Household toxicities

• Common Household Poisons


  • Oxalic acid
  • Carbamate insecticides
  • Pyrethrins and Pyrethroids
  • Organophosphates
• Environmental Poisons


  • Carbon monoxide
  • Formaldehyde
• Oxalic acid


  Used as bleaches, metal cleaners, and rust removers and in chemical synthesis and leather tanning
• Oxalates


  End product of the metabolism of plant tissues, not found in animal tissues
• High content oxalates


  • peanut
  • spinach
  • beans
  • sweet potato
• Types of oxalates


  • Soluble oxalates (Na, K)
  • Insoluble oxalates (Ca, Mg)
• Mechanism of toxicity of oxalic acid

  • Oxalic acid solutions are highly irritating and corrosives even low concentration since it is acidic
  • Ingestion and absorption of (Soluble) oxalate cause hypocalcemia resulting from precipitation of the insoluble calcium oxalate salt
  • Calcium oxalate crystals may then deposit in the brain, heart, kidneys, liver and other sites, causing serious systemic damage
  • Insoluble calcium oxalate salt found in plants causes local mucous membrane irritation
• Oxalic acid and oxalates


  • Relatively safe on the skin unless there is an open wound
  • Calcium oxalate is the major cause of kidney stones
• Clinical presentation of oxalic acid exposure


  • Acute or skin eye contact causes irritation and burning which may lead to serious corrosive injury
  • Inhalation may cause sore throat, cough and wheezing
  • Large exposure may lead to chemical pneumonitis or pulmonary edema
  • Ingestion of soluble oxalates may result in weakness, tetany, convulsions, and cardiac arrest owing to profound hypocalcemia
  • Insoluble oxalate crystals are not absorbed but can cause irritation and swelling in the oropharynx and esophagus
• Diagnosis of oxalic acid poisoning


  • Based on history of exposure and evidence of local or systemic effects or oxalate crystalluria
  • Serum oxalate levels are not available
  • Other useful laboratory studies include electrolytes, glucose, BUN, creatinine, calcium, ECG monitoring, urinalysis
• Treatment of oxalic acid poisoning


  1. Administer 10% calcium solution to counteract symptomatic hypocalcemia

  2. For insoluble oxalates, flush exposed areas and do not induce emesis or give charcoal

  3. For oxalic acid or strong commercial oxalate solutions, immediately flush with copious water, do not induce vomiting, instead give water to dilute, and perform gastric lavage

  4. For plants containing soluble oxalates, induce emesis with syrup of ipecac, consider gastric lavage, and administer calcium orally or via gastric tube

  5. Maintain a high-volume urine flow to help prevent calcium oxalate precipitation in the tubules

  6. Oxalate is removed by hemodialysis, but indications are not established
• Carbamate insecticides


  • Less toxic than organophosphates, though their clinical effects are similar
  • Found in a variety of commercial veterinary and pesticide products widely used in agriculture
  • Most household insect sprays contain carbamates
• Mechanism of toxicity of carbamates

  • Carbamates inhibit acetylcholinesterase enzyme which allows excessive accumulation of acetylcholine at muscarinic, nicotinic, and CNS receptors
  • Inhibition is short-lived and reversible
  • Carbamates are absorbed by inhalation, ingestion, and through the skin
• Toxic dose of carbamates

  • There is a wide variability in the potency of carbamates
  • Aldicarb is an important carbamate because it is relatively more potent, undergoes extensive enterohepatic recirculation, and is translocated systemically by certain plants
• Clinical presentation of carbamate poisoning

  • Signs and symptoms usually occur within 30 minutes but may not develop until 1-2 hours after exposure
  • Clinical manifestations are the same with organophosphates but the duration of toxicity is usually shorter (< 6 hours) and symptoms are self limited
• Diagnosis of carbamate poisoning

  • Based on history of exposure and the characteristic presentation of muscarinic, nicotinic, and central nervous system acetylcholine excess
  • Depression of 25% or more of red blood cell cholinesterase and plasma pseudocholinesterase from an individual's baseline value is indicative of exposure
  • Samples should be analyzed immediately, because in vitro hydrolysis of the carbamate can occur
  • Other useful laboratory studies include electrolytes, glucose, BUN, creatinine, arterial blood gases or oximetry
• Treatment of carbamate poisoning

  1. Administer atropine, 0.5-2 mg (0.01-0.04 mg/kg) IV or IM every 15 minutes until manifestations of muscarinic toxicity are reversed

  2. If a combination of carbamate and organophosphate poisoning has occurred, pralidoxime (2PAM) should be given

  3. Skin and eyes, remove all contaminated clothing and wash affected skin copiously with soap and water, including the hair and under the nails

