Predicted health effects of the Colnbrook incinerator

Predicted Health Effects of Colnbrook Incinerator
By Dr J Thompson

Lung Cancer Expected increase

In Trieste a study found a 6.7 times greater rate of lung cancer for those living near an incinerator (1). A Swedish study found that workers at a municipal waste incinerator had an 3.5 fold increased rate of lung cancer and increased ischaemic heart disease (2). Pollution from particulates is a known cause of lung cancer and a rise of particulate concentration is inevitable with an incinerator. The Six Cities study showed a 37% increase in lung cancer with a of 18.6mcg/m3 rise of PM2.5 particulates (3) and a later study showed a 8% increase in lung cancer with a 10mcg/m2 rise in PM2.5 particulates (4). Slough already has the 3rd highest rate of lung cancer in the South-East.

Other Cancers Increase expected: for children at 5 yrs, adults after 13 yrs
with large increases after 20 years

The only detailed study on an incinerator is that of the Sint Niklaas incinerator (5). Cancer was a major problem. After 5 years operation blood and glandular cancers started to appear in children. There was no increase in cancer in adults at 10 years but cancer rates had doubled at 13 years and were 5 times normal at 20 years. It could be argued that newer designs in incinerators will reduce these risks as dioxins and some other pollutants are filtered out. However the fact that the Colnbrook incinerator will be nine times larger and will include radioactive waste and greater quantities of fine particulates would suggest the opposite.
Other studies have noted a 42% increase in sarcoma and a 27% increase in non Hodgkins lymphoma near incinerators in France (6). Elliot found an excess of all cancers in UK residents within 7.5km of incinerators with a 37% excess of liver cancer (7). Knox found a doubling of childhood cancers and leukaemias within 5km of incinerators (8). Gustavsson found a 1.5 fold increase in oesophageal cancer (9) and a 2.79 fold increase in gastric cancer in incinerator workers (2)

Ischaemic Heart Disease Relative increase expected

The ability of particulates to increase cardiovascular mortality is now well-documented (3,4,10,11,12,13,14,15). A major study found an increase of cardiovascular mortality of 35-44% for an 18.6mcg/m2 increase in PM2.5s (16). Particulates can trigger myocardial infarctions (17) and admissions for heart disease(18,19). The smaller particulates, such as those produced by incinerators, have a greater effect on cardiopulmonary mortality (3). Slough has the highest rate of CHD in the South-East with an even higher rate in the Asian population. Again it would be negligent to increase this risk by building an incinerator. As cardiac mortality is decreasing nationally the effect of an incinerator may be a reverse in this trend rather than an increase.

Congenital Abnormalities Increases expected

Orofacial defects were found to be more than doubled near an incinerator at Zeeburg, Amsterdam (20). Increased congenital defects of many kinds were linked to incinerator in Neerland, Belgium and found to be 26% higher than normal (21). A 37 year study of incinerators in Cumbria found a 17% increase in spina bifida and a 12% increase in heart defects (22). Chromosomal and other major anomalies (facial clefts, megacolon, renal dysplasias) were found in a study of 70 incinerators in France (23).

Respiratory Disease Increase expected

There have been few studies of the effects of incinerators and respiratory symptoms. However there is a strong association with particulates and respiratory mortality. Particulate air pollution has been associated with:-
increased hospital admissions with asthma (24) higher incidence of asthma (25,26),
increased admissions with COPD (27,28),
increases in respiratory symptoms (29,30)
reduced immunity (31,32)
higher rates of ear, nose and throat infection (26),
loss of time from school in children through respiratory disease (33,30),
and declines of respiratory function (34,35,36).
Children who did more outdoor sport had greater declines in respiratory function.

Other Major increases in morbidity and doctor’s workload

Other symptoms noted at Sint Niklaas were: higher rate of chronic colds, bronchitis, allergies, increased infertility, spontaneous abortions, insomnia, chronic fatigue, endometriosis, hyperactivity, behaviour disturbances, learning problems, autism, hormonal complaints and stomach disorders. All this would have a dramatic impact on local health and a dramatic effect on health costs.

References:
1) Environ Health Perspect 1996; 104(7): 750-4 2) Am J Ind Med 1989; 15(3): 245-53
3) N Eng J Med 1993;329(24):1753-9 4) JAMA 2002;288(9):1132-41
5) www.milieugezondheid.be 6) Am J Epidemiol 2000;152:13-19
7) British Journal of Cancer 2000; 82(5):1103-6 8) J Epidemiol Community Health 1998;52(11):716-26 9) Archives Environ Med 1993; 48(4): 243-5
10) Environ Health Perspect 2003;111(1):39-44 11) Environ Res 2001;86(1):26-36
12) Epidemiolgy 2001;12(3):355-7 13) Environ Health Perspect 2001;109(4):487-94
14) Epidemiolgy 2001;12(1):55-61 15)N Eng J Med 2000;343(24):1742-9
16) Re-analysis of the Havard Six Cities Study and ACS Study of Particulate Air Pollution and Mortality: Special report. Cambridge, Health effects Institute.
17) Circulation 2001;103(23):2810-5 18) Epidemiology 1999;10(1):17-22
19) Am J Epidemiol 1995;142(1):23-35
20) Chemosphere 2000; 40:1263-70 21) Document 1998/TOX/R/030
22) J Epidemiol Community Health 2003;57(6):456-61
23) Risk of congenital anomalies in the vicinity of municipal incinerators, Inserm,Afssaps, Institut europeen des genomutations, not yet published
24) J Epidemiol Community Health 1996;50 Suppl 1:s59-62
25) Epidemiology 1995;5(2):137-59 26) Am J Resp Crit Care 2002;166(8):1092-8
27) Epidemiology 2001;12(1):55-61 28) Eur Resp J 1997;10(5):1064-71
29) Environ Health Perspect 2001;109(3):381-7 30 ) Am Rev Respir Dis1989;139(2):587-94
31) Environ Res 1983;31(1):201-11 32) Lancet 1995;345(8943):176-8
33) Epidemiology 2001;12(8):43-54 34) Am J Resp Critic Care 2000;162 4 Pt 1:1383-90
35) J Expo Anal 1993;3:Suppl:117-28 36) Am Resp Crit Care 2002;166(1): 76-84