![]() Sources: Yeargin-Allsopp et al. 2003, CDC 1995, Robison et al. 1995, Schecter 1999, Ananth et al. 2001, Branum and
Schoendorf 2002, Swan et al. 1998, Paulozzi et al. 1997, Dunson et al. |
Over the past 50 years, as infectious childhood diseases like polio, smallpox, rheumatic fever, and diphtheria have largely been controlled,
chronic conditions of less obvious origins have taken their place.
Asthma, autism, attention deficit and hyperactivity disorders (ADD and
ADHD), childhood brain cancer and acute lymphocytic leukemia have all
increased over the past 30 years. Five to ten percent of American
couples are infertile. Up to half of all pregnancies end in
miscarriage. Three to five percent of babies are born with birth
defects (CDC 2004, Jahnke et al. 2005, Trasande and Landrigan 2004).
Scientists cannot fully explain these increases, but early life exposure
to environmental pollutants is a leading suspect.
Fetal exposures lead to adult disease. Some chemicals are directly toxic to an exposed child — lead and mercury, for example,
which harm a developing brain — while other chemicals induce a chain of
events that may culminate in a diagnosed health problem later in life.
Hormone-mimicing chemicals like dioxins and furans, for example, could
induce delayed cancers in hormone-sensitive tissues like the breast,
testicle, or prostate gland. Chemicals like PCBs or DDT can reduce
growth rates in the womb, initiating in low birthweight babies lasting,
internal survival mechanisms that cascade into cardiovascular disease or
diabetes later in life.
The fact is, a child can bear a lifelong imprint of risks from the countless molecules of industrial pollutants that find their way through
the placenta, down the umbilical cord, and into the baby's body. The
consequences — health disorders, subtle or serious — can surface not
only in childhood but also in adulthood. Studies now support origins in
early life exposures for a startling array of adult diseases, including
Alzheimers, mental disorders, heart disease, and diabetes.
Laboratory studies show increased deposits of the Alzheimer-related protein amyloid in the brains of older animals exposed to lead as
newborns, but not in animals that were exposed to an equal amount of
lead as adults (Basha et al. 2005). And over the past two decades
numerous studies have linked low birth weight with adult onset of
coronary heart disease, diabetes, stroke, hypertension, depression and
other conditions (Barker 1995, Wahlbeck et al. 2001, Thompson et al.
2001, Hales et al. 1991). Low birth weight can arise not only from poor
maternal nutrition but also from a host of industrial pollutants,
including arsenic, mercury, lead, organic solvents, PCBs, and
pesticides, including DDT.
Recent studies shed new light on how early life chemical exposures set adult disease in motion. In laboratory studies scientists from the
University of Texas found that fetal exposures to the synthetic hormone
(and now-banned drug) DES permanently "reprogrammed" body tissues,
dramatically raising rates of uterine cancer, in this case, in later
life (Cook et al. 2005). With an estimated 75,000 chemicals registered
for use in the U.S., and an average of seven new chemicals approved each
day, many not tested for safety and certaintly not tested for their
ability to "reprogram" body tissues, the ramifications of this study are
enormous.
Fetal exposures cause disease in future generations. Remarkably, it appears that early life exposures can lead to health
problems not only in adulthood, but also down through subsequent
generations. For instance, adult diseases linked to newborns' low birth
weight, enumerated above, cause adverse effects not only in those babies
born small, but also in their children of any birth size, through
heritable changes in gene expression that result in a phenomenon known
as "epigenetic inheritance." Very different from genetic mutations,
which are physical changes in gene structure, epigenetic inheritance is
instead characterized by certain genes being turned on or off, but near
permanently in ways that can be inherited.
If a genetic mutation is like changing a light fixture, the comparable epigenitic change would involve taping the light switch on or
off. Since genes are responsible for making the chemicals that build
and repair the body, this unnatural forcing to a permanent on or off
position can have far-reaching consequences. In humans, both kinds of
genetic changes, mutations as well as epigenetic changes in gene
expression, can be passed down to a baby in the womb.
Scientists have recently found heritable epigenetic changes linked to the fungicide vinclozolin and pesticide methoxychlor, which impaired
sperm counts and sperm motility not only among animals exposed in utero,
but also in three subsequent generations (Anway et al. 2005). In other
words, what each of us was exposed to in our mother's womb might affect
the health of our great-grandchildren.
Notably, both of these pesticides were recently banned under a federal law that requires pesticides to be safe for newborns and
children. The government gives children no explicit protection under
the federal law meant to ensure the safety of other commercial chemicals
(the Toxic Substances Control Act), even though risks from childhood
exposures to industrial chemicals are no lower than those from
pesticides.
Tags:
© 2012 Created by Sway Ciaramello.
Powered by
.