Household nonpharmaceutical product ingestions

INTRODUCTION — Exploratory ingestions of nonpharmaceutical household products are common in young children. Adolescents and adults may ingest these products in self-harm attempts.

This topic discusses the approach to a patient with a nonpharmaceutical household product ingestion as well as the evaluation and management of poisoning from selected products with potential to cause toxicity.

The toxicity of many household products that are not discussed in this topic are discussed separately. (See 'Household product ingestions discussed in other topics' below.)

The general approach to the poisoned adult or child is discussed separately. (See "General approach to drug poisoning in adults" and "Approach to the child with occult toxic exposure" and "Initial management of the critically ill adult with an unknown overdose".)

EPIDEMIOLOGY — Nonpharmaceutical household products account for at least a quarter of exposures reported annually to United States poison control centers [1]. Most household ingestions occur from exploratory behavior in a young child. These generally involve a small volume or quantity and develop minimal toxicity. However, serious toxicity is more likely when a household product is ingested with the intent of self-harm, which typically occurs in an adolescent or adult patient.

Products that are widely available are the most commonly ingested, including the following:

●Cosmetics/personal care products

●Household cleaning substances

●Foreign bodies

●Vitamins

●Plants

●Pesticides

●Topical preparations

The most common household ingestions causing toxicity include the following:

●Hydrocarbons

●Caustics

●Nicotine products

●Detergent pods

●Pesticides

●Button batteries

●Automotive products

●Mothballs

●Alcohol-containing products not intended for consumption (eg, hand sanitizer, mouthwash)

APPROACH TO A PATIENT WITH A HOUSEHOLD PRODUCT INGESTION

●History of ingestion – The history is essential and should include the following:

•Character and contents of product (if available).

•Time of ingestion.

•Intent of ingestion – Exploratory ingestion by a young child will likely involve a smaller amount while a self-harm attempt suggests a larger ingestion.

•Location within the house of the incident – If the contents of the ingestion are unknown, the location of the incident may be helpful in determining what was ingested. Ingestions occurring in the kitchen may involve a detergent; those in the garage may involve pesticides or automotive products.

●Physical examination – Assess vital signs, respiratory mechanics, mental status, and general appearance. Inspect the oropharynx for lesions or burns. A hydrocarbon ingestion may cause respiratory compromise. A pesticide ingestion may cause the characteristic cholinergic toxidrome (table 1).

●Laboratory evaluation – This depends on the ingested substance (if known) or suspected substance if based on location of the ingestion. For example, serum electrolytes, serum osmolarity, and blood gas should be checked if concern for a toxic alcohol ingestion. A serum ethanol concentration should be obtained for ingestions of hand sanitizer, mouthwash, or perfume.

COSMETIC/PERSONAL CARE PRODUCTS — Cosmetics are the most common nonpharmaceutical household products involved in pediatric ingestions [1].

Toothpaste and fluoride-containing dental rinses — Fluoride toxicity is possible, albeit unlikely, from excess ingestion of toothpaste or dental rinses [2]. The estimated pediatric toxic dose of fluoride is approximately 5 mg/kg. Fluoride content in toothpaste ranges from 1000 to 1500 parts per million (ppm); one ounce of 1000 and 1500 ppm toothpaste contains 28 mg and 42 mg of fluoride, respectively [2]. Ingestion of a quarter of a standard size six-ounce tube of toothpaste is potentially toxic in a toddler.

Dental rinses and gels available for consumer purchase and at-home use have lower fluoride content compared with those provided in a dental office.

●Clinical manifestations – Fluoride toxicity can range from mild gastrointestinal symptoms (vomiting, nausea) to systemic complications of hypocalcemia (eg, seizures, tetany, decreased myocardial contractility, ventricular dysrhythmias). Excess fluoride forms insoluble calcium fluoride (CaF₂), causing hypocalcemia and hyperkalemia.

Severe fluoride toxicity is very rare following toothpaste and dental rinse ingestions. A study of 12,571 toothpaste ingestions reported to United States poison control centers found that there were no deaths and only a few patients with major effects [2].

●Evaluation – Inquire about the name of the product and estimated amount ingested as well as the timing of the ingestion. We advise contacting a regional poison control center for assistance in calculating the dose of fluoride ingested and for management recommendations. (See 'Regional poison control centers' below.)

