Air pollution is due to a variety of contaminants in the air and can occur in both indoor and outdoor environments. Outdoor contaminants include carbon monoxide, lead, sulfur dioxide, oxides of nitrogen, ozone (O3) particulate matter and biologic agents.1 Indoor air pollution is often due to many of the same contaminants but for the purposes of brevity this discussion will be restricted to outdoor agents. The sources of outdoor air pollution are divided into point sources and mobile sources.  Point sources are fixed in location and are usually factories and power plants that routinely emit gaseous and particulate matter when operating. Mobile sources include everything that uses internal combustion as a power source, most importantly motor vehicles. The Clean Air Act of 1970 as amended in 1990 established the Environmental Protection Agency (EPA) to set and monitor National Ambient Air Quality Standards (NAAQS). These standards can be found at

Asthma is reversible obstructive airway disease. Each of the contaminants above has been established to have a negative impact on asthma except for lead and carbon monoxide. 2 Particulate matter (< 10 um in diameter) has been associated with asthma exacerbations in studies performed not only in the U.S. and Europe but also in Australia, Brazil, China, and New Zealand.1 One interesting study looked at particulates and incidence of respiratory disease in a valley in Utah before, during, and after a labor strike that temporarily shut down a steel mill in the valley.2 Both particulates and respiratory diseases decreased during the strike and returned to prior levels when the mill re-opened.2

Diesel exhaust and diesel exhaust particles have been shown to have an immediate effect on lungs. Mast cells and neutrophils are increased.1 Studies have shown an increase in inflammatory markers and antioxidants like glutathione.3 More interestingly diesel exhaust has been associated with increased incidence of allergy, which is another trigger for asthma. This association was first noted in Japan. In 1951 there were 20,000 diesel cars in Japan, by 1988 there were 7,600,000. Before World War II, allergy to Japanese cedar was very rare.4 By 1974 the overall incidence had risen to 3.8% and by 1981 was 9.4%.4 The highest incidence (13.2%) occurred in schoolchildren living in areas with cedar trees and heavy traffic.4 Further studies have shown that diesel exhaust particles are associated with a switch to a T helper cell type 2 (Th2) which is associated with increased IgE production.1

Ninety three percent of sulfur dioxide comes from point sources (factories) and while studies have shown it is a potent bronchoconstrictor, its affects are often difficult to separate from particulate pollution.2 Nitrogen dioxide is a potent bronchoconstrictor as well, but it is also a precursor of ozone.2

Ozone in controlled exposure studies has been shown to drop forced vital capacity (FVC) and forced expiratory volume (FEV1) rapidly probably due to a sensory neural reflex.1    Ozone also leads to increased neutrophilic inflammation within a few hours of exposure.1 Studies have shown that there are  increased hospital admissions 24 to 48 hours after ozone exposure.1

Keeping track of these various pollutants and deciding when they are a significant threat to our respiratory health can be problematic as each one has separate values and times of exposure before they become significant (see NAAQS above).  The EPA has conveniently developed an Air Quality Index (AQI) that integrates all the various pollutants (see Figure 1). They also explain what these values mean for different populations (see Figure 2). The information can be accessed at .


Figure 1:

Air Quality Index
(AQI) Values
Levels of Health Concern Colors
When the AQI is in this range: ..air quality conditions are: …as symbolized by this color:
0 to 50 Good Green
51 to 100 Moderate Yellow
101 to 150 Unhealthy for Sensitive Groups Orange
151 to 200 Unhealthy Red
201 to 300 Very Unhealthy Purple
301 to 500 Hazardous Maroon
Note: Values above 500 are considered Beyond the AQI. Follow recommendations for the Hazardous category. Additional information on reducing exposure to extremely high levels of particle pollution is available here

Figure 2:

Air Quality Index Levels of Health Concern Numerical
Good 0 to 50 Air quality is considered satisfactory, and air pollution poses little or no risk.
Moderate 51 to 100 Air quality is acceptable; however, for some pollutants there may be a moderate health concern for a very small number of people who are unusually sensitive to air pollution.
Unhealthy for Sensitive Groups 101 to 150 Members of sensitive groups may experience health effects. The general public is not likely to be affected.
Unhealthy 151 to 200 Everyone may begin to experience health effects; members of sensitive groups may experience more serious health effects.
Very Unhealthy 201 to 300 Health alert: everyone may experience more serious health effects.
Hazardous 301 to 500 Health warnings of emergency conditions. The entire population is more likely to be affected.


The actual values for San Antonio each day and the predicted values for tomorrow can be found at .   The EPA also publishes an extensive document called the Menu of Control Measures which lists the things that can be done to reduce air pollutants (see ). When these measures are employed systematically they can reduce emissions and reduce respiratory problems. Examples of this occurred at both the Atlanta and the Beijing Olympic games. In 1996, Atlanta reduced ozone by reducing vehicle use and succeeded in reducing ozone levels and asthma morbidity during the games compared to both immediately before and immediately after the games.1  In 2008, Beijing implemented controls on both personal automobile use and industrial use of fossil fuels.1 Particulate matter smaller than 2.5 um fell from 72.3 ug/m3 before the games to 45.7 ug/m3 during the games and daily asthma events fell from 16.5/d before the games to 7.3/d during the games.1 It is apparent that improving our air quality is not only the responsibility of government and industry but of every one of us who use internal combustion engines.


  1. Hernandez ML and Peden DB. Air Pollution: Indoor and Outdoor. In Middleton’s Allergy Principles and Practice. 8th edition. Edited by Adkinson FN, Bochner BS, Burks WA et al. Elsevier. Philadelphia PA. 2014. Pages 482-484.
  2. Peden DB. Air pollution in Asthma: effect of pollutants on airway inflammation. Ann Allergy Immunol. 2001; 87 (suppl):12-17.
  3. Peden DB. The epidemiology and genetics of asthma risk associated with air pollution. J Allergy Clin Immunol. 2005; 115:213-9.
  4. Ring J, Buters J and Behrendt H. Particulate and Pollen Interactions. In Middleton’s Allergy Principles and Practice. 8th edition. Edited by Adkinson FN, Bochner BS, Burks WA et al. Elsevier. Philadelphia PA. 2014. Pages 497 – 505.

written by Theodore M. Freeman, M.D.