Human Health Effects:
Evidence for Carcinogenicity:
Classification of carcinogenicity: 1) evidence in humans: no adequate data;
2) evidence in animals: inadequate; Overall summary evaluation of carcinogenic
risk to humans is group 3: The agent is not classifiable as to its
carcinogenicity to humans. /From table/
A4; Not classifiable as a human carcinogen.
Human Toxicity Excerpts:
Harmful by inhalation, in contact with skin & if swallowed.
IN EXPTL STUDY, MALATHION WAS FOUND
TO BE A WEAK CONTACT SENSITIZER, INDUCING MILD CUTANEOUS REACTION IN HIGH
PROPORTION OF SUBJECTS.
A RELATIVELY LOW ACUTE TOXICITY OF MALATHION TO HUMANS IS INDICATED BY THE FACT
THAT A DAILY ORAL DOSAGE OF 24 MG GIVEN FOR MORE THAN 14 DAYS WAS NECESSARY TO
LOWER BLOOD CHOLINESTERASE ACTIVITIES IN ADULT VOLUNTEERS.
MALATHION POISONING IN FATAL CASES
SHOWS DAMAGE TO MYOCARDIUM WITH DILATION OF THE PERICARDIAL BLOOD VESSELS &
MARKED HEMORRHAGE IN THE SURROUNDING TISSUES, INTERSTITIAL EDEMA, INFLAMMATORY
CELLS, HEMOSIDERIN-LADEN MACROPHAGES, & FATTY INFILTRATION OF THE
MYOCARDIUM.
In a human experiment in which four men were exposed 1 hr daily for 42 days
to 84.8 mg/cu m, there was moderate irritation of the nose and conjunctiva but
there were no cholinergic signs or symptoms.
Estimated fatal oral dose for ortho-Malathion
50 Insect Spray is 60.0 g/70 kg. /From table/
Very large exposures are required to cause symptoms. After inhalation of
MALATHION, breathing and eye effects are
the first to appear. These include tightness of the chest, wheezing, a bluish
discoloration of the skin, small pupils, aching in and behind the eyes, blurring
of the vision, tearing, runny nose, headache, and watering of the mouth. After
swallowing MALATHION, loss of appetite,
nausea, vomiting, abdominal cramps and diarrhea may appear within two hr. After
skin absorption, sweating and twitching in the area of absorption may occur,
usually within 15 minutes to four hr. With severe intoxication by all routes, in
addition to the above symptoms, weakness, generalized twitching and paralysis
may occur and breathing may stop. In addition, dizziness, confusion, staggering,
slurred speech, generalized sweating, irregular or slow heartbeat, convulsions,
and coma may occur.
Immune complex nephropathy with renal dysfunction & massive proteinuria
occurred several wk after a MALATHION
exposure. /Complement 3 factor/ levels were marginally reduced & the renal
dysfunction resolved spontaneously after 1 mo.
The major signs and symptoms of malathion poisoning are attributable to the
potentiation of responses to acetylcholine released from preganglionic,
postganglionic cholinergic, and somatic motor nerve endings whenever nerve
volleys reach the periphery. In milder cases, the postganglionic stimulation may
predominate. ... Signs and symptoms include nausea, vomiting, diarrhea,
excessive sweating, salivation, miosis, increased bronchial secretion, bronchial
constriction, and the appearance of generalized muscular fasciculations followed
by weakness. Central nervous system effects may include anxiety, restlessness,
headache, and in more serious cases, tremors, confusion, drowsiness, slurred
speech, coma, loss of reflexes, and convulsions.
Alterations of the activities of serum butyrylcholinesterase (BuChE), serum
glutamic-oxalacetic transaminase, serum glutamic-pyruvic transaminase and serum
aldolase, and the concn of serum albumin in twelve agricultural workers exposed
to MALATHION over a period of six months
were examined. Two groups of controls were used, consisting of 30 blood samples
each, the first from randomly selected healthy blood donors, and the second from
healthy blood donors engaged in manual labor. The mean butyrylcholinesterase
activity of the agricultural workers at the end of the exposure period was not
significantly different from that of either group of controls. However, ... the
enzyme activity of any single subject changed significantly after exposure. A
reduction in butyrylcholinesterase activity was noted in 11 of 12 agricultural
workers, and six showed a sustained fall until the end of the study. Two showed
slight increases over their pre-exposure activities at the end. ... The largest
percent changes in the mean values of the agricultural workers during exposure
to MALATHION were decreases in the
activities of serum aldolase, serum glutamic-oxalacetic transaminase and serum
glutamic-pyruvic transaminase, with that of butyrylcholinesterase changing the
least of the four serum enzymes studied. No significant differences were
observed in serum albumin concentrations. This study indicates that
butyrylcholinesterase depression secondary to malathion exposure under field conditions does
occur.
... A 42 year old woman ingested a minimum of 120 ml of 50% malathion garden spray. She was admitted to a
hospital 30 minutes later, at which time she was comatose, markedly cyanotic,
flaccid, devoid of tendon reflexes, and markedly miotic. ... The patient was
discharged 5 weeks after admission. Laboratory investigations during the
patient's hospital course included determinations of plasma and erythrocyte
cholinesterase activities. Serum cholinesterase activity was less than 22% of
laboratory normal for the first nine days. Thereafter, the level gradually rose
to 100% by the 31st day. The erythrocyte cholinesterase activity was first
measured on the 12th day, when it was found to be 10% of normal. It remained
between 10 and 25% of normal until the 45th day after hospital admission and
then gradually rose to 100% by 130 days after admission. By this time, the
patient had been discharged. Hematocrit measurement showed a small drop after
admission, from 43 to 37%, and the reticulocyte count never rose above 2%. ...
Blood urea levels rose to 77 mg/100 ml of blood during the first 5 days,
thereafter returning to normal as the non renal uremia due to diarrhea and
hypersecretion was controlled. Electrocardiograms taken immediately after
admission and daily thereafter showed a prolongation of the P-R interval that
persisted for 5 days, as well as changes in the S-T segment which was reported
as consistent with panmyocardial ischemia. These latter changes disappeared
gradually as the patient's respiratory function improved.
To assess effects attributed to
MALATHION which escaped from an overheated
tank at a chemical plant in Linden, New Jersey, researchers surveyed seamen
subjects (n= 22) on board a nearby tanker and seamen control subjects (n= 22).
Self report measurement strategies included a medical review of body systems,
the "demoralization" scale reflecting psychological symptoms of distress,
demographics, and factors that may buffer stress, specifically, social support
and knowledge regarding toxic chemicals. Self reported postincident physical
health differences between the two groups of seamen were noted. There were no
differences between subjects and control subjects on demoralization levels.
Further analysis indicated higher levels of demoralization among less
knowledgeable seamen subjects.
Concn of up to 400 ug/ml of 95%
MALATHION failed to incr chromosomal
aberrations in human hematopoietic B411-4, RPMI-1788 & RPMI-7191 cell
cultures; however, /others/ ... reported a positive, although not dose related,
result in human lymphocytes with 99% pure
MALATHION.
A significant increase in chromosomal aberrations was found in the
lymphocytes of a group of 14 people intoxicated with a commercial formulation of
MALATHION (Fosfotion), as compared with
that in healthy controls. Aberrations observed included chromatid breaks,
chromatid isobreaks, chromatid exchanges and unstable chromosomal &
structural aberrations. No dose effect relationship was evident, since high
frequencies of aberrations were also detected in cases of mild intoxication.
(The small number of subjects involved & the inappropriateness of the
control group used does not permit the association to be established as causal.)
MALATHION is less toxic to humans
than most anticholinesterase agents because it is metabolized in the liver to an
inactive form.
To evaluate the latent neurological effects of organophosphate pesticide
poisoning, 100 matched pairs (1 black, 14 Mexican American, and 85
Anglo/Caucasian; 99 pairs were male) of individuals with previous acute
organophosphate pesticide poisoning (
MALATHION, 6 cases; results are not given for
individual chemicals) and nonpoison controls were examined. No significant
difference between the groups was found on audiometric tests, ophthalmic tests,
electroencephalograms, or the clinical serum and blood chemistry evaluations.
From the neurological examination, abnormalities were demonstrated among the
cases only on measures of memory, abstraction, and mood, and on one test of
motor reflexes. Differences between the cohorts were more apparent in the
neuropsychological tests, and occurred on tests of widely varying abilities,
including intellectual functioning, academic skills, abstraction and flexibility
of thinking, and simple motor skills. Twice as many cases as controls had
Halstead Reitan Battery summary scores in the range characteristic of cerebral
damage of dysfunction. Greater distress and complaints of disability for the
poisoned subjects were indicated by the Minnesota Multiphasic Personality
Inventory and the Patient's and Relative's Assessment of Patient Functioning
Inventories.
The cytotoxic, cytostatic, and cytogenetic effects of 14 organophosphate
pesticides, one of which was MALATHION,
on human lymphoid cells in vitro were studied. Cultures of human lymphoid
LAZ-007 cells were exposed to the test compounds at concentrations of 0.02, 0.2,
2.0, or 20 ug/ml for 48 hr with or without metabolic activation by rat liver
microsomal S9 product. At concentration of 0.2 ug/ml
MALATHION caused a significant increase in the
sister chromatid exchanges (SCE) which was elevated by exposure to 20 ug/ml.
Addition of S9 mix did not significantly increase sister chromatid exchanges
frequency. Treatment of cultures with 20 ug/ml decr the viable cell count to 53%
of control.
California collects data on most occupational and many non-occupational
illnesses and injuries related to pesticide exposure. Most of the occupational
incidents are investigated by local agencies. A thorough investigation is
conducted on all pesticide-related cases that meet "priority" guidelines: death;
hospitalization of 1 or more persons for more than 24 hours with treatment; or 5
or more people with symptoms seeking medical care as a result of the same
incident. This report summarizes the priority cases determined to be related to
pesticide exposure during 1986. Of the 67 described incidents, involving 583
people ill, 26 (38%) were related to exposure to pesticides applied indoors
(residences, offices), either by commerical pest control companies, employees or
homeowners. Nearly 200 people (33%) became ill and more than 200 people were
evacuated as a result of these types of applications. Most of these incidents
were a result of careless application techniques and not following label
instructions. Four other incidents, with 33 people ill, were the result of
spills in retail stores. In all 4 cases, store employees tried to clean the
spill without wearing protective clothing. Two other cases involved exposure via
a pesticide being put in a food container. Nineteen of these type of incidents
involved a pesticide product containing an organophosphate; most often
chlorpyrifos (8 incidents), diazinon (3 incidents), and
MALATHION (5 incidents). There were also 10
cases that resulted from suicide; eight different pesticides were involved. Five
incidents involving agricultural workers, as well as 4 incidents involving
non-agricultural workers, were primarily the result of allowing pesticides to
drift from the target field.
A 100-fold DNA amplification in the CHE gene, coding for serum
butyrylcholinesterase, was found in a farmer expressing the "silent" CHE
phenotype. Individuals homozygous for this gene display a defective serum
butyrylcholinesterase and are particularly vulnerable to poisoning by
agricultural organophosphorous insecticides, to which all members of this family
had long been exposed. DNA blot hybridization with regional
butyrylcholinesterase cDNA probes suggested that the amplification was most
intense in regions encoding central sequences within butyrylcholinesterase cDNA,
whereas distal sequences were amplified to a much lower extent. This is in
agreement with the "onion skin" model, based on amplification of genes in
cultured cells and primary tumors. The amplification was absent in the
grandparents but present at the same extent in one of their sons and in a
grandson, with similar DNA blot hybridization patterns. In situ hybridization
experiments localized the amplified sequences to the long arm of chromosome 3,
close to the site where we previously mapped the CHE gene. Altogether, these
observations suggest that the initial amplification event occurred early in
embryogenesis, spermatogenesis, or oogenesis, where the CHE gene is intensely
active and where cholinergic functioning was indicated to be physiologically
necessary. /Such/ findings demonstrate a de novo amplification in apparently
healthy individuals within an autosomal gene producing a target protein to an
inhibitor. Its occurrence in two generations from a family under prolonged
exposure to parathion indicates that organophosphorous poisons may be implicated
in previously unforeseen long-term ecological effects.
The lethal dose in mammals is about 1 g/kg.
Nearly all reported fatalities from
MALATHION have been through ingestion.
There is a single report of an association between brief anecdotal exposure
to MALATHION and subsequent fatal
aplastic anemia.
All the organophosphorus insecticides have a cumulative effect by progressive
inhibition of cholinesterase ... /Organophosphorus insecticides/
The symptoms of chronic poisoning due to organophosphorus pesticides include
headache, weakness, feeling of heaviness in head, decline of memory, quick onset
of fatigue, disturbed sleep, loss of appetite, & loss of orientation.
Psychic disorders, nystagmus, trembling of the hands & other nervous system
disorders can be observed in certain cases. Sometimes neuritis, paresis &
paralysis develop. /Organophosphorus pesticides/
Organophosphate insecticides ... are potent cholinesterase enzyme inhibitors
that act by interfering with the metabolism of acetylcholine, resulting in the
accumulation of acetylcholine at neuroreceptor transmission sites. Exposure
produces a broad spectrum of clinical effects that are indicative of massive
overstimulation of the cholinergic system, including muscarinic effects
(parasympathetic), nicotinic effects (sympathetic and motor), and CNS effects.
These effects present clinically as feelings of headache, weakness, dizziness,
blurred vision, psychosis, respiratory difficulty, paralysis, convulsions, and
coma. Typical findings are given by the mnemonic SLUD (salivation, lacrimation,
urination, and defecation). A small percentage of patients may fail to
demonstrate miosis, a classic diagnostic hallmark. The onset of the clinical
manifestation of organophosphate poisoning usually occurs within 12 hr of
exposure. /Organophosphate insecticides/
A woman at 34 to 35 weeks' gestation presented in acute respiratory distress
with cyanosis and tachypnea and bilateral rhonchi and crepitation. Her heart
rate was 78 beats per min and her blood pressure 120/80 mm Hg, with a fetal
heart rate of 140 beats per min. The mother was salivating markedly and her
pupils were reduced to "pinpoint size." An uncorrected metabolic acidosis was
diagnosed. Serum and erythrocyte acetylcholinesterase determinations were near
zero. Cholinesterase inhibitor poisoning was felt to be the likely cause of her
disorders. Administration of atropine 2.4 mg iv bolus with infusion of 0.02
mg/kg/hr lead to unacceptable fetal tachycardia. The woman had shown increased
cooperativeness and secretion control until the atropine had to be stopped. A
cesarean section was performed for delivery of a hypotonic infant with a 1 min
Apgar score of 3. The baby was mechanically ventilated for 2 days and required
atropine therapy at 0.1 mg/kg/hr for 8 days. The mother required 8 days of
mechanical ventilation and 11 days of atropine therapy. In this case, the infant
appeared relatively less poisoned than the mother by a presumed organophosphate
exposure. /Organophosphate poisoning/
A follow-up study of 232 people three years after a history of
organophosphorus pesticide poisoning disclosed only one person with slight
residual blurring of vision that might have been related to the earlier
poisoning, though at the time of poisoning over one third of the people had
blurring, which lasted only a day or two after exposure was discontinued. The
possile exceptional case had findings suggestive of basilar artery
insufficiency, rather than effects of poisoning. /Organophosphorus pesticide
poisoning/
The effects of acute intoxication by anti-cholinesterase agents are
manifested by muscarinic and nicotinic signs and symptoms and, except for
compounds of extremely low lipid solubility, by signs referable to the CNS.
Local effects are due to the action of vapors or aerosols at their site of
contact with the eyes or respiratory tract, or due to the local absorption after
liquid contamination of the skin or mucous membranes, including those of the
gastrointestinal tract. Systemic effects appear within minutes after inhalation
of vapors or aerosols. In contrast, the onset of symptoms is delayed after
gastrointestinal and percutaneous absorption. The duration of effects is
determined largely by the properties of the compound: its lipid solubility,
whether it must be activated, the stability of the organophosphorus-AChE bond,
and whether "aging" of the phosphorylated enzyme has occurred.
/Anticholinesterase agents/
Ocular effects include marked miosis, ocular pain, conjunctival congestion,
diminished vision, ciliary spasm, and brow ache. With acute systemic absorption,
miosis may not be evident due to sympathetic discharge in response to the
hypotension. /Anticholinesterase agents/
In addition to rhinorrhea and hyperemia of the upper respiratory tract,
respiratory effects consist of "tightness" in the chest and wheezing
respiration, caused by the combination of bronchoconstriction and increased
bronchial secretion. /Anticholinesterase agents/
Gastrointestinal symptoms occur earliest after ingestion, and include
anorexia, nausea and vomiting, abdominal cramps, and diarrhea.
/Anticholinesterase agents/
With percutaneous absorption of liquid, localized sweating and muscular
fasciculation in the immediate vicinity are generally the earliest
manifestations. /Anticholinesterase agents/
... Severe intoxication is manifested by extreme salivation, involuntary
defecation and urination, sweating, lacrimation, penile erection, bradycardia,
and hypotension. /Anticholinesterase agents/
The time of death after a single acute exposure may range from less than 5
minutes to nearly 24 hours, depending upon the dose, route, agent, and other
factors. The cause of death is primarily respiratory failure, usually
accompanied by a secondary cardiovascular component. Muscarinic, nicotinic, and
central actions all contribute to respiratory embarrassment; effects include
laryngospasm, bronchoconstriction, increased tracheobronchial and salivary
secretion, compromised voluntary control of the diaphragm and intercostal
muscles, and central respiratory depression. Blood pressure may fall to
alarmingly low levels and cardiac irregularities intervene. These effects
usually result from hypoxemia; they often are reversed by assisted pulmonary
ventilation. /Anticholinesterase agents/
ACCUMULATION OF ACETYLCHOLINE IN CNS IS BELIEVED TO BE RESPONSIBLE FOR
TENSION, ANXIETY, RESTLESSNESS, INSOMNIA, HEADACHE, EMOTIONAL INSTABILITY, &
NEUROSIS, EXCESSIVE DREAMING & NIGHTMARES, APATHY, & CONFUSION ...
DESCRIBED AFTER ORGANOPHOSPHATE POISONING. /ORGANOPHOSPHATE INSECTICIDES/
Three clinical syndromes of organophosphate toxicity have been described:
immediate, intermediate (1 to 4 days), and delayed (8 to 14 days) after
exposure. /Organophosphates and related compounds/
Immediate or delayed ascending paralysis (dying back axonopathy) starting in
the lower extremities may occur. This may be confused with Guillain-Barre
syndrome. /Organophosphates and related compounds/
The usual symptoms include headache, giddiness, nervousness, blurred vision,
weakness, nausea, cramps, diarrhea, and discomfort in the chest. Signs include
sweating, miosis, tearing, salivation and other excessive respiratory tract
secretion, vomiting, cyanosis, papilledema, uncontrollable muscle twitches
followed by muscular weakness, convulsions, coma, loss of reflexes, and loss of
sphincter control. The last four signs are seen only in severe cases but do not
preclude a favorable outcome if treatment is prompt and energetic. Cardiac
arrhythmias, various degrees of heart block, and cardiac arrest may occur ...
/Organic phosphorus pesticides/
Acute emphysema, pulmonary edema, pink froth in the trachea and bronchi, and
considerable congestion of the organs are found at autopsy. Slight microscopic
changes may occur in the liver and kidneys ... Petechial hemorrhages in the
organs may be present, especially if convulsions occurred during life. The
findings are not diagnostic. In a few cases in which death occurred unexpectedly
after several days of survival, multiple pericapillary and periprecapillary
hemorrhages were noted in the myocardium and medulla oblongata ... /Organic
phosphorous pesticides/
Skin, Eye and Respiratory Irritations:
Irritating to the eyes.
Drug Warnings:
MALATHION appears to have a low order
of toxicity following application to the scalp as
MALATHION 0.5% lotion. Adverse local effects
may include irritation of the scalp, pruritis, dryness of hair, and a transient
increase in dandruff.
Medical Surveillance:
1) Placement & periodic medical examinations shall include: (a)
Comprehensive initial or interim medical & work histories. (b) A physical
exam which shall be directed toward, but not limited to evidence of frequent
headache, dizziness, nausea, tightness of the chest, dimness of vision, &
difficulty in focusing the eyes. ... (d) A judgement of the worker's physical
ability to use negative or positive pressure regulators as defined in 29 CFR
1910.134.
... Examination of the respiratory system, liver, and attention to the
cholinesterase levels in the blood should be stressed. ...
MALATHION can cause depressed levels of
activity of cholinesterase in the serum and erythrocytes. The cholinesterase
activity in the erythrocytes should be measured ... before employment (or
exposure) in order to establish an individual baseline value, which should be
the mean of two cholinesterase activity measurements, taken at least one day
apart. ... The aforementioned medical examinations should be repeated on an
annual basis, with the exception of the cholinesterase determination which
should be performed quarterly or at any time overexposure is suspected or signs
and symptoms of toxicity occur.
Medical records shall be maintained for all workers engaged in the
manufacture or formulation of MALATHION
and such records shall be kept for at least 1 year after termination of
employment.
The assessment of exposure to the organophosphate pesticides, bromophos and
dicrotophos can be accomplished through measurement of these compounds in the
blood. However. since organophosphate pesticides are rapidly cleared from the
blood, it is difficult to be able to detect the pesticides in blood unless very
large quantities have been absorbed. This test may be useful for identification
of the compound in cases of severe exposure, although documented tests for
measurement of specific organophosphate pesticides in blood are very limited.
Whole Blood Reference Ranges: Normal - none detected; Exposed - not established;
Toxic -not established. Serum or Plasma Reference Ranges: Normal - not
established; Exposed - not established; Toxic - not established. Urine Reference
Ranges: Normal - not established; Exposed - not established; Toxic - not
established. /Organophosphate pesticides/
Respiratory Symptom Questionnaires: Questionnaires have been published by the
American Thoracic Society and the British Medical Research Council. These
questionnaires have been found to be useful in identification of people with
chronic bronchitis, however pulmonary function tests such as FEV1 (see pulmonary
function test section) have been found to be better predictors of chronic
airflow obstruction. /Organophosphate pesticides/
Chest Radiography: This test is widely used for assessing pulmonary disease.
Chest radiography been found to be useful for detection of early lung cancer in
asymptomatic people, especially for detection of peripheral tumors such as
adenocarcinomas. However, even though OSHA mandates this test for exposure to
some toxicants such as asbestos, there are conflicting views on its efficacy in
detection of pulmonary disease. /Organophosphate pesticides/
Pulmonary Function Tests: The tests that have been found to be practical for
population monitoring include: Spirometry and expiratory flow-volume curves;
Determination of lung volumes; Diffusing capacity for carbon monoxide;
Single-breath nitrogen washout; Inhalation challenge tests; Serial measurements
of peak expiratory flow; Exercise testing. /Organophosphate pesticides/
Sputum Cytology: Sputum cytology along with chest radiographs have been the
standard procedures for detecting early lung cancer in asymptomatic patients.
Sputum cytology has been found to be useful for detection of central tumors,
especially squamous carcinomas. For this test to be effective, exfoliated
respiratory mucosal cells must be present in the expectorated specimen. Pooling
of sputum collected over 2-3 days may enhance the sensitivity of this test by
increasing the yield of exfoliated cells in the specimen. /Organophosphorus
pesticides/
Evaluation of Peripheral Neuropathy: Nerve conduction study; Electromyography
(EMG); Quantitative sensory testing; Thermography. /Organophosphorus pesticides/
Evaluation of Central Nervous System Effects: Evaluation of CNS effects can
be performed through neuropsychological assessment, which consists of a clinical
interview and administration of standardized personality and neuropsychological
tests. The areas that the neuropsychology test batteries focus on include the
domains of memory and attention; visuoperceptual, visual scanning, visuospatial,
and visual memory; and motor speed and reaction time. There is limited data on
which components of the test batteries are best indicators of early CNS effects.
/Organophosphorus pesticides/
Evaluation of Cranial Neuropathies: Evaluation of cranial nerve damage, as
evidenced by symptoms such as loss of balance, visual function, smell, taste, or
sensation on the face, can be accomplished through a physical examination
focusing on tests such as: Smell assessment ... Vision assessment ... Facial and
Trigeminal Nerve assessment ... Vestibular assessment ... Hearing assessment.
/Organophosphorus pesticides/
Workers handling & applying pesticides must undergo an annual medical
examination at the beginning of each agricultural season. Contraindications
/meaning further clinical evaluations/ for work with /organophosphorus
pesticides/ are organic diseases of the central nervous system, mental disorders
& epilepsy, pronounced endocrine & vegetative disorders, pulmonary
tuberculosis, bronchial asthma, chronic respiratory diseases, cardiovascular
diseases & circulatory disorders, gastrointestinal diseases (peptic ulcer),
gastroenterocolitis, diseases of liver & kidneys, eye diseases (chronic
conjunctivitis & keratitis). The blood cholinesterase activity must be
determined before work starts. In the event of prolonged work periods, this
activity should be determined at intervals of 3-4 days. Persons exhibiting a
fall in cholinesterase activity of 25% or more must be transferred to other work
where they are not exposed to organophosphorus pesticides until this activity is
completely restored. Persons with initial signs of indisposition should /be
protected from exposure from/ pesticides. /Organophosphorus pesticides/
... Surveillance of workers could be carried out through measurement of blood
or urinary levels of the cmpd to which they are exposed, or through measurement
of a metabolite. /Organic phosphorus pesticides/
Populations at Special Risk:
Persons with a history of reduced pulmonary function or recent exposure to
anticholinesterase agents would be expected to be at increased risk from
exposure.
Young persons under 18 yr, expectant or nursing mothers, /alcoholics/, or
persons for whom work with toxic chemicals is contraindicated on account of
their state of health /are at elevated risk from the toxic effects of
organophosphorus pesticides. Those individuals with/ organic diseases of the
CNS, mental disorders & epilepsy, pronounced endocrine & vegetative
disorders, pulmonary tuberculosis, bronchial asthma, chronic respiratory
diseases, cardiovascular diseases and circulatory disorders, gastrointestinal
diseases (peptic ulcer), gastroenterocolitis, diseases of the liver &
kidneys, eye diseases (chronic conjunctivitis and keratitis) /are at elevated
risk from exposure/. /Organophosphorus pesticides/
Those individuals who are exposed to organophosphorus pesticides with
pre-existing/ organic diseases of the central nervous system, mental disorders
& epilepsy, pronounced endocrine & vegetative disorders, pulmonary
tuberculosis, bronchial asthma, chronic respiratory diseases, cardiovascular
diseases & circulatory disorders, gastrointestinal diseases (peptic ulcer),
gastroenterocolitis, diseases of liver & kidneys, eye diseases (chronic
conjunctivitis & keratitis) /are at elevated risk from exposure/. The blood
cholinesterase activity must be determined before work starts. In the event of
prolonged work periods, this activity should be determined at intervals of 3-4
days. Persons exhibiting a fall in cholinesterase activity of 25% or more must
be transferred to other work where they are not exposed to organophosphorus
pesticides until this activity is completely restored. Persons with initial
signs of indisposition should cease work with pesticides. /Organophosphorus
pesticides/
Probable Routes of Human Exposure:
... Skin & eye contact.
POTENTIAL DERMAL AND RESP EXPOSURES TO
MALATHION: PERSONS OUTDOORS AND INDOORS DURING
AIR APPLICATION TO POPULATED AREA. /FROM TABLE/
POTENTIAL DERMAL AND RESP EXPOSURES TO
MALATHION: OPERATING AEROSOL MACHINE, AIR
BLAST SPRAYING FRUIT ORCHARDS, PERSONS OUTDOORS AND INDOORS DURING AIR
APPLICATION TO POPULATED AREA. /FROM TABLE/
NIOSH (NOES Survey 1981-1983) has statistically estimated that 19,172 workers
(1,910 of these are female) are potentially exposed to
MALATHION in the US(1). Occupational exposure
to MALATHION may occur through
inhalation and dermal contact for persons, like pet handlers, who use
MALATHION as an insecticide to control pet and
human fleas(2), and for farmers who use
MALATHION to store grains(3). Mean of
MALATHION detected in the ambient air of
insecticide storage and office rooms of commercial pest control buildings in a 2
hr period during the winter and summer season is 0.77 ug/cu m(4). The general
population maybe exposed to MALATHION
via inhalation of ambient air, ingestion of contaminated foods, via drinking
contaminated water, and dermal contact with this compound and other products
containing MALATHION(SRC).
Body Burden:
According to a national survey performed in the US from 1976-1980,
MALATHION was detected in quantifiable amounts
from 1.6% of the urine analyses for persons 12-74 years of age(1). Trace amounts
of metabolites in urine showed 4.1% of the persons tested were exposed to
MALATHION(2). Of 267 samples of human urine,
0.4% were positive for MALATHION, at
concns < 0.1 ppm(3). MALATHION was
detected, not quantifed in the respired air of a resident in 1 of 9 residents
from 9 households sampled in Jacksonville, FL(4).
Average Daily Intake:
In 1982-84 a national study was performed that showed the average daily
intakes of MALATHION in the US for
children 6 to 11 mon of age and 2 yr old were 142.3 and 232.8 ng/kg body
weight/day, respectively(1). In 1982-84 a national study was performed that
showed the average daily intake of
MALATHION in the US for females 14-16, 25-30
and 60-65 yrs of age was 74.8, 61.8 and 53.9 ng/kg body weight/day,
respectively(1). In 1982-84 a national study was performed that showed the
average daily intake of MALATHION in the
US for males 14-16, 25-30 and 60-65 yrs of age was 107.1, 72.9 and 62.9 ng/kg
body weight/day, respectively(1).
Emergency Medical Treatment:
Emergency Medical Treatment:
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TREATMENT OF SPECIFIC CASES. Copyright 1974-1998 Micromedex, Inc. Denver,
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redistribution of all or part of the POISINDEX(R) database is a violation
of Micromedex' copyrights and is strictly prohibited.
The following Overview, *** ORGANOPHOSPHATES ***, is relevant for this HSDB record chemical. |
| Life Support: |
o This overview assumes that basic life support measures
have been instituted. |
| Clinical Effects: |
SUMMARY OF EXPOSURE
0.2.1.1 ACUTE EXPOSURE
o MUSCARINIC EFFECTS include bradycardia, bronchospasm,
bronchorrhea, salivation, lacrimation, diaphoresis,
vomiting, diarrhea, urination, and miosis.
o NICOTINIC EFFECTS include tachycardia, hypertension,
fasciculations, mydriasis, muscle cramps, weakness,
RESPIRATORY PARALYSIS.
o CENTRAL EFFECTS include CNS depression, agitation,
confusion, delirium, coma, seizures. Children may have
different predominant signs and symptoms than adults
(CNS depression, stupor, flaccidity, dyspnea, and
coma).
o ONSET - Symptoms may appear within a few minutes or up
to 12 hours (rarely longer) after exposure.
