We need to know more about the total environment ... only by reorganizing our Federal efforts can we develop that knowledge, and effectively ensure the protection, development and enhancement of the total environment itself.
—Richard Nixon, message to Congress establishing the EPA, July 9, 1970
After World War II, Donora, Pennsylvania, was a prosperous town of about fourteen thousand inhabitants located on a bend of the Monongahela River. There were many well-paying jobs in the town’s major industry, a huge complex consisting of open hearth and blast furnaces at one end and a zinc works at the other. Coal was plentiful in Pennsylvania. Coal and iron ore went in one end of the linear array of factories, and galvanized wire, nails, and other products emerged from the other end. Executives lived in plush homes on the hillside that overlooked the zinc works. Others lived in Cement Town, at the other end of the city that bristled with smoke stacks, viewed as a sign of prosperity. Nobody paid much attention to the fact that virtually all of the plants on both sides of the river had died.
Things changed dramatically and suddenly on Thursday, October 28, 1948, when a temperature inversion trapped the gases and particulates emitted by the mill. The smog was so dense that residents walking down the street could no longer see the buildings that were familiar landmarks. Then, people began to become sick and die.
Firefighters struggled to bring oxygen tanks to the afflicted. The Board of Health set up an emergency aid station and temporary morgue in the community center. The mill management refused to believe that the pollutants spewing from the factory were responsible for the crisis. After all, they said, the mill was doing what it had been doing for thirty years.
The exact death toll will probably never be known with certainty, but at least twenty-one died and hundreds were sickened. Investigations that followed linked the disaster to the oxides of sulfur, fluorine, and other unchecked emissions from the zinc works and the rest of the factory complex.
Now, if you walk down McKean Avenue past abandoned stores, it is hard to find traces of the mill. However, at the corner of McKean and Sixth Street, you will find one of the few painted storefronts: the Donora Smog Museum, located in what used to be a Chinese restaurant (http://bit.ly/1MARO0V, accessed September 28, 2015). On a lucky day, you will meet Brian Charlton, one of the town’s schoolteachers and the museum’s curator. He will tell you about the killer smog, the subsequent investigations, and how it all led to the town’s new slogan, “Clean Air Started Here.” Or he may regale you with tales of Stan “the Man” Musial, who was from Donora and whose artifacts occupy a share of the museum.
The Donora disaster was precipitated by a weather event (the formation of an inversion layer)—not climate change—and by uncontrolled emissions from the Donora mills. Its importance lies far beyond the toll on the residents of the town: this event marked the beginning of efforts to protect health by controlling hazardous air pollutants. In its analysis of the benefits of these protections, the EPA concentrates on two: particulate matter and ozone. This chapter will focus on both protections, with emphasis on ozone and how the EPA makes its decisions on air quality standards.
The Donora disaster was not the first hint that smoke is bad for health. One of the earliest recorded warnings about poor air quality was published in 1661, when John Evelyn warned “His Sacred Majestie” of “The Inconvenience of the Aer and Smoak of London” in the treatise he submitted to his king and Parliament.1 A number of more contemporary events cemented this link, including accounts of the infamous 1952 London “killer fog” that caused an estimated 12,000 deaths.2
Donorans will tell you that their tragedy led the US government to focus on the relationship between air quality and health. Multiple investigations that followed the Donora tragedy began to coalesce in 1955, when Congress passed the Air Pollution Control Act, which funded research into air pollution. The idea of controlling air pollution came into prominence in 1963 with the passage of the Clean Air Act (CAA), which provided funds for the development of air pollution monitoring and control under the auspices of the US Public Health Service. Actual controls on air pollutants were enacted seven years later.
The quote that introduces this chapter is from President Richard Nixon’s 1970 executive order that established the Environmental Protection Agency. With broad bipartisan support in Congress, the EPA was created by law, and the CAA was amended to give the new agency the authority to regulate air pollutants. The amended act required the EPA to establish National Ambient Air Quality Standards (NAAQS) for the most offensive pollutants, of which there are six, referred to together as the criteria pollutants: lead, carbon monoxide, nitrogen dioxide, sulfur dioxide, ozone, and particle pollution. For each, there are two standards. The first is referred to as the primary standard and is designed to set a concentration limit with an “adequate margin of safety,” thereby enabling the EPA to fulfill its mission, “to protect human health and the environment.” The primary standard makes special reference to “sensitive” populations, such as children, asthmatics, and the elderly. The secondary standard is designed to protect the general welfare and focuses on preventing reductions in visibility, damage to crops and other forms of vegetation, animals, and buildings. Portions of the country that meet the standards are referred to as attainment areas. Areas that fail to meet the standard are referred to as nonattainment areas.
