MSDS). When this is not the case, selection will need to
be made by a competent person, such as a certified
industrial hygienist. Factors in the selection will include
the physical, chemical, biological and toxicological
properties of the pesticide, the activities and work
conditions, and the associated hazards. Any respirator
and associated equipment which is selected for a
particular situation must comply with the joint
specifications of NIOSH & MSHA (federal agencies!.

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16
NIOSH and MSHA employ "TC" (technical
committee) numbers to assure proper selection of j
equipment. The TC numbers are imprinted on the )
equipment, cartridges, canisters etc. TC numbers for \
respirators are summarized below.
RESPIRATORY PROTECTION & TC NUMBER
TC-21C
TC-23C
TC-14G
TC-19C
TC-13F
Application-Respirator-TC number information is
provided in the text box below.
SITUATION/RESPIRATOR	TC NUMBER
~	Soil Fumiqants. Gases Applied Outside:
Cartridge with Prefilter -	TC-23C
Or Canister type - TC-14G
~	Space and Soil Fumiqants.
Gases Applied in Enclosed Spaces/
Handling Activities:
Supplied Air Respirator (hose).
Or Self-Contained-Breathing-
Apparatus {SCBA -Respirator).
»• Products Applied As Solids:
Dust/Mist Respirator -	TC-21C
~	Liquids in FIFRA Tox. Cat. I
or if in FIFRA Tox. Cat. II,
but with Tox. Cat. I Inhal. Tox.:
Org. Vap. Remov. Cartridge
& Prefilter -	TC-23C
Or a Canister Type with
MSHA/NIOSH-Approval and
TC Number prefixes -	TC-14G
»• [For a FIFRA tox. cat. II liquid:
a dust/mist filtering
respirator-	TC-21C
may be used in some activities,
provided aerosols or mists are not
generated, and overhead exposures
are not created].
When an employer provides a respirator necessary
to protect an employee's health, the employer needs
to establish a respiratory protection program. Every
worker who needs to use a respirator to safeguard
his or her health needs to participate in the
respiratory protection program.
As a guide only to setting up a program for
pesticide operations, the General Industry
requirements of OSHA (at 29 CFR 1910.134) for a
minimal acceptable program are described below:
SUMMARY OF OSHA'S MINIMUM
ACCEPTABLE RESPIRATORY PROTECTION
PROGRAM (AT 29 CFR.1910.134).
~	Written Standard Operating Procedures.
~	Respirator Selected For The Hazard.
~	Specific Instruction & Training of the User.
~	(Reserved section].
~	Regular cleaning & Disinfection.
~	Respirator Inspected During Cleaning &
Inspections are to be Routine.
~	Appropriate Surveillance of Conditions.
~	Regular Evaluation of Program
Effectiveness.
~	Physician Determines Worker's Ability To
Use A Respirator.
~	Respirators - Approved by Competent
Authority.
Different types of respirators provide different
degrees of protection. The quarter mask or
disposable mask provides the lowest degree of
protection; the self-contained-breathing-apparatus
(SCBA), the highest.
The degree of protection provided by a respirator
is measuredt in terms of "Protection Factor" (PF).
' Protection factor is measured by determining the ratio
of the outside concentration of a test aerosol (e.g., corn
oil, saccharin) to its concentration inside the mask, using
a laser optical cell device. The test involves moving the
head with the mask on in various ways, to obtain an
average PF value in the controlled test. The process is
known as quantitative fit testing. The ratio of (average!
concentrations in the test is known as the protection
factor, PF. For negative pressure respirators a more
appropriate performance descriptive term than PFis "face
fit factor", since it is the quality of the face fit, not the
filter, which determines the overall efficacy of the
respirator.
~	Dust/Mist Filter Respirator -
~	Respirator with an Organic
Vapor-Removing Cartridge and
a Pre-Filter Approved
for Pesticides -
or if a Canister -
~	Supplied Air Hose Mask -
~	Self-Cont.-Suppl.-Air Resp:

