- Email: [email protected]
LEAD-GLAZED EARTHENWARE
662 the cab
company’s depot "
so we
must
ask whether, in
exposure to lead in the home environment is not very similar to that during work and virtually identical for both groups of drivers. Diurnal patterns of lead in U.S urban areas show that the average values are slightly lower during the day (1100-1900)3 in Cincinnati and Los
addition,
Angeles than
at other times. This probably reflects the smaller volume in which pollutants are dispersed at night. Urban/rural differencesi Iso consistently show urban residents to have high blood-lead levels, and one reasonable explanation is the increased exposure to motor-vehicle exhaust. What we might do in order to estimate how much bloodlead is affected by inhalation of motor-vehicle exhaust is to compare the levels in these taxi drivers with residents or drivers in rural areas. The data suggest that (assuming analytical methods and population samples are comparable) the average blood-level of 28-7 fg. per 100 ml. is sufficiently in excess of average levels found in the " Three City Study " in Cincinnati, Philadelphia, and Los Angeles (22 g. per 100 ml. for smokers, 20 µg. per 100 ml. for non-smokers) that a substantial part of their lead body burden does come from motor-vehicle exhaust fumes. Utilising the regression relationship we have found generally applicable4 we would predict a 24-hour average respiratory exposure of 6-1 .g. per c.m. While this value is higher than the daytime average of 3-2 reported for Fleet Street by Waller et al.5 for 1961-62, there has been a steep (approximately 60%) increase in atmospheric lead levels in Los Angeles in this interval. This estimate therefore does not seem unreasonable if similar emission increases due to use of leaded petrol have occurred in London.
Environmental Epidemiology Unit, Bureau of Occupational Health and Environmental Epidemiology,
Berkeley, California 94704, U.S.A.
JOHN R. GOLDSMITH.
SIR,-Your correspondent Dr. Howard (Sept. 9, p. 545) in his criticism of the paper by Dr. Jones and his colleagues presumes that tetraethyl lead, because of its presence in petrol, will have appeared in this form in the taxi drivers. During the combustion of leaded petrol in motor vehicles, tetraethyl lead decomposes to give inorganic-lead compounds which appear in the exhaust gas. Many authoritative studies have been made of the inorganic-lead content of the air of cities, 6-8 but there is, unfortunately, little information regarding the organo-lead concentrations. Such results as are available 6,9,10 suggest that the organolead content of the atmosphere is at most 10% of the total lead content and is usually considerably less. Most of this lead can be accounted for from losses associated with the evaporation of fuel. An analysis of the lead composition of motor-vehicle exhaust emissions has shown that, under the conditions of an idling engine, 1 % of the total lead is in organic form, reducing to less than 0-05% when a vehicle 3. U.S. Department of Health, Education and Welfare, Publ. no 999-AP-12, Survey of Lead in the Atmosphere of Three Urban Communities, 1965. 4. Goldsmith, J. R., Hexter, A. C. Science, 1967, 158, 132. 5. Waller, R. E., Commins, B. T., Lawther, P. J. Br. J. ind. Med
1965, 22, 128.
Health, Education and Welfare. Publ. no 999-AP-12, Survey of Lead in the Atmosphere of Three Uurbar Communities, 1965. 7. Tepper, L. B., Levin, L. S. A survey of air and population lead levels in selected American communities. Department of Environmental Health, Kettering Laboratory, University of Cincinnati 6. U.S. Department of
1972.
Lawther, P. J., et al. in Lead in the Environment (edited by P Hepple). London, 1972. 9. Snyder, L. J. Analyt. Chem. 1967, 39, 591. 10. Laveskog, A. Paper presented to Second International Clean Ai Congress, Washington, D.C., December, 1970. 8.
is travelling at 30 m.p.h.ll Moreover, since lead alkyls are readily decomposed by light and heat, their presence in the atmosphere is transient. Dr. Howard is correct when he says that blood-lead estimations are unreliable as a measure of absorption of lead-alkyl compounds. The urinary lead concentration provides a much more reliable index of absorption of these compounds, but, in quoting Kehoe,12 Dr. Howard does not make it clear that Kehoe was referring to industrial exposure to tetraethyl lead at atmospheric concentrations far in excess of anything that could be expected to occur in the ambient air of city streets. The same criticism can be levelled in respect of Dr. Howard’s reference to the paper by Beattie et al. 13 on a recent series of cases of lead-alkyl
poisoning. The suggestion
that a control group was necessary for of purposes comparison, before the conclusions drawn by Jones et al. could be justified, is superfluous in view of the wealth of information published on the background blood-lead concentrations of unexposed population groups in a varietv of countries. 6,7,14-16 Associated Octel Co. 20
Ltd., Berkeley Square,
London W1X 6DT.