The removal of lead, a potent neurotoxin, from gasoline was one of the earliest and most important accomplishments of the CAA. Although this was controversial at the time, we now take lead-free gasoline for granted. The action led to a dramatic drop in the lead burden of children and an increase in the average IQ of over five points per child.3
The CAA was amended again in 1990, during the administration of George H. W. Bush. This amendment also passed with broad bipartisan support in the House of Representatives (401 to 21) and the Senate (89 to 11). This is the so-called acid rain amendment. Although the focus of the amendment was on the authority to regulate the sources of oxides of nitrogen (NOx) and sulfur (SOx) that were causing acid rain and damaging lakes and forests, it also enabled the EPA to regulate NOx and SOx along with chemicals that were depleting the ozone layer—most notably, the chlorofluorocarbons.
Under the authority of the CAA, the EPA has promulgated and amended a variety of regulations that establish NAAQS for each of the criteria pollutants. The CAA also requires the EPA to publish periodic reports to Congress that quantify the CAA’s costs and benefits. These reports are one of the most important sources of data that make clear-cut links between improvements in air quality and subsequent savings in the total costs associated with poor health. In the most recent of these reports, the EPA predicts that by 2020 the CAA will result in nearly $2 trillion in health benefits each year, at an annual cost to industry of $65 billion.4 These benefits are due largely to reductions in the atmospheric concentrations of particulate matter and ozone, two criteria pollutants. An account of the deaths prevented, asthma attacks averted, and other health benefits attributable to the CAA and the anticipated new ozone standards are presented in table 7.1 and table 7.2. The importance of these pollutants provides the rationale for the focus of this chapter and why the Intergovernmental Panel on Climate Change includes air quality as a climate change health target (for more details, see figure 10.1).
Table 7.1 Annual health benefits attributable to the Clean Air Act5
Health effect reduction
Adult PM2.5 deaths
Infant PM2.5 deaths
Emergency room visits
Restricted activity days
Lost school days
Lost work days
Table 7.2 Annual health benefits expected after new ozone air quality standard, year 2025; includes ozone and particle-reduction effects6
Range of expected effects
Asthma attacks, children
Missed days of school—children
Missed work days—adults
Emergency room visits—asthma
Ozone (O3) is a pale blue gas. It has a distinctive pungent odor similar to that of chlorine. It is formed in the lowest layer of the atmosphere, the troposphere, which extends from the surface of the earth to an altitude of about eleven miles. The troposphere is thicker near the equator and thinner at the poles. In the troposphere, ozone is an important constituent of ground-level smog. Ozone is also formed in the next-highest layer, the stratosphere, which extends upward above the troposphere to an altitude of just over thirty miles at the equator and to just over eight miles at the poles. In the stratosphere, ozone protects us from the ultraviolet rays of the sun that cause skin cancer and damage crops and other plants. Hence the phrase, “Ozone: good up high, bad nearby.”
Ozone is both formed and destroyed in the stratosphere as the result of the actions of ultraviolet (UV) light.7 UV light from the sun splits molecular oxygen (O2) into two atoms of oxygen (O) in the middle portion of the stratosphere. This highly reactive form of oxygen combines rapidly with O2 to form ozone (O3). In upper layers of the stratosphere, high-energy UV rays from the sun attack ozone to form O2 and O, thus creating a cycle of formation and degradation. The heat generated by these reactions and the associated trapping of the energy from the sunlight that drives them warms the upper portions of the stratosphere.
The chemical reactions involving tropospheric ozone are much more complex. The basic reactions involve the criteria pollutants nitric oxide and carbon monoxide along with volatile organic compounds (VOCs) in the presence of heat, sunlight, and diatomic or regular oxygen. Methane is one of the VOCs involved in these reactions. Because of the importance of methane as a global warming gas, VOCs are commonly subdivided into (1) methane; and (2) everything else, or nonmethane VOCs (NMVOCs). Isoprene is the most important of the naturally occurring NMVOCs, with estimated annual emissions of between four and six hundred million metric tons per year, an amount that is thought to be similar to natural emissions of methane.8 Isoprene concentrations are likely to increase due to more exuberant plant growth stimulated by increases in the atmospheric carbon dioxide concentration and warming due to climate change. Many NMVOCs are created by human activity. Some come from petroleum products, whereas others come from the transportation industry, paint, and industrial chemicals. Uncertainties in the prediction of future emissions of VOCs contribute to problems in forecasting future ozone levels. Finally, some ozone is formed from oxides of nitrogen in bolts of lightning. This mechanism is also likely to become more important as climate change causes an increase in the number of severe storms.
