|
|
| 1. |
Proceedings of the Society of Public Analysts and other Analytical Chemists |
| |
Analyst,
Volume 59,
Issue 705,
1934,
Page 785-786
Preview
|
PDF (137KB)
|
|
摘要:
WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock. Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given.However, potatoes had been given to horses in limited quantities without bad results. Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent. Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it.In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes.Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock.Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given.However, potatoes had been given to horses in limited quantities without bad results. Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent.Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it. In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes. Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.
ISSN:0003-2654
DOI:10.1039/AN9345900785
出版商:RSC
年代:1934
数据来源: RSC
|
| 2. |
The determination of traces of lead in biological materials, with special reference to bone |
| |
Analyst,
Volume 59,
Issue 705,
1934,
Page 787-806
G. Roche Lynch,
Preview
|
PDF (1542KB)
|
|
摘要:
LYNCH SLATER AND OSLER DETERMINATION OF LEAD IN BONE ETC. 787 The Determination of Traces of Lead in Biological Materials with Special Reference to Bone BY G. ROCHE LYNCH O.B.E. M.B. B.S. D.P.H. F.I.C. R. H. SLATER D.Sc. PH.D. F.R.S.E. A.I.C. AND T. G. OSLER M.B. CH.B. M.R.C.S. L.R.C.P. (Read at the Meeting October 3 1934) INTRODUCTION.-The great importance of the detection and determination of lead in the human body and in biological and industrial materials generally, has been realised for a considerable time; the interest taken in investigations of this nature is shown by the voluminous literature and frequent articles published on the subject ( c j ANALYST 1932 57 775). It has been definitely established from chemical investigation of experimentally lead-poisoned animals and from clinical cases of plumbism that when lead is taken into the organism and absorbed, that part which is not excreted by the kidneys liver and intestine and which in chronic plumbism represents nearly all the absorbed lead is taken up from the circulating blood by the bones under normal conditions and held there in a comparatively innocuous and permanent form.In spite of this knowledge very little work appears to have been done on the lead-content of “normal” bones. The difficulty of devising a satisfactory method for the determination of lead in biological materials especially bone has been emphasised by numerous authors in the past. The methods previously described (with one or two notable exceptions) involve ashing at some stage or other often for prolonged periods at dangerously high temperatures which involve the possibility of loss of lead by volatilisation ; this constitutes a very serious criticism of these methods and their results.In undertaking this work it was therefore essential to devise an accurate and if possible simple process which would avoid or overcome the defects present in previous methods and so establish the limits of lead present in normal bones with more certainty and accuracy than are afforded by former methods. These “normal” figures having been established it would then be possible to draw comparisons with the results of analyses of bones from cases of frank or suspected plumbism; this in OUT opinion constitutes a question of considerable clinical and toxicological importance.DISCUSSION OF METHOD OF ANALYSIS BoNE.-we have used wet oxidation with nitric and sulphuric acids and in our hands this has proved very satisfactory 4 grms. of bone taking 4 to 7 hours for oxidation which is a shorter time than that usually required for complete ashing. We stress the importance of wet oxidation as opposed to ashing for it must be emphasised that destruction at a temperature above 560” C. will resul 788 LYNCH SLATER AND OSLER THE DETERMINATION OF TRACES OF in loss of lead and it is possible that prolonged heating at even lower temperatures may result in some loss. Where very small amounts of lead are involved this becomes a possible source of serious error. After resolution of the bone to its inorganic constituents in sulphuric acid, the next stage was the determination of the lead.It was thought that extraction of the lead by means of diphenylthiocarbazone (Allport and Skrimshire, ANALYST 1932 57 440) might prove to be simple and satisfactory and would thus avoid the more complicated electrolytic deposition methods. The use of diphenylthiocarbazone for extraction of lead has been described by the above-mentioned workers who employed it in the determination of traces of lead in dyestuffs and suggested its use for other organic materials. Lead can be extracted quantitatively by this reagent only from its alkaline solution which must be absolutely clear and free from adsorbing substances. When a large amount of lead is present a smaller initial quantity of the material than would usually be employed should be taken on account of the insolubility of certain lead salts under these conditions and the method and quantities of reagents modified accordingly.We have not determined the maximum amount of lead that can be extracted under the conditions of our experiments and on this account have avoided wherever possible working with quantities of material containing more than 1.0 mgrm. of lead. We have found that 0.25 to 0.50 mgrm. of lead is a convenient amount to extract and determine. I t is obvious that the diphenylthiocarbazone process of extraction cannot be applied at once to the products of wet oxidation of bone since large amounts of calcium and phosphate ions are present in the mixture which would result in a bulky precipitate of calcium phosphate separating out on alkalisation.Calcium phosphate can be held in solution in alkaline medium by means of ammonium citrate but its use here is impracticable on account of the large quantity of citrate which would be necessary to ensure complete solution of the great amount of calcium phosphate present in the bone and the consequent large volumes which would have to be extracted.* In order to obtain the conditions required for this extraction using small volumes we have separated the calcium component of the bone from the phosphorus component by appropriate chemical manipulations, as suggested to us in a private communication from Dr. Dyer. Each component can then be readily held in alkaline solution in a convenient volume under the necessary conditions and the lead extracted by diphenylthiocarbazone (0.1 per cent.w/v in chloroform). This reagent extracts only lead and bismuth under these conditions; should bismuth be present it must be subsequently dealt with as it forms a black sulphide which would interfere with the colorimetric determination of the lead. The bismuth-content of bone (and other tissues) has been assumed by several investigators to be negligible except where medication by bismuth has been practised especially by parenteral administration. Its possible presence however, * Subsequently to the commencement of this work an article appeared on the determination of lead in acid calcium phosphate by Kent-Jones and Herd (ANALYST 1933,58,162) which applies the method of lead extraction of Allport and Skrimshire from the calcium phosphate directly, the latter being held in alkaline solution by ammonium citrate LEAD IN BIOLOGICAL MATERIALS WITH SPECIAL REFERENCE TO BONE 789 must be borne in mind in any method which extracts bismuth as well as lead (such as the diphenylthiocarbazone process) and in which the lead is determined colorimetrically as the sulphide.In order to detect the presence or absence of bismuth we have used the potassium chromate and the pyridine thiocyanate methods (Hamence ANALYST 1933 58 461) either of which may be conveniently applied to the residues with suitable modifications after determination of the lead or the bismuth or both. No bismuth has been found in our experiments and therefore the necessity for removing it did not occur; but had bismuth been present, we should have been compelled to separate it from the lead.This can be done by electrolysis of a solution of the mixed nitrates or by the pyridine thiocyanate method of separation. The method for the determination of lead in marrow is the same as for bone. Wet oxidation takes a longer time on account of the large proportion of fat present. FOR OTHER BIOLOGICAL MATERIALS.