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Featured stories in this issue...

The Deadliest Air Pollution Isn't Being Regulated or Even Measured
  For 20 years, scientific and medical studies have been showing that
  the tiniest particles of airborne soot are by far the most dangerous
  ones. But the government has consistently refused to regulate or even
  measure these invisible killers. Now there is evidence that "stricter"
  government regulations are allowing the numbers of these particles to
  increase.
Research Links Lead Exposure, Criminal Activity
  This research analyzes crime rates and lead poisoning levels across
  a century. The United States has had two spikes of lead poisoning: one
  at the turn of the 20th century, linked to lead in household paint,
  and one after World War II, when the use of leaded gasoline increased
  sharply. Both times, the violent crime rate went up and down in
  concert, with the violent crime peaks coming two decades after the
  lead poisoning peaks.
Asia-Pacific Countries See Effects of Climate Change on Health
  The World Health Organization estimates climate change has already
  directly or indirectly killed more than 1 million people globally
  since 2000.

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From: Rachel's Democracy & Health News #915, Jul. 12, 2007
[Printer-friendly version]

THE DEADLIEST AIR POLLUTION ISN'T BEING REGULATED OR EVEN MEASURED

By Peter Montague

In the U.S., the deadliest air pollution is not being regulated or
even measured as it kills tens of thousands of people each year.

The culprit is the smallest particles of airborne soot, known as
"ultrafines," which are emitted routinely by diesel engines,
automotive traffic, garbage incinerators, and power plants burning
coal, oil, natural gas, and biomass.[1,2]

Ultrafine particles kill in at least a half-dozen different ways,
including (but not limited to) cancer, heart attack and stroke
(initiating and worsening atherosclerosis), by narrowing the airways
(contributing to chronic obstructive pulmonary disease (COPD) and
asthma), and by causing a systemic inflammation response and
initiating "oxidative stress," which drastically alters the chemistry
inside cells and sets off a cascade of serious problems. Damaged lungs
retain a higher proportion of ultrafines, compared to healthy lungs,
and retaining more ultrafines causes more lung damage -- a positive
feedback loop with negative consequences. For the past 20 years, new
dangers from ultrafines have come to light each year, with no end in
sight. [3,4,5,6,7,8,9,10,11,12,13]

The people most endangered by ultrafines are urban dwellers,
especially the elderly and anyone with a chronic illness (e.g.,
asthma, diabetes, COPD, heart problems)[14,15] but there is evidence
that commuters in their cars[16] and children at play[17] are also
being harmed. Children exposed continuously to low levels of
ultrafines can grow into adults with diminished lung function and
shortened lives.[18]

Furthermore there is growing evidence that women are affected somewhat
more than men,[19] and that people of color are affected more than
whites,[20] women probably because of smaller lung volume and people
of color probably because of stress piled on more stress in their
lives.[21,22]

Finally, there is no observable safe level -- no threshold level below
which symptoms disappear. Any exposure to ultrafines seems to cause
some harm.[18] The only safe level of exposure is zero.

Research over the past 18 years has revealed again and again that the
greatest damage from air pollution is coming from the very smallest
airborne particles of soot, yet government regulators continue to
focus attention on the larger and less harmful particles, which are
easier to measure. It's like the drunk searching for his keys under a
street lamp, even though he knows he lost them many blocks away. "The
light's better over here," he explains.

Airborne particles are classified into three groups -- coarse, fine
and ultrafine. Coarse particles are those that measure between 10
micrometers in diameter down to 2.5 micrometers. A micrometer is a
millionth of a meter and a meter is about 39 inches. A human hair
typically measures about 100 micrometers in diameter, so the largest
particles are about 1/10th the thickness of a human hair. These coarse
particles are usually referred to as PM10 (particulate matter 10).[1]

Your nose and throat can trap these large particles (on sticky
surfaces, for example), to prevent them from entering your lungs.
After they are trapped, you eventually excrete them.

"Fines" are particles that measure between 2.5 micrometers and 0.1
micrometers; they are typically referred to as PM2.5. The smallest of
these particles are small enough to get into the lower portions of
your lungs. There they may be removed by several clearance mechanisms,
but very slowly. Their "half-life" in the human lung is five years,
meaning that a certain dose today will have diminished by half five
years from now.[23] At that rate, a dose today will stay with you for
50 years.

