2. What are Agricultural Poisons?
POISON -- substances that cause disturbances in
organisms, usually by chemical reaction or other activity on
the molecular scale, when an organism absorbs a sufficient
quantity
Herbicide - plant killer
Insecticide - insect killer
Rodenticide - rodent killer
Fungicide - fungus killer
3. Types of pests:
PESTS
Animal Pest Plant Pest
1. Rodents 1. Weeds
2. Insects 2. Fungi
*Biting 3. Microbes
*Sucking
4. A. Halogenated Insecticides
• a combination of one or
more chemical elements
that includes a HALOGEN
HALOGEN GROUP
Fluorine
Chlorine
Bromine
Iodine
Astatin
Tennessine
5. Properties of Halogens
HALOGENS COLOR STATE MOLECULAR
SIZE
DENSITY REACTIVITY
Fluorine Yellow Gas ^ ^ l
Chlorine Green Gas l l l
Bromine Orange Liquid l l l
Iodine Gray/Black Solid l l l
Astatin Black Solid l l v
8. DDT is an organochlorine insecticide
discovered by the Swiss chemist Paul
Hermann Müller in 1939
Used to control mosquito-borne malaria &
vectors, crops, control insect typhus then
extensively used as an agricultural
insecticide after 1945
DDT was banned for use in Sweden in
1970 and in the United States in 1972.
9. • Available as
aerosols,
dustable
powders,
emulsifiable
concentrates,
granules and
wettable
powders.
Commercial product
concentrate containing
50% DDT, circa 1960s
Commercial product
(Powder box, 50 g)
containing 10% DDT
"Destroys parasites
such as fleas, lice,
ants, bedbugs,
cockroaches, flies,
etc.. Néocide
Sprinkle caches of
vermin and the
places where there
are insects and their
places of passage.
Leave the powder in
place as long as
possible.
10. Acute Toxicity
DDT is moderately to slightly toxic to studied mammalian
species via the oral route.
Reported oral LD50s range from:
113-800 mg/kg in rats 150-300 mg/kg in mice
300 mg/kg in guinea pigs 400 mg/kg in rabbits
500-750 mg/kg in dogs >1,000 mg/kg in sheep &goats
DDT is readily absorbed through the gastrointestinal tract, with increased
absorption in the presence of fats.
11. • Low to moderate exposure : nausea, diarrhea, increased
liver enzyme activity, irritation (of the eyes, nose or throat),
disturbed gait, malaise and excitability
• Higher doses : tremors and convulsions are possible
• While adults appear to tolerate moderate to high ingested
doses of up to 280 mg/kg, a case of fatal poisoning was
seen in a child who ingested one ounce of a 5%
DDT:kerosene solution
12. Chronic Toxicity
• Effects on the nervous system, liver, kidneys,and immune
systems in experimental animals
Tremors in rats at doses of
16-32 mg/kg/day over 26
weeks
Tremors in mice at doses of
6.5-13mg/kg/day over 80-140
week
Changes in cellular
chemistry in the central
nervous system of monkeys
at doses of 10 mg/kg/day
over 100 days
loss of equilibrium in
monkeys at doses of 50
mg/kg/day for up to 6
months
13. Emergency Measures :
Emesis.
Give activated charcoal followed by gastric lavage,
then with saline cathartic.
Do not give fats or oil.
Scrub skin with soap and water to remove skin
contamination.
Give artificial respiration ig respiration is slowed
14. General Measures
1) Anticonvulsants - give Diazepam. If convulsion persist,
use a neuromuscular blocking agent.
2) For hypersensitivity or tremor - give Phenobarbital
Sodium
Don't give stimulants, Epinephrine, since it sometimes
induce ventricular fibrillation
15. • Trade name: Lindane, KWELL
• Benzene Hexacloride has been used both as
an agricultural insecticide and as a
pharmaceutical treatment for lice and scabies.
• The World Health Organization classifies
lindane as "Moderately Hazardous"
16. • It is named after the Dutch chemist Teunis van
der Linden, the first to isolate and describe γ-
Hexachlorcyclohexane in 1912.
• In 2009, the production and agricultural use of
lindane was banned under the Stockholm
Convention on persistent organic pollutants.
• In exemtion to the ban, Lindane is used as
second-line treatment for lice and scabies.
18. • The EPA and WHO both classify lindane as moderately
toxic.
