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Heavy metals (Bergfelt)--lead Flashcards

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1
Q

What is a toxic heavy metal?

A

Dense metal or metalloid that is noted for its potential toxicity, especially in environmental contexts

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2
Q

What are 4 elements on the World Health Organization’s list of 10 chemicals of major public concern?

A

Cadmium (Cd)

Mercury (Hg)

Lead (Pb)

Arsenic (As)

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3
Q

What characteristics must a metal have to be considered a ‘heavy metal?’

A

Metal having an atomic weight greater than sodium (23) and specific gravity (density) > 5 g/cm3

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4
Q

On the health effects basis, which heavy metals are essential?

A

Cu, Zn, Co, Cr, Mn, Fe

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5
Q

On the health effects basis, which heavy metals are non-essential?

A

Ba, Li, Zr

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6
Q

On the health effects basis, which heavy metals are highly toxic and which are less toxic?

A

Highly toxic = Pb, Hg, Cd

Less toxic = Sn, Al

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7
Q

What are the 7 toxicological properties of heavy metals?

A
  • Persistence–long residual and half-life
  • Soil residence time–> 1000 years
  • Acute toxicity–plants, animals, microorganisms
  • Bioaccumulation and biomagnification–through food chain
  • Chronic and sub-lethal effects at low conc.
  • Synergistic effects
  • Teratogenic and carcinogenic properties
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8
Q

Is lead readily degraded in the environment?

A

No

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9
Q

T/F: Lead is easily absorbed and metabolized

A

FALSE

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10
Q

What occurs with oral exposure to lead?

A

Forms insoluble compounds in GIT–small amount absorbed (acidic environment)

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11
Q

How does the type of lead affect absorption?

A

Organic lead is more readily absorbed than metallic lead

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12
Q

What conditions favor dissolution and absorption?

A

Acid conditions

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13
Q

What was the Flint water crisis (in a nutshell)?

A
  • Allowable lead levels in water = 15ppb
  • What comes out of faucets = 2ppb
  • What came out of Flint’s faucets = 13,200ppb
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14
Q

What is an anthropogenic source of lead toxicity?

A

Aerial emission from combustion of leaded fuel, batteries waste, insecticides and herbicides

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15
Q

What is the most common source of lead toxicosis in animals?

A

Lead-based paints

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16
Q

T/F: A thumbnail sized chip of lead-based paint may contain 50-200 mg of lead

A

TRUE–the lowest lethal dose in dogs is 191 mg/kg!

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17
Q

Sources of exposure to lead toxicity?

A
  • Paint (old painted surfaces, fences)
  • Old batteries
  • Plumbing, solder, putty
  • Galvanized wire
  • Some linoleum, imported ceramics/pottery
  • Contamination from industry (lead oxide)
  • Lead shots, weights, fishing sinkers
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18
Q

T/F: An estimated 10-20 million birds and other animals die from lead poisoning each year in the US

A

TRUE

:(

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19
Q

Which birds are most vulnerable to lead toxicosis?

A

Waterfowl–can ingest spent pellets or lost fishing tackle

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20
Q

What can become a source of secondary lead poisoning for wild animals?

A

Birds shot with lead pellets and not retrieved

(bioaccumulation/biomagnification)

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21
Q

How common is lead toxicosis?

A

It is one of the most common toxicoses! Acute to chronic, Pb displaces Ca and Zn!

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22
Q

Why are young animals more sensitive to lead toxicosis than adults?

A

Greater GIT absorption and immature BBB

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23
Q

Which species are most susceptible?

