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FERTILIZERS

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Fertilizers are any organic or inorganic material of natural or synthetic origin (other than liming materials) that is added to soil to supply one or more plant nutrients essential to the growth of plants. They contain three primary elements - nitrogen, phosphorus, and potassium - usually represented by their chemical symbols: N, P and K, respectively.

Specific Substances

    1) FERTILIZER
    2) FERTILIZER AMMONIATING SOLUTION, WITH MORE THAN 35% FREE AMMONIA

Available Forms Sources

    A) SOURCES
    1) Fertilizers contain three primary elements - nitrogen, phosphorus, and potassium - usually represented by their chemical symbols: N, P and K, respectively.
    2) Gardeners and farmers use another shortened term - three numbers in a row (eg: 10-8-6), representing the percentages of N, P and K by weight. A fertilizer that contains all three of these primary elements is called a complete fertilizer.
    3) Superphosphate is a phosphate rock treated with sulfuric acid, calcium hydrogen phosphate, calcium phosphate, and calcium sulfate. It contains calcium fluoride 3 to 4% and calcium sulfate 50% (Gosselin et al, 1984).
    4) Triple superphosphate contains all calcium as calcium phosphate (Gosselin et al, 1984).
    5) Sources of nitrogen (N) include (Tech Info, 1986)
    1) Bone meal
    2) Ammonium nitrate
    3) Ammonium sulfate
    4) Diammonium phosphate
    5) Fish meal
    6) Monoammonium phosphate
    7) Process sewage
    8) Seaweed
    9) Sulfur-coated urea
    10) Urea
    6) Sources of phosphorus (P) include
    1) Bone meal
    2) Diammonium phosphate
    3) Monoammonium phosphate
    4) Process sewage
    5) Superphosphate
    6) Triple super phosphate
    7) Sources of potassium (K) include
    1) Muriate of potash
    2) Sulfate of potash
    8) Trace elements may include
    1) Boron
    2) Calcium
    3) Copper
    4) Iron
    5) Magnesium
    6) Manganese
    7) Molybdenum
    8) Sulfur
    9) Zinc
    B) USES
    1) Fertilizers are any organic or inorganic material of natural or synthetic origin (other than liming materials) that is added to soil to supply one or more plant nutrients essential to the growth of plants.

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Fertilizers are any organic or inorganic material of natural or synthetic origin (other than liming materials) that is added to soil to supply one or more plant nutrients essential to the growth of plants.
    B) TOXICOLOGY: In general, liquid and granular fertilizers have a low degree of toxicity, causing mild gastrointestinal irritation. Conversion of nitrates to nitrites by bacterial action in the intestine may result in methemoglobinemia.
    C) EPIDEMIOLOGY: This is a relatively uncommon poisoning, with approximately 5400 exposures reported to US poison centers in 2012. Severe poisoning is exceedingly rare, with only 35 patients (less than 1%) experiencing moderate clinical outcomes or major clinical outcomes, and there were no reported deaths. Large fertilizer overdoses produce mild to moderate symptoms with very few confirmed fatalities reported in the literature. The exception to this rule is anhydrous ammonia, which can cause severe corrosive injuries.
    D) WITH POISONING/EXPOSURE
    1) All information about adverse effects following fertilizer exposure is from a few case reports with most useful information coming from the primary component of each fertilizer. Please refer to appropriate management for further information for each major ingredient (eg, phosphorus, potassium, iron, copper, zinc, ammonia).
    2) MILD TO MODERATE TOXICITY: In some cases, nausea, vomiting, and diarrhea may be noted. Inhalation can cause mild irritation of oral or nasal mucous membranes. Skin and eye irritation, corneal edema, and contact dermatitis may also develop.
    3) SEVERE TOXICITY: Anhydrous ammonia can cause severe corrosive injuries and because of its prevalence on farms should be suspected as a causative agent in all corrosive injuries. Methemoglobinemia may develop due to the presence of nitrates in some fertilizers. ECG abnormalities, hyperkalemia, metabolic acidosis, and acute renal failure have developed with some fertilizers that contain metals and electrolytes.
    0.2.21) CARCINOGENICITY
    A) A link between nitrate exposure and gastric carcinoma has been suggested but not borne out by studies. One study suggests a possible association between occupational exposure to phosphate fertilizers and lung cancer.

