About Mad Cow Disease (The Crisis That Never Was

Note: As an organic farmer, Mark Purdey resisted the order to spray his cattle with organophosphates for warble fly and went to court for a judicial review; he won and was exempted from using the spray. No cows born in his herd developed BSE (mad cow disease). He has contributed numerous articles on the subject of BSE to scientific journals. He farms in Somerset, UK. This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Spring 2000

As the first snowstorm of winter hit the isolated hill where I farm, I pitched out the last forkfuls of hay to my cattle before nightfall. Much like the whirlwinds of snow surging all around me, my brain was turning over and over the catalogue of injustices that successive governments had levied onto the farming community over BSE. I felt paralysed and powerless in the encroaching snowstorm.

My confidence to carry on was battered to pieces by the recent ban on beef-on-the-bone. The announcement—based on the whims of a mere handful of government “experts”—renders my hard graft over the last twenty years in farming into pathetic insignificance. But how can there be any true “experts” from academia when the most basic facets of the Bovine Spongiform Encephalitis (BSE) disease process remain a total mystery? One would have thought that all of those farmers and independent vets living and working in the front line with BSE cattle would have been the first to be consulted. But strangely, their observations have been completely ignored by officialdom.

Cows frequently partake in the bizarre habit of eating their colleagues’ afterbirths after calving, and I was particularly intrigued to watch my own home-reared, BSE-free cows positively relishing the delicacies of afterbirth tissues derived from a group of pedigree cows that I purchased into my farm in 1989. As the majority of these imported cows went on to develop BSE, it is interesting that BSE has not surfaced in my home-reared cows, despite their overzealous exposure to the allegedly “infectious” blood and lymph found in the afterbirths of the BSE cows. Other farmers sharing the same experience report the same outcome.

Another anecdote hails from the farming community of Shetland, where the island folk are free of Creutzfeld-Jakob disease (the human form of BSE), despite their ancient custom of eating “potted sheep’s brain.” Interestingly, the equivalent of BSE in sheep, called scrapie, has been rife in the sheep flock on Shetland for centuries.

The anecdotes are ever-flowing, and all point to a hypothesis based upon some environmental causal factor that falls a long way short of the current government’s nightmare infectious “ingestion” scenario. If the spongiform agent is as infectious as the authorities would have us believe, why has chronic wasting disease (the BSE equivalent in deer) remained uniquely confined to a small cluster zone in the Rocky Mountains for thirty years now, without spreading across to the neighboring deer herds roaming the rest of the Rockies? Why has no spongiform developed in the various predators of those affected deer?

From the very beginning of the crisis, the farming community has been the unfortunate victim of the whole BSE campaign. Yet, ironically, the same presiding authorities who are responsible for foisting off the burden of BSE are, no doubt, totally oblivious to the fact that more farmers have committed suicide as a result of official BSE blunderings than people have died of new variant Creutzfeld-Jakob disease (nvCJD).

A body of government experts was quick to take exclusive control of BSE research, and very rapidly the cause of the disease was attributed to the feeding of scrapie-diseased sheep brains to cattle. In other words, scrapie was said to jump from sheep to cattle by virtue of some sort of infectious agent. And it naturally followed that this same assumption of disease cause was extrapolated into the human CJD context—the presumed “microorganism” had now jumped from cows into humans. But this was no more than unproven hypothesis, and it still remains that way today.

Not surprisingly, only a handful of folk had insight into the unsavory world of the meat and bone meal (MBM) rendering business. But for anyone who had scratched the mere surface of the global distribution of British MBM products, it became strikingly obvious that the very mainstay of the official hypothesis was radically flawed. For instance, during the 1980s thousands of tons of this very same incriminated MBM was exported to cattle farms in BSE-free countries such as the Middle East, Malta and South Africa. Officials have always brushed this challenge aside, arguing that the cattle in these countries did not receive sufficiently large doses of scrapie to contract BSE. But this contradicts their current official explanation for the 30,000-plus cases of BSE that have developed in cattle born after the 1988-ban on MBM, where government scientists conveniently claim that leakage of micro amounts of MBM (destined for pig and poultry feed) into the cattle rations, caused the 30,000 cases.

Furthermore, USA and Scandinavian rendering systems duplicated exactly the same prerequisites that were supposed to kick off BSE in Britain—scrapie affected brains being milled into feed—yet their livestock remained BSE-free.

