The dashboard indicated that several compounds reported to occur in PCL formulations i.e., caprolactone, 2-ethylhexanoic acid, and common phthalates were not PXR activators, or their bioassay profiles did not match those of the consumer-grade PCL extracts. Nonetheless, common phthalates can activate PPAR, suggesting that they may contribute to the PPAR activity. Several common phthalates (e.g., benzyl butyl phthalate (CAS# 85-68-7) and di(2ethylhexyl) phthalate (CAS# 117-81-7) ) also elicit estrogen or androgen nuclear receptor activity, which was not observed for the extracts (Figure ). These phthalates tend to be orders of magnitude more acutely toxic (benzyl butyl phthalate, EC50 = ~50 ng/mL 65 ) to developing zebrafish embryos than those without sex hormone activity (e.g., di-n-octyl phthalate (CAS# 117-84-0) 66 , EC50 = ~150 µg/mL ), suggesting that any phthalates associated with the PCL are those that are less acutely toxic. Additionally, phthalates minimally leach from PCL in aqueous media, further limiting their potential as the source of harm, and phthalates were not detected by the GC analyses. Collectively, these arguments suggest that it is unlikely that phthalates were the source of acute toxicity for the zebrafish embryos following exposure to consumer-grade PCL.