CANK has read the interview given by Dr Roberts in the Evening Leader on 27th January, and we are astonished that he is able to make such statements.

Dr Roberts' report was prepared with the benefit of information supplied by Castle Cement, and neither CANK, nor, so far as we are aware,any other objectors' group, was given the opportunity to present evidence to him before he finalised his report.

Furthermore, no references were quoted in his report - the conclusions are, in CANK'S view, questionable.

In the circumstances we do not see how a decision on the planning application can be reliably made in reliance on Dr Roberts' report.

As CANK has done all along, it has sought the views of its own experts on Castle's claims, and it has done so also in relation to Dr Roberts' report.
You will find atached a copy of a report prepared by Drs. Howard and de Yanis of Liverpool University, raising significant questions about Dr Roberts' report.

These comments were sent to Flintshire County Council on January 13th,

BUT, SO FAR AS CANK IS AWARE, HAVE NOT BEEN MADE AVAILABLE TO COUNCILLORS
DESPITE THE FACT THAT THE OFFICERS' REPORT TO THE PLANNING COMMITTEE WAS
ONLY RELEASED LAST WEDNESDAY, 26th JANUARY.

Index
 Glossary
 General
 Section 3, Particulates
 Section 3, Dioxins & Furans
 Section 4

Glossary of abbreviations used

IQ  Intelligence quotient
kg  kilogram (1000 grams)
µm  micrometre (a thousandth of a millimetre)
pg  picogram (10-12 grams, or a millionth of a millionth of a gram)
PM10  Particulate matter less than 10 µm aerodynamic diameter
SO2  sulphur dioxide
TDI  tolerable daily intake
TEQ Toxic Equivalent - a method of relating the toxicity of all the different forms of dioxin-like substance back to the toxicity of TCDD, the most toxic dioxin.
VOC  Volatile organic compound
WHO  World Health Organisation
wt  weight
 
 
 

General

In general the document is under referenced.  Many of the opinions and statements are unsupported by any citations from the literature.  There is no list of references provided.
 

Section 3, Particulates (page 3)

Quote: “Significant increases in PM10 concentrations result in a small increase in deaths and acute hospital admissions for chest and heart problems”.

Comment: In this statement the author does not define the words “significant” or “small increase”.  Nor does he give any references.  The work of Dockery et. al. (1993) in a very large epidemiological study in the USA led to the attribution of 60,000 deaths per year (3% of all deaths) to the inhalation of PM10 particles.
 

Section 3, Dioxins and furans (page 3)

Quote: “We are exposed to them every day in our diet, which is the main source of most of our dioxin exposure”.

Comment: This is part of a circular argument, the nature of which the author does not acknowledge.  The reason why most dioxin intake is through food is because of deposition of dioxin-like substances on the land through anthropogenic activity of precisely the type which is proposed at Padeswood.  It is widely accepted that the majority of dioxin deposition to date has come about through the incineration of waste (Fiedler, 1999).
 

Quote: “...the average daily dioxin exposure in the UK is about 125 pg TEQ/ day”.

Comment: Given an average body weight of 70 kg, this would mean a daily intake of 125/70 = 1.8 pg TEQ/kg body wt/day.  This is lower than that reported by MAFF (from an AEA study) of 2.6 pg TEQ/kg/day (ENDS, 1999), which would lead to a total intake of 2.6 x 70 = 180 pg/day.  This latter figure includes the total TEQ for dioxins and those PCBs which have dioxin-like properties.  Intakes for high level consumers eating large quantities of fish intakes were 5.6 pg/kg/day, which is well over the WHO guideline 1-4 pg/kg/day.

It is acknowledged by some that the TDI is not a good metric to use when the pollutant bioaccumulates and persists. Dr. Linda Birnbaum (1998), a senior official in the USEPA,  stated that ‘Total Body Burden’ is the most relevant metric to apply to human health, when dealing with persistent bioaccumulative chemicals. Dioxin-like substances are avidly absorbed from the gastro-intestinal and respiratory tracts. Birnbaum confirmed that its most sensitive effects observed in multiple species appear to be developmental, including effects on the developing immune, nervous and reproductive systems. However, alterations have been noted in adult immune systems and also in some biochemical indices. Among the most important observations in recent years is that of functional developmental toxicity; for example, lifelong changes in behaviour as a result of exposure in the womb to low doses of dioxin-like substances.

Most importantly, Birnbaum pointed out that the endpoints of chronic and acute exposure are the same.  In other words, it doesn’t matter how you get dioxin into the body, the effects are identical. Therefore, the total body burden (i.e. the total amount of dioxin in the body) is the single most relevant measurement that can be made. Most current regulations, however, are based on the TDI, which Birnbaum acknowledged was less than adequate.

There are a number of other groups of chemicals which bind to the aryl hydrocarbon receptor.  For example recent research (Van Birgelen, 1999) suggests that another dioxin-like substance, the widely dispersed environmental pollutant hexachlorobenzene (HCB) is increasing the total TEQ of dioxin-like substances to human breast milk in Germany, by up to 50%. Therefore, for adults, the chosen estimate for dioxin TDI is out of date (no citation is given by Dr Roberts in his report) and does not address all the known inputs.

Dr Roberts makes no mention of the daily intake of breast fed infants of dioxin-like substances.  The AEA study (ENDS, 1999) found that, for first-born infants, their average daily dioxin intakes were between 27 - 144 times above the WHO guideline. This estimate does NOT take into account dioxin-like PCBs, which would tend to double the estimate.
 

Section 4

Quote: “SO2 and particulates do not have a lower threshold below which they have no health effect, it is not possible to say that emissions of these compounds will have no effect on health”.

