28th October 2003
To Chemical Safety and Toxicology Branch ,Food Standards Agency
The COT report on the “Risk Assessment of Mixtures of Pesticides and Similar Substances” is reported to have concluded that “the probability of any human health hazard from exposure to mixtures (combined exposure), each present at a low level, is likely to be small and that effects of mixtures of substances are unlikely to be other than additive.”
Written records show that I used over 100 different pesticides, and other chemicals including veterinary medicines, resins and other toxins, and I have first-hand knowledge of the effects of mixtures. Since my submission to the COT study on risk assessments of the 2nd May 2001 proof was sent to me that my ill health was caused by just such a mixture, regarded by some as being at a “low dose”. This proves that one person’s idea of “low dose” is far from the same as another’s but that is only part of the problem.
This raises serious concerns as to the potential adverse effects of the chemicals in that mixture.
It should be noted that if Farmer A treats his grain with Actellc D, Farmer B treats his with Reldan and then they both send their grain to a central store, where the grain may be treated again, there will inevitably be a mixing of those two chemicals. It is therefore a disgrace that the regulatory authorities are obviously ignorant of the toxins produced by such mixtures. Safety is not assured.
In this one aspect alone the statement made by COT on the risk assessment of mixtures is incorrect.
I suggest that the deliberate adding of these pesticides to grain should be a priority for research and that research should be performed by individuals, who are completely independent of those who approved the chemicals for use, so as to avoid “research bias”.
In the COT report on the “Risk Assessment of Mixtures of Pesticides and Similar Substances” in section 1.5 it is stated that “There are no substantiated accounts of adverse reactions to such exposures except under laboratory conditions.”
In 1.6 of the report it was stated that ”of specific concern, include the anticholinesterase insecticides
(organophosphates and carbamates) and certain groups of fungicides, as well as a broad range of endocrine disruptors.”
It is beyond belief that despite evidence to the contrary the COT claim that there is uncertainty over the evidence but presumably this has resulted in the action plan, which will delay any preventative action.
Section 11.4 of the action plan states that “There are already restrictions on tank mixing of anticholinesterase compounds” but, as is seen above, the restrictions do not prevent the users acting outside of the regulations – and when they do no action is taken against them. In fact, as seems to be the normal approach, the HSE failed to find the unlawful action, even though they had been warned that it might have taken place. Instead of enforcing the regulations they attacked the victim, with full force.
In 11.5 it is suggested that the “PSD will take the lead” in the assessment of organophosphate exposures but it is they who refuse to address the issues raised above. Can we trust them?
11.7 states that “HSE will lead on non-food sources of exposure” and yet in almost every case I know the HSE has made every effort to avoid recognising any pesticide exposures. Their position in my case is that there was no exposure to OPs and yet there are written records proving daily exposures over decades, admitted by the employer, and there are further admissions to the exposure to the illegal mixture of OPs.
11.9. Research is suggested to “Develop methods to provide cost effective biomarkers of …exposure” but it is obvious to those of us who have attempted to have such biomarkers used that there is a reluctance to perform tests which would prove exposure.
In Annex A 11.3 it is again stated that it will be assumed that “chemicals with different toxic actions will act independently (simple dissimilar action)” but it is well known that one form of chemical can neutralize the detoxification processes for a different chemical, and that the effect of this action is to make the second chemical far more toxic to the exposed individual.
I am not at all sure how any “analysis of all sources of exposure to pesticides” can be made as suggested in 11.5 unless there is an enormous improvement in the monitoring of pesticide use and residues.
In 11.12 under the sub-heading “Research” it is stated that “Such work might include the identification of sites of action at molecular level, to identify those groups of compounds that would be expected to show simple similar action” and studies of protein and RNA and gene expression plus enzyme and hormonal activity are also suggested.
Section 1.14 of the “Risk Assessment of Mixtures of Pesticides and Similar Substances” states that “assessment of any toxic effects of chemical mixtures is extremely difficult.”