-Having found the method to be satisfactory for bone we applied it to other biological materials e.g. urine faeces, blood and organs. The process for bone and other biological materials takes 1 to 2 days to complete this depending upon the type and the amount of tissue to be analysed, and by this method 0-02mgrm. of lead can be accurately determined. DESCRIPTION OF THE METHOD PRELIMINARY NOTE.-AS the amounts of lead present in biological materials are very small it is essential to prevent as far as possible adventitious gain of traces of lead and to know accurately the amount so picked up during the course of an experiment.Distillation or careful selection or both will enable samples of the reagents required to be obtained either free from lead or containing such small amounts of the metal that these may be neglected or compensated by small equivalent subtractions and checked by blank experiments. Periodical blank determinations should also be made for lead in order to ascertain if any lead is being taken up from the apparatus or any other source. Precautions must be taken against lead contamination of the distilled water. The process has been tested rigorously by blank and control experiments as follows : Since it appears impossible to obtain lead-free bone blank experiments have been carried out using as the initial material a practically lead-free sample of potassium carbonate (4 grms.).In addition controls on bones and other tissues have been undertaken by taking two or more portions and adding a known amount of lead in some experiments prior to the commencement of wet oxidation. In every case it was found that the added lead was satisfactorily recovered. The residues obtained from solutions A and B (see Fig. 1) in one bone experiment after extraction of the lead by the diphenylthiocarbazone reagent were ashed a t a bright red heat for many hours and then re-extracted after addition of known amounts of lead to different fractions.Here again it was found that the added lead was satisfactorily recovered. The results of the control experiments on bone and other organic materials appear in the respective Tables and those from the other control experiment 790 LYNCH SLATER AND OSLER THE DETERMINATION OF TRACES OF and the “blanks” are given in Table I. the conditions of our experiments the lead is completely extracted. These results demonstrate that under TABLE I BLANKS AND CONTROLS Twenty grms. of a sample of potassium carbonate were found to contain 0.01 mgrm. of lead by direct colorimetric estimation; hence 4 grms. contain 0.002 mgrm. of lead. Experiment. Lead added Mgrm. Lead found M P . Blank 4grms. of K&Og Nil 0.025 to 0.05 (derived from other chemicals Control 4 grms.of &CO 0.02 0.024 (These figures were obtained after 8 0.02 0.026 allowance had been made for the ,. 0-05 0.045 lead picked up from the other , 0.20 0.19 chemicals a blank having been , 0.50 0.50 performed in each case) , 1.00 1.05 Control bone solution A 0.05 0.055 (Ditto) I* , A 0.50 0.476 , , €3 0.05 0.05 9 3 0.20 0.2 1 6 expts. performed used) A=Ca” fraction (v. Fig. 1) B = PO?’ fraction (v. Fig. 1) REAGENTS 1. 2. 3. 4. 6. 6. 7. 8. 9. 10. 11. 12. 13. 14. Nitric acid A.R. . . Sulphuric acid A.R. Rectified spirit redistilled . . Acid-alcohol mixture (H,SO 1 per cent. in redist. rect. spirit 80 per cent.) Potassium carbonate A.R. Glacial acetic acid A.R. redistilled.. Ammonium hydroxide A.R. (d 04380) . . Ammonium acetate reagent (5 ml. = 2 grms. H Z ) . Prepared from the above reagents Ammonium citrate reagent (5 ml. = 2 grms. citric acid). Prepared from the above ammonia and citric acid A.R. . . Sodium cyanide solution (5 per cent. w/v) . . Diphenylthiocarbazone 0.1 per cent. w/v in chloroform . . Chloroform A.R. redistilled . . Potassium sulphate CU) . . Copper sulphate solution (1 ml. = 1 mgrm. 100 ml. found to contain 0.02 mgrm. of lead 20 I I * I , 2 8 , ,, 100 , I > * 200 9 1 ,- I , 26mgrms. ,, 10 ml. , 3 , - I 0.02 9 , Nil , Nil , 0.01 mgrm. , Nil , 0.01 mgrm. , Nil , 0.02mgrm. , Nil , 0.02mgrm. , Nil , 0.01 mgrm. , Nil THE METHOD.-BONES MARROW TEETH (see Fig.1). Stage I.-The material (2 to 4 grms.) is dissolved in concentrated nitric acid (5 ml.) in a 200-ml. long-necked silica flask by gentle heating. The flask is then cooled concentrated sulphuric acid (5 ml.) is added and the flask carefully heated until oxidatioii commences after which it proceeds vigorously. When all the nitric acid has been used up in this process as shown by charring and by the disappearance of brow LEAD I N (Stage I) (Stage 11) (Stage 111) (Stage IV) (Stage V) (Stage VI) BIOLOGICAL MATERIALS WITH SPECIAL REFERENCE TO BONE 791 BONE HNO, I Filtrate “ B ” (H,PO,). I I f i l t r a t h . j. c a y (PPt.1 CaG solution “A ’’ Filtrate “ B ” (&SO,). I Acetic acid. Solution “A ” extracted with diphenylthiocarbazone under the re-quired conditions.Solutions “ B ” and ‘‘ B ’’ combined and extracted similarly. Extracts oxidised. Lead determined colorimetrically as sulphide. Residues examined for bismuth. FIG. 1. nitrous fumes which are replaced by white sulphur trioxide fumes the flask is allowed to cool concentrated nitric acid (1 to 2 ml.) is added and careful heating recommenced. When oxidation is complete all remaining nitric acid is driven off by boiling with water until fumes of sulphuric acid appear. The contents of the flask consisting of a white precipitate of calcium sulphate and a supernatant fluid containing phosphoric and sulphuric acids are transferred to a 250-ml. beaker and the flask is washed out with water and dilute ammonium acetate solution made faintly alkaline with ammonia.(The total volume in the beaker at this stage should be about 50 ml.) Rectified spirit (about 25 ml.) is now added and the mixture is allowed to stand in the refrigerator overnight; this permits of the almost complete precipitation of the calcium sulphate. Stage 11.-The calcium sulphate precipitate (see Fig. 1) is filtered off on a small Hirsch funnel and washed with a minimum volume of the acid-alcohol mixture (about 50ml.) and the filtrate (B,) is then evaporated down to about 50ml. The precipitate is washed back with distilled water into the same beaker using about 50 ml. heated to boiling and potassium carbonate (4 grms.) in solution in boiling water (50 ml.) added. After being boiled this mixture is placed on the boiling water-bath for 2 to 4 hours when the conversion of calcium sulphate into calcium carbonate is complete and the volume has been reduced to 25 to 50ml.Stage 111.-On cooling the calcium carbonate is filtered off on the same Hirsch funnel and washed with a minimum volume of potassium carbonate solution (0.5 per cent.). The filtrate (B,) is added to B, which is again evaporated to approximately 50 ml. The calcium carbonate precipitate is washed back into the original beaker with distilled water (about 50 ml.) and sufficient glacial acetic acid is added to effect solution (A). All carbon dioxide is driven off by boiling. Stage IV.