Human Health Effects:
Toxicity Summary:
Food represents the major source of carbaryl intake for the general population.
... The general population can be exposed to carbaryl during pest control operations in
both the home & recreation areas. Workers can be exposed to carbaryl during its manufacture, formulation,
packing, transportation, storage, & during & after application. ...
Significant dermal exposure may occur in industrial & agricultural workers
if protective measures are inadequate. Carbaryl is rapidly absorbed in the lungs
& digestive tract. ... The principal metabolic pathways of carbaryl are ring hydroxylation &
hydrolysis. As a result, numerous metabolites are formed & subjected to
conjugation with the formation of water-soluble sulfates, glucuronides, &
mercapturates, excreted in the urine. Hydrolysis results in the formation of
1-naphthol, carbon dioxide & methylamine. Hydroxylation produces
4-hydroxycarbaryl, 5-hydroxycarbaryl, N-hydroxymethylcarbaryl,
5-6-dihydro-5-6-dihydroxycarbaryl & 1,4-naphthalendiol. The principal
metabolite in humans is 1-naphthol. Under normal exposure conditions, the
accumulation of carbaryl in animals is
unlikely. Carbaryl is excreted primarily
via the urine, since the product of its hydrolysis, 1-naphthol, is mainly
detoxified to water-soluble conjugates. Enterohepatic cycling of carbaryl metabolites is also considerable,
especially after oral administration. ... Carbaryl metabolites are also present in a
small percentage of the absorbed doses in saliva & milk. ... The acute
toxicity for birds is low. ... Carbaryl
is very toxic for honey-bees & earthworms. ... The acute toxicity ... varies
considerably according to species, formulation & vehicle. ... Carbaryl is a mild eye irritant & has
little or no sensitizing potential. ... Carbaryl has a low cumulative potential. Carbaryl has been shown to affect mammalian
reproduction & perinatal development adversely in a number of species.
Effects on reproduction include impairment of fertility, decreased litter size,
& reduced postnatal viability. Developmental toxicity is seen as increased
in utero death, reduced fetal weight, & the occurrence of malformation. With
the exception of a small number of studies, all adverse reproductive &
developmental effects were noted only at doses that caused overt maternal
toxicity, &, in a number of cases, the maternal animal was more sensitive to
carbaryl than the conceptus. The
maternal toxic effects included lethality, decreased growth, & dystocia.
...The available evidence indicates that carbaryl does not have any DNA-damaging
properties. ... Negative results were obtained in tests for gene mutations in a
large number of bacterial assays ... The available database does not support the
presumption that carbaryl poses a risk
of inducing genetic changes in ... humans. Carbaryl has been studied for its carcinogenic
potential in numerous studies on rats & mice. The results of most of these
studies were negative ... The effects of carbaryl on the nervous system are primarily
related to cholinesterase inhibition & are usually transitory. ... Carbaryl has been reported to affect
coagulation ... Carbaryl binds free
blood amino acids. Disturbances have been reported in the carbohydrate
metabolism & protein synthesis & detoxification function of the liver in
mammals. Carbaryl is a weak inducer of
hepatic microsomal drug-metabolizing activity. ... Carbaryl has been reported to incr the
gonadotropic function of the hypophysis of rats. Carbaryl is an inhibitor of cholinesterase
activity. This effect is dose-related & quickly reversible. ... All
identified metabolites of carbaryl are
appreciably less active cholinesterase inhibitors than carbaryl itself. Carbaryl is easily absorbed /in humans/
through inhalation & via the oral route & less readily by the dermal
route. Since the inhibition of cholinesterase is the principal mechanism of
carbaryl action, the clinical picture of
intoxication is dominated by ... symptoms, such as: increased bronchial
secretion, excessive sweating, salivation, & lacrimation; pinpoint pupils,
bronchoconstriction, abdominal cramps (vomiting & diarrhea); bradycardia;
fasciculation of fine muscles (in severe cases, diaphragm & respiratory
muscles also involved); tachycardia; headache, dizziness, anxiety, mental
confusion, convulsions, & coma; & depression of the respiratory center.
Signs of intoxication develop quickly after absorption & disappear rapidly
after exposure ends.... In cases of occupational overexposure to carbaryl, mild symptoms are observed long
before a dangerous dose is absorbed, which is why severe cases of occupational
intoxication with carbaryl are rare.
During agricultural application, dermal exposure may play an important role. ...
The appearance of a skin rash after accidental splashing with carbaryl formulations has been described. ...
The most sensitive biological indicator of carbaryl exposure is the appearance of
1-naphthol in the urine & the decr of cholinesterase activity in the blood.
... The hazards of carbaryl for human
beings are judged to be low, because of its low vapor pressure, rapid
degradation , rapid spontaneous recovery of inhibited cholinesterase, & the
fact that symptoms usually appear well before a dangerous dose has accumulated
in the body. ...
Evidence for Carcinogenicity:
No data are available in humans. Inadequate evidence of carcinogenicity in
animals. OVERALL EVALUATION: Group 3: The agent is not classifiable as to its
carcinogenicity to humans.
A4; Not classifiable as a human carcinogen.
Human Toxicity Excerpts:
MALE VOLUNTEERS WHO CONSUMED DOSES UP TO 0.13 MG/KG/DAY FOR 6 WK HAD NO
SUBJECTIVE EFFECTS THAT COULD BE RELATED TO CARBARYL, ALTHOUGH THEY EXHIBITED SLIGHT,
TRANSIENT DECR IN THEIR ABILITY TO REABSORB AMINO ACIDS.
INHIBITION OF MITOSIS & SPINDLE FIBER FORMATION HAS ... BEEN REPORTED IN
CULTURED HUMAN EMBRYONIC FIBROBLASTS. AFTER TREATMENT WITH 20-80 UG/ML OF A
TECHNICAL PRODUCT CONTAINING 84% CARBARYL.
SYMPTOMATOLOGY: Except for diminished intensity and duration, particularly of
the central nervous signs and symptoms, carbamate poisoning resembles parathion
intoxication in its clinical manifestations. 1. Nausea, vomiting, abdominal
cramps, diarrhea, and excessive salivation (sialorrhea) and sweating. 2.
Lassitude and weakness. 3. Rhinorrhea and a sensation of tightness in the chest
may occur with respiratory exposures. 4. Blurring or dimness of vision, miosis
(with fixed pinpoint pupils), tearing, ciliary muscle spasm, loss of
accommodation, and ocular pain. None of these eye signs, however, is dependable
for diagnosis. Mydriasis may be seen secondary to sympathoadrenal discharge. 5.
Loss of muscle coordination, slurring of speech, fasciculations and twitching of
muscles. 6. Difficulty in breathing, excessive secretions of saliva and of
respiratory tract mucus, oronasal frothing, cyanosis, pulmonary rales and
rhonchi, and hypertension (presumably due to asphyxia). 7. Random jerky
movements, incontinence, convulsions, and coma. 8. Death primarily due to
respiratory arrest of central origin, paralysis of the respiratory muscles,
intense bronchoconstriction, or all three.
... Epidemiological studies have not demonstrated delayed neurotoxic effects,
dysmorphic sperm, or viral enhancement in humans exposed to carbaryl.
Male human volunteers were given daily po doses of either 0.06 or 0.12 mg/kg
of carbaryl. After six weeks of
exposure, no EEG changes were found attributable to carbaryl exposure.
The observation of neurotoxicity in a subject with long-term exposure to high
levels of carbaryl has prompted the
review of the potential for carbaryl to
cause toxicity. The information available about carbaryl's disposition in humans is inadequate
to interpret the relevance of animal studies to humans. Published information on
the effects of long-term exposure to carbaryl in humans is limited and has not
identified any adverse effects. It is concluded that not enough information is
available to exclude the possibility that sustained high levels of exposure to
carbaryl could be associated with
neurotoxic or myotoxic responses in humans.
Carbaryl, a widely used insecticide,
is reputed to have a wide safety margin. It can induce acute cholinesterase
poisoning, which is rapidly reversible on discontinuation of exposure. Long-term
sequelae from long-term exposure have not previously been described in humans.
This report describes the experience of a 75-year-old man who had long-term
excessive exposure to carbaryl and in
whom a debilitating syndrome, including headaches, memory loss, proximal muscle
weakness, muscle fasciculation, muscle cramps, and anorexia with marked weight
loss developed. At the time of diagnosis, serum pseudocholinesterase levels were
low, and his major symptoms resolved on termination of exposure. Late clinical
features were sleep apnea and progressive development of a periheral neuropathy.
The difficulty in diagnosing the cause of a group of relatively nonspecific
symptoms raises the question of whether chronic carbaryl neurotoxicity might be occurring more
frequently than previously suspected.
A SINGLE ORAL DOSE OF 250 MG (ABOUT 2.8 MG/KG) CARBARYL PRODUCED MODERATE ILLNESS IN A MAN.
Carbaryl ... appears to have caused
no eye disturbance except in one case of suicidal poisoning in which disturbance
of vision was complained of but not explained. ... Splash contact of an
insecticide liquid containing both carbaryl & dimethoate in one patient on
two different occasions caused transient injury of the corneal epithelium &
much swelling of the lids, but recovery was rapid & complete. This suggests
that carbaryl is not particularly
dangerous to the eye.
A patient ingested 21 g (500 mg/kg) of carbaryl (1-naphthyl N-methylcarbamate. After
he recovered from acute cholinergic toxicity, acute weakness of arms and legs
was accompanied by electrophysiologic findings consistent with axonal peripheral
neuropathy. Recovery began at 1 week and continued for 9 months. A similar
delayed neuropathy has been described with organophosphates.
Carbamate insecticides and herbicides were tested for their ability to affect
human blood platelet aggregation and arachidonic acid metabolism in platelets.
The herbicides of the carbamate type have no, or only little, influence up to a
concentration of 100 uM; the carbamate insecticides, however, inhibit both
aggregation and arachidonic acid metabolism in a dose- and time-dependent
manner. Carbaryl, the most effective
compound, inhibits platelet aggregation and cyclooxygenase activity completely
at 10 uM. The liberation of arachidonic acid from phospholipids and the
lipoxygenase pathway are not affected, whereas the products of the
cyclooxygenase pathway are drastically decreased. By using (14)C-carbaryl labelled in the carbamyl or in the
ring moiety, it was shown that the carbamyl residue binds covalently to platelet
proteins. In contrast with acetylsalicylic acid, which acetylates only one
protein, carbaryl carbamylates a
multitude of platelet proteins. One of the carbamylated proteins was found to be
the platelet cyclooxygenase, indicating that carbaryl resembles in this respect
acetylsalicylic acid, which is known to inhibit this enzyme specifically by
acetylation.
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/
Skin, Eye and Respiratory Irritations:
Irritating to skin & eyes.
Medical Surveillance:
Initial Medical Examination: A complete history and physical examination: The
purpose is to detect pre existing conditions that might place the exposed
employee at increased risk, and to establish a baseline for future health
monitoring. Examination of the respiratory system, cardiovascular system, and
central nervous system should be stressed. The skin should be examined for
evidence of chronic disorders. Urinalysis: Carbaryl may cause kidney damage. A urinalysis
should be performed to include, at a minimum, specific gravity, albumin,
glucose, and a microscopic /examination/ of centrifuged sediment. Medical
warning: Exposure should be minimized during pregnancy. Periodic Medical
Examination: The aforementioned medical examinations should be repeated on an
annual basis.
Intact carbaryl is not routinely
measured in human blood. ... Exposure to anticholinesterase agents such as carbaryl is frequently monitored by
determination of blood cholinesterase activity. A preexposure cholinesterase
level should be obtained for each employee so that the postexposure level may be
expressed as a percentage of that subject's normal cholinesterase activity. A
postexposure blood cholinesterase level that is less than 70% of normal is
considered indicative of excessive exposure to carbaryl.
Carbaryl is known to be metabolized
by N-demethylation, ring hydroxylation, hydrolysis & conjugation. The
hydrolysis pathway results in the urinary excretion of free & conjugated
1-naphthol, which accounts for over 20% of an ingested dose & which may be
measured as an index of exposure to the chemical. Another 4% of a dose is
excreted as conjugated p-hydroxycarbamyl. Urine concn of 1-naphthol in unexposed
subjects avg less than 0.01 mg/l & do not exceed 0.23 mg/l. Exposed but
asymptomatic workers exhibited 1-naphthol urine concn of less than 0.1 to more
than 42 mg/l; air concn of carbaryl
during these exposures ranged from 0.2 to 31 mg/cu m. In another study of
formulating plant workers, asymptomatic individuals excreted 1-naphthol in urine
at concn of 0.2 to 65 mg/l, avg 8.9 mg/l. ... Although standards have not been
developed for carbaryl metabolites in
urine, it is probable that urinary 1-naphthol concentrations in excess of 4 mg/l
represent significant exposure to carbaryl.
Whole Blood Reference Ranges: Normal - not established; 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. /Carbamate pesticides/
Respiratoty Symptom Questionnaires: Questionnaires have been published by the
American Thoracic Society (ATS) and the British Medical Research Council. These
questionnaires have been found to be usead in identiEcation of people with
chronic bronchitis, however certain pulmonary function tests such as FEV1 (see
pulmonary function test section) have been found to be better predictors of
chronic airflow obstruction. /Carbamate pesticides/
Chest Radiography: This test is widely used for assessing pulmonary disease.
Chest radiographs have 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. /Carbamate 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. /Carbamate 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. /Carbamate pesticides/
Evaluation of Peripheral Neuropathy: Nerve conduction study; Electromyography
(EMG); Quantitative sensory testing; Thermography. /Carbamate 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.
/Carbamate pesticides/
Evaluation of Cranial Neuropathies: Evaluation of cranial nerve damage, as
evidenced by symptoms such as loss of balance, visual function, smell, taste,
orsensation on the face, can be accompolished through a physical examination
focusing on tests such as: Smell assessment ... Vision assessment ... Facial and
Trigeminal Nerve assessment ... Vestibular assessment .. Hearing assessment.
/Carbamate pesticides/
Probable Routes of Human Exposure:
Workers engaged in production, formulation and application of carbaryl as a contact insecticide for fruits,
vegetables, cotton, and other crops.
Mean dermal exposure to carbaryl
ranged from 0.50 mg/hr (lower arms) - 1.90 mg/hr (hands) in strawberry
harvesters(1). Individuals performing production, collection, and bagging of
carbaryl were exposed to 0.23-31 mg
dust/cu m(2). The hourly dermal exposure (HDE) of agricultural workers to carbaryl applied by air or ground equipment
was studies. HDE was highest for the aerial flagger, next highest for the mixed
loader, followed by the applicator and the bystander. The exposure of the three
types of workers was limited mainly to the hands. The hand exposure of the mixed
loader was greater when gloves were not worn. HDE on hands of thinners working
in apple orchard treated with carbaryl
correlated with total extractable from apple leaves(4). The mean rates of carbaryl exposure for professional applicators
were 3.85 and 0.26 ug/sq cm-hr, respectively for outside of the clothing and the
skin beneath the clothing. The hand exposures for the applicators were 2.36 and
24.9 ug/cm-hr, respectively for gloved and bare hands. The max air concentration
in application area was 0.28 ug/l(3). The mean dermal and respiratory exposure
for applicators was 59.4-128 mg/hr and 0.1 mg/hr(5).
NIOSH (NOES Survey 1981-1983) has statistically estimated that 16,544 workers
(3,228 of these are female) are potentially exposed to carbaryl in the US(1). The NOES Survey,
however, does not include farm workers. Workers engaged in production,
formulation and application of carbaryl
as a contact insecticide for fruits, vegetables, cotton, and other crops are
especially prone to exposure(2). Occupational exposure to carbaryl may occur through inhalation and
dermal contact with this compound at workplaces where carbaryl is produced or used(SRC). The general
population may be exposed to carbaryl
via inhalation of ambient air(3), ingestion of food(4,5) and drinking water(6,7)
and pesticide products(8) containing carbaryl(SRC).
To evaluate the exposure of farmers to carbaryl during pesticide application, a study
was conducted that measured the personal air, dermal contact, indoor residue
content, urine and serum from a single farmer(1). Before carbaryl was applied to the crops, the
personal air samples contained 0.008-0.016 ug/cu m carbaryl; a dermal patch contained
0.0014-0.010 ug/sq cm carbaryl; handwipe
sample of the farmer and family contained 9-20 ug carbaryl; urine samples contained 270 ug/g
creatinine 1-naphthol (breakdown product of carbaryl); while serum samples contained 0.260
ug/l 1-naphthol and 0 detection for carbaryl(1). On the day of application, the
carbaryl concns changed to: personal air
samples contained 640 ug/cu m; dermal patch contained 11 ug/cm sq; handwipe
samples contained 20,100 ug; urine samples contained 140-9,300 ug/g creatinine
1-naphthol; while serum samples contained 510 ug/l 1-naphthol and 0.12 ug/l
carbaryl(1). In a year long study, from
March 1986 to February 1987, of carbaryl
exposure to tree nursery workers in the Pacific Northwest and Central United
States, 18 out of 3,134 urine samples analyzed contained detectable amounts of
carbaryl(2). Of these, the total amount
of carbaryl adsorbed was determined to
range from 0.0075-0.0238 mg/kg person(2). Airborne levels of pesticides were
measured during and following the mixing, loading, or application of
pesticides(3). Measurements included breathing zone air, indoor air of pesticide
warehouse facilities and offices, indoor air of residential properties and
ambient air of residential properties(3). Approximately 500 samples were taken
in 14 cities in the U.S. and Canada(3). Breathing zone air samples contained
carbaryl in 8 out of 17 air samples with
a time weighted avg of 0.005 mg/cu m(3). Office, operations room and warehouse
air samples did not contain any detectable amount of carbaryl in 82 samples(3). For residential
indoor air samples, carbaryl was the
most frequently detected pesticide with a time waited avg of 0.013 mg/cu m in 16
out of 38 samples(3). Carbaryl was
detected in 13 out of 28 residential outdoor ambient air samples with a time
waited avg of 0.013 mg/cu m(3).
Body Burden:
Carbaryl does not accumulate in
tissues or persist in blood. It is quickly metabolized into a nontoxic compound,
1-naphthol, which is excreted in urine as the glucuronide or sulfate ester(1).
Average Daily Intake:
FOOD: The avg adult daily dietary intake for the years 1980-84 was in the
range 0.12-0.032 ug/kg body weight(1-3). Insufficient data are available to
calculate avg daily carbaryl intakes
from water and air ingestion. Avg daily intake per unit of body weight of carbaryl between 1984-1986 in the United
States was 0.0704 ug (age group: 6-11 month), 0.0565 ug (2 yr), 0.0087 ug (14-16
yr female), 0.0088 ug (14-16 yr male), 0.0123 ug (25-30 yr female), 0.010 ug
(25-30 yr male), 0.0134 ug (60-65 yr female), and 0.012 ug (60-65 yr male)(4).
Emergency Medical Treatment:
Emergency Medical Treatment:
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The following Overview, *** CARBAMATE INSECTICIDES ***, 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 Carbamates are well absorbed from all routes of
exposure. Exposure may lead to cholinergic crisis with
increased salivation, lacrimation, urinary
incontinence, diarrhea, gastrointestinal cramping, and
emesis (SLUDGE syndrome). The syndrome may be
indistinguishable from that seen after organophosphate
poisoning. Generally, clinical effects are not as
severe as those seen with organophosphate poisoning;
carbamates do not as effectively penetrate the CNS as
do organophosphates, thus they produce more limited CNS
toxicity.
o The usual cause of death is respiratory failure.
Predominant serious toxicity is related to central
nervous system depression and nicotinic effects. CNS
effects may include stupor, coma, seizures and
hypotonicity. Hypertension and tachycardia or
cardiorespiratory depression may occur.
o Children may be more likely to develop CNS depression,
seizures and hypotonia than typical SLUDGE syndrome.
Absence of classic muscarinic effects has been
reported in a series of 36 children intoxicated with
carbamate insecticides. The presence of either a
cardiac dysrhythmia or respiratory failure is
associated with a higher incidence of fatal poisoning.
HEENT
0.2.4.1 ACUTE EXPOSURE
o Miosis and blurred vision are common. Mydriasis may
occur.
CARDIOVASCULAR
0.2.5.1 ACUTE EXPOSURE
o Bradycardias, ST depression, tachycardias, and
hypertension have been reported.
RESPIRATORY
0.2.6.1 ACUTE EXPOSURE
o Dyspnea, wheezing, rales, increased bronchial
secretions, respiratory muscle weakness and respiratory
failure may occur. Usual cause of death is
respiratory failure.
o Aspiration pneumonitis may occur.
o Laryngeal irritation and associated cough is common
following inhalation of dusting powders.
NEUROLOGIC
0.2.7.1 ACUTE EXPOSURE
o In severe poisoning, respiratory depression, mental
confusion, unconsciousness, brain hemorrhages, and
seizures may occur. Children may be more susceptible
to seizures than adults.
o Headache, blurred vision, tremor, paresis, mental
depression, coma, delayed neuropathies, various
dystonias, weakness, muscle twitching may be noted.
GASTROINTESTINAL
0.2.8.1 ACUTE EXPOSURE
o Nausea, vomiting, diarrhea, and abdominal cramping have
been reported and are common.
o Pancreatitis has been reported.
HEMATOLOGIC
0.2.13.1 ACUTE EXPOSURE
o Disseminated intravascular coagulation has been
reported in humans. Brain hemorrhages were seen in one
case. Animals have experienced decreased hemoglobin,
RBC count, platelets, and erythrocyte sedimentation.
DERMATOLOGIC
0.2.14.1 ACUTE EXPOSURE
o A possible occupational effect is contact dermatitis.
Diaphoresis may be seen after exposure. Cellulitis was
seen after injection of household spray.
MUSCULOSKELETAL
0.2.15.1 ACUTE EXPOSURE
o Rhabdomyolysis may occur. |
| Laboratory: |
o Determine plasma and red blood cell cholinesterase. o Obtain a chest x-ray in symptomatic patients. |
| Treatment Overview: |
ORAL EXPOSURE
o Emesis is NOT recommended because of the possibility of
seizures or respiratory depression developing prior to
or during emesis.
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 ADMINISTER ATROPINE SULFATE - in repeated doses
intravenously until atropinization is achieved
(indicated by drying of pulmonary secretions).
1. ADULT DOSE - 2 to 4 milligrams every 10 to 15 minutes.
2. CHILD - 0.05 milligram/kilogram every 10 to 15 minutes.
o Administer pralidoxime if severe toxicity develops.
1. 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.
a. 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.
b. Repeat these doses in 1 hour and then every 6 to 12
hours if muscle weakness or fasciculations persist,
or begin continuous infusion.
c. CONTINUOUS INFUSION: Administer as a 2.5% solution in
0.9% saline. ADULT: 500 mg/hour. CHILD: 9 to 19
mg/kg/hour.
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.
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.
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.
DERMAL EXPOSURE
o DECONTAMINATION: Remove contaminated clothing and
jewelry. Wash the skin, including hair and nails,
vigorously; do repeated soap washings. Discard
contaminated clothing. |
| Range of Toxicity: |
o Acute toxicity depends on kinetics of absorption i.e.,
sudden absorption of a low toxicity compound may have a
greater effect. Aldicarb is considered the most toxic
carbamate.
o In children, the presence of either a cardiac dysrhythmia
or respiratory failure is associated with a poor
prognosis. |
Antidote and Emergency Treatment:
Basic treatment: Establish a patent airway. Suction if necessary. Aggressive
airway management 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 shock and treat if necessary ... . Monitor for
pulmonary edema 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 and the patient can swallow, has a strong gag reflex, and
does not drool. Administer activated charcoal ... . /Carbamates and related
compounds/
Advanced treatment: Consider orotracheal or nasotracheal intubation for
airway control in the unconscious patient. 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. For hypotension if signs of hypovolemia are present, administer
fluid cautiously. Watch for pulmonary edema ... . Administer atropine. Correct
hypoxia before administration ... . In severely poisoned patients, administer
pralidoxime chloride (2 PAM). DIRECT PHYSICIAN ORDERS ONLY ... . Treat seizures
with adequate atropinization and correction of hypoxia. Rarely is diazepam
necessary ... . Use proparacaine hydrochloride to assist eye irrigation ... .
