The Medical Research Council (MRC)
(Formerly the Medical Research Committee)

The Medical Research Committee (MRC) was formed from its origins in the Royal Commission into the Relations of Human and Animal Tuberculosis, which existed from 1901 to 1919.
That Commission recommended the creation of a permanent medical research body and a National Health Insurance scheme was devised to provide health and unemployment insurance for workers. In establishing that scheme there was an option of using the money raised for research purposes. The Medical Research Committee, and an Advisory Council for Research were established in August 1913.

Scientific experts formed the MRC and the Advisory Council included staff from universities and government departments and they were funded by the National Health Insurance (Medical Research Fund) Regulations, under the Minister for Health.

The Medical Research Council was formed in 1920 and conducts co-ordinated research for governmental bodies such as the Department of Health and the armed services.
They were also responsible for Radiological Protection Board with interests in industrial health.

To this end the MRC was a key source of advice for Lord Solly Zuckerman and his Committee when they were asked to report on the risks of pesticides, including organophosphates, to human health.
The danger presented by phosphorus had long been known following the deadly effects induced in workers making matches.
Phosphorus-induced “phossy jaw” was an horrific symptom of exposure to the poison.
The Zuckerman Committee’s first report was published in 1951 and the MRC provided sufficient information on the dangers of organophosphates for them to recommend that all OPs should be labelled as “Deadly Poison” and that hospitals in the area should be notified BEFORE the chemicals were used.
They wrote of organophosphates -
Parathion is representative of the group ; it can be absorbed through the skin and by inhalation and ingestion. Death can occur as a result of a single exposure ; but chronic toxicity is the main problem.
Repeated absorption of parathion may result in cumulative poisoning. Parathion appears to inactivate the enzyme cholinesterase. This enzyme is intimately concerned in the transmission of impulses between the nerves and muscles.
When the cholinesterase level falls below 50 per cent of normal, symptoms are to be expected. Cholinesterase is present at the motor nerve endings, and inactivation of the enzyme results in muscular twitchings and weakness that may develop into paralysis. Death may follow from paralysis of the respiratory muscles. That part of the nervous system which controls automatic body processes is also affected.
Successive small doses of parathion may progressively lower the cholinesterase level without producing symptoms, but may render the individual increasingly susceptible to further doses. Owing to the slow restoration of cholinesterase to its normal level, this susceptibility will persist for a long time, maybe for some weeks.

The risks were clearly known and the committee further recommended that -

Medical supervision should include routine medical examinations at weekly intervals, with suspension of workers who show any trace of early toxic symptoms. Also expert super-vision of first-aid and prophylactic measures.
(iv) A limit should be placed on the period during which any one worker may be engaged on spraying operations.
(v) The smallest possible number of workers should be exposed to risk arising from the mixing or other handling of the chemicals. Only the most responsible employees should be given these duties.
(vi) All workers and other persons handling the materials or otherwise exposed to risk should receive detailed instruction on dangers and precautions from a qualified instructor. Instruction should include demonstrations and lectures,
(vii) Research should be undertaken into the safest types of protective equipment, containers, spraying equipment, etc.
(viii) A notification should be sent to the local doctor before spraying operations are undertaken in his area in order that he may look for symptoms of DNC and parathion poisoning in patients who may report to him after using the sprays.
(ix) Information on the pharmacology of toxic chemicals and the treatment of casualties should be made specially available to general practitioners.
(x) Research should be undertaken in order to find antidotes for DNC and parathion poisoning.
(xi) Chemical manufacturers should not market any new insecticide or other preparation until they have thoroughly studied the acute and chronic toxicity of the compound, and issued extensive information about its toxic nature and prevention of accidents.
(xii) manufacturers should be required to state on the labels of containers;
(a) the name of the active ingredient ;
(b) the percentage of active ingredient ;
(c) its toxic nature and mode of action ;
(d) precautions and antidotes, and the safe intervals which must be observed between spraying and harvesting, also whether danger to other workpeople exists after the crop has been sprayed.
(xiii) Research should be instituted in order to find insecticides and weedkillers which are fully effective in their agricultural use but are harmless to man.
(viii) Warning to Local Doctors
The Ministry of Agriculture and Fisheries should consult the British Medical Association about the practicability of medical practitioners being circularized by the Association about the dangers and appropriate treatments.
Medical practitioners and hospitals should be warned when spraying operations are to be undertaken on farms in their vicinity.

Those phrases indicate how much the MRC knew about the dangers in the 1940s.

