Monthly Archives: October 2015

PROOF: Beddington incinerator is not needed

STI flyer for printing back 3 Jan 2015

The simplest and most effective argument against the incinerator is: it is not needed (see above flyer from 2009).  However, the authorities and Viridor have always presented the case as an either/or situation: landfill or incineration.  Yet, respected environmental consultants Eunomia, who work for the South London Waste Partnership, have long been reporting that residual waste over-capacity is around the corner.

Then at last month’s South London Waste Partnership Joint Committee meeting, the Contract Manager pointed out that the  judicial review had delayed the incinerator’s construction. Those present heard her indicate that for 8 months all the residual waste would be sent to Viridor’s Colnbrook incinerator (45,000 tonnes of our waste is already being transported there). Evidently, it is not so either/or. I asked for clarification and finally received the emails below from Andrea Keys.

In short, waste produced by the South London Waste Partnership can all be shipped just 12 miles away to Colnbrook, which has available capacity.  WE DON’T NEED AN INCINERATOR IN BEDDINGTON. 

Starts:

Good morning Mr Khan,

I believe you raised the following clarification question around the Beddington landfill:
Q – When will landfilling cease at Beddington Farmlands?
A – The section 106 states that Viridor and Thames will ….
“cease the landfill of non-inert waste at the Site by 31st December 2017…”.
I have also attached a link to the section of the Viridor website that contains planning documentation associated with Beddington Lane landfill and the ERF.
I hope this is of assistance.
Kindest regards,
Andrea
*** I then asked when the incinerator (ERF) would be operational  and subsequently received this reply….***

Good afternoon,

It is estimated that the ERF will be operation in the financial year 2018/19.
Kindest regards,
Andrea
Andrea Keys
Contract Manager 
South London Waste Partnership
Email Ends.
 —
With so much over-capacity, there is little doubt that once operational, the incinerator in Beddington will burn waste imported from overseas and recyclables, bearing in mind we are stuck with it for a minimum of 25 years.
By Shasha Khan
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We can’t say it will kill people, we can’t say it will not.

colour flyer for printing front

An investigation into the South London ERF Health Impact Assessment by Craig (A-Level Physics teacher)

Introduction

This investigation is a critical review of Viridor’s Health Impact Assessment (HIA) for the South London Energy Recovery Facility, highlighting gaps in analysis, careful selection of evidence from papers, and the use of careful wording, including the use of caveats (‘get out clauses’). The HIA has informed the planning process, and this investigation highlights how a more favourable impression of the evidence base has been created, allowing public regulatory bodies –the Environment Agency (EA)and Public Health England – to deem it acceptable to locate the incinerator in a highly densely populated area, and to assert that there is no evidence that modern, well monitored, well run incinerators pose a risk to public health.

This investigation is an attempt to seek out any intrinsically positive spin on the HIA, taken from the basic viewpoint that the chimneys are there for a reason. They do work, insofar as they spread pollution sufficiently far afield to reduce pollution exposure to individuals. However, they could also be said to work in a more insidious way – they make it more difficult to get a clear picture of the epidemiological evidence, enabling doubt to be placed on any claims of public health impact.

The following is a summary of the possible weaknesses in the HIA :

  1. places where wording refers to absence of effect in immediate vicinity; health effects may not occur in the immediate vicinity of incinerators, but will be detectable further afield, albeit at a lower level;
  2. places where the HIA has taken advantage of inadequate collection of low level exposure data; so that, although there may be a significant pattern of health effects around incinerators, the public can’t prove that it was the incinerators that did it;
  3. comparisons with diesel emissions , as a way of normalising health impacts; this should no longer be acceptable. The World Health Organisation has finally managed to reclassify diesel particulates, from ‘probable carcinogen’ to ‘carcinogen’, and we are now trying to ban diesels from central London;
  4. furthermore, nanoparticles from incinerators are more likely than not to be more dangerous than diesel particles, as they are known to be coated in trace metals;
  5. claims that ‘newer’ incinerators are safer than ‘older’ ones, gives an impression that public health issues have been fixed; however, without a clear definition of ‘old’ and ‘newer’ however, it is unclear whether identified health effects might come from ‘newer’ incinerators. There is an implied definition that ‘older’ incinerators refers to those of the 1950s and 60s only, and that therefore 1970s onwards are ‘newer’.

All of these points could make a case that we should be using more precaution. Although there is no certain evidence of harm to the public, there is equally no certain evidence of safety –further research is necessary. It is left up to the public to prove that the 4 hour pollution windows, typically permitted in incinerator contracts, are causing harm over a long time period.

Appendix A5 (Incineration and Public Health, p94-103) is copied here, with comments embedded in blue, sometimes referring to the 5 main points given above.

A4 AIR QUALITY

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A4.2.2 COMEAP Advice and Reports

The Committee on UK Medical Effects of Air Pollution (COMEAP) published a report in February 2006 that assessed the possible effects of outdoor air pollutants on cardiovascular disease within the UK (1).

The report presents a comprehensive review of the available literature on the cardiovascular effects of air pollution that leads to the following conclusions:

Clear associations have been reported between daily and long term exposure to air pollutants and the effects on the cardiovascular system, including death and hospital admission.

The association seen between air pollution and cardiovascular effects is likely to be causal and therefore the precautionary principle (2) should be adopted.

That it is not possible to be certain which components of the ambient pollution mixture is responsible for the health effects, but that particulate matter is likely to play a part.