1. Organophosphates are absorbed across the lung, mucous
membranes (including gut), and skin. Poisoning
depends upon inherent toxicity, dosage, rate of
absorption, rate of metabolic breakdown, and prior
exposure to other cholinesterase inhibitors.
2. Onset of cholinergic crisis following exposure to very
lipophilic organophosphates may be delayed.
3. Recurrence of toxicity after apparent improvement has
been described.
o INHALATION EXPOSURE - Organophosphate vapors rapidly
produce mucous membrane and upper airway irritation
and bronchospasm, followed by systemic muscarinic,
nicotinic and central effects if exposed to significant
concentrations.
o INTERMEDIATE SYNDROME characterized by paralysis of
respiratory, cranial motor, neck flexor, and proximal
limb muscles 1 to 4 days after apparent recovery from
cholinergic toxicity, and prior to development of
delayed peripheral neuropathy. Treatment is
respiratory support; atropine and pralidoxime are
ineffective. Recovery begins 5 to 15 days after onset.
o DELAYED POLYNEUROPATHY - Distal sensory-motor
polyneuropathy may develop 6 to 21 days following
exposure.
o HYDROCARBONS - The hydrocarbon diluent may contribute
to the overall toxicity.
Refer to "HYDROCARBONS" management for further
information.
VITAL SIGNS
0.2.3.1 ACUTE EXPOSURE
o Hypothermia or hyperthermia may occur. Bradycardia and
hypotension may develop after moderate to severe
poisoning. Tachycardia, hypertension, and changes in
respiratory rate may also occur.
HEENT
0.2.4.1 ACUTE EXPOSURE
o Miosis, lacrimation, and blurred vision are common;
mydriasis and opsoclonus may occur.
o Salivation commonly occurs.
CARDIOVASCULAR
0.2.5.1 ACUTE EXPOSURE
o Bradycardia and tachycardia are common. Hypotension or
hypertension may be seen with moderate to severe
poisoning. Other dysrhythmias, conduction delays and
ventricular dysrhythmias, are less common and
associated with severe poisonings. Myocarditis occurs
rarely.
RESPIRATORY
0.2.6.1 ACUTE EXPOSURE
o Increased bronchial secretions, bronchospasm and
dyspnea occur in moderate to severe exposures.
Respiratory failure and acute lung injury
(non-cardiogenic pulmonary edema) may occur with severe
poisonings. Acute respiratory insufficiency is the
main cause of death in acute poisonings. The
hydrocarbon vehicle may cause chemical pneumonitis.
o Transient vocal cord paralysis with complete airway
occlusion has been reported.
NEUROLOGIC
0.2.7.1 ACUTE EXPOSURE
o EARLY EFFECTS - Giddiness, anxiety headache, and
restlessness followed by ataxia, drowsiness, and
confusion are common with moderate to severe exposures.
Fasciculations, profound weakness, coma and seizures
may develop in severe cases. CNS depression and
seizures may be more common in children than adults.
o INTERMEDIATE SYNDROME - characterized by the
development of proximal weakness and paralysis 12 hours
to 7 days after exposure and following resolution of
cholinergic symptoms. It is unresponsive to
pralidoxime or atropine; treatment is supportive.
o DELAYED POLYNEUROPATHY - Distal sensory-motor
polyneuropathy may develop 6 to 21 days following
exposure; recovery may be slow or incomplete.
o SEQUELAE - Sequelae may include subtle
neuropsychological deficits.
o EXTARPYRAMIDAL SIGNS - may rarely develop in patients
with acute organophosphate poisoning, especially with
highly lipid soluble compounds such as fenthion.
GASTROINTESTINAL
0.2.8.1 ACUTE EXPOSURE
o Nausea, vomiting, abdominal cramps, and diarrhea are
common muscarinic effects. Both painless and frank
clinical pancreatitis have been reported. Anorexia,
Fecal and urinary incontinence, and esophagitis have
been reported with organophosphate intoxication.
GENITOURINARY
0.2.10.1 ACUTE EXPOSURE
o Increased urinary frequency is common; urinary
incontinence may occur.
ACID-BASE
0.2.11.1 ACUTE EXPOSURE
o Metabolic acidosis has occurred in severe poisonings.
FLUID-ELECTROLYTE
0.2.12.1 ACUTE EXPOSURE
o Hypokalemia may occur in severe poisonings.
HEMATOLOGIC
0.2.13.1 ACUTE EXPOSURE
o Alterations in PT and clotting factor levels may occur
but are rarely clinically significant.
DERMATOLOGIC
0.2.14.1 ACUTE EXPOSURE
o
Profuse sweating is common. Pallor may be noted.
Dermal sensitization has been reported.
MUSCULOSKELETAL
0.2.15.1 ACUTE EXPOSURE
o Organophosphate compounds cause skeletal muscle
weakness. Rhabdomyolysis has been reported following
exposure to fenitrothion.
ENDOCRINE
0.2.16.1 ACUTE EXPOSURE
o Hyperamylasemia, hyperglycemia, and glycosuria without
ketosis may occur in severe poisonings.
PSYCHIATRIC
0.2.18.1 ACUTE EXPOSURE
o Decreased vigilance, defects in expressive language and
cognitive function, impaired memory, depression,
anxiety or irritability and psychosis have been
reported as delayed effects, more commonly in persons
having other clinical signs of organophosphate
poisoning or pre-existing psychological conditions.
REPRODUCTIVE HAZARDS
o Most organophosphates are not teratogenic in animals,
but some cause lower fetal birth weights and/or higher
neonatal mortality.
o Sporadic reports of human birth defects related to
organophosphates have not been fully verified.
CARCINOGENICITY
0.2.21.2 HUMAN OVERVIEW
o Generally, organophosphates are thought not to be
carcinogenic; some controversy exists. |
| Laboratory: |
o Determine plasma and red blood cell cholinesterase
activities. Depression in excess of 50 percent of
baseline is generally associated with severe symptoms.
Correlation between cholinesterase levels and clinical
effects in milder poisonings may be poor.
o Monitor electrolytes, ECG and serum pancreatic isoamylase
levels in patients with significant poisoning. Patients
who have increased serum amylase levels and those who
develop a prolonged QTc interval or PVCs are more likely
to develop respiratory insufficiency and have a worse
prognosis. |
| Treatment Overview: |
ORAL EXPOSURE
o Ipecac is CONTRAINDICATED because of possible
respiratory depression and seizures.
o ACTIVATED CHARCOAL: Administer charcoal as a slurry
(240 mL water/30 g charcoal). Usual dose: 25 to 100 g
in adults/adolescents, 25 to 50 g in children (1 to 12
years), and 1 g/kg in infants less than 1 year old.
o GASTRIC LAVAGE: Consider after ingestion of a
potentially life-threatening amount of poison if it can
be performed soon after ingestion (generally within 1
hour). Protect airway by placement in Trendelenburg and
left lateral decubitus position or by endotracheal
intubation. Control any seizures first.
1. CONTRAINDICATIONS: Loss of airway protective reflexes
or decreased level of consciousness in unintubated
patients; following ingestion of corrosives;
hydrocarbons (high aspiration potential); patients at
risk of hemorrhage or gastrointestinal perforation; and
trivial or non-toxic ingestion.
o Suction oral secretions and emesis to avoid aspiration.
o ATROPINE THERAPY - If symptomatic, administer IV
atropine until atropinization is achieved. Adult - 2 to
5 mg every 10 to 15 minutes; Child - 0.05 mg/kg every 10
to 15 minutes. Atropinization may be required for hours
to days depending on severity.
o PRALIDOXIME (Protopam, 2-PAM): Treat moderate to severe
poisoning (fasciculations, muscle weakness, respiratory
depression, coma, seizures) with 2-PAM in addition to
atropine; most effective if given within 48 hours, but
has had efficacy up to 6 days. May require
administration for several days.
1. INITIAL DOSE: ADULT: 1 to 2 g in 100 to 150 ml 0.9%
saline IV over 30 min. CHILD: 20 to 50 mg/kg as a 5%
solution IV over 30 min.
2. Repeat these doses in 1 hour and then every 6 to 12
hours if muscle weakness or fasciculations persist, or
begin continuous infusion.
3. CONTINUOUS INFUSION: Administer as a 2.5% solution in
0.9% saline. ADULT: 500 mg/hour. CHILD: 9 to 19
mg/kg/hour.
o CONTRAINDICATIONS - Succinylcholine and other
cholinergic agents.
o SEIZURES: Administer a benzodiazepine IV; DIAZEPAM
(ADULT: 5 to 10 mg, repeat every 10 to 15 min as
needed. CHILD: 0.2 to 0.5 mg/kg, repeat every 5 min
as needed) or LORAZEPAM (ADULT: 2 to 4 mg; CHILD: 0.05
to 0.1 mg/kg).
1. Consider phenobarbital if seizures recur after diazepam
30 mg (adults) or 10 mg (children > 5 years).
2. Monitor for hypotension, dysrhythmias, respiratory
depression, and need for endotracheal intubation.
Evaluate for hypoglycemia, electrolyte disturbances,
hypoxia.
o ACUTE LUNG INJURY: Maintain ventilation and oxygenation
and evaluate with frequent arterial blood gas or pulse
oximetry monitoring. Early use of PEEP and mechanical
ventilation may be needed.
o HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid,
place in Trendelenburg position. If hypotension
persists, administer dopamine (5 to 20 mcg/kg/min) or
norepinephrine (0.1 to 0.2 mcg/kg/min), titrate to
desired response.
o PERSONNEL PROTECTION - Rescuers should avoid dermal
contact with contaminated patients to avoid poisoning
themselves.
INHALATION EXPOSURE
o INHALATION: Move patient to fresh air. Monitor for
respiratory distress. If cough or difficulty breathing
develops, evaluate for respiratory tract irritation,
bronchitis, or pneumonitis. Administer oxygen and
assist ventilation as required. Treat bronchospasm with
beta2 agonist and corticosteroid aerosols.
o If respiratory tract irritation or respiratory
depression is evident, monitor arterial blood gases,
chest x-ray, and pulmonary function tests.
o Carefully observe patients with inhalation exposure for
the development of any systemic signs or symptoms and
administer symptomatic treatment as necessary.
o Treatment should include recommendations listed in the
ORAL EXPOSURE section when appropriate.
EYE EXPOSURE
o DECONTAMINATION: Irrigate exposed eyes with copious
amounts of tepid water for at least 15 minutes. If
irritation, pain, swelling, lacrimation, or photophobia
persist, the patient should be seen in a health care
facility.
o Patients symptomatic following exposure should be
observed in a controlled setting until all signs and
symptoms have fully resolved.
o Treatment should include recommendations listed in the
ORAL EXPOSURE section when appropriate.
DERMAL EXPOSURE
o Systemic effects can occur from dermal exposure to
organophosphates.
o Remove contaminated clothing and jewelry; wash skin,
hair and nails vigorously with repeated soap washings.
Leather absorbs pesticides; all contaminated leather
should be discarded. Rescue personnel and bystanders
should avoid direct contact with contaminated skin,
clothing, or other objects.
o Treatment should include recommendations listed in the
ORAL EXPOSURE section when appropriate. |
| Range of Toxicity: |
o Acute toxicity is variable and depends upon absorption
kinetics and whether or not metabolic activation is
required. Sudden absorption of a less toxic compound may
have a more severe effect. |
Antidote and Emergency Treatment:
Basic treatment: Establish a patent airway. Suction if necessary. Aggressive
airway control may be needed. Watch for signs of respiratory insufficiency and
assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10
to 15 L/min. Monitor for pulmonary edema and treat if necessary ... Monitor for
shock and treat if necessary ... Anticipate seizures and treat if necessary ...
For eye contamination, flush eyes immediately with water. Irrigate each eye
continuously with normal saline during transport ... Do not use emetics. For
ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution
if the patient can swallow, has a strong gag reflex, and does not drool.
Administer activated charcoal ... /Organophosphates and related compounds/
Advanced treatment: Consider orotracheal or nasotracheal intubation for
airway control in the patient who is unconscious or has severe pulmonary edema.
Positive pressure ventilation techniques with a bag valve mask device may be
beneficial. Monitor cardiac rhythm and treat arrhythmias if necessary ... .
Start an IV with D5W /SRP: "To keep open", minimal flow rate/Use lactated
Ringer's if signs of hypovolemia are present. Administer atropine. Correct
hypoxia before giving atropine ... Administer pralidoxime chloride (2 PAM). USE
UNDER DIRECT PHYSICIAN ORDERS ONLY ... Treat seizures with adequate
atropinization and correction of hypoxia. Rarely is diazepam necessary ... For
hypotension with signs of hypovolemia, administer fluid cautiously and consider
vasopressors for hypotension with a normal fluid volume. Watch for signs of
fluid overload (refer to shock protocol in Section Three). Use proparacaine
hydrochloride to assist eye irrigation ... /Organophosphates and related
compounds/
A comatose patient who is diaphoretic, has pinpoint pupils and the odor of an
insecticide on clothing or breath, and is noted to have muscle fasciculations
represents the classic presentation of organophosphate poisoning. ... Specific
steps in management include the following. 1. Decontamination. ... 2 Airway.
Establish an airway if necessary. ... 3. Respiratory Status. Respiratory
distress, in fact, is commonly found in these patients from multiple causes. ...
4. Cardiac Monitoring. ... 5. Cholinesterase Level. ... 6. Pralidoxime.
Pralidoxime is the treatment of choice for organophosphate poisoning and should
be used for nearly all patients with clinically significant orgnophosphate
poisoning, particularly whose patients with muscular fasciculations and
weakness. ... 7. Atropine. Atropine is the physiologic antidote for
organophosphate poisoning. A trial dose of atropine should be instituted on
clinical ground when one suspects organophosphate intoxication. /Organophosphate
poisoning/
1. INSURE THAT A CLEAR AIRWAY EXISTS BY ASPIRATION OF SECRETIONS IF
NECESSARY. ADMIN OXYGEN BY MECHANICALLY ASSISTED PULMONARY VENTILATION IF
RESPIRATION IS DEPRESSED. IMPROVE TISSUE OXYGENATION AS MUCH AS POSSIBLE BEFORE
ADMIN ATROPINE TO MINIMIZE RISK OF VENTRICULAR FIBRILLATION. IN SEVERE
POISONINGS, IT MAY BE NECESSARY TO SUPPORT PULMONARY VENTILATION MECHANICALLY
FOR SEVERAL DAYS. 2. ADMIN ATROPINE SULFATE IV, OR IM IF IV INJECTION IS NOT
POSSIBLE. ... /ORGANOPHOSPHATE PESTICIDES/
2. SEVERELY POISONED INDIVIDUALS MAY EXHIBIT REMARKABLE TOLERANCE TO
ATROPINE; TWO OR MORE TIMES THE DOSAGES SUGGESTED ABOVE MAY BE NEEDED. THE DOSE
OF ATROPINE MAY BE INCREASED AND THE DOSING INTERVAL DECREASED AS NEEDED TO
CONTROL SYMPTOMS. CONTINUOUS INTRAVENOUS INFUSION OF ATROPINE MAY BE NECESSARY
WHEN ATROPINE REQUIREMENTS ARE MASSIVE. REVERSAL OF MUSCARINIC SYMPTOMS AND
SIGNS, NOT AN ARBITRARY DOSE LIMIT, IS THE DESIRED END-POINT. PRESERVATIVE-FREE
ATROPINE PRODUCTS SHOULD BE USED WHENEVER POSSIBLE. NOTE: PERSONS NOT POISONED
OR ONLY SLIGHTLY POISONED BY ORGANOPHOSPHATES MAY DEVELOP SIGNS OF ATROPINE
TOXICITY FROM SUCH LARGE DOSES. FEVER, MUSCLE FIBRILLATIONS, AND DELIRIUM ARE
THE MAIN SIGNS OF ATROPINE TOXICITY. IF THESE APPEAR WHILE THE PATIENT IS FULLY
ATROPINIZED, ATROPINE ADMINISTRATION SHOULD BE DISCONTINUED, AT LEAST
TEMPORARILY, WHILE THE SEVERITY OF POISONING IS REEVALUATED. /ORGANOPHOSPHATE
PESTICIDES/
3. DRAW BLOOD SAMPLE (HEPARINIZED) FOR CHOLINESTERASE ANALYSIS BEFORE
ADMINISTRATION OF PRALIDOXIME, WHICH TENDS TO REVERSE THE CHOLINESTERASE
DEPRESSION. 4. ADMIN PRALIDOXIME (PROTOPAM, 2-PAM) IN CASES OF SEVERE POISONING
... IN WHICH RESP DEPRESSION, MUSCLE WEAKNESS & TWITCHINGS ARE SEVERE. ...
/ORGANOPHOSPHATE PESTICIDES/
4. BE PREPD TO ASSIST PULMONARY VENTILATION MECHANICALLY IF RESP ...
DEPRESSED ... . 5. IN PATIENTS WHO HAVE BEEN POISONED BY ORGANOPHOSPHATE
CONTAMINATION OF SKIN, CLOTHING, HAIR, AND/OR EYES, DECONTAMINATION MUST PROCEED
CONCURRENTLY WITH WHATEVER RESUSCITATIVE AND ANTIDOTAL MEASURES ARE NECESSARY TO
PRESERVE LIFE. ... 6. IF ... INGESTED IN QUANTITY PROBABLY SUFFICIENT TO CAUSE
POISONING, THE STOMACH AND INTESTINE MUST BE EMPTIED. A. EMPTY THE STOMACH BY
INTUBATION, ASPIRATION, AND LAVAGE, USING SLURRY OF ACTIVATED CHARCOAL IN
ISOTONIC SALINE. RIGOROUS PRECAUTIONS MUST BE TAKEN TO PROTECT THE AIRWAY FROM
ASPIRATION OF REGURGITATED. IF VICTIM IS UNCONSCIOUS OR OBTUNDED, INSERT A
CUFFED ENDOTRACHEAL TUBE PRIOR TO GASTRIC INTUBATION. KEEP VICTIM'S HEAD BELOW
LEVEL OF STOMACH DURING GASTRIC INTUBATION AND LAVAGE ... KEEP VICTIM'S HEAD
TURNED TO THE LEFT. /ORGANOPHOSPHATE PESTICIDES/
6B. AFTER ASPIRATION OF STOMACH CONTENTS AND LAVAGE, INSTILL ACTIVATED
CHARCOAL ... TOGETHER WITH A CATHARTIC IN THE CHARCOAL SLURRY. ... ALTERNATIVE
CATHARTICS THAT MAY BE USED INSTEAD ARE SODIUM OR MAGNESIUM SULFATE OR CITRATE:
DOSAGE OF SODIUM OR MAGNESIUM SULFATE ... C. IF GASTRIC ASPIRATION AND LAVAGE IS
NOT PERFORMED DUE TO DELAY IN TREATMENT, AND IF PATIENT IS FULLY ALERT,
ADMINISTER DOSES OF CHARCOAL AND CATHARTIC ORALLY. WHEN SORBITOL IS GIVEN
ORALLY, IT SHOULD BE DILUTED WITH AN EQUAL VOLUME OF WATER TO YIELD A 35%
SOLUTION. D. SAVE A SAMPLE OF EMESIS OR INITIAL GASTRIC WASHINGS FOR CHEMICAL
ANALYSIS. E. IN SOME CASES OF ORGANOPHOSPHATE INGESTION THERE MAY BE BENEFIT
FROM REPEATED ADMINISTRATION OF ACTIVATED CHARCOAL, EITHER BY INGESTION OR
STOMACH TUBE ... /ORGANOPHOSPHATE PESTICIDES/
7. OBSERVE PATIENT CLOSELY FOR AT LEAST 72 HOURS (LONGER IN CASES OF
ORGANOPHOSPHATE INGESTION) TO INSURE THAT SYMPTOMS (SWEATING, VISUAL
DISTURBANCES, VOMITING, DIARRHEA, CHEST AND ABDOMINAL DISTRESS, AND SOMETIMES
PULMONARY EDEMA) DO NOT RECUR AS ATROPINIZATION IS WITHDRAWN. IN VERY SEVERE
POISONINGS BY INGESTED ORGANOPHOSPHATES, PARTICULARLY THE MORE LIPOPHILIC AND
SLOWLY HYDROLYZED COMPOUNDS, METABOLIC DISPOSITION OF TOXICANT MAY REQUIRE AS
MANY AS 5-14 DAYS. /ORGANOPHOSPHATE PESTICIDES/
8. PARTICULARLY IN POISONINGS BY LARGE INGESTED DOSES OF ORGANOPHOSPHATE,
MONITOR PULMONARY VENTILATION CAREFULLY, EVEN AFTER RECOVERY FROM MUSCARINIC
SYMPTOMATOLOGY, TO FORESTALL RESPIRATORY FAILURE. 9. IN SEVERELY POISONED
PATIENTS, MONITOR CARDIAC STATUS BY CONTINUOUS ECG RECORDING. /ORGANOPHOSPHATE
PESTICIDES/
10. FUROSEMIDE MAY BE CONSIDERED FOR RELIEF OF PULMONARY EDEMA IF RALES
PERSIST IN THE LUNGS EVEN AFTER FULL ATROPINIZATION. ... 11. THE FOLLOWING DRUGS
ARE PROBABLY CONTRAINDICATED IN NEARLY ALL ORGANOPHOSPHATE POISONING CASES:
MORPHINE, THEOPHYLLINE, PHENOTHIAZINES, AND RESERPINE. ADRENERGIC AMINES SHOULD
BE GIVEN ONLY IF THERE IS A SPECIFIC INDICATION, SUCH AS MARKED HYPOTENSION.
/ORGANOPHOSPHATE PESTICIDES/
For immediate first aid: ensure that adequate decontamination has been
carried out. If victim is not breathing, start artificial respiration,
preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket
mask as trained. Perform CPR if necessary. Immediately flush contaminated eyes
with gently flowing water. Do not induce vomiting. If vomiting occurs, lean
patient forward or place on left side (head-down position, if possible) to
maintain an open airway and prevent aspiration. Keep victim quiet and maintain
normal body temperature. Obtain medical attention. /Organophosphates and related
compounds/
Preservative-free atropine should be used to avoid toxicity from preservative
agents. Mydriasis may occur early in the administration of atropine; however the
endpoint for atropine administration is the drying of pulmonary secretions.
/Organophosphates and related compounds/
Never give morphine, theophylline, and theophylline ethylenediamine ... Large
amounts of iv fluids generally are contraindicated because of the threat of
pulmonary edema. /Organic phosphorous pesticides/
Succinylcholine, other cholinergic agents, and aminophylline are
contraindicated. /Organophosphates and related compounds/
Animal Toxicity Studies:
Evidence for Carcinogenicity:
Classification of carcinogenicity: 1) evidence in humans: no adequate data;
2) evidence in animals: inadequate; Overall summary evaluation of carcinogenic
risk to humans is group 3: The agent is not classifiable as to its
carcinogenicity to humans. /From table/
A4; Not classifiable as a human carcinogen.
Non-Human Toxicity Excerpts:
DIPPING 4 TIMES AT 4 DAY INTERVALS IN A 2% SOLUTION OF 57% 'EMULSIFIABLE
SOLUTION' OF MALATHION HAD NO EFFECT
UPON DOGS.
AT 100 PPM /IN RATS/, NO EFFECTS WERE OBSERVED, EVEN ON RED CELL
CHOLINESTERASE ACTIVITY. IN TWO STUDIES, 500 PPM FOR 8 WK ALSO PRODUCED NO
ADVERSE EFFECT ON WHOLE BLOOD CHOLINESTERASE ACTIVITY. AT 1000 PPM & HIGHER,
HOWEVER, RED CELL CHOLINESTERASE ACTIVITY WAS SIGNIFICANTLY DECR. IP INJECTION
... FOR 60 DAYS RESULTED IN A NO ADVERSE EFFECT LEVELS OF 100 MG/KG WITHOUT
MORTALITY, BUT DOSAGES OF 200 & 300 MG/KG/DAY RESULTED IN MORTALITY RATES OF
60 & 100%, RESPECTIVELY.
NO TERATOGENIC EFFECTS WERE OBSERVED WHEN RATS WERE TREATED IP WITH
MALATHION AT 900 MG/KG. ... ON DAY 11 AFTER
INSEMINATION, PREGNANT RATS WERE GIVEN SINGLE IP INJECTION OF
MALATHION. NO SIGNIFICANT DIFFERENCE BETWEEN
TREATED FEMALES & CONTROLS RELATIVE TO DEAD FETUSES/LITTER, RESORPTIONS, AVG
WT OF FETUSES, AVG WT OF PLACENTA, OR FETAL MALFORMATIONS WERE OBSERVED.
WHEN ACUTE TOXICITY OF A NUMBER OF ORGANOPHOSPHATE INSECTICIDES IN 23 DAY OLD
WEANLING MALE RATS WAS COMPARED WITH THAT IN ADULTS. WEANLINGS WERE FOUND TO BE
APPROX TWICE AS SUSCEPTIBLE TO ...
MALATHION ...
UNDILUTED TECHNICAL LIQ MALATHION
DROPPED ON RABBIT'S EYE CAUSED SLIGHT IMMEDIATE IRRITATION WITH CONJUNCTIVAL
HYPEREMIA & EDEMA OF LIDS ...
THE ORAL TOXIC DOSE TO CALVES ... IS 10-20 MG/KG & TO ADULT CATTLE &
SHEEP, 50-100 MG/KG. THE LETHAL DOSE IN GIVEN AS 200 MG/KG IN CATTLE & 150
MG/KG IN SHEEP. SPRAYS CONTAINING 1%
MALATHION WERE LETHAL TO CALVES.
PERSISTENT MUSCLE WEAKNESS HAS BEEN DESCRIBED IN CHICKENS FOLLOWING SINGLE
DOSES OF 100 MG/KG. ... USED IN CONCN OF 1.25% AS SPRAY OR 4% AS DUSTING POWDER,
MALATHION APPEARS TO BE HARMLESS TO
POULTRY. ... 100 PPM MALATHION IN DIET
OF CHICKENS DOES NOT AFFECT THEIR GROWTH OR FEED CONVERSION. UP TO 15 PPM DOES
NOT AFFECT HATCHABILITY OF PULLETS' EGGS. DOSES OF 400 MG/KG GIVEN TO FOWLS
CAUSED A PRONOUNCED RISE IN THE BLOOD GLUCOSE LEVELS.
BLOOD CHOLINESTERASE LEVELS IN CALVES GIVEN 2 MG/KG OF
MALATHION DAILY FOR UP TO 13 DAYS FELL TO 50%,
BUT PROMPTLY RETURNED TO NORMAL WHEN ADMIN CEASED.
... TREATMENT WITH 15% SOLN /
MALATHION/ ... CAUSED DEATHS OF 16 DOGS. IN
SOME CASES CLINICAL SIGNS (MALAISE, SALIVATION, ANOREXIA, & VOMITING) DID
NOT START UNTIL 12TH DAY; DEATH CONTINUED FOR UP TO 12 WK.
/WHEN MALATHION WAS/ ... GIVEN TO
RATS IN AMT OF 240 MG/KG, NO TERATOGENIC ACTIVITY WAS DETECTED. THERE WAS ...
INCR IN MORTALITY RATE OF NEWBORNS FROM TREATED MOTHERS. ... /IN ANOTHER EXPT/
... PREGNANT RATS /WERE FED BY GAVAGE/ ... 300 MG/KG ON DAYS 6 THROUGH 15 &
... NO TERATOGENICITY /FOUND/.
Six pesticides, one of which was
MALATHION, induced a significant increase of
sister chromatid exchange frequencies in a dose dependent fashion in cultured
Chinese hamster cell line V79. The six in decreasing order of sister chromatid
exchanges induction are methyl parathion, demeton, trichlorfon, dimethoate,
MALATHION, & methidathion. Cells
were exposed to MALATHION for 28 hr at
concn of 10, 20, 40, ug/ml, respectively. All test cmpd caused a delay in cell
cycle.
PURE MALATHION WAS TESTED FOR DNA
DAMAGING & MUTAGENIC ACTIVITY IN BACILLUS SUBTILIS & SALMONELLA
TYPHIMURIUM TESTER STRAINS & WAS WAS FOUND TO BE MODERATELY MUTAGENIC
WITHOUT METABOLIC ACTIVATION.
GROUPS OF 50 MALE AND 50 FEMALE WEANLING CHARLES RIVER B6C3F1 MICE WERE FED
DIETS CONTAINING 8000 OR 16000 MG/KG
MALATHION (PURITY 95%, IMPURITIES UNSPECIFIED)
FOR 80 WK AND OBSERVED FOR 14-15 WK. A MATCHED CONTROL GROUP COMPRISING 10
ANIMALS OF EACH SEX WAS OBSERVED FOR 95 WK ... AN ADDITIONAL POOLED CONTROL
GROUP OF 50 ANIMALS OF EACH SEX WAS USED ... IN HIGH DOSE GROUP, WHICH RECEIVED
A MAX TOLERATED DOSE, 94% OF THE MALES & 88% OF THE FEMALES WERE STILL ALIVE
AT END OF THE EXPT; SURVIVAL WAS ... LOWER IN LOW DOSE & CONTROL ... IN
FEMALE MICE, NO STATISTICALLY SIGNIFICANT INCR IN TUMOR INCIDENCE WAS FOUND. IN
MALE MICE THE INCIDENCES OF HEPATOCELLULAR CARCINOMAS PLUS NEOPLASTIC NODULES
WERE: 2/10 IN MATCHED CONTROLS, 8/49 IN POOLED CONTROLS, 7/48 IN THE LOW DOSE
GROUP AND 17/49 IN THE HIGH DOSE GROUP (COCHRAN ARMITAGE TEST FOR POS TREND, P=
0.041 (USING MATCHED CONTROLS) OR P= 0.019 (USING POOLED CONTROLS); FISHER EXACT
TEST, HIGH-DOSE VERSUS POOLED CONTROLS, P= 0.031). WHEN A TIME ADJUSTED ANALYSIS
WAS PERFORMED, ELIMINATING ... MALE MICE THAT DIED BEFORE WK 52 OF STUDY, THE
FOLLOWING INCIDENCES RESULTED: MATCHED CONTROLS, 2/9; POOLED CONTROLS, 8/48;
LOW-DOSE, 7/47; & HIGH-DOSE 17/49. ... /TESTS DID NOT SHOW/ THESE INCIDENCES
TO BE SIGNIFICANT ... .
