Peter Montague
A new peer-reviewed study in England shows that children have an increased danger of getting cancer if they live within three to five kilometres of certain kinds of industrial facilities. The study, by E.G. Knox and E.A. Gilman, finds that the danger is greatest within a few hundred metres of pollution sources and tapers off with distance.
The incidence of childhood cancers per 100,000 children in England and the US has been rising steadily for at least 20 years.
The new study examined data for 22,458 children who died of leukaemia or of other cancers during the years 1953 to 1980 in England. The study looked at home address at time of birth and home address at time of death, then measured the physical distance from these addresses to nearby industrial facilities.
Excesses of leukaemia and other cancers among children were found near the following kinds of industries:
- oil refineries, major oil storage installations, railside oil distribution terminals and factories making bitumen;
- car factories, car body construction factories and car body repair shops;
- major users of petroleum products including paint sprayers, fibreglass fabricators, paint and varnish makers, manufacturers of solvents, plastics and detergents and galvanisers;
- users of kilns and furnaces, including steel mills, power plants, cement manufacturers, brick makers, crematoria and foundries for iron and steel, aluminium and zinc;
- airfields, railways, highways and harbours.
This study was also interesting for what it did not find:
- Rubber manufacturers showed slight increases in childhood cancers nearby, but tire manufacturing plants did not. Likewise, brake manufacturing showed no excessive childhood cancers nearby.
- Despite the use of solvent-based cleaning, electroplating plants showed no childhood cancer increases nearby.
- Twenty-two factories making chlorinated and fluorinated hydrocarbons had no apparent effect, but 32 other solvent manufacturers showed cancer effects up to five kilometres away.
- Metal casting (aluminium and zinc), metal forming and welding probably account for the effects seen near car manufacturing plants, the authors say. However, casting and refining of lead showed no childhood cancer effects. The manufacture of car batteries, on the other hand, exhibited strong effects. The authors speculate that it may be the manufacture of battery casings (plastics forming, and use of solvents) that create the cancer effect, rather than the lead itself.
- Other industries that did not seem to be associated with childhood cancers included agricultural fertiliser rail terminals, TV transmitters, cake and biscuit bakers, dry cell battery manufacturers, magnetic tape makers, nuclear power plants, PVC manufacturers and the makers of wood preservatives.
- Benzene manufacturing plants were not associated with nearby clusters of childhood cancers. The known leukaemia hazard from benzene may have led to special containment measures.
The findings for leukaemia and for other cancers were the same.
Among children who had changed addresses between birth and death, the cancer hazard could be seen only near the birth address, implying that exposure to pollutants shortly before or after birth caused the cancers.
Knox and Gilman have spent several years developing analytic techniques for identifying small-scale cancer clusters, usually cancers occurring within 150 to 300 metres of each other. The authors say they are sure their techniques can now identify cancer clusters at the neighbourhood level.
The authors conclude that childhood cancers cluster around two general kinds of facilities:
- producers, refiners, distributors and industrial users of petroleum fuels and volatile petroleum products; and
- manufacturing processes using high temperature furnaces, kilns and combustion chambers.
Some operations, notably internal combustion engines and oil-fired furnaces, meet both criteria.
The authors say there may be three mechanisms by which childhood cancers are caused:
- gases and volatile organic compounds reaching children or their pregnant mothers directly;
- parents' germ cells being harmed during occupational exposures, giving rise to children who are predisposed to cancers;
- occupational contamination carried home on clothing, skin or breath.
Of the three mechanisms, the authors say they believe direct exposure of children or their pregnant mothers is the most likely.
These latest findings contradict the official view of childhood cancer in the US. The National Cancer Institute (NCI) wrote in 1993, "Time trends in childhood cancer are not likely to be affected by environmental agents because very few are known that cause cancer within the pediatric age-span, and exposures have been rare or limited".
And: "Clusters of childhood cancer occur very often by chance and almost never because of environmental agents".
Nevertheless, the NCI does say that children exposed to radiation (as at Hiroshima and Nagasaki) can develop cancers. Exposure to benzene could cause childhood leukaemia, says NCI, because benzene affects chromosomes the same way that radiation does. The children of mothers treated with diethylstilbestrol (DES) — a drug given to women in the 1950s to prevent miscarriage — can develop childhood cancers, NCI acknowledges.
NCI reports that the incidence of many childhood cancers has increased steadily during the period 1973-1990. All childhood cancers combined have increased at the rate of 0.9% per year.
However, thanks to surgery, radiation treatments and chemotherapy, death rates for all these childhood cancers have declined steadily since 1973, at an average rate of 2.9% per year, even as the incidence rates have increased.
US environmental officials discourage the kind of study reported here. Each year the US Environmental Protection Agency (EPA) collects data on toxic releases as self-reported by industrial polluters, thus creating the annual Toxics Release Inventory, or TRI database, which is authorised by federal law.
However, EPA has never assigned any staff to check the quality of the self-reported data, thus making any studies based on the TRI data suspect. Furthermore, when John R. Stockwell, a physician employed by the EPA, developed a technique for linking data from the TRI database with disease rates near pollution sources in Chattanooga, Tennessee, EPA officials immediately tried to fire him.
Because of protests, Stockwell managed to keep his job, but he has not undertaken any similar studies since then, and neither has anyone else within EPA.
EPA chief Carol Browner has issued a memo specifically ordering EPA staff to "stay away from linking human health effects and the TRI data".
Another EPA official who tried to link industrial toxic releases to human health has also found himself in serious trouble. Brian Holtzclaw, an environmental engineer employed by EPA but "on loan" to the state of Kentucky, urged the study of massive toxic releases from an Ashland Oil refinery to see if they correlated with disease rates in neighbouring communities.
He tried to bring in John Stockwell to study Ashland's toxic discharges, and he himself released some pollution data to local citizens. Holtzclaw was immediately terminated from his Kentucky projects and reassigned to Atlanta, Georgia.
Holtzclaw fought the reassignment. Hundreds of environmental groups and individuals all across the country signed letters and petitions on Holtzclaw's behalf. After a legal battle, EPA — without admitting any wrongdoing — settled with Holtzclaw for $20,000 and a written promise that he could continue to work on environmental justice issues.
[From Rachel's Environment & Health Weekly. Like 91×ÔÅÄÂÛ̳ Weekly, Rachel's is a non-profit publication which distributes information without charge on the internet and depends on the generosity of readers to survive. If you are able to help keep this valuable resource in existence, send your contribution to Environmental Research Foundation, PO Box 5036, Annapolis, Maryland 21403-7036, USA. In the United States, donations to ERF are tax deductible.]