#OpYeshua – Roman Catholic deputy head Peter Allott jailed for 3 months for paedophile drug parties

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Cambridge-educated deputy head of £15,000-a-year Catholic private school who blew £600 a week on paedophile drug parties is jailed for horrific stash of porn images featuring children as young as two

  • Peter Allott, 37, led a double life working as a devout Christian headteacher
  • At weekends, deputy head indulged in drug-fuelled paedophile sex orgies
  • Became addicted to child sex images and MDMA at £600 ‘chemsex’ parties
  • Amassed nearly 400 horrific images of children as young as two on iPhone
  • He worked at £15,000-a-year school in London but now jailed for 33 months
Peter Allott, 37, deputy head of the £15,000-a-year St Benedict's School in Ealing, west London, became addicted to child sex images and Class A drugs after being introduced to both at 'chemsex' parties

Peter Allott, 37, deputy head of the £15,000-a-year St Benedict’s School in Ealing, west London, became addicted to child sex images and Class A drugs after being introduced to both at ‘chemsex’ parties

The deputy head of a scandal-hit Catholic private school was jailed today after admitting getting hooked on child pornography blowing £600 a week on paedophile drug parties.

Peter Allott, 37, led a double life working as a high-flying devout Christian headteacher, while at the weekends he indulged in drug-fuelled sex orgies, swapping sickening images of children with other perverts.

The Cambridge–educated deputy headteacher became addicted to child sex images and Class A drugs after being introduced to both at ‘chemsex’ parties organised on gay dating app Grindr.

He amassed nearly 400 horrific images of children as young as two, which he kept on his iPhone and on a hard drive in his office at the £15,000-a-year St Benedict’s School.

Investigators also found the Class A drug MDMA, otherwise known as ecstasy, in a raid of his home, a property owned by the school.

The private school in Ealing, West London, which counts comedian Julian Clary, Tory peer Chris Patten and actor Andy Serkis amongst its alumni, has been dogged by scandal after one teacher was convicted of nearly four decades of sexual abuse of children and another priest is still on the run from a child abuse charge.

The school and its linked Benedictine monastery, Ealing Abbey, was condemned four years ago for a ‘lengthy and cumulative failure’ to protect pupils in its care from child abuse.

The scandal, which did not involve Allott, led to five monks and three former teachers being linked to child abuse.

Although Allott was working at the school at the time of the abuse, investigators do not believe he abused any children in his care.

Blackfriars Crown Court heard how the former Tory councillor, who served on the Perivale ward from 2006-2010, fooled parents with his devout Christian public persona, while in private he indulged in drug-fuelled orgies with other perverts.

Jailing Allott for 33 months, Judge Peter Hillen said: ‘You are someone who has degrees and Master’s degrees and studying for a doctorate.

‘Someone who had early ambitions to enter the church and then education, who rose to be a deputy head of a prestigious school.

‘Someone who has engaged in public service and political service. Someone who has engaged in charity work. Someone who was a high flyer.

‘All of that has been destroyed and is fully in ruins by what, in the words of your own counsel, was an addiction to debauchery.

‘Two years after you sadly lost your mother and shortly after the death of your grandmother, you started to seek relief from your grief in chemsex parties, talking to other potential sexual partners on the Grindr networking site and meeting them, using Class A drugs, crystal meth and M-Cat, then engaging in sexual activity.

The Cambridge¿educated deputy head became addicted to child sex images and Class A drugs after being introduced to both at 'chemsex' parties. He amassed nearly 400 horrific images of children as young as two, which he kept on his iPhone and on a hard drive in his office at the £15,000-a-year St Benedict's School (above)

The Cambridge–educated deputy head became addicted to child sex images and Class A drugs after being introduced to both at ‘chemsex’ parties. He amassed nearly 400 horrific images of children as young as two, which he kept on his iPhone and on a hard drive in his office at the £15,000-a-year St Benedict’s School (above)

‘It was at the drug parties that you became aware of, and addicted to, indecent images of children. I use the phrase of a paedophile ring, that’s precisely what that was.

‘You were leading in effect a double life that over the weekends you would engage in chemsex parties using crystal meth and M-Cat and having sex with multiple partners but also watch these images.

‘Then on Monday morning you would put on your suit and you would be the brilliant, high-flying deputy headmaster doing your public duty and your work for society.

‘A split personality, the devoted life on one side but the bespectacled deputy head master was a lie because the other side of your life was one of debauchery.’

Bespectacled Allott sat quietly with his lip trembling as the court heard of his two-years of paedophilia.

When detectives from the National Crime Agency’s specialist child abuse team arrested Allott in December last year, they found nearly 700 illegal images and videos of children and extreme pornography.

You were leading in effect a double life that over the weekends you would engage in chemsex parties and then on Monday morning you would put on your suit and be the brilliant, high-flying deputy headteacher
Judge Peter Hillen

Michael Shaw, for the prosecution, said: ‘He found himself in a spiral of addiction to drugs and took part in ‘chemsex’ parties whereby he would binge on drugs at the weekend and engage in viewing these images with likeminded individuals.’

Mr Shaw said when Allott was asked about the fate of the children in the images, he said: ‘I would be surprised if some of them were still alive.’

Allott admitted possessing 25 ‘grossly offensive’ images on a hard drive and sharing the images with other offenders. He also pleaded guilty to possession of drugs.

In mitigation, Daniel Taylor said Allott offended after losing his mother to cancer and then his grandmother.

A spokesman for the school said the community was ‘shocked’ by the former deputy head’s offending.

Allott, who taught there from 2004 and was promoted to deputy head in 2012, often defended the school’s legacy, assuring prospective parents touring the school that the culture of child abuse had been eradicated.

Father David Pearce, the former head of the junior school, was jailed for eight years in 2009 after being convicted of abusing five boys over a period of 36 years.

