resorcinol publications

The proposed toxicity of resorcinol has been the subject of many articles, but recent studies confirm a low level of concern regarding it's toxicity. See these two references published in January 2008, which detail the studies and results.

"Two-Generation Reproductive Toxicity Study of Resorcinol Administered Via Drinking Water to Crl:CD(SD) Rats"
Welsch, F.; Nemec, M. D.; Lawrence, W. B.
International Journal of Toxicology, Volume 27, Issue 1, January 2008, pages 43-57

The potential adverse effects of resorcinol, delivered via drinking water at 0, 120, 360, 1000, and 3000 mg/L (palatability limit), were assessed in a regulatory guideline compliant two-generation reproduction study in Crl:CD(SD) rats. Expanded end points of thyroid gland (TG) function were added because of clinical case reports indicating human TG toxicity. Average daily resorcinol intake (mg/kg) at the 3000 mg/L concentration was 233 in F0 and F1 males, whereas in females it was 304 (premating/gestation) and 660 (lactation). No resorcinol ingestion-related clinical signs of toxicity were observed. Furthermore, neither gross morphologic anomalies nor effects on reproductive function or thyroid hormone levels were detectable. Body weight reductions occurred in 3000 mg/L F0 and F1 animals and were more pronounced in males. However, there was no evidence of either cumulative toxicity in the second generation or of enhanced sensitivity to resorcinol in pregnant/lactating females. Water intake was lower in 3000 mg/L rats of both generations and intermittently, to a lesser extent, at 1000 mg/L; however, concurrent feed intake and utilization were unaffected. Decreased TG follicular colloid content (conventional histopathology; confirmed by quantitative stereomicroscopy) in the 3000 mg/L F0 males was attributed to resorcinol but not considered adverse. The 3000 mg/L intake level appeared to have caused an adaptive thyroid response to a new homeostatic level with no adverse physiological consequences in either males (the more susceptible gender) or females. There were no differences in TG histology in F0 rats of either sex at 1000 mg/L. Thus, resorcinol intake at maximum palatability via a route and mode relevant to potential human exposures via contaminated drinking water at presently unknown environmental concentrations caused no detectable adverse effects on any reproduction or TG end points. The 3000 mg/L resorcinol exposure level was the no-observed-adverse-effect level (NOAEL) for parental systemic and offspring toxicity, while 1000 mg/L was the no-observed-effect level (NOEL).

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"Routes and Modes of Administration of Resorcinol and Their Relationship to Potential Manifestations of Thyroid Gland Toxicity in Animals and Man"
Welsch, Frank
International Journal of Toxicology, Volume 27, Issue 1, January 2008, pages 59-63

Medical case reports published in the 20th century over the course of several decades show that resorcinol caused reversible adverse effects on the human thyroid gland (TG) manifested as hypothyroidism. Affected patients had ulcerating leg varicosities and underwent prolonged treatment with ointments containing high concentrations of resorcinol. In animal studies resorcinol failed to induce TG toxicity, unless pharmacokinetic/toxicokinetic (PK/TK) conditions were manipulated (e.g., injection of resorcinol in oil or application in a slow release formulation). A recently completed two-generation reproductive toxicity study in rats did not detect any adverse effects on either reproductive or TG end points (Welsch, Nemec, and Lawrence, 2008, Int. J. Toxicol. 37, this issue). Resorcinol intake via drinking water up to the palatability limit had resulted in average daily intakes (mg/kg) of 233 in F0 and F1 males and 304 (premating/gestation) or 660 (lactation) in females. Free resorcinol in blood plasma was barely detectable in a few parental animals, indicating rapid metabolism. This short review communication offers a perspective on compromised human skin barrier function as a likely cause of drastic increases in resorcinol absorption. In conjunction with multiple daily applications over many months to hyperemic, inflamed, and lesioned human skin much higher absorption was likely responsible for the reported human TG toxicity.

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