Contact Us    Contact Us     |     Feedback
MOBILE VIEW  | 

SODIUM CHLORIDE

Export To Excel

Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Sodium chloride is a natural source of chlorine and sodium. It is commonly used as an additive for meals (ie table salt), for electrolyte replacement during sport or outdoor activity. Sodium chloride is also used in medicine in the treatment of extracellular volume depletion, dehydration, and sodium depletion. It is also used in industry in various chemical processes (ie road salt for deicing roads).

Specific Substances

    1) Sodium chloride
    2) Chlorure de Sodium
    3) Cloreto de Sodio
    4) Common salt
    5) Molecular Formula: NaCl
    6) Natrii Chloridum
    7) Salt
    8) CAS 7647-14-5
    9) SODIUM (SALTS)
    1.2.1) MOLECULAR FORMULA
    1) Cl-Na NaCl

Available Forms Sources

    A) FORMS
    1) SUMMARY
    a) 1 Level tablespoon (17.85 grams) contains approximately 305 mEq of Na+ and of Cl-.
    2) FOODS AND BEVERAGES
    a) Sodium chloride is found in a wide variety of common foods and beverages. Some examples of approximate concentrations of sodium are as follows (US Department of Agriculture, Agricultural Research Service, 2004):
    PRODUCTAMOUNT
    BEVERAGES
    Beer, regular14 mg/12 ounces
    Wine (white or red) 5 mg/3.5 ounces
    Apple juice7 mg/cup
    Cranberry juice5 mg/8 ounces
    Tea brewed or herbal 2 to 5 mg per 6 ounces
    Tea, instant sweetened with artificial sweetener 24 mg per 8 ounces
    Soup, beef broth or bouillon (1 packet) 1019 mg
    Milk, 2% milkfat100 mg/cup
    Soy milk135 mg/cup
    SAUCES
    Miso2563 mg/cup
    Soy Sauce 902 mg/tbsp
    Teriyaki Sauce690 mg/tbsp
    Sauce, tomato, pasta ready to serve1284 mg/cup
    FOOD
    Apple (raw) 1 mg
    Cottage cheese (1% or 2%) 918 mg/cup
    Chili con carne with beans941 mg/cup
    Cornmeal (self rising) 1860 mg/cup
    Fast food, English muffin with eggs, cheese and Canadian bacon 729 mg
    Fast food, corn dog973 mg
    Fast food, submarine sandwich with cold cuts (6 in roll) 1651 mg
    Taco (1 large) 1233 mg
    Tuna Salad 824 mg
    Pickles (1) 833 mg
    Salt, table 2325 mg/tsp
    Pretzels (10) 1029 mg
    Potato chips, plain, salted 168 mg per 1 ounce
    Soup, onion mix, dehydrated form3132 mg per packet

    3) INTRAVENOUS FLUIDS
    a) Sodium Chloride Injection
    b) Bacteriostatic Sodium Chloride Injection
    c) 0.45% Sodium Chloride Injection (Hypotonic solution)
    1) 77 mEq/L each of chloride and sodium
    2) Osmolarity (calculated): 154 mOsm/L
    d) 0.9% Sodium Chloride Solution (Normal Saline - Isotonic solution)
    1) 154 mEq/L each of chloride and sodium
    2) Osmolarity (calculated): 308 mOsm/L
    e) 3% Sodium Chloride Solution (Hypertonic solution)
    1) 513 mEq/L each of chloride and sodium
    2) Osmolarity (calculated): 1710 mOsm/L
    f) 5% Sodium Chloride Injection (Hypertonic solution)
    g) 20% Sodium Chloride Injection - Abortifacient
    4) ORAL PRODUCTS
    a) Sodium Chloride Tablets 650 mg, 1 gram, and 2.25 grams
    b) Sodium Chloride Slow Release Tablets 600 mg
    c) Sodium Chloride Enteric Coated Tablets 1 gram
    d) Heatrol(R), Otis Clapp: Each tablet contains 635 mg sodium chloride, 40.6 mg potassium chloride, 31.5 mg calcium phosphate, and 9.1 mg magnesium carbonate
    5) NASAL PRODUCTS
    a) 0.4% Sodium Chloride (Salinex(R), Muro)
    b) 0.6% Sodium Chloride (Pretz(R), Parnell)
    c) 0.65% Sodium Chloride (many)
    6) OPHTHALMIC PRODUCTS
    a) 2% or 5% Solution of Sodium Chloride (Hypertonic)
    b) 5% Sodium Chloride Ointment (Hypertonic)
    c) Isotonic solutions for rinsing and storing soft contact lenses
    7) SODIUM CHLORIDE PICA: Secondary to iron-deficiency anemia has been reported. Once anemia was properly treated, excessive salt ingestion ceased (Shapiro & Linas, 1985).
    B) USES
    1) Table salt, rock salt, salt tablets, normal saline, sea water, etc, as well as varying amounts in the majority of protein-containing food substances.
    2) While occasional acute poisonings have been reported from ingestion of plain salt, others have followed the use of NaCl as an emetic, of saline for gastric lavage, and saline for enemas or infused into the uterus to induce abortion.

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: Used therapeutically as a parenteral crystalloid substitute for volume replacement or for maintenance therapy in the hospital setting. Also, commonly used as an additive for meals (ie, table salt) for electrolyte replacement during sports or outdoor activity, in water softening solutions, and in road salt for deicing roads.
    B) EPIDEMIOLOGY: Exposure is common, serious toxicity is very rare.
    C) PHARMACOLOGY: Sodium chloride can lead to increases in intravascular volume by adrenal glandular hormonal action. Also, potentially attenuates nitric oxide production.
    D) TOXICOLOGY: Sodium chloride can cause direct irritation to mucosal membranes, if ingested and may cause hypernatremia and hyperchloremia.
    E) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Nausea, vomiting, diarrhea and abdominal discomfort may develop. Patients may complain of excessive thirst.
    2) SEVERE TOXICITY: Restlessness, seizures, mental status depression, coma, hypotension, and respiratory arrest are rare effects of severe sodium chloride toxicity. Acute ulcerative gastritis has been reported. Hypernatremia and hyperchloremia may develop, with associated fluid retention, and the potential for pulmonary and cerebral edema can occur. Hyperosmolarity of cerebral fluids may lead to cellular crenation and irreversible neurologic damage.
    3) PEDIATRIC: Poisoning from sodium chloride has resulted from gastric lavage with hypertonic saline and errors in the formulation of infant feeds. Intentional pediatric salt poisonings have been reported. Infants with hypernatremia may develop a flat anterior fontanelle.

Laboratory Monitoring

    A) Monitor vital signs and mental status.
    B) Monitor serum electrolytes frequently.
    C) Monitor renal function and urine output. Urinary sodium excretion will be high in all cases of hypernatremia and cannot be used to differentiate salt poisoning from dehydration.
    D) Monitor for evidence of volume overload, pulmonary edema and cerebral edema.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Dilute with milk or water.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treat hypernatremia with an IV solution containing 30 to 50 mEq/L sodium. Longstanding hypernatremia should be corrected slowly. Treat seizures with benzodiazepines. Treat cerebral edema with mannitol. Hemodialysis should be performed in patients with severe toxicity.
    C) DECONTAMINATION
    1) DILUTION: Immediately dilute with 4 to 8 ounces (120 to 240 mL) of water (not to exceed 4 ounces (120 mL) in a child).
    2) OCULAR EXPOSURE: Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. If irritation, pain swelling, lacrimation, or photophobia persist, the patient should be seen in a health care facility.
    D) AIRWAY MANAGEMENT
    1) Airway management is unlikely to be necessary unless severe toxicity occurs. Maintain airway patency and adequate oxygenation. Endotracheal intubation and assisted mechanical ventilation may be required.
    E) HYPERNATREMIA
    1) For longstanding hypernatremia, IV administration of a solution containing 30 to 50 mEq/L of sodium (half as chloride and half as bicarbonate) should be administered slowly. The rate of administration is critical (usually 2/3 of a daily maintenance) and should proceed to lower serum sodium to normal range no sooner than 24 to 36 hours after institution of therapy. If a decrease in serum sodium occurs more rapidly, seizures are likely to ensue. For acute, severe hypernatremia secondary to acute ingestion of large amounts of sodium chloride, more rapid correction of serum sodium with intravenous D5W or other hypotonic solutions, oral free water, or hemodialysis may be appropriate.
    F) SEIZURE
    1) Administer a benzodiazepine IV. Diazepam: Adult: 5 mg to 10 mg, repeat every 10 to 15 min as needed. CHILD: 0.2 to 0.5 mg/kg, repeat every 5 minutes as needed OR lorazepam: Adult: 2 to 4 mg; Child: 0.05 to 0.1 mg/kg. Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children older than 5 years). Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Monitor for hypoglycemia, electrolyte disturbances and hypoxia.
    G) HYPOTENSION
    1) Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (Adult: Begin infusion at 0.5 to 1 mcg/min; Child: Begin infusion at 0.1 mcg/kg/min); titrate to desired response.
    H) CEREBRAL EDEMA
    1) Monitor intracranial pressure. IV mannitol (0.5 to 1 g/kg) may be administered to remove excess intracellular water from the brain.
    I) ENHANCED ELIMINATION
    1) Hemodialysis can effectively remove sodium chloride. It should be considered early in patients with severe hypernatremia or severe clinical manifestations, and in patients with renal insufficiency.
    J) PATIENT DISPOSITION
    1) HOME CRITERIA: Asymptomatic patients with ingestions of less than 8 mEq/kg (0.5 g/kg) sodium chloride can probably be managed at home.
    2) OBSERVATION CRITERIA: Symptomatic patients, those with deliberate ingestions, and patients ingesting 8 mEq/kg (0.5 g/kg) sodium chloride or more should be referred to a healthcare facility.
    3) ADMISSION CRITERIA: All patients with evidence of systemic toxicity from sodium chloride, severe hypernatremia not responding to hydration, or those with intractable vomiting should be admitted.
    4) CONSULT CRITERIA: Consult a medical toxicologist or poison center for patients with severe hypernatremia or severe clinical manifestations.
    K) PITFALLS
    1) Clinicians need to aware that despite the benign reputation of sodium chloride, serious toxicity can occur from overdose.
    L) DIFFERENTIAL DIAGNOSIS
    1) Organic neurologic toxicity, seizure disorder or diabetes insipidus.
    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.

Range Of Toxicity

    A) TOXICITY: Ingestion of 0.5 to 1 g/kg (8.6 to 17.2 mEq/kg) of sodium chloride is probably toxic in the majority of patients. Central nervous system signs and symptoms are common with serum sodium concentrations above 150 to 160 mEq/L. At such levels, there is a 10% chance of seizures which increases when serum sodium concentration reaches 160 to 185 mEq/L. Death is a frequent occurrence at serum sodium concentrations above 185 mEq/L. A teenager survived a serum sodium concentration of 196 mmol/L following the ingestion of soy sauce (quart size bottle; equivalent to 160 to 170 g salt) following aggressive supportive care; no permanent sequelae occurred. PEDIATRIC: One level tablespoon (17.85 g) is approximately 305 mEq of sodium, and if retained, would raise serum levels by 30.5 mEq/L in a 3-year-old (15 kg) child. A toddler died after ingesting 400 mEq/kg and an adolescent died after absorbing an estimated 45 g sodium chloride as salt water.
    B) RECOMMENDED DAILY CONSUMPTION: ADULT: It is recommended an adult consume no more than 2300 mg of sodium daily.

