Featured stories in this issue...
Twiddling Our Thumbs as We Turn Our Boys into Girls
Chemicals widely used in toys, cosmetics and pharmaceutical drugs
can interfere with the sexual development of male rodents. In recent
years, studies have began to accumulate showing similar effects on the
sexual development of baby boys. Spokeswomen for the chemical
industry, supported by risk assessors within the U.S. Environmental
Protection Agency, deny there's evidence of harm.
Sick of Poverty: A Broader Vision of Environmental Health
Many, many studies suggest that social exclusion, relative
poverty, and pyramids of status create stresses that have a strongly
harmful influence on health. Thus the "social determinants of
health" is a bridging idea, anchored in science, that could allow
environmentalists to get beyond their single issues and contribute to
a larger social movement for change. The social determinants of
health can connect people concerned about justice, fairness, poverty,
inequality, urban decay, sprawl, shabby housing, rising personal debt,
racism, sexism, mysogyny, homophobia, intolerance, white privilege,
street crime, corporate power, public health, hunger, access to a
decent diet, obesity, lousy schools, depression, suicide, domestic
violence, waste (of all kinds), economic growth, and low-wage jobs
that are boring and stressful -- plus many other aspects of our
culture that make people insecure, unhappy, stressed out and sick.
This is what "environmental health" really means. It's not just about
The Richest Americans Are Getting Richer
Getting rich by owning stock in publicly traded corporations has
gotten easier over the last twenty years. As taxes on income from
stock sales have declined -- so-called 'capital gains' tax rates are
now only 15% -- the few who have wealth to invest in stocks have
More Bad News About Common Household and Lawn-care Pesticides
"The Environmental Protection Agency needs to take a closer look at
pyrethroids" with an eye toward changing how those 22 compounds are
marketed and used, argues Michael J. Lydy, an environmental
toxicologist at Southern Illinois University in Carbondale. Ample and
growing data, he says, challenge "the suggestion that in the
environment, pyrethroids will be innocuous."
From: Rachel's Democracy & Health News #841, Feb. 9, 2006
TWIDDLING OUR THUMBS AS WE TURN OUR BOYS INTO GIRLS
By Peter Montague
[DHN introduction: One of the watershed events of 2005 was a four-part
series on chemicals published in the Wall Street Journal (WSJ),
written by Peter Waldman, a WSJ reporter. The series basically showed
that the U.S. chemical regulation system is utterly broken and is not
much more than a public relations scam. In Rachel's News #839 and
#840 we discussed the first two parts of Mr. Waldman's WSJ series;
here we discuss part 3. In some quotations from WSJ we have added
explanatory links.--DHN Editors]
In part 3 of his series, Peter Waldman begins by offering his mostly
male audience a lesson in reproductive biology:
"In the 12th week of a human pregnancy, the momentous event of gender
formation begins, as X and Y chromosomes trigger biochemical reactions
that shape male or female organs. Estrogens carry the process forward
in girls, while in boys, male hormones called androgens do."
"Phthalate syndrome" in rodents
Mr. Waldman goes on: "Now scientists have indications the process may
be influenced from beyond the womb, raising a fresh debate over
industrial chemicals and safety. In rodent experiments, common
chemicals called phthalates, used in a wide variety of products from
toys to cosmetics to pills, can block the action of fetal androgens.
The result is what scientists call demasculinized effects in male
offspring, ranging from undescended testes at birth to low sperm
counts and benign testicular tumors later in life. 'Phthalate
syndrome,' researchers call it."
In other words, these common chemicals, phthalates -- found in toys,
cosmetics, and pharmaceutical drugs -- can interfere with the
development of male rodents so reliably that there's a name for the
effect: "phthalate syndrome."
Now I don't know about you, but it I were a scientist studying a group
of chemicals commonly found in toys, cosmetics and drugs, and I
discovered that my chemicals could reliably demasculinize male baby
rodents, I'd be asking myself, "Wouldn't it be smart to keep these
chemicals away from human babies?" That would be called a
"precautionary approach" to phthalates -- but this is a noxious idea
to U.S. chemical executives and regulators alike. In the U.S., you've
got to prove harm to a scientific certainty before you are officially
allowed to become concerned about a chemical. And even then the
chemical corporations have the right to drag you into court for a
decade or two while they continue to sell product (because the
corporations are considered legal "persons" and they have arranged for
the burden of proof of harm to rest on the public, not on the
So what kind of evidence do we have about harm from phthalates?
First WSJ tells us that "...last year, federal scientists found gene
alterations in the fetuses of pregnant rats that had been exposed to
extremely low levels of phthalates, levels no higher than the trace
amounts detected in some humans."
OK, so it isn't just high doses that causes problems in rodents.
Next we learn that two studies in 2005 found "direct links" to humans:
"First, a small study found that baby boys whose mothers had the
greatest phthalate exposures while pregnant were much more likely than
other baby boys to have certain demasculinized traits."
And: "...another small study found that 3-month-old boys exposed to
higher levels of phthalates through breast milk produced less
testosterone than baby boys exposed to lower levels of the chemicals."
Testosterone is male sex hormone and it is what turns boys into boys
instead of girls during the 12th week of pregnancy.
"Testicular dysgenesis syndrome" in humans
WSJ goes on to explain that scientists in Europe "have identified what
some see as a human counterpart to rodents' phthalate syndrome, one
they call "testicular dysgenesis syndrome," which they think may be
due in part to exposure to phthalates and other chemicals that
interfere with male sex hormones.
These problems begin while the baby is still in the womb. Richard
Sharpe of the University of Edinburgh in Scotland, a researcher on
male reproduction, told the WSJ, "We know abnormal development of the
fetal testes underlies many of the reproductive disorders we're seeing
in men. We do not know what's causing this, but we do know high doses
of phthalates induce parallel disorders in rats."
Now the chemists who make this stuff have known for a long time that
it leaks into the environment and then gets into people. How could it
not? Phthalates were measured in the Charles and Merrimack Rivers in
Massachusetts in 1973. That same year, a study reported finding
phthalates in environmental samples. That same year, 1973,
researcher reported measuring phthalates in cosmetics. The following
year, 1974, we find an article describing phthalates measured in
food. So it's definitely no surprise that they're in our mothers'
WSJ acknowledges all this:
"It isn't surprising to find traces of phthalates in human blood and
urine, because they are used so widely. Nearly five million metric
tons [11 billion pounds] of phthalates are consumed by industry every
year, 13% in the U.S. They are made from petroleum byproducts and
chemically known as esters, or compounds of organic acid and alcohol.
The common varieties with large molecules are used to plasticize, or
make pliable, otherwise rigid plastics -- such as polyvinyl chloride,
known as PVC -- in things like construction materials, clothing, toys
and furnishings. Small-molecule phthalates are used as solvents and in
adhesives, waxes, inks, cosmetics, insecticides and drugs."