• Oral LD50 of 88 mg/kg in rats and a dermal LD50 of
1000 mg/kg
• Lindane affects the nervous system, liver and kidneys,
and may well be a carcinogen.
19. • Exposure to small amounts by skin contamination or
ingestion: headaches, nausea, dizziness, tremors and
muscular weakness.
• Exposure to large amounts: can harm the nervous
system, producing a range of symptoms from headache
and dizziness to seizures, convulsions, coma,
respiratory depression, and, more rarely death.
20. • Based primarily on evidence from
animal studies, most evaluations
of lindane have concluded that it
may possibly cause cancer. In
2015, the International Agency for
Research on Cancer (IARC)
classified lindane as a known
human carcinogen.
21. • If in skin contact: Remove patient clothing and discard
in well-sealed pouches. Wash immediately with soap
and water.
• Orally: DO NOT INDUCE EMESIS
Gastric lavage
Give Activated Charcoal
Secure airway
22. • No known antidote.
• Cholestyramine may be used to bind these highly
lipophilic agents. It reduces reabsorption and retains
bound agent in the GI tract for fecal elimination.
• Beta-adrenergic blocking agents and magnesium are
administered initially for organochlorine-induced
ventricular dysrhythmias
• Olestra has also been shown to increase excretion of fat-
soluble organic chlorine chemicals.
23. • Includes: Aldrin, Endrin,
Thiodan, and Chlordane
• Insecticide treating
approximately 30 million
homes for termites for
crops like corn and citrus,
and on lawns and
domestic gardens.
24. • CHLORDANE:
– LD50 in rats is 283 mg/kg
– LD50 in rabbits is 580
mg/kg
• ALDRIN:
– LD50 in rats is 39 mg/kg
– LD50 in rabbits is 65 mg/kg
• THIODAN:
– LD50 in rats is 80-110mg/kg
– LD50 in rabbits is 359
mg/kg
• ENDRIN:
– LD50 in rats is 40 mg/kg
– LD50 in rabbits is 65 mg/kg
25. • Acute poisoning: timid,
hypersensitivity,
nystagmus, clonus of
muscles, seizures,
salivation, gnashing,
collapse of breathing
• Chronic poisoning: same
signs, longer and gradual
coming, possibility of
death.
26. • ORAL: DO NOT INDUCE
VOMITING. Do not give any
liquid to the person. Gastric
lavage is recommended.
• EYE CONTACT: Hold eye
open and rinse slowly and
gently with water for 15–20
minutes. Remove contact
lenses, if present, after the
first 5 minutes, then continue
rinsing eye.
• SKIN CONTACT: Take off
contaminated clothing. Rinse
skin immediately with plenty of
water for 15–20 minutes.
• INHALED: move person to
fresh air. If person is not
breathing, call an ambulance,
then give artificial respiration,
preferably by mouth-to mouth,
if possible.
27. • There is no specific antidote.
• Amobarbital-sodium or thiopental sodium may be given
intravenously for convulsion
• DO NOT GIVE STIMULANTS
29. Cholinesterase
• Cholinesterase is a family of enzymes that catalyzes the hydrolysis of the
neurotransmitter acetylcholine into choline and acetic acid
Acetylcholine
• Acetylcholine is the neurotransmitter used at the neuromuscular
junction—in other words, it is the chemical that motor neurons of the
nervous system release in order to activate muscles
Inhibitor
• is a molecule that binds to an enzyme and decreases its activity
30. How does it work? causing a "jam" in the
nervous system
Repeated and unchecked firing of electrical signals can cause
uncontrolled, rapid twitching of some muscles, paralyzed
breathing, convulsions, and in extreme cases, death
32. Organophosphate
• Organophosphate insecticides are derived from phosphoric acid
• Organophosphate insecticides include some of the most toxic pesticides and
widely used
• Malathion is widely used in agriculture, residential landscaping, public recreation
areas, and in public health pest control programs such as mosquito eradication
• Dichlorodiphenyltrichloroethane
• The mainstays of medical therapy in organophosphate poisoning include atropine,
pralidoxime and benzodiazepines
33. Organophosphate Poisoning
Signs and symptoms of organophosphate poisoning can be divided into three broad
categories:
• muscarinic effects
• nicotinic effects
• central nervous system effects
37. Carbamates
• A carbamate is an organic compound derived from carbamic acid
• They are relatively unstable compounds
• Carbamates are commonly used as surface sprays or baits in the control of
household pests
• Carbaryl the first successful carbamate, was introduced in 1956
• Propoxur (Baygon) is highly effective against cockroaches that have developed
resistance to organophosphates
38. Carbamate Poisoning
• If a carbamate insecticide is ingested, vomiting should be induced. If absorbed
through the skin, contaminated clothing should be removed and the skin washed
thoroughly with soap and water. In carbamate poisoning, the use of atropine is
indicated, but oximes are contra-indicated.
