NeuroTalk Support Groups - PD and air pollution

I have wondered about whether or not PD has been around as long as is sometimes claimed and even engaged in a mini-debate with an infamous duck on this forum about it. <Apologies to those who have joined since :) > Now comes the paper below. Keep in mind that the two most-cited references to what might have been PD (but not at all certain) are ancient India and China, both of which had advanced metal smelting technologies and the pollution that goes with it. Then came Dr. Parkinson on the smoggy streets of London in 1817.

These particles are incredibly tiny. So much so, in fact, that they could possibly move along the transport systems INSIDE the neurons. They also act like tiny sponges and can carry things like bacterial toxins along with them. And note that they disrupt the BBB as well.

1: Toxicol Pathol. 2008 Mar 18 [Epub ahead of print]

Long-Term Air Pollution Exposure Is Associated with Neuroinflammation, an Altered
Innate Immune Response, Disruption of the Blood-Brain-Barrier, Ultrafine
Particulate Deposition, and Accumulation of Amyloid {beta}-42 and
{alpha}-Synuclein in Children and.

Calderón-Garcidueñas L, Solt AC, Henríquez-Roldán C, Torres-Jardón R, Nuse B,
Herritt L, Villarreal-Calderón R, Osnaya N, Stone I, García R, Brooks DM,
González-Maciel A, Reynoso-Robles R, Delgado-Chávez R, Reed W.

Air pollution is a serious environmental problem. We investigated whether
residency in cities with high air pollution is associated with
neuroinflammation/neurodegeneration in healthy children and young adults who died
suddenly. We measured mRNA cyclooxygenase-2, interleukin-1beta, and CD14 in
target brain regions from low (n = 12) or highly exposed residents (n = 35) aged
25.1 +/- 1.5 years. Upregulation of cyclooxygenase-2, interleukin-1beta, and CD14
in olfactory bulb, frontal cortex, substantia nigrae and vagus nerves; disruption
of the blood-brain barrier; endothelial activation, oxidative stress, and
inflammatory cell trafficking were seen in highly exposed subjects. Amyloid
beta42 (Abeta42) immunoreactivity was observed in 58.8% of apolipoprotein E
(APOE) 3/3 < 25 y, and 100% of the APOE 4 subjects, whereas alpha-synuclein was
seen in 23.5% of < 25 y subjects. Particulate material (PM) was seen in olfactory
bulb neurons, and PM < 100 nm were observed in intraluminal erythrocytes from
lung, frontal, and trigeminal ganglia capillaries. Exposure to air pollution
causes neuroinflammation, an altered brain innate immune response, and
accumulation of Abeta42 and alpha-synuclein starting in childhood. Exposure to
air pollution should be considered a risk factor for Alzheimer's and Parkinson's
diseases, and carriers of the APOE 4 allele could have a higher risk of
developing Alzheimer's disease if they reside in a polluted environment.

PMID: 18349428 [PubMed - as supplied by publisher]