A

Cattle, horses, pets, waterfowl, and pet/wild birds

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24
Q

T/F: Dogs are more frequently poisoned because of their indiscriminate eating habits

A

TRUE

(freakn labs)

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25
Which species are more resistant to lead toxicosis?
Goats, swine, and chickens | (avian plumbism or avian saturnism)
26
What is the most common route of lead poisoning?
**Ingestion**
27
How can lead be absorbed?
Dermal (poor), inhalation (rare), ingestion (oral absorption is poor, but is **increased by GI acidity**)
28
What decreases led absorption?
Calcium, zinc, or protein
29
What is the mechanism of lead absorption?
Absorbed by active transport using the same carrier protein as calcium --\> If patient is deficient in Ca, vitamin D, Zn, or Fe, then Pb is more readily absorbed
30
Which species is GIT absorption of lead greater in?
GIT absorption is greater in non-ruminants (~10%) than in ruminants (~3%)
31
What *age* is GIT absorption greater in?
Greater in immature animals (up to \>50%) compared to adults (5-15%)
32
Where/how is lead distributed?
Throughout the body by systemic circulation--binds to erythrocyte membranes for transport (60-90%, depending on species)
33
What is the main route of absorption?
GIT
34
T/F: Lead crosses the BBB, placenta, and binds to proteins in soft tissues for 8-10 weeks
FALSE--it binds to proteins in soft tissues for **4-6 weeks** Everything else is true
35
What is metallothionein?
Liver protein involved in cellular detoxification of inorganics--sequesters metal ions present in elevated concentrations
36
Where does lead accumulate?
Active bone matrix--a reserve for several **years** ~83-95% in mature animals ~70-75% in immature animals Activated by pregnancy, lactation, chelating agents
37
How is lead excreted?
Primarily through urine, but also in milk and bile
38
What does lead interfere with? What can it substitute for?
Interferes with biological structure and function Can substitute for Ca2+, Mg2+, Fe2+
39
What does lead form complexes with?
* Forms complexes with nucleophilic functional groups (COOH, NH2, SH) * Most stable complex with sulfhydryl groups (-SH) * Increases stability (S-S to S-P to S-P-S) * Pb may displace Zn in some enzymes
40
What does lead compete with?
Ca2+ in bone and alters Ca2+ movement across membranes (e.g., BBB)
41
T/F: Alterations in cerebral endothelium due to lead competing with Fe2+ may lead to edema
FALSE--it's due to lead competing with **Ca2+**
42
What are the target tissues of toxicity?
**GIT, blood, and CNS**
43
What might lead interfere with in the CNS?
GABA neurotransmission
44
What does chronic exposure inhibit?
Heme synthesis that leads to anemia
45
What else might lead to anemia?
Delayed erythrocyte maturation and fragility--short lifespan
46
T/F: Lead can alter the release of neurotransmitters (dopamine, acetylcholine, GABA)
TRUE
47
How can lead cause brain edema?
Breakdown of the BBB through toxic effect on the endothelial cells and alteration of microvascular systems
48
How long can clinical signs take to appear?
A few hours, days, weeks, to months, depending on amount, duration, species, and other factors
49
What are the main systems effected by lead poisoning?
GIT, hematologic, CNS
50
What GIT signs are seen in lead toxicosis?
* Anorexia, maybe salivation, vomiting, 'lead colic,' diarrhea, constipation, or rumen atony * Rarely megaesophagus has been reported in small animals
51
What hematologic signs are seen in lead toxicosis?
* Clinical signs related to anemia * Basophilic stippling of erythrocytes * Blood analysis * Antemortem: whole blood conc. in mammals \<0.1 ppm for background and **\>0.35 for lead toxicosis** * Postmortem: **kidney and liver \>10ppm** for lead toxicosis
52
What CNS signs are seen in lead toxicosis?
* Anxiety, hyperexcitability, vocalization, head pressing, circling, running, maniacal behavior, seizures, tremors, blindness (more acute) * Pharyngeal paralysis and 'roaring' and seizure-like activity in the horse w/ more acute toxicity * CNS depression may be seen in horses and sheep and in chronic toxicosis
53
What CNS signs are seen in avians with lead toxicosis?
* Raptors and waterfowl show peripheral neuropathy and chronic wasting * Psittacines show neuro and GIT abnormalities