In 1953 the Committee issued its second report on the dangers of residues in food.
They wrote “Unfortunately, almost all the insecticides and weed-killers are toxic to forms of life other than the pests they were designed to control and, if improperly used, they may constitute a serious hazard, not only to domestic animals and many wild creatures, but also to man - although here the risks can sometimes be greatly reduced by the correct timing of the treatments.
The Working Party hope that further research will disclose alternative pest-controlling substances which will have a greater selective toxicity to insects, weeds and fungi. Until, however, such compounds are discovered, the only way in which the present danger can be mitigated is by efficient control of the operations.
3. Our first report* (January, 1951) dealt with the protection of the men who spread the new pesticides and weed—killers, and particularly with the problem of offsetting the hazards they run when applying the more noxious of these crop-protecting chemicals.
This problem was fairly straightforward since the dangers were obvious, and since all people engaged in the work, from the farm worker to the spraying contractor, were equally anxious to devise reasonable measures of protection.
Legislation has now been enacted to embody our recommendations. Our second task, that of considering the possible hazards run by the consumer who eats food which, at an earlier stage in its history, was treated with, or exposed to, some toxic chemical, has proved far more difficult, and is the subject of this report……
…We also recommended that it would be in the interest of the retailers of chemical formulations, as well as of the public, that the sale of preparations containing dinitro and organo-phosphorus substances should either be brought under statutory control, or restricted.
This recommendation has now been implemented.
In the present report we take the problem of the risk to the consumer as far as we believe we legitimately can on the basis of real information. In the next part of our work we propose to consider the dangers to which animal and plant life are exposed as a consequence of the use of various pesticides.

But the Zuckerman recommendations were NOT implemented and in the 1953 report the Committee admitted that -
Further, there is a lack of information concerning the decomposition products of systemic insecticides within plants, and of their effects, if any, on the composition of the final food. In any event, it is impossible to conceive of animal experiments which will provide complete information about the toxic effects of chemicals on human beings.
25. The magnitude of the risk to the consumer obviously depends on the nature of the foods that are treated and on the intensity of the treatment.
A real danger may arise occasionally from the gross misuse of a pesticide when applied in excessive quantities to a crop just before consumption. The intermittent consumption of very small and undetermined quantities of toxic chemicals constitutes a more hypothetical danger. The greatest threat of chronic toxicity would therefore arise from the widespread treatment with materials of group (ii) (d) and (e) of foods which form the major part of the nation’s diet. In seeking information about this point we were immediately faced by the difficulty that, while we might be able to discover how the food we grow ourselves is treated, we were likely to remain incompletely informed about the previous history of the food we import, which is still 60 per cent of what we consume and which contains a large proportion of our staple foods.
26. Although we have not been able to obtain as much information as we should have liked about the proportion of different home-grown crops which receive spray treatment, such information as we have received shows that very little of our staple foods is treated with the materials comprised in group (ii) (d) and (e).
[NOTE this reference is to
(d) Compounds capable of leaving residues in food and which, as little is yet known about their toxicity to man or animals, constitute a possible hazard of unknown degree, e.g., some of the more recently introduced organo-phosphorus compoundsv and chlorinated hydrocarbons.
(e) Compounds reacting with the natural constituents of food to produce compounds which may be toxic, or destroying an essential factor in the food. No chemical at present used for crop protection is known to have the first of these properties.
The second is manifested to a limited extent by methyl bromide when used to protect stored wheat.]

Note that after this time treating grain post-harvest with those compounds became the norm.

Of the Medical Research Council they wrote -
(vi) The Medical Research Council
Two units formed by the Council carry out research work in the field of toxic chemicals :
(a) THE TOXICOLOGY RESEARCH UNIT was formed to assist in the solution of toxicological problems and to pursue research in fundamental questions arising from the problems referred to it. It has been concerned with the mode of action of toxic agents, and with the design of tests rather than with the carrying out of routine examinations.
(b) THE DEPARTMENT FOR RESEARCH IN INDUSTRIAL MEDICINE, among its other interests, is concerned with cases of poisoning that have occurred in factories and amongst agricultural workers. It is interested in the general problem of the use of agricultural chemicals.
The Toxicology Committee is a standing advisory committee appointed by the Medical Research Council to advise it on research in problems in toxicology.
On occasions the advice of this independent committee on toxicity has been sought by Government Departments, industrial firms and private individuals.”

It is clear then that the MRC was a major player in advising the committee as to the known danger of these chemicals.

