Toxic gases Flashcards
what happens when ammonia comes in contact with MM?
- forms ammonium hydroxide which is irritating and caustic
how does an animal become exposed to ammonia?
- inhalation***
- environmental conditions
- decomposing manure in confined animal houses
- burning plastics
- used in agricultural fertilizer
at what level of NH3 will eyes burn?
25-35ppm
what exposure of NH3 can cause acute death?
5000ppm
what are the toxicokinetics of NH3?
- converted to a strong base irritant (ammonium hydroxide) on MM
- primarily absorbed by inhalation and is distributed to tissue cells
what is the MOA of NH3?
- direct irritation of MM
- causes pulmonary edema and lung congestion
3 alkalosis and compensatory acidosis - inhibit TCA cycle
- increased susceptibility can lead to resp infections due to continuous exposure - irritation - inflammation - secondary infections
- 50-75ppm: decreased ability to clear bacteria from the lungs –> resp dysfunction - decreased growth of young animals
- 100ppm: decreased growth rate by 32% in swine
what are the CS with acute NH3 toxicity?
red MM, lacrimation, coughing, sneezing, nasal discharge, keep eyes shut
what are the CS with chronic NH3 toxicity?
- decreased growth rate and production
- dyspnea - fluid in the lungs caused by pulmonary edema/congestion
what are the CS with terminal NH3 toxicity?
CNS stimulation, clonic convulsions, cyanosis
how do we diagnose NH3 toxicity?
- history
- odor of ammonia
- CS
- lesions (blisters on MM)
how do we treat NH3 toxicity?
- remove source
- fresh air
- soothing ointments for eyes
- antibiotics may prevent secondary infections
- diuretics for pulm edema
- treat any secondary infections
what are the main properties of hydrogen sulfide gas (H2S?)
- colorless
- odor of rotten eggs
- heavier than air
- flammable
- water soluble
- irritant because converted to sulfuric acid
- forms black or dark colored compounds in GIT and tissues
what are the main routes of exposure for H2S?
- INHALATION
- by product or waste material from industry **
- may be liberated in coal pits, gas wells, or sulfur springs
- also associated with natural gas and crude oil production
humans can detect H2S at what level?
0.025ppm
at what level does H2S cause eye irritation?
20ppm
at what level is H2S possibly fatal?
400ppm
what does 1000ppm H2S cause?
rapid unconsciousness and death in about 1 hour
> 2000ppm H2S cause what?
resp paralysis after 1-2 breaths
what are the toxicokinetics of H2S?
- readily absorbed through the lungs and GIT
- converted to alkali sulfides in the blood
- hydrosulfide radical is normally oxidized to sulfate and is excreted in urine
- some sulfide is excreted in feces
what is the MOA of H2S?
- direct irritation of MM
- inhibition of cellular respiration
- decreased cytochrome oxidase
- stimulation of the chemoreceptorsof the carotid body - depressed resp drive
- DIE FROM ASPHYXIATION
what are the CS from acute H2S exposure?
- sudden collapse
- cyanosis
- dyspnea
- convulsions
- rapid death
what are the CS from chronic H2S exposure?
- eye, resp, and lung irritation
what are the CS from chronic H2S exposure?
- eye, resp, and lung irritation
what are the lesions associated with H2S poisoning?
- blood is dark and may not clot
- tissues may be dark or greenish purple
- carcass may have sewage odor
- if ingested, the GI contents may be black or dark gray and smel of sewage
how do we treat H2S toxicity?
- removal of source
- sodiun nitrite IV may be partly effective by forming methemoglobin - binds sulfide radicals and reactivates cytochrome oxidase
- oxygen therapy, ventilation
- educate about prevention (get H2S monitors!)
what are the properties of carbon monoxide (CO)?
odorless, colorless, not water soluble
what are common exposure routes for CO?
- accidental exposure with fires (incomplete combustion of carbon containing products - wood, paper, petroleum products)
- propane powered equipment, space heaters, portable cookers, de-icers
- automobile exhaust in confined spaces
what is the MOA of CO?
- CO combines with hemoglobin to form carboxyhemoglobin and reduced the level of O2 (hemoglobin has a 240x higher affinity for CO)
- carboxyhemoglobin interferes with release and availability of O2 carried by hemoglobin
- some intereference with cellular resp
- also competes with O2 for binding sites on myoglobin
what is death due to from CO poisoning?
hypoxia
what are the main CS with CO poisoning?
- sudden death at 60-70% COHb
- in low exposure (30-60% COHb) signs = hypoxia, drowsiness, incoordination, dyspnea, lethargy, coma
what are the lesions associated with CO toxicity?
- blood is bright red and the MM are pink
- no significant lesions in acute cases
- in chronic cases there may be brain edema, hemorrhage, and necrosis which may cause deafness in dogs/cats
what lab diagnostics can we run to confirm CO toxicity?
- measuring CO in air
- percentage of COHb in the blood (correlation to CS is poor)
how do we treat CO toxicity?
- oxygen or 5% CO2 in oxygen administered with positive pressure
- blood transfusion
- fluid for acidosis but bicarb use is controversial
what are the common sources of Nitrogen Oxide gases?
