Particulate Matters
Our Air, Our Laws, and COVID-19
Pollution — Image by NRCS Montana (licensed under CC PDM 1.0)
A breath of fresh air might be just what we need right now. With COVID-19 lockdowns keeping us cooped up all day, a walk down the street can be a welcome change of scenery. During my walks, I’ve noticed the air in Boston feels cleaner, even during a time when my allergies would normally bring tears to my eyes. With the lockdown came lower levels of ambient air pollutants, which are known to exacerbate respiratory diseases such as COVID-19. The regulation of one notable pollutant, particulate matter with a diameter smaller than 2.5 micrometers, or PM2.5, can provide a glimpse into what environmental factors may have contributed to the COVID-19 pandemic and what the future of air quality and infectious diseases might hold.
The U.S. Environmental Protection Agency (EPA) regulates six “criteria” air pollutants, a name that comes from the Clean Air Act in 1971, which requires that the EPA review new research on these pollutants every 5 years, and update regulations based on new criteria. These criteria are used to set the National Ambient Air Quality Standards (NAAQS) for nitrogen dioxide (NO2), ozone, sulfur dioxide (SO2), lead, carbon monoxide (CO), and particulate matter (PM). PM is regulated at two sizes, coarse and fine PM at 10 and 2.5 micrometers in diameter, respectively. PM2.5 is almost 7 times smaller than the finest human hair and is composed of particles made from vehicle emissions, biofuel fumes, pollen and more. There are many anthropogenic and natural sources, but human-derived particles make up the majority. But while a growing body of research shows that our current regulations don’t protect public health sufficiently, PM2.5 regulation is unlikely to change, even during a global health crisis that acutely manifests the harm that these fine particles may have on our health.
PM2.5 and COVID-19
The link between respiratory infections and pollutants such as PM2.5 has been established in the scientific literature for decades. The biological impact of PM2.5 on the lungs necessitates the continual reevaluation of the laws meant to protect our health. PM2.5 can reach deep into our lungs, where these tiny particles can inhibit normal respiratory function and even pass into the bloodstream, where it can impact cardiovascular, kidney, and other important body functions. A review by UNC Chapel Hill researchers described the relationship between exposure to PM2.5 and susceptibility to respiratory viral infections. The article hypothesizes several possibilities for this link: increased oxidative stress, decreased activity of the innate immune system and macrophages, and decreased production or a change in function of surfactant proteins, in the lungs.
Surfactant proteins, called SP-A, B, C, and D, are secreted by one of the three kinds of cells in the alveoli,type II alveolar cells, and serve multiple functions. SP-B and SP-C reduce surface tension, which makes gas exchange more efficient and prevents alveolar collapse, a critical function that provides our bodies with oxygen and expels carbon dioxide.SP-A and SP-D opsonize, or tag, pathogens to promote their destruction via phagocytosis, and are known to tag the SARS-CoV spike protein, a piece of the virus responsible for the 2003 SARS pandemic. SARS-CoV and SARS-CoV-2, the virus responsible for COVID-19, have similar spike proteins and use the same cell surface receptor to infect lung cells. That receptor, called ACE2, is found primarily on the same type II alveolar cells that produce surfactant protein. Both mechanical and immunological surfactant activities are critical to healthy lung function, therefore type II alveolar cells are essential to the respiratory system.
PM2.5 could, theoretically, make the body more susceptible to SARS-CoV-2 infection by decreasing expression or changing the function of surfactant proteins. The virus could then intensify the problem by infecting and destroying the cells that produce surfactant. In a pre-print study, Harvard researchers found that increasing PM2.5 exposure by 1 µg/m3, about 1 part per billion, is correlated with an 8% increase in COVID-19 mortality. It’s likely that a constellation of consequences from PM2.5 exposure both facilitates SARS-CoV-2 infection, but the mutual relationship between pollutant and virus through type II alveolar cells is an interesting potential subject of future research.
Oxidative Stress refers to the presence of radical oxygen molecules. These free radicals can attach body tissues. The resulting damage is implicated in aging, heart disease, and many other disease processes.
Gas Exchange refers to the process of binding oxygen to molecules of hemoglobin – found in red blood cells – and releasing CO2 out of the body. This exchange occurs between the lungs and the pulmonary arteries and veins.
Alveolar Collapse: Tiny sacs, called alveoli (plr.), found at the tips of the branching respiratory system in the lungs are the location of gas exchange in the body. Their thin cell walls allow the bloodstream to be close to the oxygen in inhaled air. Keeping the alveoli open, fluid-free, and functional is essential for breathing. Surfactant proteins facilitate this by reducing surface tension, which would normally constrict alveoli.
PM2.5 Regulation Under Attack
PM2.5 regulation has recently been on the EPA’s chopping block, despiteinternal assessments that reaffirm the dangers of PM2.5 pollution. In the past, the Report to Congress on the Benefits and Costs of Federal Regulations analysis of PM2.5 regulation found that it was the most financially beneficial EPA regulation, saving upwards of $167 billion annually. In 2017, the authors removed the section on PM2.5 benefits from the report. The most recent iteration of that report highlights only the uncertainty surrounding PM2.5 exposure, distorting the benefits of the regulation.
