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Environmental Medicine: Integrating a Missing Element into Medical Education
cular and pituitary hormone production in these workers.
The 2 women workers not currently using oral contraceptives had normal F.S.H. and L.H. results.
Preliminary evaluation of the testicular-biopsy results of the severely affected men indicated loss of spermatogonia, with no evidence of inflammation or severe fibrosis.
The 3 men not included in the comparison who had sperm-counts of 10 million–30 million had exposures between one and three years—an observation that supports the notion of a direct relationship between length of exposure and degree of oligospermia.
Chemically reduced male infertility related to occupation has seldom been reported. Lancranjan et al.3 reported that lead-poisoned workers had lowered sperm-counts, decreased sperm motility, and a higher propertion of abnormal forms. Diminished libido and difficulty in erection and ejaculation were also found. Kepone, an organochlorine insecticide, severely poisoned workers in Virginia in 1975. Most of the affected workers had severe neurological abnormalities, and some were also reported to be infertile.4
The chemical suspected in the present investigation to be the cause of infertility had previously been shown to produce sterility in animals. D.B.C.P. was shown by Torkelson et al.5 to be toxic to the testes of rats, guineapigs, and rabbits. In the rat testis it caused degeneration of the seminiferous tubules, increase in Sertoli cells, reduced sperm-count, and abnormal sperm morphology. Rats with these effects also showed hepatic and renal degeneration. D.B.C.P. was found to produce these changes through skin absorption as well as ingestion or inhalation. Faidysh et al.6 showed that D.B.C.P. damaged the testes, liver, and kidneys of rats, but these organs regenerated in the survivors.
Airborne concentrations of D.B.C.P. in the factory we investigated are believed to be lower than the 1 p.p.m. limit recommended by Torkelson et al.5 D.B.C.P. levels measured in early 1977 in the A.C.D. were 0·4 p.p.m. (averaged for an eight-hour day). These measurements were made with personal air-sampling devices.7
Research is being continued at this plant, together with studies in other areas. Follow-up studies of the affected workers are being planned. Our findings have raised a number of important issues. One is the significance of duration and intensity of exposure. Although all severely affected workers (group A) were, or had been, production workers for at least three years, the shortest time of exposure associated with oligospermia was only one year. Another question is whether the observed sterility is reversible in man as it has been shown to be in animals. Finally, since D.B.C.P. is carcinogenic in animals8 and mutagenic in bacterial systems,9 the possibility of such damage in man must also be considered seriously.
How big a problem D.B.C.P.-induced infertility is we do not yet know, but our communications with medical officers of other companies manufacturing D.B.C.P. clearly indicate that it extends beyond the formulating plant described here.
This study would not have been possible without the support and cooperation of the Occidental Chemical Company, Western Division, and the Oil, Chemical, and Atomic Workers Union, Local 1–5. We thank Dr William Palmer, Dr Louis Brahen, and Dr Edward Smuckler for advice on pathology, Dr John Linfoot for assistance with endocrine assays, and Dr Ken Dod, Claire Lalor, and Mary Ann Gustavson for administrative support.
Requests for reprints should be addressed to D.W., 2521 Channing Way, University of California, Berkeley, California 94720, U.S.A.