Clinical Effects

Summary Of Exposure

    A) USES: Used therapeutically as a parenteral crystalloid substitute for volume replacement or for maintenance therapy in the hospital setting. Also, commonly used as an additive for meals (ie, table salt) for electrolyte replacement during sports or outdoor activity, in water softening solutions, and in road salt for deicing roads.
    B) EPIDEMIOLOGY: Exposure is common, serious toxicity is very rare.
    C) PHARMACOLOGY: Sodium chloride can lead to increases in intravascular volume by adrenal glandular hormonal action. Also, potentially attenuates nitric oxide production.
    D) TOXICOLOGY: Sodium chloride can cause direct irritation to mucosal membranes, if ingested and may cause hypernatremia and hyperchloremia.
    E) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Nausea, vomiting, diarrhea and abdominal discomfort may develop. Patients may complain of excessive thirst.
    2) SEVERE TOXICITY: Restlessness, seizures, mental status depression, coma, hypotension, and respiratory arrest are rare effects of severe sodium chloride toxicity. Acute ulcerative gastritis has been reported. Hypernatremia and hyperchloremia may develop, with associated fluid retention, and the potential for pulmonary and cerebral edema can occur. Hyperosmolarity of cerebral fluids may lead to cellular crenation and irreversible neurologic damage.
    3) PEDIATRIC: Poisoning from sodium chloride has resulted from gastric lavage with hypertonic saline and errors in the formulation of infant feeds. Intentional pediatric salt poisonings have been reported. Infants with hypernatremia may develop a flat anterior fontanelle.

Vital Signs

    3.3.2) RESPIRATIONS
    A) WITH POISONING/EXPOSURE
    1) CASE REPORT: A 14-year-old boy presented with tachypnea (60 breaths/minute) approximately 1 hour after ingesting an unknown amount of saltwater in an attempt to induce emesis. The patient was severely hypernatremic with an initial sodium level of 195 mmol/L (Casavant & Fitch, 2003).
    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) FEVER
    a) CASE REPORT: A 19-year-old developed severe hypernatremia (peak serum sodium 196 mmol/L) after drinking a liter of soy sauce on a dare. He developed mental status depression, seizures, clonus, disconjugate gaze, tachycardia (147 beats/minute) and fever (39.4 degrees C rectally). He was treated with 6 L D5W over 30 minutes 4.5 hours after ingestion, and a further 5.2 L of D5W intravenously and 215 mL of free water through the NG tube, as well as 2.4 L of other hypotonic solutions over the next 24 hours. Plasma sodium was normal (145 mmol/L) 32 hours after the ingestion and the patient had a good neurologic outcome with no evidence of central pontine myelonecrosis on MRI (Carlberg et al, 2013).
    b) A 12-month-old toddler became febrile following nasogastric administration of 400 mEq sodium chloride over 12 hours (El-Dahr et al, 1987).
    c) Hyperthermia (peak temperature of 105.1 degrees F) was reported in a 14-year-old boy who became severely hypernatremic (195 mmol/L) following ingestion of an unknown amount of saltwater in an attempt to induce emesis (Casavant & Fitch, 2003).
    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) HYPOTENSION
    a) Hypernatremia may present with hypotension (Quereshi et al, 2010; Caillaux et al, 2006) which may be refractory to fluid replacement (Ellenhorn & Barceloux, 1988).
    b) CASE REPORT: A 14-year-old boy, who developed severe hypernatremia (sodium 195 mmol/L) following ingestion of an unknown amount of saltwater, initially developed hypertension (160/90 mmHg) that subsequently progressed to severe hypotension (systolic 40) refractory to high-dose pressors. The patient continued to deteriorate clinically, with absent neurological reflexes and poor peripheral pulses. He died within 48 hours postingestion (Casavant & Fitch, 2003).
    3.3.5) PULSE
    A) WITH POISONING/EXPOSURE
    1) TACHYCARDIA
    a) Tachycardia may be present with hypernatremia (Casavant & Fitch, 2003).