Laboratory Monitoring

    A) Most patients do not require laboratory evaluation.
    B) Measurement of methemoglobin concentrations, CBC, and electrolytes should be determined based on clinical signs.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive. Patients with mild to moderate exposure, through either dermal, inhalational, or oral exposure, are usually asymptomatic.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Patients with severe toxicity, through either dermal, inhalational, or oral exposure, can develop methemoglobinemia due to the presence of nitrates, ECG abnormalities, hyperkalemia, metabolic acidosis, and acute renal failure. Treat patients with aggressive supportive care; an investigation into the offending fertilizer's active ingredients should be undertaken. Please refer to appropriate management for further information for each major ingredient (eg, phosphorus, potassium, iron, copper, zinc, ammonia). Given the corrosive nature of anhydrous ammonia and other compounds, there should be a high clinical suspicion for corrosive injury. Other metals and electrolytes can cause nausea and vomiting as well as ECG abnormalities, hyperkalemia, metabolic acidosis, and acute renal failure. With significant ingestion, endoscopy should be considered early in these patients.
    C) DECONTAMINATION
    1) PREHOSPITAL: No oral decontamination is indicated. DERMAL EXPOSURE: Wash exposed areas with soap and water. EYE EXPOSURE: Irrigate exposed eyes with copious amounts of room temperature normal saline or water.
    2) HOSPITAL: No oral decontamination is indicated. DERMAL EXPOSURE: Wash exposed areas with soap and water. EYE EXPOSURE: Irrigate exposed eyes with copious amounts of room temperature normal saline or water.
    D) AIRWAY MANAGEMENT
    1) Exposures should be treated according to their active ingredients; however, given the corrosive nature of some fertilizers, intubation may be indicated for airway protection based on clinical signs.
    E) ANTIDOTE
    1) Methemoglobinemia from nitrate exposure may be treated with methylene blue. There is no specific antidote for other common fertilizer components.
    F) METHEMOGLOBINEMIA
    1) Initiate oxygen therapy. Treat with methylene blue if patient is symptomatic (usually at methemoglobin concentrations greater than 20% to 30% or at lower concentrations in patients with anemia, underlying pulmonary or cardiovascular disease). METHYLENE BLUE: INITIAL DOSE/ADULT OR CHILD: 1 mg/kg IV over 5 to 30 minutes; a repeat dose of up to 1 mg/kg may be given 1 hour after the first dose if methemoglobin levels remain greater than 30% or if signs and symptoms persist. NOTE: Methylene blue is available as follows: 50 mg/10 mL (5 mg/mL or 0.5% solution) single-dose ampules and 10 mg/1 mL (1% solution) vials. Additional doses may sometimes be required. Improvement is usually noted shortly after administration if diagnosis is correct. Consider other diagnoses or treatment options if no improvement has been observed after several doses. If intravenous access cannot be established, methylene blue may also be given by intraosseous infusion. Methylene blue should not be given by subcutaneous or intrathecal injection. NEONATES: DOSE: 0.3 to 1 mg/kg.
    G) ENHANCED ELIMINATION PROCEDURE
    1) Enhanced elimination is rarely required for fertilizer exposures.
    H) PATIENT DISPOSITION
    1) HOME CRITERIA: Asymptomatic patients can be managed at home. Any patient with altered mental status, weakness, pain or syncope should be evaluated at a healthcare facility. Patients with ocular exposure and/or severe dermal exposure to anhydrous ammonia should be evaluated at a healthcare facility.
    2) OBSERVATION CRITERIA: Patients with altered mental status, weakness, pain or syncope should be evaluated at a healthcare facility and observed until signs and symptoms improve. Patients with ocular exposure and/or severe dermal exposure to anhydrous ammonia should be evaluated at a healthcare facility.
    3) ADMISSION CRITERIA: Only rarely will patients require hospital admission. Patients may require admission for significant methemoglobinemia, hemolysis, hypotension, signs of severe corrosive injury, or other signs of significant illness.
    4) CONSULT CRITERIA: If patients develop respiratory failure, hemodynamic instability, or any other symptoms not expected with this exposure, consult a toxicologist or regional poison center. If patients have signs of oropharyngeal burns or a high suspicion of gastric injury, ENT and/or GI specialists should be consulted. Consult an ophthalmologist for cases of significant ocular exposure to anhydrous ammonia.
    I) PITFALLS
    1) Common errors for managing these patients include failing to identify the active ingredients, rapidly irrigating skin and eyes exposed to anhydrous ammonia, and recognizing corrosive injuries.
    J) DIFFERENTIAL DIAGNOSIS
    1) Other chemicals or drugs that cause methemoglobinemia or GI tract irritation.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) TOXICOLOGY: In general, liquid and granular fertilizers have a low degree of toxicity, causing mild gastrointestinal irritation. However, anhydrous ammonia (frequently used on farms) is very corrosive and can cause significant burns to skin and mucous membranes. See ammonia management for further information. An elderly adult was found dead following an intentional ingestion of an unknown amount of fertilizer containing ammonium sulfate. Ingestion of 700 mL of a fertilizer, consisting of nitrogen, phosphorus, potassium, manganese, iron, copper, and zinc, resulted in the development of ECG abnormalities, hyperkalemia, metabolic acidosis, acute renal failure, and mild methemoglobinemia. The patient recovered with supportive care. Please refer to appropriate management for further information for each major ingredient (eg, phosphorus, potassium, iron, manganese, copper, zinc, ammonia).