-The two clear solutions A containing the calcium component and most of the lead (80 per cent. or more) and B the phosphorus component, are extracted separately by the diphenylthiocarbazone reagent under the require 792 LYNCH SLATER AND OSLER THE DETERMINATION OF TRACES OF conditions viz.in alkaline solution and in the presence of ammonium citrate, ammonium acetate and sodium cyanide. To obtain these conditions ammonium acetate solution (5 ml.) and a noted volume of ammonium citrate solution (5 to 10 ml.) are added to A and B which are then made alkaline with ammonia. Sodium cyanide solution (2 ml. of 5 per cent.) is then added to A and B and each solution transferred to a 150-ml. separating funnel the volume being made up to about 100 ml. with water and the extraction proceeded with immediately. Precautions must be taken to ensure that the reaction of the mixture remains definitely alkaline throughout the whole of the extraction.Three extractions are made with the dye solution (using 10 7.5 and 5 ml.) shaking for 2 to 3 minutes, after which 2 to 4 (or more) extractions are made with chloroform only (using 15 10 5 ml. etc.) until the last traces of the dye are completely removed from the aqueous mixture. Each extract is washed with water in another separating funnel and run off into a Pyrex tube (8 x 1 in.) containing a small crystal of potassium sulphate. The chloroform is distilled off and collected for future use. (N.B.-The extracts from A and B may be collected in the same Pyrex tube.) The residue in the Pyrex tube is oxidised by heating with concen-trated nitric acid (1 ml.) in the boiling water-bath for 30 minutes after which concentrated sulphuric acid (0-5 ml.) is added and the tube is heated over a low flame more nitric acid being added as required.In the presence of potassium sulphate oxidation proceeds rapidly. Copper sulphate (0.5 mgrm.) may be added as a catalyst with advantage although we have avoided its use when the residue is to be tested for bismuth. When oxidation is complete all remaining nitric acid is boiled off and after cooling water (about 20 ml.) is added. Stage V.-The lead in the residue is determined colorimetrically as sulphide by comparison with a standard solution of lead acetate (1 ml. = 0-01 mgrm. of Pb), according to the method described by Francis Harvey and Buchan (ANALYST, 1929,54,725). We have found it convenient to prepare the unknown lead solution as follows: The contents of the Pyrex tube are made alkaline with ammonia and ammonium acetate reagent (5 ml.) and sodium cyanide solution (2 ml.of 5 per cent.) are added when a clear colourless solution results. If the amount of lead is known to be small e.g. up to 0-06 mgrm. the whole of this solution is transferred to the Nessler cylinder and the comparison made directly with the standard lead solution, which is run in from a burette. When the amount of lead is unknown or known to be large the solution is made up to a definite volume e.g. 50 ml. and aliquot portions are taken the necessary adjustments of reagents being made where necessary in the Nessler cylinders before adding any sodium sulphide solution. The reason for this is that the most accurate comparisons can be made with 0.04 to 0.06 mgrm.Pb 3 4 to 6 ml. of the standard lead acetate solution when we have found it possible to read correctly to 0.5 ml. (i.e. 0-005 mgrm. of Pb). Stage V I (Detection of Bism.uth).-(a) When the chromate method is to be used for the detection of bismuth the residues remaining after the lead or bismuth, or both have been determined are combined lead and bismuth (if present) are precipitated as their sulphides by hydrogen sulphide under proper conditions, and dissolved in nitric acid. From this a solution in dilute acetic acid is eventuall LEAD IN BIOLOGICAL MATERIALS WITH SPECIAL REFERENCE TO BONE 793 obtained and chromate added when lead and bismuth (if present) are precipitated as their insoluble chromates. Sodium hydroxide solution (10 per cent.) is then added drop by drop.The sodium hydroxide converts these insoluble metallic chromates into their hydroxides. The lead hydroxide being soluble in excess of the alkali rapidly dissolves and any bismuth present remains in suspension; we have found it possible by this means to detect 0.05 to 0.02 mgrm. of bismuth in the presence of large amounts of lead (1.0 to 0.2 mgrm.) in control experiments. ( b ) When the pyridine thiocyanate method as described by Hamence (vide su$ra) is to be used the oxidation of the diphenylthiocarbazone residue must be carried out in the absence of copper and furthermore ammonium acetate and sodium cyanide must not be added before the bismuth has been extracted. The reason for this is that we have found that these substances interfere with the extraction of the bismuth.When the diphenylthiocarbazone residue has been completely oxidised the determination of the lead is carried out as follows Am-monia is added until alkaline and excess is boiled off after which concentrated nitric acid (0-5 to 1 ml.) is added and the Pyrex tube heated if necessary to effect solution of all the lead if this has separated (as it sometimes does especially when a considerable amount is present). This solution is made up to a definite volume, which is such that 5 to 10 ml. contain a suitable quantity of lead for determination (viz. 0.04 to 0.07 mgrm. of Pb). The lead is then determined by placing an aliquot portion in the Nessler cylinder rendering alkaline with ammonia adding am-monium acetate reagent (5ml.) 5 per cent.sodium cyanide solution (2ml.) and sodium sulphide and comparing with the standard lead solution from the burette. A suitable reading having been obtained an equal volume is placed in a separating funnel and subjected to the pyridine thiocyanate process for removal of bismuth under the required conditions. In our work we have adjusted the hydrogen-ion concentration of the solution to pH 5-0 to 5.5 prior to extraction with amyl alcohol and ether. After the extraction the aqueous fraction is filtered into the Nessler cylinder the filter being washed twice with hot water. This fraction is then made alkaline with ammonia and the lead is determined in the usual manner after addition of ammonium acetate and sodium cyanide etc. We have found that the presence of a small amount of ammonium nitrate does not interfere with the determination of lead and that the method is efficient and satisfactory viz.that traces of lead are not removed and that small amounts of added bismuth are extracted. If a mixture of bismuth and lead is present the amount of bismuth can be determined only approximately by this method for 0.05 mgrm. of bismuth produces with sulphide a colour slightly deeper than that given by the same amount of lead. FOR ORGANS BLOOD URINE FAECES.-(~) Organs.-The tissue (10 to 20 grms.) is dissolved in concentrated nitric acid (5 to 10 ml.) by gentle heating. After cooling a noted volume of concentratedsulphuric acid (5 to 7.5 ml.) is added, and oxidation proceeded with as in the case of bones. The lead is subsequently extracted from the oxidation mixture after dilution with water (50 ml.) addition of ammonium citrate and acetate ammonia and sodium cyanide (as for bone) and transference to a separating funnel 794 LYNCH SLATER AND OSLER THE DETERMINATION OF TRACES OF ( b ) Blood.-Blood (50 to 100 ml.) is evaporated down in a beaker on the boiling water-bath or boiled down with concentrated nitric acid (10 to 20 ml.) in a silica flask.In the former case the residue is transferred to the silica flask the beaker being washed out with concentrated nitric acid (10 to 20 ml.) and the flask gently boiled to effect solution. After cooling a noted volume of concentrated sulphuric acid (5 to 7 ml.) is added and oxidation commenced by gentle heating. When this is complete all nitric acid is boiled off and extraction proceeded with in the usual way.( c ) Urine.-Urine (500ml.) is evaporated down to about 25ml. and transferred to a silica flask all the residue being washed from the evaporating dish with concentrated nitric acid (10 to 20 rnl.). Subsequently the process is the same as for blood and organs. (Note.-On account of the small amounts of calcium phosphate usually present in the portions of organs blood and urine taken for analysis it is not necessary to separate the calcium ion from the phosphate ion prior to extraction of the lead by the diphenylthiocarbazon. It is sufficient to ensure that the calcium phosphate is retained in alkaline solution by the addition of a little ammonium citrate.) (d) Faeces.