February 1999, Questions on Aldicarb
Questions for Evaluation and Incorporation of the Time for
Reversibility of the Adverse Effects of Aldicarb
- A major assumption underlying the proposed analytical process
is that if the behavioral and neurochemical effects are fully
recovered, that sensitivity to subsequent exposures to aldicarb
has returned to baseline. However, there are no systematic data
evaluating multiple within-day exposures and differences in sensitivity.
The data used to support the assumption of return to baseline
status is inferred from indirect evidence. Specifically, repeated
dose studies in rats show no decrease in effect level with time.
Is the assumption that recovery from the effects of aldicarb is
directly related to the recovery of cholinesterase inhibition
reasonable and valid?
- Do the available toxicological data reasonably support the conclusion
that the adverse effects of anticipated acute dietary exposure
to aldicarb are fully reversible within 8 hours following the
- The Office of Pesticide Programs (OPP) uses data from the Continuing
Survey of Food Intakes by Individuals (CSFII) to provide the consumption
data needed to estimate dietary exposure to pesticides. These
data are collected in the form of diaries that outline food consumption
throughout the course of the day as recalled by individuals interviewed.
OPP typically treats the consumption data as a daily aggregate
of foods consumed. However, conducting assessments on an 8 hour
basis requires a more detailed use of the consumption data, i.e.,
an hourly breakout of food reported to be consumed. Are the data
in the CSFII sufficiently robust to attempt to model behavior
below the daily level of exposure? If so, what are the limitations
of this extrapolation?
- Aldicarb presents a very extensive data base for evaluating its behavior both toxicologically and with regard to potential concentration in foods. In particular, the information surrounding the pharmacokinetics of aldicarb make it possible to detail the time course of adverse effects to a greater extent than for most other pesticides. Given appropriate data for other carbamate pesticides, particularly pharmacokinetic data, is this decision making process a reasonable approach for increasing the precision of dietary risk assessments for those chemicals?