In a patient with vomiting after toothpaste/dental rinse ingestion, we obtain an electrocardiogram (ECG), serum electrolytes, and calcium concentration. Hypocalcemia suggests the diagnosis of fluoride toxicity. Results of quantitative serum fluoride concentrations are typically not available in a clinically meaningful timeframe.

●Management – In a patient with hypocalcemia, signs or symptoms consistent with hypocalcemia (eg, carpopedal spasm, laryngospasm, bronchospasm, seizure), or ECG changes (prolongation of QT interval), we administer intravenous (IV) calcium to prevent dysrhythmia. We prefer calcium gluconate instead of calcium chloride, which is a vesicant following extravasation. Calcium gluconate should be infused intravenously over 10 to 20 minutes (starting doses 100 to 200 mg/kg per dose in children; 1 to 2 grams in adults). If calcium gluconate is not available, calcium chloride can be given via central venous access (10 to 20 mg/kg per dose IV in children, or 1 to 2 grams IV in adults). The management and physiology is similar to systemic toxicity from hydrofluoric acid poisoning. (See "Treatment of hypocalcemia", section on 'Therapeutic approach' and "Topical chemical burns: Initial evaluation and management", section on 'Hydrofluoric (HF) acid'.)

Hydrogen peroxide — Poisoning can cause air-gas embolism with potentially life-threatening toxicity. The formulation used for wound care and first aid is a 3 percent hydrogen peroxide solution. However, hydrogen peroxide products used for disinfecting food or "wellness" purposes can contain high concentrations (eg, 10 to 35 percent). Air embolism is formed from metabolism of hydrogen peroxide by catalase into water and oxygen; 1 mL of 35 percent hydrogen peroxide releases 100 cc of oxygen [3].

●Clinical manifestations – Although serious outcomes are rare, exposure to concentrated products (ie, >10 percent solution), either from ingestion or irrigation of surgical wounds, is more likely to cause clinically significant toxicity [4-6]. Ingesting concentrated hydrogen peroxide can cause caustic injury, pneumobilia, pneumatosis of the intestinal wall, and intestinal perforation. Complications of air-gas embolism include hypoxia, seizures, cerebrovascular infarction, ventricular tachycardia, hypotension, and myocardial infarction.

Ingesting 3 percent hydrogen peroxide solution may cause mild gastrointestinal irritation, nausea, and vomiting. Most exploratory ingestions have a benign course but large-volume (>150 mL) ingestion has been reported to cause severe toxicity similar to a concentrated product ingestion [7,8].

A systematic review of hydrogen peroxide exposure cases identified 126 patients (including 17 fatalities) with embolic phenomena [7]. Symptoms from air embolism occurred immediately (within 15 minutes) in 61 percent and were evident in 90 percent within 10 hours. No fatalities occurred in patients with delayed onset (>6 hours) of symptoms. Almost all patients with portal venous air had abdominal pain, nausea, or vomiting.

●Evaluation – We obtain abdominal imaging in a patient with any gastrointestinal symptoms (eg, abdominal pain, nausea, vomiting) after hydrogen peroxide exposure. Our preferred study is an abdominopelvic computed tomography (CT) scan. In a young child with an exploratory ingestion of household hydrogen peroxide (eg, 3 to 5 percent) who has transient abdominal pain or nausea and a normal physical examination, it is reasonable to obtain abdominal and chest radiographs, instead of CT, to evaluate for portal venous gas [9].

For a symptomatic patient following a hydrogen peroxide exposure or an asymptomatic patient with either a large-volume, low-concentration or a concentrated product exposure, we encourage discussion with a medical toxicologist, poison control center, and/or hyperbaric oxygen (HBO) center director. (See 'Regional poison control centers' below.)

●Management – We initiate HBO in exposed patients with any signs/symptoms attributed to systemic emboli (eg, stroke, myocardial infarction, obstructive shock) or if abdominal or chest imaging, if obtained, demonstrates extraluminal air, although consensus does not exist regarding the optimal timing or efficacy of HBO [5,6,10]. Some experts will recommend HBO for any highly concentrated (eg, 35 percent) product exposure. (See "Hyperbaric oxygen therapy", section on 'Hydrogen peroxide exposure'.)

