Memorandum submitted by Dr C V Howard
(X6)
Please note that the comments which follow
are my personal opinion and should not be construed to be any
policy of the University of Liverpool or any part thereof.
EXECUTIVE SUMMARY
As a medically qualified toxico-pathologist
specialising in developmental toxicology, my research has made
me very aware of the health impacts of the types of pollutants
emitted during waste incineration and landfill. A number of these
can affect the many ways in which hormones regulate development
in the womb and early childhood, with effects which can last throughout
life. I am of the opinion that there is no place for incineration
in municipal waste management. It is a totally unsustainable use
of resources and the inevitable emissions of particulates and
toxic organic chemicals such as dioxin-like substances are likely
to have harmful effects on health, especially the health of the
most vulnerable members of society. These pollutants remain as
a legacy for future generations. We should instead adopt two strategies.
Firstly, the substitution of products which include potentially
hazardous chemicals, by more harmless alternatives. Secondly,
adopt a Zero Waste policy throughout the UK, thus avoiding the
necessity for incineration or much landfill.
DETAILED COMMENTS
1. I am a medically qualified toxico-pathologist.
I supervise the activities of the Developmental Toxico-Pathology
Research Group at the University of Liverpool. For over 12 years,
I have been studying human and mammalian fetal and neonatal development,
ie the development of babies in the womb and young children. This
has led to my becoming involved in investigating the effects of
a number of global environmental pollutants which have their maximal
impact upon the fetus. Many of these chemicals are persistent
and bio-accumulative, ie they build up in our bodies over time.
Mothers pass these chemicals to their babies in the womb and in
breast milk, and many of them disrupt the action of the hormone
systems, affecting babies' development in many different ways.
All of these effects have been well documented, and many have
been shown to be happening at current background levels of dioxins
and PCBs, which are the most well studied of the hormone-disrupting
chemicals.
2. The so-called "background"
levels of dioxin-like compounds are almost totally caused by anthropogenic
activities, mainly through combustion of organohalogenated products.
Even the cleanest, most modern incinerators still emit an amount
of dioxins and other products of incomplete combustion (PICs).
3. Even though the "background"
levels of dioxins have been reducing in recent years, this does
not mean that it is safe to add a little more into the environment,
through new incinerators. Defra acknowledges in their recent dioxin
consultation, that infants still receive many times the dose currently
deemed "safe". Unfortunately, further evidence seems
to indicate that there may be no safe dose below which health
effects will not occur. As the effects on the fetus occur at extremely
low levels, always in combination with many other anthropogenic
chemicals, policy should be to reduce dioxin levels to as low
as possible, not just to below the current TDI. Certainly, safety
limits have steadily been revised downwards in the past few years,
as more becomes known about these chemicals mode of action.
4. There is general agreement that the fetus
is the stage of life which is the most vulnerable to damage from
hormone disrupting chemicals. Dioxins and similar compounds affect
the many ways in which hormones regulate development in the womb
and early childhood, with effects which can last throughout life.
These effects can range from an increased likelihood of respiratory
problems or allergies, to reduced IQ, less efficient kidneys,
reproductive problems or a higher probability of contracting cancer.
5. Effects on the intelligence, immune status
and hormonal status of infants have been related quantitatively
to the amount of dioxin-like substance in the mother's body, by
Koppe et al.[3]
Furthermore, the effects, including altered latency times in brain
function and altered lung function, appear to persist past the
age of seven.[4]
Neurobehavioural and immune system deficits have been shown to
be correlated with the level of PCBs and dioxins that infants
receive from their mothers while in the womb. 22, 20, [5],[6]
,[7]
,[8]
,[9]
The documented neurobehavioural effects include altered play behaviour
as well as general mental and psychomotor development. Other papers
also document a variety of reproductive dysfunctions.[10],[11]
, [12]There
is general acceptance that male reproductive health is under threat.
26,[13]
, [14],
[15]
Exposure to dioxin-like substances has also been related to changes
in the proportion of boys to girls being born[16],[17]
, there being a decrease in the number of boys.