By 1955 when the Committee released its third and final report they wrote -
The use of chemicals to destroy pests and weeds is becoming more and more widespread, and as it increases, so too does the fear that these chemical treatments may be masking a number of undesirable, or even dangerous, side-effects.
The risks run by the operatives who handle the poisons were dealt with in our first report (January, 1951),* and our recommendations on measures by which these dangers could be minimized have now been incorporated in legislation. We have also dealt, in our report to Ministers, of May, 1953,+ with the possible hazards run by the person who eats food which, at an earlier stage in its production, was exposed to some toxic chemical. Here, too, steps have been taken to implement our main recommendations.
2. Our present report deals with a third set of problems — the dangers which the toxic chemicals now used in agriculture bring to the wild life, plant and animal. of our countryside.
This comes last in the list of our enquiries, not because we or the authorities by whom we were appointed do not share the concern to which it gives rise, but because it was immediately apparent that the subject constitutes an extremely difficult field of enquiry. There is certainly no lack of statement about game birds and other animals dying after having fed in fields treated with toxic chemicals, and about unwanted, changes in verges and hedgerows following the use of toxic sprays. The difficulty has all along been the impossibility of measuring the extent of the danger.
We wish to make this clear at the outset so as to obviate any impression that the presentation of our Report implies that we have been able to give an exact scientific answer to the questions put to us. But at the same time we also wish to say that we believe that dangers do exist, and that even if they cannot be defined precisely, measures should be taken to minimize the possibility of the new toxic chemicals used in agriculture spoiling our countryside.

But the use of these poisons in the countryside and even in cities INCREASED after these reports and hospitals and doctors were not pre-warned of their use.

In 1958 Poisoning by organophosphorus insecticides was added to the Industrial Injuries legislation.
Once again it was officially confirmed that both acute and chronic poisoning by these compounds were recognised.
It also confirmed that repeated low dose exposures could result in the symptoms of acute poisoning from which some of those exposed may not recover.

In 1961 Rachel Carson published her book “Silent Spring”, which simply confirmed what the Zuckermam reports had stated, but the industry and its allies made a concerted effort to undermine her credibility in order to protect themselves.

However, also in 1961 one D.F. Heath of the Toxicology Research Unit of the Medical Research Council published a book titled “Organophosphorus Poisons” - subtitled “Anticholinesterases and related compounds”.
Interestingly the first chapter of the book refers to the problem of experimentation using these compounds and the unreliability of results caused by potential impurities, isomers and products of oxidisation, some of which may be 1000 times more active than the pure active ingredient.
Such compounds have reportedly been found in chemicals approved for use by regulators relying on those flawed testing methods.
The adverse effects of the compounds on the nerves and the paralysing of the muscles is described and given as a cause of respiratory failure, compounded by the excessive excretions in the lacrimatory and salivary glands and gastro-intestinal tract disturbances.
The main signs of poisoning by organophosphorus compounds are listed as:
Lacrimation, salivation, violent contractions of the gastro-intestinal tract and bladder, bronchoconstriction and bradycardia resulting from acetylcholine (ACh) effects on the parasympathetic nerve endings.
Muscular twitchings and paralysis resulting from excess ACh at the myoneural junctions of the striated muscles.
Convulsions, hyperexcitability and central paralysis of the respiratory system involving complex effects including the central nervous sytem.
Vasoconstriction, caused by excess ACh in the sympathetic ganglia and adrenal glands. The immediate cause of death is usually asphyxia.

Reactions triggered by ion exchange are explained in detail, (the ion of AChE being ACh, the substrate of AChE). The biochemistry and the actions of enzyme bonding and blocking by the chemicals, is also detailed, listing many of those enzymes which are inhibited by phosphorus compounds.
The importance of molecular shape to the effect of enzyme inhibition is noted as is the need for new enzymes to be created if the inhibited enzyme has become stable. This process can take months.
The brain contains a high proportion of lipids in which phosphorus compounds may persist for many hours.
Successive doses may increase susceptibility. With some compounds successive small doses can reduce AChE in man to under 5% with no obvious signs yet that degree of inhibition with a single dose can be fatal.
This is explained as a combination of A-esterase action and adaptation by the body as shown in feeding trials.
A compound is said to show cumulative action when a succession of small doses, given at intervals, is as toxic as a single dose equal to the sum of the successive doses
- in other words, repeated small doses can trigger acute poisoning.
Parasympathetic innervation triggers excessive salivation, retching, vomiting, lacrimation, borborygmus (belly rumblings), diarrhoea, tenesmus (anal spasms) lacrimation, chromodacryorrhea (weeping of red tears) in rats, myosis, bronchosecretion, cardiac slowing (bradycardia), and frequent micturition with urinary incontinence.
Voluntary innervation triggers fibrillations, fasciculations, muscular weakness, ataxia and paralysis.
More complex innervation triggers transient hyperpnoea (rapid and deep breathing), followed by gasping and respiratory failure, changes in blood pressure, failure of circulation, convulsions, hyperexcitability to sensory stimuli, acidosis and hyperglycaemia.