/Carbamates and related compounds/
Animal Toxicity Studies:
Toxicity Summary:
Food represents the major source of carbaryl intake for the general population.
... The general population can be exposed to carbaryl during pest control operations in
both the home & recreation areas. Workers can be exposed to carbaryl during its manufacture, formulation,
packing, transportation, storage, & during & after application. ...
Significant dermal exposure may occur in industrial & agricultural workers
if protective measures are inadequate. Carbaryl is rapidly absorbed in the lungs
& digestive tract. ... The principal metabolic pathways of carbaryl are ring hydroxylation &
hydrolysis. As a result, numerous metabolites are formed & subjected to
conjugation with the formation of water-soluble sulfates, glucuronides, &
mercapturates, excreted in the urine. Hydrolysis results in the formation of
1-naphthol, carbon dioxide & methylamine. Hydroxylation produces
4-hydroxycarbaryl, 5-hydroxycarbaryl, N-hydroxymethylcarbaryl,
5-6-dihydro-5-6-dihydroxycarbaryl & 1,4-naphthalendiol. The principal
metabolite in humans is 1-naphthol. Under normal exposure conditions, the
accumulation of carbaryl in animals is
unlikely. Carbaryl is excreted primarily
via the urine, since the product of its hydrolysis, 1-naphthol, is mainly
detoxified to water-soluble conjugates. Enterohepatic cycling of carbaryl metabolites is also considerable,
especially after oral administration. ... Carbaryl metabolites are also present in a
small percentage of the absorbed doses in saliva & milk. ... The acute
toxicity for birds is low. ... Carbaryl
is very toxic for honey-bees & earthworms. ... The acute toxicity ... varies
considerably according to species, formulation & vehicle. ... Carbaryl is a mild eye irritant & has
little or no sensitizing potential. ... Carbaryl has a low cumulative potential. Carbaryl has been shown to affect mammalian
reproduction & perinatal development adversely in a number of species.
Effects on reproduction include impairment of fertility, decreased litter size,
& reduced postnatal viability. Developmental toxicity is seen as increased
in utero death, reduced fetal weight, & the occurrence of malformation. With
the exception of a small number of studies, all adverse reproductive &
developmental effects were noted only at doses that caused overt maternal
toxicity, &, in a number of cases, the maternal animal was more sensitive to
carbaryl than the conceptus. The
maternal toxic effects included lethality, decreased growth, & dystocia.
...The available evidence indicates that carbaryl does not have any DNA-damaging
properties. ... Negative results were obtained in tests for gene mutations in a
large number of bacterial assays ... The available database does not support the
presumption that carbaryl poses a risk
of inducing genetic changes in ... humans. Carbaryl has been studied for its carcinogenic
potential in numerous studies on rats & mice. The results of most of these
studies were negative ... The effects of carbaryl on the nervous system are primarily
related to cholinesterase inhibition & are usually transitory. ... Carbaryl has been reported to affect
coagulation ... Carbaryl binds free
blood amino acids. Disturbances have been reported in the carbohydrate
metabolism & protein synthesis & detoxification function of the liver in
mammals. Carbaryl is a weak inducer of
hepatic microsomal drug-metabolizing activity. ... Carbaryl has been reported to incr the
gonadotropic function of the hypophysis of rats. Carbaryl is an inhibitor of cholinesterase
activity. This effect is dose-related & quickly reversible. ... All
identified metabolites of carbaryl are
appreciably less active cholinesterase inhibitors than carbaryl itself. Carbaryl is easily absorbed /in humans/
through inhalation & via the oral route & less readily by the dermal
route. Since the inhibition of cholinesterase is the principal mechanism of
carbaryl action, the clinical picture of
intoxication is dominated by ... symptoms, such as: increased bronchial
secretion, excessive sweating, salivation, & lacrimation; pinpoint pupils,
bronchoconstriction, abdominal cramps (vomiting & diarrhea); bradycardia;
fasciculation of fine muscles (in severe cases, diaphragm & respiratory
muscles also involved); tachycardia; headache, dizziness, anxiety, mental
confusion, convulsions, & coma; & depression of the respiratory center.
Signs of intoxication develop quickly after absorption & disappear rapidly
after exposure ends.... In cases of occupational overexposure to carbaryl, mild symptoms are observed long
before a dangerous dose is absorbed, which is why severe cases of occupational
intoxication with carbaryl are rare.
During agricultural application, dermal exposure may play an important role. ...
The appearance of a skin rash after accidental splashing with carbaryl formulations has been described. ...
The most sensitive biological indicator of carbaryl exposure is the appearance of
1-naphthol in the urine & the decr of cholinesterase activity in the blood.
... The hazards of carbaryl for human
beings are judged to be low, because of its low vapor pressure, rapid
degradation , rapid spontaneous recovery of inhibited cholinesterase, & the
fact that symptoms usually appear well before a dangerous dose has accumulated
in the body. ...
Evidence for Carcinogenicity:
No data are available in humans. Inadequate evidence of carcinogenicity in
animals. OVERALL EVALUATION: Group 3: The agent is not classifiable as to its
carcinogenicity to humans.
A4; Not classifiable as a human carcinogen.
Non-Human Toxicity Excerpts:
MUTAGENICITY: MUTATION RESEARCH 76: 169 (1980). ESCHERICHIA COLI WP2 -
REVERSE MUTATION STUDIES: NEGATIVE.
MUTAGENICITY: MUTATION RESEARCH 87: 211 (1981). DNA REPAIR-DEFICIENT
BACTERIAL TESTS: NEGATIVE.
MUTAGENICITY: MUTATION RESEARCH 87: 81 (1981). CHINESE HAMSTER LUNG (V79)
CELLS IN CULTURE - GENE MUTATION, OUABAIN LOCUS STUDIES: POSITIVE.
GROUPS OF 18 MALE AND 18 FEMALE (C57BL/6XC3H/ANF)F1 MICE AND 18 MALE AND 18
FEMALE (C57BL/6XAKR)F1 MICE RECEIVED COMMERCIAL CARBARYL (MP 141-142 DEG C) AT 7 DAYS OF AGE
BY STOMACH TUBE AND THE SAME AMOUNT (NOT ADJUSTED FOR INCR BODY WT) DAILY UP TO
4 WK OF AGE; SUBSEQUENTLY, THE MICE WERE GIVEN 14 MG CARBARYL/KG OF DIET. ... THE EXPT WAS
TERMINATED WHEN THE ANIMALS WERE ... 78 WK OF AGE, AT WHICH TIME 16, 18, 17 AND
18 MICE IN THE FOUR GROUPS, RESPECTIVELY, WERE STILL ALIVE. TUMOR INCIDENCES
WERE COMPARED WITH THOSE OBSERVED AMONG 79-90 NECROPSIED MICE OF EACH SEX AND
STRAIN, WHICH EITHER HAD BEEN UNTREATED OR HAD RECEIVED GELATINE ONLY; THE
INCIDENCES WERE NOT SIGNIFICANTLY GREATER FOR ANY TUMOR TYPE IN ANY SEX-STRAIN
SUBGROUP OR IN THE COMBINED SEXES OF EITHER STRAIN.
OF 60 RANDOM-BRED RATS GIVEN 30 MG/KG BODY WT COMMERCIAL CARBARYL (97.7% PURE) IN WATER BY STOMACH TUBE
DAILY FOR UP TO 22 MO, 12 SURVIVORS WERE EXAM: 3 HAD FIBROSARCOMAS, & 1 HAD
OSTEOSARCOMA. 1 FIBROSARCOMA OCCURRED AMONG 46 UNTREATED CONTROLS.
GROUPS OF 20 MALE AND 20 FEMALE CF-N RATS WERE FED DIETS CONTAINING 0
(CONTROL), 0.005 (2 MG/KG BODY WT/DAY), 0.01 (4 MG/KG BODY WT/DAY), 0.02 (8
MG/KG BODY WT/DAY) OR 0.04% (16 MG/KG BODY WT/DAY) CARBARYL; SURVIVORS WERE KILLED AFTER 732-736
DAYS. THE MEAN AGES AT DEATH FOR BOTH SEXES AT THE 0.04 AND 0.02% LEVELS WERE
656 AND 630 DAYS, AND THAT FOR CONTROLS, 585 DAYS. THE INCIDENCE OF TUMORS ...
WAS NO DIFFERENT FROM THAT IN CONTROLS; TUMOR TYPES WERE NOT REPORTED.
GROUPS OF 18 MALE AND 18 FEMALE (C57BL/6XC3H/ANF)F1 MICE AND 18 MALE AND 18
FEMALE (C57BL/6XAKR)F1 MICE WERE GIVEN SINGLE SC INJECTIONS OF 100 MG/KG BODY WT
COMMERCIAL CARBARYL (MP 141-142 DEG C)
IN DIMETHYL SULFOXIDE ON THE 28TH DAY OF LIFE AND WERE OBSERVED UNTIL ... 78 WK
OF AGE, AT WHICH TIME 15, 18, 18 AND 17 MICE IN THE FOUR GROUPS, RESPECTIVELY,
WERE STILL ALIVE. TUMOR INCIDENCES WERE COMPARED WITH THOSE IN GROUPS OF 141,
154, 161 AND 157 UNTREATED OR VEHICLE-INJECTED CONTROLS THAT WERE NECROPSIED.
INCIDENCES WERE NOT SIGNIFICANTLY INCREASED ... FOR ANY TUMOR TYPE IN ANY
SEX-STRAIN SUBGROUP OR IN THE COMBINED SEXES OF EITHER STRAIN.
GROUPS OF 30 3-MO OLD MALE A/JAX OR C3H MICE GIVEN SC INJECTIONS WEEKLY OVER
5 MO OF 10 MG/ANIMAL CARBARYL IN 0.2 ML
AGAR SUSPENSION, AGAR SUSPENSION ALONE OR LEFT UNTREATED. NUMBER OF LUNG TUMORS
SEEN @ 8 MO OF AGE WAS NO GREATER IN TREATED THAN IN CONTROL MICE.
OF 48 RANDOM-BRED RATS GIVEN SC IMPLANT OF 20 MG/KG COMMERCIAL CARBARYL (97.7% PURE) IN 250 MG PARAFFIN
PELLET, 10 SURVIVED 22 MO; 2 HAD SC SARCOMAS @ SITE OF IMPLANTATION. 1
FIBROSARCOMA OCCURRED AMONG 46 CONTROLS, WHICH DID NOT RECEIVE PARAFFIN PELLETS
& WERE STILL ALIVE @ 22 MO.
NO TOXIC EFFECTS WERE SEEN IN RATS ADMIN UP TO 200 MG CARBARYL/KG OF DIET FOR 2 YR. WITH HIGHER
DIETARY LEVELS (1500 & 2250 MG/KG OF DIET), DIFFUSE, CLOUDY SWELLING OF
KIDNEY TUBULES WAS SEEN AFTER 96 DAYS.
NEUROTOXICOLOGICAL EFFECTS OF CARBARYL (200 MG/KG OF DIET/DAY FOR 50 DAYS)
... IN WISTAR RATS ... AFFECT LEARNING (AFTER 25 DAYS) & PERFORMANCE (AFTER
15 DAYS) ... AFFECT ELECTROENCEPHALOGRAPHIC PATTERNS UNDER RESTING &
LIGHT-STIMULATED CONDITIONS, & ... INHIBIT ACETYLCHOLINESTERASE ACTIVITY IN
ERYTHROCYTES & IN ... THE BRAIN.
MARKED FUNCTIONAL & STRUCTURAL CHANGES OF PITUITARY GLAND WITH IMPAIRMENT
OF THYROID & GONADAL FUNCTION ... FOUND IN RATS ADMIN 7, 14 OR 70 MG CARBARYL/KG BODY WT FOR UP TO 12 MO.
INGESTION OF CARBARYL BY BEAGLE DOGS
THROUGHOUT GESTATION CAUSED TERATOGENIC EFFECTS @ ALL BUT LOWEST DOSE LEVEL
(3.125 MG/KG BODY WT/DAY). EMBRYOPATHIES IN 21 OUT OF TOTAL OF 181 PUPS WERE
CHARACTERIZED BY ABDOMINAL-THORACIC FISSURES WITH VARYING DEGREES OF
BRACHYGNATHIA, ECAUDATE PUPS, FAILURE OF SKELETAL FORMATION & SUPERFLUOUS
PHALANGES.
... /Carbaryl was admin to/ guinea
pigs, hamsters & rabbits. Only in guinea pigs were defects produced. ... a
near lethal dose for the mother (300 mg/kg) from day 11 to day 20 ... /produced/
vertebral anomalies in about one half of the surviving fetuses; ... /In another
study/ no teratogenicity in the rat /was observed/; ... 3.1 to 50 mg/kg /were
fed/ to Beagle /dogs/ during pregnancy. At levels of 6.25 & above the defect
rate was increased in the offspring. Midline abdominal wall defects &
skeletal defects were the most common type. Reduced conception was found at the
50 m/kg level.
CARBARYL INHIBITS SPINDLE FIBER
FORMATION IN PLANTS.
Carbaryl (85% purity) caused an
increased number of recessive lethals in Drosophila melanogaster.
PIGS CAN BE POISONED BY 1.5 G/KG, SHOWING SALIVATION, TREMORS, VOMITING,
DEPRESSION, ANOREXIA, DYSPNEA & CYANOSIS. CONTINUED ADMIN OF ... LOWER
LEVELS (150-300 MG/KG) PRODUCES CHRONIC POISONING OF NEUROMUSCULAR TYPE
CHARACTERIZED BY INCOORDINATION, ATAXIA, RECUMBENCY, & PROSTRATION.
CARBARYL DOES NOT PRODUCE
DEMYELINATION ... IN CHICKENS, BUT POISONED FOWL DID HAVE FAT DROPLETS IN
EPITHELIAL CELLS OF PROXIMAL TUBULES.
POST MORTEM FINDINGS IN ACUTE POISONING ARE USUALLY LIMITED TO CONGESTION
& EDEMA OF LUNGS, LIVER & KIDNEY & PETECHIAL HEMORRHAGES OF GASTRIC
MUCOSA.
ADMIN OF A SINGLE DOSE (200 MG/KG, ORALLY) OF CARBARYL TO RATS PRODUCED AN INCREASE IN
ADRENAL & PLASMA CORTICOSTERONE LEVELS & AN INCREASE OF TYROSINE
ALPHA-KETOGLUTARATE TRANSAMINASE ACTIVITY IN THE LIVER CYTOSOL. SYNAPTOSOMAL
ACETYLCHOLINESTERASE ACTIVITY OF THE HYPOTHALAMIC & THE STRIATAL REGIONS OF
RAT BRAIN WAS DECREASED BY CARBARYL
TREATMENT UNDER SIMILAR CONDITIONS.
EXPOSURE OF A FRESHWATER CYPRINID (PUNTIS CONCHONIUS) TO 2.142 & 4.784
PPM OF CARBARYL FOR 24 HR, SERIOUSLY
AFFECTED CARBOHYDRATE & CHOLESTEROL METABOLISM. HYPERGLYCEMIA &
GLYCOGENOLYSIS IN LIVER, BRAIN, & HEART WERE MANIFESTED IN THE TREATED FISH.
HYPERCHOLESTEROLEMIA & RISE IN LIVER CHOLESTEROL ALSO OCCURRED. LONG-TERM
EXPOSURE, 15-30 DAYS, TO CHRONICALLY SUBLETHAL CONCN, 0.194 & 0.306 PPM
CARBARYL ELICITED HYPOGLYCEMIA &
DEPLETION OF LIVER GLYCOGEN, TOGETHER WITH ENHANCED GLYCOGENESIS IN THE HEART.
THE GLYCOGEN LEVEL IN BRAIN FELL IN RESPONSE TO CARBARYL EXPOSURE.
THE 48-HR MEDIAN LETHAL CONCN OF CARBARYL FOR THE FRESHWATER FISH, TILAPIA
MOSSAMBICA, WAS 5.495 PPM. THE SLOPE VALUE OF CARBARYL TOXICITY (5.6) IS INDICATIVE OF A
HETEROGENOUS RESPONSE OF THIS FISH TO ITS TOXICITY.
MOTOR ACTIVITY & NEUROMOTOR FUNCTION WERE EXAMINED IN ADULT CD RATS
EXPOSED TO CARBARYL, & BEHAVIORAL
EFFECTS WERE COMPARED WITH THE TIME COURSE OF CHOLINESTERASE INHIBITION. RATS
RECEIVED AN IP INJECTION OF 0, 4, 8, 16, OR 28 MG/KG CARBARYL IN CORN OIL 20 MIN BEFORE TESTING.
DOSAGES OF 8, 16, & 28 MG/KG DECREASED RAT MAZE ACTIVITY WHEREAS 16 & 28
MG/KG REDUCED OPEN FIELD ACTIVITY. MAX EFFECTS OF CARBARYL ON BLOOD & BRAIN CHOLINESTERASE
& MOTOR ACTIVITY WERE SEEN WITHIN 15 MINUTES. MAZE ACTIVITY HAD RETURNED TO
CONTROL LEVELS WITHIN 30 & 60 MIN WHEREAS CHOLINESTERASE LEVELS REMAINED
DEPRESSED FOR 240 MIN.
THE MUTAGENIC ACTIVITY OF CARBARYL
& 4 OTHER METHYL CARBAMATE INSECTICIDES WAS INVESTIGATED USING HISTIDINE
AUXOTROPHS (HIS TA98, HIS TA100, HIS TA1535, HIS TA1537 AND HIS TA1538) OF
SALMONELLA TYPHIMURIUM LT2 DERIVED BY AMES. THE METHYL CARBAMATE INSECTICIDES
DID NOT CAUSE A SIGNIFICANT INCR IN THE NUMBER OF REVERTANT COLONIES IN THE
STRAINS USED. THE NITROSO DERIV OF THE TESTED INSECTICIDES ARE POTENT MUTAGENS.
PARENT INSECTICIDES ARE NON-MUTAGENIC.
The LC50 of herbicides and insecticides in aq emulsion were measured for
mallards by egg immersion. Carbaryl and
methomyl were only slightly toxic or not toxic (LC50s of 178 to greater than 500
lb/acre; 199-560 kg/ha).
Oral administration of 200 mg/kg of carbaryl for three days a week for 90 days
produced no significant histological changes in testes, epididymis, liver, and
kidney of male rats. No marked biochemical changes were observed in testes,
liver, and brain. Acetylcholine esterase activity in blood was found to be
decreased. This dosage of carbaryl did
not affect the fertility of male rats.
A study was undertaken to determine the toxicity of eight pesticides to
respiration and nitrifying activity of sewage microorganisms. Carbaryl, malathion, diazinon, chlorpyrifos,
dichlorvos, beniocarb, and 2,4-D concentrations of 0.1-100 mg/ml had little or
no /effect on/ the oxygen depletion caused by microbial degradation of organic
matter in sewage. No suppression of microbial activity was evident, except for
propoxur.
The effects of the insecticide carbaryl on the survival, behavior, food
intake, growth, and conversion efficiency of the catfish, Mystus vittatus, were
studied. At a concentration of 32.5 ppm, carbaryl caused 100% mortality within 24 hr.
No mortalities at concentrations of 12.5 ppm or less occurred within 72 hr. A 27
day exposure to sublethal concentrations led to a decrease in feeding and growth
rate. This insecticide is considered to be a metabolic stressor.
OF 16 7-9 WK OLD MALE A/HE MICE GIVEN 12 IP INJECTIONS OF CARBARYL ... IN TRICAPRYLIN OVER 4 WK (TOTAL
DOSE, 6 MG/ANIMAL), 6 OUT OF 15 MICE STILL ALIVE 20 WK AFTER END OF TREATMENT
... DEVELOPED LUNG TUMORS. OF TRICAPRYLIN-INJECTED CONTROLS, 7/28 ... DEVELOPED
TOTAL OF 8 LUNG TUMORS; 2/31 UNTREATED ... HAD 1 LUNG TUMOR EACH.
Cats which inhaled carbaryl at 40
mg/cu m showed decreased responsiveness to a classical food reward paradigm, but
this deficit was pronounced only immediately following the first administration
of carbaryl.
A decrease in body temperature in mice was observed after carbaryl administration. /50 or 250 mg/kg, ip/
Carbaryl was orally admin to rats at
doses of 7, 14 & 70 mg/kg/day for 12 months to determine the
endocrinological effects by the analysis of semen. The toxic effects observed
were reduced motility of sperm & alterations in spermatogeneis. /From table/
Carbaryl was administered in the diet
of three generations of gerbils at levels of 0, 2000, 4000, 6000, and 10,000
ppm. Reduced fertility was noted as low as 2000 ppm, although a clear
dose-response trend was not observed. A decrease in average litter size at all
dose levels /was observed/. A weak trend toward reduced litter size in the
10,000 ppm was noted, however reduced fertility and neonatal survival resulted
in too few litters for rigorous evaluation. Other trends from this study
included reduced postnatal viability and weaning weights. The reduced postnatal
survival (ie, survival to day 4) was dose-responsive, and is probably the most
significant finding of the study.
Carbaryl, a broad spectrum
insecticide with anticholinesterase activity, was tested for its ability to
disturb resident peritoneal macrophages stimulated by opsonized zymosan. The
effect of carbaryl on superoxide
production and on the release of 1-(14)C-labeled arachidonic acid and
(14)C-labeled prostaglandins was dose-dependent. For 2.5x10-6 M of carbaryl, superoxide production and
prostaglandin release were not significantly inhibited. At 12.5x10-6 M, the
inhibitory effect was apparent for superoxide production (33%) and for the
release of 6-keto-PGF1alpha (60%), PGE2 (42%), PGF2alpha (38%), PGD2 (33%).
Carbaryl had no effect on the level of
free arachidonic acid. Insecticide at 12.5x10-6 M significantly decreased the
deacylation of the phosphatidylcholine (20%). Incubation of resident peritoneal
macrophages with indomethacin studied conjointly decreased only the
prostaglandin release. Evidently carbaryl decreases the sequence of events
following the binding of an agent to its receptor and leading to the induction
of phospholipase activity. The effect of this pesticide on phospholipid
metabolism and its consequences on macrophage stimulation are discussed.
Ecto-serine esterase inhibition in the mechanism of the pesticide was suggested.
The insecticide ... carbaryl ... was
examined for its ability to induce chromosomal aberrations in the bone marrow
cells of the Syrian hamster treated in vivo. Mutagenicity of comparable
preparations was examined at 4 doses: LD50; 0.5, 0.2, and 0.1 LD50. The positive
control was an ip injection of cyclophosphamide to hamsters at a dose of 40
mg/kg. ... The mixture of carbaryl and
lindane were negative in this test.
/Data obtained from acute toxicity studies of fathead minnows exposed to LC50
concn of carbaryl (99% pure) for 96 hr
indicated that/ affected fish lost schooling behavior, were hypoactive & had
increased resp. They were also darkly colored, had edema, were hemorrhaging, had
spinal deformities & lost equilibrium prior to death.
