Tag Archives: lung function

EPA’s New Ozone Rule: Part 9

Posted on July 26, 2012 | 1 comment

Exactly what was the EPA’s reasoning behind lowering the maximum ground-level ozone concentration from 75 ppb to 70 ppb? This is the opening paragraph of the discussion in EPA’s National Ambient Air Quality Standards for Ozone, 2011, page 35.

This section presents the rationale for the Administrator’s final decision that the O3 primary standard, which was set at a level of 0.075 ppm in the 2008 final rule, should instead be set at 0.070 ppm. In developing this rationale, the Administrator recognizes that the CAA [Clean Air Act — MHK] requires her to reach a public health policy judgment as to what standard would be requisite to protect public health with an adequate margin of safety, based on scientific evidence and technical assessments that have inherent uncertainties and limitations. This judgment requires making reasoned decisions as to what weight to place on various types of evidence and assessments, and on the related uncertainties and limitations. Thus, in selecting a final level, the Administrator is seeking not only to prevent O3 levels that have been demonstrated to be harmful but also to prevent lower O3 levels that may pose an unacceptable risk of harm, even if the risk is not precisely identified as to nature or degree.

What the EPA is saying is that it isn’t enough for the maximum concentration of ground-level ozone allowable to be set just below the minimum known to cause harm. Rather, the limit must be low enough so that even if the harm is not certain but only possible, the risk of harm is low enough to be acceptable. Question is, how low must the risk be to considered acceptable? The document itself states that risk must be taken into consideration even when it can’t be precisely identified. But does that mean that any level of risk, no matter how low, is unacceptable? That would be setting a very high standard indeed. And if that is not so, what is the maximum level of risk that is acceptable? What is the cutoff point?

Unspoken is the realization that it is politically unwise to try to impose tougher rules on the public than is necessary to achieve the objective. To do so is to impose unnecessary economic hardship that could provoke a backlash. And indeed, we saw that backlash in September 2011. The EPA can’t admit that fact, but it is nevertheless true.

There have been a number of controlled studies examining human exposure to ozone, but most have been at the 80 ppb level1. However, studies by William C. Adams, researcher (now retired) at the University of California at Davis did expose humans to ozone at average concentrations as low as 40 ppb2. Besides exposing his subjects to steady concentrations, Adams attempted to mimic the natural environment by slowly increasing and then decreasing the ozone concentration, much as the ambient ozone concentration grows in the morning, peaks in midday, and then declines toward evening. Adams found no statistically significant difference in lung function compared to breathing filtered (ozone-free) air at the 40 ppb and 60 ppb levels. However, a later analysis of Adam’s data by the EPA did find a small statistical difference at the 60 ppb level3. EPA finds this of concern, because a small statistical drop of lung function among healthy adults could manifest itself much more forcefully among those with lung disease4.

Still, most controlled studies on ozone exposure do not test beneath the 80 ppb level. Yet the EPA notes that there is no evidence that the harmful effects of ozone stop at the 80 ppb level (start with a very high concentration of ozone and slowly lower it. The concentration level where harmful effects would stop is known as the threshold). In fact, it can be inferred that such effects extend well below that level, because of the variability of responses of the test subjects5. I believe this means that if 80 ppb was the threshold level, then if you exposed test subjects to that concentration, you would see a number of small responses, but they would all be roughly equal to each other. If, on the other hand, some test subjects experience effects much more than others, even though the effects are still small, that indicates that the effects occur well below the 80 ppb level. And small effects for healthy people can mean big effects for those with respiratory disease.

The above concerned controlled studies of subjects of laboratory experiments. EPA also looked at epidemiological studies, studies of what is happening to populations in their day-to-day lives6. Some found thresholds between 25 and 50 ppb. Other studies never found a threshold because the damage that ozone inflicted seemed linear with the concentration. As I understand this, this means that if the concentration was reduced by a specific percentage (for example, a 20% reduction), measureable effects are reduced by the same percentage multiplied by fixed factor (say a 2% reduction in concentration results in a 3% decrease in effects, a 4% reduction results in a 6% decrease in effects, and so on). On the other hand, you might expect that at a concentration near the threshold level, a further reduction would result in a greater decrease of effects (say a 2% reduction results in a 3% in effects, but a 3% reduction results in a 25% decrease in effects, and a 4% reduction results in a 95% decrease in    effects)6. These studies never saw this sort of effect, so they could not conclude there was any threshold for ozone.

The EPA also looked at studies that did subset analysis looking only at days whose ozone concentration did not exceed certain ozone concentrations (such as 80 ppb and 61 ppb), and still found associations between those concentrations and lung function decrements)6.

