Industrial Pollution And
The Country Doctor

Dr. Dick van Steenis M.B.B.S. (10/23/01)

[Reprinted with permission.  Contact Dr. Steenis for his latest version of this document]

Well over 14 common diseases involving perhaps 90,000 deaths a year could be conservatively linked to the results of industrial air pollution in the UK, at a cost of some 16 billion annually, representing 35% of the total NHS budget, plus social security and social costs. A recent French hospital survey found 40% attendances linked to industrial pollution. In Wales, waiting lists to see a hospital consultant rose 800% in the 4 years to October 2001. Regarding cigarettes, the tax collected exceeds the estimated medical damage, similarly fuel tax is greater than health damage from vehicle pollution, but the NHS is subsidising industrial air polluters. The rationale began as "deaths for jobs", but became "deaths and misery" for excess maximised profits, sometimes linked to "conflict-of-interest payments".

Section EA95 7 (1) c iii of the Environment Act 1995 instructs ministers to help the Environment Agency carry out its function in poor areas, which an EA chief explained meant siting the lethal processes in disadvantaged areas to create in effect "killing fields", with the DOH then alleging "deprivation" and "life-style" for the resultant illnesses and premature deaths, contrary to published research in USA and UK. The DETR in IPPC2000 diluted the standards for industrial emissions to air, while the DOH refuses to undertake epidemiology by postcode to identify source(s) and culprits. Government "spin doctors" refuse to publish anything not in line with government policy, and also mislead the public and doctors with unsubstantiated allegations concerning house dust mites, imported PM 10s &/or SO2, promoting theories including inadequate dirt exposure when young (while injecting multiple vaccines at very early ages), etc. Victims of chemical/radiological poisoning are referred to the psychiatrist because the National Poisons Unit has stated "pollution does not exist". Concurrent evidence of raised incidence of cancers (and other conditions including birth defects) in polluted zones has been removed by deleting and with-holding names from the cancer register, and by fraudulently calling half the affected wards "exposed" while the others are labelled "control" to allege "no difference", and by altering dates and zones to dilute key data. Essential data such as terminations done for defects, is omitted in published reports rendering conclusions invalid or plain fraudulent. Vital anonymised health statistics are also deliberately hidden from the public by health authorities, in defiance of article 8 of the Human Rights Act and Appeal Court ruling of December 1999. Some members of regulatory committees and organisations such as the National Poisons Unit, National Asthma Campaign and others, have had financial involvement with pharmaceutical companies whose profits are affected by their decisions, while Friends of the Earth was established by an oil company (now BP-Amoco). The Environment Agency is reluctant to enforce the 1990 Environment Protection Act or prosecute large companies due to conflicts of interest: eg 70% of its income derives from the polluters, plus "payments". The EA in Wales continues to work to 1989 "black smoke" pollution limits instead of 1999 laws. Due to a prior deal with the power company by "new labour" and E.C. lobbying, Aberthaw power station was exempted in July 2001 from a new EC abatement directive, ignoring resultant deaths and illnesses in Wales.

There is a total paucity of anybody properly trained in toxicology in councils, EA, Health Authority Public Health Departments, consultants and GPs. Yet public health doctors have requested unqualified developers or environment agency officers &/or local authorities to assist them to write reports using fake figures based on fraud and abysmal ignorance, including government "spin doctor" reports in determining crucial proposals and situations. One doctor in 1997 told the environment agency to reopen a hazardous waste site knowing it would mean killing over 200 per year. The USA War Department published on 30 October 1943 details concerning the lethal actions of inhaled PM1s, yet the UK DOH, DETR and many consultants are still determined to ignore them, compared with the USEPA, which has established generous limits in 1997 for PM2.5s of 15ug/M3, while WHO stated in October 1994 that there was no safe lower limit. The USA Supreme Court stated in 2001 that public health must come first in all government decisions, which must be compared with the UK, where profits are maximised regardless of illnesses & deaths. The largest polluters such as specific oil refineries, power stations, hazardous waste burning cement works and old intercity trains are authorised to do virtually whatever they like, even when emissions exceed the law.

PM2.5 are manmade particles smaller than 2.5 microns, which have increased enormously due to the switch from coal to waste oil mixes (SLF) as fuel in the UK in incinerators, factories, cement works and even JCBs and other equipment, especially since 1992. A switch to residual oils increases the weight of nickel emissions by some 55 times, but the particle numbers increase by some 55000 times. Cement works burning a mix of SLF, coal and petcoke, even with scubbers, would emit some 34880 times the carcinogenic heavy metal particles at say PM0.5 size compared with coal at PM5. Only those smaller than PM3 enter the lungs. Scrubbers only remove effectively particulates larger than PM3, so are only useful in reducing acidic SO2 emissions, which limits secondary particle formation in the air after exit. Emission data published by Powergen revealed an increase in respirable particle numbers from burning "Orimulsion" compared with coal at another power station with similar abatement, calculated at 197000 times higher. These emitted particles, smaller than PM2, usually comprise acidic pH2 carbon, with adsorbed heavy metals and VOCs, which all enter the lungs, with vanadium affecting bronchioles, and nickel the alveoli, and initiate a 7 day inflammation (maximum on day 4), which results in increased infant mortality, asthma in 2 to 12 year olds with their small bronchi and relatively higher air intake; depression, lassitude and cardiovascular problems in those aged from 13 to 45, and respiratory and cardiovascular problems in the over 46s. Allergens are dealt with by mast cells in the lung. In contrast, inhaled PM2.5 particles are dealt with by macrophages. Knock-on effects can even affect the lungs following inflammatory particulate/allergen reaction initiated in the nasal lining. In the UK genetic research has suggested up to 20% of asthmatic children are potentially linked to allergic responses with genetic involvement, while the remaining 80% plus would be victims of particulate foreign body reactions. In USA due to lower and falling particulate levels, the proportions were 40%/60%. Pollen allergens have increased in amount due to the switch to male plants, with the PM15 pollen split open by acidic particulates or thunderstorms, so that allergenic PM1.5 starches can be carried into the lungs as well as the nose, stuck to particulates. Tyre latex PM1.5 bits abraded from road wear are also carried into lungs stuck to acidic PM2.5s. Nickel, platinum (in car catalysts) and cobalt are also potent allergens, stimulating IgE. The immune, as well as nervous system, has been affected by OP pesticide formulations, resulting in enhancement of increased aero-allergens effects. Finally pertussis vaccine has been demonstrated to increase immunoglobulins E & G and incidence of atopy, perhaps aggravated by mercury exposure from thiomersal containing vaccines and UK waste burning chimney/crematoria emissions.

