What you are saying is dangerous. We had a serious set of exactly these transmission events in Britain only a few decades ago. Clearly the risk is not infinitesimal.
Dangerous? The hypothesized connection is not remotely clear. In vitro transformation of human PrP into PrP(Sc) by bovine PrP(Sc) is a necessary for the causal model. The fact that a strong species barrier exists, in vitro and in vivo, points towards a spurious association.
It's understandable why one might infer from the correlation that there's a relationship but this is confounded by observation. The baseline expectation for CJD in a population is 1-2 cases/million [0]. vCJD cases in the UK never exceeded 30/yr [1, Fig 2. a]. Yes, vCJD occurs primarily in younger people - but that's circular as vCJD is defined as CJD-like disease with early onset. If cross-species transmission were common, one would expect a similar spike in age >40.
The incidence of vCJD, even at its peak, was exceedingly rare. Many things, such as observation bias, pollution, or rare side-effects from faddish street drugs could be at fault here. It's tempting to jump to conclusions, a la "eating fats makes you fat," but it's totally unwarranted in the face of the in vitro and in vivo data demonstrating strong species barriers.