Heent

    3.4.2) HEAD
    A) WITH POISONING/EXPOSURE
    1) ANTERIOR FONTANELLE FLATTING
    a) Infants with hypernatremia may develop flat anterior fontanelle (Quereshi et al, 2010; Caillaux et al, 2006; Ellenhorn & Barceloux, 1988).
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) LACRIMATION
    a) Reduced lacrimation may be seen with hypernatremia (JEF Reynolds , 1989).
    2) STINGING
    a) Sodium chloride instilled into the eye in concentrations greater than that in tears causes a stinging sensation (Grant, 1986).
    3) CORNEAL EPITHELIUM PERMEABILITY
    a) Corneal epithelium permeability was not altered by solutions of sodium chloride up to 10%, but solutions less than 0.9% increased permeability (Maurice, 1955).
    3.4.5) NOSE
    A) WITH THERAPEUTIC USE
    1) EPISTAXIS
    a) Epistaxis has been associated with use of sodium chloride eye drops in a single case report (Kushner, 1987).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) DRY MUCOUS MEMBRANES
    a) Parched mucous membranes were noted in a 12-month-old child who developed dehydration from hypernatremia (El-Dahr et al, 1987).
    2) SUNKEN EYES
    a) A 12-month-old child developed dehydration with sunken eyes following nasogastric administration of 400 mEq sodium chloride over 12 hours (El-Dahr et al, 1987). It was also observed in a 17-day-old infant who developed sodium chloride poisoning after receiving an incorrectly reconstituted infant formula (Caillaux et al, 2006).
    3) THIRST
    a) Thirst is associated with excess sodium chloride (Quereshi et al, 2010; Finberg et al, 1963).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Hypernatremia may present with hypotension (Quereshi et al, 2010; Caillaux et al, 2006) which may be refractory to fluid replacement (Caraccio & McGuigan, 2004).
    b) CASE REPORTS: In India, a 7-month-old breastfed boy developed watery stools and fever and was started on supplemental feedings with oral rehydration solution (ORS). The 21 g packet of ORS was incorrectly constituted in 200 mL of water instead of 1 L. A week later the child was readmitted with severe dehydration, hypernatremia (Na 196 mEq/L), acidosis, and an unrecordable blood pressure. Shock was treated aggressively and BP normalized with adrenaline and dopamine. However, hypotension reoccurred which was unresponsive to treatment and the infant died (Quereshi et al, 2010).
    1) In a second case, an 8-month-old breastfed boy developed similar GI symptoms and was started on ORS which was again reconstituted incorrectly (21 g packet in 200 mL water instead of 1L). Two days after starting treatment, the patient was admitted with dehydration, hypotension (BP 80/40 mmHg) and hypernatremia (Na 176 mEq/L). Sodium normalized within 24 hours with treatment and oral feeds as appropriate. Blood cultures were negative. Recovery was uneventful (Quereshi et al, 2010).
    c) CASE REPORT/NEONATE: A 17-day-old infant was admitted with severe malaise, hypotonia, dehydration and hypovolemic shock. Upon admission, blood pressure was 69/49 mm Hg and heart rate was 200 beats/minute. Laboratory analysis revealed hyperchloremic metabolic acidosis and hypernatremia. Sodium chloride poisoning had occurred due to incorrectly reconstituted infant formula. Following supportive care, including oral and intravenous hydration the infant recovered (Caillaux et al, 2006).
    d) CASE REPORT: A 14-year-old boy, who developed severe hypernatremia (serum sodium 195 mmol/L) following ingestion of an unknown amount of saltwater, initially developed hypertension (160/90 mmHg) that subsequently progressed to severe hypotension (systolic 40) refractory to high-dose pressors. The patient continued to deteriorate clinically, with absent neurological reflexes and poor peripheral pulses. He died within 48 hours postingestion (Casavant & Fitch, 2003).
    B) HYPERTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) A cross-sectional study of non-brine workers (workers who worked with dry salt in the vicinity of salt milling plants; n=474) and brine workers (those working in brine pans located far away from milling plants; n=284) was conducted to determine the effects on blood pressure. Mean systolic blood pressure for non-brine workers was 122.1 +/- 13.3 mmHg, compared with 118.8 +/- 12.8 mmHg for the brine workers. Mean diastolic blood pressure was 71.5 +/- 10.4 mmHg for the non-brine workers, compared with 69.7 +/- 9.4 mmHg for the brine workers. The prevalence of hypertension was 12.2% for the non-brine workers, compared with 7.0% for the brine workers.
    1) Nineteen non-brine workers were monitored for 6 days when using face masks and spectacles. Both systolic and diastolic blood pressures began to decline on the third day and continued to decline on the fourth day (mean systolic blood pressure decreased from 127.8 +/- 11.1 mmHg to 117.5 +/- 9.9 mmHg on day 4; mean diastolic blood pressure decreased from 80.7 +/- 8.8 mmHg to 62.6 +/- 7.8 mmHg on day 4). After day 4, blood pressure remained stationary (Haldiya et al, 2005).
    C) TACHYCARDIA
    1) WITH POISONING/EXPOSURE
    a) Hypernatremia may present with tachycardia (Casavant & Fitch, 2003).
    b) CASE REPORT: A 19-year-old developed severe hypernatremia (peak serum sodium 196 mmol/L) after drinking a liter of soy sauce on a dare. He developed mental status depression, seizures, clonus, disconjugate gaze, tachycardia (147 beats/minute) and fever (39.4 degrees C rectally). He was treated with 6 L D5W over 30 minutes 4.5 hours after ingestion, and a further 5.2 L of D5W intravenously and 215 mL of free water through the NG tube, as well as 2.4 L of other hypotonic solutions over the next 24 hours. Plasma sodium was normal (145 mmol/L) 32 hours after the ingestion and the patient had a good neurologic outcome with no evidence of central pontine myelonecrosis on MRI (Carlberg et al, 2013).
    D) CONGESTIVE HEART FAILURE
    1) WITH THERAPEUTIC USE
    a) Sodium chloride should be administered with care in patients with congestive heart failure or in clinical conditions in which edema occurs with sodium retention (Prod Info Sodium Chloride IV injection, 2005).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) Pulmonary edema may occur due to retention of sodium and fluid accumulation (Turk et al, 2005).
    b) CASE REPORT: Pulmonary edema requiring mechanical ventilation was reported in a 5-week-old infant who developed severe hypernatremia (211 mmol/L) after ingesting formula reconstituted with water containing sodium chloride 23 g/L for 72 hours (Paut et al, 1999).
    B) APNEA
    1) WITH POISONING/EXPOSURE
    a) Respiratory arrest may occur (Kupiec et al, 2004).
    b) CASE REPORT: A 6-year-old child, with a history of pica (ingestion of nonfood items) and a seizure disorder, presented to the hospital, following a seizure, with respiratory failure and altered mental status. Laboratory analysis revealed hypernatremia (serum sodium level of 234 mEq/L) and hyperchloremia (serum chloride level of 205 mEq/L), as well as hypokalemia and metabolic acidosis. The patient recovered and electrolyte levels normalized with supportive care. A search of the patient's house revealed the presence of table salt on the counter top and rock salt in a closet. Based on his serum sodium level, it is believed that he ingested approximately 4 tablespoons of rock salt (total amount of sodium chloride ingested is estimated to be 86.4 grams) (Kupiec et al, 2004).
    C) DYSPNEA
    1) WITH POISONING/EXPOSURE
    a) INFANTS may have respiratory distress with flaring nostrils and tachypnea (Caillaux et al, 2006).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) FEELING NERVOUS
    1) WITH POISONING/EXPOSURE
    a) IRRITABILITY: Hypernatremia may produce restlessness, irritability, dizziness, headache, weakness, and muscular twitching and rigidity (Quereshi et al, 2010).
    B) COMA
    1) WITH POISONING/EXPOSURE
    a) Progressive obtundation leading to coma may be a symptom of hypernatremia (Turk et al, 2005; Casavant & Fitch, 2003).
    b) CASE REPORT: A 19-year-old developed severe hypernatremia (peak serum sodium 196 mmol/L) after drinking a liter of soy sauce on a dare. He developed mental status depression, seizures, clonus, disconjugate gaze, tachycardia (147 beats/minute) and fever (39.4 degrees C rectally). He was treated with 6 L D5W over 30 minutes 4.5 hours after ingestion, and a further 5.2 L of D5W intravenously and 215 mL of free water through the NG tube, as well as 2.4 L of other hypotonic solutions over the next 24 hours. Plasma sodium was normal (145 mmol/L) 32 hours after the ingestion and the patient had a good neurologic outcome with no evidence of central pontine myelonecrosis on MRI (Carlberg et al, 2013).
    C) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Seizures may occur with hypernatremia (Turk et al, 2005; Kupiec et al, 2004; Casavant & Fitch, 2003; Smith & Palevsky, 1990).
    b) CASE REPORT: A 19-year-old developed severe hypernatremia (peak serum sodium 196 mmol/L) after drinking a liter of soy sauce on a dare. He developed mental status depression, seizures, clonus, disconjugate gaze, tachycardia (147 beats/minute) and fever (39.4 degrees C rectally). He was treated with 6 L D5W over 30 minutes 4.5 hours after ingestion, and a further 5.2 L of D5W intravenously and 215 mL of free water through the NG tube, as well as 2.4 L of other hypotonic solutions over the next 24 hours. Plasma sodium was normal (145 mmol/L) 32 hours after the ingestion and the patient had a good neurologic outcome with no evidence of central pontine myelonecrosis on MRI (Carlberg et al, 2013).
    c) CASE REPORT: Seizures were observed in a 5-week-old infant who developed severe hypernatremia (211 mmol/L) after ingestion of formula reconstituted with water containing sodium chloride 23 grams per liter for 72 hours (Paut et al, 1999).
    D) CEREBROVASCULAR DISEASE
    1) CEREBRAL CHANGES: Rapid loss of intracellular water from the brain results in subsequent cellular damage, which can lead to irreversible neurologic damage (JEF Reynolds , 1989).
    2) Retention of sodium leads to accumulation of fluids with cerebral edema (Turk et al, 2005; Caraccio & McGuigan, 2004).
    3) Habbick et al (1984) observed low-density areas bilaterally in the putamen on a CT brain scan of a 6-month-old child. Eleven hours after the CT scan, serum sodium was 182 mEq/L. A CT scan repeated when serum sodium had normalized showed resolution of this abnormality.
    4) Cerebral edema and herniation were reported in a 14-year-old boy who became severely hypernatremic (195 mmol/L) following ingestion of an unknown amount of saltwater in an attempt to induce emesis. Despite supportive care, the patient died within 48 hours postingestion (Casavant & Fitch, 2003).
    E) HYPERREFLEXIA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 12-month-old child became hypotonic and hyperreflexic following nasogastric administration of 400 mEq of sodium chloride over 12 hours (El-Dahr et al, 1987).
    F) ABNORMAL GAIT
    1) WITH POISONING/EXPOSURE
    a) GAIT IMBALANCE was seen in a 3-year-old child with a serum sodium concentration of 210 mmol/L (Puczynski et al, 1983).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Vomiting and nausea are symptoms of hypernatremia (Puczynski et al, 1983).
    B) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Diarrhea is a symptom of hypernatremia (JEF Reynolds , 1989).
    C) ABDOMINAL PAIN
    1) WITH POISONING/EXPOSURE
    a) ABDOMINAL CRAMPS are symptoms of hypernatremia (JEF Reynolds , 1989). Hyperosmotic solutions are irritating to the GI tract.
    D) ACUTE GASTRITIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 20-year-old man ingested an estimated 16 g (estimated amount: approximately 1 tablespoon) of coarse salt with a small amount of wine and developed acute epigastric pain, vomiting, and watery diarrhea 48 hours after exposure. An initial physical exam and laboratory and diagnostic studies (e.g., abdominal ultrasound ) were normal. On day 3, an endoscopic exam showed intense congestive antral gastritis and a deep antral ulcer, along with smaller ulcers around the entire circumference. The esophagus, duodenal bulb and descending duodenum appeared normal. There was also no evidence of Helicobacter pylori, malignancy or chronic gastritis. Treatment included an intravenous proton pump inhibitor and sucralfate with resolution of epigastric pain by day 7. By day 70, gastric changes and ulcerations had completely healed (Coton et al, 2009). The authors suggested that the effects of alcohol were minimal in this case, and the patient denied any prior use of gastrotoxic medications.
    E) VASCULAR INSUFFICIENCY OF INTESTINE
    1) WITH POISONING/EXPOSURE
    a) An adult patient developed massive necrosis of gastric, duodenal and jejunal mucosa following ingestion of 1 kg of sodium chloride in 600 mL of water as an emetic (Calam et al, 1982).
    b) Transmural necrosis of the stomach was noted at autopsy following ingestion of 3 to 4 heaping tablespoons of salt added to each of 4 cups of jam (Johnston & Robertson, 1977).
    F) BEZOAR
    1) WITH POISONING/EXPOSURE
    a) CONCRETION: Salt crystals formed a radiopaque concretion in the stomach of a child (Dockery, 1992).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ABNORMAL RENAL FUNCTION
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Renal insufficiency (urea 15.8 mmol/L, serum creatinine 94 micromol/L) was reported in a 5-week-old infant ingesting formula reconstituted with water containing sodium chloride 23 g/L (Paut et al, 1999).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) BICARBONATE DEPLETION: Excess chloride intake may cause bicarbonate depletion (Caillaux et al, 2006; Paut et al, 1999).
    b) CASE REPORT: Metabolic acidosis (base excess -12, pH 7.19) was reported in a 5-week-old infant after ingestion of formula reconstituted with water containing sodium chloride 23 g/L (Paut et al, 1999). In another case, metabolic acidosis (base excess -22.9; pH 7.03) occurred in a 17-day-old infant given infant formula that was incorrectly reconstituted using 6 scoops of powdered formula for each 70 mL feed instead of 2 1/3 scoops of formula. Hyperchloremia (150 mmol/L) was responsible for producing the acidosis observed in this patient; serum lactic acid was not elevated. Metabolic acidosis resolved with oral and intravenous hydration (Caillaux et al, 2006).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) EXCESSIVE SWEATING
    1) WITH POISONING/EXPOSURE
    a) SWEATING may occur with hypernatremia (JEF Reynolds , 1989).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) TREMOR
    1) WITH POISONING/EXPOSURE
    a) Symptoms of sodium chloride overdose may include muscular twitching (Prod Info Thermotab(R), 1990).

Endocrine

    3.16.2) CLINICAL EFFECTS
    A) DIABETES INSIPIDUS
    1) WITH POISONING/EXPOSURE
    a) Diabetes insipidus may occur with hypernatremia (Casavant & Fitch, 2003).
    b) CASE REPORT: Diabetes insipidus with massive diuresis (1250 mL in 1 hour) was reported in a 14-year-old boy who became severely hypernatremic (195 mmol/L) following ingestion of an unknown amount of saltwater in an attempt to induce emesis. Despite supportive care, the patient died within 48 hours postingestion (Casavant & Fitch, 2003).

Reproductive

    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) When injected in mice at high doses (1,900 or 2,500 mg), it was embryotoxic and teratogenic in a study designed to pursue a laboratory animal teratogenicity study to its limits (Nishimura & Miyamoto, 1969). In other studies, it was not teratogenic in rats (Grollman & Grollman, 1962; Minor & Becker, 1971; Singh, 1973), hamsters (Ferm, 1965) or pigs (Rosenkrantz, 1970). It was nontoxic when injected into chick embryos (McLaughlin, 1963).
    2) In experimental animals, sodium chloride has caused delayed effects on newborns, has been fetotoxic, and has caused birth defects and abortions in rats and mice (RTECS , 1997).
    3.20.3) EFFECTS IN PREGNANCY
    A) HUMANS
    1) PLACENTAL DISORDER
    a) Hypertonic solutions of sodium chloride injected into the amniotic fluid can cause disseminated intravascular coagulation, renal necrosis, uterine and cervical lesions, pulmonary embolism, pneumonia, hemorrhage, and death (JEF Reynolds , 1989; Frost, 1968).
    2) PREGNANCY DISORDER
    a) A high intake of sodium chloride may increase the risk of TOXEMIA OF PREGNANCY in susceptible women (Bishop, 1978).
    B) ANIMAL STUDIES
    1) Sodium chloride has been used as a negative control in experimental animal reproductive studies, but has also caused abortions, delayed effects in newborns, fetotoxicity, and birth defects in rats and mice (Nishimura & Miyamoto, 1969; RTECS , 1997).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7647-14-5 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.3) HUMAN STUDIES
    A) GASTRIC CARCINOMA
    1) High dietary intake of sodium chloride has been linked with stomach cancer. In a group of 136 Puerto Rican patients with gastric cancer, a strong dose-related relationship was seen with dietary salt intake (odds ratio = 3.34), as compared to a group of 151 controls; differences in sex, education, and cigarette smoking were taken into account (Nazario et al, 1993).
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) Pre-treatment of Wistar rats with 1 mL of 4.5M sodium chloride given orally enhanced the ability of oral N-METHYL-N'-NITRO-N-NITROSOGUANIDINE (MNNG) to induce squamous cell carcinoma of the forestomach (Sorbye et al, 1994). Sodium chloride at 5 percent in the diet increased the number of hyperplasias and adenocarcinomas induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in the glandular stomach of rats; its effect was synergistic with potassium chloride (Nishikawa et al, 1995).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs and mental status.
    B) Monitor serum electrolytes frequently.
    C) Monitor renal function and urine output. Urinary sodium excretion will be high in all cases of hypernatremia and cannot be used to differentiate salt poisoning from dehydration.
    D) Monitor for evidence of volume overload, pulmonary edema and cerebral edema.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Serum sodium levels are available in most hospital laboratories; sodium concentrations may also be determined in gastric contents, stool contents, and urine.
    a) Severity of toxicity will vary depending upon hydration, amount absorbed, and biological variability. Monitor serum sodium and chloride levels as frequently as required.
    2) Plasma or serum osmolarity is increased with sodium chloride excess (Ellenhorn, 1997).
    3) Blood calcium decreases in patients with hypernatremia which can lead to the development of seizures and tetany (Ellenhorn, 1997).
    4) After fluid correction, serum potassium will be decreased (Ellenhorn, 1997).
    5) Sodium and chloride levels can be measured in human sweat by enzyme activation methods based on beta-galactosidase and alpha-amalyse, and are used clinically to differentiate between persons having and not having cystic fibrosis (Taylor & James, 1996).
    4.1.3) URINE
    A) Urinary sodium excretion will be high in all cases of hypernatremia and cannot be used to differentiate salt poisoning from dehydration. However, the fractional excretion of sodium will be greater than 2% with salt poisoning and less than 1% in dehydration (Coulthard & Haycock, 2003).
    4.1.4) OTHER
    A) OTHER
    1) CEREBROSPINAL FLUID
    a) An increase in cerebral spinal fluid protein has been associated with sodium chloride excess (Caraccio & McGuigan, 2004).
    2) EEG
    a) A diffusely abnormal EEG has been associated with hypernatremic states (Caraccio & McGuigan, 2004).
    3) HEAD CT
    a) A computed axial tomography of the head has revealed hypodensity in the basal ganglion in infants with salt poisoning (Caraccio & McGuigan, 2004).

