Consider this theory by Mark Purdey, British researcher of TSE.
From his website http://www.markpurdey.com/faqs_4.htm

TSE's [such as Bovine Spongiform Encephalopathy or Mad Cow] result in degeneration of the brain.


QUESTION 1.

The pathology of the copper deficient brain is completely different from the pathology of TSE diseased brain, so how can you claim that copper deficiency is linked to the cause of TSE ?

ANSWER

People get me wrong - my thesis promotes a multifactorial aetiology involving a combination of factors. I am saying that sporadic TSEs are essentially trivalent manganese toxicity on top of subclinical copper deficiency, so you would get an entirely different pathological profile than what you would observe in straight Cu deficiency. For instance, the classic Mn toxicity hallmarks such as amyloid fibrils, neuronal loss, astrogliosis and shrunken basal ganglia (caudate nucleii, putamina). are precisely present in TSE neuropathology.

Most normal prion proteins bond onto five copper atoms per molecule in the healthy individual; but the different strains of scrapie are largely dictated by the number of copper atoms that bond to prion protein. Some TSE susceptible genes only encode for synthesis of prion proteins that will bond 3 copper atoms; thus predisposing that mammal to scrapie susceptibility which will take some time to incubate, etc, etc.

On the other hand, the copper deficit in the more aggressive, short lived BSE and variant CJD syndromes is not caused by primary copper deficiency due to environmental deficiencies , but is caused by certain organo pollutants such as systemic insecticides (eg OP warble fly chemicals , which actually directly modify the histidine ligands (via generation of singlet oxygen) which bond copper to the prion protein. So basically, no copper can bond to prion protein any longer; whether copper is abundant in the brain or not! This is why vCJD/BSE is so much more rapid than traditional scrapie, simply because no copper can bond at all; whereas the more protracted incubation period in sporadic TSEs, such as scrapie, is genetically mediated by a maximum of only one, two or three copper atoms being able to bond to the prion protein - thereby creating the scrapie susceptible genotypes where susceptibility is activated once environmental copper becomes deficient

Copper has long been recognized as an essential element in human health, but like many things including metals, the difference between "essential for health" and toxicity is dose.

So there are no "long years of considering copper a poison" to reconsider.

.

Ok, so what's this?

Copper Poisoning ~Medline

Where Found -

Copper wire
Some aquarium products
Clinitest tablets (see Clinitest tablets overdose)
Vitamin and/or mineral supplements
Note: This list may not be all inclusive.

Symptoms

Acute overdose by ingestion may cause vomiting, abdominal pain, diarrhea, and jaundice. External contamination from copper can result in hair discoloration (green).

Body as a whole
Burning sensation
Metallic taste
Pain
Shock
No urine output
Convulsions
Fever
Muscular aches
Chills
Weakness
Anemia
Yellow eyes
Yellow skin
Gastrointestinal
Nausea and/or vomiting
Diarrhea

I think excessive copper intake is more likely from taking supplements, or eating and drinking out of copper implements or pipes.
Natural levels of copper in plants would be unlikely to poison you, and are the best way for your body to assimilate copper. The copper is presented in a bioavailable form which can also be easily excreted.