Red Dye No. 3, Iodine and Fluoride
FDA Revokes Authorization for FD&C Red No. 3: A Closer Look at the Decision
Background
On January 15, 2025, the U.S. Food and Drug Administration (FDA) announced it would no longer permit the use of FD&C Red No. 3 in food products, ingested pharmaceuticals, and other applications.
First approved in 1907 (USDA, 1907), this dye has been a staple in a wide range of products, including candy, breakfast cereals, baked goods, fruit snacks, frozen foods, vegan “meats,” protein shakes, and medications. To many, it is perhaps best known for its role in colouring maraschino cherries.
The FDA’s decision to revoke authorization for FD&C Red No. 3 is grounded in the Delaney Clause of the Federal Food, Drug, and Cosmetic Act (FD&C Act) (FDA, 2025). Introduced in 1960 as part of the Color Additives Amendment, the Delaney Clause prohibits the FDA from approving any food or colour additive shown to cause cancer in humans or animals.
In 1990, the FDA banned the dye from use in cosmetics, such as lipsticks, and externally applied drugs specifically due to safety concerns about carcinogenicity. Plans to prohibit its use in food and pharmaceuticals faced strong resistance from the agricultural sector, particularly canned fruit manufacturers and the maraschino cherry industry. This led the U.S. House of Representatives to delay the ban pending further studies (CSPI, 2023; Master, 1989).
Following the FDA’s recent announcement, misinformation about FD&C Red No. 3 and the reasons behind its prohibition has circulated widely, including inaccuracies from the FDA itself.
What is FD&C Red No. 3?
FD&C stands for Food, Drug, and Cosmetic, referring to dyes approved by the US FDA for use in these categories. FD&C Red No. 3, commonly known as erythrosine in other parts of the world, is a highly iodinated compound containing approximately 58% iodine by weight. For simplicity, this article will refer to it as erythrosine.
Why was it banned?
The FDA's ban on erythrosine stems from two studies conducted in the 1980s, which linked the dye to thyroid cancer (specifically follicular cell adenomas) in male rats (FDA, 1990). These findings placed the dye under the scope of the Delaney Clause, which prohibits the approval of substances shown to cause cancer in humans or animals.
What is Known About the Mechanism?
The mechanism leading to thyroid cancer in erythrosine-exposed rats involves disruptions in peripheral thyroid hormone conversion (outside the thyroid gland), resulting in elevated thyroid-stimulating hormone (TSH) levels. Erythrosine interferes with the conversion of T4 to T3 (deiodination), reducing circulating T3 levels and increasing reverse T3 (rT3), an inactive form of T3 (Capen et al., 1996; 1997; Jennings et al., 1990; Borzelleca et al., 1987; Poulsen, 1993).
This disruption in peripheral thyroid hormone metabolism perturbs the thyroid/pituitary feedback loop, leading to increased TSH secretion by the pituitary gland. Chronic TSH elevation has long been recognized as a driver of thyroid follicular cell stimulation, leading to hypertrophy, hyperplasia, and, ultimately, neoplasia in both rodents and humans (Axelrod & Leblond, 1955; Jennings et al., 1990; Capan, 1997, 1999).
Erythrosine's effects on thyroid hormone activity are attributed to its high iodine content. Studies indicate that it significantly disrupts both iodine and thyroid hormone levels in humans and animals (i.e., Anderson et al., 1964; Gardner et al., 1987; Vought et al., 1972; Shen et al., 2003; Capen & Martin, 1989; Jennings et al., 1990; Shimizu et al., 2013; Paramasivam et al., 2024; Cody, 1985; Ruiz & Ingbar, 1982). Unlike its non-iodinated parent compound, fluorescein, erythrosine interferes with thyroid hormone metabolism, supporting the conclusion that its iodine content or iodinated metabolites are responsible for these effects (Cody et al., 1985; Jennings et al., 1990).
The thyroid-disrupting effects of erythrosine are not unique. The heart drug amiodarone is another iodinated compound known to cause follicular cell adenomas in males (Su et al., 2013). It also interferes with deiodination, increases rT3 levels, and elevates TSH levels (Ursella et al., 2006), while its non-iodinated derivative, dronedarone, does not affect thyroid hormone metabolism (Pantos et al., 2002). This reinforces the conclusion that erythrosine’s impact on thyroid function is directly tied to its iodine content.