1.15 states “Direct chemical reactions can occur between the components of a mixture: there are relatively few studies of these substances that have investigated such reactions”.
1.17 that “Some interactions may not be easy to predict”
And 1.18 that “The type of combined action or interaction found at clearly toxic effect levels may not predict what will happen at non-toxic effect levels, including levels only slightly lower than the lowest observed adverse effect levels (LOAELs).”
In 3.4 “The interactive effects of mixtures has been known and indeed exploited for some time. Synergists have been important in the formulations of pesticides (particularly the synthetic pyrethroids) Although the regulatory authority is aware of the content of formulations, the presence of synergists is not always disclosed on the product label or in published documents on the active substance.”
3.8 admits, “Many chemicals including some pesticides are linked with hormone disrupting effects.”
In 3.9 “Guidance is needed on issues such as exposure, persistence, potency and potential availability in the human body”, which again admits knowledge gaps, and in 3.10 “Most of the anticholinesterase pesticides also have impacts on other enzyme systems.“
In 3.4 “These pesticides do not share a common mechanism of action, and human health implications of the effects observed in animals is unclear.“ Mechanisms not properly understood.
4.27 admits “Current UK and international assessments of pesticides do not routinely take any specific account of the risk to consumers from the potential for interaction of residues of different pesticides or to operators from the potential effects of simultaneous or sequential exposure to different active substances.”
“Fig 4.1 Flow diagram of the approvals process for pesticides in the UK” indicates a major problem with the way pesticides are approved. The chemical companies generate the data for the pesticides and no other body checks the accuracy of that data.
“4.19 Once a pesticide has been approved, it is important to check that its use does not give rise to
problems that were not foreseen when the approval was granted.“
Additionally the comment that “The HSE Pesticide Incidents Appraisal Panel (PIAP) aims to consider all incidents investigated by HSE and local authorities in which the use of pesticides may have affected a person’s health” is misleading since PIAP is part of the HSE and both have a poor record of investigation and acceptance of poisoning by pesticides. In my own case both HSE and PIAP refused to accept the facts of my exposure. Their deliberate misinformation was accepted at the highest levels, and has now been proven beyond doubt to be totally fabricated in order to hide the facts.
In 4.20 “it is therefore necessary to bring the data packages up to modern standards.
With Veterinary Medicines it is claimed that “4.34 As with pesticides, it is necessary to identify the toxic properties of the active ingredients” and yet as long ago as 1988 the VPC had to demand the withdrawal of Sheep Dips, which were already on the market, because they had not been properly tested for safety.
Under Risks the paper admits that “4.48 The most significant user safety risks are; accidental ingestion, self-injection, dermal, ocular, inhalational exposure and are often acute effects. Hypersensitivity reactions can be a problem with repeated exposure to sensitising chemicals. Multiple, repeated and/or frequent exposures are possible from occupational use e.g., veterinary staff and farm workers. Intimate and/or prolonged exposure is possible in the case of pet owners, particularly children.”
Under the heading of “Human Medicines” it is said that “The basis for risk assessment of human
pharmaceuticals is different from that for pesticides and human exposure to veterinary medicines as it is based upon balancing risk, including toxicological risk, against expected benefit. Combined exposure with pesticides and other substances is not normally considered.”
“Although known cases of synergism and potentiation are considerably less common than the other types of behaviour in mixed exposures, they are the most serious in their effects and require the most strict control. They are also the most difficult to assess and whenever there is reason to suspect such an interaction, specialist advice will be required.”
The pesticides residue surveillance programme is said to ensure that “no unexpected residues are occurring” and that “those residues do not exceed statutory maximum residue levels” but accidental excess applications of grain treating chemicals were never reported as being found, not even when such excesses were reported to the regulatory bodies. When Actellic Dust was approved for use there were repeated reports of excess applications, including whole bags accidentally dropped into grain stores.