6. It is not feasible to do a realistic
cost-benefit analysis of the health benefits arising from dioxin
reduction, as the potential developmental health effects are so
diverse, and can occur in synergy with other chemicals.[18],[19]
It will never be possible to develop an accurate algorithm to
quantify the cost to society of, for example, a reduction in IQ
levels[20],
or the reduction in quality of life due to fetal kidney growth
impairment[21],
immune system[22],
[23],
[24]
or reproductive system[25],
[26],[27]
developing less than optimally, causing reduced potential, occasional
illness throughout life or a higher risk of cancer.[28],[29]
A precautionary approach would be to reduce human exposure to
all chemicals which persist and bioaccumulate or are capable of
hormonal disruption, down to the absolutely unavoidable level,
especially as mixtures of chemicals may have synergistic effects.
7. However good the pollution abatement
equipment is, large quantities of particles will still escape
from an incinerator; they will simply be smaller, consisting of
large numbers of tiny particles known as ultrafine or nano-particles.
Unfortunately, these prove to have a size-related toxicity regardless
of what material they comprise. As well as publishing a recent
book on the health effects of particulates in 1999[30],
I more recently reviewed the potential health effects of nano-particles
and participated in an EU workshop which produced a risk analysis
of nanoparticles.[31],[32]
Many of the conclusions in these reports apply equally to the
nanoparticles arising from the incineration of waste. There is
strong human epidemiological evidence to show that chronic exposure
to particulate aerosols through polluted air carries health consequences.[33]
There is considerable evidence that inhaled nanoparticles can
gain access to the blood stream and are then distributed to other
organs in the body.[34],[35]
,[36]
Once internalised, nanoparticles appear to be able to penetrate
more rapidly into interstitial sites than larger particles can,
and therefore to be trans-located to distant sites within the
body. 31 There appears to be a natural "passageway"
for them to travel around the body. This is through "caveolar"
openings in natural cell membranes, which separate the body compartments.
When environmental nanoparticles (such as from incineration or
traffic pollution) gain unintentional entry to the body, it appears
that there is a pre-existing mechanism which can deliver them
to vital organs.[37]
The body is then "wide open" to any toxic effects that
they can exert. The probable reason that we have not built up
any defences is that any such environmental toxic nanoparticles
were not part of the prehistoric environment in which we evolved
and therefore there was no requirement to develop defensive mechanisms.
8. There are two fundamental approaches
to handling wasteeither try to reduce the amount and the
toxicity of inputs to the waste stream or to attempt to deal with
wastes once they have been produced. Clearly there is scope to
combine the two.
9. Substitution of hazardous substances:
Instead of simply considering how to dispose of waste, much of
which is hazardous, we need to start by considering pollution
from the beginning of each product lifecycle. We can only control
the health hazards from toxic pollutants throughout the product
lifecycle, and minimise the production of hazardous waste, by
substituting the production of goods which use potentially hazardous
chemicals, with alternatives that use more benign chemicals. For
most of the known hormone-disrupting chemicals, there are substitutes
which are less obviously problematic. The only effective way to
make the necessary effective permanent reductions to environmental
levels of dioxin-like chemicals, is by substitution of all major
uses of organochlorine and other halogenated chemicals (eg pesticides
and chlorinated plastics) with safer alternatives. Clearly, this
is a major step to take, but the costs to society of allowing
the continuing health consequences, which are evident already
in the general population, is likely to far outweigh the apparent
costs to industry. While these chemicals are still produced in
bulk, there will be inevitable release of dioxins during their
manufacture, use, accidental fires and disposal, a significant
amount of which will eventually find its way into our food chain
and hence our bodies. A good use of the Precautionary Principle
is to avoid the use of any persistent bioaccumulative chemicals,
as these often tend to be linked to health problems. There need
to be regulatory changes so that the necessity for a particular
process is considered as part of the authorisation process, together
with a comprehensive life-cycle analysis of the potential emission
dangers throughout the product lifecycle. This should include
a realistic assessment of the likely emissions caused by its eventual
disposal, whether via controlled disposal or through accidental
fires or uncontrolled home bonfires.
