Iodine (atomic weight 126.9 g per atom) is a micronutrient that is required for the synthesis of the thyroid hormones.
Globally, iodine supplementation has been the primary method to decrease iodine deficiency, which is the leading cause of preventable mental retardation.
The recommend a daily iodine intake is 150 μg whereas the tolerable upper level (the approximate threshold below which no adverse effects are expected) is 1,100 μg per day in adults (Leung AM and Braverman LE, 2014).
However, iodine is present in several magnitude higher in medications (Amiodarone 75,000 μg/ 200 mg; povidone iodine, often 1–5%), supplements (75–200 μg) and in the iodinated contrast agents used for radiologic studies (13,500 μg) (Leung AM and Braverman LE, 2014).
Polymer carriers such as polyvinylpyrrolidone (povidone iodine) bind I2 to keep it stable in aqueous solutions yet afford slow release of I2 that prevents toxicity to exposed tissues.
Iodine is found in certain foods such as sea weeds. However, there is normally not enough iodine in foods to cause harm.
Iodine is less reactive than other halogens, such as chlorine or fluorine, because it has a larger atomic radius and a weaker attraction for electrons. Iodide is a mild reducing agent that can donate electrons to other substances and be oxidized to iodine. A reducing agent is a chemical term for an antioxidant.
Iodine serves important biologic functions including basal intracellular metabolism by its incorporation into T3 and T4; co-substrate for neutrophilic lysosomal myeloperoxidase, thereby potentiating the bactericidal capacity of polymorphonuclear leukocytes. The germicidal activity of iodine involves the electrophilic reactions with enzymes of respiratory chain and amino acids from the cell membrane proteins located in the bacterial cell wall. The germicidal activity may also result from oxidizing capacity of iodine (Ramaswamykanive et al., 2011).
After absorption, iodine is rapidly converted into the far less toxic iodide (iodine is an oxidant). Most of the iodine (97%) is excreted by the kidneys with a half-life of 2 days (Liang et al., 2020).
Often poisoning result from exposure to non-food items that contain iodine.
Iodide is proposed to have an ancestral antioxidant function in iodide-concentrating cells in all living organisms (from primitive seaweeds to mammalians. In these cells iodide acts as an electron donor in the presence of H2 O2 and peroxides, the remaining iodine readily iodinates the tyrosine and (more slowly) the histidine or some specific lipid, and so, neutralizes its own high oxidant power.
The acute toxicity of iodine (pure) in mammals is quite low. For example, in rats the oral LD50 is 14,000 mg/kg, and in mice it is even lower – 22,000 mg/kg (Ilin A and Nersesyan A,2013). The lethal dose varies from 200 mg to > 20 g (mean 2–4 g) (Liang et al., 2020).
Sodium salt of iodine (NaI) is much toxic than iodine and its LD50 in rats (oral treatment) is 4,340 mg/kg, and 1,000 mg/kg in mice (Ilin A and Nersesyan A,2013).
When given intravenously to rats, iodate is quantitatively reduced to iodide by nonenzymatic reactions and thus it becomes available to the body as iodide. Therefore, except for the gastrointestinal mucosa, exposure of tissues to iodate might be minimal. At much higher doses given intravenously (i.e., above 10 mg/kg), iodate is highly toxic to the retina (Ilin A and Nersesyan A,2013).
Oral exposures to high doses of iodine produces corrosive effects (chemical burns associated with esophageal edema and gastric ulcers) in the gastrointestinal tract, hemolysis, nephrotoxicity, and hepatic injury (Ilin A and Nersesyan A,2013).
Iodine toxicity may lead to thyroiditis, hypothyroidism (eg acute Wolff–Chaikoff effect, transient reduction lasting ~24 h), hyperthyroidism and thyroid storm, and thyroid papillary cancer. In people with dysfunctional thyroid follicular cell, iodine overdose can impair thyroid function, which might be transient or permanent (Leung AM and Braverman LE, 2014).
It has been reported that aspiration of povidone-Iodine can trigger lung injury or pulmonary fibrosis (Liang et al., 2020).
In some susceptible patients, an excess iodine load provides a rich substrate for increased production of thyroid hormones. Iodine-induced hyperthyroidism risk factors include nontoxic or diffuse nodular goiter, latent Graves' disease and long-standing iodine deficiency.