Nor were we told of the numerous unsuccessful attempts by US scientists to induce BSE in cattle that had been experimentally fed or injected with massive amounts of scrapie brain material. Apparently, the cattle either just “got fat” or went down with a sickness more akin to motor neurons disease than BSE.

Despite millions of pounds worth of scientific research failing to ascertain a link between BSE and scrapie, the whole propaganda myth that BSE was caused by scrapie became gospel in mainstream public mentality.

The media loved the theory because they could drum up a viral holocaust-horror scoop. The vegetarian and green lobbies found themselves landed with a powerful propaganda weapon on their plate— turning cows into cannibals. And the UK scientific establishment could go on drawing generous grant funding for their viral witch-hunt without the embarrassment of having to account for years of barking up the wrong tree. And then the government could foist the blame of BSE onto a naturally occurring agent for which no significant vested interest or official body could be held accountable.

Whilst the maligned renderers and feed merchants got the full brunt of blame for BSE, it surprises me that neither were held accountable for the financial damages of the crisis. Instead, they all received generous compensation payments to the tune of millions.

Almost on a weekly basis we are now finding ourselves listening to the same experts regurgitating the same stereotype claims of how BSE has now jumped from cattle into humans. On Channel 4 Dispatches (last December), despite no reported cases of BSE in the British sheep flock, it was assumed that sheep must be affected with BSE because they had eaten meat and bone meal. We are now warned of the danger of eating sheep. Professor Blakemore summed up the programme by saying that we should all eat chicken and avoid beef and mutton. But as poultry received their fair share of meat and bone meal as well, should we not be cutting chicken out of our diet too, according the dictates of the official theory?

These spokespeople would do better to start questioning the entire foundation of their hypothesis, rather than squeezing the last drop of “infected” blood out of the sinking stone. What is more, the conventional consensus on BSE is ignoring that well-recognized academic yardstick, Koch’s postulates, which is employed for assessing the cause of disease. The first postulate dictates that a theory begins to carry weight once the hypothetical causal agent can be identified in every victim of the disease in question. The conventional hypothesis on scrapie/BSE/CJD certainly fails to fulfil this basic postulate on several counts. In this respect it is particularly interesting that spongiform disease has been experimentally induced in animals after receiving injections of brain tissue derived from people who have died of Alzheimer’s and Parkinson’s Disease. Why is nobody freaking out about Alzheimer’s disease?

In the case of BSE where no viral cause has been identified, it is illogical to assume that one animal has to eat another in order to catch the same disease. Initially, the direction of any epidemiological research programme should follow elementary logic and investigate the most likely assumption that the various different species of mammals suffering from the same disease have all been exposed to the same causal factor in the environment. But it seems that nobody has investigated this route. Sheep did not cannibalize each other in order to catch scrapie, nor did wild deer in the Rocky Mountains cannibalize each other in order to catch their BSE-equivalent disease, chronic wasting disease.

The reductionist mindset of government scientists is betrayed by the narrow scope of questions that have been put to the relatives of the new variant Creutzfeld-Jakob disease victims. The questionnaire is almost entirely focused on the carnivorous perspective of the victims’ diets, and therefore tailored to suit their own hypothesis from the outset. The Establishment’s assessment of nvCJD etiology seem to have completely ignored the fact that adolescent CJD was recorded well before the 1980s. And why do they move the goal posts every time a new challenge confronts their theory—like extending nvCJD’s incubation period to tally with the long term vegetarian victim from Kent? Take note that they have completely ignored the case of the lifelong vegetarian nvCJD victim from France.

The British government’s Spongiform Encephalitis Advisory Committee (SEAC), seems to have thrown aside one of its most relevant long standing observations on CJD epidemiology—people who are occupationally involved with pets and farm animals are at greater risk of developing CJD. And it is this observation that may well hold the key to the true cause of these diseases.

During the 1980s and early 1990s, cattle and cats (the species of animals that have developed BSE) were exclusively treated with systemically acting types of Organophosphate (OP) insecticide which were designed to penetrate the entire physiological system of the animal, transforming the bloodstream into a toxic medium so as to kill off any unwanted parasites present. In the context of cattle, the use of these systemic OP’s was subject to a compulsory government order for the eradication of warble fly. The UK government was unique in compelling a substantially higher biannual dose of this OP by comparison with the few other countries around the world that were following similar, less intensive measures to control this fly. Interestingly, these other countries, including Switzerland, France and Ireland, comprise the few other countries that are suffering from very small epidemics of BSE in their home-reared cows.

