Higher levels of PM2.5 have been shown to cause negative cardiovascular and respiratory health effects. Consequently, commercial and residential standards are being set to reduce PM2.5 exposures with the intent of improving health outcomes. This may or may not be a valid approach. Here’s why:
All PM2.5 is not the same. The negative health effects of PM2.5 vary by region. If it was just the prevalence of small particles, the health effects would relate more closely with the level of particulate pollution. Some regions with higher levels of PM2.5 have relatively low levels of illness. Others have substantially higher levels of illness. So it stands to reason that it is not just the size of the particles or the mass and number of the particles, but also the composition of the particles that is important. The fact is – some PM2.5 has a higher level of toxicity than others.
The question is – Why? A primary line of research in the medical community concerns the “oxidative potential” of PM2.5 particles. Oxidative potential refers to the concentration of Reactive Oxygen Species (ROS) in the air. The best known ROS is ozone, but there are many others including hydroxyl radicals (OH), superoxides and peroxides. All are characterized by being unstable molecules that are highly reactive with other molecules. They are also known to attack human cells. The major health problems related to ROS are caused by what is known as “oxidative stress.” Oxidative stress leads to increased inflammation and can manifest itself in such things as asthma, arthritis, heart disease, cancer and accelerated aging.
Many studies have been conducted over the past 10 years to determine if the “oxidative potential” of particles is actually a better predictor of negative health outcomes than the gross measure of PM2.5. Most, if not all, of these studies have come from the medical community. For example, a recently published study – Children’s Respiratory health and oxidative potential of PM2.5: the PIAMA birth cohort study; Yang A., Janssen NAH, Brunekreef B, et al. in the journal Occupational Environmental Medicine (January 11, 2016) – found that asthma incidence, prevalence of asthma symptoms and rhinitis were positively associated with higher levels of oxidative potential. These associations were sensitive to adjustment for NO2 (Nitrogen Dioxide). However, “respiratory health was not significantly associated with PM2.5 mass.”
This well-designed study was conducted in the Netherlands included 3,701 participants. Respiratory measurements were made by spirometry and included forced expiratory volume, forced vital capacity, and mid-respiratory flows. Airway inflammation was also measured.
Another recent medical study may shed some light on the effects of “oxidative potential” and air quality. The study entitled Particle Depletion Does Not Remediate Acute Effects of Traffic-related Air Pollution and Allergen. A Randomized, Double-Blind Crossover Study by Wooding et al. was published in the American Journal of Respiratory Care Medicine, Sept. 2019. It’s purpose was to assess the effectiveness of diesel exhaust “particulate-filtering technologies” in reducing the effects of diesel exhaust traffic related air pollution (TRAP). An analysis of the results of the study tells us much more about what could be causing many of the problems with high levels of PM2.5 and how some “air cleaning” technologies could actually be increasing the negative health effects of air pollution.
Many diesel trucks are manufactured with diesel exhaust control devices. These consist of a very high efficiency particle filter followed by a “catalytic converter” that reduces or “eliminates” the gaseous portion of the exhaust.
The randomized double-blinded crossover study was conducted by medical researchers at the Air Pollution Exposure Laboratory, Department of Respiratory Medicine, University of British Columbia. The 14 volunteer participants were atopic (allergic) and 9 had airway hyper-responsiveness (asthma). They were exposed to 3 different “air conditions” including filtered air, air with diesel exhaust and diesel exhaust air that went through a HEPA filter and then was treated by a “simulated” catalytic converter. After two hours of this exposure, they were given an allergen challenge. This was done based on prior findings that diesel exhaust plus allergen had a synergistic effect in allergic individuals. Participants were assessed after exposure for lung function, airway responsiveness and circulating white blood cells (that are activated by the body in allergic reactions). Participants were given one month between exposures. The full study took several years to complete.
Exposures were conducted in a laboratory at the University and the “simulated catalytic converter” was actually a name-brand electrostatic precipitator like those used in homes and commercial buildings. This is very important in that it has a bearing on the interpretation of the results and the increasing use of electronic “air cleaning” devices in indoor spaces.