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17
PF values for some respirators are provided below: ,
A.P. RESPIRATORS & NOMINAL PF VALUES
~- Quarter Mask Filter -	5
~	Half-Mask, Reusable Or Dispos.- 10
Full-Face Mask -	50
~	PAPR as a Half-Mask -	100
I
Many well-fitted air-purifying respirators including \
disposable masks provide an order of magnitude
higher PF-values than the nominal PF. Also, about \
98% of the work force can be suitably fitted with one
of the three sizes of half-mask or full-face mask which \
are available. Visually judging fit is unreliable; \
minimally, a qualitative fit-test (QLFT) is needed. A
QLFT pass equates to a fit factor of 10 or more for \
most people. Special care is needed in fitting people
with small or large faces, noses, or nose-bridges. j
[These comments are based on the writer's
experience in performing more than a thousand
quantitative fit tests on male and female shipyard
workers in the 1970's.]
|
i
Information on replacing filters, equipment and fit- j
checking a respirator are provided below:
~	Disposable Half-Mask Respirator.
This type of respirator offers a limited degree of
personal protection (PF 10). It is used for short-
term, minimal hazard control when disposability
is desirable to avoid decontamination etc., \
(replace twice daily, at least).
~	Reusable, Negative Pressure,
Air-purifying, HALF-MASK Respirator.
Three sizes of mask and hypo-allergenic masks
are available. They are reliable in prolonged use j
conditions and can provide at least a PF of 10.
~	Negative Pressure, Air-Purifying,
FULL FACE-MASK Respirator.
Used when eye irritation and respiratory impairment j
are to be protected against. Three sizes of mask and
hypo-allergenic masks are available. When the face-
fit is satisfactory, this type of respirator gives the \
best protection of all the negative pressure types. ~ \
Positive Pressure, Air-Purifying Respirator.
This (PAPR) respirator is available as a half-mask \
or a full head covering fabricated either as hard
or a soft construction. The PAPR-type respirator
offers good comfort, and has a lower risk of
inward leakage than a negative pressure
respirator. It requires daily battery-charging.
~	Replacement and Care of Air-Purifying
Equipment: Single-Use & Reusable.
For single-use respirators: replace when -
. Material stiffness is lost, or
. The straps lose their elasticity, or
. The immediate job is finished, or
. The morning or afternoon shift ends.
For any type of reusable, air-purifying respirator:
. The cartridges and pre-filters should be
exchanged daily. [Chemical cartridge service
life is drastically reduced with 65% or greater
relative humidity.]
. The cartridges, filters, or canister if used, must
be exchanged immediately when break-
through occurs, as evidenced by taste or odor
inside the mask.
. The mask must be decontaminated after each
use, and cleaned, dried and stored in a clean
plastic bag.
. It must not be used in atmospheres which (i)
have less than 19.5% oxygen, or (ii) have an
airborne concentration of the relevant pesticide
which is greater than the prescribed limit.
. Eyeglasses when worn must not interfere with
the seal on the face.
. Men need to be clean-shaven.
. It is not to be used in a potentially oxygen-
deficiency space, e.g., a silo, tank, or bin.
. Chemical cartridges must not be used to try to
protect against (i) a toxic substance which does
not have a warning quality, such as odor or
taste, at a concentration which is appreciably
lower than the concentration which is the
permissible exposure limit or is otherwise
dangerous, (ii) a toxic pesticide used in any
enclosed fumigation operation, or (iv) arsine,
stilbene, acrylonitrile, formaldehyde,
chloropicrin, ethylene, sulphur dioxide,
phosphine, hydrogen cyanide, TDI — all of
which are extremely toxic and have poor or no
warning properties (enclosed spaces must be
vacated before actual fumigation starts).
~	Positive Pressure, Supplied Air Respirators.
Two quite separate types of these kinds of
respirators are available and used for sustained,
work: the hose-mask respirator: and the self-
contained-breathing-apparatus (SCBA).
[Short-term, escape cylinder-respirators are
available].

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~	The Hose-Mask Respirator.
The hose-mask respirator is used, but only very
rarely, in manufacturing. Hose lengths of 75 feet
(non-blower type), and 300 feet (blower type) are
available. The air supply must be tested and meet:
Grade D quality of the Compressed Gas
Association (CGA)f; a minimum supply rate of 4
cubic feet/minute; and a maximum pressure limit,
not to exceed 125 psi on the supply line. The
buddy system is employed if the hose-mask is to
be used in an immediately dangerous to life or
health (IDLH) situation.
' CGA Grade D equates to: CO at 20 ppm as a
maximum; C02 at 1000 ppm as a maximum, and
odorless.
~	The SCBA Respirator.
The SCBA provides the highest degree of
respiratory protection of all the commercial
respirators (an order of magnitude greater than
the best air-purifying device). Air which far
exceeds Grade D quality is used. In practice the
minimum allowable grade is always exceeded.
The SCBA high pressure tanks have a nominal
one-hour supply. However, in arduous work, the
air supply time is less than nominal. SCBAs are
equipped with special safety devices, including
audible alarms. The SCBA respirator is used
when exposures exist or are likely to exist which
are potentially life-threatening. Responding to a
pesticide fire requires an SCBA to be used. The
SCBA user needs to have specific safety
instruction and training. Also, the equipment
needs to be inspected and maintained on a regular
basis. A buddy-system must be used when a
SCBA respirator is employed.
~	Fit Checking A Negative Pressure, Air
Purifying Respirator (Reusable Type).
Fit-Checking a negative pressure, air purifying
respirator is performed with the half-mask or full-
face mask donned, using the following two steps,
which must both be successful to pass the check:
STEP 1: Cover the exhalation valve with the
palm of the hand, exhale with moderate force,
sense the mask bulging outward slightly before
any air escapes under the pressure of
exhalation. Bulging indicates a satisfactory test
in this nhase.
STEP 2: Cover the cartridge(s) with the
palms, inhale, and sense the mask pulling
inward. This indicates a satisfactory test.
An air-purifying respirator should be supplied as a
proper fit. As a minimum, each user should be
qualitatively fit-tested with an individually assigned unit.
Qualitative fit testing is done by spraying banana oil or
saccharin aerosol outside of the donned mask, having the
wearer report any breakthrough of smell or taste. The
mask is worn for several minutes before testing.
Workers' Risks and Information on Safeguards
Workers who handle agricultural pesticides or who
harvest or cultivate treated plants may become
significantly exposed to pesticides in their jobs. They
need to be aware of how to avoid health risks. They
should read and understand the provisions in the
EPA Pesticide Worker Protection Standard.
Personal Protection Practices
The EPA Worker Protection Standard specifically
covers (i) workers who perform hand labor
operations in fields treated with pesticides, (ii)
employees in forests, and (iii) workers in nurseries
and greenhouses who mix, load, or apply pesticides.
WPS-requirements cover personal protection;
provision of warnings; restriction of entry;
decontamination; emergency assistance; control of
personal contact; labeling and statements, and
pesticide safety training.
Specific information on the WPS's provisions, and the
time-table for its required, phased-in compliance, as well
as assistance in understanding attaining compliance, are
available from (i) the regional EPA Air, Pesticides, and
Toxics Management Divisions, and (ii) State pesticide
offices.
Some important points and industrial hygiene
aspects for assuring personal protection and general
safety in handling pesticides, are as follows:
~	When handling any pesticide, carefully read, and
follow, the label instructions.
~	Mix and dilute pesticides outdoors when
practicable. Mix only the amount needed.
~	Do not over-apply, and limit treatment area.
~	Follow the applications and re-entry restrictions.
~	Use the correct clothing for personal protection.
~	Use the correct respirator for the job.
~	Employ proper decontamination procedures.
~	Participate ftilly in the provided safety training.
~	Keep children and pets off newly treated areas.
~	Do not spray in windy conditions, avoid trees,
plants, bee-hives, water sources and wells.
Do not smoke, eat or drink around pesticides.