Let's see now. In the U.S. we use 1,430,000,000 (1.43 billion) pounds
of this stuff each year in products that everyone knows will end up in
our homes, then in our bodies, and we know it causes baby boy rats to
start to turn into sickly baby girl rats -- and we don't have the
sense to call a halt? I suppose the Bible had it right: "The love of
money is the root of all evil" -- because the actions of chemists,
corporate executives and risk assessors who allow this to continue
surely qualify as evil by any normal definition.
Marian Stanley of the American Chemistry Council (formerly the
Chemical Manufacturer's Association) told the WSJ that phthalates are
among the most widely studied chemicals and have proved safe for more
than 50 years. So the chemical manufacturers admit they have been
pumping this stuff into the public for 50 years while evidence of harm
has accumulated. You have to appreciate their candor, and marvel at
Government researcher L. Earl Gray told the WSJ that -- even today --
EPA is "moving cautiously" because, "All this work on the effects of
phthalates on the male reproductive system is just five years old."
But wait. Mr. Gray himself published his first studies of the ability
of certain industrial chemicals to interfere with hormones and alter
the development of rodent fetuses at least 25 years ago.
If you go to the government's oldest database on chemicals and health,
known as Pub Med, and type in "phthalates" your retrieve 467
scientific and medical articles going back to 1965.
Back in 1987 -- almost 20 years ago -- U.S. EPA listed one phthalate
(bis(2-ethylhexyl)phthalate) as among the 100 most toxic chemicals
found at Superfund sites.
In 1991, Mr. Gray signed the Wingspread Statement, which was titled,
"Chemically Induced Alterations in Sexual Development: The
Wildlife/Human Connection." Why were phthalates identified as a major
problem in 1987 and then ignored for 15 years? Surely the EPA had
knowledgable staff who must have suspected a problem. Were they
ignored? Silenced? What?
Last summer Mr. Gray told WSJ, "There appears to be clear disruption
of the androgen pathway, but how? What are phthalates doing?"
Who CARES exactly what phthalates are doing? Pregnant moms don't want
the government to sit around while its scientists tease out the
precise mechanism by which phthalates cause undescended testicles,
hypospadias (a malformation of the penis, often requiring surgery),
reduced sperm count, diminished sperm quality, and testicular cancer.
They just want phthalates kept out of their babies. Is this too
difficult for government scientists and corporate spokeswomen to
But here's a breath of fresh air. At least one corporate scientist,
Dr. Rochelle Tyl, a toxicologist, told the WSJ that the broader
question is: "If we know something bad is happening, or we think we
do, do we wait for the data or do we act now to protect people?"
Exactly so. But U.S. EPA and the Chemical Manufacturers Association
both give the same answer: "Definitely, let's wait for something bad
Now I can understand why corporations would want to wait for something
bad to happen -- most companies in the business of making harmful
chemicals also have some fiduciary interest in medical technology, or
in "environmental remediation." Many of them have figured out that
they can get paid to create problems and then get paid again to fix
them. It's that love of money thing again -- it keeps the wheels
turning and the economy growing. But why would government not ask the
same precautionary question that Dr. Tyl asked and answer it in a way
that protects public health? Very mysterious. Perhaps the government
is beholden to the corporations at election time and there is no
longer any such thing as an independent moral agent making decisions
inside the regulatory system. I'm speculating because I don't know.
The Japanese have banned phthalates in certain food-handling
equipment. The Europeans have banned phthalates from cosmetics and
toys. Last summer the European Parliament asked the European
Commission (the regulatory body of the European Union) to review
products "made from plasticised material which may expose people to
risks, especially those used in medical devices." Late last year,
Unilever, Revlon Inc., and L'Oreal SA's American subsidiary -- hounded
wonderfully by the safe cosmetics campaign -- agreed to go along
with whatever the Europeans decide to ban from products. Procter &
Gamble Co. said last year it would no longer use phthalates in nail
polish. It's a start.
Other firms are resisting. Exxon Mobil Corp. and BASF dominate the
$7.3 billion phthalates market. According to WSJ, "An Exxon Mobil
spokeswoman says risk assessments by government agencies in Europe and
the U.S. confirm 'the safety of phthalates in their current
applications.'" Risk assessment is definitely the polluter's most
useful pseudo-scientific tool. As first EPA administrator William
Ruckelshaus said in 1984, "We should remember that risk assessment
data can be like the captured spy: If you torture it long enough, it
will tell you anything you want to know."
Despite these assurances from the polluters' spokeswomen, the WSJ
raises serious concerns about the safety of phthalates: "For instance,
a 2003 study divided 168 male patients at a fertility clinic into
three groups based on levels of phthalate metabolites in their urine.
The study found that men in the highest third for one of the
phthalates were three to five times as likely as those in the lowest
third to have a low sperm count or low sperm activity. Men highest in
a different phthalate also had more abnormally shaped sperm, according
to the study, which was done by researchers at the Harvard School of
Public Health and published in the journal Epidemiology," WSJ reports
And "The latest human study, on 96 baby boys in Denmark and Finland,
found that those fed breast milk containing higher levels of certain
phthalates had less testosterone during their crucial hormonal surge
at three months of age than baby boys exposed to lower levels."
Of course, as you would expect, not all studies of phthalates show
health effects in humans, so industry clings to these "negative"
studies and keeps pumping out the pollutants. Studies that create
doubt about the science allow polluters to continue polluting for
decades -- so there's now a large and growing industrial enterprise
devoted simply to ginning up faulty studies that don't find anything
because they were designed not to, thus creating doubt. No one could
ever accuse the Chemical Manufacturers of missing a trick.
But -- to its credit -- the WSJ keeps offering new evidence:
"A human study of 85 subjects published in June linked fetal exposure
to phthalates to structural differences in the genitalia of baby boys.
"Researchers measured phthalate levels in pregnant women and later
examined their infant and toddler sons. For pregnant women who had the
highest phthalate exposure -- a level equivalent to the top 25% of
such exposure in American women -- baby sons had smaller genitalia, on
average. And their sons were more likely to have incompletely
"Most striking was a difference in the length of the perineum, the
space between the genitalia and anus, which scientists call AGD, for
anogenital distance. In rodents, a shortened perineum in males is
closely correlated with phthalate exposure. A shortened AGD also is
one of the most sensitive markers of demasculinization in animal
studies," WSJ reported.
And: "Males' perineums at birth are usually about twice as long as
those of females, in both humans and laboratory rodents. In this
study, the baby boys of women with the highest phthalate exposures
were 10 times as likely to have a shortened AGD, adjusted for baby
weight, as the sons of women who had the lowest phthalate exposures."
WSJ continued to explore the meaning of this study: "Some
endocrinologists call this the first study to link an industrial
chemical measured in pregnant women to altered reproductive systems in
offspring. 'It is really noteworthy that shortened AGD was seen,' says
Niels Skakkebaek, a reproductive-disorder expert at the University of
Copenhagen, who wasn't an author of the study. 'If it is proven the
environment changed the [physical characteristics] of these babies in
such an anti-androgenic manner, it is very serious.'
Then the WSJ drops a bombshell from the Chemical Manufacturers: "Ms.
Stanley of the American Chemistry Council doubts that any study can
'tease out' the cause of a human health condition, given the wide
variety of chemical exposures in people's lives."
