The UK epidemic of BSE: Slow virus or chronic pesticide-initiated modification of the prion protein? Part 2: An epidemiological perspective

Insecticide use: Contexts and ecological consequences

“…The accumulation of pesticide residues in the food chain through the consumption of crabs and fishes from pesticide-sprayed rice paddy fields was thought to be the cause of a musculo-skeletal condition in humans (Krishnamachari and Bhat, 1978;Mohan, 1987), but more recent studies have shown that the disease was the result of a high rate of inbreeding among affected communities (Agarwal et al, 1997). The BSE crisis in the UK was improbably attributed on occasion to OP use (Gordon et al, 1998;Purdey, 1996). The recent decline in vulture populations in India was thought to be pesticide induced (Anon., 1999b;Nair, 1999;Prakash, 1999) until it was found to be the result of an unexpected interaction between a veterinary medicine (diclofenac) and vulnerable avian kidneys (Green et al, 2004;Oaks et al, 2004).…”

Effect of the Dimethoate Administration on a Scrapie Murine Model

“…To our knowledge, Phosmet is the only organophosphate insecticide that has been assessed as a triggering factor for TSEs because of its possible interaction with PrPsc. No other studies involving other organophosphate compounds are described in the literature; consequently, although the involvement of these compounds in the development of TSEs has been suggested on several occasions (Purdey, 1996), the lack of experimental data in support of this hypothesis has cast doubt into the causal role of these compounds in TSE (Rachidi et al., 2005). Only a scarce amount of epidemiological data or experimental research performed in other frameworks has been described by previous authors.…”

“…These pesticides are suggested to block the activity of a PrP‐specific protein kinase, which results in abnormally phosphorylated PrP. The resulting abnormally phosphorylated PrP would carry an extra charged phosphate group that would block both proteolytic cleavage and chaperone binding sites, potentially leading to protease‐resistant and misfolded PrPsc isoforms respectively (Purdey, 1996). The UK exclusively practised compulsory use of a high‐dose systemic Phosmet insecticide formulation directly upon cattle for warble eradication during the late 1970s/1980s.…”

Critical Evaluation of Phosmet's Breast Cancer Risk

“…An irreversible modification of the prion protein has been implicated as the causative agent for these diseases. The following papers present a unique medical hypothesis that a mutagenic trigger (phosmet) led to the post-translational covalent modification of prion proteins, and the onset of the BSE epidemic in the UK (Purdy, 1998;Purdy, 1996). The correlation between the use of phosmet and the onset of the BSE epidemic has been outlined as evidence.…”

“…No studies of inhalation exposure of experimental animals were found. A hypothesis implicating phosmet exposure of cattle as the trigger for the BSE epidemic in the UK (Purdy, 1998;Purdy, 1996) was based on inadequate evidence. The results of studies in isolated cells indicate that phosmet has the potential to induce mutations and DNA damage in the absence of metabolic activation (JMPR, 1994;Slamenova et al, 1992).…”