- Email: [email protected]
LEAD IN PETROL AND ELSEWHERE
1464 with pentamidine again. At that time pentamidine isethionate was the only effective drug available. With daily blood sugar checks and repeated glucose tolerance tests, she was treated with pentamidine isethionate 200 mg i.m. every other day for a month. Her leishmaniasis improved markedly and her parasite load diminished. Diabetes did not develop. From 1974 to 1979 we successfully treated over a hundred cutaneous leishmaniasis patients with pentamidine isethionate 200 mg i.m. daily for 15 days. Blood sugar levels and glucose tolerance were monitored before, during, and after treatment. No diabetes mellitus developed. After 1978 no more pentamidine isethionate was available and the mesylate (lomidine) had to be used again. In the ,ensuing two years diabetes was seen in two of the thirty patients treated. In 1981 the original patient had to be treated again because of a severe deterioration in her leishmaniasis, with whole body infiltration and ulceration. She was treated with pentamidine mesylate (lomidine) and diabetes developed again. Before 1974 pentamidine mesylate was used in our hospital and severe cases of diabetes developed. In 1974-79 pentamidine isethionate was used and no cases of diabetes were recorded. Subsequently, the mesylate form having been reintroduced, several cases of diabetes mellitus have developed. Thus pentamidine isethionate seems to be less pancreatotoxic than pentamidine mesylate. Incidentally, use of the name "pentamidine" for both the isethionate (’Pentamidine’) and the mesylate (’Lomidine’) is confusing and should be avoided. Armauer Hansen Research Institute, P.O. Box 1005,
Addis Ababa, Ethiopia All Africa Leprosy and Rehabilitation Training Centre *Present address’
Department of Dermatology, University
AYELE BELEHU
BERNARD NAAFS* of Amsterdam.
LEAD IN PETROL AND ELSEWHERE
SIR,—Over the past few months medical and scientific journals have devoted considerable space to the lead-in-petrol debate and your editorial (June 12, p. 1337) is further testimony to the importance of this vital issue. During this period I think it is fair to say that the consensus of medical, opinion has shifted significantly.,’ The accuracy of the geochemical data (C. C. Patterson), the relevance of animal experiments (G. Winneke) and the complementary role of the biochemical studies (E. K. Silbergeld) provide a firm basis for the view expressed by Prof. Michael Rutter in his concluding remarks to the CLEAR symposium3 to which the above workers contributed papers-namely, that lead probably does cause the neuropsychological deficits with which it is so clearly associated in epidemiological studies. It is also apparent that the removal of lead from petrol in the United States has produced a dramatic and sustained decline in the lead levels of the American population (J. L.
more easily remedied than others. If The Lancet is not prepared to advocate the removal of lead from petrol, then how can it hope to influence society’s attitude to the seemingly intractable problems of housing and education? It is also relevant to point out that the chairman of CLEAR was formerly director of the housing action group Shelter and has done more than most to draw attention to the plight of the homeless in the U.K. There are three further aspects of this problem which we ignore at our peril. First, it cannot be assumed that social class has a greater impact than lead on neurological dysfunction since no suitable leadfree control populations exist in the modern industrialised world. Second, we have no detailed toxicological information on the organo-lead compounds, but what little is known about their mutagenicity and potential carcinogenicity would immediately prohibit their use on any significant scale if the use of lead alkyls in petrol were a proposal rather than a technological reality (P. Grandjean). Third, any further attempts by the medical establishment to delay remedial action on this issue will be viewed as ethically indefensible. The procession of arguments which have been paraded over the past decade as excuses for inertia have been systematically and comprehensibly refuted. Future generations may well forgive scientists who are slow to realise the implications of their own data but they will not forgive those who deliberately discard opportunities which may never present themselves again. ROBIN RUSSELL JONES, 2 Northdown Street,
Deputy Chairman, CLEAR
LondonNI
HERBICIDES, OCCUPATION, AND CANCER SIR,—In their review of the phenoxy herbicide/cancer controversy Dr Coggon and Professor Acheson (May 8, p. 1057) ask for more information. I have updated an occupational mortality
study’ which sheds further light on the matter. There is considerable exposure in Washington State to phenoxy herbicides and chlorophenols in agriculture and forestry and the wood products industry. 2,4-D is used extensively in wheat farming, roadside brush and weed control, management of unwanted forest growth, and in pulp mills and sawmills for control of blue staining
fungi. Table
I
shows
1. Milham S.
mortality
due
Occupational mortality publication (NIOSH) (in press).
