Those writers are not reliable. Reading their incomplete rhetoric and historic bashing of iodine/iodide AND curezone tends to get old. Each person's therapeutic range of iodine/iodide is different, it all depends on individualistic variables and applicable circumstances. There's too much bias on that site to merit serious rebuttal objectively (here too even), whether they are right or wrong.
Bias can go both ways. Look at the iodophiles here on Curezone. You cannot even mention an adverse effect of iodine without them coming down on you until they feel they squashed you. I mentioned some dangers of iodine such as the adverse effects of of too much iodine on Hashimoto's.
So I would trust the claims of the link I posted over the iodine trolls here on Curezone anytime. Especially when there are plenty of evidence readily available as to the dangers of iodine in levels much lower than the lowest levels the iodophiles here keep recommending.
So what exactly in their article is unreliable in your view?
Let's see what some of the medical abstracts show as far as toxicity:
Iodine is available in solid form, in solution, and in tinctures, e.g. Povidone iodine antiseptic solution, surgical scrub 7.5%, povidone iodine 200 mg pessaries, povidone antiseptic ointment 100 mg/g. Tincture of iodine, USP, contains 2% cent iodine and 2.4% sodium iodide diluted in 50% ethanol. Aqueous solutions of iodine are Strong Iodine Solution USP (compound iodine solution, Lugol's solution) containing 5% iodine and 10% potassium iodide, and Iodine Topical Solution (USP) containing 2% iodine and 2.4% potassium iodide. Aqueous Iodine Solution BP contains the same amount of free and combined iodine per ml (130 mg/mL) as does the USP Strong Iodine Solution. (Reynolds, 1993) Potassium iodide aqueous cough expectorant. Povidone-iodide (Betadine) is an organically bound iodide compound containing 1% iodine in a water soluble base. Other organically bound iodide compounds are undecoylium chloride, diiodo hydroxyquin, tetraglycine hydroperiodide (60% iodine). These organic iodide compounds release iodine slowly and have a toxicity of one fifth of their iodine content (Haddad & Winchester, 1983). Povidone iodine antiseptic solution and surgical scrub are in 5 litre containers, pessaries, ointment (see 1.7). 2. SUMMARY 2.1 Main risks and target organs Concentrated iodine is corrosive. Main risks in acute exposure to high iodine concentrations are largely due to the highly corrosive effect of iodine on the entire gastrointestinal tract and resultant shock. If rupture occurs mediastinitis or peritonitis develop. Target organs are mucous membranes of pharynx, larynx and oesophagus for the concentrated iodine, and thyroid for the diluted form as a systemic effect. Iodine is not a frequent cause of toxicity in the amounts available in the household. 2.2 Summary of clinical effects Ingestion of iodine may cause corrosive effects such as oedema of the glottis, with asphyxia, aspiration pneumonia, pulmonary oedema and shock, as well as vomiting and bloody diarrhoea. The CNS , cardiovascular and renal toxicity following acute iodine ingestion appear to be due to the corrosive gastroenteritis and resultant shock. Vomiting, hypotension and circulatory collapse may be noted following severe intoxication. Eye Eye exposure may result in severe ocular burns. Cardiovascular Tachycardia, hypotension and circulatory collapse may be due to the ingestion of concentrated corrosive iodine solutions. Respiratory Inhalation of iodine vapour may result in severe pulmonary irritation leading to pulmonary oedema. Oedema of the glottis and pulmonary oedema have also resulted from oral ingestion. Neurological Headache, dizziness, delirium and stupor may be noted following severe intoxication. Gastrointestinal A severe corrosive oesophagitis and gastroenteritis characterised by vomiting, abdominal pain and diarrhoea may be noted following ingestion. The vomitus is blue if starch is present in the stomach. A metallic taste may be noted. Dermatological Dermal application of strong iodine solutions may result in burns. Chronic ingestion may result in iodism characterised from acne form skin lesions and other skin eruptions. Cutaneous absorption may be significant and result in systemic symptoms and death. Endocrine Hypothyroidism, as well as hyperthyroidism, has been reported. Immunological Hypersensitivity reactions including angioedema and/ or serum sickness-like reactions