The underlying mechanism of iodine-induced hypothyroidism may be attributable to failure to adapt to the acute Wolff–Chaikoff effect because of a damaged thyroid from previous pathological insults-administration of iodine to patients with severe hyperthyroidism results in an acute decrease in the release of thyroid hormones (Leung AM and Braverman LE, 2014).
The molecular and cellular basis of iodine toxicity (Povidone-Iodine exposure) includes membrane disruption, loss of mitochondrial membrane potential, and abolition of oxidative phosphorylation, which then induce a rapid cell death. In addition, it attacks lipid rafts, leading to the failure of tight junctions and thus impairment of barrier functions of surface-lining cells (Steins et al., 2023).
Early clinical signs of acute systemic iodine/iodide toxicity stem from the stimulation of exocrine gland secretion producing rhinorrhoea, conjunctivitis and a serious exudative cough.
Other acute symptoms include:
- Acneiform skin lesions
- Time dependent damage of ocular surface (conjunctiva and cornea) including post-surgery dry eye syndrome from reduced goblet cells.
- metallic taste in the mouth, increased salivation,
- Swelling of the mucous membrane of the mouth, pharynx and upper respiratory tract
- Burning mouth and throat
- GI irritation, nausea, vomiting (blue or brown colored; may cause aspiration pneumonitis), and diarrhea
- Inhalation of vapors leads to coughing, shortness of breath, swelling of the vocal cords with the development of suffocation.
- Hematuria associated with damage to the renal tubules
Severe iodine poisoning is associated with system and multiorgan failure such as anuria from acute renal failure-tubular necrosis and interstitial nephritis, hepatomegaly, cardiovascular collapse (hypotension, atrial fibrillation, tachyarrhythmias), and bilateral vision loss from retinopathy ((Liang et al., 2020; Iodine overdose, 2021; Sani et al., 2021). Other severe symptoms include elevated urine iodine concentration, histological microaggregates (Tambuzzi et al., 2022), metabolic acidosis, hypernatraemia, hyperosmolarity,
leukocytotoxicity, delirium, fever, seizures, shock, stupor and coma.
Overdose of iodate is toxic to the retinal pigment epithelium and the photoreceptors leading to diminished vision-A retino-toxic dose of 20–40 mg/kg has been estimated in animal experiments (Venu Gopal Reddy et al., 2018).
Treatment / Management
There is no specific antidote to iodine poisoning; therefore, management is largely supportive. Ensure patent airway, breathing, and circulation.
Immediately irrigate exposed with copious amounts of fluids.
Administer normal saline bolus (20 mL/kg) to treat the hypotension (Liang et al., 2020).
Administer atropine boluses to reverse bradycardia (Liang et al., 2020).
Recent oral iodine poisoning requires gastric lavage with a solution of sodium thiosulfate 5% (10 ml every 4 hours) or in its absence pure waters or normal saline. However, some authors do not recommend gastric decontamination because of the corrosive effects of iodine (Liang et al., 2020).
Shortly after exposure, administer milk, or in its absence, substitute with corn starch or flour mixed with water every 15 minutes. Starch sequesters Iodine making it unavailable for absorption.
If the patient is stable, alert, and protecting their airway, activated charcoal should be given to decontaminate the gastrointestinal tract.
Administer antiacids such as proton pump inhibitors (esomeprazole 40 mg was given intravenously every 12 hrs) and H2 blockers as well as antacid suspensions (Liang et al., 2020).
Bread containing enriched or bromated flour can be consumed as bromated flour absorbs excess iodine.
Enhance urine flow with large amounts of normal saline (iodine is renally excreted).
Renal replacement therapy may be attempted in symptomatic patients having high iodine burden: hemodialysis using high-flux membranes followed by continuous venovenous hemodiafiltration were reported effective at clearing iodine (Kanakiriya et al., 2003)
Corticosteroid therapy (1 mg/kg/day) in cases of inflammatory kidney injury (Chang et al., 2017).
Administration of antioxidants such vitamin C and E may be justified.
Retinopathies treated with prednisolone, vitamin B1, B6 and B12 reported visual recovery (Venu Gopal Reddy et al., 2018).
NOTE
Avian work and use in individuals under 18 years of age exposed to radioactive iodine following Chernobyl nuclear accident in Belarus, has provided evidence that oral bromide salts can reverse toxic effects of iodine. Thus, bromide therapy may have a place in Iodine toxicity (Baker DH2004).
Narrow anion gap has been associated with presence of halogens. Overestimation of
chloride is due to the presence of the second halide such as iodine (Ramaswamykanive et al., 2011)
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