Micturation results because the bladder empties reflexly but with lower volumes than usual. This process is complex involving not only the effect of ACh on the smooth muscle of the bladder but also effects in the CNS and ganglia.
Broncho-constriction is an important contribution to fatalities.
Bradycardia occurs at an early stage of poisoning and develops into A-V block until the heart stops beating.

The compounds can penetrate the skin without damaging it and may be as toxic by that route as by being taken orally. Several fatal cases of poisoning have been seen in the children of users.

The induced symptoms have been studied on human volunteers, as part of chemical warfare programmes and on casualties.
They included anorexia, mild abdominal cramps, excessive sweating, excessive dreaming, nausea, epigastrial and substernal tightness, tightness in the chest, bradycardia, dyspneoa, muscle twitching, giddiness, tension, anxiety, nightmares, depression, withdrawal, restlessness, emotional lability, tremors, fasciculations, pallor, infections of the upper respiratory tract, severe bronchial secretions and salivation, cyanosis, convulsions, and easily fatigued.
Symptoms do not vary much by compound.
Coma appears in man but not in animals and man can describe many symptoms such as nausea, colic, and anxiety which cannot be observed in animals but which may give early warning of poisoning.

Blood pressure is raised moderately and death is caused by paralysis of the muscles and not of the respiratory centre.
The apparent greater importance of central systems in man may only reflect his unique capacity to describe them.
Diagnosis in man depends on recognising the very general nervous symptoms.
Atropine in normal subjects causes marked unpleasant symptoms at about 0.03 mg/kg. Prognosis is markedly more favourable the sooner the treatment is begun and the slower the onset of symptoms and once the crisis is past recovery is normally complete but a few compounds, not used as insecticides, cause permanent lesions.

Some compounds cause paralysis or narcotic effects which do not cause any cholinergic symptoms. Many thousands of cases of paralysis in man have been reported mostly by tri-tolyl phosphates, also known as tri-cresyl phosphates or tri-orthocresyl phosphate abbreviated to TOCP. Some do not cause paralysis and some homologues do, often absorbed through the skin in processes involved in the manufacture of plastics or hydraulic oils.
The first signs of paralysis are seen as weakness in the feet about a fortnight after exposure. It is a flaccid paralysis mainly confined to the arms and legs, beginning at the extremities with the feet affected before the hands and persists for several months.
The primary lesion appears to involve demyelination of the nerves leading to axon degeneration but the severity of signs depends upon how many and which tracts are affected. In mild cases in the hen the spinal cord is more damaged than the sciatic nerve at all stages of poisoning and is the only part damaged in mild poisoning.
It is similar to the effects in hens of thiamine deficiency.
In man mild poisoning produces paralysis of the flaccid type only which disappears within 2 years. Flaccid paralysis results from the degeneration of peripheral nerves while degeneration of the CNS causes spastic paralysis.
De-myelinating and other phosphorus compounds inhibit glucose and pyruvate oxidation at high concentrations.
All compounds produced narcotic effects ranging from incoordination and weakness to deep anaesthesia.Some do not cause cholinergic signs. Some compounds block nerve conduction and motor end plates and can also block the passage of sodium ions through the membranes of red blood cells.

Given the above it is clear that even in 1961 the MRC was very well aware of the actions of these organophosphate compounds. and the danger they pose to man.

In 1972 B. J. Walker published book designed for students of organic chemistry.
Titled “Organophosphorus Chemistry” extracts are found in a pdf file here
The publication gave detailed descriptions of the actions of these compounds, including the effects on DNA, RNA and the energy transfer systems within the metabolism.
The history of phosphorus was explained from the early beginnings in 1669 through the white phosphorus match-making disasters from 1851 to the discovery of red phosphorus in 1847 and the discovery of the first organophosphorus compounds from the 1880s onwards.
The two types of reactions of the phosphorus atom in the OPs are explained - first the action of the atom itself and second the way the presence of the atom in organic substituents modifies the reactions.
The chemistry is explained in great detail and diagrams are supplied to aid understanding.
There is a section explaining how phosphorus is vital to the processes involving adenosine diphosphate (ADP) and adenosine triphosphate (ATP) which is essential to life itself, to the ribonucleic acids (RNA) and deoxyribonucleic acids (DNA).
Phosphates and organophosphates are therefore packets of energy and processes involving phosphates are targeted by OPs, including DNA itself.