Therefore, COMEAP concluded that there is a causal link between air pollution and cardiovascular effects which is important for public health. However, the impact of factors such as family history, smoking and hypertension will have a greater impact. The subsequent COMEAP reports, published in 2009 and 2010, on the effects on mortality of long-term exposure to air pollution (3)(4)4, also contain important material on the cardiovascular effects, since it is thought that much of the mortality observed is attributable to cardiovascular effects.

A4.2.3 Mechanism of Action

Two principal mechanisms have been proposed to explain the association between particulate matter and cardiovascular effects which are not mutually exclusive. The first suggests that particles cause inflammation in the lung and that this can trigger changes in blood clotting and also that chemical changes in the blood affect the stability of fatty deposits(plaques) found on artery walls, especially those around the heart muscle. The second suggests that inhalation of particles, or some gases, could trigger a reflex that leads to a

(1) COMEAP (2006) Cardiovascular Disease and Air Pollution. Department of Health. Available at http://comeap.org.uk/documents/reports.html

(2) The precautionary principle is the ‘better safe then sorry’ approach to assessing and managing health risks especially those associated with environmental hazards. Wherethere is sufficient evidence to believe that a risk exists, prudence and ethical norms and values require that action be taken to reduce or minimise that risk, even if the evidence is not conclusive (A Dictionary of Epidemiology, Fourth edition, Last)

(3) COMEAP (2009) Long term exposure to air pollution: effect on mortality. Department of Health. Available at: : http://comeap.org.uk/documents/reports.html

(4)4COMEAP (2010) The Mortality Effects of Long Term Exposure to Particulate Air Pollution in the United Kingdom Available at: http://comeap.org.uk/documents/reports.html

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subtle change in the rhythm of the heart. Both are based on the suggestion that inhaled pollutants will cause an inflammatory response but have yet to be proved and do not explain the relationship between

cardiovascular diseases and gaseous pollutants.

A4.2.4 Effects of Short Term Exposure

Evidence exists of an association (of similar strength and statistical significance) between daily average concentrations of a number of ‘classical’ pollutants and the daily number of deaths and hospital admissions related to cardiovascular disease. There is, however, no evidence to suggest daily ozone levels are associated with hospital admissions for cardiovascular disease.

A4.2.5 Effects of Long Term Exposure

The evidence of the effects of long term exposure to air pollutants on cardiovascular disease is growing and current thinking is that such exposure contributes to a loss of life years. Even if the associations are relatively weak, in terms of the number of people exposed, the public health impact is large and therefore the precautionary principle has been adopted by COMEAP. For the population of Great Britain, COMEAP estimates that the effect on lost life years is greater than passive smoking or motor vehicle traffic accidents.

A4.2.6 Attributable Air Pollutant

It is not possible to determine which ambient pollutant(s) are exerting the effect, but the COMEAP report suggests that fine particles play a part. The Committee also notes that;

•“Particles are likely to be playing an important part in causing the health outcomes described.”

•“Our tentative conclusion is that neither nitrogen oxides nor carbon monoxide, at ambient concentrations, are as likely to be causally linked with cardiovascular disease as are fine particles.”

•“We are unable to come to firm conclusions regarding the importance of the associations between ozone and cardiovascular disease. “

•“As regards sulphur dioxide, evidence from both short and long term studies suggests an association with cardiovascular disease.”

A4.3 OTHER HEALTH EFFECTS ASSOCIATED WITH POLLUTANTS

A4.3.1 Particulate Matter

Particulate matter describes airborne solid particles and/or droplets which vary in size, composition and origin. PM is a mixture of particles that can adversely affect human health, damage materials, and form atmospheric haze

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that degrades visibility. PM is usually divided into different classes based on size, ranging from total suspended matter (TSP) to PM2.5(particles less than 2.5 microns in aerodynamic diameter) (1). The source of the particulate matter will affect the toxicity of the particles. Evidence suggests that fine particle size fractions (eg PM2.5) are more hazardous to health than larger particle size fractions (eg PM10), although the

latter still have a negative health effect. Positive implications of reductions in ambient PM concentrations on public health have been shown after the introduction of clean air legislation (2).

Health outcomes associated with short term exposure to particulate matter include:

Lung inflammatory reactions;

Respiratory symptoms;

Adverse effects on the cardiovascular system;

Increased medication usage;

Increased hospital admissions; and

Increase in mortality.

Long term exposure to particulate matter is associated with;

Increase in lower respiratory symptoms;

Reduction in lung function in children;

Increase in chronic obstructive pulmonary disease (COPD);

Reduction in lung function in adults; and

Reduction in life expectancy, owing mainly to cardiopulmonary mortality and probably to lung cancer.

The available evidence indicates, in summary, that:

there is strong evidence that exposure to particulate matter brings forward all non traumatic deaths;

there is moderate evidence that long term exposure increases death from respiratory and cardiovascular diseases and that and COPD and asthma in the over 65s;

there is moderate evidence that particulate matter increases emergency hospital admissions for all circulatory, respiratory and heart diseases;

chronic exposure to increased concentrations of particulate matter also increases deaths; and

(1) Definition of PM from http://envirocitizen.inknoise.com/cleanenergy/2005/02/14/0001

(2) Health aspects of air pollution with Particulate matter, ozone and Nitrogen dioxide. Report on a WHO working group Bonn Germany January 2003

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there is a linear relationship (1)between and health effects with no known threshold (2), a result supported by the WHO but with a cautionary note that the linear relationship cannot be extrapolated below 20 μgm-3

or above 200 μgm-3 as these are outside the range of the observed PM10 (3)The public health implications of the long-term effects of exposure to PM are an order of magnitude greater than those of the short-term effects as measured by life years lost, although it is difficult to disentangle the two entirely (4). The WHO, therefore, recommends guidelines for both short and long term exposure levels.

