Parkinsons' disease (PD) is the most common neurodegenerative movement disorder that is a consequence of premature death of dopamine-containing neurons in the substantia nigra. A number of observations have led to the hypothesis that environmental factors, including pesticides, play a significant role in the development of PD. Among pesticides, most commonly herbicides (paraquat in particular) and insecticides have been considered. The aim of this study is to address the uncertainties provided by epidemiological studies on the role of pesticide exposures in the development of PD, with the help of experimental toxicological data. Animal models that reproduce all clinical and pathological features of human PD are not available. In addition, the fundamental questions relate to the extrapolation from experimental to actual human exposure, taking also into account the role of genetic factors. Available measurements or estimates of human exposure levels that are significantly lower than those used in animal experimentation provide little support for a causal correlation between pesticide exposure and development of PD in humans. A possible role of acute poisonings or episodes of excessive exposure, and/or of combined exposures especially at early age and/or in the presence of certain genetic variants can be hypothesised. Follow up of survivors of acute poisonings by pesticides would provide information useful in this respect. According to the available data, from a public health point of view, prevention of "high" exposures, even asymptomatic ones, especially in utero and during early age is a priority.