Insecticidal OPs were discovered in 1930 and their first use commercially was in 1942.
Compounds were developed as war gases during WW2 and were produced at the rate of several hundred tons of nerve agent every month.
In agriculture systemic OPs became part of the system of the target organism but the mechanism of poisoning in insects, mammals and man are closely related.
The phenomenon of “potentiation” was also discovered in that a mixture of two insecticides may have a much higher potency than the same two acting separately.
Another form of potentiation occurs when compounds of low toxicity are converted by the metabolism of the insect or animal into much more toxic compounds.
e.g. Parathion is rapidly oxidised to form Paraoxon, which is extremely toxic.
The effects of the poisons at every nerve junction in every muscle, gland and organ in the body and diffusion into the central nervous system leads to complete confusion of cause and effect.

Symptoms include rapid twitching (fasciculation) of muscles, followed by paralysis, intense pupil contraction, excessive saliva production and more complex effects, such as loss of coordination, caused by fundamental blockages in the central nervous system.
Some insects killed by pesticides are found to have their cholinesterase uninhibited yet some remain healthy with all their cholinesterase inhibited, which would kill mammals. Ultraviolet irradiation can greatly increase the the toxicity to mammals and this process may involve the production of dangerous phosphorus radicals.

Clearly then scientists, and Universities, have been aware of the dangers of OPs for many decades.

In 1980 the UK Health and Safety Executive released the first edition of its Medical Series of papers giving advice to medical practitioners, Known as MS 17 it gave details of the known adverse effects of the organophosphorus compounds and the long-term risks, including those from repeated low-dose exposures.
OP Poisoning became a Notifiable Disease.

In 1984 the UK Department of Health released its first publication of “Pesticide Poisoning” in which it listed all the adverse health effects triggered by exposure.
With comprehensive details about OP poisoning it listed all the hospitals holding the antidotes and where the vital blood testing could be done.

In 1987 the second edition of MS17 was published, again giving details of all the known adverse effects following exposure to the poisons with recommendations for the regular testing of those occupationally exposed to avoid cumulative effects.

In 1992 two senior toxicologists, Timothy Marrs, the UK’s Chief Medical Officer, and Professor of Toxicology, University of West Virgina USA, Bryan Ballantyne published their reference work "Clinical & Experimental Toxicology of Organophosphates and Carbamates.
This book detailed the varied adverse health effects caused by exposure to these poisons including neurological, cardio-respiratory, immunotoxic, ophthalmic, genotoxic, carcinogenic, developmental and reproductive issues.
A very long list of contributors included members of the Medical Research Council; senior toxicologists from National Poisons Units; military experts from around the world, including Porton Down, UK and Aberdeen Proving Ground, USA; veterinarians; and chemical company representatives.
Of particular interest, given that many OPs mutate bacteria and alter vital proteins, is that the book confirms the adverse effects on the immune system, which “can increase host susceptibility to viral, bacterial and parasitic infections and increase the incidence of tumours and possibly lengthen the course of an infection.
Conversely, enhancement of the immune system can lead to exacerbation of autoimmune disease or non-specific tissue damage (e.g. elevated pulmonary leucocyte function may lead to pulmonary fibrosis), and general malaise or lethargy.
Perturbation of normal homeostasis of the immune system may lead to deleterious side-effects that may not be observed until the facet of the immune system that was affected is required to defend the host from a foreign antigen.

[Note that the UK Committee on Toxicity itself warned of the risks of vaccination to those exposed to OPs a decade later, quoting the Lancet from 1996 and a World Health Authority document which indicated an OP eliciting auto-immune respoinse.]

Acute symptoms are listed as -
Muscarinic - Cough, wheezing, dyspnoea, broncho-constriction, bronchial hypersecretion, pulmonary oedema, cyanosis, rhinitis, salivation, lacrimation, diaphoresis, urinary and faecal incontinence, nausea, vomiting, abdominal cramps, diarrhoea, tenesmus, bradycardia, hypotension, hyperaemia, blurred vision, miosis.
Nicotinic - Muscle fasciculation, including diaphragm, muscle weakness, tachycardia, pallor, mydriasis, hyperglycaemia.
CNS - Anxiety, insomnia, nightmares, headaches, drowsiness, confusion, tremor, ataxia, dysarthia, dystonic reactions, hypotension, respiratory depression, convulsions, coma.