Ozone is removed from the troposphere by several chemical reactions. The ozone–water vapor reaction is critical and is expected to help keep ozone levels from rising in humid southern portions of the United States To a large degree, the ozone–water reaction is expected to balance the effects of an increase in temperature that would otherwise lead to an increase in the concentration of ozone.
Tropospheric ozone is also a short-lived greenhouse gas. It is responsible for about 15 percent of the increase in the greenhouse effect that has taken place since the beginning of the industrial age and the onset of our warming climate. From a technical perspective, tropospheric ozone accounts for about 0.35 W/m2 in its role as an RF agent, a quantitative measure of the greenhouse effect (see chapter 2 for more details). To place this in a broader perspective, total RF has increased by about 2.4 W/m2 since the onset of the industrial age, according to the most recent IPCC report (see also chapter 2).9
Ozone is a powerful oxidizing agent. It combines chemically with a wide variety of other molecules. In our bodies, these chemical reactions damage tissues—particularly in the respiratory system, where they cause inflammation and trigger immunological reactions. These responses are the link between ground-level ozone and asthma, one of the most prevalent diseases in the United States. The CDC estimates that 7.3 percent of adults and 8.0 percent of children suffer from asthma.10
Because of the importance of ground-level ozone, its concentration is monitored closely using a variety of ground- and satellite-based techniques. The EPA uses these ozone concentration data to compute an air quality index (AQI) that provides health warnings and guidance to individuals and communities. Interested parties can access the AQI at the EPA’s Enviroflash website (www.enviroflash.info), and the AQI is commonly included in weather forecasts. The AQI ranges from 0 to 500, where 0–50 means good air with no health concerns, 51–100 indicates moderate health concerns, 101–150 indicates unhealthy air for sensitive groups, 151–200 indicates unhealthy air, and 201–300 and 301–500 indicate very unhealthy and hazardous air, respectively.
This is a story that goes beyond the realm of health and climate change to include history, science, politics, and the law. Like oil and water, these elements do not always mix well.
Emission controls focused largely on the criteria pollutants have improved the quality of the air in the United States. Ozone levels are 33 percent lower now than they were in 1980, and 90 percent of the areas that failed to meet ozone air quality standards in 1988 comply with the 75 parts per billion (ppb) standard.11 The situation is similar in Europe, where there have also been air quality improvements. However, ozone levels have more than doubled in Asia as a direct result of the economic expansions in that region in the absence of controls on air emissions (see section 184.108.40.206 of the IPCC Fifth Assessment Report for details).12
The primary, or health-based, air-quality standard for ozone was set at 75 ppb in 2008 (i.e., there are seventy-five ozone molecules in every billion air molecules). The EPA’s language that defines standards is often convoluted—and this is particularly true for ozone. As of December 28, 2015, the primary standard was set as the “annual fourth-highest daily maximum 8-hour concentration, averaged over 3 years.”13 Translated, this means that the average ozone concentration in any given eight-hour time interval may not be greater than 75 ppb on more than three occasions during any given three-year period. Understandably, this is usually shortened to “the 8-hour standard.” As required by the CAA and in order to update required health protections, the EPA began a review of the standard in the fall of 2014. The intent was to lower the standard to somewhere between 60 ppb and 70 ppb. Based on 2011–2013 monitoring data, 358 counties—including most major metropolitan areas in the United States—would have been noncompliant if a 70 ppb standard had been in effect. If the standard were 65 ppb, a total of 558 counties would be in violation and classified as nonattainment areas.14 California is excluded from these data because the Air Resources Board has set their eight-hour standard at 70 ppb.
The path to the 2014 reevaluation is complicated and heavily influenced by political considerations. In 1971, the very first primary standard was 80 ppb, averaged over one hour and not to be exceeded by more than one hour per year. The standard was revised in 1997, when it was lowered to 80 ppb averaged over eight hours. In 2008, the eight-hour standard was lowered to 75 ppb, where it remained until 2015. This is where the story becomes complex as political considerations emerge.