The goal of early HBO initiation is to prevent more consequential toxicity from systemic air embolism. Evidence is based on case reports, case series, and HBO's physiological mechanism of reducing embolism size and enhancing reabsorption in the bloodstream. In the systematic review of embolism from hydrogen peroxide exposure, none of the 30 patients with portal venous air who received HBO suffered air emboli compared with 24 percent (8 out of 33, including three deaths) who did not receive HBO [7]. In patients with air emboli, 57 percent (13 out of 23) who received HBO had a full recovery compared with 42 percent (23 out of 55) who did not receive HBO. In patients with a full recovery, the mean time from air embolism onset to HBO was nine hours compared with 18 hours in patients with partial recovery or death.

Other aspects of managing a patient with an air embolism, such as cardiorespiratory support and positioning, are discussed separately. (See "Air embolism", section on 'Treatment'.)

Hair straighteners and curlers — Products used to straighten or curl hair are often highly alkaline liquids or creams. The liquid formulation can cause esophageal ulceration and/or perforation. Since the cream preparations are more viscous, the injury is more likely to be confined to the mouth and lips and less likely to involve the hypopharynx, larynx, and esophagus. A child with signs or symptoms consistent with esophageal injury (eg, drooling, stridor, dysphagia) should undergo endoscopy regardless of the viscosity of the product. In a child with a viscous product exposure without clinical suspicion of injury outside the oral cavity, it is reasonable to forego endoscopy [11].

The evaluation and management of caustic ingestions is summarized in the algorithm (algorithm 1) and discussed separately. (See "Caustic esophageal injury in children" and "Caustic esophageal injury in adults".)

Topical preparations — Small-volume ingestion of most household topical preparations, as may be encountered by a curious young child, does not cause toxicity. This includes products such as moisturizers, ointments, baby products, bath oil, shampoo, hair conditioner, deodorants, diaper cream, suntan lotion, shaving cream, and petroleum jelly.

CLEANING PRODUCTS

Toilet bowel and oven cleaner, drain opener, and degreaser — Products used to clean porcelain, remove grease buildup from drains and other surfaces, and clean or degrease ovens can be highly corrosive and cause caustic injury if ingested. These products are sufficiently acidic or alkaline to cause injury even though packaging regulations prohibit highly concentrated products from being sold for household use. The approximate pH of selected cleaning products are presented in the table (figure 1).

The evaluation and management of caustic ingestions is summarized in the algorithm (algorithm 1) and discussed separately. (See "Caustic esophageal injury in children" and "Caustic esophageal injury in adults".)

Bleach, ammonia, detergents — Exploratory ingestions of standard household cleaners (eg, bleaches, ammonia) and liquid detergents are not expected to cause serious caustic injury. Mild gastrointestinal irritation or burns can occur and are typically managed with observation or endoscopy if symptoms worsen or persist (algorithm 1). (See "Caustic esophageal injury in children", section on 'Esophageal injury'.)

A large-volume ingestion with self-harm intent or an ingestion of an industrial-strength product that was brought into the home is likely to cause significant gastrointestinal or pulmonary caustic injury [12]. Also, ingestion of concentrated single-use detergent packets ("capsules," "gel packs," or "pods") can cause esophageal and airway injury. Packets containing dishwasher detergent are generally less harmful compared to those containing laundry detergent. Management includes early tracheal intubation if there are signs of airway or respiratory involvement, upper endoscopy, and/or surgical resection for transmural necrosis or perforation. (See "Caustic esophageal injury in adults", section on 'Initial management'.)

AUTOMOTIVE PRODUCTS — Some products used in automotive maintenance contain alcohols (eg, methanol, ethylene glycol, propylene glycol), including antifreeze and windshield washer fluid. In addition, some automotive cleaning products used for removing brake dust and other dirt from the surfaces of wheels and tires are highly corrosive. The evaluation and management of ethylene glycol and methanol is discussed separately. (See "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis" and "Methanol and ethylene glycol poisoning: Management".)

Propylene glycol ("non-toxic" antifreeze) — Most antifreeze contains ethylene glycol, but some antifreeze marketed as "non-toxic" contains propylene glycol, which is generally less toxic compared with ethylene glycol. Propylene glycol can also be found in cosmetics, processed foods, and e-cigarettes [13]. It is a common pharmaceutical solvent in oral, topical, and parenteral medications and can cause toxicity following high-dose intravenous (IV) infusions (eg, lorazepam). (See "Sedative-analgesia in ventilated adults: Medication properties, dose regimens, and adverse effects", section on 'Propylene glycol toxicity' and "Serum osmolal gap", section on 'Other alcohols'.)