The National Farmers Union, the Meat and Livestock Commission and The British Veterinary Association formed a united front with MAFF (Ministry of Agriculture, Fish and Forestry) to ensure that all farmers complied with the law and treated their cattle. Systemic OP’s are recognized as exerting their toxic effect by entering the central nervous system and deforming the molecular shape of various nerve proteins. These chemically-mutilated mutant proteins are subsequently rendered incapable of performing their proper function in the nerves.

The known toxic effects of OP’s lead me to wonder whether the use of systemic OP’s on British cattle have caused the malformation of another newly discovered brain protein called prion protein—the phenomenon that US scientists have proposed as the cause of spongiform encephalopathies. Whilst some types of spongiform disease have been attributed to genetically acquired damage to the shape of the prion protein, the underlying cause of protein damage in the BSE and new variant CJD strain of the disease remains a mystery—amongst “open-minded” scientific circles, at any rate.

OP’s are known to generate a highly reactive type of “free radical” in the tissues that they intoxicate. And it is this free radical legacy of OP poisoning which is capable of instigating a chain reaction of lethal attacks on nerve membranes and proteins in the central nerves of susceptible individuals.

Once tissues become ‘infected’ with free radical chain reactions, the introduction of freezing, heat or radioactive conditions to the affected cells does not arrest such an ‘infection.’ In fact, irradiation, heating and homogenizing of such tissue (brain tissue from spongiform affected animals is homogenized before it is inoculated into healthy animals in transmission trials) actually proliferates the free radical phenomena. This suggests that these free radicals may constitute the as yet unidentified “infectious” transmissible agent of these diseases.

Concerned members of the public helped me to fund a £14,000 experimental research project at the Department of Neuroscience, Institute of Psychiatry in London, where living tissue culture cells which express the prion protein were exposed to low doses of the OP chemical; so as to stimulate the context of a living cow undergoing OP treatment. Significantly some of the recognized changes of the prion protein which appear in the early stages of spongiform disease were induced in these OP-treated cells.

Clearly, these results go some way towards proving that OP’s represent a primary or partial cause of BSE. Yet it was this very same simple test that the government had always assured me was too expensive for the tax payer to fund and, besides, impossible to set up anyway, even with the most updated lab technology.

In December 1996 Lord Lucas, MAFF’s spokesman in the House of Lords, gave a written answer stating that the government had asked the SEAC committee to revisit the OP-BSE theory as a result of the recent research findings conducted at the Institute of Psychiatry.

After being invited to deliver my thesis to a SEAC meeting in April, 1997, I was disturbed that at no stage during the protracted enquiry that followed was the experimental evidence of the Institute’s work addressed—the prime purpose behind this hearing. The committee dismissed the evidence that I presented, which had been drawn from independent peer-reviewed, published science literature. I was not surprised to learn that the outcome of this enquiry—the proceedings of which were described as “confidential” to any enquiring journalist—was a recommendation to government that any applications for funding research into the OP-BSE theory should not be supported.

I still shudder each time I visit our local farm stores and see the canisters of systemic OP products up for sale. Although the warble fly is eradicated and BSE is on the wane, farmers can still apply these chemicals in a voluntary capacity for controlling lice and other pests. I shudder further when I see the bottles of OP head lice shampoo and OP systemics for pets and gardens still in the shops for human use.

The real madness of the mad cow fracas would seem to lie with the deadlock that has kept these products on the open market for a full year since experimental evidence first linked their use to the cause of BSE. Perhaps the government is so scared of compensation claims that it employs everything at its disposal to prevent any degree of acceptance of the idea that their compulsory warble fly programme caused the biggest catastrophe in the history of British agriculture.

The brave new SEAC committee appears to be totally preoccupied with “effect” rather than “cause.” Such a back-to-front approach betrays their sensitivity with anything to do with “cause.” But how can any government programme seriously hope to eradicate BSE or nvCJD if it has failed to eradicate, let alone recognize, the disease’s true cause?

Mad Cow Update Those in charge of public health policy in the US do not really understand what I am demonstrating about bovine spongiform encephalopathy (BSA) and Creutzfeld-Jakob Disease (CJD). They get the main linchpin of the work wrong by stating “manganese deficiency” instead of “manganese excess.” Then they seem to marginalize my position in the BSE debate by falsely suggesting that I am at odds with Stanley Prisiner’s prion concept that has now been accepted as mainstream.

