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IODATES

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) TOXICOLOGICAL CLASS: Iodates are powerful oxidizing agents.
    B) Refer to "ACIDS" management for information on iodic acid.

Specific Substances

    A) POTASSIUM IODATE
    1) Iodic acid, potassium salt
    2) CAS 7758-05-6
    3) NIOSH/RTECS NN 1350000
    4) Molecular Formula: IO3.K
    POTASSIUM PERIODATE
    1) IODATES - PERIODATES
    2) Molecular Formula: IKO4
    SODIUM IODATE
    1) Iodic acid, sodium salt
    2) CAS 7681-55-2
    3) NIOSH/RTECS NN 1400000
    4) Molecular Formula: IO3.Na
    SODIUM PERIODATE
    1) Sodium metaperiodate
    2) CAS 7790-28-5
    3) NIOSH/RTECS SD 4441050
    4) Molecular Formula: IO4.Na

Available Forms Sources

    A) USES
    1) Iodate (oxidized form of iodine or IO3) has long been recommended by international health authorities, including the WHO, as an additive to salt for the public health purpose of correcting iodine deficiency.
    2) Potassium iodate is used for the prophylaxis and treatment of iodine deficiency disorders (S Sweetman , 2001).
    3) In areas endemic for goiter, potassium iodate is used for iodine supplementation. In Thailand, a 24-g packet of potassium iodate is dissolved in 725 mL of water in a Thai whiskey bottle (a concentration of 20 g/L of iodine or approximately 1000 mcg of iodine per one drop of solution) . In a water cooler, 2 drops of this concentrated iodate solution are mixed with 10 L of pure water which gives a supplemented water solution for drinking that has an iodine concentration of approximately 200 mcg/L (Singalavanija et al, 2000).

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: Iodates are used for the prevention and treatment of iodine deficiency and goiter.
    B) TOXICOLOGY: Concentrated iodates are powerful oxidizing agents. Toxicity is primarily due to corrosive injury (GI tract) and direct toxicity to retinal cells.
    C) EPIDEMIOLOGY: Overdose is not common and severe toxicity is quite rare. Deaths have not been reported.
    D) WITH THERAPEUTIC USE
    1) Nausea may occur with therapeutic dosing.
    E) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Potassium iodate can cause nausea, vomiting, diarrhea, and abdominal pain. Skin irritation may occur with dermal exposure.
    2) SEVERE TOXICITY: Vomiting, diarrhea, and severe corrosive injury to the GI tract have been reported. Acute renal failure, CNS depression, metabolic acidosis, and rhabdomyolysis have been reported after large overdose. Acute visual loss may occur after large ingestion. Vision may improve over several months but usually does not return to normal.
    0.2.21) CARCINOGENICITY
    A) No information concerning the evaluation of iodates or sodium iodates was located (IARC, 1987; US DHHS, 1991; US DHHS, 1994).

Laboratory Monitoring

    A) Monitor vital signs and mental status.
    B) In symptomatic patients and those with large ingestions, monitor serum electrolytes, CK, renal function, and liver enzymes.
    C) Monitor urine output.
    D) Monitor visual acuity. Perform a slit lamp exam in patients with visual complaints. Electroretinography and visual evoked potentials may be useful to evaluate visual loss.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) TREATMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive. Administer IV fluids and antiemetics for nausea and vomiting. Administer humidified oxygen as needed for respiratory distress. Irrigate exposed skin thoroughly.
    B) TREATMENT OF SEVERE TOXICITY
    1) Treatment is symptomatic and supportive. Administer IV fluids for hypotension. Early (within 12 hours) endoscopy is recommended for patients with large ingestions and concern for GI mucosal injury (pain with swallowing, vomiting, abdominal pain).
    C) DECONTAMINATION
    1) PREHOSPITAL: GI decontamination is generally not warranted. Toxicity is not expected from small ingestions. GI mucosal injury may develop after large ingestions. Wash exposed skin and irrigate exposed eyes.
    2) HOSPITAL: ORAL EXPOSURE: GI decontamination is generally not warranted. Toxicity is not expected from small ingestions. INHALATIONAL EXPOSURE: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer humidified oxygen and assist ventilation as needed for respiratory distress. Treat bronchospasm with inhaled beta2-agonist and oral or parenteral corticosteroids. EYE EXPOSURE: Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. If irritation, pain, swelling, lacrimating, or photophobia persist, perform a slit lamp exam.
    D) ANTIDOTE
    1) None.
    A) PATIENT DISPOSITION
    1) HOME CRITERIA: Asymptomatic patients with inadvertent, small ingestions can be monitored at home.
    2) OBSERVATION CRITERIA: Patients with deliberate ingestions, those with more than mild GI irritation should be referred to a healthcare facility for evaluation and should be observed for 4 to 6 hours. Patients can be discharged when their symptoms are controlled and they are tolerating oral hydration.
    3) ADMISSION CRITERIA: Patients with persistent vomiting, abdominal pain, renal injury, concern for GI mucosal injury, or visual impairment should be admitted.
    4) CONSULT CRITERIA: Consult a medical toxicologist or poison center for patients with large ingestions, or persistent symptoms. Consult a gastroenterologist for endoscopic evaluation of patients with large overdose or symptoms of GI mucosal injury. Consult an ophthalmologist for patients with very large ingestions (greater than 10 grams) or visual loss.
    ENHANCED ELIMINATION PROCEDURE
    5) Exchange transfusions combined with hemodialysis or peritoneal dialysis should be considered in severely poisoned patients.