MALATHION WAS INEFFECTIVE IN INDUCING
SEX LINKED RECESSIVE LETHAL MUTATIONS IN DROSOPHILA MELANOGASTER FED SOLN
CONTAINING 0.25 OR 0.5 MG/L OF THE CMPD.
The clastogenic effect of MALATHION
was studied in mice given ip injections of 115, 230, or 460 mg/kg. Results in
mice injected with 115 mg/kg of
MALATHION were not different from controls. At
230 mg/kg, increasing the frequencies of abnormal metaphases and chromosomal
aberrations were noted in animals killed 6 or 24 hr after injection. Mice
injected with 460 mg/kg, exhibited significant increments of abnormal
metaphases, gaps, breaks, and chromatid exchanges in relation to controls.
Oral single & repeated doses of
MALATHION affected the activities of serum
glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, acid
phosphatase, & cholinesterase in rats, depending on sex and duration of
exposure. The first three enzymes were much more sensitive than cholinesterase.
The serum cholesterol & bilirubin contents of female rats were more
susceptible to these insecticides than those of males.
THREE GROUPS OF 50 MALE AND 50 FEMALE FISCHER 344 RATS, SIX WK OLD, WERE FED
DIETS CONTAINING MALATHION (PURITY, 95%;
IMPURITIES UNSPECIFIED) AT CONCN OF 0, 2000, OR 4000 MG/KG FOR 103 WK. THEY WERE
OBSERVED FOR A FURTHER 2 TO 3 WK & THEN KILLED; SURVIVING RATS IN THE
MATCHED CONTROL GROUP WERE KILLED AFTER 105-106 WK OF STUDY. OF THE MALE RATS,
88% OF THE CONTROL GROUP, 86% OF THE LOW DOSE GROUP & 80% OF THE HIGH DOSE
GROUP SURVIVED THE EXPERIMENTAL PERIOD; WHILE OF THE FEMALES, 94% OF THE CONTROL
GROUP, 98% OF THE LOW DOSE GROUP & 90% OF THE HIGH DOSE GROUP WERE STILL
ALIVE AT TERMINATION OF THE EXPT. FEMALES MAY NOT HAVE RECEIVED A MAX TOLERATED
DOSE, AS INDICATED BY GAIN IN BODY WT. NO STATISTICALLY SIGNIFICANT INCR IN
TUMOR INCIDENCE WAS FOUND IN FEMALE RATS. IN MALE RATS, THE INCIDENCE OF ADRENAL
PHEOCHROMOCYTOMAS APPEARED TO INCR IN THE LOW DOSE GROUP (11/48) COMPARED WITH
THE CONTROL GROUP (2/49, P= 0.006), WHEREAS IN THE HIGH DOSE GROUP ONLY 6/49
PHEOCHROMOCYTOMAS WERE SEEN.
To determine the effects of low dosage administration on exercise in a hot
environment, MALATHION (7.5 mg/day, 4
days) was administered ip to rats, and affected a 35% reduction in plasma
cholinesterase /activities/. Treadmill endurance was unaffected when the animals
were exercised to hyperthermic exhaustion (rectal temp approx 45 deg). While
rates of heat gain were similar,
MALATHION treated rats displayed higher tail
skin temp at a number of sampling times during the treadmill run.
Female Sprague Dawley rats were placed on a drinking soln of 1 ppm
MALATHION dissolved in water for 6 mo. Hepatic
morphology, basically hepatocyte degeneration, was altered. Prolonged
prothrombin time and partial thromboplastin time were the only changes in
clotting activity.
The Tradescantia micronucleus (Trad-MCN) bioassay was utilized to determine
the genotoxicity of MALATHION. Results
of sixteen experiments indicated that
MALATHION vapors at 0.15-0.25% induced
significantly higher (0.05) micronucleus frequencies above the controls and
altered the nuclear structure to form unequal sized nuclei and multiple breaks
in each of the 4 cells of a tetrad. It also caused degeneration of nuclei,
protrusions on nuclei, and inhibition of cell growth. Higher doses (greater than
0.25%) were toxic.
MALATHION at 10 and 20% LD50 doses,
ip, impaired learning and memory retrieval of rats.
IgE antibody mediated and cell mediated hypersensitivity to
MALATHION was evaluated in BALB/c mice. To
elicit MALATHION specific antibodies of
the IgE class, a conjugate of the anhydride of the diacid metabolite of
MALATHION with keyhole limpet hemocyanin was
administered ip with aluminum hydroxide as adjuvant. Serums collected following
3 sequential sensitizations were tested for specific IgE with the passive
cutaneous anaphylaxis (PCA) test in rats. Anhydride coupled to bovine serum
albumin was used as the challenge antigen. Specific IgE was produced following
the second and third sensitization in the mice receiving 1 ug of conjugate.
MALATHION applied epicutaneously for 2
days or over 4 wk failed to elicit delayed type hypersensitivity. Anhydride
specific IgE antibodies were not detected by the passive cutaneous anaphylaxis
test in the serum of mice treated epicutaneously for 4 wk.
MALATHION was injected at concn of
3.99 or 6.42 mg/egg into the yolk sacs of 50 hen eggs incubated for 5 days.
Twenty five control eggs were used. The eggs injected with
MALATHION produced chicks exhibiting sparse
plumage, micromelia, overall growth retardation, and beak defects.
MALATHION in concn greater than 1
ug/ml was toxic to primary cultures of chick embryo fibroblasts.
... It is concluded that under the conditions of this bioassay, there was no
clear evidence of the association of the tumor incidence with the administration
of MALATHION to Osborne Mendel rats.
Levels of Evidence for Carcinogenicity: Male Rats: Negative; Female Rats:
Negative.
A daily dose of 46 mg/kg MALATHION ip
for fifteen days affected the activity of the adrenal gland & liver glycogen
in rats. The decr in the level of adrenaline, noradrenaline, and dopamine
indicate that MALATHION causes incr
adrenal medullary function without affecting the cortical activity. The incr
glycogen levels in the liver of
MALATHION exposed animals could be attributed
to the release of adrenal catecholamines.
Daily administration of MALATHION (46
mg/kg, ip) to female rats for 15 days prior to mating caused a significant
reduction in the litter size and survival of pups. Though different traits of
reproduction were not affected significantly, a slight effect was observed in
viability index and lactation index in
MALATHION treated animals.
The effect of in vivo administration of
MALATHION on cellular, humoral, and mitogenic
responses was examined. Acute (50% LD50) or subacute (10% LD50/day for 14 days)
treatment with MALATHION in vivo did not
affect the in vivo generation of specific antibody secreting cells to sheep red
blood cells or cytotoxic T-lymphocytes to allogeneic tumor. Acute treatment with
50% LD50 purified MALATHION did not
affect body weight, splenic cell number, or thymus size. However, mitogenic
responses to concanavalin A and lipopolysaccharide was significantly enhanced on
all days tested following acute administration of
MALATHION. In contrast, subacute treatment
with MALATHION did not affect mitogenic
response to concanvalin A or lipopolysaccharide, but led to a significant
decrease in thymic cell number.
MALATHION admin orally at 20-40 mg/kg
for 2-19 days to juvenile rats caused a reduction of spermatogenic cells and
Leydig cells. /From table; purity not given/
Embryos of the sheepshead minnow, exposed to 10 mg/l
MALATHION, developed skeletal deformities that
rendered them incapable of normal swimming. Fry also manifested convulsive,
uncoordinated movements, characteristic of the exposed embryos. Such fry, though
sometimes normal looking, usually developed a bent appearance akin to scoliosis
(lateral curvature of the spine).
Exposure to MALATHION caused little
alteration of hepatic protein in Clarias batrachus, but there was marked incr in
the free amino acid level, with the incorporation of lysine into the protein of
liver being drastically reduced.
A single treatment of the Atlantic silverside with ...
MALATHION or carbaryl induced optical
malformations, although not dose related. In treated groups the axis formation
& heartbeat initiation were impaired. Microphthalmia (reduced size of eyes),
unilateral or bilaterial anophthalmia (absence of eyes), & cyclopia (median
eye) were some of the observed deformities. After hatching, lordotic fry were
seen in the 10 ug/l carbaryl or
MALATHION ... groups. The ... insecticides
reduced the survival time of the embryos. ... Carbaryl and
MALATHION ... caused abnormalities in the
circulatory system of the embryos of medaka.
Growth of oyster, Crassostrea virginica, was reduced 32% by 96 hr exposure to
1 mg/l.
... Inhibition of acetylcholinesterase (AChE) and mortality were noted in
pinfish 24, 48, and 72 hours at measured concentrations of 142, 92, and 58 ug/l,
respectively. A concentration of 31 ug/l caused 34 percent acetylcholinesterase
inhibition in pinfish but no deaths in 72 hours.
... Moribund mullet, Mugil cephalus, in an estuary sprayed with
MALATHION (3 oz/acre) during a large scale
mosquito control operation had about 98% inhibition of brain
acetylcholinesterase (AChE).
FOLLOWING THE ADMIN OF (3)H-O,O,S-TRIMETHYL PHOSPHOROTHIOATE (OOS-TMP), AN
IMPURITY OF MALATHION, TO RATS,
SUBSTANTIAL AMT OF RADIOLABELED MATERIAL WERE COVALENTLY BOUND TO LUNG WITH A
CONCOMITANT DEPLETION OF GLUTATHIONE (GSH). OTHER ORGANS SHOWING SIGNIFICANT
RADIOACTIVITY WERE LIVER, KIDNEYS, & ILEUM. THE MAX ACCUM OCCURRED IN THE
TISSUES WITHIN 6 HR, & REACHED A PLATEAU BETWEEN 6-12 HR. THE COVALENT
BINDING WAS POSSIBLY DUE TO A METABOLITE(S) OF (3)H-O,O,S-TRIMETHYL
PHOSPHOROTHIOATE AND THE METABOLITE(S) WAS INVOLVED IN THE MECHANISM OF TOXICITY
OF (3)H-O,O,S-TRIMETHYL PHOSPHOROTHIOATE. PULMONARY GLUTATHIONE MAY HAVE PLAYED
A PROTECTIVE ROLE AGAINST (3)H-O,O,S-TRIMETHYL PHOSPHOROTHIOATE INDUCED LUNG
TOXICITY. /(3)H-O,O,S-TRIMETHYL PHOSPHOROTHIOATE/
White leghorn cockerels were fed a diet containing 0, 400, 800, and 1600 ppm
of MALATHION for 90 days.
MALATHION at 800 and 1600 ppm caused a
significant decrease in body weights. There was a significant increase in
liver/body weight ratio. A marked inhibition of aniline hydroxylation and
demethylation of p-chloro N-methylaniline was observed in the S9 fraction of the
liver. Protein contents of liver supernatant of the treated group were
significantly lower than control. Plasma half lives of antipyrine in cockerels
receiving MALATHION at 800 and 1600 ppm
were increased. Pentobarbital sleeping time was longer in
MALATHION treated cockerels.
The effect of O,O,S-trimethyl phosphorothioate (OOS-TMP), an impurity in
MALATHION, on immune responses such as
antigen presentation, antibody production, and cytotoxic T-lymphocyte (CTL)
function was examined in vitro. The roles of non enzymatic and enzymatic
glutathione (GSH) conjugation of O,O,S-trimethyl phosphorothioate in these
responses were studied. Antibody responses to T-dependent and T-independent
antigens were evaluated after (i) direct culture with spleen or B cells; (ii)
cocultivation of B cells with T cells with and without preincubation of
O,O,S-trimethyl phosphorothioate with glutathione fortified cytosol. Antigen
presentation by macrophages was also assessed after such treatment as compared
to untreated controls. O,O,S-trimethyl phosphorothioate preincubated with
glutathione had an inhibitory effect on the cytotoxic T lymphocyte and the
direct hemolytic plaque forming cell responses. This was found to be mediated by
a direct inhibitory effect on macrophages, T and B cells of the immune system
and not through the generation of regulatory suppressor T cells. Thus, the mode
of suppressive action of O,O,S-trimethyl phosphorothioate in vitro is due to
inhibition of lymphocytic proliferation. This is only possible in the presence
of glutathione which was determined to be a prerequisite for the induction of
O,O,S-trimethyl phosphorothioate suppressive effect.
WITH IMPROVED SYNTHETIC METHODS PURITY OF THIS CMPD NOW EXCEEDS 99%. INCR IN
PURITY HAS RESULTED IN CORRESPONDING DECR IN ACUTE TOXICITY SO THAT RECENT ORAL
AE (A underlined) LD50'S FOR RATS TEND TO CLUSTER AROUND 2500 MG/KG ...
beta- Glucuronidase activity increased in the liver of adult male rats in a
dose dependent manner with MALATHION
treatment (orally, for 3 wk). Low protein diets, however, appeared to reduce the
enzyme activity. In protein deprived rats, there was initially a decrease in the
activity of the enzyme which was greater after pesticide treatment.
There has been much debate concerning the teratogenic potential of the
organophosphate pesticides, including
MALATHION, although few experimental studies
have been performed on mammals. This study was designed to expand the range of
animal species used in the testing of
MALATHION and to further evalutate
MALATHION's teratogenic potential. A 100 mg/kg
dose regimen from /days/ 7 to 12 of gestation was administered to New Zealand
white rabbits. This produced no detectable differences in the number of
resorptions, fetal size, and external or visceral anomalies between the treated
and control groups. This suggests, as has been previously reported, that
MALATHION has little or no teratogenic
potential in the mammal.
The time course of immune modulation induced by acute treatment with
O,S,S-trimethyl phosphorodithioate, an impurity in techincal formulations of
MALATHION, was examined in female
C57BL/6 mice. The immune parameters studied included the generation of cytotoxic
T lymphocytes to alloantigen (H-2 incompatible) and antibody secreting cells to
sheep red blood cells, proliferative response to the mitogens, and interleukin-2
production. Acute administration of the non-toxic doses of O,S,S-trimethyl
phosphorodithioate, ie 20 or 40 mg/kg, led to an elevation in the generation of
a cytotoxic T lymphocyte response on day 1 or 7, respectively. At 20 mg/kg
O,S,S-trimethyl phosphorodithioate, the antibody response was elevated at day 3.
However, at a dose of 40 mg/kg O,S,S-trimethyl phosphorodithioate, the antibody
response was suppressed at day 1 following treatment. Following acute
administration of 60 or 80 mg/kg O,S,S-trimethyl phosphorodithioate, the
generation of an antibody and cytotoxic T lymphocytes responses was suppressed
at all time points tested with 1 exception. One day following treatment at a
dose of 60 mg/kg O,S,S-trimethyl phosphorodithioate, there was no change in the
cytotoxic T lymphocytes response. At day 7 following treatment, the mitogenic
responses to lipopolysacharide and phytchemagglutinin were elevated at
administered. ... The proliferative response to concanavalin A was elevated in a
dose dependent manner. Interleukin-2 production was suppressed following acute
administration of 60 or 80 mg/kg O,S,S-trimethyl phosphorodithioate all doses of
O,S,S-trimethyl phosphorodithioate at all time points tested and at all doses
tested on day 5 following treatment.
The glutathione dependent degradation of salithion, which is one of the
effective insecticide against organophosphate-resistant housefly (Musca
domestica L.) and that of the ineffective insecticcides, fenitrothion and
MALATHION, was studied. The most degradable
insecticide was MALATHION (22% and 97%
with susceptible SRS and organophosphate-resistant 3-Y homogenates,
respectively), then fenitrothion (9% and 26%), and the least was salithion (3%
and 9%). Ethacrynic acid inhibited the in vitro degradation of all three
organophosphate-insecticides by both LSRS and 3-Y homogenates, and lowered the
degradation level to the same as that existing under conditions without the
addition of glutathione.
Results from the testing of 108 coded chemicals in Chinese hamster ovary
cells for the induction of chromosome aberrations and sister chromatid exchanges
are presented. All chemicals were tested with and without exogenous metabolic
activation, using protocols designed to allow testing up to toxic doses. Cell
harvest times could also be extended if chemical-induced cell cycle delay was
seen. Chromosome aberrations were induced by 43 of the chemicals, and 66 induced
sister chromatid exchanges; 37 of the chemicals were positive for both
endpoints.
Exposure to 0.5 of the 96 hr median lethal concentrations of endrin and
MALATHION formulations retarded the
gonadotrophin secretion in Heteropneustes fossilis & this led to a reduced
ovarian (32)P uptake. The fish had reduced thyroid activity. After 4 wk of
exposure to a concn of endrin or
MALATHION that had no effect in 96 hr, the
thyroid (131)I uptake and the conversion ratio of protein bound (131)I in blood
serum, in relation to total serum were significantly reduced. At half the 96 hr
median lethal concn both cmpd reduced the pituitary and serum thyroid
stimulating hormone content. ... After 4 wk of exposure to half the 96 hr median
lethal concn ... ovarian (32)P uptake was reduced in preparatory, prespawning,
& spawning phases. ... These two pesticides seem to interfere with
gonadotrophin secretion.
... It was concluded that under the conditions of this bioassay,
MALATHION was not carcinogenic in male or
female rats, but the females may not have received a maximum tolerated dose. ...
Levels of Evidence of Carcinogenicity: Male Rats: Negative Female Rats:
Negative.
Storage of technical MALATHION for
3-6 months at 40 deg C resulted in materials that were noticeably more toxic to
mice.
The lethal dose in mammals is about 1 g/kg.
/MALATHION/ can be detoxified by
hydrolysis of the carboxyl ester linkage by plasma carboxylesterases, and plasma
carboxylesterase activity dictates species resistance to
MALATHION. The detoxification reaction is much
more rapid in mammals and birds than in insects.
MALATHION (technical grade, 95% pure)
was fed to rats at a dietary concentration of 4000 mg/kg (approximate daily
intake, 240 mg/kg bw) for two generations. Males and females 70-100 days of age
were bred after 10 weeks on test; survival of the progeny of days 7 and 21 after
birth was found to be reduced, and the surviving offspring showed growth
retardation and an increased incidence of ring-tail disease.
The clinical signs associated with organophosphorus cmpd poisoning are due to
accumulation of acetylcholine & hence over-stimulation of the
parasympathetic nervous system. It is usual to divide them under 3 categories,
namely, muscarinic, nicotinic & central effects. Muscarinic signs ...
consist of hypersalivation, lacrimation, sweating & nasal discharge. Miosis,
dyspnea, vomiting, diarrhea & frequent urination also occur. The nicotinic
effects consist of fasciculation of the muscles, weakness & paralysis. The
central effects include nervousness, apprehension, ataxia, convulsions &
coma. Death is due to resp failure, or sometimes cardiac arrest. There is little
difference between the signs produced by the different organophosphorus
compounds, but the route of absorption may influence one system more than
another. /Organophosphorus insecticides/
In adult cattle the minimum toxic oral dose of organophosphate pesticides
varies from 1 to 125 mg/kg; the minimum toxic dermal concentration varies from
0.5 to 3%, but these figures are not sacred. The literature is not complete with
regard to animal toxicity of organophosphates; even if it were, toxicity values
would not be reliable because of the number of factors that influence toxicity
of these chemicals under different conditions of use. /Organophosphorus
pesticides/
Biologic factors also influence toxicity of organophosphates. Species is very
important here. ... Age of the animal is another biologic factor that alters
toxicity of organophosphate pesticides. Compounds that do not require enzymatic
activation are more toxic in very young animals in which the enzymes of
pesticide degradation are deficient. Compounds that require enzymatic activation
are not so toxic for very young animals because the enzymes of activation are
deficient during the early weeks of life. Sex of the animals can also alter
toxicity of organophosphates ... . /Organophosphate pesticides/
Some anticholinesterase organic phosphorous compounds interfere with
temperature control and make the body temperature of rats and mice abnormally
dependent on the environmental temperature ... No such effect was observed in
guinea pigs or rabbits. The effect in rats .. and in mice ... was partially
prevented by atropine, suggesting that it is related to cholinesterase
inhibition. /Organic phosphorous pesticides/
The cause of death in poisoning by organic phosphorous compounds is usually
respiratory failure and consequent anoxia but may be cardiovascular in origin.
Four factors (excessive secretion of the respiratory tract, bronchoconstriction,
weakness of the muscles of respiration, and failure of the respiratory center)
may contribute to respiratory failure. ... In a few instances, death has
followed profound brain damage that occurred, usually early in the course of
poisoning, as a result of severe anoxia ... . /Organic phosphorous pesticides/
Some organic phosphorous compounds produce an immediate /CNS depressant/
effect, ranging from incoordination to deep anesthesia following iv injection.
At the same time respiration may be affected. A large dosage is required for all
compounds for which the effect has been demonstrate and, by necessity, all of
them are of low toxicity. /Organic phosphorous pesticides/
Although some anticholinergic compounds are teratogenic, most are not.
/Organic phosphorous pesticides/
National Toxicology Program Studies:
A bioassay of technical grade
MALATHION for possible carcinogenicity was
conducted by admin the test chemical in feed to Osborne-Mendel rats and B6C3F1
mice. Groups of 50 rats of each sex were admin
MALATHION at one of two doses for 80 wk, then
observed for 33 wk. Time weighted avg doses were 4,700 or 8,150 ppm. Matched
controls consisted of groups of 15 untreated rats of each sex; pooled controls
consisted of the matched controls combined with 40 untreated male and 40
untreated female rats from similar bioassays of four other test chemicals. All
surviving rats were /sacrificed/ at 108-113 wk. Groups of 50 mice of each sex
were administered MALATHION at one of
two doses, either 8,000 or 16,000 ppm, for 80 wk, then observed for 14-15 wk.
Matched controls consisted of groups of 10 untreated mice of each sex; pooled
controls consisted of the matched controls combined with 40 untreated male and
40 untreated female mice from similar bioassays of four other test chemicals.
All surviving mice were /sacrificed/ at 94 or 95 wk. ... It is concluded that
under the conditions of this bioassay, there was no clear evidence of the
association of the tumor incidence with the admin of
MALATHION to Osborne-Mendel rats or B6C3F1
mice. Levels of Evidence of Carcinogenicity: Male Rats: Negative; Female Rats:
Negative; Male Mice: Negative; Female Mice: Negative.
A bioassay of MALATHION for possible
carcinogenicity was conducted by admin the test chemical in feed to F344 rats.
Groups of 49 or 50 rats of each sex were fed diets containing 2,000 or 4,000 ppm
MALATHION for 103 weeks and were then
observed for an additional 2 or 3 weeks. Matched controls consisted of 50
untreated rats of each sex. All surviving rats were killed at 105 or 106 weeks.
... It was concluded that under the conditions of this bioassay,
MALATHION was not carcinogenic in male or
female rats, but the females may not have received a maximum tolerated dose. ...
Levels of Evidence of Carcinogenicity: Male Rats: Negative Female Rats:
Negative.
Non-Human Toxicity Values:
LD50 Rat (male) oral 5,843 mg/g
LD50 Mice (male) oral 4,059 mg/mg
LD50 Rat male oral 1375 mg/kg /purity of cmpd not stated/
LD50 Rat (female) oral 1000 mg/kg /purity of cmpd not stated/
LD50 Dog intraperitoneal 1.51 ml/kg (19% soln)
LD50 Rabbit percutaneous 4100 mg/kg /purity of cmpd not stated/
LD50 Rat intraperitoneal 750 mg/kg /purity of cmpd not stated/
LD50 Mouse intraperitoneal 420-474 mg/kg /purity not stated/
LD50 Chicken subcutaneous 1400 mg/kg /purity of cmpd not stated/
LD50 Guinea pig oral 570 mg/kg /purity not stated/
LD50 Rat subcutaneous 1000 mg/kg /purity not stated/
LD50 Rat percutaneous > 4444 mg/kg /purity not stated/
LD50 Rat oral 290 mg/kg
LC50 Rat ihl 43,790 ug/cu m/4 hr
LD50 Rat ip 250 mg/kg
LD50 Rat iv 50 mg/kg
LD50 Mouse oral 190 mg/kg
LD50 Mouse skin 2330 mg/kg
LD50 Mouse ip 193 mg/kg
LD50 Mouse sc 221 mg/kg
LD50 Mouse iv 184 mg/kg
LD50 Dog ip 1857 mg/kg
LD50 Rabbit oral 250 mg/kg
LD50 Rabbit skin 4100 mg/kg
LD50 Rat (female) oral 1400 mg/kg
LD50 Rabbit dermal 2460 to 6150 mg/kg
Ecotoxicity Values:
LD50 ANAS PLATYRHYNCHOS (MALLARD) ORAL 1485 MG/KG (95% CONFIDENCE LIMIT
1020-2150 MG/KG), 3-4 MO OLD FEMALES (SAMPLE PURITY 95%)
LC50 ASELLUS BREVICAUDUS (SOWBUGS) 3000 UG/L/96 HR @ 21 DEG C (95% CONFIDENCE
LIMIT 1500-8500 UG/L), MATURE, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 GAMMARUS FASCIATUS (SCUD) 0.76 UG/L/96 HR @ 21 DEG C (95% CONFIDENCE
LIMIT 0.63-0.92 UG/L), MATURE, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 ORCONECTES NAIS (CRAYFISH) 180 UG/L/96 HR @ 15 DEG C (95% CONFIDENCE
LIMIT 140-230 UG/L), EARLY INSTAR, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 PALAEMONETES KADIAKENSIS (GLASS SHRIMP) 90 UG/L/96 HR @ 21 DEG C (95%
CONFIDENCE LIMIT 67-120 UG/L), MATURE, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 PTERONARCYS CALIFORNICA (STONEFLY) 10 UG/L/96 HR @ 15 DEG C (95%
CONFIDENCE LIMIT 7.0-13 UG/L), SECOND YEAR CLASS, STATIC BIOASSAY /TECHNICAL,
95%/
LC50 PTERONARCELLA BADIA (STONEFLY) 1.1 UG/L/96 HR @ 15 DEG C (95% CONFIDENCE
LIMIT 0.8-1.5 UG/L), NAIAD, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 CLAASSENIA SABULOSA (STONEFLY) 2.8 UG/L/96 HR @ 15 DEG C (95% CONFIDENCE
LIMIT 1.4-4.3 UG/L), SECOND YEAR CLASS, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 ISOPERLA SPECIES (STONEFLY) 0.69 UG/L/96 HR @ 15 DEG C (95% CONFIDENCE
LIMIT 0.20-2.4 UG/L), SECOND YEAR CLASS, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 LESTES CONGENER (DAMSELFLY) 10 UG/L/96 HR @ 15 DEG C (95% CONFIDENCE
LIMIT 6.5-15 UG/L), JUVENILE, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 HYDROPSYCHE SPECIES (CADDISFLY) 5.0 UG/L/96 HR @ 15 DEG C (95%
CONFIDENCE LIMIT 2.9-8.6 UG/L), JUVENILE, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 LIMNEPHILUS SPECIES (CADDISFLY) 1.3 UG/L/96 HR @ 15 DEG C (95%
CONFIDENCE LIMIT 0.8-2.0 UG/L), JUVENILE, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 ATHERIX VARIEGATA (SNIPE FLY) 385 UG/L/96 HR @ 15 DEG C (95% CONFIDENCE
LIMIT 246-602 UG/L), JUVENILE, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 ONCORHYNCHUS KISUTCH (COHO SALMON) 170 UG/L/96 HR @ 12 DEG C (95%
CONFIDENCE LIMIT 160-180 UG/L), WT 0.9 G, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 SALMO CLARKI (CUTTHROAT TROUT) 280 UG/L/96 HR @ 12 DEG C (95% CONFIDENCE
LIMIT 270-310 UG/L), WT 1.0 G, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 SALMO GAIRDNERI (RAINBOW TROUT) 200 UG/L/96 HR @ 12 DEG C (95%
CONFIDENCE LIMIT 160-240 UG/L), WT 1.4 G, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 SALMO TRUTTA (BROWN TROUT) 101 UG/L/96 HR @ 12 DEG C (95% CONFIDENCE
LIMIT 84-115 UG/L), WT 1.1 G, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 SALVELINUS NAMAYCUSH (LAKE TROUT) 76 UG/L/96 HR @ 12 DEG C (95%
CONFIDENCE LIMIT 47-123 UG/L), WT 0.3 G, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 CARASSIUS AURATUS (GOLDFISH) 10700 UG/L/96 HR @ 18 DEG C (95% CONFIDENCE
LIMIT 8340-13800 UG/L), WT 0.9 G, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 CYPRINUS CARPPIO (CARP) 6590 UG/L/96 HR @ 18 DEG C (95% CONFIDENCE LIMIT
4920-8820 UG/L), WT 0.6 G, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 PIMEPHALES PROMELAS (FATHEAD MINNOW) 8650 UG/L/96 HR @ 18 DEG C (95%
CONFIDENCE LIMIT 6450-11500 UG/L), WT 0.9 G, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 ICTALURUS MELAS (BLACK BULLHEAD) 12900 UG/L/96 HR @ 18 DEG C (95%
CONFIDENCE LIMIT 10700-15600 UG/L), WT 1.2 G, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 ICTALURUS PUNCTATUS (CHANNEL CATFISH) 8970 UG/L/96 HR @ 18 DEG C (95%
CONFIDENCE LIMIT 6780-12000 UG/L), WT 1.5 G, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 LEPOMIS CYANELLUS (GREEN SUNFISH) 175 UG/L/96 HR @ 18 DEG C (95%
CONFIDENCE LIMIT 134-228 UG/L), WT 1.1 G, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 LEPOMIS MACROCHIRUS (BLUEGILL) 103 UG/L/96 HR @ 18 DEG C (95% CONFIDENCE
LIMIT 87-122 UG/L), WT 1.5 G, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 LEPOMIS MICROLOPHUS (REDEAR SUNFISH) 62 UG/L/96 HR @ 24 DEG C (95%
CONFIDENCE LIMIT 58-67 UG/L), WT 3.2 G, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 MICROPTERUS SALMOIDES (LARGEMOUTH BASS) 285 UG/L/96 HR @ 18 DEG C (95%
CONFIDENCE LIMIT 254-320 UG/L), WT 0.9 G, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 PERCA FLAVESCENS (YELLOW PERCH) 263 UG/L/96 HR @ 18 DEG C (95%
CONFIDENCE LIMIT 205-338 UG/L), WT 1.4 G, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 STIZOSTEDION VITREUM VITREUM (WALLEYE) 64 UG/L/96 HR @ 18 DEG C (95%
CONFIDENCE LIMIT 59-70 UG/L), WT 1.3 G, STATIC BIOASSAY /TECHNICAL, 95%/
LC50 COLINUS VIRGINIANUS (BOBWHITE) ORAL 3497 PPM IN 5 DAY DIET (95%
CONFIDENCE LIMIT 2959-4117 PPM), AGE 14 DAYS /TECHNICAL 95%/
LC50 PHASIANUS COLCHISUS (RING-NECKED PHEASANT) ORAL 2639 PPM IN 5 DAY DIET
(95% CONFIDENCE LIMIT 2220-3098 PPM), AGE 10 DAYS /TECHNICAL 95%/
LC50 COTURNIX JAPONICA (JAPANESE QUAIL) ORAL 2128 PPM IN 5 DAY DIET (95%
CONFIDENCE LIMIT 1780-2546 PPM), AGE 2 WK /TECHNICAL 95%/
LC50 Tilapia mossambica 0.367 ppm/48 hr /Conditions of bioassay not
specified/
LC50 Macrobrachium lamarrei 2.907 mg/l/24 hr; 1.687 mg/l/48 hr; 1.454 mg/l/72
hr; 1.261 mg/l/96 hr. /Static bioassay/
LD50 Bee topical 0.710 ug/bee
LC50 Crangon septemspinosa (sand shrimp) 33 ug/l/96 hr static bioassay
LC50 Palaemonetes vulgaris (grass shrimp) 82 ug/l/96 hr static bioassay
LC50 Pagurus longicarpus (hermit crab) 83 ug/l/96 hr static bioassay
LC50 Eastern mudminnows 0.24 mg/l/96 hr in a static bioassay
LC50 Eastern mudminnows 0.14 mg/l/14 days in a flow through bioassay
LC50 Salmo gairdneri (rainbow trout) 170 ug/l/96 hr /Conditions of bioassay
not specified/
LC50 Oncorhynchus kisutch (coho salmon) 101 ug/l/96 hr /Conditions of
bioassay not specified/
LC50 Lepomis macrochirus (bluegill) 120 ug/l/24 hr /Conditions of bioassay
not specified/
LC50 Salmo gairdneri (rainbow trout) 100 ug/l/24 hr /Conditions of bioassay
not specified/
LC50 Roccus soxatilis (striped bass) 0.039 mg/l/96 hr in a static bioassay
LC50 Banded killifish 0.24 mg/l/96 hr in a static bioassay
LC50 Lepomis gibbosus (pumpkinseed) 0.48 mg/l/96 hr in a static bioassay
LC50 White perch 1.1 mg/l/96 hr /Static bioassay/
LC50 American eel 0.50 mg/l/96 hr /Static bioassay/
LC50 Cyprinus carpio (carp) 1.9 mg/l/96 hr /Static bioassay/
LC50 Lebistes reticulatus (guppy) 1.2 mg/l/96 hr /Static bioassay/
LC50 Cyprinodon variegatus (sheepshead minnows) 51 ug/l/96 hr /Flow through
bioassay/
LC50 Flagfish 349 ug/l/96 hr /Flow through bioassay/
LC50 Chingatta 7.0; 7.4 mg/l/96 hr /Static bioassay/
LC50 Salmo gairdneri (rainbow trout) 68 ug/l/96 hr /Static bioassay/
LC50 Micropterus salmoides (largemouth bass) 50 ug/l/96 hr /Static bioassay/
LC50 Oncorhynchus tschawytscha (chinook salmon) 23 ug/l/96 hr /Static
bioassay/
LC50 Lepomis macrochirus (blue gill) 110 ug/l/96 hr /Flow-through bioassay/
LC50 Gammarus lacustris 1.0 ug/l/96 hr. /Conditions of bioassay not
specified/
LC50 Pteronarcella badia 1.1 ug/l/96 hr /Conditions of bioassay not
specified/
LC50 Simocephalus serrulatus 3.5 ug/l/48 hr /Conditions of bioassay not
specified/
LC50 Daphnia (water flea) 0.9 ug/l/50 hr /Conditions of bioassay not
specified/
LC50 Menidia menidia 125 ug/l/96 hr /Static bioassay/
LC50 Mugil cephalus (mullet) 550 ug/l/96 hr /Static bioassay/
LC50 Fundulus majalis (mummichog) 250 ug/l/96 hr /Static bioassay/
LC50 Fundulus heteroclitus (mummichog) 240 ug/l/96 hr /Static bioassay/
LC50 Sphaeroides maculatus 3250 ug/l/96 hr /Static bioassay/
LC50 Anguilla rostrata (eel) 82 ug/l/96 hr /Static bioassay/
LC50 Thalassoma bifasciatum 27 ug/l/96 hr /Static bioassay/
LC50 Gasterosteus aculeatus 76.9 ug/l/24 hr static bioassay.
