Trace Amounts, Time
excerpted from the book
by Sandra Steingraber
Vintage Books, 1998 (paper)
To the 89 percent of Illinois that is farmland, an estimated 54
million pounds of synthetic pesticides are applied each year.
Introduced into Illinois at the end of World War II, these chemical
poisons quietly familiarized themselves with the landscape. In
1950, less than 10 percent of cornfields were sprayed with pesticides.
In 1993,99 percent were chemically treated.
Pesticides do not always stay on the fields where they are
sprayed. They evaporate and drift in the jetstream. They dissolve
in water and flow downhill into streams and creeks. They bind
to soil particles and rise into the air as dust. They migrate
into glacial aquifers and buried river valleys and thereby enter
groundwater. They fall in the rain. They are detectable in fog.
Little is known about how much goes where. In 1993, 91 percent
of Illinois's rivers and streams showed pesticide contamination.
These chemicals travel in pulses: pesticide levels in surface
water during the months of spring planting-April through June-are
sevenfold those during winter, although detections never fall
to zero. Even less is known about pesticides in groundwater. A
recent pilot study found that one-quarter of private wells tested
in central Illinois contained agricultural chemicals...
Some of the pesticides inscribed into the Illinois landscape
promote cancer in laboratory animals. Some, including one of the
most commonly used pesticides, atrazine, are suspected of causing
breast and ovarian cancer in humans. Other probable carcinogens,
such as DDT and chlordane, were banned for use years ago, but
like the islands in preglacial river valleys, their presence endures.
A lot goes on in the 11 percent of Illinois that is not farmland.
Approximately fifteen hundred hazardous waste sites are in need
of remediation-a list that does not include several thousand pits,
ponds, and lagoons containing liquid industrial waste. And each
year Illinois injects some 250 million gallons of industrial waste-which,
until recently, included pesticides-through five deep wells that
penetrate into bedrock caverns. These geological formations are
overlain by aquifers and farmland. Illinois exports hazardous
waste but also imports it-almost 400,000 tons in 1992-from every
state except Hawaii and Nevada. In this same year, Illinois industries
legally released more than 100 million pounds of toxic chemicals
into the environment.
Like pesticides, industrial chemicals have filtered into the
groundwater and surface waters of streams and rivers. Metal degreasers
and dry-cleaning fluids are among the most common contaminants
of glacial aquifers. Both have been linked to cancer in humans.
A recent assessment of the Illinois environment concluded that
chemical contamination "has become increasingly dispersed
and dilute (and thus less visible)," leaving residues that
are "increasingly chemically exotic and whose health effects
are not yet dearly understood."
Moreover, even after its ban, DDT has continued to be shipped
abroad. Laws banning the use of particular pesticides in this
country do not prohibit their export. U.S. Customs records from
1992 reveal that several million pounds of unregistered, canceled,
or suspended pesticides were loaded on ships and exported from
the United States that year. As of 1994, nine tons per day of
domestically banned pesticides left U.S. shores for foreign lands.
Lindane, chlordane, dieldrin, aldrin, heptachlor. These names,
unfamiliar to us now, are a roll call of the other pesticides
Rachel Carson featured in Silent Spring. All are now classified
as known, probable, or possible carcinogens. All are now prohibited
or heavily restricted for domestic use. Many are still manufactured
Banned pesticides, like fugitives from justice, have not entirely
disappeared. We have forgotten about them, but they are still
among us. They frequent foreign ports. They languish underground.
But they are beginning to surface again in the tissues of women
with breast cancer, sometimes under different names-DDT is metabolized
in the human body into other chemicals, including one called DDE-
and sometimes along with banned industrial chemicals belonging
to the same chemical clan.
Four years after DDT was banned, researchers reported that
women with breast cancer had significantly higher levels of DDE
and PCBs in their tumors than in the surrounding healthy tissues
of their breasts. Similar but weaker trends held for lindane,
heptachlor, and dieldrin. The study was small-involving only fourteen
women-but the findings provocative, because DDT and PCBs were
already linked to breast cancer in rodents.