10. Another concern is the major issue of
the unsustainable use of resources if waste is incinerated or
landfilled. Incineration is rather worse than landfill in that
respect, as future generations could at least recover certain
materials such as metals from a landfill, if the shortage of resources
made this necessary. The planetary resources of many raw materials
are finite, and the energy consumed in retrieving raw materials
often outweighs the energy recovered by incinerating products,
which could have been reused or recycled.
11. In summary, my researches have led me
to the firm conclusion that there is no place for incineration
in municipal waste management. It is a totally unsustainable use
of resources and the inevitable emissions of particulates and
dioxin-like substances are likely to have harmful effects on health,
especially the health of the most vulnerable members of society.
12. Strong emphasis should be focussed on
waste minimisation rather than concentrating wholly on the debate
over what method to use for the disposal of waste. Many local
authorities worldwide are starting to adopt "Zero-Waste"
policies. The concept of Zero Waste may sound impractical, but
California, Toronto, Canberra, and New Zealand have already adopted
a Zero Waste policy. The first two local authorities to adopt
Zero Waste policies in England were Bath and North Somerset and
Braintree.
13. We need to adopt a policy of maximal
waste minimisation, reuse and recycling, by adoption of a Zero
Waste policy throughout the UK and developing suitable financial
and regulatory incentives. This would thus avoid the necessity
for any incineration or much landfill.
Dr C V Howard MB. ChB. PhD. FRCPath
Head of Research, Developmental Toxico-Pathology
Research Group
4 October 2004
3 Koppe, JG, ten Tusscher, G, and de Boer, P. (2000)
"Background exposure to dioxins and PCBs in Europe and the
resulting health effects" in P Nicolopoulou-Stamati, L Hens,
and CV Howard (eds) Health Impacts of Waste Management Policies,
Kluwer Academic Publishers, Dordrecht, the Netherlands, pp 135-154. Back
4
ten Tusscher, G (2002) "Later childhood effects of perinatal
exposure to background levels of dioxins in The Netherlands",
PhD Thesis, University of Amsterdam, ISBN: 90-9016271-2. Back
5
Vreugdenhil, HJ, Slijper, FM, Mulder, PG, Weisglas-Kuperus, N.
(2002) "Effects of Perinatal Exposure to PCBs and Dioxins
on Play Behavior in Dutch Children at School Age." Environ
Health Perspect.; 110(10): A593-8. Back
6
Huisman, M, Koopman-Esseboom, C, Lanting, CI, van der Paauw, CG,
Th Tuinstra, LGM, Fidler, V, Weisglas-Kuperus, N, Sauer, PJJ,
Boersma, ER and Towen, BCL (1996). "Neurological condition
in 18-month-old children perinatally exposed to polychlorinated
biphenyls and dioxins." Early Human Development 43:
165-176. Back
7
Koopman-Esseboom, C, Weisglas-Kuperus, N, de Ridder, MAJ, van
der Paauw, CG, Th Tuinstra LGM, and Sauer PJJ (1996). "Effects
of Polychlorinated Biphenyl/Dioxin Exposure and Feeding Type on
Infants' Mental and Psychomotor Development." Pediatrics
97(5): pgs 700-706. Back
8
Patandin, S, Lanting, CI, Mulder, PG, Boersma, ER, Sauer, PJ,
Weisglas-Kuperus N (1999). "Effects of environmental exposure
to polychlorinated biphenyls and dioxins on cognitive abilities
in Dutch children at 42 months of age." J Pediatr.
134(1):33-41. Back
9
Weisglas-Kuperus, N, Patandin, S, Berbers, GA, Sas, TC, Mulder,
PG, Sauer, PJ, Hooijkaas, H (2000) "Immunologic effects of
background exposure to polychlorinated biphenyls and dioxins in
Dutch preschool children." Environ Health Perspect.