LC50 Morone saxatilis (striped bass) 14 ug/l/96 hr /Flow through bioassay/
TSCA Test Submissions:
MALATHION (CAS # 121-75-5) was
evaluated for cytotoxicity in study to evaluate the validity of in vitro testing
for direct reuse water toxicity in mammalian systems. As a quick, inexpensive,
reproducible, and sensitive means of detection, if this test is also a valid
reflection of toxicity in mammals, it would be highly beneficial in assessing
the potability of direct reuse water and in prescribing mode of water treatment.
Continuous L-cell cultures (mouse or rat, 26 cultures/assay, >200,000
cells/culture) in minimal medium with 1% fetal bovine serum were exposed to 12
graded doses (unspecified) in ethanol solution for 72 to 96 hours. A reflection
of effects on growth and reproduction of the indicator cells, the change in
protein synthesis as determined by calorimetric Lowry method was chosen to
quantify the cytotoxicity in 6 cultures/assay at 24, 48, 72 and 96 hours after
initiation of study. A concentration of 32 mg/L was toxic to L-cells. Levels
greater than 1 mg/L inhibited protein production in a time-dependent manner;
cells exposed in vitro to 18 mg/L demonstrated static protein synthesis by the
third day, with protein loss evident at Day 4. The effect was less pronounced in
response to a 10 mg/L MALATHION
exposure, although this level halved protein synthesis (LC50). An LC10 was 2.0
mg/L. The authors suggested that the timed response might be due to altered
cellular metabolism or intracellular accumulation of
MALATHION. The LC50 (10 mg/L) was both
significantly lower than the NOEL in chronic animal studies (100-1000 and 100
ppm in rats and dogs, respectively) and higher than WHO/FAO's maximum daily
intake standard (0.02 mg/kg/day). However, a positive relationship was
established in both instances by a two-way ANOVA statistical method, indicating
a relevant toxicological result with the cell culture bioassay.
MALATHION, a non-persistent (biodegradable)
and poorly soluble insecticide of low relative mammalian toxicity that is rarely
found in drinking water, bears no EPA-derived drinking water standard limit.
Using an EPA convention for calculation of drinking water maximum limits and
either the same historical minimal effect level or WHO/FAO data, the resultant
standard (0.03 or 0.15 mg/L respectively) would be undetectable with the tissue
culture bioassay.
MALATHION (CAS # 121-75-5) was
evaluated for acute oral toxicity in study of strain-specific differences in
Fischer 344-derived (CDF) and Sprague-Dawley (SPB) rats (5/sex/strain/group)
administered single oral doses of 252 to 3980 mg/kg by oral gavage. Groups of
female rats of both strains received doses of 252, 500, 1000, 2000, and 3980
mg/kg, while groups of male rats also received doses of 2520 mg/kg. Additional
groups of Sprague-Dawley males only received doses of 2100 and 2250 mg/kg.
Single-dose oral LD50's, based on a moving average method, were 2101 and 2102
mg/kg for SPB males and females and 1875 and 1898 mg/kg for CDF male and female
rats, respectively. Clinical signs of toxicity, associated with doses of 500 and
above throughout 14-day post-gavage observation, included lethargy, total body
tremors, bluish face (1000-3980 mg/kg, SPB females only), piloerection,
heightened tail color (2000 mg/kg, 5/5 SPB males only), gasping, and
convulsions. No significant treatment-related changes in bodyweight were noted
in either strain. Upon necropsy of both surviving and decedent rats, gross
lesions were limited to focal corneal cloudiness, which was more prevalent in
the CDF males. The authors concluded, however, that the overall response between
these strains of rat were comparable.
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
SELECTIVE TOXICITY TO INSECTS HAS BEEN ACCOUNTED FOR BY DIFFERENCES IN
METABOLISM. (32)P-MALATHION IS RAPIDLY
METABOLIZED IN MICE, RATS, & DOGS, PRINCIPALLY BY HYDROLYSIS OF THE ETHYL
ESTER BONDS TO GIVE MALATHION MONOESTER
& MALATHION DIACID, WHEREAS IN
INSECTS OXIDN TO MALAOXON & CLEAVAGE OF THE PHOSPHATE THIOESTER BOND TO GIVE
O,O-DIMETHYL-PHOSPHORODITHIONATE & -PHOSPHOROTHIONATE ARE THE PRINCIPAL
ROUTES OF METAB. THE TOXICITY OF
MALATHION IS PROBABLY DUE TO ITS OXIDATION TO
MALAOXON, WHICH IS SOME 1000 TIMES MORE ACTIVE THAN
MALATHION AS AN ANTI CHOLINESTERASE.
MALATHION ... REQUIRES ACTIVATION TO
/MALAOXON/ ... TO BECOME AN ACTIVE ANTICHOLINESTERASE AGENT. ... THE CONVERSION
OF MALATHION TO MALAOXON IS A REACTION
CARRIED OUT BY THE LIVER MICROSOMAL MONOOXYGENASE SYSTEM. COMPETING WITH THE
ACTIVATION OF MALATHION ARE ENZYMES
RESPONSIBLE FOR ITS DEGRADATION TO NON-TOXIC METABOLITES. THESE ARE ...
CHARACTERIZED AS PHOSPHATASES AND CARBOXYLESTERASES OR ALIESTERASES. PRODUCTS OF
REACTIONS CATALYZED BY THESE ENZYMES ARE
MALATHION MONOESTER, VARIOUS PHOSPHORIC ACIDS
& DEMETHYLATED PRODUCT. ... THE DEGRADATION RATE OF MALAOXON EXCEEDS THE
ACTIVATION RATE OF MALATHION, SO THERE
IS ... LITTLE ACCUMULATION OF THE TOXIC ACTIVATION PRODUCT IN MAMMALIAN SYSTEMS.
STUDIES /SHOWED/ ARTHROBACTER SP ... WAS CAPABLE OF DEGRADING
MALATHION. LAB STUDIES IDENTIFIED METABOLITES
AS MALATHION HALF ESTER, DICARBOXYLIC
ACID, DIMETHYL PHOSPHORODITHIOATE, & DIMETHYL PHOSPHOROTHIOATE.
WHEN LARVAL HOMOGENATES OF
MALATHION-RESISTANT & ... SUSCEPTIBLE
STRAIN OF INDIAN MEAL MOTH (PLODIA INTERPUNCTELLA HUBNER) WERE TESTED FOR
ESTERASE ACTIVITY, RESISTANT STRAIN HAD GREATER ALPHA-NAPHTHYL ACETATE ESTERASE
THAN SUSCEPTIBLE STRAIN; LESS CARBOXYLESTERASE & BUTYRYLCHOLINESTERASE;
& SIMILAR ACETYLCHOLINESTERASE ACTIVITY.
Metabolite of MALATHION found in cow
feces: dimethyl phosphate. /From table/
Metabolites of MALATHION in cow, rat,
and dog urine and serum are desmethyl
MALATHION and
MALATHION diacid. /From table/
A metabolite of MALATHION in mouse
urine and serum is desmethyl MALATHION.
/From table/
In plants ... /the/ MALATHION
carboxylic acids /MALATHION mono &
dicarboxylic acids/ are ... formed.
MALATHION ... is broken down by the
mammalian liver. ... MALATHION`s
selectivity is due to the presence of the carboxyl groups, which are susceptible
to mammalian hydrolysis.
Two organophosphorus impurities of technical
MALATHION (insecticide), isomalathion and
O,S,S-trimethyl phosphorodithioate, were examined for their effects on the in
vivo metabolism of MALATHION in rats.
Both impurities were confirmed to be potent in vivo inhibitors of plasma, liver,
and kidney MALATHION carboxylesterases
at relatively low doses. Pretreatment of rats with these impurities followed by
administration of (14)C MALATHION
resulted in changes in the quantities of certain
MALATHION metabolites excreted in the urine.
Compared to the corn oil pretreated controls, the most notable change in the
impurity pretreated animals was in the decrease in the amount of
MALATHION diacid excreted along with a
commensurate increase in the amount of excreted
MALATHION alpha monoacid. An increase in
malaoxon metabolites in the urine of impurity pretreated rats was indicated,
suggesting that more malaoxon was originally produced in these animals.
BY USING HIGH SPECIFIC ACTIVITY
MALATHION & ION EXCHANGE CHROMATOGRAPHY, A
TOTAL OF 11 METABOLITES WERE ISOLATED FROM THE GERMAN COCKROACH, AMERICAN
COCKROACH, & THE COMMON HOUSEFLY, & SEVEN METABOLITES FROM THE WHITE
MOUSE. THE PRINCIPAL METABOLITES ISOLATED FROM THE MOUSE WERE MONOETHYL ESTER OF
MALATHION (86%), DIMETHYL
PHOSPHOROTHIOIC ACID (13%), DIMETHYL PHOSPHORODITHIOIC ACID (5%), 10% OF AN
UNKNOWN METABOLITE. RELATIVE AMT OF VARIOUS METABOLITES OBTAINED WERE SIMILAR
BETWEEN ROACHES, WHICH IN TURN WERE SLIGHTLY DIFFERENT FROM FLIES. ... LEVEL OF
MALAOXON WAS ... GREATER IN COCKROACH THAN IN MOUSE @ ANY TIME AFTER INJECTION,
EG, @ 1 HR AFTER INJECTION /OF
MALATHION/ THERE WAS 10 TIMES MORE MALAOXON
PER G OF ANIMAL. RELATIVE PROP OF METABOLITES INDICATES GREATER PS TO PO
ACTIVATION IN INSECTS COMPARED TO MAMMALS ...
The conversion of many organophosphates with a P=S group to P=O is another
instance of activation by MFO /mixed function oxidase/ resulting in an incr in
toxicity. This process explains the greater toxicity of metabolites like
paraoxon, malaoxon, fenitrooxon, etc than that of their parent compounds.
The hydrolysis of MALATHION by rabbit
liver oligomeric and monomeric carboxylesterase results in the formation of a
mixture of an alpha and beta monoacid. The oligomeric carboxylesterase produced
an alpha/beta ratio of monoacids of 4.55, and the monomeric carboxylesterase
produced an alpha/beta ratio of monoacids of 2.33. Kinetic studies demonstrated
that the Km values were the same for the corresponding reactions which produced
alpha monoacid, or beta monoacid with the same enzyme. Since both
carboxylesterases are electrophoretically pure, the kinetic data strongly
supports the theory that the reactions which produced alpha and beta monoacids
are catalyzed by the same active site.
In man, MALATHION is metabolized by
(1) hydrolytic cleavage of ethyl groups from the succinic acid moiety of the
molecule by carboxylesterase enzymes; and (2) hydrolysis of the succinate moiety
from the dialkyl thiophosphate.
Plasma and tissue enzymes are responsible for hydrolysis /of organophosphorus
compounds/ to the corresponding phosphoric and phosphonic acids. However,
oxidative enzymes are also involved in the metabolism of some organophosphorus
compounds. /Anticholinesterase agents/
The organophosphorus anticholinesterase agents are hydrolyzed in the body by
a group of enzymes known as A-esterases or paraoxonases. These enzymes are found
in the plasma and liver and hydrolyze a large number of organophosphorus
compounds ... by cleaving the phosphoester, anhydride, P-F, or P-CN bonds.
/Anticholinesterase agents/
Absorption, Distribution & Excretion:
THE LESS VOLATILE AGENTS THAT ARE COMMONLY USED AS AGRICULTURAL INSECTICIDES
(EG PARATHION, FENTHION, DIAZINON,
MALATHION) ARE GENERALLY DISPERSED AS AEROSOLS
OR AS DUSTS CONSISTING OF THE ORGANOPHOSPHORUS COMPOUND ADSORBED TO AN INERT,
FINELY PARTICULATE MATERIAL. CONSEQUENTLY, THE COMPOUNDS ARE ABSORBED RAPIDLY
AND EFFECTIVELY BY PRACTICALLY ALL ROUTES, INCLUDING THE GASTROINTESTINAL TRACT,
AS WELL AS THROUGH THE SKIN AND MUCOUS MEMBRANES FOLLOWING CONTACT WITH
MOISTURE, AND BY THE LUNG AFTER INHALATION.
... WHEN (14)C-MALATHION ... WAS
APPLIED /TO HUMAN SKIN/ 7, 9, & 23% WERE ABSORBED THROUGH FOREARM, ABDOMEN,
& FOREHEAD, RESPECTIVELY.
THE INSECTICIDE (14)C-MALATHION WAS
ABSORBED & RAPIDLY EXCRETED IN RATS. 8 HR AFTER ORAL DOSE, 44% OF (14)C HAD
BEEN EXCRETED IN URINE & 47% STILL REMAINED IN GI TRACT, WHEREAS AFTER 24
HR, 83% HAD BEEN EXCRETED IN URINE, 6% IN FECES, 3% IN EXPIRED AIR, & 8%
REMAINED IN GI TRACT. EXCRETION OF (32)P AFTER AN ORAL DOSE OF (32)P-
MALATHION TO LACTATING COW WAS LESS RAPID. 69%
WAS EXCRETED IN 4 DAY URINE, 8% IN FECES, & 0.2% IN MILK. SINCE EXCRETION OF
(32)P WAS VERY SLOW AFTER THAT TIME, ITS INCORPORATION INTO BODY TISSUES HAD
PROBABLY OCCURRED, & ITS RELEASE WAS DEPENDENT ON TURNOVER RATES OF THOSE
TISSUES.
Percutaneous absorption of chronically applied
MALATHION was determined in man and chronic
absorption was compared to single dose absorption. (14)C-
MALATHION was applied topically to the ventral
forearm of human male volunteers. This procedure was followed by repeated
administration of non radioactive
MALATHION to the same site. (14)C-
MALATHION was reapplied on day 8 when urinary
excretion of radioactivity from the first application reached minimum detectable
levels. Percutaneous absorption from the first admin was 4.48% of the applied
dose. Absorption from the second administration was 3.53%. Therefore, the single
dose application data are relevant for predicting toxic potential for long term
exposure.
EIGHT AUTOPSY SAMPLES FROM AN INDIVIDUAL WHO HAD INGESTED A LARGE AMT OF
MALATHION WERE ANALYZED.
MALATHION WAS PRESENT IN ALL SAMPLES EXCEPT
LIVER. THE HIGHEST CONCN WERE FOUND IN GASTRIC CONTENTS (8621 PPM) & ADIPOSE
TISSUE (76.4 PPM). MALAOXON WAS IDENTIFIED IN SOME TISSUES AT VERY LOW LEVELS; A
SIGNIFICANT AMT WAS FOUND ONLY IN FAT (8.2 PPM).
MALATHION MONOCARBOXYLIC ACID &
MALATHION DICARBOXYLIC ACID WERE FOUND IN
GREATER ABUNDANCE: 221 PPM IN BILE, 106 PPM IN KIDNEY, & 103 PPM IN THE
GASTRIC CONTENTS.
/Measurement was made of/ the ether extractable phosphates in the urine of an
adult man who had been administered
MALATHION in a single oral dose of 58 mg (0.84
mg/kg). A total of 23% of the ingested dose was recovered in the ether
extractable, urinary phosphate fraction of the urine during the first 16.3
hours. 97% of this recovered dose was excreted in the first 7.5 hours. ... Based
on experiments in rats injected ip or fed (32)P-labeled
MALATHION, /it was/ found that an average of
69 and 36%, respectively, of the
MALATHION excreted in the urine to be
recoverable in the ether extractable fraction.
... 7% OF TOTAL METABOLITES IN FECES /FROM COW GIVEN
MALATHION ORALLY/ WAS CHLOROFORM SOLUBLE, OF
WHICH 85% WAS MALATHION & 12%
MALAOXON. THE MILK CONTAINED A SMALL AMOUNT OF
MALATHION METABOLITES (9.2% OF TOTAL DOSE
AFTER 7 DAYS); OF THIS, ONLY 29% WAS EXTRACTABLE OUT OF MILK AND PARTITIONED IN
FAVOR OF WATER OVER BENZENE, INDICATING THE ABSENCE OF EITHER
MALATHION OR MALAOXON.
No MALATHION residues were found 24
hr after the exposure of pinfish to 75 ug/l; only
MALATHION monoacid was detected in the gut.
The American cockroach was treated by topical application of (14)C-
MALATHION. The distribution of the label
within the body tissues was found to be both rapid and extensive. As much as 40%
of the applied label was still present superficially in the cuticle even 24 hr
post-application. The overall tissue ranking order for (14)C label was found to
be: foregut > digestive tract contents > skeletal muscle > fat body
> hidout > midgut > nerve cord > brain > malpighian tubules.
MALATHION, malaoxon and
MALATHION monoacids were detected in the nerve
cord plus brain, the digestive tract, skeletal muscle and fat body at 1, 2 and
24 hr after topical application of the insecticide. At 24 hr post-application a
significant proportion of MALATHION
remained unmetabolized in all tissues examined. The highest levels of metabolic
transformation were found in the digestive tract and fat body. Insects were
prostrate 24 hr after topical application of (14)C-
MALATHION. In these insects the greatest
concentration of MALATHION and monoacids
(expressed in relation to unit tissue wt) was found in the digestive tract. On
the other hand, the nerve cord and brain contained the greatest concentration of
malaoxon. About 18% of applied (14)C-
MALATHION label partitioned into the tissue
aqueous phase up to 24 hr after topical application but very little applied
label was expired as (14)CO2 or excreted. Although a neurotoxic action may be
the cause of prostration and death, the extensive dissemination of
MALATHION and its products belies the concept
of any tissue specificity. The haemolymph, after an initial sharp rise in
MALATHION content, maintained a steady
MALATHION level over the 24 hr experimental
periods suggesting that the hemolymph is the main distributor of the insecticide
to the various body tissues.
Most organophosphate compounds are ... absorbed from skin, conjunctiva,
gastrointestinal tract, & lung. /Organophosphate compounds/
The rate of dermal absorption /of organophosphorus pesticides/ may be ...
influenced by the solvent used. /Organophosphorus insecticides/
Many of /the organophosphorus insecticides/ are excreted in the milk ...
/Organophosphorus insecticides/
Following their absorption, most organophosphorus cmpd are excreted almost
entirely as hydrolysis products in the urine. /Anticholinesterase agents/
TOXICANTS CAN BE ABSORBED BY INHALATION, INGESTION, AND SKIN PENETRATION. ...
ALL UNDERGO HYDROLYTIC DEGRADATION IN LIVER AND OTHER TISSUES, USUALLY WITHIN HR
OF ABSORPTION. DEGRADATION PRODUCTS ARE OF LOW TOXICITY, AND ARE EXCRETED IN
URINE AND FECES. /ORGANOPHOSPHATE CHOLINESTERASE-INHIBITING PESTICIDES/
/THEY/ ... ARE RAPIDLY ABSORBED THROUGH MUCOUS MEMBRANE OF DIGESTIVE SYSTEM,
RESPIRATORY SYSTEM & THE SKIN, & CONVEYED BY THE BLOOD TO VARIOUS BODY
TISSUES. ... THE MAIN ROUTE OF ELIMINATION ... /IS/ THE KIDNEYS.
/ORGANOPHOSPHORUS PESTICIDES/
Organic phosphorous insecticides are absorbed by the skin, as well as by the
respiratory and GI tracts. Absorption by the skin tends to be slow, but, because
the insecticides are difficult to remove, such absorption is frequently
prolonged. Skin absorption is somewhat greater at higher temperatures and may be
much greater in the presence of dermatitis. /Organic phosphorous pesticides/
Mechanism of Action:
Signs and symptoms of intoxication by anticholinesterase agents /such as
MALATHION/ are caused by the
inactivation of the enzyme cholinesterase, which results in the accumulation of
acetylcholine at synapses in the neuromuscular system, and secretory glands.
MALAOXON, ACTIVE ANTICHOLINESTERASE METABOLITE OF
MALATHION ... HAS ALIESTERASES INHIBITING
ACTIVITY.
Organophosphorus derivatives act by combining with and inactivating the
enzyme acetylcholinesterase (AChE). ... The inactivation of cholinesterase by
cholinesterase inhibitor pesticides allows the accumulation of large amounts of
acetylcholine, with resultant widespread effects that may be ... separated into
4 categories: (1) Potentiation of postganglionic parasympathetic activity. ...
(2) Persistent depolarization of skeletal muscle ... (3) Initial stimulation
following depression of cells of central nervous system ... (4) Variable
ganglionic stimulation or blockade ... /Cholinesterase inhibitor pesticides/
The characteristic pharmacological effects of the anti-ChE agents are due
primarily to the prevention of hydrolysis of ACh by AChE at sites of cholinergic
transmission. Transmitter thus accumulates, and the response to ACh that is
liberated by cholinergic impulses or that is spontaneously released from the
nerve ending is enhanced. With most of the organophosphorus agents ... virtually
all the acute effects of moderate doses are attributable to this action.
/Anticholinesterase agents/
The cardiovascular actions of anticholinesterase agents are complex, since
they reflect both ganglionic and postganglionic effects of accumulated ACh on
the heart and blood vessels. The predominant effect on the heart from the
peripheral action of accumulated ACh is bradycardia, resulting in a fall in
cardiac output. Higher doses usually cause a fall in blood pressure, often as a
consequence of effects of anticholinesterase agents on the medullary vasomotor
centers of the CNS. /Anticholinesterase agents/
The main feature of the toxic mechanism of organophosphorus pesticides is
inhibition of the esterase enzyme activity, in particular of cholinesterase,
which plays an important physiological part. Organophosphorus pesticides can
also indirectly interact with the biochemical receptors of acetylcholine.
/Organophosphorus pesticides/
... The serum cholinesterase activity of 14 men and 16 women at seven
approximately equal intervals throughout one 24 hr day was measured. The lowest
average value, ... was 92% of the mean of all values at other sampling times.
The next lowest value was 98.7% of the same mean. /It was/ concluded that the
small variation observed did not take the form of a regular curve but was
entirely individual without correspondence to hour. /Organic phosphorus
pesticides/
... There is no change in red blood cell cholinesterase activity in adults
associated with age. ... Activity of this enzyme increases progressively during
the first year of life, it is higher in children under 3 yr of age than in older
children, and it is markedly higher in 5 yr old children than in 3 yr olds.
/Organic phosphorus pesticides/
Cholinesterase activity of plasma is significantly higher in men than in
women, and this is true no matter which of several choline esters are used as
substrate in measuring the enzyme activity. According to some, the difference is
confined to young people. There is no sex difference in the red cell enzyme
activity. Serum cholinesterase activity of blacks tends to be lower than whites
of the same sex. /Organic phosphorus pesticides/
Phosphorylated enzymes, like acetylated acetylcholinesterase, are esters and
may be hydrolyzed by nucleophilic agents, including water. The rate at which
phosphorylated enzymes are reactivated by water is extremely low, compared to
the rate for acetylcholinesterase combined with acetate. When inhibition is by
isopropyl phosphate, the rate is essentially zero. /Organic phosphorous
pesticides/
Organophosphates poison insects and humans primarily by phosphorylation of
the acetylcholinesterase enzyme at nerve endings. /Organophosphate
Cholinesterase-inhibiting pesticides/
Interactions:
Of five N-methylcarbamate insecticides tested, only
2-sec-butylphenyl-N-methylcarbamate exhibited marked synergism with
MALATHION when a mixture was tested for the
combined acute oral toxicity toward mice. The mixture exhibited less potent
synergism toward male rats.
TOXICITY OF MALATHION IS POTENTIATED
BY O-ETHYL O-PARA-NITROPHENYL PHOSPHOROTHIOATE, TRI-O-TOLYLPHOSPHATE, & SOME
OTHER ORGANOPHOSPHORUS CMPD. IT IS POSTULATED THAT THIS POTENTIATION RESULTS
FROM THE INHIBITION OF CARBOXYLESTERASE OR ALIESTERASE ENZYMES RESPONSIBLE FOR
DEGRADATION OF MALATHION IN MAMMALS.
PRESUMABLY, THIS MECHANISM WOULD LEAD TO INCR FORMATION OF MALAOXON, THE
ACTIVATION PRODUCT, BECAUSE THE ENZYMES RESPONSIBLE FOR DEGRADATION OF MALAOXON
WOULD BE INHIBITED.
Twelve organophosphorus insecticides were tested for toxicity and
mutagenicity in the forward mutation test system (ade6) of the yeast
Schizosaccharomyces pombe. Trichlorfon, tested in combination with
MALATHION, produced clearly synergistic
effects for toxicity and mutagenicity.
Impurities such as O,S,S-trimethyl phosphorodithioate (TMPD) and the S-methyl
isomer of MALATHION (iso-
MALATHION) strongly potentiated the mammalian
toxicity of MALATHION. The potentiation
was attributed to inhibition of mammalian liver and serum carboxylesterase.
O,O,S-Trimethyl phosphorothioate (TMP), another impurity present in technical
grade MALATHION, proved to be highly
toxic. Rats given a single oral dose of O,O,S-trimethyl phosphorothioate at a
level as low as 20 mg/kg died over a period of 3 wk, with death occurring with
non cholinergic signs of poisoning. O,S,S-Trimethyl phosphorodithioate also
caused similar delayed death in rats, O,O,O-trimethyl phosphorothioate, another
impurity in technical MALATHION, was a
potent antagonist to the delayed toxicity of O,O,S-trimethyl phosphorothioate.
/Impurities of technical grade
MALATHION/
The disposition and metabolism of pesticides used in combination, especially
carbaryl and MALATHION, is of
considerable toxicological importance. Radioactivity was rapidly absorbed from
the rat gastrointestinal tract following the administration of 0.25 ml of 10
mg/kg (14)C-carbaryl (0.80 microCi), 10/10 mg/kg (14)C-carbaryl/
MALATHION (0.80 microCi), 10 mg/kg (14)C-
MALATHION (1.03 microCi), or 10/10 mg/kg
(14)C-MALATHION/carbaryl (0.86 microCi).