Other small studies followed. Some showed an association between
breast cancer and residues of pesticides or PCBs; some did not.
In 1990, Finnish researchers reported that women with breast cancer
had higher concentrations of a lindane-like residue in their breasts
than women without breast cancer. Indeed, women whose breasts
sequestered the highest levels were ten times more likely to have
breast cancer than women with lower levels. Moreover, the pooled
blood from women with breast cancer contained 50 percent more
of this pesticide residue than the blood from women without breast
cancer. Similarly, in 1992, a study of forty Connecticut women
revealed that levels of PCB, DDE, and DDT in the breasts of women
with breast cancer were 50 to 60 percent higher than in women
who did not have breast cancer.
In 1993-seventeen years after the first pilot study-the biochemist
Mary Wolff and her colleagues conducted the first carefully designed,
major study on this issue. They analyzed DDE and PCB levels in
the stored blood specimens of 14,290 New York City women who had
attended a mammography screening clinic. Within six months, fifty-eight
of these women were diagnosed with breast cancer. Wolff matched
each of these fifty-eight women to control subjects-women without
cancer but of the same age, same menstrual status, and so on-who
had also visited the clinic. The blood samples of the women with
breast cancer were then compared to their cancer-free counterparts.
On average, the blood of breast cancer patients contained
35 percent more DDE than that of healthy women. (PCB levels were
only slightly higher.) The most stunning discovery was that the
women with the highest DDE levels in their blood were four times
more likely to have breast cancer than the women with the lowest
levels. The authors concluded that residues of DDE "are strongly
associated with breast cancer risk."
... women born in the United States between 1947 and 1958 ...
now have almost three times the rates of breast cancer than their
great-grandmothers did when they were the same age.
At the end of the 1950s, death certificates showed that a far
greater proportion of people were dying of cancer than had been
true at the turn of the century. Most ominously, children's cancers,
once a medical rarity, were becoming commonplace-as revealed both
by statistics and by doctors' observations.
In 1982, 90 out of every 100,000 women living in the state of
Massachusetts were diagnosed with breast cancer. By 1990, the
incidence rose to 112 out of 100,000.
... [a] 24 percent rise in breast cancer in Massachusetts ...
occurred between 1982 and 1990
While still a, matter of some debate, the most widely accepted
estimate is that between 25 and 40 percent of the recent upsurge
in breast cancer incidence is attributable to earlier detection.
Underlying this acceleration exists still a gradual, steady, and
long-term increase in breast cancer incidence that has just recently
begun to level off. This slow rise-between 1 and 2 percent each
year since 1940- predates the introduction of mammograms as a
common diagnostic tool. Moreover, the groups of women in whom
breast cancer incidence is ascending most swiftly-blacks and the
elderly-are among those least served by mammography. Between 1973
and 1991, the incidence of breast cancer in females over sixty-five
in the United States rose nearly 40 percent, while the incidence
of breast cancer in black females of all ages rose more than 30
percent. Therefore, the majority of the increase in breast cancer
cannot be explained by mammograms.
This kind of analysis is possible only when many years of
data are available. Unfortunately, many state cancer registries
are new; they cannot look back across fifty years as I could with
my tree inventories. The Illinois State Cancer Registry was created
in 1985. My own diagnosis, which took place in 1979, is therefore
not part of the collective story of cancer in Illinois. Unless
I die from the disease, I will never be officially counted among
those touched by cancer. The first year of reliable data in the
Illinois State Cancer Registry is 1986. Moreover, like many state
registries, Illinois's is about five years behind in analyzing
and publishing its data. Currently, therefore, Illinois residents
have only a four-year picture of cancer incidence in their home
state. Studying these time trends is like watching four minutes
of a feature-length movie and trying to figure out the whole story.
Regional comparisons are often difficult because cancer registries
in neighboring states can vary wildly in their length of operations.