Radiographic Studies

    A) ABDOMINAL RADIOGRAPH
    1) Dockery (1992) found that a mass of crystallized salt was radiopaque in the stomach.

Treatment

Monitoring

    A) Monitor vital signs and mental status.
    B) Monitor serum electrolytes frequently.
    C) Monitor renal function and urine output. Urinary sodium excretion will be high in all cases of hypernatremia and cannot be used to differentiate salt poisoning from dehydration.
    D) Monitor for evidence of volume overload, pulmonary edema and cerebral edema.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Large ingestions often produce spontaneous vomiting.
    B) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    C) ACTIVATED CHARCOAL
    1) Activated charcoal is not likely to be of use, due to molecular size and strong ionic dissociation of sodium chloride.
    D) OCULAR EXPOSURE
    1) Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. If irritation, pain swelling, lacrimation, or photophobia persist, the patient should be seen in a health care facility.
    6.5.2) PREVENTION OF ABSORPTION
    A) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    B) ACTIVATED CHARCOAL
    1) Activated charcoal is not likely to be of use, due to molecular size and strong ionic dissociation of sodium chloride.
    6.5.3) TREATMENT
    A) SUPPORT
    1) Dilute with milk or water.
    2) Treat hypernatremia with an intravenous solution containing 30 to 50 mEq/L sodium. Longstanding hypernatremia should be corrected slowly. Treat seizures with benzodiazepines. Treat cerebral edema with mannitol. Hemodialysis should be performed in patients with severe toxicity.
    B) AIRWAY MANAGEMENT
    1) Maintain airway patency and adequate oxygenation. Endotracheal intubation and assisted mechanical ventilation may be required.
    C) MONITORING OF PATIENT
    1) Monitor vital signs and mental status.
    2) Monitor serum electrolytes frequently.
    3) Monitor renal function and urine output. Urinary sodium excretion will be high in all cases of hypernatremia and cannot be used to differentiate salt poisoning from dehydration.
    4) Monitor for evidence of volume overload, pulmonary edema and cerebral edema.
    D) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    E) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    7) PHENYTOIN/FOSPHENYTOIN
    a) Benzodiazepines and/or barbiturates are preferred to phenytoin or fosphenytoin in the treatment of drug or withdrawal induced seizures (Wallace, 2005).
    b) PHENYTOIN
    1) PHENYTOIN INTRAVENOUS PUSH VERSUS INTRAVENOUS INFUSION
    a) Administer phenytoin undiluted, by very slow intravenous push or dilute 50 mg/mL solution in 50 to 100 mL of 0.9% saline.
    b) ADULT DOSE: A loading dose of 20 mg/kg IV; may administer an additional 5 to 10 mg/kg dose 10 minutes after loading dose. Rate of administration should not exceed 50 mg/minute (Brophy et al, 2012).
    c) PEDIATRIC DOSE: A loading dose of 20 mg/kg, at a rate not exceeding 1 to 3 mg/kg/min or 50 mg/min, whichever is slower (Loddenkemper & Goodkin, 2011; Prod Info Dilantin(R) intravenous injection, intramuscular injection, 2013).
    d) CAUTIONS: Administer phenytoin while monitoring ECG. Stop or slow infusion if dysrhythmias or hypotension occur. Be careful not to extravasate. Follow each injection with injection of sterile saline through the same needle (Prod Info Dilantin(R) intravenous injection, intramuscular injection, 2013).
    e) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over next 12 to 24 hours for maintenance of therapeutic concentrations. Therapeutic concentrations of 10 to 20 mcg/mL have been reported (Prod Info Dilantin(R) intravenous injection, intramuscular injection, 2013).
    c) FOSPHENYTOIN
    1) ADULT DOSE: A loading dose of 20 mg phenytoin equivalent/kg IV, at a rate not exceeding 150 mg phenytoin equivalent/minute; may give additional dose of 5 mg/kg 10 minutes after the loading infusion (Brophy et al, 2012).
    2) CHILD DOSE: 20 mg phenytoin equivalent/kg IV, at a rate of 3 mg phenytoin equivalent/kg/minute, up to a maximum of 150 mg phenytoin equivalent/minute (Loddenkemper & Goodkin, 2011).
    3) CAUTIONS: Perform continuous monitoring of ECG, respiratory function, and blood pressure throughout the period where maximal serum phenytoin concentrations occur (about 10 to 20 minutes after the end of fosphenytoin infusion) (Prod Info CEREBYX(R) intravenous injection, 2014).
    4) SERUM CONCENTRATION MONITORING: Monitor serum phenytoin concentrations over the next 12 to 24 hours; therapeutic levels 10 to 20 mcg/mL. Do not obtain serum phenytoin concentrations until at least 2 hours after infusion is complete to allow for conversion of fosphenytoin to phenytoin (Prod Info CEREBYX(R) intravenous injection, 2014).
    8) Hyperthermia, lactic acidosis, and muscle destruction may necessitate immediate use of neuromuscular blocking agents. If hyperkalemia is suspected, DO NOT administer succinylcholine. Monitor EEG to ensure cessation of cerebral seizure activity.
    F) HYPERNATREMIA
    1) CHRONIC HYPERNATREMIA
    a) If hypernatremia is longstanding, administer an IV solution containing 30 to 50 mEq/L of sodium (half as chloride and half as bicarbonate) slowly.
    1) This solution may be prepared by adding 6 to 10 mL (15 to 25 mEq) sodium chloride 2.5 mEq/mL for injection and 15 to 25 mL (15 to 25 mEq) sodium bicarbonate 1 mEq/mL for injection to 1000 mL D5W or other suitable solution.
    2) The rate of administration is critical (usually 2/3 of daily maintenance) and should lower serum sodium to normal range no sooner than 24 to 36 hours after institution of therapy. If serum sodium is decreased more rapidly, seizures are likely to ensue.
    b) Goal of therapy is to lower serum sodium level at a rate of 10 mEq/L per day (Caraccio & McGuigan, 2004).
    c) Monitor fluid status carefully. Diuretics, such as furosemide, may be of benefit to enhance diuresis in some cases (Caraccio & McGuigan, 2004).
    2) ACUTE HYPERNATREMIA
    a) For acute, severe hypernatremia secondary to acute ingestion of large amounts of sodium chloride, more rapid correction of serum sodium with intravenous D5W or other hypotonic solutions, oral free water, or hemodialysis may be appropriate.
    b) CASE REPORT: A 19-year-old developed severe hypernatremia after drinking a liter of soy sauce on a dare. He developed mental status depression and seizures. On transfer to a tertiary care facility 4 hours after ingestion, he was comatose (Glasgow coma score 3), had clonus, disconjugate gaze, tachycardia (147 beats/minute) and fever (39.4 degrees C rectally) and serum sodium was 196 mmol/L (corrected for hyperglycemia). He was intubated and treated with 6 L D5W over 30 minutes 4.5 hours after ingestion, after which he had spontaneous eye opening, began coughing in response to the endotracheal tube, and plasma sodium had decreased to 170 mmol/L. A further 5.2 L of D5W intravenously and 215 mL of free water through the NG tube, as well as 2.4 L of other hypotonic solutions was administered over the next 24 hours. Plasma sodium was normal (145 mmol/L) 32 hours after the ingestion and the patient had a good neurologic outcome with no evidence of central pontine myelonecrosis on MRI (Carlberg et al, 2013).
    c) Administration of hypotonic dextrose solution (to correct the volume deficit and restore normal serum sodium over 48 hours) produced a good outcome in a 5 week old infant with severe hypernatremia (serum sodium 211 mEq/L) from unintentional poisoning (Paut et al, 1999). In a second case in a very low birthweight infant also suggests that IV fluid administration to restore normal serum sodium levels over several days can produce a good outcome (Roscelli et al, 1994).
    G) CEREBRAL EDEMA
    1) Intravenous mannitol (0.5 to 1 g/kg) may be administered to remove excess intracellular water from the brain. This can be used when the hypotonic saline treatment is administered too rapidly.

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).

Enhanced Elimination

    A) PERITONEAL DIALYSIS
    1) Peritoneal dialysis with 7% dextrose should be considered in infants with salt poisoning; 4 mEq of potassium chloride/liter may be administered, but careful electrolyte monitoring is imperative.
    2) Peritoneal dialysis removed 53 mEq of sodium over 14 hours and reduced the serum sodium concentration from 189 mEq/L to 160 mEq/L (El-Dahr et al, 1987).
    3) Peritoneal dialysis may be required for more than 24 hours of continuous exchanges to effect clinical improvement (Caraccio & McGuigan, 2004; Hey & Hickling, 1982).
    B) HEMODIALYSIS
    1) Hemodialysis should be considered to restore normal and electrolyte relationships if standard measures are ineffective. Indications may include:
    1) Serum sodium greater than 200 mEq/L
    2) Renal impairment
    3) Moribund patient
    2) CASE REPORTS: Three adult patients with severe hypernatremia (serum sodium levels of 178, 172, and 182 mEq/L, respectively) that was associated with cardiopulmonary or hepatorenal complications were treated with acute hypotonic hemodialysis (standard commercial dialysate was modified to a final concentration of 110 mEq/L sodium). Serum sodium was decreased successfully in all 3 patients from 178 to 152, 172 to 153 and 182 to 148 mEq/L, respectively. Each patient was admitted in an obtunded state and improved neurologically within 24 hours or less following dialysis. However, one patient died despite a reduction in serum sodium due to progressive hepatic failure, the other 2 patients recovered uneventfully (Pazmino & Pazmino, 1993).
    3) CASE REPORT: A 65-year-old woman who developed acute hypernatremia (serum sodium 176 mEq/L) after drinking 1150 mL of soy sauce was treated successfully with emergent hemodialysis. Her serum sodium decreased to 146 mEq/L after hemodialysis without significant neurologic complications (Sakai et al, 2004).
    C) HEMOFILTRATION
    1) Continuous arteriovenous hemofiltration may be useful to manage hypernatremia (Caraccio & McGuigan, 2004).