Another former abbot, Father Laurence Soper, jumped bail before he could be charged with child abuse offences and remains on the run.

A spokesman for the school said: ‘St Benedict’s has been shocked and saddened by the offences committed by Mr Allott. He has already resigned and will not be returning to it.

‘We would reiterate that there remains no evidence any pornographic material was found on school computers or that any other members of the school community have been involved in or exposed to the material Mr Allott was using.’

Source: http://www.dailymail.co.uk/news/article-3575806/Cambridge-educated-deputy-head-15-000-year-Catholic-private-school-blew-600-week-paedophile-drug-parties-jailed-horrific-stash-porn-images-featuring-children-young-two.html

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#OpMurderForHire – Cooking with vegetable oil increases the risk of heart disease, type 2 diabetes & cancer

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The toxic truth about vegetable oil: Cooking with ‘healthy’ fats increases the risk of heart disease, type 2 diabetes and cancer

  • Dr Aseem Malhotra is a consultant cardiologist, advisor on the National Obesity Forum and contributor to the Hippocratic Post
  • Cooking vegetable oils at high temperatures changes chemical compounds
  • Studies found it can produce potentially harmful levels of adelhyde
  • Experts: Dairy products and olive oil are more beneficial to heart health 

When I go to my local curry restaurant, I always ask the waiter to make sure my chicken jalfrezi, spinach curry and lentil daal is cooked in ghee, not vegetable oil.

They know me now so I don’t get rolling eyes and shrugs any more.

It helps that I leave a generous tip. But it’s worth it.

As a cardiologist with an interest in obesity and heart health, there is no way I am going to put my health at risk by eating poisonous compounds that are created when vegetable oils are cooked at high heat.

When Dr Aseem Malhotra orders a lentil daal (pictured), he insists it is cooked in ghee, not vegetable oil. This is because vegetable oils can produce dangerous chemical compounds when cooked at high temperatures

When Dr Aseem Malhotra orders a lentil daal (pictured), he insists it is cooked in ghee, not vegetable oil. This is because vegetable oils can produce dangerous chemical compounds when cooked at high temperatures

Unfortunately, curry lovers in the UK, and the vast majority of Indians on the subcontinent are doing just that – they have abandoned traditional ghee (a kind of clarified butter) in favour of ‘healthier’ vegetable oils.

The outcome of this trend has been disastrous – driving higher rates of heart disease, type 2 diabetes and cancer.

GOLDEN RULES FOR SAFE COOKING

So what can you do to minimise any potentially harmful effects?

Professor Martin Grootveld, works in bio-analytical chemistry at De Montfort University in Leicester, came up with the following tips.

  • Cut down on frying, particularly at high temperatures or above the so-called ‘smoke point’. If you are frying, minimise the amount of oil you use.
  • To reduce production of harmful aldehydes, go for a product high in mono or saturated fat (preferably greater than 60 per cent) and low in polyunsaturates (less than 20 per cent).
  • The ideal compromise for cooking purposes is olive oil ‘because it is about 76 per cent monunsaturates, 14 per cent saturates and 10 per cent polyunsaturates’.
  • If cooking, there is no health benefit paying extra for extra virgin olive oil.
  • In view of its high saturate content, coconut oil is also recommended.
  • Always keep your oils in a cupboard, out of the light, and try not to reuse oils because that leads to the accumulation of nasty side products.

Studies now show that sunflower oil, corn oil and other vegetable oils are unstable at high temperature and quickly break down into toxic adelhyde which is linked to an increased risk of developing getting cancer among other things.

A recent study showed that cooking in vegetable oil for just 20 minutes, produced 20 times the permitted levels of adelhyde recommended as a maximum limit by the World Health Organisation.

When I see someone who is otherwise healthy frying healthy kale and tofu in sunflower oil, I despair how good intentions can go so wrong.

For years, we have thought that vegetable oils, including sunflower oil and corn oil, were better than butter and animal based fats.

But the tide of opinion has changed and the latest scientific evidence reveals that dairy products actually protect against heart disease and type 2 diabetes.

Sadly, the news has come too late for the millions of people who now shun full-fat milk and butter because they think it is bad for them.

I now always advise my patients to actively avoid eating any industrial vegetable oils.

Cold pressed extra virgin olive oil however will protect your heart and give you a bit of a boost when it comes to antioxidants which help to mop up damaging free radicals in the blood.

But the vast majority of vegetable oils are not going to help, despite claims that they help reduce cholesterol.

A recent BMJ analysis found that even if cholesterol levels do decline on a diet of vegetable oil margarines, there is no knock-on benefit to heart health and a more worrying trend to increasing the risk of death.

So my message is drizzle your cold pressed olive oil on your chorizo to your (healthy) heart’s content but stick to butter (and ghee) when you want to create a bit of a sizzle.

This article has been reproduced with the permission of The Hippocratic Post

WHY COOKING OIL AT HIGH TEMPERATURES CAN STOP THEM BEING ‘HEALTHY’ – By Michael Mosley

The problem is that when fats and oils are heated they change, and as they do so they produce chemicals that may cause heart disease and cancer.

Take olive oil, for example, championed by so many as the reason why the lucky folk of the Mediterranean live such long, healthy lives.

When fats and oils are heated they change, and as they do so they produce chemicals that may cause heart disease and cancer

When fats and oils are heated they change, and as they do so they produce chemicals that may cause heart disease and cancer

This has a lower ‘smoke point’ – the point at which an oil begins to smoke and change – than some other oils, meaning it will start to alter more quickly.

As olive oil heats up and reaches its smoke point, the beneficial compounds start to degrade, and potentially health-harming compounds form.

At least, that was the accepted theory before we began our research – that the lower the smoke point, the more dangerous the oil as the more quickly it will start producing harmful chemicals when heated.