54
What are the gross lesions associated w/ Pb toxicosis?
Non-specific; lead objects may be found in GIT
55
What microscopic lesions are seen in Pb toxicosis?
* May see cerebral cortical necrosis and poliomalacia in cattle * Acid-fast eosinophilic intranuclear inclusion bodies in renal tubular epithelium or hepatocytes
56
What hematology changes are seen?
* Increased nucleated RBCs: high demand for bone marrow to produce RBCs--\> immature nRBCs released into circulation * Non-regenerative anemia w/ inappropriate release of nRBCs * 5-140 nRBCs/100WBCs * Basophilic stippling of erythrocytes in dogs, rabbits--differentiate from regenerative anemias * Fluorescence of plasma or urine porphyrins
57
What is seen on radiographs following lead toxicosis?
* Objects in the GIT * Metaphyseal sclerosis in young animals w/ chronic toxicosis * Rarely megaesophagus
58
Urinalysis?
* Inc. delta aminolevulinic acid dehydrase levels (porphyroobilinogen synthase--involved in heme synthesis) * Inc. urinary lead (4x or more) following EDTA administration--can result in kidney damage
59
What is the specimen of choice for an antemortem chemical analysis?
Whole blood \>90% of circulating lead is bound to erythrocytes
60
What are the blood Pb levels?
* Blood Pb \>0.4 ppm along w/ clinical signs is considered diagnostic * Blood Pb \>0.6 ppm is considered diagnostic * **Blood levels may not correlate w/ clinical signs**
61
T/F: Liver, kidney, and GI contents can be tested as well for chemical analysis
TRUE
62
DDx?
* Other toxicants that cause neuro signs * Other causes of anemia--assoc. w/ nRBCs * Lupinosis (acute liver atrophy) may be a differential
63
Treatment: what should be done to stabilize the patient?
Fluid/electrolyte therapy (and ensure point of exposure is removed)
64
Treatment: how can you eliminate Pb if present?
* Wash it if in haircoat * Remove any lead from the gut **before** chelation * **Chelation may enhance absorption further** * Cathartics--magnesium sulfate may bind with Pb to form Pb-sulfate (harder to absorb and accelerates defecation)
65
T/F: Activated charcoal is recommended to remove lead
FALSE--**it is NOT recommended--**does not bind well to heavy metals!
66
Treatment: what is chelation therapy?
Use of chelating agents to detoxify an exposure to heavy metals (e.g., Pb, Hg, As) by **converting them to a chemically inert form that can be excreted** w/o further interaction w/ the body
67
Treatment: should you be cautious w/ chelating agents?
YES--chelating agents can also be dangerous Use of disodium-EDTA instead of Ca-disodium-EDTA has resulted in fatalities due to hypocalcemia and kidney damage
68
What is the most common chelating agent used?
Calcium-disodium-EDTA
69
How is Ca-disodium-EDTA administered?
IV--diluted and given in multiple doses (painful when used IM or SC in large animals)
70
What is the primary concern with Ca-disodium-EDTA?
Renal injury Treat max 5 days--if longer treatment is needed, 'rest' for 5 days, then resume
71
Does Ca-disodium-EDTA bind to other minerals?
YES--Zn, Cu, Fe, and Ca; concurrent Zn supplementation is recommended
72
What is 'rebound?'
Pulling the lead out of the bone --\> increases blood levels Must be distinguished from re-exposure
73
What is DMSA?
* Dimercaptosuccinic acid (Succimer) * Structurally analogous to BAL (Dimercaprol)
74
How is DMSA administered? What is it used for?
* Orally administered, can be used alone or after treatment with EDTA or BAL * Used in children to treat lead toxicity
75
Dimercaprol (BAL)
* Can be used alone or w/ CaEDTA * May improve effect--crosses BBB and enhances excretion * Avoid if liver or renal disease * Given by IM injection--**painful**
76
D-penicillamine
* Given orally (can bind oral minerals) * Used following EDTA for **chronic toxicosis** * May be less effective * Potentially nephrotoxic, vomiting common
77
What can be used to treat neuro signs?
Mannitol, diazepam or barbiturates, glucocorticoids (?)
78
Adjunct therapies?
Taurine (inc. depleted glutathione), thiamine, Zn supplementation (if treating w/ EDTA)
79
Prognosis?
Guarded--better if caught early ## Footnote **Animals may act as sentinels for human exposure--house pets**

Toxicology (22 decks)

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