-The dried material (2 to 4 grms.) is dissolved in nitric acid (5 to 10ml.) in a silica flask by gentle heating.After cooling a noted volume of concentrated sulphuric acid (5 to 7.5 ml.) is added and the method proceeded with as for organs. If only a small amount of calcium phosphate was present extraction can be carried out at once (as in the case of organs) but if not the calcium and phosphorus components must be separated as described for bone prior t o extraction of the lead. The following results were obtained : TABLE IIt BONE MARROW TEETH Weight of Lead in Ash Leadin fresh- bone Exp. analysed Grms. 1 S.F. 2 3 S.F. 2 4 S.F. 4 16 S.F. 4 17 S.F. 4 Lead found as Pb Mgrms. 0.22 0.22 0-32 0.34 0-3 1 fresh bone p.p.m. 110 100 80 82.5 77.5 5 S.F.4 0.155 39 6 S.F. 4 0.16 40 9 S.F. 4 10 S.F. 4 0.07 0.045 18 11 from ashed Average bone bone2 p.p.m. Per Cent. p.p.m. 105 80 60 39.5 61.9 14.5 56.8 133.5 64 25.5 Case Clinical No. details 1 }Unknown. 2 }Unknown. Female. aet. 26. Housewife. Haemon-hage after child-birth. Male. aet. 26. No occupa-Pneumonia head injury. 4 tion. following 1 LEAD IN BIOLOGICAL MATERIALS WITH SPECIAL REFERENCE TO BONE 795 0.48 120 33-2 324 } 0.38 95 0.53 133 J Weight of fresh bone Exp. analysed Grms. 11 S.F. 4 12 S.F. 2 13* S.F. 4 +0.1 mgrm. Pb. added 18 S.F. 4 26 S.F. 4 dead. aneurysm. Ruptured 61 UE.F. 4 62 UE.F. 4 64 LE.F. 4 65 LE.F. 4 19 S.F. 2 20 S.F. 4 21* S.F. 4 + 0.2 mgrm. Pb.added 27 S.F. 4 28 S.F. 4 29* S.F. 4 + 0.2 mgrm. Pb. added 30 S.F. 4 31 S.F. 4 32 S.F. 4 33 S.F. 4 34 S.F. 4 35 S.F. 4 36 S.F. 4 37 S.F. 4 38 S.F. 4 39 S.F. 4 41 S.F. 4 42 S.F. 4 43 UE.F. 2 44 UE.F. 4 45 LE.F. 2 46 LE.F. 796 Exp. 47 48 49 50 51 52 53 54 67 68 66 66 80 81 87 88 83 84 77 78 79 102 103 110 111 106 107 104 119 126* LYNCH SLATER AND OSLER THE DETERMINATION OF TRACES OF TABLE II-cofitin/ued. Lead in Ash Lead in ashed Case Clinical Weight of fresh bone analysed Grms . S.F. 4 S.F. 4 Lead found as Pb Mgrm. 0.43 Expt. abandoned Expt. abandoned 0.18 fresh bone p.p.m. 107.5 45 107.5 120 51 49 20 57.6 51 117.5 107.5 55 61 57-5 67.5 26 20 21 20 27.5 27.6 25 67.6 62-5 50 40 42.6 50 47.6 62.5 50 60 17-5 from Average bone p.p.m.Per Cent. bone1 No. details p.p.m. man. Gas-107.5 45 114 50 20 64 112.6 63 62.5 23 29 26 65 50 41 50 62 47 41 62.9 36.3 40.4 62 26.2 24.6 -54-6 20.6 20 -59 68.9 27 27-1 -UE.F. 4 UE.F. 4 0.43 0.48 LE.F. 4 LE.F. 4 S.F. 4 S.F. 4 0.205 0.195 Expt. abandoned 0.08 UE.F. 4 UE.F. 4 Lymphosar-LE.F. 4 LE.F. 4 0.23 0.205 coma. 136.5 ) J S.F. 4 S.F. 4 0.47 0.43 UE.F. 4 UE.F. 4 0.22 0.205 aet. 67. Pneumonia. LE.F. 4 LE.F. 4 0.23 0.27 M.F. 4 M.F. 4 M.F. 4 0.10 0.08 0.085 S.F. 4 S.F.4 0.12 0.11 Male. aet. 3*. +No occupa-tion Acute pneumonic tuberculosis. UE.F. 4 UE.F. 4 0.11 0.10 127 1 1 7 325 } LE.F. 4 LE.F. 4 0-27 0.26 M. 4 0.21 - J S.H. 4 S.H. 4 0.16 + 0-3 mgrm. Pb. added 121 S.F. 4 122* S.F. 4 + 0.25 mgrm. Pb. added + 0.30 mgrm. Pb. added 127* S.F. 4 124 UE.F. 4 123 LE.F. 4 125 M.F. 4 1 0.20 Male. aet. 72. Occupation unknown. Intestinal obstruction. 185 221.6 0.20 0.24 0-0 LEAD I N BIOLOGICAL MATERIALS WITH SPECIAL REFERENCE TO BONE 797 Weight of fresh bone Exp. analysed Grms. 136 S.H. 4 129 S.F. 4 131* S.F. 4 + 0-25 mgrm. Pb. added 133 M.F. 4 TABLE II-continued. Lead in Lead found as fresh Pb bone Mgrm. p.p.m. 0.22 55 0.21 52.5 0.44 0.095 24 Ash Lead in from ashed Case Clinical Average bone bone No.details p.p.m. Per Cent. p.p.m. 60.4 91 Male. aet. 65. Occupation unknown. Broncho-pneumonia. 50 24 137 S.H. 4 Expt. abandoned 139 S.H. 4 160 S.H. 4 0.15 0.17 37.5 42.5 41 59.9 67 } 1 140 S.F. 4 153 S.F. 4 59-5 73 } 0.175 44 0.175 44 44 30 loo >20 142 UE.F. 4 0.12 30 30 143 UE.F. 4 Expt. abandoned 146 LE.F. 4 0-13 32.5 - 32.5 26.3 123.5 ) 32.5 0.23 147* LE.F. 4 + O s l o mgrm. -o.lo} =Om13 Pb. added Female. aet. 38. -Housewife. Heart failure. 152 F.M. 4 0.08 20 20 - - 1 158 Teeth 4 0.24 60 66 90 26 Unknown. 159 I 2 0.085 42.5 60 71 27 Unknown. 167 I 4 Male. assistant. 0.42 105 63 157 28 } aet. 49. Shop Male. Kitchen porter. 66 370.5 29 168 ,I 4 0.99 247.5 Male.169 I 2 0.155 77.5 aet. 21. Carpenter’s 60 129 30 } J mate. S-Shaft. F-Femur. p.p.m.-Parts per million. LE-Lower end. H-Humerus. * in margin indicates control experiment to UE-Upper end. M-Marrow. which lead has been added. $ Note.-The percentage of ash of the bone was determined independently of the lead determination by ashing a known weight of the respective sample of bone and the results given in column 7 are the values for lead expressed in terms of the ash so determined. This was done in order to ascertain whether the amounts of lead in “normal” bones bore any definite relationship to their inorganic constituents 798 LYNCH SLATER AND OSLER THE DETERMINATION OF TRACES OF TABLE I11 ORGANS AND BLOOD* Material analysed Lead found as Exp.Fresh weight Pb. Grms. Mgrm. 66 Blood 20 0.015 67 I 10 nil 68* I # 2o +On05 mgrm. -::::5} = 0.005 Pb. added 69 Liver 10 70 , 20 72 J 9 lo 0.01 0.015 0.026 71* Pb. added 73 Kidney 10 74 3 20 76 I . 10 nil nil nil 75 I* 10 +0.05 mgrm. -::;:} = -0.02 Pb. added 80 Shaft femur (See Table 11) 81 3 Average amount of lead in Case fresh tissue No. p.p.m. 0.33 } '" ] 16 I nilt 116 Liver 10 nil 1 120 Kidnev 10 0.015 12 1 122 96 109 112 95* 06* 108* 97 115 98* 114* Shaft femur Liver 10 I 10 , 10 10 + 0-050 mgrm. Pb. added Liver 10 + 0.05 mgrm. Pb. added Liver 10 +Om10 mgrm. Pb. added Kidney 10 8 10 9 9 10 + 0.05 mgrm. Pb. added Kidney 10 +Om10 mgrm.Pb. added , ? P 48.5 } (See Table 11) 0.015 0.01 0.025 1 lg6 I 17 - 8 i:5} = 0.005 J 0.015 0.020 - ::;:6} = 0.005 1.25 1 Clinical details Male. aet. 57. Cook. Broncho-pneumonia. '(See Table 11 Exp. 80. etc. Male. aet. 72. Occupation unknown. . Intestinal obstruction. (See Table 11 Exp.121, etc. Male. aet. 34. No occupation. Acute .pulmonary tubercu-losis. (See Table 11, Exp. 102 etc.) ?? J I 102 Shaft femur (See Table 11) 10 LEAD IN BIOLOGICAL MATERIALS WITH SPECIAL REFERENCE TO BONE 799 TABLE III-continued. Average amount of lead in Case fresh tissue No. Clinical details p.p.m. .\ Material analysed Fresh weight Grms . Liver 10 , 10 +O-10 mgrm. Pb. added Lead found as Pb . M P . 0.01 Exp.130 128* 129 131 134 149 148* 132 138 141 144* 145* 140 163 164 1, 50 1 19 Male. aet. 65. Occupation unknown. + Broncho-pneumonia. (See Table 11 Exp. 129 etc.) Shaft femur (See Table 11) 0.01 Blood 20 Liver 10 , 10 + 0.30 mgrm. Pb. added 0.01 -;:;;} = 0.02 Kidney 10 3 10 + 0.05 mgrm. Pb. added Kidney 10 + 0-25 mgrm. Pb. added 1 ) lo J I lo 1 5 2o Female. aet. 38. Housewife. Heart 'failure. (See Table 11, Exp. 140 etc.) Shaft femur , >, (See Table 11) 44 1 J Male. aet. 40. Occupation unknown. Head iniurv. 0.06 0-6 Blood 100 I . . * in margin indicates control experiment with added lead. t Yellow colour but readings possible. + Yellow colour readings impossible. + Exp.22 23 24* 63 TABLE IV URINE AND FAECES* Lead found as Pb. Average Lead Mgrm. Mgrm. p.p.m. Material anal ysed Case No. Clinical details Urine 500 ml. , 500 ml. , 500 ml. +O.lO mgrm. Pb. added Telephone cable engineer. Blue line on gums. Ex-tensor weakness. Male. aet. 40. Occupation un-known. Indefinite symptoms. Male. aet. 60. Plumber. Lead Urine 500 ml. 0.04 0-08 154 155 Urine 500 ml. , 500 ml. 0.07 0.05 0.06 0-12 162 I. 63 Male. aet. 27. symptoms. 9 Student. No Dried faeces 2 grms. 0.05 , 4grms. 0.11 0.105 26-25 (for 4 grm.) (dried faeces) * in margin indicates control experiment with added lead 800 LYNCH SLATER AND OSLER THE DETERMINATION OF TRACES OF DIscussIoN.-The material used in these experiments was taken from post-mortem cases at St.Mary’s Hospital and from patients attending for treatment. Some were cases of sudden death due to accident or disease in which a complete history could not be obtained but in others it was possible to elicit information regarding occupation illness etc. In none of the cases excepting the three whose wines were examined was any exposure to lead discovered beyond the every-day hazard. So far it has not been possible to obtain bone or teeth from an established case of plumbism. Bone.