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~	Use coveralls, long-sleeved shirts, head covering,
rubber or vinyl gloves, goggles or a face shield,
rubber shoe covering and pesticide respirators for
needed protection in agricultural activities with
FIFRA toxicity category I and II pesticides.
~	Use full-length neoprene or plastic gloves, and a
rubber apron in mixing and loading activities.
~	When handling a pesticide with dermal toxicity,
completely cover the arms, legs and feet.
~	Avoid inhaling pesticide dusts mists or vapors.
Use an appropriate respirator.
~	Whenever a non-disposable type respirator is to
be used, check the respirator mask for cracks and
breaks. Check the straps for elasticity. Check the
valve diaphragms for proper seating. Check the
valves themselves and their seals before each use.
~	Fit-Check a negative pressure respirator before
every use, when making a check is practicable.
~	Use the respirator which provides the level of
protection which is necessary for the situation.
~	Keep the respirator clean and covered when not in
use. Use soap and water, and a brush for
cleaning. Rinse, dry and store in a plastic bag.
~	At the first sign of difficulty with wearing a
respirator, go to a fresh-air area and remove it.
Obtain medical help immediately if you are ill.
Controlling Skin Exposures
Preventing pesticide exposure and skin absorption
of pesticide is crucial in handling, mixing and
loading activities. The chest, stomach, back and
upper arms have large surface areas, and high
absorption capabilities. The scrotal area and eye
areas have very high absorptivity. Significant
amounts of deposited pesticides can be absorbed
through the skin. Reportedly, as much as about ten
percent of malathion deposited on the skin may be
absorbed directly. Properly selected clothing and
equipment when used prevent skin exposure.
Liquid pesticide penetration* and vapor permeation
of clothing and gloves varies considerably. Factors
of penetration or permeation are:
. The pesticide and its form
. The material composition, type and weave
. The quality of construction.
t
Penetration poses a potential health problem whenever
lightweight cotton or worn clothing is used in handling a
highly toxic liquid or wettabfe pesticide.
To control the hazard in handling a pesticide which
has a high dermal toxicity rating, heavy-weight,
woven-fabric coveralls with lapped, zippered
closures and tight seams need to be worn. [Plastic-
coated, and fluorocarbon-film finished coveralls
provide superior protection against both penetration
and permeation. They are hot to wear, however].
Cotton gloves and canvas shoes are easily penetrated
and permeated by pesticides, and they can act as
reservoirs of pesticide. This creates an on-going risk
of dermal pesticide absorption. Wearing vinyl or
rubber gloves and shoes or overshoes helps prevent
this problem.
Gloves which extend to the mid-forearm should be
used in handling or applying pesticides. Full-arm-
length gloves should be used in mixing and loading.
Care must be taken to avoid contaminating gloves
on the inside; do not place your hands into them if
you have pesticide on your skin.
Regardless of the type of gloves used, they should
not be actually soaked by or immersed in pesticides.
Gloves which are swollen (a sign of permeation),
hardened or cracked should be discarded promptly.
Heavily used gloves even if they appear to be
unaffected should be discarded periodically.
Controlling dermal risks is best achieved by
preventing clothing from becoming contaminated in
the first instance; by washing clothing promptly after
use, and by using only the recommended equipment.
Decontamination and Related Practices.
Decontamination of equipment and related
permissible practices are addressed in the EPA
Worker Protection Standard (at section 170.150).
Key points on decontamination of personnel,
equipment and locations, and on preventing on-going
contamination are:
~	Keep work clothing and street clothing separated
at all times to avoid cross-contamination.
~	If you become contaminated by a pesticide,
remove the contaminated clothing, and wash
yourself immediately, using only soap and water.
Do not use organic solvents.
~	Be alert to possible adverse effects occurring over
the following 12 hours.
~	Discard and properly dispose of extensively
contaminated (and damaged or evidently
permeated) gloves.