Propylene glycol is metabolized by alcohol dehydrogenase and aldehyde dehydrogenase to L-lactate, D-lactate, and methylglyoxal [13]. These are further metabolized to glucose, pyruvate, and carbon dioxide. Propylene glycol is cleared by hemodialysis, similar to ethylene glycol.

●Clinical manifestations – Following intentional propylene glycol ingestion, patients can develop mild central nervous system depression, confusion, and hyperlactemia (with or without a metabolic acidosis) [13,14]. Large-volume ingestions have been reported to cause seizures, hemolysis, and kidney failure.

●Evaluation – In a patient with an antifreeze ingestion and the exact ingredients of the antifreeze are unknown (or any intentional antifreeze ingestion in self-harm attempt), we obtain serum chemistries, lactate, calcium, osmolality, blood gas, and ethanol, methanol, isopropyl alcohol, and ethylene glycol concentrations. Immediately following an antifreeze ingestion, it can be challenging to differentiate propylene glycol versus ethylene glycol poisoning since both cause an elevated osmolar gap, and most hospital laboratories cannot provide results of serum concentrations within a clinically meaningful timeframe. The evaluation is therefore the same for ethylene glycol ingestion and is discussed separately. (See "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis", section on 'Laboratory evaluation'.)

In a child with an exploratory ingestion of antifreeze that can be reliably identified to contain propylene glycol and not ethylene glycol, we obtain only serum chemistries and lactate.

We do not routinely obtain propylene glycol serum concentrations, but they are available at some laboratories if definitive confirmation is needed. Patients with propylene glycol ingestion have had good outcomes even with reported concentrations >350 mg/dL [14].

In a patient with dyspnea, cyanosis, or hypoxia not improving with supplemental oxygen, we also obtain a serum methemoglobin concentration. Some antifreezes contain nitrites/nitrates (anticorrosion agents required for some diesel engines) that have caused methemoglobinemia following large ingestion [15]. These may not be listed on the product label or safety data sheet if concentrations are sufficiently low. (See "Methemoglobinemia", section on 'How to detect (measure) methemoglobin'.)

●Management – In a child with an exploratory ingestion of antifreeze that can reliably be identified to contain propylene glycol and not ethylene glycol, we provide supportive care alone, since we would not expect significant toxicity to develop. If they are symptomatic or have an elevated lactate, we observe until asymptomatic and the lactate normalizes. An asymptomatic child with normal serum chemistries and lactate can be discharged.

In a patient with an antifreeze ingestion and the exact ingredients of the antifreeze are unknown or an adult with an intentional antifreeze ingestion (regardless of the ingredients), we recommend cautiously managing the patient by assuming that the more toxic ethylene glycol was ingested (ie, alcohol dehydrogenase inhibition with fomepizole, hemodialysis for metabolic acidosis), even though alcohol dehydrogenase inhibition may not be required for an isolated propylene glycol ingestion. (See "Methanol and ethylene glycol poisoning: Management".)

Methemoglobinemia, if present, may require antidotal therapy (algorithm 2). (See "Methemoglobinemia", section on 'Management (acquired/toxic)'.)

Wheel and tire cleaner — Cleaning products to remove brake dust and dirt from wheels are potentially highly corrosive and may contain ammonium bifluoride or hydrofluoric acid (HF). Ingestion can cause caustic injury and fluoride toxicity (eg, hypocalcemia, hyperkalemia, ventricular dysrhythmia); life-threatening toxicity and fatality can occur with pediatric exploratory ingestion [16]. Symptomatic HF burns are managed with irrigation and calcium (topical calcium gel applied to burned areas; IV calcium for systemic toxicity). These are discussed in detail separately. (See "Topical chemical burns: Initial evaluation and management", section on 'Hydrofluoric (HF) acid'.)

Other potential contents of wheel and tire cleaner include phosphoric, glycolic, and oxalic acids, alcohols, and glycol ethers and may cause caustic injury and/or toxic alcohol poisoning. The evaluation and management of caustic ingestions is summarized in the algorithm (algorithm 1). The management of caustic ingestions and toxic alcohol poisoning are discussed separately. (See "Caustic esophageal injury in children" and "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis" and "Methanol and ethylene glycol poisoning: Management".)