-From a study of Table I1 it will be observed that we have never failed to detect lead in any of the twenty bones examined and that the amounts of lead present vary from 14.5 to 146.0 p.p.m. of fresh bone (which is equivalent to 25.5 to 232 p.p.m.of ashed bone) ; 25 per cent. of these cases have a lead-content of over 100 p.p.m. of fresh bone.* Our results for lead in teeth in the five “normal” cases examined are 42.5 to 247-5 p.p.m. of fresh specimen (71 to 370.5 p.p.m. of ash). These figures (for bone and teeth) are considerably higher than those given by other workers in this field e.g. Amount of lead detected Aub Fairhall Minot Reznikoff (Lead Poisoning 1926, Specimens of bone from 26 “normal” cases examined; Bone from 7 cases of plumbism. Bone from 40 “normal” persons. p. 56). lead found in 17. Barth (Virchow Arch. path. Anat. 1931,281 146). Lead found in all Cases. Jowett Dilling Bell (Lancet 1929 i 126). Bone from patients treated for carcinoma with col-loidal lead injections.Animals experimentally lead-poisoned. Danckwortt and Jurgens (Arch. Pharm. 1928,266,492). Dogs experimentally lead-poisoned. (Cranium most lead bones of limbs least ribs intermediate.) Tannahill (Australian Med. J. 1929 1 216). Bone from two lead workers. Weyrauch ( Z . Hyg. und Inf. 1930 111 162). Pfrieme (Arch. Hyg. 1934 232). Bones of rabbits experimentally lead-poisoned. Teeth from 60 “normal” persons. Teeth from 3 cases of plumbism; average. (Lead found in teeth of normal and experimentally Lead found in all. lead-poisoned animals.) 0.9 to 20-8 p.p.m. fresh bone. 21.7 to 153 p.p.m. fresh bone. 10 to 60 p.p.m. ashed bone. 4 to 53 p.p.m. ( ? fresh) bone. Up to 100 p.p.m. whole bone ( ? fresh). 8.4 to 51 p.p.m. ( ? fresh) bone. 32.6 and 652 p.p.m.( ? fresh) bone. 10 to 23.3 p.p.m. fresh bone. 23 to 73 p.p.m. ashed teeth. 140 p.p.m. ashed teeth. The discrepancy between our results for “normal” bones and teeth and those of other workers may be due to a higher lead-content of the bones examined by us or as we think more likely to our method of analysis which by the avoidance of ashing of the organic matter and by the use of diphenylthiocarbazone to extract the lead gives more accurate results. We have found that bone is very refractory to ashing at temperatures about 500” C. and we suspect that many workers may have lost lead at this stage of the process on account of ashing for prolonged periods * The highest figure for lead in bone was obtained from Expts. 64 65 viz. 451-5 p.p.m. of ashed bone.(See note to Table 11. LEAD IN BIOLOGICAL MATERIALS WITH SPECIAL REFERENCE TO BONE 801 at high temperatures ; alternatively incomplete ashing would result in the persistence of some residual organic matter upon which the lead might readily be adsorbed and consequently lost. It is stated in a recent publication (Leschke CZinicaE Toxicology 1934 p. 10) that most of the lead is stored in the bone marrow. We have not found this to be so in our cases our figures for marrow being 23 to 50 p.p.m. The results of Aub and his co-workers (Zoc. cit. p. 69) agree with ours and they state in their exhaustive work on this subject (Chap. XI) that the anaemia of plumbism is due to peripheral destruction of red blood cells and not to a local action of lead on the bone marrow.Investigation of bone marrow is complicated by the fact that it is difficult to obtain uniform samples. In a number of femora examined the lead-content of the ends as well as of the shaft and the marrow was determined. Here again it was found difficult to obtain uniform samples as the ends are composed of cancellous bone which, unlike compact bone cannot be uniformly sampled after crushing owing to expression of oily marrow. On this account portions were split off from the ends of the bone and subjected to analysis without removal of the marrow. The results obtained from analysis of the ends of bone do not permit of any significant conclusions although in nearly all cases the lower end was found to contain more lead than the upper end. When expressed in terms of ashed bone, the ends almost always have a higher figure than the shaft.The difference between the lead-content of the upper and lower ends and the ends and the shaft is probably to be explained by the way in which growth of bone takes place in relation to the epiphyseal lines and to the periosteum and also to the association between deposition of lead and calcification. It has been demonstrated radiologically (Rogers Peck Jupe Lancet 1934 11 29; Waters Kaplan Year Book of Radiology, 1932) in clinical and experimental cases of plumbism that in growing individuals lead produces a subcortical sclerosis most marked at the ends of the bones and at the epiphyseal lines where growth is most active and where calcium and any circulating lead is being deposited under normal conditions.To discuss the disposition of the epiphyseal lines and their duration would be out of place here and it will be sufficient to point out that if an individual is exposed to lead in early youth while bone-growth is most active a t the ends these will probably be found to contain relatively more lead than the shaft (if bone from the actual region of the epiphyseal line is analysed as has been done with the lower end and not with the upper end). On account of the practical difficulties of obtaining uniform specimens of marrow and ends of bone only a few such analyses were made. In three cases the lead-content of the shaft of the humerus was determined, as well as that of the shaft of the femur; the former was found in every case to contain slightly less lead than the latter.Danckwortt and Jurgens (Zoc. cit.) give the following figures from experimentally lead-poisoned dogs :-Bones of limbs 8.4; ribs 46; skull 51 p.p.m. (fresh bone). Although these figures are open to question by reason of the method of analysis used they do suggest that the lead-content of different bones varies. It is perhaps worthy of note that the total amount of lead in the bones may reach considerable proportions. If we take for example a 12-stone man who ha 802 LYNCH SLATER AND OSLER THE DETERMINATION OF TRACES OF 100p.p.m. of lead in his bones he will have in his whole skeleton 7.6grms. (117 grains) of lead (as Pb) or 9-9 grms. (153 grains) of lead phosphate Pb,(PO,),. Lead stored in the bones remains there under normal conditions in a harmless form.In cases of chronic plumbism or after prolonged exposure to lead when the amount of lead in the bones may be assumed to be much higher than our figures show, mobilisation will aggravate the existing condition or may give rise to definite symptoms of plumbism. Such mobilisation may result from a number of causes, viz. medication changes in diet pathological conditions e.g. disturbance of calcium metabolism acute infections shock starvation etc. These may produce small changes in the hydrogen-ion concentration of the blood which presumably affect the stability of the tertiary phosphate. OTHER BIOLOGICAL MATERIALS-It will be observed that in only a compara-tively few cases have organs and blood been analysed the reason for this being that we were more concerned with the applicability of the method to these substances than to the actual amount of lead present in them.Our figures show that traces of lead are present in organs and blood from “normal” persons. When applied to organs the method occasionally gave rise to difficulties. Wet oxidation although troublesome in some cases did not offer any real difficulty, and extraction of the 1ead.was easy. It was found however that in some cases, after oxidation of the diphenylthiocarbazone residues a yellowish colour persisted, which made the colorimetric reading either impossible or unreliable. It will be noted from the Tables that there is considerable variation in results