Zinc Phosphide

Zinc phosphide is an inorganic compound with the molecular formula Zn3P2 that combines phosphorus with zinc. [fusion_builder_container hundred_percent=”yes” overflow=”visible”][fusion_builder_row][fusion_builder_column type=”1_1″ background_position=”left top” background_color=”” border_size=”” border_color=”” border_style=”solid” spacing=”yes” background_image=”” background_repeat=”no-repeat” padding=”” margin_top=”0px” margin_bottom=”0px” class=”” id=”” animation_type=”” animation_speed=”0.3″ animation_direction=”left” hide_on_mobile=”no” center_content=”no” min_height=”none”][1] The IUPAC chemical name is trizinc diphosphide, and the CAS registry number is 1314-84-7. Zinc phosphide is a grey-black powder with an odour similar to garlic. It is practically insoluble in water and insoluble in alcohol. [2]

 

Uses [3]

 

Zinc phosphide is used for rodent control on crops including grapes, sugarcane, artichoke, sugar beet, alfalfa, barley, berries, oats, sugar maple, wheat, corn, and hay. It is also used on grasses such as home lawns, rangeland, and golf courses. Zinc phosphide targets household rodent pests, such as mice and rats, in addition to field rodents including voles, ground squirrels, pocket gophers, prairie dogs, and jack rabbits.

 

Ecological & Environmental Effects [2,3,4]

 

Zinc phosphide converts to phosphine gas in the presence of moisture and acid in the stomach. The toxicity of zinc phosphide is due to phosphine gas exposure. Thus, zinc phosphide must be ingested to become toxic. After phosphine is absorbed in the gastrointestinal tract, it inhibits cytochrome C oxidase, which is vital to mitochondrial respiration. It is suspected that there are other modes of action in its toxicity.

 

Zinc phosphide is highly toxic to wild birds and also to freshwater fish. Zinc phosphide is also toxic to non-target mammals when ingested directly. Secondary toxicity to mammalian predators (animals eating other animals that had been exposed to the compound) from zinc phosphide is rather low, primarily because the compound does not significantly accumulate in the muscles of target species. Some of the toxic effects to predators have been due to the ingestion of zinc phosphide that was in the digestive tract of the target organism.

 

Zinc phosphide may be applied as an active ingredient in either bait or a dust. Under average conditions, toxic activity persists for approximately 2 weeks. Soil acidity and moisture tend to accelerate the breakdown of the compound. Phosphine gas may be liberated as a result of this process.

 

Sources & Routes of Exposure

 

Sources of Exposure [1]

 

Exposure can occur via contact to a pesticide containing zinc phosphide including contact with skin, breathe it in, or if you accidentally eat or drink a product containing it. This can happen if you get some on your hands and eat or smoke without washing your hands first. Young children and pets are most likely to be exposed to zinc phosphide by eating the bait pellets if they find them. Baits often have peanut butter, molasses, or other flavours that may attract dogs or children. You may also be exposed if you apply bait with your bare hands, or breathe in any dust or crumbled, powdery bait.

 

Routes of Exposure [5]

 

The main routes of exposure to zinc phosphide are:

  • Inhalation
  • Skin contact
  • Eye contact
  • Ingestion

 

Health Effects [2]

 

Acute Toxicity

 

Humans

 

  • Zinc phosphide dust may release phosphine once it contacts the moist tissues of the respiratory tract if the dust is inhaled, resulting in pulmonary oedema and cardiotoxicity.
  • If ingested, zinc phosphide releases phosphine in the gut and may cause headache, dizziness, fatigue, nausea and vomiting, cough, dyspnea, chest tightness, and thirst. Other signs include liver failure, jaundice, loss of ability to urinate, tetany, delirium, convulsions, coma, and death.
  • Death in humans from fatal doses may be delayed for 30 hours after exposure, with the majority of tissue damage occurring in the liver, kidneys and heart.
  • Victims of lethal phosphine exposure were found to have liver, myocardial, and alveolar cell necrosis, pulmonary oedema and microscopic pulmonary congestion, and anoxic damage in the brain.
  • Hyperglycaemia following exposure to phosphine has also been reported. Elevated levels of the enzyme creatine phosphokinase were found in two instances of severe poisoning by phosphine.28,29
  • Phosphine have been shown to interfere with acetylcholinesterase in humans, but the impact of this inhibition on the toxicity is not clear.

 

Animals

 

  • Animals that ingest zinc phosphide may begin showing clinical signs within 1 to 4 hours. Early signs of exposure include loss of appetite and depressed activity followed by vomiting and painful retching. These signs progress to anxiousness, ataxia or uncoordinated movements, weakness, laboured breathing, thrashing, muscle tremors and convulsions.
  • Onset of signs may be delayed for up to 12 hours or more in animals who consumed the bait without any other food in their stomachs. Gastric acid release in animals that have recently eaten causes more rapid release of phosphine.
  • The vomit of poisoned animals may contain blood. The vomit can also include phosphine, which can be dangerous to humans at levels below which its odour can be detected.

 

Chronic Toxicity

 

Humans

 

  • Chronic, low-level inhalation or oral exposures to zinc phosphide in people have been associated with weakness, anaemia, toothache, necrosis of the jaw bones and associated swelling, weight loss, and spontaneous fractures.
  • Blood samples taken from fumigant applicators and control subjects were examined for chromosomal abnormalities. Researchers collected samples during the application season, and 6 weeks to 3 months after application. Fumigant applicators who had been exposed to phosphine had more chromosome abnormalities than control subjects during the application season. Chromosomal rearrangements were more common in phosphine applicators than in controls 3 months after exposure.
  • More recent investigations repeated the earlier work above, but found no such differences. One group of researchers hypothesised that improved personal protective equipment practices were responsible for the change. Other researchers reported that chromosomal breaks were more prevalent in men who used fumigants relative to controls, but these applicators also used insecticides and herbicides.