... Short-term studies in animal species confirm that carbaryl can cause toxicity due to
cholineterase inhibition. Wide variations in the dosage required to induce
toxicity in either different species or in one species by different routes of
administration can in part be explained by differences in drug disposition. ...
Limited long-term exposure studies in rats and dogs have not demonstrated
unexpected adverse effects. However, long-term exposure in pigs results in a
progressive neuromyopathy that is associated with structural damage and is not
acutely reversible with atropine. ...
... In mice ip carbaryl has produced
disturbances in ERG.
Toxic to bees ... /&/ beneficial insects.
The primary breakdown product of carbaryl (1-naphthol) is believed to be
nontoxic in the terrestrial environment. But in the few cases where its toxicity
to the aquatic organisms /molluscs, and 3 species of marine fish/ has been
tested, it was found to be more toxic than the parent compound. ... the growth
of juvenile cockleclams (Clinocardium nuttalli) was reduced more by 1-naphthol
than by carbaryl, and ... 1-naphthol was
more toxic to juvenile clams. ... for 6 species of fish, 1-naphthol was about 2
times as toxic as carbamyl, but in the case of Mystus cavasius ... the
degradation product /was/ 14 times as toxic as the parent cmpd (96 hr LC50s
being, respectively, 0.33 and 4.6 mg/l). /1-Naphthol/
... Retardation of the generation of the caudal fins of Fundulus heteroclitus
/was observed/ following a treatment with 10 ug/l ... carbaryl. ... A relationship between
acetylcholinesterase inhibition and retardation of the fin regeneration was
suggested. ... the relative usefulness of Atlantic silverside, sheepshead
minnows, and the killifish /were evaluated/ for monitoring pesticide-induced
deformities, and ... the killifish /was considered/ the most useful species for
... /this/ purpose.
Respiratory distress is one of the early symptoms of pesticide poisoning.
Exposure to sublethal concn is reported to increase resp activity, resulting in
increased ventilation and ... increased uptake of the toxicant. ... Therapon
/perch/ exposed to ... carbaryl consumed
more oxygen than controls.
A single treatment of embryos of the Atlantic silverside with ... carbaryl induced optical malformations,
although not dose-related. In treated group the axis formation and heartbeat
initiation were impaired. Microphthalmia (reduced size of eyes), unilateral or
bilaterial anophthalmia (absence of eyes), and cyclopia (median eye) were some
of the observed deformities. After hatching, lordotic fry were seen in the 10
ug/l carbaryl ... treatment groups. ...
the survival time of the embryos /were reduced/. These effects were observed at
concn that may occur as were noticed.
Following the aerial /carbaryl/
spraying of forests in the Boulder River drainage in Montana, large-scale
mortality and drift of aquatic insects in the adjoining streams were noticed.
The activities of rat brain isocitrate dehydrogenase and succinate
dehydrogenase generally inhibited after pesticide treatment. Carbaryl brought about a significant p<
0.01 rise in the ketone bodies level. The inhibition of isocitrate dehydrogenase
and succinate dehydrogenase activities inhibit the TCA-cycle resulting into
diversion of non-utilized acetyl-CoA units towards ketogenesis.
The potencies of various xenobiotics for induction of monooxygenases and
their influence on the rat liver microsomal metabolite profile of the weak
carcinogen, chrysene, was determined. Carbaryl was found to be inefficient or weak
inducers.
The genotoxic potential of the insecticide carbaryl-beta-naphthol was investigated using
the sperm abnormality assay comparatively with the conventional chromosomal
aberration analysis, after chronic administration in rats, for a period of 3, 6,
9, 12, 15 and 18 months. The sperm and bone marrow cells seemed to have the same
sensitivity, carbaryl showing genotoxic
effects in both the assays performed.
A study was made of the effects of long term exposure of mouse-3T3
fibroblasts to carbaryl on
mixed-function-oxidase activity as represented by benzo(a)pyrene metabolism.
Carbaryl was used at 10(-6) molar.
Individual cell activities were assessed by microspectrofluorimetry. Two groups
of cells were identified, one (70%) with high benzo(a)pyrene metabolism and the
other (30%) with little or no benzo(a)pyrene metabolizing capability. Carbaryl, which does not require metabolism to
be toxic, decreased the number of cells in the low benzo(a)pyrene metabolizing
category without changing rate constants, when exposure was for 9 to 11 days.
Longer exposure (14 to 31 days) caused complete elimination of this class of
cells, and some rate constants were increased in the high metabolism class. Both
compounds activate the same mixed-function-oxidase system and there are two 3T3
cell subpopulations which present different responses to treatment with carbaryl, reflecting differences in
aryl-hydrocarbon-hyrdoxylase activity.
The physiological mechanisms of resistance to carbaryl were investigated in a carbaryl-resistant strain of the fall armyworm
Spodoptera frugiperda. Piperonyl butoxide greatly reduced the resistance level
from 90-to 6-fold, indicating that microsomal cytochrome p450-dependent
monooxygenases may play a major role in resistance. This finding is consistant
with metabolic data in which the oxidative metabolism of carbaryl by midgut homogenates was five times
more active in the resistant strain than in the susceptible strain. In addition,
the resistant strain showed increased activities of microsomal hydroxylation and
epoxidation compared to the susceptible strain. Cuticular penetration studies
using (14)C-carbaryl revealed that 55%
of the applied radioactivity remained on the cuticle of resistant larvae while
32% remained on susceptible larvae 24 hr after topical treatment. The resistance
appeared to be unrelated to target site insensitivity. The high level of
resistance to carbaryl in this insect
was mainly due to enhanced oxidative metabolism of the insecticide (via
hydroxylation and epoxidation) with reduced cuticular penetration playing a very
minor role, if any.
Hematological responses of bluerock pigeon (Columba livia) were studied after
oral administration of carbaryl (a
carbamate) for one week. Hematological disorders were induced which include
reduction in total count of peripheral erythrocytes, hemoglobin content,
hematocrit and total cellularity of spleen. Total count of peripheral
leukocytes, on the otherhand, increased with marked heterophilia together with
lymphopenia and monocytopenia. Both bleeding and clotting time became
conspicuously prolonged in the experimental birds.
A functional observational battery of tests of autonomic, sensory, and motor
integrity of rodents was used to examine the effects of carbaryl in rats. ... In Long Evans hooded
rats carbaryl was injected ip at doses
of 0, 3, 10, or 30 mg/kg, with testing after 0.5, 3, 24, and 48 hr. Assessments
were made of spontaneous activity, central nervous system excitability,
autonomic function, muscle tone and equilibrium, motor and sensory affective
function, and physiologic responses. Carbaryl caused changes in muscle tone and
equilibrium, righting reflex and forelimb and hindlimb grip strength. Numerous
signs of autonomic dysfunction were seen with carbaryl. Carbaryl produced decreased reactivity to all
stimuli. Carbaryl treated rats were limp
and easily handled. Carbaryl produced a
general prostration. Dose related decreased general exploratory activity was
found for carbaryl in both sexes. Carbaryl caused hypothermia and body weight
loss.
A possible structure/activity relationship was investigated for 12 chemicals,
including phenyl-N- methylcarbamate, p-biphenylyl-n-methyl-carbamate,
1-naphthyl-N-methyl-carbamate, 9-phenanthryl-N-methylcarbamate, and their
mammalian enzyme activated mutagenic activity. The study measures the reversion
of histidine dependent Salmonella-typhimurium (TA-98) and (TA-1535) in the
presence of a rat liver 9000-g supernatant fraction. Methylcarbamates were
effective versus (TA-98). Methylcarbamates appeared efficient in frameshift
strains.
In vitro incorporation of (14)C-glucose/acetate into lipids and (14)C-leucine
into proteins by liver of Channa punctatus, exposed to safe application rate and
sublethal concentrations of malathion and carbaryl for 30 days during preparatory phase
declined more in the fish exposed to sublethal concentrations than in safe
application rate concentrations of the pesticides. The decline in the
incorporation was more in malathion-exposed than in carbaryl-exposed fish. Hence, malathion is
considered more toxic than carbaryl in
inhibiting the de novo synthesis of lipids and proteins by liver.
Observations on the effect of endrin (0.0015 pm) and carbaryl (5 ppm) on the tissues and activity
of acid and alkaline phosphatases in the stomach, intestine and liver of Mystus
tengara were made. The fish treated with endrin showed severe histopathological
changes and greater inhibition in enzyme activity as compared with carbaryl.
Four groups of goats were poisoned by different levels of sevin given as a
drench. Clinical signs included inappetance, profused diarrhea, dullness,
weakness of the hindlimbs, frothing, nasal discharge, recumbancy and death.
Histopathology revealed severe, moderate or slight hyperaemia of the lung,
heart, liver, kidney brain, and spinal cord depending on the dose given. Fatty,
myocardial or neuronal degenarations and chromatolysis were seen. Focal
necrosis, chronic proliferative and chronic interstital glomerulonephritis were
evident. SGOT, SGPT and alkaline phosphatase activities and sodium, potassium,
and urea concentrations had increased, while cholinesterase activity and total
protein concentrations decreased. Hematology showed reductions in Hb, PCV, and
RBC values, but total and differential leukocyte counts were not affected. It is
conclude that sevin is toxic to goats by causing nephrotoxic, endothelio-toxic,
neurotoxic and pulmonary-toxic effects and hepato-cellular injury.
Laboratory trials for the control of North Indian snail pests, Lymnaea
acuminata (a livestock parasite vector) and Plia globosa (a rice pest) were
carried out. Three carbamate compounds were tested for molluscicidal activity.
On the basis of LD50 values calculated for exposure times ranging from 48 to 240
hr the order to toxicity for the carabamates was zectran > carbaryl > aldicarb. Lymnnaea acuminata was
more sensitive to all the pesticides tested.
The acute toxicity of 3 carbamate pesticides, aldicarb, carbaryl and mexacarbate, on a population of
Paramecium multimicronucleatum was studied. The toxicity was evaluated by the
Warburg respirometer and the static acute plate assay. Aldicarb, carbaryl and mexacarbate were shown to
significantly inhibit cumulative O2 uptake at 24 hr in the Paramecium culture at
160, 120 and 100 ppm, respectively. Aldicarb, carbaryl and mexacarbate concentrations of 60,
20 and 10 ppm demonstrated no inhibition of cumulative O2 uptake when compared
to a paramecium control at 24 hr. Pesticide concentrations intermediate to the
high and low concentratins demonstrated varying degrees of inhibition. Static
plate assay data for aldicarb demonstrated LC50 values of 93, 104, 122 and 145
ppm at 24, 17, 13 and 9 hr, while carbaryl demonstrated LC50 values of 28, 34,
46, 65 and 105 ppm at 24, 17, 13, 9 and 7 hr respectively. Mexacarbate LC50
values were 19, 25, 35, 57 and 83 ppm at 24, 17, 13, 9 and 7 hr. O2 uptake
values compared favorably with the static assay data. Scanning electron
micrographs demonstrated several morphologic changes in Paramecium with
increased pesticide concentration and exposure in Paramecium with increased
pesticide concentration and exposure time including ciliary abnormalities and
disruption of surface structure.
Continuous-flow laboratory bioassays were used to assess the acute toxicities
of four formulated insecticides to representative stream invertebrates
(Orconectes propinquus, Simulium venustum, Pycnopsyche sp, Phasganophora sp,
Isonychia sp and Ophiogomphus sp). Toxicities (48 hr, LC50) ranged from 478 to
2863 ug/l for aminocarb, and from 99 to 492 ug/l for mexacarbate.
Carbaryl was applied in spring to
concrete ponds to study its effects on zooplankton communities. The population
density of Cladocera (Daphnia sp) was nearly constant before application of the
chemical. Carbaryl at 1 ppm killed all
zooplankton species, including Chaobrus larvae.
Mutagenic effects of carbaryl, a
contact insecticide with slight systemic properties, have been investigated
employing histidine reversion assay in Salmonella typhimurium strains and in
vivo chromosomal aberrations in root meristems of Allium cepa. Carbaryl did not enhance significantly the
frequency of histidine revertants in any of the strains of Salmonella ie
frameshift mutagen tester (TA98), base pair substitution tester strain (TA1535)
and ochre mutant strain (TA102). The supplementation with S9 mix did not enhance
the reversion frequency significantly. However, carbaryl induced both clastogenic and
physiological types of chromosomal aberration. The spectrum of chromosomal
aberrations included c-mitosis, stickiness, vagrant chromosomes, polyploidy
multipolarity, delayed anaphases, end to end joining of chromosomes, chromosome
breaks, ring chromosomes and anaphase bridges. The frequency of chromosomal
aberrations was reduced by transferring the carbaryl treated bulbs to distilled water for
24 an 48 hr. The differences between the two assays may be attributed to
differences in the metabolism of the test organisms.
The reactivities of carbaryl,
N-methyl 1-naphthylcarbamate insecticide was investigated on the microsomal
hepatic lipid peroxidation and NADPH-dependent reductase activities. Carbaryl did not affect lipid peroxidation
under in vivo conditions. Moreover, following administratin of the compound, the
activities of NADPH-cytochrome reductase as well as NADPH-neotetrazolium
reductase was not influenced by carbaryl.
Acutely sublethal concentrations of carbaryl induced alterations in the
cholesterol levels in Barbus conchonius. Carbaryl poisoning leads to a fall in blood,
kidney and testis cholesterol but liver and ovarium cholesterol levels were
markedly elevated. The pesticide interferes with cholesterol homeostasis in this
fish.
Biochemical and behavioral effects of carbaryl were investigated in chicks.
Six-day-old birds received 100 mg/kg body weight (bw) per day carbaryl for 7 days. Brain
acetylcholinesterase (AChE) and neuropathy target esterase (NTE) were measured
at 24 hr after the first, third, and fifth dose during the 1 wk of treatment,
and then at 1, 3, 6, 10, 20, 30, and 40 after the last dose. Gait analysis was
evaluated on each posttreatment day. No significant reduction in both neuropathy
target esterase and acetylcholinesterase activities was noticed throughout the
experiment. However, carbaryl altered
the locomotion of the chicks from day 1 until day 40 after last treatment.
Treated chicks walked with abnormal gait. Delayed ataxia and paralysis occurred
20 days after the last treatment and lasted until the end of the experiment.
Activation of the human complement (C') system, requires the participation of
serine esterases. Since the anticholinesterase insecticides inhibit serine
esterases, the C'-mediated lysis of sheep red cells was measured. At 0.5, to 3.0
mM, carbaryl, carbofuran, dichlorvos,
and DFP produced a dose-dependent inhibition of lysis, whereas paraoxon was not
inhibitory. On a molar basis, carbaryl
was three times more potent than DFP, and inhibited lysis 15-25 and 26-54% at
1.0 and 3.0 mM, respectively. Carbofuran, dichlorvos, and DFP were equipotent.
Young chickens were administered oral doses of either aldicarb (0.2 mg/kg
body wt/day) or carbaryl (100 mg/kg body
wt/day) for 7 days because this regimen had been demostrated to alter locomotor
activities. Activities of brain acetylcholinesterase (AChE) and neurotoxic
esterase (NTE), liver and plasma cholinesterase (ChE), and carboxylesterase were
measured to determine whether these parameters could be used to indicate,
predict, or monitor changes in locomotor activity. Activities of brain
acetylcholinesterase, plasma cholinesterase, plasma carboxylesterase, nad liver
cholinesterase were inhibited in young chicks by both carbaryl and aldicarb, with inhibitions
greater after carbaryl treatments.
Enzyme activities were not, however, inhibited in adult chickens. Carbamate
treatment did not cause histological damage nor did it inhibit activities of
neurotoxic esterase and liver carboxylesterase activities either in young or
adult chickens. Esterase determinations and histological studies could not be
used to predict or support carbamate-induced functional deficits.
In a subchronic study with cats, cholinergic signs appeared during the first
2 hr of each 6-hr inhalation exposure to carbaryl at 63 mg/cu m; at 40 mg/cu m blood
acetylcholinesterase inhibition and behavioral effects were noted ...
In a 1 yr study with dogs, carbaryl
in the diet at 1250 ppm reduced body weight gain, increased liver weight,
increased leukocyte and segmented neutrophil counts, decreased albumin levels,
and inhibited acetylcholinesterase in the plasma, erythrocytes, and brain.
Acetylcholinesterase inhibition was also observed at a dosage of 400 ppm, but
not at 125 ppm.
Carbaryl, when fed to hogs (150
mg/kg/day for 72 or 83 days), caused a rear leg paralysis, minimal at rest but,
when the animals were forced to move, resulting in marked incoordination,
ataxia, tremors, clonic muscle contractions, and prostration, with histological
evidence of lesions in the CNS and in skeletal muscle.
Non-Human Toxicity Values:
LD50 Rat oral 230 mg/kg
LD50 Rat skin 4000 mg/kg
LD50 Rat ip 64 mg/kg
LD50 Rat sc 1400 mg/kg
LD50 Rat iv 41,900 ug/kg
LD50 Mouse oral 128 mg/kg
LD50 Mouse ip 25 mg/kg
LD50 Mouse sc 6717 mg/kg
LD50 Rabbit skin 2000 mg/kg
Ecotoxicity Values:
LD50 PHEASANT ORAL GREATER THAN 2000 MG/KG, 3 MO OLD MALES /95% PURE/
LD50 PHEASANT ORAL 707 MG/KG, 3-4 MO OLD FEMALES /FORMULATION/
LD50 COTURNIX ORAL 2290 MG/KG, 2 MO OLD MALES (95% CONFIDENCE LIMITS
1740-3020 MG/KG) /85% PURE/
LD50 SHARP-TAILED GROUSE ORAL 780-1700 MG/KG, 3-12 MO OLD FEMALES /95% PURE/
LD50 CANADA GOOSE ORAL 1790 MG/KG (95% CONFIDENCE LIMITS 1480-2180 MG/KG)
/50% PURE/
LD50 BULLFROG ORAL GREATER THAN 4000 MG/KG, MALES /50% PURE/
LC50 ASELLUS 280 UG/L/96 HR (95% CONFIDENCE LIMIT 214-367 UG/L), MATURE
/TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 GAMMARUS LACUSTRIS 22 UG/L/96 HR (95% CONFIDENCE LIMIT 16-30 UG/L),
MATURE /TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 GAMMARUS FASCIATUS 26 UG/L/96 HR (95% CONFIDENCE LIMIT 16-39 UG/L),
MATURE /TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 PROCAMBARUS 1900 UG/L/96 HR (95% CONFIDENCE LIMIT 1160-3110 UG/L), EARLY
INSTAR /TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 PALAEMONETES 5.6 UG/L/96 HR (95% CONFIDENCE LIMIT 3.6-8.3 UG/L), MATURE
/TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 PTERONARCELLA 1.7 UG/L/96 HR (95% CONFIDENCE LIMIT 1.4-2.4 UG/L), NAIAD
/TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 PTERONARCYS 4.8 UG/L/96 HR (95% CONFIDENCE LIMIT 3.0-7.7 UG/L), SECOND
YR CLASS /TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 CLAASSENIA 5.6 UG/L/96 HR (95% CONFIDENCE LIMIT 3.9-8.1 UG/L), SECOND YR
CLASS /TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 SKWALA 3.6 UG/L/96 HR (95% CONFIDENCE LIMIT 2.4-5.5 UG/L), NAIAD
/TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 COHO SALMON 4340 UG/L/96 HR (95% CONFIDENCE LIMIT 3310-5690 UG/L), WT
1.0 G /TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 CHINOOK SALMON 2400 UG/L/96 HR (95% CONFIDENCE LIMIT 1620-3550 UG/L),
FINGERLING /TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 CUTTHROAT TROUT 7100 UG/L/96 HR (95% CONFIDENCE LIMIT 5240-9620 UG/L),
WT 0.5 G /TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 RAINBOW TROUT 1950 UG/L/96 HR (95% CONFIDENCE LIMIT 1450-2630 UG/L), WT
1.5 G /TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 ATLANTIC SALMON 4500 UG/L/96 HR (95% CONFIDENCE LIMIT 3820-5310 UG/L),
WT 0.4 G /TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 BROWN TROUT 6300 UG/L/96 HR (95% CONFIDENCE LIMIT 5520-7190 UG/L), WT
0.6 G /TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 BROOK TROUT 2100 UG/L/96 HR (95% CONFIDENCE LIMIT 1680-2620 UG/L), WT
0.8 G /TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 LAKE TROUT 690 UG/L/96 HR (95% CONFIDENCE LIMIT 520-910 UG/L), WT 1.7 G
/TECHNICAL MATERIAL 99.5%; STATIC BIOASSAY/
LC50 GOLDFISH 13200 UG/L/96 HR (95% CONFIDENCE LIMIT 8310-20800 UG/L), WT 0.9
G /TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 CARP 5280 UG/L/96 HR (95% CONFIDENCE LIMIT 4620-6050 UG/L), WT 0.6 G
/TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 FATHEAD MINNOW 14600 UG/L/96 HR (95% CONFIDENCE LIMIT 11700-19800 UG/L),
WT 0.8 G /TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 BLACK BULLHEAD 20000 UG/L/96 HR (95% CONFIDENCE LIMIT 18000-24000 UG/L),
WT 1.2 G /TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 CHANNEL CATFISH 15800 UG/L/96 HR (95% CONFIDENCE LIMIT 13900-18000
UG/L), WT 1.5 G /TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 GREEN SUNFISH 11200 UG/L/96 HR (95% CONFIDENCE LIMIT 8140-15500 UG/L),
WT 1.1 G /TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 BLUEGILL 6760 UG/L/96 HR (95% CONFIDENCE LIMIT 5220-8760 UG/L), WT 1.2 G
/TECHNICAL MATERIAL 99.5%; STATIC BIOASSAY/
LC50 LARGEMOUTH BASS 6400 UG/L/96 HR (95% CONFIDENCE LIMIT 4400-9200 UG/L),
WT 0.9 G /TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 BLACK CRAPPIE 2600 UG/L/96 HR (95% CONFIDENCE LIMIT 1180-5700 UG/L), WT
1.0 G /TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 YELLOW PERCH 5100 UG/L/96 HR (95% CONFIDENCE LIMIT 4520-5760 UG/L), WT
0.6 G /TECHNICAL MATERIAL, 99.5%; STATIC BIOASSAY/
LC50 SKWALA 9.2 UG/L/96 HR (95% CONFIDENCE LIMIT 7.4-12.0 UG/L), 1ST CLASS
INSTAR /OIL DISPERSION, 49%; STATIC BIOASSAY/
LC50 BROOK TROUT 4500 UG/L/96 HR (95% CONFIDENCE LIMIT 3948-5066 UG/L), WT
1.3 G /OIL DISPERSION, 49%; STATIC BIOASSAY/
LC50 BLUEGILL 39000 UG/L/96 HR (95% CONFIDENCE LIMIT 29732-51157 UG/L), WT
0.7 G /OIL DISPERSION, 49%; STATIC BIOASSAY/
LC50 BOBWHITES 23 DAYS OLD, MORE THAN 5000 PPM IN AD LIBITUM DIET
LC50 JAPANESE QUAIL 7 DAYS OLD, MORE THAN 5000 PPM IN AD LIBITUM DIET
LC50 RING-NECKED PHEASANT 23 DAYS OLD, MORE THAN 5000 PPM IN AD LIBITUM DIET
LC50 MALLARD 24 DAYS OLD, MORE THAN 5000 PPM IN AD LIBITUM DIET
LD50 MULE DEER ORAL 200-400 MG/KG, 11 MO OLD FEMALES /95% PURE/
LD50 PIGEON ORAL 1000-3000 MG/KG /85% PURE/
LC50 Coturnix japonica (Japanese quail) oral in 5 day diet ad libitum
>10,000 ppm /Technical grade, 98% AI/
LC50 Coturnix japonica (Japanese quail) oral in 5 day diet at libitum
>10,000 ppm /Commercial formulation, 50% AI (Sevin 50)/
LC50 Coturnix japonica (Japanese quail) oral in 5 day diet at libitum
>10,000 ppm /Commercial formulation as carbaryl-zineb (3.0% carbaryl AI and 5.2% zineb AI)/
LC50 Pimephales promelas (fathead minnows) 29 days old 6.67 mg/l/96 hr at
25.8 deg C, 6.7 mg/l dissolved oxygen, 45.4 mg/l CaCO3 water hardness, 43.4 mg/l
CaCO3 alkalinity, pH 7.7, 1.0 l tank volume, tank additions 14.4 vol/day (98%
confidence limit 6.05 to 7.34 mg/l), flow-through bioassay /Purity, 99%/
EC50 Pimephales promelas (fathead minnows) 29 days old 5.29 mg/l/96 hr at
25.8 deg C, 6.7 mg/l dissolved oxygen, 45.4 mg/l CaCO3 water hardness, 43.4 mg/l
CaCO3 alkalinity, pH 7.7, 1.0 l tank volume, tank additions 14.4 vol/day (95%
confidence limit 4.80 to 5.82 mg/l), flow-through bioassay /Purity, 99%/
LC50 Pimephales promelas (fathead minnows) 28 days old 8.93 mg/l/96 hr at
26.0 deg C, 6.7 mg/l dissolved oxygen, 45.4 mg/l CaCO3 water hardness, 43.4 mg/l
CaCO3 alkalinity, pH 7.7, 1.0 l tank volume, tank additions 14.4 vol/day (98%
confidence limit 8.43 to 9.46 mg/l), flow-through bioassay /Purity, 99%/
LC50 Pimephales promelas (fathead minnows) 28 days old 7.47 mg/l/96 hr at
26.0 deg C, 6.7 mg/l dissolved oxygen, 45.4 mg/l CaCO3 water hardness, 43.4 mg/l
CaCO3 alkalinity, pH 7.7, 1.0 l tank volume, tank additions 14.4 vol/day (95%
confidence limit 6.00 to 9.30 mg/l), flow-through bioassay /Purity, 99%/
LC50 Pimephales promelas (fathead minnows) 28 days old 10.4 mg/l/96 hr at
24.5 deg C, 7.0 mg/l dissolved oxygen, 44.1 mg/l CaCO3 water hardness, 44.9 mg/l
CaCO3 alkalinity, pH 7.7, 1.0 l tank volume, tank additions 14.4 vol/day (98%
confidence limit 9.55 to 11.3 mg/l), flow-through bioassay /Purity, 99%/
EC50 Pimephales promelas (fathead minnows) 28 days old 6.40 mg/l/96 hr at
24.5 deg C, 7.0 mg/l dissolved oxygen, 44.1 mg/l CaCO3 water hardness, 44.9 mg/l
CaCO3 alkalinity, pH 7.7, 1.0 l tank volume, tank additions 14.4 vol/day (98%
confidence limit 5.20 to 7.87 mg/l), flow-through bioassay /Purity, 99%/
LC50 Pimephales promelas (fathead minnows) 31 days old 9.47 mg/l/96 hr at
24.2 deg C, 7.0 mg/l dissolved oxygen, 43.8 mg/l CaCO3 water hardness, 41.5 mg/l
CaCO3 alkalinity, pH 7.7, 1.0 l tank volume, tank additions 14.4 vol/day (98%
confidence limit 8.60 to 10.4 mg/l), flow-through bioassay /Purity, 99%/
LC50 Pimephales promelas (fathead minnows) 31 days old 6.42 mg/l/96 hr at
24.2 deg C, 7.0 mg/l dissolved oxygen, 43.8 mg/l CaCO3 water hardness, 41.5 mg/l
CaCO3 alkalinity, pH 7.7, 1.0 l tank volume, tank additions 14.4 vol/day (98%
confidence limit 5.57 to 7.40 mg/l), flow-through bioassay /Purity, 99%/
TSCA Test Submissions:
Carbaryl (CAS # 63-25-2) 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 unspecified, 26 cultures/assay,
>200,000 cells/culture) in minimal medium with 1% fetal bovine serum were
exposed to 12 graded doses (unspecified) for 72 to 96 hours. A reflection of
effects on growth and reproduction of the indicator cells, the change in protein
synthesis 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 3.6 mg/L killed all L-cells within 4 days. Levels
greater than 0.56 mg/L inhibited protein production, and an LC50 was 2.0 mg/L.