for organs, and that added lead is not always completely recovered; this error doubtless arose on account of the difficulty of making accurate readings in the presence of this colour.What this interfering substance is we do not know definitely (it may be some very resistant fatty substance which is extracted by the chloroform), and we have not as yet devised a method for its removal. This yellow colour may be due to the presence of nitro-bodies which are resistant to further oxidation by nitric and sulphuric acids. (Since this work was completed it was suggested to us that treatment with ammonium oxalate might destroy the colour.) The method when applied to blood was also found to be rapid and simple, even when a large quantity was used e.g. 100 ml. The amount of lead found in the 100-ml. specimen of blood examined (Expt. 164) vix. 0.06 mgrm.per 100 ml., or 0-6 p.p.m. is significant because whilst this was a “normal” case the lead-content of the blood is above the normal range given by Litzner and Weyrauch (Med. Klin. 1933 29 381) vix. up to 0.04mgrm. per 100ml. When applied to urine the method was found to be very satisfactory although the oxidation process may occasionally prove to be tedious. The amounts of lead found in the three cases examined (Table IV) compared with the limits of lead in “normal” urine given by Francis Harvey and Buchan (Zoc. cit.) viz. up to 0.133 mgrm. per litre are in accordance with the clinical findings in our cases. The analysis of the specimen of faeces by this method presented no difficulty. SIGNIFICANCE OF ANALYTICAL FINDINGS.-The presence of a high lead-conten t in bone is not in itself evidence that the lead was a contributing factor in the cause of death but is a “silent witness” of exposure to and absorption of lead at som LEAD IN BIOLOGICAL MATERIALS WITH SPECIAL REFERENCE TO BONE 803 stage or other.It must be remembered that lead after reacting with the tissues and causing damage does not remain there but is removed by the blood-stream, and either excreted or stored in the skeleton. This explains the failure to find lead in certain tissues e.g. brain in lead encephalopathy after fairly definite evidence clinically of lead poisoning and in such cases determination of lead in the bones would doubtless be of great value. It must also be remembered that the kidney which is damaged by nephritis may fail to excrete the lead circulating in the blood, and this again may be a possible cause of failure to detect excess of lead in the urine in some cases of plumbism; in such a case analysis of the blood for lead might be of use.A spectrographic method of blood analysis has been used with success by Shipley Scott and Blumberg (Bull. Johns Hopkins Hosp. 1932 51 327) in the diagnosis of plumbism in children. The diagnosis of lead poisoning at autopsy is notoriously difficult owing to the lack of positive evidence and in the living subject it is often largely a matter of guesswork. It has been our endeavour to elaborate a technique for the accurate determination of lead in bone and other tissues and to set forth the “normal” figures which may be found. These may require modification when further information is available but we trust that they may be of assistance in the study and the diagnosis of chronic lead poisoning.SUMMARY.-An accurate and comparatively simple method for the deter-mination of lead in bones has been devised. The process involves wet oxidation (instead of ashing) followed by diphenylthiocarbazone extraction of the lead and subsequent colorimetric determination as sulphide. Special precautions must be taken to exclude bismuth if present. By the use of this method we have found that the limits of lead in a series of twenty “normal” bones are 14.5 to 146.0 parts per million of “fresh” bone and in teeth froin five “normal” persons 42-5 to 247.5 parts per million of “fresh” teeth. These figures are considerably higher than those given by other workers.The method has been successfully applied to other biological material (marrow, organs blood urine and faeces). We desire to express our thanks to the Pathological Department St. Mary’s Hospital (Director Dr. W. D. Newcomb) for a supply of post-mortem material. One of us (T. G. 0.) is indebted to the Pathological Institute of the Hospital for the award of a Research Studentship which has enabled him to take part in this work. DISCUSSION Sir WILLIAM WILLCOX congratulated the Society on the very valuable work that it was doing particularly in relation to toxicology. As Senior Physician at St. Mary’s Hospital he could testify that papers published in THE ANALYST had been of very great value in clinical medicine. The present paper by Dr. Roche Lynch and his co-workers would upset many of their preconceived ideas.Bone had not been systematically investigated in toxicology and it was difficult to find in the literature any really reliable information about metals being deposited in bones; the statements in textbooks had been copied from one to another for many years. The question of lead was very important and difficult ; he was constantly being faced with it in clinical work. As they knew under the Workmen’s Compensation Act a person suffering from lead poisoning received higher compensation than h 804 LYNCH SLATER AND OSLER THE DETERMINATION OF TRACES OF could otherwise obtain; the result was that when workmen were ill they hcped that some doctor would diagnose lead poisoning. Such a diagnosis might tend to prevent a patient ever doing any work again.He had recently had a case in which a man’s illness five years previously had been diagnosed as lead poisoning, but the man showed no clinical indications of it now and it was doubtful whether he had ever suffered from it. The problem came before the Departmental Com-mittee appointed three or four years ago to enquire into the possibility of danger from the use of lead ethyl and it was found when the analytical figures were considered that lead was present in normal persons. I t was most interesting to find that the authors’ investigation showed that relatively high amounts of lead were normally present in the bones. The quantity taken into the system must have been appreciable and the authors appeared to suggest that it was stored in the bone in an innocuous form.The quantities now recorded were much higher than those found by other chemists which was doubtless due to the greater accuracy of the method of determination. I t was very difficult to disprove in Court the possibility of lead poisoning. In a recent case amounts of lead much lower than those found by the authors for normal persons had been determined in the faeces and the illness had been diagnosed as lead poisoning. The new method should prove a valuable test for certain clinical diagnoses. The authors had given certain figures for the amount of lead in the blood of a person not exposed to lead; he had no doubt that the blood of persons exposed to lead poisoning would be much greater. The behaviour of calcium was most important in connection with many diseases of which little was known.If parathyroid extract were injected into the veins it mobilised the calcium; it would be a most interesting experiment if Dr. Roche Lynch would determine the lead in the blood of a normal person then give parathyroid and see if the lead increased. If lead behaved in the same way as calcium there should be considerable increase. Regarding the question of controls he was never quite sure what was meant by a “normal” person. Where did this lead come from in a so-called “normal” person? As far as possible, apparently by the history lead from drinking water had been excluded; did it come from food or to what extent was it present normally in the body? Had the authors for instance found any present in the new-born child? He assumed that so far as bones were concerned the presence of lead found post mortem must be evidence of chronic absorption-not necessarily of lead-poisoning-as the two