The comment that “6.4 It is clear that an accurate measurement of the amount of a chemical to which a human is exposed is crucial in any study of the effects of chemicals on the human population” is of particular interest because there is evidence that those investigating poisoning by pesticides actually avoid using the correct procedures in order to deny any adverse effects. In my own case the tests used were those for the organochlorine, lindane, when in fact the correct procedure was for organophosphates.
In 7.16 the paper states incorrectly that ”as long as exposure is at a suitable margin below these NOAELs, consumers will be protected from the effects of any potential interactions that might occur within the mixture, providing there is an adequate margin of safety” but that assumes that it is possible to establish the true safety levels. It is not possible, because adverse effects on living tissues are created at much lower levels than those that cause observable adverse effects. For example only small changes are required to seriously disrupt hormone levels and those changes may not show as observable effects until the symptoms of hormone imbalance develop. Again, small changes in proteins are known to cause mutations, which can in turn trigger cancers. The development of some cancers takes a considerable time and there are many instances where individuals have never felt more healthy, with no obvious symptoms, when those life-threatening cancers have been detected by scans or screening.
It seems to me that this statement makes several assumptions of questionable accuracy.
(i) That the exposure levels “are likely to be small” when in reality the true exposure levels are unknown and most calculations are based on statistical theory and not actual measurements.
(ii) That the effects of those exposures “are likely to be small” and that such small changes do not indicate adverse health effects, even though very small effects can actually cause serious ill-health.
(iii) That the effects of mixtures are “unlikely to be other than additive” which is untrue.
In my case I was exposed to an illegal mixture of pesticides. The illegal use of pesticides in agriculture and horticulture is more common than the regulators might think, or hope. In fact one of two farmers locally who have been shown to be using pesticides unlawfully was fined some £250,000 for 11 breaches of pesticide regulation. The other escaped by giving the Health and Safety Executive false information.
I was exposed to an interesting mixture of Actellic D (pirimiphos methyl), Reldan 50 (chlorpyrifos methyl) and their solvents, Solvesso 100 and 1,1,-trichloroethane.
It is clear then that what happened to me might not be as unusual as might be thought but in my case this was a mixture of two organophosphorus chemicals, described as “illegal”, and condemned by both the chemical companies involved.
Claims that the breakdown products of these chemicals are “known” proved to be false but it is what happened after the exposure that is more worrying.
Because the poison badly affected my breathing – a problem acknowledged by the VMD in respect to OP sheep dips as long ago as the 1980’s – my GP treated me symptomatically with theophylline and erythromycin. This drug combination is known to be dangerous – even at low levels – but the former chemical is contraindicated in organophosphorus poisoning, giving a triple strength adverse effect.
No one knows whether or not this caused what has now developed but the results are very serious and should send warning signals to all those who are complacent about the dangers of chemical mixtures.
Some 7 years after the exposure medical experts in 1999 observed the worsening signs of serious neurological problems and peripheral neuropathy was confirmed earlier this year.
I am assured that no chemical is permitted for use in agriculture if it can cause peripheral neuropathy.
However transcripts of the Hill v Tomkins trial suggest serious doubts as to the potential to cause peripheral neuropathy for both pirimiphos methyl and chlorpyrifos, which is similar in most respects to the related compound chlorpyrifos methyl.
Furthermore it is possible that the breakdown products of both chemicals can be even more toxic than the parent chemical.
There are doubts therefore, despite official assurances, about each of these compounds alone but when mixed all sources contacted to date admit that nothing is known for certain although comments from scientists vary from “no additional effect” to “worse than Sarin”. Clearly, since it is officially admitted that my disability resulted from the exposure, some aspect of that mixture caused the peripheral neuropathy but when I approached the regulators they refused to answer my queries.
This hardly inspires confidence, especially since that refusal followed the issue of denials that some chemicals considered as potential breakdown products had ever been approved as active ingredients when in fact both those chemicals, about which denials were made, were listed by government in 1984.
There has been persistent misinformation and refusal to address the true toxicity of these chemicals.