P. S. I. BARRY, Chief Medical Officer.
LEAD-GLAZED EARTHENWARE SIR,-Dr. Williams’s account of a patient with lead poisoning (Sept. 2, p. 480) draws attention to the dangers arising from the use of lead-glazed earthenware. In the past such vessels have been the chief cause of many large epidemics of colic and paralysis," but the public is still by no means fully aware of the risk. In July this year a young Civil Servant came to hospital for a blood-count. He was suffering from increasing malaise, aching muscles, depression, and insomnia. These symptoms had begun insidiously several weeks earlier. A few days before his visit to the laboratory he had an attack of severe abdominal pain which lasted about 36 hours. It was thought that he might be suffering from a viral infection, possibly glandular fever. His haemoglobin was 12-5 g. per 100 ml., red blood-cells 4-25 x 106 per µl., mean corpuscular volume 89 fl. and mean corpuscular haemoglobin 29 pg. Because stippled cells were found in a routine blood-film, a wet preparation was immediately examined by fluorescence microscopy. Virtually all the red cells showed porphyrin fluorescence, typical of lead poisoning. Estimates of the patient’s blood-lead by independent laboratories gave results of 79 µg. and 59 µg. per 100 ml. A urine sample contained 1880 µg. of coproporphyrin per litre. Examination of the patient’s table and kitchen ware did not immediately reveal the source of the poison, but eventually a reddish-brown jug was produced. This had first been brought into use about five months beforehand, as a serving-vessel for cider drawn from a barrel, and was badly blackened and pitted inside. Extraction for 4 hours with 1-5 litres of 5% acetic acid (pH 2-4) dissolved the equivalent of 683 mg. of elemental lead from the interior. Although dilute acetic acid is not comparable to fresh cider (pH 3-3), it was evident from this test that the jug was a highly dangerous source of lead. 11. Associated Octel Co. Ltd. Engine Laboratory, Bletchley, 1972. 12. Kehoe, R. A. in Industrial Hygiene and Toxicology (edited by F. A. Patty); vol. II, p. 955. New York, 1963. 13. Beattie, A. D., Moore, M. R., Goldberg, A. Lancet, July 1, 1972, p. 12. 14. Goldwater, L. J., Hoover, A. W. Archs envir. Hlth, 1967, 15, 60. 15. Swiss Leaded Gasoline Commission, Mitt. Geb. Lebensmittelunters.
16. 17.
u. Hyg. 1961, 52, 135. Kehoe, R. A. J. R. Inst. publ. Hlth Hyg. 1961, 24, 81, 101, 129, 177. Childs, St. J. R. Bull. Hist. Med. 1970, 44, 213.
663 The patient’s wife was symptomless, but more than 90% of her red cells were fluorescytes. Her hxmoglobin was 14-0 g. per 100 ml., blood-lead 69 µg. per 100 ml., and urine coproporphyrin 295 ;ig. per litre. Like her husband, she had often drunk cider after it had stood in the jug. Their 2-year-old son was well, and his blood picture normal. His blood-lead was 38 µg. per 100 ml. (2 µg. above the upper limits of normal for the laboratory which performed the test), but no fluorescytes were found and coproporphyrin was not detected in a random sample of his urine. For some months the child had used a pewter goblet as a drinking-cup. This may have contributed to the lead content of his blood. The patient became symptom-free shortly after discarding his earthenware jug. At first his haemoglobin continued to fall, reaching 11.7 g. per 100 ml. before rising again. His wife’s hxmoglobin level has risen to 15-0 g. per 100 ml. It is probable that the onset and severity of lead poisoning is related to the rate of absorption as well as to the total dose. Lead levels greater than 80 µg. per 100 ml. of blood are considered unacceptably dangerous in industrial workers, but lower levels are sometimes associated with
poisoning and must not be disregarded. The jug described was purchased in France, and its purpose was clearly functional rather than decorative. Many of the patient’s relatives and friends had drunk from it, including several who were medically qualified. Since such items are popular tourist souvenirs, it is likely that serious poisoning from this traditional source will be met with for many years to come. Casual inquiries amongst friends and acquaintances have disclosed that in recent times articles of this kind have sometimes been used casseroles, salad bowls, or dishes for babv food. Department of Hæmatology, King’s College Hospital Medical School, London S.E.5.