The LC50 (2 mg/L) was lower than the NOEL in chronic animal studies (200 ppm in
rats and dogs) and higher than WHO/FAO's maximum daily intake standard (0.02
mg/kg/day). A positive relationship was established by a two-way ANOVA
statistical method in both instances, however, indicating a relevant
toxicological result with the cell bioassay. Unstable and not considered a
serious pollutant in an aqueous environment, carbaryl 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 (0.06 or 3.0 mg/L, respectively) would be primarily
undetectable with the tissue culture bioassay.
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
SEVIN, LABELED WITH (14)C, IS METABOLIZED IN INSECTS, IN RAT, AND BY
MICROSOMAL PREPN OF MOUSE, RAT & RABBIT LIVER, BY AROMATIC HYDROXYLATION,
N-METHYL HYDROXYLATION, HYDROLYSIS OF CARBAMYL GROUPING, & BY CONJUGATION.
SINGLE ORAL DOSE OF CARBARYL WAS
ADMIN TO RATS. AFTER EXTRACTION OF ... URINE, COLUMN & TLC CHROMOTOGRAPHY,
TENTATIVE IDENTIFICATION WAS MADE FOR 1,5-NAPHTHALENEDIOL WITH SMALL AMT OF
CARBARYL, 5-HYDROXYCARBARYL, & TRACE
OF N-HYDROXYMETHYLCARBARYL WAS ALSO PRESENT. A MAJOR METAB ... IDENTIFIED AS
5,6-DIHYDRO-5,6-DIHYDROXYCARBARYL, WAS FOUND FREE (1.4% OF THE DOSE) & AS
THE GLUCURONIDE (10.5% OF THE DOSE). NAPHTHYL GLUCURONIDE & SULFATE WERE
ALSO OBSERVED.
IN URINE OF RATS IN ADDN TO 1-NAPHTHOL, 1-NAPHTHYL METHYLCARBAMATE
N-GLUCURONIDE, 1-NAPHTHYL METHYLIMIDO-CARBONATE O-GLUCURONIDE,
4-(METHYLCARBAMOYLOXY)-1-NAPHTHYL GLUCURONIDE, 1-NAPHTHYL GLUCURONIDE,
1-NAPHTHYL SULFATE, 4-(METHYLCARBAMOYLOXY)-1-NAPHTHYL SULFATE, 3 UNIDENTIFIED
CMPD & CMPD BELIEVED TO BE 1-NAPHTHYL N-HYDROXYMETHYLCARBAMATE WERE
OBSERVED. SIMILAR RESULTS WERE OBSERVED WITH GUINEA PIGS.
Using rat tissue fractions, carbaryl
metabolism was greater in hepatic microsomal fraction than in any other
preparation/ 1-Naphthol was the major metabolite in all rat tissue fractions.
However, in the postmitochondrial fraction of liver, 1-naphthyl-N-hydroxymethyl
carbamate & 1-naphthol were ... produced. With carbaryl & rat blood, lung, kindey &
testis tissues, 1-naphthol, 5-hydroxycarbaryl, hydroxymethylcarbaryl, & two
unknowns were formed; with liver, 4-hydroxycarbaryl &
5,6-dihydro-5,6-dihydroxycarbaryl were also observed.
AFTER ADMIN OF (14)C-LABELED CARBARYL
TO LACTATING COWS RADIOACTIVE RESIDUES WERE OBSERVED IN WHOLE MILK & IN MILK
FAT, TISSUES, URINE & FECES. IN ADDN TO 1-NAPHTHOL IN URINE, 5 COMPOUNDS
WERE OBSERVED IN FECES & MILK: 5,6-DIHYDROXY-5,6-DIHYDRONAPHTHYL
N-METHYLCARBAMATE; 1,5,6-TRIHYDROXY-5,6-DIHYDRONAPHTHALENE;
1-NAPHTHYL-N-HYDROXYMETHYLCARBAMATE; 4-HYDROXY-1-NAPHTHYL N-METHYLCARBAMATE;
& UNCHANGED CARBARYL.
WHITE LEGHORN LAYING HENS WERE TREATED WITH CARBARYL (SEVIN) BY DIPPING IN A 0.5 OR 1.0%
(ACTIVE INGREDIENT) WATER SUSPENSION OF AN 80%, COMMERCIALLY AVAILABLE, WETTABLE
POWDER FORMULATION. RESIDUES OF CARBARYL
& TWO OF ITS METABOLITES, 1-NAPHTHOL & N-HYDROXYMETHYL CARBARYL, WERE DETECTED IN EGGS WITHIN 1 DAY
& REACHED MAX LEVELS 5-7 DAYS AFTER DIPPING. AFTER THAT TIME RESIDUES
STEADILY DECLINED BUT WERE STILL DETECTABLE 56 DAYS POSTTREATMENT IN THE EGGS OF
THE HIGH-DOSE HENS.
THE BILIARY SECRETION OF (14)C WAS OBSERVED IN CONSCIOUS, BILE-FISTULATED
RATS GIVEN SINGLE ORAL DOSES OF (14)C-LABELED CARBARYL (1.5, 30, & 300 MG/KG). OVER 94%
OF THE (14)C WAS ABSORBED AFTER 12 HR. FROM 15 TO 46% OF THE (14)C WAS SECRETED
IN BILE, 10-40% IN URINE, & LESS THAN 1% IN FECES 12 HR AFTER DOSING. THREE
METABOLITES WERE ISOLATED FROM BILE & IDENTIFIED BY MASS &/OR NMR
SPECTROMETRIC METHODS. THESE METABOLITES WERE: 5,6-DIHYDRO-5,6-DIHYDROXYCARBARYL
GLUCURONIDE (12-18% OF THE BILIARY (14)C), A CONJUGATE(S) OF CARBARYL (12% OF THE BILIARY (14)C), &
CONJUGATED ISOMERS OF HYDROXYCARBARYL (2% OF THE BILIARY (14)C). THE MAJORITY OF
THE BILIARY (14)C REMAINS TO BE IDENTIFIED.
At an alkaline pH and in aqueous solution, carbaryl hydrolyzes to form 1-naphthol,
methylamine and carbon dioxide, but it is much more stable at an acid pH. Two
bacteria isolated from garden soil, Pseudomonas sp (NCIB 12042) and rhodococcus
sp (NCIB 12038), could grow on carbaryl
as sole carbon and nitrogen source at pH 6.8 but failed to metabolize carbaryl rapidly. Both could use 1-naphthol as
sole carbon source and NCIB 12042 metabolized 1-naphthol via salicyclic acid
which induced higher expression of enzymes in the pathway. Strain NCIB 12038
metabolized 1-naphthol via salicylic and gentisic acids. In contrast,
Pseudomonas sp (NCIB 12043) was selected in a soil perfusion column enrichment
at pH 5.2 and metbaolized carbaryl
rapidly to 1-naphthol and methylamine. 1-Naphthol was metabolized via gentisic
acid. Neither salicylate nor gentisate induced higher expression of enzymes for
1-naphthol catabolism in NCIB 12038 and NCIB 12043.
Liver tissue from a man, guinea pig & dog was incubated with carbaryl. Identified metabolites were the same
in each case: naphthyl sulfate, naphthyl glucuronide, hydroxycarbaryl sulfate,
hydroxycarbaryl glucuronide, & 5,6-dihydroxycarbaryl glucuronide. Three
compounds were not identified.
Studies with perfused lung tissue /of rabbits/ indicated that lungs were able
to take up carbaryl & metabolize it.
Metabolism was rapid with over 22% of the dose metabolized within 5 min. Only
alpha-naphthol & 4-hydroxycarbaryl were identified.
In rainbow trout (Salmo gairdneri), carbaryl gave rise to 1-naphthyl glucuronide
& 5,6-dihydro-5,6-dihydroxycarbaryl.
Larvae of resistant Anopheles albimanus metabolized carbaryl to N-hydroxymethylcarbaryl, the
5,6-dihydrodihydroxycarbaryl & an unidentified metabolite.
Tobacco cells in suspension culture were incubated with (14)C-carbaryl labeled in the C1-naphthyl, carbonyl,
or N-methyl position. About 18% of the characterized metabolites was in the form
of N-hydroxymethylcarbaryl, which was excreted by the cells into the culture
medium. Within the cells, the metabolites consisted mostly of conjugates of
1-naphthol (about 73% of characterized metabolites), N-methylhydroxycarbaryl,
7-hydroxycarbaryl, 4-hydroxycarbaryl, 5-hydroxycarbaryl. A new type of plant
conjugate was identified as O-1-naphthylcholesterol
(cholest-5-en-3beta-yl-1-naphthol). An unconjugated metabolite was tentatively
identified as 1,4-dihydro-1,4-epiperoxynaphthalene. Not completely characterized
but also observed was a beta-glucosidase-resistant conjugate of a
cis-dihydrodiol.
The effect of phenobarbital pretreatment on the metabolism of carbaryl was studied in male Sprague-Dawley
rats given intraperitoneal doses of phenobarbital at 75 mg/kg daily for 5 days.
On day five (14)C labeled carbaryl was
administered orally at 1.64 or 16.4 mg/kg, 4 hr following the phenobarbital
dose. About half of the administered carbaryl was excreted in the urine in the
first 24 hr. Carbaryl underwent hydrolys
is followed by conjugation of hydrolytic products forming 1-naphthyl-sulfate and
1-naphthyl-glucuronide conjugates. At the higher carbaryl dose level rats showed typical signs
of acetylcholinesterase inhibition, but no mortality. Neither the oxidative nor
conjugative biotransformation of carbaryl was induced by phenobarbital dosing
when carbaryl was administered at the
low dose level. Phenobarbital pretreatment at the higher carabaryl dose level
enhanced only sulfate conjugation of carbaryl, which may be due to either a higher
affinity and accessibility of the carbaryl to the cytosolic sulfotransferase or
saturation of the glucuronide conjugation pathway.
An enzyme that hydrolyzes the carbamate linkage of carbofuran
(2,3-dihydro-2,2-dimethyl-7- benzofuranyl N-methylcarbamate) was detected in
crude extracts of a carbofuran degrading Achromobacter sp. It was soluble with a
molecular size of 105,000 Da. No cofactor requirement could be demonstrated. The
optimum pH was broad (9.0-10.5), Km values of 56, 15, and 2800 uM were
determined for carbofuran, carbaryl
(1-naphthyl N-methylcarbamate), and aldicarb (2-methyl-2-
(methylthio)propionaldehyde O-(N-methylcarbamoyl)oxime), respectively. A product
of carbofuran hydrolysis was identified as 2,3-dihydro-2,2-dimethyl-7-
benzofuranol. A product carbaryl
degradation cochromatographed with 1-naphthol. The enzyme was unable to
hydrolyze prathion (O,O-diethyl O(p-nitrophenyl) phosphorothioate), or EPTC
(S-ethyl dipropylthiocarbamate).
The in vitro interaction of carbaryl
with rat liver microsomal monooxygenase activities was studied. The inhibition
induced by the parent amide is found to be competitive on aminopyrine
N-demethylase and p-nitroanisole O-demethylase. In vitro studies of the
metabolism of the compound was carried out: it yielded formaldehyde.
Absorption, Distribution & Excretion:
EXCRETION--RETENTION OF ... CARBARYL
LABELED IN 3 DIFFERENT POSITIONS ... STUDIED 48 HR AFTER IP ADMIN TO RATS. 65%
OF (14)C OF CARBONYL-(14)C-CARBARYL WAS
EXCRETED IN URINE, 25% IN EXPIRED AIR, 2% IN FECES, & 10% WAS RETAINED ...
HIGHEST LEVELS OF (14)C WERE PRESENT IN LIVER, KIDNEYS, HEART, & CORPUSCLES
(ERYTHROCYTES & LEUCOCYTES). 58% OF (14)C OF N-METHYL-(14)C-CARBARYL WAS EXCRETED IN URINE, 12% IN EXPIRED
AIR, 4% IN FECES, & 13% WAS RETAINED ... (14)C WAS MAXIMAL IN LIVER,
KIDNEYS, HEART, LUNGS, & SPLEEN, ORGANS WITH HIGH BLOOD FLOW. 77% OF (14)C
OF NAPHTHYL-(14)C-CARBARYL WAS EXCRETED
IN URINE, 9% IN FECES, & 7% WAS RETAINED ... LEVELS OF (14)C IN TISSUE WERE
HIGHEST IN KIDNEYS, SPLEEN, BONE, & FAT ... ABOUT 50% OF (14)C HAD BEEN
EXCRETED IN 4 HR ... .
OF ORAL DOSE OF (1-NAPHTHYL-1-(14)C)-N-METHYLCARBAMATE GIVEN TO RATS, 53%
& 82% WERE ABSORBED AFTER 20 MIN & 1 HR, RESPECTIVELY. CARBARYL IS ABSORBED VERY RAPIDLY FROM LUNG,
2.5 TIMES FASTER THAN FROM SMALL INTESTINE.
(14)C-CARBARYL LABELED IN N-METHYL
GROUP HAS BEEN FOUND IN FETUSES OF PREGNANT RATS, & MICE. ...
AUTORADIOGRAPHIC STUDY OF (14)C-METHYL-CARBARYL IN PREGNANT RAT HAS SHOWN THAT
RADIOLABEL WAS LOCALIZED IN EYE, LIVER, & BRAIN OF FETUS.
WORKERS ENGAGED IN PRODUCTION, COLLECTION & BAGGING OF CARBARYL WERE EXPOSED BY INHALATION TO 0.23-31
MG DUST/CU M; THEY EXCRETED UP TO 80 MG 1-NAPHTHOL/DAY ... LARGE PROPORTION OF
CARBARYL APPLIED TO FOREARMS OF HUMAN
VOLUNTEERS WAS ABSORBED, & 74% OF DOSE WAS EXCRETED IN URINE.
THE BILIARY SECRETION OF (14)C WAS OBSERVED IN CONSCIOUS, BILE-FISTULATED
RATS GIVEN SINGLE ORAL DOSES OF (14)C-LABELED CARBARYL (1.5, 30, & 300 MG/KG). OVER 94%
OF THE (14)C WAS ABSORBED AFTER 12 HR. FROM 15 TO 46% OF THE (14)C WAS SECRETED
IN BILE, 10-40% IN URINE, & LESS THAN 1% IN FECES 12 HR AFTER DOSING.
Bean plants were treated with carbaryl & the bound residues were fed to
rats. About 98% of the dose was eliminated in feces within 48 hr. Urinary
excretion amounted to 1.3%.
In rats, carbaryl was absorbed more
rapidly from the intestine than from the stomach. Absorption was most rapid when
dimethyl sulfoxide was the vehicle and was more rapid with oil than with gum
tragacanth or milk.
Dogs excreted in their urine none of the metabolites found in rat urine.
Biological Half-Life:
... The half-life of carbaryl was 6.4
min in the empty small intestines and 2.6 min in the lungs of rats.
Mechanism of Action:
The mode of action of carbaryl is
inhibition of the acetylcholinesterase, although there is evidence that the
inhibition is reversible under some conditions, in contrast with that caused by
the organophosphorus insecticides.
It inactivates cholinesterase, resulting in the accumulation of acetylcholine
at synapses in the nervous system, at neuromuscular junctions of the skeletal
and smooth muscles, and secretory glands.
The carbamate insecticides are reversible cholinesterase-inhibitors. They
cause this effect by reversible carbamylation of the enzyme
acetylcholinesterase, allowing accum of acetylcholine, as with the
organophosphate insecticides. ... While the organophosphate insecticides cause
irreversible inhibition of the cholinesterase enzymes, the carbamyl-enzyme
complex is reversible & dissociates far more readily than the
organophosphate complex. The clinical syndrome is more benign & of much
shorter duration with the carbamate insecticides. Unlike the the
organophosphates, the carbamates poorly penetrate the CNS. Thus, the clinical
presentation of the carbamates resembles that of the organophosphates with
exception of prominent CNS effects, such as convulsions. Convulsions are
uncommon with the carbamate insecticides. Serum & red cell cholinesterase
values are not reliable in "capturing" the diagnosis of carbamate poisoning, as
they are with the organophosphates, for enzyme activity ... returns to normal
within a few hours. A patient may show symptoms in the emergency room 6 hr after
exposure, but the cholinesterase levels already may have returned to normal.
/Carbamate insecticides/
Interactions:
ANTIDIURETIC AGENT DIAZOXIDE ... INCR 20-FOLD TOXICITY OF CARBARYL IN PIG.
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.
Diquat was reported to be a potential inhibitor of aldrin epoxidation by the
microsomal mixed function oxidases in the goldfish & mosquito fish. After
mosquito fish were exposed to aldrin for 24 hr, dieldrin accounted for 23% of
the residues extracted from the tissues. Addition of diquat to the test water at
8X10-4 molar concn led to the finding of negligible quantities of dieldrin in
the water as well as hexane extracts of the tissues. The aldrin epoxidase system
of various tissue homogenates of mosquito fish & goldfish was inhibited by
/In the goldfish and mosquito/ the 24 hr toxicity of DDT, aldrin, &
parathion was not affected by 275 mg/l diquat, whereas the acute toxicity of
carbaryl was increased at this concn.
Inhibition of acetylcholinesterase and accumulation of acetylcholine were
observed in tissues of fish, Channa punctatus, during carbaryl and/or phenthoate toxicity. Carbaryl in combination with phenthoate
exerted synergism on the acetylcholinesterase system during their interaction.
Malathion-induced marked potential of 2-sec-butylphenyl N-methylcarbamate
toxicity (about fivefold) was analyzed by measuring LD50 as an index of acute
toxicity. The acute lethality of 2-sec-butylphenyl N-methylcarbamate was
decreased by muscarinic blockers (atropine, methylatropine, or trihexyphenidyl)
or a monoamine oxidase inhibitor (pargyline) and increased by a monoamine
depleter (reserpine) or a dopaminergic blocker (haloperidol). The potentiation
observed with 2-sec-butylphenyl N-methylcarbamate and malathion was decreased by
the muscarinic blockers, monoamine depleters (reserpine,
alpha-methyl-p-tyrosine), an alpha-noradrenergic blocker (phentolamine), or
haloperidol. The acute toxicities of other N-methylcarbamates MPMC
(3,4-dimethlphenyl N-methylcarbamate) MTMC (3-methylphenyl N-methylcarbamate),
NAC (1-naphthyl N-methylcarbamate), and XMC (3,5-dimethylphenyl
N-methylcarbamate) were potentiated by malathion to a lesser degree than that of
2-sec-butylphenyl N-methylcarbamate. Atropine protected against the lethalities
of all N-methylcarbamates. Reserpine or haloperidol potentiated the lethalities
of N-methylcarbamates with a similar tendency toward malathion. When the
inhibitory effect of each N-methylcarbamate or brain acetylcholinesterase (AChE)
was compared with its LD50, among five N-methylcarbamates 2-sec-butylphenyl
N-methylcarbamate had particularly strong anti-AChE activity. This
characteristic of 2-sec-butylphenyl N-methylcarbamate was not observed after the
treatment with reserpine. 2-sec-Butylphenyl N-methylcarbamate may act not only
on cholinergic nerves as an anti-AChE but also on monoaminergic nerves which
antagonize the lethal cholinergic effect. Malathion might inhibit the effect of
2-sec-butylphenyl N-methylcarbamate on the monoaminergic nerves, thereby
markedly potentiating the lethal effect of 2-sec-butylphenyl N-methylcarbamate.