Some fine particles can cause serious harm before they are excreted
because their surfaces are typically covered with organic chemicals
and metals, which are carried into your airways. And some of these
PM2.5 particles can pass directly into your blood stream, carrying
their load of metals and organics with them, and distributing them
throughout your body.

The federal government began setting standards for PM10 in 1987 and
for PM2.5 in 1997 after several studies revealed that fines were
killing an estimated 60,000 people each year in the U.S.[8] -- far
more than were being killed by traffic accidents. A much larger number
of people were (and are) being made sick with lung and heart problems.
Corporations challenged the 1997 rules, which were finally upheld by
the U.S. Supreme Court in 2001.[18]

But long before the government began to regulate "fines," many studies
had revealed that the actual killing was really being done by the
smallest particles of all, called "ultrafines," which the government
has so far refused to regulate or even measure.[8]

Ultrafines vary in size from 0.1 micrometers down to 0.001 micrometers
(or 100 nanometers down to 1 nanometer in diameter; a nanometer is a
billionth of a meter). The largest of these particles has a diameter
1/1000th of the width of a human hair, and the smallest has a diameter
1/100,000th of a human hair. Relatively few such particles occur in
nature, so our bodies have evolved no efficient means for protecting
us against them.[1]

In typical urban air, ultrafines account for only 1 to 5 percent of
all airborne particles by weight, yet a typical person breathing the
air in Los Angeles will inhale 200 billion (2E11) ultrafine particles
every day and retain half of those in their lungs.[26]

As particles get smaller, their surface area gets larger in relation
to their volume (a physicist might say, as their diameter decreases,
their surface-to-volume ratio increases). The very smallest particles,
which are present in the largest numbers, have an enormous surface
area compared to larger particles. This large surface area provides a
perfect place for airborne toxicants to glom on and be carried
efficiently into the deepest portions of your lungs.[1]

Of course your lungs are in the business of transferring oxygen from
the air directly into your blood stream. Unfortunately, they do the
same thing with ultrafines. healthy lungs retain about of 50% of the
ultrafines you breathe[26] and a substantial number of those are
passed directly into your blood stream. While in your lungs,
ultrafines cause an inflammation response by creating "free radicals"
from oxygen, which then combine with your lung tissues in destructive
ways.[13,4] Ultrafines in your blood stream provoke an immune response
that can include coagulation (thickening) of the blood -- leading in
some cases to heart attacks and strokes.

Current government regulations do not take into consideration the
number of particles present in air -- only the total weight of the
particles. So, for example, the government says it is OK for local air
to contain 35 micrograms of PM2.5 in each cubic meter of air averaged
over one hour, or 15 micrograms of PM2.5 in each cubic meter averaged
over a year's time. A microgram is a millionth of a gram and there are
28 grams in an ounce.

The assumption of this approach is that the total weight of particles
is related in some consistent way to the number of particles in the
air. Unfortunately in the few cases where this assumption has been
tested, it has found to be false.[15,24,25,26] The total number of
particles in the air can vary independently of the total weight of
particles in the air. This means that, if you want to know the level
of danger from fine particles in the air, you need to count particles,
not weigh them. [9,15]

Worse, regulating the weight of particles instead of the number of
particles may actually make air pollution more dangerous. Reducing the
number of large particles (which is the easiest way to reduce the
weight of pollution, to comply with the law) can lead to an increase
in the release of ultrafine particles because larger particles serve
as a "magnet" for the smallest particles. As the larger particles are
removed from air emissions, ultrafine particles have fewer "magnets"
to hook onto and thus can enter the ambient air in greater numbers,
increasing the danger to human health.

A writer in Science magazine observed in 2005, "Controlling only mass
[of airborne particles], as EPA does now, might actually be
counterproductive. For example, if larger PM2.5 particle levels go
down but levels of ultrafines do not, "that could make things worse,"
[Mark W.] Frampton says. That's because ultrafines tend to glom onto
larger PM2.5 particles, so they don't stay in the air as long when
more larger particles are around."[8]

So the most dangerous forms of air pollution -- ultrafines -- which
are killing tens of thousands of people each year, are not regulated
and are not even being measured.