Soluble heavy metals migrate through the blood stream, with resultant DNA mutations producing cancer risk in the patient or unborn child (if patient is pregnant). The particles with adsorbed contaminants, are mopped up by macrophages and transferred to the lung lymph nodes during the following 6 weeks. An inflammatory response is initiated by the macrophages, including release of cytokines and increased blood coaguability within 2 hours, followed by leukocytes and T-cell lymphocytes within 6 hours. If the inhaled load of particles is too great for macrophages to cope with, or if the inhaled particles are insoluble such as insoluble uranium oxides or beryllium, or wrong shape such as asbestos or quartz, the lung inflammation produces fibrosis. Recent published data from Californian children confirmed a significant permanent reduction in peak flow from this fibrosis even at age 10 years, entirely resulting from inhalation of exterior PM2.5 particulates from transport and industry, not household items, as often alleged. A county athlete in Pembrokeshire had her peak flow reduced from around 525 to 330 by PM2.5 emissions from oil refineries and power station (burning residual fuel oil without abatement). When plumes grounded at her school or home, peak flow fell further, necessitating oxygen tent and intensive therapy. She was proven via extensive testing to have no known allergies.

Exposure to PM2.5s leads to a reduction in lifespan of some 1.5 years for every 10ug/M3, which explains the 5 to over 12 year average differential in longevity between upper social classes in places like Arundel, compared with polluted lower class areas, which have become killing fields. However in unpolluted places in southern Italy and Tonga, lifespan averages 90 fit years irrespective of class. On 17 October 2000, the US Clean Air Task Force published an analysis of effects on mortality and health damage by US power stations, limited just to respiratory and cardiac systems, which revealed 30000 premature deaths, plus asthma, respiratory and cardiac problems, from those PM2.5 particles. Analysis has confirmed that the deaths are not simply expediting those who were about to die anyway, but new victims were being harmed. Ambient PM2.5s recorded in Derbyshire in 1999/2000 were consistent with at least 3 years reduction in lifespan, while analysis of content of the particles identified the major sources as open-casting of coal, demolition at a brown-field site and chimney emissions. Earlier Derbyshire data had revealed an average 325% rise in all deaths, 334% rise in heart attack deaths, 289% rise in all cancer deaths with 550% rise in breast cancer deaths in 7 polluted wards compared with a less polluted ward (that had an incidence of 5% children taking asthma inhalers to school with prevailing winds over the national park). Admissions to the hospital at Chesterfield resulted in deaths 42% above the national average, with all the increase arising from victims from heavily polluted villages. In Merthyr Tydfil 25% of the workforce is drawing sickness benefits. Attic dust analysis may be undertaken to confirm human exposure to unusual pollutants, noting that most exterior PM2.5s enter houses and adhere to surfaces. Hair analysis can reveal heavy metal prolonged exposure. At Bacton in 2000/1 PM2.5 levels were up to 8 times PM10 levels, with analysis revealing excesses of cobalt and mercury in the ambient air from the gas plants. Hair analysis confirmed these 2 metals while analysis of household ducted air filters also revealed cobalt. Numbers of exposed victims developed rashes from the cobalt exposure, confirmed by consultant skin testing. The reanalysis of previous studies of 550000 people regarding pulmonary and cardiac damage published by the Health Effects Institute in May 2000, confirmed PM2.5 particles as the prime causative mechanism, not deprivation, lifestyle or social factors. USEPA prosecution of oil & power companies followed to enforce reduction of PM2.5s.

The UK is still ignoring published research, preferring manipulated PM10 printouts massaged downwards by using recalibrated equipment and computer adjustments (instead of accurate factory-set PM2.5 beta-monitors). This scam was admitted by a DETR official in mid 1998. UK monitors have been stated as only measuring PM10 to PM4 inclusive, which do not enter the lungs. PM2.5s stay in the air for up to a week and result in maximum adverse health effects at some 0.5 miles from road vehicles; 3 miles from earthmoving equipment in open-casting and waste sites; and about 7 miles per 100 feet of chimney height. Hence from 700 feet chimneys, full effect is seen up to 49 miles downwind (plus another 100 miles at lower concentration, and a further 100 miles at still lower concentration). The maximum grounding of a 700 feet chimney would be at some 17 miles, where as anticipated, 38% of 4 & 5 year olds had been diagnosed as chronic asthmatics at Whitland school in the plume grounding zone from Pembroke oil complex, with similar findings elsewhere, (dependant on weather and terrain). Similarly, increased heart attacks in at least young women were reported in a corridor from Merseyside to Hull; excess cancer and heart attack deaths in a corridor from eastern Ulster through central Scotland in the plume-grounding zone of BP Grangemouth and 2 Ulster power stations. The highest standardised death rates in the UK in 1990 were hence around Glasgow but following conversion of their waste sires to hazardous content in 1993 and 1995, the highest 2 death rates became within 3 miles of the Merthyr Tydfil and Rhondda waste sites with high prevalence also of heart attacks. Hospital admissions for cancers downwind of the oil complex in Pembrokeshire, and Mid-Glam were reported as being 20 times higher in high asthma incidence postcodes, compared with less polluted low asthma incidence postcodes. In consequence, downwind of Pembrokeshire's oil complex is found the industrial world's highest breast cancer incidence, with a revelation in June 2001 that 80% of all deaths being registered in Pembroke area were due to cancer. All this carnage results from the virtually unregulated minimally- abated emissions. One monitor was turned off during maximum pollution episodes in 2001 blaming "foot and mouth" when the nearest cases were 100 miles downwind. The good news is that Salford's standardised mortality improved following closure of Ince power station. At a public inquiry in Flintshire the environment agency's agents ENTEC alleged all emissions would cease at 500m from a high chimney, the health authority doctor alleged 5000m, and EPAQS comments alleged 500km. The real truth of extent of downwind spread was nearer 180km with highest zone of 36km. Similarly in Swansea October 2001, emissions from a proposed incinerator were falsely claimed to only move 200 metres then presumedly, vanish. Daily deaths from high particulate episodes in USA were discovered to be greater prior to attending hospital due to outside exposure and were only related to fine particulate levels irrespective of weather or socio-economic circumstances. The` EC Okopol report in 1999 agreed with USEPA in stating that for every $1 spent on the pollution abatement (not CO2), there would be expected to follow a $6 saving on health cost subsequently, plus social and misery cost savings. A new 3mm thickness membrane electrostatic precipitator system developed in Ohio, traps small particles in coal-fired plant efficiently at greatly reduced cost and weight, cost-effective for electricity generation.