For example, Connecticut has the oldest functioning registry,
one started in 1941. The Connecticut Tumor Registry provides one
of the only truly long-term views of U.S. cancer incidence. Massachusetts,
on the other hand, established its cancer registry in 1982. Nearby
Vermont is one of ten states that had no cancer registry at all
until 1992, when Congress established the National Program of
This patchwork of state-based registries is afflicted with
another problem that we who count plants never have to worry about.
People, unlike trees, move. Lifelong residents of one state, for
example, may migrate to another upon retirement and become statistics
in their new community. Without a comprehensive national cancer
registry-which the United States does not have-state registries
must rely on an elaborate system of data exchange. This is especially
crucial for my elongated home state of Illinois, which shares
a border with five other states. When faced with a serious health
problem, many rural folk in the central and southern counties
wind up being diagnosed across the Mississippi and Wabash Rivers
because they would rather travel to cities in Iowa, Missouri,
Indiana, or Kentucky than make the long trek north to Chicago.
Illinois recently began trading registry data with its neighbors,
thereby considerably boosting cancer incidence figures in its
many east and west border counties.
Five state registries also contribute data to the federal
cancer registry. The so-called SEER Program (Surveillance, Epidemiology,
and End Results), overseen by the National Cancer Institute, does
not attempt to record all cases of cancer in the country, but
instead samples about 14 percent of the populace. SEER is a child
of the War on Cancer as declared by President Richard Nixon and
codified as the National Cancer Act of 1971. SEER has been collecting
cancer diagnoses since 1973 and currently represents the states
of Connecticut, Hawaii, Iowa, New Mexico, and Utah, as well as
five specific metropolitan areas: Atlanta, Detroit, San Francisco-Oakland,
Seattle, and Los Angeles. Everyone living in one of these states
or cities who is diagnosed with cancer becomes a bit of data in
the SEER Program registry, and their tumors stand in for all of
Without a nationwide registry, no one can know exactly how
many new cases of cancer are diagnosed in the United States every
year. Instead, such numbers are estimated by applying rates from
the SEER registry to the population projection for any particular
year. To generate estimates before 1973, statisticians combine
data from older individual state and city registries across the
country. In this way, we now have reasonably reliable incidence
figures going back to 1950.
Incidence data were not available to Rachel Carson when she
first documented what she believed was the beginnings of a cancer
epidemic. Instead, Carson focused on rising death rates from cancer.
She was most disturbed by evidence that childhood cancer had jumped
from the realm of medical rarity to the most common disease killer
of American schoolchildren within a few decades.
Some researchers believe that mortality rates-which are also
adjusted for age and population size-are still a more reliable
indicator than incidence because they are less affected by changes
in diagnostic technique. Death, after all, is certain and absolute.
Moreover, causes of death, duly noted in all states of the union,
have been tallied for far longer than tumors have been registered.
We have a much deeper and wider view when we examine cancer trends
over time using information gleaned from death certificates.
But mortality is ... an imperfect measure of the prevalence
of cancer. Not everyone diagnosed with cancer, thankfully, goes
on to die from it. If treatment improves, mortality can decline
even as incidence rises. This is certainly the case for childhood
cancers, which, according to SEER data, jumped in incidence by
10.2 percent between 1973 and 1991 even as the death rate fell
by almost 50 percent. Long-term trends show that childhood cancers
have risen by one-third since 1950. Using mortality to measure
the occurrence of cancer in children today would create a falsely
rosy picture. Heroic measures may be saving more children from
death, but every year more children are diagnosed with cancer
than the year before. Increases are most apparent for leukemia
and brain tumors. At present, eight thousand children are diagnosed
with cancer each year; one in every four hundred Americans can
expect to develop cancer before age fifteen.
