Environmental lung diseases are caused by harmful particles, mists, vapors, or gases that are inhaled, usually while people work. If the lung disease is due to inhaled particles, the term pneumoconiosis is often used. Where within the airways or lungs an inhaled substance ends up and what type of lung disease develops depend on the size and kind of particles inhaled. Large particles may get trapped in the nose or large airways, but very small ones may reach the lungs. There, some particles dissolve and may be absorbed into the bloodstream. Most solid particles that do not dissolve are removed by the body's defenses.
The body has several means of getting rid of inhaled particles. In the airways, an accumulation of secretions (mucus) coats particles so that they can be coughed up more easily. Additionally, tiny cells lining the airways (cilia) are able to brush inhaled particles upward, out of the lungs. In the small air sacs of the lungs (alveoli), special scavenger cells (macrophages) engulf most particles and render them harmless.
Many different kinds of particles can harm the lungs. Some are organic, meaning that they are made of materials that contain carbon and are part of living organisms (such as grain dusts, cotton dust, or animal dander). Some are inorganic, meaning that they usually come from nonliving sources, such as metals or minerals (for example, asbestos).
Different types of particles produce different reactions in the body. Some particles—animal dander, for example—can cause allergic reactions, such as hay fever–like symptoms or a type of asthma. Other particles cause harm not by triggering allergic reactions but by being toxic to the cells of the airways and air sacs in the lung. Some particles, such as quartz dust and asbestos, may cause chronic irritation that can lead to scarring of lung tissue (pulmonary fibrosis—see see Overview of Idiopathic Interstitial Pneumonias). Certain toxic particles, such as asbestos, can cause lung cancer, especially in people who smoke, or cancer of the lining of the chest and lung (mesothelioma), regardless of the person's smoking history.
Air Pollution-Related Illness
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), and suspended solid or liquid particles. Burning of biomass fuel is an important source of particulate matter indoors in developing countries. Secondhand smoke is also an important source of indoor air pollution.
High levels of air pollution can trigger exacerbations in people with asthma or chronic obstructive pulmonary disease. People living in areas with high traffic are at particular risk. Most air pollutants cause airways to narrow (airway hyperreactivity). Long-term exposure may increase respiratory infections and symptoms in the general population, especially children.
Ozone, which is the major component of smog, is a strong lung irritant. Levels tend to be highest in the summer compared to other seasons and relatively higher in the late morning and early afternoon compared to other times of the day. Short-term exposures can cause breathing difficulties, chest pain, and airway hyperreactivity. Children who participate in outdoor sports on 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.
Combustion of fossil fuels that are high in sulfur can create acid particles that are easily deposited in the upper airway. These particles, called sulfur oxides, can cause the airways to become inflamed and constricted and increase the risk for chronic bronchitis.
Particulate air pollution derived from fossil fuel combustion (especially diesel fuel) is a complex mixture. The particles can cause inflammation of the airways or can affect other parts of their body, such as the heart. Data from some studies suggest that particulate air pollution increases death rates from all causes, especially heart and lung disorders.
Last full review/revision April 2008 by Lee S. Newman, MD, MA