When the EPA lowered the eight-hour standard to 75 ppb, it did so against the unanimous advice of its own Clean Air Scientific Advisory Committee (CASAC), which had urged setting the standard to between 60 ppb and 70 ppb. This deviation was deemed a political decision made by the George W. Bush administration. The standard was revisited again from 2009 to 2010 during the administration of Barack Obama. However, on a Friday afternoon, a time apparently chosen to minimize media scrutiny, the EPA announced that it had suspended plans to revise the standard in spite of the formal publication of a proposed rule in the Federal Register and the receipt of numerous comments from the public and other stakeholders. Again, this was viewed as a political decision. This time, it seemed to be designed to take political heat off the EPA and to shield candidates during the forthcoming election cycle. On the Wednesday prior to the US Thanksgiving holiday in 2014, the EPA announced that it was once again reconsidering the standard and opened a new round of comments on a proposed rule.
Lawsuits ensued, and an October 1, 2015, deadline to publish a final standard was imposed via a consent decree. The new standard was set at 70 ppb. After intense lobbying, industry leaders complained, advocating leaving the standard at 75 ppb. Public health groups and environmentalists that had advocated for a more stringent rule with a standard of 60 ppb argued that the EPA had failed to protect public health adequately. The new standard does not take effect immediately. Nonattainment areas have until 2020 or late 2037 to meet the new standard. By then, the EPA will be required to reevaluate the standard. More lawsuits seem likely.
So what is the evidence that concentrations of ozone higher than the 75 ppb standard are bad for health? During the course of my medical career, I reviewed many articles for a variety of scientific and medical journals as part of the peer-review process, and for many years I was a member of my hospital’s science review and ethics committees, including three years as chair of the ethics committee, formally known as the institutional review board (IRB). The primary review considerations are related to methodology, results, and conclusions—that is, whether the science is sound. However, there is more to consider, such as the ethics involved. Usually this means that there is a declaration that an independent review committee, such as the one I chaired, has approved the research. It is also important to ask whether potential issues related to conflicts of interest and bias have been managed properly, which may involve determining the source of the funds used to sponsor the study. Therefore, when I reviewed the human inhalation studies, I saw them from my perspective as a university professor who worked in a medical environment in which I taught a course in evidence-based medicine and chaired the research ethics committee in my hospital.
Because the route for exposure is via the lungs and numerous studies have linked ozone exposure to exacerbations of asthma and other respiratory conditions, several ozone-inhalation studies in normal volunteers have been published. The authors stated that federal and international standards for the ethical conduct of research involving human participants were met and informed consent had been obtained. Importantly, the brief administration of ozone to healthy individuals was thought to pose little risk. Unhealthy individuals and children were excluded. These studies appear to have had two objectives: to better understand the effects of ozone on the human respiratory system and to influence the EPA as it seeks to update the air quality standard for ozone.
In its proposed rule, the EPA appears to rely on many of the studies that I have reviewed. Some were funded in part by the American Petroleum Institute, an industry-supported group.15 This fact creates the potential for bias even though the results were published in peer-reviewed scientific literature. It is virtually certain that research participants were paid. This is permissible, but setting an appropriate level for reimbursement is tricky. The ethics committee must decide that the amount does not create the possibility for coercion. Coercively high payments discourage dropouts from the study and underreporting of adverse effects that could result in dismissal from the study and a loss of income. Both have the possible effect of introducing bias into the results. The study volunteers were healthy men and women free of respiratory problems who had not been exposed to high ozone concentrations. Some were competitive athletes; those who were not were commonly regular exercisers. Thus the research participants were healthier than typical Americans. This creates yet another opportunity for bias when research results are extrapolated to the American population as a whole.
Participants were exposed to ozone concentrations that ranged from 40 ppb to 120 ppb during several 6.6-hour intervals. Participants exercised during exposures and underwent basic pulmonary function tests. Participants also completed a questionnaire known as the total symptom score (TSS) inventory as a part of the evaluation. Although some of the inhalation protocols and statistical analyses seemed somewhat contorted in a way that minimized explaining the effects of the ozone inhalation, a close evaluation of the data shows that virtually all studies found effects on the pulmonary function tests, the TSS, or both at relatively low O3 concentrations. A reevaluation of one of these studies focused on just one of the many inhalation protocols and found clear effects of 60 ppb ozone on breathing function.16
Another study I examined was conducted by EPA scientists, reported in 2011, and again evaluated young healthy adults who were exposed to 60 ppb of O3.17 In addition to significant reductions in two standard breathing tests, these investigators found evidence for inflammation in the airway by studying white blood cells (polymorphonuclear leukocytes) in the sputum sixteen to eighteen hours after O3 exposure. Because ozone is a potent oxidizing agent, investigators also measured a gene called glutathione S-transferase mu 1 that affects responses to oxidative stress. Participants who carried this gene experienced significant effects on one of the breathing tests. They concluded that inhaling O3 at a concentration of 60 ppb affects lung function and triggers an immunological response. These are hallmarks of asthma.