Cardiac manifestations of OP Poisoning - Bradycardia, tachycardia EEG - S-T changes; A-V block; Q-T prolongation; Ventricular arrhythmias; torsades de pointes; Ventricular fibrillation; Asystole
Myocarditis - Lysis of myofibrils; Z-band abnormalities
Long-term sequelae

Delayed mixed sensorimotor peripheral neuropathies can result from acute poisonings to some OPs and can include parasthesia in the distal lower extremities, fatigue and cramps.
Gait disturbances can develop and remain for months, occasionally with permanent injury.
Both transient and persistent behavioural abnormalities have been associated with OP toxicity and include depression, irritability, confusion and emotional lability, most of them resolve within a year.

Much of the above represents an admission of potential long-term, life threatening effects of exposure to these poisons.

Also in 1992, in the USA Robert Engel published his book titled the “Handbook of Organophosphorus Chemistry”, which is a comprehensive study of the chemical group and the actions in the metabolism.
The chapter on fire retardants states -

The neurotoxic character of tri-cresyl phosphate was traced principally to the presence of the ortho-cresyl isomer, although the p-ethylphenyl group was also shown to produce this effect.
The structure-activity relationships and the mechanism of action have been studied extensively as well as the clinical manifestations in animal and human poisoning.
The basis for the specific toxicity is believed to be biooxidation of the ortho-alkyl group to form a cyclic phosphate ester which has phosphorylation capabilities for a membrane-bound enzyme “neurotoxic esterase” (NTE).
Phosphorylation of NTE appears to initiate delayed peripheral neuropathy……
it is not necessary to have tri-o-cresyl phosphate (TOCP) in the composition to have a neurotoxic effect…..

The chapter studying phosphorus containing insecticides confirms that organophosphorus compounds may inhibit not only AChE but also other serine enzymes and that their ability to inhibit enzymes is due to molecular shape.

In 1996 the UK Department of Health released its second edition of the “Pesticide Poisoning" publication, edited by Proudfoot. Extracts in pdf file here.
Again it gave details of the toxic action of various groups including organophosphates and the available tests and treatments.
Interestingly the list of hospitals holding the antidotes and able to test for poisoning was not included.
Although the publication stated that glyphosate is an organophosphate and that the chemical has had adverse effects it wrongly suggests that the chemical has no anticholinesterase action and that it only affects amino acids found in plants.
This was disproven by attempts to approve the compound as a cancer treatment.

In 1997 American scientists released a publication titled Overexposed - organophosphate insecticides in children’s food which called for an immediate ban on all OPs used on food crops because of the danger to children posed by cumulative residues of multiple OPs.

In 1999 the UK Committee on Toxicity released its publication “Organophosphates
Disgracefully it suggested that there were no long-term adverse health effects caused by repeated low-dose exposure to OPs.
But they did admit that effects other than those on cholinesterase could trigger the reported long-term effects.
Despite evidence given in a high profile court case the report claimed that no compounds giving a positive result in the hen test (for NTE inhibition) were approved for use.
Some approved chemicals inhibit NTE and cause peripheral neuropathy.
Given that information from the MRC was referred to in the report the conclusion is difficult to comprehend but perhaps more importantly, given the information above, the suggestion the more research is required is simply astounding. Many of the members of the Committee had direct links to chemical companies which manufactured OPs.

Criticisms of the COT report on OPs were brushed aside even though it was clear that the committee found any excuse possible to dismiss science which supported the poisoned victims and yet supported questionable studies dismissing dangerous adverse effects and called for more expensive publicly funded research.

According to Parliamentary written answers to questions the MRC was involved in that research, which cost the taxpayers some £4 million only to reach conclusions calling for more research. At best they can only re-discover what was known by them for decades.

In 2000 the third and latest version of MS17 was released.
Although now some 8 pages instead of just 4 the paper was not as comprehensive as the earlier editions.
Now it would merely be "helpful to report OP poisoning cases, which "may be investigated...."
Clesrly poisoning by these "Deadly Poisons" is no longer considered important.

Sinister developments followed as the COT report on OPs was used to halt the ongoing High Court cases in which plaintiffs sought compensation for the long-term harm caused to them by OP exposure. Deception and perversion of justice were frequently used to prevent a successful outcome for the plaintiffs.
Worse was to come when the Industrial Injuries legislation was changed in order to prevent any further successful claims for poisoning by OP chemicals.