3. 4.
5. 6. 7.
Department of Applied Pharmacology, School of Pharmacy, Hebrew University, Jerusalem, Israel.
Sulman, F. G., Hirschman, N., Pfeifer, Y. Proceedings of Lucknow Symposium on Arid Zones; p. 89. UNESCO, 1964. Danon, A., Weller, C. P., Sulman, F. G. Int. J. Biometeorol. 1969, 13, 95. Weller, C. P., Sulman, F. G. ibid. suppl. 4, part 2, p. 30. Danon, A., Weller, C. P., Sulman, F. G. ibid. p. 71. Sulman, F. G., Danon, A., Pfeifer, Y., Tal, E., Weller, C. P. ibid. 1970, 14, 45. Dikstein, S., Kaplanski, Y., Koch, Y., Sulman, F. G. Life Sci. 1970, 9, 1191. Sulman, F. G. Aerztl. Praxis, 1971, 23, 998.
F. G. SULMAN E. SUPERSTINE.
Obituary KENNETH HERBERT TAYLOR M.B.Lond., F.R.C.S.
Mr. K. H. Taylor, senior surgeon to High and Amersham hospitals, died on Sept. 8.
Wycombe
direct line of doctors for four generations, and his son carries on the line. He was educated at Epsom College and St. Thomas’s Hospital, London, qualified in 1938, and after house appointments joined the Welsh Guards at the outbreak of war and was in their rearguard action at Boulogne. He next served with the 57th Anti-tank Regiment from El Alamein through North Africa and Italy until the end of the war. He returned to St. Thomas’s in January, 1946, and took his F.R.C.S. He held junior posts at the Royal Berkshire Hospital, Reading, and the Royal Free Hospital, London, until apconsultant surgeon in 1952 to the Aylesbury and
He was in
K. G. A. CLARK.
SIR,—The findings of Dr. Robinson and his colleagues (Feb. 5, p. 290) seem to confirm our observations. 1-7 Daily urinalysis in 500 people5 has shown that from the age of 30, as well as in old age, life in hot climates and other forms of heat stress can cause lack of adrenaline and noradrenaline. We have found in such people all the symptoms of tropical lethargy-i.e., hypotension, fatigue, exhaustion, apathy, depression, lack of concentration, confusion, hypoglycæmic spells, and ataxia. The most typical complaint is that the heat stress becomes worse each year. In hot dry winds excessive sweating is avoided by contraction of skin blood-vessels. This rapidly induces exhaustion of the adrenal medulla and very low adrenaline output. Noradrenaline is also reduced but never reaches zero level (as adrenaline does) because of its extra-adrenal production as a sympathetic transmitter. The results of 3 years’ experience in treating such patients have shown that very low doses (¼-1 tablet per 2.
these disabilities without any risk of a reaction with The M.A.O.I. chosen must be one with an immediate effect. We have found that mebanazine (’ Actomol ’) and isocarboxazid (’ Marplan ’) produce relief within 30 minutes without producing tolerance or addiction. We are now trying tranylcypromine (’ Parnate ’). cure
tyramine-containing foods.
as
AGEING AND ADRENAL-MEDULLA EXHAUSTION DUE TO LACK OF MONOAMINES AND RAISED MONOAMINEOXIDASE LEVELS
1.
day) of monoamine-oxidase inhibitors (M.A.O.I.S) completely
pointed Wycombe A
a
group.
colleague writes:
"
As a surgeon Kenneth was skilful and gentle; he had great stamina, his skill and judgment remaining keen at the end of unusually long lists and outpatient sessions. " He was seen at his best in consultation with physicians and family doctors, readily understanding their problems and making up his mind quickly and with reasons for his decision given clearly. He had superb clinical judgment. He was loved by his patients both for his skill and for his good manners and wit; he gave them clear explanations of what he had done and why he had done it. He had the rare gift of expressing meaning in the fewest possible words, which was one of the reasons why he was so excellent a teacher. He was a founder member and past-president of the flourishing Chiltern Medical Society. He served long periods on the hospital management committee and the Oxford Regional Hospital Board, and was a member of the British Association of Paediatric Surgeons. " Kenneth was a strong simple man, who drew his strength from his love for his family, his home, and his church. He had an innate sweetness of character. To all his colleagues, medical, nursing, and lay, he was always "
available, always ready Mr. Taylor is daughters.
to
help."