Emissions ground as a plume affecting rural and urban areas of most of the UK. A special NASA satellite is currently mapping gross CO movements as an indicator of associated other pollutants. Not only are PM2.5 particulates emitted, but in addition, secondary particles form in the air by complex reactions, beginning at PM0.02 in size then coalescing to PM1. Those who inhale the particles and assorted gasses are then put at risk of toxic effects, the morbidity depending on their genes, nutrition status, integrity of the immune system and their state of mind and presence/absence of godly faith (both of which influence outcomes sometimes, via hormone systems). Deficiency of excess antioxidant vitamins C and E leaves oxidising pollutant free radicals (including those arising from paracetamol breakdown) able to cause cell damage, especially if the cell wall quality has been deteriorated by dietary transfatty hydrogenated fats instead of omega-3 oils. Incidence of Alzheimer's Disease has been discovered substantially lower in those ingesting extra vitamins C&E. These paracetamol breakdown radicals also increase the burden from PM2.5 inhalation in asthmatics who take paracetamol for other conditions. Depression and stress both put strain on the hypothalamo-pituitary-adrenal axis, opening up the blood-brain barrier and affecting calcium homeostasis, hence brain cell health. Brain cells can also be compromised by OP pesticide attachment or viruses. Brain cells may die as in some Gulf War victims or may produce amyloid deposition typical of Alzheimers dementia. Deficiency of selenium depletes six vital enzymes required in the body's immune and toxicology systems, resulting in cancer becoming more likely, from inhaled or ingested carcinogens. Selenium supplementation in one trial reduced incidence of the main 4 cancers by some 56%. Folic acid and vitamins B6 & B12 deficiency result in excess homocysteine, linked to premature vascular disease. A less varied and poorer quality non-organic diet of deprived victims explains why they are more seriously affected when exposed to relevant pollution. German research has been indicating that those on an organic diet have 20% lower NHS costs due to higher essential mineral content, plus freedom from pesticides and contaminants. The UK diet is deficient in selenium. Half of UK teenage girls are deficient in zinc. Essential minerals in UK vegetables have reduced by 75% during recent years, due to acid rain and OP pesticides affecting soil chemistry. The USA adds folic acid to flour, and Finland adds selenium to the soil. Cell wall quality appears protective with olive oil as dietary fat, along with adequate essential omega fatty acids.

To clarify the results of the industrial air pollution on disease patterns, I now list some of the effects.

ASTHMA. About 0.3% of children a generation ago suffered from allergic reactions acting via mast cells to moulds, pollen starches, and other inspired allergens, and certain foods or short peptide chains absorbed from a leaking bowel wall. This allergic proportion has risen in the UK to some 3% by last year probably due to OP pesticide/herbicide intake exacerbated by allergenic items such as nickel, cobalt and platinum, interfering with the immune system. BBC TV Watchdog showed the rise in asthma and other illnesses from crop spraying in USA. A study in Mississippi revealed an incidence of diagnosed asthma in African American children of average 6.0% in a zone of heavy pesticide agricultural use, compared with 3.3% in a zone of lighter pesticide use. OP pesticide use and excess ozone in sunny cities could explain the asthma rise in Australasia. Exposure to irritant scorching items such as ozone at levels over 80ug/M3, or SO2 in smogs or chlorine based cleaning materials also cause intense bronchial inflammation, as can viral bronchiolitis. In addition we now have the effects of PM 2.5 particles from vastly increased vehicle traffic emissions (affecting some 9% of primary schoolchildren near busy roads). These comprise contaminated carbon from inadequate quality fuels, platinum from catalysts and tyre particulates. In addition we inhale cocktails of industrial emissions of heavy metals especially nickel, vanadium, cadmium, lead and mercury with acidic carbon (affecting up to 35% of primary schoolchildren with asthma). PM2.5s are also produced by open-casting quartz and coal (causing asthma in up to 30% of primary schoolchildren). Coal particles have been found down to PM1. Hospital admissions per 1000 population hence have been as high as 17 in rural Pembrokeshire in the Texaco/defunct power station plume grounding area, 11 in Eastern Sheffield some 1.5 miles from the Orgreave opencast site, 3 in Sheffield city centre, and 1 in Worcestershire. Ozone effects last 24 to 48 hours, exacerbating particulate inflammation (which lasts acutely for 6 days). Hence it takes 6 days away from the polluted zone to recover. At a school in Derbyshire, PM 2.5 levels were as high as 137ug/M3 in 1999, rising to 156 ug/M3 in 2000. When analysed, cadmium levels were equivalent to smoking 300 cigarettes daily. This analysis often pinpoints the source(s). In USA since October 2000, prosecutions and rulings have defined ways forward by more effective industrial chimney abatement and opportunities for safer systems like plasma gasification, installation of particle traps on heavy vehicles, use of bio-diesel in buses (20% soya or other oil with 80% low sulphur diesel), low-sulphur cleaner fuel for cars, some with ethanol.

Pollens & sea salt are larger than PM 4 as are the average particulates from coal burning. Coal burning plants require scrubbers (FGD) plus Ohio electrostatic membranes, while waste oil burning cement works, power stations & other industry require Ohio electrostatic membranes, scrubbers with activated charcoal in the stream, bag filters and after-burners. The Canadian Health Dept. requested my help with an orimulsion-fired power station that had caused an increase in asthma incidence from 0.5% to 22%, acted on my advice, and altered abatement equipment. Waste oil with solvents and other mixes of hazardous waste called SLF, where burnt all over the UK, produce particulates less than PM 1 in size, all entering the lungs with some 70% being retained in the lung. The effective solution to reduce dangerous emissions from burning waste is a high tech gasification plant. The UK has NONE while Italy has built three in recent years. Sampling of metals in Birmingham near the M6 motorway revealed ambient levels of nickel unconnected with the motorway exceeding HSE limits. Those allergic to nickel respond immediately. Hence the UK's asthma epidemic is limited to areas with high PM 2.5 particulate pollution, with unpolluted areas having childhood asthma incidence as low as 1%. With denial of the true causes by vested interests allowing virtually no regulatory mitigation, it is hardly surprising that the UK has developed the industrial world's highest incidence of asthma and other diseases. Current policy for erection of incinerators to handle mixed waste will cause yet further rises in ambient PM2.5 particulates, dioxins and VOCs as they represent the unsafe alternative. Far better to sort waste with a recycling of relevant categories, compost organic household waste in a semi-sealed system to collect methane, treat the burnable matter in a gasification system with the gases being burned with the methane in a gas-turbine to produce electricity. This is being done in an economic low-tech manner in Wollongong, Australia. Any hazardous waste is best dealt with by higher-tech gasification with the most dangerous waste dealt with very safely by plasma-gasification as in Ottawa, Canada. The ash from gasification is only 10% of the input and is vitrified so will not leach. Ash from UK incinerators fired with SLF (hazardous waste mixes), exceeds 28% of the input and hazardous, NOT safe for reuse, fit only for special landfills. Hazardous kiln dust from cement works using toxic waste as fuel, has since 1995 been stupidly used in cattle feed and in fertiliser to contaminate the food chain.

