Occupational hazard among veterinary workers: exposure to phosphine gas

April 28, 2012, 2:34 pm


Occupational Phosphine Gas Poisoning at Veterinary Hospitals from Dogs that Ingested Zinc Phosphide — Michigan, Iowa, and Washington, 2006—2011. MMWR 2012 April 27;61:286-288.

Full Text

This article reports on the CDC National Institute  for Occupational Health (NIOSH) investigation into cases of phosphine (PH3) poisoning among veterinary workers treating dogs who had swallowed zinc phosphide rodenticide. A poisoning case was defined as “two or more acute adverse health effects consistent with PH3 toxicity in a person exposed to PH3 generated from zinc phosphide”.

When zinc phosphide contacts stomach acid, phosphine gas is produced. Phosphine is a colorless flammable gas. It inhibits oxidative phosphorylation and can by toxic to the lungs, liver, kidney, heart, and nervous system. Although massive exposure can be fatal, victims who do not die recover completely.

There were eight human poisoning cases identified stemming from four separate incidents. All were classified as low severity exposures and all workers recovered. (All the dogs recovered also.) Symptoms included dyspnea, headache, nausea, abdominal pain, lightheadedness, and chest pain.

Many of the more pronounced symptoms occurred when treating veterinarians induced dogs to vomit or initiated gastric lavage in enclosed treatment areas. The authors recommend that “[v]eterinarians who induce vomiting in animals that have ingested zinc phosphide should do so outdoors”. By I wonder:  with physicians and toxicologists no longer recommending induced emesis or (to a great extent) gastric lavage in cases of human ingestions, is there any evidence that such interventions improve outcomes in pets?

Related posts:

Deaths from phosphine gas exposure

Methemoglobinemia and intravascular hemolysis after aluminum phosphide exposure

Review of aluminum phosphide pesticide poisoning

Methemoglobinemia in aluminum phosphide ingestion: an effect of toxin or treatment?

What toxin causes a patient to spontaneously combust?





  1. Rosalind Dalefield Says:

    As a Diplomate of the American Board of Veterinary Toxicology (as well as the American Board of Toxicology), I can say that there is no evidence whatsoever that emesis or gastric lavage improve outcomes in pets. In fact many of the studies showing the futility of these procedures were conducted in dogs! The problem is that the veterinary profession continues to cling to outdated,futile and potentially harmful procedures.

  2. Leon Says:


    Thank you for your comment. I agree, and it didn’t seem plausible to me that interventions thought to have just about zero benefit in humans would suddenly become useful just because the patient has four legs.

  3. Rosalind Dalefield Says:

    Dogs provide a nice example of the futility of inducing emesis in that they vomit very readily, and ingestion of fluoroacetate (Compound 1080) reliably and promptly causes emesis, yet dogs remain extremely susceptible to fatal fluoroacetate poisoning.
    I’m giving a course on this subject in a few weeks but I don’t expect a warm reception.