Clinical Effects

Summary Of Exposure

    A) USES: Fertilizers are any organic or inorganic material of natural or synthetic origin (other than liming materials) that is added to soil to supply one or more plant nutrients essential to the growth of plants.
    B) TOXICOLOGY: In general, liquid and granular fertilizers have a low degree of toxicity, causing mild gastrointestinal irritation. Conversion of nitrates to nitrites by bacterial action in the intestine may result in methemoglobinemia.
    C) EPIDEMIOLOGY: This is a relatively uncommon poisoning, with approximately 5400 exposures reported to US poison centers in 2012. Severe poisoning is exceedingly rare, with only 35 patients (less than 1%) experiencing moderate clinical outcomes or major clinical outcomes, and there were no reported deaths. Large fertilizer overdoses produce mild to moderate symptoms with very few confirmed fatalities reported in the literature. The exception to this rule is anhydrous ammonia, which can cause severe corrosive injuries.
    D) WITH POISONING/EXPOSURE
    1) All information about adverse effects following fertilizer exposure is from a few case reports with most useful information coming from the primary component of each fertilizer. Please refer to appropriate management for further information for each major ingredient (eg, phosphorus, potassium, iron, copper, zinc, ammonia).
    2) MILD TO MODERATE TOXICITY: In some cases, nausea, vomiting, and diarrhea may be noted. Inhalation can cause mild irritation of oral or nasal mucous membranes. Skin and eye irritation, corneal edema, and contact dermatitis may also develop.
    3) SEVERE TOXICITY: Anhydrous ammonia can cause severe corrosive injuries and because of its prevalence on farms should be suspected as a causative agent in all corrosive injuries. Methemoglobinemia may develop due to the presence of nitrates in some fertilizers. ECG abnormalities, hyperkalemia, metabolic acidosis, and acute renal failure have developed with some fertilizers that contain metals and electrolytes.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) SUMMARY: Eye contact may produce irritation. Alkaline fertilizers can produce severe corneal injury (see ammonia or alkaline corrosive management).
    2) IRRITATION: Eye contact with fertilizers may produce irritation and pain (Anon, 1979). Granular products may cause corneal abrasion (Blake, 1975).
    3) ANIMAL STUDY: Brief exposure to rabbit eyes of neutral ammonium salts used in fertilizers (ammonium nitrate or ammonium phosphate) produced no adverse effects. Prolonged exposure to continuous drops for 3 hours or longer produced corneal epithelium edema (Grant & Schuman, 1993).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) IRRITATION: Inhalation of dusts or mists of fertilizer mixtures may cause nose and throat irritation (Tech Info, 1986).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) ELECTROCARDIOGRAM ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Right bundle branch block with peaked T-waves in V3 - V6 leads were observed on the ECG of a 64-year-old man, with a history of right bundle branch block, who developed hyperkalemia (7.3 mEq/l) following ingestion of approximately 700 mL of a fertilizer. The fertilizer consisted of nitrogen, phosphorus, potassium, manganese (222,000 mcg/L), iron (276,000 mcg/L), zinc (104,000 mcg/L), and copper (80,000 mcg/L). Following a 4-hour hemodialysis session, his renal failure, hyperkalemia, and the peaked T-waves resolved, although his complete right bundle branch block remained (Huang & Lin, 2004).
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CARDIAC ARREST
    a) Cardiac and respiratory arrest were reported in rabbits within 60 minutes of exposure to ammonium sulfate (used in agricultural and home fertilizers) after receiving a total dose of 1500 mg/kg (Sato et al, 1999a).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) INJURY DUE TO ASPHYXIATION
    1) WITH POISONING/EXPOSURE
    a) A feeling of suffocation is common as well as the inability to speak due to laryngeal edema which occurs almost immediately on exposure to anhydrous ammonia (Anon, 1979).
    B) STRIDOR
    1) WITH POISONING/EXPOSURE
    a) LARYNGEAL STRIDOR: Laryngeal stridor is almost universally present after exposure to anhydrous ammonia (Anon, 1979).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) NEUROLOGICAL FINDING
    1) WITH POISONING/EXPOSURE
    a) LACK OF EFFECT
    1) ALS RISK ASSESSMENT: Using a small survey study of 54 patients with amyotrophic lateral sclerosis, Norris & Padia (1989) determined that these patients had no more exposure to Milorganite fertilizer than matched controls (Norris & Padia, 1989).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SEIZURES
    a) In a toxicological study using rabbits, a total dose of 1500 mg/kg of ammonium sulfate (used in agricultural and home fertilizers) was given and generalized seizures were reported within 15 to 25 minutes of ingestion. All rabbits died within approximately 1 hour of exposure from cardiac and respiratory arrest (Sato et al, 1999a).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) GASTRITIS
    1) WITH POISONING/EXPOSURE
    a) Generally, ingestion of fertilizers containing only the 3 main elements (nitrogen, phosphorus and potassium) usually causes no symptoms other than nausea, with possible vomiting, cramps, and diarrhea (Tech Info, 1986; (Haddad et al, 1998).
    b) CASE REPORT: Crampy abdominal pain was reported in a 64-year-old man who ingested 700 mL of a fertilizer containing nitrogen, phosphorus, potassium, manganese, iron, zinc, and copper. An endoscopy revealed superficial gastritis (Huang & Lin, 2004).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ACUTE RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Acute renal failure was reported in a 64-year-old man following ingestion of approximately 700 mL of a fertilizer. The fertilizer consisted of nitrogen, phosphorus, potassium, manganese (222,000 mcg/L), iron (276,000 mcg/L), zinc (104,000 mcg/L), and copper (80,000 mcg/L). Laboratory analysis showed elevated serum creatinine and BUN levels (3.4 mg/dL and 43 mg/dL, respectively) and hyperkalemia (7.3 mEq/L). A urinalysis revealed proteinuria (25 mg/dL), hematuria (RBC 10/mcL), and glucosuria (300 mg/dL). The patient's whole blood manganese level was 195 mcg/L (total amount of manganese ingested was approximately 155 mg). Following supportive care and hemodialysis, the patient recovered and was discharged 1 week post-ingestion (Huang & Lin, 2004).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Metabolic acidosis (pH 7.214, pCO2 22.5 mmHg, pO2 88.6 mmHg, HCO3 8.9 mm/L) was reported in a 64-year-old man following ingestion of approximately 700 mL of a fertilizer. The fertilizer consisted of nitrogen, phosphorus, potassium, manganese (222,000 mcg/L), iron (276,000 mcg/L), zinc (104,000 mcg/L), and copper (80,000 mcg/L). Following ingestion, the patient also developed acute renal failure (creatinine 3.4 mg/dL and BUN 43 mg/dL), hyperkalemia (7.3 mEq/L), and mild methemoglobinemia (2.4%). The patient's whole blood manganese level was 195 mcg/L (total amount of manganese ingested was approximately 155 mg). Following supportive care and hemodialysis, the patient recovered and was discharged 1 week post-ingestion (Huang & Lin, 2004).
    3.11.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ACIDOSIS
    a) Sato et al (1999) studied the effects of ammonium sulfate used in many agricultural and home fertilizers and reported that seizure activity (untreated) was followed by severe metabolic acidosis (pH 6.629, pCO2 mmHg 44.1, pO2 75.4 mmHg, HCO3 4.2 (mM/I)). The total dose was 1500 mg/kg with fatal cardiac arrest occurring in all animals exposed (Sato et al, 1999).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) METHEMOGLOBINEMIA
    1) WITH POISONING/EXPOSURE
    a) Conversion of nitrates to nitrites by bacterial action in the intestine may result in methemoglobinemia in a child less than one year of age.
    b) CASE REPORT: A methemoglobin level of 2.4% (normal 1.4% to 1.5%) was reported in a 64-year-old man following ingestion of approximately 700 mL of a fertilizer. The fertilizer consisted of nitrogen, phosphorus, potassium, manganese (222,000 mcg/L), iron (276,000 mcg/L), zinc (104,000 mcg/L), and copper (80,000 mcg/L) (Huang & Lin, 2004).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) Repeated or prolonged exposure may cause irritation, redness, and dermatitis (Tech Info, 1986).
    B) CONTACT DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Contact dermatitis has been reported from use of calcium ammonium nitrate and nickel containing fertilizers (Pasricha & Gupta, 1983) Petcegueiro, 1990).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) FLUOROSIS
    1) WITH POISONING/EXPOSURE
    a) Skeletal fluorosis has been described in workers in superphosphate fertilizer production (Grandjean, 1982).

