32 - Industrial Chemicals Flashcards
1
Q
Petroleum products
A
- Concern for livestock and wildlife
- Oil products are mixtures of chemicals with varying health issues
- Light crude oil is more toxic than heavy crude oils
- Weathered oil is also less toxic
o Many of the volatile components have evaporated.
2
Q
Light crude oil
A
- More toxic than heavy crude oils
- Contains more volatile oil components
- Frequently produce aspiration pneumonia
3
Q
What does sweet crude oil contain more of?
A
- Gasoline, naptha and kerosene
4
Q
What does sour creed oil contain more of?
A
- Lubricating distillates and sulfur
5
Q
What are the components of oil in general?
A
1) short-chain aliphatics – methane, propane
2) long-chain aliphatics – gasoline, kerosene
3) chlorinated alphatics – chloroform, trichloroethylene
4) aromatic hydrocarbons – benzene, toluene, xylene
5) phenols
6
Q
Both crude and refined oils may contain a variety of highly toxic impurities. What are some examples?
A
1) metals
2) catalysts
3) hydrate inhibitors – ethylene glycol
4) corrosion inhibitors – sodium arsenite
5) scrubbers
6) salt
7) HCL
8) Dyes
9) Polycyclic aromatic hydrocarbons
10) Tri-o-cresyl phosphate (TOCP)
7
Q
Toxicokinetics of petroleum products
A
- Most are lipophilic and readily absorbed from all routes including the respiratory system
- Most are metabolized and conjugated with sulfate glucuronides or glycine in the liver
o These agents are generally not considered as persistent chemicals.
8
Q
Petroleum products: Mechanism of action
A
- irritation
- GIT dysfunction through stimulation or microorganism alteration
- bone marrow suppression – anemia, leucopenia
9
Q
Petroleum products: Clinical manifestations MAJOR concerns
A
- *Aspiration pneumonia is the most significant concern associated with oil ingestion.
- Oil is approximately 100 fold more toxic if INHALATION of the oil occurs, particularly the volatile components.
o The normal defense mechanisms including ciliary action and coughing do not function. - GI dysfunction
10
Q
Petroleum products: GIT signs
A
- bloat
- vomiting
- anorexia, weight loss, ketosis
- oil smell in rumen contents
11
Q
Petroleum products: respiratory signs
A
- increased lung sounds
- coughing (possibly persistent)
- dyspnea
- pleuritis
12
Q
Petroleum products: other signs
A
- ataxia, incoordination
- abortion
- elevated body temperature
13
Q
Petroleum products: Clinical pathology
A
- leucopenia followed by a neutrophilia
- anemia
- marrow depression
- elevated BUN and liver enzymes
14
Q
Petroleum products: Pathology
A
- evidence of oil in the rumen
- bloat
- GIT irritation
- Mild degeneration of liver and fatty change
- Nephrosis
- Pulmonary congestion and consolidation
- Occasional pulmonary abscesses
- Fibrinous pleuritis
- Dermal irritation
15
Q
Petroleum products: Other Concerns
A
- milk taint and meat residues
- low vitamin E/A status
- impaired reproduction
- cancer
- endocrine disruption
16
Q
Petroleum products: Treatment
A
- activated charcoal
- mineral oil
- antibiotics for secondary infections
- in wildlife, bathing with detergents to remove oil from hair or feather is helpful to prevent hypothermia
- do not induce vomiting
- if aspiration has occurred the prognosis is poor
17
Q
Coal Tar and Phenol Compounds
A
- derived from coal processing
- frequently used as fungicides, disinfectants or antiseptics
- absorbed well orally and reasonably well absorbed through the skin
- metabolized in the liver to form glucuronide conjugates
- *Cats are unable to form glucuronide metabolites=more susceptible to poisoning
18
Q
Coal Tar and Phenol Compounds: Mechanism of action
A
- liver necrosis and renal tubular necrosis
- Historically, the ingestion of clay pigeons used for trap shooting by swine resulted in idiopathic hemorrhagic hepatitis
19
Q
Coal Tar and Phenol Compounds: Clinical manifestations
A
- High dose=sudden death with few symptoms
- Low to moderate levels
o anorexia
o depression, weakness, tremors
o jaundice
o secondary anemia
o Photosensitization may develop over time.
20
Q
Coal Tar and Phenol Compounds: Pathology
A
1) necrosis or ulceration of the skin
2) kidney – enlarged, pale, tubular necrosis
3) liver – centrilobular degeneration and necrosis
- enlarged, friable, hemorrhagic
4) icterus
21
Q
Coal Tar and Phenol Compounds: Clinical pathology
A
- Urinalysis
o proteinuria, hematuria
o epithelial cells or casts - Liver
o elevated liver enzymes
22
Q
Coal Tar and Phenol Compounds: Diagnosis
A
- Based on pathological and circumstantial information
- Chemical analysis is often difficult
23
Q
Coal Tar and Phenol Compounds: Treatment
A
- activated charcoal
- gastric lavage
- wash the skin with detergents
- vitamin E supplementation – reduces oxidative damage
24
Q
Coal Tar and Phenol Compounds: Differential Diagnosis
A
- Agents associated with liver or kidney disease
25
Polyhalogenated Biphenyls
- polybrominated biphenyls (PBB) and the polychlorinated biphenyls (PCB) produce similar toxic effects
- *PBBs are more toxic
- used as flame retardants, electrical insulators, chemical sealants, oxidation inhibitors, etc.