In other words, the Chemical Manufacturers are pumping out 1.43
billion pounds of a chemical that is increasingly linked to sexual
dysfunction, including genital cancer in boys, and they don't believe
there is any way to definitively learn the truth about that chemical
-- or any other chemical -- because the Chemical Manufacturers are
pumping out so many other chemicals!
Think about that. The U.S. regulatory system requires a very high
level of proof of harm before action can be taken to curtail
production of a chemical. And the chemical manufacturers don't believe
science can EVER "tease out the cause of a human health condition"
because we're all exposed to too many industrial poisons
simultaneously. So the Chemical Manufacturers must think they're home
free -- no amount of scientific study can ever trip them up.
And of course the Chemical Manufacturers are right. Science cannot
definitively "tease out" the effects of a single chemical when we are
all exposed to a toxic soup of industrial poisons from the moment of
conception onward. Scientists who insist otherwise are either fooling
themselves, or trying to fool us. No matter how many studies are
done, some uncertainty will always remain -- some variable that wasn't
studied could always confound the results.
The only way to pull back from the edge of this cliff is to alter our
standards of proof, shift the burden onto the polluter to show that
each of his or her products is the least-harmful one available to do
the job -- and take precautionary action by insisting on safer
substitutes for chemicals that seem harmful based on the weight of the
evidence, not waiting for scientific certainty. Insist that every
chemical on the market be accompanied by rigorous and thorough data.
No data? No market.
But of course different people will weigh the evidence differently.
WSJ quotes Dr. Tyl, the chemical-industry toxicologist, saying "her
own rat studies confirm that AGD is very sensitive to phthalates. She
says that in rats that had very high phthalate exposures, a shortened
AGD at birth was closely associated with a number of serious
reproductive disorders later in life. However, in rats exposed to much
lower doses of phthalates, a shortened AGD at birth did not always
lead to later troubles. Many of these rats grew up to breed normally,
she says, despite their slightly altered anatomy."
And, says WSJ, "Dr. Tyl suggests that the same may be true of
humans.... Dr. Tyl theorizes, that the boys with shortened AGD will
grow up normally. 'At what point do changes like this cross the line'
to become dangerous, she asks." And she answers her own question: "We
don't know yet."
OK, we don't know. We may never know. But we can ask 1000 pregnant
moms one question: "Is it OK with you if I pump teensy amounts of a
few dozen industrial poisons into your womb and alter the anatomy of
your baby?" How many women out of a thousand would say, "Yes?"
Maybe a few. Perhaps the wives of chemical company executives would
answer, "Of course!. I love having those industrial chemicals in my
baby. I'm tickled with the idea of Exxon-Mobil and BASF altering my
child's anatomy before birth!" Maybe Marian Stanley (the flak for the
Chemical Manufacturers) and the anyonymous spokeswoman for Exxon Mobil
would say they are happy to have their babies' anatomy altered so
their bosses can continue to consummate their love of money.
But somehow I doubt it.
Return to Table of Contents
From: Scientific American, Dec. 15, 2005
SICK OF POVERTY
By Robert Sapolsky
[DHN introduction: We have added a few explanatory links to the text.
Rudolph Virchow, the 19th-century German neuroscientist, physician
and political activist, came of age with two dramatic events -- a
typhoid out-break in 1847 and the failed revolutions of 1848. Out of
those experiences came two insights for him: first, that the spread of
disease has much to do with appalling living conditions, and second,
that those in power have enormous means to subjugate the powerless. As
Virchow summarized in his famous epigram, "Physicians are the natural
attorneys of the poor."
Physicians (and biomedical scientists) are advocates of the
underprivileged because poverty and poor health tend to go hand in
hand. Poverty means bad or insufficient food, unhealthy living
conditions and endless other factors that lead to illness. Yet it is
not merely that poor people tend to be unhealthy while everyone else
is well. When you examine socio-economic status (SES), a composite
measure that includes income, occupation, education and housing
conditions, it becomes clear that, starting with the wealthiest
stratum of society, every step downward in SES correlates with poorer
This "SES gradient" has been documented throughout Westernized
societies for problems that include respiratory and cardiovascular
diseases, ulcers, rheumatoid disorders, psychiatric diseases and a
number of cancers. It is not a subtle statistical phenomenon. When you
compare the highest versus the lowest rungs of the SES ladder, the
risk of some diseases varies 10-fold. Some countries exhibit a five-
to 10-year difference in life expectancy across the SES spectrum. Of
the Western nations, the U.S. has the steepest gradient; for example,
one study showed that the poorest white males in America die about a
decade earlier than the richest.
So what causes this correlation between SES and health? Lower SES may
give rise to poorer health, but conversely, poorer health could also
give rise to lower SES. After all, chronic illness can compromise
one's education and work productivity, in addition to generating
Nevertheless, the bulk of the facts suggests that the arrow goes from
economic status to health -- that SES at some point in life predicts
health measures later on. Among the many demonstrations of this point
is a remarkable study of elderly American nuns. All had taken their
vows as young adults and had spent many years thereafter sharing diet,
health care and housing, thereby controlling for those lifestyle
factors. Yet in their old age, patterns of disease, incidence of
dementia and longevity were still significantly predicted by their SES
status from when they became nuns, at least half a century before.
So, to use a marvelous phrase common to this field, how does SES get
"under the skin" and influence health? The answers that seem most
obvious, it turns out, do not hold much water. One such explanation,
for instance, posits that for the poor, health care may be less easily
accessible and of lower quality. This possibility is plausible when
one considers that for many of the poor in America, the family
physician does not exist, and medical care consists solely of trips to
the emergency room.
But that explanation soon falls by the wayside, for reasons made
clearest in the famed Whitehall studies by Michael G. Marmot of
University College London over the past three decades. Marmot and his
colleagues have documented an array of dramatic SES gradients in a
conveniently stratified population, namely, the members of the British
civil service (ranging from blue-collar workers to high-powered
executives). Office messengers and porters, for example, have far
higher mortality rates from chronic heart disease than administrators
and professionals do. Lack of access to medical attention cannot
explain the phenomenon, because the U.K., unlike the U.S., has
universal health care. Similar SES gradients also occur in other
countries with socialized medicine, including the health care Edens of
Scandinavia, and the differences remain significant even after
researchers factor in how much the subjects actually use the medical
Another telling finding is that SES gradients exist for diseases for
which health care access is irrelevant. No amount of medical checkups,
blood tests and scans will change the likelihood of someone getting
type 1 (juvenile-onset) diabetes or rheumatoid arthritis, yet both
conditions are more common among the poor.