42. Organophosphates (OP)
• CHLORPYRIFOS, DIAZINON AND MALATHION
• Inhibits the action of acetylcholinesterase.
• causes the acetylcholine to remain coupled to the nerve cell, causing the cell to fire
repeatedly. [Irreversible]
• Hyperactivity, Uncoordinated Movements, Tremors, Convulsions Or Paralysis
49. Patients with suspected exposure, insert IV line &
commence atropinisation to minimise bronchorrhoea:
• 0.02-0.05mg/kg (max 2mg) can be given every 10-15min until
atropinised:
• ie. warm, dry, flushed skin; dilated pupils, dry mouth, tachycardia
• signs of atropine excess appear to be reversing:
• OP - at least 24hrs with tapering of dose after 12hrs if clinically OK
• lipophilic OP - longer duration Rx
• carbamates - shorter duration of Rx
50. The Role Of Pralidoxime:
• Cholinesterase reactivator at the NM junction, and is
effective for some of the nicotine effects but does not
cross BBB
• Dose of pralidoxime:
• 25-50mg/kg IV over 15-30min up to 0.5-1g (adult dose)
• Repeat dose in 1-2hrs & then at 6-12hr intervals
• Administration should commence within 36hrs
• Adverse effects of pralidoxime:
• dizziness, headache, nausea, blurred vision, muscle weakness.
51. Summary of Differences between organophosphate &
carbamate insecticides:
• shorter effect - usually only lasting 24hrs in carbamates
• Carbamates do not pass BBB & thus have less CNS
effects
• use pralidoxime makes carbamate toxicity worse unlike
OP
53. Miscellaneous Pesticides
As a result of their rather high degree of specificity, they might be regarded
as less important than many of the more broad-spectrum chemicals that are
in such wide use.
Miscellaneous pesticides classified as miscellaneous vary in their chemical
structures, toxicities, physical, and chemical properties. Nevertheless, some
members of this class might share common mechanisms of action.
Methyl Bromide
Bromopropylate
Ethylene oxide
Ethylene dibromide
are some of the well-known
miscellaneous pesticides.
55. Methyl Bromide
chemical name for this fumigant is bromomethane.
A non-inflammable, colorless gas at ordinary temperatures and pressures
Fairly easily compressible into liquid form
Extensively used as an insecticides, fire extinguisher, fumigant and refrigerant
It is without smell in low concentrations
3.3 times as heavy as air
it constitutes a very real industrial hazard
56. Methyl Bromide
Toxic effects
1. On the skin – giving the rise to a vesicular irritative dermatitis and second
degree burns
2. On the respiratory system – produces bronchitis , broncho-pneumonia,
pulmonary congestion and edema
3. On the alimentary system – gastro-intestinal upset and hepatic dysfunction
4. On the nervous system – both an acute and a chronic symptomatology
57. Methyl bromide
Human experience indicates:
acute fatal intoxication can result from exposures to vapor levels as low
as 1164 to 1552 mg/cu m
harmful effects can occur at 388 mg/cu m or more
Systemic poisoning has been reported to occur from a two week exposure
(8 hr/day) at about 136 mg/cu m
Sublethal poisoning cases a latency period of 2 to 48 hr (usually about 4 to
6 hr) occurs between exposure and onset of symptoms.
58. In most instances, the onset of the symptoms is delayed and this latent period varies from 1/2
to several hrs and occasionally 12, 24, or 48 hr.
The symptoms may be fatigue, headache, dizziness, nausea and vomiting, disturbances of
hearing, vision, mental confusion, muscular weakness, collapse, respiratory difficulties and
coma. Death is usually due to lung damage, but damage to the CNS may accompany pulmonary
damage.
