Front Page VSPN Message Boards Chat Library Continual Education Search MyVSPN Help Frequently Asked Questions Send us Feedback! Industry VetQuest Search & Referral and Classifieds The Pet Care Forum Y2Spay
Menu bar   Go to the Portal
Back Print Save Bookmark in my Browser Top of Page. Front Page : Library : Toxicology Of Household Hazards
Toxicology Of Common Household Hazards

Sharon Gwaltney-Brant DVM, PhD

Acids and Alkalis


Products containing acids include cleaning agents (e.g. toilet bowl cleaners), anti-rust compounds, etching compounds, automotive batteries, and pool sanitizers. The relative toxicity of an acid is related to its concentration and decreases with dilution. Acids produce localized coagulative necrosis of tissue and generally produce immediate pain upon exposure, which helps to limit ingestion.

In most cases, clinical signs occur almost immediately upon exposure. Oral exposure results in oral pain, vocalization, dysphagia, vomiting (+/- blood), abdominal pain, and irritation or ulceration of oral and/or esophageal mucosa. Lesions often appear milky white to gray initially, then gradually turn black. Esophageal lesions are less common than with alkaline products. With high levels of exposure, gastric ulceration is also possible. Dermal exposure results in dermal irritation or ulceration, accompanied by intense local pain. Inhalation of acid fumes may result in dyspnea, pulmonary edema, tracheobronchitis or pneumonitis. Ocular exposure may result in corneal erosion or ulceration.

Attempts to chemically neutralize with a weak alkali are contraindicated, as this may stimulate an exothermic reaction that will exacerbate tissue injury. Treatment of oral exposure includes immediate dilution with water or milk. Gastric lavage and induction of emesis are contraindicated due to the risk of increasing corrosive injury. Activated charcoal is ineffective for caustic agents and should not be used. Treatment of oral lesions is symptomatic, and should include antibiotics to prevent infection; pain management (butorphanol), sucralfate slurries to treat oral, esophageal or gastric ulcers; intravenous fluids to maintain hydration; and provision for nutritional support (e.g. gastrostomy tube). The use of corticosteroids to decrease inflammation and esophageal stricture formation is controversial, as steroids will delay wound healing and may increase susceptibility to infection. Dermal exposures should be treated with copious flushing with clear water for 15 minutes. For ocular exposures, eyes should be flushed with room temperature water or sterile saline solution for 15 minutes. Fluorescein staining of the eyes should be performed, and corneal erosion or ulceration should be treated as needed. Animals with significant respiratory signs (coughing, dyspnea, etc.) should be monitored for a minimum of 24 hours for the development of pulmonary edema. Supplemental oxygen or other respiratory supportive care should be used as needed.


Alkaline products include sodium or potassium hydroxide, ammonium hydroxide, sodium or potassium hydroxide, and potassium permanganate. Common sources of alkaline products include drain openers, automatic dishwasher detergents, alkaline batteries, toilet bowl cleaners, swimming pool products and radiator cleaning agents. Agents with pH greater than 11 should be considered to be capable of causing significant corrosive injury. Alkaline agents penetrate local tissue rapidly and deeply, causing liquefactive necrosis. Unlike acidic products, very little pain may be evident upon initial contact with an alkaline product, which may encourage further contact and ultimately result in more extensive exposures.

Clinical signs may not develop immediately, and it may require up to 12 hours for the full extent of tissue damage to become apparent. Acute signs include depression, hypersalivation, anorexia, oral inflammation or ulceration, smacking of lips, tongue flicking, dysphagia, vomiting (+/- blood), abdominal pain, and melena. Significant hyperthermia (>104° F) may accompany oral inflammation. Esophageal and/or pharyngeal ulceration may occur. Inhalation of corrosive material may result in coughing, dyspnea, and moist lung sounds. Sequelae can include esophageal perforations or strictures and pleuritis or peritonitis from leakage of ingesta through perforated mucosa.