Any cumulative risk assessments calculated on the basis of those assumptions will also be unsafe.
What is clear from the above is that if both chemicals were approved as being incapable of causing peripheral neuropathy, but in the mixture they have indeed caused that problem, then the mixing of the two has caused a more than additive toxic effect. Similarly, if the drugs used over such a short time after exposure worsened the effect of the exposure then they too had more than additive effects.
Whatever way this matter is examined it would seem that safety data is flawed, just as described in the above mentioned court hearing.
Urgent research should also include the other organophosphorus pesticides used on food crops, particularly glyphosate formulations, for which safety data is in doubt, as reported in earlier submissions.
Reports on the GM crop trials demonstrate that far from acting only on “amino acids found in plants” there are detrimental effects on insect and bird life, just as I reported long ago. This chemical has also been linked to a cause of Non-Hodgkin’s Lymphoma and from two scientific sources there has been experimental confirmation of the same neurological effects as other OPs via anticholinesterase action.
Why the regulators have attempted to deny these effects is a mystery, unless they are influenced by their desire to support the industry, no matter what the consequences to human health.
I wonder how the authors explain this comment given government advice as long ago as the 1970s, which warned workers who suffered adverse effects from one group of chemicals not to work with another group because of the known dangers to health.
How can there be “no substantiated accounts” when the VMD itself admitted in the 1980s that some parts of formulations enhanced the dangers of the active ingredients? It is obvious that phenols in one formulation could enhance the toxicity of OPs in another and some researchers state that the increase in toxicity could be as much as a thousand-fold.
These effects were and are employed by the formulators to enhance the effectiveness of their pesticides and yet those who regulate the industry were denying this basic fact. Why?
It has been known for decades that organophosphorus compounds interfere with the ADP/ATP energy transfer process within the body. Cyclic AMP is linked to that process and that in turn triggers hormone actions, and many other processes. As admitted many chemicals are endocrine disruptors in their own right and it has been known for half a century, that a slight imbalance in hormone levels can trigger serious effects on health. A combination of the actions of cAMP limiting OPs and chemicals with direct endocrine disrupting or hormone mimicking effects have the potential to cause more than additive effects.
Had the COT and the PSD/ACP/VPC etc acted on the reports of those who have suffered from the effects of these chemicals at an early stage much suffering could have been avoided.
I do not believe that it is an excuse to say that we are controlled or restrained by the EU, or the wider International community. Our regulators have a duty to protect those of us who live in the UK and if necessary they should have acted unilaterally when safety data was shown to be inadequate, or false.
Can we trust them to identify the chemicals for review – or will they protect industry again?
Can we trust them to properly assess the risks when they have had a history of denial of evidence?
The comment “Tank mixes are relevant to people exposed at the time of application, but not to residues in food as they do not differ from those arising from sequential applications” is also incorrect since experimental evidence demonstrates prolonged activity of commercial formulations extending for years beyond the claimed half-lives for the active ingredient. Therefore, as in the grain store chemical situation explained above, mixed chemicals will still be active, despite denials, and may be more than additive in effect, especially if residues of glyphosate are additionally present. I understand that researchers in this country have established firm evidence that glyphosate enhances the toxicity of other OP chemicals.
Despite that the HSE refuses to admit that they got things wildly wrong or to correct the records.
I for one will never be convinced that we can trust the HSE on any aspects of chemical safety.
Perhaps the regulators would be happy to use them for study purposes, provided the subject of the tests are unable to use them in court actions?
Certainly we are told that there are no tests for OP poisoning beyond cholinesterase testing and the measurement of metabolites in urine, both soon after exposure, but it is becoming obvious that a number of testing procedures could have been employed which would have proved exposure. The world- renowned expert Professor Abou-Donia, who gave the evidence mentioned in the Hill v Tomkins case, has just such a test which demonstrates damage to brain cells. Neurological tests are available which have shown damage to nerve function some years after exposure. Why are these tests denied to the exposed?
