Please consider the following chain of events. While a good portion of the research has been with rat and primate models, each link in this chain is well established. Like RLSmi I will be happy to provide references:

1- As embryos we have certain windows of vulnerability when particular parts of our nervous system are forming. These windows may only be "open" a few hours or maybe a few days. If exposed to certain chemicals during these times our development is altered with the extent determined by the combination of who (genetics), what (chemicals), when (which window), where (the embryonic area within the window), and how long (exposure length).

2- Two common chemicals have a particular relevance to PD - bacterial toxins (LPS) and maternal stress hormones, particularly cortisol.

3- Embyonic exposure to LPS has three key effects-
a- a lowered density of neurons in the substantia nigra
b- a post-puberty hypersensitivity of the microglia (brain immune defenders) to further LPS contact
c- an altered HPA axis, the center of our stress response, resulting in chronically high levels of cortisol in the adult. This effect also results from exposure to maternal cortisol if at the right time.

4- Elevated cortisol causes systemic inflammation which opens both the BBB and the equivalent in the GI tract. The net result is entry of toxins into the brain. Among those toxins is LPS.

5- The microglia, already "primed", overreact to the LPS and destroy nearby neurons (the SN has one of the greatest densities of microglia in the brain).

6- This process repeats, ebbs and flows, life-long. Eventually we notice a tremor...

This is part of a broader theory to be published later this year and is, IMHO, the most important part. Given that LPS is everywhere and that the BBB-opening stress is too, I think Ron's concerns are well founded.

-Rick