Hi,
Although Lyn's message below seem to target metallic irritants, the
association with woodturning comes from the microscopic particles generated
with the sanding operations. The PM 2.5 regulations, if they are ever
enacted in this country will help in the public and industrial areas, but it
is up to individuals to take care of themselves. The effects of ultra small
particles are shown in the illnesses of silicosis (white lung, found in
workes around crushed stone and quarries), black lung found in coal miners
and the thousands who die of lung cancer every year from smoking. These
smallest particles go so much deeper into the minute air passages that they
can not be expelled by normal breathing or coughing. So they remain there,
carcinogenic or not, blocking all areas past where they stop, blocking air
that would normally be absorbed into the blood stream. Even if they are not
carcinogenic, they cause significant damage.
It's up to each of us to learn to take care of ourselves.

Ken Moon
Webberville, TX
************************************************** ****

"Lyn J. Mangiameli" wrote in message
link.net...
Science News

Week of Aug. 2, 2003; Vol. 164, No. 5

Air Sickness

How microscopic dust particles cause subtle but serious harm

Janet Raloff

On Oct. 26, 1948, a temperature inversion laid a blanket of cold,
stagnant air over Donora, Pa., a tiny mill town on the Monongahela
River. Over the next 5 days, the buildup of pollution cloaked the sun,
sometimes restricting vision to just a few feet. Twenty people died
outright and 50 more perished within a month from lingering health
damage, says consulting epidemiologist Devra Davis, a former Donora
resident whose own family survived the tragedy.

As bad as her hometown's pollution had been, its impact would pale
against a 5-day killer smog that settled on London in December 1952. It
killed some 12,000 people within 3 months, according to calculations in
a June 2001 report by Davis and Michelle L. Bell of Johns Hopkins
University in Baltimore. "With a death rate more than three times the
norm for this period, the London fog of 1952 is widely regarded as a
catalyst for the study of air pollution epidemiology," the pair noted.

That science would eventually show that even the diffuse dust wafting in
seemingly clear air could kill. Its victims are just harder to identify
than those in the London and Donora catastrophes because most who
succumb are elderly or already in ill health. Indeed, a trailblazing
1991 analysis by Joel Schwartz, then at the Environmental Protection
Agency, concluded that some 60,000 U.S. residents die from heart attacks
and respiratory problems each year because of the effects of airborne
dust at concentrations within federal pollution limits (SN: 4/6/91, p.
212).

Stunning as those numbers were at first, they're now accepted by most
researchers. In that 1991 study and subsequent ones, Schwartz, now at
the Harvard School of Public Health in Boston, has shown that community
death rates rise and fall nearly in lock-step with local changes in
concentrations of tiny dust particles—even when concentrations of those
particulates are just one-quarter of the federal limit for outdoor air.

Yet more than a decade later, nagging questions remain: What makes dust
and smoke particles, especially small ones, toxic? Is particulate
matter, as scientists call it, inherently poisonous, regardless of its
composition? Or does a large surface area per unit mass make those
particles robust vehicles for ferrying toxicants such as metal atoms
deep into the lungs?

In the past 2 years, a flurry of new data has finally begun answering
these questions. The research links the greatest harm to the tiniest
dust: particulate matter no more than 2.5 micrometers in diameter,
called the PM-2.5 fraction. Some studies suggest that the most dangerous
of all may be ultrafines, particles less than 0.1 micrometer across—a
class of dust that environmental studies and regulations have generally
ignored.

Remodeled airways

Although most people who die from particulate pollution had heart
disease or respiratory problems, the new data are showing that even
young and healthy people aren't immune to the violence that dust can
perpetrate on lung tissue.

In Fresno, Calif., for instance, outwardly robust people routinely
harbor damage in their lungs' small airways, setting the stage for
respiratory and cardiovascular disease. These lung effects appear to
trace to Fresno's high level of PM-2.5 pollution, which is as bad as
that in Los Angeles and worse than that in nearly any other U.S. city,
according to Kent E. Pinkerton of the University of California, Davis
and his colleagues. They surveyed the airways of more than 80 men who
had been longtime residents of Fresno—many of them in their 20s to
40s—who died from auto accidents and other events unrelated to pollution.