Comment: I agree with this comment.  However we do know quite a lot about the toxicology of ultrafine particles (Donaldson et. al., 1999) and the report could have made reference to it.  For example particles become more toxic if they are smaller and/or more insoluble.  In addition particles comprised of transitional metals are more likely to give rise to free radicals, which increases their toxicity (Donaldson et. al., 1999, Fig 8.2).  Examination of the table showing the composition of Cemfuel clearly demonstrates the increased presence of transitional and heavy metals.  Therefore the ultrafine particulate aerosol that would be produced by this plant will, by definition, have a higher proportion of nanoparticles comprised of transitional metals and therefore be more toxic than, say, a plant powered by coke.  There is no discussion of any of these factors in this health assessment.
 

Quote: “For metals and dioxins, current medical knowledge does not allow us to estimate the effects on health of any specific level of these pollutants in the environment”.

Comment: This is not correct for dioxin and dioxin-like substances.  We do know that a proportion of the population is exceeding the WHO recommended TDI.  In addition we know that virtually all breastfed babies are exceeding the WHO TDI, some in excess of 100-fold.  In addition population-based epidemiology has been performed which demonstrates adverse effects in infants in relation to the dose of dioxin-like substances that they are receiving from their mothers (Lanting, 1999; Patandin, 1999).  These effects include a loss of IQ up to 4 points, immunosuppression and hormone disruption.
 

Quote: "Using the methodology developed by the Environment Agency, emissions of metals, including heavy metals, from the proposed kiln are expected to be very low and are unlikely to have significant effect on health”.

Comment: What methodology? The terms “unlikely” and “significant” are undefined.  Does the “Methodology” treat the metals as if they were ingested doses or inhaled doses?  If they are considered as part of a TDI for an ingested dose, that would be a totally unrealistic comparison if they were in fact being inhaled as nanoparticles. For all the reasons discussed above their toxicity, weight for weight, would be much higher as inhaled particles.

The only hope of detecting population shifts in the pattern of disease is to have a) good base-line data and b) monitor for changes.  As the former has never been done and the latter is not recommended the conclusion must be that if this plant was built and it did have an adverse health impact, it would be impossible to detect, unless the effect was absolutely massive, which is unlikely.
 

Quote: "The emissions of volatile organic compounds (VOCs) are also reported to be “very small””.

Comment:  This is uninterpretable.  Which VOCs, and what is “very small”?
 

Quote: “Those calculations showed the hypothetical individual would take in 131 pg/day of dioxins, compared to the average intake in the UK of 125 pg/day.”

Comment:  This paragraph starts “First, calculations of “worst case” dioxin exposure ...”.  However the hypothetical individual only has an average dioxin intake (in fact lower than the true average, as discussed above).

Surely a “worst case” scenario would be to have a ‘maximally exposed’ individual, just as was practised in this type of risk assessment in the past (e.g. Bridges, 1992). What would happen if the hypothetical individual was a person, who enjoyed eating fish, taking in 5.6 x 70 = 392 pg/day? The additional exposure attributable to this plant would then, by WHO guidelines, be unacceptable.  What this would mean to a breast-fed infant also needs to be considered. In addition the occupationally and accidentally exposed individual should be considered. In my opinion the regulations need to protect all citizens and not only those with an “average intake”.

Quote: “...add less than 0.1% to the “normal” background intake of dioxins and furans in local people”.

Comment: This is based on the old WHO TDI of 10 pg/kg bw/day and is therefore unacceptable, in light of the new WHO standard 1-4 pg/kg bw/day.  Furthermore the use of the word “normal” is inappropriate.  The term “average” dioxin intake would be more realistic.  The “normal” intake of these substances is in fact very close to zero, as was the case prior to industrialisation.
 

Dr C. Vyvyan Howard. MB. ChB. PhD. FRCPath.
Dr G. Staats de Yanes  Dr. Vet. Med.
Toxico-Pathology, University of Liverpool

10th January 2000
 
 

References

Birnbaum, L.S. (1998) Sensitive non-carcinogenic effects of TCDD in animals, Organohalogen Compounds 38, 291-294, ISBN 91-89192-07-9.

Bridges J W (1992).  Consideration of possible impact on human health – Volume 1.  Proof of Evidence, Document A13, submitted in evidence to the UK Department of the Environment Public Inquiry into an application for Planning Permission for a Refuse to Energy Plant in Belvedere, Bexley, Kent.

Dockery, D.W., and Pope, C.A. III (1994) Acute respiratory effects of particulate air pollution, Annual Review of Public Health 15, 107-132.

Donaldson, J., Stone, V., and MacNee, W. (1999) The toxicology of ultrafine particles, in R.L. Maynard and C.V. Howard (eds) Particulate Matter: Properties and Effects Upon Health, BIOS Scientific Publishers Ltd., Oxford, UK, pp. 115-129, ISBN 1-85996-172X.

ENDS (1999) November Vol 298. ‘Infants face huge dietary exposure to dioxins’.

Fiedler H (1999). National and regional dioxin and furan inventories.  Organohalogen Compounds. 41: 473-476.

Lanting, C.I. (1999) Effects of Perinatal PCB and Dioxin Exposure and Early Feeding Mode on Child Development, PhD Thesis, Printpartners Ipskamp B.V., Enschede, ISBN 90-367-1002-2.

Patandin, S. (1999) Effects of Environmental Exposure to Polychlorinated Biphenyls and Dioxins on Growth and Development in Young Children, PhD Thesis, Microweb, Saasveld, ISBN 90-9012306-7.

van Birgelen A.P.J.M (1998). Hexachlorobenzene as a possible major contributor to the dioxin activity of human milk. Environmental Health Perspectives 106: 683-688.