That action is far from “simple” and such interactions are well known in drug therapy. Since many pesticides have similar actions as medical preparations dangerous interactions must occur with pesticides.
It is difficult to understand why COT and other regulatory bodies have denied such actions take place.
More importantly recent correspondence suggests that those who monitor residues do not test for all the potential breakdown products of pesticides, some of which are admitted to be unknown.
If no checks are made on the records kept by pesticide users, and, if reports of unlawful use are never investigated, it will be impossible to obtain accurate residue and exposure data. Without that accurate information all recommendations will be no better than guesses based on unreliable information.
Interestingly it has been known for decades that the action of the organophosphorus compounds takes place at the phosphorus atom and yet the dangers of such actions on the vital metabolic processes have been ignored. Biologically important phosphate groups include sugars and phospholipids that are vital for cell membranes. Cholesterol the precursor for vital hormones is also dependent upon phosphate groups for both production and hormone activation. There are literally hundreds of phosphorus-dependant processes that are vital for life, and which are vulnerable to the organophosphorus group of pesticides.
Damage to any of these processes may cause long-term harm.
It is unlikely that a system damaged by this pesticide group will withstand attack from another group, and government papers confirmed that long ago.
It is inconceivable that influential Government groups such as COT and the PSD could be ignorant of these basic biological processes, or the risks to them posed by pesticides.
Could it be that the denials of knowledge are made for ulterior motives and not for the purpose of protecting public health?
If COT are not aware of the full formulations how can they be confident about mixing two or more together during and after application or in store? The synergists in one pesticide may greatly enhance the effects of the active ingredient in the other, producing unpredictable results, and as they write in 3.6 “two pesticides have entirely different mechanisms of mammalian toxicity, the mechanism of the combined action being enzyme induction.” One can destroy the enzyme processes that detoxify the other.
Given the admitted lack of knowledge how was it possible to suggest that risks are small?
Despite that, and the track record of poisonings and withdrawals of approvals through lack of sound data, the regulatory bodies still approve pesticides without any serious checks on the claims made by those who will profit from the sales.
My own experiments regarding the activity of stored diluted pesticide demonstrated that the official figures were massively understated and that insecticidal activity lasted for years instead the days quoted from chemical company figures. The length of time that chemicals remain actively toxic is vital when making exposure assessments. If it is assumed that an application would be inactive after days when in fact it remains active for months, or years, then all exposure figures will be increased proportionately.
This must also be taken into account when making calculations in respect to exposures to mixtures and repeated applications of different pesticides, as experienced by those living near regularly sprayed areas.
In the light of the doubts over the safety of chemicals mentioned in this submission this comment appears to overstate the safety protocol. This year many chemical approvals have been withdrawn but it must be asked if that action would have been taken if it were not for the order being imposed by Europe?
There has certainly been a determined effort in this country to ignore all reports of adverse effects.
This is achieved by programmes reviewing older compounds.“
When pirimiphos methyl was reviewed the PSD were aware of the errors regarding half-life and the data gaps regarding the potential to cause mutations but the chemical was still approved despite the doubts.
Likewise I requested that glyphosate should be reviewed because of its anticholinesterase properties but once again the PSD refused to include the chemical, suggesting that it did not have the property, but in 2001 further confirmation was obtained by science. Officials still deny the truth.
Most were reformulated with the phenols omitted but the doubts over the accuracy of the data remain.
Amazingly all these issues are denied when those poisoned by these chemicals report them to the authorities. Studies of exposure risks often ignore inhalation completely.
However it is vitally important for the health of those who have been exposed to pesticides that the treating doctors are aware of the drugs which may be contraindicated, and therefore enhance the actions of the poisons. These issues must be considered, as they are vitally important for the safety of human life.