The dangers of turning up the heat

It is this assumption that has consistently seen health experts warn people not to cook with olive oil and advise that vegetable and sunflower oil are safer for cooking as they have a higher smoke point, so can resist greater heat without producing cancer-causing agents.

That point is 225c for sunflower oil and 230c for corn oil, compared to 160c to 190c for extra virgin olive oil.

A study found that cooking fats at high temperaturesleads to oxidation - they react with oxygen in the air to form substances such as aldehydes and lipid peroxides - linked to heart disease and cancer

A study found that cooking fats at high temperaturesleads to oxidation – they react with oxygen in the air to form substances such as aldehydes and lipid peroxides – linked to heart disease and cancer

That was the theory when we began our research.

To test it out we asked some volunteers, local residents in Leicester, to use a variety of fats and oils, provided by us, in their everyday cooking.

The volunteers were asked to collect any leftover oil after cooking, which we would then have analysed.

They were given sunflower oil, vegetable oil, corn oil, cold-pressed rapeseed oil, olive oil (refined and extra virgin), butter, goose fat and lard.

Samples were then sent to De Montfort University in Leicester, where Martin Grootveld, professor of bio-analytical chemistry and chemical pathology, got to work in the lab analysing their contents.

His team also ran a parallel experiment where they heated up these oils and fats to frying temperatures.

The findings were surprising, to say the least.

Indeed, for many who have followed traditional advice on cooking with oils and fats it will prove to be a case of ‘everything you think you know is wrong’.

What about olive oil?

Cooking with olive oil could be better than was previously thought, a study found

Cooking with olive oil could be better than was previously thought, a study found

Is cooking with olive oil a no-no? Not according to Professor Grootveld.

In fact, it is, on balance, unquestionably the best compromise.

Sunflower oil, supposedly the healthier alternative, is far worse. Even lard, so demonised it has entered common usage as an insult, is preferable to sunflower oil and its closely related cousin, corn oil.

To understand why, we must look closely at what happens to fats and oils when heated to a high temperature.

They undergo what is called oxidation: they react with oxygen in the air to form substances such as aldehydes and lipid peroxides. At room temperature something similar happens, though more slowly.

When fats go rancid they have been oxidised, and it results in the same by-products. It is these aldehydes they form that are the problem.

Consuming or inhaling them, even in small amounts, has been linked to increased risk of cancer and heart disease.

‘We found that oils which were polyunsaturated-rich – corn oil and sunflower oil – generated very high levels of aldehydes,’ Professor Grootveld told me.

This surprised me. Like so many others, I had always thought of sunflower oil as being healthy.

‘Sunflower and corn oil are fine, but only as long as you don’t subject them to heat, such as frying or cooking,’ said Professor Grootveld.

‘It’s a simple chemical fact that something which is thought to be healthy for us is converted into something that is unhealthy at frying temperatures.’

Aldehydes, which are known promoters of cancer, heart disease and dementia when eaten or inhaled, were present in levels up to 20 times higher than recommended by the World Health Organisation.

Not only that, but Professor Grootveld’s team also identified two previously unknown aldehydes in the samples of these oils – a world first and cause of some excitement for scientists, but bad news for consumers.

Cooking with sunflower oil and corn oil was found to produce even more toxic compounds than ever before

Cooking with sunflower oil and corn oil was found to produce even more toxic compounds than ever before

Put simply, cooking with these oils is producing even more toxic compounds than has ever before been realised. In contrast, the olive oil and cold-pressed rapeseed oil produced far fewer aldehydes, as did butter and goose fat.

The reason being that these fats are richer in monounsatured and saturated fats, and are much more stable when heated.

‘Far lower levels of toxic compounds were generated by these oils and the compounds that were are actually less threatening to the human body,’ says the professor.

And as one in the eye for those who have eschewed old-fashioned fats, his research also suggests that when it comes to cooking, frying in animal fats may be preferable to sunflower or corn oil.

Toxic by-products

The study showed that cooking in vegetable oil for just 20 minutes produced potentially dangerous levels of toxic compounds

The study showed that cooking in vegetable oil for just 20 minutes produced potentially dangerous levels of toxic compounds

His personal cooking choice is unequivocal. ‘If I had a choice between lard and polyunsaturates, I’d use lard every time,’ he says.

Staying true to the science, it must be stressed that as long as they are not heated, polyunsaturated fats (vegetable and sunflower oils) are still seen as a healthy option.

These fats reduce bad cholesterol and lower the risk of stroke and heart disease.

And while the most stable fats of all are the saturated ones, such as butter, these should still be used sparingly as they can increase bad cholesterol and the risk of narrowed arteries and heart disease.

So far, so interesting, but the discoveries were not over.

Along the way our study had thrown up additional bad news about the destructive compounds hidden in our food – even storing oils in the wrong way can change them, as sunlight creates the same damaging chemical reactions as heat, only more slowly.

So storing oils in a dark cupboard is highly recommended to avoid formation of these dangerous by-products.

The research hasn’t just changed my thinking on oils – it’s changed the way I use them, too. I am considering giving lard a try – and I never thought I would hear myself say that.