The administration of carbaryl or
MALATHION, individually and in combination,
followed a two phase elimination model. The presence of
MALATHION decreased the rate constants of
absorption and beta phase elimination of (14)C-carbaryl. In the mean time, the
length of the distribution phase and the area under the curve of (14)C-carbaryl
were decreased by MALATHION
administration. Although (14)C-
MALATHION's absorption half life was unchanged
in the presence of carbaryl, increases were noted in the length of the
distribution phase, beta phase elimination half life, and area under the curve
for MALATHION when administered
simultaneously with carbaryl. Both combinations caused an increase in (14)C
activity to be deposited in the fat as compared to the respectively labeled
pesticide. However, only MALATHION
increased the concentration of (14)C-carbaryl remaining in the gastrointestinal
tract tissues after the administration of the combined pesticides. The
subcellular distribution of the liver indicated that the highest activity was
present in the cytosol. These pesticides and their combinations were excreted
primarily by the kidney, followed by the lung and the intestinal route. Although
there was no alteration in the metabolic pathways due to the combinations, an
increase in malaoxon and MALATHION
diacid concentration in urine was observed after the administration of
(14)C-MALATHION/carbaryl as compared to
(14)C-MALATHION. The results from this
study revealed that the combination of these pesticides altered fundamental
pharmacokinetic parameters, which may explain some of the toxicities associated
with exposure to these chemicals in combination.
Pretreatment of rats with chloramphenicol (100 mg/kg, ip) 30 min prior to a
single oral LD50 dose of MALATHION at
340 mg/kg completely protected against
MALATHION induced inhibition of
cholinesterase. It appears that the inhibition of
MALATHION toxicity by chloramphenicol
pretreatment is attributable to inhibition by chloramphenicol of the metabolic
activation of MALATHION to malaoxon.
Pretreatment with MALATHION augmented
the effect of chlorpromazine and diazepam on learning and retrieval in rats.
The various ne-oils, /such as/ mahua, neem, karanj or pongam, undi, kokum
butter, gamboge, dhupa fat and rubber oil generally synergised
MALATHION when malathin and oils,
respectively, were tested at 1:1 and 1:5 levels. The synergism is probably
because of desulfuration of MALATHION
into malaoxon by ne-oils due to their oxidising nature.
Some phenothiazines may antagonize & some may potentiate the toxic
anticholinesterase effects of ... /organophosphorus insecticides/.
/Organophosphate cholinesterase inhibitors/
In long term therapy, adrenocorticoids antagonize the antiglaucoma effects of
anticholinesterases (incr ocular pressure). ... Anticholinergics antagonize the
miotic (antiglaucoma) & other muscarinic effects of anticholinesterases on
the autonomic & central nervous systems. Tricyclic antidepressants
(anticholinergic effects) antagonize the antiglaucoma (miotic) effects of
anticholinesterases in glaucoma. ... Antihistamines with anticholinergic effects
antagonize the miotic (antiglaucoma) & CNS effects of anticholinesterases.
Anticholinesterases potentiate tranquilizing & behavioral changes induced by
antihistamines. The actions of anticholinesterase agents on autonomic effector
cells, & to some extent those on CNS, are antagonized by atropine, an
antidote of choice. Barbiturates are potentiated by anticholinesterases. ...
Dexpanthenol potentiates the effects of anticholinesterases. Fluorophosphate
insecticides potentiate the effects of other anticholinesterases.
/Anticholinesterases/
BARBITURATES ARE POTENTIATED BY ANTICHOLINESTERASES. ALTHOUGH BARBITURATES
MAY BE USED CAUTIOUSLY IN TREATING CONVULSIONS, EXTREME CARE IS ESSENTIAL IN
HANDLING POISONINGS DUE TO ANTICHOLINESTERASES, PARTICULARLY ORGANOPHOSPHORUS
PESTICIDES. ECHOTHIOPHATE, A CHOLINESTERASE INHIBITOR USED AS MIOTIC,
POTENTIATES OTHER SUCH INHIBITORS ... USED FOR OTHER PURPOSES (ADDITIVE EFFECTS)
OR POSSIBLY SYNERGISTIC. THOSE EXPOSED TO ORGANOPHOSPHATE INSECTICIDES MUST TAKE
STRICT PRECAUTIONS. ... ORGANOPHOSPHORUS INSECTICIDES: ADDITIVE
ANTICHOLINESTERASE EFFECTS. HAZARDOUS. PATIENTS ON ANTICHOLINESTERASES (EVEN
TOPICAL, SUCH AS EYE DROPS) SHOULD AVOID AREAS WHERE ORGANOPHOSPHORUS
INSECTICIDES ... RECENTLY ... USED. /ANTICHOLINESTERASE/
ANTICHOLINESTERASE (ORGANOPHOSPHORUS) INSECTICIDES ANTAGONIZE POLARIZING
MUSCLE RELAXANTS. PHENOTHIAZINES /AND THIOXANTHENES/: ... MAY ENHANCE TOXIC
EFFECTS OF ORGANOPHOSPHORUS INSECTICIDES. /INSECTICIDES, ORGANOPHOSPHORUS/
Pharmacology:
Therapeutic Uses:
For treatment of pediculosis capitis (head lice) a quantity of
MALATHION 0.5% lotion sufficient to thoroughly
wet the hair and scalp is applied topically.
MALATHION lotion is sprinkled on dry hair ...
until hair and scalp are thoroughly wet, special care should be taken to ensure
the application of the lotion to the back of head and neck. The hair should be
left uncovered and allowed to dry naturally for at least 8 hr after application
... of lotion. ... After 8 hr the hair should be shampooed, rinsed thoroughly,
and combed with a fine toothed comb to remove dead lice and eggs. Although first
treatment is usually successful, application of ... lotion may be repeated after
7-9 days if live lice, or eggs are detected.
Vet: Kil-A-Mite /which contains 15.34%
MALATHION is used to treat/ ... sarcoptic
mange on dogs.
MEDICATION (VET): Flair ... /which contains/ 0.50%
MALATHION /is used/ for fleas, ticks, &
lice on dogs & cats.
A comparison study of the therapy of scabies in 67 patients, both adults and
children, who received one or two applications of either
MALATHION, as a 0.5% topical emulsion, or
benzyl benzoate, as a 25% topical emulsion, was reported. A cure rate of 92.3%
was achieved with /the former/, as opposed to 68.8% for /the latter/.
PEDICULICIDE
MEDICATION (VET): ECTOPARASITICIDE
Drug Warnings:
MALATHION appears to have a low order
of toxicity following application to the scalp as
MALATHION 0.5% lotion. Adverse local effects
may include irritation of the scalp, pruritis, dryness of hair, and a transient
increase in dandruff.
Interactions:
Of five N-methylcarbamate insecticides tested, only
2-sec-butylphenyl-N-methylcarbamate exhibited marked synergism with
MALATHION when a mixture was tested for the
combined acute oral toxicity toward mice. The mixture exhibited less potent
synergism toward male rats.
TOXICITY OF MALATHION IS POTENTIATED
BY O-ETHYL O-PARA-NITROPHENYL PHOSPHOROTHIOATE, TRI-O-TOLYLPHOSPHATE, & SOME
OTHER ORGANOPHOSPHORUS CMPD. IT IS POSTULATED THAT THIS POTENTIATION RESULTS
FROM THE INHIBITION OF CARBOXYLESTERASE OR ALIESTERASE ENZYMES RESPONSIBLE FOR
DEGRADATION OF MALATHION IN MAMMALS.
PRESUMABLY, THIS MECHANISM WOULD LEAD TO INCR FORMATION OF MALAOXON, THE
ACTIVATION PRODUCT, BECAUSE THE ENZYMES RESPONSIBLE FOR DEGRADATION OF MALAOXON
WOULD BE INHIBITED.
Twelve organophosphorus insecticides were tested for toxicity and
mutagenicity in the forward mutation test system (ade6) of the yeast
Schizosaccharomyces pombe. Trichlorfon, tested in combination with
MALATHION, produced clearly synergistic
effects for toxicity and mutagenicity.
Impurities such as O,S,S-trimethyl phosphorodithioate (TMPD) and the S-methyl
isomer of MALATHION (iso-
MALATHION) strongly potentiated the mammalian
toxicity of MALATHION. The potentiation
was attributed to inhibition of mammalian liver and serum carboxylesterase.
O,O,S-Trimethyl phosphorothioate (TMP), another impurity present in technical
grade MALATHION, proved to be highly
toxic. Rats given a single oral dose of O,O,S-trimethyl phosphorothioate at a
level as low as 20 mg/kg died over a period of 3 wk, with death occurring with
non cholinergic signs of poisoning. O,S,S-Trimethyl phosphorodithioate also
caused similar delayed death in rats, O,O,O-trimethyl phosphorothioate, another
impurity in technical MALATHION, was a
potent antagonist to the delayed toxicity of O,O,S-trimethyl phosphorothioate.
/Impurities of technical grade
MALATHION/
The disposition and metabolism of pesticides used in combination, especially
carbaryl and MALATHION, is of
considerable toxicological importance. Radioactivity was rapidly absorbed from
the rat gastrointestinal tract following the administration of 0.25 ml of 10
mg/kg (14)C-carbaryl (0.80 microCi), 10/10 mg/kg (14)C-carbaryl/
MALATHION (0.80 microCi), 10 mg/kg (14)C-
MALATHION (1.03 microCi), or 10/10 mg/kg
(14)C-MALATHION/carbaryl (0.86 microCi).
The administration of carbaryl or
MALATHION, individually and in combination,
followed a two phase elimination model. The presence of
MALATHION decreased the rate constants of
absorption and beta phase elimination of (14)C-carbaryl. In the mean time, the
length of the distribution phase and the area under the curve of (14)C-carbaryl
were decreased by MALATHION
administration. Although (14)C-
MALATHION's absorption half life was unchanged
in the presence of carbaryl, increases were noted in the length of the
distribution phase, beta phase elimination half life, and area under the curve
for MALATHION when administered
simultaneously with carbaryl. Both combinations caused an increase in (14)C
activity to be deposited in the fat as compared to the respectively labeled
pesticide. However, only MALATHION
increased the concentration of (14)C-carbaryl remaining in the gastrointestinal
tract tissues after the administration of the combined pesticides. The
subcellular distribution of the liver indicated that the highest activity was
present in the cytosol. These pesticides and their combinations were excreted
primarily by the kidney, followed by the lung and the intestinal route. Although
there was no alteration in the metabolic pathways due to the combinations, an
increase in malaoxon and MALATHION
diacid concentration in urine was observed after the administration of
(14)C-MALATHION/carbaryl as compared to
(14)C-MALATHION. The results from this
study revealed that the combination of these pesticides altered fundamental
pharmacokinetic parameters, which may explain some of the toxicities associated
with exposure to these chemicals in combination.
Pretreatment of rats with chloramphenicol (100 mg/kg, ip) 30 min prior to a
single oral LD50 dose of MALATHION at
340 mg/kg completely protected against
MALATHION induced inhibition of
cholinesterase. It appears that the inhibition of
MALATHION toxicity by chloramphenicol
pretreatment is attributable to inhibition by chloramphenicol of the metabolic
activation of MALATHION to malaoxon.
Pretreatment with MALATHION augmented
the effect of chlorpromazine and diazepam on learning and retrieval in rats.
The various ne-oils, /such as/ mahua, neem, karanj or pongam, undi, kokum
butter, gamboge, dhupa fat and rubber oil generally synergised
MALATHION when malathin and oils,
respectively, were tested at 1:1 and 1:5 levels. The synergism is probably
because of desulfuration of MALATHION
into malaoxon by ne-oils due to their oxidising nature.
Some phenothiazines may antagonize & some may potentiate the toxic
anticholinesterase effects of ... /organophosphorus insecticides/.
/Organophosphate cholinesterase inhibitors/
In long term therapy, adrenocorticoids antagonize the antiglaucoma effects of
anticholinesterases (incr ocular pressure). ... Anticholinergics antagonize the
miotic (antiglaucoma) & other muscarinic effects of anticholinesterases on
the autonomic & central nervous systems. Tricyclic antidepressants
(anticholinergic effects) antagonize the antiglaucoma (miotic) effects of
anticholinesterases in glaucoma. ... Antihistamines with anticholinergic effects
antagonize the miotic (antiglaucoma) & CNS effects of anticholinesterases.
Anticholinesterases potentiate tranquilizing & behavioral changes induced by
antihistamines. The actions of anticholinesterase agents on autonomic effector
cells, & to some extent those on CNS, are antagonized by atropine, an
antidote of choice. Barbiturates are potentiated by anticholinesterases. ...
Dexpanthenol potentiates the effects of anticholinesterases. Fluorophosphate
insecticides potentiate the effects of other anticholinesterases.
/Anticholinesterases/
BARBITURATES ARE POTENTIATED BY ANTICHOLINESTERASES. ALTHOUGH BARBITURATES
MAY BE USED CAUTIOUSLY IN TREATING CONVULSIONS, EXTREME CARE IS ESSENTIAL IN
HANDLING POISONINGS DUE TO ANTICHOLINESTERASES, PARTICULARLY ORGANOPHOSPHORUS
PESTICIDES. ECHOTHIOPHATE, A CHOLINESTERASE INHIBITOR USED AS MIOTIC,
POTENTIATES OTHER SUCH INHIBITORS ... USED FOR OTHER PURPOSES (ADDITIVE EFFECTS)
OR POSSIBLY SYNERGISTIC. THOSE EXPOSED TO ORGANOPHOSPHATE INSECTICIDES MUST TAKE
STRICT PRECAUTIONS. ... ORGANOPHOSPHORUS INSECTICIDES: ADDITIVE
ANTICHOLINESTERASE EFFECTS. HAZARDOUS. PATIENTS ON ANTICHOLINESTERASES (EVEN
TOPICAL, SUCH AS EYE DROPS) SHOULD AVOID AREAS WHERE ORGANOPHOSPHORUS
INSECTICIDES ... RECENTLY ... USED. /ANTICHOLINESTERASE/
ANTICHOLINESTERASE (ORGANOPHOSPHORUS) INSECTICIDES ANTAGONIZE POLARIZING
MUSCLE RELAXANTS. PHENOTHIAZINES /AND THIOXANTHENES/: ... MAY ENHANCE TOXIC
EFFECTS OF ORGANOPHOSPHORUS INSECTICIDES. /INSECTICIDES, ORGANOPHOSPHORUS/
Environmental Fate & Exposure:
Environmental Fate/Exposure Summary:
MALATHION's production and use as an
insecticide is expected to result in its direct release to the environment. If
released to air, a vapor pressure of 1.78X10-4 mm Hg at 25 deg C indicates
MALATHION will exist solely as a vapor in the
ambient atmosphere. Vapor-phase
MALATHION will be degraded in the atmosphere
by reaction with photochemically-produced hydroxyl radicals; the half-life for
this reaction in air is estimated to be 5 hr.
MALATHION absorbs light at >290nm and thus
has the potential for direct photolysis. If released to soil,
MALATHION is expected to have very high
mobility based upon an estimated Koc of 30. Volatilization from moist soil
surfaces is not expected to be an important fate process based upon a Henry's
Law constant of 4.9X10-9 atm-cu m/mole.
MALATHION is not expected to volatilize from
dry soil surfaces based upon its vapor pressure. Biodegradation in soil is rapid
with 80-95% biodegradation detected in 10 days. The rate of degradation
increased with organic matter content, and half-lives in the 1-6 day range. If
released into water, MALATHION is not
expected to adsorb to suspended solids and sediment in water based upon the
estimated Koc. Biodegradation of 90% in 2 weeks was reported in raw river water.
Volatilization from water surfaces is not expected to be an important fate
process based upon this compound's Henry's Law constant. An estimated BCF of 13
suggests the potential for bioconcentration in aquatic organisms is low.
Hydrolysis half-lives range from 2-11 days in seawater and freshwater.
Occupational exposure to MALATHION may
occur through inhalation and dermal contact with this compound at workplaces
where MALATHION is produced or used. The
general population can be exposed to
MALATHION after a spraying event, via
inhalation and dermal contact with this compound when using it for household
purposes. (SRC)
Probable Routes of Human Exposure:
... Skin & eye contact.
POTENTIAL DERMAL AND RESP EXPOSURES TO
MALATHION: PERSONS OUTDOORS AND INDOORS DURING
AIR APPLICATION TO POPULATED AREA. /FROM TABLE/
POTENTIAL DERMAL AND RESP EXPOSURES TO
MALATHION: OPERATING AEROSOL MACHINE, AIR
BLAST SPRAYING FRUIT ORCHARDS, PERSONS OUTDOORS AND INDOORS DURING AIR
APPLICATION TO POPULATED AREA. /FROM TABLE/
NIOSH (NOES Survey 1981-1983) has statistically estimated that 19,172 workers
(1,910 of these are female) are potentially exposed to
MALATHION in the US(1). Occupational exposure
to MALATHION may occur through
inhalation and dermal contact for persons, like pet handlers, who use
MALATHION as an insecticide to control pet and
human fleas(2), and for farmers who use
MALATHION to store grains(3). Mean of
MALATHION detected in the ambient air of
insecticide storage and office rooms of commercial pest control buildings in a 2
hr period during the winter and summer season is 0.77 ug/cu m(4). The general
population maybe exposed to MALATHION
via inhalation of ambient air, ingestion of contaminated foods, via drinking
contaminated water, and dermal contact with this compound and other products
containing MALATHION(SRC).
Body Burden:
According to a national survey performed in the US from 1976-1980,
MALATHION was detected in quantifiable amounts
from 1.6% of the urine analyses for persons 12-74 years of age(1). Trace amounts
of metabolites in urine showed 4.1% of the persons tested were exposed to
MALATHION(2). Of 267 samples of human urine,
0.4% were positive for MALATHION, at
concns < 0.1 ppm(3). MALATHION was
detected, not quantifed in the respired air of a resident in 1 of 9 residents
from 9 households sampled in Jacksonville, FL(4).
Average Daily Intake:
In 1982-84 a national study was performed that showed the average daily
intakes of MALATHION in the US for
children 6 to 11 mon of age and 2 yr old were 142.3 and 232.8 ng/kg body
weight/day, respectively(1). In 1982-84 a national study was performed that
showed the average daily intake of
MALATHION in the US for females 14-16, 25-30
and 60-65 yrs of age was 74.8, 61.8 and 53.9 ng/kg body weight/day,
respectively(1). In 1982-84 a national study was performed that showed the
average daily intake of MALATHION in the
US for males 14-16, 25-30 and 60-65 yrs of age was 107.1, 72.9 and 62.9 ng/kg
body weight/day, respectively(1).
Natural Pollution Sources:
MALATHION is not known to occur as a
natural product.
Artificial Pollution Sources:
/Release of MALATHION to the
environment may result from/ its production, formulation & widespread use as
insecticide ... and /from/ household applications ... .
MALATHION's production and use as an
insecticide to protect crops, control ectoparasites and human head and body
lice(1) is expected to result in its direct release to the environment.
Environmental Fate:
TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value
of 31(SRC), determined from a structure estimation method(2), indicates that
MALATHION is expected to have very high
mobility in soil(SRC). Volatilization of
MALATHION from moist soil surfaces is not
expected to be an important fate process(SRC) given a Henry's Law constant of
4.9X10-9 atm-cu m/mole(3). MALATHION is
not expected to volatilize from dry soil surfaces(SRC) based upon a vapor
pressure of 1.78X10-4 mm Hg(4).
MALATHION soil half-lives range from 1 to 6
days depending on soil pH's in the range of 3.8 to 7.0(5). Half-lives for
MALATHION for radish and carrot soil for the
seasons of winter, summer, and post-monsoon were determined to be 6.4, 2.1, and
5.3 days, and 6.6, 2.6, and 5.6 days, respectively(6).
MALATHION levels found in Southern California
after a single spraying event at soil depths of 1 and 0.1 cm were 1.4 ug/g and
14.1 ug/g, respectively(5).
AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of
31(SRC), determined from an estimation method(2), indicates that
MALATHION is not expected to adsorb to
suspended solids and sediment in water(SRC). Volatilization from water surfaces
is not expected(3) based upon a Henry's Law constant of 4.9X10-9 atm-cu
m/mole(4), developed using a fragment constant estimation method(5). According
to a classification scheme(6), an estimated BCF of 13(SRC), from its log Kow of
2.36(7) and a regression-derived equation(8), suggests the potential for
bioconcentration in aquatic organisms is low. Hydrolysis and biodegradation are
important processes. Hydrolysis half-lives in seawater/sediment systems at pH
7.3-7.7 are 2.0 days and in freshwater, at pH 7.4 and 20 deg C, 11 days(9).
Products of hydrolysis include malaoxon,
MALATHION alpha and beta monoacid,
O,O-dimethylphosphorodithioic acid, diethyl fumarate, diethyl thiomalate,
O,O-dimethylphosphorothionic acid. Photodegradation may compete with hydrolysis
as an important degradation process in certain waters, however, photolysis has
been shown to be sensitized only in water from 1 river, half-life 16 hr,
compared to a half-life of 6 weeks in distilled water(10).
MALATHION sorbed by algae was photodegraded
> 25 times faster than MALATHION in
distilled water(11). Biodegradation is especially important in waters < pH
7.0 where the rate of hydrolysis may be slow relative to the rate of
biodegradation. Persistence of MALATHION
in water from 4 rivers ranged from 52% still present after 11 days to 21% after
14 days(12). Degradation of 90%
MALATHION within 2 weeks in raw river water
(pH 7.3-8.0) compared to no change in distilled water over 3 weeks suggests that
degradation was biological(13).
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of
semivolatile organic compounds in the atmosphere(1),
MALATHION, which has a vapor pressure of
1.78X10-4 mm Hg at 25 deg C(2), is expected to exist solely as a vapor in the
ambient atmosphere. Vapor-phase
MALATHION is degraded in the atmosphere by
reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for
this reaction in air is estimated to be 5 hr(SRC), (calculated) from its rate
constant of 77X10-12 cu cm/molecule-sec at 25 deg C(3) (determined using a
structure estimation method(3).
MALATHION absorbs light at wavelengths >290
nm(4) and is therefore susceptible to photolysis(SRC).
MALATHION sorbed by algae was photodegraded
> 25 times faster than MALATHION in
distilled water(5). Half-lives for thin films (concn, ug/cm squared) of
MALATHION irradiated at environmentally
important wavelengths were found to be 2.1 days at 0.67 nm, 5.0 days at 3.3 nm,
and 7.3 days at 6.7 nm(6).
Environmental Biodegradation:
Soil fungus, Trichoderma viride, ... degraded
MALATHION by 2 paths that did not incl oxidn
product malaoxon. Presence of ... carboxyesterases was suggested by fact that
carboxylic acid deriv of MALATHION
constituted major portion of metabolites. Some variants of T viride also showed
... demethylation activity.
MALATHION is rapidly degraded in
soils with reported degradation in 10 days in various non sterile (sterile) loam
soils: 92% (8%), 94% (5%), and 81% (19%)(1). The rate of degradation increased
with increasing soil organic matter and was related to soil pH(2). Degradation
of 50-90% of MALATHION reported in 24 hr
in both sterile and non sterile soil systems with no lag phase detected(3).
Complete degradation of MALATHION in 25
days reported in both sterile and non sterile estuarine water and 97% and 99%
degradation in 18 days, respectively(4). Degradation of 90%
MALATHION within 2 weeks in raw river water
(pH 7.3-8.0) compared to no change in distilled water over 3 weeks suggests that
degradation was biological(5). Degradation was complete in 3 days in non-sterile
estuarine sediments, and 57% in 11 days in sterilized sediment(4). Products of
degradation include alpha and beta monocarboxylic acids, and dicarboxylic
acid(6). The major metabolite in soil was
MALATHION beta monoacid(6). Two organisms,
Trichoderma viride and Pseudomonas sp. metabolize
MALATHION by two pathways that do not yield
malaoxon. Biochemical reactions utilitzed include desulfuration, oxidation,
hydrolysis, transfer of alkyl or aryl groups, alkylation, dealkylation,
reduction and conjugation(1).
Environmental Abiotic Degradation:
/DEGRADATION/ ... IN SOIL WAS RAPID & WAS RELATED TO DEGREE OF
ABSORPTION, SUGGESTING CHEMICAL MECHANISM. ... STUDIES HAVE SHOWN THAT RATE OF
MALATHION HYDROLYSIS INCR ... ABOVE
CRITICAL MOISTURE LEVEL. AT TEMP OF 70 DEG F & 90 DEG F, CRITICAL MOISTURE
LEVEL WAS ... 11.6% & 11.8%, RESPECTIVELY.
IN SOIL FREE ACID SYSTEMS (MORE THAN PH 2) HYDROLYSIS DID NOT OCCUR, WAS SLOW
AT PH 9 (LESS THAN 50% IN 20 DAYS), & RAPID AT PH 11 (MORE THAN 99% IN 1
DAY). AT PH 9 HYDROLYSIS PRODUCED THIOMALIC ACID, DIMETHYL THIOPHOSPHATE, &
DIETHYL THIOMALATE. IN SOIL BOTH ESTERS WERE HYDROLYZED BUT NOT AT SAME RATE,
& DIETHYL THIOMALATE ACCUMULATED IN SOME SOILS.
The rate constant for the vapor-phase reaction of
MALATHION with photochemically-produced
hydroxyl radicals has been estimated as 77X10-12 cu cm/molecule-sec at 25 deg
C(SRC) using a structure estimation method(1). This corresponds to an
atmospheric half-life of about 4.974 hr at an atmospheric concentration of
5X10+5 hydroxyl radicals per cu cm(1). A base-catalyzed second-order hydrolysis
rate constant of 6X10-2 L/mole-sec(SRC) was estimated using a structure
estimation method(2); this corresponds to half-lives of 3.6 years and 130 days
at pH values of 7 and 8, respectively; 120 days at 20 deg C, pH 6.1(2). 8.1 and
91% degradation by hydrolysis of
MALATHION was observed immediately and after 4
weeks, respectively, at pH 6.0(4).
MALATHION hydrolysis half-life in water was
shown to be 11 and 1.3 days at 20 and 37.5 deg C, respectively, pH 7.4(5). Very
little or no hydrolysis of MALATHION was
observed at pHs <7.0(6). Hydrolysis of
MALATHION occurs at higher rates under
alkaline conditions, indicating that hydroxide-catalyzed hydrolysis is more
effective than hydronium- or water-catalyzed hydrolysis(7).
MALATHION had a half-life of 2.0 days in
seawater/sediment system at pH 7.3-7.7 and a half-life of 11 days at pH 7.4 and
20 deg C in freshwater(7). Hydroxide-catalyzed hydrolysis is the major pathway
for MALATHION degradation in marine
systems(7). Products of hydrolysis and oxidation include
O,O-dimethylphosphorodithioic acid and diethyl fumarate in basic solution, and
diethyl thiomalate and O,O-dimethylphosphorothionic acid in acidic solution(11).
MALATHION absorbs light at wavelengths
>290nm(8) and is therefore susceptible to photolysis(SRC).
MALATHION sorbed by algae was photodegraded
> 25 times faster than MALATHION in
distilled water(9). Half-lives for thin films (concn, ug/cm squared) of
MALATHION irradiated at environmentally
important wavelengths: were found to be 2.1 days at 0.67 nm, 5.0 days at 3.3 nm,
and 7.3 days at 6.7 nm(10).
Environmental Bioconcentration:
Motsugo fish exposed to 0.6 to 1.2 mg/l of diazinon, fenitrothion,
MALATHION ... or XMC attained highest body
concn (mg/kg) of various compounds as follows: diazinon, 211, after 3 days,
fenitrothion, 162, after 3 days;
MALATHION, 2.4, after 1 day ... Only diazinon
(17 mg/kg), fenitrothion (4.9 mg/kg) ... & XMC (0.55 mg/kg) persisted longer
than 4 wk in the fish.
An estimated BCF of 13.1 was calculated for
MALATHION(SRC), using log Kow of 2.36(1) and a
regression-derived equation(2). According to a classification scheme(3), this
BCF suggests the potential for bioconcentration in aquatic organisms is low
(SRC). The BCF for egg masses of the Triaenodes tardus was found to be 10(4).
MALATHION did not bioconcentrate in the
freshwater fish, Pseudorasbora parva(5).
Soil Adsorption/Mobility:
Using a structure estimation method based on molecular connectivity
indices(1), the Koc for MALATHION can be
estimated to be 31(SRC). According to a classification scheme(2), this estimated
Koc value suggests that MALATHION is
expected to have very high mobility in soil. An experiment conducted to see how
much MALATHION leaches at depths of 50cm
in soil found that most of the MALATHION
is degraded in the higher layers of soil (within the polar carboxylic acid
groups) and only small degradation products, that are usually biodegradable,
move to the groundwater(3). MALATHION
was given a leaching index of 2.0-3.0 in soil (<20 cm to >35 cm) with an
annual rainfall of 150 cm(4).
Volatilization from Water/Soil:
The Henry's Law constant for
MALATHION is 4.9X10-9 atm-cu m/mole(1). This
Henry's Law constant indicates that
MALATHION is expected to be essentially
nonvolatile from water surfaces(2). Based on this Henry's Law constant, the
volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind
velocity of 3 m/sec)(2) is estimated as 2X10+5 hr(SRC). The volatilization
half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5
m/sec)(2) is estimated as 2X10+6 hr(SRC).
MALATHION's Henry's Law constant(1) indicates
that volatilization from moist soil surfaces will not occur(SRC).
MALATHION is not expected to volatilize from
dry soil surfaces(SRC) based upon a vapor pressure of 1.78X10-4 mm Hg(3).
Environmental Water Concentrations:
... Residues of MALATHION have
reportedly been identified in the Rhine River in the Federal Republic of Germany
at levels of 0.01-0.1 ug/kg. In the Virgin Islands, where
MALATHION is used extensively ... only 2 of 49
water samples taken from cisterns contained
MALATHION, at levels of 0.14 and 0.01 ug/kg.
DRINKING WATER: MALATHION was not
detected in 54 of 54 California wells near areas where telone or D-D had been
applied for several years(2). MALATHION
was not detected in Ottawa, Ontario, Canada, with a detection limit of 10-15
pg/l(1); however, it was detected in 4 of 91 ground wells at an average concn of
0.1 ug/l in Southern Ontario, Canada(3). The Arno River in Italy, which supplies
drinking water to the people of Florence, was tested for
MALATHION from 1992 to 1995 and found to have
a maximum concn of 0.17 ug/l with 6 and 8 positive samples in 1193 and 1995,
respectively, detection limit = 0.01 ug/l(4).
SURFACE WATER: National surface water monitoring program, 1976-80, 0.3% pos
samples, max concn 0.18 ppb(3). USA Pesticide Monitoring Network, 1975-80, 174
stations, 0.6% pos, 2,85 samples, 0.1% pos(5). Lake Erie watershed, 1971-72, 157
river water and bottom sediment samples, not detected(2). Ontario, Canada, 11
agricultural watersheds, 0.8% samples pos 1975-76, not detected, 1976-77, not
detected-1.80 parts per trillion, overall avg < 0.01 parts per trillion max
avg 1.80(1). Raw bank filtered Rhine water, West Germany, occasionally detected,
not quantified(4). MALATHION was
detected at 0.6% of 174 sampling stations of the nations river(6).