conditions should be distinguished.How far would it be possible to use this method for examination of excreta in cases of acute lead-poisoning? With reference to the large amount of lead in faeces the statement that in cases of lead-poisoning it was useless to examine the faeces for the first week or so was of practical importance. Was the lead found in the cases under consideration, ingested or inhaled? Inhalation was the most important cause of lead absorption and poisoning in industrial cases. He asked why the authors had confined themselves to the use of nitric and sulphuric acids in oxidising the bone.He had oxidised urine with nitric acid and potassium chlorate and found it a very quick and very good method. The lead had then been extracted by the electrolytic process. He had also found it successful for the determination of lead in livers etc. In one case of suspected lead-poisoning he had found only 0-12 p.p.m in the liver-an amount which Dr. Roche Lynch had found in a normal person. On the other hand he had found ten to twelve times this amount in cases of chronic lead-poisoning. He would certainly test the process thoroughly as it might be much simpler in practice than it appeared although he did not like oxidising with nitric and sulphuric acids every time. When there was plenty of material available it would be well to use both methods.In cases of suspected chronic lead-poisoning it seemed that it Dr. S. A. HENRY also congratulated the authors. Professor W. H . ROBERTS added his congratulations. Had the authors ever tried this method LEAD IN BIOLOGICAL MATERIALS WITH SPECIAL REFERENCE TO BONE 805 would be a good idea to get the patient into hospital draw some of his teeth, analyse them and thus settle the matter once and for all. He had always had difficulty in stating in evidence the amounts of lead normally present and in giving these the paper was a very valuable contribution to the subject. Mr. J. R. NICHOLLS adding his congratulations especially with regard to the neat way of overcoming the interfering effect of such large proportions of calcium phosphate said that Dr.Roche Lynch had rightly stressed the fact that the solution to be extracted must be perfectly clear. How was this to be ensured in all cases? If the final solution contained traces of iron phosphate or magnesium phosphate the liquid might appear clear to the eye and yet might have a very slight turbidity sufficient to adsorb lead and prevent its extraction. Also small quantities of aluminium might similarly interfere. Some caution was therefore needed before the process was adopted as a general method. Mr. A. L. BACHARACH welcomed the work that had been presented partly because it put an important instrument into the hands of biochemists for investigat-ing the metabolism of lead. It should now be possible to conduct the essential preliminary animal experiments by making use of a diet significantly free from lead for the methods brought before the Society would enable the necessary analyses of foodstuffs to be made with an accuracy previously unobtainable.It would be possible to add to this lead-free diet small or large quantities of lead, with a view to examining the rate of storage and the method of excretion. It would be important to discover to what extent the kidneys could “take care of” lead and whether there was any significant variation in the time taken by different individuals to get rid of lead. I t might be that varying susceptibility to lead poisoning was due to variation in the efficiency with which the metabolic machinery of different individuals could cope with excess lead. The matter was one of importance in the veterinary as well as in the clinical field because of the well-known abortifacient action of lead and the prevalence of habitual and other forms of abortion among domestic animals.Dr. OSLER replying to Dr. Henry’s questions about lead in the bones of infants said that he had had a case of a male 3?$ years of age the shaft of whose femur contained 29 parts per million of lead. Infants obtained their calcium from their mothers and he thought that the same applied to lead. The diagnosis of plumbism still remained a clinical question. He had used this method in several cases of lead-poisoning and it had worked very well indeed the results being in accordance with the clinical findings. With regard to the lead in the faeces of the student investigated being due to inhalation or ingestion he knew the student personally and he had not been exposed to inhalation of lead; in all probability he had derived the lead by ingestion in his lodgings e.g.from solder in a frying-pan. The reason why it was useless to examine the faeces for lead from a case of suspected lead-poisoning during the first week or so after removal (e.g. to hospital) from the source of the lead was because the lead present in these specimens might be due to ingestion of lead alone. After some time had elapsed any excess of lead found in the faeces might be taken with more or less certainty to arise from the excretion of previously-absorbed lead. Replying to Professor Roberts Dr. Osler said that he had not tried the potassium chlorate and nitric acid method of oxidation or the electrolytic method of separating lead. With regard to the question raised by Mr. Nicholls of the interference of certain substances Allport and Skrimshire had found that it was possible to avoid the interference of most of the substances in the long list of those which they had tested. So far as he and his colleagues could find there were no interfering substances in their experiments. Mr. Bacharach had referred to the amount of lead that the kidneys could excrete. I t had been found by Aub and his co-workers that the maximum quantit 806 TANKARD BAGNALL AND MORRIS THE COMPOSITION OF excreted in the urine in lead-poisoning was not very great and that most of the lead was excreted in faeces. The question of abortion in animals had many points of interest and he thought that Mr. Bacharach was quite right in saying that abortion might somehow or other be associated with lead because of its known action upon the sexual organs. The wives of workers in factories where lead was extensively used were rather liable to abortion but this tendency ceased when the workers changed their occupation. When deer grazed upon lead-contaminated fields the growth of their antlers was affected and chickens kept on the same land had been known to lay addled eggs. Lead had a very definite harmful effect upon animals. DEPARTMENT OF CHEMICAL PATHOLOGY ST. MARY’S HOSPITAL LONDON w.
ISSN:0003-2654
DOI:10.1039/AN9345900787
出版商:RSC
年代:1934
数据来源: RSC
|
| 3. |
The composition of the amniotic fluid |
| |
Analyst,
Volume 59,
Issue 705,
1934,
Page 806-808
Arnold R. Tankard,
Preview
|
PDF (234KB)
|
|
摘要:
WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock. Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given.However, potatoes had been given to horses in limited quantities without bad results. Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent. Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it.In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes.Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock.Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given.However, potatoes had been given to horses in limited quantities without bad results. Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent.Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it. In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes.Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock.Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given. However, potatoes had been given to horses in limited quantities without bad results.Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent.Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it. In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes. Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.