As with oral acid exposures, emesis should NOT be induced and activated charcoal should not be given. Complete evaluation of the oral cavity and pharynx for ulceration or irritation should be performed upon presentation of the animal to the veterinarian, although with very recent exposures the oral cavity may appear normal. Evidence of oral discomfort and inflammation generally develop within 2 to 4 hours, although the full extent of injury may not be evident until 12 hours post exposure. It is important to remember that the absence of oral burns does not preclude the development of esophageal burns. Endoscopy may be elected for cases in which esophageal damage is a concern, although delaying endoscopy for 12 hours will allow the full extent of the burns to develop. Should mucosal burns develop, treatment should include antibiotics, pain medication as needed, gastrointestinal protectants (e.g. sucralfate), anti-inflammatories (corticosteroid use is controversial) and general supportive care. In cases with severe oral burns or esophageal burns, placement of a gastrostomy tube will facilitate nutritional support while allowing for mucosal healing. Esophageal lesions may take weeks to heal and there is risk of stricture formation, leading to impairment of esophageal function.

Albuterol Inhalers

Albuterol is a synthetic sympathomimetic amine that primarily has beta-2 adrenergic agonist activity. Albuterol inhalers are used for relief of bronchospasm in humans with obstructive airway disease, and they generally contain approximately 15-20 g of albuterol that is designed to be released in 90 microgram increments. When small animals puncture inhalers with their teeth, some or all of the contents may be propelled into the oral cavity, where it is rapidly absorbed.

Signs of albuterol toxicosis may develop within minutes of exposure to the inhaler. The most common signs associated with albuterol toxicosis are tachycardia, vomiting, depression, tachypnea, hyperactivity, muscle tremors, and weakness. A not infrequent comment regarding symptomatic dogs is that one can see their heart beating through the chest wall “from across the room,” signifying severe increase in the force of myocardial contraction. In addition, agitation, arrhythmia, nervousness, hypertension or hypotension, collapse, weakness, seizures, and death may occur. Some animals may experience an initial phase of hyperactivity, hypertension, and tachycardia that gives way to a “collapse” phase of depression, hypotension, bradycardia and, possibly, circulatory failure. Clinical laboratory abnormalities that have been associated with albuterol include profound hypokalemia (can be life-threatening), hypoglycemia, and hyperglycemia. In experimental exposures in dogs, doses of albuterol in excess of 0.28 mg/kg have been associated with myocardial fibrosis.

Because of the rapidity of absorption of albuterol from inhalers, decontamination is generally not feasible. Animals that have bitten into inhalers should be examined for evidence of tachycardia or other signs; if more than an hour has passed and the animal is asymptomatic, it is unlikely that signs will develop. Treatment for foreign body ingestion may be required in cases where parts of the inhaler have been ingested. Symptomatic animals often require prompt and aggressive care. Seizures, hyperactivity, tremors and agitation will generally respond to diazepam. Propranolol (preferred) or other beta-blocker should be used to manage severe tachycardia and/or arrhythmias. Fluid therapy should be initiated and maintained while the animal is symptomatic. Potassium and glucose levels should be closely monitored, and abnormalities, particularly hypokalemia, should be treated as needed. In dogs, signs generally resolve within 12 hours, although in some individuals, signs may persist up to 48 hours. The prognosis is generally good for cases where veterinary intervention is prompt and appropriate. Animals with pre-existing cardiac disease may be at increased risk for severe cardiac complications or death.


The alcohol toxicoses that veterinarians most commonly deal with involve ethanol, isopropanol, or methanol. Ethanol is present in a variety of products, including certain rubbing alcohols, drug formulations (especially elixirs), alcoholic beverages, and fermenting bread dough (see below). Isopropanol, which is twice as toxic as ethanol, is commonly used as a rubbing alcohol, a base for perfumes and cosmetics, and in alcohol-based flea sprays for pets. Methanol is most commonly encountered in the form of windshield washer fluid (windshield “antifreeze”). All are rapidly and completely absorbed from the GI tract, requiring that decontamination be done very soon following ingestion (within the first 20-30 minutes). Dermal absorption also occurs, and alcohol toxicosis is not uncommon in small cats or dogs that are over-treated with isopropanol alcohol based flea sprays; the presence of flea anemia or other debilitating condition enhances susceptibility to the effects of alcohol-based sprays.