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) All patients with evidence of systemic toxicity from sodium chloride, severe hypernatremia not responding to hydration, or those with intractable vomiting should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Asymptomatic patients with ingestions of less than 8 mEq/kg (0.5 g/kg) sodium chloride) can probably be managed at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a medical toxicologist or poison center for patients with severe hypernatremia or severe clinical manifestations.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Symptomatic patients, those with deliberate ingestions, and patients ingesting 8 mEq/kg (0.5 g/kg) sodium chloride or more should be referred to a healthcare facility.

Abstracts

Case Reports

    A) ADULT
    1) A 20-year-old woman ingested large amounts of salt water as part of a ritual to treat depression. Over the course of approximately 11 hours the patient became progressively obtunded. A the time of presentation her serum sodium was 255 mEq/L. She was treated aggressively with hypotonic fluid but died several hours after arrival. The authors reviewed 19 additional deaths reported in the literature. They noted the vast majority of cases are women, that all the patients had cognitive or psychiatric impairment, and that saline was most often taken as an emetic or by mistake and over a short period of time (Ofran et al, 2004).
    B) PEDIATRIC
    1) TODDLER: A 3-year-old child developed hypernatremia (188 mEq/L sodium chloride) following consumption of 2 glasses of water containing an unknown amount of table salt administered to induce emesis. The child died despite treatment with mechanical ventilation, fluid therapy, and peritoneal dialysis (Barer et al, 1973).
    2) INFANT: A 5-week-old infant developed hypernatremia (211 mmol/L) after ingesting improperly made infant formula reconstituted with water containing 23 g sodium chloride per liter for 72 hours. Upon admission, the child had moderate dehydration, lethargy, and lateral deviation of the eyes. Metabolic acidosis, renal insufficiency, and natriuresis (238 mmol/L) were also noted. During management of the child with dextrose and hypotonic saline infusions, the child developed pulmonary edema requiring mechanical ventilation, neurological dysfunction, and seizures. The child eventually recovered with no sequelae noted after 10 months (Paut et al, 1999).

Range Of Toxicity

Summary

    A) TOXICITY: Ingestion of 0.5 to 1 g/kg (8.6 to 17.2 mEq/kg) of sodium chloride is probably toxic in the majority of patients. Central nervous system signs and symptoms are common with serum sodium concentrations above 150 to 160 mEq/L. At such levels, there is a 10% chance of seizures which increases when serum sodium concentration reaches 160 to 185 mEq/L. Death is a frequent occurrence at serum sodium concentrations above 185 mEq/L. A teenager survived a serum sodium concentration of 196 mmol/L following the ingestion of soy sauce (quart size bottle; equivalent to 160 to 170 g salt) following aggressive supportive care; no permanent sequelae occurred. PEDIATRIC: One level tablespoon (17.85 g) is approximately 305 mEq of sodium, and if retained, would raise serum levels by 30.5 mEq/L in a 3-year-old (15 kg) child. A toddler died after ingesting 400 mEq/kg and an adolescent died after absorbing an estimated 45 g sodium chloride as salt water.
    B) RECOMMENDED DAILY CONSUMPTION: ADULT: It is recommended an adult consume no more than 2300 mg of sodium daily.

Therapeutic Dose

    7.2.1) ADULT
    A) ROUTE OF ADMINISTRATION
    1) ORAL REPLACEMENT DOSE - 1 to 2 grams three times daily, orally with food or as a solution (JEF Reynolds , 1989).
    2) PARENTERAL REPLACEMENT - Dose varies depending on several factors including age, weight, and clinical condition of the patient (JEF Reynolds , 1989).

Minimum Lethal Exposure

    A) CASE REPORTS
    1) HISTORY: A traditional method of suicide among the Chinese was drinking a pint of saturated salt water (Elton et al, 1963).
    2) Deaths have been associated with administration of salt water to induce emesis (Calam et al, 1982; Hey & Hickling, 1982; Gresham & Mashru, 1982; Streat, 1982).
    3) ADULT
    a) An adult with Down Syndrome developed a grand mal seizure 2 hours after ingesting a supersaturated salt solution (estimated amount 70 to 90 g of salt {1,200 to 1500 mEq of sodium}; serum sodium 209 mEq/L) intended for gargling. Upon admission he was in status epilepticus and responding only to painful stimuli. Despite supportive care and a normalizing serum sodium by the third day, oliguria, severe edema, a cumulative fluid balance of more than 24 L and neurologic deterioration were present. Seventy-two hours after admission cardiac asystole occurred and resuscitation was unsuccessful. Postmortem exam revealed severe cerebral edema, bilateral pleural effusions and pulmonary congestion, along with ascites of 3.7 L (Moder & Hurley, 1990).
    4) PEDIATRIC
    a) TODDLER: An estimated dose of over 400 mEq/kg resulted in brain injury leading to death in a 2-year-old child given a salt water solution to induce emesis (DeGenaro & Nyhan, 1971).
    b) TEENAGER: A 14-year-old boy developed severe hypernatremia (195 mmol/L) with associated complications (coma, seizures, tachycardia, hyperthermia, hypotension, and cerebral edema) after ingesting an unknown amount of saltwater in an attempt to induce emesis. Despite aggressive supportive care, the patient's clinical condition continued to deteriorate with subsequent death within 48 hours postingestion. An autopsy revealed cerebral edema and hemorrhagic gastritis. It was later determined that the patient had absorbed at least 45 g (5 tablespoons) of sodium chloride (Casavant & Fitch, 2003).

Maximum Tolerated Exposure

    A) SUMMARY
    1) RECOMMENDED DAILY CONSUMPTION: ADULT: It is recommended an adult consume no more than 2300 mg of sodium daily (US Food and Drug Administration, 2012).
    2) When serum sodium ranges between 150 and 160 mEq/L, CNS symptoms are common and seizures occur in approximately 10% of patients.
    3) With serum sodium concentrations greater than 160 to 185 mEq/L, seizures occur more commonly, particularly if treatment precipitates a rapid decrease in serum sodium. Death is a frequent occurrence at serum sodium concentrations greater than 185 mEq/L (Caraccio & McGuigan, 2003).
    4) One level tablespoonful of salt contains about 305 mEq of sodium and, if retained and absorbed, would raise the serum sodium level by 30.5 mEq/L in a 3-year-old (15 kg) child (Caraccio & McGuigan, 2003).
    5) Ingestion of 0.5 to 1 g/kg (8.6 to 17.2 mEq/kg) of sodium chloride is probably toxic in the majority of patients (Caraccio & McGuigan, 2003).
    B) CASE REPORTS
    1) ADULT
    a) SURVIVAL/TEENAGER: A 19-year-old healthy man (72 kg) drank a quart sized bottle of soy sauce (equivalent to 160 and 170 g salt; considered to be a lethal dose based on weight) following a challenge by his friends and survived. Two hours after ingestion he was unresponsive to verbal or painful stimuli with evidence of seizure-like activity. He was treated aggressively and was transferred to a tertiary care center. His serum sodium concentration peaked at 196 mmol/L (corrected for hyperglycemia) 4.5 hours postingestion. The patient was intubated and received 6 L of D5W rapidly infused over 30 minutes. A head CT was consistent with dehydration (ie, hyperdensity of the venous sinuses), but otherwise normal. Over the next 24 hours, the patient received an additional 5.2 L of D5W and 215 mL of free water via a NG tube and an additional 2.4 L of other hypotonic solutions. The patient maintained an adequate urine output and hemodialysis was not performed. Thirty-two hours after ingestion serum sodium normalized. During the second day, the patient self-extubated and was noted to be confused. By day 3, his mental status had normalized. He completely recovered and was discharged on day 4 neurologically intact (Carlberg et al, 2013).
    b) A 20-year-old man developed acute ulcerative gastritis following the ingestion of approximately 16 g (estimated amount: approximately 1 tablespoon) of coarse salt. Symptoms resolved within 1 week of IV treatment with a proton pump inhibitor and sucralfate. The patient was asymptomatic within 1 week with complete healing by day 70 (Coton et al, 2009).
    c) A 63-year-old woman was found unresponsive after ingesting 1150 mL of soy sauce with an initial blood sodium concentration of 176 mEq/L. Following emergent hemodialysis, serum sodium decreased to 146 mEq/L and the patient recovered without sequelae (Sakai et al, 2004).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) CASE REPORTS
    a) PEDIATRIC
    1) Lethal doses are generally estimated at about 3 grams/kilogram, but doses as low as 0.75 gram/kilogram have been fatal (Elton et al, 1963).
    2) Fatal hypernatremia, with a serum sodium concentration of 245 mmol/L was reported in a 4-year-old girl who consumed large amounts of a salt solution in order to induce emesis following ingestion of bathing foam. The patient developed seizures, became unresponsive, and was pronounced dead within 2 hours post-ingestion. Autopsy showed cerebral and pulmonary edema (Turk et al, 2005).
    b) INFANT
    1) A 12-month-old child had an initial serum sodium concentration of 189 milliequivalents/Liter and serum osmolality of 381 milliosmoles/kilogram water following nasogastric administration of 400 milliequivalents of sodium chloride over 12 hours (El-Dahr et al, 1987).
    2) An infant accidently poisoned by substitution of salt for sugar in infant formula had a serum sodium concentration of 274 milliequivalents/Liter but survived (Finberg et al, 1963).
    c) ADULT
    1) Initial serum sodium concentration was 209 milliequivalents/liter in a 41-year-old man with Down's syndrome who ingested the contents of a glass containing approximately one-third cup of salt (Moder & Hurley, 1990a).
    2) Fatal hypernatremia (serum sodium concentrations up to 196 mmol/L) was reported in two patients who were ingested large amounts of salt solution in order to induce emesis. Both patients developed severe cerebral edema and were pronounced dead within 48 hours post-ingestion (Turk et al, 2005).

Workplace Standards

    A) ACGIH TLV Values for CAS7647-14-5 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS7647-14-5 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS7647-14-5 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS7647-14-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (ORAL)RAT:
    1) 3.32 to 4.18 g/kg (Boyd & Shanas, 1963)

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Together with H2O, NaCl constitutes the basic internal milieu of mammals. A contributor to stability of extracellular and thus intracellular osmolarity, the sodium ion is distributed virtually exclusively in the extracellular compartment.
    1) When the ratio of sodium to water in that compartment exceeds normal, hypernatremia is said to exist; while this is much more commonly due to water deficiency than sodium excess, ingestion of excessive amounts of sodium chloride per se can lead to the condition.
    B) HYPERNATREMIA FROM EXERCISE - A study reported that short burst of intensive exercise (100 meter swim) lasting approximately one minute resulted in hypernatremia (serum sodium > 150 mEq/L) in 30 to 40 percent of well-trained athletes.
    1) This short exercise burst resulted in a 12-fold increase in blood lactate levels, an increase in serum osmolality of 14 +/- 2 mosm/L, and a mean increase in serum sodium of 7 +/- 1 mEq/L.
    2) Hypernatremia may be a consequence of a shift of hypotonic fluid from the extracellular to the intracellular compartment (Felig et al, 1982).