Such actions are impossible to assess if the actual mixtures are unknown or the risks of known mixtures have never been assessed. In most cases approved mixes of pesticides are those using two or more products from the same manufacturer. The true potentials of other mixtures are largely unknown but when other factors for exposure, such as pesticide residues in foods and water, post application exposures, prescription drugs, solvents, glues, paints, and other industrial chemicals are involved, either in the work place, or by living in homes in pesticide spraying areas, the accurate assessment of risk is impossible.
To say otherwise is misleading and dangerous, especially for the sick, children, and pregnant mothers, but the denial of occupational poisoning in workers regularly exposed at work, and via the normal domestic routes, and who live within areas frequently sprayed, does not fit with reality and needs investigation.
Such accidental excesses would raise the residue levels many hundreds of times over the set MRL for the chemical and yet such excesses were never discovered in testing. Incredibly, despite the ban on the dust form, the chemical and others like it are still permitted for addition to food grains as liquid applications. There remains ample scope for excess dosing through bad calculations or poorly designed, calibrated, or maintained, equipment. It is unlikely that those excesses will be discovered either.
This failure to detect very high levels could be due to the small quantities tested.
A few grams taken from a couple of hundred loaves of varying type is an insignificant fraction of the total tonnage of wheat eaten every day in the UK. The samples are nowhere near representative.
Similarly, when the supermarkets were notified of illegal pesticide use locally, action was taken which exposed failure to adhere to pre-harvest intervals and the use of illegal pesticides, but none of those pesticides were found by any monitoring process, either government or supermarket.
If these high levels are not found doubt is cast over all subsequent safety claims and calculations.
Additionally, most residue testing is an “after the event” procedure and by the time the results are obtained any adverse health effects in the human population have already been triggered.
Worst-case scenarios should consider the implications of accidental or illegal pesticide excesses but what is obvious is that, apart from DDT and tecnazene metabolites, there is little or no testing for the chemical breakdown products, which could in fact be more dangerous than the original active ingredients.
Since many of the chemicals formed by mixtures and the breakdown of those mixtures are unknown then testing is impossible and any calculations based on the active ingredients will be useless.
This is important since the residues of the active ingredient found may be low only because the chemical has broken down post-treatment. The overall toxic potential of the residue of the active ingredients and those breakdown chemicals may be far greater than had the original chemical formed the entire residue.
It is of interest that no lindane was found even though it is known to be present in people who have never used the chemical and I had used various forms of the chemical regularly over decades.
Assessing human exposure requires honesty and the correct use of available testing procedures but as in 7.2 “It is clear that, because of the complexity and variability of chemical mixtures that may occur in the environment, risk assessment of their potential toxic effects is an extremely difficult task.”
The question that must be asked therefore is how can anyone be certain that the risk of harm is low, especially if the chemicals involved have suffered breakdown into more toxic compounds?
I suggest that the NOAEL system does not indicate safety. It merely indicates a point in the exposure curve indicating toxic effects, which do not result in observable symptoms. In fact when the exposure curve and the adverse effect curve meet at the point where symptoms are observable it is likely that even if all exposures are stopped the adverse effect curve will show increasing effects from the toxins.
The risks are increased if the exposure follows others, raising the entry point on the effects curve, or, if the exposed person already has sub-clinical symptoms as the result of disease or illness, in which case lower exposures are required to reach critical effect points.
Two or more additive exposures will also bring forward those critical points, as will cumulative effects.
It is not possible to honestly argue against the effects as described above since it is known that with repeated exposures to organophosphorus compounds, for example, there is considerable danger of acute symptoms developing if the exposed person is re-exposed before the enzyme levels have recovered.
Nor can anyone claim that we are not continuously exposed to these pesticides since they are in our food, our water, and the environment. If, as seems to be the case, the pesticide formulations maintain persistent activity long after the claimed half-lives, then the potential for repeated and cumulative exposure is greater than has been assumed by those responsible for calculations based on assumed short half-lives.
Figure 2 below is an attempt to illustrate that it is wrong to suggest that the calculations for life time exposure ensure safety, as official figures suggest. In reality large sections of the population are exposed even before they are born as the result of their mothers’ regular intake of toxins in food, water, and in the environment. Each of us therefore begins life with low-level damage caused by those toxins.