survived
by
his
wife, his
son, and two
company’s depot "
so we
must
ask whether, in
exposure to lead in the home environment is not very similar to that during work and virtually identical for both groups of drivers. Diurnal patterns of lead in U.S urban areas show that the average values are slightly lower during the day (1100-1900)3 in Cincinnati and Los
addition,
Angeles than
at other times. This probably reflects the smaller volume in which pollutants are dispersed at night. Urban/rural differencesi Iso consistently show urban residents to have high blood-lead levels, and one reasonable explanation is the increased exposure to motor-vehicle exhaust. What we might do in order to estimate how much bloodlead is affected by inhalation of motor-vehicle exhaust is to compare the levels in these taxi drivers with residents or drivers in rural areas. The data suggest that (assuming analytical methods and population samples are comparable) the average blood-level of 28-7 fg. per 100 ml. is sufficiently in excess of average levels found in the " Three City Study " in Cincinnati, Philadelphia, and Los Angeles (22 g. per 100 ml. for smokers, 20 µg. per 100 ml. for non-smokers) that a substantial part of their lead body burden does come from motor-vehicle exhaust fumes. Utilising the regression relationship we have found generally applicable4 we would predict a 24-hour average respiratory exposure of 6-1 .g. per c.m. While this value is higher than the daytime average of 3-2 reported for Fleet Street by Waller et al.5 for 1961-62, there has been a steep (approximately 60%) increase in atmospheric lead levels in Los Angeles in this interval. This estimate therefore does not seem unreasonable if similar emission increases due to use of leaded petrol have occurred in London.
Environmental Epidemiology Unit, Bureau of Occupational Health and Environmental Epidemiology,
Berkeley, California 94704, U.S.A.
JOHN R. GOLDSMITH.
SIR,-Your correspondent Dr. Howard (Sept. 9, p. 545) in his criticism of the paper by Dr. Jones and his colleagues presumes that tetraethyl lead, because of its presence in petrol, will have appeared in this form in the taxi drivers. During the combustion of leaded petrol in motor vehicles, tetraethyl lead decomposes to give inorganic-lead compounds which appear in the exhaust gas. Many authoritative studies have been made of the inorganic-lead content of the air of cities, 6-8 but there is, unfortunately, little information regarding the organo-lead concentrations. Such results as are available 6,9,10 suggest that the organolead content of the atmosphere is at most 10% of the total lead content and is usually considerably less. Most of this lead can be accounted for from losses associated with the evaporation of fuel. An analysis of the lead composition of motor-vehicle exhaust emissions has shown that, under the conditions of an idling engine, 1 % of the total lead is in organic form, reducing to less than 0-05% when a vehicle 3. U.S. Department of Health, Education and Welfare, Publ. no 999-AP-12, Survey of Lead in the Atmosphere of Three Urban Communities, 1965. 4. Goldsmith, J. R., Hexter, A. C. Science, 1967, 158, 132. 5. Waller, R. E., Commins, B. T., Lawther, P. J. Br. J. ind. Med
1965, 22, 128.
Health, Education and Welfare. Publ. no 999-AP-12, Survey of Lead in the Atmosphere of Three Uurbar Communities, 1965. 7. Tepper, L. B., Levin, L. S. A survey of air and population lead levels in selected American communities. Department of Environmental Health, Kettering Laboratory, University of Cincinnati 6. U.S. Department of
1972.
Lawther, P. J., et al. in Lead in the Environment (edited by P Hepple). London, 1972. 9. Snyder, L. J. Analyt. Chem. 1967, 39, 591. 10. Laveskog, A. Paper presented to Second International Clean Ai Congress, Washington, D.C., December, 1970. 8.
is travelling at 30 m.p.h.ll Moreover, since lead alkyls are readily decomposed by light and heat, their presence in the atmosphere is transient. Dr. Howard is correct when he says that blood-lead estimations are unreliable as a measure of absorption of lead-alkyl compounds. The urinary lead concentration provides a much more reliable index of absorption of these compounds, but, in quoting Kehoe,12 Dr. Howard does not make it clear that Kehoe was referring to industrial exposure to tetraethyl lead at atmospheric concentrations far in excess of anything that could be expected to occur in the ambient air of city streets. The same criticism can be levelled in respect of Dr. Howard’s reference to the paper by Beattie et al. 13 on a recent series of cases of lead-alkyl
poisoning. The suggestion
that a control group was necessary for of purposes comparison, before the conclusions drawn by Jones et al. could be justified, is superfluous in view of the wealth of information published on the background blood-lead concentrations of unexposed population groups in a varietv of countries. 6,7,14-16 Associated Octel Co. 20
Ltd., Berkeley Square,
London W1X 6DT.