Worst of all, the "nanotechnology" industry is now ramping up
manufacturing facilities to intentionally make ultrafines in ton
quantities. Until recently, ultrafines have been created as an
unwanted byproduct of combustion. But now ultrafines are being
purposefully manufactured for use in tires, fuel cells, electronics,
personal care products like sun screens, and many other products.[1,2]
This will certainly create new occupational hazards -- and will
certainly lead to release of ultrafines into the general environment,
through products discarded and through spills, leaks and other
glitches.

Do we know everything we need to know about the hazards of ultrafines?
We do not. Do we know enough to act? We certainly do. As Jocelyn
Kaiser summarized it in Science magazine in 2005, "Environmental and
health groups, as well as many scientists, say that, as with tobacco
smoke and lung cancer, policymakers can't wait for all the scientific
answers before taking action to prevent deaths from dirty air."[8]
Tens of thousands of lives stand to be saved each year by aggressive
action to curb ultrafines. Prevention is possible -- and that's good
news.[18]

With 20 years of data to rely on, it is long past time for ultrafines
to be strictly controlled -- and controlled by number, not merely by
weight.

Citizens concerned about new power plants, new diesel engines, or new
incinerators have a right to insist on detailed information about
ultrafine emissions. Will new technologies make things worse by
emitting larger numbers of deadly ultrafines, even as they reduce the
total weight of emissions? Given the available data, it's a fair
question.

=========================================================

[1] Oberdorster, Gunter, and others. "Nanotoxicology: An Emerging
Discipline Evolving from Studies of Ultrafine Particles."
Environmental Health Perspectives Vol. 113, No. 7 (July 2005), pgs.
823-839. http://tinyurl.com/2vkvbr

[2] Oberdorster, Gunter, and others. 2005b. "Nanotoxicology: An
Emerging Discipline Evolving from Studies of Ultrafine Particles;
Supplemental Web Sections." http://tinyurl.com/3942au

[3] Oberdorster, Gunter. "Pulmonary effects of inhaled ultrafine
particles." International Archives of Occupational and Environmental
Health Vol. 74 (2001), pgs. 1-8. http://tinyurl.com/2jwrvb

[4] Vinzents, Peter S., and others. "Personal Exposure to Ultrafine
Particles and Oxidative DNA Damage." Environmental Health Perspectives
Vol. 113, No. 11 (November 2005), pgs. 1485-1490.
http://tinyurl.com/2nf2sa

[5] Zhang, Qunwei, and others. "Differences in the Extent of
Inflammation Caused by Intracellular Exposure to Three Ultrafine
Metals: Role of Free Radicals." Journal of Toxicology and
Environmental Health, Part A Vol. 53 (1998), pgs. 423-438.
http://tinyurl.com/2lygc6

[6] Frampton, Mark W. "Systemic and Cardiovascular Effects of Airway
Injury and Inflammation: Ultrafine Particle Exposure in Humans."
Environmental Health Perspectives Vol. 109 Supplement 4 (August 2001),
pgs. 529-532. http://tinyurl.com/3d39ff

[7] Goldberg, Mark S., and others. "Associations between ambient air
pollution and daily mortality among persons with congestive heart
failure." Environmental Research Vol. 91 (2003), pgs. 8-20.
http://tinyurl.com/2wv8kt

[8] Kaiser, Jocelyn. "Mounting Evidence Indicts Fine-Particle
Pollution." Science Vol. 307 (March 25, 2005), pgs. 1858-1861.
http://tinyurl.com/385hdc

[9] Li, Ning, and others. "Ultrafine Particulate Pollutants Induce
Oxidative Stress and Mitochondrial Damage." Environmental Health
Perspectives Vol. 111, No. 4 (April 2003), pgs. 455-460.
http://tinyurl.com/2jy5al

[10] Brook, Robert D., and others. "Air Pollution and Cardiovascular
Disease." Circulation Vol. 109 (2004), pgs. 2655-2671.
http://tinyurl.com/2nbpja

[11] Brown, D.M., and others. "Size-Dependent Proinflammatory Effects
of Ultrafine Polystyrene Particles: A Role for Surface Area and
Oxidative Stress in the Enhanced Activity of Ultrafines." Toxicology
and Applied Pharmacology Vol. 175 (2001), pgs. 191-199.
http://tinyurl.com/2zclcp

[12] Churg, Andrew, and others. "Chronic Exposure to High Levels of
Particulate Air Pollution and Small Airway Remodeling." Environmental
Health Perspectives Vol. 111, No. 5 (May 2003), pgs. 714-718.
http://tinyurl.com/2emfar