Source: http://www.dailymail.co.uk/health/article-3574810/The-toxic-truth-vegetable-oil-Cooking-healthy-fats-increases-risk-heart-disease-type-2-diabetes-cancer.html

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#OpMurderForHire -Fluoride classified as a neurotoxin

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Summary

Neurodevelopmental disabilities, including autism, attention-deficit hyperactivity disorder, dyslexia, and other cognitive impairments, affect millions of children worldwide, and some diagnoses seem to be increasing in frequency. Industrial chemicals that injure the developing brain are among the known causes for this rise in prevalence. In 2006, we did a systematic review and identified five industrial chemicals as developmental neurotoxicants: lead, methylmercury, polychlorinated biphenyls, arsenic, and toluene. Since 2006, epidemiological studies have documented six additional developmental neurotoxicants—manganese, fluoride, chlorpyrifos, dichlorodiphenyltrichloroethane, tetrachloroethylene, and the polybrominated diphenyl ethers. We postulate that even more neurotoxicants remain undiscovered. To control the pandemic of developmental neurotoxicity, we propose a global prevention strategy. Untested chemicals should not be presumed to be safe to brain development, and chemicals in existing use and all new chemicals must therefore be tested for developmental neurotoxicity. To coordinate these efforts and to accelerate translation of science into prevention, we propose the urgent formation of a new international clearinghouse.

Introduction

Disorders of neurobehavioural development affect 10–15% of all births,1 and prevalence rates of autism spectrum disorder and attention-deficit hyperactivity disorder seem to be increasing worldwide.2 Subclinical decrements in brain function are even more common than these neurobehavioural developmental disorders. All these disabilities can have severe consequences3—they diminish quality of life, reduce academic achievement, and disturb behaviour, with profound consequences for the welfare and productivity of entire societies.4

The root causes of the present global pandemic of neurodevelopmental disorders are only partly understood. Although genetic factors have a role,5 they cannot explain recent increases in reported prevalence, and none of the genes discovered so far seem to be responsible for more than a small proportion of cases.5 Overall, genetic factors seem to account for no more than perhaps 30–40% of all cases of neurodevelopmental disorders. Thus, non-genetic, environmental exposures are involved in causation, in some cases probably by interacting with genetically inherited predispositions.

Strong evidence exists that industrial chemicals widely disseminated in the environment are important contributors to what we have called the global, silent pandemic of neurodevelopmental toxicity.6, 7 The developing human brain is uniquely vulnerable to toxic chemical exposures, and major windows of developmental vulnerability occur in utero and during infancy and early childhood.8 During these sensitive life stages, chemicals can cause permanent brain injury at low levels of exposure that would have little or no adverse effect in an adult.

In 2006, we did a systematic review of the published clinical and epidemiological studies into the neurotoxicity of industrial chemicals, with a focus on developmental neurotoxicity.6 We identified five industrial chemicals that could be reliably classified as developmental neurotoxicants: lead, methylmercury, arsenic, polychlorinated biphenyls, and toluene. We also noted 201 chemicals that had been reported to cause injury to the nervous system in adults, mostly in connection with occupational exposures, poisoning incidents, or suicide attempts. Additionally, more than 1000 chemicals have been reported to be neurotoxic in animals in laboratory studies.

We noted that recognition of the risks of industrial chemicals to brain development has historically needed decades of research and scrutiny, as shown in the cases of lead and methylmercury.9, 10 In most cases, discovery began with clinical diagnosis of poisoning in workers and episodes of high-dose exposure. More sophisticated epidemiological studies typically began only much later. Results from such studies documented developmental neurotoxicity at much lower exposure levels than had previously been thought to be safe. Thus, recognition of widespread subclinical toxicity often did not occur until decades after the initial evidence of neurotoxicity. A recurring theme was that early warnings of subclinical neurotoxicity were often ignored or even dismissed.11 David P Rall, former Director of the US National Institute of Environmental Health Sciences, once noted that “if thalidomide had caused a ten-point loss of intelligence quotient (IQ) instead of obvious birth defects of the limbs, it would probably still be on the market”.12 Many industrial chemicals marketed at present probably cause IQ deficits of far fewer than ten points and have therefore eluded detection so far, but their combined effects could have enormous consequences.

In our 2006 review,6 we expressed concern that additional developmental neurotoxicants might lurk undiscovered among the 201 chemicals then known to be neurotoxic to adult human beings and among the many thousands of pesticides, solvents, and other industrial chemicals in widespread use that had never been tested for neurodevelopmental toxicity. Since our previous review, new data have emerged about the vulnerability of the developing brain and the neurotoxicity of industrial chemicals. Particularly important new evidence derives from prospective epidemiological birth cohort studies.

In this Review, we consider recent information about the developmental neurotoxicity of industrial chemicals to update our previous report.6 Additionally, we propose strategies to counter this pandemic and to prevent the spread of neurological disease and disability in children worldwide.

Unique vulnerability of the developing brain

The fetus is not well protected against industrial chemicals. The placenta does not block the passage of many environmental toxicants from the maternal to the fetal circulation,13 and more than 200 foreign chemicals have been detected in umbilical cord blood.14 Additionally, many environmental chemicals are transferred to the infant through human breastmilk.13 During fetal life and early infancy, the blood–brain barrier provides only partial protection against the entry of chemicals into the CNS.15

Moreover, the developing human brain is exceptionally sensitive to injury caused by toxic chemicals,6 and several developmental processes have been shown to be highly vulnerable to chemical toxicity. For example, in-vitro studies suggest that neural stem cells are very sensitive to neurotoxic substances such as methylmercury.16 Some pesticides inhibit cholinesterase function in the developing brain,17 thereby affecting the crucial regulatory role of acetylcholine before synapse formation.18 Early-life epigenetic changes are also known to affect subsequent gene expression in the brain.19 In summary, industrial chemicals known or suspected to be neurotoxic to adults are also likely to present risks to the developing brain.

Figure 1 shows the unique vulnerability of the brain during early life and indicates how developmental exposures to toxic chemicals are particularly likely to lead to functional deficits and disease later in life.

Thumbnail image of Figure 1. Opens large image

Figure 1

Effect of neurotoxicants during early brain development

Exposures in early life to neurotoxic chemicals can cause a wide range of adverse effects on brain development and maturation that can manifest as functional impairments or disease at any point in the human lifespan, from early infancy to very old age.