MOTHBALLS

Determining active ingredient — Mothballs and other fragrant pesticides are common household products. Mothballs may contain one of three active ingredients (naphthalene, paradichlorobenzene, or camphor) which should be clearly stated on the packaging. Camphor mothballs are the most toxic and least commonly available.

If the mothball packaging is not available or illegible, the active ingredient can be determined using the "float test." The test is performed by dropping the mothball into a cup of tap water and another cup with a saturated salt or sugar solution (eg, table salt dissolved in warm water until saturated or 50 percent dextrose in water intravenous fluid) [17]:

●Camphor mothballs will float in both

●Paradichlorobenzene mothballs will sink in both

●Naphthalene mothballs will sink in water and float in saturated salt or sugar solution

Camphor — Ingestion of a camphor mothball or other aromatic block characteristically causes seizures. Other toxicity can include vomiting, abdominal pain, agitation, confusion, myoclonus, hyperreflexia, lethargy, and/or coma. Camphor mothballs are not commonly sold in the United States, but camphor products may still be found from internet retailers, for home décor, and for wellness purposes (table 2). The evaluation and management of camphor poisoning is discussed separately. (See "Camphor poisoning in children".)

Paradichlorobenzene, naphthalene — Paradichlorobenzene is the most common active ingredient in mothballs and may also be found in other products such as toilet bowl cleaner/freshener and commercial urinal cakes. Naphthalene is a component of petroleum and coal tar as well as mothballs.

●Clinical manifestations

•Paradichlorobenzene – Acute ingestions rarely causes significant toxicity. Patients may develop nausea, vomiting, abdominal pain, and/or mucous membrane irritation. Ichthyosiform eruption, hemolysis, methemoglobinemia, hepatotoxicity, and pulmonary edema have been reported [18,19]. Chronic consumption can lead to an irreversible leukoencephalopathy [20].

•Naphthalene – Acute naphthalene ingestions may cause nausea, vomiting, abdominal pain, and headache. Large ingestions can cause methemoglobinemia and hemolysis from red blood cell oxidant stress due to naphthalene and its metabolites. Patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency are most susceptible.

●Evaluation – Laboratory testing is targeted towards specific signs and symptoms (eg, methemoglobin concentration for cyanosis/dyspnea; complete blood count, blood smear, reticulocyte count, lactate dehydrogenase, bilirubin, haptoglobin for pallor/jaundice/dark or red urine (table 3)). In a patient with methemoglobinemia associated with a mothball ingestion, we also investigate for other causes such as nitrite-containing foods and high-risk medications (eg, dapsone) (table 4). (See "Methemoglobinemia", section on 'How to detect (measure) methemoglobin' and "Drug-induced hemolytic anemia", section on 'Evaluation'.)

Paradichlorobenzene and a naphthalene metabolite (1-napthol) can be measured in serum, but the results are typically not available to impact acute management.

●Management – Toxicity is managed with supportive care. Methemoglobinemia, if present, may require antidotal therapy (algorithm 2). Transfusion may be needed for hemolysis. If the patient is suspected to have G6PD deficiency, we advise consultation with a hematologist and toxicologist/poison control center since antidotal therapy (ie, methylene blue) can cause hemolysis. (See "Methemoglobinemia", section on 'Management (acquired/toxic)' and "Drug-induced hemolytic anemia", section on 'Management'.)

PESTICIDES/INSECTICIDES/HERBICIDES — "Pesticide" is a broad term that describes a compound used to kill harmful or unwanted organisms. These are grouped according to the intended target (eg, insecticide, herbicide, rodenticide), although there is considerable overlap between categories. A complete discussion of pesticides, as well as long-term risks following chronic exposure, are beyond the scope of this topic.

Toxicity following acute exposure to some of the pesticides that may be encountered in the household are reviewed below. The World Health Organization provides a report of pesticides classified by acute oral and dermal toxicity.

Pyrethroid insecticides — These commonly used insecticides are derived from the chrysanthemum plant. They specifically target the insect exoskeletons and are generally nontoxic to humans and other non-target species (eg, domestic pets). Pyrethroids are classified into Type I (eg, permethrin) and Type II (eg, cypermethrin) compounds based on the presence or absence of a cyano group. Type II pyrethroids contain a cyano group but do not cause cyanide toxicity. Type II pyrethroids are more toxic to humans compared with Type I. Toxicity can occur from dermal or inhalational exposure or from ingestion.