Elevated TSH levels are commonly associated with iodine deficiency, and prolonged iodine deficiency can lead to the development of follicular cell adenomas (Boorman, 1983). However, iodine excess may also disturb peripheral thyroid hormone metabolism and cause increased TSH levels. Both iodine deficiency and iodine excess have been linked to thyroid cancer in animals and humans (Kolonel et al., 1990; Zhu et al., 2009; Takegawa et al., 2000). In male rats specifically, both conditions - iodine deficiency and iodine excess - are known to cause elevated TSH levels (Boorman, 1983; Li et al., 2012; Arbez-Evangelista et al., 2024).
Excessive TSH secretion alone (without any chemical exposure) has also been shown to result in a high incidence of thyroid tumours in rodents (Caplan, 1997).
Erythrosine and Neurobehaviour
While the FDA ban of erythrosine was based only on the cancer data (Delaney Clause) it should be noted that there have been many studies in the last 30 years documenting the effects of erythrosine on neurobehaviour at doses much lower than those documented in the cancer studies, or deemed “acceptable daily intakes” (ADI) (Sing & Chada, 2024; Miller et al., 2022; Dalal & Poddar, 2009, 2010; Erickson et al., 2010).
These findings align with the many recent studies linking prenatal iodine supplementation to ADHD and neurobehavioural issues in offspring (PFPC, 2023).
Food for Thought - Fluoride
While the FDA has banned erythrosine due to its cancer-promoting effects via TSH stimulation, a similar yet more extensively documented mechanism has been established for fluoride. Like erythrosine, fluoride can raise reverse T3 (rT3) levels and increase TSH secretion. In fact, rT3 has been identified as a biomarker for fluoride poisoning (Lin et al., 1991, 1992; Shashi & Singla, 2013). When iodine deficiency is present, even low concentrations of fluoride in drinking water can elevate rT3 and TSH levels in both children and adults (Lin et al., 1991, 1992; Kheradpisheh et al., 2018). Elevated TSH levels are one of the most consistently observed abnormalities in fluoride poisoning (PFPC, 2021). An increased incidence of follicular cell adenomas in rodents has been observed in studies involving fluoride (Bucher et al., 1990) and PFAS (Butenhoff et al., 2012).
Fluoride’s effects extend beyond peripheral thyroid hormone metabolism and deiodination. It has been shown to act directly as a TSH analog. Fluoride has been extensively used in studies to examine how TSH promotes cancer growth (PFPC, 2003), with evidence indicating that thyroid neoplasms sometimes exhibit a stronger response to fluoride than to TSH itself (i.e. Clark & Gehrend, 1984, 1985). Moreover, hundreds of studies have now documented fluoride’s effects on cancer-promoting pathways such as Cox-2, MAPK, and PI3K/Akt.
The body of scientific literature on fluoride’s impact on thyroid hormone metabolism far exceeds that on erythrosine, by an estimated ratio of 40 to 1. This research includes data on humans, animals, endocrine disruptor models, and detailed investigations of molecular pathways. Spanning over 150 years, this evidence highlights fluoride’s role as a potent disruptor of thyroid function. Despite this, the FDA has taken no significant action to regulate fluoride exposure through oral care products, such as fluoridated toothpaste, which fall under its purview.
While the food industry delayed the FDA’s ban on erythrosine in food for 35 years, the dental industry has played a similarly obstructive role regarding fluoride. Since the advent of water fluoridation, public health dentists and industry-funded nutritionists have manipulated public perception and policymaking. Even during the 1950-1952 Delaney hearings - which helped set the stage for later legislative actions - the issue of water fluoridation was added to the agenda. However, dental public health advocates and industry interests ensured that the potential risks associated with fluoride exposure were downplayed or dismissed.
This stark discrepancy between the regulation of erythrosine and fluoride raises critical questions about public health priorities and industry influence on regulatory decisions.
Canada
Finally, a few words about Canada’s reaction to the FDA’s announcement banning erythrosine. Health Canada issued a statement confirming it would not follow the FDA’s lead in banning the dye. Erythrosine remains approved for use in cosmetics, food, and drugs in Canada. The National Post reported that Health Canada justified its stance by stating that the two 1980s studies linking erythrosine to cancer were “due to a rat-specific hormonal mechanism which does not exist in humans.”
