Toxic Gases Causing Pulmonary Toxicity in Animals

What are the gases known to cause pulmonary toxicity in animals

 Gaseous Ammonia (NH3)

 Hydrogen Sulfide (H2S)

 Polytetrafluoroethylene (PTFE) Fumes

 Carbon Monoxide (CO)

What are the routes of exposure for ammonia ?

• Animal Production Facilities: Decaying Fecal Material as Source of NH3 (THIS IS THE MAIN ONE)… but theres also other sources such as

• Accidental release of ammonia

• Ammonia theft in the farm

What are the clinical signs and symptoms for Ammonia Toxicity

• Respiratory symptoms

• Eye symptoms

• Foot pad symptoms

In Ammonia Toxicity what do we see in Respiratory symptoms (THIS IS Ammonia Toxicity)

- Rhinitis and dyspnea

- Acute respiratory distress

In Eye symptoms what do we see in Respiratory symptoms (THIS IS Ammonia Toxicity)

- Swollen eyes, keratoconjunctivitis

- Corneal opacity, ulcers, blindness

In Foot pad symptoms what do we see in Respiratory symptoms (THIS IS Ammonia Toxicity)

- Foot pad dermatitis

What are the diagnosis for Ammonia Toxicity

• Monitor Ammonia levels

• Supportive evidence

In ammonia toxicity what do we mean by Monitor Ammonia levels:

• Using colorimetric tube assays

- Frequently performed in poultry farms

- Ammonia concentration at ≥ 25 ppm is considered toxic to birds

In ammonia toxicity what do we mean by Supportive evidence:

history, clinical signs, and lesions

What are the treatments for Ammonia Toxicity

 No antidote

 Prompt removal of patient from source of exposure

 Irrigate mucus membranes with copious amount of water

 Management of burns and respiratory distress

What are the Prevention of Ammonia Toxicity

 Reduce litter material buildup

 Reduce moisture and improve ventilation

 Routinely monitor NH3 levels in the animal facility

Whare the routes of Exposure to Hydrogen sulfide (H2S)

Confined manure pits: Agitation releases hydrogen sulfide gas

What is the Mechanism of Toxicity with Hydrogen Sulfide (H2S)

 Inhibits Cytochrome C oxidase in mitochondria

 Impairs aerobic respiration in the cell

Suppresses ATP synthesis

What do we see if the Exposure to lower concentration of hydrogen sulfide

 Irritation of eyes and upper respiratory tract

 Cardiac arrythmia

 Gastrointestinal complications- nausea, vomition, diarrhea

What do we see if the Exposure to high concentration of hydrogen sulfide (>750 ppm)

 Knockdown effect- apnea, loss of consciousness, collapse, and death

 Acute respiratory distress due to pulmonary edema

 Recovered animals: Long term neurological complications

 Recovered animals: Euthanasia is recommended

What are the Diagnosis of Hydrogen Sulfide Toxicity

Lab tests are NOT readily available for H2S detection

History of agitation of manure pit and animal exposure

Clinical evidence of hydrogen sulfide toxicity

What are the Differential diagnosis of Hydrogen Sulfide Toxicity

- Polioencephalomalecia in cattle (ruminants only)

- Caused by ingestion of high level of sulfur (water or feed)

- Hydrogen sulfide gas is produced in rumen by bacteria

What is the treatment for Hydrogen Sulfide Toxicity

There is no clinically effective antidote availble

Prompt removal of patient from source of exposure

Resuscitation and oxygen therapy

 Recovered animals develop CNS complications

What are the prevention of Hydrogen Sulfide Toxicity

Avoid exposure to manure pits, sludge tank, settling ponds

Ensure adequate ventilation during manure agitation

What are the sources of Polytetrafluoroethylene (PTFE; Teflon®) toxicity

• PTFE Coated Cookware and Appliances

• PTFE Coated Heating Lamp (Poultry Farm)

• PTFE fumes cause toxicity

Which animals is highly susceptible to Polytetrafluoroethylene (PTFE; Teflon®) toxicity

• birds

• Budgerigars- most sensitive

What is the mechanism for PTFE Fumes

PTFE toxicity mechanism is not very clear

Pyrolysis products and fine particles (<1 μm) contribute to toxicity

Direct irritation and oxidative damage to fine blood vessels in lungs

Cause hemorrhage and edema of lungs

 Sudden death is observed in most cases

What are the clinical presentation of PTFE Toxicity

Begins with with frequent eyelid movement

Signs of anxiety, respiratory distress, and breathing difficulty

Rapid escalation of respiratory signs leading to sudden death

In most cases, birds found dead without visible clinical signs

What is the diagnosis for PTFE Toxicity

Diagnostic tests are NOT available to detect PTFE products

Diagnosis made based on history of exposure, signs, and lesions

What are the treatments for PTFE Toxicity

Peracute death with PTFE toxicity leaves no time for intervention

Place affected bird in warm and oxygenated incubator

Provide supportive care: NSAIDs, diuretics, and brancondilators

What are the preventions for PTFE Toxicity

Owner education: avoid bird exposure to PTFE fumes

- Replace PTFE coated cookware and utensils

- Move birds to a safe and well ventilated location

What is the source of Carbon Monoxide (CO) Toxicity

• Incomplete Combustion Releases CO (limited Oxygen Supply)

• Sources of CO in Animal Facilities (Gas Powered Forklift, Catalytic Radiant Heater, Kerosine Heater, Diesel Generator)

In carbon monoxide toxicity what is the major cause of the toxicity

Carboxyhemoglobin Formation

Which are the major drivers of toxicity for the Mechanism of Carbon Monoxide Toxicity

CO + Hemoglobin = Carboxyhemoglobin

Carboxyhemoglobin unable to carry O2

CO exposure leads to tissue hypoxia

What are the other that Contribute to toxicity

CO cause brain microvascular damage

CO cause lipid peroxidation in brain cells

Are there clinical signs for CO toxicity ?

• Highly Nonspecific

Examples

• nausea

• vomit

• tachycardia

• hypotension

• ataxia

• syncope

What are the diagnosis for Carbon Monoxide Toxicity

A detailed history of physical surroundings of animals

”Red Cherry” coloration of mucus membrane- rarely useful

Pulse oximeter readings may remain normal- do not use

Elevated carboxyhemoglobin levels in blood suggest CO toxicity

What is the Treatment of Carbon Monoxide Toxicity

Antidote: 100% oxygen by endotracheal tube, mask, or cage

Supportive therapy may be necessary to address:

• Cardiovascular complications

• Acidosis (use of bicarbonates is controversial)

What are the prevention for carbon Monoxide Toxicity

Avoid exposure to source of carbon monoxide

 Provide adequate ventilation to minimize the exposure

Monitor exposure with inhouse CO detection devises

WHat is the Mechanism of Toxicity with Ammonia

• NH3 + H20 = Ammonium hydroxide= toxicity

• Mucus membrane irritation

• Liquefactive necrosis

• Tissue damage and ulceration