may be noted.""Contraindications Iodine preparations should not be taken regularly during pregnancy and lactation. Because iodine may cause burns on occluded skin, an iodine- treated wound should be covered with a light bandage. As iodine and iodides can affect the thyroid gland, the administration of such preparations may interfere with tests of thyroid functions (Reynolds 1989; McEvoy, 1990). Potassium iodide should not be used in adolescent patients because of its potential to induce acne and its effects on the thyroid gland (Bouillon ,1988). Iodine or iodides should not be administered to patients with a history of hypersensitivity to such compounds.""Teratogenicity Iodides diffuse across the placenta. Infant and neonatal death from respiratory distress secondary to goitre has been reported in mothers taking iodides(Parmalee et al., 1940; Galima et al., 1962). Chronic topical maternal use of povidone-iodine during pregnancy has been associated with clinical and biochemical hypothyroidism in the infant (Danziger et al., 1987). Exposure to I 131 can damage or ablute the developing thyroid of the human foetus. Hypothyroidism, either congenital or of late onset, has been reported in at least 5 children whose mothers were exposed to I 131 during pregnancy (Shepard, 1980)""Main adverse effects Endocrine system effects Iodine and iodides produce goitre, hypothyroidism as well as hyperthyroidism. These effects have also been reported in infants born to mothers who had taken iodides during pregnancy (Reynolds, 1989). Side effects of iodine given for radioprotection In iodine-induced goitre and iodine-induced hypothyroidism, special risk groups are foetus and neonates. Iodine-induced hyperthyroidism special risk group are people living in iodine deficient areas and people with a history of hyperthyroidism, (Bouillon, 1988). Extrathyroidal side effects are gastrointestinal complaints (nausea, pain), taste abnormalities, cutaneous and mucous membrane such as irritation, rash, oedema (including face and glottis), allergic-like reactions such as fever, eosinophilia, serum- sickness-like symptoms, vasculitis. Special risk groups are patients with hypocomplementic vasculitis, (Bouillon, 1988). Allergic effects Whether iodine is administered topically or systematically, iodine and iodides can give rise to allergic reactions: urticaria, angioedema, cutaneous haemorrhage or purpuras, fever, arthralgia, lymphadenopathy and eosinophile, acne-form or severe eruptions. Iodism effects A mild toxic syndrome called iodism results from repeated administration of small amount of iodine. Iodism is characterised by hyper-salivation, coryza, sneezing, conjunctivitis, headache, laryngitis, bronchitis, stomatitis, parotitis, enlargement of the submaxillary glands, skin rashes and gastric upsets, (Reynolds, 1989, Gosselin et al, 1984). In rare cases jaundice, bleeding from mucous membranes and bronchospasm may occur. Inflammatory states may be aggravated by these adverse reactions, (Bouillon, 1988). Gastrointestinal effects Acute effects due to ingestion of iodine are mainly due to its corrosive effects or action which arises at least in part from oxidizing potential of this element on the gastrointestinal tract. Symptoms include a metallic taste, vomiting, abdominal pain, and diarrhoea. Oesophageal stricture may occur if the patient survives the acute stage, (Reynolds, 1989; Gosselin et al., 1984). Cardiovascular and respiratory effects Death may occur due to circulatory failure, oedema of the glottis resulting in asphyxia, aspiration pneumonia, or pulmonary oedema, (Reynolds, 1989, Sittig 1981). Kidney effect Anuria may occur 1 to 3 days after exposure, (Reynolds, 1989).""Acute poisoning 9.1.1 Ingestion Ingestion of iodine may cause corrosive effects such as oedema of the glottis, with asphyxia, aspiration pneumonia, pulmonary oedema and shock, vomiting and bloody diarrhoea. The CNS, cardiovascular and renal toxicity following acute iodine ingestion appear to be due to the corrosive gastroenteritis and resultant shock. Vomiting, hypotension and circulatory collapse may be noted following severe intoxication. 9.1.2 Inhalation Inhalation of iodine vapour is very irritating to mucous membranes. Headache, dizziness, delirium, collapse and stupor, death due to circulatory collapse, asphyxia from oedema of glottis, aspiration pneumonia or pulmonary oedema has been reported. Occasionally haemorrhagic nephritis may occur within 1 to 3 days, oesophageal and pyloric stenosis have been reported, (Gosselin et al., 1984). 