    F) PITFALLS
    1) The absence of oral burns does not preclude GI mucosal injury. Failure to test visual acuity and visual fields.
    G) PHARMACOKINETICS
    1) Rapidly absorbed orally.
    H) DIFFERENTIAL DIAGNOSIS
    1) Any exposure which causes nausea, vomiting, and diarrhea.
    0.4.3) INHALATION EXPOSURE
    A) Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer humidified oxygen and assist ventilation as needed for respiratory distress. Treat bronchospasm with inhaled beta2-agonist and oral or parenteral corticosteroids.
    B) Refer to ORAL SECTIONS for information on specific treatments.
    0.4.4) EYE EXPOSURE
    A) Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. If irritation, pain, swelling, lacrimating, or photophobia persist, perform a slit lamp exam.
    B) Refer to ORAL SECTIONS for information on specific treatments.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    2) Refer to ORAL SECTIONS for information on specific treatments.

Range Of Toxicity

    A) TOXICITY: Severe visual impairment has developed in adults after ingestion of doses of 12 grams or 187 mg/kg or more.

Clinical Effects

Heent

    3.4.3) EYES
    A) IRRITATION: Eye irritation may occur (Technical Information, 1985; Technical Information, 1985a).
    B) IMPAIRED VISION, BLINDNESS: Literature prior to 1940 reported the use of a sodium iodate containing solution, Septojod (R), IV or IP to prevent infection in humans. Temporary reduction of vision or blindness developed within 24 hours of administration in some patients (Grant & Schuman, 1993).
    1) A case of iodate-induced blindness has occurred in China; the dose calculated was 10 to 20 mg/kg (Tong, 1995).
    C) VISUAL FIELD CONSTRICTION: Constriction of the visual fields was reported in some patients who had received IV or IP Septojod(R), an antiseptic which contained sodium iodate (Grant & Schuman, 1993). This product is no longer in use.
    D) RETINAL EFFECTS following exposures are reported as retinal edema, retinitis pigmentosa, degeneration of retinal pigment epithelium, increased permeability of the blood-retinal barrier and degeneration of rods and cones:
    1) RETINAL EDEMA developed in some patients treated prior to 1940 with iv or IP Septojod(R), a sodium iodate containing antiseptic (Grant & Schuman, 1993).
    2) RETINITIS PIGMENTOSA: A condition similar to retinitis pigmentosa developed in some patients treated prior to 1940 with iv or IP Septojod(R), a sodium iodate containing antiseptic (Grant & Schuman, 1993).
    3) DEGENERATION OF RETINAL PIGMENT EPITHELIUM (ANIMALS): Sodium iodate produces degeneration of the retinal pigment epithelium of animals (Grant & Schuman, 1993; Potts, 1991).
    a) Intravenous injection in mice of 40 mg/kg sodium iodate produced degeneration of the pigment epithelial cells 4 hours post injection (Hosada et al, 1993).
    b) Changes in the electrical activity of the eye which are attributed to damage of the retinal pigment epithelium have been reported in animal studies (Grant & Schuman, 1993).
    1) Intravenous injection in mice of 40 mg/kg sodium iodate produced changes in the amplitude of alpha and beta waves as measured by electroretinography (Hosada et al, 1993).
    4) BLOOD-RETINA, BLOOD-VITREOUS BARRIER EFFECTS: Iodate causes increased permeability of the blood-retina or blood-vitreous barrier (Grant & Schuman, 1993).
    5) DEGENERATION OF THE RODS AND CONES: Systemic administration of iodate in animals produces degeneration of the rods and cones as a secondary effect (Grant & Schuman, 1993).
    E) CASE REPORT: A 34-year-old man developed unconsciousness, dehydration, hypothermia (rectal temperature of 28.7 degrees C), metabolic acidosis (anion gap of 26 mmol/L and normal osmolar gap), rhabdomyolysis (CK maximum of 18500 U/L), and anuric renal failure after ingesting approximately 2 liters of Seristrip liquid (5100 mg of iodate/kg of body weight), a cleansing agent containing large amounts of sulfuric acid and sodium metaperiodate. In addition, he experienced major corrosive injuries in the esophagus and stomach, transient hyperphosphatemia and hypocalcemia, and central amaurosis (blindness) in both eyes (some peripheral vision in both eyes). The eye examination showed atrophic pigmented changes in the central part of the retina with a normal peripheral retina. The authors suggested that toxic effect on retinal photoreceptor cells (retinopathy) and optic nerve injury may have caused the blindness. His peripheral vision improved after 3 weeks of treatment (Solberg et al, 2003).