We then accumulate the effects of thousands of chemicals throughout our lifetime. In fact those over retirement age are likely to be receiving higher exposures than they did in their youth and it is probable that their exposures now put them at the level where some of their symptoms are due to the toxins.
Those occupationally exposed, and others repeatedly exposed, will be at greater risk since their exposures are in addition to those in the general population. Each new exposure is likely to come before the last has been resolved and, as time passes, ever-lower levels of exposure will exceed the critical levels at which symptoms will show. Unless there have been serious high-dose acute effects such exposures are likely to trigger symptoms during the ages of 40 years onwards with the peak being in the 50 to 60 year age bracket. After that time illness or retirement will reduce the risk of higher than average exposures but the overall body burden will still be greater than that of the general population and early death is likely.
It is easy to see how the critical levels will be reached if the warnings of adverse health effects are not headed by those in the 40 to 50 year age group who must reduce their exposures to remain in the “safe(r) zone” below the observable effect level. If they continue to be exposed at the levels they could tolerate at a younger age they will show symptoms and require medical treatment to maintain life.
As the Government has admitted for decades by Act of Parliament “The neuro behavioural symptoms of late organo-phosphorus poisoning are common in the unpoisoned population.”
It is difficult to know how those who wrote that managed to determine this “unpoisoned” group since everyone is exposed to some degree and there are no known levels at which no adverse effects take place.
Although it is claimed that the effects of organophosphates, for example, decline in time there is evidence to show that the damage caused in the meantime is not reversible, leading to irreversible and lasting harm.
It is possible that the exposures to these chemical toxins may themselves corrupt the processes of enzyme regeneration. More importantly it is admitted that “7.25 The precise mechanisms of interactions between constituents of mixtures, in most cases, are not known.”
The reported effects are often denied, even when there is officially recognised documentary evidence in support of links between ill health and such mixtures.
This is the case where the document states that “8.9 Very few reports were identified regarding toxic effects on the respiratory system of mixtures containing pesticides.”
Interestingly in its review of the use of phenols in OP Sheep Dips the VPC admitted as long ago as 1988 that those with respiratory problems should not use such chemicals because they would be at risk from the muscarinic effects of the OPs. They ordered that the Sheep Dips should be withdrawn or reformulated demonstrating that the knowledge of the respiratory risks from such mixtures was admitted even then.
Once sensitised, very low levels of the triggering chemicals are required to cause serious adverse effects, as was seen in the documentary on the asthma deaths in Barcelona, which were eventually put down to the unloading of soya from ships in the docks. This was supported by the COT mixtures report statement that “The levels of exposure required for the effective acquisition of sensitisation (induction) and for the subsequent provocation of an allergic reaction in a previously sensitised subject (elicitation), may be very different. The view is that, in most cases, the amount of chemical required for sensitisation is greater than that required for the elicitation of an allergic reaction in sensitised individuals.”
Again this demonstrates that those already exposed may then be susceptible to very low doses and that those in areas regularly sprayed may be at or just below the danger levels because of the constant exposure to repeated doses of various mixed pesticides and their co-formulants.
In 1998 The USA publication “Overexposed – Organophosphate Insecticides in Children’s Food” referred to the dangers of cumulative exposures to a variety of OP compounds in the diet. All pesticides were at or below their own set maximum residue limits but taken collectively they massively exceeded the recommended maximum intakes of OPs for humans. The paper called for an immediate ban on OPs.
A PSD contact at the time referred to that paper as “a challenging document” but no action was taken.
Perhaps the challenge was in fact how to avoid taking action despite the powerful arguments presented?
Those who promote the view that there is no real risk from mixtures of pesticides should read the European Environment Agency publication “Late lessons from early warnings: the precautionary principle 1896-2000” in which they will see that scientists forged ahead with confident predictions of safety in numerous areas of interest, only to be proven dangerously wrong in the fullness of time.