A4.3.2 Nitrogen Dioxide

Health effects associated with short term exposure to ambient levels of nitrogen dioxide include;

effects on pulmonary function, particularly in asthmatics;

an increase in airway allergic inflammatory reactions;

an Increase in hospital admissions; and

an increase in mortality.

The health effects associated with long term exposure include;

reduction in lung function; and

increased probability of respiratory symptoms.

In summary, the evidence suggests that:

a linear relationship between health outcomes and NO2 exists and no threshold level has yet been established;

causality has yet to be established between health effects and NO2;

health risks from nitrogen dioxide may result from NO2 itself or its reaction products, including O3 and secondary particles;

associations between NO2 and health effects need to be interpreted with caution, since it could be that NO2 is in fact acting as a ‘marker’ for other pollutants associated with road traffic emissions;

•‘uncertainty remains about the significance of nitrogen dioxide as a pollutant with a direct impact on human health at the currentambient air concentrations in

(1) This means that the percentage chance of an outcome remains the same for a given increment in the pollutant

(2) Health Aspects of Air Pollution with Particulate Matter, Ozone and Nitrogen Dioxide. Report of a WHO working group Bonn Germany January 2003

(3) WHO Regional Office for Europe (2000) Air Quality Guidelines for Europe, 91 (2nd ed) edn

(4) WHO (2004) Health Aspects of Air Pollution- results from the WHO project “systematic review of health aspects of air pollution in Europe” available at www.who.euro.int

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the EU and there is still no firm basis for selecting a particular concentration as a long term guideline for nitrogen dioxide’ (1), according to the WHO;

the setting of a 40μgm-3 as an annual average may not be justified, although it may be a useful precautionary principle;

nitrogen dioxide is associated with circulatory deaths, emergency admissions for asthma in younger adults and emergency admissions for cardiac diseases; and

there have been no recent peer reviewed studies which have shown that a reduction in NO2 has a positive impact on public health (2)

.

A4.3.3 Sulphur Dioxide

In summary, the evidence on health effects from exposure to sulphur dioxide states that:

there is linearity in the dose response relationships and reports conclude that there is no evidence that there is any threshold below which the effects do not occur;

there is evidence that sulphur dioxide causes symptoms in asthmatics, as it is a potent irritant and induces reversible change in lung function in both children and adults; and

sulphur dioxide is also related to all cause mortality, cardiovascular deaths and respiratory deaths and admissions.

A4.3.4 Other Pollutants

A wide variety of other pollutants are also known to result in health effects at sufficiently high oncentrations, but they are of less significance in terms of health for populations, as their ambient concentrations tend to be extremely small for most locations. Many of these have to be considered in terms of risk,

since they are carcinogens, such as some volatile organic compounds and some metals.

A4.4THE CLEAN AIR FOR EUROPE PROGRAMME

Clean Air for Europe (CAFE) was a European Commission programme of technical analysis and policy development, initiated in 2001. The CAFE programme developed a methodology for assessing the

health impacts of changing air pollution and for cost benefit analysis of any change. CAFE

(1) WHO (2004) Health Aspects of Air Pollution- results from the WHO project “systematic review of Health aspects of air pollution in Europe” available at www.who.euro.int.

(2) Health aspects of air pollution with Particulate matter, ozone and Nitrogen dioxide. Report on a WHO working group Bonn Germany January 2003

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adopts a no threshold assumption as the primary basis for its quantification methodology; an assumption consistent with a variety of other studies. CAFE uses the following linear equation to quantifying acute health effects for air for those pollutants where epidemiology has identified an association:

E = βx ∆C x P x E, where: (∆)E = (change in) background rate of events; β= exposure-response coefficient; ∆C = change in concentration of pollutant; P = population exposed.

Although the time series epidemiological studies are based on 24-hour concentrations of pollutants, an assumption of no lower threshold of effect means that the relative risk ratios can be applied

to annual average concentrations, making the computation much simpler.

Acute morbidity related to exposure to particulate matter is considered by CAFE for the following outcomes:

Chronic bronchitis (adults);

Respiratory hospital admissions;

Cardiac hospital admissions;

Restricted activity days (adults);

Respiratory medication use (adults);

Respiratory medication use (children);

lower respiratory system symptom days (children) and;

Lower respiratory system symptom days (adults).

For mortality, takes the view that the results should be expressed in terms of life years lost, rather than numbers of deaths. This represents the current consensus view of the subject and is also consistent with the view of COMEAP. The CAFE methodology takes the increased incidence of certain heath

outcomes (based on relative risks) for exposure to particulate matter as shown in

Table A4.1 below. These increased incidences are from studies that are statistically significant at a conventional 5% level, with one exception.

Table A4.1 Increases in Health Outcomes from Exposure to an Additional 1 μg m-3 PM

Health Outcome

Increase (based on Relative Risk)(1)

PM type

Chronic exposure

Change in mortality hazards

0.6%

PM2.5

Chronic bronchitis (attack rates)

0.7%

PM10

Acute Exposure

Cardiovascular hospital admissions

0.06%

PM10

Respiratory hospital admissions

0.114%

PM10

Consultation with GPs (asthma, April –Sept, 15 –64 years age)

0.25%

PM10

Restricted Activity Days

0.0475%

PM2.5

Lower respiratory symptoms (wheeze, shortness of breath , phlegm production) (in children)

0.0004%

PM10

Lower respiratory symptoms (in adults)

0.0017

% PM10

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(1)Relative Risk: The relative risk estimates the magnitude of an association between exposure and disease and indicates the likelihood of developing the disease in an exposed group relative to those who have not been exposed. It is defined as the ratio of the incidence of disease in the exposed group divided by the corresponding incidence of disease in the non exposed group.