9.1.3 Skin exposure Skin contact with iodine may give rise to hypersensitivity reaction, fever and skin eruption. Death following skin contact covering one third of body surface is reported to have occurred, (Gosselin et al., 1984). 9.1.4 Eye contact Iodine vapour causes irritation and lachrymation in human eyes, (Grant, 1974). 9.1.5 Parenteral exposure Injection of iodine compounds may cause sudden fatal collapse (anaphylaxis) as a result of hypersensitivity. Symptoms are dyspnea, cyanosis, fall of blood pressure, unconsciousness and convulsions, (Dreisbach & Robertson, 1987). 9.1.6 Other No data available. 9.2 Chronic poisoning 9.2.1 Ingestion Repeated administration of small amounts of iodine may result in a mild toxic syndrome called "iodism". It is characterised by hyper-salivation, coryza, sneezing, conjunctivitis, stomatitis, parotitis, enlargement of the submaxillary glands, and skin rashes (Barker & Wood, 1940; Ehrich & Seifter, 1949). Hypotension, tachycardia, cyanosis and signs of shock are frequent symptoms of iodine ingestion. (Gosselin et al., 1984). Iodated glycerol used as a mucolytic expectorant in the treatment of respiratory disorders inhibited the biosynthesis of thyroid hormone and induced hypothyroidism (Drinka & Nolten, 1988; Gommolin, 1987). Amiodarone, an iodine rich drug widely used in the treatment of tachyarrhythmias, represents one of the most common sources of iodine-induced thyrotoxicosis (Martino et al., 1987; Regouby et al., 1985). Tablets of seaweed, sold over the counter, is one of the less common sources of iodine-induced hyperthyroidism (Shilo & Hirsch, 1990). 9.2.2 Inhalation No data available. 9.2.3 Skin exposure Intact skin Irritant contact dermatitis caused by povidone-iodine has been reported, (Okano, 1989). Liberal application of the tincture or povidone-iodine to the skin resulted in significant plasma and urine iodine levels and may cause systemic iodine toxicity (Luckhardt et al., 1920; Smerdely et al., 1989; Pyati et al., 1977; Chabrolle & Rossier, 1978; Coakley et al., 1989; L'Allemand et al., 1987; Dantzigen et al., 1987; Schoenberger & Grim, 1982). Injured skin Continuous postoperative wound irrigation with povidone-iodine resulted in death of a patient. Toxic manifestations of systemic iodine absorption appeared to cause the death, (D'Auria et al., 1990; Glick et al., 1985). Application of povidone-iodine on skin burns may cause systemic iodine toxicity (Lavelle et al., 1975; Peitsch & Meakins, 1976). 9.2.4 Eye contact Iodine-containing eye drops caused hyperthyroidism (Geisthoevel, 1984). 9.2.5 Parenteral exposure Iodine-containing contrast media may cause hyperthyroidism; the most frequent thyroid disorders, usually of a temporary nature, occur after choledochal contrast media (Steidle, 1989). In premature infants they cause hypothyroidism (L'Allemand et al., 1987). 9.2.6 Other No data available. 9.3 Course, prognosis, cause of death If the patient survives 48 hours after the ingestion of iodine, recovery is likely, although stricture of the oesophagus or pyloric sphincter may be a complication, (Dreisbach & Robertson 1987). It is probable that the pathological changes recorded in fatal cases of iodine poisoning and attributed to the systemic effects of iodine are largely the result of shock due to massive loss of fluid from the gastrointestinal tract and tissue hypoxia (Gilman et al.,1990). 9.4 Systematic description of clinical effects 9.4.1 Cardiovascular Cardiovascular effects are not due directly to iodine or iodide. Hypotension, tachycardia circulatory collapse may occur secondary to corrosive gastroenteritis due to ingestion of highly concentrated iodine solutions. In acute iodine inhalation, hypotension and tachycardia have been reported, (Gosselin et al., 1984). 9.4.2 Respiratory Inhalation of fumes leads to irritation of mucous membranes of the respiratory tract, which may result in asphyxia. Oedema of the glottis from ingestion was reported in early literature as a frequently mentioned cause of death, (Finkelstein & Jacobi, 1937). Pulmonary oedema and tachypnoea have been reported following ingestion of an unspecified large quantity of Lugol's solution, (Dyck et al., 1979). 