I have no doubt that the failure to prevent exposures to mixtures of dangerous pesticides will be seen as another momentous error which will have caused suffering to countless numbers of innocent people.
I hope that honest and independent research will be done to establish a knowledge base of the real and increasing risks, and that action will be taken to eliminate the dangers.
Although many Universities are now linked to chemical and drug companies for their funding or equipment it must be possible to find a way to employ their facilities as part of the education process to assist the authorities in the study of pesticide mixtures and their effects. Samples could be taken from the farms or horticultural sectors so that there is real independence from the chemical companies and a true representation of the types of chemicals used in the field.
The effects of treated tap water on diluted chemical mixtures could also be assessed, instead of relying on experiments using almost pure water, as used by the chemical companies in their studies.
It was not possible for me to obtain straight answers from the PSD on the effects of fluoride and chlorine in the tap water used to dilute agricultural pesticides for spraying.
Again it seems that chemical company data is accepted as accurate and apparently never checked.
Further evidence in support of this view has come this year with the withdrawal by the EU regulators of a large percentage of the active ingredients, said to have been considered and approved as “safe” when in reality there was insufficient data to support those claims.
Even when all those chemicals were withdrawn the EU then added to the list when it ordered the withdrawal of Atrazine long after concerns were first raised about the dangers of the chemical.
Interestingly one of the chemicals banned was Actellic Dust but the use of the liquid form, Actellic D, as an undeclared food additive continues, despite reported safety concerns, including failures of the Ames Test by mutation of Salmonella typhimurium, and evidence of irreversible brain damage in rats, in tests performed almost 30 years ago. Oddly, given the evidence, the deadly paraquat also escaped the ban.
If those responsible cannot get things right in regard to single pesticides how can they be trusted with the largely unknown effects of mixtures?
This situation must not continue. The decision making process must be made more open and accessible.
A good starting point would be to revisit all the cases of reported poisoning, including those denied by PIAP, the VMD, and the Poisons Units, in order to get accurate data on the effects of these chemicals.
Currently there appears to be no follow-up at all on these cases and so the long-term effects are not known. Often the victims are abandoned to their fate by the medical profession who offer no or inappropriate treatments, often implying mental illness. Certainly many of the pesticides used and involved in these poisoning cases are known to cause serious and irreversible brain damage but it is insulting in the extreme to imply that the sufferers are mentally ill. In fact many of the antidepressants prescribed to these people are known to seriously worsen their symptoms – as described by experts for the defendants in the Hill v Tomkins case. By prescribing inappropriate drugs the medical profession could be causing the very mental problems they then use as an excuse to deny poisoning. This is disgraceful.
As I have suggested in the past I believe that there should be a major change in the way chemical poisonings are reported, treated, and processed.
There is no doubt that all reports of illness with suspected pesticide involvement should be recorded, whether recognised or not, so that early trends can be spotted before too many people are harmed. In this way if a chemical is implicated in an unusually high number of pesticide poisoning complaints it will be seen as a potential for further problems, enabling the authorities to keep a closer watch over its use and safety. This early warning system should be reinforced by a second record of cases that have a strong link to those pesticide exposures and if any confirmed cases are found then those pesticides listed as having caused poisoning should be carefully reviewed and withdrawn from the market as soon as possible.
I believe that the recent changes to the reporting system, in which all cases of suspected adverse reactions must be reported to the chemical companies, is a retrograde step, and it is dangerous.
We need independent assessments of incidents. There are already too many close links to the industry but at least there was a middle line, which supposedly added a layer of protection from false reporting.
The public pays for, and expects to be protected by, the approval and regulatory systems.
The failures of those systems are becoming increasingly evident as the cost of the process increases.
Could we please have a rapid return to honest, and accurate, independent science, which has as its first priority the safety of the health of users and consumers and not the profit of industry?
Dated 28/10/2003 Updated 29/10/2005
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