108(12):1203-7. Back
10
Mably TA, Moore RW, and Peterson RE (1992) "In Utero and
Lactational Exposure of Male Rats to 2,3,7,8-Tetrachlorodibenzo-p-dioxin",
Toxicology and applied Pharmacology 114, 97-107. Back
11
Gray, LE Jr, Kelce, WR, Monosson, E, Ostby, JS and Birnbaum, L
(1995) "Exposure to TCDD during development permanently alters
reproductive function in male Long Evans rats and hamsters: reduced
ejaculated and epididymal sperm numbers and sex accessory gland
weights in offspring with normal androgenic status.", Toxicol
Appl Pharmacol. 131(1):108-118. Back
12
Johnston, P, Comhaire, F, Krumbiegel, P, Boerjan, ML, Hanf, V,
Bock, KW, Abel, J, Gutzeit, HO, Groot, MJ, Fischer, B (1997).
"Effects of environmental pollutants on reproduction",
Proceedings of conference held 11-13 April 1997, Halle (saale)
Germany. Back
13
Swan, SH, Elkin, EP, and Fenster, L (2000) "The question
of declining sperm density revisited: an analysis of 101 studies
published 1934-96", Environ Health Perspect. 108(10),
961-966. Back
14
Skakkebaek, NE, Rajpert-de Meyts, E and Main, KM (2001), "Testicular
dysgenesis syndrome: an increasingly common developmental disorder
with environmental aspects", Human Reproduction, 16
(5): 972-978. Back
15
Hardell L, van Bavel B, Lindstrm G, Carlberg M, Dreifaldt AC,
Wijkstrm H, Starkhammar H, Eriksson M, Hallquist A, Kolmert T.
(2003) "Increased Concentrations of Polychlorinated Biphenyls,
Hexachlorobenzene and Chlordanes in Mothers to Men with Testicular
Cancer." Environ Health Perspect: doi:10.1289/ehp.5816.
(Online 19 December 2002) available at http://ehpnet1.niehs.nih.gov/docs/2003/5816/abstract.html Back
16
Williams FLR, Lawson AB and Lloyd OL (1992). "Low Sex Ratios
of Births in Areas at Risk from Air Pollution from Incinerators,
as Shown by Geographical Analysis and 3-Dimensional Mapping."
International Journal of Epidemiology, 21(2): 311-319. Back
17
Mocarelli P, Gerthoux PM, Ferrari E, Patterson G, Kieszak SM,
Brambilla P, Vincoli N, Signorini S, Tramacere P, Carreri V, Sampson
EJ, Turner WE and Needham LL (2000). "Paternal concentrations
of dioxin and sex ratio of offspring". The Lancet,
27 May 2000, 355: 1858-1863. Back
18
Lang, L (1995) "Strange brew: assessing risk of chemical
mixtures", Environ Health Perspect. 103, 142-145. Back
19
Howard, CV (1997) "Synergistic effects of chemical mixtures-Can
we rely on traditional toxicology?", The Ecologist
27(5), 192-195. Back
20
Lanting, CI (1999) "Effects of Perinatal PCB and Dioxin Exposure
and Early Feeding Mode on Child Development", PhD Thesis,
Printpartners Ipskamp BV, Enschede, the Netherlands, ISBN 90-367-1002-2. Back
21
Hinchliffe, SA, Lynch, MRJ, Sargent, PH, Howard CV, and van Velzen
D (1992). "The effect of human intrauterine growth retardation
on the development of renal nephrons." British Journal
of Obstetrics and Gynaecology, 99: 296-301. Back
22
Baccarelli, A, Mocarelli, P, Patterson, DG Jr, Bonzini, M, Pesatori,
AC, Caporaso, N and Landi1, MT (2002). "Immunologic Effects
of Dioxin: New Results from Seveso and Comparison with Other Studies."
Environmental Health Perspectives 110:1169-1173. Back
23
Koppe, J, and De Boer, P (2001) "Immunotoxicity by dioxins
and PCBs in the perinatal period" in P Nicolopoulou-Stamati,
L Hens, and CV Howard (eds), Endocrine Disrupters: Environmental
Health and Policies, Kluwer Academic Publishers, Dordrecht,
The Netherlands, pp 69-80. Back
24
Weisglas-Kuperus, N, Patandin, S, Berbers, GA, Sas, TC, Mulder,
PG, Sauer, PJ, Hooijkaas, H (2000) "Immunologic effects of
background exposure to polychlorinated biphenyls and dioxins in
Dutch preschool children." Environ Health Perspect.