This assertion is difficult to reconcile with decades of scientific evidence showing that the mechanism exists in humans. The disruption of the thyroid-pituitary feedback loop due to interference with thyroid hormone metabolism is well-documented and supported by thousands of studies. Moreover, the principle that elevated TSH drives thyroid cell growth and potential malignancy is foundational in thyroid medicine. This is evidenced by TSH-suppressive therapy - a standard treatment for thyroid cancer survivors, which is approved by Health Canada.
Health Canada further claimed that “the use of this colour in food puts people’s health at risk is not supported by the available scientific evidence.” Such statements reflect an alarming disregard for well-established science, consistent with other recent Health Canada publications on fluoride, PFAS, and other substances.
At the same time, the majority of Canadian children aged 3–5 consume too much iodine, with 40% consuming excessive amounts (CHMS, 2009–2011). Similarly, 90% of pregnant women take prenatal supplements containing iodine, leading to more-than-adequate or excessive iodine intake in a significant proportion of expectant mothers (Krzeczkowski et al., 2023). To date, Health Canada has entirely failed to address this critical public health issue.
Is it any wonder that trust in public health agencies continues to erode?
PFPC Canada
REFERENCES
Anderson CJ, Keiding NR, Nielson AB - “False elevation of serum protein-bound-iodide caused by red colored drugs and foods” Scand J Clin Lab Invest 16:249 (1964)
https://www.tandfonline.com/doi/10.1080/00365516409060512
Arbez-Evangelista C, Arroyo-Xochihua O, Ortega-Ibarra IH, Ortega-Ibarra E, De León-Ramírez YM, Cuevas-Romero E, Arroyo-Helguera O - “Excess Iodine Consumption Induces Oxidative Stress and Pancreatic Damage Independently of Chemical Form in Male Wistar Rats: Participation of PPAR-γ and C/EBP-β” Biology (Basel) 13(7):466 (2024). doi: 10.3390/biology13070466
https://www.mdpi.com/2079-7737/13/7/466
Axelrad AA, Leblond CP - “Induction of thyroid tumors in rats by a low iodine diet” Cancer 8(2):339-67 (1955) doi: 10.1002/1097-0142(1955)8:2<339::aid-cncr2820080214>3.0.co;2-m.
https://acsjournals.onlinelibrary.wiley.com/doi/10.1002/1097-0142(1955)8:2%3C339::AID-CNCR2820080214%3E3.0.CO;2-M
Borzelleca JF, Capen CC, Hallagan JB - “Lifetime toxicity/carcinogenicity study of FD & C Red No. 3 (erythrosine) in rats” Food Chem Toxicol 25(10):723-33 (1987). doi: 10.1016/0278-6915(87)90226-2
https://www.sciencedirect.com/science/article/abs/pii/0278691587902262
Boorman GA - “Follicular Cell Adenoma, Thyroid, Rat” In: Jones, T.C., Mohr, U., Hunt, R.D., Capen, C.C. (eds) Endocrine System. Monographs on Pathology of Laboratory Animals. Springer, Berlin, Heidelberg (1983)
https://doi.org/10.1007/978-3-642-96720-7_41
Brehaut L - “The U.S. banned red dye No. 3. Why is it still allowed in Canada?” National Post, January 20, 2025
https://nationalpost.com/life/food/the-u-s-banned-red-dye-no-3-why-is-it-still-allowed-in-canada
Bucher JR, Hejtmancik MR, Toft JD 2nd, Persing RL, Eustis SL, Haseman JK - "Results and conclusions of the National Toxicology Program's rodent carcinogenicity studies with sodium fluoride" Int J Cancer 48(5):733-7 (1991) doi: 10.1002/ijc.2910480517
https://pubmed.ncbi.nlm.nih.gov/2071234/
Butenhoff JL, Chang SC, Olsen GW, Thomford PJ - "Chronic dietary toxicity and carcinogenicity study with potassium perfluorooctanesulfonate in Sprague Dawley rats" Toxicology 293(1-3):1-15 (2012) doi: 10.1016/j.tox.2012.01.003
https://pubmed.ncbi.nlm.nih.gov/22266392/
Butterworth KR, Gaunt IF, Grasso P, Gangolli SD - “Acute and short-term toxicity studies on erythrosine BS in rodents” Food Cosmet Toxicol 14(6):525-31 (1976). doi: 10.1016/s0015-6264(76)80001-6.