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~	Promptly wash actually or possibly contaminated ,
clothing. Use hot water and a heavy duty j
detergent. Use hot air for drying.
~	Promptly clean diked concreted work areas which j
become contaminated. Wash with a strong I
alkaline solution or a recommended cleaner.
~	Quickly arrange for the immediate collection of j
spilled pesticide by the designated first-responder I
(in some cases, incineration of the waste will be \
required, per 40 CFR Part 165).
~	Decontaminate empty pesticide containers which |
can stand up to the rigors of washing, using either \
a triple-rinsing or a pressure-washing.
Certain containers are required to be returned to the j
supplier or manufacturer, under penalty in law. The
requirement will be stated on the pesticide label.
Providing Health And Safety Information
EPA and the States set and enforce standards for
pesticide worker protection. These include j
requirements on employers to: post danger signs,
provide notices of applications, provide workers with
specific information about applications, provide each
worker with prescribed training, assure training, j
provide personal protective equipment, provide \
washing facilities (soap, water, and single-use towels
placed at appropriate locations), and provide \
emergency assistance.
Apart from the EPA Worker Protection Standard,
the federal OSHA Hazard Communication Standard
(at 29 CFR. 1910.1200) may be relevant and
applicable to a particular pesticide operation or
activity. This General Industry standard requires
covered employers to give workers specific \
information and training on materials, hazard j
identification, safety practices and equipment. |
Material safety data sheets must be made available.
Emergency Response Information
i
Only designated trained persons should respond to j
an actual emergency situation. Information on \
responding to a pesticide personal exposure, spill or I
fire is given in the respective DOT Emergency j
Guide, the pesticide label, and the pesticide MSDS. j
24 hour Emergency information service is available
from: the National Pesticide Telecommunications j
Network (NPTN), and Chemtrec:
NPTN: 1-800-858-7378
CHEMTREC: 1-800-424-9300
Medical Monitoring & A Rise-Based Program
Federal pesticide regulations do not require
medical monitoring. In industrial pesticide
operations, medical monitoring could be required as
a duty under OSHA. Regardless of a question of
regulatory requirement, workers who are exposed to
pesticides could benefit from participation in a risk-
based medical monitoring program (with subsequent
analysis of group data to identify subtle health
changes, i.e., medical surveillance). A medical
monitoring program is described summarily below.
A BASIC PESTICIDE RISK-BASED
MEDICAL MONITORING PROGRAM
~	Exposure Profile Assessment &
Baseline Examination
. Medical History, as appropriate.
. Comprehensive Physical Examination, &
Screening based on risk factors,
medically recommended practice, and
actual and potential exposures.
. Respiratory Protection Program.
. Confidential Employee Counselling.
. Medical Referral, as appropriate.
~	Exposure Profile Assessment &
Periodic Examination
. A Core Medical Examination & Screening
. Exposure-Specific Biological Monitoring.
. Confidential Employee Counselling.
. Medical Referral, as appropriate.
~	EpisodicTreatment Program (per contract).
This framework is based on the author's experience.
With this program, examinations would be "no cost" to
the worker and conducted during regular working hours.
Procedurally, the worker would complete an exposure
profile questionnaire and give it to the physician before
every examination. In the baseline examination:
~	neurological status, blood chemistry, cardio-vascular
system status, liver and kidney functional status, skin
status, ability to wear a respirator, a relevant biological
profile, counselling and any needed medical referral
would be undertaken.
~	Medical risks, a plan for biological monitoring and the
frequency for re-examination (the periodic examination)
would be established by the physician. Biological
monitoring would be non-invasive, whenever practicable.
This would in some situations, the program would be
complemented by industrial hygiene surveillance and area
and personal exposure monitoring.