- *very stable resulting in significant environmental and residue concerns.
- Banned in 1979
- The greater percentage of halogen content, the more resistant the agent is to degradation.
26
Polyhalogenated Biphenyls: Why have these agents been banned?
1) embryotoxic
2) teratogenic
3) carcinogenic
4) immunosuppressive
5) residues
6) potent enzyme inducers – mixed function oxidases
27
Polyhalogenated Biphenyls: impurities
- dioxins are often associated with these chemicals
- Herbicides, in the past, contained dioxins
o TCDD – tetra-chloro-dibenzo-dioxin
o TCDD produces chloracne in addition to many of the toxic effects of PCBs or PBBs except at much lower levels.
28
Polyhalogenated Biphenyls: Mechanism of action
- Enzyme induction
- Degenerative and membrane changes in a variety of tissues
- Clinical syndromes may be non-specific.
29
Polyhalogenated Biphenyls: Clinical manifestations (Michigan incident)
1) insidious, vague onset
2) anorexia
3) weight loss, reduced milk production
4) udder atrophy
5) abnormal hoof development
6) increased urination and lacrimation*
7) hematomas thrombocytopenia
8) abscesses
9) reproduction - metritis, abortion
- abnormal estrous
- prolonged gestation
10) alopecia
11) chloracne (follicular pyodermatitis)* (Vit A responsive)
12) anemia
30
Polyhalogenated Biphenyls: Pathology
- emaciation
- thymic atrophy
- hepatic fatty change
- renal tubular degeneration
- other non specific degenerative changes
- ascites, possibly mild pulmonary edema
31
Polyhalogenated Biphenyls: Treatment
- Residue and reproductive effects and associated long half life
o Slaughter and disposal are recommended
- Vitamin supplementation is useful.
32
Fluoride
- Acute poisoning=rare event
- Chronic fluorosis is often seen in cattle
o fluoride is often a byproduct of the aluminum industry
o Forages contaminated by airborne sources, feed supplements and water contamination are the primary sources of exposure
o Usually the fluorine is ingested.
33
Fluoride: Factors influences Toxicity
1) amount ingested
2) duration of exposure
3) solubility - sodium fluoride highly toxic
4) age – young and fetus more susceptible
5) nutritional status – high calcium protective
6) stress
34
Fluoride: Toxicokinetics
- well absorbed
- *cumulative poison that has a predisposition for calcified tissues (bone, teeth)
- Requires many months to deplete F from bone
- Fetus will accumulate F
35
Fluoride: Mechanism of action broad
- delays and alters normal mineralization of bones and teeth
36
Fluoride: Mechanism of action, teeth during development
- The ameloblasts (enamel) and the odentoblasts (dentine) are damaged
- Matrix, which is laid down by these cells will NOT mineralize=teeth wear very rapidly and are discolored
37
Fluoride: Mechanism of action, bone
- fluoride alters osteoblastic activity resulting poor matrix formation and defective mineralization
o Exostoses and osteoporosis may be observed
o bones appear chalky white with thickened periosteum, uneven mineralization with excessive osteoid and areas of immature bone
38
Fluoride: Clinical manifestations, acute poisoning
- Symptoms may appear within 30 minutes
- irritation, colic, salivation
- vomiting
- hemorrhagic gastroenteritis
- stiffness, muscle weakness
- convulsions
- cardiac failure
- weight loss
39
Fluoride: Clinical manifestations, chronic poisoning
- onset may be months depending upon the dose
- lameness
- stiffness
- unthrifty
- mottled, brown and uneven tooth enamel
- exostoses
- lapping of water (dental pain)
40
Fluoride: Diagnosis
- based on a history of lameness and dental problems
- Typically, a herd problem manifested by unthrifty animals
41
Fluoride: treatment
- Once the lesions have developed, treatment is ineffective
- Administration of aluminum salts at about ten times the level of fluoride may PREVENT the problem
42
Fluoride: DDx, acute poisoning
The syndrome is characterized by severe GIT signs and terminal clonic convulsions.
1) arsenic (inorganic)
2) mercury (inorganic)
3) selenium
4) cadmium
5) vitamin D (monogastrics)
6) chlorinated hydrocarbon insecticides
7) lead
8) herbicides
43
Fluoride: DDx, chronic poisoning
The syndrome is characterized by unthrifty lame animals.
1) Molybdenum
2) Chronic selenium
3) Chronic cadmium
4) Chronic arsenic
5) Ergot
6) PCBs
44
What are some non-toxicological syndromes that may be confused with fluorosis?
- other lameness problems
- arthritis
- vitamin D deficiency
- parathyroid disease and Ca/P imbalances
