Predicted health effects of the Colnbrook incinerator

Incinerators: The Effect on Children
By Dr J Thompson

The report on the Sint Niklaas incinerator states “we have dedicated this report to all the deceased children who died from cancer as well as the numerous children who have numerous serious health complaints caused by the waste incinerator in Sint Niklaas. A society that does not take care of its children is less than primitive.
This report, funded by the Belgian government, is the only complete study ever done on incinerators. Although the proposed incinerator at Colnbrook will have a lower dioxin output than that at Sint Niklaas, the fact that it would be nine times larger, will emit higher volumes of particulates and will foolishly be allowed to incinerate radioactive material gives little cause for comfort.
Children are more vulnerable to the pollutants produced by incinerators, breathing in more air than adults relative to their size, and are likely to be the first to suffer from adverse effects. The foetus and newborn are uniquely vulnerable (see below).

Cancer

The report on the Sint Niklaas incinerator showed that blood and glandular cancers appeared in children about 5 years after the incinerator started operating. This preceded the increase in adult cancers by 7 years. Adults cancers showed a five-fold increase over 20 years. Knox found a doubling of childhood cancers and leukaemias within 5km of municipal incinerators (2) greatly exceeding the risk around non-combustion urban sites.

Congenital Abnormalities

A recent large study by Dummer over a 37 year period showed that the incidence of spina bifida was 17% higher and heart defects 12% higher near incinerators (3). Congenital defects of many kinds were found at Sint Niklass (1). Orofacial defects were found to be more than doubled near an incinerator at Zeeberg, Amsterdam (4). Dolk found a 33% higher incidence of birth defects, (86% higher neural tube defects, 50% higher incidence of cardiac septal defects) and a higher risk of chromosomal abnormalities within 3 km of municipal waste sites (5). The same pattern of increased congenital defects (12%) with a higher excess of neural tube defects (54%) was found in a study of ethnic minorities near waste sites in the US (6). Chromosomal and other major anomalies (facial clefts, megacolon, renal dysplasias) were found in a study of 70 incinerators in France.

Asthma and Respiratory Disorders

Incinerators produce vast amounts of fine particulates. Particulate pollution has been shown to increase the incidence of asthma in children (7,8), to reduce immunity (9,10,11), to be associated with higher rates of ear, nose and throat infections (7), increased frequency of respiratory symptoms (12,13), increased duration of infections (14), loss of time from school (16) and significant permanent reduction in peak flow from fibrosis with progressive declines in respiratory function (16,17). The greatest declines have been shown to occur in those who spend more time outdoors. Similarly with asthma the greatest effect is on children who do outdoor sports who have a threefold increase (compared to no increase in unpolluted areas) (18).

Other Illness

The Sint Niklaas study showed an excess of autism, hyperactivity, allergies, asthma, repeated infections and congenital defects. Data from this country shows increased autism rates near incinerators: being 1 in 85 near the Edmonton incinerator and 1 in 30 in parts of Birmingham sandwiched between two incinerators (Tysley and Dudley). Average in UK 1 in 180.

Effects on the Foetus

Chemicals and pollutants that the mother is exposed to during her lifetime will build up in her fatty tissues and in pregnancy these will be actively transported across the placenta into the tiny body of the foetus. Foetuses have virtually no protection against toxic chemicals as they have no fat stores. They store them in the only fatty tissue they have: the brain and nervous system. During the first 12 weeks of life the foetus will be affected by miniscule amounts of chemicals, particularly oestrogenic chemicals and these can be neurotoxic and lead to behavioural disorders (19). Small amounts of PCBs and dioxins can affect neurological development, sexual development of the brain and cause altered expression of genes (20) and alter thyroid status (19,21). These chemicals can affect immunity and be associated with high incidences of middle ear infections and recurrent respiratory infections (22).

Breast Feeding

The situation with breast feeding is already extremely serious as it is known that 90% of samples contain about 350 chemicals. This is higher in industrialised areas showing that inhalation of toxic substances is important (23). The daily dose of toxic substances taken in from breast-feeding can be 50 times greater than that taken in by an adult (24). This has been shown to affect neurological development (25). Sadly breast-feeding is one of the few effective ways of reducing the mother’s toxic load. There is no question that an incinerator would add to this already dangerous chemical load and there is no justification for this as safe technology exists for waste disposal.

The Next Generation

It has been clearly demonstrated in animal studies that chemicals can cause cancer in not only the exposed animals but also its offspring for several generations (26). We now know that both chemicals and heavy metals can form DNA adducts and these can be passed on to the foetus. This is very worrying scenario and demonstrates the importance of the precautionary principle and avoiding further pollution.

1) www.milieugezondheid.be 2) Int J Epidemiol 2000;29(3):391-7
3) J Epidemiol Community Health 2003;57(6): 456-61 4) Chemosphere 2000;40:1263-70
5) Lancet 1998;352(9126):417 and 2002;359(9309):320-2 6) Int J Hyg Environ Health 2002;205(1-2):19-27
7) Am J Resp Critic Care 2002;166(8):1092-8 8) J Community Health 1996;50 Supp 1S59-62
9) Environ Toxicology 2002;17(3):219-31 10) Environ Res 1983;31(1):201-11
11) Lancet 1999;353 (9156):859-66 12) Environ Health Perspect 2001; 109Sup 3 381-7
13) Am Rev respire Dis 1989; 139(3)587-94 14) Am Rev Respir Dis 1992;145(1):42-7
15) Epidemiology 2001;12(1):43-54 16) Am J Respir Care 2000;162 4Pt1:1383-90
17) Am J Respir Care 2002;166(1):76-84 18) Lancet 2002;359(9304):386-91
19) Environ Health Perspect 1994;102 Sup 2:125-30
20) Evol Dev 2003; 5(1):67-75 21) Paed Res 1994;36(4):469-73
22) Environ Health Perspect 2000:108(12):1203-7 23) Chemosphere 1994;29(9-11):2327-38
24) Environ Health Perspect 1999;107(1):45-51 25) Environ Health Perspect 2003;111(10):357-76
26) Int J Cancer 1969;4:219-25