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Toxicology > Toxic Gases > Flashcards

Toxic Gases Flashcards

1
Q

What are the local responses to toxic gases?

A
  • Iritation
  • inflammation
  • edema
  • necrosis
  • fibrosis
  • emphysema
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2
Q

What are farm sources of toxic gases?

A
  • Uncontrolled decomposition of feeds (eg - NO2 from silage)
  • Anaerobic decomposition of animal wastes inside confinement buildings
    • NH3, CO2, CH4, H2S
  • Incomplete combustion of fossil fuels (CO)
  • Accidental/intended release of anhydrous NH3
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3
Q

What is the source of Nitrogen Dioxide?

A
  • Fermentation of corn/forages high in nitrate
  • NO2 is formed in the first 2 weeks after the ensiling.
    • Incomplete Reduction of NO3
    • Highest concentration in the first 48 hrs of ensiling
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4
Q

What are the characteristics of NO2

A
  • Brownish in color
  • Pungent irritating odor
  • Heavier than air - accumulates in low areas
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5
Q

What happens to NO2 when exposed to H2O in the air?

A
  • forms nitric acid
  • direct toxicant and strong irritant to eyes, respiratory tract and lungs
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6
Q

What is Silo Fillers Disease?

A
  • Nitrogen Dioxide toxicosis
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7
Q

What is the MOA of NO2

A
  • Direct irritant - forms HNO3
  • Oxidant ⇢ lipid peroxidation
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8
Q

What are the effects of NO2

A
  • Ocular and upper airway irritation, coughing, chocking at > 50 ppm
  • Pulmonary edema, tachycardia, fever, dyspnea, hypoxia are delayed effects
  • Chronic bronchitis or emphysema
    • “Silo Fillers disease”
  • Rapid progression, may be fatal
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9
Q

What are the clinical signs of NO2 exposure

A
  • Reddened mucous membranes
  • Lacrimation
  • Salivation
  • ⇣ Food and water intake
  • coughing, paning
  • Dyspnea - flyid sounds in chest
  • Hypoxia
  • Fever
  • Pneumonia
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10
Q

What lung lesions are common to NO2 exposure?

A
  • Edema
  • Hyperemia + hemorrhage
  • Emphysema
  • Bronchiolar inflammation
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11
Q

How is NO2 exposure diagnosed and treated?

A
  • Dx - clinical signs, history, few tox tests
  • Rx - Move to ventilated places
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12
Q

What are the characteristics of Methane gas?

A
  • Lighter than air
  • Odorless
  • Explosive at 5% in the atmosphere
  • Toxicity by displacing O2
    • very high levels (rare) ⇢ asphyxiation
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13
Q

What are the sources of Methane gas?

A
  • Natural Gas:
    • 85% methane
    • 9% ethane
    • 3% propane
    • 2% nitrogen
    • 1% butane
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14
Q

What are the characteristics of CO2

A
  • Odorless
  • Heavier than air
  • 0.03% (300 ppm) in atmosphere
  • 1540 ppm - recommended maximal concentration in environmental air for swine
  • 10% distress, increased respiratory rate
  • 25% coma
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15
Q

What are the characteristics of Ammonia (NH3)

A
  • Lighter than air
  • Colorless
  • Sharp pungent odor
    • 5ppm very slight
    • 20pp, easily detected
    • 6-35ppm found in confinement units
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16
Q

What are the sources for NH3

A
  • Fertilizers - NH3 rarely a problem
    • NH4NO3, NH42CO3, NH43PO4
  • Manure - slurry pits
    • chicken or horses
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17
Q

What are the effects of NH3 at 50 ppm?

A
  • Chronic stressor
    • Exacerbated respiratory disease
    • Reduces pulmonary bacterial clearance
    • Feed intake, growth rate decreased by ≥10%
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18
Q

What are the effects of NH3 at 100 ppm?

A
  • Strong odor
  • Eye and respiratory irritation
  • Salivation, lacrimation, corneal damage
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19
Q

What are the effects of NH3 in poultry?