HEART ATTACKS AND STROKES. The lung inflammation from inhaling particulates or irritants results in enhanced clotting, increasing the likelihood of heart attacks and strokes. Any increase in PM2.5 particles halves the time needed for an ischaemic heart attack. Measurements on Boston volunteers exposed to 3-hour increase of only 14.3ug/m3 of PM2.5s, proved vagal tone decreased resulting in reduced heart rate variability, which is a predictor of increased risk of cardiovascular mortality or morbidity (p=0.006). These levels are below the monthly averages of 19 ug/m3 at 8.5km downwind of Texaco's Pembrokeshire refinery. Ozone excess induced lung inflammation also decreased vagal tone (p=0.03). Nickel in PM2.5 particulates in the lung enters the bloodstream and excites the heart's electrical system leading to tachycardia, while lead and iron particulates harm heart muscle (e.g. from London's Northern Line old trains, and emissions from burning SLF). Lead exposure can elevate blood pressure. Cadmium (from cigarettes, waste sites, plants using cadmium, and from burning SLF) and manganese (eg Rhondda hazardous waste site) PM2.5 particulate exposure produces arteriosclerosis plus damage to vessel walls resulting in aortic aneurisms near the base in young adults, and abdominal area in older victims. Vehicle pollution is alleged to cause 20,000 heart deaths in the UK annually, but just one oil refinery according to USEPA emits as many VOCs as 5 million cars with other emissions in similar proportions. Industrial emissions from those industries using mixed waste as fuel, which even include some earth-moving equipment used on waste sites and opencasting, all exceed car emissions (which government cites as a prime culprit). This mixed waste SLF comprises both home-sourced and some 73000 shiploads of imported hazardous waste a year coming from many countries, including what Germany, Denmark and the Ireland would not dare incinerate or bury themselves, now mostly used as "fuel" in the UK.

Detailed analysis in Boston of patients suffering myocardial infarcts revealed an increase in odds ratio of 1.48 after 2 hours of an increase of just 25ug/m3 of PM2.5 particulates, with a second peak from further inflammatory responses amounting to odds ratio of 1.69 at 24 hours exposure to a rise of only 20ug/m3 PM2.5s. Excess UK deaths annually would exceed 200 in Rhondda, 500 at Merthyr and 8000 in Central Scotland compared with Western Europe, mostly from heart attacks, because of presumed PM2.5 pollution as described earlier. Inflammation in the lungs from PM2.5 particulates, or peptic ulcers with H.pylori, or autoimmune conditions all cause increased blood coaguability, and/or sticky red blood cells and/or sticky platelets. In susceptible individuals the result would be coronary occlusion or stroke or even DVT. Hence the value of preventive indomethacin, or aspirin plus clopidogrel in selected patients. The biggest risk group for inducing hospital admissions from PM2.5 damage are those with acute respiratory infections or defects in the heart electrical control system.

CANCERS Coking works were responsible for increased incidence of lung cancer in the oven workers, plus leukaemia, breast and other cancers in the surrounding population from heavy metals, phenols, benzine and PCBs dumped as waste. A detailed survey in NSW Australia of a steelworks, coking works and adjacent waste site, illustrated how the plume of carcinogens settled, with some fourfold incidence of leukaemias and ninefold increase in general cancers at 1 mile tailing off to background rates at 11 miles. USA and UK studies around hazardous waste sites revealed a rise in cancers within 3 miles, the mix depending on the items dumped. The same principles apply to inhaled carcinogenic PM 2.5 particles and organic gases from chimneys. The lung cancer rate in West Glam. has been double that of Powys, but the difference in incidence of smoking is only 3%. The difference might be explained by emissions from BP Llandarcy plus the Clydach nickel works as nickel inhalation with or without PAHs adds to the carcinogenic effects of cadmium and PAHs in cigarettes. Cadmium causes cancers of lung, bladder, prostate & breast. Radioactive sea spray from Sellafield's waste resulted in up to 450% rise in cancer incidence within 2 km of the Irish Sea Welsh coastline. Excess cancer deaths at present in the plume grounding zone of the oil complex in just Pembrokeshire could be as high as 800 annually. Exposure to heavy metals such as arsenic, nickel, cadmium and chromium, or to radioactivity or dioxins or pesticides such as dieldren and OPs, all cause DNA mutations which would progress to cancer if the protective P53 gene is damaged by certain polyaromatic hydrocarbons inhaled from cigarettes, industrial or vehicle emissions, or if the immune system is deficient in selenium. Selenium also is used in the thyroid gland and binds some heavy metals, preventing cell damage. PM2.5 particles become enhanced in carcinogenic effect under high voltage power lines with the effect dispersing after 400 metres. One would expect minimal effects where PM2.5 levels are lower than UK, such as Finland. The Millenium Dome site excavation at Greenwich removed 240000 tons of carcinogenic waste from an old gas works, chemical and benzol plants. Who will dare trace future cancer incidence among the site workers and residents living within 3 miles? Many workers on the roof developed RASHES presumedly due to the nickel and phenols excavated below, while hospital and HSE did not have a clue. An incinerator at Killamarsh near Sheffield burned 20 tons of arsenate in a 6 month period with high soil levels confirming excess emissions. In 1986 a Berkshire fire by a reactor was apparently cooled with water from an adjacent lake. Subsequently the lake was infilled, and new houses erected upon it. Large number of victims of leukaemia (with >400 deaths) and other cancers ensued between Earley and Bracknell. Analysis of property soil and dust samples confirmed levels of manmade plutonium 239/240 some 1000 times background levels elsewhere in UK, with presence of other manmade nucleotides as one might expect. The effects on breast and other cancer incidence resulting from hormone manipulation by tablet or oestrogen-mimics in non-organic food also need further rigorous investigation. With print and sewage waste & kiln dust from toxic waste burning cement works laden with arsenic being dumped on farmland, plus grounding of dioxins and other emissions, there is plenty of scope for contaminated milk and other food. Crankcase oils in the feed, colorants and banned pesticides hardly made for safe salmon. The FSA admitted in 2001 that UK milk contains PCBs & dioxins, which accumulate.

DEPRESSION. Raised levels of ultrafine particulates under PM 2.5 were proven in a German study to increase incidence of depression. Some PAHs, some metals and some other organic compounds also initiate depression. A high incidence is hence found in the high-asthma plume-grounding zone in Pembrokeshire and other areas afflicted with high pollutant levels of the type described, such as Merthyr Tydfil. Dioxins will deteriorate brain function making children's IQ drop the equivalent of some 2 classes at school, perhaps explaining findings at Blyth school near the power station or at Grimsby or Cefn Mawr. Febrile convulsions following DPT or MMR immunisations in USA also resulted in almost every affected child suffering low IQ and learning difficulties or ADHD. Lead exposure can also reduce IQ. Welsh depression incidence in polluted postcodes has been the highest in the industrialised world, for example 9 times higher in polluted parts of Pembrokeshire. Depression, apathy, mood swings and aches & pains can result from OP exposure in farmers, pesticide workers and others. OP flame-retardants on computer circuit-boards could explain increased symptoms and surgery attendances in 20 year olds in the UK during recent years. Depression along with hypothyroidism, reduced exercise and dioxin contaminated milk could explain much of the rise in OBESITY incidence in the UK.