https://www.sciencedirect.com/science/article/abs/pii/S0015626476800016
Capen CC, Martin SL - "The effects of xenobiotics on the structure and function of thyroid follicular and C-cells" Toxicol Pathol 17(2):266-93 (1989) doi: 10.1177/019262338901700205
https://pubmed.ncbi.nlm.nih.gov/2675279/
Capen CC - “Hormonal imbalances and mechanisms of chemical injury of thyroid gland” In: Jones TC, Capen CC, Mohr U, editors. Endocrine System. Monographs on Pathology of Laboratory Animals. Berlin, Heidelberg: Springer (1996) https://doi.org/10.1007/978-3-642-60996-1_23
Capen CC - “Mechanistic data and risk assessment of selected toxic end points of the thyroid gland” Toxicol Pathol 25(1):39-48 (1997). doi: 10.1177/019262339702500109.
https://journals.sagepub.com/doi/epdf/10.1177/019262339702500109
rT3 graph: https://poisonfluoride.com/dir/wp-content/uploads/Capen-erythrosine-rT3-1997-e1737832828495.png
Canadian Health Measures Survey (2009–2011)
https://www150.statcan.gc.ca/n1/en/pub/82-625-x/2012001/article/11733-eng.pdf?st=ESvkDMd5
Center for Sciene in the Public Interest (CSPI) - “Red 3: Why hasn’t the FDA banned this carcinogenic food dye?” (2023)
https://www.cspinet.org/cspi-news/red-3-why-hasnt-fda-banned-carcinogenic-food-dye
Clark OH, Gerend PL - “Thyrotropin regulation of adenylate cyclase activity in human thyroid neoplasms” Surgery 97(5):539-46 (1985)
Clark OH, Gerend PL, Nissenson RA - “Mechanisms for increased adenylate cyclase responsiveness to TSH in neoplastic human thyroid tissue” World J Surg 8(4):466-73 (1984) doi: 10.1007/BF01654915
https://onlinelibrary.wiley.com/doi/10.1007/BF01654915
Cody V - "Conformational analysis of erythrosine B (FD&C Red No. 3) and its comparison with thyroid hormone structures" Endocr Res 11(3-4):211-24 (1985) doi: 10.3109/07435808509032979
https://pubmed.ncbi.nlm.nih.gov/3009171
“The observed potency of erythrosine B as an inhibitor of iodothyronine deiodinase, and its structural homology with the active thyroid hormone conformation, suggest that many of its antithyroid effects are mediated by interference with thyroid hormone metabolic pathways.”
Dalal A, Poddar MK - "Short-term erythrosine B-induced inhibition of the brain regional serotonergic activity suppresses motor activity (exploratory behavior) of young adult mammals" Pharmacol Biochem Behav 92(4):574–82 (2009)
https://linkinghub.elsevier.com/retrieve/pii/S0091305709000720
Erickson ZT, Falkenberg EA, Metz GA - "Lifespan psychomotor behaviour profiles of multigenerational prenatal stress and artificial food dye effects in rats" PLoS One 9(6):e92132 (2014)
https://pmc.ncbi.nlm.nih.gov/articles/PMC4061018/
Food and Drug Administration (FDA) - FDA to Revoke Authorization for the Use of Red No. 3 in Food and Ingested Drugs (January 15, 2025)