[13] Dick, Colin A.J., and others. "The Role of Free Radicals in the
Toxic and Inflammatory Effects of Four Different Ultrafine Particle
Types." Inhalation Toxicology Vol. 15 (2003), pgs. 39-52.
http://tinyurl.com/3c4cah

[14] Brown, James S., and others. "Ultrafine Particle Deposition and
Clearance in the Healthy and Obstructed Lung." American Journal of
Respiratory and Critical Care Medicine Vol. 166 (2002), pgs.
1240-1247. http://tinyurl.com/ywwcev

[15] Penttinen, P., and others. "Ultrafine particles in urban air and
respiratory health among adult asthmatics." European Respiratory
Journal Vol. 17 (2001), pgs. 428-435. http://tinyurl.com/2v9xc4

[16] Zhu, Yifang, and others. "In-Cabin Commuter Exposure to Ultrafine
Particles on Los Angeles Freeways." Environmental Science and
Technology Vol. 41, No. 7 (2007), pgs. 2138-2145.
http://tinyurl.com/22g98l

[17] Gauderman, W. James, and others. "The Effect of Air Pollution on
Lung Development from 10 to 18 Years of Age." New England Journal of
Medicine (NEJM) Vol. 351, No. 11 (September 9, 2004), pgs. 1057-1067
plus correction from NEJM Vol. 352 (2005), pg. 1276a.
http://tinyurl.com/32vv9e

[18] Pope, C. Arden III. "Air Pollution and Health -- Good News and
Bad." New England Journal of Medicine Vol. 351, No. 11 (September 9,
2004), pgs. 1132-1133. http://tinyurl.com/yntrmk

[19] Jacques, Peter A., and Chong S. Kim, "Measurement of Total Lung
Deposition of Inhaled Ultrafine Particles in Healthy Men and Women."
Inhalation Toxicology Vol. 12 (2000), pgs. 715-731.
http://tinyurl.com/2jm4cv

[20] Gwynn, R. Charon, and George D. Thurston. "The Burden of Air
Pollution: Impacts among Racial Minorities." Environmental Health
Perspectives Vol. 109 Supplement 4 (August 2001), pgs. 501-506.
http://tinyurl.com/3dnbeq

[21] Gee, Gilbert C., and Devon C. Payne-Sturges. "Environmental
Health Disparities: A Framework for Integrating Psychosocial and
Environmental Concepts." Environmental Health Perspectives Vol. 112,
No. 17 (December 2004), pgs. 1645-1653. http://tinyurl.com/3ylzmp

[22] deFur, Peter L., and others. "Vulnerability as a Function of
Individual and Group Resources in Cumulative Risk Assessment."
Environmental Health Perspectives Vol. 115, No. 5 (May 2007), pgs.
817-824. http://tinyurl.com/3dexxs

[23] Lundborg, Margaret, and others. "Human Alveaolar Macrophage
Phagocytic Function is Impaired by Aggregates of Ultrafine Carbon
Particles." Environmental Research Section A Vol. 86 (2001), pgs.
244-253. http://tinyurl.com/36rp2r

[24] Peters, A., and others. "Respiratory effects are associated with
the number of ultrafine particles." American Journal of Respiratory
and Critical Care Medicine Vol. 155 (1997), pgs. 1376-1383.
http://tinyurl.com/2pbhap

[25] von Klot, S., and others. "Increased asthma medication use in
association with ambient fine and ultrafine particles." European
Repiratory Journal Vol. 20 (2002), pgs. 691-702.
http://tinyurl.com/2mm2jn

[26] Hughes, Lara S., and others. "Physical and Chemical
Characterization of Atmospheric Ultrafine Particles in the Los Angeles
Area." Environmental Science & Technology Vol. 32, No. 9 (1998), pgs.
1153-1161. http://tinyurl.com/33d8kb

Additional reading

Brauer, Michael, and others. "Air Pollution and Retained Particles in
the Lung." Environmental Health Perspectives Vol. 109, No. 10 (October
2001), pgs. 1039-1043. http://tinyurl.com/2uzp2d