A4.5 VULNERABLE GROUPS

Groups that are particularly vulnerable to exposurefrom air pollution include foetuses, young children, the elderly, those with cardio-respiratory disease and the socio-economically deprived.

A4.6QUANTIFICATION OF HEALTH EFFECTS FROM INCINERATOR EMISSIONS

The existence of exposure-response relationships for pollutants such as PM2.5, PM10 and NO2 make the quantification of health effects resulting from EfW plant emissions a feasible task. Several examples exist in several Environmental Statements submitted in recent years,but also in scientific literature, such as Mindell and Barrowcliffe (1), and more recently, Forastiere et al (2). Such studies find that the impact of waste incineration emission on the population, in terms of mortality, is quite low, when seen in the proper context. Estimates of life years lost tend to range from minutes to days on a per person basis. Such numbers can seem alarming to a reader not acquainted with such statistics, but are in fact not at all high when compared

with other forms of environmental pollution or hazards encountered in everyday life. The Forastiere et al study produced an estimate for life years lost that was strongly influenced by the assumption that NO2 contributes to mortality. Not all experts would agree with this assumption, including COMEAP. Roberts and Chen (2006) (3) assessed the potential health impacts of a waste to energy plant, designed to burn 52,500 tons of refuse derived fuel (RDF) annually (assuming current EU regulations on emissions are in force). Making the worst case scenario that the plant could emit the maximum permitted levels of every chemical of interest throughout the normal operating period,

(1) Mindell J and Barrowcliffe R (2005) Linking environmental effects to health impacts: a computer modelling approach for air pollution Journal of Epidemiology and Community Health 59 1092-1098

(2) ForastiereF et al Health impact assessment of waste management facilities in three European countries Environmental Health 10 53

(3) Roberts RJ, Chen M (2006)’Waste incineration – how big is the health risk? A quantitative method to allow comparison with other health risks’ J of Public Health 28(3):261-266

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they calculated the impact on the local population of 25,000. They estimated that if the plant operated for 25 years it might contribute to a cancer increase of 0.018 per million of population. In addition, 0.46 deaths per million of the population might be brought forward due to sulphur dioxide and 0.02 deaths per million brought forward due to particles (this study did not consider the effect of PM2.5 in terms of life years lost or the most recent COMEAP exposure response relationship for mortality). The overall risk of dying as a

consequence of the plants operation calculated to be 2.49×10-7. The overall conclusion is that the impact of the proposed planton the health of the local community would be negligible.

A4.7 DUST

A4.7.1 Introduction

The potential for dust to be emitted during construction is strongly dependent on the type of activities taking place, on wind speed and on whether winds carry emitted particles towards sensitive receptors, such as hospitals, schools and residential property.

A4.7.2 Health Effects of Dust

Dust emissions arising from construction activities can cause outside the site boundary causing annoyance to neighbours by the soiling of property, in particular, windows, cars and washed clothes that have been hung out to dry.

Construction sites are a temporary operation and some degree of nuisance would normally be tolerated if the activity lasts for no more than a few months. Recent studies by the Building Research Establishment also suggest that nuisance is unlikely to occur at distances greater than 50 metres from a construction site boundary (1). One particular study (2)has also shown that at least half the people living within 50 metres of the site boundary of a road construction scheme were seriously bothered by construction nuisance due to

dust, but that beyond 100 metres less than 20 percent of the people were seriously bothered.

(1)Buildings Research Establishment (BRE) (2003). Control of dust from construction and demolition activities. Kukadia, V., Upton, S. and Hall, D. BRE Bookshop, London. February 2003.

(2) Baughan, C.J. (1980) Nuisance from road construction : a study at the A31 Poulner Lane Diversion, Ringwood: TRRL Supplementary Report 562. In: Design Manual for Roads and Bridges, 1994.

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A5 INCINERATION AND PUBLIC HEALTH

A5.1 INTRODUCTION

A dominant concern and anxiety within host communities where a new EfW plant is proposed relates to the emissions to atmosphere of a number of substances. In recent times, the emerging knowledge relating to particles and health has reinforced such concerns. In terms of the available evidence, this is more than adequately addressed by the preceding section on general air pollution. There is nothing unique about particles generated by EfW facilities relative to other combustion processes and every reason to suppose that the effect of such particles on human health at the population level around any facility is entirely similar to that observed in the large scale epidemiological studies.

A more long standing concern relates to substances such as dioxins and metals, which have been associated with waste incineration. Any health effects from exposure to these substances would be

through prolonged exposure and manifest themselves as chronic effects. Some of the substances are carcinogens and a fear commonly expressed is that the incidence of cancer will increase.

Unsurprisingly, given that waste incineration is a waste treatment practice with a long history, there is a wealth of scientific literature examining the evidence for health effects in the vicinity of such plant. In excess of 650 peer reviewed papers on the subject can be found in the literature. This section provides a review of the most useful of these, concentrating on those that are reviews and those that relate to modern EfW facilities. It is not intended as a comprehensive review, which would occupy a report in itself.

A number of literature reviews have been carried out and these provide a useful point of reference for the range of literature available (1)(2)(3)(4). The conclusions drawn are variable and sometimes reflect the views and affiliations of the authors.