https://www.fda.gov/food/hfp-constituent-updates/fda-revoke-authorization-use-red-no-3-food-and-ingested-drugs
Food and Drug Administration (FDA) - Color Additives History (2003)
https://www.fda.gov/industry/color-additives/color-additives-history
Food and Drug Administration (FDA) - Color Additives in Foods (2023)
https://www.fda.gov/food/color-additives-information-consumers/color-additives-foods
Food and Drug Administration (FDA). Color Additives; Denial of Petition for Listing of FD&C Red No. 3 for Use in Cosmetics and Externally Applied Drugs; Withdrawal of Petition for Use in Cosmetics Intended for Use in the Area of the Eye. Federal Register 55 FR 3520-01 55(22):3520-4 (1990) https://www.cspinet.org/sites/default/files/2022-12/Dyes%20Red-3-FDA-Delisting-Cosmetics-2-1-90%20%2813%29.pdf
ALSO: https://archives.federalregister.gov/issue_slice/1990/2/1/3512-3541.pdf
Gardner DF, Utiger RD, Schwartz SL, Witorsch P, Meyers B, Braverman LE, Witorsch RJ - "Effects of oral erythrosine (2',4',5',7'-tetraiodofluorescein) on thyroid function in normal men" Toxicol Appl Pharmacol 91(3):299-304 (1987) doi: 10.1016/0041-008x(87)90052-4
https://pubmed.ncbi.nlm.nih.gov/2447681/
Gardner DF, Centor RM, Utiger RD - "Effects of low dose oral iodide supplementation on thyroid function in normal men" Clin Endocrinol (Oxf) 28(3):283-8 (1988) doi: 10.1111/j.1365-2265.1988.tb01214.x. https://pubmed.ncbi.nlm.nih.gov/3139337/
Hiasa Y, Ohshima M, Kitahori Y, Konishi N, Shimoyama T, Sakaguchi Y, Hashimoto H, Minami S, Kato Y - "The promoting effects of food dyes, erythrosine (Red 3) and rose bengal B (Red 105), on thyroid tumors in partially thyroidectomized N-bis(2-hydroxypropyl)-nitrosamine-treated rats" Jpn J Cancer Res 79(3):314-9 (1988). doi: 10.1111/j.1349-7006.1988.tb01593.x
https://pubmed.ncbi.nlm.nih.gov/2836348/
Jennings AS, Schwartz SL, Balter NJ, Gardner D, Witorsch RJ - "Effects of oral erythrosine (2',4',5',7'-tetraiodofluorescein) on the pituitary-thyroid axis in rats" Toxicol Appl Pharmacol 103(3):549-56 (1990) doi: 10.1016/0041-008x(90)90327-q https://pubmed.ncbi.nlm.nih.gov/2160137/
Kanno J, Onodera H, Furuta K, Maekawa A, Kasuga T, Hayashi Y - “Tumor-promoting effects of both iodine deficiency and iodine excess in the rat thyroid” Toxicol Pathol 20(2):226-35 (1992) doi: 10.1177/019262339202000209
https://journals.sagepub.com/doi/10.1177/019262339202000209
Kheradpisheh Z, Mirzaei M, Mahvi AH, Mokhtari M, Azizi R, Fallahzadeh H, Ehrampoush MH - "Impact of Drinking Water Fluoride on Human Thyroid Hormones: A Case-Control Study" Scientific Reports Volume 8:2674 (2018)
https://www.nature.com/articles/s41598-018-20696-4
Kobylewski S, Jacobson MF - "Toxicology of food dyes" Int J Occup Environ Health 18(3):220-246 (2012) doi:10.1179/1077352512Z.00000000034.
