What is not clear are which data were used under which circumstances. Results from the PDP and TDS programs are much more statistically representative while those from the FDA's Surveillance program are not, as is addressed in the accompanying analysis of their previous report. Even with the PDP data, there is considerable room to skew findings based upon choice of data used. Consider peaches, for example, which were considered by EWG to be the second riskiest food item after apples. But in kids five years and under, peaches are often not consumed raw but rather as canned peaches.
Apples are another good example.
Large differences in residues are associated with the different apple forms. Again, it is impossible to determine which data were used in which ways by the authors. At the risk of getting too technical, it is well established that ethyl parathion should be much more toxic than methyl parathion because mammalian systems have an easier time hydrolyzing methyl parathion to non-toxic products than they do ethyl parathion. Less hydrolysis of ethyl parathion means that more ethyl parathion is likely to be oxidized to ethyl paraoxon which is presumably the chemical that exerts the effect on cholinesterase enzymes. All in all, I would conclude that the EPA's reference dose for methyl parathion may be much lower than appropriate, and could explain why the risks attributed to methyl parathion may be artifacts of this abnormally low reference dose.