9.4.3 Neurological 184.108.40.206 Central nervous system (CNS) Headache, dizziness and delirium have been reported in severe intoxications. Altered sensorium (agitation, confusion, hallucinations) have occurred in association with elevated serum iodine concentrations, (Alvarez, 1979; Gosselin et al., 1984). Continued administration of iodine may lead to mental depression, nervousness and insomnia (Reynolds, 1989). 220.127.116.11 Peripheral nervous system No data available. 18.104.22.168 Autonomic nervous system No data available. 22.214.171.124 Skeletal and smooth muscle No data available. 9.4.4 Gastrointestinal Excessive ingestion of iodine solutions can lead to gastrointestinal irritation, vomiting and ulceration at various levels of the upper gastrointestinal tract. Late oesophageal and pyloric stenosis have been reported, (Gosselin et al., 1984). If the stomach contains starch the emesis is coloured blue. 9.4.5 Hepatic Elevated serum transaminases and bilirubin concentrations have been reported occasionally in patients with elevated serum iodine concentrations, (Lavelle et al., 1975; Peitsch & Meakins, 1976). 9.4.6 Urinary 126.96.36.199 Renal Poisoning is manifested by serum creatine and levels up to 3.5 mg/dL (309 mmol/L) has been reported, (Dela Cruz et al., 1987). The renal lesions, which sometimes resemble acute tubularnecrosis, may be exacerbated by haemolytic anaemia, (Gosselin et al., 1984). Nephrotoxicity by iodine contrast media is reported by Cacoub et al., (1987). 188.8.131.52 Others No data available. 9.4.7 Endocrine and reproductive systems Transient hypothyroidism characterised by elevated urinary iodide concentrations, elevated serum iodine concentrations, elevated TSH concentrations, and low T4 concentrations have been demonstrated in povidone- iodine exposed mothers and their infants (L'Allemand et al., 1987). Iodine induced thyrotoxicosis is a condition that may develop in older patients with long-standing iodine deficiencies who receive high doses of iodine (Kobberling et al., 1985; Fradkin, 1983; Klein & Levey, 1983). Iodine containing drugs caused thyrotoxic crisis (Mackenroth, 1990). Excessive iodine intake can cause thyroid autoimmunity in endemic goitre, (Boyages et al., 1989). Organically bound iodine in the form of iodinated glycerol used as a mucolytic expectorant can inhibit the biosynthesis of thyroid hormone and induce hypothyroidism, (Drinka & Nolten, 1988). Hypothyroidism has also been described in neonates treated with topical povidone-iodine (Cosman et al., 1988). Topical iodine containing antiseptics may induce hypothyroidism in very-low-birthweight infants, (Smerdely et al., 1989). Multiple applications of povidone iodine in pregnancy, and lactation caused transient congenital hypothyroidism in a 6 week old girl, (Danziger et al., 1987). Iodine in contrast agents and skin disinfectants is the major cause for hypothyroidism in premature infants during intensive care, (L'Allemand et al., 1987). Iodated glycerol, an organic form of iodine, prescribed as a mucolytic-expectorant induced a mild hypothyroidism in a patient with a previous history of severe potassium iodide-induced hypothyroidism. Amiodarone, an iodine-rich drug widely used in the treatment of tachyarrhythmias, represents one of the most common sources of iodine-induced thyrotoxicosis. It developed not only in patients with underlying thyroid disorders, but also in subjects with apparently normal thyroid gland. Thyrotoxicosis occurred either during treatment with or at various intervals after withdrawal of amiodarone. Classical symptoms were often lacking, the main clinical feature being a worsening of cardiac disorders, (Martino et al., 1987). Tablets of seaweed, sold over the counter, is a real source of iodine. A 72-year-old female developed hyperthyroidism while ingesting these tablets. After stopping, the symptoms of hypothyroidism disappeared, (Shilo & Hirsch, 1990). Continuous povidone-iodine irrigation caused iodine toxicity with symptoms of metabolic acidosis, changes in mental status and the patient died (Glick et al., 1985). Administration of iodine containing eye-drops used as a cataract treatment caused hyperthyroidism (Geisthoevel, 1984). 