Comments on the COT Report on Organophosphates

Part 1. The first six comments on the COT Report and replies.

30th November 1999, the reply of 24th January 2000 and the response of 25th January 2000

The Working Party has produced an unprincipled document in its attempts to escape criticism for the failure of its members to protect the health of our people. The evidence is presented before you in their own document but the reason why such a disgrace l report was ever issued is much more worrying.

There are several important questions which are raised by the Document.

1. Why does the Working Group profess to have incomplete knowledge of toxicological processes 8.2 when the group is made up of the Chairman and members p252 of the Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment which by definition should be expert in toxic reactions?
They were, after all, responsible for attempting to ban B6 and as such must have understood biological processes other than those involving cholinesterase. I seem to recall that questions were asked then too?
The concerns that led to the establishment of the COT Working Group related primarily to the possibility that OPs reduced(sic) chronic neurotoxicity following exposure to low levels ie below those producing overt toxicity. The composition of the Working Group was chosen to enable a detailed assessment to be made of the scientific evidence for such effects in humans. Thus it included experts in clinical neurology, clinical neurophysiology and neuropsychology together with 3 experts in epidemiology. The work of the Group related to class effects of OPs (ie effects due to a common mechanism) rather than compound specific effects. the latter are being covered in the ongoing comprehensive reviews of all compounds acting by inhibition of cholinesterase activity by the regulatory Authorities concerned with pesticides and veterinary medicines.
It is pertinent that the bulk of the published scientific data concerning class effects of OPs related to neurotoxic effects. In addition this was the type of illness most frequently of concern to those who made submissions to the Group. A search of the scientific literature revealed little evidence of other class effects of OPs. To cover all other areas in depth would have significantly delayed completion of the COT Report and was not felt warranted.
Point 1. While the effects of individual OPs may be slightly different it is clear that they have common ancestry and all have adverse effects on life at the atomic level. I suspect that the authorities restrict studies to the anticholinesterase action because they are aware that there is no safe level as regards action on the other vital enzyme processes upon which our lives depend. This is perhaps why studies on the neurotoxic effects have become the bulk of the technical data but it misses the real problem - I suspect this is intentional.
Although "not warranted" such investigation was vital but there was no need for delay. The information is readily available even to the likes of me. Those who wish to see it can do so easily.

2. Why did the Working Group claim that insufficient evidence existed to enable them to determine how OP pesticides and medicines might adversely affect the long-term health of individuals? 9.6 They admit that the processes which they refused to consider could cause long term damage5.21 and they admit that such conditions as OPIDN are recognised long-term 5.8 health effects which follow exposure.
They were aware of MS17 and PDC3 which are Government papers of long standing which recognise that long-term damage may follow single or repeated low-dose exposures and warn of the dangers.p25
They were aware of the Hong-Kong case p11 which confirmed in British Law that the dangers of exposures, even via a single episode of inhalation, were known and recognised as resulting in long-term injury.
Their "Blood-brain barrier" 41 is easily permeated by lipophillic OPs and the CNS toxic a narcotic solvents.d
They knew that the basic toxic information is to be found in standard text books which will clearly show to anyone who understands the action of OPs that a wide range of adverse effects can result from exposure.
The Working Group recognised that there were a number of limitations in the available data, and they could not exclude the possibility that at least some of the illnesses that were described to them as following low level exposure to OPs were indeed a manifestation of toxicity (para 8-11). It was for this reason that they recommended that further research be carried out to address those outstanding issues.
Point 2. Further research is therefore unnecessary. The work has already been done which is why papers such as the Industrial Injuries Acts have recognised the dangers for decades.
The only outstanding issue is the question asking why top scientists deliberately ignore the obvious.

3. Why did the Working Group restrict its deliberations to individuals who were exposed but still able to work?7.29 They knew that many of us had evidence of our physical ill-health and cognitive changes and that those changes had left those of us who survive to tell the tale unable to work. They knew that other departments within Government had cause to hide these truths and perhaps that is why we were ignored? Certainly the claim that no supporting medical evidence exists is not true in several cases.
As you know the Working Group sought information from as wide a range of sources as possible in addition to the information available in the scientific literature. They were faced however with a major problem relating to the data available. This is discussed in Chapter 6 of the Report and particularly in the conclusions to this section. The Group recognised the distressing illness reported by many sufferers, but noted that few had long term medical observations or results of tests to present with their accounts. Similar the data available from the various adverse reactions scheme, or the NPIS, was of very limited value in terms of the remit of the Group, namely does low level exposure to OPs produce chronic neurotoxic effects.
In order to draw definite conclusions regarding the above, the Group considered the results of a very comprehensive literature search of published scientific data. in addition the results of the COM epidemiology study published in July 1999 were considered. The Group identified 27 reports as being most informative to their remit and these were considered in depth. Reasons why the other studies were considered less important were also given.
One of the limitations of the available data was that the epidemiology studies essentially all involved working populations. It was not the case that the Group restricted deliberations to individuals at work. A comprehensive search of the literature did not find any studies that had followed-up populations after leaving work. This limitationwas highlighted in the conclusions of the Report, and was an area addressed in their recommendations for further research.
Response Many of the victims who gave evidence to the Working Group did so because they had been notified of the call for information. My understanding is that the call for submissions was made only through an advert in the BMJ which would have succeeded in preventing sufferers bypassing the screening system for information.
The admission that the information from the Poisons Units was of limited help is proof enough that the DoH is failing in its duty to properly monitor the effects of chemicals on human health. Low level exposure which results in ill-health would be missed by the units because few GPs would relate the symptoms presented to chemical toxicity. First because of the delay in onset of symptoms, second because GPs are not properly trained to recognise them and third because when they do refer to the Poisons Units the commercial and Governmental pressures to hide the truth over-ride both clinical need and Patient Rights.
Epidemiological studies become flawed and follow-up studies are not performed for the same reasons.