●Clinical manifestations – Most exposures are well tolerated, although large ingestions with self-harm intent can be life-threatening or fatal. Ingestion commonly causes nausea, vomiting, abdominal pain, and sore throat. Large ingestions may cause neuroexcitatory symptoms such as tremor, the "CS: syndrome (choreoathetosis and salivation), respiratory compromise, and metabolic acidosis with elevated lactate. Toxicity can also overlap with cholinergic insecticides and include fasciculations, altered mental status, and seizures [21].

Allergic signs and symptoms can also occur from cross-reactivity with chrysanthemum and ragweed allergy.

●Evaluation – Laboratory testing is targeted towards specific signs and symptoms (eg, serum chemistries, blood gas). There are no useful quantitative tests specifically for pyrethroid exposure.

●Management – Toxicity is managed with supportive care. A patient who remains asymptomatic for several hours after exposure can be safely discharged. Delayed onset effects are not expected.

Glyphosate herbicides — This is the most commonly available household herbicide in the United States. Glyphosate inhibits a plant-specific enzyme used in protein synthesis that is not present in humans or other species. Typical household formulations in ready-to-use spray bottles contain 1 to 5 percent glyphosate while commercial preparations may contain 41 percent or greater and a variety of surfactants [22].

●Clinical manifestations – Exploratory small-volume ingestions do not usually cause significant toxicity. Patients may develop nausea, vomiting, and abdominal pain. Concentrated product ingestion with self-harm intent, particularly if in excess of 85 mL, can cause severe toxicity such as corrosive injury, acute kidney injury, acute respiratory distress syndrome, and other multiorgan derangements [23].

●Evaluation – In a symptomatic patient, laboratory testing should be performed to assess for kidney and other organ dysfunction. A patient with respiratory symptoms should have a chest radiograph, which may demonstrate infiltrates. A patient with signs of corrosive injury should undergo endoscopy. Quantitative testing for glyphosate is not helpful. (See "Caustic esophageal injury in children" and "Caustic esophageal injury in adults".)

●Management – Toxicity is managed with supportive care. There is no specific therapy for glyphosate poisoning.

Organochlorines — Compounds such as dichlorodiphenyltrichloroethane (DDT), chlordecone, and lindane are neuroexcitatory toxins but are not readily available in US households. Lindane may still be prescribed for the treatment of scabies and lice, with the potential for adverse effects, especially if ingested [24]. In some locations, chlordecone is a contaminant in soil and water although unlikely to cause acute toxicity [25].

●Clinical Manifestations – Acute toxicity is rarely reported, but signs and symptoms may include paresthesias, tremor, ataxia, altered mental status, and seizures [26].

●Evaluation – Organochlorine compounds can be measured in blood, plasma, and tissue, but diagnostic testing is not likely to be helpful in a clinically meaningful timeframe. It is important to investigate alternate causes of neuroexcitatory symptoms.

●Management – Neuroexcitatory symptoms (eg, seizures) are treated with benzodiazepines. (See "Management of convulsive status epilepticus in children", section on 'Emergency antiseizure treatment' and "Convulsive status epilepticus in adults: Management", section on 'Emergency antiseizure treatment'.)

Chlorphenoxy herbicides — Compounds such as 2,4-dichlorophenoxyacetic acid (2,4-D) and 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) are used industrially but are not available for household use in the US.

●Clinical Manifestations – Ingestion may cause vomiting, diarrhea, headache, confusion, and, in severe cases, fasciculations, metabolic acidosis, rhabdomyolysis, kidney injury, and multiorgan failure [27].

●Evaluation – In a patient with a history of exposure, we obtain serum chemistries and creatine kinase. Further testing is targeted towards signs and symptoms (eg, chest radiograph for dyspnea). These compounds can be measured in urine, but the results are not available in a clinically meaningful timeframe.

●Management – Supportive care is the priority. In addition, we administer intravenous (IV) sodium bicarbonate to alkalinize the urine, which enhances elimination similar to salicylate poisoning [26]. (See "Salicylate (aspirin) poisoning: Management", section on 'Serum and urine alkalinization'.)

Others – Other insecticide classes include triazene derivatives (eg, prometryn) and thiocarbamates (eg, cartap), which are generally less toxic following acute exposure.

