Black clouds

New Scientist, 28 March 1985:

There is much in Sir Douglas Black’s article on Sellafield (7 March, p 12) with which even his sternest critics would agree. Thus, there is no doubt about the inability of epidemiological studies to provide indisputable evidence of causality. Equally, no one disputes that a causal relationship between Sellafield discharges and local cases of childhood leukaemia is biologically possible.

It is widely realised that radioactive contamination along the Cumbrian coast is unique, both in terms of level, and duration of exposure, that the alpha discharges result in bone marrow exposures which are unparalleled in any other civilian population, and that the placenta does not offer an effective barrier to fetal exposure. Consequently, if nuclear establishments are going to produce any biological effects at all, it is in the population of Cumbria that those effects will be most apparent.

Black’s inquiry identified some biological phenomena, but omitted several others. For example, it failed to mention that of the 675 electoral wards surveyed in the North of England, four of the ten with the highest incidence of leukaemia are located along the Cumbrian coastline. It excluded two cases of leukaemia diagnosed in Seascale in 1983, and did not update its information on the other “top ten” electoral wards. It failed to observe that leukaemia was not the only malignancy present in excess around Sellafield. It failed to draw the obvious parallel between Cumbria and Denver, where an increased rate of malignancy, including leukaemia, has been documented downwind of a local plutonium production plant, which also caught fire in the late 1950s.

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Catalytic cancer

New Scientist, 13 December 1984:

The headline of your article, “Catalytic converters may cause cancer” is seriously misleading (This Week, 22 November, p 6). There is no evidence that catalytic converters increase hydrocarbon emissions. It may be that they have little or no effect on hydrocarbon-coated particles generated by poorly tuned engines. But that does nothing to alter the fact that catalytic converters reduce gaseous hydrocarbon emissions by over 90 per cent. Indeed, in the case of the major carcinogen, benzo-apyrene, gaseous emissions are reduced by over 99 per cent.

Nor is it true to argue that lean-burn engines are a better solution to emission control. Lean-burn technology may be effective at reducing carbon-monoxide emissions, but it is less effective at dealing with NOX, and has only a minimal effect on hydrocarbon emissions, the main concern of your article. Apart from their known carcinogenic potential, hydrocarbon emissions are of major environmental concern as they are ozone precursors and therefore contribute substantially to the forest damage observed in central Europe.

The proper solution to vehicle emissions is to combine lean-burn engines with catalysts which function as a three-way catalytic converter when the engine is running rich, and as an oxidative catalyst when the engine is running lean. Toyota already has such a car on the market.

Robin Russell-Jones
Stoke Poges

How much lead?

New Scientist, 22 September 1983:

It is the right of every scientist to criticise the work of others, and Peter Elwood’s recent contribution to the lead debate (“Labs accused of deplorable conduct in lead debate”, 8 September, p. 671) takes issue with virtually every major study of the past decade. Whilst it is true that no study can be epidemiologically perfect, most of the studies mentioned in your article are far more reliable than those emanating from Elwood’s laboratory. To give but one example; earlier this year Elwood obtained considerable publicity by claiming that blood-lead levels in a remote traffic-free island in the Irish Sea were only slightly lower than those found on the UK mainland. From this it was concluded that petrol lead cannot be an important contributor to human lead intake. However, what Elwood did not say, was that the islanders have a very much increased reliance on tinned food, a well-known source of dietary lead which would invalidate any meaningful comparison between the two populations in terms of petrol lead. Elwood’s selective use of these data casts serious doubt on his scientific credibility. His recent contributions to the lead debate have nothing to restore his reputation as an epidemiologist.

Robin Russell Jones
Campaign for Lead-free Air
London N1

How scandalous is the lead scandal?

Hans Eysenck book review in New Scientist, 14 April 1983:

Lead versus health, Edited by M.Rutter and R.Russell-Jones, Wiley, pp 379, £18.50
The lead scandal, By Des Wilson, Heinemann Educational, pp182, £12.50, pbk £3.95

Both these books deal with the question of whether low-level exposure to lead has important effects on behaviour and intelligence, and both come to a rather positive conclusion. Apart from these similarities they could not be more different.

Des Wilson is not a scientist but an activist; he is indeed, as is said in the book, “one of Britain’s most experienced and best-known campaigners on social issues”. The Lead Scandal is manifestly a propaganda effort, as the title suggests, and his presentation of the evidence is rather one-sided, as well as being emotional and full of accusations of scientists and politicians with whom he disagrees.

It is a very effective package, paperbacked with a threatening kind of picture on the cover: it has a subtitle (“The fight to save children from damage by lead in petrol”) which begs the question, and although it contains nothing but the truth, it certainly does not contain the whole truth.

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Lead in children

New Scientist, 20 May 1982:

Those who are familiar with David Otto’s work on lead and its effects upon evoked brain wave potentials in early childhood (Monitor, 15 April, p 144) will realise that the subsequent communication from Alexander Macnair (Letters, 29 April, p 312) confuses the issue. His version of Otto’s work differs in several respects from the original papers (Electroencephalography and Clinical Neurophysiology, vol. 52, pp 229 and 240).

First, the population, studied was not drawn entirely from the families of lead workers. Children were also included as part of a routine screening programme. Secondly, all children were asymptomatic at the time of study: there are no data to substantiate Macnair’s statement that the children had been previously exposed to levels high enough to cause permanent brain damage. Furthermore, there is no reference from their source of exposure. Both statements represent pure conjecture by Macnair and it is difficult to imagine what he hopes to achieve by writing letters which contain so many inaccuracies. Macnair should declare his allegiances, if any.

Robin Russell-Jones
Member of CLEAR Scientific and Medical Advisory Board