A
  • 20 ppm - decreased egg production
  • 50 ppm - increased incidence of respiratory disease
  • 60-75 ppm - corneal injury (keratoconjunctivitis)
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20
Q

What are the clinical signs of NH3 exposure?

A
  • Reddened mucous membranes
  • Keratoconjunctival lesions
  • Lacrimation
  • Nasal discharge (⇡ pulmonary infection)
  • Sniffling, sneezing, coughing
  • Pulmonary edema, congestion
  • Dyspnea - fluid sounds
  • hypoxia
  • Electrolyte and A/B imbalance
  • Decreased egg production in birds
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21
Q

What are the Terminal signs of NH3 exposure?

A
  • Cyanosis
  • Violent struggling
  • Clonic convulsions
22
Q

How is NH3 exposure diagnosed?

A
  • Clinical signs
  • Odor
  • No reliable analytical tests for the field
23
Q

How is NH3 exposure treated?

A
  • Remove from the source
  • Ointment for eyes
  • Antibiotics
24
Q

What are the characteristics of Hydrogen sulfide (H2S)

A
  • Colorless
  • Heavier than air, collects in low places
  • Odor of rotten eggs
25
Q

What are the sources for H2S?

A
  • Formed by anaerobic decomposition of sulfur containing AA
  • Held as tiny bubbles deep within manure slurry in pit and released when the slurry is agitated prior to pumping
  • Also from oil drilling and industrial sources
  • Feed related - high sulfur diets
26
Q

What are the toxic levels of H2S

A
  • 0.1-0.2 ppm - odor threshold
  • 3-5 ppm - offensive odor
  • 50-100 ppm - irritating to eyes, respiratory tract
  • 200 ppm - olfactory paralysis
  • > 500 ppm - pulmonary edema, potentially lethal
  • >1000 ppm - respiratory paralysis, collapse
  • > 3000ppm - death after a few violent gasps
27
Q

What is the MOA of H2S

A
  • Direct irritant to eyes and lungs
  • CNS effects - inhibition of respiratory center (??), seizures, unknown MOA
  • General metabolic: inhibition of cytochrome oxidase
28
Q

What are the clinical signs of H2S exposure?

A
  • Coughing, lacrimation, nasal discharge
  • Dyspnea
  • Depression
  • Fluid sounds in lungs
  • Terminal cyanosis, convulsions
  • Lesions:
    • Edema in lungs (intestine and brain)
    • Dark blood
    • Smell of H2S in tissues
29
Q

How can H2S exposure be diagnosed?

A
  • Difficult
  • Clinical signs
  • Odor
  • Hx of exposure
  • Gas detectors - $$$
  • Necropsy and tests to eliminate other causes:
    • neurodegeneration in the brainstem
  • Humans: sulfide, thiosulfate in serum/urine
30
Q

What is the treatment for H2S exposure?

A
  • Remove from source
  • No antidotes
  • Experimental Tx:
    • Nitrites
    • Cobinamide
    • Hydroxycobolamine
    • Thiamine
31
Q

What are the characteristics of Carbon Monoxide (CO)?

A
  • Odorless
  • Colorless
  • Lighter than air
32
Q

What are the sources of CO?

A
  • Internal combustion engine exhaust:
    • automobile exhaust ( up to 9% CO)
    • Lethal CO in 10 minutes in enclosed spaces
  • Unvented or faulty heating equipment:
    • Furnaces, gas water heaters, gas or kerosene space heaters, charcoal grills
    • lethal in enclosed spaces
  • Fires:
    • CO may reach 10% in the atmosphere in burning building
33
Q

What is the MOA of CO?

A
  • Co absorbed from lung, combines with Hb to from COHb ⇢ Anoxia
  • Affinity of Hb for CO ~300x more than for O
34
Q

What are the Acute signs of CO exposure?