MALATHION was listed in the waters of Lake
Erie(7).
RAIN/SNOW/FOG: MALATHION was detected
in the atmospheric fog water from Parlier, Corcoran and Lodi, CA, and
Beltsville, MD at concn of 70, 110, 350 and 2740 ng/l, respectively(1).
Effluent Concentrations:
Conc within 800 m of 2 formulation plants in Arkansas: 1970, 66 samples,
33.3% pos, 0.6-5.7 ng/cu m, avg 1.9 ng/cu m; 1971, 60 samples, 18.3% pos,
0.4-4.1 ng/cu m, avg 1.6 ng/cu m; 1972, 64 samples, 17.2% pos, 0.8-38.1 ng/cu m,
avg 10.4 ng/cu m(1). Concn within 275 m of formulation plant in Tennessee, 1971,
56 samples, 46.4% pos, 0.8-198.2 ng/cu m, avg 10.9 ng/cu m(1).
Sediment/Soil Concentrations:
SEDIMENTS: USA National Surface Water Monitoring Program, 1976-80, not
detected(4). SOILS: USA National Soils Monitoring Program, Fiscal Year
1973(FY73), 1483 sites, 0.2% pos, 0.08-0.13 ppm dry wt, avg <0.01 ppm(2);
FY71, 1,486 samples, 1 sample pos, 0.19 ppm dry wt(3). Southwestern Ontario,
Canada, farm soil, < 0.01-0.02 ppm(1).
MALATHION was detected at concn ranging from 7
to 1 ppm in dry soils from West Bengal at 15 days after treatment(5).
MALATHION was detected at concn ranging from
6.5 to 25 ppm in waterlogged soils from West Bengal at 15 days after
treatment(5). MALATHION levels of 1.4
and 14.1 ug/g were detected in Southern California at a soil depth of 1 and 0.1
cm, respectively(6).
Atmospheric Concentrations:
CONCN OF MALATHION OBSERVED IN WORK
AREAS AND IN THE AIR OF AN AGRIC COMMUNITY AS A RESULT OF CROP TREATMENT HAVE
BEEN REPORTED AS 0.01-0.60 MG/CU M AND 0.1 NG/CU M, RESPECTIVELY. ...
MALATHION HAS BEEN DETECTED AT A LEVEL OF
126-130 NG/CU M IN AMBIENT AIR SAMPLES FROM INSECTICIDE STORAGE ROOMS, AND AT
LEVELS OF 48-106 NG/CU M FROM THE AMBIENT AIR OF VEHICLES USED IN COMMERCIAL
PEST CONTROL.
RESIDUAL LEVELS OF MALATHION WERE
MEASURED IN 31 SAMPLES OF GRAIN DUST COLLECTED FROM 6 TERMINAL GRAIN ELEVATORS
ALONG THE MISSISSIPPI RIVER IN THE NEW ORLEANS AREA. SAMPLES CONTAINED 0.17-32
UG MALATHION/G DUST.
SOURCE DOMINATED: Concn in work areas and in an agricultural community as a
result of crop treatment were 0.01-0.60 mg/cu m and 0.1 ng/cu m, respectively.
Ambient air from insecticide storage rooms had 126-130 ng/cu m and vehicles used
in commercial pest control contained 48-106 ng/cu m(1).
MALATHION levels on outdoor surfaces in
California after a single application were recorded as 21.2 mg/sq m(2).
MALATHION level found in outdoor air in
California after a single application was 0.091 ug/cu m(2).
MALATHION level found in indoor air after a
single aerial application in residential areas of southern Califonria was 0.022
ug/cu m(2).
URBAN/SUBURBAN: 10 USA locations, 1980, 123 samples, 50% were positive for
MALATHION, avg 7.5 ng/cu m, max concn
220 ng/cu m(1). USA, 16 states, 17.94% were positive samples, avg of pos, 19.7
ng/cu m, max concn 7,090 ng/cu m(2). In 1970,
MALATHION was detected in 26.94% of the air
samples from 14 states at an average concn of 12.1 ng/cu m with a maximum concn
of 587.2 ng/cu m(2). In 1971, MALATHION
was detected in 19.00% of the air samples from 16 states at an average concn of
38.9 ng/cu m with a maximum concn of 57090.0 ng/cu m(2). In 1972,
MALATHION was detected in 21.26% of the air
samples from 16 states at an average concn of 8.2 ng/cu m with a maximum concn
of 38.1 ng/cu m(2). MALATHION was
detected, not quantified in the outdoor air of 2 of 9 homes sampled in
Jacksonville, FL(3).
RURAL/REMOTE: Rural Orlando, FL, 1971, 99 samples, 4.0% were positive for
MALATHION, max 2.0 ng/cu m(1). Pekin,
IL, Feb-Sept, 1980, 11 samples, 18.2% pos, 1.2(Mar) and 6.2 ng/cu m(May)(2).
INDOOR AIR: MALATHION was detected,
not quantified in the inside air in 4 of 9 homes sampled in Jacksonville, FL(1).
Food Survey Values:
Market basket surveys USA Fiscal Year 1965(FY65) through FY69, respectively,
number of samples/percent positive composites: FY65 216/not detected, FY66
312/5.3%, FY67 360/3.6%, FY68 360/1.9%, FY69 360/5.8%; daily intake ug: FY65 not
detected, FY66 9, FY67 10, FY 68 3, FY69, 12(1). The number of samples/percent
positive composites for 1971 through 1976: 360/13.6% (1971), 420/16.7% (1972),
360/15.0% (1973), 360/14.7% (1974), 240/14.2% (1975), 240/12.1% (1976); daily
intake - ug: 15 (1971), 10 (1972), 11 (1973), 9 (1974), 9 (1975), 9 (1976),
respectively(2). The adult total diet composites/percent pos (range): FY77,
300/14.7% pos (3-115 ppb)(3), FY78, 240/16.3% pos (3-54 ppb)(4).
MALATHION was detected in 1 composite
sample of tomatoes with an average concn of 0.01 mg/kg(1).
MALATHION was detected by the FDA Los Angeles
District on 249 various agricultural commodities at concn ranging from less than
0.05 to over 2 ppm(2). MALATHION was
found in 9 of 10 grain and cereal samples for infants at a mean concentration
less 0.0236 ppm, with a range from 0.006 to 0.044 ppm, and in 1 of 10 vegetable
samples for infants at a mean concentration of 0.0001 ppm, with a range from
0.001 to 0.0091 ppm, and in 1 of 10 oil and fat samples for infants at a mean
concentration of 0.0320 ppm, with a range from 0.320 to 0.651 ppm (FDA: Total
Diet Study)(3). MALATHION was found in 1
of 20 grain and cereal samples for adults at a mean concentration of 0.0001 ppm,
with a range from 0.009 to 0.079 ppm, and in 1 of 20 meat, fish and poultry
samples for adults at a mean concentration of 0.0001 ppm, with a range from 0 to
0.002 ppm, and in 4 of 20 fruit samples for adults at a mean concentration of
0.0002 ppm, with a range from trace amounts to 0.001 ppm, and in 13 of 20 oil
and fat samples for adults at a mean concentration of 0.0167 ppm, with a range
from 0.003 to 0.080 ppm, and in 6 of 20 sugar and adjuncts samples for adults at
a mean concentration of 0.0031 ppm, with a range from trace amounts to 0.0037
ppm (FDA: Total Diet Study)(4).
MALATHION was found in 20 of 20 grain
and cereal samples for adults at a mean concentration of 0.0412 ppm, with a
range from 0.007 to 0.149 ppm, and in 1 of 20 garden fruit samples for adults at
a mean concentration less than 0.0001 ppm, with a range from 0 to trace amounts,
and in 1 of 20 fruit samples for adults at a mean concentration of 0.0001 ppm,
with a range from 0 to 0.002 ppm, and in 15 of 20 oil and fat samples for adults
at a mean concentration of 0.0138 ppm, with a range from 0.001 to 0.051 ppm, and
in 8 of 20 sugar and adjunct samples for adults at a mean concentration of
0.0018 ppm, with a range from 0.001 to 0.008 ppm (FDA: Total Diet Study) for Oct
1978 - Sept 1979(1).
MALATHION was also found in 13 of 13
grain and cereal samples for infants at a mean concentration of 0.0335 ppm, with
a range of 0.008 to 0.0158 ppm, and in 3 of 13 oil and fat samples for infants
at a mean concentration of 0.0038 ppm, with a range from 0.010 to 0.021 ppm, and
in 13 of 13 grain and cereal samples for toddlers at a mean concentration of
0.0179 ppm, with a range from 0.005 to 0.040 ppm, and in 2 of 13 fruit and fruit
juice samples for toddlers at a mean concentration of 0.0003 ppm, with a range
from 0 to 0.002 ppm, and in 8 of 13 oil and fat samples for toddlers at a mean
concentration of 0.0321 ppm, with a range from 0.002 to 0.240 ppm, and in 5 of
13 sugar and adjuncts samples for toddlers at a mean concentration of 0.003 ppm,
with a range from trace amounts to 0.003 ppm, and in 1 of 13 beverage samples
for toddlers at a mean concentration of 0.0001 ppm, with a range from 0 to trace
amounts (FDA: Total Diet Study) for Oct 1980 - March 1982(1).
MALATHION was found in 1 of 27 meat,
fish and poultry samples for adults at a mean concentration of 0.0003 ppm, with
a range from 0 to 0.008 ppm, and in 27 of 27 grain and cereal samples for adults
at a mean concentration of 0.0360 ppm, with a range from 0.009 to 0.108 ppm, and
in 1 of 27 root vegetable samples for adults at a mean concentration of 0.0001
ppm, with a range from 0 to 0.001 ppm, and in 1 of 27 garden fruit samples for
adults at a mean concentration of 0.0003 ppm, with a range from 0 to 0.008 ppm,
and in 3 of 27 fruit samples for adults at a mean concentration of 0.0002 ppm,
with a range from trace amounts to 0.004 ppm, and in 17 of 27 fruit samples for
adults at a mean concentration of 0.0196 ppm, with a range from 0.001 to 0.102
ppm, and in 9 of 27 sugar and adjunct samples for adults at a mean concentration
of 0.0011 ppm, with a range from trace amounts to 0.007 ppm (FDA: Total Diet
Study) for Oct 1980 - March 1982(1).
USA Market basket surveys: avg daily intake (ug/kg body weight/day): FY65-69,
overall, 0.3(1), 1971-76, overall, 0.07(2), FY77, 0.154(3), FY78, 0.1423(4),
FY79, 0.265(7), FY80, 0.203(8), Oct 1980-March 1982, 0.243(9); infant and
toddler total diet: avg daily intake (ug/kg body wt/day), infant (toddler):
FY75, 0.2028 (0.1374), FY76, 0.0865 (0.1488)(5), FY77, 0.0643 (0.2097), FY78,
0.3305 (0.2985)(6), FY79, 0.126 (0.126) (0.259)(10), FY80, 0.191 (0.234)(11),
Oct 1980-March 1982, 0.177 (0.193)(12).
US 1969-76, number of samples/percent pos (avg,ppm): large fruits, domestic
3281/21.3% (0.057), import 1048/not detected; small fruits, domestic 1145/15-7%
(0.009), import 2119/24% (0.022); leaf and stem vegetables, domestic, 5319/36.2%
(0.071), import 312/18.8% (0.028); whole grains domestic 947/53.1% (0.790);
processed vegetables, domestic 631/12.7% (0.028), import, 929/6.9% (0.007); corn
and corn products, domestic, FY64-69, 1314/not detected, peanuts, domestic
FY64-69, 229/not detected, FY70-76, 148/14.8% (0.712); soybeans, FY64-69,
690/not detected, FY70-76, 104/42.1% (0.051)(1).
MALATHION resiudes found on
strawberries after 0, 2, 4, 7, 11 and 18 days of treatment are 4.630, 0.125,
0.022, 0.015, 0.009, and 0.001 ppm in 1986 and 1.272, 0.012, 0.009, 0.007,
0.001, 0.001 ppm, in 1987 and respectively(1).
MALATHION was detected on oranges 0, 2, and 7
days after treatment at respective concentrations of 1.7, 1.5, and 1.1 ppm(2).
MALATHION levels on backyard
vegetation in California after a single application were recorded as 3.7
ug/g(1).
Plant Concentrations:
In the USA National Soils Monitoring Program (1970 & 1972), the following
levels ... were detected in crops that were mature &/or ready for harvest
(mg/kg): alfalfa/bur clover, 0.03-0.26; corn stalks, 0.04-0.25; cotton ...
0.01-2.17; grass hay, 0.02-0.22; mixed hay, 0.02-0.09 ... & sorghum ...
0.04-0.29.
MALATHION was detected on oranges 0,
2 and 7 days after treatment at respective concn of 1.7, 1.5 and 1.1 ppm(1).
MALATHION undergoes extensive
degradation in plants via enzymatically, hydrolytically and photocatalytically
induced reactions to produce products such as hydrogen sulfide, methyl and ethyl
compounds and more complex compounds(2). A summarized half-life of
MALATHION on plants ranged from <1 to 9
days(3).
Fish/Seafood Concentrations:
MALATHION was detected in tissue
samples from fish from 144 estuaries throughout USA.
Other Environmental Concentrations:
A mean content of 4 ng/g MALATHION
was measured in cured tobacco leaves from farms in southern Ontario, /Canada/ in
1978.
Environmental Standards & Regulations:
FIFRA Requirements:
Tolerances are established for residues of the insecticide
MALATHION in or on the following raw
agricultural commodities (expressed in ppm): alfalfa (pre-harvest); almond hulls
(pre-harvest); almonds (pre- and post-harvest); almonds, shells; apples
(pre-harvest); apricots (pre-harvest); asparagus (pre-harvest); avocados
(pre-harvest); barley, grain (pre- and post-harvest); beans (pre-harvest); beets
(including tops) (pre-harvest); beets, sugar, roots (pre-harvest); beets, sugar,
tops (pre-harvest); birdsfoot, trefoil, forage (pre-harvest); birdsfoot,
trefoil, hay (pre-harvest); blackberries (pre-harvest); blueberries
(pre-harvest); boysenberries (pre-harvest); broccoli (pre-harvest); brussels
sprouts (pre-harvest); cabbage (pre-harvest); carrots (pre-harvest); cattle, fat
(pre-slaughter); cattle, mbyp (pre-slaughter); cattle, meat (pre-slaughter);
cauliflower (pre-harvest); celery (pre-harvest); cherries (pre-harvest);
chestnuts (pre-harvest); clover (pre-harvest); collards (pre-harvest); corn,
forage (pre-harvest); corn, fresh (including sweet kernel plus cob with husk
removed) (pre-harvest); corn, grain (post-harvest); cottonseed (pre-harvest);
cowpea, forage (pre-harvest); cowpea, hay (pre-harvest); cranberries
(pre-harvest); cucumbers (pre-harvest); currants (pre-harvest); dandelions
(pre-harvest); dates (pre-harvest); dewberries (pre-harvest); eggplants
(pre-harvest); eggs (from application to poultry); endive (escarole)
(pre-harvest); figs (pre-harvest); filberts (pre-harvest); flax seed; flax
straw; garlic (pre-harvest); goats, fat (pre-slaughter); goats, mbyp
(pre-slaughter); goats, meat (pre-slaughter); gooseberries (pre-harvest);
grapefruit (pre-harvest); grapes (pre-harvest); grass (pre-harvest); grass, hay
(pre-harvest); guavas (pre-harvest); hogs, fat (pre-slaughter); hogs, mbyp
(pre-slaughter); hogs, meat (pre-slaughter); hops (pre-harvest); horseradish
(pre-harvest); horses, fat (pre-slaughter); horses, mbyp (pre-slaughter);
horses, meat (pre-slaughter); kale (pre-harvest); kohlrabi (pre-harvest);
kumquats (pre-harvest); leeks (pre-harvest); lemons (pre-harvest); lentils
(pre-harvest); lespedeza, hay (pre-harvest); lespedeza, seed (pre-harvest);
lespedeza, straw (pre-harvest); lettuce (pre-harvest); limes (pre-harvest);
loganberries (pre-harvest); lupine, seed (pre-harvest); macadamia nuts
(pre-harvest); mangoes (pre-harvest); melons (pre-harvest); milk, fat (from
application to dairy cows); mushrooms (pre-harvest); mustard greens
(pre-harvest); nectarines (pre-harvest); oats, grain (pre- and post-harvest);
okra (pre-harvest); onions (including green onions) (pre-harvest); oranges
(pre-harvest); papayas (pre-harvest); parsley (pre-harvest); parsnips
(pre-harvest); passion fruit (pre-harvest); peaches (pre-harvest); peanut,
forage (pre-harvest); peanut, hay (pre-harvest); peanuts (pre- and
post-harvest); pears (pre-harvest); peas (pre-harvest); peavine, hay
(pre-harvest); peavines (pre-harvest); pecans (pre-harvest); peppermint
(pre-harvest); peppers (pre-harvest); pineapples (pre-harvest); plums
(pre-harvest); potatoes (pre-harvest); poultry, fat (pre-slaughter); poultry,
mbyp (pre-slaughter); poultry, meat (pre-slaughter); prunes (pre-harvest);
pumpkins (pre-harvest); quinces (pre-harvest); radishes (pre-harvest);
raspberries (pre-harvest); rice, grain (pre- and post-harvest); rice, wild;
rutabagas (pre-harvest); rye, grain (pre- and post-harvest); safflower, seed
(pre-harvest); salsify (including tops) (pre-harvest); shallots (pre-harvest);
sheep, fat (pre-slaughter); sheep, mbyp (pre-slaughter); sheep, meat
(pre-slaughter); sorghum, forage (pre-harvest); sorghum, grain (pre- and
post-harvest); soybeans (dry and succulent) (pre-harvest); soybeans, forage
(pre-harvest); soybeans, hay (pre-harvest); spearmint (pre-harvest); spinach
(pre-harvest); squash, summer and winter (pre-harvest); strawberries
(pre-harvest); sunflower seeds (post-harvest); sweet potatoes (pre-harvest) 1;
swiss chard (pre-harvest); tangerines (pre-harvest); tomatoes (pre-harvest);
turnips, (including tops); vetch, hay (pre-harvest); vetch, seed (pre-harvest);
vetch, straw (pre-harvest); walnuts (pre-harvest); watercress (pre-harvest);
wheat, grain (pre- and post-harvest). The tolerance level shall not be exceeded
in any cut of meat or in any meat byproduct from cattle, goats, hogs, horses,
poultry, or sheep.
MALATHION may be safely used in
accordance with the following conditions: it is incorporated into paper trays in
amounts not exceeding 100 mg/sq ft; treated paper trays are intended for use
only in the drying of grapes (raisins); total residues of
MALATHION resulting from drying of grapes on
treated trays and from application to grapes before harvest shall not exceed 12
ppm on processed ready-to-eat raisins.
Residues of MALATHION in refined
safflower oil from application to the growing safflower plant shall not exceed
0.6 ppm.
As the federal pesticide law FIFRA directs, EPA is conducting a comprehensive
review of older pesticides to consider their health and environmental effects
and make decisions about their future use. Under this pesticide reregistration
program, EPA examines health and safety data for pesticide active ingredients
initially registered before November 1, 1984, and determines whether they are
eligible for reregistration. In addition, all pesticides must meet the new
safety standard of the Food Quality Protection Act of 1996.
MALATHION is found on List A, which contains
most food use pesticides and consists of the 194 chemical cases (or 350
individual active ingredients) for which EPA issued registration standards prior
to FIFRA, as amended in 1988. Case No: 0248; Pesticide type: Insecticide;
Registration Standard Date: 02/15/88; Case Status: OPP is reviewing data from
the pesticide's producers regarding its human health and/or environmental
effects, or OPP is determining the pesticide's eligibility for reregistration
and developing the Reregistration Eligibility Decision (RED) document.; Active
ingredient (AI): MALATHION; Data Call-in
(DCI) Date(s): 06/15/92, 06/07/94, 01/10/95, 03/03/95, 10/13/95; AI Status: The
producers of the pesticide has made commitments to conduct the studies and pay
the fees required for reregistration, and are meeting those commitments in a
timely manner.
Acceptable Daily Intakes:
... 0.02 MG/KG /IN DRINKING WATER/ ...
CERCLA Reportable Quantities:
Persons in charge of vessels or facilities are required to notify the
National Response Center (NRC) immediately, when there is a release of this
designated hazardous substance, in an amount equal to or greater than its
reportable quantity of 100 lb or 45.4 kg. The toll free number of the NRC is
(800) 424-8802; In the Washington D.C. metropolitan area (202) 426-2675. The
rule for determining when notification is required is stated in 40 CFR 302.4
(section IV. D.3.b).
Clean Water Act Requirements:
MALATHION is designated as a
hazardous substance under section 311(b)(2)(A) of the Federal Water Pollution
Control Act and further regulated by the Clean Water Act Amendments of 1977 and
1978. These regulations apply to discharges of this substance. This designation
includes any isomers and hydrates, as well as any solutions and mixtures
containing this substance.
Federal Drinking Water Guidelines:
EPA 200 ug/l
State Drinking Water Guidelines:
(AZ) ARIZONA 140 ug/l
(CA) CALIFORNIA 160 ug/l
(FL) FLORIDA 140 ug/l
(ME) MAINE 40 ug/l
Allowable Tolerances:
Tolerances are established for residues of the insecticide
MALATHION in or on the following raw
agricultural commodities (expressed in ppm): alfalfa (pre-harvest) 135; almond
hulls (pre-harvest) 50; almonds (pre- and post-harvest) 8; almonds,shells 50;
apples (pre-harvest) 8; apricots (pre-harvest) 8; asparagus (pre-harvest) 8;
avocados (pre-harvest) 8; barley, grain (pre- and post-harvest) 8; beans
(pre-harvest) 8; beets (including tops) (pre-harvest) 8; beets, sugar, roots
(pre-harvest) 1; beets, sugar, tops (pre-harvest) 8; birdsfoot, trefoil, forage
(pre-harvest) 135; birdsfoot, trefoil, hay (pre-harvest) 135; blackberries
(pre-harvest) 8; blueberries (pre-harvest) 8; boysenberries (pre-harvest) 8;
broccoli (pre-harvest) 5; brussels sprouts (pre-harvest) 8; cabbage
(pre-harvest) 8; carrots (pre-harvest) 8; cattle, fat (pre-slaughter) 4; cattle,
mbyp (pre-slaughter) 4*; cattle, meat (pre-slaughter) 4*; cauliflower
(pre-harvest) 8; celery (pre-harvest) 8; cherries (pre-harvest) 8; chestnuts
(pre-harvest) 1; clover (pre-harvest) 135; collards (pre-harvest) 8; corn,
forage (pre-harvest) 8; corn, fresh (including sweet kernel plus cob with husk
removed) (pre-harvest) 2; corn, grain (post-harvest) 8; cottonseed (pre-harvest)
2; cowpea, forage (pre-harvest) 135; cowpea, hay (pre-harvest) 135; cranberries
(pre-harvest) 8; cucumbers (pre-harvest) 8; currants (pre-harvest) 8; dandelions
(pre-harvest) 8; dates (pre-harvest) 8; dewberries (pre-harvest) 8; eggplants
(pre-harvest) 8; eggs (from application to poultry) 0.1; endive (escarole)
(pre-harvest) 8; figs (pre-harvest) 8; filberts (pre-harvest) 1; flax seed 0.1;
flax straw 1.0; garlic (pre-harvest) 8; goats, fat (pre-slaughter) 4; goats,
mbyp (pre-slaughter) 4*; goats, meat (pre-slaughter) 4*; gooseberries
(pre-harvest) 8; grapefruit (pre-harvest) 8; grapes (pre-harvest) 8; grass
(pre-harvest) 135; grass, hay (pre-harvest) 135; guavas (pre-harvest) 8; hogs,
fat (pre-slaughter) 4; hogs, mbyp (pre-slaughter) 4*; hogs, meat (pre-slaughter)
4*; hops (pre-harvest) 1; horseradish (pre-harvest) 8; horses, fat
(pre-slaughter) 4; horses, mbyp (pre-slaughter) 4*; horses, meat (pre-slaughter)
4*; kale (pre-harvest) 8; kohlrabi (pre-harvest) 8; kumquats (pre-harvest) 8;
leeks (pre-harvest) 8; lemons (pre-harvest) 8; lentils (pre-harvest) 8;
lespedeza, hay (pre-harvest) 135; lespedeza, seed (pre-harvest) 8; lespedeza,
straw (pre-harvest) 135; lettuce (pre-harvest) 8; limes (pre-harvest);
loganberries (pre-harvest) 8; lupine, seed (pre-harvest) 8; macadamia nuts
(pre-harvest) 1; mangoes (pre-harvest) 8; melons (pre-harvest) 8; milk, fat
(from application to dairy cows) 0.5; mushrooms (pre-harvest) 8; mustard greens
(pre-harvest) 8; nectarines (pre-harvest) 8; oats, grain (pre- and post-harvest)
8; okra (pre-harvest) 8; onions (including green onions) (pre-harvest) 8;
oranges (pre-harvest) 8; papayas (pre-harvest) 1; parsley (pre-harvest) 8;
parsnips (pre-harvest) 8; passion fruit (pre-harvest) 8; peaches (pre-harvest)
8; peanut, forage (pre-harvest) 135; peanut, hay (pre-harvest) 135; peanuts
(pre- and post-harvest) 8; pears (pre-harvest) 8; peas (pre-harvest) 8; peavine,
hay (pre-harvest) 8; peavines (pre-harvest) 8; pecans (pre-harvest) 8;
peppermint (pre-harvest) 8; peppers (pre-harvest) 8; pineapples (pre-harvest) 8;
plums (pre-harvest) 8; potatoes (pre-harvest) 8;poultry, fat (pre-slaughter) 4;
poultry, mbyp (pre-slaughter) 4*; poultry, meat (pre-slaughter) 4*; prunes
(pre-harvest) 8; pumpkins (pre-harvest) 8; quinces (pre-harvest) 8; radishes
(pre-harvest) 8; raspberries (pre-harvest) 8; rice, grain (pre- and
post-harvest) 8; rice, wild 8; rutabagas (pre-harvest) 8; rye, grain (pre- and
post-harvest) 8; safflower, seed (pre-harvest) 0.2; salsify (including tops)
(pre-harvest) 8; shallots (pre-harvest) 8; sheep, fat (pre-slaughter) 4; sheep,
mbyp (pre-slaughter) 4*; sheep, meat (pre-slaughter) 4*; sorghum, forage
(pre-harvest) 8; sorghum, grain (pre- and post-harvest) 8; soybeans (dry and
succulent) (pre-harvest) 8; soybeans, forage (pre-harvest) 135; soybeans, hay
(pre-harvest) 135; spearmint (pre-harvest) 8; spinach (pre-harvest) 8; squash,
summer and winter (pre-harvest) 8; strawberries (pre-harvest) 8; sunflower seeds
(post-harvest) 8; sweet potatoes (pre-harvest) 1; swiss chard (pre-harvest) 8;
tangerines (pre-harvest) 8; tomatoes (pre-harvest) 8; turnips, (including tops)
8; vetch, hay (pre-harvest) 135; vetch, seed (pre-harvest) 8; vetch, straw
(pre-harvest) 135; walnuts (pre-harvest) 8; watercress (pre-harvest) 8; wheat,
grain (pre- and post-harvest) 8. * The tolerance level shall not be exceeded in
any cut of meat or in any meat byproduct from cattle, goats, hogs, horses,
poultry, or sheep.
Chemical/Physical Properties:
Molecular Formula:
C10-H19-O6-P-S2
Molecular Weight:
330.36
Color/Form:
Clear colorless liquid when pure
Deep brown to yellow liquid
Deep-brown to yellow liquid ... [Note: A solid below 37 degrees F].
Odor:
SKUNK-LIKE ODOR
... Garlic-like odor ...
Mercaptan odor
Boiling Point:
156-157 deg C @ 0.7 mm Hg
Melting Point:
2.9 deg C
Corrosivity:
Corrosive to iron & some other metals
MALATHION will attack some forms of
plastics, rubber, and coatings
Corrosive to metals
Density/Specific Gravity:
1.23 @ 25 deg C/4 deg C
Octanol/Water Partition Coefficient:
log Kow= 2.36
Solubilities:
145 ppm in water @ 20 deg C
Miscible with alcohols, esters, ketones, ethers, aromatic and alkylated
aromatic hydrocarbons and vegetable oils. Limited solubility in paraffin
hydrocarbons
Soluble in ethanol and acetone; very soluble in ethyl ether
> 10% in ethanol
> 10% in ethyl ether
> 10% in benzene
Spectral Properties:
Index of refraction: 1.4985 @ 25 deg C/D
Index of refraction: 1.4960 @ 20 deg C/D
IR: H587 (Sadtler Research Laboratories Prism Collection)
MASS: 239 (Aldermaston, Eight Peak Index of Mass Spectra, UK)
MALATHION absorbs light at
wavelengths > 290 nm
Intense mass spectral peaks: 125 m/z (100%), 173 m/z (98%), 93 m/z (96%), 158
m/z (54%)
Intense mass spectral peaks: 127 m/z, 285 m/z, 330 m/z
Surface Tension:
37.1 DYNES/CM @ 24 DEG C
Vapor Pressure:
1.78X10-4 mm Hg @ 25 deg C
Other Chemical/Physical Properties:
LIQUID WATER INTERFACIAL TENSION: 19 DYNES/CM @ 24 DEG C
Hydrolyzed at pH >7.0 or <5.0. Stable in an aqueous solution buffered
to pH 5.26.
Henry's Law constant= 4.9X10-9 atm cu-m/mole @ 25 deg C
Chemical Safety & Handling:
DOT Emergency Guidelines:
Health: Toxic; may be fatal if inhaled, ingested or absorbed through skin.
Inhalation or contact with some of these materials will irritate or burn skin
and eyes. Fire will produce irritating, corrosive and/or toxic gases. Vapors may
cause dizziness or suffocation. Runoff from fire control or dilution water may
cause pollution. /Organophosphorus pesticide, liquid, flammable, poisonous;
Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus
pesticide, liquid, poisonous, flammable; Organophosphorus pesticide, liquid,
toxic, flammable/
Fire or explosion: Highly flammable: Will be easily ignited by heat, sparks
or flames. Vapors may form explosive mixtures with air. Vapors may travel to
source of ignition and flash back. Most vapors are heavier than air. They will
spread along ground and collect in low or confined areas (sewers, basements,
tanks). Vapor explosion and poison hazard indoors, outdoors or in sewers. Those
substances designated with a "P" may polymerize explosively when heated or
involved in a fire. Runoff to sewer may create fire or explosion hazard.
