Propylene Glycol vs Red Dye 3: which is worse?

What is Propylene Glycol?

Propylene glycol is a synthetic organic compound used as a humectant, solvent, and emulsifier in food, pharmaceuticals, cosmetics, and industrial applications. It is produced from propylene oxide (derived from petroleum). Its chemical formula is C3H8O2.

What is Red Dye 3?

Red Dye 3 (erythrosine) is a synthetic cherry-pink fluorescent dye belonging to the xanthene class. It contains approximately 58% iodine by weight, distinguishing it from azo dyes. Its chemical formula is C20H6I4Na2O5. Approved since 1907, it is one of the oldest certified US food colorants and was notably the first synthetic food dye formally revoked by the FDA in decades.

Documented risks

Propylene Glycol: Propylene glycol is generally considered safe by the FDA and is metabolized by the liver to lactic acid and pyruvate (normal metabolites). However, at high doses — particularly from intravenous pharmaceutical formulations — propylene glycol can accumulate and cause lactic acidosis, kidney toxicity, and CNS effects. These effects are seen in critically ill patients receiving high-dose PG-containing intravenous medications, not from food consumption. In children and people with impaired liver or kidney function, PG accumulation may occur at lower doses than in healthy adults. Animal studies have found reproductive and developmental effects at high doses. EFSA's 2018 re-evaluation found no concerns at typical food use levels but noted the EU limits PG use as a direct food additive, using it only as a carrier solvent for permitted additives.

Red Dye 3: The FDA revoked Red Dye 3 authorization in January 2025, marking the first synthetic food dye ban by the FDA since Red Dye 2 in 1976. The revocation was triggered by the Delaney Clause, which mandates revocation of any food additive found to cause cancer in animals regardless of dose. The carcinogenicity data stems from studies showing that high doses of erythrosine caused thyroid follicular cell tumors in male rats. The mechanism is indirect: erythrosine suppresses thyroid-stimulating hormone (TSH) feedback by elevating thyroxine (T4) levels, causing chronic TSH suppression that promotes thyroid cell proliferation and ultimately tumor formation. This is a rat-specific mechanism related to their thyroxine-binding protein system, which differs from human biology. EFSA's 2011 comprehensive safety assessment concluded erythrosine was unlikely to be genotoxic at typical food use levels and set an ADI of 0.1 mg/kg body weight — one of the lowest for any food color. EFSA restricted EU use to cocktail cherries only (max 200 mg/kg). The high iodine content (58% by weight) raises concerns for thyroid-sensitive individuals. Excessive erythrosine intake could theoretically contribute to iodine overload and thyroid disruption, particularly in individuals with hyperthyroidism or Hashimoto's disease. The FDA had been aware of the rat thyroid tumor data since 1990 but delayed action for 35 years. Advocacy groups including CSPI petitioned for a ban since 1983. The January 2025 revocation finally addressed this long-standing regulatory gap.