59. High concentrations of methyl bromide can produce rapid
unconsciousness during exposure, leading to a prompt "anesthetic"
death.
The delay in onset usually is several hours, but a delay of only a few
min & a delay of 48 hr have been observed.
In fatal cases with delayed onset, death generally occurs within 4-6 hr
but sometimes after 24-48 hr.
In rare instances, death may be delayed as much as 18 days. The
cause of death in these cases usually is circulatory failure.
60. LD50 and LC50
The inhalation LC50 for rats is:
3,120 ppm/15 minutes
2,700 ppm/30 minutes, and
1,164 ppm/60 minutes.
LD50 administered in liquid is 20 mg/L for rats
61. TOXICOLOGICAL EFFECTS
ACUTE TOXICITY
Methyl bromide, labeled with a DANGER signal word, is an extremely toxic vapor.
In humans, methyl bromide is readily absorbed through the lungs.
Most problems occur as a result of inhalation.
Inhalation of 1,600 ppm for 10-20 hours, or 7,900 ppm for 1.5 hours is lethal to
humans
The lowest inhalation level found to cause toxicity in humans is 35 ppm in air.
62. First symptoms often are due to damage to the nervous system, and may be delayed from 48
hours to as long as several months after exposure. This delay, combined with methyl
bromide's lack of odor, means that the victim may not realize that exposure is occurring until
much time has passed.
Soon after inhalation of large doses, symptoms may include headache, dizziness, nausea,
chest and abdominal pain, and a dry throat.
Three to 12 hours after vapor inhalation symptoms include slurred speech, blurred vision,
temporary blindness, mental confusion, and sweating.
More severe symptoms may include lung swelling; congestion; hemorrhaging of the brain,
heart, and spleen; severe kidney damage; and numbness.
Death may occur within 1-30 hours, usually from respiratory failure.
63. CHRONIC TOXICITY
Chronic exposures to methyl bromide can cause dizziness, vision and hearing disturbances,
depression, confusion, hallucinations, euphoria, personality changes, and irritability. If exposure
is severe enough, lung irritation followed by lung swelling and bronchial pneumonia may occur
Reproductive Effects
No reproductive problems involving methyl bromide have been observed in test animals, though
few experiments have been performed.
Teratogenic Effects
Inhalation of methyl bromide for 6-7 hours per day during gestation was reported to cause no
birth defects on rabbits and rats
Mutagenic Effects
The overall scientific evidence indicates that methyl bromide is a mutagen, but that its potential
to cause genetic mutations is relatively low.
Carcinogenic Effects
Methyl bromide is considered to be a potent cell growth stimulant and is thus a potential
promoter of cancerous growth.
64. Organ Toxicity
Chronic low level exposure causes depression of the central nervous system,
injury to the kidneys, and may cause respiratory problems, and irritate the skin
and eyes.
65. Prehospital Management
Victims exposed only to methyl bromide gas do not pose substantial risks of
secondary contamination to personnel outside the Hot Zone; however, some
methyl bromide may permeate clothing. Victims whose clothing or skin is
contaminated with liquid methyl bromide (i.e., ambient temperature less
than 38.5°F) can secondarily contaminate response personnel by direct
contact or through off-gassing vapor.
Methyl bromide is a neurotoxic gas that may cause headaches, dizziness,
visual disturbances, ventricular fibrillation, pulmonary edema, ataxia,
convulsions, coma, and death.
Exposures to high concentrations of methyl bromide can cause eye, skin, and
respiratory tract irritation, as well as chemical pneumonitis. Dermal
absorption may contribute to systemic toxicity.
There is no antidote for methyl bromide. Treatment consists of support of
respiratory and cardiovascular functions.
67. Bromopropylate
Also known as Isopropyl 4,4'-dibromobenzilate; Phenisobromolate
A white solid compound that is almost insoluble in water but soluble
in most organic solvents
An acaricide used to control mites on fruit and other crops
The major crops on which it is recommended are citrus, vines, pome
and stone fruits, sugar beet, sugarcane and tea.
The target mite species include European red mite, two-spotted mite,
carmine mite, apple-rust mite
68. Probable Routes of Human Exposure:
BROMOPROPYLATE was applied directly to some fruit crops as an acaricide
and exposure to this compound was primarily dermal and via inhalation for
workers.