Ironically, both my own studies and those of Dr. David Brown largely open up the final door of evidence in support of Prisiner’s concept. We have shown what causes the prion protein to transform into its protease-resistant form (the disease-associated form). Prisiner first identified the abnormal prion as the hallmark of the BSE-diseased brain and he hypothesized that his abnormal protein somehow caused the disease. Where I do differ from the Prisiner brigade is only in one point—I don’t believe that the “prion” is highly infectious as they are suggesting; that is, I don’t believe that it can infect those who eat prion-contaminated meat. I believe that it is the manganese 3+ attached to the prion that is the infectious agent and only when it is transmitted by injection, etc., into susceptible genotypes. Prisiner himself is skeptical of “the-BSE-feed-caused-new-variant-CJD” hypotheses. He was the only person (apart from myself) who suggested this to the BSE inquiry!

I just hope that the beef industry in America realizes that we’re not as “way out” as has been suggested. The industry is shooting itself in the foot by rejecting the link to toxic mineral excess and organophosphate pesticides. We have accumulated so much hard evidence now—more than all other theories.

I have been to Calabria in Southern Italy looking at the case of 20 CJD victims in a hamlet of 150 population since 1995. Intriguing stuff! But I was warned that the Mafia controls the property market and meat market in this part of Italy and would be hostile to me. So I was unable to get soil samples at that time.

Things are so desperate in farming in Europe at present. We are so concerned by the totalitarian, global control that is molding the direction of agriculture into complete ecological and economic crisis. The “arable aid payments scheme” has caused acres of former livestock grassland to be ploughed up. The global warming flash flood storms have caused an unprecedented degree of soil erosion, with its attendant self-perpetuating drain on human reserves.

Here's more, from Corporate Watch -- http://www.corporatewatch.org.uk/magazine/issue12/cw12f5.html :

12 Autumn 2000
Issue12

Organophosphate Madness?

When a cluster of new variant (nv) CJD victims were discovered in and around the Leicestershire village of Queniborough in June, fingers began to point at local butchers and school meal caterers. The government line has always been that Mad Cow Disease came about by feeding scrapie infected meat and bone meal to cows. However there is a different theory. One that the authorities and the pesticide producers have gone to great lengths to silence. Si Mitchell unveils the other elements at work in the Leicestershire countryside.

Since 1982 British farmers have been forced by law to treat their cows for warble fly with a pour-on systemic organophosphate called phosmet1 - originally formulated as a weapon by Nazi chemists during World War II[2]. The money men were soon to realise its profit potential and after the war it was exclusively marketed as an agricultural pesticide by ICI, and later their renamed subdivision Zeneca[3].

One farmer, Mark Purdey, refused to treat his Somerset herd with the nervous system-attacking toxin after observing how his own organically reared cows never developed BSE, but phosmet-treated cattle brought onto the farm did. In 1984 the Ministry of Agriculture, Fisheries and Food (MAFF) took him to the High Court, but a judicial review found in his favour, ruling that the government couldn't enforce treatment as it was neither a vaccine or serum.[4]

"Before 1982 farmers could treat warbles with an organic ground-up root compound called derris. This was outlawed, so they could sell more organophosphates," said Purdey. "You can pick warbles out by hand, they don't really harm the cows, just make skin holes which the leather industry don't like."

Organophosphates (OPs), used to treat headlice in school children, have been identified as one potential cause of Gulf War Syndrome[5] (Purdey managed to allieviate symptoms in a BSE infected cow by injecting oxime, an antidote to pesticide poisoning. The cure was never completed as MAFF turned up and destroyed the cow). For years schools advised parents to treat lice with malthion (an OP similar to phosmet) - since the Queniborough Mad Cow Disease cluster's exposure, the local authority have been questioning parents. However whether lice treatment appears on their question -naire is not known - the document is being kept under wraps. Phosmet also contains thalimide[6], the chemical base of thalidomide, a drug which caused severe birth defects in the 1960s.

Unconvinced by the accepted cause of Transmissible Spongiform Encephalopathy (TSEs - the kind of brain disease that includes BSE and CJD), Purdey set about studying the epidemiology of these diseases and how their clustering reflected OP usage.