A5.2 SOURCES AND CHARACTERISTICS OF DIOXINS

Dioxins are emitted from many sources including vehicles, bonfires, domestic and industrial combustion process. Uncontrolled burning of waste is a major

(1) Allsopp M, Costner P and Johnston P. Incineration and human health: State of knowledge of the impacts of waste incinerators and human health, Environmental science and pollution research 8(2) 141-145 (2001)

(2) Health effects of waste incineration: A review of Epidemiologic studies. Hu and Shy, Journal of air and waste management association 51:1100-1109 July 2001

(3) Health Risks of Air Pollution from Incincerators: a perspective. Rabl and Spadaro Waste Management and Research;16;365-388 1998

(4) Incineration and Human Health, State of Knowledge of the impacts of waste incinerators on Human Health. Michelle Allsopp et al Greenpeace research laboratories

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source of dioxin emissions. The main route of dioxin exposure is through food. Each year, many new publications on aspects of the toxicology and epidemiology of dioxins appear. Dioxin concentrations in food and the general environment throughout the western world have been falling, but public concern and new research results in frequent evaluations of acceptable levels of these chemicals ( by national and international bodies). Many of the new studies showing effects of dioxins come from the Far East, where general pollution levels have been rising. The overall conclusion of many studies is that at body burden levels, within an order of magnitude of those found in the general western population, subtle adverse effects may occur. However, it should be noted that body burden of dioxins have been falling over the past two decades in Europe and this trends appears to be continuing. This is confirmed by a DEFRA review (2004) (1), which stated that even in a rural environment any increased deposition of dioxins from an incinerator would be too small to be of concern with regard to health. The consensus view is that dioxins increase the risk for all cancers combined. However, the magnitude of this increase appears to be low and no statistically significant increase in any particular type of cancer has been identified. A substantial dioxin exposure leads to elevated incidence of cardiovascular disease and diabetes although other studies challenge this conclusion. In workers a persistent skin condition (termed chloro-acne) may occur handling contaminated materials. In animals, dioxin is a teratogen. There is clear evidence of immune suppression following exposure as a foetus. However, there is no good evidence among exposed communities such as the Seveso population of impaired immune competence. In other human studies there is some rather limited evidence of effects on the immune system. There is insufficient information from human studies to determine the threshold level directly. In a number of studies dioxins were found to be endocrine disrupters, a property it has in common with a number of persistent polyhalogenated aromatic chemicals.

Dioxins are generated from many processes as trace contaminants. The levels of individual congeners (related structures) of dioxins vary considerably by source. In view of this fact a standardised form of expressing the overall toxicity is required. The internationally accepted form is to use Toxicological

Equivalents (TEQs), which is based on an allocation of a toxicity rating to each congener (so called toxic equivalency factor TEF)).The most potent – 2, 3 , 7, 8- tetrachlorodibenzodioxane (TCDD) – is assigned a

value of 1 and the remaining 17 dioxin congeners with chlorine in the 2, 3, 7 and/or 8 positions are assigned a value lower than 1. A TEQ for a particular source can be calculated using measurements of the percentage of each congener in the total amount of dioxin, and its concentration.

(1) DEFRA (2004) Review of environmental and health effects of waste management, HMSO: London

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Ingestion is the primary exposure route in relation to dioxins. In 1998, the World Health Organization (WHO) proposed a revised Tolerable Daily Intake (TDI) of 1-4 pg/kg body weight for dioxins, on the

basis of a comprehensive review of the health effects of these chemicals. The WHO emphasised, in its

analysis of the risks from dioxin exposure at different levels, that (as far as the protection of the public is concerned), it is the exposure over a prolonged period of time (rather than short term fluctuations in levels) that is important. In the UK, the Committee on Toxicity has recommended a Tolerable Daily Intake of 2 pg/kg body weight, over a lifetime. It reached this decision on the basis of developmental effects, not carcinogenicity, which would have produced a higher number. Most countries have not set ambient air quality guidelines or standards for dioxins in air and have concentrated on applying the WHO standards for dioxins in food instead.

A5.3 EXPOSURE AND BIOMONITORING STUDIES

An evaluation of the likely impacts arising from emissions from the operation of an EfW facility can be made by considering the available publications on:

Measurements of the concentrations of certain chemicals of interest (exposure investigations)in air, soil and plants; and

Measurements of certain chemicals of interest in human blood and breast milk (biological monitoring).

The focus of research in the last two decades has been on measurements of dioxins and metals as these are most likely to persist in the local environment. Dioxin concentrations in ambient air are very low, in part a reflection of their very low volatility and declining emissions. Maximum quarterly concentrations of dioxins and furans in major cities in the UK are currently in the range (approximately) 10-100 fgTEQ m-3. Rural concentrations are in the range 5-15 fg TEQ m-3(1).Part of the reason for the decline in ambient concentrations is that the emissions from modern EfW facilities in the EU countries are a minimum of 2 -3 orders of magnitude lower than was the case in the 1950s and 1960s. An investigation of dioxin concentrations in soil and vegetation around a municipal waste (MSW) EfW plant in Spain by Domingo

et al (2001) (2), that emitted somewhat higher levels of dioxins that are currently permitted, resulted in the conclusion that, “in comparison with other emission sources of PCDD/Fs in the same area” (traffic, other industrial activities, bonfires) “the current PCDD/F emissions from the MSW incinerator would be of small significance for the population living in the neighbourhood of the MSW incinerator”.