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Poisoning By Pesticides
The mode of biological action and poisoning is
well known for many pesticides, however, for some
pesticides, the mechanisms are not completely
understood. Pesticide poisoning may involve:
interference with an enzyme in some essential
pathway; competition with an essential substance;
inhibition of blood clotting (anticoagulation with
internal hemorrhaging); interference with the ionic
processes with sodium channels in cell membranes;
interference with cell metabolism, or inhibition of
synthesis or alteration of purine, or DNA synthesis.
' ¦ Most of what is known about commercial pesticide
poisoning comes from accidental or deliberate
ingestion, and from cases of accidental inhalation
and skin absorption. Information on toxic dosages,
metabolism and enzymatic pathways has been
obtained from the use of pesticides as human
therapeutic agents, and from earlier tests on
volunteers. Toxicity information gained in these
ways exist for atrazine, baygon, carbaryl, dacthal,
diazinon, dicamba, disulfoton, glyphosate, fonofos,
turbufos, propachlor and 2,4,5-T.
In pesticide poisoning cases in hospital emergency
rooms, physicians with first-hand knowledge have told
me that it is not uncommon that the name of the
pesticide involved was not known, or that the claimed
exposure was inconsistent with the clinical picture. The
(illegal) use of an obsolete pesticide or °cocktail* is a
likely cause of the poisoning. Also, in some cases, there
is a question of the affected person being especially
sensitive because of an existing genetic pre-disposition
(in this situation, exposure need not be excessive to
cause a problem).
Reported symptoms of poisoning by the thio- and
organo-phosphates and the carbamates are weakness,
headache, sweating, nausea, salivation, difficult
breathing, nose-bleed, muscle problems, speech
problems, fever, cyanosis, cramps and stomach pain
(some of these signs of poisoning are easily confused
with heart attack). However, not everyone manifests
the same symptoms or even the same extent of a
particular symptom (reportedly, the latter point is
especially relevant when cholinesterase activity is
already depressed). The usual symptoms may vary
in intensity, unrelated to plasma cholinesterase level.
Reportedly, in volunteer-tests with propoxur, with
single dosing, in some cases, evident poisoning
. (nausea, tremors) was accompanied by an initial
decrease in nlasma ChE of 50 percent or more,
while in others, no cholinergic crisis arose with as
much as a 70 percent decrease occurring in plasma
cholinesterase. The dose sufficient to cause clinical
poisoning need not be "excessive," if a body burden
or enzyme deficiency pre-exists.(7, 34)
In pesticide poisoning, the onset of clinical signs
may be delayed for several hours, depending on the
type of pesticide, the physical, chemical properties,
the dose involved, transport across body membranes,
the stomach being empty or full at the time, the
metabolites involved, and other factors.
In poisoning with the thio-/organophosphates or the
carbamates, the onset of symptoms or clinical signs
may be delayed up to several hours after an acute
exposure, but not more than 12 hours (except that
leg weakness might take several days to develop).
Any significant depletion of red blood cell-ChE
will not completely restored until weeks or months
afterward. Red blood ceU-ChE replenishment rate is
about one percent per day. As an example, a 60%
loss of RBC-ChE would require about two months
for replenishment. Slow restoration of lost RBC-ChE
may account for the long durations of some adverse
effects seen with organophosphate poisoning,
including long-lasting abnormalities in
electroencephalograms and behavior which can arise
after a cholinergic crisis.(33)
First Aid, and Medical Treatment
If pesticide poisoning is suspected, and in every
pesticide accident involving a personal exposure-
medical help must he obtained immediately.
First aid (and immediately seeking medical help} is
indicated whenever general weakness, headache,
sweating, nausea, salivation, difficult breathing,
muscle problems, speech problems, fever, cyanosis,
cramps, nose-bleeds, or stomach pain occurs in
association with a suspected pesticide exposure.
NOTE. Immediate medical attention is also needed
whenever leg weakness, loss of feeling in the
fingers, or any other nerve problems arise in
association with pesticide exposure, regardless of the
interval between an exposure and the onset.
Neuropathy caused by pesticides may be delayed
days or weeks.
In an accident involving significant personal
contamination to a pesticide, IMMEDIATELY:
~	remove all contaminated clothing
~	Wash the body and hair vigorously
DO NOT USE ANY ORGANIC SOLVENT