P. S. I. BARRY, Chief Medical Officer.
LEAD-GLAZED EARTHENWARE SIR,-Dr. Williams’s account of a patient with lead poisoning (Sept. 2, p. 480) draws attention to the dangers arising from the use of lead-glazed earthenware. In the past such vessels have been the chief cause of many large epidemics of colic and paralysis," but the public is still by no means fully aware of the risk. In July this year a young Civil Servant came to hospital for a blood-count. He was suffering from increasing malaise, aching muscles, depression, and insomnia. These symptoms had begun insidiously several weeks earlier. A few days before his visit to the laboratory he had an attack of severe abdominal pain which lasted about 36 hours. It was thought that he might be suffering from a viral infection, possibly glandular fever. His haemoglobin was 12-5 g. per 100 ml., red blood-cells 4-25 x 106 per µl., mean corpuscular volume 89 fl. and mean corpuscular haemoglobin 29 pg. Because stippled cells were found in a routine blood-film, a wet preparation was immediately examined by fluorescence microscopy. Virtually all the red cells showed porphyrin fluorescence, typical of lead poisoning. Estimates of the patient’s blood-lead by independent laboratories gave results of 79 µg. and 59 µg. per 100 ml. A urine sample contained 1880 µg. of coproporphyrin per litre. Examination of the patient’s table and kitchen ware did not immediately reveal the source of the poison, but eventually a reddish-brown jug was produced. This had first been brought into use about five months beforehand, as a serving-vessel for cider drawn from a barrel, and was badly blackened and pitted inside. Extraction for 4 hours with 1-5 litres of 5% acetic acid (pH 2-4) dissolved the equivalent of 683 mg. of elemental lead from the interior. Although dilute acetic acid is not comparable to fresh cider (pH 3-3), it was evident from this test that the jug was a highly dangerous source of lead. 11. Associated Octel Co. Ltd. Engine Laboratory, Bletchley, 1972. 12. Kehoe, R. A. in Industrial Hygiene and Toxicology (edited by F. A. Patty); vol. II, p. 955. New York, 1963. 13. Beattie, A. D., Moore, M. R., Goldberg, A. Lancet, July 1, 1972, p. 12. 14. Goldwater, L. J., Hoover, A. W. Archs envir. Hlth, 1967, 15, 60. 15. Swiss Leaded Gasoline Commission, Mitt. Geb. Lebensmittelunters.
16. 17.
u. Hyg. 1961, 52, 135. Kehoe, R. A. J. R. Inst. publ. Hlth Hyg. 1961, 24, 81, 101, 129, 177. Childs, St. J. R. Bull. Hist. Med. 1970, 44, 213.
663 The patient’s wife was symptomless, but more than 90% of her red cells were fluorescytes. Her hxmoglobin was 14-0 g. per 100 ml., blood-lead 69 µg. per 100 ml., and urine coproporphyrin 295 ;ig. per litre. Like her husband, she had often drunk cider after it had stood in the jug. Their 2-year-old son was well, and his blood picture normal. His blood-lead was 38 µg. per 100 ml. (2 µg. above the upper limits of normal for the laboratory which performed the test), but no fluorescytes were found and coproporphyrin was not detected in a random sample of his urine. For some months the child had used a pewter goblet as a drinking-cup. This may have contributed to the lead content of his blood. The patient became symptom-free shortly after discarding his earthenware jug. At first his haemoglobin continued to fall, reaching 11.7 g. per 100 ml. before rising again. His wife’s hxmoglobin level has risen to 15-0 g. per 100 ml. It is probable that the onset and severity of lead poisoning is related to the rate of absorption as well as to the total dose. Lead levels greater than 80 µg. per 100 ml. of blood are considered unacceptably dangerous in industrial workers, but lower levels are sometimes associated with
poisoning and must not be disregarded. The jug described was purchased in France, and its purpose was clearly functional rather than decorative. Many of the patient’s relatives and friends had drunk from it, including several who were medically qualified. Since such items are popular tourist souvenirs, it is likely that serious poisoning from this traditional source will be met with for many years to come. Casual inquiries amongst friends and acquaintances have disclosed that in recent times articles of this kind have sometimes been used casseroles, salad bowls, or dishes for babv food. Department of Hæmatology, King’s College Hospital Medical School, London S.E.5.
