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Air Pollution–Related Illness


Abigail R. Lara

, MD, University of Colorado

Last full review/revision May 2020| Content last modified May 2020

The major components of air pollution in developed countries are

  • Nitrogen dioxide (from combustion of fossil fuels)
  • Ozone (from the effect of sunlight on nitrogen dioxide and hydrocarbons)
  • Suspended solid or liquid particles
  • Sulfur oxides

(See also Overview of Environmental Pulmonary Disease.)

Indoor air pollution has additional sources, particularly

  • Passive smoking
  • Burning of biomass fuel (eg, wood, animal waste, crops) in developing countries (eg, for cooking and heating).

High levels of air pollution can adversely affect lung function and trigger asthma and COPD (chronic obstructive pulmonary disease) exacerbations and increase risk of lung cancer. Air pollution also increases risk of acute cardiovascular events (eg, myocardial infarction) and development of coronary artery disease. People living in areas with a large amount of traffic, especially when stagnant air is created by thermal inversions, are at particular risk.

All of the so-called criteria air pollutants (oxides of nitrogen, oxides of sulfur, ozone, carbon monoxide, lead, particulates), except carbon monoxide and lead, cause airway hyperreactivity. Long-term exposure may increase respiratory infections and respiratory symptoms in the general population, especially in children, and can decrease lung function in children.

Ozone, which is the major component of smog, is a strong respiratory irritant and oxidant. Ozone levels tend to be highest in the summer and in the late morning and early afternoon. Short-term exposures can cause dyspnea, chest pain, and airway reactivity. Children who regularly participate in outdoor activities during days on which ozone pollution is high are more likely to develop asthma. Long-term exposure to ozone produces a small, permanent decrease in lung function.

Oxides of sulfur, resulting from combustion of fossil fuels that are high in sulfur content, can create acid aerosols with high solubility, which are likely to be deposited in the upper airways. Sulfur oxides can induce airway inflammation, possibly increasing the risk of chronic bronchitis as well as inducing bronchoconstriction.

Particulate air pollution is a complex mixture, derived from fossil fuel combustion (especially diesel). The particles can have both local and systemic inflammatory effects, suggesting an explanation for their impact on both pulmonary and cardiovascular health. So-called PM2.5 (particulate matter < 2.5 micrometer diameter) produce a greater inflammatory response per mass than do larger particles. Data suggest that particulate air pollution increases death rates from all causes, especially cardiovascular and respiratory illness.

Air pollution data have raised concerns regarding the potential health effects of even smaller particles, so-called nanoparticles, which are particles manufactured via a controlled engineering process, and ultrafine particles. Nanoparticles and ultrafine particles are generally defined as < 0.1 micrometer (< 100 nanometer) in diameter. Certain nanoparticles and ultrafine particles can induce oxidative stress, airway inflammation, and toxicity in animal models and have been associated with increased respiratory symptoms in patients with asthma; however, direct causation has yet to be reported.

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