Soy isoflavones have been a component of the diet of certain populations for centuries. The consumption of soy generally has been considered beneficial, with a potentially protective effect against a number of chronic diseases; because of their estrogenic activity, however, negative effects of isoflavones have been postulated. This review examines the literature associated with the safety of soy isoflavones, including dietary soy isoflavone exposure data of populations with high soy intakes, human studies in which soy protein or isoflavones were provided, and toxicologic studies investigating the potential genotoxicity, carcinogenicity, and reproductive and developmental toxicity of soy isoflavones. Whereas results in some studies are limited or conflicting, when viewed in its entirety, the current literature supports the safety of isoflavones as typically consumed in diets based on soy or containing soy products.

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Cyclopiazonic acid (CPA) is an indol-tetramic acid mycotoxin and is produced by the nearly ubiquitous molds, Aspergillus and Penicillium. CPA produced by these molds has been identified in a number of food sources (including, but not limited to, grain, legumes, meat, milk, and cheese) and from parasitic infections of man and other animals. Few incidents of CPA mycotoxicoses have been reported because of the benign nature of the intoxication, the small amounts present, and its effects may be disguised with concurrent aflatoxicosis (some toxicity data may have been generated using aflatoxin-contaminated CPA). CPA is absorbed in the gastrointestinal tract and following oral administration; it has a half-life of approximately 30 hours and is excreted largely unchanged in the urine and feces. Cyclopiazonic acid is not considered to be a potent acute toxin as its oral LD50 in rodents is in the range of 30 to 70 mg/kg. Multiple dose studies also show a range of effects in several species and among mammalian models, the pig appears to be the most sensitive with a no-observable-effect level (NOEL) in the range of 1.0 mg/kg/day. The preponderance of evidence from the rat and other test animals supports this dose as a defensible estimate of a no effect level. The target organs of CPA toxicity appear to be muscle, hepatic tissue, and spleen, with a localization in the former, although a more apparent toxic change in the latter two. The toxicity and symptoms of CPA poisoning can be attributed to its ability to alter normal intracellular calcium flux through its inhibition of the reticular form of the Ca2+-ATPase pump. CPA was not teratogenic in mice. CPA is not considered a carcinogen and the weight of evidence militates against its characterization as a mutagen. Despite CPA-induced pathological changes ascribed to the spleen or bursa of Fabricius, there does not appear to be an effect on the immune system. In vitro studies imply a potential immunomodulatory effect of CPA, but in all of those reports very high concentrations of CPA were required and none of these findings have been supported with in vivo studies. Therefore, based on a NOEL of 1 mg/kg/day and accounting for species variation, an appropriate acceptable daily intake (ADI) would be approximately 10 μg/kg/day or 700 μg/day. In the context of human exposure, if the uppermost limit of CPA found in cheese is 4 μg/g and the average individual consumes 50 g of cheese daily, this allows an intake of 200 μg, less than one third of a traditionally established ADI.

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