Carcinogenicity

    3.21.2) SUMMARY/HUMAN
    A) A link between nitrate exposure and gastric carcinoma has been suggested but not borne out by studies. One study suggests a possible association between occupational exposure to phosphate fertilizers and lung cancer.
    3.21.3) HUMAN STUDIES
    A) GASTRIC CARCINOMA
    1) A link between nitrate exposure and gastric carcinoma has been suggested but not borne out by studies. One study suggests a possible association between occupational exposure to phosphate fertilizers and lung cancer.
    a) NITRATES - There was no increased risk in mortality from carcinomas in a study of 1327 male workers in a fertilizer production plant using nitrates (Al-Dabbagh et al, 1986).
    b) Fraser (1985) concluded that there is no convincing epidemiological evidence that dietary nitrate is associated with the development of stomach cancer.
    c) A cohort of 862 men who worked in the nitrate fertilizer-producing industry was followed from 1961 through 1985. Results showed a low mortality from all causes and all cancers and no evidence of excess morbidity from any type of cancer when compared to the control population (Fraser et al, 1989).
    d) A slight increase in stomach cancer incidence was seen in a group of 1756 male workers at a nitrate fertilizer plant; no increased risk for total cancers was seen (Zandjani et al, 1994).
    B) PULMONARY CARCINOMA
    1) PHOSPHATES - An excess in lung cancer mortality was seen in a retrospective study of 3,199 workers in a phosphate fertilizer production facility. Only workers with more than 10 years of employment had an increased risk and the study did not control for smoking (Stayner et al, 1985).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Most patients do not require laboratory evaluation.
    B) Measurement of methemoglobin concentrations, CBC, and electrolytes should be determined based on clinical signs.