Regarding the existence of a threshold for the effects of ozone, the EPA concluded:

Based on the above considerations, the 2007 Staff Paper recognized that the available evidence neither supports nor refutes the existence of effect thresholds at the population level for morbidity and mortality effects, and that if a population threshold level does exist, it would likely be well below the level of the then current standard and possibly within the range of background levels. Taken together, these considerations also support the conclusion that if a population threshold level does exist, it would likely be well below the level of the 0.075 ppm, 8-hour average, standard set in 2008.7

But if the EPA needed to pick the lowest allowable concentration, should it have chosen the lowest threshold found by the studies, 25 ppb? That would not be possible, because the background level of ground-level ozone (the concentration of ozone in the U.S. that is either naturally occurring or coming from outside the U.S. and over which the U.S. government has no control. The background level varies with location and season8.) is often above that level of 25 ppb9. This being the case, setting the standard at 25 ppb would have been an impossible demand. (In fact, the 2007 Staff Paper found that below 35 ppb, it was difficult to tell effects from ozone from effects from other air pollutants9.) Even 50 ppb would be an extremely difficult and expensive goal to meet.

Footnotes:

  1. U.S. Environmental Protection Agency, National Ambient Air Quality Standards for Ozone, Final Preamble, 2011, p.38
  2. Adams,W.C., Comparison of chamber 6.6-h exposures to 0.04-0.08 ppm ozone via square-wave and triangular profiles on pulmonary responses Inhalation Toxicology vol. 18: pp. 127-136. For the abstract, click here.
  3. U.S. Environmental Protection Agency, National Ambient Air Quality Standards for Ozone, Final Preamble, 2011, p.38
  4. ibid.p.39
  5. ibid.p.40
  6. ibid.p.42
  7. ibid.p.43
  8. For a detailed discussion of background ozone levels, see U.S. Environmental Protection Agency, Integrated Science Assessment for Ozone and Related Photochemical Oxidants, Third External Review Draft, June 2012, Section 3.4, “Background Ozone Concentrations”, p.3-32ff.
  9. U.S. Environmental Protection Agency, National Ambient Air Quality Standards for Ozone, Final Preamble, 2011, p.42, p.107

1 Comment

Posted in EPA's New Ozone Rule

Tagged , , , , , , , , , , , , , , , ,

EPA’s New Ozone Rule: Part 7

Posted on July 19, 2012 | 1 comment

Before discussing why EPA should lower the limit on maximium ground-level ozone concentration from 75 ppb to 70 ppb, we need to explain why EPA needs to regulate ozone in the first place. Just to clarify, we are not dealing with stratospheric ozone high above the earth’s surface 10 miles up that protects us from harmful ultraviolet radiation from the sun. Rather, we are strictly speaking about ground-level ozone, the only ozone that people have direct exposure to.

Ozone is a highly corrosive chemical, one of the most chemically active known (reaction potential = 2.07 volts in an acid solution at 25°C)1. When breathed in, it attacks the upper respiratory tract and the lungs2. Breathing 100% ozone is quickly fatal, in fact, breathing air with as little as 50 ppm (50,000 ppb) ozone will likely kill a human within a half-hour3. It has been observed that people inhaling 9 ppm ozone along with other air pollutants developed pulmonary edema3.

Ozone at much lower concentrations can also cause problems. To quote EPA’s Integrated Science Assessment:

…short-term O3 exposures induced or were associated with statistically significant declines in lung function. An equally strong body of evidence from controlled human exposure and toxicological studies demonstrated O3-induced inflammatory responses, increased epithelial permeability, and airway hyperresponsiveness. Toxicological studies provided additional evidence for O3-induced impairment of host defenses. Combined, these findings from experimental studies provided support for epidemiologic evidence, in which short-term increases in O3 concentration were consistently associated with increases in respiratory symptoms and asthma medication use in children with asthma, respiratory-related hospital admissions, and ED [emergency department – MHK] visits for COPD [chronic obstructive pulmonary disease, including chronic bronchitis and emphysema – MHK] and asthma. Additionally, recent evidence supports the range of respiratory effects induced by O3 by demonstrating that short-term increases in ambient O3 concentrations can lead to respiratory mortality. The combined evidence across disciplines supports a causal relationship between short-term O3 exposure and respiratory effects4.

The decrease in lung function caused by short-term exposure to ozone quickly fade when the ozone is removed5. However, repeated exposure to ozone over a long period of time may cause more chronic problems such as reduced lung function6. Ozone has also been implicated in causing problems to the cardiovascular, central nervous, and reproductive systems, although these have not been conclusively proven. 6. There is not enough evidence to suggest that ozone causes cancer6.

