The EPA recently announced stronger standards for fine particulate matter, described as reducing pollution by airborne "soot." However, an examination of its supporting documentation reveals a lack of focus on particulate composition, neglect of actual exposures – as well as no mention of any health effects of soot. Here we explore the implications of these shortcomings.
“EPA finalizes stronger standards for harmful soot pollution, significantly increasing health and clean air protection for families, workers, and communities…”
– EPA
This was national news, but only the New York Times got it right; this regulatory action refers not to soot but the total mass of size-classified particulate matter as collected by filtration, PM2.5. “Soot” is not mentioned anywhere in the massive seven hundred and fifteen-page technical support document, but the press release boldly proclaimed “fine particle pollution, also known as soot.” As I wrote in 2021,
“PM2.5 is a mixture of many types of particles classified only by size, while soot is confined to unburned carbon.”
Soot lines the insides of coal- or wood-fired chimneys, belches out of poorly tuned diesel tailpipes and coated my mother’s outside laundry lines in the era of coal-fired space heating. PM2.5 is a mixture that does not exist as an atmospheric entity; these disparate particles meet for the first time on the filter of an EPA air sampler. In the world of air pollution, soot, and PM2.5 are at opposite trends of the spectrum:
- PM2.5 can be high in soluble sulfates and nitrates that may appear white, with median diameters of ~ 1 micrometer.
- Soot particles are smaller (<0.15 micrometers), insoluble, and black.
By this unwarranted juxtaposition, EPA seeks to cover it all.
Does particle size matter?
Fundamentally, yes. Particulate toxicity depends on its composition, acidity, solubility, and size, which determines the degree of penetration and dwell time in our respiratory system. Air pollution particle sizes vary tremendously by many orders of magnitude, from microscopic grains of sand to “ultrafine” that are too small to be captured and weighed but must be counted as electronic disturbances.
Once inhaled, penetration is inversely related to particle size. Particles larger than 2.5 micrometers in diameter tend to be deposited in the upper respiratory tract; the smaller PM2.5 particles may enter the lower tract. Only much smaller particles can enter the bloodstream and potentially affect the cardiovascular system, and only even smaller ones, < 0.15 micrometers, can “defeat” the blood-brain barrier and potentially affect neurology. Neither of these size restrictions is discussed in the technical support document, nor is the fact that, as with smoking, chronic effects may depend on decades of internal deposition.
Pollution Sources
Where does PM2.5 come from? Virtually everywhere. There are outdoor sources, the bulk from inorganic ions (sulfates and nitrates) and organic compounds formed in the atmosphere that can only be controlled indirectly, plus smaller contributions from windblown dust. Soot and smoke, on the other hand, are produced by incomplete combustion of carbon. Because of cost and reduced efficiency, soot is not produced in powerplant boilers or other major industrial facilities under normal operating conditions.
Indoor sources of PM2.5 are ubiquitous and largely uncontrolled. They include cigarette smoke, fireplaces, household dust, pet dander, cooking, cleaning, and candle smoke. Their contributions to human health are largely unquantified.
Tighter restrictions on emissions to improve ambient air quality
This is a familiar story. As a regulatory agency, which problems would you prefer to tackle?
- Riding herd on a few large facilities.
- Inspecting individual vehicle exhausts.
- Restricting outdoor barbecues and trash disposal.
- Licensing indoor air pollution sources.
PM2.5 is a perfect whipping boy:
- Emissions from a variety of sources can be targeted without documenting toxicity.
- Ambient community levels are relatively uniform.
- Sampling equipment and analytical methods are well-developed.
- No special technological skills are required.
Determining the contributions of specific components of ambient PM2.5 can be much more difficult. Although elemental particles (Fe, Pb, Ca, etc.) are relatively easy to quantify, organic compounds, including soot, are much more difficult. The need to characterize atmospheric carbon concentration goes back a century when various analog methods were developed based on the blackness of samples. Ambient particle counters are now available, including inexpensive models suitable for home use. Given an adequate instrumentation market, I do not doubt the sampling problem can be solved.
PM2.5 monitoring is a good example of the well-known “lamp-post problem. EPA chooses to monitor it routinely because it is relatively straightforward, i.e., “the light is better.” And why is that? Because of the decades of development required to meet the agency’s regulations. By contrast, lacking the need to comply with regulatory requirements, soot monitoring has been totally neglected. The EPA operating cycle is thus complete: Only regulated pollutants deserve monitoring, and only monitored pollutants can be regulated. This guarantees the maintenance of the status quo regardless of new scientific developments.
Health effects
In searching the EPA’s technical support document, I found no mentions of
- soot
- lag-time, an essential component for short-term exposures
- cumulative exposure and latency measures necessary for long-term effects
- indoor or personal measurements that comprise ~85% of our exposures.
The most thorough comparison of mortality associations with “soot” vs. PM2.5 was presented by a group of European authors in 2011 who identified four long-term studies, including my studies of US veterans. Associations with mortality were much stronger for elemental carbon (soot) than for PM2.5, with about ten times the risk. This critical study was not discussed in the EPA technical support document.
Most long-term air pollution studies have been based on geographic differences, e.g., urban vs. rural, east vs. west. One study compared changes in health with changes in air quality around coal-fired power plants, but not soot. It found no relationships with short-term exposures and was not discussed by EPA.
The New York Times published a review of the potential health effects of wildfire exposure, including premature mortality. Guess what? Despite the copious press reports of “bad air,” no such deaths have been reported. How can this be given the black carbon and soot concentrations involved in these fires? Possible explanations involve ease of detection and avoidance of even limited durations of exposure and low probability of exposure for extremely frail and sensitive individuals.
What To Do Now?
As both a long-time taxpayer and student of air pollution, I am incensed by this attempt to justify new regulatory actions. It is unsupported by scientific evidence, and its statistical “associations” are insufficient. We all want clean air. These remarks are about the air that we actually breathe and the control of the pollutants that truly matter. I can only hope that other interested observers will take note.