Clinical signs of intoxication occur within 30-60 minutes of exposure and may include vomiting, diarrhea, ataxia, disorientation (inebriation), depression, tremors, and dyspnea. More severe signs include coma, hypothermia, seizures, bradycardia, premature ventricular contractions, and respiratory depression. Death is generally due to respiratory failure, hypothermia, hypoglycemia, and/or metabolic acidosis. The blindness that has been reported in humans with methanol toxicosis is not an issue in non-primates due to differences in methanol metabolism. Pneumonia secondary to aspiration of vomitus is possible.

Decontamination via emesis and/or activated charcoal is generally effective only within the first 20-40 minutes following ingestion due to the rapid GI absorption of alcohol. Bathing of animals with dermal exposures is recommended. Once signs develop, aggressive supportive care consisting of intravenous fluid therapy (diuresis enhances excretion), thermoregulation, and cardiovascular and respiratory support will be required. For seizures, diazepam is recommended, but it should be used with care as it will enhance CNS depression. Anecdotally, yohimbine has been used successfully to help reverse profound coma in dogs. Most animals given prompt, aggressive care will recover within 4 to 24 hours.

Ant and Roach Baits

Ant and roach baits are commonly used in homes and other buildings to control or eliminate ant/roach populations. The product names may vary, and the containers may be referred to as chambers, discs, stations, systems, traps, baits, or trays. Most ant/roach baits use some form of attractant, often peanut butter, some type of sweetening agent, and bread (a peanut butter and jelly sandwich for the insects). Pets are attracted by the odor of the peanut butter or other attractant and will chew open the bait to get at the attractant. In many instances, the risk of foreign body obstruction from the plastic or metal part of the bait is of larger concern than the ingredients. While these baits once could contain compounds of relatively high mammalian toxicity (e.g. arsenic trioxide, lead arsenate), most manufacturers now use ingredients that, in the amounts used in ant/roach baits, pose little to no hazard to most mammalian pets. Birds vary in their sensitivity to the individual ingredients, and, due to their size, birds may ingest a potentially harmful dose of insecticide from ant and roach baits.

Some of the more common active ingredients in roach/ant baits include avermectins (e.g. abamectin B), bendiocarb, boric acid, chlorpyrifos, fipronil, hydramethylnon, propoxur, sodium borate, and sulfluramid. Dr. Wismer discussed several of these compounds in a previous session, and further information on these agents may be found by using the EXTOXNET web search engine ( These agents have very high mammalian LD50s and are present in very small quantities within the baits, making them of low toxicity hazard to dogs and cats. Some, such as boric acid and sodium borate, can cause mild gastrointestinal upset, as can the stale peanut butter. Generally any gastrointestinal signs that might develop from ingestion of ant/roach bait contents will occur within an hour of ingestion. No specific treatment is needed other than management for potential foreign body obstruction if the plastic or metal part of the bait is ingested.


Flashlights, remote controls, battery-operated toys, watches, calculators, hearing aids, etc. all provide the opportunity for pets, especially dogs, to be exposed to alkaline or disc batteries. Most alkaline dry cell batteries use potassium hydroxide or sodium hydroxide to generate current, and disc, nickel-cadmium, and silver batteries are generally of the alkaline type. The alkaline gel within a battery cause liquefactive necrosis of tissue, resulting in burns that can penetrate deeply into the local tissue. Lithium disc batteries tend to lodge in the esophagus, increasing the risk of esophageal ulceration. In addition, batteries casings may result in respiratory or gastrointestinal obstruction if inhaled or swallowed.