Pinkerton's team found that PM-2.5 has little effect on the lungs'
larger passages but injures the deeper, smaller, thin-walled bronchioles
that mark where the body begins to extract oxygen from air. The damage
was apparently caused by the ravages of molecular fragments called free
radicals. The affected tissue exhibited a kind of scarring called
fibrosis and an abnormal thickening, two features that make breathing
more difficult.

To confirm the role of particulate pollution in these subtle changes to
the lung, Pinkerton's colleague Kevin R. Smith exposed young-adult rats
for 4 hours on 3 consecutive days to air deliberately concentrated with
the particulates in Fresno's atmosphere. The amount of PM-2.5 in the
test air, Pinkerton notes, reflected "what can exist in Fresno on
bad-air days."

After the exposures, Smith examined areas of the rats' lungs and
extracted unusually large numbers of inflammatory cells, called
neutrophils, as well as hosts of dead cells.

"It's not unusual to see an occasional dead cell" in the lungs of rats
that had breathed only clean air, Pinkerton notes, but the dust-exposed
rats showed many dead lung cells, including macrophages—the organ's
housekeeping cells. Because macrophages normally gobble up cellular
trash such as pollutant particles, their loss could prove important, the
Davis team notes in the June Environmental Health Perspectives.

In the May issue of that journal, Andrew Churg of the University of
British Columbia in Vancouver and his colleagues report similar findings
in the autopsied lungs of 11 nonsmoking women from Mexico City, but not
in an equal number from Vancouver. Though the Canadian city's air is
relatively clear of particulates, Mexico City's air carries a dense haze
of fine dust much of the year.

The scientists focused on the lungs' smallest, oxygen-absorbing airways.
Compared with those from the Canadian women, the tiny airways from
residents of Mexico City "were very abnormal," Churg says. They were
twisted and exhibited significantly more fibrosis and thickness than
normal lung tissue. "A heavy smoker could have airways that look very
much the same," he told Science News.

Churg's colleague David Bates plans to test whether the effects the team
documented translate into breathing problems in healthy Mexico City
adults.

Lilian Calderón-Garcidueñas of the University of North Carolina at
Chapel Hill says she knows what Bates will find. At the Experimental
Biology meeting in San Diego last April, she documented mildly
obstructed breathing in 10 percent of the 174 ostensibly healthy Mexico
City children she examined. All the children came from middle- to
upper-class nonsmoking families living where the air wasn't the city's
dustiest.

Heart of the matter

Despite the natural expectation that lungs should be especially
vulnerable to dust, "the worst effects, it turns out, are on the
cardiovascular system," observes particle toxicologist Ken Donaldson of
the University of Edinburgh.

Some of the most intriguing clues to what underlies these effects are
emerging from studies on endothelin. This small protein, produced in
healthy lungs, ordinarily prompts blood vessels to constrict to maintain
proper blood pressure.

Renaud Vincent of Health Canada in Ottawa, Ont., and his colleagues had
been wondering what makes some people particularly vulnerable to an
increase in pollution, even in a relatively unpolluted Canadian city. To
find out, the researchers exposed healthy volunteers to high
concentrations of PM-2.5. They found that endothelin concentrations
doubled in healthy people's blood when their exposures tripled from 50
micrograms per cubic meter (µg/m3) to 150 µg/m3, a range typical for the
world's most polluted cities.

Although the endothelin jolt didn't hurt these healthy volunteers,
previous studies have shown that people with artery-clogging
atherosclerosis have a higher risk of dying after a heart attack if they
had endothelin concentrations comparable to the spikes observed in the
volunteers' blood.

Interestingly, Vincent notes, his team could trigger increases of
endothelin only with the kind of dirty dust usually encountered
outside—particles that carry some chemical hitchhikers, including metals
and hydrocarbons. When the researchers washed the particles to remove
those hitchhikers, the PM-2.5 exposures had no impact on blood
concentrations of endothelin.