Methods

    A) OTHER
    1) If methemoglobinemia is suspected, initial bedside determination can be made by placing a drop of blood on filter paper with a control drop of blood nearby. If there is greater than 15% methemoglobinemia, then the affected blood will have a chocolate brown color in comparison with control blood.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Only rarely will patients require hospital admission. Patients may require admission for significant methemoglobinemia, hemolysis, hypotension, signs of severe corrosive injury, or other signs of significant illness.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Asymptomatic patients can be managed at home. Any patient with altered mental status, weakness, pain or syncope should be evaluated at a healthcare facility. Patients with ocular exposure and/or severe dermal exposure to anhydrous ammonia should be evaluated at a healthcare facility.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) If patients develop respiratory failure, hemodynamic instability, or any other symptoms not expected with this exposure, consult a toxicologist or regional poison center. If patients have signs of oropharyngeal burns or a high suspicion of gastric injury, ENT and/or GI specialists should be consulted. Consult an ophthalmologist for cases of significant ocular exposure to anhydrous ammonia.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with altered mental status, weakness, pain or syncope should be evaluated at a healthcare facility and observed until signs and symptoms improve. Patients with ocular exposure and/or severe dermal exposure to anhydrous ammonia should be evaluated at a healthcare facility.

Monitoring

    A) Most patients do not require laboratory evaluation.
    B) Measurement of methemoglobin concentrations, CBC, and electrolytes should be determined based on clinical signs.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ORAL EXPOSURE
    1) No oral decontamination is indicated.
    B) DERMAL EXPOSURE
    1) Wash exposed areas with soap and water.
    C) EYE EXPOSURE
    1) Irrigate exposed eyes with copious amounts of room temperature normal saline or water.
    6.5.2) PREVENTION OF ABSORPTION
    A) No oral decontamination is indicated in most cases. Given the corrosive nature of anhydrous ammonia and other compounds, there should be a high clinical suspicion for corrosive injury. Other metals and electrolytes can cause nausea and vomiting as well as ECG abnormalities, hyperkalemia, metabolic acidosis, and acute renal failure. With significant ingestion, endoscopy should be considered early in these patients.
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment is symptomatic and supportive. Patients with mild to moderate exposure, through either dermal, inhalational, or oral exposure, are usually asymptomatic.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Patients with severe toxicity, through either dermal, inhalational, or oral exposure, can develop methemoglobinemia due to the presence of nitrates, ECG abnormalities, hyperkalemia, metabolic acidosis, and acute renal failure. Treat patients with aggressive supportive care; an investigation into the offending fertilizer's active ingredients should be undertaken. Please refer to appropriate management for further information for each major ingredient (eg, phosphorus, potassium, iron, copper, zinc, ammonia). Given the corrosive nature of anhydrous ammonia and other compounds, there should be a high clinical suspicion for corrosive injury. Other metals and electrolytes can cause nausea and vomiting as well as ECG abnormalities, hyperkalemia, metabolic acidosis, and acute renal failure. With significant ingestion, endoscopy should be considered early in these patients.
    B) MONITORING OF PATIENT
    1) Most patients do not require laboratory evaluation.
    2) Measurement of methemoglobin concentrations, CBC, and electrolytes should be determined based on clinical signs.
    C) GASTROENTERITIS
    1) Ingestion of fertilizers usually causes limited gastrointestinal symptoms. Some fertilizers may contain insecticides or herbicides - see specific managements for treatment recommendations.
    D) METHEMOGLOBINEMIA
    1) SUMMARY
    a) Determine the methemoglobin concentration and evaluate the patient for clinical effects of methemoglobinemia (ie, dyspnea, headache, fatigue, CNS depression, tachycardia, metabolic acidosis). Treat patients with symptomatic methemoglobinemia with methylene blue (this usually occurs at methemoglobin concentrations above 20% to 30%, but may occur at lower methemoglobin concentrations in patients with anemia, or underlying pulmonary or cardiovascular disorders). Administer oxygen while preparing for methylene blue therapy.
    2) METHYLENE BLUE
    a) INITIAL DOSE/ADULT OR CHILD: 1 mg/kg IV over 5 to 30 minutes; a repeat dose of up to 1 mg/kg may be given 1 hour after the first dose if methemoglobin levels remain greater than 30% or if signs and symptoms persist. NOTE: Methylene blue is available as follows: 50 mg/10 mL (5 mg/mL or 0.5% solution) single-dose ampules (Prod Info PROVAYBLUE(TM) intravenous injection, 2016) and 10 mg/1 mL (1% solution) vials (Prod Info methylene blue 1% intravenous injection, 2011). REPEAT DOSES: Additional doses may be required, especially for substances with prolonged absorption, slow elimination, or those that form metabolites that produce methemoglobin. NOTE: Large doses of methylene blue may cause methemoglobinemia or hemolysis (Howland, 2006). Improvement is usually noted shortly after administration if diagnosis is correct. Consider other diagnoses or treatment options if no improvement has been observed after several doses. If intravenous access cannot be established, methylene blue may also be given by intraosseous infusion. Methylene blue should not be given by subcutaneous or intrathecal injection (Prod Info methylene blue 1% intravenous injection, 2011; Herman et al, 1999). NEONATES: DOSE: 0.3 to 1 mg/kg (Hjelt et al, 1995).
    b) CONTRAINDICATIONS: G-6-PD deficiency (methylene blue may cause hemolysis), known hypersensitivity to methylene blue, methemoglobin reductase deficiency (Shepherd & Keyes, 2004)
    c) FAILURE: Failure of methylene blue therapy suggests: inadequate dose of methylene blue, inadequate decontamination, NADPH dependent methemoglobin reductase deficiency, hemoglobin M disease, sulfhemoglobinemia, or G-6-PD deficiency. Methylene blue is reduced by methemoglobin reductase and nicotinamide adenosine dinucleotide phosphate (NADPH) to leukomethylene blue. This in turn reduces methemoglobin. Red blood cells of patients with G-6-PD deficiency do not produce enough NADPH to convert methylene blue to leukomethylene blue (do Nascimento et al, 2008).
    d) DRUG INTERACTION: Concomitant use of methylene blue with serotonergic drugs, including serotonin reuptake inhibitors (SRIs), selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), norepinephrine-dopamine reuptake inhibitors (NDRIs), triptans, and ergot alkaloids may increase the risk of potentially fatal serotonin syndrome (U.S. Food and Drug Administration, 2011; Stanford et al, 2010; Prod Info methylene blue 1% IV injection, 2011).
    3) TOLUIDINE BLUE OR TOLONIUM CHLORIDE (GERMANY)
    a) DOSE: 2 to 4 mg/kg intravenously over 5 minutes. Dose may be repeated in 30 minutes (Nemec, 2011; Lindenmann et al, 2006; Kiese et al, 1972).
    b) SIDE EFFECTS: Hypotension with rapid intravenous administration. Vomiting, diarrhea, excessive sweating, hypotension, dysrhythmias, hemolysis, agranulocytosis and acute renal insufficiency after overdose (Dunipace et al, 1992; Hix & Wilson, 1987; Winek et al, 1969; Teunis et al, 1970; Marquez & Todd, 1959).
    c) CONTRAINDICATIONS: G-6-PD deficiency; may cause hemolysis.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