ISSN:0003-2654
DOI:10.1039/AN9345900806
出版商:RSC
年代:1934
数据来源: RSC
|
| 4. |
Determination of impurities in commercial carbon monoxide |
| |
Analyst,
Volume 59,
Issue 705,
1934,
Page 809-811
H. R. Ambler,
Preview
|
PDF (240KB)
|
|
摘要:
WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock. Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given.However, potatoes had been given to horses in limited quantities without bad results. Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent. Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it.In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes.Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock.Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given.However, potatoes had been given to horses in limited quantities without bad results. Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent.Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it. In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes.Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock.Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given. However, potatoes had been given to horses in limited quantities without bad results.Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent.Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it. In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes. Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.
ISSN:0003-2654
DOI:10.1039/AN9345900809
出版商:RSC
年代:1934
数据来源: RSC
|
| 5. |
The detection and identification of metallic particles in manufactured products |
| |
Analyst,
Volume 59,
Issue 705,
1934,
Page 812-814
H. C. Lockwood,
Preview
|
PDF (464KB)
|
|
摘要:
WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock. Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given.However, potatoes had been given to horses in limited quantities without bad results. Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent. Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it.In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes.Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock.Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given.However, potatoes had been given to horses in limited quantities without bad results. Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent.Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it. In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes.Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock.Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given. However, potatoes had been given to horses in limited quantities without bad results.Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent.Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it. In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes.Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock.Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given. However, potatoes had been given to horses in limited quantities without bad results.Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent.Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it. In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes. Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.
ISSN:0003-2654
DOI:10.1039/AN9345900812
出版商:RSC
年代:1934
数据来源: RSC
|
| 6. |
Notes |
| |
Analyst,
Volume 59,
Issue 705,
1934,
Page 815-818
S. Gordon Liversedge,
Preview
|
PDF (378KB)
|
|
摘要:
WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock. Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given.However, potatoes had been given to horses in limited quantities without bad results. Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent. Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it.In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes.Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock.Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given.However, potatoes had been given to horses in limited quantities without bad results. Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent.Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it. In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes.Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock.Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given. However, potatoes had been given to horses in limited quantities without bad results.Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent.Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it. In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes.Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock.Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given. However, potatoes had been given to horses in limited quantities without bad results.Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent.Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it. In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes. Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.
ISSN:0003-2654
DOI:10.1039/AN9345900815
出版商:RSC
年代:1934
数据来源: RSC
|
| 7. |
Notes from the Reports of Public Analysts. City and County of Kingston-upon-Hull |
| |
Analyst,
Volume 59,
Issue 705,
1934,
Page 819-819
A. R. Tankard,
Preview
|
PDF (114KB)
|
|
摘要:
WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock. Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given.However, potatoes had been given to horses in limited quantities without bad results. Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent. Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it.In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes. Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.
ISSN:0003-2654
DOI:10.1039/AN9345900819
出版商:RSC
年代:1934
数据来源: RSC
|
| 8. |
Ministry of Health. Sale of food and drugs |
| |
Analyst,
Volume 59,
Issue 705,
1934,
Page 820-821
Preview
|
PDF (218KB)
|
|
摘要:
WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock. Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given.However, potatoes had been given to horses in limited quantities without bad results. Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent. Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it.In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes.Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock.Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given.However, potatoes had been given to horses in limited quantities without bad results. Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent.Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it. In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes. Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.
ISSN:0003-2654
DOI:10.1039/AN9345900820
出版商:RSC
年代:1934
数据来源: RSC
|
| 9. |
Report of the Government Chemist upon the work of the Laboratory. For the year ending 31st March, 1934 |
| |
Analyst,
Volume 59,
Issue 705,
1934,
Page 822-824
Preview
|
PDF (244KB)
|
|
摘要:
WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock. Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given.However, potatoes had been given to horses in limited quantities without bad results. Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent. Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it.In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes.Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock.Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given.However, potatoes had been given to horses in limited quantities without bad results. Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent.Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it. In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes.Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock.Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given. However, potatoes had been given to horses in limited quantities without bad results.Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent.Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it. In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes. Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.
ISSN:0003-2654
DOI:10.1039/AN9345900822
出版商:RSC
年代:1934
数据来源: RSC
|
| 10. |
Western Australia. Annual Report of the Chemical Branch Mines Department for the year 1933 |
| |
Analyst,
Volume 59,
Issue 705,
1934,
Page 824-825
Preview
|
PDF (147KB)
|
|
摘要:
WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock. Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given.However, potatoes had been given to horses in limited quantities without bad results. Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent. Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it.In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes.Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.WILLIMOTT AN INVESTIGATION OF SOLANINE POISONING 439 DISCUSSION The PRESIDENT remarked that it seemed somewhat strange that potatoes in certain states (old potatoes, green potatoes, etc.) were often described as highly toxic to stock.Many hundreds of tons had been used as stock feed, and he had never actually known of any stock poisoning. Of course, it could be argued that the potatoes used for feeding were often cooked, and much of the solanine dissolved out, but, on the other hand, a large number of these potatoes were used uncooked, and, therefore, stock did consume this vegetable with its full content of solanine, and, so far as he knew, without detriment. During the war a circular was issued, stating that potatoes were an injudicious feed for horses, and setting out the maximum amount that should be given.However, potatoes had been given to horses in limited quantities without bad results. Mr. C. E. SAGE said that cases of solanine poisoning were not infrequent, but he knew of no fatal one, caused by eating the bright red berries of Solanum dulcamara, which grew plentifully in this country. Solanum nzgrum, which had white flowers and black fruits, were sometimes eaten by country children, but he had never met with any casualties. Until recently the fruits of Solanum carolinense were used in America for the preparation of a tincture for medicinal use. I t grew plentifully as a weed in the Southern States, and the orange-coloured fruits were known as Sodom apples. The alkaloids, solanine and solanidine, existed in the fruits, and, as the negroes had used it for a long time as a remedy for falling sickness, the alkaloid could not be particularly toxic, although it was undoubtedly potent.Solanum chenopodium was a native of Queensland, and some thirty years ago he had isolated the alkaloid solanine from it. In Brazil, S. aculeatissimum was the plant yielding Sodom apples. It also contained solanine. With all these sources of solanine, and with potatoes and tomatoes containing it, there seemed to be no great danger from its toxicity. The leaves of S. nigrum were boiled and eaten in the Hawaii Islands, and the fruits known as “fox’s grapes’’ could be eaten in small quantities without any harmful effects. With sprouting potatoes it did not seem beyond the bounds of possibility that some product of decomposition might have caused the illness of people recorded in the paper.Mr. W. PARTRIDGE said that his only experience in the determination of solanine was in connection with a case in which it was alleged that potatoes had been tampered with and had caused illness. He had used the Meyer process, as outlined by Harris and Cockburn (ANALYST, 1918,43, 133) , but with the improve- ments (including the correction for solubility in ammonia wash-water) of Borner and Mattis (ANALYST, 1924, 49, 284). The potatoes in question, substantial areas of which were green, contained 19 mgrms. of solanine per 100 grms. Taking the attitude that normal potatoes contained about 2 mgrms., and never niore than 8 mgrms. per 100 grms., and that 25 mgrms. per 100 grms. were known to be dangerous, he had felt justified in associating the symptoms, minor though they were, with green potatoes. Mr. E. M. HAWXINS remarked that there seemed to be something in the wisdom of old-fashioned country folk. Thirty years ago when, fresh from the town, he went to live in a rural district, the old country folk instructed him that a potato which was allowed to get green through exposure above the earth was likely to be dangerous to human beings and to animals, and he, therefore, never used them. He thought it significant, in the Glasgow case, that more solanine was contained in potatoes which were green from exposure to sunlight than in the white tubers, and the paper certainly bore out this same contention.
ISSN:0003-2654
DOI:10.1039/AN9345900824
出版商:RSC
年代:1934
数据来源: RSC
|
|