New findings about known hazards

Recent research on well-documented neurotoxicants has generated important new insights into the neurodevelopmental consequences of early exposures to these industrial chemicals.

Joint analyses that gathered data for lead-associated IQ deficits from seven international studies20, 21 support the conclusion that no safe level of exposure to lead exists.22 Cognitive deficits in adults who had previously shown lead-associated developmental delays at school age suggest that the effects of lead neurotoxicity are probably permanent.23 Brain imaging of young adults who had raised lead concentrations in their blood during childhood showed exposure-related decreases in brain volume.24 Lead exposure in early childhood is associated with reduced school performance25 and with delinquent behaviour later in life.26, 27

Developmental neurotoxicity due to methylmercury occurs at much lower exposures than the concentrations that affect adult brain function.28 Deficits at 7 years of age that were linked to low-level prenatal exposures to methylmercury were still detectable at the age of 14 years.29 Some common genetic polymorphisms seem to increase the vulnerability of the developing brain to methylmercury toxicity.30 Functional MRI scans of people exposed prenatally to excess amounts of methylmercury showed abnormally expanded activation of brain regions in response to sensory stimulation and motor tasks (figure 2).31 Because some adverse effects might be counterbalanced by essential fatty acids from seafood, statistical adjustment for maternal diet during pregnancy results in stronger methylmercury effects.32, 33

Thumbnail image of Figure 2. Opens large image

Figure 2

Functional MRI scans show abnormal activation in the brain

Average activation during finger tapping with the left hand in three adolescents with increased prenatal methylmercury exposure (A) and three control adolescents (B). The control participants activate the premotor and motor cortices on the right, whereas participants exposed to methylmercury activate these areas bilaterally.31

Prenatal and early postnatal exposures to inorganic arsenic from drinking water are associated with cognitive deficits that are apparent at school age.34, 35 Infants who survived the Morinaga milk arsenic poisoning incident had highly raised risks of neurological disease during adult life.36

The developmental neurotoxicity of polychlorinated biphenyls has been consolidated and strengthened by recent findings.37 Although little new information has been published about the developmental neurotoxicity of toluene, much has been learned about the developmental neurotoxicity of another common solvent, ethanol, through research on fetal alcohol exposure. Maternal consumption of alcohol during pregnancy, even in very small quantities, has been linked to a range of neurobehavioural adverse effects in offspring, including reduced IQ, impaired executive function and social judgment, delinquent behaviour, seizures, other neurological signs, and sensory problems.38

Newly recognised developmental neurotoxicants

Prospective epidemiological birth cohort studies make it possible to measure maternal or fetal exposures in real time during pregnancy as these exposures actually occur, thus generating unbiased information about the degree and timing of prenatal exposures. Children in these prospective studies are followed longitudinally and assessed with age-appropriate tests to show delayed or deranged neurobehavioural development. These powerful epidemiological methods have enabled the discovery of additional developmental neurotoxicants.

Cross-sectional data from Bangladesh show that exposure to manganese from drinking water is associated with reduced mathematics achievement scores in school children.39 A study in Quebec, Canada, showed a strong correlation between manganese concentrations in hair and hyperactivity.40 School-aged children living near manganese mining and processing facilities have shown associations between airborne manganese concentrations and diminished intellectual function41 and with impaired motor skills and reduced olfactory function.42 These results are supported by experimental findings in mice.43

A meta-analysis of 27 cross-sectional studies of children exposed to fluoride in drinking water, mainly from China, suggests an average IQ decrement of about seven points in children exposed to raised fluoride concentrations.44 Confounding from other substances seemed unlikely in most of these studies. Further characterisation of the dose–response association would be desirable.

The occupational health literature45 suggests that solvents can act as neurotoxicants, but the identification of individual responsible compounds is hampered by the complexity of exposures. In a French cohort study of 3000 children, investigators linked maternal occupational solvent exposure during pregnancy to deficits in behavioural assessment at 2 years of age.46 The data showed dose-related increased risks for hyperactivity and aggressive behaviour. One in every five mothers in this cohort reported solvent exposures in common jobs, such as nurse or other hospital employee, chemist, cleaner, hairdresser, and beautician. In Massachusetts, USA, follow-up of a well-defined population with prenatal and early childhood exposure to the solvent tetrachloroethylene (also called perchlorethylene) in drinking water showed a tendency towards deficient neurological function and increased risk of psychiatric diagnoses.47

Acute pesticide poisoning occurs frequently in children worldwide, and subclinical pesticide toxicity is also widespread. Clinical data suggest that acute pesticide poisoning during childhood might lead to lasting neurobehavioural deficits.48, 49 Highly toxic and bioaccumulative pesticides are now banned in high-income nations, but are still used in many low-income and middle-income countries. In particular, the organochlorine compounds dichlorodiphenyltrichloroethane (DDT), its metabolite dichlorodiphenyldichloroethylene (DDE), and chlordecone (Kepone), tend to be highly persistent and remain widespread in the environment and in people’s bodies in high-use regions. Recent studies have shown inverse correlations between serum concentrations of DDT or DDE (which indicate accumulated exposures), and neurodevelopmental performance.50, 51

Organophosphate pesticides are eliminated from the human body much more rapidly than are organochlorines, and exposure assessment is therefore inherently less precise. Nonetheless, three prospective epidemiological birth cohort studies provide new evidence that prenatal exposure to organophosphate pesticides can cause developmental neurotoxicity. In these studies, prenatal organophosphate exposure was assessed by measurement of maternal urinary excretion of pesticide metabolites during pregnancy. Dose-related correlations were recorded between maternal exposures to chlorpyrifos or other organophosphates and small head circumference at birth—which is an indication of slowed brain growth in utero—and with neurobehavioural deficits that have persisted to at least 7 years of age.52, 53, 54 In a subgroup study, MRI of the brain showed that prenatal chlorpyrifos exposure was associated with structural abnormalities that included thinning of the cerebral cortex.55

Herbicides and fungicides might also have neurotoxic potential.56 Propoxur,57 a carbamate pesticide, and permethrine,58 a member of the pyrethroid class of pesticides, have recently been linked to neurodevelopmental deficits in children.

