Toxicology
Reference guide to toxic elements, poisonous compounds, mechanisms of toxicity, and clinical antidotes.
Toxic Elements
Pb
Lead
TOXICSources: Lead-based paint, old plumbing pipes, batteries, ammunition, contaminated soil.
Effects: Neurotoxicity with cognitive impairment, developmental delays in children, peripheral neuropathy, abdominal pain, anemia, nephropathy.
Mechanism: Mimics Ca²⁺ and Zn²⁺ ions, disrupting calcium-dependent signaling. Inhibits δ-aminolevulinic acid dehydratase (δ-ALAD), blocking heme synthesis. Crosses the blood-brain barrier.
Treatment: Chelation therapy with EDTA (CaNa₂EDTA) or DMSA (succimer) for elevated blood lead levels.
Hg
Mercury
TOXICSources: Fish consumption (methylmercury), dental amalgams, thermometers, industrial emissions, artisanal gold mining.
Effects: Neurological damage including tremor, memory loss, and sensory impairment. Organic forms (methylmercury) cause Minamata disease with severe CNS damage. Renal toxicity from inorganic forms.
Mechanism: Binds sulfhydryl (-SH) groups on proteins and enzymes, disrupting their function. Methylmercury bioaccumulates in the food chain and readily crosses the blood-brain barrier.
Forms: Elemental (Hg⁰), inorganic (Hg²⁺), organic (methylmercury CH₃Hg⁺)
Treatment: Chelation with DMSA or BAL (dimercaprol). Remove exposure source.
As
Arsenic
TOXICSources: Contaminated groundwater (endemic in Bangladesh, West Bengal), pesticides, treated wood (CCA), mining runoff.
Effects: Acute: severe GI distress, garlic breath, rice-water diarrhea. Chronic: peripheral neuropathy, keratoses, increased cancer risk (skin, lung, bladder).
Mechanism: Arsenate (As⁵⁺) mimics phosphate, uncoupling oxidative phosphorylation. Arsenite (As³⁺) binds sulfhydryl groups, inhibiting pyruvate dehydrogenase and disrupting ATP production.
Treatment: Dimercaprol (BAL) for acute poisoning. DMSA for chronic exposure. Supportive care.
Cd
Cadmium
TOXICSources: Nickel-cadmium batteries, cigarette smoke, mining and smelting, phosphate fertilizers, contaminated rice.
Effects: Kidney damage (proximal tubular dysfunction), bone demineralization leading to itai-itai disease, lung damage from inhalation, possible carcinogen (IARC Group 1).
Mechanism: Displaces zinc in metalloenzymes, inducing metallothionein production. Accumulates in kidneys with a biological half-life of 10–30 years. Generates oxidative stress.
Treatment: No effective chelation. Treatment is symptomatic and supportive. Prevention of further exposure is critical.
Tl
Thallium
TOXICSources: Historical rat poison (now banned in many countries), industrial processes, semiconductor manufacturing.
Effects: Alopecia (characteristic hair loss after 2–3 weeks), painful peripheral neuropathy, GI symptoms, cardiac arrhythmias, CNS effects.
Mechanism: Mimics K⁺ ions due to similar ionic radius, entering cells via potassium channels and disrupting potassium-dependent enzymes. Binds sulfhydryl groups.
Treatment: Prussian blue (potassium ferric hexacyanoferrate) traps thallium in the GI tract, preventing reabsorption.
Cr
Chromium (VI)
TOXICSources: Industrial processes, stainless steel production, chrome plating, leather tanning, contaminated drinking water.
Effects: Hexavalent chromium (Cr⁶⁺): lung cancer, nasal septum perforation, skin ulcers, contact dermatitis. IARC Group 1 carcinogen.
Mechanism: Cr(VI) crosses cell membranes via sulfate/phosphate transporters. Intracellular reduction generates reactive intermediates (Cr⁵⁺, Cr⁴⁺) that damage DNA. Note: Cr(III) is an essential trace element.
Treatment: Remove from exposure. Supportive care. Ascorbic acid may reduce Cr(VI) to less toxic Cr(III) in the GI tract.
Toxic Compounds
Carbon Monoxide
CID 281CO
Mechanism: Binds hemoglobin with approximately 200× greater affinity than oxygen, forming carboxyhemoglobin (COHb). Shifts the oxygen-hemoglobin dissociation curve left, impairing O₂ delivery to tissues. Also inhibits cytochrome c oxidase.
Symptoms: Headache, confusion, cherry-red skin, loss of consciousness, death.
Treatment: 100% oxygen; hyperbaric oxygen for severe cases.
Hydrogen Cyanide
CID 768HCN
Mechanism: Cyanide ion (CN⁻) binds to the iron center of cytochrome c oxidase (Complex IV) in mitochondria, blocking the electron transport chain and halting aerobic ATP production. Cells switch to anaerobic metabolism.
Symptoms: Rapid onset: headache, seizures, lactic acidosis, cardiac arrest.
Treatment: Hydroxocobalamin (binds CN⁻) or sodium thiosulfate (provides sulfur for rhodanese-mediated detoxification).
Hydrogen Sulfide
CID 402H₂S
Mechanism: At high concentrations, inhibits cytochrome c oxidase similar to cyanide. At low concentrations, acts as a gaseous signaling molecule. Detectable by characteristic rotten-egg odor, but olfactory fatigue occurs at dangerous levels.
Symptoms: Eye irritation, pulmonary edema, sudden collapse (“knockdown”) at high concentrations.
Treatment: Remove from exposure, supportive care, oxygen. Nitrite therapy may help by forming sulfmethemoglobin.
Antidote Reference
| Toxin | Antidote | Mechanism of Antidote |
|---|---|---|
| Lead | EDTA, DMSA | Chelation — binds metal ions for renal excretion |
| Mercury | DMSA, BAL | Chelation — binds mercury via sulfhydryl groups |
| Arsenic | BAL | Chelation — competes for sulfhydryl binding sites |
| Cyanide | Hydroxocobalamin, Na thiosulfate | Binds CN⁻ directly / provides sulfur donor for rhodanese detoxification |
| Organophosphates | Atropine + pralidoxime | Blocks muscarinic effects / reactivates acetylcholinesterase (AChE) |
| Opioids | Naloxone | Competitive μ-opioid receptor antagonist |
| Acetaminophen | NAC | Replenishes hepatic glutathione stores to detoxify NAPQI metabolite |
| Iron | Deferoxamine | Chelation — binds free iron to prevent oxidative tissue damage |