He found Britain, the only country enforcing phosmet use, to have the highest rate of TSEs. Ireland had some BSE, but OP use was voluntary, and given at a lower dose (6mg/kg annually, compared to Britain's twice yearly 20mg/kg - British phosmet is also produced at a higher initial concentrate). Brittany began to develop BSE following an enforced phosmet trial, after which the disease began to appear across France, reflecting the spread of OP use too. Purdey also found nvCJD in people to be clustered in the Weald Valley in Kent, where hop and top fruit growth attract a hundred-fold levels of systemic OP spraying[7].

Similarly meat and bone meal feed is peddled all over the world, including the Middle East where there hasn't been a single case of Mad Cow Disease, and US scientists have been force-feeding scrapie-infected gunk to cows for years without managing to give them BSE.

Agitated by Purdey's discoveries, the pesticide industry hit back. The dubiously named National Office of Animal Health (NOAH), a lobby group representing the UK animal medicine industry (whose membership reads like a White House dinner party invite list[8] - includes Bayer, Monsanto, Novartis, Pfizer, Roche, Schering-Plough, Intervet) published documents discrediting Purdey's work[9].

In a briefing paper to Lord Philips' BSE inquiry[10] - who were due to publish a year ago, but are still taking statements - NOAH said Purdey's facts "do not add up". They said: "Many independent experts [have said] a relationship between OPs and BSE does not exist." To back it up NOAH claimed that warble treatment took place in Jersey but not Guernsey, yet there was five times the BSE in Guernsey than Jersey. They wrote to science editors explaining that phosmet was licensed in New Zealand and Australia, yet no cases of BSE had occurred there. Purdey dismisses their argument: "They twist the facts - phosmet was used in Guernsey, but as a lice treatment. And the stuff used in Australia and New Zealand was non-systemic (ie it doesn't penetrate the skin and subsequently every organ) as it was dissolved in water, not oil as in Britain."

NOAH's independent expert, Dr David Ray, turned out to be receiving funding from Zeneca for his Medical Research Council toxicology unit[11].

"I don't think this affected my judgement," says Ray. "You may not believe it, but I didn't realise Zeneca produced phosmet at the time."

Ray chose not to test with phosmet, but with another organophosphate, DFP. He also used synthetic brain proteins, which Purdey believes would have reacted differently to their natural counterparts.

In January Ray was appointed to the Veterinary Products Committee (VPC), a quango of academics and farmers, whose job is to scrutinise the safety of animal medicines before licences are issued (and review existing-licences, like phosmet's).

Ray said that the interests he has with pesticide producers will not affect his judgement on the VPC. He admitted that Astra (now merged with Zeneca) still fund a research post in his unit, as does the pharmaceutical company Bayer. Neither of these corporate links are listed in Ray's declared interests.[12] "There are two ways to get bad pesticides off the market: ban them, or get the companies to develop better pesticides," he says.

Food Safety Minister Baroness Hayman, reportedly told the committee that she recognised the need for 'experts' with links to industry. Less than a quarter of VPC members have no declared financial interest in the pharmaceutical industry. Professor Karl Linklater, for example, holds commercial consultancies with pharmaceutical producers including Intervet, Novartis, Roche and Shering-Plough[13] (when approached about their funding sources, the Scottish Agricultural College - of whom Linklater is Principal and Chief Executive - refused to co-operate, citing 'commercial confidentiality'). Pfizer has two consultants on the committee as does Grampian Pharmaceuticals.

Hoechst, SmithKline Beecham, the Wellcome Trust and Merck, are all represented in the declarations of interests of VPC members. A similar picture is painted by the declarations of the Spongiform Encephalopathy Advisory Committee (SEAC), which advise the government on CJD and BSE, and the other committees set up under the Medicines Act to ensure pharmaceutical safety.

According to Richard Young of the Soil Association, the Thatcher government's withdrawal of state funding for research into medicines that were nearing a marketable state left only industry-funded research, or no research at all: "There are very few academics who aren't in some way beholden to industry," he says. During the 1980's, when the academic/industry grip was weaker, a VPC sub-committee attempted to scrutinise the merit of antibiotic livestock feed additives. When hindered by the VPC, the committee's chair James Howie wrote to the then MAFF Minister, Peter Walker, who immediately disbanded the committee.

In March 1996 - one week before the UK government admitted to a link between BSE and nvCJD - Zeneca 'sold' the phosmet (trade name Imidan) patent to a previously unheard of PO Box company in the Arizona desert called Gowan[14]. As Ray says: "Zeneca are not keen to be sued."