Cancer among children provides a particularly intimate glimpse
into the possible routes of exposure to contaminants in the general
environment and their possible significance for rising cancer
rates among adults. The lifestyle of toddlers has not changed
much over the past half century. Young children do not smoke,
drink alcohol, or hold stressful jobs. Children do, however, receive
a greater dose of whatever chemicals are present in air, food,
and water because, pound for pound, they breathe, eat, and drink
more than adults do. In proportion to their body weight, children
drink 2.5 times more water, eat 3 to 4 times more food, and breathe
2 times more air. They are also affected by parental exposures
before conception, as well as by exposures in the womb and in
All types combined, the incidence of cancer in the United States
rose 49.3 percent between 1950 and 1991. This is the longest reliable
view we have available. If lung cancer is excluded, overall incidence
still rose by 35 percent. Or, to express these figures in another
way: at mid-century a cancer diagnosis was the expected fate of
about 25 percent of Americans-a ratio Carson found so shocking
that it inspired the title of one of her chapters-while today,
about 40 percent of us (38.3 percent of women and 48.2 percent
of men) will contract the disease sometime within our lifespans.
Cancer is now the second leading cause of death overall, and the
leading cause of death among Americans aged thirty-five to sixty-four.
More of the overall upsurge has occurred in the past two decades
than in the previous two, and increases in cancer incidence are
seen in all age groups-from infants to the elderly. If we exclude
cancer of the lung and restrict our view to the period covered
by SEER, overall incidence rose 20.6 percent between 1973 and
1991, while mortality declined 2.8 percent.
Adding lung cancer to the picture, overall cancer mortality
rose by 6.9 percent from 1973 until 1991-a difference that testifies
to the deadly nature of this disease. Happily, the decline in
smoking is finally affecting the cancer death rate. In a recent
study of cancer mortality rates from 1991 to 1995, researchers
found a small but decisive decline in overall cancer mortality
(about 3 percent) during this period. The single largest factor
behind this decline is a decrease in lung cancer deaths.
One-fourth of all cancer deaths are from lung cancer. Because
the fatality rate is so high, lung cancer incidence and lung cancer
mortality are very nearly the same statistic, and, in the United
States, both closely mirror historical patterns of cigarette consumption.
(Among American women, who began smoking in large numbers later
in the century than did men, lung cancer mortality is still rising.)
Overall, approximately 87 percent of the deaths from lung cancer
can be attributed to cigarette smoking.
This also means, of course, that 13 percent of all lung cancer
deaths occur among people who do not smoke. Thus, although smoking
dominates the lung cancer picture, additional mysteries need sleuthing
here. And, while smoking remains the largest single known preventable
cause of cancer, the majority of cancers cannot be traced back
to cigarettes. Indeed, many of the cancers now exhibiting swift
rates of increase-cancers of the brain, bone marrow, lymph nodes,
skin, and testicles, for example-are not related to smoking. Testicular
cancer is now the most common cancer to strike men in their twenties
and thirties. Among young men both here and in Europe, it has
doubled in frequency during the past two decades. These increases
cannot be attributed to improved diagnostic practices. Brain cancer
rates have risen particularly among the elderly. Between 1973
and 1991, brain cancers among all Americans rose 25 percent. Those
over sixty-five suffered a 54 percent rise.
Mortality and incidence do not always track each other. No
cancers are increasing in mortality while decreasing in incidence,
but several cancers have increased in incidence even as their
death rates have declined due to more effective treatments. According
to SEER data, these include cancers of the ovary, testicle, colon
and rectum, bladder, and thyroid. There are eight cancers whose
incidence and mortality are both on the decline: those of the
stomach, pancreas, larynx, mouth and pharynx, cervix, and uterus,
as well as Hodgkin's disease and leukemia. Stomach cancer has
been declining for decades, probably owing to improvements in
food handling and the increased consumption of fresh foods made
possible when refrigeration replaced more toxic methods of food
preservation, such as smoking, salting, and pickling. Pap smears
have been credited with bringing down the incidence of cervical
cancer because precancerous lesions can be detected and cut out
before they are transformed into invasive tumors.