When batteries are chewed and the contents released, alkaline burns result (see Alkali section). Signs of foreign body obstruction (vomiting, anorexia, tenesmus, etc) may occur when casings are swallowed; disc batteries may be inhaled, resulting in acute dyspnea and cyanosis.

Treatment of battery exposures is as for exposure to any alkaline product (see Alkali section). In the case of lithium batteries, administration of tap water in 20 ml boluses every 15 minutes has been shown to decrease the severity and delay the development of current-induced tissue injury in dogs. Radiography to determine the location of the battery casing should be performed in cases where the casing is missing. The decision to remove a battery present in the stomach depends on the size of the animal, battery size, and evidence of battery puncture. Batteries that are small relative to the size of the animal will often pass uneventfully through the GI tract and into the stools. Bulky diets may assist in the passage of the battery. If the battery is not seen in the stools within 3 days of ingestion, radiography is recommended to verify the location of the battery. Batteries that have not passed thorough the pylorus within 48 hours are unlikely to do so and may require endoscopic or surgical removal, although endoscopic removal is not recommended in cases where there is suspicion that the battery has been punctured.

Birth Control Pills

Birth control pills are oral contraceptives that contain combinations of progesterone and estrogen. There are 4 main types of birth control pills: monophasic, biphasic, triphasic, and third generation. The "phasic" birth control pills have different concentrations of progesterone for each phase. The "phasics" also may have different concentrations of estrogen for each phase as well. Remember that in most cases, a 28-pill pack will contain 7 placeboes. Some birth control pills contain iron in addition to the hormones. In general, the levels of progesterone in birth control pills are not a concern for single acute exposures, as relatively high doses of progesterones may be used in dogs and cats for behavior disorders. The primary concerns are the estrogen levels and the iron levels, if any.

Estrogen levels in birth control pills may range from 0.035 mg to 40 mg per pill. High doses of estrogens have been associated with blood dyscrasias in small animals, although this is most commonly seen with multiple doses or chronic administration of estrogens. In general, single acute doses below 1 mg/kg of estrogen should be considered to be unlikely to cause bone marrow changes. Animals ingesting >1 mg/kg of estrogen should be decontaminated (emesis, activated charcoal) if within 2 hours of ingestion. Depending on the dose and whether the animal was promptly decontaminated, monitoring of the CBC may be indicated to detect evidence of bone marrow suppression. A baseline CBC should be obtained, then the CBC should be repeated twice weekly for 2-3 weeks. If evidence of bone marrow suppression exists (sequential decreases in WBC), the CBC should be monitored over the next 4-6 weeks. Should the WBC level drop to dangerously low levels, the use of filgrastim (NeupogenÒ), a granulocyte colony stimulating factor, may be considered to attempt to stimulate the bone marrow. Platelets and RBCs should be similarly monitored; epoetin alfa (EpogenÒ) may be considered if non-regenerative anemia develops.

Iron levels of 20 mg/kg or more may be associated with corrosive gastroenteritis; at 40 mg/kg or more, significant hepatic damage may occur. Decontamination should consist of early emesis. Activated charcoal will generally not bind iron, but magnesium hydroxide (milk of magnesia) may decrease iron absorption by binding to iron in the GI tract.

Bread Dough

Raw bread dough made with yeast poses mechanical and biochemical threats to animals ingesting it. The warm, moist gastric environment stimulates yeast growth, resulting in expansion of the dough mass, resulting in gastric distention, which if severe, can result in respiratory and vascular compromise. Perhaps more significant is the release of alcohol from yeast fermentation, resulting in profound metabolic acidosis, CNS depression and death.

Early clinical signs may include unproductive attempts at emesis, abdominal distention, and depression. As alcohol intoxication develops, the animal becomes ataxic and disoriented. Eventually, profound CNS depression, weakness, recumbency, coma, hypothermia may occur.