In her submission to the BSE inquiry, dairy farmer Joanna Wheatley says: "The initial epidemiological study carried out in 1988 that identified meat and bonemeal as the cause of BSE was flawed. It recorded 68 per cent of farms affected by the disease had not used chemicals or weed killers. This could not possibly be the case." Wheatley points out that OP treatment was enforced on all farms and organic farming was rare and viewed with suspicion by the majority of farmers in the 1980s.

Taking his research overseas Purdey discovered clusters of CJD downwind of large ferromanganese and glass factories in Slovakia; around a missile production plant in Tucson; and around the scene of the Seveso disaster in Milan - where a pesticide factory exploded in 1976. Similar scrapie clusters appeared in sheep in certain volcanic areas of Iceland. Soil, water and plant samples in all these areas showed high levels of manganese and low levels of copper.

Intrigued by Purdey's findings, a Cambridge university chemist, Dr David Brown, carried out tests which found that not only could manganese replace copper in the brain proteins, but it transformed them into the protease resistant isoforms that are found in TSE diseased brains[15]. Purdey reckons that phosmet prevents the brain proteins bonding with the copper, which is subsequently replaced by manganese - readily available to cows in high dose mineral licks. The CJD and BSE symptoms also mirror 'manganese madness', an irreversible fatal neuro-psychiatric degenerative syndrome that plagued manganese miners in the first half of the last century[16].

Queniborough has an agricultural college and experimental farm nearby[17]. It is situated on an outfold of pre-cambrian manganese-heavy rock that is being quarried locally, and a chemical distribution company, Omnichem, is based in the area. None of these activities have been mentioned in reports.

"If phosmet is proven to have caused BSE, the worldwide use of organophosphates could be put into jeopardy, costing the chemical industry billions. The government know more than they're letting on. They've stuck to the scrapie theory to placate people and give the impression they've got it under control," says Purdey.

Whether Purdey is a genius or a paranoiac, MAFF's continued reluctance to explore the OP link to BSE is significant. According to a spokesman: "Anyone with a suitable proposal [concerning the cause of BSE] can approach MAFF for funding." However Brown could not continue his research as he couldn't get more funding, and another chemist, Steven Whatley, had to stop similar tests a year ago for the same reasons.

Richard Young, of the Soil Association, says: "If it could be established that BSE was caused by OPs it would be a major liability issue for both the government and manufacturers."

More sinister is the attention that Purdey, and those who have taken up his theory, have received. Purdey's house was mysteriously burnt down and a structurally sound barn collapsed onto the caravan that housed his science library. He's been shot at[18] (another anti OP campaigner's husband had his fingers broken), and following the publication of an Independent newspaper article in 1993, he awoke to find his telephone lines cut - preventing him receiving follow-up media calls. He says strangers with in-depth knowledge of his movements appear on his farm freaking out his wife, and when he travels to talk about his theory he is constantly tailed. The solicitor who defended his High Court action died when his car went inexplicably out of control. Purdey's vet (who said Purdey's theory should be taken seriously) was killed in what the local paper described as: 'Mystery Vet Death Riddle' when his car was "magnetised" into the front of an oncoming lorry on a clear straight road.

"I'm easier to marginalise as a crank," said Purdey, "but these people were professionals."

Anyone familiar with the start of the anti-nuclear movement, may recall the discrediting of Alice Stewart who discovered the link between radiation and cancer. Scientists who aligned themselves with her had their cars rammed off the road.19 In 1978 four children belonging to anti-herbicide activist Carol Van Strum were killed in a house fire in Five Rivers, USA. In 1993, also in America, a couple who filed a suit against Merck - claiming contamination from their plant had caused the death of their unborn baby - had their house broken into eleven times and a doctor who was helping them had his dog's throat cut.20

Officials from MAFF met with Purdey in the spring, to 'help' him apply for funding to further his research, though a promised meeting with the Food Safety Minister never materialised.

The MRC's David Ray says he is interested in identifying OP toxicity and that all new scientific theories should be tested. Except for Purdey's which is "implausible". "I'm not the only scientist around," says Ray. Though, of course, uncovering their own complicity in a killer disease is not the sort of research that chemical companies flock to fund. In February of this year the US Environmental Protection Agency began reassessing phosmet as a health hazard to farm workers. Sources within MAFF say they are about to take the possibility of linking OPs and BSE seriously - but whether they wish to take the issue up in order to discredit it, remains to be seen.

