91996E2410

WRITTEN QUESTION E-2410/96 by Ian White (PSE) to the Commission (11 September 1996)

Subject: BSE - the alternative theory associated with organophosphorus concentrate insecticides

1. Considering that recently reported experimental work in the United States has conclusively failed to induce BSE in cattle exposed to material from scrapie-afflicted sheep, both through routes of ingestion and intra-cerebral infusion, what detailed scientific evidence can be forwarded to substantiate the claim that the rogue prion responsible for inducing BSE has originated in the nervous system of sheep, rather than having arisen as a result of induced mutation of the native bovine prion protein, as outlined in the alternative BSE theory associated with organophosphorus concentrate insecticides?

2. How is it possible to distinguish that the rogue prion responsible for induction of BSE is of ovine origin, as has been suggested, and that it could not be a mutant form of the indigenous bovine prion protein?

3. Considering that organophosphorus chemicals have been documented as being both potentially teratogenic (embryo-deformative) and mutagenic, and that prion-related conditions are known to arise through forces of mutation, what research has been undertaken into the theory that organophosphorus concentrate-induced mutation is the root cause of BSE?

Answer given by Mr Fischler on behalf of the Commission (23 October 1996)

1. & 2. The origin of bovine spongiforme encephalopathy (BSE) remains unclear. Scientific advice to the Commission is that there is at present no firm evidence to indicate whether it derived from scrapie in sheep or originated in cattle. Available data cannot disprove either of these hypotheses. If it originated in cattle, there is no evidence to implicate any particular factor involved in its appearance.

3. When BSE was first recognised, an intensive epidemiological study was undertaken to determine the factors associated with its transmission. The use of agricultural chemicals, including organophosphate compounds, was among the factors examined. However, no significant association has been found between exposure to these compounds and the development of BSE. The disease occurred in animals which had not been exposed to organophosphates and did not occur in the great majority of animals which had been exposed, both in the United Kingdom and elsewhere.

The spatial and temporal distribution of BSE suggests an extended common source epidemic. This is unlikely to have been caused by a single mutation, which has a single point of origin from which it spreads slowly.

In addition, the Commission would refer to its answer to Written Question P-1454/96 ((OJ C 345, 15.11.1996. )) by Mr Skinner on organochlorides and organophosphates and their impact on agricultural workers and the public health of consumers.