Air pollution remains a contentious issue. While everyone is in favor of cleaner air, there is less unanimity over which pollutants, in what concentrations, can harm our health. The linkage between air pollution and disease is beset with problems of accurately identifying a dose-response (a biologic gradient), a clear temporal connection, and, most importantly, biologic plausibility – how does a pollutant cause a disease.
Over time as our understanding and instrumentation have changed and improved, we have reframed the villain from particulate matter as a whole to its various components. The evil du jour has been PM2.5, the smaller particles, but some scientists are focusing on the even smaller components of PM2.5 as the bad actors. A new paper in the Journal of Physiology feels it has identified a new culprit, polycyclic aromatic hydrocarbons (PAH). To say that PAH's, as a class is a new concern is not entirely true, levels at the World Trade Center site increased 65-fold and raised questions of cancer risk. More recently, and relevant to this study, PAH levels were a concern as a water pollutant entering the food chain after the Deepwater Horizon blowout. And this is the starting point for this latest study.
Despite "clear differences in air pollutants and aquatic environmental pollution (e.g., physicochemical properties of the pollutants, interaction between pollutants and the environment, the biology of the species exposed and the route of exposure) it has become apparent that parallels exist, especially in terms of the ability of these pollutants to cause cardiovascular toxicity."
While the lung is the gateway for air pollution, the researchers put to the side any linkage of pollution to asthma or chronic obstructive pulmonary disease. Instead, they focus on the presumptive impact of air polluted with PM2.5s on the heart and its roles in cardiovascular disease. But how to explain how these particles affect more distant organs?
Within the lung, particles captured by alveolar macrophages trigger an inflammatory response, and it is hypothesized that a "sufficient particle dose, reactivity, or lack of clearance leads to amplification of the response … causing systemic inflammation." Or that these particles, by an unknown mechanism, "stimulate alveolar sensory receptors" to ultimately altering the autonomic function of the heart and vasculature. Finally, advances in our understanding of the composition of PM2.5 have identified ultrafine particles (UFP), paving the way for a third hypothesis. The tiny size of UFPs allows them to translocate across the thin alveolar-capillary wall (by an as-yet-undetermined mechanism) and enter the circulation themselves to directly affect cardiovascular function." 
These statements have significant limitations. First, these mechanisms are theoretical, and as their citation states, "There is a wealth of evidence for and against each of these hypotheses." That the mechanisms are not explicitly described as theoretical can be forgiven because they are writing to their peers who presumably already are aware of the hypothetical nature of their argument. But there is an additional deal-breaking limitation, the PAH's an "ultrafine" particle within the PM2.5, and "Ultrafine PM cannot presently be routinely measured in the environment." Without a quantifiable measure, no amount of statistical sophistry will yield a dose-response curve, the biologic gradient necessary for an epidemiologic study.
"The translocation pathway is of importance as it provides a biological basis that could account for the widespread effects of inhaled PM across the cardiovascular system, and elsewhere in the body."
The evidence they do cite comes from the translocation of gold nanoparticles in both rats and human subjects. Here, volunteers inhaled gold particles off and on over two hours, and subsequent blood and tissue analysis found that at best, 0.2% of the inhaled gold translocated. But translocation is size-dependent, with smaller particle being translocated more readily. PAHs are five times the size of the gold particles so that the translocation pathway may be more important to the researcher's beliefs and funding than to a biologic pathway.
The heart of their argument begins with the 1989 Exxon Valdez spill putting a lot of PAHs into the water and the subsequent finding of significant cardiotoxic effects on the herring and salmon of the area. These effects involved not only the cardiac structure but the heart's rhythm and ability to pump. The Deepwater Horizon disaster demonstrated an additional reduction of cardiac work in fish spawning in the area. They also detail in vitro studies showing an effect by PAHs on electrical excitation of fish heart cells
The Path from Fish to Humans
The researcher point out that core function and physiologic properties, like those of the heart, are conserved evolutionarily. Vertebrates share some common characteristics; we are similar in some ways to fish. Their argument is bolstered by the "similar" cardiotoxic effects of some drugs, like tricyclic anti-depressants, on fish and humans. But those similarities need to be balanced by the "significant differences between human and zebrafish hearts." And of course we need not forget the "differences in routes of uptake between fish (water/gill/gut) and terrestrial mammals (air/lung/gut).
With ambiguity firmly in hand, they point to tantalizing, unproven, threads of possibility. The general format of their argument is that PAHs cause these particular effects in fish, that PM2.5 has been implicated in adverse cardiac health, that PAHs are contained in PM2.5 and therefore may well be the smoking gun. In writing about the general process of atherosclerosis, "These results suggest tissue-specific cytotoxic effects by individual PAHs and PM warrants further study."
At times they point out that in the PM2.5 studies considered, "specific PAHs were not described," at other times they are more disingenuous.
"Mammalian (including human) studies from urban areas around the world implicate PM2.5 and its associated tricyclic PAHs in the induction of cardiac arrhythmias, the exacerbation of heart failure, the triggering of myocardial infarction and other atherosclerotic/ischemic complications."
No ambiguity in that statement, and in writing those words, the authors cite two papers. Neither has any information linking PAH's to these outcomes. At best, the only comment I could find was this.
"Although there is only limited epidemiological evidence directly linking UFPs [ultrafine particulates, the fraction in which PAH would be found] with cardiovascular health problems, the toxicological and experimental exposure evidence is suggestive that this size fraction may pose a particularly high risk to the cardiovascular system." 
So, where are we left?
There are a few key messages.
- Studying air pollution is difficult and everchanging. Our increasing understanding, especially about how factors relate to one another, means that our target questions keep changing and are more refined.
- As with any incremental process, the changes in our thinking are found in the nuance, paradigm shifts are rare. As a result, communicating air pollution “science” isn’t straightforward. Experts rely on jargon, and subtlety that we “civilians” do not appreciate; science communicators, including this one, are left to do the heaving lifting. In many instances, despite our best efforts, both experts and the curious provide “a tale, told by an idiot, full of sound and fury, signifying nothing.”
- To understand the background and put the message into a proper perspective, you have “to read the plaque.” You have to look back at the citations, and few of us are willing to read the entire paper, let alone the references. In those instances where I did pursue those prior studies, they did not support, at least in my mind, the statements being made. That inaccuracy, intentional or not, is exceedingly problematic. We understand intuitively that a number without a context has little meaning; is four big or small? Words, too, require a framework, often it is hiding in the references.
What is the impact of air pollution on our health? The short answer is we do not know, although, as I have said before, it is hard to argue against cleaner air. Nor do we understand the underlying biological plausible mechanisms and their relationship to one another. Our understanding is in its infancy, and perhaps we should be more humble in our declarations.
 Nanomaterials Versus Ambient Ultrafine Particles: An Opportunity to Exchange Toxicology Knowledge Environmental Health Perspectives DOI: 10.1289/EHP424.
Source: Polyaromatic hydrocarbons in pollution: a heart-breaking matter Journal of Physiology DOI: 10.1113/JP278885.