Organophosphates (eg, malathion) and carbamates (eg, carbaryl), which are acetylcholinesterase inhibitors, are sold in US retail stores and sometimes encountered in the household. Acetylcholinesterase inhibitors cause a cholinergic toxidrome (seizures, salivation, urinary and fecal incontinence, vomiting, diarrhea, bronchorrhea, bronchoconstriction, muscle fasciculation, paralysis) and are treated with atropine, pralidoxime, and benzodiazepines. Organophosphate and carbamate poisoning is discussed separately. (See "Organophosphate and carbamate poisoning".)

Paraquat, diquat, and inorganic arsenic (eg, sodium arsenate ant killer, cacodylic acid herbicide) are highly toxic but not readily available in US households and are discussed separately. (See "Paraquat poisoning".)

HOUSEHOLD PRODUCT INGESTIONS DISCUSSED IN OTHER TOPICS — The evaluation and management of the following household product ingestions are discussed separately:

●Foreign bodies, including button batteries and magnets (see "Foreign bodies of the esophagus and gastrointestinal tract in children")

●Hydrocarbons (eg, lighter fluid, lamp/torch fuel, kerosene, gasoline, turpentine, pine oil, furniture polishes) (see "Acute hydrocarbon exposure: Clinical toxicity, evaluation, and diagnosis" and "Acute hydrocarbon exposure: Management")

●Plants (see "Potentially toxic plant ingestions in children: Clinical manifestations and evaluation" and "Toxic plant ingestions in children: Management")

●Mushrooms (see "Clinical manifestations and evaluation of mushroom poisoning" and "Management of mushroom poisoning (except amatoxin-containing mushrooms)" and "Amatoxin-containing mushroom poisoning (eg, Amanita phalloides): Clinical manifestations, diagnosis, and treatment")

●Nicotine products (eg, cigarette butts) (see "Nicotine poisoning (e-cigarettes, tobacco products, plants, and pesticides)")

●Caustics (see "Caustic esophageal injury in children" and "Caustic esophageal injury in adults")

●Isopropyl alcohol (eg, rubbing alcohol, isopropyl-based hand sanitizers) (see "Isopropyl alcohol poisoning")

●Alcohol-containing products not intended for consumption (eg, perfumes, colognes, mouthwash, glass cleaner, ethanol-based hand sanitizers) (table 5) (see "Ethanol intoxication in children: Epidemiology, estimation of toxicity, and toxic effects" and "Ethanol intoxication in children: Clinical features, evaluation, and management" and "Ethanol intoxication in adults")

●Methanol (eg, windshield washer fluid) and ethylene glycol (eg, antifreeze) (see "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis" and "Methanol and ethylene glycol poisoning: Management")

●Organophosphate and carbamate insecticides (see "Organophosphate and carbamate poisoning")

●Paraquat and diquat herbicides (see "Paraquat poisoning")

●Arsenic-based insecticides/herbicides (see "Arsenic exposure and chronic poisoning")

●Rodenticides (see "Overview of rodenticide poisoning" and "Anticoagulant rodenticide poisoning: Management" and "Anticoagulant rodenticide poisoning: Clinical manifestations and diagnostic evaluation")

●Vitamins and dietary elements (see "Acute iron poisoning" and "Overview of water-soluble vitamins" and "Overview of dietary trace elements" and "Overview of vitamin D", section on 'Excess' and "Overview of vitamin A", section on 'Excess')

●High-risk dietary supplements (see "High-risk dietary supplements: Patient evaluation and counseling")

PREVENTION — Prevention of poisoning in children is discussed in detail separately and includes the following measures (see "Prevention of poisoning in children"):

●Caregivers should be encouraged to survey the home periodically to evaluate all injury hazards, not just those related to poisoning (table 6).

●In each room, caregivers should consider whether toxic or poisonous substances are necessary; those that are deemed necessary should be safely stored, and those that are not should be appropriately discarded. Special attention should be paid to storage of products in the garage.

●Caregivers should be encouraged to buy the least toxic product that will accomplish the desired task.

ADDITIONAL RESOURCES

Regional poison control centers — Regional poison control centers in the United States are available at all times for consultation on patients with known or suspected poisoning and who may be critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have medical toxicologists available for bedside consultation. Whenever available, these are invaluable resources to help in the diagnosis and management of ingestions or overdoses. Contact information for poison centers around the world is provided separately. (See "Society guideline links: Regional poison control centers".)

Society guideline links — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: General measures for acute poisoning treatment" and "Society guideline links: Treatment of acute poisoning caused by specific agents other than drugs of abuse".)

