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Professional Version

Carbon Monoxide as a Veterinary Workplace Hazard


Rhian B. Cope

, BVSc, BSc, PhD, DABT, DABVT, FACTRA, Australian Pesticides and Veterinary Medicines Authority, Australian Government

Reviewed/Revised Mar 2021 | Modified Nov 2022

Carbon monoxide (CO) will most commonly be encountered by veterinarians working in enclosed spaces (eg, intensive animal production facilities) being heated by combustion sources (eg, gas space heating). Accordingly, this exposure most commonly occurs during cold weather and winter. Indeed, epidemics of fatal CO poisoning notoriously occur during extreme winter weather conditions, especially in conjunction with electrical power failures (ie, use of combustion heaters, electrical generators, combustion engines, combustion power tools, wood heaters, etc, in enclosed spaces without adequate ventilation). Like cyanide, CO is also a component of smoke inhalation poisoning. Inhalation is the main route of exposure to CO. CO poisoning is the most common form of fatal air poisoning in many countries.

CO is colorless and tasteless and has no odor, making it especially hazardous in occupational settings, particularly in enclosed spaces with inadequate ventilation. The use of CO monitors and/or testing of breathing air with a Drӓger tube apparatus or similar test method are strongly recommended before entry into any environment where CO might be present. The use of CO monitors in animal production facilities being heated by combustion sources is strongly recommended.

CO binds to hemoglobin, forming carboxyhemoglobin and disrupting blood oxygen transport. The development of impaired hemoglobin oxygen transport can cumulatively progress over time because of the relatively slow reversal of carboxyhemoglobin to normal hemoglobin. Thus, CO poisoning can “creep up unexpectedly and without being noticed” over time.

The signs and symptoms of CO poisoning in people are relatively nonspecific. One of the early and important indicators of exposure to excessive amounts of CO is development of a severe and persistent headache. Other common early clinical signs include dizziness, weakness, nausea, vomiting, chest pain, shortness of breath, irritability, and altered mental status. Loss of consciousness, coma, and death can occur. Other signs and symptoms include tachycardia, tachypnea, hypotension, various neurologic findings (including impaired memory and cognitive and sensory disturbances), metabolic acidosis, arrhythmias, myocardial ischemia or infarction, and noncardiogenic pulmonary edema; any organ system can be involved. Many survivors of severe CO poisoning 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).

Persons with significant CO poisoning have been described as having a “healthy” red complexion and mucous membranes because of the presence of high levels of carboxyhemoglobin. Normal pulse oximeters will not detect the presence of carboxyhemoglobin; pulse CO-oximetry is required. Additionally, blood carboxyhemoglobin levels correlate poorly with the clinical severity of the poisoning.

There is no specific antidote for CO poisoning. Resuscitation combined with oxygen is the only known effective approach to treatment. Rescue and treatment of individuals with CO poisoning is a matter for properly equipped and trained professionals.

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