HYPOTHYROIDISM Certain organic emissions bind the building blocks in the body, which produce thyroid hormone. This fact along with selenium deficiency, would explain why 15% of UK women now suffer from this condition. Industrial fluorides, inhaled or swallowed, also depress thyroid hormone production. The TSH test done by some doctors may be within the upper range of normal because the pituitary does not realise the building blocks or production system are blocked. T3 and T4 levels will reveal any deficiency requiring thyroxin treatment.

ENDOMETRIOSIS 12.5% of UK women now have this condition, blamed on a rise in dioxin intake, either inhaled from waste incinerators or ingested from for example dioxin contaminated milk. A mycoplasma infection of the uterus has also been described as a possible causative agent.

INSULIN DEPENDANT DIABETES Dioxin intake by inhalation and/or ingestion has been revealed in published journals to be associated with an increased incidence of diabetes. In Sheffield the hospital admissions for diabetes were recorded per 1000 population as 4 in the city centre but as high as 11 in the eastern zone affected by pollution from opencasting of dioxin-contaminated land, and dioxins emitted by the city incinerator & a castings plant. Diabetics given gamma-linoleic acid supplements were proven in a Glasgow study to be totally protected from small blood vessel damage in eyes and peripheries, due to improved blood flow from less sticky platelets and more flexible red blood cells. The evening primrose oil supplements reduce elevated total cholesterol levels found in many diabetics. Fish oil supplements, which contain eicosapentaenoic acid, reduce elevated triglycerides, restore red blood cell flexibility after 8 weeks and platelets in 2 weeks. So, is it not prudent to give diabetics with lipid disorders, supplements of fish oil and evening primrose oil to reduce the raised heart attack incidence risk? Mycoplasma pancreatitis leads to cessation of insulin production. Raised incidence of diabetes has also been documented following hepatitis-B vaccine and the rubella complexes from MMR vaccine.

POLYMYALGIA RHEUMATICA AND SOME REACTIVE ARTHRITIS An increase has been noted in the plume grounding area of 2 oil refineries in Pembrokeshire, possibly due to an auto-immune response to haptens formed from fluoride emissions. Exposure to radioactivity causes deterioration in cartilage.

BIRTH DEFECTS, PERINATAL DEATHS, and INFANT MORTALITY. The Dolk report concerning selected European hazardous waste sites revealed a rise in birth defects within 3 miles (5km). A more recent report compared births under 2km with those affected between 3-5km (with some outside) to fraudulently minimise any differential. Within 5km of Trecatti waste site following conversion to hazardous, the birth defects, perinatal deaths and infant mortality all doubled. Similarly within 5 km of Nantygwyddon following conversion to hazardous the birth defects soared and infant mortality doubled. At Corby the public discovered 28 birth defect babies, again associated with hazardous waste sites, with the infant mortality in 2000 reaching 12.4 which is virtually identical to those 2 Welsh sites compared to Helsinki 3.3 and Belarus after Cherobyl 14/1000 births. Some sites are clearly worse than others depending on topography and content. Perinatal deaths in Cardiff and downwind of the plant emitting tritium were raised significantly, with a 7-month time lag, relating to early pregnancy exposure. The existence of styrene, vinyl, lead, ethylene oxide and tritium, apparently with spent uranium and other radioactive waste at the Nantygwyddon tip (Rhondda) inevitably resulted in huge numbers of birth defects with as many as one pregnancy in three or more being terminated for such defects plus several live children with assorted birth defects. At Warrington (downwind of the Wirral) about one pregnancy in four was ending in miscarriage or stillbirth. Mutations can be passed on to the next generation, as has been identified in veterans exposed to nuclear radiation. Birth defect clusters were noted after the Sea empress crude oil spill as was found in Ecuador. Another cluster was reported between Trawsfynydd nuclear power station and Conwy. Pesticide drift has been blamed for birth defects 9 miles downwind in California.

CARBON MONOXIDE AND HYDROGEN SULPHIDE emanate from cars and from many industrial chimneys. Both, and also mercaptens, block the P450 cytochrome in the liver so the recipient can no longer break down toxins inhaled or ingested. The damage may last for 2.5 years. Tests are available in California in this field. Subsequent pollution will thus have unabated effects on the immune system, neurological system and elsewhere, resulting in conditions such as ME, whether from reactivation of Epstein Barr virus, mycoplasma or chemicals. Seven hospital staff developed ME following installation of a faulty hospital incinerator in Bristol that leaked CO and burned inadequately. The P450 cytochrome is controlled by 70 genes, allowing genetic variability and damage. Toxins are detoxified in 2 phases. Phase 1 requires B-vitamins, flavinoids, phospholipids, amino acids, selenium and vitamin C. Phase 2 requires glycine, glutathione, magnesium, vitamins E, B6, B5, B12 & folic acid flavinoids and other amino acids. Hydrogen sulphide also inactivates cytochrome A3 which leads to inactivation of mitochondria electron transport resulting in inhibited oxidative phosphorilation hence reduced energy production resulting in FATIGUE. Hydrogen sulphide causes conjunctivitis at concentrations below 10 ppm found near some waste sites (eg Rhondda) and oil refineries (eg Pembroke), with headaches, nausea, permanent eye damage and cough above 50ppm, which was recently recorded in a victim's house near that Rhondda Nantygwyddon hazardous waste site. Hydrogen sulphide is noticeable above 0.13 ppm.

GRANULOMATOUS CONDITIONS such as probable berylliosis and sarcoidosis were discovered around Nantygwyddon (Rhondda) hazardous waste site, the former from the metal dumped on site, the latter most likely from Mycobacterium a.Paratuberculosis. Victims near Nantygwyddon site probably comprise both, as attic dust analysis revealed beryllium excess (presumed ex-MOD nuclear weapon facility) and there are high levels of M.a.P. in the river Taff downstream of the tip. Workers at a beryllium plant in Milford Haven exposed to inside levels of beryllium up to 333 times the HSE limit, have complained of symptoms of berylliosis.