Toxicologic Mechanism

    A) Acute salt poisoning produces central nervous system damage when brain cells become dehydrated following the acute osmotic shift of intracellular fluids to the extracellular space (Habbick et al, 1984).
    B) Brain cell damage may also occur after idiogenic osmoles have been established and vigorous therapeutic hydration leads to cerebral edema. This may result in a diffuse encephalopathy with multiple small hemorrhages or thromboses.
    1) No gross neurologic deficit may be noted in surviving children with this condition, however, there may be general cerebral dysfunction (Macaulay & Watson, 1967).

Physicochemical

Physical Characteristics

    A) This compound exists as a colorless, translucent, cubic, odorless crystals, granules, or powder (Windholz, 1983; (JEF Reynolds , 1989; HSDB , 1997).

Ph

    A) 6.7-7.3 (Windholz, 1983)

Molecular Weight

    A) 58.4 (Windholz, 1983; (JEF Reynolds , 1989)

Animal Toxicology

Clinical Effects

    11.1.1) AVIAN/BIRD
    A) SANDHILL CRANE - Franson et al (1981) observed muscle weakness, paresis, dyspnea, and depression in sandhill cranes given drinking water containing a sodium chloride concentration of 1 percent.
    B) CHICKEN - Ingestion of water containing 0.9 percent NaCl in young chickens produced signs and symptoms of weakness, polydypsia, dyspnea, and 100 percent mortality within 5 days (Blaxland, 1946).