    F) CASE SERIES: Five patients (age 22 to 65 years) developed retinal toxicity following the ingestion of potassium iodate solution at a concentration between 187 and 470 mg/kg body weight. Ocular examinations revealed the visual acuity range from light perception with projection to counting fingers; the visual acuity decreased from 2 to 12 hours after ingestion. Bilateral extensive areas of retinal pigment epithelial (RPE) window defects were noted following fundus fluorescein angiography. Marked impairment of retinal function was seen following electroretinography and visual evoked potential (VEP) studies. Following 3 months of supportive care, these patients regained ambulatory vision. The authors concluded that retinal function recovery depends on the amount of chemical absorption, the regeneration of RPE, and the recovery function of photoreceptor cells (Singalavanija et al, 2000).
    3.4.6) THROAT
    A) IRRITATION of mucous membranes may occur. Sodium periodate may produce coughing and possible shortness of breath (Technical Information, 1985a).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) GASTROINTESTINAL COMPLICATION
    1) WITH POISONING/EXPOSURE
    a) GI irritation may occur (Technical Information, 1985).
    b) CASE SERIES: Five patients (age 22 to 65 years) developed retinal toxicity following the ingestion of potassium iodate solution at a concentration between 187 and 470 mg/kg body weight. In addition, they experienced nausea, vomiting, abdominal pain, and diarrhea (Singalavanija et al, 2000).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ACUTE RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 47-year-old woman developed acute renal failure (BUN 140 mg/dL, creatinine 15.6 mg/dL) after ingesting approximately 12 grams potassium iodate. Renal failure improved in two weeks without dialysis (Singalavanija et al, 2000).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RENAL FAILURE
    a) Acute renal failure has occurred in animals (Gosselin et al, 1984).
    2) HEMOLYSIS
    a) Hemoglobinuria has occurred in animals (Gosselin et al, 1984).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) Skin irritation may occur (Technical Information, 1985; Technical Information, 1985a).

Carcinogenicity

    3.21.2) SUMMARY/HUMAN
    A) No information concerning the evaluation of iodates or sodium iodates was located (IARC, 1987; US DHHS, 1991; US DHHS, 1994).

Summary Of Exposure

    A) USES: Iodates are used for the prevention and treatment of iodine deficiency and goiter.
    B) TOXICOLOGY: Concentrated iodates are powerful oxidizing agents. Toxicity is primarily due to corrosive injury (GI tract) and direct toxicity to retinal cells.
    C) EPIDEMIOLOGY: Overdose is not common and severe toxicity is quite rare. Deaths have not been reported.
    D) WITH THERAPEUTIC USE
    1) Nausea may occur with therapeutic dosing.
    E) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Potassium iodate can cause nausea, vomiting, diarrhea, and abdominal pain. Skin irritation may occur with dermal exposure.
    2) SEVERE TOXICITY: Vomiting, diarrhea, and severe corrosive injury to the GI tract have been reported. Acute renal failure, CNS depression, metabolic acidosis, and rhabdomyolysis have been reported after large overdose. Acute visual loss may occur after large ingestion. Vision may improve over several months but usually does not return to normal.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs and mental status.
    B) In symptomatic patients and those with large ingestions, monitor serum electrolytes, CK, renal function, and liver enzymes.
    C) Monitor urine output.
    D) Monitor visual acuity. Perform a slit lamp exam in patients with visual complaints. Electroretinography and visual evoked potentials may be useful to evaluate visual loss.

