toxicology environmental or occupational exposure

• Carbon Monoxide • Caustic Agents • Cyanide • Metals and Metalloids

• 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

typical in non- smokers 0.5% smokers 5-10% immediately fatal 80%

• 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

• 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

• 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

• 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

• 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

• 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)

• 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)