to
in
soft tissue sarcomas, Washington State,
TABLE I-OBSERVED/EXPECTED DEATHS
Hodgkin’s
1950-1979
HEW
(AND PMRS) FOR SELECTED
CANCERS* IN OCCUPATIONS WITH EXPOSURE TO PHENOXY HERBICIDES AND CHLOROPHENOLS: WASHINGTON STATE WHITE MALE DEATHS, AGE
20 +, 1950-79
Annest). In the face of this remarkable convergence of scientific evidence, the last paragraph of your editorial seems strangely out of place. You seem to suggest that having accumulated this synthesis of highquality data we can now ignore it since other factors may have an even greater impact on neurological development in early childhood. This sort of logic falls far short of the standard one can normally expect from The Lancet. More is known about lead than about any. other environmental pollutant. If there is no mechanism for translating that knowledge into effective remedial action, then why bother to gather the information in the first place? Carried to its logical conclusion, one might as well abandon all attempts at preventive medicine on the grounds that old age correlates more closely with death than any other single determinant. Obviously there are many ways of ruining a child’s environment, but some are 1 Editorial Lead 2. Editorial Lead
3
petrol Br Med J 1982; 284: 529. petrol: Again. Br Med J 1982; 284: 1506 Rutter MA, Russell Jones R, eds. Lead versus health- Proceedings of an international symposium on low level lead exposure and its effects on human beings (London, May 10-12, 1982). Chichester: John Wiley (in press) in
in
p<0.05 *ICD nos are, respecnvely, 197,201; 200.0-200. 1,202-202. 2. Expected deaths based on age-at-death and year-of-death specific proportionate mortality (rounded to nearest whole number). PMR=Obs/Expx100
Addis Ababa, Ethiopia All Africa Leprosy and Rehabilitation Training Centre *Present address’
Department of Dermatology, University
AYELE BELEHU
BERNARD NAAFS* of Amsterdam.
LEAD IN PETROL AND ELSEWHERE
SIR,—Over the past few months medical and scientific journals have devoted considerable space to the lead-in-petrol debate and your editorial (June 12, p. 1337) is further testimony to the importance of this vital issue. During this period I think it is fair to say that the consensus of medical, opinion has shifted significantly.,’ The accuracy of the geochemical data (C. C. Patterson), the relevance of animal experiments (G. Winneke) and the complementary role of the biochemical studies (E. K. Silbergeld) provide a firm basis for the view expressed by Prof. Michael Rutter in his concluding remarks to the CLEAR symposium3 to which the above workers contributed papers-namely, that lead probably does cause the neuropsychological deficits with which it is so clearly associated in epidemiological studies. It is also apparent that the removal of lead from petrol in the United States has produced a dramatic and sustained decline in the lead levels of the American population (J. L.
more easily remedied than others. If The Lancet is not prepared to advocate the removal of lead from petrol, then how can it hope to influence society’s attitude to the seemingly intractable problems of housing and education? It is also relevant to point out that the chairman of CLEAR was formerly director of the housing action group Shelter and has done more than most to draw attention to the plight of the homeless in the U.K. There are three further aspects of this problem which we ignore at our peril. First, it cannot be assumed that social class has a greater impact than lead on neurological dysfunction since no suitable leadfree control populations exist in the modern industrialised world. Second, we have no detailed toxicological information on the organo-lead compounds, but what little is known about their mutagenicity and potential carcinogenicity would immediately prohibit their use on any significant scale if the use of lead alkyls in petrol were a proposal rather than a technological reality (P. Grandjean). Third, any further attempts by the medical establishment to delay remedial action on this issue will be viewed as ethically indefensible. The procession of arguments which have been paraded over the past decade as excuses for inertia have been systematically and comprehensibly refuted. Future generations may well forgive scientists who are slow to realise the implications of their own data but they will not forgive those who deliberately discard opportunities which may never present themselves again. ROBIN RUSSELL JONES, 2 Northdown Street,
Deputy Chairman, CLEAR
LondonNI
HERBICIDES, OCCUPATION, AND CANCER SIR,—In their review of the phenoxy herbicide/cancer controversy Dr Coggon and Professor Acheson (May 8, p. 1057) ask for more information. I have updated an occupational mortality
study’ which sheds further light on the matter. There is considerable exposure in Washington State to phenoxy herbicides and chlorophenols in agriculture and forestry and the wood products industry. 2,4-D is used extensively in wheat farming, roadside brush and weed control, management of unwanted forest growth, and in pulp mills and sawmills for control of blue staining
fungi. Table
I
shows
1. Milham S.
mortality
due
Occupational mortality publication (NIOSH) (in press).
to
in
soft tissue sarcomas, Washington State,
TABLE I-OBSERVED/EXPECTED DEATHS
Hodgkin’s
1950-1979
HEW
(AND PMRS) FOR SELECTED
CANCERS* IN OCCUPATIONS WITH EXPOSURE TO PHENOXY HERBICIDES AND CHLOROPHENOLS: WASHINGTON STATE WHITE MALE DEATHS, AGE
20 +, 1950-79
Annest). In the face of this remarkable convergence of scientific evidence, the last paragraph of your editorial seems strangely out of place. You seem to suggest that having accumulated this synthesis of highquality data we can now ignore it since other factors may have an even greater impact on neurological development in early childhood. This sort of logic falls far short of the standard one can normally expect from The Lancet. More is known about lead than about any. other environmental pollutant. If there is no mechanism for translating that knowledge into effective remedial action, then why bother to gather the information in the first place? Carried to its logical conclusion, one might as well abandon all attempts at preventive medicine on the grounds that old age correlates more closely with death than any other single determinant. Obviously there are many ways of ruining a child’s environment, but some are 1 Editorial Lead 2. Editorial Lead
3
petrol Br Med J 1982; 284: 529. petrol: Again. Br Med J 1982; 284: 1506 Rutter MA, Russell Jones R, eds. Lead versus health- Proceedings of an international symposium on low level lead exposure and its effects on human beings (London, May 10-12, 1982). Chichester: John Wiley (in press) in
in
p<0.05 *ICD nos are, respecnvely, 197,201; 200.0-200. 1,202-202. 2. Expected deaths based on age-at-death and year-of-death specific proportionate mortality (rounded to nearest whole number). PMR=Obs/Expx100