Insecticide
linked to increased
breast cancer risk — 40 years after exposure
Melinda
Lewis remembers splashing in the irrigation canals that outlined her grandpa's
walnut and almond groves in the late 1960s.
Two
decades earlier, her mother had played in those same Escalon, California, farm
fields as crop dusters flew overhead, releasing a new "miracle"
chemical—a war-time innovation—the insecticide known as DDT.
Since a bout with atypical hyperplasia, a pre-cancerous breast condition, in 1997 at age 36, Lewis often has wondered whether exposures to farm chemicals in childhood—her own and her mother's—may have heightened her health risks.
Since a bout with atypical hyperplasia, a pre-cancerous breast condition, in 1997 at age 36, Lewis often has wondered whether exposures to farm chemicals in childhood—her own and her mother's—may have heightened her health risks.
In
recent decades, it's become increasingly clear that certain adult diseases may
have their origins in childhood—or before. Early-life exposures—including those
that take place in the womb—may hold the key to understanding who gets diseases
such as breast cancer or heart disease, say environmental researchers.
Some of the most reliable evidence for this link comes from exposures that took place during World War II. Years after the Dutch "Hunger Winter" of 1944-1945, babies conceived during the famine were more likely to suffer from obesity, diabetes, and heart disease in adulthood than their peers born shortly afterwards.
Teenage
girls in Hiroshima and Nagasaki were far more likely to develop breast cancer
years after the atomic bombings than women who had been 35 years or older when
the radiation exposures occurred.
Yet
such ailments often take decades to develop, making the link between
environment and disease difficult to study—and prove.
Lewis,
and her mother, who passed away in 2013 after suffering from a rare blood
disorder, are part of a 60-year-long study of Northern California women, their
children and grandchildren, that's now yielding clues on some of science's most
vexing questions about environmental influences on health—including the
long-debated role of DDT in breast cancer.
"What
we've learned over the years is that environmental exposures that occur during
important periods of breast development can play a role in later-life breast
cancer risk," Barbara Cohn, director of the Berkeley-based Child Health
and Development Studies, told EHN.
Risk
manifests four decades later
Cohn
and colleagues showed recently that pre-puberty
exposures to DDT may have increased the breast cancer risk for
women through their early postmenopausal years.
DDT
was used heavily on farms in the U.S. and around the world from the 1940s
through 1960s, but banned in 1972 after it was found to accumulate in wildlife.
The chemical, along with the other chemicals it breaks into as the body metabolizes it, also appeared to mimic the hormone estrogen.
After discovery in the 1970s that another synthetic estrogen, diethylstilbestrol (DES), increased the risk of breast cancer in women who took the drug during pregnancy, scientists questioned whether DDT exposure might have a similar effect.
The chemical, along with the other chemicals it breaks into as the body metabolizes it, also appeared to mimic the hormone estrogen.
After discovery in the 1970s that another synthetic estrogen, diethylstilbestrol (DES), increased the risk of breast cancer in women who took the drug during pregnancy, scientists questioned whether DDT exposure might have a similar effect.
Yet
by the early 2000s, numerous studies, including a major research effort to
determine whether certain environmental contaminants increased the risk of
breast cancer among Long Island, New York, women, failed to find a link between
DDT and breast cancer.
But
there was a problem with the Long Island study. Science was beginning to show
that breast cancer may have its origins early in life—while the breast tissue
is still developing—and that exposures to pollutants during critical windows of
breast development may matter most.
Since
the researchers couldn't go back in time to measure what chemicals the women
might have been exposed to years ago, they did the next best thing. They
measured DDT levels in the bodies of the Long Island women during the current
period—when most were middle-age or later.
"We
knew at the time that measuring certain environmental exposures late in life
wasn't going to give us an absolute final answer on risk," Regina
Santella, a biochemist at Columbia University in New York, who was involved in
the Long Island Breast Cancer Study Project, told EHN.
The
Child Health and Development Studies—with its 60-year-long dataset of 15,000
California families—offered a unique opportunity to fill in some of the blanks
about early life exposures that the Long Island study couldn't answer.
Researchers had blood samples from women who had been pregnant during the late 1950s and early 1960s, when DDT use was at its peak—and when the women were much closer in age to those key windows of breast development. Cohn notes that pregnancy, itself, may also be an important window of susceptibility.