A
  • Drowsiness, lethargy, weakness, deafness, incoordination
  • Reduced heart excitability
  • Cherry red color to skin, mucous membranes
  • Dyspnea, coma, terminal clonic spasms, acute death
35
Q

What are the clinical signs of CO exposure?

A
  • Based on degree of anoxia:
    • Acute -
      • pregnant animals may abort
      • CO crosses placenta ⇢ Fetal hypoxia
        • fetal Hb even more susceptible to CO than maternal Hb
    • Chronic
      • low exercise tolerance
      • Abnormal posture and gait
      • ECG abnormalities consistent with anoxia and necrosis of heart muscle fibers
36
Q

How is CO exposure diagnosed?

A
  • Hx of exposure
  • Clinical signs
  • Necropsy shows bright red blood or pink mm
  • Anoxia causes necrosis of cerebral cortex and white matter, globus pallidus and brain stem
  • Measure CO in environments
  • Measure COHb in whole blood
    • <5% normal
    • 10-20% headache, fatigue, irritability
    • 20-30% weakness, dizziness, mild symptoms
    • 30-60 % confusion, increased heart and respiratory rate, coma
    • >60% usually fatal
  • COHb in fetal serosanguinous thoracic fluid (>8% is significant)
37
Q

What is the treatment for CO exposure?

A
  • Main goal - restore adequate oxygen supply to the brain and heart
  • Move patient to fresh air to stop further CO exposure
  • Maintain patent airway and provide artificial respiration if necessay
  • Patients breathing hyperbaric or 100% O2 recover more quickly
38
Q

How can CO exposure be prevented?

A
  • Maintain properly functioning heaters, exhaust systems and adequate ventilation
  • Use CO detectors
  • Do Not operate automobile engines and other cources of CO in or near enclosed spaces
39
Q

What are the sources of Anhydrous Ammonia?

A
  • Agricultural fertilizer - injected into soil as source of N
  • Used as a commercial refrigerant
  • Used in meth labs
40
Q

What is the MOA of Anhydrous Ammonia?

A
  • Released gas seeks water
    • attacks moisture rich tissues - cornea, mm, respiratory epithelium
  • Gas NH3 + H2O = NH4OH
  • Produces strong alkali burns in the tissue
41
Q

What are the clinical effects of Anhydrous Ammonia?

A
  • Acute death from laryngospasm
  • Fluid accumulation in lungs
  • Sloughing epithelium or respiratory system
  • Corneal opacity, blindness
  • Secondary bacterial invasion
42
Q

What pathological affects are common with Anhydrous Ammonia

A
  • necrosis of superficial layers
    • dermis of muzzle
    • epithelium of trachea
43
Q

What are the effects of ventilation failure on animals?

A
  • Hyperthermia - from
    • Metabolic activity of large animals
    • thermal inpute from exterior (summer)
    • Inadequate building ventilation
    • Heat generation from manure stored in pits
44
Q

What are the sources for Polytetrafluoroethylene (PTFE)

A
  • Overheated Teflon or Silverstone coated cooking pans
  • Ironing board covers, electric irons, range top drip pans, self-cleaning ovens
45
Q

What temperature do Pyrolysis products form from PTFE?

A
  • at >280-530C (535-985F)
  • Pyrolysis products = particulates + acidic volatile gases
46
Q

What animal is the most sensitive to PTFE?

47
Q

What are the clinical signs of PTFE exposure?

A
  • Acute respiratory distress
  • Audible respiration
  • Dyspnea
  • Rapidly fatal
48
Q

What lesions are seen with PTFE exposure?

A
  • Pulmonary hemorrhage and congestion
  • Particles my be seen on lung sections
49
Q

How is PTFE exposure prevented?

A
  • Do not use non stick cookware around pet birds
  • Have good ventilation
  • Remove birds from house when cooking
50
Q

What is the treatment for PTFE exposure?

A
  • Difficult unrewarding
  • Move immediately to fresh air
  • Corticosteroids to reduce shock, pulmonary edema
  • Fluids, broad spectrum antibbiotics

Toxicology (25 decks)

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