However, recent monitoring data indicate that consumers may be exposed to
bromopropylate via ingestion of some imported fruits and vegetables.
69. TOXICOLOGICAL INFORMATION
Dermal Exposure: irritation
Eye Exposure: irritation
Inhalation: irritation to the respiratory tract
Ingestion: harmful
Effects for chronic exhibition: The product is belonging to low pesticide for
human; it has no reproductive, teratogenic and carcinogenic effects. But it
can irritate the skin of humans, and if ingest large, can be harmful to body.
70. FIRST AID TREATMENT:
SKIN: Wash with soap and water.
EYES: Flush with plenty of water for at least 15 minutes.
See medical attention if irritation develops.
INHALATION: Move to fresh air. Do not breathe spray mist.
INGESTION: Drink 1-2 glasses of water and milk.
Call physician/poison control center immediately
71. DERMAL EXPOSURE
DECONTAMINATION:
Remove contaminated clothing and jewelry and place them in
plastic bags. Wash exposed areas with soap and water for 10 to 15
minutes with gentle sponging to avoid skin breakdown. A physician
may need to examine the area if irritation or pain persists.
Treat dermal irritation or burns with standard topical
therapy. Patients developing dermal hypersensitivity
reactions may require treatment with systemic or topical
corticosteroids or antihistamines.
72. EYE EXPOSURE
DECONTAMINATION:
Remove contact lenses and irrigate exposed eyes with copious
amounts of room temperature 0.9% saline or water for at least 15
minutes. If irritation, pain, swelling, lacrimation, or photophobia
persist after 15 minutes of irrigation, the patient should be seen in
a healthcare facility.
73. INHALATION EXPOSURE
DECONTAMINATION
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 an inhaled
beta2-adrenergic agonist. Consider systemic corticosteroids in
patients with significant bronchospasm.
Respiratory tract irritation, if severe, can progress to
pulmonary edema which may be delayed in onset up to
24 to 72 hours after exposure in some cases.
74. ORAL EXPOSURE
Immediate dilution with milk or water may be of benefit.
DILUTION: If no respiratory compromise is present, administer milk or water
as soon as possible after ingestion. Dilution may only be helpful if performed
in the first seconds to minutes after ingestion. The ideal amount is unknown;
no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is
recommended to minimize the risk of vomiting.
75. EXPOSURE CONTROLS/PERSONAL
PROTECTION:
Personal protective equipment
Respiratory protection: Approved respirator
Protective gloves: Rubber gloves
Eye protection: Goggles
Industrial hygiene:
Wear face shield or goggles, elbow length PVC gloves, cotton overalls
buttoned to the neck and wrist, washable hat and half face respirator with
dust and vapor cartridge.
After use and before eating, drinking or smoking, wash hands, arms and
face thoroughly with soap and water.
76. HANDLING AND STORAGE:
HANDLING: Do not apply to humans, their clothing, or bedding.
Do not contaminate food or use on household tanks.
STORAGE: Store in original container only in cool, dry, well ventilated, secure
area out of reach of children and animals.
77. DISPOSAL CONSIDERATIONS:
Do not reuse product containers.
Dispose of product containers, waste containers, and residues according to all
state and local haws and regulation.
Use proper protective equipment to minimize exposure.
Take all necessary action to prevent and to remedy the adverse effect of the
spill.
79. ETHYLENE OXIDE
Properly called OXIRANE
Colorless and flammable gas at room temperature and pressure
Toxic gaseous cyclic ether with a sweet ether-like smell
Bactericidal, fungicidal and sporocidal disinfectant
Fumigant and insecticide
Sterilant for food and cosmetic
A chemical intermediate in industry
81. Ethylene oxide
ACUTE EFFECTS
-nausea, vomiting, bronchitis, neurological disorders
-irritation of the eyes and mucous membranes
CHRONIC EFFECTS
-Irritation of the eyes, skin and mucous membrane
-problems in functioning of the brains and nerves.
