As for the stereoselectivity of in vivo hepatic metabolism of ethanol and methylphenidate into EPH, I couldn't find much information other then that
these researchers believe the racemic to be active and that it is formed under 'higher level dosing'.
I can't see why the liver would prefer to metabolize into l-EPH, but I will stand corrected if I see evidence of it.
Well I'll be damned it was John Markowitz that actually informed me of the preferential transesterfication. It's carried out by the same enzyme as the MPH>ritilinic acid. Anyway here's an excerpt from a paper of his about the stereoselectivity of CES1.
Profound differences between d- and l-MPH metabolism
and disposition have consistently been demonstrated in
enantiospecific investigations. The major pathway mediating
the metabolism of MPH is rapid de-esterification to the
inactive metabolite, ritalinic acid. This process seems to be
exclusively mediated by the carboxylesterase 1 enzyme
(hCE-1), encoded for by CES1.3 In addition, Sun et al3 have
demonstrated in vitro that this hydrolytic process is highly
stereospecific with the catalytic efficiency of hCE-1 up to
6-fold higher, favoring l-MPH over d-MPH. This finding is
consistent with that of extensive enantiospecific pharmacokinetic
studies that have measured both isomers and found
the l-isomer to generally attain only a small fraction of that of
circulating concentrations of d-MPH