Containers may explode when heated. Many liquids are lighter than water.
/Organophosphorus pesticide, liquid, flammable, poisonous; Organophosphorus
pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid,
poisonous, flammable; Organophosphorus pesticide, liquid, toxic, flammable/
Public safety: Call Emergency Response Telephone Number. ... Isolate spill or
leak area immediately for at least 100 to 200 meters (330 to 660 feet) in all
directions. Keep unauthorized personnel away. Stay upwind. Keep out of low
areas. Ventilate closed spaces before entering. /Organophosphorus pesticide,
liquid, flammable, poisonous; Organophosphorus pesticide, liquid, flammable,
toxic; Organophosphorus pesticide, liquid, poisonous, flammable;
Organophosphorus pesticide, liquid, toxic, flammable/
Protective clothing: Wear positive pressure self-contained breathing
apparatus (SCBA). Wear chemical protective clothing which is specifically
recommended by the manufacturer. It may provide little or no thermal protection.
Structural firefighters' protective clothing provides limited protection in fire
situations ONLY; it is not effective in spill situations. /Organophosphorus
pesticide, liquid, flammable, poisonous; Organophosphorus pesticide, liquid,
flammable, toxic; Organophosphorus pesticide, liquid, poisonous, flammable;
Organophosphorus pesticide, liquid, toxic, flammable/
Evacuation: ... Fire: If tank, rail car or tank truck is involved in a fire,
isolate for 800 meters (1/2 mile) in all directions; also, consider initial
evacuation for 800 meters (1/2 mile) in all directions.
Fire: CAUTION: All these products have a very low flash point. Use of water
spray when fighting fire may be inefficient. Small fires: Dry chemical, CO2,
water spray or alcohol-resistant foam. Large fires: Water spray, fog or
alcohol-resistant foam. Move containers from fire area if you can do it without
risk. Dike fire control water for later disposal; do not scatter the material.
Use water spray or fog; do not use straight streams. Fire involving tanks or
car/trailer loads: Fight fire from maximum distance or use unmanned hose holders
or monitor nozzles. Cool containers with flooding quantities of water until well
after fire is out. Withdraw immediately in case of rising sound from venting
safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in
fire. For massive fire use unmanned hose holders or monitor nozzles; if this is
impossible, withdraw from area and let fire burn. /Organophosphorus pesticide,
liquid, flammable, poisonous; Organophosphorus pesticide, liquid, flammable,
toxic; Organophosphorus pesticide, liquid, poisonous, flammable;
Organophosphorus pesticide, liquid, toxic, flammable/
Spill or leak: Fully encapsulating, vapor protective clothing should be worn
for spills and leaks with no fire. ELIMINATE all ignition sources (no smoking,
flares, sparks or flames in immediate area). All equipment used when handling
the product must be grounded. Do not touch or walk through spilled material.
Stop leak if you can do it without risk. Prevent entry into waterways, sewers,
basements or confined areas. A vapor suppressing foam may be used to reduce
vapors. Small spills: Absorb with earth, sand or other non-combustible material
and transfer to containers for later disposal. Use clean non-sparking tools to
collect absorbed material. Large spills: Dike far ahead of liquid spill for
later disposal. Water spray may reduce vapor; but may not prevent ignition in
closed spaces. /Organophosphorus pesticide, liquid, flammable, poisonous;
Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus
pesticide, liquid, poisonous, flammable; Organophosphorus pesticide, liquid,
toxic, flammable/
First aid: Move victim to fresh air. Call 911 or emergency medical service.
Apply artificial respiration if victim is not breathing. Do not use
mouth-to-mouth method if victim ingested or inhaled the substance; induce
artificial respiration with the aid of a pocket mask equipped with a one-way
valve or other proper respiratory medical device. Administer oxygen if breathing
is difficult. Remove and isolate contaminated clothing and shoes. In case of
contact with substance, immediately flush skin or eyes with running water for at
least 20 minutes. Wash skin with soap and water. Keep victim warm and quiet.
Effects of exposure (inhalation, ingestion or skin contact) to substance may be
delayed. Ensure that medical personnel are aware of the material(s) involved,
and take precautions to protect themselves. /Organophosphorus pesticide, liquid,
flammable, poisonous; Organophosphorus pesticide, liquid, flammable, toxic;
Organophosphorus pesticide, liquid, poisonous, flammable; Organophosphorus
pesticide, liquid, toxic, flammable/
Health: Highly toxic, may be fatal if inhaled, swallowed or absorbed through
skin. Contact with molten substance may cause severe burns to skin and eyes.
Avoid any skin contact. Effects of contact or inhalation may be delayed. Fire
may produce irritating, corrosive and/or toxic gases. Runoff from fire control
or dilution water may be corrosive and/or toxic and cause pollution.
/Organophosphorus pesticide, liquid, poisonous; Organophosphorus pesticide,
liquid, toxic; Organophosphorus pesticide, solid, poisonous; Organophosphorus
pesticide, solid, toxic/
Fire or explosion: Combustible material: may burn but does not ignite
readily. Containers may explode when heated. Runoff may pollute waterways.
Substance may be transported in a molten form. /Organophosphorus pesticide,
liquid, poisonous; Organophosphorus pesticide, liquid, toxic; Organophosphorus
pesticide, solid, poisonous; Organophosphorus pesticide, solid, toxic/
Public safety: CALL Emergency Response Telephone Number. ... Isolate spill or
leak area immediately for at least 25 to 50 meters (80 to 160 feet) in all
directions. Keep unauthorized personnel away. Stay upwind. Keep out of low
areas. /Organophosphorus pesticide, liquid, poisonous; Organophosphorus
pesticide, liquid, toxic; Organophosphorus pesticide, solid, poisonous;
Organophosphorus pesticide, solid, toxic/
Protective clothing: Wear positive pressure self-contained breathing
apparatus (SCBA). Wear chemical protective clothing which is specifically
recommended by the manufacturer. It may provide little or no thermal protection.
Structural firefighters' protective clothing provides limited protection in fire
situations ONLY; it is not effective in spill situations. /Organophosphorus
pesticide, liquid, poisonous; Organophosphorus pesticide, liquid, toxic;
Organophosphorus pesticide, solid, poisonous; Organophosphorus pesticide, solid,
toxic/
Evacuation: ... Fire: If tank, rail car or tank truck is involved in a fire,
ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial
evacuation for 800 meters (1/2 mile) in all directions. /Organophosphorus
pesticide, liquid, poisonous; Organophosphorus pesticide, liquid, toxic;
Organophosphorus pesticide, solid, poisonous; Organophosphorus pesticide, solid,
toxic/
Fire: Small fires: Dry chemical, CO2 or water spray. Large fires: Water
spray, fog or regular foam. Move containers from fire area if you can do it
without risk. Dike fire control water for later disposal; do not scatter the
material. Use water spray; do not use straight streams. Fire involving tanks or
car/trailer loads: Fight fire from maximum distance or use unmanned hose holders
or monitor nozzles. Do not get water inside containers. Cool containers with
flooding quantities of water until well after fire is out. Withdraw immediately
in case of rising sound from venting safety devices or discoloration of tank.
ALWAYS stay away from tanks engulfed in fire. For massive fire, use unmanned
hose holders or monitor nozzles; if this is impossible, withdraw from area and
let fire burn. /Organophosphorus pesticide, liquid, poisonous; Organophosphorus
pesticide, liquid, toxic; Organophosphorus pesticide, solid, poisonous;
Organophosphorus pesticide, solid, toxic/
Spill or leak: Do not touch damaged containers or spilled material unless
wearing appropriate protective clothing. Stop leak if you can do it without
risk. Prevent entry into waterways, sewers, basements or confined areas. Cover
with plastic sheet to prevent spreading . Absorb or cover with dry earth, sand
or other non-combustible material and transfer to containers. DO NOT GET WATER
INSIDE CONTAINERS. /Organophosphorus pesticide, liquid, poisonous;
Organophosphorus pesticide, liquid, toxic; Organophosphorus pesticide, solid,
poisonous; Organophosphorus pesticide, solid, toxic/
First aid: Move victim to fresh air. Call 911 or emergency medical service.
Apply artificial respiration if victim is not breathing. Do not use
mouth-to-mouth method if victim ingested or inhaled the substance; induce
artificial respiration with the aid of a pocket mask equipped with a one-way
valve or other proper respiratory medical device. Administer oxygen if breathing
is difficult. Remove and isolate contaminated clothing and shoes. In case of
contact with substance, immediately flush skin or eyes with running water for at
least 20 minutes. For minor skin contact, avoid spreading material on unaffected
skin. Keep victim warm and quiet. Effects of exposure (inhalation, ingestion or
skin contact) to substance may be delayed. Ensure that medical personnel are
aware of the material(s) involved, and take precautions to protect themselves.
/Organophosphorus pesticide, liquid, poisonous; Organophosphorus pesticide,
liquid, toxic; Organophosphorus pesticide, solid, poisonous; Organophosphorus
pesticide, solid, toxic/
Odor Threshold:
1.00 ppm (detection in water, purity not stated)
Odor thresholds: 13.5000 mg/cu m (low); 13.5000 mg/cu m (high)
Skin, Eye and Respiratory Irritations:
Irritating to the eyes.
Fire Potential:
It is combustible though it may take some effort to ignite.
Commercially available /pharmaceutical/ preparation is flammable.
Flash Point:
ABOVE 325 DEG F (TAG OPEN CUP)
163 deg C (Pensky-Martens closed cup) /Technical/
Fire Fighting Procedures:
Dry chemicals, carbon dioxide for small fires. Water spray, foam for large
fires.
AREA SURROUNDING FIRE SHOULD BE DIKED TO PREVENT WATER RUNOFF.
WEAR SELF CONTAINED BREATHING APPARATUS (OR RESPIRATOR FOR ORGANOPHOSPHATE
PESTICIDES) AND RUBBER CLOTHING WHILE FIGHTING FIRES OF
MALATHION WITH CHLORINE BLEACH SOLN. ALL
CLOTHING CONTAMINATED BY FUMES AND VAPORS MUST BE DECONTAMINATED.
Extinguish fire using agent suitable for type of surrounding fire.
If material on fire or involved in fire: Do not extinguish fire unless flow
can be stopped or safely confined. Use water in flooding quantities as fog.
Solid streams of water may be ineffective. Cool all affected containers with
flooding quantities of water. Apply water from as far a distance as possible.
Use "alcohol" foam, carbon dioxide or dry chemical. /Organophosphorus
pesticides, liquid, NOS/
If material on fire or involved in fire: Extinguish fire using agent suitable
for type of surrounding fire. (Material itself does not burn or burns with
difficulty.) Use water in flooding quantities as fog. Use "alcohol" foam, carbon
dioxide or dry chemical. /Organophosphorus pesticides, solid, NOS/
Toxic Combustion Products:
VAPORS AND FUMES FROM FIRES ... INCL SULFUR DIOXIDE AND PHOSPHORIC ACID.
Toxic gases & vapors (such as ... carbon monoxide) may be released in
fires involving MALATHION.
Explosive Limits & Potential:
CONTAINERS MAY EXPLODE IN FIRE.
Hazardous Reactivities & Incompatibilities:
Strong oxidizers, magnesium, alkaline pesticides [Note: Corrosive to metals].
Hazardous Decomposition:
Above 100 deg C, decomposes ... explosively.
Starts to decompose at 49 deg C (140 deg F) ...
When heated to decomposition it emits toxic fumes of phosphoxides and
sulfoxides.
Decomposed by acids and alkalis.
Other Hazardous Reaction:
A portion of even the most flammable materials is likely to be lost by
vaporization. ... The smoke from an open fire used to destroy pesticides will
contain some of the poison. Burning should be attempted only in an isolated
place. Inhalation of smoke must be avoided. /Pesticides/
Immediately Dangerous to Life or Health:
250 mg/cu m
Protective Equipment & Clothing:
Employees should be provided with and required to use ... face shields (eight
inch minimum), and other appropriate protective clothing necessary to prevent
repeated, or prolonged skin contact with
MALATHION.
Any employee whose work involves likely exposure of the skin to
MALATHION or
MALATHION formulations, eg, mixing or
formulating, shall wear full body coveralls, or the equivalent, impervious
gloves, and footwear. When there is danger of
MALATHION coming in contact with the eyes,
safety goggles shall be provided and worn.
Wear appropriate personal protective clothing to prevent skin contact.
Wear appropriate eye protection to prevent eye contact.
Recommendations for respirator selection. Max concn for use: 100 mg/cu m.
Respirator Class(es): Any chemical cartridge respirator with organic vapor
cartridge(s) in combination with a dust, mist, and fume filter. Any supplied-air
respirator.
Recommendations for respirator selection. Max concn for use: 250 mg/cu m.
Respirator Class(es): Any supplied-air respirator operated in a continuous flow
mode. May require eye protection. Any chemical cartridge respirator with a full
facepiece and organic vapor cartridge(s) in combination with a high-efficiency
particulate filter. Any air-purifying, full-facepiece respirator (gas mask) with
a chin-style, front- or back-mounted organic vapor canister having a
high-efficiency particulate filter. Any powered, air-purifying respirator with
organic vapor cartridge(s) in combination with a dust, mist, and fume filter.
May require eye protection. Any self-contained breathing apparatus with a full
facepiece. Any supplied-air respirator with a full facepiece.
Recommendations for respirator selection. Condition: Emergency or planned
entry into unknown concn or IDLH conditions: Respirator Class(es): Any
self-contained breathing apparatus that has a full facepiece and is operated in
a pressure-demand or other positive-pressure mode. Any supplied-air respirator
that has a full facepiece and is operated in a pressure-demand or other
positive-pressure mode in combination with an auxiliary self-contained breathing
apparatus operated in pressure-demand or other positive-pressure mode.
Recommendations for respirator selection. Condition: Escape from suddenly
occurring respiratory hazards: Respirator Class(es): Any air-purifying,
full-facepiece respirator (gas mask) with a chin-style, front- or back-mounted
organic vapor canister having a high-efficiency particulate filter. Any
appropriate escape-type, self-contained breathing apparatus.
Respiratory protection (supplied-air respirator with full facepiece or
self-contained breathing apparatus) should be available where these compounds
are manufactured or used and should be worn in case of emergency and
overexposure. /Phosphorus compounds/
WORKERS HANDLING AND APPLYING ORGANOPHOSPHATE PESTICIDES (OPP) MUST ... BE
GIVEN PERSONAL PROTECTIVE EQUIPMENT COMPRISING OVERALLS MADE OF A TIGHT FABRIC
OR POLYVINYL CHLORIDE, GLOVES, AND RUBBER BOOTS. THEY MUST WEAR A RESPIRATOR
WITH AN ACTIVATED-CARBON GAS FILTER CARTRIDGE AFFORDING PROTECTION FOR A
DETERMINED NUMBER OF WORKING HOURS. THE EYES SHOULD BE PROTECTED BY GOGGLES. THE
SIGNALMEN FOR AERIAL DUSTING OPERATIONS SHOULD BE EQUIPPED WITH A HAT AND CAPE
MADE OF POLYVINYL CHLORIDE OR A FABRIC IMPREGNATED WITH A WATER REPELLENT.
/PESTICIDES, ORGANOPHOSPHORUS/
Preventive Measures:
If material not involved in fire: Keep material out of water sources and
sewers. Build dikes to contain flow as necessary. Keep upwind. ... Avoid
breathing vapors, or dusts. Wash away any material which may have contacted the
body with copious amounts of water, or soap and water.
Nonimpervious clothing which becomes contaminated with
MALATHION should be removed promptly and not
reworn until the MALATHION is removed
from the clothing. Employees should be provided with and required to use splash
proof safety goggles where liquid
MALATHION may contact the eyes. Where there is
any possibility that employees' eyes may be exposed to
MALATHION, an eye wash fountain should be
provided within the immediate work area for emergency use. Skin that becomes
contaminated with MALATHION should be
promptly washed or showered with soap or mild detergent and water to remove any
MALATHION. ... Eating and smoking should
not be permitted in areas where
MALATHION is handled, processed, or stored.
Good industrial hygiene practices recommend that engineering controls be used
to reduce environmental concentrations to the permissible exposure level.
However, there are some exceptions where respirators may be used to control
exposure. Respirators may be used when engineering and work practice controls
are not technically feasible, when such controls are in the process of being
installed, or when they fail and need to be supplemented. Respirators may also
be used for operations which require entry into tanks or closed vessels, and in
emergency situations. ... In addition to respirator selection, a complete
respiratory protection program should be instituted which includes regular
training, maintenance, inspection, cleaning, and evaluation.
Employees shall be required to shower at the end of each shift.
Contact lenses should not be worn when working with this chemical.
SRP: The scientific literature for the use of contact lenses in industry is
conflicting. The benefit or detrimental effects of wearing contact lenses depend
not only upon the substance, but also on factors including the form of the
substance, characteristics and duration of the exposure, the uses of other eye
protection equipment, and the hygiene of the lenses. However, there may be
individual substances whose irritating or corrosive properties are such that the
wearing of contact lenses would be harmful to the eye. In those specific cases,
contact lenses should not be worn. In any event, the usual eye protection
equipment should be worn even when contact lenses are in place.
SRP: Contaminated protective clothing should be segregated in such a manner
so that there is no direct personal contact by personnel who handle, dispose, or
clean the clothing. Quality assurance to ascertain the completeness of the
cleaning procedures should be implemented before the decontaminated protective
clothing is returned for reuse by the workers. Contaminated clothing should not
be taken home at end of shift, but should remain at employee's place of work for
cleaning.
Keep /material/ away from food, drink & animal feeding stuffs.
The worker should immediately wash the skin when it becomes contaminated.
Work clothing that becomes wet or significantly contaminated should be
removed and replaced.
Workers whose clothing may have become contaminated should change into
uncontaminated clothing before leaving the work premises.
In some situations where personnel may become accidently contaminated ... it
is necessary to provide shower bath in addition to the usual washing facilities.
Special arrangements for cleaning clothing & overalls may be necessary ...
/Pesticides/
Special aircraft should preferably be used for spraying or dusting toxic
organophosphorus pesticides. ... Aerial spraying or dusting gives rise to clouds
which spread over larger surfaces than clouds produced by ground application.
Aerial spraying should therefore be carried out on windless days only.
Residential areas, water supply sources, etc must be avoided. ... When aircraft
approaches, signalmen /guiding the aircraft/ should leave the windward side. ...
The local population should be informed about the site & time of aerial
pesticide treatment. Access of unauthorized persons & especially children to
the area to be treated must be ... forbidden. Warning signs should be placed at
the limits of the area. Ground spraying must be carried out with compressed-air
spraying equipment towed by tractors with closed cabs. /Organophosphorus
pesticides/
Small packages of pesticides are preferable for individual application in
order to limit the quantities to be weighed & metered. A special vessel with
long stirring rod for dilution & suspension of the poison must be available
in order to reduce manual handling to a minimum. The strict observance of
hygiene rules--no smoking & no food intake during work. Thorough washing
with soap after work, changing protective clothing before going home--is of
utmost importance. /Organophosphorus pesticides/
Containers ... should be cleaned with a suspension of bleaching powder in
water or with other alkaline soln after soaking for 24 hr and then be rinsed
with hot water. /Organophosphorus pesticides/
If material not on fire and not involved in fire: Keep sparks, flames, and
other sources of ignition away. Keep material out of water sources and sewers.
Build dikes to contain flow as necessary. Use water spray to knock-down vapors.
/Organophosphorus pesticides, liquid, NOS/
Personnel protection: Keep upwind. Wear appropriate chemical protective
gloves, boots and goggles. Do not handle broken packages unless wearing
appropriate personal protective equipment. Wear positive pressure self-contained
breathing apparatus when fighting fires involving this material.
/Organophosphorus pesticides, liquid, NOS/
If material not on fire and not involved in fire: Keep sparks, flames, and
other sources of ignition away. Keep material out of water sources and sewers.
/Organophosphorus pesticides, solid, NOS/
Personnel protection: Avoid breathing dusts, and fumes from burning material.
Keep upwind. Avoid bodily contact with the material. Wear appropriate chemical
protective gloves, boots and goggles. Do not handle broken packages unless
wearing appropriate personal protective equipment. Wash away any material which
may have contacted the body with copious amounts of water or soap and water.
Wear positive pressure self-contained breathing apparatus when fighting fires
involving this material. If contact with the material anticipated, wear
appropriate protective clothing. /Organophosphorus pesticides, solid, NOS/
Parathion and possibly other organophosphate insecticide residues may persist
in clothing, despite repeated laundering. /Organophosphates and related
compounds/
Do not drink alcoholic beverages before or during spraying since alcohol
promotes absorption of organic phosphates. /Organic phosphates/
Stability/Shelf Life:
BIOL ACTIVITY OF MALATHION PREMIUM
GRADE, REMAINS PRACTICALLY UNVARIED FOR 2 YR UNDER ENVIRONMENTAL CONDITIONS,
PROVIDED THE PRODUCT IS STORED IN ITS UNOPENED AND UNDAMAGED ORIGINAL
CONTAINERS, IN COOL, SHADED AND POSSIBLY WELL AIRED PLACES. RECOMMENDED 68-86
DEG F (20-25 DEG C) F0R GOOD SHELF LIFE. SHELF LIFE OF
color=red>MALATOX & VEGFRU IS 1-2 YR.
VARIOUS MALATHION WETTABLE POWDER
FORMULATIONS WERE SUBJECTED TO LONG TERM STORAGE @ AMBIENT TEMP & TO
ACCELERATED STORAGE UNDER UNIFORM PRESSURE OF 25 G/SQ CM @ 54 DEG FOR 24 HR. TWO
DEGRADATION PRODUCTS FORMED DURING STORAGE DIFFERED IN THEIR CONCN. RESULTS FROM
STUDIES USING THIN LAYER CHROMATOGRAPHY SUGGESTED THAT ESTER GROUPS MIGHT NOT
HAVE SUFFERED ANY DEGRADATION, BUT CLEAVAGE OCCURRED AT THE P-S BOND.
Conditions contributing to instability: Starts to decompose at 49 deg C (140
deg F) ...
Storage Conditions:
Biological activity of MALATHION
premium grade, remains practically unvaried for 2 yr under environmental
conditions, provided the product is stored in its unopened and undamaged
original containers, in cool, shaded, and possibly well aired places.
Recommended 68-86 deg F (20-25 deg C) for good shelf life.
THE CONTAINERS MUST BE STACKED IN SUCH A WAY AS TO PERMIT A FREE CIRCULATION
OF AIR ALSO AT THE BOTTOM AND INSIDE OF THE PILES.
Keep container tightly closed ... /&/ dry.
Protect containers against physical damage. Preferably store outdoor or in a
detached quarter; otherwise in standard combustible liq storage room.
Rooms used for storage only should be soundly constructed & fitted with
secure locks. Floors should be kept clear & pesticides clearly identified.
If repacking is carried out in storage rooms, adequate light should be
available; floors should be impervious & sound ... /Pesticides/
Pesticides containers must be provided with labels indicating the degree of
toxicity of the product they contain. The labels must not only give a short
description of how to use the prepn, but also state basic precautions to be
taken when applying it. /Organophosphorus pesticides/
Pesticides of any degree of toxicity should be transported in containers
which are clearly labelled, leak-proof, and not easily damaged. They should
never be transported /or stored/ beside, or above any type of food, and all
spillages should be immediately reported. /Pesticides/
Cleanup Methods:
1. VENTILATE AREA OF SPILL OR LEAK. 2. COLLECT FOR RECLAMATION OR ABSORB IN
VERMICULITE, DRY SAND, EARTH, OR A SIMILAR MATERIAL.
Environmental consideration: Landspill: Dig a pit, pond, lagoon, or holding
area to contain liquid or solid material /SRP: If time permits, pits, ponds,
lagoons, soak holes, or holding areas should be sealed with an impermeable
flexible membrane liner./ Dike surface flow using soil, sand bags, foamed
polyurethane, or foamed concrete. Absorb bulk liquid with fly ash or cement
powder.
Environmental consideration: Water spill: If dissolved ... apply activated
carbon at ten times the spilled amount /in region of 10 ppm or greater
concentration/. Remove trapped material with suction hoses. Use mechanical
dredges, or lifts to remove immobilized masses of pollutants and precipitates.
Spills of MALATHION on floors shall
be absorbed with absorbing clay. Sweeping compound may be utilized to facilitate
the removal of all visible traces of
MALATHION contaminated clay. Equipment and
fixtures contaminated with MALATHION
shall be decontaminated with an alkaline solution (5% sodium hydroxide).
... Alternative treatment process for spent filter cake from
MALATHION mfr requires the following steps:
(1) hydrolysis; (2) steam stripping; (3) decantation; (4) composting; & (5)
biological treatment.
Ultraviolet radiation in conjunction with ozone is a highly effective
degradation technique for MALATHION ...
Hydrolysis: The overalls polluted with
MALATHION should be shaken and soaked in a
soap-and-soda soln for 6-8 hr. Then the overalls must be washed 2-3 times in a
hot soap-and-soda soln and rinsed carefully. Containers are decontaminated with
5% caustic or washing soda (300-500 g per 10 l of water). The containers are
filled with this soln, kept for 5-12 hr, then washed with ample water. If soda
is not at hand, wood ash may be used instead.
Disposal Methods:
SRP: At the time of review, criteria for land treatment or burial (sanitary
landfill) disposal practices are subject to significant revision. Prior to
implementing land disposal of waste residue (including waste sludge), consult
with environmental regulatory agencies for guidance on acceptable disposal
practices.
MALATHION MAY BE DISPOSED OF BY
ABSORBING IN VERMICULITE, DRY SAND, EARTH, OR A SIMILAR MATERIAL ... &
/DISPOSING OF SO AS TO MEET LOCAL, STATE, & FEDERAL REGULATIONS/.
Incineration together with flammable solvent in furnace equipped with
afterburner and scrubber is recommended.
The following wastewater treatment technologies have been investigated for
MALATHION: Biological treatment and
reverse osmosis.
MALATHION is reported to be
"hydrolyzed almost instantly" at pH 12; 50% hydrolysis at pH 9 requires 12 hr.
Alkaline hydrolysis under controlled conditions (0.5 N NAOH in ethanol) /0.5 N
sodium hydroxide in alcohol/ gives quantitative yields of (CH30)2P(S)SNA,
whereas hydrolysis in acidic media yields (CH30)2P(S)OH. On prolonged contact
with iron or iron-containing material, it is reported to break down and
completely lose insecticidal activity. Incineration together with a flammable
solvent in a furnace equipped with afterburner and scrubber is recommended.
Recommendable methods: Incineration & landfill. Peer review: Only small amt
may be landfilled. (Peer-review conclusions of an IRPTC expert consultation (May
1985))
Molten salt combustion: The melts contained either sodium carbonate or
potassium carbonate. The use of potassium carbonate is of interest because the
combustion product, potassium chloride can be used as a fertilizer. Destruction
of the pesticide was greater than 99.9%. No pesticides were detected in the
melt; however, traces of pesticides were detected in the off-gas. The conc of
pesticides in the off-gas were generally well below the TLV.
All organic pesticides, whether of botanical or synthetic origin, can be
destroyed by incineration. /Organic pesticides/
Manufacturers or formulators of very large amounts of pesticides may find it
advantageous to build incinerators adequate to destroy all organic pesticides
and equipped with scrubbers to remove acid wastes. /Organic pesticides/
Occupational Exposure Standards:
OSHA Standards:
Permissible Exposure Limit: Table Z-1 8-hr Time-Weighted Avg: 15 mg/cu m.
Skin Designation. /Total dust/
Vacated 1989 OSHA PEL TWA 10 mg/cu m, skin designation, is still enforced in
some states.
Threshold Limit Values:
8 hr Time Weighted Avg (TWA): 10 mg/cu m, skin.
Excursion Limit Recommendation: Excursions in worker exposure levels may
exceed three times the TLV-TWA for no more than a total of 30 min during a work
day, and under no circumstances should they exceed five times the TLV-TWA,
provided that the TLV-TWA is not exceeded.
Biological Exposure Index (BEI): Determinant: cholinesterase activity in red
blood cells; Sampling Time: discretionary; BEI: 70% of individual's baseline.
The determinant is nonspecific, since it is also observed after exposure to
other chemicals. /Acetylcholinesterase inhibiting pesticides/
A4; Not classifiable as a human carcinogen.
Notice of Intended Change for 2002: These substances, with their
corresponding values and notations, comprise those for which a limit has been
proposed for the first time or for which a change in the Adopted value is
proposed. In each case, the proposed values should be considered trial values
for the year following ratification by the ACGIH Board of Directors. If, during
the year, no evidence comes to light that questions the appropriateness of these
proposals, the values will be reconsidered for adoption as TLVs. 8 hr Time
Weighted Avg (TWA): 1 mg/cu m, skin. /Inhalable fraction; vapor and aerosol/
NIOSH Recommendations:
Recommended Exposure Limit: 10 Hr Time-Weighted Avg: 10 mg/cu m. Skin.
Immediately Dangerous to Life or Health:
250 mg/cu m
Other Occupational Permissible Levels:
Australia: 10 mg/cu m, skin (1990); Federal Republic of Germany: 15 mg/cu m
(total particulate), short-term exposure values in preparation, Pregnancy group
C, no reason to fear a risk of damage to the developing embryo or fetus when MAK
and BAT values are adhered to (1991); United Kingdom: 10 mg/cu m, skin (1991).
Manufacturing/Use Information:
Major Uses:
Insecticide
INSECTICIDE FOR NON AGRICULTURAL USES-EG, AQUATIC USES, LIVESTOCK, POULTRY,
HOME & GARDEN USES, LAWNS, TURF & ORNAMENTALS, COMMERCIAL, HOUSEHOLD
& INDUSTRIAL USES, COTTON, VEGETABLES, & CITRUS, OTHER FIELD CROPS-EG,
CORN & SORGHUM, DECIDUOUS FRUITS/NUTS & WHEAT, STORAGE BINS &
TRANSPORTATION EQUIPMENT ACARICIDE
... MALATHION has been employed ...
for control of Mediterranean fruit flies and mosquitoes.