Summary

    A) TOXICOLOGY: In general, liquid and granular fertilizers have a low degree of toxicity, causing mild gastrointestinal irritation. However, anhydrous ammonia (frequently used on farms) is very corrosive and can cause significant burns to skin and mucous membranes. See ammonia management for further information. An elderly adult was found dead following an intentional ingestion of an unknown amount of fertilizer containing ammonium sulfate. Ingestion of 700 mL of a fertilizer, consisting of nitrogen, phosphorus, potassium, manganese, iron, copper, and zinc, resulted in the development of ECG abnormalities, hyperkalemia, metabolic acidosis, acute renal failure, and mild methemoglobinemia. The patient recovered with supportive care. Please refer to appropriate management for further information for each major ingredient (eg, phosphorus, potassium, iron, manganese, copper, zinc, ammonia).

Minimum Lethal Exposure

    A) ADULT
    1) Sato et al (1999) reported that an elderly woman died after the intentional ingestion of an unknown amount of fertilizer (presumably mixed into a solution with beer) containing ammonium sulfate (Sato et al, 1999).
    a) The authors than examined the effects of ammonium sulfate (a total dose of 1500 mg/kg) using rabbits and found that all developed seizures (untreated) followed by metabolic acidosis and subsequent fatal cardiac and respiratory arrest.

Maximum Tolerated Exposure

    A) ROUTE OF EXPOSURE
    1) Ingestion of 20 grams of a typical fertilizer mixture per kilogram (approximately one tablespoonful/kilogram) is expected to produce gastrointestinal irritation (Tech Info, 1986).
    2) Ingestion of 700 mL of a fertilizer, consisting of nitrogen, phosphorus, potassium, manganese, iron, copper, and zinc, in a 64-year-old man resulted in the development of ECG abnormalities, hyperkalemia, metabolic acidosis, acute renal failure, and mild methemoglobinemia. Following supportive care and hemodialysis, the patient recovered and was discharged 1 week post-ingestion (Huang & Lin, 2004).

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) SODIUM BORATE FERTILIZER

Animal Toxicology

Clinical Effects

    11.1.2) BOVINE/CATTLE
    A) Cattle and sheep may develop nitrate intoxication after drinking surface water contaminated by fertilizers, or grazing on grasses known to accumulate nitrates. Ruminants readily convert nitrate to nitrite by ruminal microorganisms, resulting in methemoglobinemia, with clinical signs of anxiety, polypnea, and dyspnea (Burrows, 1980).
    B) BORON FERTILIZER - 26 cattle in a herd being grazed on a peanut field died after eating boron fertilizer from a bag left in the field. Clinical signs included ataxia, fasciculations, seizures, bloat, greenish diarrhea, and dehydration. Two pregnant cows appeared to be aborting. Ingestion of this fertilizer in monogastric animals may cause protective emesis; this effect has not been seen in ruminants (Sisk et al, 1988).
    11.1.3) CANINE/DOG
    A) Dogs given extreme amounts (10 mL/kg) orally of urea-based fertilizer mixtures used routinely in lawn applications did not develop any clinical signs of illness. Ingestion of grass or walking or laying on lawns treated with fertilizers, alone or in combination with herbicides or insecticides, is expected to be safe (Yeary, 1984).
    11.1.4) CAPRINE/GOAT
    A) BORON FERTILIZER - A kid goat intentionally dosed with 3.6 g/kg boron fertilizer died 8 hours later after experiencing depression, diarrhea, and tremors (Sisk et al, 1988).
    11.1.10) PORCINE/SWINE
    A) Swine with nitrate intoxication may develop gastrointestinal irritation with little or no methemoglobin formation (Burrows, 1980).

