lindane became monstrously deformed with tumorlike swellings on their roots. Their cells grew
in s ize, being s wollen with chromos omes which doubled in numbe r. The doubling continue d
in future divisions until further cell division became mechanically impossible. The herbicide 2,4-
D has als o produced tumorlike s wellings in treated plants. Chromos omes become s hort, thick,
clumped togethe r. Cell divis ion is s erious ly retarded. The general effect is said to parallel closely
that produced by X rays.
Thes e are but a few illus trations ; many more could be cited. As yet the re has been no
comprehe ns ive s tudy aimed at tes ting the mutagenic effects of pes ticides as s uch. The facts
cited above are by-products of research in cell phys iology or genetics. What is urgently needed
is a direct attack on the proble m. Some scientists who are willing to concede the potent effect
of environmental radiation on man neve rtheles s ques tion whethe r mutagenic chemicals can, as
a practical propos ition, have the s ame effect. They cite the great penetrating powe r of
radiation, but doubt that che micals could reach the germ cells. Once again we are hampere d by
the fact that the re has been little direct investigation of the problem in man. Howeve r, the
finding of large res idues of DDT in the gonads and germ cells of birds and mammals is strong
evidence that the chlorinate d hydrocarbons , at leas t, not only become widely dis tributed
throughout the body but come into contact with genetic materials. Professor David E. Davis at
Penns ylvania State Univers ity has recently dis covered that a potent chemical which preve nts
cells from dividing and has had limited use in cancer therapy can also be used to cause sterility
in birds. Sublethal levels of the chemical halt cell division in the gonads. Professor Davis has had
s ome s uccess in field trials. Obvious ly, then, the re is little bas is for the hope or belief that the
gonads of any organism are shielded from chemicals in the environmen t.
Recent medical findings in the field of chromosome abnormalities are of extreme interest and
s ignificance. In 1959 s everal Britis h and French res earch teams found thei r inde pende nt s tudies
pointing to a common conclus ion—that s ome of humanity’s ills are caus ed by a dis turbance of
the normal chromosome number. In certain diseases and abnormalities s tudied by thes e
investigators the number differed from the normal. To illustrate: it is now known that all typical
mongoloids have one extra chromos ome. Occasionally this is attached to another so that the
chro mos o me nu mbe r remains the normal 46. As a rule, however, the extra is a separate
chromos ome, making the numbe r 47. In s uch individuals , the original caus e of the defect mus t
have occurred in the generation preceding its appearance. A different mechanism seems to
operate in a numbe r of patie nts , both in A merica and G reat Britain, who are s uffering fr o m a
chronic form of leukemia. Thes e have bee n found to have a cons is tent chromos ome
abnormality in some of the blood cells. The abnormality consists of the loss of part of a
chromosome. In these patients the skin cells have a normal co mpl e ment of ch ro mos o mes. Thi s
indicates that the chromos ome defect did not occur in the germ cells that gave ris e to thes e
individuals, but represents damage to particular cells (in this case, the precursors of blood cells)
that occurre d during the life of the individual. The loss of part of a chromos ome has perhaps
deprive d thes e cells of their ‘ins tructions ’ for normal behavior.
The lis t of defects linked to chromos ome dis turbances has grown with s urpris ing s peed s ince
the opening of this territory, hithe rto beyond the boundaries of medical res earch. One, known
only as Klinefelter’s syndrome, involves a duplication of one of the s ex chromos omes. The
resulting individual is a male, but because he carries two of the X ch ro mos o mes (becomi ng X XY
instead of XY, the normal male complement) he is somewhat abnormal. Excessive height and
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