Hunt, Andrew. "Toxicologic and Epidemiologic Clues from the
Characterization of the 1952 London Smog Fine Particulate Matter in
Archival Autopsy Lung Tissues." Environmental Health Perspectives Vol.
111, No. 9 (July 2003), pgs. 1209-1214. http://tinyurl.com/3yuf27

Nemmar, Abderrahim, and others. "Ultrafine Particles Affect
Experimental Thrombosis in an In Vivo Hamster Model." American Journal
of Respiratory and Critical Care Medicine Vol. 166 (2002), pgs.
998-1004. http://tinyurl.com/374q2g

Renwick, L.C., and others. "Impairment of Alveolar Macrophage
Phagocytosis by Ultrafine Particles." Toxicology and Applied
Pharmacology Vol. 172 (2001), pgs. 119-127.
http://tinyurl.com/2knz9z

Seaton, A., and M. Dannenkamp. "Hypothesis: Ill health associated with
low concentrations of nitrogen dioxide -- an effect of ultrafine
particles?" Thorax Vol. 58 (2003), pgs. 1012-1015.
http://tinyurl.com/35muq4

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From: Washington Post (pg. A2), Jul. 8, 2007
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RESEARCH LINKS LEAD EXPOSURE, CRIMINAL ACTIVITY

By Shankar Vedantam, Washington Post Staff Writer

Rudy Giuliani never misses an opportunity to remind people about his
track record in fighting crime as mayor of New York City from 1994 to
2001.

"I began with the city that was the crime capital of America,"
Giuliani, now a candidate for president, recently told Fox's Chris
Wallace. "When I left, it was the safest large city in America. I
reduced homicides by 67 percent. I reduced overall crime by 57
percent."

Although crime did fall dramatically in New York during Giuliani's
tenure, a broad range of scientific research has emerged in recent
years to show that the mayor deserves only a fraction of the credit
that he claims. The most compelling information has come from an
economist in Fairfax who has argued in a series of little-noticed
papers that the "New York miracle" was caused by local and federal
efforts decades earlier to reduce lead poisoning.

The theory offered by the economist, Rick Nevin, is that lead
poisoning accounts for much of the variation in violent crime in the
United States. It offers a unifying new neurochemical theory for
fluctuations in the crime rate, and it is based on studies linking
children's exposure to lead with violent behavior later in their
lives.

What makes Nevin's work persuasive is that he has shown an identical,
decades-long association between lead poisoning and crime rates in
nine countries.

"It is stunning how strong the association is," Nevin said in an
interview. "Sixty-five to ninety percent or more of the substantial
variation in violent crime in all these countries was explained by
lead."

Through much of the 20th century, lead in U.S. paint and gasoline
fumes poisoned toddlers as they put contaminated hands in their
mouths. The consequences on crime, Nevin found, occurred when
poisoning victims became adolescents. Nevin does not say that lead is
the only factor behind crime, but he says it is the biggest factor.

Giuliani's presidential campaign declined to address Nevin's
contention that the mayor merely was at the right place at the right
time. But William Bratton, who served as Giuliani's police
commissioner and who initiated many of the policing techniques
credited with reducing the crime rate, dismissed Nevin's theory as
absurd. Bratton and Giuliani instituted harsh measures against
quality-of-life offenses, based on the "broken windows" theory of
addressing minor offenses to head off more serious crimes.

Many other theories have emerged to try to explain the crime decline.
In the 2005 book "Freakonomics," Steven D. Levitt and Stephen J.
Dubner said the legalization of abortion in 1973 had eliminated
"unwanted babies" who would have become violent criminals. Other
experts credited lengthy prison terms for violent offenders, or
demographic changes, socioeconomic factors, and the fall of drug
epidemics. New theories have emerged as crime rates have inched up in
recent years.

Most of the theories have been long on intuition and short on
evidence. Nevin says his data not only explain the decline in crime in
the 1990s, but the rise in crime in the 1980s and other fluctuations
going back a century. His data from multiple countries, which have
different abortion rates, police strategies, demographics and economic
conditions, indicate that lead is the only explanation that can
account for international trends.

Because the countries phased out lead at different points, they
provide a rigorous test: In each instance, the violent crime rate
tracks lead poisoning levels two decades earlier.

"It is startling how much mileage has been given to the theory that
abortion in the early 1970s was responsible for the decline in crime"
in the 1990s, Nevin said. "But they legalized abortion in Britain, and
the violent crime in Britain soared in the 1990s. The difference is
our gasoline lead levels peaked in the early '70s and started falling
in the late '70s, and fell very sharply through the early 1980s and
was virtually eliminated by 1986 or '87.

