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Arsenic
there are inorganic and organic forms
can cause acute (GI) or chronic (CNS, kidney) signs
valence affects toxicity
trivalent (As3+) is more toxic, pentavalent (As5+) is less toxic
readily absorbed from GI tract, lungs, and intact skin
accumulates in the liver, then distributes to other tissues
can be excreted in urine, feces, sweat, and milk
Common sources of arsenic
herbicides/rodenticides
antifungal agents on seed grains
wood preservatives
growth enhancers, medications
Which form of arsenic is the most toxic?
trivalent (As3+)
Copper
an essential nutrient that can be toxic with high intakes
species differences related to dose
SHEEP ARE VERY SENSITIVE → readily accumulate it and have trouble excreting it
>15 ppm is toxic to them
chemical interactions and toxicity depend on Cu availability
most consistent acute sign is liver dysfunction ± hemolytic anemia (in sheep)
gunmetal kidneys are a pathologic finding
Cu is readily mobilized during times of stress
all animal groups are at risk to Cu toxicity
Common sources of Cu
poisoning is more likely to occur where multiple sources exist
feed additives
concentrate mixes
forages
trace mineralized salts
foot baths
medicinals
Flourine
sources
soil types, mine drainage
rock phosphates
water sources
1080 rodenticide (NaF)
deposits in teeth and bones, can cause abnormal formation and mineralization by interfering with Ca
clinical signs
mottle teeth
arthritic joints
Lead (Pb)
acute poisoning
GI signs
poorly absorbed by GI
chronic poisoning
not excreted very efficiently
CNS signs
anemia
ruminants may be more sensitive - lead is solubilized in the rumen
Common sources of lead
storage batteries (cattle like to lick them)
leaded solder and lead water pipes
lead shot used in hunting
old lead based paints
industrial pollution
pollution from vehicle exhaust when leaded gasoline was in use
lead can be persistent in the soil
Mercury (Hg)
a cumulative poison → biomagnification in food chain (Hg levels increase the higher you go in the food chain)
elemental mercury → inhaled → respiratory disease, neurologic issues, renal toxicity
inorganic mercury salts → ingested → severe damage to GI tract and kidneys
methylmercury is far more toxic
Sources of mercury
fungicidal seed treatments
environmental sources
medicinals
devices → thermometers
Where is mercury mainly a concern?
All over the U.S.; every state has at least one mercury advisory, with many northern/midwest states having a statewide advisory
Selenium (Se)
narrow margin of safety → especially for ruminants
acute toxicity
syndromes vary
acute respiratory, cardiovascular collapse
chronic toxicity - “alkali disease”
associated with highly alkaline soil
hair loss
abnormal hoof growth
emaciation, roughness of coat
stiffness, lameness
Selenium sources
highly alkaline soils are high in Se
improperly mixed feeds
accumulator plants → Astragulus spp.
parenteral products
How does soil pH affect Se availability?
toxic Se soils
very alkaline pH, low rainfall
nontoxic Se soils
acidic pH 4.5-6.5
non-water soluble forms are bound to Fe, Al
low Se soils
recent volcanic deposits
weathered land
Sodium Chloride
“Salt intoxication”
sodium chloride toxicity is mainly due to water deprivation, not excess salt intake
CNS signs that can result in an eosinophilic meningoencephalitis
pigs are highly susceptible
Nitrate
nitrate is the substance, but the toxic agent is nitrite
nitrate is converted to nitrite by rumen microbes
nitrite crosses the rumen wall and binds to hemoglobin, blocking O2 from binding
results in methemoglobin (blood is dark and brown) and cyanosis (lack of O2 delivery to tissues)
nitrite can cross the placenta and bind fetal hemoglobin, causing abortions
acute onset within 4 hours of consumption
early signs: anxiety, polypnea, dyspnea, rapid and weak pulse
advanced signs: weakness, ataxia, low exercise tolerance
Source of nitrates
primary source is from nitrate in plants
accumulates in roots and lower parts of the stem
nitrate accumulation is higher under drought conditions
nitrates can also be high in water (may be from fertilization runoff)
Urea
source of non-protein nitrogen in ruminant rations
urea is hydrolyzed to ammonia in the rumen
excess ammonia can cross the rumen wall into the bloodstream and overwhelm the liver
ammonium ion is highly toxic to cells
early signs: frothy salivation, blepharospasm, incoordination, weakness
recumbency, bloat, regurgitation of rumen contents
hyperthermia, anuria, and cyanosis just prior to death
Sources of urea and effects
acute toxicity
ration formulation mistakes
ration deficient in energy
chronic toxicity
infertility in cattle - early embryonic mortality
Prevention for inorganic toxins
minimize the potential for exposure
identify potential risks for the specific molecule
dietary formulation - Cu, Se, nitrates, Mo
environmental risks - Pb, As, Nitrates, Hg
water risks - Pb, As, NaCl, MO, F
therapeutics - As, Cu, Se, Hg, F
limited therapy options (i.e. chelation), must focus on prevention of exposure
diagnostic testing
dietary evaluation