However, these modest gains are swamped by the cancers that
show both increasing incidence and increasing mortality: cancers
of the brain, liver, breast, kidney, prostate, esophagus, skin
(melanoma), bone marrow (multiple myeloma), and Iymph (non-Hodgkin's
Iymphoma) have all escalated over the past twenty years and show
long-term increases that can be traced back at least forty years.
In recent years, breast cancer mortality among white women has
begun to slow down, declining 6.8 percent from 1989 to 1993. However,
the death rate is still higher than it was when Rachel Carson
died of the disease in 1964, and it is still rising for black
women. Moreover, breast cancer incidence rates are still rising
for localized disease even as they are falling for more advanced-stage
diagnoses (a shift probably indicating that breast cancer is being
detected and treated earlier); the proportion of women developing
the disease at all remains at the highest level ever recorded.
"Explanations for these increases do not exist,"
according to Philip Landrigan, a pediatrician and leading public
health researcher. Medical literature is accustomed to summations
more temperate and indirect, but this one has been echoed again
and again in recent research papers on trends in cancer rates.
In a 1995 assessment of the situation, a research team at the
National Cancer Institute similarly concluded, "Some trends
remain unexplained . . . and may reflect changing exposures to
carcinogens yet to be identified and clarified."
Clarification about carcinogens, Landrigan believes, requires
an environmental line of inquiry:
The possible contribution to recent cancer trends of the substantial
worldwide increases in chemical production that have occurred
since World War II (and the resulting increases in human exposure
to toxic chemicals in the environment) has not been adequately
assessed. It needs to be systematically evaluated.
I have read the preceding two sentences many times. Most of
my life spans the time between Carson's call for a systematic
evaluation of the contribution of toxic chemicals to increased
human cancers and Landrigan's repetition of this call. Both give
I am struck also by the symmetry between Landrigan's recommended
course of action and an observation made thirty years earlier
by two senior scientists at the National Cancer Institute, Wilhelm
Hueper and W. C. Conway : "Cancers of all types and
all causes display even under already existing conditions, all
the characteristics of an epidemic in slow motion." This
unfolding crisis, they asserted, was ) being fueled by "increasing
contamination of the human environment with chemical and physical
carcinogens and with chemicals sup- ~ porting and potentiating
their action." And yet the possible ) relationship between
cancer and what Hueper and Conway called "the growing chemicalization
of the human economy" has not been pursued in any systematic,
The environment, it seems, keeps falling off the cancer screen.
After lung cancer in women, the three cancers ascending most swiftly
in the United States are melanoma of the skin, non-Hodgkin's lymphoma,
and multiple myeloma. These are not the most prevalent cancers-breast
cancer remains the most frequently diagnosed cancer in women,
for example-but these are the ones galloping forward at the fastest
Melanoma accounts for only 5 percent of all skin cancers,
but it is the most dangerous kind, accounting for 75 percent of
skin cancer deaths. The U.S. incidence of melanoma rose nearly
350 percent between 1950 and 1991, and mortality rose by 157 percent.
Between 1982 and 1989 alone, melanoma incidence jumped 83 percent.
Each year, about 4 percent more people contract melanoma than
the year before, and the average age at diagnosis is going down.
Melanomas are clearly associated with exposure to ultraviolet
radiation (albeit in a complicated way that is a matter of some
debate), and here is where individual behavior and changes in
the global environment come together. Basal and squamous cell
cancers, which arise from keratinocytes, appear to increase in
proportion to one's cumulative lifetime exposure to sunlight.
Melanomas, by contrast, are thought to be initiated by acute exposures,
such as a bad sunburn in childhood. In essence, the cells designed
to protect us from the chromosome-breaking effects of the sun
are themselves damaged by an overdose of the very element they
strive to shield us from. Decades later, another insult of some
kind causes wild cell divisions within the damaged melanocyte
to commence. A melanoma forms. A borderline is crossed. This second
event may be more sunlight, but it may also include exposure to
certain chemicals. Excess rates of melanoma are found in rubber
and plastics workers, as well as in those employed in electronics
and metal industries.