(1) The Lancaster Environment Centre (2010) Annual |Report on the UK Toxic Organic Micro-Pollutants Monitoring and Analysis Network, for Defra

(2) Domingo JL, Schuhmacher M, Granero S and De Kok HAM (2001)’Temporal variation of PCDD/PCDF levels in environmental samples collected near an old municip

al waste incinerator’ Environ Monitoring and Assessment, 69:175-193

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Caserini et al(2004) (1)examined air and soil concentrations of dioxins around three MSW EfW facilities in Italy. At all three sites, dioxin concentrations in soil were at the lower limit of the average values for rural areas. Mari et al (2007) carried out a temporal assessment of environmental contamination around a modern hazardous waste incinerator. The authors’ conclusion was that the EfW Facility did not significantly increase dioxin concentrations in soils around the plant. Marti-Cid et al(2008) (2)measured PCDD/PCDFs in foodstuffs in Tarragona (Spain) near a hazardous waste incinerator (in operation since 1998). The authors concluded that the concentrations of dioxin were higher prior to the installation of the EfW facility and concluded that‘the notable decrease in the atmospheric levels of PCDD/PCDFs over the world would explain notable differences between the results in the dietary intake in the base line, 2002 and current surveys’.

Both for humans and animals the intake of dioxins (and dioxin-like materials) is influenced by the nature of their diet, regardless of age. Diet high in fat (particularly oily fish) will lead to relatively high intake of dioxins. In an investigation of the blood levels of dioxins in a local population, Spanish authors compared measurements made in individuals before and for two years after a new MSW EfW plant became operational (Gonzales et al 2000) (3). Two population groups were selected: one living within 1.5km of the plant and the other 3.5-4 km away. There was a control group, which lived in an area without an EfW facility. All three populations showed increased blood levels of dioxins over the two-year period regardless of the distance from the incinerator. A similar,

(1) Caserini S, Cernuschi S, Giugliano M, Grosso M,Lonati G, Mattaini P (2004) ‘Air and soil dioxin levels at three sites in Italy in proximity to MSW incinerator plants’ Chemosphere 54, 1279-1287

(2) Marti-Cid, Bocio A and Domingo JL (2008) Dietary exposure to PCDD/PCDFs byindividuals living neara hazardous waste incinerator in Catalonia, Spain: temporal trend’ Chemosphere 70, 158-159

(3) Gonzales CA, Kogevinas M, Gadea E, Huici A, Basch A, Bleda MJ, Ergo OP (2000)’Biomonitoring study of people living near or working at a municipal solid-waste incinerator before and after two years of operation’ Arch Environ Health 55, 259-267

(4) Yoshida K, Ikeda S, Nakanishi J (2000)’Assessment of human health risk of dioxins in Japan Chemosphere 40:177-185

(5)Evans RG, Shadel BN, Roberts DW, Clardy S, Jordan-Izaguirre D, Patterson DD, Needham LL,(2000)’Dioxin incinerator emissions exposure study Times Beach, Missouri’ Chemosphere, 40: 1063-107

but smaller, reduction was also found in the control population. Two studies conducted in Portugal found no increase in either blood levels or in breast milk in the local population in the vicinity of modern incinerators compared to a control population (Reis et al2007a, 2007b) (1)(2).

Measurements of dioxin in air around waste incinerators that are performing to current EU emission standards indicate ambient air levels that are indistinguishable from those in other urban locations. There is little or no indication of increased blood or other breast milk levels of dioxins. Numerous studies also show that background dioxin levels have been falling in food over the past decade. Kulkarni et al(2008) (3)stated ’over the past several years there has been a shift in the major sources of dioxins in large part due to

regulations and focused voluntary efforts.’

The published literature in relation to dioxins in the local environment around modern incinerators may be summarised as follows:

No detectable increases in blood levels, breast milk levels or umbilical cord blood samples;

No detectable increases in contamination of plants or animals;

No measurable increases in soil or air concentrations.

These studies are useful and persuasive, because they the most direct measure available of the ‘imprint’ that an EfW plant might have on the local environment. It is much harder to isolate and measure any health outcomes in a local population that might be directly attributable to the emissions than it is to isolate and measure a ‘marker’ substance strongly associated with the emission.

A5.4 EPIDEMIOLOGICAL STUDIES

A great many epidemiological investigations have looked at various diseases in populations living around incinerators compared with the incidence of the same diseases in ‘control populations’ in terms of the incidence of:

effects on the lung;

cancers; and

reproductive effects.

An important constraint in reviewing the data is that the key studies are all retrospective and therefore are focussed on incinerators that are poorly performing by today’s standards. A selection of papers from the literature are briefly summarised here. A complete review would form a report in itself.

(1) Reis MF, Miguel JP, Sampaio C, Aguiar P, Melim JM, Papke O (2007a)’Biomonitoring of PCDD/Fs in populations living near Portuguese solid waste incinerators: Levels inhuman milk’ Chemosphere 67: S231- 237

(2) Reis MF, Miguel JP, Sampaio C, Aguiar P, Melim JM, Papke O (2007b)’Determinants of dioxins and furans in blood of non-occupationally exposed populations living near Portuguese solid waste incinerators’ Chemosphere 67: S224- 230

(3) Kulkarni Ps, Crespo JG and Afonso CAM (2008)’ Dioxin sources and current remediation technologies-A review’ Environ Int 34, 139-153

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Hu et al, (2001)(1)investigated chronic health effects in communities living near to three separate MSW EfW plant in the USA (which performed to levels that are substandard to the current EU ones between1992 and 1994). Participants in the study were assessed each year by a spirometric test. The results were not statistically significant between lung function and proximity of residence to any of the three incinerators.