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22
DO NOT	,
. Give the victim coffee or tea
. Induce vomiting in (i) a conscious person, j
unless this is medically specified, or (ii) an
affected person who is unconscious.
DO
. Follow the first aid guidance on the
pesticide label and the pesticide MSDS.
First aid guidance is provided in the U.S. I
Department of Transportation's Guides, numbers 27, \
28,31,33,55 and 60, and is summarized below:
A SUMMARY of D.O.T FIRST AID GUIDANCE
PESTICIDE CONTACT:
. Wash with Soap and Water.
. Flush Eyes for 15 Minutes.
. Remove Contaminated Clothing.
TREATING THE VICTIM:
. Remove to Fresh Air.
. Keep Victim Quiet.
. Maintain Normal Body Temperature.
. Artificial Respiration if Breathing Stopped.
. Oxygen for Labored Breathing.
. Watch For Delayed Reaction.
TO OBTAIN HELP:
. Contact Chemtrec or nearest Poison
Control Center.
Specific antidotes are available for the anti-
cholinesterase type pesticides and some others, but not
for the organochlorines and many other pesticides.
OP-pesticide and carbamate workers who have antidote }.
kits available must not be allowed to use them j
prophytactically. Such use may cause acute illness and is
itself hazardous.
Medical treatment for OP and Carbamate poisoning is: \
~	For Thio-/Organophosphate Poisoning:
Quickly emptying the stomach, keeping the airways \
dear, administering atropine; and in severe poisoning,
administering pralidoxime: 2-PAM, except that 2-PAM |
is counter-indicated after a significant delay because
ageing of the 2-PAM, receptor complex occurs, the
altered complex is not affected by 2-PAM, and 2-PAM
is itself toxic (as is atropineI. A fter aspiration of the j
stomach, charcoal instillation may be employed.
~	For Carbamate Poisoning:
Administering atropine (but without 2-PAM). Rapid
lavage, and aspiration.
~	In Every Pesticide Poisoning Case:
Maintaining supportive therapy for 72 hours to ensure
that pulmonary ventilation, and cardiac and neural \
status are satisfactory.	\
Responding To a Pesticide Fire or a Spill
Everyone who might make an initial response to a
fire or spill which could involve a pesticide must be
informed, and be truly aware, that their actions must
be limited to raising an alarm and doing only
minimal remedial actions. They must not incur the
risk of pesticide poisoning. In the case of a fire,
provided a pesticide is not initially involved in the
initial conflagration, they can use an extinguisher.
However, they may not attempt to Fight a pesticide
fire, regardless of how small it is. The combustion
products of many pesticides, including those which
ordinarily are relatively low in toxicity, are
potentially lethal.They should immediately sound the
fire alarm, and report to the supervisor. They must
not make any unprotected "heroic" effort. It almost
certainly will lead to their own serious injury. In a
spill, a person present at its start may only attempt
to control and isolate it, if this can be done safely.
Absorbent pads can be used to contain the spill.
The risks of becoming contaminated or inhaling
gases, vapors or particles must be avoided. People
must stay upwind of the spill.
Only a designated first-responder or a member of
an emergency response team should undertake an
actual response to a fire or spill. Employers need to
designate personnel to respond to emergencies.
Anyone who is exposed to pesticide particles from
a fire must decontaminate themselves immediately
and seek first aid. They must watch for signs of
poisoning, which could be delayed for several hours
after exposure. Medical help should be obtained at
the first suspicion of a problem, and the supervisor
needs to be told.
The designated (and trained) first-responder, in
every response, must use the correct personal
protective equipment. If personal contamination
occurs, all contaminated clothing must be removed,
and the responder needs to be washed thoroughly.
One must watch for signs of poisoning, and medical
help must be obtained at the first sign of poisoning.
Reporting Releases
Most pesticides are designated as hazardous or
extremely hazardous substances. They have assigned
reporting quantities (RQ's) which trigger formal
reporting to EPA of a significant release.

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23
Reporting requirements of releases of extremely
hazardous substances, toxic chemicals, - and
hazardous wastes are contained in:
~	CERCLA, the Comprehensive Environmental
Response and Liability Act.
» SARA, Title 111, the Superfund Amendments and
Reauthorization Act of 1986. SARA (111) § 313.
~	EPCRA, the Emergency Planning and
Community Right-To-Know Act. Section 302.
~. RCRA, the Resource Conservation and Recovery
Act of 1976, Part 261.
Some common pesticides have a CERCLA-
established reporting quantity (R.Q.) of either one,
ten, or one hundred pounds, as follows:
~	Pesticides with a R.Q. of One Pound:
These include acrolein, aldicarb, amitrole,
diallate, azinphosmethyl, DDT, diazinon,
dieldrin, diclone, 1,2 - dichloropropane,
l,2-dimethylhydrazide,l,l,2,2-tetrachloroethene,
2-nitropropane, parathion, pyrethrins and
toxaphene.
~	Pesticides With a R.Q. of Ten Pounds:
These include pentachlorobenzene, captan,
dichIorvos,kelthane,ethion,bis(dimethylthiocarb-
amoyl)disu!phide, carbofiiran, cupric sulphate,
dimethoate, dinitro-cresol, methiocarb,
mevinphos, pentachlorophenol, naled, propargite
and sodium fluoroacetate.
~	Pesticides with a R.Q. of 100 pounds:
These include acrylonitrile, allyl alcohol,
aluminum phosphide, antu, mono and di-
chlorobenzene, carbaryl, dichlobenil, 2,4-D
(acid), dichlobenil, diuron, fluoacetamide,
hexachlorophene, malathion, methomyl,
sulphotep, p-nitrophenol, thionazin, trichlorophon -
and zineb.
~ * •
Sources of Information
A.	The Pesticides Hot-Line. 1-800-858-PEST.
B.	The EPA. OPP Pesticide Information Network (PIN): a
free, data base accessible by data-phone. (703)305-5919.
C.	U.S. EPA Health Advisories (EPA Office of Drinking
Water). These advisories contain information on
structure, fate, pharmokinetics, health effects, dosage
limits, cancer potential, and more.
D.	U.S. EPA Pesticide Fact Sheets. They provide data on
science, characteristics, toxicology, and more.
E.	OSHA 29 CFR.1910 Subpart I, PPE standards.
F.	U.S. EPA Worker Protection Standard, 40 CFR.170.
G.	Computer Data Bases (available through EPA.)
CHRIS U.S. D.O.T
HSED U.S. National Library of Medicine
HSELINE U.K. Health and Safety Executive
MHIDA U.K. Atomic Energy Authority
NIOSTIC U.S. Dept. Health and Human Services
OHMTADS U.S. Environmental Protection Agency
TOXL1NE U.S. National Library of Medicine
NPURG The University of Massachusetts, Amherst.
H.	Books. Journals and Standards: Recognition and
Management of Pesticide Poisoning. 4th edition, Donald
Morgan. U.S. EPA, 1989. Pesticides Studies in Man.
Williams and Wilkins, 1982. Drinking Water Health
Advisory: Pesticides. Lewis Publishers, Inc, Chelsea,
MI. Toxicology. Casarett and Doull. Macmillan
Publishing Company. Nanogen Index: a dictionary of
pesticides. Nanogens Company, Watsonville, Ca.
Pesticide Handbook - Entoma, Entomological Society of
America, College Park, Maryland. Herbicide Handbook
of the Weed Society of America, WSA, Champaign, 11.
Environmental Toxicology & Chemistry. Pergamon
Press, Bulletin of Environmental Contamination &
Toxicology, Springler-Verag, New York, Inc. Farm
Chemicals Handbook. Meister Publishing Company,
Modesto, California. Pesticide Transformation
Products. ACS Series 459, 1991. L. Somasudaram.
End Notes and References
I.	Ortho-dichlorobenzene, for example, is a herbicide,
insecticide and bactericide. Also, replacement of the
methoxy group in trichlorfon by a normal butoxy group
creates a substance with high neurotoxicity. The normal
butoxy group is associated with neurotoxicity in other
compounds. Also, optical isomers of a pesticide are well
know to exhibit different biological activity. Ohkawa, H.;
Mikami, N.; Okuno, Y.; and Miyamoto, J.;
Stereospecificity in toxicity of the optical isomers of
EPN, Bull. Env. Cont. Toxicol., 18:534-40, 1977.
2,3. Acetylcholinesterase and its inhibition, in Wilkinson,
C.F. (ed.): Insecticide Biochemistry and Physiology.
Plenum Press, New York, 1976,pp. 271-96.
4,5. Biotransformation of Organophosphorus insectides in
Mammals: Relationship to Acute Toxicity. J.E.
Chambers,H.E. Chambers. Pesticide Transformation
Products, L. Somasundaram ACS. Series No. 459.
6. Umetsu, N.; Grose, F.H.; Allahyari, R.; Abu-El-Haj, S.;
and Fukuto, T.R.: Effect of impurities on the mammalian
toxicity of technical malathion and acephate. J. Agr.
Food Chem., 25:946-53,1977. Also, Pellegrini, G., and
Santi, R. Potentiation of toxicity of organophosphorus
compounds containing carboxylic ester functions toward
warm-blooded animals by some organophosphorus
impurities. J. Agr. Food Chem., 20:944-49,1972. Also,
Keplinger, M.L., and Deichmann, W.B.: Acute toxicity
of combinations of pesticides. Toxicol. Appl.
Pharmacol., 10 :586-95,1967.