In 2014 the Committee on Toxicity released a new statement following their “inconclusive” 1999 report on OPs.
Headed “Statement on long-term neurological, neuropsychological and psychiatric effects of low-level exposure to organophosphates in adults
it was clear from the outset that the real danger to the unborn and to children, the sick and the elderly, was being ignored.

Despite all the evidence collected by honest scientists over decades and reported officially once again the Committee affirmed their original position denying serious adverse effects caused by OPs.
See pdf file here for this statement
One section states
Despite limitations of individual studies, current evidence suggests that there is an excess of multiple neuropsychiatric symptoms in people who have been exposed to organophosphates at levels insufficient to cause overt acute poisoning. However, it does not support the existence of a specific syndrome of “chronic organophosphate-induced neuropsychiatric disorder (COPIND)”, as has previously been hypothesised. It is unclear whether the observed excess of symptoms is a consequence of chemical toxicity or occurs through psychological mechanisms, and it is possible that people who are aware of having been exposed to potentially toxic chemicals are more inclined to notice and report symptoms. Studies on the relationship of symptoms to polymorphisms and activity of the enzyme, paraoxonase (PON1), have not clearly established a causal link with poorer capacity to detoxify organophosphate compounds, as might be expected if the illness were a consequence of toxicity.

Once again the favoured view that symptoms known to be caused by poisoning are claimed to be not caused by the chemicals but by mental health issues is used to further harm those exposed.
In fact such false claims are referenced as Fraud in the text of the Fraud Act 2006.
It would seem that £millions of taxpayer funding is handed to scientists involved in these studies.
Invariably "inconclusive" results are achieved and the scientists simply call for “more research”.
Then they again find ways to ignore and criticise the methodology etc. of independent research which supports the victims of poisoning - and call for more research.

It seems to be the standard practice and it protects those who harm us all.

The Committee on Toxicity appears to have a habit of ignoring and dismissing evidence of serious harm and implying that the symptoms are the result of a “Nocebo” effect - an invented word based on "Placebo" - and another way of implying that the symptoms are induced by the mind and not by the recognised effects of the poisons.

Their Aerotoxic report here on the potentially lethal effects of toxic fumes in the enclosed space of aircraft cabin air is a perfect example of that process.
The “Nocebo” effect is raised even though pilots have been rendered unconscious by the fumes with potentially disastrous results.

On the same lines their former Chairman is on record as suggesting that those with Multiple Chemical Sensitivity, often triggered in those poisoned by OPs, may be suffering from affects akin to “Voodoo” - again implying mentally induced symptoms.
Scientists who believe in "Voodoo" but not in the effects of poisoning are surprisingly common - when it suits their purpose.

Even with Gulf War Illness the MRC, with members from the Committee on Toxicity suggested that the symptoms were likely to be psychological in origin, despite scientific evidence from the USA confirming links to poisoning by anticholinesterase compounds - with further harm caused by other toxins such as oil fire smoke and radiation. Vaccinations also played a part - see above for the dangers of vaccination in those exposed to OPs.

Members of COT were involved when the dangers of Depleted Uranium used in the Gulf and other Wars were examined. The Committee declared that :
None of the individuals tested showed evidence of significant exposure to DU, and for both laboratories, the mean isotope ratio across all samples from veterans was almost identical to that for natural uranium. The Board is thus confident in concluding that, within the sample of veterans tested, there was no exposure to DU in the Gulf War or more recently, at a level which, according to mainstream medical and scientific thinking, would have any material impact on health. In their potential for exposure to DU, the veterans who participated in the programme may not have been representative of all those eligible for testing. Nevertheless, this finding suggests that clinically significant exposure of British military personnel to DU in the Gulf War and Balkans, if it occurred at all, was relatively uncommon. "
Not everyone in that research group agreed with the findings and their criticism is found in the pdf file here.

Another example of the COT’s failure to properly judge incidents of poisoning was seen with the Lowermoor Water Poisoning incident in which aluminium sulphate was accidentally added directly to the water supply with devastating effects on those who drank the water. The effects of the poison were dismissed by the Committee and when post mortem evidence was finally gathered the conclusion again appears to be that other sources of the toxins may have been responsible.

When the failure to properly monitor residential exposure to pesticides was exposed it was suggested that “fear of pesticides” rather than the poisons themselves, was responsible for the reported symptoms. This attitude seems to have been accepted as the normally employed means to dismiss reports of adverse effects from the poisons, even in the occupationally exposed who had no fear of the poisons - even when they were poisoned by them.

