Rachel's News #841: Turning Boys into Girls?

February 10, 2006

rachel

Fri, 10 Feb 2006 00:40:23 -0500

..

Are you coming to the Precaution Academy in New Jersey

Mar. 31-Apr.2? Let us know. Space is very limited. Time

is short. But you can still apply for a scholarship to attend free.

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Rachel's Democracy & Health News #841

" Environment, health, jobs and justice--Who gets to decide? "

Thursday, February 9, 2006

www.rachel.org -- To make a secure donation,

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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

chemicals anymore.

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

gained tremendously.

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. "

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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

corporations).

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'

wombs.

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

their gall.

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

grasp?

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

to happen. "

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

descended testicles.

" 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

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Scientific American, Dec. 15, 2005

SICK OF POVERTY

By Robert Sapolsky

[DHN introduction: We have added a few explanatory links to the text.

--DHN Editors]

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

health.

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

enormous expenses.

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.

Inadequate Explanations

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

services.

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

Gates. "

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.

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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.

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Psychosocial Stress

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

neurons.

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, © 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.

Feeling Poor

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

Deteriorated immune

===

** Acute stress: Circulatory System

Heart beats faster, and blood vessels constrict to bring more oxygen

to muscles

** 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

mathematical artifact.

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

dwarf ours.

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.

Social Capital

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,

number 29).

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.

Additional Reading:

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

Company, 2004.

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).

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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

useless.

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

tax policies.

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

Americans.

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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 rs at

http://www.sciencenews.org/articles/20031108/note14.asp).

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

ingredients.

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. "

Hunting thrins

" 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

that suffix.

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

sediments sampled.

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.

Amweg

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

manicured lawns.

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

didn't.

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.

Johnson/OSU

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

2005 ET & C.

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

fluke.

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. "

References:

2005. Pyrethroid pesticides found at toxic levels in California urban

streams. University of California, Berkeley press release. Oct. 25.

Available here.

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

available here.

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.

Abstract.

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.

Baltimore. Abstract.

Lydy, M., D. Weston, and J. You. 2005. Relative contributions of

agricultural or urban pyrethroid usage to toxicity in California

streams. SETAC North America 26th Annual Meeting. Nov. 13-17.

Baltimore. Abstract.

Talent, L.G. 2005. Effect of temperature on toxicity of a natural

pyrethrin pesticide to green anole lizards (Anolis carolinensis).

Environmental Toxicology and Chemistry 24(December):3113-3116.

Abstract available here.

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Rachel's News #841: Turning Boys into Girls?

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