The efficacy of the oximes pyridinium-2-aldoxime methochloride (2-PAM) and
1-[[[(4-aminocarbonyl)pyridinio]methoxy]methyl]-2-[(hydroxyimino) methyl)]
pyridinium dichloride (HI-6), in combination with atropine, against lethality by
either carbaryl or physostigmine was
investigated in rats. The protection by atropine, 8 mg/kg, iv, against carbaryl intoxication was reduced by
pyridinium-2-aldoxime methochloride (22 mg/kg, iv) and
1-[[[4-aminocarbonyl)pyridinio]methoxy]methyl]-2-[(hydroxyimino)methyl)]
pyridinium dichloride (50 mg/kg, iv) from a protective ratio of 6.6 to 3.5 and
2.3, respectively. However, in physostigmine-intoxicated rats, the
administration, iv, of atropine alone, atropine + pyridinium-2-aldoxime
methochloride, or atropine +
1-[[[4-aminocarbonyl)pyridinio]methoxy]methyl]-2-[(hydroxyimino) methyl]
pyridinium dichloride at 1 min following physostigmine provided good protection
and resulted in protective ratios of 7.2 and 23.3, respectively. In experiments
on decarbamylation of inhibited acetylcholinesterase (AChE),
1-[[[(4-aminocarbonyl)pyridinio]methoxy]methyl]-2-[(hydroxyimino)methyl]
pyridinium dichloride and pyridinium-2-aldoxime methochloride accelerated (p
< 0.05) the decarbamylation of physostigmine-inhibited acetylcholinesterase
in vitro, and 1-[[[(4-aminocarbonyl)pyridinio]methoxy]methyl]-2-[(hydroxyimino)
methyl] pyridinium dichloride decreased (p < 0.05) the inhibition of whole
blood acetylcholinesterase in physostigmine-intoxicated rats. The protection was
increased substantially by the use of either pyridinium-2-aldoxime methochloride
or 1-[[[(4-aminocarbonyl)pyridinio]methoxy]methyl]-2- [(hydroxyimino)
methyl]pyridinium dichloride against physostigmine-induced lethality, whereas
the use of oximes against carbaryl
poisoning was contraindicated. Furthermore, even though carbaryl and physostigmine are both N-methl
carbamates, there is no adverse interaction between pyridinium-2-aldoxime
methochloride or 1-[[[(4-aminocarbonyl)pyridinio]methoxy]-
2-[(hydroxyimino)methyl] pyridinium dichloride and physostigmine.
Mice pretreated with the liver microsomal enzyme inducer phenobarbital were
less susceptible to carbaryl poisoning,
and those pretreated with the microsomal enzyme inhibitor SKF 525A were more
susceptible. Toxicity of carbaryl was
increased by pretreatment with the drugs reserpine and chlordiazepoxide and
decreased by chlorpromazine and meprobamate.
Carbaryl caused a threefold increase
in the toxicity of coadministered niridazole to rats. Coadministration of
lindane and carbaryl to rats produced a
slight increase in their lethal effect.
Carbaryl-induced tremors in rats were
significantly reduced by pretreatment with L-dopa and exacerbated by haloperidol
...
Coadministration of malathion and carbaryl to rats altered pharmacokinetic
parameters for both pesticides and delayed the elimination of (14)C-carbaryl from gastrointestinal tissues.
Diphenyl, o-phenylphenol, piperonyl butoxide,and thiabendazole potentiated the
effects of carbaryl when administered in
equitoxic acute oral doses to mice.
In the male mouse, carbaryl treatment
increases the hydroxylation of testosterone but does not increase the formation
of polar metabolites. Carbaryl also
stimulates the conversion of testosterone to 5alpha-DHT by prostatic tissue in
vitro.
Pharmacology:
Therapeutic Uses:
Formulations of carbaryl have been
used successfully to control human lice.
TO CONTROL FLEAS, LICE, TICKS, & MITES ON ANIMALS, POULTRY, &
PREMISES, INCL SARCOPTIC MANGE ON BUFFALOES; LICE, TICKS, & MANGE MITES ON
CATTLE; FLEAS & RESISTANT FLEAS ON DOGS; & FOWL MITES, LICE, & FLEAS
ON POULTRY.
Medication (Vet): Ectoparasiticide
Interactions:
ANTIDIURETIC AGENT DIAZOXIDE ... INCR 20-FOLD TOXICITY OF CARBARYL IN PIG.
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.
Diquat was reported to be a potential inhibitor of aldrin epoxidation by the
microsomal mixed function oxidases in the goldfish & mosquito fish. After
mosquito fish were exposed to aldrin for 24 hr, dieldrin accounted for 23% of
the residues extracted from the tissues. Addition of diquat to the test water at
8X10-4 molar concn led to the finding of negligible quantities of dieldrin in
the water as well as hexane extracts of the tissues. The aldrin epoxidase system
of various tissue homogenates of mosquito fish & goldfish was inhibited by
/In the goldfish and mosquito/ the 24 hr toxicity of DDT, aldrin, &
parathion was not affected by 275 mg/l diquat, whereas the acute toxicity of
carbaryl was increased at this concn.
Inhibition of acetylcholinesterase and accumulation of acetylcholine were
observed in tissues of fish, Channa punctatus, during carbaryl and/or phenthoate toxicity. Carbaryl in combination with phenthoate
exerted synergism on the acetylcholinesterase system during their interaction.
Malathion-induced marked potential of 2-sec-butylphenyl N-methylcarbamate
toxicity (about fivefold) was analyzed by measuring LD50 as an index of acute
toxicity. The acute lethality of 2-sec-butylphenyl N-methylcarbamate was
decreased by muscarinic blockers (atropine, methylatropine, or trihexyphenidyl)
or a monoamine oxidase inhibitor (pargyline) and increased by a monoamine
depleter (reserpine) or a dopaminergic blocker (haloperidol). The potentiation
observed with 2-sec-butylphenyl N-methylcarbamate and malathion was decreased by
the muscarinic blockers, monoamine depleters (reserpine,
alpha-methyl-p-tyrosine), an alpha-noradrenergic blocker (phentolamine), or
haloperidol. The acute toxicities of other N-methylcarbamates MPMC
(3,4-dimethlphenyl N-methylcarbamate) MTMC (3-methylphenyl N-methylcarbamate),
NAC (1-naphthyl N-methylcarbamate), and XMC (3,5-dimethylphenyl
N-methylcarbamate) were potentiated by malathion to a lesser degree than that of
2-sec-butylphenyl N-methylcarbamate. Atropine protected against the lethalities
of all N-methylcarbamates. Reserpine or haloperidol potentiated the lethalities
of N-methylcarbamates with a similar tendency toward malathion. When the
inhibitory effect of each N-methylcarbamate or brain acetylcholinesterase (AChE)
was compared with its LD50, among five N-methylcarbamates 2-sec-butylphenyl
N-methylcarbamate had particularly strong anti-AChE activity. This
characteristic of 2-sec-butylphenyl N-methylcarbamate was not observed after the
treatment with reserpine. 2-sec-Butylphenyl N-methylcarbamate may act not only
on cholinergic nerves as an anti-AChE but also on monoaminergic nerves which
antagonize the lethal cholinergic effect. Malathion might inhibit the effect of
2-sec-butylphenyl N-methylcarbamate on the monoaminergic nerves, thereby
markedly potentiating the lethal effect of 2-sec-butylphenyl N-methylcarbamate.
The efficacy of the oximes pyridinium-2-aldoxime methochloride (2-PAM) and
1-[[[(4-aminocarbonyl)pyridinio]methoxy]methyl]-2-[(hydroxyimino) methyl)]
pyridinium dichloride (HI-6), in combination with atropine, against lethality by
either carbaryl or physostigmine was
investigated in rats. The protection by atropine, 8 mg/kg, iv, against carbaryl intoxication was reduced by
pyridinium-2-aldoxime methochloride (22 mg/kg, iv) and
1-[[[4-aminocarbonyl)pyridinio]methoxy]methyl]-2-[(hydroxyimino)methyl)]
pyridinium dichloride (50 mg/kg, iv) from a protective ratio of 6.6 to 3.5 and
2.3, respectively. However, in physostigmine-intoxicated rats, the
administration, iv, of atropine alone, atropine + pyridinium-2-aldoxime
methochloride, or atropine +
1-[[[4-aminocarbonyl)pyridinio]methoxy]methyl]-2-[(hydroxyimino) methyl]
pyridinium dichloride at 1 min following physostigmine provided good protection
and resulted in protective ratios of 7.2 and 23.3, respectively. In experiments
on decarbamylation of inhibited acetylcholinesterase (AChE),
1-[[[(4-aminocarbonyl)pyridinio]methoxy]methyl]-2-[(hydroxyimino)methyl]
pyridinium dichloride and pyridinium-2-aldoxime methochloride accelerated (p
< 0.05) the decarbamylation of physostigmine-inhibited acetylcholinesterase
in vitro, and 1-[[[(4-aminocarbonyl)pyridinio]methoxy]methyl]-2-[(hydroxyimino)
methyl] pyridinium dichloride decreased (p < 0.05) the inhibition of whole
blood acetylcholinesterase in physostigmine-intoxicated rats. The protection was
increased substantially by the use of either pyridinium-2-aldoxime methochloride
or 1-[[[(4-aminocarbonyl)pyridinio]methoxy]methyl]-2- [(hydroxyimino)
methyl]pyridinium dichloride against physostigmine-induced lethality, whereas
the use of oximes against carbaryl
poisoning was contraindicated. Furthermore, even though carbaryl and physostigmine are both N-methl
carbamates, there is no adverse interaction between pyridinium-2-aldoxime
methochloride or 1-[[[(4-aminocarbonyl)pyridinio]methoxy]-
2-[(hydroxyimino)methyl] pyridinium dichloride and physostigmine.
Mice pretreated with the liver microsomal enzyme inducer phenobarbital were
less susceptible to carbaryl poisoning,
and those pretreated with the microsomal enzyme inhibitor SKF 525A were more
susceptible. Toxicity of carbaryl was
increased by pretreatment with the drugs reserpine and chlordiazepoxide and
decreased by chlorpromazine and meprobamate.
Carbaryl caused a threefold increase
in the toxicity of coadministered niridazole to rats. Coadministration of
lindane and carbaryl to rats produced a
slight increase in their lethal effect.
Carbaryl-induced tremors in rats were
significantly reduced by pretreatment with L-dopa and exacerbated by haloperidol
...
Coadministration of malathion and carbaryl to rats altered pharmacokinetic
parameters for both pesticides and delayed the elimination of (14)C-carbaryl from gastrointestinal tissues.
Diphenyl, o-phenylphenol, piperonyl butoxide,and thiabendazole potentiated the
effects of carbaryl when administered in
equitoxic acute oral doses to mice.
In the male mouse, carbaryl treatment
increases the hydroxylation of testosterone but does not increase the formation
of polar metabolites. Carbaryl also
stimulates the conversion of testosterone to 5alpha-DHT by prostatic tissue in
vitro.
Environmental Fate & Exposure:
Environmental Fate/Exposure Summary:
Carbaryl's production and use as a
pesticide is expected to result in its direct release to the environment. If
released to air, a vapor pressure of 3.97X10-5 mm Hg at 25 deg C indicates carbaryl will exist in both the vapor and
particulate phases in the ambient atmosphere. Vapor-phase carbaryl 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 15 hrs. This is in agreement with various
papers citing the half-life of carbaryl
reacting with hydroxyl radical in the ambient atmosphere as less than one day.
Particulate-phase carbaryl will be
removed from the atmosphere by wet and dry deposition. Photolysis half-lives
calculated from sunlight intensity data and experimentally determined quantum
efficiencies ranged from 52 (carbaryl in
<10 cm water) to 264 hrs for a summer day at latitude 40 degrees north. If
released to soil, carbaryl is expected
to have moderate mobility based upon a Koc of 251. Carbaryl is expected to slowly photolyze on
surface soil at a rate dependent on the water content. Volatilization from moist
soil surfaces is not expected to be an important fate process based upon an
estimated Henry's Law constant of 8.8X10-8 atm-cu m/mole. Carbaryl is not expected to volatilize from
dry soil surfaces based upon its vapor pressure. Various soil fungi are able to
metabolize carbaryl and in soils
previously treated with carbamates and cloethocarb, 80% of carbaryl was completely mineralized to carbon
dioxide during a four week incubation period. If released into water, carbaryl is not expected to adsorb to sediment
and suspended solids in water based upon the Koc. Biodegradation of carbaryl occurred in a mixture of
non-acclimated sludge, field soil and river sediment at 18-22 deg C with a
half-life of 0.34 days. Volatilization from water surfaces is not expected to be
an important fate process based upon this compound's estimated Henry's Law
constant. BCF values ranging from 9-34 suggests bioconcentration in aquatic
organisms is low. At 20 deg C, hydrolysis half-lives of carbaryl in water are 10.5 days, 1.8 days, 2.5
hours, and 15 min at pH values of 7, 8, 9, and 10, respectively. Occupational
exposure to carbaryl may occur through
inhalation and dermal contact with this compound at workplaces where carbaryl is produced or used. Workers engaged
in production, formulation and application of carbaryl as a contact insecticide for fruits,
vegetables, cotton, and other crops are especially prone to exposure to carbaryl. The general population may be
exposed to carbaryl via inhalation of
ambient air, ingestion of food and drinking water and pesticide products
containing carbaryl. (SRC)
Probable Routes of Human Exposure:
Workers engaged in production, formulation and application of carbaryl as a contact insecticide for fruits,
vegetables, cotton, and other crops.
Mean dermal exposure to carbaryl
ranged from 0.50 mg/hr (lower arms) - 1.90 mg/hr (hands) in strawberry
harvesters(1). Individuals performing production, collection, and bagging of
carbaryl were exposed to 0.23-31 mg
dust/cu m(2). The hourly dermal exposure (HDE) of agricultural workers to carbaryl applied by air or ground equipment
was studies. HDE was highest for the aerial flagger, next highest for the mixed
loader, followed by the applicator and the bystander. The exposure of the three
types of workers was limited mainly to the hands. The hand exposure of the mixed
loader was greater when gloves were not worn. HDE on hands of thinners working
in apple orchard treated with carbaryl
correlated with total extractable from apple leaves(4). The mean rates of carbaryl exposure for professional applicators
were 3.85 and 0.26 ug/sq cm-hr, respectively for outside of the clothing and the
skin beneath the clothing. The hand exposures for the applicators were 2.36 and
24.9 ug/cm-hr, respectively for gloved and bare hands. The max air concentration
in application area was 0.28 ug/l(3). The mean dermal and respiratory exposure
for applicators was 59.4-128 mg/hr and 0.1 mg/hr(5).
NIOSH (NOES Survey 1981-1983) has statistically estimated that 16,544 workers
(3,228 of these are female) are potentially exposed to carbaryl in the US(1). The NOES Survey,
however, does not include farm workers. Workers engaged in production,
formulation and application of carbaryl
as a contact insecticide for fruits, vegetables, cotton, and other crops are
especially prone to exposure(2). Occupational exposure to carbaryl may occur through inhalation and
dermal contact with this compound at workplaces where carbaryl is produced or used(SRC). The general
population may be exposed to carbaryl
via inhalation of ambient air(3), ingestion of food(4,5) and drinking water(6,7)
and pesticide products(8) containing carbaryl(SRC).
To evaluate the exposure of farmers to carbaryl during pesticide application, a study
was conducted that measured the personal air, dermal contact, indoor residue
content, urine and serum from a single farmer(1). Before carbaryl was applied to the crops, the
personal air samples contained 0.008-0.016 ug/cu m carbaryl; a dermal patch contained
0.0014-0.010 ug/sq cm carbaryl; handwipe
sample of the farmer and family contained 9-20 ug carbaryl; urine samples contained 270 ug/g
creatinine 1-naphthol (breakdown product of carbaryl); while serum samples contained 0.260
ug/l 1-naphthol and 0 detection for carbaryl(1). On the day of application, the
carbaryl concns changed to: personal air
samples contained 640 ug/cu m; dermal patch contained 11 ug/cm sq; handwipe
samples contained 20,100 ug; urine samples contained 140-9,300 ug/g creatinine
1-naphthol; while serum samples contained 510 ug/l 1-naphthol and 0.12 ug/l
carbaryl(1). In a year long study, from
March 1986 to February 1987, of carbaryl
exposure to tree nursery workers in the Pacific Northwest and Central United
States, 18 out of 3,134 urine samples analyzed contained detectable amounts of
carbaryl(2). Of these, the total amount
of carbaryl adsorbed was determined to
range from 0.0075-0.0238 mg/kg person(2). Airborne levels of pesticides were
measured during and following the mixing, loading, or application of
pesticides(3). Measurements included breathing zone air, indoor air of pesticide
warehouse facilities and offices, indoor air of residential properties and
ambient air of residential properties(3). Approximately 500 samples were taken
in 14 cities in the U.S. and Canada(3). Breathing zone air samples contained
carbaryl in 8 out of 17 air samples with
a time weighted avg of 0.005 mg/cu m(3). Office, operations room and warehouse
air samples did not contain any detectable amount of carbaryl in 82 samples(3). For residential
indoor air samples, carbaryl was the
most frequently detected pesticide with a time waited avg of 0.013 mg/cu m in 16
out of 38 samples(3). Carbaryl was
detected in 13 out of 28 residential outdoor ambient air samples with a time
waited avg of 0.013 mg/cu m(3).
Body Burden:
Carbaryl does not accumulate in
tissues or persist in blood. It is quickly metabolized into a nontoxic compound,
1-naphthol, which is excreted in urine as the glucuronide or sulfate ester(1).
Average Daily Intake:
FOOD: The avg adult daily dietary intake for the years 1980-84 was in the
range 0.12-0.032 ug/kg body weight(1-3). Insufficient data are available to
calculate avg daily carbaryl intakes
from water and air ingestion. Avg daily intake per unit of body weight of carbaryl between 1984-1986 in the United
States was 0.0704 ug (age group: 6-11 month), 0.0565 ug (2 yr), 0.0087 ug (14-16
yr female), 0.0088 ug (14-16 yr male), 0.0123 ug (25-30 yr female), 0.010 ug
(25-30 yr male), 0.0134 ug (60-65 yr female), and 0.012 ug (60-65 yr male)(4).
Natural Pollution Sources:
Carbaryl is not known to occur as a
natural product.
Artificial Pollution Sources:
Carbaryl's production and use as a
contact and stomach insecticide(1-4) is expected to result in its direct release
to the environment(SRC). Carbaryl is
used against a variety of insect pests of cotton, fruits, vegetables(5),
ornamental trees, shrubs, animals and livestock(6). Release can also result from
its use to decrease the number of fruits on heavily laden trees(5) and as an
acaricide and molluscicide(6).
Environmental Fate:
CARBARYL PERSISTED LONGER IN SOIL
WATER THAN IN LAKE WATER. FOUR DAYS AFTER TREATMENT OF SOIL WATER, 1-NAPHTHOL AS
WELL AS CARBARYL WAS RECOVERED.
TERRESTRIAL FATE: Based on a classification scheme(1), a Koc value of 251(2),
indicates that carbaryl is expected to
have moderate mobility in soil(SRC). Volatilization of carbaryl from moist soil surfaces is not
expected to be an important fate process(SRC) given an estimated Henry's Law
constant of 8.8X10-8 atm-cu m/mole(SRC), from its vapor pressure 3.97X10-5 mm
Hg(3) and water solubility 120 mg/l(3). Carbaryl is not expected to volatilize from
dry soil surfaces(SRC) based upon its vapor pressure(3). Carbaryl is expected to slowly photolyze on
surface soil at a rate dependent on the water content (half-life = 97-251 hr in
dry soil, 458-688 hr in wet or saturated soil)(4). In neutral and alkaline
soils, carbaryl is expected to hydrolyze
rapidly. In acidic soils, hydrolysis is expected to occur more slowly(4).
Biodegradation is expected to be a significant degradation pathway for carbaryl in soil. Various soil fungi are able
to metabolize carbaryl(5) and in soils
previously treated with carbamates and cloethocarb, 80% of carbaryl was completely mineralized by
microorganisms to C02 during a 4-week incubation period(6). In addition to
microbes, plants are known to metabolize carbaryl to 4-hydroxycarbaryl,
5-hydroxycarbaryl and methylol-carbaryl(7).
AQUATIC FATE: One ppm of carbaryl was
incubated in autoclaved and unautoclaved creek water at 9 deg C(1). After 50
days, an avg of 39.3% and 56.9% carbaryl
was recovered from the unautoclaved and the autoclaved creek water samples,
respectively(1). Avg recoveries from creek water and bottom sediments following
addition of 1 ppm carbaryl were 11.8%
and 16.2%, respectively, in non-autoclaved samples, after 50 weeks at 9 deg
C(1). Avg recoveries from creek water and bottom sediments were 12.8% and 45.1%,
respectively, in autoclaved samples after 50 weeks at 9 deg C(1). Recovery from
pond water and bottom sediments following addition of 1 ppm carbaryl avgd 13.75% and 13.9%, respectively,
after 42 days at 9 deg C(1). Within 4 days of carbaryl addition to Fall Creek water, >60%
of the carbaryl added at 30 ug/ml and
300 ng/ml was converted to carbon dioxide compared with <10% conversion of
carbaryl added at 3.0 ug/ml and 30
ng/ml(2). Due to the rapid hydrolysis of carbaryl under the conditions of the
experiment, it is not possible to determine how much carbon dioxide resulted
from carbaryl biodegradation and how
much from biodegradation of the hydrolysis product, 1-naphthol(2). Carbaryl was completely degraded after 4 weeks
incubation in the dark at 21 deg C in water from the Holland Marsh drainage
canal(3). Carbaryl in streams, rivers
and brooks as a result of forest spraying decayed with half-lives of 25, 28 and
23 hr, respectively(4). Carbaryl was
incubated in estuarine water in the presence and absence of estuarine mud(5). In
the absence of mud, 50% of the initial carbaryl had disappeared after 38 days at 8
deg C and nearly all had disappeared after 17 days at 20 deg C with 43% being
converted to 1-naphthol(5). In the presence of mud, after 10 days at 8 deg C,
90% of the initial carbaryl had been
removed from the water. This was attributed to the adsorption of the carbaryl on the mud, in which degradation
proceeded more slowly than in the sea water(5). Carbaryl was detectable in the mud for up to 3
weeks(5). Carbaryl persisted in mud
treated with 10 pounds active ingredient per acre for up to 42 days(5). At
neutral and basic pH values, carbaryl is
expected to hydrolyze rapidly (half-life = 10.5 days at pH 7 and 20 degC;
half-life = 1.8 days at pH 8 at 20 deg C). The lifetime of carbaryl in water at pH 7 is about 70 days
(99% hydrolyzed). In acidic water, hydrolysis is not expected to be significant
(half-life = 1500 days at pH 5 and 27 deg C; half-life = 406 days at pH 6 and 25
deg C). The photolysis half-life of carbaryl calculated from experimentally
determined parameters ranged from 52-264 hr for a summer day at latitude 40
degrees north. Biodegradation may be significant, but at pH values of 7 and
above, hydrolysis is expected to predominate(SRC).
