Veterinarians and other veterinary personnel can be exposed to nonanesthetic toxic gases as part of their work, particularly when dealing with animal housing areas, waste systems, or emergency situations.
Hazardous Nonanesthetic Gases Commonly Encountered in the Veterinary Workplace
Hazardous nonanesthetic gases that veterinarians and their staff might encounter include carbon monoxide (CO), cyanide (HCN), hydrogen sulfide (H2S), nitrogen dioxide (NO2), and phosphine (PH3).
Hazardous nonanesthetic gases can arise from sources like faulty equipment, combustion engines, manure decomposition, or certain chemical agents. Awareness of potential sources of these gases, proper monitoring, and the use of appropriate safety measures are essential to minimize the risk of harmful exposure in veterinary environments.
Hazardous nonanesthetic gases are typically encountered via inhalation, particularly in confined or poorly ventilated spaces, making vigilance, environmental monitoring, and appropriate safety measures essential for veterinary personnel.
Veterinarians and their staff can be exposed during necropsy to cyanide and phosphine gas present in the GI tract of animals poisoned with cyanide (or its glycosides) or with phosphide salts (commonly zinc and aluminum). Emergency room staff and veterinary staff casualties have occurred during treatment of, respectively, human and veterinary patients poisoned with phosphide salts (1).
Exposure to some toxic gases can have a seasonal component. For example, fatal carbon monoxide poisoning often occurs during extreme cold weather conditions, especially in conjunction with electrical power failures and the use of combustion heaters, electrical generators, and other alternative heat sources in enclosed spaces with inadequate ventilation.
Exposure to these hazardous gases, even at low levels, can pose serious health risks because of their rapid effects on respiration and cellular function. The physical characteristics, common sources of veterinary exposure, primary routes of exposure, mechanisms of action, and main adverse health effects of selected toxic gases relevant in the veterinary workplace are summed up here.
Carbon Monoxide (CO) as a Toxic Gas in the Workplace
Physical characteristics: Colorless, odorless, tasteless gas; slightly lighter than air; nonirritating, making it difficult to detect without monitoring equipment.
Common sources of exposure: Incomplete combustion from gas heaters, generators, charcoal, wood-burning equipment, and vehicle exhaust in barns or enclosed areas; smoke inhalation during barn or building fires
Primary route of exposure: Inhalation
Mechanism of action: Binds to hemoglobin with high affinity, forming carboxyhemoglobin and decreasing oxygen delivery to tissues; also impairs cellular respiration. Blood carboxyhemoglobin levels correlate poorly with the clinical severity of the poisoning.
Main health effects: Headache, dizziness, weakness, confusion, loss of consciousness, cardiac stress, death in severe cases. Hypoxic brain injury in survivors. Cherry-colored skin and mucous membranes can occur. Most pulse oximeters do not detect the presence of carboxyhemoglobin; pulse CO-oximetry is required.
Cyanide (HCN) as a Toxic Gas in the Workplace
Physical characteristics: Colorless or pale-blue liquid/gas; faint bitter-almond odor (not detectable by all individuals); slightly lighter than air; highly volatile.
Common sources of exposure: Smoke from structure or barn fires (burning plastics, wool, synthetic materials); certain chemical exposures; decomposition of nitrogen-containing organic matter under specific conditions; cyanide-based pesticides.
Primary route of exposure: Inhalation (primarily); dermal also possible
Mechanism of action: Inhibits cytochrome c oxidase in mitochondria, blocking cellular respiration and preventing oxygen use (cellular hypoxia). Skin and eye irritant.
Main health effects: Rapid onset of headache, anxiety, shortness of breath, seizures, cardiovascular collapse, death. Hypoxic brain injury in survivors. Cherry-colored skin and mucous membranes can occur.
Hydrogen Sulfide (H2S) as a Toxic Gas in the Workplace
Physical characteristics: Colorless gas with characteristic rotten-egg odor at low concentrations; heavier than air; odor might disappear at high concentrations as a result of olfactory fatigue (loss of the ability to smell).
Common sources of exposure: Decomposition of manure and organic waste in manure pits, lagoons, and slurry storage systems; agitation of manure in confined animal housing.
Primary route of exposure: Inhalation
Mechanism of action: Inhibits cytochrome c oxidase; also acts as a mucosal and respiratory irritant.
Main health effects: Eye and respiratory irritation, coughing, pulmonary edema, olfactory fatigue (loss of the ability to smell), rapid unconsciousness, and death at high concentrations. Hypoxic brain injury in survivors. Cherry-colored skin and mucous membranes can occur.
Nitrogen Dioxide (NO2) as a Toxic Gas in the Workplace
Physical characteristics: Reddish-brown, water-insoluble gas with sharp, acrid odor; heavier than air; forms nitric and nitrous acid when combined with moisture. Low water solubility results in penetration into the lung, where it is reactive with lung surface fluids and acts as a pulmonary irritant.
Common sources of exposure: Formation during anaerobic fermentation of silage in silos, silage bags, and pit systems, especially in newly filled silos or poorly ventilated feed storage areas. People working in or around silo chutes and hatches or silage pits/bags during approx. the first 10 days after fill can be exposed.