https://www.tandfonline.com/doi/abs/10.1179/1077352512Z.00000000034
Kolonel LN, Hankin JH, Wilkens LR, Fukunaga FH, Hinds MW - “An epidemiologic study of thyroid cancer in Hawaii” Cancer Causes Control 1(3):223-34 (1990). doi: 10.1007/BF00117474
https://link.springer.com/article/10.1007/BF00117474
Krzeczkowski JE, Hall M, McGuckin T, Lanphear B, Bertinato J, Ayotte P, Chevrier J, Goodman C, Green R, Till C - “Iodine status in a large Canadian pregnancy cohort” Am J Obstet Gynecol MFM 5(1):100784 I (2023) doi: 10.1016/j.ajogmf.2022.100784 https://linkinghub.elsevier.com/retrieve/pii/S2589-9333(22)00214-2
Li N, Jiang Y, Shan Z, Teng W - "Prolonged high iodine intake is associated with inhibition of type 2 deiodinase activity in pituitary and elevation of serum thyrotropin levels" Br J Nutr 107(5):674-82 (2012). doi: 10.1017/S0007114511003552 LINK
Lin J, Lin FF, Zhao HX, Jiang JY, Xu XF - "A study on the relationship between serum rT3 and environmental iodine or fluoride levels" Endemic Disease Bulletin (3):68-70 (1992)
http://www.nmglib.com:8901/article/detail.aspx?id=720441
Lin FF, Aihaiti, Zhao HX, Lin J, Jiang JY, Maimaiti, Aiken - "High-fluoride and Low-iodine Environment and Subclinical Cretinism in Xinjiang" Endem Dis Bul 6(2):62-67 (1991)
English Translation in: ICCIDD Newsletter, Volume 7 Number 3 (August 1991)
https://poisonfluoride.com/dir/wp-content/uploads/Lin-FF-1991.pdf
https://poisonfluoride.com/pfpc/lin-1991.pdf
Master BA - “Dyeing to keep the cherry red” Washington Post, July 18, 1989
https://www.washingtonpost.com/archive/politics/1989/07/18/dyeing-to-keep-the-cherry-red/59c82b6b-c37c-466c-adb6-f4ce3636d0e7/
Miller MD, Steinmaus C, Golub MS, Castorina R, Thilakartne R, Bradman A, Marty MA - "Potential impacts of synthetic food dyes on activity and attention in children: a review of the human and animal evidence" Environ Health 21(1):45 (2022) doi: 10.1186/s12940-022-00849-9
https://pmc.ncbi.nlm.nih.gov/articles/PMC9052604/
Pantos C, Mourouzis I, Delbruyère M, Malliopoulou V, Tzeis S, Cokkinos DD, Nikitas N, Carageorgiou H, Varonos D, Cokkinos D, Nisato D - “Effects of dronedarone and amiodarone on plasma thyroid hormones and on the basal and postischemic performance of the isolated rat heart” Eur J Pharmacol 444(3):191-6. (2002) doi: 10.1016/s0014-2999(02)01624-2
https://www.sciencedirect.com/science/article/abs/pii/S0014299902016242
Paramasivam A, Murugan R, Jeraud M, Dakkumadugula A, Periyasamy R, Arjunan S - "Additives in Processed Foods as a Potential Source of Endocrine-Disrupting Chemicals: A Review" J Xenobiot 14(4):1697-1710 (2024). doi: 10.3390/jox14040090
https://pmc.ncbi.nlm.nih.gov/articles/PMC11587131/
PFPC - “Fluoride = TSH | 70 Studies” (2003)
https://poisonfluoride.com/Science/TSH/tsh.html
PFPC - “TSH & Fluoride Studies” (2021)
https://poisonfluoride.com/phpBB3/viewtopic.php?f=7&t=3812
PFPC - ADHD and Iodine (2023)
https://poisonfluoride.com/phpBB3/viewtopic.php?p=6075
Poulsen E - “Case study: Erythrosine” Food Additives & Contaminants 10(3):315-323 (1993) DOI: 10.1080/02652039309374154
https://www.tandfonline.com/doi/abs/10.1080/02652039309374154
Ruiz M, Ingbar SH - "Effect of erythrosine (2',4',5',7'-tetraiodofluorescein) on the metabolism of thyroxine in rat liver" Endocrinology 110(5):1613-7 (1982). doi: 10.1210/endo-110-5-1613
https://academic.oup.com/endo/article-abstract/110/5/1613/2590417
Sand G, Jortay A, Pochet R, Dumont JE - “Adenylate cyclase and protein phosphokinase activities in human thyroid. Comparison of normal glands, hyperfunctional nodules and carcinomas” Eur J Cancer 12(6):447-53 (1976)