Radiographic Studies

    A) ABDOMINAL RADIOGRAPH
    1) Iodates may be radiopaque. Abdominal x-rays may help in diagnosing large ingestions.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with persistent vomiting, abdominal pain, renal injury, concern for GI mucosal injury, or visual impairment should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Asymptomatic patients with inadvertent, small ingestions can be monitored at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a medical toxicologist or poison center for patients with large ingestions, or persistent symptoms. Consult a gastroenterologist for endoscopic evaluation of patients with large overdose or symptoms of GI mucosal injury. Consult an ophthalmologist for patients with very large ingestions (greater than 10 grams) or visual loss.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with deliberate ingestions, those with more than mild GI irritation should be referred to a healthcare facility for evaluation and should be observed for 4 to 6 hours. Patients can be discharged when their symptoms are controlled and they are tolerating oral hydration.

Monitoring

    A) Monitor vital signs and mental status.
    B) In symptomatic patients and those with large ingestions, monitor serum electrolytes, CK, renal function, and liver enzymes.
    C) Monitor urine output.
    D) Monitor visual acuity. Perform a slit lamp exam in patients with visual complaints. Electroretinography and visual evoked potentials may be useful to evaluate visual loss.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) GI decontamination is generally not warranted. Toxicity is not expected from small ingestions. GI mucosal injury may develop after large ingestions. Wash exposed skin and irrigate exposed eyes.
    6.5.2) PREVENTION OF ABSORPTION
    A) GI decontamination is generally not warranted. Toxicity is not expected from small ingestions. GI mucosal injury may develop after large ingestions.
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Monitor vital signs and mental status.
    2) In symptomatic patients and those with large ingestions, monitor serum electrolytes, CK, renal function, and liver enzymes.
    3) Monitor urine output.
    4) Monitor visual acuity. Perform a slit lamp exam in patients with visual complaints. Electroretinography and visual evoked potentials may be useful to evaluate visual loss.

Inhalation Exposure

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

Eye Exposure

    6.8.1) DECONTAMINATION
    A) Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. If irritation, pain, swelling, lacrimating, or photophobia persist, perform a slit lamp exam.

Dermal Exposure

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

Range Of Toxicity

Summary

    A) TOXICITY: Severe visual impairment has developed in adults after ingestion of doses of 12 grams or 187 mg/kg or more.

Minimum Lethal Exposure

    A) ANIMAL DATA
    1) 200 to 250 mg/kg intravenously was lethal to dogs (Gosselin et al, 1984).

Maximum Tolerated Exposure

    A) CASE REPORT: A woman developed severe visual impairment, vomiting and diarrhea after ingesting 13.35 grams of potassium iodate (247 milligrams/kilogram). Visual acuity was hand motions on presentation. Another woman developed severe visual impairment, vomiting, diarrhea and acute renal failure after ingesting approximately 12 grams potassium iodate (300 mg/kg). Visual acuity on presentation was light perception, but improved to 20/80 in the right eye and counting fingers in the left eye by 3 months(Singalavanija et al, 2000).
    B) CASE SERIES: Five patients (age 22 to 65 years) developed retinal toxicity following the ingestion of potassium iodate solution at a concentration between 187 and 470 mg/kg body weight. Ocular examinations revealed the visual acuity range from light perception with projection to counting fingers; the visual acuity decreased from 2 to 12 hours after ingestion. Bilateral extensive areas of retinal pigment epithelial (RPE) window defects were noted following fundus fluorescein angiography. Marked impairment of retinal function was seen following electroretinography and visual evoked potential (VEP) studies. Following 3 months of supportive care, these patients regained ambulatory vision. The authors concluded that retinal function recovery depends on the amount of chemical absorption, the regeneration of RPE, and the recovery function of photoreceptor cells (Singalavanija et al, 2000).
    C) A case of iodate-induced blindness has occurred in China; the dose calculated was 10 to 20 mg/kg (Tong, 1995).
    D) ANIMAL DATA
    1) 60 to 90 mg/kg of potassium iodate was tolerated in animals (Gosselin et al, 1984).
    2) Acute toxicity is 3 to 6 times that of iodides in mice.
    3) In rabbits, 12.5 mg/kg iodate intravenously did not produce retinal damage whereas 20 mg/kg did (Heike & Marmor, 1990).

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (INTRAPERITONEAL)MOUSE:
    1) 136 mg/kg
    B) LD50- (INTRAPERITONEAL)MOUSE:
    1) 119 mg/kg
    C) LD50- (INTRAPERITONEAL)MOUSE:
    1) 58 mg/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) Iodates are strong oxidizing substances in acidic solutions.
    B) Sodium iodate is widely used for studying retinal pigment epithelium (RPE) because of its toxic specificity for RPE. Iodate causes an immediate loss of the c-wave and then the development of pigmentary degeneration of the RPE and retina over ensuing days (Singalavanija et al, 2000; Heike & Marmor, 1990).

