Requests: If you need specific information on this remedy - e.g. a proving or a case info on toxicology or whatsoever, please post a message in the Request area www.homeovision.org/forum/ so that all users may contribute.
Description and Distribution
Zinc phosphide (Zn3P2) is a heavy, finely ground, crystalline gray-black powder that is practically insoluble in water and alcohol. It was first synthesized in 1740 and was first used as a rodenticide in 1911-12 by the Italians. It was not used in the U.S. as a rodenticide until 1939 when it was used in place of strychnine, which was in short supply because of rodent control in Europe during W.W.II. Zinc phosphide was popular as a rodenticide because the rats tended to die in open areas, which was psychologically rewarding to animal control personnel. The popularity of zinc phosphide decreased during the late 1940's and early 1950's when sodium monofluoroacetate (1080) and the anti-coagulants first appeared. In recent years, as problems associated with 1080 and strychnine have been recognized, interest in zinc phosphide has again increased. Currently, zinc phosphide is recognized as the slowest acting of the commonly used acute rodenticides.
Zinc phosphide is often recommended as the rodenticide of choice because it is fairly specific for rodents and there is no true secondary poisoning, except possibly in dogs and cats. Most animals that feed on rodents are unaffected because the zinc phosphide does not accumulate in the rodent's muscles or other tissues. Experimentally, several predators and scavengers have been exposed on a secondary nature, but only dogs and cats have been affected.
Nationwide, there have been poisonings of all species of domestic livestock, dogs and cats but these are usually accidental exposures and are few in number. All species of animals are subject to zinc phosphide poisoning, but avian species, specifically gallinaceous birds, are the most seriously affected. In Michigan, wild turkeys, ring-necked pheasants, black and gray squirrels, Canada geese, and possibly white-tailed deer have died from zinc phosphide poisoning. There have not been any reported cases of secondary poisoning in the state to date.
Through the years across the U.S., various types of baits have been treated with zinc phosphide. These baits include fruits (apples), vegetables (sweet potatoes), meat (hamburger, damp sausage rusks, canned dog or cat food), seeds, grains (oats, corn, wheat), cereal, and bread (bread mash). Concentrations of zinc phosphide of 0.75% to 2.0% have been used in the past.
In Michigan, technical grade (94% purity) zinc phosphide (2.0% concentration) can be used on cubed apples and hand placed. No other fruit or vegetable is authorized to be used. Zinc phosphide laced grains (corn, wheat, and oats) can be purchased from private companies (all 3 grains) or the U.S. Department of Agriculture (wheat and oats). The grains can be used for broadcast distribution. Another distribution method is through the use of T-feeders. T-feeders are pieces of PVC pipe glued together in the form of an inverted T. The feeders are attached to stakes and placed close to the ground. These feeders are filled with treated grains and are used throughout the pine plantations in the northern portion of the lower peninsula of the state. Zinc phosphide-laced baits have a strong, pungent phosphorus-like (garlic-like) odor that attracts rodents but makes the bait unattractive to other animals. Avian species, specifically wild turkeys, are not bothered by the odor and will feed on the grain.
Clinical Signs and Pathology
Poisoning occurs by the liberation and rapid absorption of phosphine gas (PH3) into the bloodstream when the zinc phosphide comes into contact with the dilute acids in the stomach. This results in damage to the blood vessels and erythrocyte membranes and eventual cardiovascular collapse and irritation of the alimentary tract. Toxicosis usually is evident in 15 minutes to 4 hours following ingestion of a toxic dose.
There are no definitive clinical signs for zinc phosphide toxicity. Clinical signs include anorexia (loss of appetite), nausea, vomiting (often containing blood), abdominal pain, colic, diarrhea, prostration, lethargy, ataxia (loss of muscular coordination), chest tightness, dyspnea (frequent rapid breathing), salivation, excitement, convulsions, paralysis, rigor, and coma. In fatal cases there is liver, kidney, heart, and brain damage. Death is usually due to anoxia (decreased amount of oxygen in organs and tissues).
Gross lesions observed at necropsy are venous congestion, capillary breakdown, pulmonary congestion, interlobular lung edema, liver and kidney congestion, and gastroenteritis. When the stomach (true stomach, crop or gizzard) is opened, an odor of carbide (acetylene) may be apparent. Yellow mottling can be seen in the liver in animals that live long enough for liver damage to occur.
Microscopic examination reveals congestion of the liver and kidney. Renal tubular necrosis can be seen in many instances and cloudy swelling and fatty degeneration can be seen in the liver