Treatment

    11.2.1) SUMMARY
    A) GENERAL TREATMENT
    1) SUMMARY -
    a) Begin treatment immediately.
    b) Keep animal warm and do not handle unnecessarily.
    c) Sample vomitus, blood, urine, and feces for analysis.
    d) Remove the patient and other animals from the source of contamination.
    e) Treatment should always be done on the advice and with the consultation of a veterinarian. Additional information regarding treatment of poisoned animals may be obtained from a Board Certified (ABVT) Veterinary Toxicologist (check with nearest veterinary school or veterinary diagnostic laboratory) or the National Animal Poison Control Center.
    2) ANIMAL POISON CONTROL CENTERS
    a) ASPCA Animal Poison Control Center, An Allied Agency of the University of Illinois, 1717 S. Philo Rd, Suite 36, Urbana, IL 61802, website www.aspca.org/apcc
    b) It is an emergency telephone service which provides toxicology information to veterinarians, animal owners, universities, extension personnel and poison center staff for a fee. A veterinary toxicologist is available for consultation.
    c) The following 24-hour phone number is available: (888) 426-4435. A fee may apply. Please inquire with the poison center. The agency will make follow-up calls as needed in critical cases at no extra charge.
    11.2.2) LIFE SUPPORT
    A) GENERAL
    1) MAINTAIN VITAL FUNCTIONS: Secure airway, supply oxygen, and begin supportive fluid therapy if necessary.
    11.2.4) DECONTAMINATION
    A) GASTRIC DECONTAMINATION
    1) DOGS/CATS
    a) DERMAL - No reports exist of toxicity due to dermal exposure to this compound; however, decontamination is advised on dermal exposure. Bathe in mild detergent (animal shampoo or Ivory liquid). Wear gloves to avoid human exposure. Clip hair as necessary to facilitate removal.
    b) CAUTION - Carefully examine patients with chemical exposure before inducing emesis. If signs of oral, pharyngeal, or esophageal irritation, a depressed gag reflex, or central nervous system excitation or depression are present, EMESIS SHOULD NOT BE INDUCED.
    1) EMESIS AND LAVAGE - Induce emesis with 1 to 2 milliliters/kilogram syrup of ipecac per os. Dogs may vomit more readily with 1 tablet (6 milligrams) apomorphine diluted in 3 to 5 milliliters water and instilled into the conjunctival sac or per os. Dogs may also be given apomorphine intravenously at 40 micrograms/kilogram. Do not use an emetic if the animal is hypoxic. In the absence of a gag reflex or if vomiting cannot be induced, place a cuffed endotracheal tube and begin gastric lavage. Pass large bore stomach tube and instill 5 to 10 milliliters/kilogram water or lavage solution, then aspirate. Repeat 10 times.
    c) ACTIVATED CHARCOAL - Administer activated charcoal, 2 grams/kilogram per os or via stomach tube. Avoid aspiration by proper restraint, careful technique, and if necessary tracheal intubation.
    d) CATHARTIC - Administer a dose of a saline cathartic such as magnesium or sodium sulfate (sodium sulfate dose is 1 gram/kilogram). If access to these agents is limited, give 5 to 15 milliliters magnesium oxide (Milk of Magnesia) per os for dilution.
    2) RUMINANTS/HORSES/SWINE
    a) DERMAL - No reports exist of toxicity due to dermal exposure to this compound; however, decontamination is advised on dermal exposure. Wash exposed animals with soap and water. If possible, shave or clip long hair to facilitate thorough cleaning. All handlers should wear gloves and protect themselves from exposure.
    b) EMESIS - Do not attempt to induce emesis in ruminants (cattle) or equids (horses).
    c) ACTIVATED CHARCOAL -
    1) Adult horses: Administer 0.5 to 1 kilogram of activated charcoal in up to 1 gallon warm water via nasogastric tube.
    2) Neonates: Administer 250 grams (one-half pound) activated charcoal in up to 2 quarts water.
    3) Adult cattle: Administer 2 to 9 grams/ kilogram of activated charcoal in a slurry of 1 gram charcoal/3 to 5 milliliters warm water via stomach tube.
    4) Sheep may be given 0.5 kilogram charcoal in slurry.
    d) CATHARTICS - Administer an oral cathartic:
    1) Mineral oil (small ruminants and swine, 60 to 200 milliliters; equids and cattle, 0.5 to 1 gallon) or
    2) Magnesium sulfate (ruminants and swine, 1 to 2 grams/kilogram; equine, 0.2 to 0.9 gram/kilogram) or
    3) Milk of Magnesia (small ruminants, up to 0.25 gram/kilogram in 1 to 3 gallons warm water; adult cattle up to 1 gram/kilogram in 1 to 3 gallons warm water or 2 to 4 boluses MgOH per os).
    4) Give these solutions via stomach tube and monitor for aspiration.
    11.2.5) TREATMENT
    A) RUMINANT
    1) Cattle and sheep with nitrate-induced methemoglobinemia may be given methylene blue 4 to 15 mg/kg IV as a 1% solution. Ruminal lavage with cold water and/or large oral doses of antibiotics may also be given (Burrows, 1980).