Harvard School of Public Health scientists also have begun exploring
dust's cardiovascular effects. Gregory A. Wellenius and his colleagues
exposed dogs to either clean filtered air or air seeded with 30 times
the concentration of particulates that local outdoor air carried that
day. The exposures lasted 6 hours on 3 or 4 consecutive days.

Right after each exposure, the researchers simulated a heart attack in
the dogs by constricting a surgically implanted balloon that temporarily
shut off a coronary artery. During this blockage, the researchers
measured the heart's growing oxygen debt.

The debt was significantly larger in animals that had been exposed to
fine airborne dust, the scientists reported in the April Environmental
Health Perspectives. A dog's other coronary arteries couldn't dilate as
well and couldn't compensate for the blocked vessel if the animal was
inhaling particulates, Wellenius speculates. Such a reaction is
"entirely consistent" with an endothelin boost from exposure to
particulate pollution, he says.

A nose for clues

The collective message from the 200-or-so Mexico City mongrels that
Calderón-Garcidueñas and her colleagues studied is also alarming.

A neuropathologist, she was concerned that if dust could damage lung
tissue, it might also break down the capacity of nasal passages to block
substances from entering the brain. She now reports tracing metals
associated with fossil fuel combustion—chiefly vanadium and nickel—from
the dogs' nasal tissue, through the olfactory bulb, and into the frontal
lobe and hippocampus of the animals' brains.

Because such metals can foster damage by generating free radicals,
Calderón-Garcidueñas looked for signs of brain changes in dogs living in
areas with heavy particulate pollution.

Dogs often serve as a model for human age-related cognitive impairments.
Some dogs at age 10 and older develop the waxy brain plaques
characteristic of Alzheimer's disease (SN: 11/3/01, p. 286: Available to
subscribers at http://www.sciencenews.org/20011103/bob17.asp). "In
Mexico City," Calderón-Garcidueñas told Science News, "we are seeing
[plaque] pathology in 11-month-old pups"—a dramatic acceleration in the
development of the signature of Alzheimer's disease.

These data are "definitely worrisome," she says, especially in light of
her preliminary findings of a similar breakdown in the nasal tissue of
many people living in Mexico City.

Another new study in mice, this one by EPA scientists, suggests that
particulates do their harm via the metals they sometimes carry. They
found signs that exposure to metal-laden PM-2.5 aggravates asthma much
more than does relatively metalfree dust.

Stephen H. Gavett of the agency's Research Triangle Park, N.C.,
laboratory and his colleagues used dust collected in two eastern German
towns—one an industrial community polluted with metals and other
combustion products and the other a farm village with relatively clean
air. The metal-rich dust, gathered by Joachim Heinrich of the GSF
Institute of Epidemiology in Neuherberg, Germany, proved far more potent
in aggravating asthmatic constrictions of an animal's airways, the
researchers will report in the September Environmental Health
Perspectives.

Ultrafines, ultrabad?

If such studies suggest that the composition of inhaled particles
affects their toxicity, other findings indicate that particle size can
greatly exacerbate the problem.

In studies with isolated lung cells, for example, ultrafine particles
proved to be between 10 and 50 times as potent as PM-2.5 or PM-10
particles in inducing free-radical damage, such as inflammation. Andre
Nel of the University of California, Los Angeles and his team reported
their findings in the April Environmental Health Perspectives.

Nel's team also found that ultrafine particles from urban air carry far
more toxic combustion hydrocarbons on their surface, per unit mass, than
larger particles do. Further probing showed that the smaller motes tend
to lodge in cells' mitochondria, the organelles that generate power. The
particles turn the mitochondria into "functionless bags," says Nel. And
when these powerhouses die, he says, so do the cells they power.

Donaldson has tested "particles that are completely naked"—motes of pure
carbon or titanium dioxide, for instance—and shown they cause no damage
when delivered to rat lungs as 10-micrometer-wide particles. But crush
them into submicron pieces, he says, and "they become highly
inflammogenic to the lungs."