AUTISM and ATTENTION DEFICIT DISORDER have been linked to exposure to mercury by pregnant mothers, arising from emissions from crematoria and cement works/incinerators burning SLF hazardous waste as fuel, affecting the foetus, exacerbated in especially lower weight babies by mercury preservative in many vaccines. Mercury sensitises the brain, which is affected by multiple live vaccines especially the measles of MMR if the immune system is deficient from being compromised by cadmium or mercury exposure or dietary selenium deficiency. Brain cells would be even more susceptible to attention deficit disorder if affected by deficiency of essential fatty acids such as found in oily fish (omega-3) or flaxseed; or exposure to tartrazine or cadmium. Even one injection of tetanus vaccine in healthy adults sufficed to utilise some in 63.6% of patients or almost all in 36.4% of patients of available T-lymphocytes. Cimetidine has been found to stimulate T-lymphocyte production and hence has shortened recovery in shingles. Is this why some babies cannot cope with multiple live vaccines like MMR with some producing antibodies to only part of the combination, leaving for example clusters of live measles virus in the bowel wall causing low-grade inflammation with leaks of partly digested bits of polypeptide chains into the bloodstream to cause yet more potential problems. Genes in Gulf War veterans have been found with fragmented, reshuffled genes of chromosome 22Q11.2, which is required in antibody production. This gene damage can result from viruses or other cell stress from chemicals, as found in ME. If an immunised baby has damaged or sensitised systems or inadequate T-lymphocytes, it is hardly surprising that problems may occur. It has been a feature of the UK MENINGITIS outbreaks, that all appear to have occurred in polluted areas, where strained immune systems could explain susceptibility. Autopsies of 80,000 New York dead birds 2000/2001 revealed the majority died from OP pesticides, while the balance succumbed to West Nile Virus due to immune systems damaged by the same OP pesticides. [Ed. Note: Dr. Steenis is reconsidering his views of those press releases, critiqued in wnvDB1 and wnvDB2 and avdieoff] A few children have succumbed to one strain of meningitis following immunisation against another in polluted areas, again probably due to overload of the immune system with T-lymphocytes diverted to dealing with the lung PM2.5 particulates from the pollution, with insufficient left over. Low pollution in Finland plus selenium crop supplements probably allowed fewer babies to have registered problems with the MMR vaccine.

Doctors must be aware of the described cocktail effects of interacting pollutants and challenges in patients of variable status. An analysis of practice and hospital databases providing anonymised postcoded data would be of great benefit. The author may, on request, provide appropriate information or advice.

Copyright Dr. Dick van Steenis M.B.B.S. 23 October 2001 Contact:


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162. Macloed-Gilford W. Personal Communication & Details of Tritium Contamination.
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164. Lopez-Abente G and Escolar A. 2001. Tobacco Consumption and Bladder Cancer in Non-Coffee Drinkers. J Epidemiol Community Health/ 55 p68-70
165. USEPA . 4 April 1998 Decade-old Study Revealed the Polluting Effects of Landfills. Rachel's Hazardous Waste News. Annapolis.
166. Mason J. 21 June 2001. Soy Sauce Cancer Warning. Financial Times.
167. Environment News Service. 16 July 2001. Power Lines, Wiring, pose Health Risks.
168. Rachel's Environment and Health News. 7 June 2001. Science, Precaution and Pesticides. Environmental Research Foundation. Annapolis.
169. Fielding N. 8 July 2001. Suburb 'Poisoned' by Plutonium. The Sunday Times.
170. Morgan O. 1 July 2001. Finger on the Nuclear Button. The Observer.
171. Downie R. 19 July 2001. Nuclear Plant Cover-Up Denied. The Daily Telegraph.
172. Jones M. 17 July 2001. BNFL Chiefs Face Grilling Over Accident. Financial Times.
173. Kluger J. 16 July 2001. Toxic Playground. Time.
174. Stavopoulos P. 10 Feb, 1999. Wollongong Steelworks Pumps Out Dangerous Dioxins. WSW.
175. Newbold RR, Banks EP, Bullock B and Jefferson WN. 2001. Uterine Adenocarcinoma in Mice Treated Neonatally with Genistein. Cancer Research 61 p4325 - 4328.
176. Gains G. Personal Communication. Re. AWRE
177. Thorlacius S., Struewing JP, Hartge P, Olafsdottir GH, Sigvaldason H, Tryggvadattir L, Wacholder S, Tulinius H and Eyfjord JE. 24 October. 1998. Population-Based Study of Risk of Breast Cancer in carriers of BRCA2 Mutation. The Lancet / 352 p1337-1339.
178. Dartmouth Medical School. 28 Feb 2001. Arsenic: A New Type of Endocrine Disrupter? Environment News Service and March 2001 Environmental Health Perspectives.
179. Newman LS. 1994. Beryllium Lung Disease. Immunotoxicolgy and Immunopharmacology, Ch 21. Cell-Mediated Immunity.2nd Ed. Raven Press.
180. Newman L. 1995. Beryllium Disease and Sarcoidosis: Clinical & Lab. Links. Sarcoidosis 1995;12:7-19
181. Newman L, Rose CS and Maier L. 24 April 1997. Medical Progress: Sarcoidosis. The New England Journal of Medicine/336/17 p1224-1234.
182. Markowski VP, Zareba G, Stern S, Cox C and Weis B. 2001. Altered Operant Responding for Moter Reinforcement and Determination of Benchmark Doses following Perinatal Exposure to Low-level 2,3,7,8-Tetrachlorodibenzo-P-Dioxin. Environmental Health Perspectives 109:621-627. (Reduced Motivation & Obesity even after single exposure).
183. Fairlie I. Sept-Oct 1992. Tritium. The Overlooked Nuclear Hazard. The Ecologist
184. Citizens Awareness Network. The Carcinogenic, Mutagenic, Teratogenic and Transmutation Effects of Tritium.
Hazardous Waste
185. Budnick LD, Sokal DC and Falk H. November/December 1984. Cancer and Birth Defects Near the Drake Superfund Site, Pennsylvania. US Dept of Health and Human Services.
186. Ozonoff D, Aschengrau A and Coogan P. 1994. Cancer in the Vicinity of a Department of Defense Superfund Site in Massachusetts. Toxicology and Industrial Health 10/3
187. Meharg A , Osborn D. 1 June 1995. Dioxins Released from Chemical Accidents. Nature/375.
188. Racette B. 23 January 2001. Researchers Link (Manganese from) Welding and Parkinson's Disease. Environment News Service.
189. Rachel's Hazardous Waste News. 23 January 1991. Why Plastic Landfill Liners Always Fail. Environmental Research Foundation.
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191. Hart A, Begley C & Taras T. 6 Feb. 2001.Village in Shadow of Death, News of the World.
192. Smith GH and Lloyd OL. Feb. 1986. Soil Pollution from a Chemical Waste Dump. Chemistry in Britain.
193. Rossington P. April 1999. A Summary of the Effects of Venting or Combusting Landfill Gas from Toxic Waste Sites. Report and Personal Communication.
194. Hale RC, La Guardia MJ, Harvey EP, Gaylor MO, Matteson T and Duff WH. 2001. Flame Retardants: Persistant Pollutants in Land-Applied Sludges. Nature/412 p140-141
195. Link A. August 1993. Living With Dioxins in North East Derbyshire. ISBN 1-874137-04-8
196. Wollongong City Council Waste Management & Recycling. 23 Oct 2000. Domestic Waste and Waste to Energy Plant.
197. Jiang S. 8 Feb 2001. Human Viruses Found in California Coastal Waters. Env. News Service.
198. AEA Technology. Aug 1996. Analysis of 216 Gases emanating from a Wiltshire Waste Site.
199. Occupational Health & Safety, Canada. Hazardous Substance Fact Sheet 14. Hydrogen Sulphide Mist.
200. Motelin G. 16 July 2001. Kenya's Pink Flamingos Weighed Down by Heavy Metals. (Lead, Cadmium, Arsenic, Mercury and Organochlorines). Environment News Service.9999
201. Gulyas H and Hemmerling L. 1990. Tetrachloroethylene Air Pollution Originating from Coin Operated Dry Cleaning Establishments. Environmental Research/53, p90-99.
202. White RF & Proctor SP. 26 April 1997. Solvents and Neurotoxicity. The Lancet/349:1239/43
203. Hellen N. 3 June 2001. Hidden Dome pollution hits sell-off price. Sunday Times.
204. Richards H. 12 July 1999. Perinatal Mortality in Cardiff. (Related to Tritium). Report to National Assembly for Wales plus subsequent reanalysis.
205. Bender M. 2 March 2001. CDC Report Finds More US Children and Pregnant Women at Risk From Mercury Exposure Than Ever Before. Sierra Club.
206. USEPA. 2 March 2001. Blood and Hair Mercury Levels in Young Children and Women of Childbearing Age. MMWR Weekly /50(8) p140-3
207. Graveling RA, Pilkington A, George JPK, Butler MP and Tannahill SN. Feb 1999. A Review of Multiple Chemical Sensitivity. Occupational and Environmental Medicine 56 (2) p73-85.
208. Nicholson GL, Nasralla M, Haier J and Nicholson NL. 1998. Gulf War illnesses: Role of Chemical, Radiological & Biolog. Exposures. War and Health (Helsinki) & Inst. for Molecular Medicine, California.
209. Khattak S, K-Moghtader G, McMartin K, Barrera M, Kennedy D and Koren G. 24 March 1999. Pregnancy Outcome Following Gestational Exposure to Organic Solvents. JAMA 281 (12) p1106-209
210. Canadian Centre for Occupational Health & Safety. May 2001. Cheminfo for Hydrogen Sulphide.
211. Piggot CS. 30 July 1987. Duncan Flockhart research concerning use of fish oil and evening primrose oil supplements in lipid disorders in diabetics. Personal letter.
212. Sanders TAB, Sullivan DR, Reeve J and Thompson GR. Sept/Oct 1985. Triglyceride-Lowering Effect of Marine Polyunsaturates in Patients in with Hypertriglyceridemia. Arteriosclerosis 5(5) p459-465
213. Sanders TAB. 1987. Fish and Coronary Artery Disease. British Heart Journal 57 p214-9
214. Lawrence F. 22 June 2001. Cancer Chemicals Found in Eggs. The Guardian.
215. Hope J. 1 June 2001. Oily Fish Can Help Ward Off Cancer. Daily Mail.
216. Hermon-Taylor J. Mycobact. A. Paratuberculosis & Crohn's. Personal communication.
217. Shamsuddin AM. 1996 IP6 & inositol mechanisms. Anticancer Research 16:3287-3292
218. Mason P. 23 Oct 1999. Folic Acid - New Roles for Well Known Vitamin. Pharm. Journal 263:673-677
219. Jones GRN. 2001. Causes of Alzheimer's Disease: Paracetamol (Acetaminophen) today? Amphetamines tomorrow? Medical Hypotheses 56: (1): 121-123
220. Orrell MW & O'Dwyer A.18 March 1995.Dementia, Ageing & the Stress Control System.Lancet 345 p666-7.
221. Rajapakse N, Ong D and Kortenkamp A. 2001. Defining the Impact of Weakly Estrogenic Chemicals On The Action of Steroidal Estrogens. Toxicological Sciences 60 p296-304.
222. Holding R. July 2001. Detoxification. The Nutrition Practitioner. 3.2 pp36-39
223. McClenaghan. July 2001. Liver health. The Nutrition Practitioner. 3.2 pp32-35
Virus And/Or Chemical?
224. Vojdani A & Lapp CW. 1999. Interferon-Induced Proteins are Elevated in Blood Samples of Patients with Chemically/Virally Induced Chronic Fatigue Syndrome. Immunopharmacology and Immunotoxicology 21 (2): 175-202 and Personal Communication.