Management of exposure includes decontamination and treatment for alcohol toxicosis. Because emesis is often unsuccessful, cold-water gastric lavage is initially recommended (the cold water may slow down yeast reproduction, thereby decreasing alcohol production). The veterinarian should be prepared to perform gastrotomy should the lavage fail to remove the bulk of the dough mass due to the glutinous nature of the dough. Treatment for alcohol intoxication should proceed as previously described.


There are a wide variety of chocolate and cocoa products to which pets may be exposed, including candies, cakes, cookies, brownies, and cocoa bean mulches. Not surprisingly, the incidence of accidental chocolate exposures in pets occurs around holidays, especially Easter, Halloween and Christmas. The active (toxic) agents in chocolate are methylxanthines, specifically theobromine and caffeine. Methylxanthines stimulate the CNS, act on the kidney to stimulate diuresis, and increase the contractility of cardiac and skeletal muscle. The relative amounts of theobromine and caffeine will vary with the form of the chocolate (see table).

Milligrams per ounce
Compound Theobromine Caffeine
White Chocolate 0.25 0.85
Milk Chocolate 58 6
Semi-sweet Chocolate chips 138 22
Baker’s Chocolate (unsweetened) 393 47
Dry cocoa powder 737 70

Cocoa beans may contain up to 255 mg theobromine per ounce of beans, although the exact amount will vary due to natural variation of the cocoa beans. The LD50’s of theobromine and caffeine are 100-300 mg/kg, but severe and life threatening clinical signs may be seen at levels far below these doses. Based on NAPCC experience, mild signs have been seen with theobromine levels of 20 mg/kg, severe signs have been seen at 40-50 mg/kg, and seizures have occurred at 60 mg/kg. Accordingly, less than 2 ounces of milk chocolate per kg is potentially lethal to dogs.

Clinical signs occur within 6-12 hours of ingestion. Initial signs include polydypsia, bloating, vomiting, diarrhea, and restlessness. Signs progress to hyperactivity, polyuria, ataxia, tremors, seizures, tachycardia, PVC’s, tachypnea, cyanosis, hypertension, hyperthermia, and coma. Death is generally due to cardiac arrhythmias or respiratory failure. Hypokalemia may occur later in the course of the toxicosis. Because of the high fat content of many chocolate products, pancreatitis is a potential sequela.

Management of chocolate ingestion includes decontamination via emesis followed by gastric lavage. Because methylxanthines undergo enterohepatic recirculation, repeated doses of activated charcoal are usually of benefit in symptomatic animals (vomiting may need to be controlled with metaclopramide). Intravenous fluids at twice maintenance levels will help maintain diuresis and enhance urinary excretion. Because caffeine can be reabsorbed from the bladder, placement of a urinary catheter is recommended. Cardiac status should be monitored via EKG and arrhythmias treated as needed; propranolol reportedly delays renal excretion of methylxanthines, so metoprolol is the beta-blocker of choice. Seizures may be controlled with diazepam or a barbiturate. In severe cases, clinical signs may persist up to 72 hours.


Non-ionic and Anionic Detergents

Non-ionic and anionic detergents are found in a wide variety of household products, including body soaps, shampoos, dishwashing detergents, various household cleaners, etc. These products are gastrointestinal and ocular irritants with few to no systemic effects.

Clinical signs consist of hypersalivation, vomiting, and diarrhea, and are generally mild and self limiting, although ingestion of large quantities may result in more severe vomiting (+/- blood) requiring veterinary intervention. Protracted vomiting may also cause dehydration and electrolyte abnormalities necessitating parenteral fluid therapy.

Management includes symptomatic treatment for gastric upset and parenteral fluid therapy, if indicated. Ocular exposures should be treated by flushing eyes with room temperature water or sterile saline solution for 5 minutes. While corneal injury is unlikely, if persistent photophobia, blepharospasm, or lacrimation should occur, the eye should be fluorescein stain to rule out corneal erosions or ulcers.

