Are the EDCs and other Synthetic Chemicals Depopulating the Human Race? 221A study by Skakkebaek et al. [129] compiled many fascinating facts. It is
predicted that Japan and the European Union will soon experience appreciable
decreases in their populations due to persistently low total fertility rates below
replacement level (2.1 children per woman). In the USA, where the total fertility
rate has also declined, there are ethnic differences. Caucasians have rates below
replacement, while total fertility rates among African‐Americans and Hispanics
are higher.
As shown in Figure 7.18a, the total fertility rate has dramatically decreased
below replacement level to between 1.0 and 1.5 in many nations of the European
Union, Japan, the USA. It is difficult to state with some degree of certainty, but
environmental factors are greatly contributing to low fertility rates in these
nations, along with other social and economic factors, including contracep
tives and access to induced abortions. Of note, total fertility rates have been
declining decades before the contraceptive pill and legal abortion were intro
duced (Figure 7.18b).
Skakkebaek et al. [129] have summarized some surprising aspects of current
trends in male reproductive disorders and fertility. They have described
possible links between environmental agents and the rising incidence of
testicular cancer, disorders of sex development, cryptorchidism, hypospadias,
low testosterone levels, poor semen quality, childlessness and changed sex
ratio [138]. Based on their review of genetic and environmental factors, we
conclude that environmental exposures arising from modern lifestyle, rather
than genetics, are the most important factors in the observed trends. These
environmental factors might act either directly or via epigenetic mechanisms.
In the latter case, the effects of exposures might have an impact for several
generations post exposure.
As we hypothesized earlier, exposure to environmental agents that specifi
cally deplete or reduce the numbers of certain progenitor neurons may con
tribute to the development of ASD. They have taken this one step further and
have hypothesized that the increasing incidence of testicular germ cell cancer
is the result of interference in spermatogenesis process mainly due to environ
mental agents. The key pathogenetic event is insufficient masculinization and
impaired function of the testicular somatic cell niche, which in fetal life is
mainly composed of Sertoli and Leydig cells. The insufficient stimulation of
developing germ cells causes arrest of gonocyte differentiation to spermatogonia
and prolonged expression of pluripotency genes (Figure 7.19). The delayed
gonocytes (pre‐germ cell neoplasia in situ or pre‐GCNIS cells) then gradually
acquire secondary genetic defects, while adapting to the changing niche, espe
cially during and after pubertal hormonal stimulation of the testis. Increased
proliferation results in malignant transformation of GCNIS cells into an
invasive tumor, either a seminoma or nonseminoma (the latter through the
reprogrammed pluripotent stage of embryonal carcinoma). Normal germ cell
development is shown in the top part of Figure 7.19.