Mark Purdey is funding his research (testing /labs/travel to cluster sites) himself (no corporate backing on his side of the fence) - any donations to his research fund will help him carry on. Send to: Mark Purdey Research Fund, High Barn Farm, Elworthy, Nr Taunton, Somerset TA4 3PX

[1] MAFF Warble Fly Order 1982
[2] IG Farben developed organophosphate sarin as chemical nerve agent weapon for the Nazis.
[3] Extonet - Extension Toxicology Network - pesticide information profiles June 1996
[4] Mark Purdey statement to BSE Inquiry 23.3.98
[5] Sarin gas (organophosphate) used by Saddam Hussein during Gulf War - in the frame as a possible cause of Gulf War Syndrome.
[6] Claire Gilbert, Blazing Tattles, New Theory, New Intrigue and the Mad Cows, June 3, 1996
[7] Mark Purdey Journal of Medical Hypotheses February 2000
[8] NOAH corporate membership list
[9] NOAH briefing notes to editors April and September 1998
[10] NOAH statement to BSE Inquiry
[11] David Ray statement to BSE Inquiry June 1998
[12] Medicines Act Advisory Bodies, Annual Report 1998
[13] Medicines Act Advisory Bodies, Annual Report 1998
[14] Department of Pesticide Regulation Branch, Notice of Proposal and Final Decisions and Directors Findings
[15] David Brown, Embojournal Spring 2000
[16] Manganese: a review of occupational and environmental toxicology - V Benko and M Cikrt, Journal of Hygeiene, Epidemiology, Microbiology and Immunology 28(2) 1984. Manganese exposure in steel smelters a health hazard to the nervous system - A Wennberg, Scandinavian Journal of Work, Environment and Health August 1991
[17] Brooksby Agricultural College
[18] The Independent 11.3.97
[19] The Woman Who Knew Too Much, Alice Stewart and the Secrets of Radiation - Gayle Green, University of Michigan Press
[20] Green Backlash – Andrew Rowell, Routledge

TOXICOLOGICAL EFFECTS of PHOSMET

ACUTE TOXICITY
Phosmet is a moderately toxic compound by ingestion but requires the signal word WARNING on the label because it is more highly toxic by other routes of exposure.

It has a moderately high toxicity through the skin and a very high toxicity through inhalation.

Typical of other organophosphates, phosmet is an inhibitor of the enzyme cholinesterase.

Symptoms of acute phosmet poisoning include nausea, vomiting, abdominal cramps and diarrhea. Acute exposure at high levels may result in muscle spasms, loss of muscle coordination, mental confusion and drowsiness. The insecticide may also adversely affect breathing and salivation.

The oral LD50 of phosmet ranges from 113 to 369 mg/kg in rats of both sexes and 23.1 to 50.1 mg/kg in mice. Signs of acute poisoning are rapid, generally occurring within 30 minutes after exposure. The dermal LD50 for phosmet in the rabbit ranges from 1,560 to 4,640 mg/kg. Inhalation experiments showed that 50 to 800 ml/l resulted in behavior changes but no mortality to rats.

The compound appears to be more toxic to many domestic animals such as cattle, sheep and goats than to rodents.

