This website was developed by undergraduate biology researchers working with Dr. Karen Bernd at Davidson College.

Your Gender, Your Lifestyle, and Your Lung's Ability to Deal with Ozone

Your body makes oxidants as part normal cellular activity and in response to things that you eat or do. Although too much these oxidants can cause all sorts of cellular damage you need some in order for cells to live. As in many parts of life--balance is important. We are interested in how tipping the scale toward or away from the cell (or the body) producing oxidants impacts the lung's cells ability to deal with ozone in airborne pollution.

To explore the role of gender and life style on lung cell's susceptibility to ozone damage we are examine the combined effect of ozone and ethanol, metabolic rate, selenium and estrogen. These different variables were chosen because

  • Alcoholics may be more likely to get Acute Respiratory Distress Syndrome (ARDS) (see our lung and ethanol pages)
  • Asthma symptoms are worsened by both increased metabolic rate and ozone exposure (see our metabolism page)
  • Selenium is an essential micronutrient that may provide protection to oxidants at low concentrations but is toxic at high ones. (see our selenium page)
  • There are gender descrepancies in the morbidity and mortality of ARDS, asthma, chronic obstructive pulmonary disease (COPD) and lung cancers as well as in reponse to oxidative stress in healthy patients (Moss et al. 2002; Omoto et al. 2001; Kwong et al. 2001; Atmospheric Chemistry; Huber et al. 2002; Chen et al. 2007; TenHoor et al. 2001; Dougherty et al. 2006). (see our estrogen page)

Resources relating to specific diseases and conditions can be found on our Resources page


The Ozone Connection

Since 1970, the United States government has been concerned with the relationship between ambient ozone and the health of the general population (Balmes 1993).

There is a positive corrleation between exposure to airborne oxidants, such as ozone, and pulmonary distress in both healthy and lung disease populations(Chen et al. 2007; Blames 1993; TenHoor et al. 2001; Urata 2006). However, we still don’t understand the cellular reason behind the correlation. More evidence would

    • Extend our understanding of cellular mechanisms of defense against oxidative damage.
    • Further clarify the the Environmental Protection Agency’s standard for permissible levels of ambient ozone (Balmes 1993) and
    • Could lead to more effective lifestyle changes for sensitive groups and development of better treatments for lung disorders where ozone is a mitigating factor

We examine the effect of ozone on cultured lung cells through several different measures.

  • Viability assays, examining mitochondrial function or secreted components, to determine if ozone exposure decreases the number of live cells
  • Necrosis / Apoptosis assays to determine, if there is a decrease in viability, how the cells die
  • GSH/GSSG assays to determine the redox state of the cell
  • PGE2 assays to determine the degree of cellular inflammation

The combination of these different measures will help us to understand the net effect of ozone on lung cells.

Rat Lung Cells as Model

We use the L2 cell culture line as our model for the effect of ozone on the lung for several reasons.

    • Rats have been shown to be an appropriate model in whole organism studies exploring the effects of ozone exposure on the lungs (Topcuoglu et al. 2009; Singhal et al. 2008; Marquez-Garban et al. 2009; Buchmuller-Rouiller et al. 1995; Wang et al. 2006; Nadadur et al. 2005). Cell culture based approaches focus in on one cell type and therefore limit external variables.
    • Type 2 pneumocytes are critical to both proper lung function and its maintentance (Wang et al. 2006). While previous research has focused on bronchiole cells, our group has chosen to focus on characterizing ozone's effect on the cells where gas exchange occurs.


Send comments, concerns or questions to Dr. Karen Bernd