"In Britain and most of Europe, they did not have meaningful
constraints [on leaded gasoline] until the mid-1980s and even early
1990s," he said. "This is the reason you are seeing the crime rate
soar in Mexico and Latin America, but [it] has fallen in the United
States."

Lead levels plummeted in New York in the early 1970s, driven by
federal policies to eliminate lead from gasoline and local policies to
reduce lead emissions from municipal incinerators. Between 1970 and
1974, the number of New York children heavily poisoned by lead fell by
more than 80 percent, according to data from the New York City
Department of Health.

Lead levels in New York have continued to fall. One analysis in the
late 1990s found that children in New York had lower lead exposure
than children in many other big U.S. cities, possibly because of a
1960 policy to replace old windows. That policy, meant to reduce
deaths from falls, had an unforeseen benefit -- old windows are a
source of lead poisoning, said Dave Jacobs of the National Center for
Healthy Housing, an advocacy group that is publicizing Nevin's work.
Nevin's research was not funded by the group.

The later drop in violent crime was dramatic. In 1990, 31 New Yorkers
out of every 100,000 were murdered. In 2004, the rate was 7 per
100,000 -- lower than in most big cities. The lead theory also may
explain why crime fell broadly across the United States in the 1990s,
not just in New York.

The centerpiece of Nevin's research is an analysis of crime rates and
lead poisoning levels across a century. The United States has had two
spikes of lead poisoning: one at the turn of the 20th century, linked
to lead in household paint, and one after World War II, when the use
of leaded gasoline increased sharply. Both times, the violent crime
rate went up and down in concert, with the violent crime peaks coming
two decades after the lead poisoning peaks.

Other evidence has accumulated in recent years that lead is a
neurotoxin that causes impulsivity and aggression, but these studies
have also drawn little attention. In 2001, sociologist Paul B.
Stretesky and criminologist Michael Lynch showed that U.S. counties
with high lead levels had four times the murder rate of counties with
low lead levels, after controlling for multiple environmental and
socioeconomic factors.

In 2002, Herbert Needleman, a psychiatrist at the University of
Pittsburgh, compared lead levels of 194 adolescents arrested in
Pittsburgh with lead levels of 146 high school adolescents: The
arrested youths had lead levels that were four times higher.

"Impulsivity means you ignore the consequences of what you do," said
Needleman, one of the country's foremost experts on lead poisoning,
explaining why Nevin's theory is plausible. Lead decreases the ability
to tell yourself, "If I do this, I will go to jail."

Nevin's work has been published mainly in the peer-reviewed journal
Environmental Research. Within the field of neurotoxicology, Nevin's
findings are unsurprising, said Ellen Silbergeld, professor of
environmental health sciences at Johns Hopkins University and the
editor of Environmental Research.

"There is a strong literature on lead and sociopathic behavior among
adolescents and young adults with a previous history of lead
exposure," she said.

Two new studies by criminologists Richard Rosenfeld and Steven F.
Messner have looked at Giuliani's policing policies. They found that
the mayor's zero-tolerance approach to crime was responsible for 10
percent, maybe 20 percent, at most, of the decline in violent crime in
New York City.

Nevin acknowledges that crime rates are rising in some parts of the
United States after years of decline, but he points out that crime is
falling in other places and is still low overall by historical
measures. Also, the biggest reductions in lead poisoning took place by
the mid-1980s, which may explain why reductions in crime might have
tapered off by 2005. Lastly, he argues that older, recidivist
offenders -- who were exposed to lead as toddlers three or four
decades ago -- are increasingly accounting for much of the violent
crime.

Nevin's finding may even account for phenomena he did not set out to
address. His theory addresses why rates of violent crime among black
adolescents from inner-city neighborhoods have declined faster than
the overall crime rate -- lead amelioration programs had the biggest
impact on the urban poor. Children in inner-city neighborhoods were
the ones most likely to be poisoned by lead, because they were more
likely to live in substandard housing that had lead paint and because
public housing projects were often situated near highways.

Chicago's Robert Taylor Homes, for example, were built over the Dan
Ryan Expressway, with 150,000 cars going by each day. Eighteen years
after the project opened in 1962, one study found that its residents
were 22 times more likely to be murderers than people living elsewhere
in Chicago.