AQUATIC FATE: Based on a classification scheme(1), a Koc value of 251(2)
indicates that carbaryl is not expected
to adsorb to sediment and suspended solids in water(SRC). Volatilization from
water surfaces is not expected(3) based upon an estimated Henry's Law constant
of 8.8X10-8 atm-cu m/mole(SRC), from its vapor pressure 3.97X10-5 mm Hg(4) and
water solubility 120 mg/l(4). According to a classification scheme(5), a BCF
ranging from 9-34(6,7), suggests the potential for bioconcentration in aquatic
organisms is low. Biodegradation of carbaryl occurred in a mixture of
non-acclimated sludge, field soil and river sediment at 18-22 deg C with a
half-life of 0.34 days(8). At 20 deg C, hydrolysis half-lives of carbaryl in water are 10.5 days, 1.8 days, 2.5
hours, and 15 min at pH values of 7, 8, 9, and 10, respectively(9). Photolysis
half-lives calculated from sunlight intensity data and experimentally determined
quantum efficiencies ranged from 52 (carbaryl in <10 cm water) to 264 hrs for a
summer day at latitude 40 degrees North(10,11).
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of
semivolatile organic compounds in the atmosphere(1), carbaryl, which has a vapor pressure of
3.97X10-5 mm Hg at 25 deg C(2), is expected to exist in both the vapor and
particulate phases in the ambient atmosphere. Vapor-phase carbaryl 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 15 hrs(SRC), calculated from its rate
constant of 2.6X10-13 cu cm/molecule-sec at 25 deg C determined using a
structure estimation method(3). This is in agreement with various papers citing
the half-life of carbaryl reacting with
hydroxyl radical in the ambient atmosphere as less than one day(4,5).
Particulate-phase carbaryl may be
removed from the air by wet and dry deposition(SRC). Carbaryl exhibits an absorption max at 312.5
nm (extinction coefficient= 378 l/mol cm)(6) and may directly photolyze in the
atmosphere.
The persistence of carbaryl in water
has been found to be dependent on pH and temperature. ... Creek and pond water
samples containing 1 ppm of carbaryl
were incubated at 9 deg C with and without sediment. Autoclaved and
non-autoclaved samples were also analyzed. Persistence of carbaryl in the creek water having a pH of 7.0
to 7.1 was greater than in the slightly alkaline pond water, pH 7.5 to 7.8.
After 21 days incubation about 66 to 62% of added carbaryl remained in creek water whereas 46 to
39% was found in pond water. Autoclaving and the presence of sediment also
increased persistence. In the pond water incubated with sediment there was a
steady decrease in the carbaryl
concentration of the water but the sediment concentration remained about the
same from 2 days after inoculation through day 21 of the experiment.
Environmental Biodegradation:
THE PERSISTENCE OF CARBARYL AT CONCN
OF 2 & 200 PPM IN 5 DIFFERENT JAPANESE RICE PADDY SOILS WAS STUDIED.
EVOLUTION OF CARBON DIOXIDE WAS NOT RAPID & VARIED BETWEEN 2% & 40% OVER
32 DAY TEST PERIOD. HYDROLYSIS OF CARBONYL LINKAGE WAS THE DOMINANT METABOLIC
PATHWAY. AN ISOLATED SOIL MICROORGANISM RAPIDLY DEGRADED NAPHTHOL & PRODUCED
A NUMBER OF UNIDENTIFIED AROMATIC COMPOUNDS.
IN POND WATER, CARBARYL RAPIDLY
HYDROLYZED TO 1-NAPHTHOL. ONE BACTERIUM, POSSIBLY FLAVOBACTERIUM, RAPIDLY
DEGRADED 1-NAPHTHOL. OF 3 CMPD OBSERVED, 2 WERE IDENTIFIED AS HYDROXYCINNAMIC
ACID & SALICYLIC ACID.
The rate of dissipation of carbaryl
from soils varied from 3 to 70% disappearance of radioactivity after 4 days.
Carbon dioxide was formed by attack on the ring. Hydroxymethylcarbaryl was
formed by a fungus SF-10 & P implicatum. P lilacinum & A elegans
produced small amounts of 5,6-dihydro-5,6-dihydroxycarbaryl.
THE RATE OF DEGRADATION OF CARBARYL
AFTER 1, 2, & 3 APPLICATIONS TO 3 SUBMERGED SOILS WAS EXAMINED. SOILS WHICH
HAD BEEN PRETREATED WITH CARBARYL WERE
ABLE TO DEGRADE THE CMPD MORE RAPIDLY THAN THOSE WITHOUT PRETREATMENT. A
DILUTION, AS LOW AS 1X10-8 OF THE ENRICHMENT CULTURE FROM 1 SOIL EFFECTED THE
DEGRADATION OF CARBARYL.
Isolated marine organisms degraded carbaryl & 1-naphthol. Metabolites were
not identified. When a Pseudomonas specie was incubated with 1-naphthol, a
dihydrodihydroxy-1(2H)-naphthalenone was observed. Of two structrues, the
spectral information favored 2,3-dihydroxy-3,4-dihydro-1(2H)-naphthalenone. An
enzyme was isolated from the fungus Rhizoctonia praticola & incubated with
1-naphthol. Mass spectra indicated polymerization to at least a pentameric
compound. A tetramer, one trimer & two dimers were purified from the
mixture. One dimer was identified as 4,4'-bi-1-naphthol.
After 30 days incubation at room temperature in a mineral salts medium
inoculated with carbaryl-enrichment
cultures from flooded or nonflooded soils, 31.5% and 26.8% of the initial carbaryl remained, respectively compared to an
uninoculated control in which 89.4% remained(1). Formation of (14-C)-carbon
dioxide from ring labeled carbaryl added
at 200 ppm to a variety of soils ranged from 2.2-37.4% after incubation at 25
deg C for 32 days(2). After application to corn seed furrows at 5.03 kg/ha
active ingredient, carbaryl was stable
for up to 116 days, at which time it degraded rapidly(3). The long period of
persistence followed by rapid degradation was said to indicate microbial
degradation(3). Incubation with activated sludge caused about 30% biodegradation
of the compound in 5 days(8). In soils previously treated with carbamates and
cloethocarb, 80% of carbaryl completely
mineralized to C02 during a 4-week incubation(9). Biodegradation was faster in
organic-amended soil than unamended soil(10,11). Soil-bound carbaryl residues mineralized faster in moist
than flooded soils(10) indicating aerobic biodegradation may be faster than the
anaerobic process. Various soil fungi metabolized carbaryl to 1-naphthyl
N-hydroxy-methylcarbamate, 4-hydroxy-1-naphthyl methylcarbamate and
5-hydroxy-1-naphthyl methylcarbamate(4). Three microbial strains isolated from
soil were able to accelerate the rate of carbaryl hydrolysis to 1-naphthol(5). Fusarium
solani degraded 82% of the initial carbaryl after 12 days and an unidentified
strain degraded 51% after 7 days(5). A mixed culture of any two or all three
strains completely metabolized the initial amount of carbaryl after about 12 days(5). All the
cultures were incubated at 26-28 deg C(5). An Aspergillus terrens culture
metabolized carbaryl to 1-naphthyl
carbamate(6). Approximately 50% of the initial amount of carbaryl was metabolized in 8 days(6).
Achromobacter sp degraded carbaryl as a
sole carbon source(7).
AEROBIC: Plants are known to metabolize carbaryl to 4-hydroxycarbaryl,
5-hydroxycarbaryl and methylol-carbaryl(1). Carbaryl at 1 ppm degraded with a half-life
ranging from 7-14 days in a sandy loam and 14-20 days in a clay loam(1).
Hydrolysis was found to be the major process for microbial degradation of carbaryl in soil enrichment cultures and
cultures of a Bacillus sp. with 1-naphthol and 1,4-naphthoquinone accumulating
in the medium(2). Carbaryl had an avg
biodegradation half-life of 10 days in four different soils (a Pliocene sand, an
organic-rich orchard soil, an agricultural soil and soil from a volcanic
area)(3). In raw seawater, carbaryl was
biodegraded to undetectable levels within 96 hrs(4).
ANAEROBIC: Carbaryl was found to
stimulate methanogenesis in anaerobic salt marsh soils and organic-rich aquifer
soils(1). The monomethylamine formed by the microbial hydrolysis of carbaryl under anaerobic conditions serves as
a substrate for methanogenic bacteria(1).
Environmental Abiotic Degradation:
UNDER CONDITIONS SIMILAR TO THOSE IN THE FIELD, THE PRINCIPAL NON-BIOLOGICAL
DEGRADATION PATHWAY OF CARBARYL IN WATER
INVOLVED BASE-CATALYZED HYDROLYSIS TO 1-NAPHTHOL FOLLOWED BY PHOTOLYTIC DECOMP
TO 1-NAPHTHOXIDE ION. IN SEA WATER, 1-NAPHTHOL UNDERWENT DEGRADATION ... THE
FORMATION OF CARBON DIOXIDE WAS OBSERVED BUT WAS PROBABLY PRODUCED BY
MICROORGANISMS. EXPOSURE TO LIGHT ENHANCED THE CARBONDIOXIDE PRODUCTION. A
REDDISH BLUE PRECIPITATE ALSO FORMED. FOUR PEAKS WERE OBSERVED ON THE TOTAL ION
MONITOR OF A MASS SPECTROMETER. ONE PEAK WAS COMPLETELY ASSIGNED TO
1,4-NAPHTHOQUINONE. THE PRESENCE OF 2-(OR 3)-HYDROXY-1,4-NAPHTHOQUINONE, &
1-NAPHTHOL WERE ALSO OBSERVED. IDENTIFICATION OF THE INTACT COMPOUND WAS NOT
MADE.
Carbaryl was irridiated at wavelength
>265 nm in various solvents. In all cases,1-naphthol was formed & in
cyclohexane it was the only product. In polar solvents (isopropanol, t-butanol,
ethanol), small amounts of naphthamides, naphthalene &
beta-naphthyl-1-naphthol were also produced. Photolysis half-life for carbaryl in sunlight was 6.6 days in distilled
water.
In aqueous medias, a number of carbaryl decomposition products were present
within 7 days; and, by the 19th day, 13 spots were visible in chromatographs of
suspensions of pH 5-10, stored at 37 deg C. In other studies, carbaryl half-life varied from 0.15 days pH 9
to 1500 days pH 5.
Carbaryl added to filter sterilized
Hickory Hills (pH 6.7) and USDA No.1 pond waters (pH 7.2) hydrolyzed with
half-lives of 30 and 12 days, respectively(1). Hydrolysis half-lives of aqueous
carbaryl calculated from kinetic data
for neutral and alkaline hydrolysis at 27 deg C are 1500, 15, and 0.15 days at
pH values of 5, 7, and 9, respectively(1). In a 99:1 water:ethanol solution at
25 deg C, carbaryl hydrolysis half-lives
are 2100, 406, 14 and 1.9 days at pH values of 4.5, 6, 7, and 8,
respectively(2). At 25 deg C, hydrolysis half-lives in water are 173, 27 and 20
min at pH values of 9, 9.8, and 10, respectively(3). The lifetime of carbaryl in pH 7 water is about 70 days (99%
hydrolyzed)(4). After 2 and 4 days in autoclaved, mildly alkaline Fall Creek
water, 60% and 90% of the added carbaryl
was hydrolyzed, respectively(5). The direct photolysis half-life of aqueous
carbaryl at 25 deg C by sunlight or 313
nm light is 6.6 days(1). In distilled water buffered at pH 5.5, the photolysis
half-life of carbaryl irradiated at
>280 nm is about 45 hr(6). Photolysis half-lives calculated from sunlight
intensity data and experimentally determined quantum efficiencies ranged from 52
(carbaryl in <10 cm water) to 264 hr
for a summer day at latitude 40 degrees North(6,7). Photolytic products were not
identified. The photolytic half-life of a thin film of carbaryl irradiated at >290 nm is 51.66 hr
at 33-36 deg C(8). Photolytic products were not identified. At wavelengths
greater than 290 nm, alpha-naphthol was the only product of photoreaction(9).
Intense UV irradiation caused the formation of five other phenols(10).
Photolytic half-life in a buffer solution at pH 5.5 by outdoor summer sunlight
in Rochester, NY was about 11 days(11). Photolysis half-lives of carbaryl in soil irradiated at >290 nm
ranged from 97 hours in dry Etowah soil (0.13% carbon) to 251 hr in dry Holston
soil (0.60% carbon) and from 458 hr in wet Holston soil (pH 6.3 slurry) to 688
hours in water saturated Holston soil(12).
The rate constant for the vapor-phase reaction of carbaryl with photochemically-produced
hydroxyl radicals has been estimated as 2.6X10-13 cu cm/molecule-sec at 25 deg
C(SRC) using a structure estimation method(1). This corresponds to an
atmospheric half-life of about 15 hrs at an atmospheric concn of 5X10+5 hydroxyl
radicals per cu cm(1). This is in agreement with various papers citing the
half-life of carbaryl reacting with
hydroxyl radical in the ambient atmosphere as less than one day(2,3). At 20 deg
C, hydrolysis half-lives of carbaryl in
water are 10.5 days, 1.8 days, 2.5 hours, and 15 min at pH values of 7, 8, 9,
and 10, respectively(4). In a study of carbaryl's stability in various water
conditions, it was found that when exposed to ultrapure water at pH 6.1 and 6
deg C no degradation was observed while at 22 deg C the half-life was 37
days(5). When exposed to river water at pH 7.3 and 6 deg C, the half-life was 31
days while at 22 deg C the half-life was 11 days(5). Using filtered river water
at pH 7.3 and 6 deg C, the half-life was 45 days while at 22 deg C the half-life
was less than 2 days(5). Finally, using seawater at pH 8.1 and 6 deg C, the
half-life was 22 days and at 28 deg C, carbaryl degraded with a half-life of less
than 2 days(5). Carbaryl degraded
rapidly under direct photolysis with a half-life in pure water of 63 hrs(6).
When carbaryl was added to a flooded
rice field at noon in July at Davis California, it had a half-life of 8.8
hrs(6). Since carbaryl has such a low
estimated Henry's Law constant and low Koc value, volatilization from water and
adsorption to sediment or suspended solids in water were not considered to
contribute to loss processes for carbaryl(6). Photolysis, hydrolysis, and
reaction with hydroxyl radical were considered to be the main degradation
pathways for carbaryl in the
environment(6).
Environmental Bioconcentration:
Carbaryl had a measured BCF value of
34, 30 and 9 in golden orfe(1), golden ide(2), and topmouth gudeon,
respectively(3). An avg BCF of 9 was determined based on data compilations of
freshwater fish at steady state with carbaryl in solution and by the kinetic method
(ratio between first-order uptake and elimination rate constants)(4). According
to a classification scheme(5), these BCF values suggest the potential for
bioconcentration in aquatic organisms is low.
Soil Adsorption/Mobility:
Carbaryl was estimated to leach
<20 cm/yr assuming an annual rainfall of 150 cm; a loam soil and a
temperature of 25 deg C were assumed(1). Soil-sorption coefficient (Koc) values
of 370 and 390 were determined using a soil slurry method and reverse phase
HPLC, respectively(2). In another study, carbaryl had a Koc value of 230(3). Freundlich
k values are 0.017 and 0.046 in kaolinite and bentonite clays, respectively(4).
In Ca-bentionite, alluvial and highly calcareous soils, the Freundlich
adsorption isotherm showed a non-linear pattern and the adsorption was found to
be temperature dependent, the adsorption being higher at lower temperature(5).
According to a classification scheme(6), these Koc values suggest that carbaryl is expected to have moderate mobility
in soil.
Volatilization from Water/Soil:
The Henry's Law constant for carbaryl
is estimated as 8.8X10-8 atm-cu m/mole(SRC) from its vapor pressure, 3.97X10-5
mm Hg(1), and water solubility, 120 mg/l(1). This Henry's Law constant indicates
that carbaryl is expected to be
essentially nonvolatile from water surfaces(2). Carbaryl's estimated Henry's Law constant(1)
indicates that volatilization from moist soil surfaces will not occur(SRC).
Carbaryl is not expected to volatilize
from dry soil surfaces(SRC) based upon its vapor pressure(1).
Environmental Water Concentrations:
SURFACE WATER: Carbaryl was detected
but not quantified in organic extracts from British or West German river water
samples(1). Carbaryl at a concn 0.003
ppm was detected in stream water adjacent to a land spraying area in Canada 5
days following an application rate of 280 g/ha(2). In a study conducted from
April 1993 to April 1994, twenty five water samples (one taken each month) were
taken at the mouths of two tributary streams of the South Platte River in
Colorado and studied for pesticide concns(3). The tributary that originated from
an agricultural region contained carbaryl ranging from <0.046-1.5 ug/L while
the tributary that originated from an urban setting contained carbaryl ranging from 0.15-2.5 ug/l(3). Carbaryl was only detected in the agricultural
tributary from July to September which corresponded to its use on beans in June
and July for beetle control(3). Urban tributary samples consistently contained
carbaryl probably as a result of
repeated applications for residential and commercial insect control(3). Forty
water samples collected between February 1992 and July 1992, from the rivers
Canyoles, Albaida, Claria, Serpis, Polop, Belcaire, Turia and Xuquer, the Lake
Albufera and the irrigation channels in Spain were analyzed for pesticide
content(4). Carbaryl was detected in 6
of the samples ranging from 1.23-6.48 ug/ml(4).
DRINKING WATER: Detected but not quantified in USA drinking water(1).
GROUNDWATER: Carbaryl was not
detected, detection limit of 1 ug/l, in 10 farm wells where the land was treated
with the pesticide(1). Carbaryl was
detected, concn not specified, in three groundwaters samples in California(2).
Carbaryl was detected in Solano and
Ventura Counties in California at a concn ranging from 10-55 ppb taken from July
1, 1994 to June 30, 1995(3). In 1986 and 1987, 103 and 76 wells, respectively,
were sampled in Southern Ontario, Canada for pesticide concns(4). Samples were
collected in late November and in mid December in both 1986 and 1987. Carbaryl was detected, concn not specified, in
10 out of 10 wells sampled in both 1986 and 1987 with a detection limit of 1.0
ug/l(4).
RAIN/SNOW/FOG: Coastal fog and air samples collected from three locations
along the Pacific coast near Monterey, CA in September 1987 were analyzed for
pesticide content(1). Carbaryl was
detected ranging from 0.069-4.0 ug/l(1).
Effluent Concentrations:
Air emisions from carbaryl
manufacture have been reported to consist of 1.5 kg of hydrocarbons & 0.5 kg
of carbaryl per metric ton of pesticide
produced.
Sediment/Soil Concentrations:
A field study in India measuring soil persistence associated with heavier
application rates of granular carbaryl
showed a slower decline in residue levels. Reductions in soil residues of 62 to
81% after 15 days and 94-98% after 60 days were measured for application rates
of 13.4, 26.8, and 40.2 lb active ingredient per acre. Residues up to 6.3 ppm
were still in the soil after 90 days. Soil samples were taken to a depth of 10
cm. A heavy application of 22.7 lb per acre of carbaryl to a sandy loam soil resulted in
residues in the first 20 cm of soil after 4 months. The upper 1 meter soil
layer, however, retained 6% of the initial carbaryl applied after 16 months.
SOIL: Carbaryl was detected in
Southwestern Ontario farm soil in 1976 ranging from 0.03-0.08 ppm(1). Five days
following a carbaryl application rate of
280 g/ha, carbaryl was detected ranging
from 0.06-0.08 ppm in forest soil located in Canada(2). Two hours following a
carbaryl application rate of 280 g/ha,
carbaryl was detected in stream sediment
located adjacent to the spraying area at a concn of 0.03 ppm. Twenty four hours
later, no carbaryl was detected (det
limit = <=0.005 ppm)(2).
Atmospheric Concentrations:
Air samples taken after spraying for budworms at 91, 96, and 107 ng Carbaryl/cu m in Maine, did not contain carbaryl(det limit = 3.5 ng/cu m)(1). The mean
concn of carbaryl in indoor air samples
taken in Jacksonville, Florida for summer(1986), spring(1987) and winter(1988)
were 68.1, 0.4, and 0 ng/cu m, respectively(2). Carbaryl was detected only in outdoor air
samples during summer at 0.2 ng/cu m(2). Carbaryl was also detected in personal air
samples during summer and spring at 28.3 and 0.8 ng/cu m, respectively(2).
Overall, an annual avg daily concn of carbaryl in Jacksonville, Florida air was
determined to be 7.5 ng/cu m(2). Carbaryl was also detected in indoor and
personal air samples taken from Springfield, Massachusetts in spring(1987) at
0.3 and 0.1 ng/cu m(2). The annual avg daily concn of carbaryl in Springfield, Massachusetts air was
0.1 ng/cu m(2).
Food Survey Values:
Average dietary intake 20 ng/kg body weight/day(1). The avg daily dietary
intake of carbaryl for the U.S.
population in 1971, 72, 73, 74, 75, and 76 was 5.6, 1.9, 3.1, 2.2, 0.8, and 2.1
ug, respectively(1). The daily intake in ug/kg body weight/day for carbaryl in 1978, 79, and 80 was 0.016, 0.016,
and 0.021, respectively(2). The daily intake in ug/kg body weight/day for carbaryl from 1982-84 ranged from
0.012-0.032(3,4,5). The daily intake (ug/kg body weight/day) for carbaryl by infants in 1977, 78, 79, and 80
was <0.001, 0.088, non detected, 0.060(2,5,6). The daily intake (ug/kg body
weight/day) for carbaryl by infants from
1981-82 was 0.129, from 1982-84 was 0.114(2,5,6). The daily intake (ug/kg body
weight/day) for carbaryl by toddlers in
1977, 78, 79, and 80 was none detected, 0.05, 0.049, and 0.035(3),
respectively(2,5,6). The daily intake (ug/kg body weight/day) for carbaryl by toddlers from 1981-82 was 0.127
and from 1982-84 was 0.117(2,5,6). In 665 samples of domestic large fruits,
13.9% tested positive for carbaryl at an
avg concn of 0.064 ppm(1). Of imported fruit, only 9.4% tested positive for
carbaryl at an avg concn of 0.001
ppm(1). Carbaryl was detected in 3.6% of
2904 domestic leaf and stem vegetables analyzed at an avg concn of 0.020 ppm(1).
Carbaryl was detected in 6.2% of 725
domestic vine and ear vegetables analyzed at an avg concn of 0.013 ppm(1). Carbaryl was detected in 11.4% of 499 domestic
beans analyzed at an avg concn 11.4%(1). Carbaryl was detected in fruit ranging from
trace amounts to 0.05 ppm with an avg concn of 0.005 ppm(2). Carbaryl was detected in infant diet,
particularly sugar and adjuncts at 0.050 ppm(3). Food samples collected from
1980-83 contained carbaryl as follows:
apples - 0.19-0.57 ppm; cabbage - <0.01-0.19 ppm; cantalope - 0.04 ppm;
celery - <0.01-0.06 ppm; eggplant - 0.01-0.03 ppm; grapes - 0.05 ppm; oranges
- 0.26 ppm; tomatoes - <0.01-0.016 ppm(7). In 21 domestic and 132 imported
agricultural commodities surveyed from 1981-1986, carbaryl was detected ranging from 0.05 to
greater than 2.0 ppm(8).
Carbaryl was found in Canadian
produce such as apples, celery, grape juice, lettuce, and parsnips ranging from
<0.05-1.0, 0.5->2.0, 0.10-0.50, <0.05, and 0.50 ppm, respectively from
Jan 1, 1992 to March 31, 1994(1). Carbaryl was also detected on produce imported
to Canada during this same time period on apples, beans, celery, cucumbers,
eggplant, canned fruit cocktail, grapes, grapefruit, lemons, lettuce, oranges,
peas, peaches, pears, sweet peppers, pineapples, radishes, snowpeas,
strawberries, tangerines and tomatoes ranging from <0.05-2.0, <0.05-0.5,
0.5, 0.5, 0.1, <0.5, <0.5->2.0, 0.5-2.0, 1.0, 0.50, 0.10->2.0,
<0.05-2.0, 0.50, <0.05-0.50, <0.05-2.0, 0.50, 0.50, 1.0, <0.05-1.0,
1.0, and <0.05-0.5 ppm, respectively(1). In an adult diet study from
1982-1986, food samples were collected from 4 geographical areas of the United
States and analyzed for pesticide content(2). Carbaryl was detected, concn not specified, in
135 out of 3744 food samples analyzed(2).