- farm
- NO2 and N2O4 gases are produced by incomplete reduction of nitrates during fermentation process in silo’s
- nitrogen oxide poisoning = Silo filler’s disease - industry
- NO2 is a major pollutant (burning of fossil fuels)
what are the major properties of Nitrogen Oxide gases?
- NO2 gas is reddish brown
- N2O4 is colorless
- NO2 is heavier than air but the gases are about as dense as air - forms layers on top of silage and settles down on the chute
- gas mixture has an irritating chlorine-like odor
- low solubility in water
which nitrogen oxide gas exposure is more toxic - acute or chronic?
acute
what are the toxicokinetics of nitrogen oxide gases?
- animal quarters that develop the irritant odor or yellow haze in the air must not be entered
- nitrogen dioxide and tetraoxide gases form nitric acid upon contact with mucus membranes
- cross resp mucosa and cause cellular damage in the lungs - pulmonary edema
what is the MOA of nitrogen oxide gases?
- direct irritation of the MM by nitric acid
- low water solubility - passes from upper to lower resp tract and causes damage in the lungs
- lung damage - due to caustic reaction with the PFAs at cellular membrane - pulmonary edema, hemorrhage
- death is from hypoxia -resp failure
what are the CS associated with nitrogen oxide gas toxicity?
- resp signs - generally similar to ammonia poisoning (irritation of MM, effects on respiration)
what lesions are associated with nitrogen gas toxicity?
- pulmonary edema
- hemorrhage
- emphysema
- cyanosis
- methemoglobinemia
- necrosis of skeletal muscle
how do we treat nitrogen oxide gas toxicity?
- supportive treatment
- diuretics if pulmonary edema
- methylene blue IV for methemoglobinemia
- antibiotic ointment for MM
at what percentage of methemoglobinemia do we normally start seeing toxic signs?
15% (normal is 1%)
what are the common sources of exposure with sulfure oxide gases?
- sulfur dioxide SO2 and sulfur trroxide (SO3) are industrial pollutants
- fossil fuel combustion at power plants
what are the main properties of sulfur oxide gases?
- highly soluble in water
- sharply irritant to MM because the form sulfurous and sulfuric acids on contact with water
- odor causes coughing, choking, and suffocation
SO2 at ___ppm is fatal to cats within 30-60mins
500
SO2 at 500ppm for __ hour(s) is dangerous to grazing animals
1
SO2 at ___ppm for 8 days causes poisoning in pigs
5-40
what is the MOA of sulfur oxide gases?
- direct irritation of the MM - primarily upper resp tract
- reflex bronchoconstriction - lung damage
- death due to hypoxia
what are the CS and lesions associated with sulfur oxide gas toxicity?
- similar to other toxic gases (irritation to MM, effects on respiration)
what all does “smoke” include?
vapors, gases, fumes, heated air and particulate matter, liquid and solid aerosols
why is there no LD50 for smoke?
it is a heterogenous mixture of gases - too many variable
inhalation of super-heated air and steam can cause?
thermal burns to resp tract and enhance absorption of gases
burns in the resp tract enhances toxicity
what are the MOAs of smoke inhalation?
- simple asphyxiants - inert (CO2) gases or vapors displace O2
- low concentration, generally have little if any physiological effect - chemical asphyxiant - prevent uptake of O2
- produce toxic local (lungs) and systemic effects
- carbon monoxide –> COHb - irritants
- chemically reactive on contact with MM to cause local effects
- sulfur dioxide –> sulfuric acid
- particle - ash and soot
what are the CS associated with chemical asphyxiants?
- resp
- cough, dyspnea, tachypnea
- wheezing, decreased breath sounds, crackles - CV
- tachycardia, hypoxemia
- hypotension, dysrhythmias - signs of irritation
- conjunctivitis, pharyngitis, rhinitis, drooling, hoarseness
- edema, mucosal ulcerations
- corneal abrasions common from ash/soot - CNS
- agitation, confusion, ataxia, abnormal posture, seizure - surface burns
what kind of lesions might we see with smoke inhalation (chemical asphyxiants?)
- burns
- pulmonary changes
- cerebral edema
how do we treat smoke inhalation (chem asphyxiants)?
- prompt removal from the smoke environment + O2 support
- B2 adrenergic agonists may benefit for bronchoconstriction
- NO STEROIDS
- remove soot from skin
- avoid cough suppressants and opioids
- maintain airway patency, ventilation, etc
____ of the toxin (gas, chemical) is the most importany determinant of resp injury
solubility
highly soluble particles (smoke inhalation) end up where in the resp tract?
upper airway
- injury to the mucosa, inflammatory mediators, free radicals –> increased permeability –> edema
low water soluble particles (smoke inhalation) end up where in the resp tract?
- lung, bronchiole, alveoli
- slower reaction, delayed effect
ammonia and sulfur dioxide have high or low water solubility?
high - end up in upper airway
- chemically reactive on contact with mucus
nitrogen oxides have high or low water solubility?
- low - end up in pulmonary parenchymal injury in the alveoli, alveolar ducts
