toxicology environmental or occupational exposure Flashcards
Toxicology of Specific Agents
- Carbon Monoxide
- Caustic Agents
- Cyanide
- Metals and Metalloids
Carbon Monoxide
•Produced by incomplete combustion of carbon-containing substances
•Primary environmental sources:
- Gasoline engines, improperly vented furnaces, wood or plastic fires
- Colorless, odorless, tasteless gas that is rapidly absorbed into blood from inspired air
- Highly toxic due to its affinity for binding to hemoglobin( 200x > O2)
- Called carboxyhemoglobin (COHb)
- Decreases the amount of oxygen to tissue, producing hypoxia
- Testing:
- Differential spectrophotometry
- Gas chromatography - reference method
- everyone has a very small amount
COHb%
typical in non- smokers 0.5%
smokers 5-10%
immediately fatal 80%
Caustic Agents
- Strong acid or alkaline substances found in household products and occupational settings
- If aspirated - pulmonary edema (excess fluid in lungs), shock with progression to death
- If ingested - lesions in esophagus and GI tract
* Results in hematemesis (vomiting blood), abdominal pain and shock
* Rapid onset of metabolic acidosis or alkalosis
•Treatment - usually dilution
Cyanide
- Supertoxic substance
- Can exist as a gas, solid, or in solution
- Exposure routes: inhalation, ingestion, transdermal absorption ( BINDS with HEME IRON)
- Found in industrial processes, insecticides/rodenticides, burning of plastics
•Low level exposure:
- Headaches, dizziness, respiratory depression
•High level exposure:
- Seizure, coma, death
- Analysis:
- Ion-selective electrodes
- Photometric analysis
Elemental Toxicities
- If found early, it is easily treatable with good outcomes.
- If not identified and reduced early, there can be irreparable damage to nervous, renal, and cardiovascular systems.
- For a diagnosis, all of the following factors must be demonstrated:
- A source of elemental exposure must be evident
- Must demonstrate signs and symptoms typical of the element
- Abnormal element concentration in the appropriate tissue must be evident
Analysis should be considered with:
- Renal disease of unexplained origin
- Bilateral peripheral neuropathy
- Acute changes of mental function
- Acute inflammation of nasal or laryngeal epithelium - History of exposure
Elemental Toxicity - Arsenic (As)
- Exist in both naturally occurring and manmade substances.
- Sources of exposure:
- Present in many foods (shellfish, cod, haddock)
- Exposures in workplace
Clinical Presentation
•Acute toxicity associated with:
- GI distress (vomiting, diarrhea)
- Cardiac arrhythmias
•Transverse white lines in fingernails (Mees’ lines)
Chronic toxicity: •Renal failure •Cardiac arrhythmias •Liver dysfunction •Peripheral neuropathy
Analysis:
•Urine is sample of choice
- Predominately excreted by kidney
•Hair - used to document time of arsenic exposure
- Deposition in hair and fingernails can be seen two weeks after an exposure.
- Inductively coupled plasma mass spectrometry (ICP-MS)
- High-performance liquid chromatography (HPLC
Elemental Toxicity - Cadmium (Cd)
- Found in industrial processes, paints and plastics, and in nickel-cadmium batteries.
- Smoking is a common route of exposure, as tobacco leaves accumulate cadmium in the soil.
- Consumption of shellfish, organ meats, lettuce, spinach, potatoes, grains, peanuts, soybeans, and sunflower seeds.
- Cadmium expresses its toxicity by binding proteins.
- Toxicity can cause:
- Renal tubular dysfunction, parathyroid dysfunction and vitamin D deficiency.
•Half life of 10 - 30 years
Elemental Toxicity - Lead (Pb)
- By-product of many industrial processes, household paints (prior to 1972), plumbing
- Ingestion of contaminated food accounts for most exposures.
•Lead combines with the matrix of bone and soft tissue and can persist for long periods of time.
•Half life of almost 20 years
(120 days in soft tissue)
•Excessive exposure:
- Hypertension, carcinogenesis, birth defects, compromised immunity, severe renal effects
Clinical Presentation
•A progressive pattern is shown in the development of lead toxicity
Children are more prone to effects of Pb
- More opportunity for exposure
Analysis:
•Venous whole blood collected in Tan or Royal Blue-top containing EDTA
•Lab Results:
- ↓ vitamin D - ↑ urinary aminolevulinic acid - Anemia - Basophilic stippling in RBCs
•Tested using inductively coupled plasma mass spectrometry (ICP-MS)
Elemental Toxicity - Mercury (Hg)
- 3 forms: elemental, inorganic salts, and component of organic compounds
- Major source of exposure: consumption of contaminated food.
Most forms can be ingested without significant effects.
•Organic mercury (methyl mercury) is extremely toxic.
- Rapidly and efficiently absorbed into hydrophobic compartments such as brain and nerves
•Clinical Presentation
Methylmercury poisoning characterized by:
•Degeneration of neurons
•Impaired speech
•Visual field constriction
•Hearing loss
•Neurodevelopmental delays to fetal death if exposed in utero
- Inorganic mercury toxicity: ulceration and necrosis of the GI tract → shock, death
- Organic mercury toxicity: neurological symptoms (tremors, behavioral changes, mumbling)
- Analysis:
- Blood, urine, or hair can be used to determine exposure
- Quantity in blood or urine corelate with degree of toxicity
- Time and peak of exposure can be determined on hair
•Atomic Absorption Spectrometry (AAS)