EPA’s New Ozone Rule: Part 7

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?


  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.

One response to “EPA’s New Ozone Rule: Part 7

  1. Pingback: EPA’s New Ozone Rule: Part 24 | Michael Klein's Environmental Essays

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