9.4.8 Dermatological A case of fatal dermatitis following the use of a 2.5% solution of resublimated iodine in pure industrial alcohol before a surgical operation has been reported. The reaction was thought to be due to idiosyncrasy to iodine. Skin disinfection with iodine has caused goitre and hypothyroidism in 5 of 30 newborns under intensive care (Bouillon, 1988). Prolonged exposure to tincture of iodine can induce superficial necrosis. At least one death has been reported consequent to extensive skin involvement. Solutions of iodine applied to the skin should not be covered with occlusive dressings. Topical application of povidone-iodine on burn patients may lead to increased iodine/iodide absorption (Lavelle et al., 1975) and the development of a metabolic acidosis, renal failure and an altered mental status although a cause and effect relationship has not been definitely established. The older literature reports systemic symptoms which occurred immediately to 24 hours later, rarely following cutaneous application of one-half to one normal strength iodine tincture. Symptoms included fever, diarrhoea, pain, headache and delirium. Skin eruptions included urticaria to erythema to exfoliative dermatitis. Mortality was 47% in those 15 cases reported (Seymour, 1937). Repeated applications of iodophors may cause contact dermatitis. Allergic reactions occur 12 to 20 hours after application (Harvey, 1985; Kudo et al., 1988). 9.4.9 Eye, ear, nose, throat: local effects Exposure to iodine vapour may cause burning in the eyes, blepharitis, and severe ocular burns (Finkelstein & Jacobi, 1937). Iodine vapour may cause rhinitis. Stomatitis and pharyngitis may result from exposure to iodine vapour or solutions and mucous membranes are coloured brown. (Finkelstein & Jacobi, 1937). 9.4.10 Haematological Neutropenia has been reported in association with elevated serum iodine concentrations, (Alvarez, 1979). Thrombotic thrombocytopenic purpura has been observed after repeated administration of small amounts of iodine, (Ehrich & Seifter, 1949) Haemolysis has also been reported (Dyck et al., 1979). 9.4.11 Immunological Reactions to iodine may occur acutely or after chronic use and may be characterised by coryza, headache, salivary gland pain, conjunctivitis, fever or skin reactions (urticaria, acneform, eruptions, erythema, bullous, ioderma). Oral and intravenous iodine containing radio-contrast media (e.g Telopaque (R); I125, I131) may cause iodine hypersensitivity reaction as well as anaphylactic type reactions, (Crocker & Vadam, 1963). 9.4.12 Metabolic 184.108.40.206 Acid-base disturbances Metabolic acidosis may be associated with iodine toxicity. There is an increased anion gap due to elevated serum lactate levels (47 micromol/L) (Dyck et al., 1979; Dela Cruz et al., 1987) 220.127.116.11 Fluid and electrolyte disturbances Elevated serum sodium (hypernatraemia) (156 mEq/L) has been reported (Dela Cruz et al., 1987). Hyperchloremia (127 mEq/L) has also been reported but probably represents a spurious elevation due to interference in the assay by iodine (Dela Cruz et al., 1987). Elevations in calculated osmolarity (340 in Osm/L) have also been reported (Dela Cruz et al., 1987). 18.104.22.168 Others No data available. 9.4.13 Allergic reactions Intolerance to iodised X-ray contrast media may cause reactions consisting of fever, chills, malaise, nausea and vomiting, skin rash, diarrhoea and even hypotension. These may be classified as idiosyncratic. In patients with a history of idiosyncratic reaction premedication with corticoids and histamines is indicated or non-ionic contrast reagents should be used,(Soyer & Levesque, 1990). After interleukin-2 administration an increased incidence of hypersensitivity to iodine was observed, (Zukiwski et al., 1990). Hypersensitivity reactions were reported in 14 cases, secondary to the application of iodine-alcohol solutions to the skin. Symptoms reported were fever and generalised skin eruption of varying types. Despite the wide use of tincture of iodine the incidence of systemic reactions is low (Seymour, 1937). 9.4.14 Other clinical effects No data available. 9.4.15 Special risks Pregnancy Maternal ingestion of iodine containing substances during pregnancy can cause (transient) primary hypothyroidism in the newborn, (Coakley et al., 1989). Exposure to iodine and radioactive iodine in pregnancy may lead to permanent hypothyroidism or goitre in the newborn. Such goitres may become very large and even create problems during delivery or mechanical compression during early postnatal life (Bouillon, 1988). Breast feeding Similar warnings to those given for pregnancy against the use of iodine or iodine-containing drugs applies during lactation since iodine is actively secreted in milk, (Bouillon, 1988).""ILLUSTRATIVE CASES 11.1 Case reports from literature Case 1 Continuous irrigation with povidone-iodine in a 34-month- old