Cationic Detergents

Cationic detergents are contained in fabric softeners, some potpourri oils, hair mousse, algaecides, germicides and sanitizers. Cationic detergents are more toxic than non-ionic/anionic detergents and can cause extensive systemic and local effects at levels as low as 2% or less.

Local tissue injury caused by cationic detergents resembles that seen with exposure to alkaline products (see Alkali section). In addition, cationic detergents can cause systemic toxicity including CNS depression, coma, seizures, hypotension, muscular weakness and fasciculations, collapse, pulmonary edema, and metabolic acidosis; the mechanism of these signs is not known.

Treatment of local exposure is similar to that for alkaline products (see Alkali section). Systemic signs should be treated symptomatically (i.e. fluids for hypotension, diazepam for seizures, etc.).

Moldy Food (Tremorgenic mycotoxins)

Tremorgenic mycotoxins produced by molds on foods are a relatively common, and possibly under-diagnosed, cause of tremors and seizures in pet animals. Because of their relatively indiscriminate appetites, dogs tend to be most commonly exposed to tremorgens. These toxins are produced from a variety of fungi, however tremorgens produced by Penicillium spp. are the most commonly encountered. These molds grow on practically any food, including dairy products, grains, nuts, and legumes; compost piles may also provide a source of tremorgens. Tremorgens have a several different mechanisms of actions: some alter nerve action potentials, some alter neurotransmitter action, and while others alter neurotransmitter levels. The overall affect is the development of muscle tremors and seizures.

Clinical signs include fine muscle tremors that may rapidly progress to more severe tremors and seizures. Death generally occurs in the first 2 to 4 hours and is usually secondary to respiratory compromise, metabolic acidosis or hyperthermia. Other signs that may be seen include vomiting (common) hyperactivity, depression, coma, behavior alterations, tachycardia, and pulmonary edema.

Asymptomatic animals exposed to moldy foods should be decontaminated via emesis or lavage followed by activated charcoal and cathartic. In symptomatic animals, control of severe tremors or seizures has priority over decontamination. Seizures may respond to diazepam, however others have had better success with methocarbamol (RobaxinÒ; 55-220 mg/kg IV to effect), especially in seizuring animals. Barbiturates may be used in animals that are unresponsive to other anticonvulsants. Supportive care should include intravenous fluids, thermoregulation, and correction of electrolyte and acid-base abnormalities. In severe cases, signs may persist for several days, and residual fine muscle tremors may take a week or more to fully resolve. Testing of stomach content, suspect foods, or vomitus for tremorgens is available through the Animal Health Diagnostic Laboratory, Michigan State University (517-355-0281).


Mothballs may be composed of either 100% naphthalene or 99% paradichlorobenzene. Naphthalene-based mothballs are approximately twice as toxic as paradichlorobenzene, and cats are especially sensitive to naphthalene. Naphthalene causes Heinz bodies, hemolysis, and, occasionally, methemoglobinemia in dogs with doses of 411 mg/kg or more (one 2.7 g mothball contains 2700 mg of naphthalene). Paradichlorobenzene primarily affects the liver and CNS, although methemoglobinemia and hemolysis have been reported in humans.

Signs of ingestion of naphthalene mothballs include emesis (early), weakness, icterus, lethargy, icterus, brown-colored mucous membranes, and collapse. Rarely, hepatitis has been reported 3-5 days post-ingestion. Paradichlorobenzene mothballs may cause GI upset, ataxia, disorientation, and depression. Elevations in liver serum biochemical values may occur within 72 hours of ingestion.

Treatment of mothball ingestion includes early emesis, activated charcoal, and cathartic. Treatment for hemolysis or methemoglobinemia (blood replacement therapy, methylene blue, etc) may be necessary. Intravenous fluid diuresis should be maintained in cases with hemolysis in order to minimize the risk of hemoglobin-induced renal nephrosis. Evidence of hepatic damage, based on biochemical values, would indicate that symptomatic therapy for general liver failure (oral antibiotics, lactulose, dietary management, etc) should be instituted.