Gray et al(1994) (2)compared the prevalence of asthma in children living around a sludge burning incinerator and in a control area. No significant differences were found. Miyake et al(2005) (3)examined the possible

contribution to respiratory symptoms (and some other effects) in young Japanese school children whose schools were near incinerators. The authors conclude that the presence of a school close to the incinerators causes a small increase in the prevalence of one or more of the symptoms. However, the

design of this study makes the interpretation of the findings very difficult.

The main contributor to foetal abnormalities appears to be genetic. The overall level of congenital abnormalities in the UK is generally rather constant from year to year. Dolk and Vrijheid (2003) (4) reviewed the epidemiological studies for correlations between congenital abnormalities and exposure to chemicals

associated with environmental pollution and considered a number of possible causes and contributory factors. The authors concluded that there are relatively few environmental pollution sources for which strong conclusions can be drawn regarding their potential to cause congenital abnormalities. Cresswell

et al, (2003) (5)conducted a study in a population around the Byker (Newcastle- upon-Tyne) waste combustion plant. No significant overall association between the number of congenital abnormalities and geographical proximity to the plant was found in the study.

Zambon et al(2007) (6)investigated the incidence of sarcomas in a case control study involving individuals living in an area which had some 22 incinerators of various kinds as well as a number of other industrial plants. The data were collected in the 1990s and relate to old incinerators. They found an increased

incidence of sarcomas which they attributed to dioxins. No direct evidence was put forward to link the sarcomas either to the incinerators or to dioxins.

A Finnish research project which studied the association between soft-tissue sarcoma and dioxin identified that the highest risk of sarcoma was found at

(1) Hu SW, Hazucha M, Shy C (2001,a) Waste incineration and pulmonary function; an epidemiologic study of six communities, Air and Waste Manage Assoc, 51, 1185-1194

(2) Gray, E.J.; Peat, J.K.; Mellis, C.M.; Harrington, J.; Woolcock, A.J (1994). Asthma Severity and Morbidity in a Population Sample of Sydney School children’ NZ J.. ed. 24, 168-175

(3) Miyake Y et al(2005) Relationship between distance of schools from the nearest municipal waste incinerator plant and child health in Japan. Environ Epidemiology 20, 1023-1029

(4) Dolk H and Vrijheid M (2003) ‘The impact of environmental pollution on congenital anomalies’ British Medical Bulletin68:25-45

(5) Cresswell PA, J. E. S. Scott, S. Pattenden and M. Vrijheid(2003)’Risk of congenital anomalies nearthe Byker vaste combustion plant’ J of Public Health 25(3):237-242

(6) Zambon P, Ricci P, Bovo E, Casula A, Gattolin M, Fiore AR, Chiosi F and Guzzinati S (2007) ‘Sarcoma risk and dioxin emissions from incinerators and industrial plants: a population-based case-control study (Italy)’ Environmental Health, 6, 19

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low levels of dioxin concentration (Tuomisto et al, 2004) (1). No increased risk associated with increased dioxin concentration was found.

One of the best conducted studies on possible adult cancer risks was that of Elliott et al, (1996) (2). They used postcode data to investigate the cancer incidence among 14 million people living near any of the 72 MSW incinerators in the UK. A statistically significant trend for a decline in risk was observed with increasing distance from the incinerators for all cancers combined (and for stomach, liver and lung cancers specifically). When allowance was made for socio-economic deprivation scores in each location no adverse effects could be identified.

Knox (2000) (3)studied possible health risks to children from both landfill and incineration emissions the study focused exclusively on child deaths from cancer (both solid tumours and leukaemias). Knox’s

view was that with proximity (7.5-km) to very old MSW waste incinerators and old hospital incinerators there was a small increased relative risk for children to develop cancer. If these very old incinerators are omitted, there is no identifiable increased cancer risk. Knox acknowledged that this‘seemed to exonerate the more modern plants’ (built in the 1960s and 1970s).

In another review, the authors stated that there is no clear relationship between childhood cancer and incinerator emissions, even if some results were statistically significant (Franchini et al, 2004) (4). In Italy, Federico et al, 2010 (5) examined cancer incidence in people with residential exposure to a municipal waste incinerator, using data recorded between 1991-2005. Three bands of increasing distance from the incinerator up to a radius of 5 km were used as surrogate markers of exposure. Over the 15 year period over 16,000 cases of cancer were identified within the three bands. Three significant clusters were identified but their shapes could not be associated with the MWI location.

The authors’ final conclusion reads as follows: ‘Bearing in mind the intrinsic limits of the study, the results suggest that there is no detectable increase of cancer risk for people living in proximity to the Modena MWI’.

There are so many published papers investigating the possible effects on health of waste incinerators that it is not surprising that there is a diversity of opinion and results. This breadth of literature also lends itself to some reviewers taking a selective or partial view of the literature, or even of

(1) Tuomisto JT, Pekkanen J, Kiviranta H, Tukianen E, Vartiainen T and Tuomisto J (2004)’ Soft-tissue sarcoma and dioxin: a case-control study’ Int J Cancer, 198:893-900

(2) Elliot t P, Shaddick G, Kleinschmidt I, Jolley D, Walls P, Beresford J and Gruny G (1996)’ Cancer incidence near municipal solid waste incinerators in Great Britain’,

Brit J Cancer, 73, 702-710

(3) Knox EG((2000)’Childhood cancers, birthplaces,incinerators and landfill sites’ in Int J of Epidemiology, 29:391-397

(4) Franchini M, Rial M, Buiatt E, Bianchi F (2004)’Health effects of exposure to waste incinerator emissions: a review of epidemiological studies’ Ann Ist Super Sanita,