SUMMARY AND RECOMMENDATIONS

●Common household ingestions producing toxicity – The most common toxic household ingestions include hydrocarbons, caustics, nicotine products, detergent pods, pesticides, button batteries, automotive products, mothballs, and alcohol-containing products not intended for consumption (eg, hand sanitizer, mouthwash). (See 'Epidemiology' above.)

●Approach to nonpharmaceutical household ingestion – Determine the character and ingredients of the product, if available, or the location within the house of the incident, which can provide clues to the type of product. Assess the intent of ingestion; exploratory ingestions by a young child will likely involve a smaller amount and typically not cause significant toxicity, while a self-harm attempt suggests a larger ingestion and greater potential for toxicity. (See 'Approach to a patient with a household product ingestion' above.)

●Cosmetics/personal care products – Exploratory cosmetic ingestions rarely cause serious toxicity even though these are the most common nonpharmaceutical household products involved in pediatric exposures. Exceptions include liquid products used to straighten or curl hair, which are highly alkaline and can cause esophageal ulceration and/or perforation. (See 'Cosmetic/personal care products' above.)

●Hydrogen peroxide – Hydrogen peroxide poisoning, especially from concentrated products (ie >10 percent solution), can cause air-gas embolism with potentially life-threatening toxicity such as hypoxia, seizures, cerebrovascular infarction, ventricular tachycardia, hypotension, and myocardial infarction. We obtain abdominal imaging in a patient with any gastrointestinal symptoms (eg, abdominal pain, nausea, vomiting) following a hydrogen peroxide ingestion. We prefer an abdominopelvic CT scan, but abdominal and chest radiographs are a reasonable alternative in a young child with an exploratory ingestion of household hydrogen peroxide who has transient abdominal pain or nausea and a normal physical examination.

In a patient with a hydrogen peroxide exposure and imaging showing extraluminal or portal venous gas (typically obtained for abdominal symptoms) or having any signs/symptoms attributed to systemic emboli (eg, stroke, myocardial infarction, obstructive shock), we suggest hyperbaric oxygen (Grade 2C). (See 'Hydrogen peroxide' above.)

●Toothpaste and fluoride-containing dental rinses – Fluoride toxicity is possible, albeit unlikely, from excess ingestion of toothpaste or dental rinses. Manifestations range from mild gastrointestinal symptoms to systemic complications of hypocalcemia (eg, seizures, tetany, decreased myocardial contractility, ventricular dysrhythmias).

A patient with a toothpaste or dental rinse ingestion with signs or symptoms of hypocalcemia (eg, carpopedal spasm, laryngospasm, bronchospasm, seizure) or electrocardiogram (ECG) changes (prolongation of the QT interval) requires intravenous (IV) calcium. We prefer calcium gluconate infused intravenously over 10 to 20 minutes (starting doses 100 to 200 mg/kg per dose in children; 1 to 2 grams in adults). (See 'Toothpaste and fluoride-containing dental rinses' above.)

●Household cleaning products – Exploratory ingestion of most standard liquid household cleaners or detergents does not cause significant toxicity. Exceptions include products used to clean porcelain, remove grease buildup from drains or other surfaces, clean or degrease ovens, concentrated single-use detergent packets ("capsules," "gel packs," or "pods"), and automotive wheel/tire cleaner. (See 'Cleaning products' above and 'Wheel and tire cleaner' above.)

●Mothballs – These may contain naphthalene, paradichlorobenzene, or camphor, and if not clearly labeled, the float test can be used to differentiate the active ingredient. Camphor mothballs are the most toxic (seizures) and least commonly available. Ingestion of naphthalene or paradichlorobenzene can cause nausea, vomiting, abdominal pain, methemoglobinemia, and/or hemolysis. (See 'Mothballs' above.)

●Pyrethroids and glyphosate pesticides – Exploratory small-volume ingestions of these common household pesticides do not typically cause significant toxicity. Large-volume pyrethroid ingestion can cause tremor, the "CS" syndrome (choreoathetosis and salivation), respiratory compromise, and metabolic acidosis with elevated lactate. Large-volume glyphosate ingestion can cause corrosive injury, acute kidney injury, acute respiratory distress syndrome, and other multiorgan derangements. Treatment is typically supportive. (See 'Pesticides/insecticides/herbicides' above.)