Ingestion of coins by pets, especially dogs, is not uncommon. Of the existing US coins currently in circulation, only pennies pose a significant toxicity hazard. Pennies minted since 1983 contain 99.2% zinc and 0.8% copper, making ingested pennies a rich source of zinc. Other potential sources of zinc include hardware such as screws, bolts, nuts, etc., all of which may contain varying amounts of zinc. In the stomach, gastric acids leach the zinc from its source, and the ionized zinc is readily absorbed into the circulation, where it causes intravascular hemolysis.

The most common clinical signs of penny ingestion are vomiting, depression, anorexia, hemoglobinuria, diarrhea, weakness, collapse and icterus. Secondarily, acute renal failure may develop. Clinical laboratory abnormalities will be suggestive of hemolysis (elevated bilirubin, hemoglobinemia, hemoglobinuria, regenerative anemia) and may also indicate the development of kidney failure. Serum zinc levels may be obtained-blood should be collected in all plastic syringes (no rubber grommets) and shipped in Royal blue top vaccutainers to minimize contamination with exogenous zinc. Radiography of the abdomen may reveal the presence of coins or other “hardware” within the stomach.

Treatment for recently ingested pennies would include induction of vomiting. Activated charcoal is not indicated, as it is of little benefit in binding metals. Removal of zinc-containing foreign bodies via endoscopy or gastrotomy/enterotomy may be required. Treatment for symptomatic animals should include blood replacement therapy as needed, intravenous fluids, and other supportive care. The use of chelators may not be necessary in cases where prompt removal of the zinc source is accomplished. If chelation therapy is instituted, careful monitoring of renal parameters is important for the duration of therapy.


Liquid potpourri may contain essential oils and cationic detergents; because product labels may not list ingredients, it is wise to assume that a given liquid potpourri contains both ingredients. Essential oils can cause mucous membrane and gastrointestinal irritation, central nervous system depression, and dermal hypersensitivity and irritation. Severe clinical signs can be seen with potpourri products that contain cationic detergents. Dermal exposure to cationic detergents can result in erythema, edema, intense pain, and ulceration. Ingestion of cationic detergents may lead to tissue necrosis and inflammation of the mouth, esophagus, and stomach. Treatment is symptomatic and supportive (see Cationic Detergent section).

Suggested Readings

Drolet R, Arendt TD, Stowe CM. Cacao bean shell poisoning in a dog. J. Am. Vet. Med. Assoc. Vol 185(8): 902, 1984.

Kore, AM, Nesselrodt A. Household cleaning products and disinfectants. Vet. Clin. North Am. Small Anim. Pract. Vol 20(2): 525-537, 1990.

Robinette CL. Zinc. Vet. Clin. North Am. Small Anim. Pract. Vol 20(2): 529-544, 1990.

Schell, MM. Tremorgenic mycotoxin intoxication. Vet. Med. Vol 95(4):

Tanaka J, Yamashita M, Yamashita M, Kajigaya H. Effects of tap water on esophageal burns in dogs from button lithium batteries. Vet. Hum. Toxicol. Vol 41(5): 279-282, 1999.

Tanaka J, Yamashita M, Yamashita M, Kajigaya H. Esophageal electrochemical burns due to button type lithium batteries in dogs. Vet. Hum. Toxicol. Vol 40(4): 193-196, 1998.

Valentine WM. Short-chain alcohols. Vet. Clin. North Am. Small Anim. Pract. Vol 20(2): 515-524, 1990.

Address (URL):

Back Print Save Bookmark in my Browser Top of Page. Front Page : Library : Toxicology Of Household Hazards

800.700.4636  |  |  530.756.4881  |  Fax: 530.756.6035
777 West Covell Blvd, Davis, CA 95616

Copyright , Veterinary Information Network, Inc.