4. Why did they repeat the claims by the National Poisons Information Service that only 6.9 asymptomatic cases or those suffering only mild transient effects had been referred? They knew very well from my own submissions that this was not a true representation of the facts. My own case was referred because the symptoms were persistent and certainly not mild. At least another six serious cases were reported as being referred at the same time. Asymptomatic is an interesting term because many of the symptoms of poisoning are those detected by doctors and of which the patient may not be aware.
Many of those symptoms such as high blood pressure, cardiac abnormalities, respiratory restriction, visual disturbance, hormone imbalance and diabetes are neither transient nor mild. Referral is through doctors.
The information available to the group from the NPIS indicated that nearly all cases arising from dermal or inhalation exposure to OPs involved at most mild transient symptoms. However the report recognised the limitations os such data and the fact that follow up data were available only in a few cases.
Point 4. The dangers of both dermal and inhalation exposures to OPs are well documented in Government papers. COT should not have required further evidence to show the dangers when the risk to those regularly exposed to OPs from further small doses was already known to science.

5. Why was it suggested that the OP poisoned patients "over-report" their symptoms? 215, 112(iv), 208 It is clear from their own document that OPs can effect multiple organs within the body and as such the patient will obviously present with a wide range of symptoms depending on which organ or organs in the body are most affected. Reference books list a wide variety of symptoms as attributable to OP poisoning.
It is arrogant and unscientific to make unfounded observations in respect to the symptoms reported.
The COT Report does not state that OP poisoned patioents over-report their symptoms. In the section on limitations of epidemiology reference is made (112 iv) to the possibility of bias due to subjects knowledge of exposure (but there is no mention of which direction this might apply). This is accepted by epidemiologists as an important factor to be considered when assessing studies. Similary in the critique of the IOM study the comment is made that there is a tendency for mildy anxious or depressed individuals to complain of neurological symptoms more readily and that the association may, in part, reflect this. It was not mentioned in the main text of the report.
Point 5. I suspect that the only bias in the reporting of symptoms is found in the corridors of the MRC where the preferred line is to pronounce that exposed groups over report. Referring to papers from that source assumes that COT agrees with such biased opinions. Poisoners throughout history have attempted to convince their victims that the symptoms they face are imaginary. I carefully studied the report and provided reference points. I would have thought the COT and MRC were above such comment. I was obviously wrong.

6. Who suggested that Post-Traumatic Stress disorder played a part in the symptomology? 5.20 The users of pesticides are not at war or suffering the effects of a sudden shocking or physically disfiguring catastrophe. They are normally relaxed in the work they know until the symptoms develop. Then they find their GP will suggest the symptoms are transient and he may even offer drugs which make matters worse.
Only then does the patient discover the real cause of his illness and by then it is too late. I suggest that each and every one of the OP sufferers reporting to the Poisons Units never believed for one moment that the chemicals could make them feel so ill. Only when further exposures prove the case do they make efforts to avoid the chemicals but by then it is too late because they have become almost unavoidable.
The trauma, if there is one, only occurs when Government backed officials attempt to hide the truth.
In the section on other punitive mechanisms for long term effects following acute poisoning the Group mentioned that psychological stress following an acute poisoning episodes could trigger psychiatric illness such as post-traumatic stress disorder. It was only listed as a possibility, and this was in the context of the sequelae of acute poisoning.
Point 6. I suggest that COT reads Government papers. After an acute phase of poisoning, not necessarily requiring hospitalisation, the victim is left vulnerable to further exposures, no matter how small. I note with interest that the COT Working Party did not cover this subject in the detail required.


p Page number in the COT Report
1.1 Numbers represent numbered paragraphs as published in the COT Report.

a Notes on the Diagnosis of Prescribed Diseases Dept of Social Security 1992
b New Scientist 27/5/1995 "Just obeying orders" Stephen Day.
c Encyclopaedia Britannica 1959 edition.
d Penguin Dictionary of Biology. Thain and Hickman1996
e HSE prosecution of former Government advisor for illegal pesticide use resulting in food contamination with illegal types and levels of pesticides. Injuries to human health, with evidence, were ignored.
f Mechanisms of Joint Neurotoxicity of n-Hexane, Methyl Isobutyl Keytoneand O-Ethyl O-4-Nitrophenyl Phenylphosphonothiate in Hens. Abou-Donia et al 1991
g Letter to PSD 11th May 1999.

Dated 16/9/2000

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