Why? Lung-defending macrophages can easily catch and discard the
occasional big particle that gets lobbed their way. Exposing the lungs
to large numbers of the smallest particles, however, "may completely
overwhelm their defenses," Donaldson says. His team's data support that
scenario.

After decades of research, says Donaldson, toxicologists are still
discovering ways that fine dust particles can kill. And as the dust
particles in their sights get ever smaller, the challenge of controlling
their release gets ever larger.

Dust Rules

A finer standard governing particulate pollution is on the horizon

Environmental agencies around the world today regulate dusty pollutants
on the basis of mass—not chemistry—and most governments focus on the
particles easiest to catch and quantify: those that are 10 micrometers
across (the PM-10 fraction), rather than 2.5-micrometer particles
(PM-2.5) and smaller ones.

Seven years ago, the U.S. Environmental Protection Agency announced it
would soon require states to regulate airborne concentrations of PM-2.5
pollution in recognition of the smaller particles' significantly greater
toxicity than larger particles and ability to move far deeper into the
lungs, (SN: 12/21/96, p. 410). Almost immediately, the agency was sued
by several industries that would be affected.

It took a Supreme Court ruling 2 years ago to get the regulations back
on track (SN: 3/10/01, p. 159: Available to subscribers at
http://www.sciencenews.org/20010310/note17.asp). Yet "we're definitely
several years away" from enforcement of any regulation limiting PM-2.5
pollution, says EPA spokesman Dave Deegan in Washington, D.C.

So, for now, federal law prohibits PM-10 concentrations in air from
exceeding an average of 150 micrograms per cubic meter (µg/m3) over any
24-hour period or a 50 µg/m3 daily average over an entire year. When
PM-2.5 rules do go into effect, they'll restrict the 24-hour average air
concentration of those small particles in any city to 65 µg/m3 and the
annual average concentration to just 15 µg/m3.

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References and Sources

References:

Bouthillier, L., R. Vincent, et al. 1998. Acute effects of inhaled urban
particles and ozone. American Journal of Pathology
153(December):1873-1884. Available at
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Brauer, M. . . . and A. Churg. 2001. Air pollution and retained
particles in the lung. Environmental Health Perspectives
109(October):1039-1043. Abstract available at
http://ehpnet1.niehs.nih.gov/docs/20.../abstract.html.

Brook, R.D. . . . R. Vincent, et al. 2002. Inhalation of fine
particulate air pollution and ozone causes acute arterial
vasoconstriction in healthy adults. Circulation 105(April 2):1534-1536.
Available at http://circ.ahajournals.org/cgi/cont...ll/105/13/1534.

Brown, D.M. . . . and K. Donaldson. 2001. 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 175(Sept. 15):191-199. Abstract available at
http://dx.doi.org/10.1006/taap.2001.9240.

Calderón-Garcidueñas, et al. 2002. Air pollution and brain damage.
Toxicologic Pathology 30(May-June):373-389. Abstract available at
http://dx.doi.org/10.1080/01926230252929954.

Churg, A., et al. 2003. Chronic exposure to high levels of particulate
air pollution and small airway remodeling. Environmental Health
Perspectives 111(May):714-718. Abstract available at
http://ehpnet1.niehs.nih.gov/docs/20.../abstract.html.

Davis, D. 2002. When Smoke Ran Like Water: Tales of Environmental
Deception and the Battle Against Pollution. New York: Perseus Books Group.

Gavett, S.H., et al. In press. Metal composition of ambient PM2.5
influences severity of allergic airways disease in mice. Environmental
Health Perspectives. Abstract available at
http://dx.doi.org/10.1289/ehp.6300.

Goldberg, M.S. . . . R. Vincent, et al. 2003. Associations between
ambient air pollution and daily mortality among persons with congestive
heart failure. Environmental Research 91(January):8-20. Available at
http://dx.doi.org/10.1016/S0013-9351(02)00022-1.