Physicochemical

Physical Characteristics

    A) POTASSIUM IODATE: Colorless, triclinic crystals (Lewis, 1996; Clayton & Clayton, 1993; Budavari, 1996)
    B) POTASSIUM PERIODATE: Colorless, tetragonal crystals (Lewis, 1996; Budavari, 1996)
    C) SODIUM IODATE: White, rhombic crystals (Lewis, 1996; Clayton & Clayton, 1993; Budavari, 1996)
    D) SODIUM PERIODATE
    1) Colorless, tetragonal crystals (Lewis, 1996)
    2) White, efflorescent, trihydrate, trigonal crystals (Budavari, 1996)

Ph

    A) Neutral (Potassium Iodate; aqueous solution) (Budavari, 1996)

Molecular Weight

    A) 214 (Potassium Iodate) (Lewis, 2000; (Clayton & Clayton, 1993)
    B) 230.01 (Potassium Periodate) (Lewis, 1996; Budavari, 1996)
    C) 197.89 (Sodium Iodate) (Lewis, 1996; Clayton & Clayton, 1993)
    D) 213.89 (Sodium Periodate) (Lewis, 1996)

References

General Bibliography

    1) Arroyave G, Pineda O, & Scrimshaw NS: The stability of potassium iodate in crude table salt. Bull World Health Organ 1956; 14(1):183-185.
    2) Budavari S: The Merck Index, 12th ed, Merck & Co, Inc, Whitehouse Station, NJ, 1996.
    3) Burgess JL, Kirk M, Borron SW, et al: Emergency department hazardous materials protocol for contaminated patients. Ann Emerg Med 1999; 34(2):205-212.
    4) Clayton GD & Clayton FE: Patty's Industrial Hygiene and Toxicology, Vol 2A, Toxicology, 4th ed, John Wiley & Sons, New York, NY, 1993.
    5) Gosselin RE, Smith RP, & Hodge HC: Clinical Toxicology of Commercial Products, 5th ed, Williams & Wilkins, Baltimore, MD, 1984.
    6) Grant WM & Schuman JS: Toxicology of the Eye, 4th ed, Charles C Thomas, Springfield, IL, 1993.
    7) Heike M & Marmor MF: L-cystein protects the pigment epithelium from acute sodium iodate toxicity. Doc Ophthal 1990; 75:15-22.
    8) Hosada L, Adachi-Usami E, & Mizota A: Early effects of sodium iodate injection on ERG in mice. Acta Ophthal 1993; 71:616-622.
    9) IARC: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans- Overall Evaluations of Carcinogenicity: An Updating of IARC Monographs Volumes 1 to 42, Supplement 7, International Agency for Research on Cancer, World Health Organization, Geneva, Switzerland, 1987.
    10) Lewis RJ: Sax's Dangerous Properties of Industrial Materials, 10th ed, John Wiley & Sons, Inc, New York, NY, 1996.
    11) National Heart,Lung,and Blood Institute: Expert panel report 3: guidelines for the diagnosis and management of asthma. National Heart,Lung,and Blood Institute. Bethesda, MD. 2007. Available from URL: http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf.
    12) Potts AM: Toxic responses of the eye. IN: Amdur MO, Doull J & Klaassen CD (Eds): Casarett and Doull's Toxicology, 4th ed, Pergamon Press, New York, NY, 1991, pp 545.
    13) S Sweetman : Martindale: The Complete Drug Reference. Pharmaceutical Press. London, UK (Internet Version). Edition expires 2001; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    14) Singalavanija A, Ruangvaravate N, & Dulayajinda D: Potassium iodate toxic retinopathy. A report of five cases. Retina 2000; 20:378-383.
    15) Solberg K, Thrane EV, Thorud LO, et al: Blindness after poisoning with sodium metaperiodate (Seristrip liquid). J Toxicol Clin Toxicol 2003; 41(4):468.
    16) Technical Information: Sodium Iodate, Material Safety Data Sheet, Mallinckrodt Inc, Paris, KY, 1985.
    17) Technical Information: Sodium Periodate, Material Safety Data Sheet, Mallinckrodt Inc, Paris, KY, 1985a.
    18) Tong Y: A case of blindness caused by acute iodine poisoning. Chin Med J (Engl) 1995; 108(7):555-556.
    19) US DHHS: Seventh Annual Report on Carcinogens - 1994 Summary, National Toxicology Program, Washington, DC, 1994.
    20) US DHHS: Sixth Annual Report on Carcinogens - 1991 Summary, National Toxicology Program, Washington, DC, 1991.