patient with mediastinitis was associated with iodine toxicity, resulting in fatalities, (Glick et al., 1985). It is suggested that povidone-iodine continuous irrigation of the mediastinum be a contraindication. Case 2 A 63-year-old woman with a suppurative mediastinitis, treated with continuous Polyvinyl-pyrrolidone-iodine (PI) irrigation developed an acute oliguric renal failure due to systemic toxicity of PI. The withdrawal of PI was followed by a complete improvement of renal function, (Campistol et al., 1988). Case 3 Two patients with leg ulcers got worse after the application of a compound mixture of sugar and povidone iodine (sugar/PI compound). Patch-tests showed positive reactions to 10% povidone-iodine in water and 5% potassium iodide in water with no response to sugar. They were also tested with sugar/PI compound containing 3% povidone iodine, resulting in another positive reaction. They improved after the application of sugar/PI compound was discontinued, (Kudo et al., 1988). Case 4 A 34-year-old male with burns covering 80% BSA and a 22- year-old female with a 45% BSA burn, showed hyperthyroidism induced by topical treatment with 1% povidone-iodine. After topical treatment with povidone-iodine was discontinued circulating thyroid hormones returned to normal values within weeks (Rath and Meissl,1988). Case 5 Fifteen episodes of infection due to Pseudomonas aeruginosa, including peritonitis and other site infections, occurred in nine patients receiving continuous ambulatory peritoneal dialysis over a 27 month period. Occurrence of P. aeruginosa infection was significantly associated with use of povidone-iodine solution to cleanse the catheter site. Local irritation and alteration in skin flora caused by antiseptic solution or low-level contamination of povidone-iodine solution are potential mechanisms of infection (Goetz and Muder, 1989) Case 6 Vaginal douching with polyvinyl pyrrolidone iodine (PVP-I) during pregnancy resulted in maternal iodine overload and increased the iodine content of amniotic fluid. The possible effect of this therapy was evaluated on the thyroid of the fetus by investigating 62 women with a mean duration of amenorrhoea of 20 weeks who solicited controlled abortion. Nineteen of them douched daily with PVP-I for 2 consecutive days before abortion (treated group). The other 43 women were not treated (control group). In both groups the iodine content was determined in the foetal thyroid and in amniotic fluid and maternal urine at the time of abortion. In addition, in the treated group the concentrations of iodine were also determined in amniotic fluid and urine before therapy and in urine after 4 days of therapy. There were no differences in the concentrations of iodine in urine and amniotic fluid in the control group and in the treated group before therapy. Iodine content increased more rapidly in the treated group (from 1 to 7.7 micrograms) than in the control group (from 1 to 2.5 micrograms) P less than 0.05 (Mahillon et al., 1989). Case 7 Approximately 570,000 newborns were tested for congenital hypothyroidism between May 1977 and December 1986. One hundred and sixty cases of primary hypothyroidism, were later found to be transient. 14 out of the transient cases were due to excessive intake of iodine. In two, this was due to maternal ingestion of iodide during pregnancy and in 12 the babies received large amounts of topical iodine antiseptic. Two cases were caused by maternal anti-thyroid antibodies and in eight instances the cause was unknown. The large number of cases due to topical application of iodine antiseptic emphasizes the need for caution when using this substance in neonates (Coakely et al., 1989)."
Supplier's contact details amended. Reissued according to Regulation (EU) No 453/2010.
Revision Date 11-2011
Supersedes date 02-2010
Risk Phrases In Full
R20/21 Harmful by inhalation and in contact with skin.
R11 Highly flammable
NC Not classified.
R23/24/25 Toxic by inhalation, in contact with skin and if swallowed.
R39/23/24/25 Toxic: danger of very serious irreversible effects through inhalation, in contact with skin and if swallowed.
R50 Very toxic to aquatic organisms.
Hazard Statements In Full
H370 Causes damage to organs <
H332 Harmful if inhaled.
H312 Harmful in contact with skin.
H225 Highly flammable liquid and vapour.
H331 Toxic if inhaled.
H301 Toxic if swallowed.
H311 Toxic in contact with skin."
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