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suring sebum secretion in the rats together with preputialgland weight and prostate and seminal vesicle weights as

androgen primed organs. We measured the response to cimeti-dine in the intact and castrate rat with and without exogenousandrogen. In the intact rat there was a decrease in prostateand seminal vesicle weights but no effect on cutaneous seba-ceous glands and only a slight effect on preputial gland. Therewas a much, smaller effect in the castrate. When given withtestesterone the cimetidine showed an androgenic action.The conclusion in my report to S.K.F. (we did not publish

the work) was that the simplest explanation of these puzzlingresults was that cimetidine was a weak androgen whichshowed either an androgenic or antiandrogenic effect (by com-petition) which varied with the target organ and ambient con-centration of androgen. More work was needed to establishthis and exclude other mechanisms; moreover, in view of thespecies and tissue differences in sebaceous gland response theeffect of cimetidine would be worth trying on the human seba-ceous gland.

Like S.K.F. we did not take our own advice, which explainshow it is we took so long to show that the human sebaceousgland is inhibited by cimetidine. Of course cimetidine is anantiandrogen-though blockade of 5-HT suggested by Burtonand Lovall does not greatly appeal as a mechanism because ourown evidence is that 5-HT is irrelevant to human sebaceousfunction-but there remain other more interesting ideas, andwe are now looking at the H2 receptor itself.

It is too soon to be other than tentative about therapeuticpossibilities but, like Burton and Lovall, we feel that it wouldbe sensible to try a number of therapeutic tricks, includingcombination with antibiotic and other inhibitors of sebum pro-duction, especially if this were done by others who have moresympathy for, and expertise with, clinical trials.

Department of Dermatology,The University of Newcastle upon Tyne,Royal Victoria Infirmary,Newcastle upon Tyne NE1 4LP SAM SHUSTER

LYMPHOMAS AND BENZENE

SIR,-Vianna and Polan! have reported an excess in death-rates from major lymphomas among men in occupations wherebenzene or coal tar fractions are handled. The death-rates theypresent were developed by relating occupational informationfrom the U.S. decennial census to occupational informationappearing on death certificates. This procedure is likely to pro-duce erroneous results since in the U.S. the census occupationis the current or last occupation while the death certificatecalls for the usual occupation. For retired persons (65 andover), relating these two items seems hopeless, and mortalitydata are not ordinarily reported by occupation for this agegroup. Where mortality at other ages has been studied, a cor-rection of population data has-been made to convert counts ofcurrent occupation to counts of usual occupation. Data pre-sented by Vianna and Polan relate to all ages and apparentlythey did not attempt any correction. The excess in death ratesthey report are for occupations more likely to be usual thancurrent (or last) and thus the excess may simply be an artefact.One solution to this problem is to look simply at propor-

tionate mortality ratios (PMRs) which are based only on occu-pation as defined on the death certificate. Milham2 has calcu-lated these ratios for the State of Washington. For twelve of

5. Archibald A, Shuster S. The measurement of sebum secretion in the rat. BrJ Dermatol 1970; 82: 146.

6. Shuster S, Thody AJ. The control and measurement of sebum secretion. JInvest Dermatol 1974; 62: 172-90.

1. Vianna NJ, Polan A. Lymphomas and occupational benzene exposure. Lan-cet 1979; i: 1394-95.

2. Milham S. Occupational mortality in Washington State 1950-71:N.I.O.S.H. research report, vols I, n, and III. U.S. Government PrintingOffice, 1976.

the fourteen occupations selected by Vianna and Polan, Lym-phoma deaths are reported in Milham’s study. For reticulumcell sarcoma, none of the PMRs for these twelve occupationsare in excess (greater than 100), for lymphosarcoma only oneout of the twelve is in excess, while for Hodgkin’s disease, onlythree out of the twelve are in excess.

I think if Vianna and Polan were to calculate PMRs, as Mil-ham did, or recalculate rates as suggested above, they may findthat the excess in mortality from lymphomas disappears.

Department of Biostatistics,University of Pittsburgh,Pittsburgh, Pennsylvania 15261, U.S.A. PHILIP E. ENTERLINE

DIETARY VITAMIN D

SiR,-The letter by D Rees (Oct. 6, p. 754), regretting theomission from the Ministry of Agriculture, Fisheries and Foodpublication Food Facts of any reference to vitamin D, is unfor-tunate in implying a role for dietary vitamin D in maintenanceof vitamin D status. Rees appears to accept that the source ofvitamin D is the action of sunlight on skin but not the coroll-ary, that dietary vitamin D contributes an unimportantamount of the total body pool of this vitamin. Intakes severaltimes greater than those currently prevailing are required toproduce a response in plasma vitamin D levels similar to thatachieved by sunlight.1-4 A lack of dietary vitamin D is not acause of rickets or osteomalacia. S

Low vitamin D states do occur, but the conditions underwhich these cause disease to develop are unknown. Low vita-min D states arise from a number of causes: for example, lackof exposure to sunlight may be the cause in the elderly6 butthis is not so in Asians.7

Dunn Nutritional Laboratory,Cambridge CB4 1XJ D. E. M. LAWSON

OVARIAN FAILURE IN GALACTOSÆMIA

SiR,—I read the letter by Dr Kaufman and his colleagues(Oct. 6, p. 737) with considerable interest because I believethat clinicians looking after treated galactosxmic girls will beable to reinforce their clinical findings. I certainly have onesuch case; she is the eldest of the small number of affected girlsunder my care. However, the next two patients have hadchildren of their own, and the fourth, now aged 12 years,seems to be a healthy young girl. My hunch is that galactose-1-phosphate, the intermediary in galactosaemia which, howeverstrict the diet, accumulates in body cells to some degree, inter-feres with the binding affinity of receptor sites for gonadotro-phins.2 18th Century House,Oakley Park,Frilford Heath,Abingdon, Oxon. GEORGE KOMROWER

1. Poskitt EM, Cole T, Lawson DEM, Diet, sunlight and 25-hydroxyvitaminD in healthy children and adults. Br Med J 1979; i: 221.

2. Stamp TCB, Haddad JG, Twigg CA. Comparison of oral 25-hydroxychole-calciferol, vitamin D and ultraviolet light as determinants of circulating25-hydroxyvitamin D. Lancet 1977; i: 1341.

3. Somerville PJ, Lien JWK, Kaye MJ. The calcium and vitamin D status inan elderly female population and their response to administered supple-mental vitamin D3. Gerontology 1977; 32: 659.

4. Pietrek J, Windo J, Preece MA, O’Riordan JLH, Dunnigan MG, McIntoshWB, Ford JA. Prevention of vitamin D deficiency in Asians. Lancet 1976;i: 1145.

5. Pittet PG, Davie M, Lawson DEM, Role of nutrition in the development ofosteomalacia in the elderly. Nutr Metab 1979; 23: 109.

6. Lawson DEM, Paul AA, Black AE, Cole TJ, Mandel AP, Davie M. Relativecontributions of diet and sunlight to vitamin D state in the elderly. BrMed J 1979; ii: 303.

7. Dunnigan M. Asian rickets and osteomalacia in Britain. In: Child nutritionand its relation to mental and physical development. London: KelloggCompany of Great Britain Ltd: 43.