The group of compounds known as polybrominated diphenyl ethers (PBDEs) are widely used as flame retardants and are structurally very similar to the polychlorinated biphenyls. Experimental evidence now suggests that the PBDEs might also be neurotoxic.59 Epidemiological studies in Europe and the USA have shown neurodevelopmental deficits in children with increased prenatal exposures to these compounds.60, 61, 62 Thus, the PBDEs should be regarded as hazards to human neurobehavioural development, although attribution of relative toxic potentials to individual PBDE congeners is not yet possible.

Other suspected developmental neurotoxicants

A serious difficulty that complicates many epidemiological studies of neurodevelopmental toxicity in children is the problem of mixed exposures. Most populations are exposed to more than one neurotoxicant at a time, and yet most studies have only a finite amount of power and precision in exposure assessment to discern the possible effects of even single neurotoxicants. A further problem in many epidemiological studies of non-persistent toxicants is that imprecise assessment of exposure tends to obscure associations that might actually be present.63 Guidance from experimental neurotoxicity studies is therefore crucial. In the assessment of potential developmental neurotoxicants, we have used a strength of evidence approach similar to that used by the International Agency for Research on Cancer for assessing epidemiological and experimental studies.

Phthalates and bisphenol A are added to many different types of plastics, cosmetics, and other consumer products. Since they are eliminated rapidly in urine, exposure assessment is complicated, and such imprecision might lead to underestimation of the true risk of neurotoxicity. The best-documented effects of early-life exposure to phthalates are the consequence of disruption of endocrine signalling.64 Thus, prenatal exposures to phthalates have been linked to both neurodevelopmental deficits and to behavioural abnormalities characterised by shortened attention span and impaired social interactions.65 The neurobehavioural toxicity of these compounds seems to affect mainly boys and could therefore relate to endocrine disruption in the developing brain.66 In regard to bisphenol A, a prospective study showed that point estimates of exposure during gestation were linked to abnormalities in behaviour and executive function in children at 3 years of age.67

Exposure to air pollution can cause neurodevelopmental delays and disorders of behavioural functions.68, 69 Of the individual components of air pollution, carbon monoxide is a well-documented neurotoxicant, and indoor exposure to this substance has now been linked to deficient neurobehavioural performance in children.70 Less clear is the reported contribution of nitrogen oxides to neurodevelopmental deficits,71 since these compounds often co-occur with carbon monoxide as part of complex emissions. Tobacco smoke is a complex mixture of hundreds of chemical compounds and is now a well-documented cause of developmental neurotoxicity.72 Infants exposed prenatally to polycyclic aromatic hydrocarbons from traffic exhausts at 5 years of age showed greater cognitive impairment and lower IQ than those exposed to lower levels of these compounds.68

Perfluorinated compounds, such as perfluorooctanoic acid and perfluorooctane sulphonate, are highly persistent in the environment and in the human body, and seem to be neurotoxic.73 Emerging epidemiological evidence suggests that these compounds might indeed impede neurobehavioural development.74

Developmental neurotoxicity and clinical neurology

Exposures in early life to developmental neurotoxicants are now being linked to specific clinical syndromes in children. For example, an increased risk of attention-deficit hyperactivity disorder has been linked to prenatal exposures to manganese, organophosphates,75 and phthalates.76 Phthalates have also been linked to behaviours that resemble components of autism spectrum disorder.77 Prenatal exposure to automotive air pollution in California, USA, has been linked to an increased risk for autism spectrum disorder.78

The persistent decrements in intelligence documented in children, adolescents, and young adults exposed in early life to neurotoxicants could presage the development of neurodegenerative disease later in life. Thus, accumulated exposure to lead is associated with cognitive decline in the elderly.79 Manganese exposure may lead to parkinsonism, and experimental studies have reported Parkinson’s disease as a result of developmental exposures to the insecticide rotenone, the herbicides paraquat and maneb, and the solvent trichloroethylene.80 Any environmental exposure that increases the risk of neurodegenerative disorders in later life (figure 1) requires urgent investigation as the world’s population continues to age.81

The expanding complement of neurotoxicants

In our 2006 review,6 we expressed concern that additional developmental neurotoxicants might lie undiscovered in the 201 chemicals that were then known to be neurotoxic to human adults, in the roughly 1000 chemicals known to be neurotoxic in animal species, and in the many thousands of industrial chemicals and pesticides that have never been tested for neurotoxicity. Exposure to neurotoxic chemicals is not rare, since almost half of the 201 known human neurotoxicants are regarded as high production volume chemicals.

Our updated literature review shows that since 2006 the list of recognised human neurotoxicants has expanded by 12 chemicals, from 202 (including ethanol) to 214 (table 1 and appendix)—that is, by about two substances per year. Many of these chemicals are widely used and disseminated extensively in the global environment. Of the newly identified neurodevelopmental toxicants, pesticides constitute the largest group, as was already the case in 2006. In the same 7-year period, the number of known developmental neurotoxicants has doubled from six to 12 (table 2). Although the pace of scientific discovery of new neurodevelopmental hazards is more rapid today than in the past, it is still slower than the identification of adult neurotoxicants.

Table 1

Industrial chemicals known to be toxic to the human nervous system in 2006 and 2013, according to chemical group

Table Thumbnail. Opens Table in new tab.

*Including ethanol.

Table 2

Industrial chemicals known to cause developmental neurotoxicity in human beings in 2006 and 2013, according to chemical group

Table Thumbnail. Opens Table in new tab.