In a 2015 report, a Taiwanese group measured pulmonary function in a group of almost 1,500 nonasthmatic children.18 They performed typical tests of pulmonary function and correlated these with ozone data from monitoring sites near the children’s schools. The average ozone concentration during the monitoring period was 29 ppb. The maximum never exceeded 58 ppb. They found that on a day after an ozone peak there was a reduction in lung function as measured by a standard breathing test. Younger children, six to ten years of age, were more affected than older children.
When new O3 concentration limits are set, it is important to consider additional factors that do not always show up in the statistical analyses found in these reports. It seems likely that individuals with asthma, other pulmonary problems, or other chronic diseases, especially of the cardiovascular system, might be more sensitive to ozone than the super-healthy adult research participants were. It is possible to make a convincing argument that the research participants in the published studies were not “normal” subjects but were in fact healthier than normal and part of a population that is the least likely to sustain an adverse effect after the inhalation of O3. Children are also likely to be more susceptible to ozone at the concentrations studied, as suggested by the observations made on Taiwanese children, because each minute they breathe more liters of air per unit weight than adults. This means that the dose of ozone at the same ozone concentration is higher in children. The dose differs from the concentration and may be a more important measure. Dose is determined by the concentration of ozone in the air multiplied by the amount of air inhaled and time. Because children and other sensitive populations were excluded from the studies, their results may have only limited applicability to the EPA’s task, which is to protect “sensitive populations ... with an adequate margin of safety.”
Global and regional modeling efforts are needed to predict the effects of climate change on future atmospheric ozone concentrations. The variables that are the most important determinants of the future ozone concentration include the temperature itself, which is likely to increase as the result of climate change; the atmospheric concentration of ozone precursors, including nitrogen oxides and natural and anthropogenic VOC concentrations, some of which will increase due to climate change; ozone produced by lightning, which may also increase in prevalence; air currents that mix stratospheric and tropospheric ozone; and the concentration of water vapor, a factor that is also likely to be altered by climate change. Water vapor is the only one of these variables that leads to a decrease in the ozone concentration.
There are typically two components to global ozone models: a global circulation model (GCM) and a chemical transport model (CTM). GCMs simulate atmospheric climatic phenomena, such as heat flow, whereas CTMs simulate the behavior of a given chemical species, such as VOCs. This GCM-CTM combination yields data that predict worldwide background ozone concentrations. Additional modeling efforts, based on local assumptions concerning emission scenarios, produce more regional data that are used to predict ozone concentrations in a given city.
The authors of a relatively recent review of twelve studies that compared data from the year 2000 with what they expected in 2050 found three investigations that predicted an increase in the global ozone concentration and nine that predicted a decrease.19 Projected changes ranged from a 12 percent decrease to a 5 percent increase. These studies focused on what the EPA terms policy-relevant background ozone concentrations, or ozone that would be found in the surface layer of the troposphere over the United States in the absence of additional North American anthropogenic emissions. Differences in assumptions, particularly the effects of lightning and emissions of isoprene (both of which are likely to increase due to climate change), account for a great deal of the variability among studies. The review’s authors conducted their own study, utilizing an IPCC scenario that assumes a balance between fossil fuel and other energy sources. Using the IPCC A1B scenario, they projected a 2 percent increase in the global ozone burden. In the eastern United States, rising emissions of ozone precursors that would drive ozone concentrations up were canceled out by increases in the tropospheric water vapor content, which removes ozone from the air, in spite of increases in temperature. In the western part of the country, which is drier, they project an increase of between 2 and 5 ppb in the ozone concentration.
