Triton Respirator

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, some species are highly toxic, and it can kill you.

Back up your respirator with a top-quality dust collection system that is based on a well-designed cyclone with ample air flow (can't always believe the "specifications" in a lot of catalogs). I produce such systems. Contact me for further info if needed.

CE

Tim Schubach wrote:

The respirator meets Australian Standard AS/NZS 1716. This standard contains three particulate filter classes: P1, P2 and P3.

P2, which is the recommended filter by Triton, is the equivalent of the American N95 class. The only difference is with marking and labelling to meet the Australian Standard.

The Triton can also take the P1 filters but it is _not_ a VOC respirator, that is, not for spraying purposes, just dust.

The short answer to the question is the P2 (N95) filters will remove 95% (i.e. N95 = 95%) of particulates down to 0.3 micron.

N95 is generally recommended for woodworking (but not for finishing). Note that the Triton also uses pre-filtering.

Greg

My thoughts, exactly.

Leslie

Chuck inquired, "ANYBODY ever know anybody who was diagnosed with cancer as a direct result of exposure to wood dust?"

*********************************************** Not sure how direct a cause the dust was, but I did know of such a case in a weekend wood turner. Working as a welder of magnesium rods in a nuclear generating facility while smoking 3 packs of bare-backed Camels a day probably played no carcinogenic role since he was protected by a 4 in. thick asbestos blanket plus keeping a lifelong heavy suntan. Besides that he was always careful to grease himself with used motor oil that was washed off after work with xylene. Sadly, he was killed while driving drunk just as the dreaded cancer was erroneously diagnosed. And so young, too., only 93. HTH, Arch

Fortiter,

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

Gee it is great to have you back Arch!

Well, uh, sure. My wife's former hairdresser's great aunt's 2nd cousin twice removed's sophmore year college roomate's ex-girlfriend's mother's step sister's fourth husband's brother in law did. At least I think it was him.

Jeepers Chuck, what more proof could a guy want?

...Kevin

Kevin, was his last name Bunyon by any chance???

-- Email evades spam Direct contact through web site

M.J. Orr

~

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

"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

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.

**************** If you have a comment on this article that you would like considered for publication in Science News, send it to snipped-for-privacy@sciencenews.org. Please include your name and location.

To subscribe to Science News (print), go to

To sign up for the free weekly e-LETTER from Science News, go to 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 M. . . . and A. Churg. 2001. Air pollution and retained particles in the lung. Environmental Health Perspectives 109(October):1039-1043. Abstract available at 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 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 et al. 2002. Air pollution and brain damage. Toxicologic Pathology 30(May-June):373-389. Abstract available at 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 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 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 N. . . . and A. Nel. 2003. Ultrafine particulate pollutants induce oxidative stress and mitochondrial damage. Environmental Health Perspectives 111(April):455-460. Abstract available at 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 L.C., K. Donaldson, and A. Clouter. 2001. Impairment of alveolar macrophage phagocytosis by ultrafine particles. Toxicology and Applied Pharmacology 172(April 15):119-127. Abstract available at 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 R. 2001. Inhalation Toxicology of Urban Ambient Particulate Matter: Acute Cardiovascular Effects in Rats. Health Effects Institute Research Report. October. Available at 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 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

2001. Reducing blood pressure in the lungs. Science News 160(Nov. 17):312. Available to subscribers at 2001. Attacking Alzheimer's. Science News 160(Nov. 3):286. Available to subscribers at 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 2003. National maps of the effects of particulate matter on mortality: Exploring geographical variation. Environmental Health Perspectives 111(January):39-43. Abstract available at 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 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 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 J. 2001. Dusty workplace may cause change of heart. Science News 160(Sept. 15):167. Available to subscribers at 2001. High court gives EPA a partial victory. Science News 159(March 10):159. Available to subscribers at 1999. Traffic may worsen hay fever and asthma. Science News 156(Nov. 20):325. Available at 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 N. 1998. Amyloid can trigger brain damage. Science News 154(July 4):4. Available at 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 . U.S. Environmental Protection Agency. Information on Particulate Matter. Available at Environmental Protection Agency. PM2.5 NAAQS Implementation. Available at Environmental Protection Agency. National Ambient Air Quality Standards. Available at Environmental Protection Agency. Air Quality Criteria for Particulate Matter (Fourth External Review Draft). Available at

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

From Science News, Vol. 164, No. 5, Aug. 2, 2003, p. 72. Copyright (c) 2003 Science Service. All rights reserved.

Chuck wrote:

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 news:MmuUb.12721$ snipped-for-privacy@newsread2.news.pas.earthlink.net...

Perspectives.

subServices.asp.>

.>

Yes. A guy in our club several year ago. Lung cancer. Made a convert out of most of the members in our club and continues to do so to this day.

Joe

That's the guy!!! What are the odds????

...Kevin

=============================== George, My point was that the smaller particles, especially those below 2.5 microns, go the deepest into the lung passages, and are the hardest to emit. Whether they are carcinogenic or not, they do reduce lung capacity for the time they're there. This may not be felt on a young healty person, but if you already have cardiovascular deficiencies, they can be a problem.

Ken Moon Webberville, TX

I don't like to bring this back, but please read this article by Terry Martin related to Fabrice Micha, who was a young turner, ITE resident in 1998. He died in 2001.

by

I expect that he is not planning on living forever, and wants to do things he loves/likes in whatever time he has left. Can relate to that! Although I think if he used LDD he might stand a better chance! *G*

No, but one of our members who is an MD had a friend who was a turner that died from fungus in his lungs that seems to have come from turning spalted woods.

Carl Abrams, Secretary Central Indiana Chapter of American Association of Woodturners (CICAAW)

I'll let you know about the respirator - I just bought one for MY use inmy shop.

It was most likely a type of pneumonia caused by the foreign bodies in the lungs and not some sort of sci-fi "attack of the killer fungus" or a cancerous condition. There are all kinds of fungal induced pneumonia's on medical record.

- Andrew

I have a Triton respirator and am quite please with it.

Features:

1. Full face mask;

1. Ear protection;

2. Dual filter, first one is washablble, second one contains two replacable cartridges;

1. Shroud improves seal around the neck;

2. Flow meter helps you figure out when to charge the battery.

Concerns

1. Some people say the hose from the fan on your belt to the helmet is a bit stiff. Triton says they are going to fix it. I haven't noticed a problem.

1. The battery is internal to the fan unit, the only way to charge it is to plug the fan unit in. I would prefer removable battery packs so that I can charge one while using another.

2. The latches that hold the fan unit together are molded plastic. I've already bent the "hook" part of the latches by misaligning them slightly. This was easily fixed but I would prefer metal latches.

All in all I am pleased with the products performaned and am very glad I got it. I wear glasses and this beats a mask or face shield hands down for comfort and lack of fog. The price was also a lot nicer than other units that I've seen.