40(1):101-115

(5) Federico M, Pirani M, Rashid I, Caranci N and Cirilli C (2010)The cancer incidence in people with residential exposure to a municipal waste incinerator: an ecological study in Modena (Italy) 1991-2005’ Waste Management,30:1362-1370

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individual papers. For example, Tango et al(1) report that there is a small but statistically significant peak decline risk with distance from 63 MSW incinerators for infant mortality beyond 2 km up to10 km. Opponents of incineration often cite this result, but fail to mention that the authors also states;

However, due to the lack of detailed exposure information to dioxins around the incinerators, the observed trend in risk should be interpreted cautiously and there is a need for further investigation to accumulate good evidence regarding the reproductive health effects of waste

incinerator exposure’, or that the study showed no significant excess of outcomes in the distance 0-2

km. Moreover, the incinerators selected were deliberately chosen as those with emissions of dioxins above 80 ng (TEQ) m-3(as compared with the current EU limit value of 0.1 ng (TEQ) m-3.) In fact, it is noticeable that many of the studies that purport to show an association between health outcomes and proximity to incinerators are based on data gathered in Asian countries where emission were historically high.

The published literature in relation to the epidemiology of health effects around incinerators is retrospective and does not include modern incinerators. The findings for older incinerators with substantially higher emissions may be summarised as follows:

No consistent increase in the incidence of respiratory effects;

No consistent increase in the incidence of reproductive effects or effects on the developing foetus;

No detectable increase in childhood cancers;

A possible small increase in sarcomas; and

No identifiable increase in other cancers.

In other words, for some outcomes, there is some degree of evidence that older forms of waste incineration were associated with adverse health outcomes, but this evidence is far from conclusive.

Finally, it should be noted that that are some reviews of the subject that are often cited by campaigners against incineration and which therefore achieve undue prominence. One such report has been publish

ed by the British Society for Ecological Medicine, in 2008 (2). This report was strongly criticised by the

Health Protection Agency in a formal response (3), part of which states, ‘The BSEM report is not a systematic review of the literature and there is no critical assessment of the quality of the included studies. Consequently, the report presents a selective and limited use of the scientific literature.

(1) Tango et al (2004) Risk of adverse outcomes associated with proximity ot municipal solid waste incinerators with high dioxin emission levels in Japan Journal of Epidemiology 14(3) 83-93

(2) Available at : http://www.ecomed.org.uk/publications/reports/the-health-effects-of-waste-incinerators

(3) Available at: http://www.ecomed.org.uk/content/IncineratorHPA.pdf

The response goes on to state:

the report does not distinguish adequately between hazard and risk, ie the intrinsic hazard associated with a chemical/s, as opposed to the likelihood of health impacts (which is dependent upon exposure).’

A5.5 ULTRAFINE PARTICLES

A topic that is often raised in applications for new EfW facilities is that of the effect of ultrafine particles on health. These are defined as being those particles with a diameter of 0.1 μm or less. Particles of such small dimension pose a potential problem for human health, as they are able to pass through the bronchial epithelium (ie the lining of the lung) into the bloodstream. Evidence is accumulating that ultrafine particles may be associated with health effects in a more potent way than larger particles.

The term nanoparticles is sometimes used interchangeably with ultrafine particles, chiefly because this term has entered the language through the debate on the safety of nanotechnology. There is no widely accepted definition of the size of nanoparticles. Strictly speaking, they should refer to particles of diameter 1 nm, but in practice, the term is taken to include particles up to 50 nm, or 0.05 μm. Ultrafine particles are generated very effectively by combustion processes and an EfW plant would be a prime source of such particles, were it not for the fact that such plant operates with fabric filters. It is commonly assumed, and

frequently asserted, that ultrafine particles are released freely and without restraint by EfW plants. This is not the case. The physics of filtration lead to the conclusion that a fabric filter is actually extremely efficient for very small particles, where the process of diffusion attracts the ultrafine particles with near 100% efficiency to the fibre and filter cake. The minimum efficiency, with respect to particles size, occurs in the range 0.1 μm to 1 μm, although even here the collection efficiency is easily in excess of 97% at the lowest point.

Until recently, the evidence base for measurements supporting the theory was very weak. In the last few years, however, a number of Italian studies have demonstrated that fabric filtration is indeed highly efficient at removing fine and ultrafine particles. The work done by Buonanno et a l (1)shows that the efficiency with which particle numbers are reduced across a fabric filter in a working EfW plant is 99.995%. This same paper also reports measurements of ultrafine particle numbers downwind of a major road and demonstrates that the road traffic is a significantly greater source of ultrafine particles than is the EfW plant. Similar observations on the magnitude of ultrafine particle numbers have been reported by Buonanno et al (2), Cernuschi et al (3) and

(1) BuonannoG et al (2010) Ultrafine particle apportionment and exposure assessment in respect of linear and point sources Atmospheric Pollution Research 1 36-43

(2) Buonanno G et al (2009) Size distribution and number concentration of particles at the stack of amunicipal waste incinerator Waste Management 29 749-755

(3) Cernuschi et al (2010) Ultrafine partciles in the flue gas from four waste to energy plants Proceedings of the Third International Symposium on Energy from Biomass and Waste, Venice, Italy, 8-11 November 2010.

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Angeluci et al(1). The use of particle number concentrations as a metric, rather than the one based on mass, is significant, as thismetric is strongly biased towards the ultrafine fraction. It is a more useful measurement if the emphasis is on the very smallest particles.

(1) Angelucci et al (2010) Ultrafine particles in emission of a municipal solid waste incinerator and wood stove Proceedings of the Third International Symposium on Energy from Biomass and Waste, Venice, Italy, 8-11 November 2010.

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