Li, N. . . . and A. Nel. 2003. Ultrafine particulate pollutants induce
oxidative stress and mitochondrial damage. Environmental Health
Perspectives 111(April):455-460. Abstract available at
http://ehpnet1.niehs.nih.gov/docs/20.../abstract.html.

Long, C.M., et al. 2001. A pilot investigation of the relative toxicity
of indoor and outdoor fine particles: In vitro effects of endotoxin and
other particulate properties. Environmental Health Perspectives
109(October):1019-1026. Abstract available at
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Renwick, L.C., K. Donaldson, and A. Clouter. 2001. Impairment of
alveolar macrophage phagocytosis by ultrafine particles. Toxicology and
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Smith, K.R. . . . and K.E. Pinkerton. 2003. Airborne particles of the
California Central Valley alter the lungs of healthy adult rats.
Environmental Health Perspectives 111(June):902-908. Abstract available
at http://dx.doi.org/10.1289/ehp.5964.

Vincent, R. 2001. Inhalation Toxicology of Urban Ambient Particulate
Matter: Acute Cardiovascular Effects in Rats. Health Effects Institute
Research Report. October. Available at
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Wellenius, G.A., et al. 2003. Inhalation of concentrated ambient air
particles exacerbates myocardial ischemia in conscious dogs.
Environmental Health Perspectives 111(April):402-408. Abstract available
at http://ehpnet1.niehs.nih.gov/docs/20.../abstract.html.

Further Readings:

1996. EPA to tighten air pollution limits. Science News 150(Dec.
21&28):410.

Christensen, D. 2002. Lingering legacy of Sept. 11, 2001 on
firefighters' health. Science News 162(Oct. 5):222. Available to
subscribers at http://www.sciencenews.org/20021005/note17.asp.

______. 2001. Reducing blood pressure in the lungs. Science News
160(Nov. 17):312. Available to subscribers
athttp://www.sciencenews.org/20011117/note12.asp.

______. 2001. Attacking Alzheimer's. Science News 160(Nov. 3):286.
Available to subscribers at http://www.sciencenews.org/20011103/bob17.asp.

Dominici, F., et al. 2003. Airborne particulate matter and mortality:
Timescale effects in four US cities. American Journal of Epidemiology
157(June 15):1055-1065. Abstract available at
http://www.aje.oupjournals.org/cgi/c...ct/157/12/1055.

______. 2003. National maps of the effects of particulate matter on
mortality: Exploring geographical variation. Environmental Health
Perspectives 111(January):39-43. Abstract available at
http://dx.doi.org/10.1289/ehp.5181.

Gavett, S.H., et al. 2003. World Trade Center fine particulate matter
causes respiratory tract hyperresponsiveness in mice. Environmental
Health Perspectives 111(June):981-991. Available at
http://ehpnet1.niehs.nih.gov/docs/20.../abstract.html.

Lippmann, M., et al. 2003. The U.S. Environmental Protection Agency
particulate matter health effects research centers program: A midcourse
report of status, progress, and plans. Environmental Health Perspectives
111(June):1074-1092. Abstract available at
http://dx.doi.org/10.1289/ehp.5750.

Osornio-Vargas, A.R., et al. 2003. Proinflammatory and cytotoxic effects
of Mexico City air pollution particulate matter in vitro are dependent
on particle size and composition. Environmental Health Perspectives
111(August):1289-1293. Abstract available at
http://dx.doi.org/10.1289/ehp.5913.

Raloff, J. 2001. Dusty workplace may cause change of heart. Science News
160(Sept. 15):167. Available to subscribers at
http://www.sciencenews.org/20010915/fob8.asp.

______. 2001. High court gives EPA a partial victory. Science News
159(March 10):159. Available to subscribers at
http://www.sciencenews.org/20010310/note17.asp.

______. 1999. Traffic may worsen hay fever and asthma. Science News
156(Nov. 20):325. Available at
http://www.sciencenews.org/sn_arc99/11_20_99/fob4.htm.

