14. air & water toxicants

source of ammonia gas (NH₃)

formed by decomposition of animal waste

• metabolism of uric acid by bacteria

mechanism of ammonia toxicity

• irritant gas

• corrosive — cellular damage

  • irritates respiratory tract, mucous membranes

• corneal injury & skin burns

where should ammonia levels be measured?

ground level (high concentration)

what is the major route of elimination for ammonia gas?

exhalation (~70-80%)

ammonia toxicity treatment

• remove from source

  • decontaminate if cleaning product was spilled on animal

• change management

  • ventilation

  • removal of old bedding

• supportive care

  • respiratory support

  • antibiotics if secondary infection

source of hydrogen sulfide

manure pit danger — released during decomposition, agitation, and pumping

mechanism of hydrogen sulfide toxicity

inactivates mitochondrial cytochrome C oxidase

• failure of oxidative metabolism — no ATP produced

• hypoxia

• metabolic acidosis

clinical signs of hydrogen sulfide toxicity

• irritant gas

• low concentrations

  • respiratory tract irritation

  • skin & eye irritation

  • CNS stimulation, nausea, headache, impaired gait, dizziness, tremors

  • arrhythmias

• high concentrations

  • sudden collapse, respiratory failure, death

why can odor alone not be used to detect hydrogen sulfide?

olfactory paralysis occurs at concentrations of 150-250 ppm (can no longer smell at higher concentrations)

what tests are used to diagnose hydrogen sulfide toxicity?

measure in blood and urine

• urinary thiosulfate = most common biomarker

how is hydrogen sulfide metabolized?

• rhodanese (enzyme) converts to thiocyanate

• detoxified to thiosulfate → excreted in urine

• can bind to RBCs → sulfhemoglobin

hydrogen sulfide toxicity treatment

• remove from source

• ventilation

• supportive care

  • nitrate therapy to induce methemoglobin

    • prevent sulfhemoglobin formation (irreversible)

    • can naturally be reversed to Hb

• prevention

source of nitrogen dioxide (silo gas)

formed in silos / pits / bags filled with fresh organic material

mechanism of nitrogen dioxide toxicity

• low water solubility — penetrates deeply into lung

  • reacts with lung surface fluids; hydrolyzes to nitrous and nitric acid → damage epithelium

  • free radicals — lipid peroxidation & oxidative stress

  • pneumonitis and pulmonary edema

nitrogen dioxide toxicokinetics

metabolized to nitrite and nitrate and excreted in urine

exposure to what 2 gases should be assumed in cases of smoke inhalation?

• carbon monoxide — incomplete combustion of organic material

• cyanide gas — burning of nitrogen containing material (nylon, wool, silk, polyurethane, plastics)

mechanism of carbon monoxide toxicity

binds hemoglobin to form carboxyhemoglobin

• cannot carry oxygen

• hypoxia

• “red gums/complexion”

“silent killer”

mechanism of cyanide gas toxicity (smoke inhalation)

inhibits mitochondrial cytochrome C oxidase — arrest of aerobic metabolism

how is cyanide metabolized?

metabolized to thiocyanate in liver by rhodanase → excreted in urine

cyanide antidotes

• hydroxocobalamin (vitamin B12a) — directly binds cyanine + helps eliminate

• sodium thiosulfate — helps conversion to thiocyanate

other sources of carbon monoxide

• occur outside of fires

  • home/garage

  • barn

• exhaust fumes / gas space heaters

• transport

  • exhaust fumes when chicks are being transported or from improper ventilation in hatchers

other sources of cyanide

• plants

• M44 cyanide device: “cyanide bombs” to kill predators

mechanism of cyanide toxicity

sodium cyanide → hydrogen cyanide gas → CNS depression; cardiac arrest; respiratory failure

how is cyanide toxicity treated?

sodium nitrite → create methemoglobin → prevent cyanomethemoglobin ?

• use for ONLY cyanide exposure, not smoke inhalation — O₂ carrying already decreased due to carbon monoxide

sources of polytetrafluoroethylene (PTFE) gas + species affected

• “teflon toxicity”

• produced when products with PTFE-based coated surfaces in household products are heated to 280°C (536°F) or higher

• species affected: humans & birds

mechanism of polytetrafluoroethylene (PTFE) gas toxicity

• PTFE pyrolysis products

  • direct injury to lung pneumocytes & endothelial cells

  • direct irritant to eye (high concentrations)

• cause massive pulmonary edema & hemorrhage

mechanism of crude oil toxicity

• irritant

• destroys insulating fur or feathers

• reduces mobility

• cell membrane damage

• reproductive toxicity

important clinical signs of crude oil toxicity

• hypothermia

• low blood glucose

crude oil toxicity treatment

• remove oil

• activated charcoal

• supportive care (antibiotics, fluids, electrolytes, monitor body temperature)

• emetics contraindicated due to aspiration risk

mechanism of fluoride toxicity

• acute — corrosive damage to tissues

• chronic (more common; esp. in dairy cattle)

  • interferes with metabolism of essential metals

  • Ca²⁺ metabolism — complex formation

  • free radical generation

• delayed/impaired mineralization of bones & teeth

  • esp. in young animals

fluoride toxicity treatment

• calcium gluconate or magnesium hydroxide

• milk — limit absorption

• supplementation with calcium carbonate, aluminum salts, magnesium metasilicate, or boron will reduce absorption or enhance excretion

• prevention is key

  • livestock consume supplements and mineral mixes with <1% fluoride