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Garry F. Gordon, MD, DO, MD(H), President
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A.M.A Archives of Industrial Health
Volume 13, 1956
pg. 366 and 371

Effect of Oral Edathamil Calcium-Disodium on
Urinary and Fecal Lead Excretion

Comparative Excretory Studies with Intravenous Therapy

Robert F. Bell, M.D.
James C. Gilliland, M.S.
J. Robert Boland, B.S.
and Beverly R. Sullivan, B.S., Denver


Before attempting any extensive clinical trial or oral edathamil calcium-disodium (calcium disodium ethylenediamine-tetra-acetate or Na2CaEDTA [Calcium Disodium Versenate]) for the prophylaxis or treatment of lead poisoning, it was felt fundamental to determine whether the oral use of the drug could effect an increase in lead excretion from the body by way of the urine or feces. To our knowledge no studies have been mad on the combined fecal and urinary lead excretion in occupational lead-poisoning cases treated with oral edathamil calcium-disodium.

During the last year three occupational lead-poisoning cases were followed, with 24-hour fecal and urinary lead-excretion rates, before, during, and after treatment with oral edathamil calcium-disodium. The patients were purposely studied while they were removed from exposure, since it has been our experience that while the worker continued at his occupational lead exposure the fecal lead excretion was high an variable.

Urine specimens were collected over approximately 24-hour intervals. Fecal specimens were collected singly, unless two or more defecations occurred within a 24-hour period. All excretion rates were corrected for time and are reported in this paper as milligrams of lead per 24 hours.

The time of urination is easily controlled. The time of defecation is not easily controlled. In the calculation of the combined lead content of feces and urine, therefore, the urinary lead values were adjusted to fecal time intervals. The feces that were collected between certain time intervals were mixed thoroughly, and weighed aliquot was taken for analysis. All specimens were prepared for analysis by wet ashing and analyzed by them mixed color dithizone technique.1 Although these cases were studied over a considerable period of time, as wil be mentioned in the individual case records, Figures 1, 2, 3, and 4 show only excretory values for the 3 days prior to oral treatment, the 10 days of oral treatment, and the 6 days following oral treatment.


Received for pulication Sept. 8th, 1955.
Division of Industrial Medicine, University of Colorado Medical Center.

* * * * *


SUMMARY AND CONCLUSIONS 

It is concluded from this study of the fecal and urinary lead excretions of three lead-poisoning cases treated daily with 3gm of edathamil calcium-disodium orally or intravenously that:

1. Oral administration given while men are out of exposure causes a significant increase in both the fecal and urinary lead excretion. There is a two-and-one-half to three-fold increase in the combined urinary and fecal lead excretion with oral administration.

2. In these cases the combined fecal and urinary lead-excretion response is approximately two-thirds as much on oral as on intravenous therapy.

3. There is a marked shift to urinary lead excretion with both oral and intravenous therapy. This shift is much greater with intravenous therapy.

4. Data on these cases suggest that fecal lead excretion is diminished during intravenous therapy, but uncontrolled environmental factors may be the cause of this observation.

Drs. Robert L. McKenna and Thomas H. Mahony, Jr. referred these cases for study, and Drs. Sherman S. Pinto, James J. Waring, and Harry Foreman offered advice and helpful criticism in the preparation of this paper.

 

REFERENCES

1. Welcher FJ: Organic Analytic Reagents, New York, D. Van Nostrand Company, Inc, 1947, Vol. 3

2. Reiders F: Effect of Oral Na2CA Ethylenediamine Tetraacetate on Urinary and Fecal Excretion of Lead in Rabbits, Fed. Proc. 13:397-398, 1954.

3. Kehoe, RA: Misuse of Edathamil Calcium-Disodium for Prophylaxis of Lead Poisoning, report of the Council on Industrial Health and the council on Pharmacy and Chemistry, JAMA 157:341-342 (Jan 22) 1955.