References

General Bibliography

    1) 40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.
    2) 40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.
    3) 49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.
    4) 62 FR 58840: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 1997.
    5) 65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    6) 65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    7) 65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    8) 66 FR 21940: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2001.
    9) 67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.
    10) 68 FR 42710: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2003.
    11) 69 FR 54144: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2004.
    12) AIHA: 2006 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook, American Industrial Hygiene Association, Fairfax, VA, 2006.
    13) AMA Department of DrugsAMA Department of Drugs: AMA Evaluations Subscription, American Medical Association, Chicago, IL, 1992.
    14) American Conference of Governmental Industrial Hygienists : ACGIH 2010 Threshold Limit Values (TLVs(R)) for Chemical Substances and Physical Agents and Biological Exposure Indices (BEIs(R)), American Conference of Governmental Industrial Hygienists, Cincinnati, OH, 2010.
    15) Ansell-Edmont: SpecWare Chemical Application and Recommendation Guide. Ansell-Edmont. Coshocton, OH. 2001. Available from URL: http://www.ansellpro.com/specware. As accessed 10/31/2001.
    16) Barer J, Hill LL, & Hill RM: Fatal poisoning from salt used as an emetic. Am J Dis Child 1973; 125:889-890.
    17) Bata Shoe Company: Industrial Footwear Catalog, Bata Shoe Company, Belcamp, MD, 1995.
    18) Best Manufacturing: ChemRest Chemical Resistance Guide. Best Manufacturing. Menlo, GA. 2002. Available from URL: http://www.chemrest.com. As accessed 10/8/2002.
    19) Best Manufacturing: Degradation and Permeation Data. Best Manufacturing. Menlo, GA. 2004. Available from URL: http://www.chemrest.com/DomesticPrep2/. As accessed 04/09/2004.
    20) Bishop C: Canad Pharm J 1978; 111:357-358.
    21) Blanchard JD & Willeke K: J Appl Physiol Resp Environ Exerc Physiol 1984; 57:1850-1856.
    22) Blaxland JD: The toxicity of sodium chloride for fowls. Vet J 1946; 102:157-173.
    23) Boss Manufacturing Company: Work Gloves, Boss Manufacturing Company, Kewanee, IL, 1998.
    24) Boyd EM & Shanas MN: The acute oral toxicity of sodium chloride. Arch Internat Pharmacodyn 1963; 144:86-96.
    25) Brophy GM, Bell R, Claassen J, et al: Guidelines for the evaluation and management of status epilepticus. Neurocrit Care 2012; 17(1):3-23.
    26) Budavari S: The Merck Index, 12th ed, Merck & Co, Inc, Whitehouse Station, NJ, 1996, pp 1474.
    27) Caillaux G, Denizot S, Roze JC, et al: Shock revealing salt poisoning in a neonate. Pediatr Emerg Care 2006; 22(10):748-750.
    28) Calam J, Krasner N, & Haqqani M: Extensive gastrointestinal damage following a saline emetic. Dig Dis Sci 1982; 27:936-940.
    29) Caraccio TR & McGuigan MA: Over-the-Counter Products. In: Dart RC ed. Medical Toxicology. 3rd ed., 3rd ed. Lippincott Williams & Wilkins, Philadelphia, PA, 2004, pp -.
    30) Caraccio TR & McGuigan MA: Over-the-Counter Products. In: Dart RC, Caravati EM, McGuigan MA, eds. Medical Toxicology, 3rd ed.. Lippincott Williams & Wilkins, Philadelphia, PA, 2003, pp 1051-1062.
    31) Caravati EM: Alkali. In: Dart RC, ed. Medical Toxicology, Lippincott Williams & Wilkins, Philadelphia, PA, 2004.
    32) Carlberg DJ, Borek HA, Syverud SA, et al: Survival of Acute Hypernatremia Due to Massive Soy Sauce Ingestion. J Emerg Med 2013; Epub:Epub.
    33) Casavant MJ & Fitch JA: Fatal hypernatremia from saltwater used as an emetic. J Toxicol Clin Toxicol 2003; 41(6):861-863.
    34) Chamberlain JM, Altieri MA, & Futterman C: A prospective, randomized study comparing intramuscular midazolam with intravenous diazepam for the treatment of seizures in children. Ped Emerg Care 1997; 13:92-94.
    35) ChemFab Corporation: Chemical Permeation Guide Challenge Protective Clothing Fabrics, ChemFab Corporation, Merrimack, NH, 1993.
    36) Chin RF , Neville BG , Peckham C , et al: Treatment of community-onset, childhood convulsive status epilepticus: a prospective, population-based study. Lancet Neurol 2008; 7(8):696-703.
    37) Choonara IA & Rane A: Therapeutic drug monitoring of anticonvulsants state of the art. Clin Pharmacokinet 1990; 18:318-328.
    38) Clayton GD & Clayton FE: Patty's Industrial Hygiene and Toxicology, Vol 2F, Toxicology, 4th ed, John Wiley & Sons, New York, NY, 1994, pp 4491-4492.
    39) Comasec Safety, Inc.: Chemical Resistance to Permeation Chart. Comasec Safety, Inc.. Enfield, CT. 2003. Available from URL: http://www.comasec.com/webcomasec/english/catalogue/mtabgb.html. As accessed 4/28/2003.
    40) Comasec Safety, Inc.: Product Literature, Comasec Safety, Inc., Enfield, CT, 2003a.
    41) Coton T, Mallaret C, Coilliot C, et al: Severe acute ulcerated gastritis induced by salt. Presse Med 2009; 38(3):499-500.
    42) Coulthard MG & Haycock GB: Distinguishing between salt poisoning and hypernatraemic dehydration in children. BMJ 2003; 326(7381):157-160.
    43) DFG: List of MAK and BAT Values 2002, Report No. 38, Deutsche Forschungsgemeinschaft, Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area, Wiley-VCH, Weinheim, Federal Republic of Germany, 2002.
    44) Dautrebande L: Arch Internat Pharm Ther 1949; 80:388-412.
    45) DeGenaro F & Nyhan WL: Salt -- a dangerous antidote. J Pediatr 1971; 78:1048-1049.
    46) Dockery WK: Fatal intentional salt poisoning associated with a radiopaque mass. Pediatrics 1992; 89:964-965.
    47) DuPont: DuPont Suit Smart: Interactive Tool for the Selection of Protective Apparel. DuPont. Wilmington, DE. 2002. Available from URL: http://personalprotection.dupont.com/protectiveapparel/suitsmart/smartsuit2/na_english.asp. As accessed 10/31/2002.
    48) DuPont: Permeation Guide for DuPont Tychem Protective Fabrics. DuPont. Wilmington, DE. 2003. Available from URL: http://personalprotection.dupont.com/en/pdf/tyvektychem/pgcomplete20030128.pdf. As accessed 4/26/2004.
    49) DuPont: Permeation Test Results. DuPont. Wilmington, DE. 2002a. Available from URL: http://www.tyvekprotectiveapprl.com/databases/default.htm. As accessed 7/31/2002.
    50) EPA: Search results for Toxic Substances Control Act (TSCA) Inventory Chemicals. US Environmental Protection Agency, Substance Registry System, U.S. EPA's Office of Pollution Prevention and Toxics. Washington, DC. 2005. Available from URL: http://www.epa.gov/srs/.
    51) El-Dahr S, Gomez A, & Campbell FG: Rapid correction of acute salt poisoning by peritoneal dialysis. Pediatr Nephrol 1987; 1:602-604.
    52) Ellenhorn MJ & Barceloux DG: Medical Toxicology: Diagnosis and Treatment of Human Poisoning, Elsevier, New York, NY, 1988.
    53) Ellenhorn MJ: Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human Poisoning, 2nd ed, Williams & Wilkins, Baltimore, MD, 1997, pp 1014-1016.
    54) Elton NW, Elton WJ, & Nazareno JP: Pathology of acute salt poisoning in infants. Am J Clin Pathol 1963; 39:252-264.
    55) Felig P, Johnson C, & Levitt M: Hypernatremia induced by maximal exercise. JAMA 1982; 248:1209-1211.
    56) Ferm VH: Lancet 1965; 1:1338-1339.
    57) Finberg L, Kiley J, & Luttrell CN: Mass accidental salt poisoning in infancy. JAMA 1963; 184:187-190.
    58) Frost AC: Death following intrauterine injection of hypertonic saline solution with hydatidiform mole. Am J Obstet Gynecol 1968; 101:342-344.
    59) Furiosi NJ: Arch Environ Health 1973; 27:405-408.
    60) Gamble J: Am J Ind Med 1983; 4:435-458.
    61) Grant WM: Toxicology of the Eye, 3rd ed, Charles C Thomas, Springfield, IL, 1986.
    62) Gresham GS & Mashru MKS: Fatal poisoning with sodium chloride. Forens Sci Internat 1982; 20:87-88.
    63) Grollman A & Grollman EF: J Clin Invest 1962; 41:710-714.
    64) Guardian Manufacturing Group: Guardian Gloves Test Results. Guardian Manufacturing Group. Willard, OH. 2001. Available from URL: http://www.guardian-mfg.com/guardianmfg.html. As accessed 12/11/2001.
    65) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 1997; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    66) Habbick BF, Hill A, & Tchang SPK: Computed tomography in an infant with salt poisoning: relationship of hypodense areas in basal ganglia to serum sodium concentration. Pediatrics 1984; 74:1123-1125.
    67) Haldiya KR, Mathur ML, Sachdev R, et al: Risk of high blood pressure in salt workers working near salt milling plants: a cross-sectional and interventional study. Environ Health 2005; 4:13-.
    68) Hegenbarth MA & American Academy of Pediatrics Committee on Drugs: Preparing for pediatric emergencies: drugs to consider. Pediatrics 2008; 121(2):433-443.
    69) Hey A & Hickling KG: Accidental salt poisoning. NZ Med J 1982; 95:864.
    70) Hvidberg EF & Dam M: Clinical pharmacokinetics of anticonvulsants. Clin Pharmacokinet 1976; 1:161.
    71) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: 1,3-Butadiene, Ethylene Oxide and Vinyl Halides (Vinyl Fluoride, Vinyl Chloride and Vinyl Bromide), 97, International Agency for Research on Cancer, Lyon, France, 2008.
    72) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol, 88, International Agency for Research on Cancer, Lyon, France, 2006.
    73) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Household Use of Solid Fuels and High-temperature Frying, 95, International Agency for Research on Cancer, Lyon, France, 2010a.
    74) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Smokeless Tobacco and Some Tobacco-specific N-Nitrosamines, 89, International Agency for Research on Cancer, Lyon, France, 2007.
    75) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Some Non-heterocyclic Polycyclic Aromatic Hydrocarbons and Some Related Exposures, 92, International Agency for Research on Cancer, Lyon, France, 2010.
    76) IARC: List of all agents, mixtures and exposures evaluated to date - IARC Monographs: Overall Evaluations of Carcinogenicity to Humans, Volumes 1-88, 1972-PRESENT. World Health Organization, International Agency for Research on Cancer. Lyon, FranceAvailable from URL: http://monographs.iarc.fr/monoeval/crthall.html. As accessed Oct 07, 2004.
    77) ILC Dover, Inc.: Ready 1 The Chemturion Limited Use Chemical Protective Suit, ILC Dover, Inc., Frederica, DE, 1998.
    78) International Agency for Research on Cancer (IARC): IARC monographs on the evaluation of carcinogenic risks to humans: list of classifications, volumes 1-116. International Agency for Research on Cancer (IARC). Lyon, France. 2016. Available from URL: http://monographs.iarc.fr/ENG/Classification/latest_classif.php. As accessed 2016-08-24.
    79) International Agency for Research on Cancer: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. World Health Organization. Geneva, Switzerland. 2015. Available from URL: http://monographs.iarc.fr/ENG/Classification/. As accessed 2015-08-06.
    80) JEF Reynolds : Martindale: The Extra Pharmacopeia. The Pharmaceutical Press. London, England (Internet Version). Edition expires 1989; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    81) Johnston JG & Robertson WO: Fatal ingestion of table salt by an adult. West J Med 1977; 126:141-143.
    82) Joossens JV: Triangle 1973; 12:916.
    83) Kappler, Inc.: Suit Smart. Kappler, Inc.. Guntersville, AL. 2001. Available from URL: http://www.kappler.com/suitsmart/smartsuit2/na_english.asp?select=1. As accessed 7/10/2001.
    84) Kaufman T, Monies-Chass I, & Hirshowitz B: Sodium poisoning: a lethal case of a burned child. Burns 1986; 12:293-294.
    85) Kimberly-Clark, Inc.: Chemical Test Results. Kimberly-Clark, Inc.. Atlanta, GA. 2002. Available from URL: http://www.kc-safety.com/tech_cres.html. As accessed 10/4/2002.
    86) Kleinman ME, Chameides L, Schexnayder SM, et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 14: pediatric advanced life support. Circulation 2010; 122(18 Suppl.3):S876-S908.
    87) Kupiec TC, Goldenring JM, & Raj V: A non-fatal case of sodium toxicity. J Analyt Toxicol 2004; 28:526-528.
    88) Kushner FH: Sodium chloride eye drops as a cause of epistaxis (Letter). Arch Ophthalmol 1987; 105:1634.
    89) LaCrosse-Rainfair: Safety Products, LaCrosse-Rainfair, Racine, WI, 1997.
    90) Loddenkemper T & Goodkin HP: Treatment of Pediatric Status Epilepticus. Curr Treat Options Neurol 2011; Epub:Epub.
    91) MAPA Professional: Chemical Resistance Guide. MAPA North America. Columbia, TN. 2003. Available from URL: http://www.mapaglove.com/pro/ChemicalSearch.asp. As accessed 4/21/2003.
    92) MAPA Professional: Chemical Resistance Guide. MAPA North America. Columbia, TN. 2004. Available from URL: http://www.mapaglove.com/ProductSearch.cfm?id=1. As accessed 6/10/2004.
    93) Macaulay D & Watson M: Hypernatremia in infants as a cause of brain damage. Arch Dis Child 1967; 42:485-491.
    94) Manno EM: New management strategies in the treatment of status epilepticus. Mayo Clin Proc 2003; 78(4):508-518.
    95) Mar-Mac Manufacturing, Inc: Product Literature, Protective Apparel, Mar-Mac Manufacturing, Inc., McBee, SC, 1995.
    96) Marigold Industrial: US Chemical Resistance Chart, on-line version. Marigold Industrial. Norcross, GA. 2003. Available from URL: www.marigoldindustrial.com/charts/uschart/uschart.html. As accessed 4/14/2003.
    97) Maurice DM: Influence on corneal permeability of bathing with solutions of differing reaction and tonicity. Br J Ophthalmol 1955; 39:463-472.
    98) McLaughlin J Jr: Toxicol Appl Pharmacol 1963; 5:760-771.
    99) Melino C & Pascone A: Folia Medica 1973; 56:53-67.
    100) Memphis Glove Company: Permeation Guide. Memphis Glove Company. Memphis, TN. 2001. Available from URL: http://www.memphisglove.com/permeation.html. As accessed 7/2/2001.
    101) Minor JL & Becker BA: Toxicol Appl Pharmacol 1971; 19:373.
    102) Moder KG & Hurley DL: Fatal hypernatremia from exogenous salt intake: report of a case and review of the literature. Mayo Clin Proc 1990a; 65:1587-1594.
    103) Moder KG & Hurley DL: Fatal hypernatremia from exogenous salt intake: report of a case and review of the literature.. Mayo Clin Proc 1990; 65:1587-1594.
    104) Montgomery Safety Products: Montgomery Safety Products Chemical Resistant Glove Guide, Montgomery Safety Products, Canton, OH, 1995.
    105) NFPA: Fire Protection Guide to Hazardous Materials, 13th ed., National Fire Protection Association, Quincy, MA, 2002.
    106) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 1, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2001.
    107) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 2, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2002.
    108) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 3, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2003.
    109) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 4, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2004.
    110) Naradzay J & Barish RA: Approach to ophthalmologic emergencies. Med Clin North Am 2006; 90(2):305-328.
    111) Nat-Wear: Protective Clothing, Hazards Chart. Nat-Wear. Miora, NY. 2001. Available from URL: http://www.natwear.com/hazchart1.htm. As accessed 7/12/2001.
    112) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,3-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    113) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,4-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    114) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Butylene Oxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648083cdbb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    115) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Dibromoethane (Proposed). United States Environmental Protection Agency. Washington, DC. 2007g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802796db&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
    116) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,3,5-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    117) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 2-Ethylhexyl Chloroformate (Proposed). United States Environmental Protection Agency. Washington, DC. 2007b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037904e&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    118) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Acrylonitrile (Proposed). United States Environmental Protection Agency. Washington, DC. 2007c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648028e6a3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    119) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Adamsite (Proposed). United States Environmental Protection Agency. Washington, DC. 2007h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    120) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Agent BZ (3-quinuclidinyl benzilate) (Proposed). United States Environmental Protection Agency. Washington, DC. 2007f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ad507&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