The LD50 values for these animals range from 25 to 50 mg/kg.
CHRONIC TOXICITY
Rats fed phosmet for sixteen weeks at moderate to very high doses (22.5 mg/kg to 300 mg/kg) suffered some mortality and exhibited a number of toxic effects. Over a six month period, doses of phosmet of 1 mg/kg/day in the diets of rats produced no observable chronic effects (NOEL). In another study conducted over two years the NOEL was 2 mg/kg/day. These two studies indicate that even small amounts of phosmet can cause chronic toxic effects.
Dogs also had a 1 mg/kg/day NOEL in a two-year feeding study. In a 20- week experiment, dogs exhibited changes in their blood enzyme activity (cholinesterase) at doses at or above 3.7 mg/kg/day.
Cattle also showed a blood enzyme activity decrease when fed varying amounts of phosmet (1 to 2 mg/kg) for eight weeks.
No delayed neurotoxic effects were noted in chickens fed diets with moderate levels of phosmet for six weeks.
Rabbits which had phosmet applied to their skin for five days a week for three weeks suffered high mortality rates at doses of 300 to 600 mg/kg/day. At 50 mg/kg/day there was significant brain enzyme (cholinesterase) depression.
Estimates place field worker exposure to the pesticide at levels ranging from 0.1 to 1.4 mg/kg/day one day following field application. The worst case estimate of homeowner exposure was no greater than 0.005 mg/kg/day. Despite its high toxicity, over an eight year reporting interval only sixteen cases of phosmet poisoning were reported in California. One year during this period (1986) approximately 240,000 pounds of phosmet were sold in the state indicating the relative safety with which the product was handled.
The signs and symptoms of chronic toxicity are generally consistent with those for the class of organophosphate insecticides.
Reproductive Effects
A three-generation study with rats indicated that there were no reproductive effects when the animals were fed small amounts (2.0 mg/kg) of the compound for the first generation and slightly higher amounts (4 mg/kg) for the second and third generations . Female rabbits given phosmet both dermally and orally for three weeks prior to mating and for 18 consecutive days of gestation showed no effects on reproductive parameters. The doses tested ranged from 10 to 60 mg/kg for both routes of exposure.
Teratogenic Effects
No birth defects were noted in studies with pregnant rabbits fed 10 to 60 mg/kg for three weeks during pregnancy or in monkeys given 8 to 12 mg/kg on days 22 to 32 of gestation.
Rats fed 10 to 30 mg/kg on days 6 through 15 of gestation suffered some maternal toxicity at the higher doses but no abnormalities appeared in the pups. In another study however, single moderate doses of 30 mg/kg administered to rats between day nine and thirteen of gestation, produced an increase in brain damage (hydrocephaly) in 33 of the 55 embryos examined. Embryo toxicity was dose-dependent. The results of these studies, viewed together, are somewhat ambiguous and make it difficult to draw firm conclusions about possible teratogenic effects in humans.
Mutagenic Effects
The tests on the mutagenicity of phosmet have produced mixed results. Several tests with bacteria did not cause any mutations though there was one positive test with one strain of bacteria (S. typhimurium). There have been no tests conducted directly on animal or human cells. However, among workers producing the compound Safidon, some changes in their chromosomes were noted.
Carcinogenic Effects
A group of rats fed diets containing 1 to 20 mg/kg/day of phosmet for two years showed no differences with respect to neoplasms when compared to the controls. However, the study has been deemed inadequate because too few rats were analyzed at the end of the test.
A two-year mouse study showed that phosmet is associated with a significant increase in liver tumors in male mice. The dose in this test was not noted in the report. In female mice, there was a positive dose-related trend for liver tumors and carcinomas. Phosmet has a "tentative" category C carcinogen rating (possible carcinogen). The EPA has requested that additional testing be conducted.
Organ Toxicity
Observations of occupationally exposed workers indicate that the compound may cause a reduction in enzyme activity (peripheral cholinesterase). No other observable adverse effects were noted among the workers.
Phosmet is a mild irritant to the eyes, and only mildly irritating to the skin.
Fate in Humans and Animals
Phosmet is rapidly absorbed, distributed, and eliminated in mammals. Rats given single doses of 23 to 35 mg/kg phosmet excreted greater than three quarters of the dose in urine, about fifteen percent in the feces. Less than three percent was found in body tissues after two days. Other figures show nearly eighty percent eliminated in the urine and twenty percent eliminated in the feces after three days.

Phosmet applied to a steer's back was moderately absorbed and rapidly broken down in the blood to phthalamic and phthalic acids.

Rat studies indicate that phosmet crosses the placenta. Phosmet also appeared in the milk of goats fed a single dose of 70 mg/kg. The level in the milk after eight hours was 0.38 mg/kg but after 24 hours and 48 hours none could be detected.
Cows fed silage with an average residue level of 19 mg/kg for nearly two months showed no residues in the milk above the detection level of 0.01 mg/kg. Cattle fed dietary levels of 20 to 100 ppm showed no residues in the tissues at levels higher than 0.005 ppm.
Metabolic breakdown is primarily by hydrolytic pathways and the breakdown products are similar to those resulting from other organophosphate pesticides. The major metabolite is phthalamic acid with phthalic acid produced in smaller quantities.

OK, I'm convinced.

Disclaimer: Opinions posted on Free Republic are those of the individual posters and do not necessarily represent the opinion of Free Republic or its management. All materials posted herein are protected by copyright law and the exemption for fair use of copyrighted works.