To begin to address the issues posed by climate change related to ozone levels in US cities, the authors of another recent study used models based on an IPCC scenario that predicts a continued high rate of CO2 emissions (the IPCC A2 scenario).20 This scenario predicts temperature increases of between 1.6°C and 3.6°C by 2050 relative to 1990 temperatures. Because of difficulties predicting anthropogenic ozone precursor emissions, these authors assumed that such emissions would remain constant in the future. Presumably, population increases and reduced per capita emissions were expected to offset each other. Emissions of natural ozone precursors were included in the authors’ modeling effort. They predicted that there would be an increase in the summertime one-hour ozone concentration of 4.8 ppb on average for the cities studied. The largest increase was 9.6 ppb. Cities with an increase of 12 percent or more included Chicago, Illinois, Cleveland, Ohio, Columbus, Ohio, and Detroit, Michigan. The authors predicted a 68 percent increase in the number of days each summer for which the ozone concentration would exceed the present eight-hour standard of 75 ppb. Although they considered the entire United States, the cities with increases were all in the Mississippi River Valley and the eastern half of the country. Because the results of ozone modeling are highly dependent on model assumptions, other studies reached different conclusions. In one of these studies, in which investigators used models that predicted an emissions decrease of more than 50 percent in oxides of nitrogen and a balanced use of fossil and nonfossil fuels, the investigators found that there would be a reduction in future ozone concentrations that ranged between 11 and 28 percent in the eight-hour ozone concentration in different regions of the United States.21
The summer of 2015 set new records for the number and severity of wildfires as a consequence of the severe drought that affected significant parts of the nation. These fires produce particulate matter (PM) and are likely to affect the concentration of ozone. The summer of 2004 was also a bad year for wildfires in North America. Significant portions of the forests in Alaska and the Yukon Territory were consumed by fires. The smoke, carbon monoxide, and other emissions drifted toward the northeastern part of the United States and Canada. To assess the impact of these fires on ozone levels, researchers employed data from aircraft-based measuring devices to estimate the additional carbon monoxide burden in the troposphere over New England that arose from these fires.22 The researchers found that around 30 percent of the carbon monoxide in the atmosphere, a criteria pollutant and an ozone precursor, could be attributed to these distant fires. In a communication with colleagues, the study authors learned that this pollution plume was also detected in Europe. It is likely that carbon monoxide plumes from 2015’s fires will affect the eastern part of the United States as they did in 2004.
From these and other studies, it seems possible—even likely—that uncontrolled emissions of greenhouse gases and ozone precursors will lead to increases in the ozone concentration in the most highly polluted portions of the country. If these increases occur, they will have important implications for the health of the exposed populations. One take-home message is clear; there are at least two ways that increases in the ground-level ozone concentration can be prevented: (1) mitigate climate change through effective controls on greenhouse gas emissions to prevent increases in surface temperatures that drive the chemical reactions that produce ozone and (2) control anthropogenic emissions of ozone precursors, particularly methane.
It is likely that the effects of climate change will lead to increases in the ozone concentration in some parts of the world, particularly in areas with high levels of air pollution due to high concentrations of VOCs and/or low levels of atmospheric water vapor, such as the Southwest. To be certain that the quality of the air at a future date meets the new standard, the initial target concentration must be lower than any new standard. An example may help to explain this point: if the new standard is set at 60 ppb and air quality modeling predicts that the ozone concentration will rise by 5 ppb in five years due to hotter weather induced by climate change, then the concentration five years after the standard is finalized will be 65 ppb and the region will be noncompliant. To remain compliant during the five-year period, the new target should be 55 ppb, so that when the predicted 5 ppb increase due to climate change is added, the ozone concentration will be 60 ppb and thus in compliance. The 5 ppb offset is referred to as the climate change penalty.23 Research by at least one group predicts that we should include a climate penalty when planning for the future.24 Of course, the additional reductions undertaken to anticipate a concentration rise would have health benefits, so perhaps the term penalty is not appropriate. A climate change protection might be a more appropriate and accurate term.
Particulate matter is one of the deadliest of all of the pollutants in the atmosphere. In addition, it is the other criteria pollutant that will be affected by climate change. PM is not a single entity but a category that includes objects with a variety of sizes, shapes, and, importantly, compositions. As science and epidemiology have progressed, it has become evident that PM is a major a risk factor for the development of a variety of diseases.25
Atmospheric modeling studies predict that there will be changes in the PM concentration due to the mixing of atmospheric layers and changes in the movement of air from tropical toward polar latitudes. These changes are likely to be more pronounced for PM than for ozone for two reasons: (1) the region-to-region concentration differences for PM are much greater than for ozone and (2) the normal background concentrations of ozone are much higher than for PM.26
PM in the atmosphere exists in the form of an aerosol—that is, a suspension of liquids and solids in a gas. At present, particle size forms the basis for the classification of PM. Size is a critical risk determinant and forms the basis for regulatory activity. Somewhat paradoxically, the smaller the particle, the greater the threat to health. Large particles are trapped in the upper airway by nasal hairs and the mucous membranes of the nose, throat, and the upper airway. The smallest particles travel deeply into the lungs and into the alveoli, the small air sacs from which oxygen is absorbed by red blood cells and CO2 is eliminated. This is also where PM triggers inflammatory and immunological responses. These responses damage tissues and organs, as shown in figure 7.1. PM is further classified by the mechanism of formation. Primary PM is generated de novo, often by combustion in coal-fired power plants, internal combustion engines, or fires. Secondary PM is formed by physical and chemical reactions among constituents of the atmospheric aerosol. The criteria pollutants—such as oxides of sulfur and nitrogen, formed by burning fossil fuels—are important precursors to these secondary particulates.