Range Of Toxicity

    11.3.2) MINIMAL TOXIC DOSE
    A) DOG
    1) Dogs given extreme amounts (10 mL/kg) orally of urea-based fertilizer mixtures used routinely in lawn applications did not develop any clinical signs of illness. Ingestion of grass or walking or laying on lawns treated with fertilizers, alone or in combination with herbicides or insecticides, is expected to be safe (Yeary, 1984).

Continuing Care

    11.4.1) SUMMARY
    11.4.1.2) DECONTAMINATION/TREATMENT
    A) GENERAL TREATMENT
    1) SUMMARY -
    a) Begin treatment immediately.
    b) Keep animal warm and do not handle unnecessarily.
    c) Sample vomitus, blood, urine, and feces for analysis.
    d) Remove the patient and other animals from the source of contamination.
    e) Treatment should always be done on the advice and with the consultation of a veterinarian. Additional information regarding treatment of poisoned animals may be obtained from a Board Certified (ABVT) Veterinary Toxicologist (check with nearest veterinary school or veterinary diagnostic laboratory) or the National Animal Poison Control Center.
    2) ANIMAL POISON CONTROL CENTERS
    a) ASPCA Animal Poison Control Center, An Allied Agency of the University of Illinois, 1717 S. Philo Rd, Suite 36, Urbana, IL 61802, website www.aspca.org/apcc
    b) It is an emergency telephone service which provides toxicology information to veterinarians, animal owners, universities, extension personnel and poison center staff for a fee. A veterinary toxicologist is available for consultation.
    c) The following 24-hour phone number is available: (888) 426-4435. A fee may apply. Please inquire with the poison center. The agency will make follow-up calls as needed in critical cases at no extra charge.
    11.4.2) DECONTAMINATION
    11.4.2.2) GASTRIC DECONTAMINATION
    A) GASTRIC DECONTAMINATION
    1) DOGS/CATS
    a) DERMAL - No reports exist of toxicity due to dermal exposure to this compound; however, decontamination is advised on dermal exposure. Bathe in mild detergent (animal shampoo or Ivory liquid). Wear gloves to avoid human exposure. Clip hair as necessary to facilitate removal.
    b) CAUTION - Carefully examine patients with chemical exposure before inducing emesis. If signs of oral, pharyngeal, or esophageal irritation, a depressed gag reflex, or central nervous system excitation or depression are present, EMESIS SHOULD NOT BE INDUCED.
    1) EMESIS AND LAVAGE - Induce emesis with 1 to 2 milliliters/kilogram syrup of ipecac per os. Dogs may vomit more readily with 1 tablet (6 milligrams) apomorphine diluted in 3 to 5 milliliters water and instilled into the conjunctival sac or per os. Dogs may also be given apomorphine intravenously at 40 micrograms/kilogram. Do not use an emetic if the animal is hypoxic. In the absence of a gag reflex or if vomiting cannot be induced, place a cuffed endotracheal tube and begin gastric lavage. Pass large bore stomach tube and instill 5 to 10 milliliters/kilogram water or lavage solution, then aspirate. Repeat 10 times.
    c) ACTIVATED CHARCOAL - Administer activated charcoal, 2 grams/kilogram per os or via stomach tube. Avoid aspiration by proper restraint, careful technique, and if necessary tracheal intubation.
    d) CATHARTIC - Administer a dose of a saline cathartic such as magnesium or sodium sulfate (sodium sulfate dose is 1 gram/kilogram). If access to these agents is limited, give 5 to 15 milliliters magnesium oxide (Milk of Magnesia) per os for dilution.
    2) RUMINANTS/HORSES/SWINE
    a) DERMAL - No reports exist of toxicity due to dermal exposure to this compound; however, decontamination is advised on dermal exposure. Wash exposed animals with soap and water. If possible, shave or clip long hair to facilitate thorough cleaning. All handlers should wear gloves and protect themselves from exposure.
    b) EMESIS - Do not attempt to induce emesis in ruminants (cattle) or equids (horses).
    c) ACTIVATED CHARCOAL -
    1) Adult horses: Administer 0.5 to 1 kilogram of activated charcoal in up to 1 gallon warm water via nasogastric tube.
    2) Neonates: Administer 250 grams (one-half pound) activated charcoal in up to 2 quarts water.
    3) Adult cattle: Administer 2 to 9 grams/ kilogram of activated charcoal in a slurry of 1 gram charcoal/3 to 5 milliliters warm water via stomach tube.
    4) Sheep may be given 0.5 kilogram charcoal in slurry.
    d) CATHARTICS - Administer an oral cathartic:
    1) Mineral oil (small ruminants and swine, 60 to 200 milliliters; equids and cattle, 0.5 to 1 gallon) or
    2) Magnesium sulfate (ruminants and swine, 1 to 2 grams/kilogram; equine, 0.2 to 0.9 gram/kilogram) or
    3) Milk of Magnesia (small ruminants, up to 0.25 gram/kilogram in 1 to 3 gallons warm water; adult cattle up to 1 gram/kilogram in 1 to 3 gallons warm water or 2 to 4 boluses MgOH per os).
    4) Give these solutions via stomach tube and monitor for aspiration.

References

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