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24
7. Pesticides Studied in Man. Williams & Wilkins Co.,
Baltimore, 1982. Also, Wills, J.H.; Jameson, E.; and
Coulston, F.: Effects of oral doses of carbaryl on man.
Clin. Toxicol., 1:265-71, 1968.
8,9. For information, refer to Pesticide Transformation
10.	Products. L. Somasundaram. ACS Series No. 459.
11.	Aldridge, W.N.: The nature of the reaction of
organophosphorus compounds and carbamates with
esterases. Bull. WHO, 44:25-30. 1971.
12.	O'Neill, J.J.: Non-cholinesterase effects of
anticholinesterases. Fufid. Appl .T oxicol. ,1:154-60,1981.
13.	Weil, C,S.: Woodside, M. D.: Carpenter, C.P.;
and Smyth, H.F., Jr.: Current status of tests ofcarbaiyl
for productive and teratogenic effects. Toxicol. Appl.
Pharmacol., 21:390-404, 1972.
14.	Hydrolysis by chemical and microbial processes is a
principal step in degradation of carbamates. 1-naphthol is
the significant hydrolysis metabolite of carbaryl [which
has a naphyl group attached to -0-C(0)-NH(CH3)].
15.	Petrova-Vergieva, T., and Ivanova-Chemishanska, L.:
Assessment of the teratogenic activity of dithiocarbamate
fungicides. Food Cosmet. Toxicol., 11:239-44, 1973.
16.	Triazine persistence and fate information. Kaufman D.D.
and J. Blake. 1970. Degradation of triazine by soil fungi.
Soil Biol. Biochem. 2:72-80.
17.	See reference 16, and L. Somasundaram et al. 1991.
Mobility of Pesticides and Metabolites in Soil.
Environmental Toxicology and Chemistry. 10:188-189.
18.	DDT may be found, at trace concentrations several times
above the background blood levels, in human populations
in areas of past manufacturing activities. For a discussion
of the point and data, see Toxic Effects of Pesticides,
pages 546, 547 in Toxicology, Cassarrett and Doull.
Macmillan Publishing Co.
19.	Van Miller, J.P.; Lalich, J.J.; and Allen, J.R.:
Increased incidence of neoplasm in rais exposed to low
levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin.
Chemosphere, 6:537-44, 1977.
20.	Egan.H.; Goulding, R.: Roburn, J.; and Tatton, J. O'G:
Organo-chlorine residues in human fat and human milk.
Br. Med. J., 2:66-69, 1965. Also, Abbott, D.C.;
Goulding, R.; and Tatton, J. O'G.: Organochlorine
pesticide residues in human fat in Great Britain. Br. Med.
J., 3:146-49, 1968.
21.	The toxicity of pesticides and their Metabolites. In
Degradation of Synthetic Molecules in the Biosphere.
Proceedings of a Conference. National academy of
Sciences, Washington, D.C. 1972, pp 313-35.
22.	Abou-Donia, M.B.: Organophosphorus ester-induced
delayed neurotoxicity. Ann. Rev. Pharmacol. Toxicol.,
21:511-48,1981. Also, Abou-Donia, M.B., andPreissig,
S.H.: Delayed neurotoxicity of leptophos: Toxic effects
on the nervous system of hens. Toxicol. Appl.
Pharmacol., 35:269-82, 1976.
23.	Durham, W.F., and Williams, C.H.: Mutagenic
teratogenic, and carcinogenic properties of pesticides.
Annu. Rev. Entomol., 17:123-48, 1972. Also, The
cancer risk assessment protocol used by the U.S.
EPA, together with highly informative background
material, is given in Risk Assessment in the Federal
Government: Managing the Process. Washington,
D.C.: National Academy Press, 1983.
24.	Smalley, H.E.; Curtis, J.M.; and Earl, F.L:
Teratogenic action of carbaryl in beagle dogs.
Toxicol. Appl. Pharmacol., 13:392-403,1968. Also,
Fishbein, L.: An overview of the structural features
of some mutagenic and teratogenic pesticides. In
Chambers, J.E., and Yarbrough, J.D. (eds.): Effects
of Chronic Exposures to Pesticides on Animal
Systems. Raven Press. New York. 1982, pp. 177-209.
25.	Street, J.C.: Pesticides and the immune system. In
Sharma, R.P. (ed.): Immunologic Considerations in
Toxicology, Vol. I. CRC Press, Inc., Boca Raton,
FL., 1981, pp. 45-66.
26.	Rodgers. K.E. and others. A Rapid In Vitro
Screening Assay For Immunotoxic Effects In The
Generation Of Cytotoxic T-Lymphocyte Responses.
Pesticide Biology and Physiology. Vol. 26, No. 3,
pages 292-301. And, Bemier J. and others.
Suppression Of Humoral Immunity In Inbred Mice By
Dieldrin. Toxicology Letters. Vol.35, No.2 & 3,
pages 231-240.
27.	Specific toxicity data for fish, freshwater
invertebrates, and estuarine and marine organisms are
provided in respective Pesticide Fact Sheets, issued by
the U.S. EPA. Office of Pesticide Programs.
28-30. Somasundaram L. and others. Pesticide
Transformation Products. ACS Symposia Series.
No.459. (and same authors and subject. International
Journal Of Environmental Toxicology and Chemistry.
Vol. 10, No. 2, 1991)
31. EPA Publication "Pesticide Spray Application and
Thermal Comfort of Protective Apparel for Pesticide
Applicators," authored by l.O. Dejonge and E.
Easter. Available from the National Technical
Information Service (703)-487-4650.
32,34. Recognition and Management of Pesticide Poisonings.
Fourth edition. Donald P. Morgan. M.D., 1989.
33. Duffy et al. The Long Term Effects Of An OP On
The Human Electroencephalogram. Toxic Applied
Pharmacology. 47:161-176, 1979.