The next "obvious" explanation centers on unhealthy life-styles. As
you descend the SES ladder in Westernized societies, people are more
likely to smoke, to drink excessively, to be obese, and to live in a
violent or polluted or densely populated neighborhood. Poor people are
also less likely to have access to clean water, healthy food and
health clubs, not to mention adequate heat in the winter and air-
conditioning in the summer. Thus, it seems self-evident that lower SES
gets under the skin by increasing risks and decreasing protective
factors. As mordantly stated by Robert G. Evans of the University of
British Columbia, "Drinking sewage is probably unwise, even for Bill
What is surprising, though, is how little of the SES gradient these
risk and protective factors explain. In the Whitehall studies,
controlling for factors such as smoking and level of exercise
accounted for only about a third of the gradient. This same point is
made by studies comparing health and wealth among, rather than within,
nations. It is reasonable to assume that the wealthier a country, the
more financial resources its citizens have to buy protection and avoid
risk. If so, health should improve incrementally as one moves up the
wealth gradient among nations, as well as among the citizens within
individual nations. But it does not. Instead, among the wealthiest
quarter of countries on earth, there is no relation between a
country's wealth and the health of its people.
Thus, health care access, health care utilization, and exposure to
risk and protective factors explain the SES/health gradient far less
well than one might have guessed. One must therefore consider whether
most of the gradient arises from a different set of considerations:
the psychosocial consequences of SES.
Sidebar: Overview: Status and Health
Researchers have long known that people with low socioeconomic status
(SES) have dramatically higher disease risks and shorter life spans
than do people in the wealthier strata of society. The conventional
explanations that the poor have less access to health care and a
greater incidence of harmful lifestyles such as smoking and obesity
cannot account for the huge discrepancy in health outcomes.
** New studies indicate that the psychosocial stresses associated
with poverty may increase the risks of many illnesses. The chronic
stress induced by living in a poor, violent neighborhood, for example,
could increase one's susceptibility to cardiovascular disease,
depression and diabetes.
** Other studies have shown a correlation between income inequality
and poor health in the U.S. Some researchers believe that the poor
feel poorer, and hence suffer greater stress, in communities with wide
gaps between the highest and lowest incomes.
Ideally, the body is in homeostatic balance, a state in which the
vital measures of human function heart rate, blood pressure, blood
sugar levels and so on are in their optimal ranges. A stressor is
anything that threatens to disrupt homeostasis. For most organisms, a
stressor is an acute physical challenge for example, the need for an
injured gazelle to sprint for its life or for a hungry predator to
chase down a meal. The body is superbly adapted to dealing with short-
term physical challenges to homeostasis. Stores of energy, including
the sugar glucose, are released, and cardiovascular tone increases to
facilitate the delivery of fuel to exercising muscle throughout the
body. Digestion, growth, tissue repair, reproduction and other
physiological processes not needed to survive the crisis are
suppressed. The immune system steps up to thwart opportunistic
pathogens. Memory and the senses transiently sharpen.
But cognitively and socially sophisticated species, such as we
primates, routinely inhabit a different realm of stress. For us, most
stressors concern interactions with our own species, and few
physically disrupt homeostasis. Instead these psycho- social stressors
involve the anticipation (accurate or otherwise) of an impending
challenge. And the striking characteristic of such psychological and
social stress is its chronicity. For most mammals, a stressor lasts
only a few minutes. In contrast, we humans can worry chronically over
a 30-year mortgage.
Unfortunately, our body's response, though adaptive for an acute
physical stressor, is pathogenic for prolonged psychosocial stress.
Chronic increase in cardiovascular tone brings stress-induced
hypertension. The constant mobilization of energy increases the risk
or severity of diseases such as type 2 (adult-onset) diabetes. The
prolonged inhibition of digestion, growth, tissue repair and
reproduction increases the risks of various gastrointestinal
disorders, impaired growth in children, failure to ovulate in females
and erectile dysfunction in males. A too-extended immune stress
response ultimately suppresses immunity and impairs disease defenses.
And chronic activation of the stress response impairs cognition, as
well as the health, functioning and even survival of some types of
An extensive biomedical literature has established that individuals
are more likely to activate a stress response and are more at risk for
a stress-sensitive disease if they (a) feel as if they have minimal
control over stressors, (b) feel as if they have no predictive
information about the duration and intensity of the stressor, (c) have
few outlets for the frustration caused by the stressor, (d) interpret
the stressor as evidence of circumstances worsening, and (e) lack
social support for the duress caused by the stressors.
Sidebar: Chronic Stress
CHRONIC STRESS may explain how poverty "gets under the skin" and
exerts a harmful influence on health. The risk of stress-sensitive
diseases increases if individuals lack social support, have no outlets
for their frustration and feel that their circumstances are worsening
exactly the conditions in many poor communities in the U.S.
Psychosocial stressors are not evenly distributed across society. Just
as the poor have a disproportionate share of physical stressors
(hunger, manual labor, chronic sleep deprivation with a second job,
the bad mattress that can't be replaced), they have a disproportionate
share of psychosocial ones. Numbing assembly-line work and an
occupational lifetime spent taking orders erode workers' sense of
control. Unreliable cars that may not start in the morning and
paychecks that may not last the month inflict unpredictability.
Poverty rarely allows stress-relieving options such as health club
memberships, costly but relaxing hobbies, or sabbaticals for
rethinking one's priorities. And despite the heartwarming stereotype
of the "poor but loving community," the working poor typically have
less social support than the middle and upper classes, thanks to the
extra jobs, the long commutes on public transit, and other burdens.
Marmot has shown that regardless of SES, the less autonomy one has at
work, the worse one's cardiovascular health. Furthermore, low control
in the workplace accounts for about half the SES gradient in
cardiovascular disease in his Whitehall population.
Three lines of research provide more support for the influence of
psychological stress on SES-related health gradients. Over the past
decade Nancy E. Adler of the University of California, San Francisco,
has explored the difference between objective and subjective SES and
the relation of each to health. Test subjects were shown a simple
diagram of a ladder with 10 rungs and then asked, "In society, where
on this ladder would you rank yourself in terms of how well you're
doing?" The very openness of the question allowed the person to define
the comparison group that felt most emotionally salient.
As Adler has shown, a person's subjective assessment of his or her SES
takes into account the usual objective measures (education, income,
occupation and residence) as well as measures of life satisfaction and
of anxiety about the future. Adler's provocative finding is that
subjective SES is at least as good as objective SES at predicting
patterns of cardiovascular function, measures of metabolism,
incidences of obesity and levels of stress hormones -- suggesting that
the subjective feelings may help explain the objective results.
Sidebar: The Good and Bad Effects of Stress
The human body is superb at responding to the acute stress of a
physical challenge, such as chasing down prey or escaping a predator.
The circulatory, nervous and immune systems are mobilized while the
digestive and reproductive processes are suppressed. If the stress
becomes chronic, though, the continual repetition of these responses
can cause major damage.