MEDICATION
Therap Cat (Vet): Ectoparasiticide
Used to control insects in a wide range of crops, including cotton, pome,
soft, and stone fruit, potatoes, rice and vegetables, major arthropod disease
vectors in public health programs, ectoparasites of cattle, poultry, dogs, cats,
human head and body lice, household insects, and for the protection of stored
grain.
Used as an insecticide to effectively combat the Mediterranean fruit fly.
Manufacturers:
Drexel Chemical Co., 1700 Channel Ave., Memphis, TN 38106-1412, (901)
774-4370; Production site: Cordele, GA 31015
SureCo, Inc., 310 Martin Luther King Dr., P. O. Box 938, Fort Valley, GA
31030, (912) 825-3351 ; Production site: Fort Valley, GA 31030
Methods of Manufacturing:
The feed materials for MALATHION
manufacture are O,O-dimethyl phosphorodithioic acid and diethyl maleate or
fumarate. ... An antipolymerization agent such as hydroquinone may be added to
the reaction mixture to inhibit polymerization of the maleate or fumarate cmpd
under reaction conditions. This reaction is ... carried out at temp within the
range of 20 deg to 150 deg C ... at atmospheric pressure.
Prepn: Johnson et al, J Econ Entomol 45, 279 (1952); Cassaday, US patent
2,578,652 (1951 to Am Cyanamid).
Reaction between O,O-dimethyl dithiophosphate (756-80-9) and diethyl maleate
produce the insecticide MALATHION.
General Manufacturing Information:
THE WHO /WORLD HEALTH ORGANIZATION/ HAS SPECIFIED THAT THE CONTENT OF
ISOMALATHION ... IN WATER DISPERSIBLE POWDERS OF
MALATHION SHALL NOT EXCEED 1.8% OF THE NOMINAL
MALATHION CONTENT AFTER STORAGE OF THE
POWDER FOR SIX DAYS @ 55 DEG C.
/MALATHION IS/ GENERALLY COMPATIBLE
WITH ALL INSECTICIDES & FUNGICIDES IN COMMON USAGE. WHEN MIXED WITH ALKALINE
MATERIALS THE INITIAL KILLS ARE SATISFACTORY BUT RESIDUAL TOXICITY MAY BE
REDUCED.
/Insecticide used for/ ... many insects. ... Particularly where a high degree
of safety to mammals is desired; a tolerance of 135 ppm for forage, grass &
green hay allows MALATHION to be applied
the same day as grazed or harvested. Generally established tolerances are for
residues of 8 ppm MALATHION. There are
specialized uses with higher & lower tolerances. Fyfanon ULV for most major
uses. MALATHION ULV Concentrate for
ultra low vol aerial application to alfalfa, clover, pasture & range
grasses, nonagricultural land, cereal crops, cotton, when it can be diluted with
vegetable oil & applied ULV, safflower, soybeans, sugar beets, corn, beans,
blueberries for the control of many insects at rate of 4 to 16 oz/acre. Cythion,
Fyfanon, Emmaots Extra are low odor products manufactured by patented
procedures, avialable for all uses of
MALATHION ULV concentrates.
Half-life values for ... MALATHION:
apple fruit (2-3 days), lettuce (3-4 days), onions (1-2 days), citrus fruit
(17-32 days), peach fruit (4-6 days), stored wheat (150-190 days). /From table/
Formulations/Preparations:
WP (25%, 50%), EC (5 LB AND 8 LB PER USA GAL); DUSTS (4%, 5%); AEROSOLS (95%)
(9.7 LB/USA GAL) FOR ULTRA LOW VOL USE ...
MALATHION ULTRA LOW VOL CONCN
CONTAINS 91% O,O-DIMETHYL S-(1,2-DICARBETHOXYETHYL) PHOSPHORODITHIDATE ...
Flair (Insecticide/Repellant) /contains:/ Pyrethrins: 0.06%; Piperonyl
butoxide (technical): 0.48%; MALATHION:
0.50%; Carbaryl: 0.50%; Butoxypropylene glycol: 5.0%; 2,3:4,5-Bis(2-butylene)
tetrahydro-2-furaldehyde: 0.14%; Petroleum distillate: 17.85%; Inert
ingredients: 75.47%.
Flea off dip contains: MALATHION ...
53.0%; xylene: 15.0%; inert ingredients: 32.0%.
Kill-A-Mite /contains:/ MALATHION:
15.34%; gamma isomer of benzene hexachloride (lindane): 2.0%; xylene: 12.00%;
mineral seal oil: 57.46%; inert ingredients: 13.20%.
Paladin contains: Pyrethrins: 0.06%; Piperonyl butoxide (technical): 0.48%;
2,3:3,5-bis(2-butylene) tetrahydro-2-furaldehyde: 0.24%;
MALATHION: 0.50%; petroleum distillate: 0.97%;
inert ingredients: 97.76%.
Mixtures include: Malatox P (Siapa),
EC (475 g MALATHION + 196 g
parathion/kg); Saitofos (Siapa), EC (20 g
MALATHION + 270 g methoxychlor + 100 g
parathion/kg). Discontinued mixtures include: Combat Vegetable Insecticide
(Fisons PLC), (MALATHION +
bioresmethrin).
Dust, emulsifiable concentrate, oil solutions, powder, ULV concentrate,
wettable powder
EC; WP; DP; UL. Mixtures (MALATHION
+) fenitrothion; parathion; parathion-methyl; dichlorvos; methoxychlor +
parathion; piperonyl butoxide + pyrethrins
Impurities:
THE FOLLOWING IMPURITIES WERE IDENTIFIED IN ONE SAMPLE: O,O,O-TRIMETHYL
PHOSPHOROTHIOATE; DIETHYL MALEATE; O,O,S-TRIMETHYL PHOSPHORODITHIOATE; DIETHYL
THIOMALATE; DIETHYL 2-METHYLTHIOSUCCINATE; O,O,O,O-TETRAMETHYL
TRITHIOPYROPHOSPHATE; AND AN UNIDENTIFIED ISOMER OF
MALATHION.
Crude or technical grade MALATHION
may contain an active metabolite of
MALATHION, malaoxon, which may account for the
increased toxicity of impure MALATHION
preparations compared with highly purified preparations.
Impurities present in technical grade
MALATHION were O,S,S-trimethyl
phosphorodithioate, S-methyl isomer of
MALATHION (iso-
MALATHION), & O,O,S-trimethyl
phosphorothioate.
The analysis of technical organophosphorus insecticides by (31)P nuclear
magnetic resonance showed the major known toxic contaminants to be simple
trialkyl phosphorothio- and -dithioic acid esters and the S-alkyl insecticide
isomers. Small amt of the bis derivatives & the dithiopyrophosphate were
also detected. These contaminants included both byproducts from the synthesis as
well as degradation products. This procedure was used to analyze the following
technical grade products: ronnel, sulfotepp, methyl parathion, dimethoate,
MALATHION, methidathion, ethion, phosalone,
& fenitrothion.
Impurities of MALATHION include
malaoxon, isomalathion, O,O,S-trimethylphosphorodithioate, O,O,O-trimethyl
phosphorothioate, O,O,S-trimethyl phosphorothioate, and diethyl fumarate,
diethyl hydroxysuccinate, ethyl nitrite, diethyl mercaptosuccinate, diethyl
methylthiosuccinate.
Consumption Patterns:
INSECTICIDE FOR AQUATIC USES, 15%; LIVESTOCK/POULTRY, 7%; OTHER NON
AGRICULTURAL USES-EG, HOME & GARDEN, LAWN, TURF, ORNAMENTAL, COMMERCIAL,
HOUSEHOLD & INDUSTRIAL USES, 33%; COTTON, 14%; VEGETABLES, 10%; ALFALFA, 4%;
TOBACCO, 3%; CITRUS, 1%; OTHER FIELD CROPS-EG, CORN, DECIDUOUS FRUITS/NUTS,
SORGHUM & WHEAT, 11% (1982)
U. S. Production:
(1978) 6.86X10+9 G (CONSUMPTION)
(1982) 6.13X10+9 G (CONSUMPTION)
U. S. Imports:
(1977) 2.93X10+6 G (PRINCPL CUSTMS DISTS)
(1982) 6.50X10+7 G (PRINCPL CUSTMS DISTS)
U. S. Exports:
(1978) 5X10+9 G (EST)
Laboratory Methods:
Clinical Laboratory Methods:
MATRIX: HUMAN TISSUE & EXCRETA; PROCEDURE: GAS CHROMATOGRAPHY/FLAME
PHOTOMETRIC DETECTION. LIMIT OF DETECTION: LESS THAN 0.1 MG/KG. MATRIX: HUMAN
TISSUE; PROCEDURE: GAS CHROMATOGRAPHY/ELECTRON CAPTURE DETECTION; LIMIT OF
DETECTION NOT GIVEN. /FROM TABLE/
Simultaneous determination of organophosphorus pesticides /including
MALATHION/ in forensic chemistry by gas-liquid
chromatography with a hydrogen-flame ionization detector.
A rapid and sensitive method for the determination of
MALATHION and malaoxon in milk and plasma was
developed. Following a simple extraction and cleanup procedure,
MALATHION and malaoxon were analyzed by gas
liquid chromatography (GLC) equipped with a phosphorus specific detector and a
glass column packed with 3% SE 30 on 80 100 mesh Chromosorb W AW DMCS. For
quantification, the internal standard technique was used with bromophos as the
internal standard. All compounds eluted within 5 min. Confirmation of the
identities was obtained by gas liquid chromatography mass spectrometry with a
flexible quartz capillary column coated with SE 54. Recoveries ranged from 85 to
98%. The detection limits of MALATHION
and malaoxon in milk were 0.002 and 0.02 ppm, respectively, and in plasma 0.004
and 0.04 ppm, respectively.
Analytic Laboratory Methods:
AOAC Method 968.24. Organophosphorus Pesticide Residues sweep codistillation
methods.
AOAC Method 970.53. Organophosphorus pesticide residues single sweep
oscillographic polarographic confirmatory method.
AOAC Method number 979.05. MALATHION
in pesticide formulations gas chromatographic method.
AOAC Method 957.15. MALATHION
pesticide residues colorimetric method.
NIOSH Method 5600. Organophosphorus pesticides. GC, flame photometric
detection (FPD).
Determination of some organophosphorus insecticides /including
MALATHION/ by flow injection with a molecular
emission cavity detector.
MATRIX: WATER. EXTRACT WITH DICHLOROMETHANE; PROCEDURE: GC/FLAME IONIZATION
DETECTION. LIMIT OF DETECTION 4 UG/KG. MATRIX: SEDIMENT; PROCEDURE: ELUTE ON
CHROMATOGRAPHIC COLUMN USING ACETONE/HEXANE, EXTRACT & CONCENTRATE, ASSAY
PROCEDURE GC/ELECTRON CAPTURE DETECTION. LIMIT OF DETECTION NOT GIVEN. /FROM
TABLE/
MALATHION & MALAOXON ARE
EXTRACTABLE FROM AQ SUSPENSIONS BY BENZENE ISOBUTANOL. ALIQUOTS OF THE EXTRACT
ARE EVAPORATED AT 110-120 DEG C, THE RESIDUE IS DISSOLVED IN METHANOL, & THE
TOTAL FERRIC HYDROXAMATE COLOR IS DETERMINED. EXTRACTION OF A SECOND ALIQUOT
WITH CYCLOHEXANE REMOVES MALATHION &
SOME MALAOXON. MALAOXON IS SELECTIVELY PARTITIONED FROM CYCLOHEXANE INTO
ALKALINE HYDROXYAMINE, LEAVING MALATHION
IN THE CYCLOHEXANE PHASE. AFTER EVAPORATION, THE AMT OF
MALATHION CAN BE EST BY THE FERRIC HYDROXAMATE
METHOD. THE DIFFERENCE IN THE COLOR FOR THE BENZENE ISOBUTANOL EXTRACT & THE
CYCLOHEXANE EXTRACT REPRESENTS THAT DUE TO MALAOXON; THE AMT OF MALAOXON MAY BE
CALCULATED FROM A STD CURVE. THE METHOD, SENSITIVE TO ABOUT 0.2 UMOLE MALAOXON,
IS USEFUL FOR MONITORING THE LAB PREPN OF MALAOXON FROM
MALATHION.
A METHOD FOR MONITORING PRESENCE OF
MALATHION & ITS METABOLITES IN AQUATIC
ENVIRONMENT IS DESCRIBED. MALATHION,
MALAOXON, MALATHION MONOACID, &
DIACID WERE DETERMINED IN FISH, OYSTER, & SHRIMP TISSUES BY GAS LIQUID
CHROMATOGRAPHY USING PHENTHOATE & PHENTHOATE ACID AS INTERNAL STD. GLC
ANALYSES WERE PERFORMED WITHOUT CLEANUP, USING A FLAME PHOTOMETRIC DETECTOR
OPERATING IN THE PHOSPHORUS MODE.
MALATHION & other organophosphate
agricultural chemicals were analyzed by high performance liquid chromatography
with on line photolysis, followed by electrochemical detection using single or
dual electrode approaches for the species generated.
SOME PROCEDURES FOR THE ENZYMATIC DETECTION OF ORGANOPHOSPHORUS PESTICIDES,
WHICH HAVE GIVEN REPRODUCIBLE RESULTS ON A ROUTINE SCALE, ARE DESCRIBED. THE
METHODS HAVE SUCCESSFULLY BEEN APPLIED TO THE DETECTION OF
MALATHION IN FRUIT OR VEGETABLE EXTRACTS. THE
METHODS INVOLE INITIAL THIN LAYER CHROMATOGRAPHY OF THE SAMPLE EXTRACTS, THEN
OXIDATION WITH BROMINE TO CONVERT THE THIOPHOSPHATES TO ACTIVE ENZYME
INHIBITORS. THE PLATES ARE THEN SPRAYED WITH ESTERASES FROM A SUITABLE SOURCE
& FURTHER SPRAYED WITH A SUITABLE SUBSTRATE WHICH WILL CAUSE THE BACKGROUND
TO BECOME COLORED FOLLOWING HYDROLYSIS. ALTERNATIVELY, THE ENZYME & AN ACID
BASE INDICATOR ARE INCORPORATED INTO AN AGAR GEL & THE DEVELOPED TLC PLATE
PRESSED AGAINST THIS FOR 1 HR AFTER ACTIVATION WITH BROMINE, THEN THE AGAR IS
SPRAYED WITH ACETYLCHOLINE, WHICH RELEASES ACETIC ACID ON HYDROLYSIS. THE LIMIT
OF DETECTION ACHIEVED FOR MOST SUBSTANCES IS 1 TO 10 NG. THE METHOD CAN BE USED
AS A SCREENING PROCEDURE FOR ROUTINE ANALYSES.
Residues determined by glc or by tlc or paper chromatography, or by single
sweep oscillographic polarography
EAD Method 1657. The Determination of Organo-Phosphorus Pesticides in
Municipal and Industrial Wastewater by Gas Chromatography.
EMSLC Method 614. The Determination of Organophosphorus Pesticides in
Municipal and Industrial Wastewater by Gas Chromatography using
Phosphorus-specific Flame Photometric Detection.
HERL Method HERL_022. The Sampling and Analysis of Water For Pesticides.
EPA Method 8141. Determination of Organophosphorus Compounds by Gas
Chromatography Using the Capillary Column Technique.
Determination of Organophosphorus Compounds by Gas Chromatography Using the
Capillary Column Technique.
Determination Semivolatile Organic compounds by Gas Chromatography/Mass
Spectrometry (GC/MS): Capillary Column Technique.
Semivolatile Organic Compounds by Gas Chromatography/ Mass Spectrometry
(GC/MS): Capillary Column Technique.
AOB Method P-006-1. Organophosphorus Pesticides in Soil by FASP Method
F050.003.
EPA PMD-MAL-LC. Determination of
MALATHION by High Performance Liquid
Chromatography.
EPA PMD-MAL. Determination of
MALATHION by IR Spectroscopy.
EPA PMD-TLC. Detection of Organothiophosphates by Thin-Layer Chromatography.
EPA PMD-TLC. Thin-Layer Chromatography Systems for Identification of
Pesticides - System 2.
FDA Method 211.1. Organochlorine Residues (Nonionic) General Method for Fatty
Foods Including Extraction of Fat, Acetonitrile Partition, Florisil Column
Cleanup, Partition Chromatography Cleanup, and Supplemental Cleanup .
Sampling Procedures:
NIOSH 5012: Analyte: MALATHION;
Matrix: air; Sampler: Filter (glass fiber); Flow rate: 1 to 2 l/min; Vol: min:
15 l, max: 130 l; Stability: at least 7 days @ 25 deg C
Special References:
Special Reports:
MULLA MS, MIAN LS; RESIDUE REV 78: 101-35 (1981). INFORMATION ON THE IMPACT
OF MALATHION ON NON TARGET FLORA AND
FAUNA IN AQUATIC ECOSYSTEMS AND THEIR PERSISTENCE & DISTRIBUTION IN AQUATIC
HABITATS IS COLLECTED AND INTERPRETED.
NIOSH; Criteria Document: MALATHION
(1976) DHEW Pub. NIOSH 76-205
Nicolson RS; J Assoc Public Anal 24 (1): 27-39 (1986). Association of Public
Analysts Survey of Pesticide Residues in Food: 1984.
Willems JL et al; Naunyn Schmiedemberg's Arch Pharmacol 330 (Suppl) (1985)
Fate of organophosphorus compounds in animals and man.
MARX JL; SCIENCE 213 (4507): 526-7 (1981). CONTROVERSY CONCERNING THE USE OF
MALATHION IN CALIFORNIA FOR CONTROL OF
THE MEDITERRANEAN FRUIT FLY (MEDFLY) IS DISCUSSED.
Anonymous ; Pesticide Fact Sheet #152:
MALATHION Govt Reports Announcements &
Index (GRA & I) Issue 14 (1988).
DHEW/NCI; Bioassay of MALATHION for
Possible Carcinogenicity (1978) Technical Rpt Series No. 24 DHEW Pub No. (NIH)
78-824
Synonyms and Identifiers:
Related HSDB Records:
Synonyms:
AI3-17034 **PEER REVIEWED**
American Cyanamid 4,049 **PEER REVIEWED**
S-(1,2-Bis(aethoxy-carbonyl)-aethyl)-O,O-dimethyl-dithiophosphat (German)
**PEER REVIEWED**
S-(1,2-bis(carbethoxy)ethyl) O,O-dimethyl dithiophosphate **PEER
REVIEWED**
S-(1,2-bis(ethoxy-carbonyl)-ethyl)-O,O-dimethyl-dithiofosfaat (Dutch)
**PEER REVIEWED**
S-(1,2-bis(ethoxycarbonyl)ethyl) O,O-dimethyl phosphorodithioate
**PEER REVIEWED**
S-1,2-BIS(ETHOXYCARBONYL)ETHYL-O,O-DIMETHYL THIOPHOSPHATE **PEER
REVIEWED**
S-(1,2-bis(etossi-carbonil)-etil)-O,O-dimetil-ditiofosfato (Italian)
**PEER REVIEWED**
BUTANEDIOIC ACID, ((DIMETHOXYPHOSPHINOTHIOYL)THIO)-, DIETHYL ESTER
**PEER REVIEWED**
Camathion **PEER REVIEWED**
Carbetovur **PEER REVIEWED**
Carbetox **PEER REVIEWED**
Carbofos **PEER REVIEWED**
Carbophos **PEER REVIEWED**
Caswell No 535 **PEER REVIEWED**
Chemathion **PEER REVIEWED**
Cimexan **PEER REVIEWED**
Compound 4049 **PEER REVIEWED**
Cythion **PEER REVIEWED**
S-(1,2-dicarbethoxyethyl) O,O-dimethylphosphorodithioate **PEER
REVIEWED**
DICARBOETHOXYETHYL O,O-DIMETHYL PHOSPHORODITHIOATE **PEER
REVIEWED**
S-(1,2-DI(ETHOXYCARBONYL)ETHYL DIMETHYL PHOSPHOROTHIOLOTHIONATE
**PEER REVIEWED**
Diethyl(dimethoxythiophosphorylthio)succinate **PEER
REVIEWED**
DIETHYL MERCAPTOSUCCINATE, O,O-DIMETHYL DITHIOPHOSPHATE, S-ESTER
**PEER REVIEWED**
DIETHYL MERCAPTOSUCCINATE, O,O-DIMETHYL PHOSPHORODITHIOATE **PEER
REVIEWED**
DIETHYL MERCAPTOSUCCINATE, O,O-DIMETHYL THIOPHOSPHATE **PEER
REVIEWED**
((Dimethoxyphosphinothioyl)thio)butanedioic acid diethyl ester
**PEER REVIEWED**
O,O-Dimethyl-S-1,2-(dicarbaethoxyaethyl)-dithiophosphat (German)
**PEER REVIEWED**
O,O-DIMETHYL S-(1,2-DICARBETHOXYETHYL) DITHIOPHOSPHATE **PEER
REVIEWED**
O,O-DIMETHYL S-(1,2-DICARBETHOXYETHYL)PHOSPHORODITHIOATE **PEER
REVIEWED**
O,O-DIMETHYL S-1,2-DI(ETHOXYCARBAMYL)ETHYL PHOSPHORODITHIOATE
**PEER REVIEWED**
O,O-dimethyl-S-1,2-dikarbetoxylethylditiofosfat (Czech) **PEER
REVIEWED**
O,O-DIMETHYLDITHIOPHOSPHATE DIETHYLMERCAPTOSUCCINATE **PEER
REVIEWED**
O,O-dimethyl dithiophosphate of diethyl mercaptosuccinate **PEER
REVIEWED**
Dithiophosphate de O,O-dimethyle et de S-(1,2-dicarboethoxyethyle) (French)
**PEER REVIEWED**
Dorthion **PEER REVIEWED**
Emmatos extra **PEER REVIEWED**
ENT 17,034 **PEER REVIEWED**
EPA Pesticide Chemical Code 057701 **PEER
REVIEWED**
Ethiolacar **PEER REVIEWED**
Etiol **PEER REVIEWED**
Extermathion **PEER REVIEWED**
Flair **PEER REVIEWED**
Fog 3 **PEER REVIEWED**
Forthion **PEER REVIEWED**
Fosfothion **PEER REVIEWED**
Fosfotion **PEER REVIEWED**
Fyfanon **PEER REVIEWED**
Hilthion **PEER REVIEWED**
IFO 13140 **PEER REVIEWED**
Insecticide No 4049 **PEER REVIEWED**
Karbofos **PEER REVIEWED**
Kill-A-Mite **PEER REVIEWED**
Kop-thion **PEER REVIEWED**
Kypfos **PEER REVIEWED**
Malacide **PEER REVIEWED**
Malafor **PEER REVIEWED**
Malagran **PEER REVIEWED**
Malakill **PEER
REVIEWED**
Malamar 50 **PEER REVIEWED**
Malasol **PEER
REVIEWED**
Malaspray **PEER
REVIEWED**
Malataf **PEER REVIEWED**
Malathiazol **PEER REVIEWED**
Ortho malathion **PEER
REVIEWED**
MALATHION E50 **PEER
REVIEWED**
MALATHION LV concentrate
**PEER REVIEWED**
Malathon **PEER
REVIEWED**
Malathyl **PEER REVIEWED**
Malation (Polish) **PEER
REVIEWED**
Malatol **PEER
REVIEWED**
Malatox **PEER
REVIEWED**
Malmed **PEER
REVIEWED**
Malphos **PEER
REVIEWED**
MERCAPTOSUCCINIC ACID DIETHYL ESTER **PEER
REVIEWED**
MERCAPTOTHION **PEER
REVIEWED**
Mercaptotion (Spanish)
**PEER REVIEWED**
Moscarda **PEER
REVIEWED**
NCI-C00215 **PEER REVIEWED**
Oleophosphothion **PEER
REVIEWED**
Paladin **PEER REVIEWED**
Phosphothion **PEER
REVIEWED**
Prioderm **PEER
REVIEWED**
Sadofos **PEER
REVIEWED**
Sadophos **PEER
REVIEWED**
SF 60 **PEER REVIEWED**
Siptox I **PEER
REVIEWED**
SUCCINIC ACID, MERCAPTO-, DIETHYL ESTER, S-ESTER WITH O,O-DIMETHYL
PHOSPHORODITHIOATE **PEER REVIEWED**
Sumitox **PEER
REVIEWED**
Tak **PEER REVIEWED**
TM-4049 **PEER REVIEWED**
Vetiol **PEER REVIEWED**
XMC **PEER REVIEWED**
Zithiol **PEER REVIEWED**
Formulations/Preparations:
WP (25%, 50%), EC (5 LB AND 8 LB PER USA GAL); DUSTS (4%, 5%); AEROSOLS (95%)
(9.7 LB/USA GAL) FOR ULTRA LOW VOL USE ...
MALATHION ULTRA LOW VOL CONCN
CONTAINS 91% O,O-DIMETHYL S-(1,2-DICARBETHOXYETHYL) PHOSPHORODITHIDATE ...
Flair (Insecticide/Repellant) /contains:/ Pyrethrins: 0.06%; Piperonyl
butoxide (technical): 0.48%; MALATHION:
0.50%; Carbaryl: 0.50%; Butoxypropylene glycol: 5.0%; 2,3:4,5-Bis(2-butylene)
tetrahydro-2-furaldehyde: 0.14%; Petroleum distillate: 17.85%; Inert
ingredients: 75.47%.
Flea off dip contains: MALATHION ...
53.0%; xylene: 15.0%; inert ingredients: 32.0%.
Kill-A-Mite /contains:/ MALATHION:
15.34%; gamma isomer of benzene hexachloride (lindane): 2.0%; xylene: 12.00%;
mineral seal oil: 57.46%; inert ingredients: 13.20%.
Paladin contains: Pyrethrins: 0.06%; Piperonyl butoxide (technical): 0.48%;
2,3:3,5-bis(2-butylene) tetrahydro-2-furaldehyde: 0.24%;
MALATHION: 0.50%; petroleum distillate: 0.97%;
inert ingredients: 97.76%.
Mixtures include: Malatox P (Siapa),
EC (475 g MALATHION + 196 g
parathion/kg); Saitofos (Siapa), EC (20 g
MALATHION + 270 g methoxychlor + 100 g
parathion/kg). Discontinued mixtures include: Combat Vegetable Insecticide
(Fisons PLC), (MALATHION +
bioresmethrin).
Dust, emulsifiable concentrate, oil solutions, powder, ULV concentrate,
wettable powder
EC; WP; DP; UL. Mixtures (MALATHION
+) fenitrothion; parathion; parathion-methyl; dichlorvos; methoxychlor +
parathion; piperonyl butoxide + pyrethrins
Shipping Name/ Number DOT/UN/NA/IMO:
NA 2783; MALATHION
Standard Transportation Number:
49 411 56; MALATHION
RTECS Number:
NIOSH/WM8400000
Administrative Information:
Hazardous Substances Databank Number: 665
Last Revision Date: 20021108
Last Review Date: Reviewed by SRP on 9/23/1999
Update History:
Complete Update on 11/08/2002, 1 field added/edited/deleted.
Complete
Update on 10/31/2002, 1 field added/edited/deleted.
Complete Update on
07/22/2002, 2 fields added/edited/deleted.
Complete Update on 01/14/2002, 1
field added/edited/deleted.
Complete Update on 08/09/2001, 1 field
added/edited/deleted.
Complete Update on 05/16/2001, 1 field
added/edited/deleted.
Complete Update on 03/28/2000, 1 field
added/edited/deleted.
Complete Update on 03/13/2000, 1 field
added/edited/deleted.
Complete Update on 03/02/2000, 71 fields
added/edited/deleted.
Field Update on 02/09/2000, 1 field
added/edited/deleted.
Field Update on 02/08/2000, 1 field
added/edited/deleted.
Field Update on 02/02/2000, 1 field
added/edited/deleted.
Field Update on 12/27/1999, 1 field
added/edited/deleted.
Field Update on 11/18/1999, 1 field
added/edited/deleted.
Field Update on 09/21/1999, 1 field
added/edited/deleted.
Field Update on 08/26/1999, 1 field
added/edited/deleted.
Complete Update on 03/19/1999, 1 field
added/edited/deleted.
Complete Update on 01/27/1999, 1 field
added/edited/deleted.
Complete Update on 11/12/1998, 3 fields
added/edited/deleted.
Field Update on 10/29/1998, 1 field
added/edited/deleted.
Complete Update on 06/02/1998, 1 field
added/edited/deleted.
Complete Update on 03/27/1998, 10 fields
added/edited/deleted.
Field Update on 10/17/1997, 1 field
added/edited/deleted.
Field Update on 05/08/1997, 1 field
added/edited/deleted.
Field Update on 05/01/1997, 2 fields
added/edited/deleted.
Complete Update on 02/27/1997, 1 field
added/edited/deleted.
Complete Update on 10/12/1996, 1 field
added/edited/deleted.
Complete Update on 09/12/1996, 1 field
added/edited/deleted.
Complete Update on 06/03/1996, 1 field
added/edited/deleted.
Complete Update on 03/01/1996, 7 fields
added/edited/deleted.
Complete Update on 01/19/1996, 1 field
added/edited/deleted.
Complete Update on 11/10/1995, 1 field
added/edited/deleted.
Complete Update on 01/23/1995, 1 field
added/edited/deleted.
Complete Update on 12/21/1994, 1 field
added/edited/deleted.
Complete Update on 07/28/1994, 1 field
added/edited/deleted.
Complete Update on 05/05/1994, 1 field
added/edited/deleted.
Complete Update on 03/25/1994, 1 field
added/edited/deleted.
Complete Update on 09/08/1993, 1 field
added/edited/deleted.
Complete Update on 08/07/1993, 1 field
added/edited/deleted.
Field update on 12/14/1992, 1 field
added/edited/deleted.
Complete Update on 09/03/1992, 1 field
added/edited/deleted.
Complete Update on 04/27/1992, 1 field
added/edited/deleted.
Complete Update on 01/23/1992, 1 field
added/edited/deleted.
Complete Update on 09/26/1991, 1 field
added/edited/deleted.
Field update on 05/18/1990, 1 field
added/edited/deleted.
Field Update on 03/06/1990, 1 field
added/edited/deleted.
Field Update on 01/15/1990, 1 field
added/edited/deleted.
Complete Update on 01/11/1990, 72 fields
added/edited/deleted.
Complete Update on 05/05/1989, 50 fields
added/edited/deleted.
Complete Update on 04/03/1989, 87 fields
added/edited/deleted.
Field Update on 03/01/1989, 1 field
added/edited/deleted.
Complete Update on 03/05/1988, 91 fields
added/edited/deleted.
Complete Update on 02/15/1985
Record Length: 331441
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