DDT=dichlorodiphenyltrichloroethane. DDE=dichlorodiphenyldichloroethylene.

*Including ethanol.

The gap that exists between the number of substances known to be toxic to the adult brain and the smaller number known to be toxic to the much more vulnerable developing brain is unlikely to close in the near future. This discrepancy is attributable to the fact that toxicity to the adult brain is usually discovered as a result of acute poisoning incidents, typically with a clear and immediate association between causative exposure and adverse effects, as occurs for workplace exposures or suicide attempts. By contrast, the recognition of developmental neurotoxicity relies on two sets of evidence collected at two different points in time: exposure data (often obtained from the mother during pregnancy), and data for the child’s postnatal neurobehavioural development (often obtained 5–10 years later). Because brain functions develop sequentially, the full effects of early neurotoxic damage might not become apparent until school age or beyond. The most reliable evidence of developmental neurotoxicity is obtained through prospective studies that include real-time recording of information about exposure in early life followed by serial clinical assessments of the child. Such research is inherently slow and is hampered by the difficulty of reliable assessment of exposures to individual toxicants in complex mixtures.

Consequences of developmental neurotoxicity

Developmental neurotoxicity causes brain damage that is too often untreatable and frequently permanent. The consequence of such brain damage is impaired CNS function that lasts a lifetime and might result in reduced intelligence, as expressed in terms of lost IQ points, or disruption in behaviour. A recent study compared the estimated total IQ losses from major paediatric causes and showed that the magnitude of losses attributable to lead, pesticides, and other neurotoxicants was in the same range as, or even greater than, the losses associated with medical events such as preterm birth, traumatic brain injury, brain tumours, and congenital heart disease (table 3).94

Table 3

Total losses of IQ points in US children 0–5 years of age associated with major risk factors, including developmental exposure to industrial chemicals that cause neurotoxicity

Table Thumbnail. Opens Table in new tab.

IQ=intelligence quotient. Data from from Bellinger.94

*From Grandjean and colleagues.95

Loss of cognitive skills reduces children’s academic and economic attainments and has substantial long-term economic effects on societies.4 Thus, each loss of one IQ point has been estimated to decrease average lifetime earnings capacity by about €12 000 or US$18 000 in 2008 currencies.96 The most recent estimates from the USA indicate that the annual costs of childhood lead poisoning are about US$50 billion and that the annual costs of methylmercury toxicity are roughly US$5 billion.97 In the European Union, methylmercury exposure is estimated to cause a loss of about 600 000 IQ points every year, corresponding to an annual economic loss of close to €10 billion. In France alone, lead exposure is associated with IQ losses that correspond to annual costs that might exceed €20 billion.98 Since IQ losses represent only one aspect of developmental neurotoxicity, the total costs are surely even higher.

Evidence from worldwide sources indicates that average national IQ scores are associated with gross domestic product (GDP)—a correlation that might be causal in both directions.99 Thus, poverty can cause low IQ, but the opposite is also true. In view of the widespread exposures to lead, pesticides, and other neurotoxicants in developing countries, where chemical controls might be ineffective compared with those in more developed countries,100, 101 developmental exposures to industrial chemicals could contribute substantially to the recorded correlation between IQ and GDP. If this theory is true, developing countries could take decades to emerge from poverty. Consequently, pollution abatement might then be delayed, and a vicious circle can result.

The antisocial behaviour, criminal behaviour, violence, and substance abuse that seem to result from early-life exposures to some neurotoxic chemicals result in increased needs for special educational services, institutionalisation, and even incarceration. In the USA, the murder rate fell sharply 20 years after the removal of lead from petrol,102 a finding consistent with the idea that exposure to lead in early life is a powerful determinant of behaviour decades later. Although poorly quantified, such behavioural and social consequences of neurodevelopmental toxicity are potentially very costly.76

Prevention of developmental neurotoxicity caused by industrial chemicals is highly cost effective. A study that quantified the gains resulting from the phase-out of lead additives from petrol reported that in the USA alone, the introduction of lead-free petrol has generated an economic benefit of $200 billion in each annual birth cohort since 1980,103 an aggregate benefit in the past 30 years of over $3 trillion. This success has since been repeated in more than 150 countries, resulting in vast additional savings. Every US$1 spent to reduce lead hazards is estimated to produce a benefit of US$17–220, which represents a cost-benefit ratio that is even better than that for vaccines.4 Furthermore, the costs associated with the late-life consequences of developmental neurotoxicity are enormous, and the benefits from prevention of degenerative brain disorders could be very substantial.

New methods to identify developmental neurotoxicants

New toxicological methods now allow a rational strategy for the identification of developmental neurotoxicants based on a multidisciplinary approach.104 A new guideline has been approved as a standardised approach for the identification of developmental neurotoxicants.105 However, completion of such tests is expensive and requires the use of many laboratory animals, and reliance on mammals for chemicals testing purposes needs to be reduced.106 US governmental agencies have established the National Center for Computational Toxicology and an initiative—the Tox 21 Program—to promote the evolution of toxicology from a mainly observational science to a predominantly predictive science.107

In-vitro methods have now reached a level of predictive validity that means they can be applied to neurotoxicity testing.108 Some of these tests are based on neural stem cells. Although these cell systems do not have a blood–brain barrier and particular metabolising enzymes, these approaches are highly promising. As a further option, data for protein links and protein–protein interactions can now be used to explore potential neurotoxicity in silico,109 thus showing that existing computational methods might predict potential toxic effects.110

In summary, use of the whole range of approaches along with clinical and epidemiological evidence, when available, should enable the integration of information for use in at least a tentative risk assessment. With these methods, we anticipate that the pace of scientific discovery in developmental neurotoxicology will accelerate further in the years ahead.