The accelerating incidence of melanoma means exposure to ultraviolet
radiation is probably increasing. This could be happening for
two reasons. First, more people are spending more time in the
sun. Second, the sunlight to which we are exposed contains more
ultraviolet rays. Since the 1974 discovery that earth's ultraviolet
shielding ozone layer is thinning, a growing group of physicians
and climatologists have come to believe both forces are at work,
especially in raising the risk for future melanomas. The U.S.
Environmental Protection Agency (EPA) projects that tens of thousands
of additional fatal skin cancers will result from the 5 percent
loss of ozone that has already occurred in the stratosphere above
Lymphomas(do)seem to be consistently associated with exposure
to synthetic chemicals, especially a class of pesticides known
as phenoxy herbicides. These synthetic chemicals were born in
1942 as part of a never-implemented plan by the U.S. military
to destroy rice fields in Japan. The most famous phenoxy is a
mixture of two chemicals, 2,4,5-trichlorophenoxyacetic acid (2,4,5-T)
and 2,4dichlorophenoxyacetic acid (2,4-D). This combination is
called Agent Orange, and it was used between 1962 and 1970 by
U.S. troops to clear brush, destroy crops, and defoliate rainforests
in Vietnam. The military career of phenoxy herbicides was thus
Linked to miscarriages and contaminated with dioxin, 2,4,5-T
was eventually outlawed. By contrast, 2,4-D went on to become
one of the most popular weed killers in lawns, gardens, and golf
courses, as well as in farm fields and timber stands. It has been
marketed under a schizophrenic collection of trade names: Ded-Weed,
Lawn-Keep, Weedone, Plantgard, Miracle, Demise.
Evidence for an association between phenoxy herbicides and
non-Hodgkin's lymphoma comes from several corners. Vietnam veterans
have high rates of non-Hodgkin's lymphoma. So do farmers in Canada,
Kansas, and Nebraska who use 2,4-D. Studies show that the risk
of lymphoma to farmers rises with the number of days per year
of use, the number of acres sprayed, and the length of time they
wear their "application garments" before changing clothes.
In Sweden, exposure to phenoxy herbicides was shown to raise one's
risk of contacting Iymphomas six-fold. In a comprehensive review
of the topic, ~e National Cancer Institute scientists Sheila Hoar
Zahm and Aaron Blair concluded:
NHL is associated with pesticide use, particularly phenoxy
herbicides. Exposure to phenoxy herbicides is widespread in the
agricultural and general populations. The use has increased dramatically
preceding and during the time period in which the incidence of
NHL has increased, which could explain at least part of the rising
Similarly, an 812-page study of herbicide-exposed Vietnam
veterans conducted by the Institute of Medicine offered the following
Evidence is sufficient to conclude that there is positive
association. That is, a positive association has been observed
between herbicides and the outcome [non-Hodgkin's lymphoma] in
studies in which chance, bias, and confounding could be ruled
out with reasonable confidence.
Dogs also acquire lymphoma. One recent study showed that pet
dogs living in households whose lawns were treated wit 2,4-D were
significantly more likely to be diagnosed with canine lymphoma
than dogs whose owners did not use weed killers. Risk rose with
number of applications: the incidence of Iymphoma doubled among
pet dogs whose owners applied lawn chemicals at least four times
From jungle warfare to suburban dandelions: our ongoing war
against plants is now waged on a domestic grid of tiny battlefields.
One in ten single-family American households now uses commercial
lawn care services, and one in five applies the chemicals themselves.
The evidence linking phenoxy compounds to non-Hodgkin's Iymphoma
is preliminary. No one knows exactly how traces of weed killer
find their way into our extracellular fluid as it is funneled
back and forth between blood and Iymph. Absorption through the
skin is considered the most likely route of exposure.