The researchers used the term Particle Depleted Diesel Exhaust (PDDE) to describe the diesel exhaust that was sent through a HEPA filter and then “cleaned” with the electrostatic precipitator. PDDE-allergen co-exposure impaired lung function more than the Diesel Exhaust (DE) – allergen co-exposure. DE-allergen and PDDE-allergen each increased airway-responsiveness (a measure of asthma) in normally-responsive participants. DE-allergen and PDDE-allergen each increased total leukocyte (white blood cell) counts. Changes in white blood cell counts correlated with lung function decline. Thus, “particulates are not necessarily the sole or main culprit responsible for the harmful effects of diesel exhaust.”
Measurements of PM2.5, Total Volatile Organic Compounds (TVOC) and Nitrogen Dioxide (NO2) were taken on the “exposure air” for all three conditions – filtered air (FA), PDDE and DE.
PM2.5 – Filtered Air – 3 ug/m3, DE – 290 ug/m3, PDDE – 16 ug/m3
TVOC – Filtered Air – 300 ppb; DE – 1,900 ppb and PDDE – 1,700
NO2 – Filtered Air – 0 ppb; DE – 50 ppb; PDDE – 170 ppb
In summary, even though the PM2.5 from the diesel exhaust was reduced by 94%, there was no reduction in negative health outcomes. In fact, by at least one measure the negative reactions of participants exposed to the Particle Depleted Diesel Exhaust plus allergen was more severe than Diesel Exhaust plus allergen.
Note: The EPA Air Quality Guide for Nitrogen Dioxide shows that levels of 150-200 ppb are “unhealthy” and that the “following groups should avoid prolonged outdoor exertion – 1. People with lung disease, such as asthma and 2. Children and older adults. Everyone else should limit prolonged outdoor exertion.”
Little attention has been paid to the “oxidative potential” of particles in the HVAC community. Unfortunately, it is one more example of where the medical and the engineering communities do not communicate with each other. At the very least, it needs to be moved up the priority list of critical issues that need to be addressed in our quest to create healthier indoor environments.
The particle depletion/diesel exhaust study also raises the issue of the indoor air chemistry created by electronic air cleaners. More and more of these cleaners are entering the HVAC market. They all use some form of “activated oxygen” and call it a variety of names from ions, to plasma, to hydroperoxides, to you name it . . . the list seems endless. All use some form of unstable molecules to create reactions that modify the air to “reduce viruses, reduce bacteria, reduce mold, reduce allergies, reduce dust, reduce odors, reduce VOC’s, etc., etc..” Most are supported either by “anecdotal” accounts or very limited tests. All seem to claim that they will not create hazardous byproducts.
Yet, we know through our own tests and those of many others that activated oxygen, like ozone, will react with organic molecules like terpenes (scents) and create massive amounts of ultrafine particles. We also know that the reactions created by the activated oxygen and various substances will create byproducts that are often more harmful than their precursors. Two good examples are the often-created carcinogen formaldehyde and the Nitrogen Dioxide (NO2) that we saw in the study above. But there are many more.
One of the claims is that the activated oxygen created by these devices reacts with molecules to break them down into carbon dioxide and water. This is hard to believe. No, it is impossible! First, the reactions are seldom complete. Secondly, all indoor air has non-organic molecules (think NO being converted into NO2) and third, the reaction paths often go in unintended directions (Formaldehyde is HCHO).
Think for a moment of the medical researcher who has just completed a study on the negative effects of the oxidative potential of outdoor air. The conclusion is that OP is a better predictor of negative cardiovascular and respiratory outcomes than PM2.5. What do you think her reaction is going to be when you tell her that your new electronic air cleaning device is ADDING activated oxygen to indoor spaces?
The minimum that needs to be done is that the manufacturers of these devices need to prove they are safe. One way to start would be expose them to diesel exhaust after it has gone through a HEPA filter. We know from experience with at least one device that it can create high levels of NO2. Users and potential users of electronic air cleaners must have the assurance that other devices will not do the same.
It is also clear that reducing PM2.5 in indoor spaces may not reduce the negative health effects. Determining and dealing with the “oxidative potential” and toxicity of the particles also should be a major consideration.