By Jan Dye
Because epithelial cells ─ the surface cells of the lung ─ are some of the first cells in the body to encounter air pollutants, they function as an important protective barrier against the numerous noxious or injurious agents found in the inspired air, including microorganisms, pollutants, and allergens.
In my laboratory, we use a relatively simple cell culture approach to investigate how gases and particles from different pollutant sources can induce differing degrees of damage to airway and lung epithelial cells. Our findings help to link air pollutant exposure to specific adverse effects on these important protective cells of the lung.
- For example, we have shown that when lung cells are exposed to certain metal mixtures (similar to that found on particles derived from steel mill emissions); cells were more damaged than if they were exposed to just one metal at a time, even at relatively high concentrations.
- We demonstrated that real-world diesel exhaust particles (which have a layer of organic carbon-rich material and road dust associated metals) are more injurious to airway epithelial cells than simple carbon particles (like that found in cartridge toner). Taken together, results show that both the particle dose and its composition are important in determining its epithelial toxicity.
- We have also shown that if lung cell cultures undergo physical injury or “wounding” prior to exposure to diesel particles, cultures are not able to “heal” the injured areas as readily or as completely as the unexposed cultures. It appears that air pollutant exposure may interfere with cell migration. Directed epithelial cell migration is critical for healing of the airways after insult (e.g., viral infection or asthma flare up) and for lung development during periods of rapid lung growth (e.g., early childhood and adolescence).
- Finally, we have shown that when epithelial cells “grow up” within an inflammatory microenvironment (not unlike that present in the airways of people with asthma), exposure to diesel particles induced significantly greater lung cell damage, resulting in a “leaky” epithelial barrier. If this were to happen within the airways of an asthmatic individual, inhaled irritants may penetrate deeper into lung tissues, potentially worsening allergen exposure and responses.
These are just a few of the ways in which exposure to air pollutants can negatively impact the health of epithelial cells lining the airways and deep lung spaces. Epithelial cells also play critical roles in controlling inflammatory and immune responses after lung insult. If damaged by air pollution, these cells are not able to do their job as effectively.
About the author: Dr. Jan Dye is a health effects researcher in EPA’s Office of Research and Development. She is a Project Lead for the Air, Climate, and Energy program’s National Ambient Air Quality Standards and Multipollutant Project on susceptibility to air pollutants.