    121) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Allyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039d9ee&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    122) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    123) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Arsenic Trioxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480220305&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    124) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Automotive Gasoline Unleaded (Proposed). United States Environmental Protection Agency. Washington, DC. 2009a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cc17&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    125) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Biphenyl (Proposed). United States Environmental Protection Agency. Washington, DC. 2005j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1b7&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    126) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bis-Chloromethyl Ether (BCME) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648022db11&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    127) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Boron Tribromide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae1d3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    128) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromine Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2007d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039732a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    129) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromoacetone (Proposed). United States Environmental Protection Agency. Washington, DC. 2008e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187bf&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    130) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Calcium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    131) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae328&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    132) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Sulfide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037ff26&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    133) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Chlorobenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803a52bb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    134) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Cyanogen (Proposed). United States Environmental Protection Agency. Washington, DC. 2008f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187fe&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    135) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Dimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbf3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    136) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Diphenylchloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    137) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091884e&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    138) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Phosphorodichloridate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480920347&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    139) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809203e7&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    140) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    141) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Germane (Proposed). United States Environmental Protection Agency. Washington, DC. 2008j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963906&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    142) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Hexafluoropropylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1f5&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    143) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ketene (Proposed). United States Environmental Protection Agency. Washington, DC. 2007. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ee7c&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    144) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    145) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    146) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Malathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2009k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809639df&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    147) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Mercury Vapor (Proposed). United States Environmental Protection Agency. Washington, DC. 2009b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a087&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    148) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Isothiocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a03&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    149) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a57&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    150) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl tertiary-butyl ether (Proposed). United States Environmental Protection Agency. Washington, DC. 2007a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802a4985&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    151) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methylchlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5f4&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    152) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    153) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c646&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    154) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN1 CAS Reg. No. 538-07-8) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    155) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN2 CAS Reg. No. 51-75-2) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    156) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN3 CAS Reg. No. 555-77-1) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    157) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Tetroxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091855b&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    158) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Trifluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e0c&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    159) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008o. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e32&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    160) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perchloryl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e268&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    161) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perfluoroisobutylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2009d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26a&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    162) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008p. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dd58&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    163) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2006d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020cc0c&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    164) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    165) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phorate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008q. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dcc8&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    166) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene (Draft-Revised). United States Environmental Protection Agency. Washington, DC. 2009e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a08a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    167) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene Oxime (Proposed). United States Environmental Protection Agency. Washington, DC. 2009f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26d&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    168) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    169) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    170) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Propargyl Alcohol (Proposed). United States Environmental Protection Agency. Washington, DC. 2006e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec91&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    171) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Selenium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec55&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    172) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Silane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d523&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    173) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    174) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    175) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Strontium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    176) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sulfuryl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec7a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    177) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tear Gas (Proposed). United States Environmental Protection Agency. Washington, DC. 2008s. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e551&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    178) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tellurium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e2a1&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    179) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tert-Octyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2008r. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5c7&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    180) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tetramethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-17.
    181) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    182) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7d608&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    183) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethylacetyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008t. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5cc&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    184) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Zinc Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    185) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for n-Butyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064808f9591&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    186) National Institute for Occupational Safety and Health: NIOSH Pocket Guide to Chemical Hazards, U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Cincinnati, OH, 2007.
    187) National Research Council : Acute exposure guideline levels for selected airborne chemicals, 5, National Academies Press, Washington, DC, 2007.
    188) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 6, National Academies Press, Washington, DC, 2008.
    189) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 7, National Academies Press, Washington, DC, 2009.
    190) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 8, National Academies Press, Washington, DC, 2010.
    191) Nazario CM, Szklo M, & Diamond E: Salt and gastric cancer -- a case-control study in Puerto Rico. Internat J Epidemiol 1993; 22:790-797.
    192) Neese Industries, Inc.: Fabric Properties Rating Chart. Neese Industries, Inc.. Gonzales, LA. 2003. Available from URL: http://www.neeseind.com/new/TechGroup.asp?Group=Fabric+Properties&Family=Technical. As accessed 4/15/2003.
    193) Nishikawa A, Furukawa F, & Mitsui M: Dose-dependent promotion effects of potassium chloride on glandular stomach carcinogenesis in rats after initiation with N-methyl-N'-nitro-N-nitrosoguanidine and the synergistic influence with sodium chloride. Cancer Res 1995; 55:5238-5241.
    194) Nishimura H & Miyamoto S: ACTA Anat Nippon 1969; 74:121-124.
    195) North: Chemical Resistance Comparison Chart - Protective Footwear . North Safety. Cranston, RI. 2002. Available from URL: http://www.linkpath.com/index2gisufrm.php?t=N-USA1. As accessed April 30, 2004.
    196) North: eZ Guide Interactive Software. North Safety. Cranston, RI. 2002a. Available from URL: http://www.northsafety.com/feature1.htm. As accessed 8/31/2002.
    197) Ofran Y, Lavi D, Opher D, et al: Fatal voluntary salt intake resulting in the highest ever documented sodium plasma level in adults (255 mmol L-1): a disorder linked to female gender and psychiatric disorders. J Intern Med 2004; 256(6):525-528.
    198) Paut O, Andre N, & Fabre P: The management of extreme hypernatremia secondary to salt poisoning in an infant. Paediatr Anaesthes 1999; 9:171-174.
    199) Pazmino PA & Pazmino BP: Treatment of acute hypernatremia with hemodialysis.. Am J Nephrol 1993; 13:260-265.
    200) Peate WF: Work-related eye injuries and illnesses. Am Fam Physician 2007; 75(7):1017-1022.
    201) Peberdy MA , Callaway CW , Neumar RW , et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care science. Part 9: post–cardiac arrest care. Circulation 2010; 122(18 Suppl 3):S768-S786.
    202) Playtex: Fits Tough Jobs Like a Glove, Playtex, Westport, CT, 1995.
    203) Product Information: CEREBYX(R) intravenous injection, fosphenytoin sodium intravenous injection. Pfizer Labs (per FDA), New York, NY, 2014.
    204) Product Information: Dilantin(R) intravenous injection, intramuscular injection, phenytoin sodium intravenous injection, intramuscular injection. Parke-Davis (per FDA), New York, NY, 2013.
    205) Product Information: Sodium Chloride IV injection, Sodium Chloride IV injection. Baxter Healthcare Corporation, Deerfield, IL, 2005.
    206) Product Information: diazepam IM, IV injection, diazepam IM, IV injection. Hospira, Inc (per Manufacturer), Lake Forest, IL, 2008.
    207) Product Information: dopamine hcl, 5% dextrose IV injection, dopamine hcl, 5% dextrose IV injection. Hospira,Inc, Lake Forest, IL, 2004.
    208) Product Information: lorazepam IM, IV injection, lorazepam IM, IV injection. Akorn, Inc, Lake Forest, IL, 2008.
    209) Product Information: norepinephrine bitartrate injection, norepinephrine bitartrate injection. Sicor Pharmaceuticals,Inc, Irvine, CA, 2005.
    210) Puczynski MS, Cunningham DG, & Mortimer JC: Sodium intoxication caused by use of baking soda as a home remedy. Canad Med Assoc J 1983; 128:821-822.
    211) Quereshi UA, Bhat JI, Ali SW, et al: Acute salt poisoning due to different oral rehydration solution (ORS) packet sizes. Indian J Pediatr 2010; 77(6):679-680.
    212) RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 1997; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    213) River City: Protective Wear Product Literature, River City, Memphis, TN, 1995.
    214) Roscelli JD, Yu CE, & Southgate WM: Management of salt poisoning in an extremely low birth weight infant. Pediatr Nephrol 1994; 8(2):172-174.
    215) Rosenkrantz JG: J Pediatr Surg 1970; 5:232-237.
    216) Safety 4: North Safety Products: Chemical Protection Guide. North Safety. Cranston, RI. 2002. Available from URL: http://www.safety4.com/guide/set_guide.htm. As accessed 8/14/2002.
    217) Sakai Y, Kato M, Okada T, et al: [Treatment of salt poisoning due to soy sauce ingestion with hemodialysis]. Chudoku Kenkyu 2004; 17(1):61-63.
    218) Sax NI: Dangerous Properties of Industrial Materials, 6th ed, Van Nostrand Reinhold Company, New York, NY, 1984, pp 2126.
    219) Scott R, Besag FMC, & Neville BGR: Buccal midazolam and rectal diazepam for treatment of prolonged seizures in childhood and adolescence: a randomized trial. Lancet 1999; 353:623-626.
    220) Servus: Norcross Safety Products, Servus Rubber, Servus, Rock Island, IL, 1995.
    221) Shapiro MD & Linas SL: Sodium chloride pica secondary to iron-deficiency anemia. Am J Kidney Dis 1985; 5:67-68.
    222) Singh AR: J Pharm Sci 1973; 62:1596-1600.
    223) Smith EJ & Palevsky S: Salt poisoning in a two-year-old child (Letter). Am J Emerg Med 1990; 8:571-572.
    224) Sorbye H, Maartmannmoe H, & Svanes K: Gastric carcinogenesis in rats given hypertonic salt at different times before a single dose of n-methyl-n'-nitro- n-nitrosoguanidine. J Cancer Res Clin Oncol 1994; 120:159-163.
    225) Sreenath TG, Gupta P, Sharma KK, et al: Lorazepam versus diazepam-phenytoin combination in the treatment of convulsive status epilepticus in children: A randomized controlled trial. Eur J Paediatr Neurol 2009; Epub:Epub.
    226) Standard Safety Equipment: Product Literature, Standard Safety Equipment, McHenry, IL, 1995.
    227) Streat S: Fatal salt poisoning in a child (Letter). NZ Med J 1982; 95:285-286.
    228) Taylor RP & James TJ: Enzymatic determination of sodium and chloride in sweat. Clin Biochem 1996; 29:33-37.
    229) Tingley: Chemical Degradation for Footwear and Clothing. Tingley. South Plainfield, NJ. 2002. Available from URL: http://www.tingleyrubber.com/tingley/Guide_ChemDeg.pdf. As accessed 10/16/2002.
    230) Trelleborg-Viking, Inc.: Chemical and Biological Tests (database). Trelleborg-Viking, Inc.. Portsmouth, NH. 2002. Available from URL: http://www.trelleborg.com/protective/. As accessed 10/18/2002.
    231) Trelleborg-Viking, Inc.: Trellchem Chemical Protective Suits, Interactive manual & Chemical Database. Trelleborg-Viking, Inc.. Portsmouth, NH. 2001.
    232) Turk EE, Schulz F, Koops E, et al: Fatal hypernatremia after using salt as an emetic-report of three autopsy cases. Legal Med 2005; 7:47-50.
    233) U.S. Department of Energy, Office of Emergency Management: Protective Action Criteria (PAC) with AEGLs, ERPGs, & TEELs: Rev. 26 for chemicals of concern. U.S. Department of Energy, Office of Emergency Management. Washington, DC. 2010. Available from URL: http://www.hss.doe.gov/HealthSafety/WSHP/Chem_Safety/teel.html. As accessed 2011-06-27.
    234) U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project : 11th Report on Carcinogens. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Washington, DC. 2005. Available from URL: http://ntp.niehs.nih.gov/INDEXA5E1.HTM?objectid=32BA9724-F1F6-975E-7FCE50709CB4C932. As accessed 2011-06-27.
    235) U.S. Environmental Protection Agency: Discarded commercial chemical products, off-specification species, container residues, and spill residues thereof. Environmental Protection Agency's (EPA) Resource Conservation and Recovery Act (RCRA); List of hazardous substances and reportable quantities 2010b; 40CFR(261.33, e-f):77-.
    236) U.S. Environmental Protection Agency: Integrated Risk Information System (IRIS). U.S. Environmental Protection Agency. Washington, DC. 2011. Available from URL: http://cfpub.epa.gov/ncea/iris/index.cfm?fuseaction=iris.showSubstanceList&list_type=date. As accessed 2011-06-21.
    237) U.S. Environmental Protection Agency: List of Radionuclides. U.S. Environmental Protection Agency. Washington, DC. 2010a. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
    238) U.S. Environmental Protection Agency: List of hazardous substances and reportable quantities. U.S. Environmental Protection Agency. Washington, DC. 2010. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
    239) U.S. Environmental Protection Agency: The list of extremely hazardous substances and their threshold planning quantities (CAS Number Order). U.S. Environmental Protection Agency. Washington, DC. 2010c. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-part355.pdf. As accessed 2011-06-17.
    240) U.S. Occupational Safety and Health Administration: Part 1910 - Occupational safety and health standards (continued) Occupational Safety, and Health Administration's (OSHA) list of highly hazardous chemicals, toxics and reactives. Subpart Z - toxic and hazardous substances. CFR 2010 2010; Vol6(SEC1910):7-.
    241) U.S. Occupational Safety, and Health Administration (OSHA): Process safety management of highly hazardous chemicals. 29 CFR 2010 2010; 29(1910.119):348-.
    242) US Department of Agriculture, Agricultural Research Service: USDA National Nutrient Database for Standard Reference, Release 17: Sodium, Na (mg) content of selected foods per common measure, sorted alphabetically. US Department of Agriculture. Washington, DC. 2004. Available from URL: www.nal.usda.gov/fnic/foodcomp/Data/SR17/wtrank/sr17a307.pdf. As accessed 2012-12-12.
    243) US Food and Drug Administration: Consumer updates: Lowering salt in your diet. US Food and Drug Administration. Silver Spring, MD. 2012. Available from URL: http://www.fda.gov/ForConsumers/ConsumerUpdates/ucm181577.htm. As accessed 2012-12-12.
    244) United States Environmental Protection Agency Office of Pollution Prevention and Toxics: Acute Exposure Guideline Levels (AEGLs) for Vinyl Acetate (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6af&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    245) Wallace KL: Toxin-Induced Seizures. In: Brent J, Wallace KL, Burkhart KK, et al, eds. Critical Care Toxicology, Elsevier Mosby, Philadelphia, PA, 2005.
    246) Wangenheim J & Bolcsfoldi G: Mouse lymphoma L5178Y thymidine kinase locus assay of 50 compounds. Mutagenesis 1988; 3:193-205.
    247) Wells Lamont Industrial: Chemical Resistant Glove Application Chart. Wells Lamont Industrial. Morton Grove, IL. 2002. Available from URL: http://www.wellslamontindustry.com. As accessed 10/31/2002.
    248) Williams K & Lovejoy FH Jr: Sodium chloride. Clin Toxicol Rev 1984; 6:1-2.
    249) Workrite: Chemical Splash Protection Garments, Technical Data and Application Guide, W.L. Gore Material Chemical Resistance Guide, Workrite, Oxnard, CA, 1997.