Primary route of exposure: Inhalation
Mechanism of action: Strong oxidant that causes direct damage to lung tissue and formation of nitric and nitrous acid in the respiratory tract.
Main health effects: Acute or delayed-onset respiratory distress, cough, wheezing, chest pain, pulmonary edema, bronchiolitis obliterans (“silo filler’s disease”). Mucous membrane and eye irritation are relatively uncommon.
Phosphine (PH3) as a Toxic Gas in the Workplace
Physical characteristics: Colorless gas with garlic or decaying fish odor (impurities); slightly heavier than air; highly toxic and flammable.
Common sources of exposure: Use of fumigants (eg, aluminum phosphide) in stored grain, feed, or pest control operations in agricultural and veterinary facility settings. Can be generated in the GI tract from zinc phosphide and aluminum phosphide.
Primary route of exposure: Inhalation
Mechanism of action: Disrupts mitochondrial function and oxidative phosphorylation; generates reactive oxygen species, causing cellular damage.
Main health effects: Acute inhalation exposure to phosphine can result in respiratory, neurological, and GI effects. Nausea, vomiting, chest tightness, pulmonary edema, cardiac arrhythmias, multiorgan failure in severe exposure.
Many of these gases act rapidly, interfering with cellular respiration or causing oxidative injury to the lungs and other organs. Understanding both the mechanisms by which these gases exert their effects and the associated health consequences is essential for recognizing early signs of exposure, initiating appropriate treatment, and implementing effective preventive measures.
Because children have higher ratios of minute volume to weight and of lung surface area to body weight, they are often more susceptible than adults to these hazardous gases.
Survivors of severe poisoning with some gases (eg, carbon monoxide, cyanide, hydrogen sulfide) might have hypoxic brain injuries, which can be associated with personality changes, memory deficits, disturbances in voluntary muscle movements, and the appearance of involuntary movements (extrapyramidal syndromes) (2, 3, 4).
The primary control method to decrease exposure to hazardous nonanesthetic gases is prevention. Preventive steps include improving ventilation (local exhaust and general dilution), deploying continuous gas monitoring systems with alarms for these gases (smell should never be relied on to detect toxic gases), and maintaining equipment to prevent leaks (pipes, tanks, engines).
Judicious use of appropriate respiratory protection is critical. Supplied-air respirators or self-contained breathing apparatus might be needed for high-risk gases (eg, cyanide, hydrogen sulfide, phosphine). Personnel should not work alone if there is any uncertainty about environmental safety, and all activities should adhere to human exposure limits set by relevant regulatory authorities.
Another consideration regarding hazardous gases is that enclosed spaces might also have decreased oxygen concentrations. For example, enclosed spaces that contain biologically respiring materials (such as freshly cut plant material, including grains and timber) might have low-oxygen environments. Oxygen sensors are readily available and are included in most multigas detectors.
Hypoxia Due to Hazardous Nonanesthetic Gases in the Veterinary Workplace
Entry into low-oxygen environments can result in rapid loss of consciousness and death. Typical signs and symptoms of hypoxia include lightheadedness, fatigue, numbness, tingling of extremities, nausea, ataxia, confusion, disorientation, hallucinations, behavioral change, severe headaches, diminished consciousness, papilledema, breathlessness, pallor, tachycardia, and tachypnea, with eventual progression to cyanosis, slow heart rate/cor pulmonale and low blood pressure, and death.
Immediate actions that can be taken in cases of hypoxia due to low-oxygen conditions include prompt evacuation of personnel from the affected area. Rescue should not be attempted without proper respiratory protection (many fatalities occur during rescue attempts), and ideally, trained emergency personnel should be called. Affected individuals should be moved to fresh air immediately.
General principles of medical management for hypoxia include provision of 100% oxygen; support of airway, breathing, and circulation; use of specific antidotes when indicated (eg, hydroxocobalamin, cyanide antidote kits for cyanide exposure); and rapid transport to medical care.
For More Information
Kirkhorn SR, Garry VF. Agricultural lung diseases. Environ Health Perspect. 2000;108 (suppl 4):705-712. doi:10.1289/ehp.00108s4705
Chemical Hazards and Toxic Substances. Occupational Safety and Health Administration (OSHA).
References
Centers for Disease Control and Prevention. Occupational phosphine gas poisoning at veterinary hospitals from dogs that ingested zinc phosphide—Michigan, Iowa, and Washington, 2006–2011. MMWR Morb Mortal Wkly Rep. 2012;61(16):286-288. https://www.cdc.gov/mmwr/preview/mmwrhtml/mm6116a3.htm
Batterman S, Grant-Alfieri A, Seo SH. Low level exposure to hydrogen sulfide: a review of emissions, community exposure, health effects, and exposure guidelines. Crit Rev Toxicol. 2023;53(4):244-295. doi:10.1080/10408444.2023.2229925
Lachowicz JI, Alexander J, Aaseth JO. Cyanide and cyanogenic compounds—toxicity, molecular targets, and therapeutic agents. Biomolecules. 2024;14(11):1420. doi:10.3390/biom14111420
Savioli G, Gri N, Ceresa IF, et al. Carbon monoxide poisoning: from occupational health to emergency medicine. J Clin Med. 2024;13(9):2466. doi:10.3390/jcm13092466