** Acute stress: Brain
Increased alertness and less perception of pain
** Chronic stress: Brain
Impaired memory and increased risk of depression
** Acute stress: Thymus Gland and Other Immune Tissues
Immune system readied for possible injury
** Chronic stress: Thymus Gland and Other Immune Tissues
** Acute stress: Circulatory System
Heart beats faster, and blood vessels constrict to bring more oxygen
** Chronic stress: Circulatory System
Elevated blood pressure and higher risk of cardiovascular disease
** Acute stress: Adrenal Glands
Secrete hormones that mobilize energy supplies
** Chronic stress: Adrenal Glands
High hormone levels slow recovery from acute stress
** Acute stress: Reproductive Organs
Reproductive functions are temporarily suppressed
** Chronic stress: Reproductive Organs
Higher risks of infertility and miscarriage
This same point emerges from comparisons of the SES/health gradient
among nations. A relatively poor person in the U.S. may objectively
have more financial resources to purchase health care and protective
factors than a relatively wealthy person in a less developed country
yet, on average, will still have a shorter life expectancy. For
example, as Stephen Bezruchka of the University of Washington
emphasizes, people in Greece on average earn half the income of
Americans yet have a longer life expectancy. Once the minimal
resources are available to sustain a basic level of health through
adequate food and housing, absolute levels of income are of remarkably
little importance to health. Although Adler's work suggests that the
objective state of being poor adversely affects health, at the core of
that result is the subjective state of feeling poor.
Being Made to Feel Poor
Another body of research arguing that psychosocial factors mediate
most of the SES/health gradient comes from Richard Wilkinson of the
University of Nottingham in England. Over the past 15 years he and his
colleagues have reported that the extent of income inequality in a
community is even more predictive than SES for an array of health
measures. In other words, absolute levels of income aside, greater
disparities in income between the poorest and the wealthiest in a
community predict worse average health. (David H. Abbott of the
Wisconsin National Primate Research Center and I, along with our
colleagues, found a roughly equivalent phenomenon in animals: among
many nonhuman primate species, less egalitarian social structures
correlate with higher resting levels of a key stress hormone an index
for worse health among socially subordinate animals.)
Sidebar: The surest way to feel poor
The surest way to feel poor is to be endlessly made aware of the haves
when you are a have-not.
Wilkinson's subtle and critical finding has generated considerable
controversy. One dispute concerns its generality. His original work
suggested that income inequality was relevant to health in many
European and North American countries and communities. It has become
clear, however, that this relation holds only in the developed country
with the greatest of income inequalities, namely, the U.S.
Whether considered at the level of cities or states, income inequality
predicts mortality rates across nearly all ages in the U.S.. Why,
though, is this relation not observed in, say, Canada or Denmark? One
possibility is that these countries have too little income variability
to tease out the correlation.
Some critics have questioned whether the linkage between income
inequality and worse health is merely a mathematical quirk. The
relation between SES and health follows an asymptotic curve: dropping
from the uppermost rung of society's ladder to the next-to-top step
reduces life expectancy and other measures much less drastically than
plunging from the next-to-bottom rung to the lowest level. Because a
community with high levels of income inequality will have a relatively
high number of individuals at the very bottom, where health prospects
are so dismal, the community's average life expectancy will inevitably
be lower than that of an egalitarian community, for reasons that have
nothing to do with psychosocial factors. Wilkinson has shown, however,
that decreased income inequality predicts better health for both the
poor and the wealthy. This result strongly indicates that the
association between illness and inequality is more than just a
Wilkinson and others in the field have long argued that the more
unequal income in a community is, the more psychosocial stress there
will be for the poor. Higher income inequality intensifies a
community's hierarchy and makes social support less available: truly
symmetrical, reciprocal, affiliative support exists only among equals.
Moreover, having your nose rubbed in your poverty is likely to lessen
your sense of control in life, to aggravate the frustrations of
poverty and to intensify the sense of life worsening.
If Adler's work demonstrates the adverse health effects of feeling
poor, Wilkinson's income inequality work suggests that the surest way
to feel poor is to be made to feel poor to be endlessly made aware of
the haves when you are a have-not. And in our global village, we are
constantly made aware of the moguls and celebrities whose resources
John W. Lynch and George A. Kaplan of the University of Michigan at
Ann Arbor have recently proposed another way that people are made to
feel poor. Their "neomaterialist" interpretation of the income
inequality phenomenon which is subtle, reasonable and, ultimately,
deeply depressing runs as follows: Spending money on public goods
(better public transit, universal health care and so on) is a way to
improve the quality of life for the average person. But by definition,
the bigger the income inequality in a society, the greater the
financial distance between the average and the wealthy. The bigger
this distance, the less the wealthy have to gain from expenditures on
the public good. Instead they would benefit more from keeping their
tax money to spend on their private good a better chauffeur, a gated
community, bottled water, private schools, private health insurance.
So the more unequal the income is in a community, the more incentive
the wealthy will have to oppose public expenditures benefiting the
health of the community. And within the U.S., the more income
inequality there is, the more power will be disproportionately in the
hands of the wealthy to oppose such public expenditures. According to
health economist Evans, this scenario ultimately leads to "private
affluence and public squalor."
This "secession of the wealthy" can worsen the SES/health gradient in
two ways: by aggravating the conditions in low- income communities
(which account for at least part of the increased health risks for the
poor) and by adding to the psychosocial stressors. If social and
psychological stressors are entwined with feeling poor, and even more
so with feeling poor while being confronted with the wealthy, they
will be even more stressful when the wealthy are striving to decrease
the goods and services available to the poor.
A third branch of support for psychosocial explanations for the
relation between income inequality and health comes from the work of
Ichiro Kawachi of Harvard University, based on the concept of "social
capital." Although it is still being refined as a measure, social
capital refers to the broad levels of trust and efficacy in a
community. Do people generally trust one another and help one another
out? Do people feel an incentive to take care of commonly held
resources (for example, to clean up graffiti in public parks)? And do
people feel that their organizations such as unions or tenant
associations actually have an impact? Most studies of social capital
employ two simple measures, namely, how many organizations people
belong to and how people answer a question such as, "Do you think most
people would try to take advantage of you if they got a chance?"
What Kawachi and others have shown is that at the levels of states,
provinces, cities and neighborhoods, low social capital predicts bad
health, bad self-reported health and high mortality rates. Using a
complex statistical technique called path analysis, Kawachi has
demonstrated that (once one controls for the effects of absolute
income) the strongest route from income inequality to poor health is
through the social capital measures to wit, high degrees of income
inequality come with low levels of trust and support, which increases
stress and harms health.
None of this is surprising. As a culture, America has neglected its
social safety nets while making it easier for the most successful to
sit atop the pyramids of inequality. More- over, we have chosen to
forgo the social capital that comes from small, stable communities in
exchange for unprecedented opportunities for mobility and anonymity.
As a result, all measures of social epidemiology are worsening in the
U.S. Of Westernized nations, America has the greatest income
inequality (40 percent of the wealth is controlled by 1 percent of the
population) and the greatest discrepancy between expenditures on
health care (number one in the world) and life expectancy (as of 2003,
The importance of psychosocial factors in explaining the SES/health
gradient generates a critical conclusion: when it comes to health,
there is far more to poverty than simply not having enough money. (As
Evans once stated, "Most graduate students have had the experience of
having very little money, but not of poverty. They are very different
things.") The psychosocial school has occasionally been accused of
promulgating an antiprogressive message: don't bother with universal
health care, affordable medicines and other salutary measures because
there will still be a robust SES/health gradient after all the
reforms. But the lesson of this research is not to abandon such
societal change. It is that so much more is needed.
