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

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