Shashi A, Singla S - "Syndrome of Low Triiodothyroinine in Chronic Fluorosis" International Journal of Basic and Applied Medical Sciences 3(1):152-160 (2013a)
Shashi A, Singla S - "Clinical and Biochemical Profile of Deiodinase Enzymes and Thyroid Function Hormones in Patients of Fluorosis" Australian Journal of Basic and Applied Sciences 7(4): 100-107 (2013b)
http://poisonfluoride.com/phpBB3/viewtopic.php?t=552
Shen L, Furuya M, Tachibana S, Kuwagata M, Kanazawa Y, Nagata T, Horiuchi S, Saegusa K, Inada H, Kojima K, Takashima H - "Alteration of Thyroid Hormone in Crj: CD (SD) IGS Rats by Repeated Administration of Erythrosine" Hatano Research Institute, Food and Drug Safety Center CD (SD) IGS-2002/2003; 38-43 (2003) [PFPC Library]
Shimizu R, Yamaguchi M, Uramaru N, Kuroki H, Ohta S, Kitamura S, Sugihara K - "Structure-activity relationships of 44 halogenated compounds for iodotyrosine deiodinase-inhibitory activity" Toxicology 314(1):22-9 (2013) doi: 10.1016/j.tox.2013.08.017
https://pubmed.ncbi.nlm.nih.gov/24012475/
Singh M, Chadha P - "Erythrosine-Induced Neurotoxicity: Evaluating Enzymatic Dysfunction, Oxidative Damage, DNA Damage, and Histopathological Alterations in Wistar Rats" J Appl Toxicol (2024) doi: 10.1002/jat.4731
https://pubmed.ncbi.nlm.nih.gov/39600142/
Singh M, Chadha P - "Gastrointestinal toxicity following sub-acute exposure of erythrosine in rats: biochemical, oxidative stress, DNA damage and histopathological studies" J Biochem Mol Toxicol 38(11):e70007 (2024). doi: 10.1002/jbt.70007
https://pubmed.ncbi.nlm.nih.gov/39400474/
Su VY, Hu YW, Chou KT, Ou SM, Lee YC, Lin EY, Chen TJ, Tzeng CH, Liu CJ - “Amiodarone and the risk of cancer: a nationwide population-based study” Cancer. 119(9):1699-705 (2013). doi: 10.1002/cncr.27881
https://acsjournals.onlinelibrary.wiley.com/doi/10.1002/cncr.27881
Takegawa K, Mitsumori K, Onodera H, Shimo T, Kitaura K, Yasuhara K, Hirose M, Takahashi M - “Studies on the carcinogenicity of potassium iodide in F344 rats” Food Chem Toxicol 38(9):773-81 (2000). doi: 10.1016/s0278-6915(00)00068-5
https://www.sciencedirect.com/science/article/abs/pii/S0278691500000685
Taylor KW, Eftim SE, Sibrizzi CA, Blain RB, Magnuson K, Hartman PA, Rooney AA, Bucher JR - "Fluoride Exposure and Children's IQ Scores: A Systematic Review and Meta-Analysis" JAMA Pediatr. Published online January 6, 2025. doi:10.1001/jamapediatrics.2024.5542
https://jamanetwork.com/journals/jamapediatrics/fullarticle/2828425
Ursella S, Testa A, Mazzone M, Gentiloni Silveri N - “Amiodarone-induced thyroid dysfunction in clinical practice” Eur Rev Med Pharmacol Sci 10(5):269-78 (2006)
https://pubmed.ncbi.nlm.nih.gov/17121321/
USDA - Food Inspection Decision (F.I.D.) 76 (1907)
Vought RL, Brown FA, Wolff J - "Erythrosine: an adventitious source of iodide" J Clin Endocrinol Metab 34(4):747-52 (1972) doi: 10.1210/jcem-34-4-747
https://pubmed.ncbi.nlm.nih.gov/5012776/
Watanabe E, Tsutsui T, Suzuki N, Homma T, Ozaki T, Arai T, Okamura T, Maizumi H - “Cytotoxicity of plaque-disclosing agents on cultured mammalian cells” Dentistry 74(5):1146-52 (1986) (Japanese)
Yankell SL, Loux JJ - “Acute toxicity testing of erythrosine and sodium fluorescein in mice and rats” J Periodontol 48(4):228-31 (1977) doi: 10.1902/jop.1977.48.4.228
https://pubmed.ncbi.nlm.nih.gov/265392/
Zhu YP, Bilous M, Boyages SC - “Excess iodine induces the expression of thyroid solid cell nests in lymphocytic thyroiditis-prone BB/W rats” Autoimmunity 20(3):201-6 (1995). doi: 10.3109/08916939508993351
https://www.tandfonline.com/doi/10.3109/08916939508993351
Thanks for this, have added as an update to
https://geoffpain.substack.com/p/fda-finally-bans-supertoxin-red-dye