Researchers had blood samples from women who had been pregnant during the late 1950s and early 1960s, when DDT use was at its peak—and when the women were much closer in age to those key windows of breast development. Cohn notes that pregnancy, itself, may also be an important window of susceptibility.
In
a series of studies, published since 2007, Cohn and other researchers who
study the California cohort, have shown that women exposed to high levels of
DDT both before and after puberty are at an increased risk of breast cancer
through age 54 and that these risks are greatest for women exposed before
puberty.
The latest study, published
earlier this month in the Journal of the National Cancer Institute, found a
40-year lag between the timing of a woman's first DDT exposure and her breast
cancer diagnosis.
Women who would first have been exposed to DDT in infancy had the highest risks of developing breast cancer before age 50, while women whose first exposure would have been between ages 3 and 13 had a three-fold increased risk of developing breast cancer between ages 50 and 54.
Women who would first have been exposed to DDT in infancy had the highest risks of developing breast cancer before age 50, while women whose first exposure would have been between ages 3 and 13 had a three-fold increased risk of developing breast cancer between ages 50 and 54.
Hormone-mimickers
derail development
The
findings fit with what we know about breast development, Ana Soto, a
developmental biologist from Tufts University who was not involved in the
research, told EHN. The mammary gland develops throughout life. The main stages
are: before birth, at puberty and in pregnancy. Hormones dictate when and how
breast tissue remodels at these key junctures.
"Cancer
is a problem of tissue organization," Soto told EHN. If you throw a
hormone-mimicking chemical into the mix at just the right time, these
developmental processes may go awry, she explained. Indeed, rodent studies have
shown that DDT and other hormone-mimicking chemicals that may increase the risk
of mammary tumors following early-life exposure.
While
we've stopped using DDT in most parts of the world, it's possible that other
hormone-disrupting chemicals we're putting in the environment today could show
a similar risk pattern, Cohn said.
For
instance, laboratory studies of cells, and some on animals, have linked
exposure to some widely used chemicals in plastics—BPA and certain phthalates,
for instance—to breast cancer, though long-term studies in humans are lacking.
These
early-life exposures may be affecting more than just cancer risk. Studies in
animals suggest that prenatal exposures to BPA, phthalates and some other
chemicals dubbed obesogens, may pre-program the way the body stores fat,
increasing the risk of obesity and related diseases later on.
Complex mix of
genetics, environment and behavior
Breast
cancer, like most other diseases, is caused by a mix of genetics, environment
and behavior. Most medical studies are designed to look at immediate
consequences or benefits—the effects of losing weight or changing one's diet,
for instance—in a tighter time frame. These kinds of studies can help show
people what they can do right now to reduce their risk of disease.
"Long-term
cohort studies like this present a rare opportunity to study disease risk from
a higher elevation where we can see the bigger picture," Dr. Kenneth
Spaeth, an occupational and environmental health specialist at Northwell Health
in New Hyde Park, NY, told EHN.
Yet the big picture is often complicated. Not every person who was exposed to DDT early on develops breast cancer—in fact, most don't—just like not every person who smokes gets lung cancer.
A
whole lifetime of different behaviors and exposures contribute to disease risk
in genetically susceptible people.
"We
know now that there are benefits and harms to the things we do and the things
we put in our bodies, and that those consequences start at a young age. We see
that here in regard to DDT," Spaeth said.
And
increasingly this seems true for many of today's endocrine disrupting chemicals
as well—but proving definitive health links remains difficult, which gives
manufacturers a pass to continue producing compounds that we know little about
with little interference from regulators.
Melinda
Lewis will never know whether exposure to DDT during those early days playing
on her grandpa's farm—or any other specific chemical or exposure she may have
experienced before or since—was tied to her breast cancer, but that doesn't
matter much to her anymore.
She's
now a grandmother. Lewis looks at her toddler grandson crumbling cheese and crackers
on the floor of her Benicia, California, home and asks, "am I now
unwittingly exposing him to chemicals or products around my house that could
impact his health?"
This
story was supported by a Lizzie Grossman Freelance Grant for
Environmental Health Reporting awarded through the Society for
Environmental Journalism's Fund for Environmental Journalism