-leukemia, stomach cancer, pancreatic cancer, Hodgkin’s disease
OTHER EFFECTS
-increase rate of miscarriage in female workers
82. Ethylene oxide
ANTIDOTE AND EMERGENCY TREATMENT (IMMEDIATE FIRST AID)
-ensure adequate decontamination
-perform CPR if necessary
-immediately flush contaminated eyes with flowing water
-do not induce vomiting
-if vomiting, lean patient forward or place on left side
-keep patient quiet and maintain normal body temperature
83. Ethylene oxide
MINIMUM/ POTENTIAL FATAL HUMAN DOSE
- 5-15g/kg, between 1pt and 1qt for 70kg person(150 Lb)
-12500 ppm/10 seconds
ANTIDOTE AND EMERGENCY TREATMENT (BASIC TREATMENT)
- patent airway, suction if necessary
-administer oxygen by nonbreather mask 10-15L/min
-anticipate seizures and treat if necessary
- for eye: flush eyes immediately with water, irrigate with 0.9% saline during transport
-administer activated charcoal
-for ingestion: rinse mouth, administer 5ml/kg up to200ml of water for dilution
-cover burns with dry sterile dressings
-treat frostbite by rewarming
84. Ethylene oxide
ANTIDOTE AND EMERGENCY TREATMENT ( ADVANCE TREATMENT)
-orotracheal/nasotracheal intubation for airway control
-lactated ringer’s if signs of hypovolemia are present
-diazepam( Valium) or lorazepam (Ativan) to treat seizures
-proparacaine hydrochloride to assist eye irrigation
86. ETHYLENE DIBROMIDE
Also known as 1,2-DIBROMOETHANE
Clear, colorless, volatile liquid
Mild, sweet, chloroform like odor that emits corrosive and toxic fumes when
heated to decomposition
Effective soil fumigant, insecticide, and nematocide
Chemical intermediate in the synthesis of resins, waxes, gums, dyes
Used in gasoline
87. Ethylene dibromide
EXPOSURE ROUTES AND SYMPTOMS
-INHALATION: burning sensation, cough, laboured breathing, shortness of breath,
vomiting, drowsiness, unconsciousness
-SKIN(ABSORBED)/ EYE: redness, pain
-INGESTION: abdominal pain, vomiting, drowsiness
TARGET ORGANS
- liver, kidneys, CNS, respiratory and reproductive system
88. Ethylene dibromide
ACUTE EFFECTS
-severe burning of skin, BLISTERS
-irritation of the eyes and respiratory tract
CHRONIC EFFECTS
-prolonged inhalation may cause liver necrosis
-impair reproduction in males by damaging sperm cells in the testicles long term
-bronchitis and depression
REFERENCE DOSE
-0.OO2MG PER CUBIC METER, BASED ON THE REPRODUCTIVE EFFETCS IN HUMANS
89. ANTIDOTE AND EMERGENCY TREATMENT (BASIC TREATMENT)
- patent airway, suction if necessary
-administer oxygen by nonbreather mask 10-15L/min
-anticipate seizures and shock and treat if necessary
- for eye: flush eyes immediately with water, irrigate with normal saline during
transport
-for ingestion: rinse mouth, administer 5ml/kg up to200ml of water for
dilution
-administer activated charcoal
-cover burns with dry sterile dressings
90. Ethylene dibromide
ANTIDOTE AND EMERGENCY TREATMENT ( ADVANCE TREATMENT)
-orotracheal/nasotracheal intubation for airway control
-lactated ringer’s if signs of hypovolemia are present
-diazepam(valium) to treat seizures
-proparacaine hydrochloride to assist eye irrigation
Editor's Notes
Do not penetrate the CNS hence CNS toxicity is limited
Rest s/s same as OP
T/t : ATROPINE is the specific antidote
Pralidoxime may diminish the severity of the symptoms
S/S: begin within 15 minutes to 2 hrs.
and help prevent some morbidity
It improves respi functions and patient well being
Atropine will not affect nicotinic (skel. muscle & symp. ganglia) receptors.
Adverse effects of atropine include:
fever, muscle fasciculations, delirium, dry eyes, adynamic bowel, unresponsive pupils
There is evidence that pralidoxime may increase the toxicity of carbamates & thus should only be used in organoP poisonings, after adequate atropinisation & only if resp. depression or unresponsive cardiac arrhythmias, although some feel it is appropriate to use if more than 2 doses of atropine have been needed in organoP poisonings.
- In severe cases, respiratory tract irritation can progress to ARDS/acute lung injury, which may be delayed in onset for up to 24 to 72 hours in some cases.
- It can produce an allergic hypersensitivity dermatitis or asthma with bronchospasm and wheezing with chronic exposure.
- If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.