PM size would be a simple concept if all particles were spherical and had the same density. Although some particles are spherical and easily described in terms of their size, others are elongated fibers, flakes, or almost any other shape imaginable. Because of this variability, atmospheric scientists use the term aerodynamic diameter to describe PM size. Thus, regardless of their size, shape, composition, or density, all particles with the same aerodynamic diameter behave similarly in the atmosphere. More precisely, under the influence of gravity, all particles with the same aerodynamic diameter reach the same final speed as they settle under laboratory conditions. As indicated previously, the smallest particles have the greatest impact on health. These are referred to as PM2.5 and have an aerodynamic diameter of 2.5 microns (millionths of a meter) or less. Like ozone, PM2.5 concentrations are monitored closely and used to compute air quality indices. The EPA website Enviroflash displays the index for major cities.
A 2009 review article suggests that the relationship between temperatures of the future and PM concentrations is much weaker than the relationship between temperature and ozone concentrations.27 This conclusion is derived in part from an analysis of data collected between 1990 and 2005 in five cities in the southwestern part of the United States.28 As expected, since temperature is a force that drives reactions that form ozone, the authors of the aforementioned study found a link between temperature and ozone concentration. There was no link between temperature and PM concentrations. Although there were large variations in the PM concentration, these were thought to be due to between-city differences in the transportation sector, construction, and industrialization after the passage of the North American Free Trade Agreement (NAFTA), not due to differences in climate.
PM concentrations in the southwest were correlated with relative humidity and may rise and fall in parallel with the water content of the atmosphere.29 This effect is related to the mechanisms that remove PM from the atmosphere. PM acts as a nidus for the formation of water droplets, which become drops of rain that fall to the ground.30 As a corollary to this observation, the rate of PM removal from the atmosphere is more highly correlated with the frequency with which it rains than with the intensity of rainfall.31 Frequent brief rains remove more PM from the atmosphere than rarer more intense rains. Based on predictions of future increases in precipitation in the northeastern United States and decreases in the southwest, PM clearances and hence concentrations are likely to decrease and increase, respectively, in these regions.32 These results need to be correlated with future emissions of PM in order to gain an accurate perspective on future PM concentrations.
As the result of climate change, severe droughts will probably continue in the southwestern part of the country. As a result, wildfires are likely to become an increasingly serious problem. These wildfires have become a major source of PM discharges into the atmosphere. A glimpse into a future characterized by more wildfires occurred during the 2003 European drought and heatwave. The fires and the resulting discharges of PM into the atmosphere were due to a combination of below-normal rainfall, extreme temperatures, and stagnation of the air that precluded dilution of PM by mixing it uniformly with other parts of the troposphere.33 A 2008 report of the wildfires in California in 2003 demonstrated the health toll that fire-induced PM can exact.34 Using satellite-derived PM data, the investigators found increases in PM2.5 concentrations of up to seventy micrograms per cubic meter during fires compared to prefire concentrations. These peaks were associated with a 34 percent increase in hospital admissions. Those between the ages of sixty-five and ninety-nine years were the most likely to be affected. During the month of October 2003, the investigators’ analysis identified over forty-thousand hospital admissions due to increased PM2.5 concentrations.
