Document Nen3aajrkZRXywObmad9qOZnE

John T . L e v is and B ro s . Co , 2545 Aram ingo Avenue, P h ila d e lp h ia P ennsylvania < My 21, 1^47 Dr-. Kenne th A , Koerber, Plant , hysician, John i. Lewis and Brothers Company, 2345 Arajaingo Avenue* Philadelphia , Penney iwania. Bear r. Koerber*. 2 send you herewith ay beet interpretation of the analytical results obtained by us in the- case of Biaery Koblnaon * as veil as a general opinion on the case, i'heae axe in triplicate as you requested. In order to leftre argument out of the opinion, I call your attention herein to vhat say be regarded as incorrect statements or interpre tations in your last letter. Our results as reported on January 8, 1.947 shoved a definitely abnormal lead concentration in the blood, ss so indicated in th report forwarded with my letter of January 13, 1347. the urinary lead concentration vas at the upper level of normal values, but was regarded dubiously because of ine ri-i f * e of the sample. Our second set of analyses, reported on March X, 1347 and transmit te-G with my letter or March 4* 194-7, shoved scaaewhat higher but not centred!tory values in the blood, and an even loiter value for the urine. In neither Instance was the urinary lead concentration beyond the limits of normal variation for samples of ail volume, nor vere they in any way remarkable in view of the volume of sample submitted. the status of this man, however, with respect to lead exposure, was shown not by the analyses of the urine but by those on the blood. `ihe blood results confirm each other quite adequately, unci defaonistrat beyond any reasonable doubt that .r.ohinson * a leoa exposure during the months immediately preceding the taking of those samples was signifi cant. ihe superintendent * a statement does not show that he had no lead exposure. On the contrary, it specifically refers to work which could have, and clearly did actually result in lead exposure and absorption. Moreover, the lead concentration in the blood in both instances is such that symptomatology from lead absorption could have existed. -he result of this situation is that th diagnosis must bo mad on purely clinical grounds. I agree with your diagnosis and that of KE 0013761 Dr. Kenneth A. Koerber - (2) - May 21, 19^7 Ir. Hollander, that this man la suffering from gout and hypertension. I see no reason for supposing that he lias lead poisoning in addition. Uis present symptomatology and the present hematological findings of anemia vlthout stippling or abnormal numbers of other young forms, fail to indicate the existence of lead poisoning* Therefore, the evidence of lead exposure and absorption is, at present, incidental, from the diagnostic viewpoint. As to the relationship of lead absorption to gout, the evidence is of poor quality, and unsatisfactory the British clinicians, especially, considered lead absorption to be a precipitating factor in gout, but their evidence lay purely in the coincidental occurrence of the two phenomena of gouty diathesis or the onset of gout, with load exposure in the lead trades. Gout was and is common in England and the relationship, in my opinion, was fortuitous. I wiusrc that this clarifies my opinion in this case. Vdiat your ihiladelphia colleagues fail to recognise is that they and no one else can make the diagnosis of lead poisoning by analytical or any other than clinical means, head exposure and leac absorption are not synonymous with lead intoxication. They confuse the issue by not sticking to clinical consideratIona Cordially yours , -AS ef Enc. -.obort A. Ec-hoe, M. t-, K % 0013762 .... . Interpreta tion of Analytical r.t-aulfca and Clinical Syndrome Case of This man v&a exposed to appreciable quantities of lead in the course of his occupation in the period immediately prior to December 21, ip47 and thereafter. The exposure v&s not highly hazardous, but it led to his nbsorption of potentially dangerous quantities of lead, as shown by the lead concentrations in the blood on tvo occasional namely i.j 35 mg. Fh per luu grams of vhole blood os reported by us on January 8, 1947, and j.lj5 mg. f'b per lu.v grams of vhole blood as reported by us on March 1, 1947* In our opinion, these results, taken with the relatively low (normal ranges lead concentration in the urine on both occasions, strongly suggests that lobinson's lead exposure was of a low but significant order of magnitude over a long period of time (years). The occupational history indicates that this was the case. A diagnosis of lead poisoning is not justified by the symptomatology and the clinical facts, including the hematological findings. A diag nosis of gout is tenable and reasonable, thereby making it wholly unnecessary to explain any of the symptomatology on the highly dubious basis of atypical pltunbisia* An biologic relatioaship between lead absorption and the onset of gout is, X should say, purely speculative. I obert A KehOfc k eT o U I O i !> I N16581.01