108(12):1203-7. Back
25
Skakkebaek, NE, Rajpert-de Meyts, E and Main, KM (2001), "Testicular
dysgenesis syndrome: an increasingly common developmental disorder
with environmental aspects", Human Reproduction, 16
(5): 972-978. Back
26
Toppari, J, Larsen, JC, Christiansen, P, Giwercman, A, Grandjean,
P, Guillette, LJ, Jr, Jegou, B, Jensen, TK, Jouannet, P, Keidig,
N, Leffers, H, McLachlan, JA, Meyer, O, Muller, J, Rajpert-De
Meyts, E, Scheike, T, Sharbe, R, Sumpter, J, and Skakkebaek, NE
(1996) "Male reproductive health and environmental chemical
xenoestrogen", Environ Health Perspect. 104(4),
741-803. Back
27
Gray, LE Jr, Kelce, WR, Monosson, E, Ostby, JS and Birnbaum, L
(1995) "Exposure to TCDD during development permanently alters
reproductive function in male Long Evans rats and hamsters: reduced
ejaculated and epididymal sperm numbers and sex accessory gland
weights in offspring with normal androgenic status.", Toxicol
Appl Pharmacol. 131(1):108-118. Back
28
Mackie, D, Liu, J, Loh, Y and Thomas V (2003) "No Evidence
of Dioxin Cancer Threshold" Environ Health Perspect:
doi:10.1289/ehp.5730 Online 25 November 2002 (available
at http://dx.doi.org/) Back
29
Lichtenstein, P, Holm, NV, Verkasalo, PK, Iliadou, A, Kaprio,
J, Koskenvuo, M, Pukkala, E, Skythe, A and Hemminki, K (2000)
"Environmental and Heritable Factors in the Causation of
Cancer-Analyses of Cohorts of Twins from Sweden, Denmark, and
Finland" New England Journal of Medicine, 343,
78-85. Back
30
Maynard RL and Howard CV (1999). (Eds) Particulate Matter:
Properties and effects upon health. Bios Scientific Publishers,
Oxford. ISBN 1 85996 172X. Back
31
Howard CV (2003) Nanoparticles and Toxicity. Annex to No Small
Matter II: The Case for a Global Moratorium Size Matters!
ETC Group, Occasional Paper Series 7:1 April 2003, pp 15-20.
Available on ETC Group website at http://www.etcgroup.org/documents/Occ.Paper_Nanosafety.pdf Back
32
Howard CV (2004) A briefing note on Nanoparticles, in Nanotechnologies:
A Preliminary Risk Analysis on the Basis of a Workshop Organized
in Brussels on 1-2 March 2004 by the Health and Consumer Protection
Directorate General of the European Commission. Published
on the EU website at http://europa.eu.int/comm/health/ph_risk/documents/ev_20040301_en.pdf Back
33
Wichmann, HE, and Peters, A (2000) "Epidemiological evidence
of the effect of ultrafine particle exposure." Phil Trans
Roy Soc Lond. 358: 2751-2769. Back
34
Kreyling WG, Semmler M, Erbe F, Mayer P, Takenaka S, Schulz H,
Oberdrster G,and Ziesenis A. (2002) "Translocation of ultrafine
insoluble iridium particles from lung epithelium to extrapulmonary
organs is size dependent but very low." J Toxicol Environ
Health A. 25 Oct; 65(20): 1513-1530. Back
35
Oberdrster G, Sharp Z, Atudorei V, Elder A, Gelein R, Lunts A,
Kreyling W, Cox C. (2002a) "Extrapulmonary translocation
of ultrafine carbon particles following whole-body inhalation
exposure of rats." J Toxicol Environ Health A. 25
Oct 2002; 65(20): 1531-43. Back
36
Oberdrster G, and Utell MJ. (2002b) "Ultrafine particles
in the urban air: to the respiratory tract and beyond?" Environ
Health Perspect. Aug; 110(8): A440-441. Back
37
Gumbleton M (2001) "Caveolae as potential macromolecule trafficking
compartments within alveolar epithelium", Advanced Drug
Delivery Reviews 49: 281-30. Back
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