The EPA’s National Ambient Air Quality Standards 2011 document on ozone states these concerns with some passion:

These physiological effects [inflammation and damage to the respiratory system and impaired host defense capabilities – MHK] have been linked to aggravation of asthma and increased susceptibility to respiratory infection, potentially leading to increased medication use, increased school and work absences, increased visits to doctors’ offices and emergency departments, and increased hospital admissions. Further, pulmonary inflammation is related to increased cellular permeability in the lung, which may be a mechanism by which O3 exposure can lead to cardiovascular system effects, and to potential chronic effects such as chronic bronchitis or long-term damage to the lungs that can lead to reduced quality of life. These are all indicators of adverse O3-related morbidity effects, which are consistent with and lend plausibility to the adverse morbidity effects and mortality effects observed in epidemiological studies.7

Ozone has also been shown to injure plants and reduce their growth. This reduces agricultural yields and the productivity of ecosystems8. Ozone is a significant greenhouse gas, and is probably contributing to global warming9. However, I would think that it would be less than a threat than carbon dioxide, because ozone tends to quickly decompose into oxygen whereas carbon dioxide can linger in the atmosphere for a century or more10. Nevertheless, if society is constantly generating more ozone, the contribution to climate change could be significant. If it reduced its ozone production, this contribution would fade almost instantaneously.

To demonstrate the extent of scientific research documenting the effects of ozone on human health, I excerpted the reference section of Chapter 6 of EPA's Integrated Science Analysis, the chapter that discusses the health effects of short-term ozone exposure. This reference section lists some 500 scientific papers on the effects of ozone. I have not read these papers except for one, so I cannot vouch for them; nevertheless, the list taken together is formidable. Take a look yourself by clicking on the link below. You can click on any reference in the list to see the paper’s abstract.

Reference Section of Chapter 6

The next question we must discuss is: Granted that trace amounts of ozone in the ground-level atmosphere is injurious to human welfare, how do we know that 75 ppb (the former limit) is still injurious? Why wasn’t that level good enough? Why did the EPA think it should lower it?

Footnotes

  1. Rein Munter, Ozone: Science and Technology,Encyclopedia of Life Support Systems. To view, click here.
  2. U.S. Environmental Protection Agency, Integrated Science Assessment for Ozone and Related Photochemical Oxidants, Third External Review Draft, Section 6.2: Respiratory Effects, p. 6-1ff.
  3. Ozone Levels and Their Effects, edited by Den Rasplicka, OzoneLab Instruments website. To view, click here.
  4. U.S. Environmental Protection Agency, Integrated Science Assessment for Ozone and Related Photochemical Oxidants, Third External Review Draft, Chapter 1: Executive Summary, p.1-6.
  5. Ibid., Chapter 6: Integrated Health Effects of Short-Term Ozone Exposure, pp. 6-14, 6-27, 6-165.
  6. Ibid., Table 1-1: Summary of ozone causal determinations by exposure duration and health outcome, p. 1-5. Table 2-2: Summary of evidence from epidemiologic, controlled human exposure, and animal toxicological studies on the health effects associated with short- and long-term exposure to ozone, pp 2-25 — 2-26.
  7. U.S. Environmental Protection Agency, National Ambient Air Quality Standards for Ozone, Final Preamble, 2011, p.40.
  8. U.S. Environmental Protection Agency, Integrated Science Assessment for Ozone and Related Photochemical Oxidants, Third External Review Draft, Table 1-2: Summary of ozone causal determination for welfare effects, p. 1-8. Table 2-3: Summary of ozone causal determination for vegetation and ecosystem effects, p.2-40.
  9. Ibid., Section 2.7.1: Tropospheric Ozone as a Greenhouse Gas, pp. 2-49 — 2-50.
  10. I don’t have a single source for this. Wikipedia quotes M.Z. Jacobson in a 2005 letter to the Journal of Geophysical Research, 110 pp. D14105, as estimating the atmospheric lifetime of carbon dioxide as 300 years (click here to view the Wikipedia article). David Archer, in his article Fate of Fossil Fuels in Geologic Time, Journal of Geophysical Research, Volume 110 C09S05, argues, “A better approximation of the lifetime of fossil fuel CO2 for public discussion might be ‘300 years, plus 25% that lasts forever.'” He claims that when additional carbon dioxide is added to the atmosphere, some of it lingers for tens of thousands of years. To see the article, click here. See also Archer, David et al, Atmospheric Lifetime of Fossil Fuel Carbon Dioxide, Annual Review Earth Planet Sci. 2009 37:117-34 (click here to view). For a lively discussion of the topic, see the Skeptical Science website, which you can read by clicking here.

1 Comment

Posted in EPA's New Ozone Rule

Tagged , , , , , , , , , , , , ,