Because most PM enters the body via the lungs, that is where many of its effects are found. However, many other organs are also affected, as shown in figure 7.1. In the nose, some very small particles may enter the brain directly via the nerve cells that mediate the sense of smell. These neurons originate in the nose, pass through tiny holes in the bone at the base of the frontal lobes of the brain known as the cribiform plate, and then pass directly to the limbic system of the brain.35 Among other things, the limbic system plays an important role in memory and emotion. In the brain, these particles trigger inflammatory reactions and increase the activity of enzymes that are a part of the immunological system. This causes changes in the brain that are similar to those found in patients with Alzheimer’s disease.36
PM-induced inflammatory and immunological responses that are similar to those in the brain are also evident in the lungs. These responses produce a condition known as oxidative stress, which damages tissues to varying degrees, depending on its intensity.37 Oxidative stress in the nervous system affects neural reflexes that control blood pressure and other functions that are not a part of conscious activity. Thus, the seemingly innocuous entry of particles into the lungs can result in a constriction of blood vessels and increases in blood pressure. Altered reflex activity also affects heart rate and rhythm and produces atherosclerosis in the arteries to the heart and brain. Atherosclerosis and high blood pressure are major risk factors for strokes and heart attacks and major contributors to the global burden of disease, as discussed in chapter 1. In addition, other changes in the autonomic nervous system help control how our bodies metabolize glucose and insulin, as well as a variety of other abnormalities depicted in figure 7.1.
When the vast epidemiological data linking air pollution and human disease are tallied, it is clear that the four most common causes of death among Americans—heart disease, cancer, diseases of the respiratory system, and stroke—all are caused in part by air pollution. Furthermore, as epidemiological research progresses, the spectrum of disease caused by pollution is likely to widen to include type 2 diabetes mellitus, Alzheimer’s disease, and other degenerative diseases of the nervous system.38
Climate change seems virtually certain to have some adverse effects on air quality due to expected changes in temperature, humidity, the emission of naturally-occurring VOCs such as isoprene, the flow of air currents, droughts, and related wildfires, and so on. Predicting all of these variables is difficult, so precise estimates are associated with uncertainties. This is particularly true for ground-level ozone. There is much to learn about this aspect of climate change. The literature linking air pollutants with diseases has always been limited by methodology. As techniques for measuring PM have improved, the data about these particles have become more sophisticated and informative. The ability to subdivide particles by size is a perfect example. Three decades ago, many reports referred only to particles with an aerodynamic diameter of ten microns or less. As technology has advanced, it has become possible to measure smaller particles accurately and more frequently. Now, hourly pollution reports focus on those with an aerodynamic diameter of 2.5 microns or less, with the awareness that the smallest particles in that range are the most threatening.
As atmospheric science and epidemiology evolve, it seems likely that analyses of the chemical composition of PM2.5 will become more widely available and incorporated into ambient air quality standards. One study of the chemical composition of PM linked higher disease risks to particles produced by burning coal, compared to particles from other sources.39 The investigators did this by using a statistical technique called factor analysis and identified a “silicon factor” linked to particles arising from the earth’s crust, a “lead factor” linked to exhaust from motor vehicles, and a “selenium factor” linked to coal combustion. Using additional statistical techniques, the PM from mobile and coal sources was found to increase the risk of death. As a preview of the future, short-duration (thirty-minute) sequential measurements of PM2.5 in Killarney, Ireland, demonstrated evening peak concentrations that were more than fifteen times greater than the WHO guideline.40 These peaks correlated with when workers return to their homes and light coal fires for heat and cooking. No linkages to health outcomes were attempted, although such consequences are likely to happen, as shown by reports linking transient peaks in pollutants to cardiovascular diseases and stroke becoming more widespread, as discussed below. These peaks may disappear or at least become less prominent as the Irish ban on “smoky coal” (bituminous coal) begins to take effect.
Policy always lags behind science—and this is particularly true when air quality standards are revised. Currently, the concentration of ozone is averaged over an eight-hour period. Today’s state-of-the-art epidemiological methods have shown, for example, that the risk of an acute stroke rises significantly after a brief spike in the concentration of particulates.41 There also are other examples in which disease appears after a pollutant spike.42 An increasing number of Americans have implanted cardiac pacemaker defibrillators, and when these devices detect a potentially fatal heart rhythm disturbance (such as ventricular fibrillation), they attempt to pace the heart to restore a viable rhythm. If that fails, the device delivers a shock to the heart to defibrillate the cardiac muscle. Post-defibrillation data show a close correlation with prior spikes in nitrogen dioxide levels in the air. Among patients who have had ten or more defibrillator discharges, nitrogen dioxide, carbon monoxide, black carbon, and fine particle mass all were linked to the cardiac events. Very large short-duration peaks in the concentration of pollutants may lurk and remain undetected when only the eight-hour average concentration is considered. It is likely that future studies will emerge that firmly establish links between transient peaks in the concentration of air pollutants and diseases. This in turn will require further changes in air quality standards.