Plant Concentrations:
Residues on spinach and chicory were measured. Four applications of 1 lb
active ingredient per acre resulted in an average residue 8 days after the last
application of 16.5 ppm on spinach and 18 ppm on chicory. The calculated percent
reduction in carbaryl from 1 day to 8
days after treatment are comparable: 1 lb active ingredient/acre, spinach 88%,
chicory 82% and 2 lb active ingredient/acre, spinach 81%, chicory 85%. The rate
of dissipation of carbaryl on plants
appears to be independent of initial concentration.
Carbaryl residues /were measured/ on
the surface of apple leaves from trees treated with an aqueous solution
containing 0.5 and 1.0 lb active ingredient per 100 gallons of water. Each test
plot consisted of three apple trees which were sprayed until insecticide runoff
was produced. Average surface residues on leaves measured 0.70 and 1.71 ug/sq cm
the day of treatment. By day 31, the average surface residue had decreased by
90% to 0.07 and 0.18 ug/sq cm. The calculated half-life of carbaryl for apple leaves for this study was
13.33 days.
Carbaryl was detected, concn not
specified, in roots, stems and leaves 10 days following the application of 150
mL of 500-800 ppm Carbaryl suspension
solution(1). Carbaryl was detected five
days following an application rate of 280 g/ha in Fir foilage at concns ranging
from 0.42-0.48 ppm(2).
Animal Concentrations:
Carbaryl at concns ranging from
0.02-5.80 ppm was detected in dead honey bees from poisoned apiaries in
Connecticut in 1983-1985(1).
Other Environmental Concentrations:
House dust collected from four houses in two residential areas of Seattle, WA
contained carbaryl at an avg concn of 54
ppm(1).
Environmental Standards & Regulations:
FIFRA Requirements:
Tolerances are established for residues of the insecticide carbaryl (1-naphthyl N-methylcarbamate),
including its hydrolysis product 1-naphthol, calculated as 1-naphthyl
N-methylcarbamate, in or on the following raw agricultural commodities: alfalfa;
alfalfa, hay; almonds; almonds, hulls; apricots; asparagus; bananas; barley,
grain; barley, green fodder; barley, straw; beans; beans, forage; beans, hay;
beets, garden (root); beets, garden (tops); birdsfoot trefoil, forage; birdsfoot
trefoil, hay; blackberries; blueberries; boysenberries; broccoli; brussels
sprouts; cabbage; carrots; cauliflower; celery; cherries; chestnuts; chinese
cabbage; citrus fruits; clover; clover, hay; collards; corn, fresh (including
sweet) kernel plus cob with husk removed; corn, fodder; corn, forage; cotton,
forage; cottonseed; cowpeas; cowpeas, forage; cowpeas, hay; cranberries;
cucumbers; dandelions; dewberries; eggplants; endive (escarole); filberts
(hazelnuts); flax, seed; flax, straw; grapes; grass; grass, hay; horseradish;
kale; kohlrabi; lentils; lettuce; loganberries; maple sap; melons; millet,
proso, grain; millet, proso, straw; mustard greens; nectarines; oats, fodder,
green; oats, grain; oats, straw; okra; olives; oysters; parsley; parsnips;
peaches; peanuts; peanuts, hay; peas (with pods); pea vines; pecans; peppers;
pistachio nuts; plums (fresh prunes); poultry, fat; poultry, meat; potatoes;
prickly pear cactus, fruit; prickly pear cactus, pods; pumpkins; radishes;
raspberries; rice; rice, straw; rutabagas; rye, fodder, green; rye, grain; rye,
straw; salsify (roots); salsify (tops); sorghum, forage; sorghum, grain;
soybeans; soybeans, forage; soybeans, hay; spinach; squash, summer; squash,
winter; strawberries; sugar beets, tops; sunflower seeds; sweet potatoes; swiss
chard; tomatoes; turnips, roots; turnips, tops; walnuts; wheat, fodder, green;
wheat (grain); wheat, straw.
Tolerances are established for residues of the insecticide carbaryl (1-naphthyl N-methylcarbamate)
including its metabolites 1-naphthol (naphthyl-sulfate), 5,6-dihydrodihydroxy
carbaryl, and 5,6-dihydrodihydroxy
napthol, calculated as 1-naphthyl N-methylcarbamate in or on the following raw
agricultural commodities: cattle, fat; cattle, kidney; cattle, liver; cattle,
meat; cattle, meat by-products; goats, fat; goats, kidney; goats, liver; goats,
meat; goats, meat by-products; horses, fat; horses, kidney; horses, liver;
horses, meat; horses, meat by-products; sheep, fat; sheep, kidney; sheep, liver;
sheep, meat; sheep, meat by-products; swine, fat; swine, kidney; swine, liver;
swine, meat; and swine, meat by-products.
A tolerance is established for residues of the insecticide carbaryl, including its metabolites 1-naphthol
(naphthyl sulfate), 5,6-dihydrodihydroxycarbaryl and
5-methoxy-6-hydroxycarbaryl, calculated as 1-naphthyl N-methylcarbarmate in or
on the raw agricultural commodity milk.
Tolerances are established for residues of the insecticide carbaryl in or on the following raw
agricultural commodities: pineapples and pome fruits.
Tolerances with regional registration are established for the insecticide
carbaryl in or on the following raw
agricultural commodities: avocados and dill (fresh).
Pesticide chemicals that cause related pharmacological effects will be
regarded, in the absence of evidence to the contrary, as having an additive
deleterious action. Many pesticide chemicals within the following groups have
related pharmacological effects: chlorinated organic pesticides,
arsenic-containing chemicals, metallic dithiocarbamates,
cholinesterase-inhibiting pesticides. Where residues from two or more chemicals
in the same class are present in or on a raw agricultural commodity the
tolerance for the total of such residues shall be the same as that for the
chemical having the lowest numerical tolerance in this class, unless a higher
tolerance level is specifically provided for the combined residues by a
regulation in this part. Carbaryl is a
member of the class of cholinesterase-inhibiting pesticides.
While petitions for tolerances for negligible residues are pending and until
action is completed on these petitions, an interim tolerance is established for
the residues of carbaryl and its
metabolite 1-naphthol (calculated as carbaryl) for its use as an insecticide in or
on the raw agricultural commodity of eggs.
A tolerance is established for residues of the insecticide carbaryl (1-naphthyl N-methyl carbamate) in or
on the feed commodity pineapple bran (wet and dry).
As the federal pesticide law FIFRA direct, 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. Carbaryl 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 88. Case No: 0080; Pesticide type: Insecticide; Registration Standard
Date: 03/30/84; Case Status: PreRED - 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
RED document. Active ingredient (AI): Carbaryl; Data Call-in (DCI) Date(s):
04/30/91, 01/09/95, 03/03/95, 10/13/95, 03/01/96; AI Status: Supported - The
producers of the pesticide have made commitments to conduct the studies and pay
the fees required for reregistration, and are meeting those commitments in a
timely manner.
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).
RCRA Requirements:
U279; As stipulated in 40 CFR 261.33, when carbaryl, as a commercial chemical product or
manufacturing chemical intermediate or an off-specification commercial chemical
product or a manufacturing chemical intermediate, becomes a waste, it must be
managed according to Federal and/or State hazardous waste regulations. Also
defined as a hazardous waste is any residue, contaminated soil, water, or other
debris resulting from the cleanup of a spill, into water or on dry land, of this
waste. Generators of small quantities of this waste may qualify for partial
exclusion from hazardous waste regulations (40 CFR 261.5).
Atmospheric Standards:
Listed as a hazardous air pollutant (HAP) generally known or suspected to
cause serious health problems. The Clean Air Act, as amended in 1990, directs
EPA to set standards requiring major sources to sharply reduce routine emissions
of toxic pollutants. EPA is required to establish and phase in specific
performance based standards for all air emission sources that emit one or more
of the listed pollutants. Carbaryl is
included on this list.
Clean Water Act Requirements:
Carbaryl 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 700 ug/l
State Drinking Water Guidelines:
(AZ) ARIZONA 700 ug/l
(CA) CALIFORNIA 60 ug/l
(ME) MAINE 164 ug/l
(WI) WISCONSIN 960 ug/l
Allowable Tolerances:
Tolerances are established for residues of the insecticide carbaryl (1-naphthyl N-methylcarbamate),
including its hydrolysis product 1-naphthol, calculated as 1-naphthyl
N-methylcarbamate, in or on the following raw agricultural commodities
(expressed in ppm): alfalfa 100; alfalfa, hay 100; almonds 1; almonds, hulls 40;
apricots 10; asparagus 10; bananas 10; barley, grain 0; barley, green fodder
100; barley, straw 100; beans 10; beans, forage 100; beans, hay 100; beets,
garden (root) 5; beets, garden (tops) 12; birdsfoot trefoil, forage 100;
birdsfoot trefoil, hay 100; blackberries 12; blueberries 10; boysenberries 12;
broccoli 10; brussels sprouts 10; cabbage 10; carrots 10; cauliflower 10; celery
10; cherries 10; chestnuts 1; chinese cabbage 10; citrus fruits 10; clover 100;
clover, hay 100; collards 12; corn, fresh (including sweet) kernel plus cob with
husk removed 5; corn, fodder 100; corn, forage 100; cotton, forage 100;
cottonseed 5; cowpeas 5; cowpeas, forage 100; cowpeas, hay 100; cranberries 10;
cucumbers 10; dandelions 12; dewberries 12; eggplants 10; endive (escarole) 10;
filberts (hazelnuts) 1; flax, seed 5; flax, straw 100; grapes 10; grass 100;
grass, hay 100; horseradish 5; kale 12; kohlrabi 10; lentils 10; lettuce 10;
loganberries 12; maple sap 0.5; melons 10; millet, proso, grain 3; millet,
proso, straw 100; mustard greens 12; nectarines 10; oats, fodder, green 100;
oats, grain 0; oats, straw 100; okra 10; olives 10; oysters 0.25; parsley 12;
parsnips 5; peaches 10; peanuts 5; peanuts, hay 100; peas (with pods) 10; pea
vines 100; pecans 1; peppers 10; pistachio nuts 1; plums (fresh prunes) 10;
poultry, fat 5; poultry, meat 5; potatoes 0.2 (negligible residue); prickly pear
cactus, fruit 12; prickly pear cactus, pods 12; pumpkins 10; radishes 5;
raspberries 12; rice 5 ; rice, straw 100; rutabagas 5; rye, fodder, green 100;
rye, grain 0; rye, straw 100; salsify (roots) 5; salsify (tops) 10; sorghum,
forage 100; sorghum, grain 10; soybeans 5; soybeans, forage 100; soybeans, hay
100; spinach 12; squash, summer 10; squash, winter 10; strawberries 10; sugar
beets, tops 100; sunflower seeds 1; sweet potatoes 0.2; swiss chard 12; tomatoes
10; turnips, roots 5; turnips, tops 12; walnuts 1; wheat, fodder, green 100;
wheat (grain) 3; wheat, straw 100.
Tolerances are established for residues of the insecticide carbaryl (1-naphthyl N-methylcarbamate)
including its metabolites 1-naphthol (naphthyl-sulfate), 5,6-dihydrodihydroxy
carbaryl, and 5,6-dihydrodihydroxy
napthol, calculated as 1-naphthyl N-methylcarbamate in or on the following raw
agricultural commodities (expressed in ppm): cattle, fat 0.1; cattle, kidney 1;
cattle, liver 1; cattle, meat 0.1; cattle, meat by-products 0.1; goats, fat 0.1;
goats, kidney, 1; goats, liver 1; goats, meat 0.1; goats, meat by-products 0.1;
horses, fat 0.1; horses, kidney 1; horses, liver 1; horses, meat 0.1; horses,
meat by-products 0.1; sheep, fat 0.1; sheep, kidney 1; sheep, liver 1; sheep,
meat 0.1; sheep, meat by-products 0.1; swine, fat 0.1; swine, kidney 1; swine,
liver 1; swine, meat 0.1; and swine, meat by-products 0.1.
A tolerance is established for residues of the insecticide carbaryl, including its metabolites 1-naphthol
(naphthyl sulfate), 5,6-dihydrodihydroxycarbaryl and
5-methoxy-6-hydroxycarbaryl, calculated as 1-naphthyl N-methylcarbarmate in or
on the raw agricultural commodity milk at 0.3 ppm.
Tolerances are established for residues of the insecticide carbaryl in or on the following raw
agricultural commodities (expressed in ppm): pineapples 2.0 and pome fruits
10.0.
Tolerances with regional registration are established for the insecticide
carbaryl in or on the following raw
agricultural commodities: avocados at 10.0 ppm and dill (fresh) 0.2 ppm.
Pesticide chemicals that cause related pharmacological effects will be
regarded, in the absence of evidence to the contrary, as having an additive
deleterious action. Many pesticide chemicals within the following groups have
related pharmacological effects: chlorinated organic pesticides,
arsenic-containing chemicals, metallic dithiocarbamates,
cholinesterase-inhibiting pesticides. Where residues from two or more chemicals
in the same class are present in or on a raw agricultural commodity the
tolerance for the total of such residues shall be the same as that for the
chemical having the lowest numerical tolerance in this class, unless a higher
tolerance level is specifically provided for the combined residues by a
regulation in this part. Carbaryl is a
member of the class of cholinesterase-inhibiting pesticides.
While petitions for tolerances for negligible residues are pending and until
action is completed on these petitions, an interim tolerance is established for
the residues of carbaryl and its
metabolite 1-naphthol (calculated as carbaryl) at 0.5 ppm for its use as an
insecticide in or on the raw agricultural commodity of eggs.
A tolerance is established for residues of the insecticide carbaryl (1-naphthyl N-methyl carbamate) in or
on the feed commodity pineapple bran (wet and dry) at 20 ppm.
Chemical/Physical Properties:
Molecular Formula:
C12-H11-N-O2
Molecular Weight:
201.22
Color/Form:
Colorless solid
White or gray ... solid.
Colorless to light-tan crystals
Odor:
... Odorless ...
Boiling Point:
Decomposes
Melting Point:
145 deg C
Corrosivity:
Non-corrosive
Density/Specific Gravity:
1.232 @ 20 deg C/20 deg C
Octanol/Water Partition Coefficient:
log Kow= 2.36
Solubilities:
120 mg/l water at 20 deg C; dimethylformamide 400-450, dimethyl sulfoxide
400-450, acetone 200-300, cyclohexanone 200-250, isopropanol 100, xylene 100
(all in g/kg at 25 deg C)
Moderately sol in isophorone
SOL IN ETHANOL, PETROLEUM ETHER, DIETHYL ETHER, FREELY SOL IN CHLOROFORM
Soluble in most polar organic solvents such as acetone and mixed cresols.
Spectral Properties:
Intense mass spectral peaks: 144 M/z (100%), 115 M/z (44%), 116 M/z (37%),
145 M/z (14%)
MASS: 1193 (National Bureau of Standards EPA-NIH Mass Spectra Data Base,
NSRDS-NBS-63)
Vapor Pressure:
4.1X10-2 mPa @ 23.5 deg C
Other Chemical/Physical Properties:
Carbaryl decomposes at its boiling
point.
Chemical Safety & Handling:
DOT Emergency Guidelines:
Health: Highly toxic, may be fatal if inhaled, swallowed or absorbed through
skin. 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.
Fire or explosion: Non-combustible, substance itself does not burn but may
decompose upon heating to produce corrosive and/or toxic fumes. Containers may
explode when heated. Runoff may pollute waterways.
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.
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.
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: 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 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. 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.
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.
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.
Skin, Eye and Respiratory Irritations:
Irritating to skin & eyes.
Fire Potential:
... FLAMMABILITY POINT OF 193 DEG C.
Material itself does not burn or burns with difficulty.
Fire Fighting Procedures:
/Wear/ self-contained breathing apparatus with a full facepiece operated in
pressure-demand or other positive pressure mode /when fighting fire/.
Extinguish fire using agent suitable for type of surrounding fire. (Material
itself does not burn or burns with difficulty.) /Carbamate pesticid, solid,
toxic, not otherwise specified
If material /is/ on fire or involved in /a/ 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, dry chemical or carbon dioxide. /Carbamate
pesticide, liquid, nos/
Do not extinguish fire unless flow can be stopped. Use water in flooding
quantities as fog. Cool all affected containers with flooding quantities of
water. Apply water from as far a distance as possible. Solid streams of water
may be ineffective. Use foam, dry chemical, or carbon dioxide. /Carbamate
pesticide, liquid nos ; carbamate pesticides, liquid, flammable, toxic, nos/
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, dry chemical or carbon dioxide. /Carbamate
pesticide, solid, nos/
Toxic Combustion Products:
Toxic gases and vapors such as oxides of nitrogen, methylamine, and carbon
monoxide may be released in a fire involving carbaryl.
Hazardous Reactivities & Incompatibilities:
... Incompatible with alkaline materials such as Bordeaux mixture, lime, and
lime sulfur.
Strong oxidizers, strongly alkaline pesticides.
Hazardous Decomposition:
When heated to decomposition it emits toxic fumes of nitroxides.
Immediately Dangerous to Life or Health:
100 mg/cu m
Protective Equipment & Clothing:
Employees should be provided with and required to use impervious clothing,
gloves, face shields (eight-inch minimum), and other appropriate protective
clothing necessary to prevent repeated or prolonged skin contact with carbaryl or liquids containing carbaryl.
Wear appropriate chemical protective gloves, boots and goggles. /Carbamate
pesticide, liquid, flammable, toxic, nos; carbamate pesticide, solid, toxic,
nos/
Wear positive pressure self-contained breathing apparatus. ... Wear
appropriate chemical protective clothing. /Carbamate pesticide, liquid, not
otherwise specified; carbamate pesticides, liquid, flammable, toxic, nos/
Wear appropriate chemical protective gloves, boots and goggles. ... Wear
positive pressure self-contained breathing apparatus when fighting fires
involving this material. /Carbamate pesticide, liquid, flammable, nos; carbamate
pesticide, solid, toxic, nos/
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: 50 mg/cu m).
Respirator Class(es): Any supplied-air respirator. May require eye protection.
Recommendations for respirator selection. Max concn for use: 100 mg/cu m.
Respirator Class(es): Any supplied-air respirator operated in a continuous flow
mode. 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 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.
Preventive Measures:
Smoking, eating, and drinking before washing should be absolutely prohibited
when any pesticide of moderate or higher toxicity is being handled or used.
/Pesticides/
Persons not wearing protective equipment and clothing should be restricted
from areas of spills until cleanup has been completed.
Clothing contaminated with carbaryl
should be placed in closed containers for storage until it can be discared or
until provision is made for the removal of carbaryl from the clothing. If the clothing is
to be laundered or otherwise cleaned to remove the carbaryl, the person performing the operation
should be informed of the hazardous properties of carbaryl.
Employees, including those in agricultural operations, who handle carbaryl or liquids containing carbaryl, should wash their hands thoroughly
with soap or mild detergent and water before eating, smoking, or using toilet
facilities. Eating and smoking should not be permitted in areas where solid
carbaryl is handled, processed, or
stored.
A complete respiratory protection program should be instituted which includes
regular training, maintenance, inspection, cleaning, and evaluation.
If clothing may have become contaminated with carbaryl, employees should change into
uncontaminated clothing before leaving the work premises. Non impervious
clothing which becomes contaminated with carbaryl should be removed promptly and not
reworn until the carbaryl is removed
from the clothing.
Good industrial hygiene practices recommend that engineering controls be used
to reduce environmental concentrations to the permissible exposure levels.
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.
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.
If material /is/ not involved in fire keep material out of water sources and
sewers. Build dikes to contain flow as necessary. /Carbaryl (agricultural insecticides, nec,
liquid); Carbaryl (agricultural
insecticides, nec, other than liquid); Carbaryl (insecticides, other than
agricultural, nec)/
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. /Carbaryl (agricultural
insecticides, NEC, liquid)/; /Carbaryl
(agricultural insecticides, NEC, other than liquid)/; Carbaryl (insecticides, other than
agricultural, NEC/
If material /is/ 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. Attempt to stop leak if
without undue personnel hazard. Use water spray to knock-down vapors. /Carbamate
pesticide, liquid, nos; carbamate pesticides, liquid, flammable, toxic, nos/
If material /is/ 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. /Carbamate pesticide, liquid, flammable, toxic, nos/
If material /is/ 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. /Carbamate pesticide, solid, toxic, nos/
Avoid breathing vapors. Keep upwind. ... Avoid bodily contact with the
material. ... 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. /Carbamate pesticide, liquid,
nos; carbamate pesticides, liquid, flammable, toxic, nos/
Avoid breathing dusts, and fumes from burning material. Keep upwind. Avoid
bodily contact with the material. ... 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. ...
If contact with the material anticipated, wear appropriate chemical protective
clothing. /Carbamate pesticide, solid, toxic, nos/
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.
Stability/Shelf Life:
STABLE TO HEAT, LIGHT, ACIDS; HYDROLYZED IN ALKALIES
UNSTABLE ABOVE 70 DEG C
Stable under neutral and weakly acidic conditions.
Shipment Methods and Regulations:
No person may /transport,/ offer or accept a hazardous material for
transportation in commerce unless that person is registered in conformance ...
and the hazardous material is properly classed, described, packaged, marked,
labeled, and in condition for shipment as required or authorized by ... /the
hazardous materials regulations (49 CFR 171-177)./
The International Air Transport Association (IATA) Dangerous Goods
Regulations are published by the IATA Dangerous Goods Board pursuant to IATA
Resolutions 618 and 619 and constitute a manual of industry carrier regulations
to be followed by all IATA Member airlines when transporting hazardous
materials.
The International Maritime Dangerous Goods Code lays down basic principles
for transporting hazardous chemicals. Detailed recommendations for individual
substances and a number of recommendations for good practice are included in the
classes dealing with such substances. A general index of technical names has
also been compiled. This index should always be consulted when attempting to
locate the appropriate procedures to be used when shipping any substance or
article.
Storage Conditions:
KEEP IN COOL, DRY PLACE. STORE AWAY FROM FEED & FOODSTUFFS. KEEP OUT OF
REACH OF CHILDREN.
Cleanup Methods:
1. VENTILATE AREA OF SPILL. 2. ... LARGE QUANTITIES MAY BE RECLAIMED;
HOWEVER, IF THIS IS NOT PRACTICAL, DISSOLVE IN FLAMMABLE SOLVENT (SUCH AS
ALCOHOL) & ATOMIZE IN SUITABLE COMBUSTION CHAMBER EQUIPPED WITH APPROPRIATE
EFFLUENT GAS CLEANING DEVICE.