Wilkinson, Richard. Mind the Gap: Hierarchies, Health and Human
Evolution. London, UK: Weidenfeld and Nicolson, 2000.
Kawachi, Ichiro and Bruce P. Kennedy, The Health of Nations: Why
Inequality Is Harmful to Your Health. New York: New Press, 2002.
Marmot, Michael. The Status Syndrome. New York: Henry Holt and
Sapolsky, Robert. Why Zebras Don't Get Ulcers: A Guide to Stress,
Stress-Related Diseases and Coping. Third edition. New York: Henry
Holt and Company, 2004.
Robert Sapolsky is professor of biological sciences, neurology and
neurological sciences at Stanford University and a research associate
at the National Museums of Kenya. In his laboratory work, he focuses
on how stress can damage the brain and on gene therapy for the nervous
system. In addition, he studies populations of wild baboons in East
Africa, trying to determine the relation between the social rank of a
baboon and its health. His latest book is Monkeyluv and Other Essays
on Our Lives as Animals (Scribner, 2005).
Return to Table of Contents
From: Mercury News (San Jose, Calif.), Jan. 29, 2006
CORPORATE WEALTH SHARE RISES FOR TOP-INCOME AMERICANS
By David Cay Johnston
New government data indicate that the concentration of corporate
wealth among the highest-income Americans grew significantly in 2003,
as a trend that began in 1991 accelerated in the first year that
President Bush and Congress cut taxes on capital.
In 2003 the top 1 percent of households owned 57.5 percent of
corporate wealth, up from 53.4 percent the year before, according to a
Congressional Budget Office analysis of the latest income tax data.
The top group's share of corporate wealth has grown by half since
1991, when it was 38.7 percent.
In 2003, incomes in the top 1 percent of households ranged from
$237,000 to several billion dollars.
For every group below the top 1 percent, shares of corporate wealth
have declined since 1991. These declines ranged from 12.7 percent for
those on the 96th to 99th rungs on the income ladder to 57 percent for
the poorest fifth of Americans, who made less than $16,300 and
together owned 0.6 percent of corporate wealth in 2003, down from 1.4
percent in 1991.
The analysis did not measure wealth directly. It looked at taxes on
capital gains, dividends, interest and rents. Income from securities
owned by retirement plans and endowments was excluded, as were gains
from noncorporate assets such as personal residences.
This technique for measuring wealth has long been used in standard
economic studies, though critics have challenged that tradition.
Among them is Stephen J. Entin, president of the Institute for
Research on the Economics of Taxation in Washington, which favors
eliminating most taxes on capital and teaches that an unintended
consequence of the corporate income tax is depressed wage rates. Mr.
Entin said the report's approach was so flawed that the data were
He said reduced tax rates on long-term capital gains may have prompted
wealthy investors to sell profitable investments. That would show up
in tax data as increased wealth that year, even though the increase
may have built up over decades.
Long-term capital gains were taxed at 28 percent until 1997, and at 20
percent until 2003, when rates were cut to 15 percent. The top rate on
dividends was cut to 15 percent from 35 percent that year.
The White House said it did not believe that the 2003 tax cuts had
much influence on wealth shares. It also said that since wealth is
transitory for many people, a more important issue is how incomes and
wealth are influenced by the quality of education.
''We want to lift all incomes and wealth,'' said Trent Duffy, a White
House spokesman. ''We are starting to see that the income gap is
largely an education gap.''
''The president thinks we need to close the income gap, and he has
talked about ways in which we can do that,'' especially through
education, Mr. Duffy said.
The data showing increased concentration of corporate wealth were
posted last month on the Congressional Budget Office Web site. Isaac
Shapiro, associate director of the Center on Budget and Policy
Priorities in Washington, spotted the information last week and wrote
a report analyzing it.
Mr. Shapiro said the figures added to the center's ''concerns over the
increasingly regressive effects'' of the reduced tax rates on capital.
Continuing those rates will ''exacerbate the long-term trend toward
growing income inequality,'' he wrote.
The center, which studies how government affects the poor and supports
policies that it believes help alleviate poverty, opposes Mr. Bush's
The center plans to release its own report on Monday that questions
the wisdom of continuing the reduced tax rates on dividends and
capital gains, saying the Congressional Budget Office analysis
indicates that the benefits flow directly to a relatively few
Return to Table of Contents
From: Science News (Vol. 169, No. 5, pg. 74), Feb. 5, 2006
A LITTLE LESS GREEN?
HN Are Pyrethroid Insecticides Dangerous?
Studies challenge the benign image of pyrethroid insecticides
By Janet Raloff
Rachel Carson turned the pest-control world upside down in 1962. In
Silent Spring, she documented how long-lived organochlorine
pesticides, most notoriously DDT, were not only ridding croplands of
insects, streets of mosquitoes, and homes of spiders but also exacting
a high toll on songbirds and other nontargeted species. The chemicals'
broad-spectrum potency and resistance to breakdown, advantages in
their use against pests, emerged as hazards.
Shortly after the publication of Carson's book, industrialized
countries began phasing out such persistent organic pollutants, or
POPs. There's now a United Nations treaty aiming at their global
elimination (SN: 11/8/03, p. 301: Available to subscribers at
In the wake of organochlorine pesticides came organophosphate agents.
Although these agents are highly effective, their toxicity to
nontarget animals -- including people -- echoed the perils of DDT.
Regulators responded, and by the middle 1990s, once-popular members of
this class of agents -- such as dursban, malathion, and chlorpyrifos
-- were being phased out or severely restricted in their uses.
In recent years, farmers and others have increasingly turned to
products based on pyrethrins, chemicals made by certain members of the
chrysanthemum family. Farmers in various parts of the world have for
millennia used preparations from these flowers to protect crops from
insects. Since the 1960s, manufacturers have produced synthetic
analogs -- called pyrethroids -- of the herbal products' active
Although pyrethroids have greater toxicity to insects and somewhat
more resistance to breakdown than their natural counterparts do,
studies have demonstrated that these synthetic chemicals pose little
risk to most vertebrates, from songbirds to people.
Pyrethroids stand poised to overtake organophosphate insecticides for
farm use and are already the leading insecticides sold to homeowners.
However, emerging data show that even pyrethroids can pose serious
environmental hazards. At concentrations found in streams, the
chemicals can kill beneficial insects and crustaceans and may even be
acting -- below the radar screen -- to poison fish and lizards.
Most of these findings came to light in some dozen presentations in
Baltimore last November at the Society of Environmental Toxicology and
Chemistry (SETAC) annual meeting. The research described there
suggests that, at least where the mum-based pesticides might enter
streams, these compounds should be used sparingly.
"The Environmental Protection Agency needs to take a closer look at
pyrethroids" with an eye toward changing how the 22 such compounds
that it has registered are marketed and used, argues Michael J. Lydy,
an environmental toxicologist at Southern Illinois University in
Carbondale. Ample and growing data, he says, challenge "the suggestion
that in the environment, pyrethroids will be innocuous."