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Acknowledgments
The review and suggestions (on an earlier
related draft) of Gershon Bergeison M.D. are
acknowledged with thanks.
/ am grateful to Professor L Somasundaram,
Iowa State University of Science and Technology,
for his review and comments, and for the
information and data on persistence, fate and
mobility which he gave me on an earlier draft.
The reviews, comments and access to various
data bases provided by my colleagues Robert
Kalayjian, Robert Koethe, and Wayne Toland are
gratefully acknowledged.
The review and help ofAlvero J. OCampo, M.D.
MPH and the review and comments that Dr.
Ames of the State of California, Pesticide and
Environmental Toxicology Section provided to Dr.
OCampo are acknowledged with pleasure.
Information and data from the following sources
have been used: for the oral and dermal toxicity
data, the Pesticide Dictionary, of the Farm
Chemicals Handbook; for toxicity information, the
U.S. EPA "Pesticides" book - a publication from
the Office of Drinking Water health advisories
(Lewis Publishers, Inc.), and Casarett and Doull's
"Toxicologyfor structural information and
formulae, the "Nanogen Index", a publication by
the Nanogen Company, of Watsonville, California,
and the "Pesticides Handbook", a publication of
the Entomological Society Of America.

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26
onA
-CH-
ca,
O-Na O-Na
DDT
O-Na O-Na
-CH-
—SUBSTITUTION Of -CI By -OH—
2,4,5-TRICHLOROPHENOLATE
(TCDD) DIOXIN
ATRAZINE
+
-CH(CH3)j222
HYDROXY ATRAZINE

DESETHYL-ATRAZINE

DESISOPROPYL-ATRAZINE

	LOSS OF ETHYL-

	LOSS OF ISOPROPYL-

-UOT

CI CI CI CL CI cL cL cL


-------