On Mobile phone radiation former COT Chairman and MRC member David Coggon reportedly said, while Chairman of the Mobile and Telecommunications Research Programme (MTHR) that :

When the MTHR programme was first set up, there were many scientific uncertainties about possible health risks from mobile phones and related technology. This independent programme is now complete, and despite exhaustive research, we have found no evidence of risks to health from the radio waves produced by mobile phones or their base stations.
Thanks to the research conducted within the programme, we can now be much more confident about the safety of modern telecommunications systems. To be sure that there are no delayed adverse effects, which only become apparent after many years, the programme provided funding to set up an epidemiological investigation (the COSMOS study) which will follow-up a large population of mobile phone users long-term.
Future Government support for this study and any new research on mobile phones and health will be managed by the Department of Health.

That Research Programme received approximately £13.6 million in funding.
There are on-line videos of people cooking popcorn and even steak using only the radiation from mobile phones.

The former COT Chairman was the former chairman of the Advisory Committee on Pesticides and a member of the Medical Research Council.

He was also influential on the Industrial Injuries Advisory Committee which has now made it almost impossible to obtain a recognised diagnosis of OP poisoning as an Industrial Disease.

Were vested interests involved once again in the production of the report which denied known evidence?

Regarding Parkinson’s Disease their OP report actually admits that the known action of OPs on the mitochondria and oxidative stress trigger the disease but the link is dismissed.
Parkinson’s disease results from degeneration of dopaminergic neurons in the substantia nigra (a part of the midbrain), which often is accompanied by the presence of protein-containing, eosinophilic inclusion bodies (Lewy bodies) in the neurons that survive. Clinical manifestations, which typically do not develop until the neuronal loss is advanced, include resting tremor, bradykinesia, rigidity and postural imbalance. The mechanisms leading to neuronal loss are not well understood, but mitochondrial dysfunction and oxidative stress are likely to have a role in the pathogenesis.
In the 1990s the UK regulators admitted that even the organophosphorus compound glyphosate "damaged the mitochondria at all dose levels tested" -
But they protected the chemical from re-appraisal and being banned and still do..."

For information on the multiple adverse health effects caused by mitochondria damage see here.

With Dementia, which they admit is a rapidly growing problem, and is now reported as the main cause of premature death, they simply call for more research.
But a telling statement indicates that this report was an attempt to hide poisoning by OPs for the foreseeable future.
Given the evidence that is now available, it seems unlikely that further research on neurophysiological, neuropsychological and psychiatric outcomes would identify any important hazard from low-level exposure to organophosphates. Research to explore the possibility of more subtle, minor effects would require rigorous assessment of exposure, and better methods for assessment of the health outcomes than are currently available .

Even though the researchers apparently find it impossible to confirm the chemical causes of the above symptoms they are not averse to finding very large sums of money in vain attempts to treat those symptoms.
Sadly unless the cause of these illnesses is removed from the environment the numbers of people suffering with cancers, neurological, cardio-respiratory, autoimmune and hormonal illnesses will simply grow exponentially.

In 2016 Her Majesty the Queen and the Duke of York opened a new research centre, the Francis Crick Institute in London.
The Crick building cost around £700 million to build.
Its annual budget is reported to be £130 million.
It is the biggest research building under one roof in the entire European Union employing some 1500 scientists and staff.
Those involved include the MRC, Cancer Research UK, Wellcome, University College London, Imperial College London and King's College London.
It is claimed to be "a world-leading centre of biomedical research and innovation, it has scale, vision and expertise to tackle the most challenging scientific questions underpinning health and disease.
The aim is to find new ways to prevent, diagnose and treat conditions such as cancer, heart disease and stroke, infections and neurodegenerative conditions like motor neurone disease.

As seen in the text above the cause of these illnesses is already well-known and has been known for a very long time but nothing is done to remove those causes.
Protecting the poisons industry seems to be the real aim.
Poisoned people earn the industry £millions in drug sales and research.
The Biochemistry is clear. The treatments are designed to target the same processes as those damaged by the chemicals which trigger the illnesses,
In most medicines very low doses of active ingredient are used, often at levels far below those found in the chemical exposures that trigger poisoning cases.

Why is the Medical Research Council now implying that it does not understand the ever present danger not only to the occupationally exposed but to everyone, adult, child and unborn, exposed as we are in our food, clothes, furniture, fuels paints, oils and our environment?

Dated 14/11/2016

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