 

Carcinogenicity

 

Humans

 

  • The U.S. EPA determined that chronic exposure to zinc phosphide should be negligible and therefore waived carcinogenicity testing requirements for reregistration.
  • No human data were found on carcinogenic effects of zinc phosphide or phosphine.

 

Endocrine Disruption

 

  • No data were found on the ability of zinc phosphide or phosphine to disrupt the endocrine system.

 

Reproductive or Teratogenic Effects

 

  • No human data were found on the teratogenic or reproductive effects of zinc phosphide or phosphine exposure.

 

Safety [5,6]

 

First Aid Measures

 

For Inhalation:

  • Move victim to fresh air. Emergency personnel should avoid self-exposure to zinc phosphide.
  • Evaluate vital signs including pulse and respiratory rate and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. If breathing is laboured, administer 100% humidified oxygen or other respiratory support.
  • Rush to a health care facility.
  • Obtain authorisation and/or further instructions from the local hospital for performance of other invasive procedures.

 

For Skin and Eyes

  • Remove victims from exposure. Emergency personnel should avoid self-exposure to zinc phosphide.
  • Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. If breathing is laboured, administer 100% humidified oxygen or other respiratory support.
  • Remove contaminated clothing as soon as possible.
  • If eye exposure has occurred, eyes must be flushed with lukewarm water for at least 15 minutes.
  • Wash exposed skin areas thoroughly with soap and water.
  • Rush to a health care facility.
  • Obtain authorisation and/or further instructions from the local hospital for performance of other invasive procedures.

 

For Ingestion

  • Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. If breathing is laboured, administer 100% humidified oxygen or respiratory support.
  • Rush to a health care facility.
  • Obtain authorisation and/or further instructions from the local hospital for performance of other invasive procedures.
  • DO NOT INDUCE VOMITING or attempt to neutralise.

 

Fire & Explosion Information

 

  • The product is not readily flammable. If there is a build-up of phosphine gas it may ignite when in contact with atmospheric oxygen if the concentration exceeds 1.79%. While kept dry the product is stable for long periods and the fire/explosion risk is minimal.
  • Suitable extinguishing media: Use carbon dioxide or extinguishing powder. Do not use water. Move containers from the area if possible and if safe to do so. Fight fire in early stage only if safe to do so.
  • Hazards from combustion: Oxides of phosphorous and oxides of zinc and hydrogen phosphide (phosphine) may be formed in a fire situation.

 

Exposure Controls & Personal Protection

 

Engineering Controls

 

  • Use only in a well ventilated area.
  • After handling zinc phosphide and before eating, drinking or smoking, wash hands, arms and face thoroughly with soap and water.

 

Personal Protective Equipment

 

The following personal protective equipment is recommended when handling zinc phosphide:

  • PVC gloves.
  • Full face-piece respirator with combined dust and gas cartridge or supplied air respirator. For help in selecting a suitable mask consult AS/NZS 1715.
  • After each day’s use, wash gloves and respirator and if rubber, wash with detergent and warm water.

 

Regulations [6,7]

 

United States

 

No occupational exposure limits have been established for zinc phosphide. However, as zinc phosphide can be converted to phosphine gas the following exposure limits apply to phosphine:

 

OSHA Permissible Exposure Limit (PEL):

 

  • General Industry: 29 CFR 1910.1000 Table Z-1 — 0.3 ppm, 0.4 mg/m3 TWA
  • Construction Industry: 29 CFR 1926.55 Appendix A — 0.3 ppm, 0.4 mg/m3 TWA
  • Maritime: 29 CFR 1915.1000 Table Z-Shipyards — 0.3 ppm, 0.4 mg/m3 TWA

 

American Conference of Governmental Industrial Hygienists (ACGIH) Threshold Limit Value (TLV): 0.3 ppm, 0.42 mg/m3 TWA; 1 ppm, 1.4 mg/m3 STEL

 

National Institute for Occupational Safety and Health (NIOSH) Recommended Exposure Limit (REL): 0.3 ppm, 0.4 mg/m3 TWA; 1 ppm, 1 mg/m3 STEL

 

Australia

 

There is no exposure standard allocated for zinc phosphide bait or zinc phosphide powder. However, the product may evolve phosphine gas, which presents a serious toxic risk. The time-weighted average (TWA) for phosphine gas is 0.42 mg/cubic metre (0.3ppm). The TWA is the average airborne concentration of the material which must not be exceeded when calculated over a normal 8-hour day and a 5 day working week. The short term exposure limit (STEL) for phosphine gas is 1.4mg/ cubic metre (1.0ppm). The STEL is a value, which should not be exceeded for more than 15 minutes and which should not be equalled on more than four occasions per day. There should be a period of at least 60 minutes between successive exposures at the STEL.

 

References

 

  1. http://npic.orst.edu/factsheets/znpgen.html
  2. http://npic.orst.edu/factsheets/znptech.html
  3. http://www.toxipedia.org/display/toxipedia/Zinc+Phosphide
  4. http://extoxnet.orst.edu/pips/zincphos.htm
  5. http://www.pesticideinfo.org/Detail_Chemical.jsp?Rec_Id=PC34737
  6. http://www.animalcontrol.com.au/pdf/MOUSEOFF_ZP_2013.pdf
  7. http://nj.gov/health/eoh/rtkweb/documents/fs/2041.pdf

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