"Walk down the pesticide aisle of your local hardware store and read
the active ingredients in insecticides. Nearly every one ends in
'thrin,'" a dead giveaway that it is a pyrethroid, observes Donald P.
Weston, an environmental toxicologist at the University of California,
Berkeley. Only a few pyrethroids -- most notably esfenvalerate -- lack
Although many of these compounds have been used for decades,
especially on farms, "no one had looked for them in the environment,"
Weston notes. In the past few years, he and his colleagues launched
several surveys to check whether pyrethroids were causing harm in
streams. Because these pesticides don't readily dissolve, but instead
glom on to particles and quickly settle out of water, his team focused
its analyses on sediments.
Their findings proved eye-opening, Weston told Science News.
In one study of creeks adjacent to farmlands across a 10-county area
in California's Central Valley, researchers looked for five
pyrethroids and found one or more in at least three-quarters of the 70
The researchers then tested two stream dwellers: the amphipod Hyalella
azteca, which is a small, shrimplike crustacean, and a larval midge of
the species Chironomus tentans. Ecologists use these tiny "lab rats of
the sediment-testing world" for toxicity assessments, Weston explains.
At 42 percent of the sampled sites, the sediment proved deadly to at
least one of two species, his group reported 2 years ago.
In a follow-up study, the scientists spiked sediment samples from
clean sites with six common pyrethroids to compare their toxic effects
on H. azteca. They measured each compound's LC50 -- the concentration
lethal to 50 percent of animals exposed in a test.
In the April 2005 Environmental Toxicology and Chemistry (ET&C), the
team reported that permethrin's LC50 was 60 to 110 parts per billion
(ppb), depending on how much organic carbon the sediment contained.
The LC50 for the remaining pyrethroids was far lower, indicating
greater toxicity. The most toxic: lambda-cyhalothrin and bifenthrin,
which have an LC50 of 2 to 6 ppb.
The crustaceans' growth was significantly retarded at concentrations
just one-third of a pyrethroid's LC50.
Lawn pollution Farm runoff isn't the only -- or perhaps even the most
important -- way in which these agents get into streams. Weston and
his Berkeley colleague Erin L. Amweg reported data at the SETAC
meeting showing that pyrethroids are washed into waterways from
suburban yards by rain and lawn watering.
RUNAWAY RUNOFF. Lawn-watering runoff at this home in Roseville,
Calif., illustrates how pyrethroids used on the yard would be washed
into storm drains, which are a direct conduit to neighborhood streams.
In one recent study, Weston, Lydy, and others surveyed streams in
Roseville, a suburb of Sacramento, Calif. Only a decade earlier, land
along these creeks had been arid grassland. Since then, much of it has
been converted to subdivisions sporting four homes per acre, most with
Roughly 90 percent of the stream sediments sampled contained
bifenthrin, and the majority of them had bifenthrin concentrations
toxic to Hyalella, the scientists report in the Dec. 15, 2005,
Environmental Science & Technology. Often, one to five more
pyrethroids were present.
In contrast, the pesticides didn't show up in waters draining
Roseville sites free of residential development.
In toxicity, bifenthrin dominated the suburban sediments. Indeed, Lydy
told Science News, "80 percent of our samples had enough toxicity due
to bifenthrin alone to cause at least half of our [amphipods] to die."
The team recorded pesticide concentrations as high as 437 ppb—that's
about 100 times as great as its LC50 for H. azteca and 15 times the
highest bifenthrin concentration seen in sediments of creeks running
through Central Valley croplands.
This indicates, Weston says, that the highest concentrations of
pyrethroids in creek sediments trace to "classic suburbia -- we're
talking Mom, Dad, two kids, and a dog."
Although pesticides applied by professional exterminators around the
perimeters of homes are a possible source of the creek contamination,
the research group strongly suspects that much of the bifenthrin comes
from lawn-care products. Some fertilizers even include bifenthrin, so
that homeowners can feed their grass and kill bugs in one pass.
In the Roseville study, the pesticides didn't appear to travel far
once they reached a creek, with the high concentrations appearing only
within 100 yards or so of storm-drain outfalls.
What's not clear, Weston and others observe, is whether the California
data reflect what's occurring nationally or might instead represent a
worst-case scenario. For instance, Amweg presented data at the SETAC
meeting indicating that creeks near Sacramento and San Francisco
showed substantial sediment contamination but streams in Nashville
The California sites, unlike Nashville, get little summer rainfall to
dilute stream pollutants. Moreover, many of California's urban areas
rely on concrete storm drains to channel lawn runoff directly into
streams, whereas the Nashville sites were separated from waterways by
a corridor of greenery.
Too excited Joel R. Coats of Iowa State University in Ames and his
colleagues have been probing why pyrethroids "are as nasty as DDT [is]
to a lot of aquatic life -- including fish."
HOW NEAT? Aquatic caddis fly nymphs build protective cases from plant
debris. Ordinarily, a nymph cuts and stacks materials, log-cabin
style, into an orderly, well-aerated covering (top inset). Pyrethroid-
exposed nymphs, however, make chaotically structured dwellings from
uncut parts (bottom inset) or forgo such protection altogether.
Pyrethroids poison pests by wreaking havoc on their nervous systems,
as most insecticides do. When nerves transmit an impulse, Coats
explains, "there's an electrical ripple that's triggered by sodium
gates in [each cell] opening in sequence." Pyrethroids perturb the
nerve cells' sodium gates, however, so that once open, they never
fully close, Coats says. The resulting sodium leaks maintain nerve
cells in a state of overexcitation that kills the insects.
Because the nervous systems of crustaceans and many other soft-bodied
aquatic animals resemble those of insects, these nontargeted animals
are also vulnerable to pyrethroids.
Coats observes that mammals and birds gain some protection from
pyrethroid poisoning by two mechanisms: production of esterase enzymes
that inactivate the poisons by splitting them in half, and another
metabolic process that employs oxidation. He reported at the SETAC
meeting that although rainbow trout, bluegill, and fathead minnows can
all oxidize pyrethroids, their esterase enzyme activity doesn't break
apart the pesticides.
Although these pesticides may induce ill effects that fall short of
lethality, toxicologists have generally been forced to focus on their
deadliness, Weston says, because fatal concentrations tend to be at or
near the minimum value at which current technology can detect the
pesticides. If the pesticides cause sickness, therefore, it's likely
to happen at concentrations too low to measure, he says. To get around
this difficulty, some scientists have added minute amounts of the
compounds to tanks of water containing aquatic animals.
At Oregon State University (OSU) in Corvallis, Katherine R. Johnson
and her colleagues administered esfenvalerate to aquatic nymphs of the
caddis fly (Brachycentrus americanus) -- an insect eaten by many fish.
For protection from predators, these nymphs enshroud themselves in
hard cases. As the OSU researchers increased pyrethroid concentrations
above 0.05 ppb, formerly resting animals began fleeing their cases in
increasing numbers, notes coauthor Jeffrey J. Jenkins. Among nymphs
that fled, three-quarters of those exposed to as little as 0.2 ppb
esfenvalerate didn't rebuild their cases. Rebuilt cases were
disordered and much weaker than the originals, the scientists reported
at the SETAC meeting.
