An important consideration would be as to the type of binding that pyriproxyfen has to target molecules - e.g. retinoid receptor molecules - if there is high affinity binding low concentrations may still lead to very adverse effects. Also, pyriproxyfen may accumulate in the body - it is fat soluble and evidence in the literature suggests it may also bind to DNA - so may reach a saturation point in sequestration and binding sites if there is continued intake via drinking water where sudden release of significant concentrations into circulation could occur. This occurring during early pregnancy could be very damaging if pyriproxyfen does indeed bind to retinoid receptors.
The authors should be commended for a thorough and nuanced analysis of a pressing health emergency.
However, I am struck by the conclusion that doses in animal models of 100 mg/kg or 300 mg/kg dosage have any relevance to what is almost certainly ppm exposure in humans. Eg, 300 mg/kg for an adult woman (assuming 60 kg) would be 18g of pyriproxyfen!
The estimated exposure from drinking water is only ~1 mg.
While animal models are indeed models, and human pk/pd can be dramatically different, I find it implausible for humans be to several orders of magnitude more sensitive to teratogenic effects.
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