Effect Measure

A small air pollution risk. Nano sized.

The particles are smaller but the risks appear to be bigger. We’re talking air pollution, here, folks. Not so long ago EPA regulations were on the basis of pretty large partiles, ten microns in size. Then a considerable body of work indicated that much smaller particulate matter, size around 2.5 microns were a much better measure of risk. Like a lot of things, though, as our measurements get better we are finding effects, sometimes big ones, with ever smaller particles. A recent study published in Circulation Research and reported by Bloomberg says that unregulated extremely fine particles, less then 0.2 microns particles not measured at all by most methods, produce serious cardiovascular effects. The work is with animal models but the model used has been quite informative about human health:

Nano-size pollutants from vehicles can lead to plaque buildup in the arteries, putting people at risk of cardiovascular problems, researchers said in a study published today in Circulation Research, a journal of the American Heart Association. The pollutants may cause arteries to harden by impairing the protective qualities of so-called good cholesterol.

The U.S. Environmental Protection Agency doesn’t regulate the nano-size particles, which can’t be captured using current filtering technology. The pollutants, abundant in urban areas, are less than 0.18 micrometers in size and cause four times more artery buildup than particles four times larger, said Jesus Araujo, director of environmental cardiology at University of California, Los Angeles. (Bloomberg)

The apparent mechanism involves the promotion of inflammation in artery walls. The inflammatory cytokines caused by the nanoparticles promoted the development of arterial plaques that obstructed blood flow. The role of inflammation in plaque formation has been known for some time but this connects it with the ultrafine particles characteristic of urban air. While the study was done with mice (what did you expect, they’d use people?), the air was good old Los Angeles freeway, vintage 2007. Mice breathed either downtown LA freeway air or the same air filtered to remove the ultrafines. The mice breathing freeway air had 55% more plaquing and the plaques were 25% bigger than the filtered air mice. And it all happened pretty quickly.

So far large scale epidemiologic studies haven’t been able to find a “no effect” level for air pollution. If there is one, we are a long way away from it in most urban areas.

Does this kind of news make you anxious? Just take a couple of deep breaths.


  1. #1 6EQUJ5
    January 25, 2008

    Think of all the diesel particulates — soot — that we’ve been breathing all our lives,

  2. #2 daedalus2u
    January 25, 2008

    I think the mechanism is likely via inhibition of nitric oxide synthase. The nasal passages produce a couple hundred ppb NO in the air which reaches the lungs. This NO production is inhibited by particle inhalation. This is eNOS, which typically is found in caveolae which might well be more sensitive to particles than other forms of NOS.



    A more recent paper


    Found the same thing, but they donít seem to quite appreciate it. They are looking for higher exhaled NO to be pathologic (which it can be, but isnít in non-pathologic situations). High exhaled NO is a sign of lung inflammation in asthma. NO is also a very good anti-inflammatory agent.

    Nasal NO is likely more important than FE(NO) (in this circumstance), but is a lot harder to measure because it is much more variable. Normal NO in air passing through the nasal passages is a couple hundred ppb (not the ~10 ppb measured in FE(NO). If the nasal passages are occluded NO levels can reach 20 ppm (yes, ppm, not ppb).

    I think the effect of particulates on heart disease is probably the same as the effects due to cold. Low humidity air does reduce NO production in the nose, I would think that cold air would too.


  3. #3 Scrambler
    January 25, 2008

    How do you filter ultrafine particles without also removing the more coarse particles? Just asking …

  4. #4 revere
    January 25, 2008

    scrambler: You can fractionate by size via a compactor, but in this case I think all the particulates were filtered out.

  5. #5 phisrow
    January 26, 2008

    It looks like mechanical filtration is pretty hopeless on any reasonable scale with particles that small. Are they small enough to permit approaching them with tactics used on things like viruses? Could we, in theory at any rate, develop a “smog vaccine” to induce the immune system to attack or encapsulate such particles when they enter the body?

  6. #6 revere
    January 26, 2008

    phisrow: You are correct that you can’t feasibly filter out particles that small for individuals if they are in community air. The preventive measure is not to generate them. Many are probably (my speculation) generated by gas to particle conversion in situ. By eliminating the precursors you would eliminate the particles. So much work needs to be done to identify the ultrafines and their sources. We know they are in urban “smog” (photochemical oxidants). What else? And what are they in smog?

  7. #7 Frank Mirer
    January 26, 2008

    Maximum filter penetration is at 300 nm (0.3 micron). Below that, air is cleaned by sedimentation, also lung deposition becomes dominated by sedimentation.

    In environment, nanoparticles are generated by combustion processes, then agglomerate to ultrafines with a mmd of about 1 micron. The EPA fine particle size of PM2.5 sits in between the combustion 1 u peak and the crustal mmd peak at 10 u. OSHA respirable, about 4 u, is picking up the back end of the crustal distribution. (Respirable may be defended as health based, based on mass deposition. Particle area and number may be a different story.)

    News of penetration of ultrafine and fine particles into the systemic circulation to cause cardiac effects is about 10 years old. The American Heart Association scientific statement concludes that particles are a cause of heart problems.