Conditional toxicity Environmental stressors can sabotage pesticide-
detoxification systems, even in animals that would otherwise withstand
the chemicals, notes Larry G. Talent. At Oklahoma State University in
Stillwater, he studied adult green anole lizards (Anolis
carolinensis), 6 to 8 inches long, exposed to a pyrethroid product
used to treat birds for mites and lice.
When he doused the lizards with a solution of the pesticide and then
maintained the reptiles at a comfortable 95°F, none died. However, 70
percent of treated lizards died within 2 days when they were instead
housed at a cool 68°F. Without pesticide exposure, the lizards showed
no mortality at the lower temperature, Talent reports in the December
Low temperatures, which might mimic night or winter environments, pose
a double whammy for pyrethroid effects: Not only is the lizard's
nervous system more vulnerable to poisoning but its metabolic
breakdown of pollutants also slows.
Mark A. Clifford last year reported a similar synergy between two
environmental stressors—pyrethroid exposure and a viral infection --
in young salmon. The University of California, Davis fish pathologist
exposed 2-month-old chinook salmon for 4 days to either esfenvalerate
or chlorpyrifos, an organophosphate pesticide. He then seeded some of
the aquariums holding the fish with infectious hematopoietic necrosis
virus, which can kill juveniles.
Fish exposed to low doses of the virus survived, as did those exposed
to either pesticide alone, Clifford's team reported in the July 2005
ET&C. Deaths occurred only in fish exposed to high concentrations of
the virus or to both the pyrethroid and virus. Within 3 days of being
exposed to either dose of virus, roughly 70 percent of the pesticide-
exposed salmon fry were dead.
The pyrethroid's impact "was totally unexpected," Clifford says. Two
follow-up trials confirmed that the initial observation was not a
Winds of change? EPA considers new data when it periodically reviews
its approvals of pesticides registered before 1984. Reevaluations for
permethrin, resmethrin, and cypermethrin are slated for completion
this year, and three other pyrethroids are to be reviewed by 2008.
Because bifenthrin was registered in late 1985, it's not scheduled for
such a reevaluation. In a statement to Science News, however, EPA's
Office of Pesticide Programs (OPP) notes that this pesticide's
manifestation of "certain toxic properties at the level of detection
[makes it] challenging for the agency to determine whether risks from
the use of this pesticide are acceptable."
In fact, the statement says, to better understand pyrethroids'
toxicity and bioavailability to nontarget organisms, OPP is "reviewing
the sediment toxicity studies on bifenthrin, cypermethrin, cyfluthrin,
and esfenvalerate that were recently submitted [by Weston's group and
others]." These pesticides were chosen as "surrogates," the statement
says, for assessing the exposures and toxicity of other pyrethroids.
Indeed, OPP notes, despite their use on some 50 agricultural crops,
some pyrethroids have only "conditional" approval from EPA, pending
future evaluation of their sediment toxicity and of the value of
buffer zones in keeping treated areas from tainting streams.
OPP says that it anticipates completing a "comparative assessment for
pyrethroids" by December.
Pyrethroid manufacturers are already bracing for change.
Jim Fitzwater, a spokesman for bifenthrin-maker FMC Corp. of
Philadelphia, says that homeowners need to be educated about how and
when to apply lawn-care products containing pyrethroids. He notes that
his company sells to consumer-products companies rather than consumers
and says, "We're looking at working with [these] end-use manufacturers
to do a better stewardship job."
2005. Pyrethroid pesticides found at toxic levels in California urban
streams. University of California, Berkeley press release. Oct. 25.
2004. Sediments in many Central Valley streams contain toxic levels of
pyrethroid pesticides. University of California, Berkeley press
release. May 6. Available here.
Amweg., E.L., D.P. Weston, J. You, and M.J. Lydy. In press. Pyrethroid
insecticides and sediment toxicity in urban creeks from California and
Tennessee. Environmental Science & Technology.
Abstract available here.
Amweg, E.L., and J. You. 2005. Pyrethroid pesticide distribution and
toxicity in urban creeks. SETAC North America 26th Annual Meeting.
Nov. 13-17. Baltimore. Abstract.
Amweg, E.L., D.P. Weston, and N.M. Ureda. 2005. Use and toxicity of
pyrethroid pesticides in the Central Valley, California, USA.
Environmental Toxicology and Chemistry 24(April):966-972. Abstract
Clifford, M.A., et al. 2005. Synergistic effects of esfenvalerate and
infectious hematopoietic necrosis virus on juvenile chinook salmon
mortality. Environmental Toxicology and Chemistry 24(July):1766-1772.
Abstract available here.
Coats, J.R. 2005. Toxicology of synthetic pyrethroids to fish. SETAC
North America 26th Annual Meeting. Nov. 13-17. Baltimore. Abstract.
DeLorenzo, M.E., et al. 2005. Toxicity of the pyrethroid insecticide
permethrin to adult and larval grass shrimp (Palaemonetes pugio).
SETAC North America 26th Annual Meeting. Nov. 13-17. Baltimore.
Johnson, K.R., J.J. Jenkins, and P.C. Jepson. 2005. Exposure to
esfenvalerate induces case-leaving in the caddisfly Brachycentrus
americanus. SETAC North America 26th Annual Meeting. Nov. 13-17.
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agricultural or urban pyrethroid usage to toxicity in California
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Talent, L.G. 2005. Effect of temperature on toxicity of a natural
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Abstract available here.
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Weston, D.P., R.W. Holmes, and T. English. 2005. A tale of two creeks:
an intensive study of pyrethroids and related toxicity in urban
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SETAC North America 26th Annual Meeting. Nov. 13-17. Baltimore.
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Erin L. Amweg University of California, Berkeley Building 102-RFS
Berkeley, CA 94720-3140
Mark Clifford Fish Health Laboratory Medicine and Epidemiology
University of California, Davis Davis, CA 95616
Joel R. Coats Iowa State University Department of Entomology Ames, IA
Jim Fitzwater FMC Corporation 1735 Market Street Philadelphia, PA
Jeffrey J. Jenkins Department of Molecular Toxicology Oregon State
University 1007 Ag and Life Science Building Corvallis, OR 97331-7301
Katherine R. Johnson Department of Environmental and Molecular
Toxicology 1007 ALS Building Corvallis, OR 97331-7301
Michael J. Lydy Department of Zoology Southern Illinois University
Carbondale, IL 62901-6501
Mah Shamin Environmental Risk Branch 5 Environmental Fate & Effects
Division 1200 Pennsylvania Avenue, N.W. Washington, DC 20460
Society of Environmental Toxicology and Chemistry 1010 North 12th
Avenue Pensacola, FL 32501-3368
Donald P. Weston University of California, Berkeley Building 102-RFS
Berkeley, CA 94720-3140
From Science News, Vol. 169, No. 5, Feb. 4, 2006, p. 74.
Copyright 2006 Science Service.
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