Nevin's finding implies a double tragedy for America's inner cities:
Thousands of children in these neighborhoods were poisoned by lead in
the first three quarters of the last century. Large numbers of them
then became the targets, in the last quarter, of Giuliani-style law
enforcement policies.

Copyright 2007 The Washington Post Company

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From: Associated Press, Jul. 3, 2007
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ASIA-PACIFIC COUNTRIES SEE EFFECTS OF CLIMATE CHANGE ON HEALTH

By Margie Mason

KUALA LUMPUR, Malaysia (AP) -- Rising temperatures are contributing to
more landslides in Nepal, dengue fever cases in Indonesia and flooding
in India, threatening to put an even greater strain on health systems
across the Asia-Pacific region.

Health officials from more than a dozen countries, ranging from tiny
Maldives to China, met Tuesday in Malaysia to outline health problems
they are experiencing related to climate change. They discussed ways
to work together to limit the impact in a region expected to be hit
hard by flooding, drought, heat waves, and mosquito- and waterborne
diseases.

The World Health Organization estimates climate change has already
directly or indirectly killed more than 1 million people globally
since 2000. More than half of those deaths have occurred in the Asia-
Pacific, the world's most populous region. Those figures do not
include deaths linked to urban air pollution, which kills about
800,000 worldwide each year, according to WHO.

"We're not going to have a magic bullet to fix climate change in the
next 50 years. We need to motivate an awful lot of people to change
their behavior in a lot of different ways," said Kristie Ebi of WHO's
Global Environmental Change unit, a lead author of the health chapter
in a report by the Intergovernmental Panel on Climate Change, a U.N.
network of 2,000 scientists.

Ebi said health officials are about a decade behind other sectors,
such as water and agriculture, in taking a look at what climate change
could mean and how to deal with it. She said countries seeing the
effects firsthand are now starting to realize that any problems with
air, water or food will directly affect people's health. The poorest
countries in Asia and Africa are expected to suffer the most.

Scientists have predicted droughts will lower crop yields and raise
malnutrition in some areas, dust storms and wildfires will boost
respiratory illnesses, and flooding from severe storms will increase
deaths by drowning, injuries and diseases such as diarrhea. Rising
temperatures could lead to the growth of more harmful algae that can
sicken people who eat shellfish and reef fish. People living in low-
lying coastal areas will also face more storms, flooding, and
saltwater intrusion into fresh groundwater that is vital for drinking.

Many health systems in poor Asian countries are already overwhelmed
with diseases like HIV/AIDS and tuberculosis, and officials have been
under intense international pressure to combat bird flu outbreaks and
prepare for a pandemic despite limited resources.

But tackling current pressing diseases, and investing more in public
health systems overall, will help prepare countries for the future
effects of global warming while saving money in the long run, said Dr.
Shigeru Omi, head of the WHO's Western Pacific region.

"The economic impact will be seen eventually," he said, adding water
scarcity could create a worst-case scenario that produces political
instability. "I think it will pay off if we take action now."

Globalization, urbanization and the rapid development of many Asian
countries are also fueling climate change that's already noticeable.
Last month, China passed the United States to become the largest
greenhouse gas emitter, according to the Netherlands Environmental
Assessment Agency.

Singapore saw mean annual temperatures increase 2.7 degrees Fahrenheit
between 1978 and 1998, while the number of dengue fever cases jumped
10-fold during the same period.

Malaria has recently reached Bhutan and new areas in Papua New Guinea
for the first time. In the past, mosquitoes that spread the disease
were unable to breed in the cooler climates there, but warmer
temperatures have helped vector-borne diseases to flourish.

Melting of glaciers in the Himalayas has also created about 20 lakes
in Nepal that are in danger of overflowing their banks, which could
create a torrent of water and debris capable of wiping out villages
and farms below.

Omi said governments can offer tax incentives to help motivate
companies to become more environmentally friendly, while pushing for
energy-efficient technologies and greener buildings. Promoting walking
and bicycling, instead of driving, can also improve overall health
while saving the environment.

The four-day workshop in Malaysia lays the groundwork for a
ministerial-level meeting on the topic next month in Bangkok,
Thailand.

Copyright 2007 The Associated Press

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