The EPA proposed the “Strengthening Transparency in Regulatory Science” rule, which would require all data used to justify EPA regulations to be publicly available. This rule has been widely disputed by researchers and public health faculty who point out that personal health information used to study the impacts of pollutants can’t be made publicly available without an unprecedented breach of privacy, leading to weaker regulations for lack of health data.On the other side, members of groups such as the Heartland Institute, a climate-change denial group, have written letters in support of the new ruling.
While a final decision has not been made, there is a clear danger in limiting the scope of the EPA’s scientific analysis to only those studies with public information. The EPA’s 2019 final policy assessment on PM2.5 air quality standards concluded that recent studies have “reduced key uncertainties and broadened our understanding” surrounding the health impacts of PM 2.5 and that “current primary PM2.5 standards could allow a substantial number of PM2.5-associated deaths.” This finding was largely ignored by the Chartered Clean Air Scientific Advisory Committee (CASAC), a group of 7 external EPA advisors, many of whom have long histories of opposing regulatory action on pollutants and ties to the industry giants that would be impacted by that regulation.
The uncertainty surrounding studies that predict the benefits of PM2.5 regulation have often been a talking point for anti-regulation proponents. Through arguments that mirror those of COVID-19 or climate change deniers, PM2.5 deniers point to the fallibility of models as a way to criticize any conclusions drawn therefrom. And, like COVID-19 mortality models, new data, assumptions, and methodologies can influence the final statistical conclusions of those models. But when realistic models find significant health risks from PM2.5, the response should not be to wait and see. The economic toll of PM2.5 (and climate broadly) regulation is another common argument against regulation, but the 2001 Whitman v. American Trucking Assns. Supreme Court Ruling determined that the EPA is not allowed to “consider financial effects when making environmental regulations.” Additionally, PM2.5 is a classification solely of size and not of a specific chemical, allowing dissenters to argue that regulation is punishing industry for ambient PM2.5 pollution for which they are not responsible. One study that disputes this argument analyzed the chemical makeup of PM2.5 and found ammonium sulfate, primarily from diesel engines, accounted for over 80% of ambient PM2.5. Another study found toxic trace elements in PM2.5 along heavily trafficked roads in New Jersey. Regardless of the source or composition, the link between PM2.5 and premature mortality necessitates action to reduce the burden of air pollution.
Current regulations hold that the daily concentration of PM2.5 must be less than 35 µg/m3 for 98% of days within the last three years, and the average annual concentration must be less than 12 µg/m3 to protect vulnerable populations, such as those with asthma, and less than 15 µg/m3 to protect everyone. 12 micrograms, spread around an area about 90 times bigger than a basketball, could seem like an insignificant concentration, but we don’t know how many individual particles are in the air without knowing their densities. This complicated system of rules for PM2.5 pollution aims to mitigate adverse health risks from exposure, but if 12 µg/m3 is already too high, does the rest of it matter?
Especially in regions with high air pollution and high COVID-19 mortality, such asnorthern Italy, cleaner skies might mean more than just an enjoyable walk outside; it could help with future respiratory disease epidemics. All around the United States, PM2.5 concentrations have dropped, a likely result of stay-at-home orders. The EPA provides data on PM2.5 and other criteria pollutant concentrations and allows quick comparisons across time. A quick look at Suffolk County, MA shows that in the past few months, PM2.5 levels have remained low, with few days with concentrations above the 12 µg/m3 standard. The areas around New York City show dramatic reductions in high PM2.5 detections in 2020 compared to the levels over the past few years. Any color that isn’t green represents a time when PM2.5 was detected at a level above the 12 µg/m3 maximum, a standard that is likely not restrictive enough.
COVID-19 lockdowns around the world have changed local environments significantly over the past few months. A decrease in air pollution in the Northeast US, India and China has been detected by satellites. Carbon emissions are projected to drop by an unprecedented 8%. And, as governments around the world investigate how to reopen, keeping people safe from infection while maintaining the beneficial changes, such as decreased manufacturing and travel, that lowered pollution should be at the top of the agenda. Despite the opportunity for change towards a more sustainable future, the EPA has instead rolled back emissions regulations in an attempt to keep the economy afloat. There’s a realistic fear that the economic damage caused by the pandemic will put climate change policy on the back burner, despite evidence that climate change will exacerbate the spread and impact of infectious diseases. However, if our politicians are serious about mitigating or preventing future, economy-destroying pandemics, then keeping our air and water clean, protecting wild spaces, and decreasing our impact on the natural world is essential.
So, as lockdowns are lifted and you peek your head outside, take a breath of fresh air. It’s likely healthier than when the lockdown started. And if we want to keep it that way, we can’t return to the old normal. We must build a new normal that addresses the environmental indifference that contributed to and exacerbated the current crisis. Only then can we breathe freely without a pandemic locking us down.
Hugh Shirley is a recent graduate from Northeastern University with a BS in Biochemistry. He organized two global health conferences with a team of undergrads, led an undergraduate research project on remediating estrogen contamination in groundwater, and founded a sustainability action committee. He has written for NUSci, PHU and the Johns Hopkins Outbreak Observatory. Currently, he is working for Atalanta Therapeutics before matriculating into Harvard Medical School in the fall, where he will pursue an MD. In his free time, he swims, writes, and is playing Mario Odyssey on his brand new quarantine Switch.