225. White P. 1998. Glandular Fever ME. British Journal of Psychiatry, reported in The Times of 1 Dec. 1998.
226. Hooper M. 2000. Report for UK MOD on extensive exposures to chemical and biological insults by Gulf War Veterans, and Personal Communication.
227. Henderson M. 18 April 2001. Nuclear Disaster Software Tracks Disease. The Times.
228. Buttram HE & Yazbak FE. 1 July 2001. Shaken Baby Vaccine-Induced Encephalitis? The Story of Baby Alan. The Journal of Degenerative Diseases. Vol.3 Number 1.
229. Hughes G. January 2001 Autoimmune induced sticky blood as risk factor for DVT. Personal Communication.
Relevant Death Data
230. Dorling D. July 1997. Death in Britain -How Local Mortality Rates Have Changed. ISBN 1 95935 0931 3.
231. Federal Dept of Environment , Transport, Energy and Communications. Based on 1993 Data. Monetarization of the External Health Costs Attributable to Transport. GVF-Report 272. Switzerland.
232. Dynes M. 4 May 1998. Life Goes On and On For the People Who Time Forgot. The Times.
233. Lynch J, Smith GD, Hillemeier M, Shaw M, Raghunathan T and Kaplan G. 21 July 2001. Income Inequality, the Psychosocial Environment and Health: Comparisons of Wealthy Nations. The Lancet 358 p194-200.
234. Office of Health Economics. 13 Aug. 1999. Britain is Doomed to Head Europe Heart Deaths Table. Times.
235. WHO Statistics Annual. 18 Oct 1995. Coronary Heart Disease Deaths. Daily Mail.
236. NHS Statistics. Jan 2001. NHS Available beds drop 31% since 1990. Country Doctor.
237. Dunn N. 16 March 2000. Getting Right to the Heart of the Matter. Western Mail.
238. Burns G, Broxbourne Council. 22 Sept 1998. Shock warning the Tube's toxic Dust Could Kill. London Evening Standard.
239. Rogers L. Britain Has The Worst Baby Death Rate in North Europe. The Times
240. Thompson R. 13 November 1998. Alarm over Infant-Death Figures. The Western Mail.
241. Ecocide in the USSR. 1991. Dark Satanic Mills p105. ISBN 1854 10 2303
Pesticides, Herbicides and GM Genes
242. Mae-Wan Ho. 1997. Genetic Engineering Dreams or Nightmares. Research Foundation for Science, Technology and Ecology, New Delhi.
243. Didricksen N. June 2000. Use of the Halstead-Reitan Neuropsychological Test Battery to Measure Neurotoxic Effects in Chemically-Poisoned Individuals. Symposium, Dallas, Texas.
244. Davies R, Ahmed G & Freer T. 2000. Chronic Exposure to Organophosphates: Background and Clinical Picture. Advances in Psychiatric Treatment 6 p187-192.
245. Davies DR, Ahmed GM and Freer T. 1999. Chronic Organophosphate Induced Neuropsychiatric Disorder (COPIND): Results of two postal questionnaire surveys. Journal of Nutritional & Environmental Medicine. 9/ p123-134.
246. Beavais SL, Jones SB, Brewer SK and Little E. 2000. Physiological Measures of Neorotoxicity of Diazinon and Malathion to Larval Rainbow Trout and their Correlation with Behavioural Measures. Environmental Toxicology and Chemistry 19(7) p1875-1880.
247. Environmental Working Group. 20 Feb 2001. Toxic Pesticide Found in California Air Samples (Chlorpyrifos @ 9 miles). Environment News Service.
248. Grimes G, Farm Worker Association of Florida. 23 February 2001. Toxic Pesticide Drifts Onto Florida Church Properties. Environment News Service.
249. Routledge L. 19 Sept 1999. Pesticides 'Making half a million ill'. The Observer.
250. Stone W. 22 June 2001. Pesticides Causes More Bird Deaths Than West Nile Virus - 80,000 Birds Examined. Environment News Service.
251. Lazaroff C. 20 Dec 2000. $73 Million Cleanup Targets DDT-Contaminated Ocean Floor. US Justice Department/State of California court settlement. Environment News Service.
252. Sao Paula State EPA. 16 Feb 2001. Shell Ordered to Decontaminate Brazilian Pesticide Plant. (Endrin, Aldrin and Dieldrin). Environment News Service.
253. Tvedten S. The Best Control. 2nd Ed.
254. Glynn P. 5 July 1999. Neural Development and Neurodegeneration: two faces of neuropathy Target Esterase. Progress in Neurobiology 61 p61-74.
255. Ho Mae Wan. 4 May 2001. Horizontal Gene Transfer Happens - 2. Inst.of Science in Society
256. Greunke G. July/Aug. 2001. The Cooking Oil Conspiracy. The Ecologist. Were the health effects really due to OP agrochemical contamination, also the Barcelona soya dust asthmas??
257. Natural Resources Defense Council. ?1999. A Summary of the hazards of Chlorpyrifos.
258. Natural Resources Defense Council. 1998. Trouble on the Farm- Growing Up with Pesticides in Agricultural communities (with 170 references).
259. Benbrook CM, Northwest Science and Environmental Policy Centre, Idaho. 3 May 2001. Troubled Times Amid Commercial Success for Roundup Ready Soybeans. AgBio InfoNet Technical Paper Number 4.
260. Richards P, Johnson M, Ray D and Walker C. 1999. Novel Protein Targets for Organophosphorus Compounds. Chemico-Biological Interactions 119-120 p503-511
261. Cox C. Autumn 1998.Responding to Chemical Goliath (Glyphosate). Journal of Pesticide Reform 18 (3).
262. Demerdash E, Yousef and Elagamy EI. Jan 2001. Glyphosate Demonstrated Toxicity on the Vital Enzymes. J Environmental Science Health 36 (1) p29-42. Note: Bruce R. has revealed that Glyphosate escaped the UK review of anticholinesterase compounds. (letter 5 May 2001).
263. Myhill S. 4 Dec 1996. Review of article-Chronic Organophosphate Syndrome as a Delayed Reaction to Chronic Low-Dose Organophosphate Exposure. Journal of Nutritional and Environmental Medicine 6 (4) p341-350. Also personal communications.
264. Park D, Hempleman SC and Propper CR. 2001. Endosulfan Exposure Disrupts Pheromonal Systems in the Red-Spotted Newt: A Mechanism for Subtle Effects of Environmental Chemicals. Environmental Health Perspectives 109 p669-73.
265. Box SA and Lee MR. 1996. A Systematic Reaction Following Exposure to a Pyrethroid Insecticide. Human and Experimental Toxicology 15 p389-390.
266. Black's Veterinary Dictionary 10th Ed. 1973. Warbles - Atropine is an Antidote for OP Crufomate overdosage in cattle.
267. Health and Safety Executive. Oct 1987. Revised Guidance Note MS 17 - Biological Monitoring of workers exposed to Organo-Phosphorus Pesticides.
268. MacLeod-Gilford W. 10 October 1998. Report on Use of Pesticides and Other Chemicals at WinterBrook Pig Farm, Blewbury. Blewbury Environmental Research Group.
269. Abou-Donia MB and Garettson LK. 2000. Detection of Neurofilament Autoantibodies in Human Serum following Chemically Induced Neurologic Disorder: A Case Report. Environmental Epidemiology and Toxicology 2 p37-41.
270. Ungoed-Thomas J. 20 Aug 2000. Passengers at risk from jet engine fumes. Sunday Times.
271. Cory-Slechta D. 15 Dec 2000. Combination of Pesticides Linked to Parkinson's Disease (Paraquat and Fungicide Maneb). Journal of Neuroscience.
272. Menegon A, Board PG, Blackburn AC, Mellick GD & LeCouteur DG. 24 Oct 98. Parkinson's Disease, Pesticides & Glutathione Transferase Polymorphisms. The Lancet 352 pp 1344-6.
273. Hardell L and Eriksson M. 15 March 1999. A Case-Control Study of Non-Hodgkin Lymphoma and Exposure to Pesticides. Cancer 85 (6) P1353-60
274. Lewis DL, Garrison AW, Wommack KE, Whittemore A, Steudler P and Melillo (USEPA). 28 Oct. 1999. Influence of Environmental Changes on Degradation of Chiral Pollutants in Soils. Nature 401 p898-901.
275. Miller CS & Mitzel HC March/April 1995. Chemical Sensitivity Attributed to Pesticide Exposure Versus Remodeling. Archives of Environmental Health. Vol.50 No.2. pp 119-129.
276. Frate DA. January 2001. Implementing a Chronic Noninfectious Disease Surveillance System. (Asthma Incidence in Children in area of high pesticide agricultural use, compared with low use area.) Report.

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