In case of OPs, the issues are whether the young may be more susceptible to the acute toxicity of OPs (AChE inhibition), and whether OPs may cause developmental neurotoxicity. Experimental data indicate that the acute toxicity of OPs is influenced by age, with young animals being more sensitive to the effects of exposure [66] and [67]. Indeed, when comparing lethal dose levels or maximum tolerated doses (MTD) of various OPs, young rats have consistently been shown to be more sensitive (Table 4). This increased sensitivity is not due to intrinsic differences in AChE, whose catalytic properties are not influenced by age [67], but rather to lower metabolic abilities of young animals. For example, in case of parathion and methylparathion, low detoxication by CYPs appeared to be most relevant for the age-dependent susceptibility [68]. In case of chlorpyrifos and diazinon, a lower hydrolytic detoxication by PON1, and perhaps carboxylesterase, accounts for the differential age-related in their acute toxicity [69] and [70]. As these enzymatic systems are believed to show a developmental curve also in humans (see for example Ref. [71] with regard to PON1), young children would be expected to be more sensitive than adults to acute OP toxicity. On the other hand, with regard to OPIDP, the young appear to be more resistant [19] and [72]. Furthermore, these is also some evidence suggesting that enhanced sensitivity to AChE inhibition may not extend to situations of repeated sublethal exposures to OPs [73].