3. 4.
5. 6. 7.
Department of Applied Pharmacology, School of Pharmacy, Hebrew University, Jerusalem, Israel.
Sulman, F. G., Hirschman, N., Pfeifer, Y. Proceedings of Lucknow Symposium on Arid Zones; p. 89. UNESCO, 1964. Danon, A., Weller, C. P., Sulman, F. G. Int. J. Biometeorol. 1969, 13, 95. Weller, C. P., Sulman, F. G. ibid. suppl. 4, part 2, p. 30. Danon, A., Weller, C. P., Sulman, F. G. ibid. p. 71. Sulman, F. G., Danon, A., Pfeifer, Y., Tal, E., Weller, C. P. ibid. 1970, 14, 45. Dikstein, S., Kaplanski, Y., Koch, Y., Sulman, F. G. Life Sci. 1970, 9, 1191. Sulman, F. G. Aerztl. Praxis, 1971, 23, 998.
F. G. SULMAN E. SUPERSTINE.
Obituary KENNETH HERBERT TAYLOR M.B.Lond., F.R.C.S.
Mr. K. H. Taylor, senior surgeon to High and Amersham hospitals, died on Sept. 8.
Wycombe
direct line of doctors for four generations, and his son carries on the line. He was educated at Epsom College and St. Thomas’s Hospital, London, qualified in 1938, and after house appointments joined the Welsh Guards at the outbreak of war and was in their rearguard action at Boulogne. He next served with the 57th Anti-tank Regiment from El Alamein through North Africa and Italy until the end of the war. He returned to St. Thomas’s in January, 1946, and took his F.R.C.S. He held junior posts at the Royal Berkshire Hospital, Reading, and the Royal Free Hospital, London, until apconsultant surgeon in 1952 to the Aylesbury and
He was in
K. G. A. CLARK.
SIR,—The findings of Dr. Robinson and his colleagues (Feb. 5, p. 290) seem to confirm our observations. 1-7 Daily urinalysis in 500 people5 has shown that from the age of 30, as well as in old age, life in hot climates and other forms of heat stress can cause lack of adrenaline and noradrenaline. We have found in such people all the symptoms of tropical lethargy-i.e., hypotension, fatigue, exhaustion, apathy, depression, lack of concentration, confusion, hypoglycæmic spells, and ataxia. The most typical complaint is that the heat stress becomes worse each year. In hot dry winds excessive sweating is avoided by contraction of skin blood-vessels. This rapidly induces exhaustion of the adrenal medulla and very low adrenaline output. Noradrenaline is also reduced but never reaches zero level (as adrenaline does) because of its extra-adrenal production as a sympathetic transmitter. The results of 3 years’ experience in treating such patients have shown that very low doses (¼-1 tablet per 2.
these disabilities without any risk of a reaction with The M.A.O.I. chosen must be one with an immediate effect. We have found that mebanazine (’ Actomol ’) and isocarboxazid (’ Marplan ’) produce relief within 30 minutes without producing tolerance or addiction. We are now trying tranylcypromine (’ Parnate ’). cure
tyramine-containing foods.
as
AGEING AND ADRENAL-MEDULLA EXHAUSTION DUE TO LACK OF MONOAMINES AND RAISED MONOAMINEOXIDASE LEVELS
1.
day) of monoamine-oxidase inhibitors (M.A.O.I.S) completely
pointed Wycombe A
a
group.
colleague writes:
"
As a surgeon Kenneth was skilful and gentle; he had great stamina, his skill and judgment remaining keen at the end of unusually long lists and outpatient sessions. " He was seen at his best in consultation with physicians and family doctors, readily understanding their problems and making up his mind quickly and with reasons for his decision given clearly. He had superb clinical judgment. He was loved by his patients both for his skill and for his good manners and wit; he gave them clear explanations of what he had done and why he had done it. He had the rare gift of expressing meaning in the fewest possible words, which was one of the reasons why he was so excellent a teacher. He was a founder member and past-president of the flourishing Chiltern Medical Society. He served long periods on the hospital management committee and the Oxford Regional Hospital Board, and was a member of the British Association of Paediatric Surgeons. " Kenneth was a strong simple man, who drew his strength from his love for his family, his home, and his church. He had an innate sweetness of character. To all his colleagues, medical, nursing, and lay, he was always "
available, always ready Mr. Taylor is daughters.
to
help."
survived
by
his
wife, his
son, and two