A system for removing pesticides from the wash water produced by pesticide
applicators as they clean their equipment has been developed. The first step is
the flocculation/coagulation and sedimentation of the pesticide-contaminated
wash water. The supernatant from the first step is then passed through activated
carbon columns. /Pesticides/
Land spill: Dig a pit, pond, lagoon, 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, cement powder, or commercial sorbents. /Carbaryl (agricultural insecticides, nec,
liquid)/
Water spill: If dissolved, in region of 10 ppm or greater concentration,
apply activated carbon at ten times the spilled amount. Use mechanical dredges
or lifts to remove immobilized masses of pollutants and precipitates. /Carbaryl (agricultural insecticides, nec,
liquid)/
Land spill: Dig a pit, pond, lagoon, 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./ Cover
solids with a plastic sheet to prevent dissolving in rain or fire fighting
water. /Carbaryl (agricultural
insecticides, nec, other than liquid); Carbaryl (insecticides, other than
agricultural, nec/
Water spill: If dissolved, in region of 10 ppm or greater concentration,
apply activated carbon at ten times the spilled amount. Remove trapped material
with suction hoses. Use mechanical dredges or lifts to remove immobilized masses
of pollutants and precipitates. /Carbaryl (agricultural insecticides, nec,
other than liquid); Carbaryl
(insecticides, other than agricultural, nec)/
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.
Hydrolysis & landfill: For each 2.265 kg of actual carbaryl, add 0.906 kg of flake caustic
(sodium hydroxide) (this amt was stated to be a 50% excess over the minimum
required) and allow about 24 hr for completion of the reaction. The first step
of the degradation would be: aryl-O-CO-NHR + H2O --- NaOH ---> aryl-OH- +
(HO-CO-NHR). The carbamic acid at the right would decompose to the amine and
carbon dioxide in neutral soln, or to sodium carbonate in excess base. In excess
base the phenol would be converted to the salt, that is, NaO-aryl. Phenolic
decomposition products of some carbamate pesticides may, under some
circumstances, persist in the environment and harm specific ecosystems. ...
Hence, the hydrolysis should be followed by soil burial of the products in
disposal.
The heavy residue solid wastes are burned. One shutdown for cleaning is made
per year, but numerous maintenance cleanups are made and the washings go to the
process waste treatment system. Carbaryl
may be disposed of: 1) By making packages of carbaryl in paper or other flammable material
and burning in a suitable combustion chamber equipped with an appropriate
effluent gas cleaning device. 2) By dissolving carbaryl in a flammable solvent (such as
alcohol) and atomizing in a suitable combustion chamber equipped with an
appropriate effluent gas cleaning device. Recommendable methods: Alkaline
hydrolysis, landfill & incineration. Peer-review: Use 1 part by weight NaOH
/sodium hydroxide/ (as a 10% wt/vol soln in 50% ethanol:water) per 4 parts of
carbaryl plus 50% excess of NaOH. Leave
for 24 hr. Dissolve carbaryl in
flammable solvent such as ethanol, then spray the soln in an incinerator with
effluent gas scrubbing. (Peer-review conclusions of an IRPTC expert consultation
(May 1985))
Hydrolysis & landfill: Under the influence of sunlight, the reversal
reaction of carbaryl to 1-naphthol and
methylisocyanate (CH3NCO) has been found to take place. Methylisocyanate is a
poisonous and highly reactive substance. Accordingly, carbaryl should always be submitted to
alkaline hydrolysis before disposal. For the decontamination of carbaryl containers triple rinse and use of a
rinse soln containing caustic soda and detergent may be considered. "Triple
rinse" means the flushing of containers three times, each time using a volume of
the normal diluent equal to approx ten percent of the container's capacity, and
adding the rinse liquid to the spray mixture or disposing of it by a method
prescribed for disposing of the pesticide.
Occupational Exposure Standards:
OSHA Standards:
Permissible Exposure Limit: Table Z-1 8-hr Time Weighted Avg: 5 mg/cu m.
Threshold Limit Values:
8 hr Time Weighted Avg (TWA): 5 mg/cu m.
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.
A4; Not classifiable as a human carcinogen.
NIOSH Recommendations:
Recommended Exposure Limit: 10 Hr Time-Weighted Avg: 5 mg/cu m.
Immediately Dangerous to Life or Health:
100 mg/cu m
Other Occupational Permissible Levels:
Australia: 5 mg/cu m, substance under review (1990); Federal Republic of
Germany: 5 mg/cu m as total dust, skin (1990); United Kingdom: 5 mg/cu m, 10-min
STEL 10 mg/cu m (1991).
Manufacturing/Use Information:
Major Uses:
INSECTICIDE FOR CORN, ALFALFA, LIVESTOCK, POULTRY, OTHER NON-AGRICULTURAL
USES (EG, HOME USE), GARDENS, LAWNS, & FOR COMMERCIAL/INDUSTRIAL USE;
ACARICIDE & MOLLUSCICIDE
Insecticide; plant growth regulator
Medication (Vet)
Use in medical facilities, & in sewage treatment plants. /Former use/
Carbaryl /has been used/ to treat
oyster grounds.
Manufacturers:
Drexel Chemical Co., 1700 Channel Ave., Memphis, TN 38106-1412, (901)
774-4370; Production site: Cordele, GA 31015
HACCO, Inc., 537 Atlas Ave., Madison, WI 53714, (608) 221-6200; Production
site: Randolph, WI 53956
Rhone-Poulenc Ag Co., 2 T.W. Alexander Dr., P.O. Box 12014, Research Triangle
Park, NC 27709, (919) 549-2000; Production site: Institute, WV 25112
Chunchu; Crystal; Drexel; Jin Hung; Kuo Ching; Makhteshim-Agan;
Thone-Poulenc; Shenzhen Jiangshan
Methods of Manufacturing:
In a first step, sodium 1-naphthoxide is reacted with phosgene ... and in a
second step that intermediate is reacted with methylamine to give
1-naphthyl-N-methyl carbamate ... (Lambrech JA; US patent 2,903,478, September 8
(1959), assigned to Union Carbide Corp; and US patent 3,009,855, November 21
(1961), assigned to Union Carbide Corp).
Synthesized directly from 1-naphthol and methyl isocyanate or from naphthyl
chloroformate (1-naphthol and phosgene) plus methylamine.
General Manufacturing Information:
COMPATIBLE WITH MOST OTHER PESTICIDES EXCEPT THOSE STRONGLY ALKALINE SUCH AS
BORDEAUX MIXT OR LIME SULFUR, DECOMP TO FORM ALPHA-NAPHTHOL.
Crude or semirefined coal tar or petroleum naphthalene can be used for carbaryl manufacture.
Formulations/Preparations:
Aqueous dispersions, baits, dusts, emulsifiable concentrates, flowables,
granules, oil based flowables, powder, soluble concentrate, suspension
concentrate, wettable powder, water based flowables, water based dispersible
granules.
Carbaryl is available in the USA in a
technical grade of at least 99% purity or a technical grade of 95% purity for
use in manufacture of formulations
Carbaryl formulations include ...
wettable powders ...
Formulation types: TK; WP; DP; RB; SC; GR; OF. Mixtures: (carbaryl +) rotenone: propanil; tetrdifor;
diazinon; chlorfenson; lindane; sulfur; maneb; malathion; lindane + maneb;
propaphos
Consumption Patterns:
INSECTICIDE FOR CORN, 14%; VEGETABLES, 13%; SOYBEANS, 11%; COTTON, 4%;
DECIDUOUS FRUITS & NUTS, 4%; TOBACCO, 4%; SORGHUM, 2%; ALFALFA, 1%; CITRUS,
1%; OTHER FIELD CROPS, 17%; FORESTS, 2%; LIVESTOCK & POULTRY, 1%; OTHER
NON-AGRICULTURAL USES, 28% (1982)
1.5 million lbs on soybeans, 0.2 million lbs on corn, 0.2 million lbs on
peanuts, 0.1 million lbs on tobacco, & 0.1 million lbs on other small grains
(1982)
In 1988, about 25 million pounds of carbaryl was applied to crops on farms in the
United States.
In 1979, carbaryl was used on 50% of
the sweet corn acres at 2.7 lbs/acre. In 1992, no carbaryl use was reported for Minnesota. In
New York and Pennsylvania, carbaryl was
used at 4 lbs/acre while in 1991, it was used at 31 lbs/acre.
U. S. Production:
(1978) 2.27X10+10 TO 2.72X10+10 G (EST)
(1982) 1.59X10+10 TO 2.04X10+10 G (EST)
U. S. Imports:
(1982) 5.55X10+8 G (PRINCPL CUSTMS DISTS)
Laboratory Methods:
Clinical Laboratory Methods:
A method is presented for the determination of cholinesterase activity in
whole blood by colorimetry; at least 80% of the activity measured by this
technique is erythrocyte cholinesterase, & the method is applicable to all
anticholinesterase agents. A small volume of blood is incubated with a soln
containing 4 umoles of acetylcholine. Hydroxylamine is added to stop the
reaction & to react with the remaining acetylcholine, forming a colored
complex. The absorbance of this solution is measured in a spectrophotometer at
540 nm. The cholinesterase activity of a blood specimen is expressed as the
number of micromoles of acetylcholine hydrolyzed during the 10 min incubation,
& is calculated using the formula: umoles acetylcholine hydrolyzed=
4(1-As/Ac) where As represents the absorbance of the sample & Ac represents
the absorbance of the control. Quality control materials are not applicable to
this procedure. Sensitivity, 0.2 umoles; linearity, 0.2 to 4 umoles; coefficient
of variation, 1%; relative recovery, not applicable. Interferences: the avg
cholinesterase activity in whole blood using this technique is 2.38 umoles
(range 1.93-2.83) for adult males & 2.18 umoles (range 1.73-2.63) for
females. Approx 80% of the activity measured by this method is due to
erythrocyte cholinesterase, which is less subject to random variation than
plasma esterase activity. This method is useful for the routine monitoring of
worker exposure to carbaryl.
A method is presented for the determination of total 1-naphthol in urine by
colorimetry. Conjugated 1-naphthol in urine is released by acid hydrolysis &
the free substance is extracted into an organic solvent. The solvent is removed
by evaporation & the residue dissolved in methanolic alkali. The 1-naphthol
is reacted with p-nitrobenzene diazonium fluoroborate & the resulting color
determined spectrophotometrically at 590 nm. Calculation is based on a response
factor derived from a standard curve. A quality control specimen containing 2
mg/l 1-naphthnol is analyzed daily. Sensitivity, 0.2 mg/l; linearity, 0.5 to 16
mg/l; coefficient of variation, not established; relative recovery, not
established. Interferences: Urinary 1-naphthol concn have not exceeded 0.3 mg/l
in healthy unexposed subjects. Concentrations in excess of 4 mg/l may be
considered to represent significant exposure to carbaryl.
Analytic Laboratory Methods:
AOAC Method 985.23. N-Methylcarbamate insecticide and metabolite residues.
Liquid chromatographic method.
AOAC Method 975.40. N-Methylcarbamate insecticide residues. Gas
chromatographic method.
AOAC Method 964.18. Carbaryl
pesticide residues. Colorimetric method.
AOAC Method 968.26. Carbaryl
pesticide residues. Qualitative and semiqualitative method.
AOAC Method 991.06. N-Methylcarbamoyloximes and N-Methylcarbamates in
Finished Drinking Water by Liquid Chromatography.
NIOSH Method 5006. Determination of Carbaryl by Visible Absorption
Spectrophotometry in the Workplace .
METHOD IS DESCRIBED FOR DETERMINING CARBARYL ON FRUITS, VEGETABLES, & GRAINS.
RESIDUES ARE SEPARATED BY REVERSE PHASE HIGH PERFORMANCE LIQ CHROMATOGRAPHY
& DETECTED USING IN-LINE POST-COLUMN FLUOROMETRIC DETECTION TECHNIQUE.
DETERMINATION OF SOME CARBAMATE PESTICIDES, INCLUDING CARBARYL, IN WATER & SOIL BY
HIGH-PERFORMANCE LIQUID CHROMATOGRAPHY. AVERAGE RECOVERIES FROM THE HPLC COLUMN
WERE GREATER THAN 80% FOR WATER & SOIL SAMPLES WITH SOME EXCEPTIONS.
EPA Method 8270B-W. Determination Semivolatile Organic compounds by Gas
Chromatography/Mass Spectrometry (GC/MS): Capillary Column Technique.
EPA Method 8318-W. Determination of N-Methylcarbamates by High Performance
Liquid Chromatography (HPLC).
Sampling Procedures:
NIOSH 5006: Air samples containing carbaryl are taken with a 37 mm filter
cassette Type A glass fiber connected to a sampling pump calibrated at a flow
rate between 1 to 3 l/min for a sample size of 20 to 400 l. This technique has
an overall precision of 0.057 in a range of 2 to 13 mg/cu m using 90 liter
samples. Ship filters in 25 ml scintillation vials. Sample is stable for at
least 7 days at 25 deg C.
Special References:
Special Reports:
Vettorazzi G; Pest Rev 63 (44): 1 (1976). The criteria for evaluating
cholinesterase-inhibiting substances and other important aspects that have been
taken as the basis for formulating toxicological decisions on carbamate and
organophosphorus pesticides are reviewed. Criteria are viewed in the light from
published documents resulting from the activities or the joint meeting of the
FAO working party of experts on pesticide residues and the WHO expert committee
on pesticide residues. Short toxicological summaries and profiles reiterate the
current thinking on the toxicity of carbamate and organophosphorus
compounds.
Kingsbury PD; ACS Sym Series 238: 365 (1984). Environmental impact assessment
of insecticides /including carbaryl/
used in Canadian Forests is considered.
Hoffman DJ et al; Arch Env Contam Toxicol 13 (1): 15 (1984). Evaluation of
potential embryotoxicity and teratogenicity of 42 herbicides, (including carbaryl), insecticides, and petroleum
contaminants to mallard eggs.
Cranmer MF; Carbaryl A Toxicological
Review and Risk Analysis. Neurotoxicology 7 (1): 247-328 (1986).
Santodonato J; Govt Reports Announcements & Index (GRA&I) ISS 7
(1986)] The report presents a summary and evaluation of information relevant to
an occupational hazard assessment of /carbaryl/. Pertinent toxicologic data were
located through on-line and manual literature searches for the period extending
back approximately ten years from 1984. No attempt was made to exhaustively
review the toxicologic literature; where appropriate the reader is referred to
comprehensive reviews on this topic. Special attention in this report was
focused on summarizing the available information regarding the carcinogenic
potential of the chemical.
USEPA; Health and Environmental Effects Profile for Carbaryl (1984) ECAO-CIN-039.
Ghassemi M et al; Environmental Fates and Impacts of Major Forest Use
Pesticides TRW Environmental Division (1981) EPA/68-02-3174.
USEPA; Health Advisories for 50 Pesticides (1988) PB88-245931.
Synonyms and Identifiers:
Synonyms:
ARILAT **PEER REVIEWED**
ARILATE **PEER REVIEWED**
ARYLAM **PEER REVIEWED**
ATOXAN **PEER REVIEWED**
BERCEMA NMC50 **PEER REVIEWED**
CAPROLIN **PEER REVIEWED**
CARBAMIC ACID, METHYL-, 1-NAPHTHYL ESTER **PEER
REVIEWED**
Carbamine **PEER REVIEWED**
Carbaril **PEER
REVIEWED**
Carbaril (Italian) **PEER
REVIEWED**
CARBATOX **PEER REVIEWED**
CARBATOX-60 **PEER REVIEWED**
CARBATOX 75 **PEER REVIEWED**
CARBAVUR **PEER REVIEWED**
CARPOLIN **PEER REVIEWED**
Carylderm **PEER REVIEWED**
Cekubaryl **PEER REVIEWED**
COMPOUND 7744 **PEER REVIEWED**
Crag sevin **PEER REVIEWED**
Denapon **PEER REVIEWED**
Devicarb **PEER REVIEWED**
DICARBAM **PEER
REVIEWED**
DYNA-CARBYL **PEER REVIEWED**
ENT 23,969 **PEER REVIEWED**
ENT-23969 **PEER REVIEWED**
EXPERIMENTAL INSECTICIDE 7744 **PEER
REVIEWED**
Gamonil **PEER REVIEWED**
GERMAIN'S **PEER REVIEWED**
Hexavin **PEER
REVIEWED**
KARBARYL (POLISH) **PEER
REVIEWED**
Karbaspray **PEER REVIEWED**
KARBATOX **PEER
REVIEWED**
KARBATOX 75 **PEER
REVIEWED**
KARBOSEP **PEER
REVIEWED**
MENAPHTAM **PEER
REVIEWED**
N-METHYLCARBAMATE DE 1-NAPHTYLE (FRENCH) **PEER
REVIEWED**
N-METHYL-1-NAFTYL-CARBAMAAT (DUTCH) **PEER
REVIEWED**
N-METHYL-1-NAPHTHYL CARBAMATE **PEER
REVIEWED**
N-METHYL-1-NAPHTHYL-CARBAMAT (GERMAN) **PEER
REVIEWED**
N-METHYL-ALPHA-NAPHTHYLURETHAN **PEER
REVIEWED**
N-Metil-1-naftil-carbammato (Italian) **PEER
REVIEWED**
MONSUR **PEER
REVIEWED**
Mugan **PEER
REVIEWED**
MURVIN **PEER
REVIEWED**
NAC **PEER REVIEWED**
1-NAPHTHALENOL, METHYLCARBAMATE **PEER
REVIEWED**
ALPHA-NAPHTHALENYL METHYLCARBAMATE **PEER
REVIEWED**
1-NAPHTHOL N-METHYLCARBAMATE **PEER REVIEWED**
ALPHA-NAPHTHYL METHYLCARBAMATE **PEER
REVIEWED**
ALPHA-NAPHTHYL N-METHYLCARBAMATE **PEER
REVIEWED**
1-NAPHTHYL N-METHYLCARBAMATE **PEER REVIEWED**
1-NAPHTHYL METHYLCARBAMATE **PEER REVIEWED**
NMC 50 **PEER REVIEWED**
Olititox **PEER REVIEWED**
OMS-29 **PEER REVIEWED**
PANAM **PEER
REVIEWED**
POMEX **PEER
REVIEWED**
Prosevor 85 **PEER REVIEWED**
Ravyon **PEER
REVIEWED**
Rylam **PEER REVIEWED**
SEFFEIN **PEER
REVIEWED**
Septene **PEER REVIEWED**
SEVIMOL **PEER
REVIEWED**
SEVIN 4 **PEER REVIEWED**
Sok **PEER REVIEWED**
Tercyl **PEER
REVIEWED**
Toxan **PEER
REVIEWED**
Tricarnam **PEER
REVIEWED**
UC 7744 **PEER REVIEWED**
UNION CARBIDE 7,744 **PEER REVIEWED**
VIOXAN **PEER
REVIEWED**
Formulations/Preparations:
Aqueous dispersions, baits, dusts, emulsifiable concentrates, flowables,
granules, oil based flowables, powder, soluble concentrate, suspension
concentrate, wettable powder, water based flowables, water based dispersible
granules.
Carbaryl is available in the USA in a
technical grade of at least 99% purity or a technical grade of 95% purity for
use in manufacture of formulations
Carbaryl formulations include ...
wettable powders ...
Formulation types: TK; WP; DP; RB; SC; GR; OF. Mixtures: (carbaryl +) rotenone: propanil; tetrdifor;
diazinon; chlorfenson; lindane; sulfur; maneb; malathion; lindane + maneb;
propaphos
Shipping Name/ Number DOT/UN/NA/IMO:
NA 2757; Carbaryl
IMO 6.1; Carbamate pesticides, solid, toxic, nos; carbamate pesticides,
liquid, toxic, flammable, nos, flashpoint between 23 deg C and 61 deg C;
carbamate pesticides, liquid, toxic, nos; carbamate pesticides, liquid, nos
IMO 3.2; Carbamate pesticides, liquid, flammable, toxic, nos, flashpoint less
than 23 deg C
UN 2757; Carbamate pesticides, solid, toxic, not otherwise specified;
carbamate pesticides, liquid, nos
UN 2758; Carbamate pesticides, liquid, flammable, toxic, nos, flashpoint less
than 23 deg C
UN 2991; Carbamate pesticides, liquid, toxic, flammable, nos, flashpoint
between 23 deg C and 61 deg C
UN 2992; Carbamate pesticides, liquid, toxic, nos
Standard Transportation Number:
49 411 21; Carbaryl (agricultural
insecticides, nec, liquid)
49 411 22; Carbaryl (agricultural
insecticides, nec, other than liquid)
49 411 20; Carbaryl (insecticides,
other than agricultural, nec)
49 105 28; Carbamate pesticide (compounds and preparations), flammable
liquid
49 216 25; Carbamate pesticide (compounds and preparations), liquid (poison
b) (insecticides, agricultural, nec, liquid)
49 216 27; Carbamate pesticide (compounds and preparations), solid (poison b)
(insecticides, agricultural, nec, other than liquid)
49 105 27; Carbamate pesticide (compounds and preparations), liquid
(flammable liquid)
49 216 24; Carbamate pesticide (compounds and preparations), liquid (poison
b) (insecticides, nec, other than agricultural)
49 216 26; Carbamate pesticide (compounds and preparations), solid (poison b)
(insecticides, nec, other than agricultural)
RTECS Number:
NIOSH/FC5950000
Administrative Information:
Hazardous Substances Databank Number: 952
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 10/16/2002, 5 fields added/edited/deleted.
Field Update on
01/14/2002, 1 field added/edited/deleted.
Field Update on 08/08/2001, 1 field
added/edited/deleted.
Field Update on 05/15/2001, 1 field
added/edited/deleted.
Complete Update on 08/29/2000, 2 fields
added/edited/deleted.
Field Update on 06/12/2000, 1 field
added/edited/deleted.
Field Update on 06/12/2000, 1 field
added/edited/deleted.
Complete Update on 03/28/2000, 1 field
added/edited/deleted.
Complete Update on 03/02/2000, 72 fields
added/edited/deleted.
Field Update on 02/02/2000, 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 01/27/1999, 1 field
added/edited/deleted.
Complete Update on 11/12/1998, 2 fields
added/edited/deleted.
Complete Update on 06/02/1998, 1 field
added/edited/deleted.
Complete Update on 03/26/1998, 4 fields
added/edited/deleted.
Field Update on 10/20/1997, 1 field
added/edited/deleted.
Field Update on 09/17/1997, 1 field
added/edited/deleted.
Field Update on 08/12/1997, 5 fields
added/edited/deleted.
Field Update on 05/08/1997, 1 field
added/edited/deleted.
Complete Update on 03/19/1997, 1 field
added/edited/deleted.
Complete Update on 02/27/1997, 1 field
added/edited/deleted.
Complete Update on 10/13/1996, 1 field
added/edited/deleted.
Complete Update on 05/10/1996, 1 field
added/edited/deleted.
Complete Update on 04/23/1996, 1 field
added/edited/deleted.
Complete Update on 04/09/1996, 8 fields
added/edited/deleted.
Field Update on 01/19/1996, 1 field
added/edited/deleted.
Complete Update on 05/04/1995, 1 field
added/edited/deleted.
Complete Update on 04/20/1995, 1 field
added/edited/deleted.
Complete Update on 04/20/1995, 1 field
added/edited/deleted.
Complete Update on 01/18/1995, 1 field
added/edited/deleted.
Complete Update on 12/22/1994, 1 field
added/edited/deleted.
Complete Update on 06/30/1994, 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 08/17/1993, 1 field
added/edited/deleted.
Complete Update on 08/07/1993, 1 field
added/edited/deleted.
Field update on 12/16/1992, 1 field
added/edited/deleted.
Complete Update on 12/02/1992, 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 01/07/1991, 70 fields
added/edited/deleted.
Field Update on 01/15/1990, 1 field
added/edited/deleted.
Complete Update on 01/11/1990, 67 fields
added/edited/deleted.
Field Update on 05/05/1989, 1 field
added/edited/deleted.
Field Update on 03/01/1989, 1 field
added/edited/deleted.
Field Update on 05/12/1988, 1 fields
added/edited/deleted.
Complete Update on 03/04/1988, 76 fields
added/edited/deleted.
Complete Update on 03/31/1986
Record Length: 270566
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