  4. Irrigate exposed eyes with copious tepid water or saline

  5. For ingestion, administer activated charcoal, do not induce emesis

  6. Repeat-dose activated charcoal is theoretically applicable to aldicarb poisoning, because aldicarb undergoes enterohepatic recirculation
• Pyrethrins and pyrethroids


  • Pyrethrins are naturally occurring insecticides derived from the chrysanthemum plant
  • Pyrethroids are synthetically derived compounds
  • Inhalation frequently causes upper airway irritation and hypersensitivity reactions
  • Common pyrethrin containing pediculicides are A-200, triple-X and RID
• Mechanism of toxicity of pyrethrins and pyrethroids

  • In insects, pyrethrins and pyrethroids paralyzes the nervous system through disruption of the membrane ion transport system in nerve axons
  • Pyrethroids prolong sodium influx and also may block inhibitory pathways
  • Mammals are generally able to metabolize these compounds rapidly and thereby render them harmless
• Toxic dose of pyrethrins and pyrethroids


  • Toxic oral dose in mammals is greater than 100-1000 mg/kg
  • Potentially lethal acute oral dose is 10-100 g
  • Pyrethrins are not well absorbed across the skin or from the GIT
• Clinical presentation of pyrethrin and pyrethroid exposure

  • Anaphylactic reactions including bronchospasm, oropharyngeal edema, and shock may occur in hypersensitive individuals
  • Inhalation may precipitate wheezing in asthmatics and cause hypersensitivity pneumonitis
  • Skin exposure may cause burning, tingling, numbness, and erythema (paresthesia)
  • Accidental eye exposure may cause corneal injury including keratitis and denudation
  • Ingestion of large amounts may cause seizures, coma, or respiratory arrest
• Decontamination and treatment of pyrethrin and pyrethroid exposure

  1. Inhalation: Remove victim from exposure and give supplemental oxygen

  2. Skin: Wash with copious soap and water, topical application of vitamin E may relieve paresthesia

  3. Eyes: Irrigate with copious water, perform fluorescein examination and refer to ophthalmologist if corneal injury

  4. Ingestion: Administer activated charcoal and ipecac-induced emesis for initial treatment, in hospital administer activated charcoal and a cathartic
• Organophosphates are widely used pesticides that may cause acute or chronic poisonings after accidental or suicidal exposure
• Mechanism of toxicity of organophosphates

  • They inhibit the enzyme acetylcholinesterase, allowing the accumulation of excessive acetylcholine at muscarinic receptors, nicotinic receptors, and in the CNS
  • Are well absorbed by inhalation and ingestion
• Paresthesia


  Abnormal skin sensation, such as burning, prickling, or tingling
• Irrigate eyes


  1. Irrigate with copious water

  2. Perform fluorescein examination

  3. Refer to ophthalmologist if corneal injury
• Ingestion treatment


  1. Administer activated charcoal

  2. Administer ipecac-induced emesis
• Hospital ingestion treatment


  1. Administer activated charcoal

  2. Administer cathartic
• Enhanced elimination for ingestion - None
• Organophosphates


  Widely used pesticides that may cause acute or chronic poisonings after accidental or suicidal exposure
• Organophosphates often contain


  Solvents such as toluene or xylene (aromatic hydrocarbon) that can themselves produce toxic effects in an overdose
• Mechanism of organophosphate toxicity

  1. Inhibit acetylcholinesterase enzyme

  2. Allow accumulation of excessive acetylcholine at muscarinic receptors, nicotinic receptors, and in the CNS
• Organophosphates are well absorbed by inhalation, ingestion, and through the skin
• Some organophosphates are highly lipophilic and are stored in fat tissue for longer duration of action
• Toxic dose of organophosphates


  • Wide spectrum of relative potency
  • Degree of intoxication affected by rate of exposure, metabolic degradation, and rate of metabolism to more toxic '-oxon' derivative
• Signs and symptoms of acute organophosphate poisoning

  • Muscarinic: Vomiting, Diarrhea, Abdominal cramping, Bronchospasm, Miosis, Bradycardia, Excessive salivation, Sweating
  • Nicotinic: Muscle fasciculation, Tremor, Weakness, Increased blood pressure and pulse rate
  • Central nervous: Agitation, Seizures, Coma, Delayed peripheral neuropathy, Intermediate syndrome
• Diagnosis is based on history of exposure and characteristic muscarinic, nicotinic, and CNS manifestations
• There is frequently a solvent odor, and some describe a garlic-like odor of the organophosphate
• Specific diagnostic tests


  • Measure decreases in plasma pseudocholinesterase (PChE) and red blood cell acetylcholinesterase (AChE) activities
  • 25% or greater depression in activity from baseline generally indicates true exposure
• Other useful laboratory studies

  • Electrolytes, glucose, BUN, creatinine, liver transaminases, arterial blood gases or oximetry, ECG monitoring, chest x-ray