Air Pollution–Related Illness

ByCarrie A. Redlich, MD, MPH, Yale Occupational and Environmental Medicine Program Yale School of Medicine;
Efia S. James, MD, MPH, Bergen New Bridge Medical Center;Brian Linde, MD, MPH, Yale Occ and Env Medicine Program
Reviewed/Revised Oct 2023
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Air pollution–related illness is disease caused by harmful pollutants in the air or exacerbation of preexisting disease by those pollutants.

Air pollution contributes significantly to a number of adverse health effects. Ambient air pollution can adversely affect lung function and trigger asthma and COPD (chronic obstructive pulmonary disease) exacerbations and increase the risk of lung cancer. Air pollution also increases the risk of acute cardiovascular events (eg, myocardial infarction) and strokes, and the development of coronary artery disease. People living in areas with a large amount of traffic have an elevated risk of pollution-related health effects.

Pollution may affect the air within or outside a building. The causes of indoor and outdoor air pollution may be different.

(See also Overview of Environmental and Occupational Pulmonary Disease.)

The major components of air pollution are

  • Nitrogen dioxide (from combustion of fossil fuels)

  • Ozone (from the effect of sunlight on nitrogen dioxide and hydrocarbons)

  • Carbon monoxide

  • Particulate air pollution

  • Sulfur oxides

Outdoor air pollution is an important contributor to indoor air pollution. In addition, important sources of indoor air pollution include environmental tobacco smoke, indoor cooking (including gas stoves), construction, and renovation. Burning of biomass fuel (eg, wood, animal waste, crops) for cooking and heating is an important pollution source in countries that rely on biomass fuel.

The US Environmental Protection Agency (EPA) sets ambient air quality standards for so-called criteria air pollutants (oxides of nitrogen, ozone, oxides of sulfur, carbon monoxide, lead, particulates) that can harm human health or the environment. All of the EPA's criteria pollutants except carbon monoxide and lead cause airway hyperreactivity. Long-term exposure to those that cause airway hypersensitivity may increase respiratory infections and respiratory symptoms in the general population, especially in children, and can decrease lung function.

Ozone, which is the major component of smog, is a strong respiratory irritant and oxidant. Ozone levels are 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.

Oxides of nitrogen form primarily from vehicle emissions and are associated with respiratory irritation and asthma.

Carbon monoxide is a product of incomplete combustion of fossil fuels and interferes with oxygen delivery to tissues by binding to hemoglobin. Very high levels of carbon monoxide are not likely to occur outdoors.

With removal of lead from motor vehicle gasoline, lead levels in the air markedly decreased.

Particulate air pollution is a complex mixture derived from fossil fuel (especially diesel) combustion. Wildfire smoke, another important source of particle air pollution, can impact populations hundreds of miles from the source of the fire. The particles can have both local and systemic inflammatory effects, consistent with their impact on both pulmonary and cardiovascular health. Smaller, PM2.5 (particulate matter < 2.5 micrometer diameter) produce a greater inflammatory response per mass than do larger particles. It is widely recognized that particulate air pollution increases all-cause mortality, especially due to cardiovascular and respiratory illnesses.

In addition to being an important source of particulate matter, wildfire smoke also contains carbon dioxide, water vapor, carbon monoxide, hydrocarbons, nitrogen oxides, and trace minerals.

Air pollution data have raised concerns regarding the potential health effects of even smaller particles < 0.1 micrometer (< 100 nanometer) in diameter (ie, nanoparticles), which are particles manufactured via a controlled engineering process, and ultrafine particles, which are incidentally generated. 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.

Prevention of Air Pollution–Related Illness

Air pollution is a leading cause of mortality worldwide (1). Preventing or reducing exposure to outdoor air pollutants is central to both acute and chronic risk modification.

Patients should be educated on air quality resources, such as airnow.gov in the United States and should be encouraged to regularly check air quality in their location and modify activity according to the recommendations made in the air quality alerts.

Examples of risk modification include reducing strenuous outdoor exercise and/or staying indoors in spaces with high-efficiency particulate air (HEPA) filtration systems on days when air quality is poor (2).

Reducing exposure to indoor sources such as smoking and cooking and optimizing ventilation are also recommended.

Prevention references

  1. 1. Fuller R, Landrigan PJ, Balakrishnan K, et al. Pollution and health: a progress update [published correction appears in Lancet Planet Health 2022 Jun 14]. Lancet Planet Health 2022;6(6):e535-e547. doi:10.1016/S2542-5196(22)00090-0

  2. 2. Sorensen C, Lehmann E, Holder C, et al. Reducing the health impacts of ambient air pollution BMJ 2022; 379 :e069487. doi:10.1136/bmj-2021-069487

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