______. 1991. Dust to dust: A particularly lethal legacy. Science News
139(April 6):212.

Samet, J.M., et al. 2000. Fine particulate air pollution and mortality
in 20 U.S. cities, 1987-1994. New England Journal of Medicine 343(Dec.
14):1742-1749. Abstract available at
http://content.nejm.org/cgi/content/...ct/343/24/1742.

Seppa, N. 1998. Amyloid can trigger brain damage. Science News 154(July
4):4. Available at http://www.sciencenews.org/sn_arc98/7_4_98/fob1.htm.

Zelikoff, J.T., et al. 2002. A role for associated transition metals in
the immunotoxicity of inhaled ambient particulate matter. Environmental
Health Perspectives 119:Supplement 5(October):871-875. Abstract
available at

http://ehpnet1.niehs.nih.gov/docs/20.../abstract.html
.

U.S. Environmental Protection Agency. Information on Particulate Matter.
Available at http://www.epa.gov/oar/oaqps/regusmog/infpart.html.

U.S. Environmental Protection Agency. PM2.5 NAAQS Implementation.
Available at http://www.epa.gov/ttn/naaqs/pm/pm25_index.html.

U.S. Environmental Protection Agency. National Ambient Air Quality
Standards. Available at http://www.epa.gov/airs/criteria.html.

U.S. Environmental Protection Agency. Air Quality Criteria for
Particulate Matter (Fourth External Review Draft). Available at
http://cfpub.epa.gov/ncea/cfm/record...cfm?deid=58003.

Sources:

David Bates
University of British Columbia
4891 College Highroad
Vancouver, BC V6T 1G6
Canada

Andrew Churg
Department of Pathology
University of British Columbia
2211 Wesbrook Mall
Vancouver, BC V6T 2B5
Canada

Ken Donaldson
MRC Centre for Inflammation Research
University of Edinburgh Medical School
Edinburgh, Midlothian EH8 9AG
Scotland

Stephen Gavett
U.S. Environmental Protection Agency
Mail Code: B142-02
Research Triangle Park, NC 27711

Christopher Long
Gradient Corporation
238 Main Street
Cambridge, MA 02142

Andre Nel
Department of Medicine
University of California, Los Angeles
52-175 CHS
10833 Le Conte Avenue
Los Angeles, CA 90095

Kent E. Pinkerton
Center for Health and the Environment
University of California, Davis
One Shields Avenue
Davis, CA 95616

Joel Schwartz
Harvard School of Public Health
Department of Environmental Health
665 Huntington Avenue
Boston, MA 02115

Kevin R. Smith
Center for Health and the Environment
University of California, Davis
One Shields Avenue
Davis, CA 95616

Renaud Vincent
Room 332
Environmental Health Centre
0803 Tunney's Pasture
Ottawa, ON K1A 0L2
Canada

Gregory A. Wellenius
Physiology Program
Department of Environmental Health
Harvard School of Public Health
665 Huntington Avenue
Building II, Room 227
Boston, MA 02115

http://www.sciencenews.org/20030802/bob8.asp

From Science News, Vol. 164, No. 5, Aug. 2, 2003, p. 72.

Copyright (c) 2003 Science Service. All rights reserved.


Chuck wrote:
On Tue, 03 Feb 2004 21:30:02 -0700, Clarke Echols
wrote:


I'd suggest you get some evidence that the filters are rated at 99.97%
efficient at 0.3 microns for ANY respirator, with certification from an
independent testing lab. Wood dust is carcinogenic,


Yeah, yeah, yeah, along with grilled hamburgers, mother's milk, sodium
cyclamates, paraquat....others?

oh yeah, and opportunistic advertisers.

Anybody every know ANYBODY who was diagnosed with cancer as a direct
result of exposure to wood dust?
--
Chuck *#:^)
chaz3913(AT)yahoo(DOT)com
Anti-spam sig: please remove "NO SPAM" from e-mail address to reply.


September 11, 2001 - Never Forget


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