Conclusions and recommendations

The updated findings presented in this Review confirm and extend our 2006 conclusions.6 During the 7 years since our previous report, the number of industrial chemicals recognised to be developmental neurotoxicants has doubled. Exposures to these industrial chemicals in the environment contribute to the pandemic of developmental neurotoxicity.

Two major obstacles impede efforts to control the global pandemic of developmental neurotoxicity. These barriers, which we noted in our previous review6 and were recently underlined by the US National Research Council,111 are: large gaps in the testing of chemicals for developmental neurotoxicity, which results in a paucity of systematic data to guide prevention; and the huge amount of proof needed for regulation. Thus, very few chemicals have been regulated as a result of developmental neurotoxicity.

The presumption that new chemicals and technologies are safe until proven otherwise is a fundamental problem.111 Classic examples of new chemicals that were introduced because they conveyed certain benefits, but were later shown to cause great harm, include several neurotoxicants, asbestos, thalidomide, diethylstilboestrol, and the chlorofluorocarbons.112 A recurring theme in each of these cases was that commercial introduction and wide dissemination of the chemicals preceded any systematic effort to assess potential toxicity. Particularly absent were advance efforts to study possible effects on children’s health or the potential of exposures in early life to disrupt early development. Similar challenges have been confronted in other public health disasters, such as those caused by tobacco smoking, alcohol use, and refined foods. These problems have been recently termed industrial epidemics.113

To control the pandemic of developmental neurotoxicity, we propose a coordinated international strategy (panel). Mandatory and transparent assessment of evidence for neurotoxicity is the foundation of this strategy. Assessment of toxicity must be followed by governmental regulation and market intervention. Voluntary controls seem to be of little value.11

Panel

Recommendations for an international clearinghouse on neurotoxicity

The main purpose of this agency would be to promote optimum brain health, not just avoidance of neurological disease, by inspiring, facilitating, and coordinating research and public policies that aim to protect brain development during the most sensitive life stages. The main efforts would aim to:

  • Screen industrial chemicals present in human exposures for neurotoxic effects so that hazardous substances can be identified for tighter control

  • Stimulate and coordinate new research to understand how toxic chemicals interfere with brain development and how best to prevent long-term dysfunctions and deficits

  • Function as a clearinghouse for research data and strategies by gathering and assessing documentation about brain toxicity and stimulating international collaboration on research and prevention

  • Promote policy development aimed at protecting vulnerable populations against chemicals that are toxic to the brain without needing unrealistic amounts of scientific proof

The three pillars of our proposed strategy are: legally mandated testing of existing industrial chemicals and pesticides already in commerce, with prioritisation of those with the most widespread use, and incorporation of new assessment technologies; legally mandated premarket evaluation of new chemicals before they enter markets, with use of precautionary approaches for chemical testing that recognise the unique vulnerability of the developing brain; and the formation of a new clearinghouse for neurotoxicity as a parallel to the International Agency for Research on Cancer. This new agency will assess industrial chemicals for developmental neurotoxicity with a precautionary approach that emphasises prevention and does not require absolute proof of toxicity. It will facilitate and coordinate epidemiological and toxicological studies and will lead the urgently needed global programmes for prevention.

These new approaches must reverse the dangerous presumption that new chemicals and technologies are safe until proven otherwise. They must also overcome the existing requirement to produce absolute proof of toxicity before action can be started to protect children against neurotoxic substances. Precautionary interpretation of data about developmental neurotoxicity should take into account the very large individual and societal costs that result from failure to act on available documentation to prevent disease in children.114 Academic research has often favoured scepticism and required extensive replication before acceptance of a hypothesis,114 thereby adding to the inertia in toxicology and environmental health research and the consequent disregard of many other potential neurotoxicants.115 Additionally, the strength of evidence that is needed to constitute “proof” should be analysed in a societal perspective, so that the implications of ignoring a developmental neurotoxicant and of failing to act on the basis of available data are also taken into account.

Finally, we emphasise that the total number of neurotoxic substances now recognised almost certainly represents an underestimate of the true number of developmental neurotoxicants that have been released into the global environment. Our very great concern is that children worldwide are being exposed to unrecognised toxic chemicals that are silently eroding intelligence, disrupting behaviours, truncating future achievements, and damaging societies, perhaps most seriously in developing countries. A new framework of action is needed.

Search strategy and selection criteria

We identified studies published since 2006 on the neurotoxic effects of industrial chemicals in human beings by using the search terms “neurotoxicity syndromes”[MeSH], “neurotoxic”, “neurologic”, or “neuro*”, combined with “exposure” and “poisoning” in PubMed, from 2006 to the end of 2012. For developmental neurotoxicity, the search terms were “prenatal exposure delayed effects”[MeSH], “maternal exposure” or “maternal fetal exchange”, “developmental disabilities/chemically induced” and “neurotoxins”, all of which were searched for with the limiters “All Child: 0–18 years, Human”. We also used references cited in the publications retrieved.

Contributors

Both authors did the literature review, wrote and revised the report, and approved the final version.

Conflicts of interest

PG has provided paid expert testimony about mercury toxicology for the US Department of Justice. PJL has provided paid expert testimony in cases of childhood lead poisoning. We declare that we have no other conflicts of interest.

Acknowledgments

This work was supported by the National Institutes of Health, National Institute for Environmental Health Sciences (ES09584, ES09797, and ES11687). The funding source had no role in the literature review, interpretation of data, writing of this Review, or in the decision to submit for publication. The contents of this paper are solely the responsibility of the authors and do not represent the official views of the National Institutes of Health. We thank Mary S Wolff (Icahn School of Medicine at Mount Sinai, New York, NY, USA) and Linda S Birnbaum (US National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA) for their critical reading of the report.

Supplementary Material

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pdf iconSupplementary appendix pdf .34 MB

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