Citation:

Gibbs-Flournoy, E., J. Richards, E. Hines, K. Kraft, J. Norwood, G. Hatch, M. Madden, AND J. Dye. Neonatal rat age, sex, and strain modify acute antioxidant response to ozone. In Proceedings, American Physiologic Society Conference on Cardiovascular, Renal and Metabolic Diseases: Physiology and Gender, Annapolis, MD, November 17 - 20, 2015. Inhalation Toxicology, 291-303, (2017). https://doi.org/10.1080/08958378.2017.1369602

Impact/Purpose:

This pilot study evaluates lung antioxidant levels in air- and O3-exposed neonatal FIS, SD, and W pups to determine which strain/sex may be most susceptible to early life oxidative insult. Abstract for Submission to Ameican Physiologic Society (APS) Meeting on Physiology and Gender, Annapolis MD, Nov. 17-20, 2015.

Description:

ABSTRACT - For Paper in Non-EPA Proceeding-Early life exposure to an adverse environment during critical or sensitive periods of respiratory and immune development may increase risk of developing chronic diseases of various organ systems, including respiratory conditions, throughout the life course (Duijts et al., 2014; Martinez, 2016; Miller & Marty, 2010; Postma et al., 2015). Currently, chronic obstructive pulmonary disease (COPD) is the third leading cause of death in the US, hence more people die from COPD than any other condition except cardiovascular disease and cancer (Blanchette et al., 2012; Xu et al., 2016). COPD is also the third leading cause of death globally — in large part due to exposure to household air pollution generated by rudimentary stoves used for cooking and heating (Burney et al., 2015). Stove emissions disproportionately impact women and children (Gordon et al., 2014). In developed countries, cigarette smoking remains the primary known cause of COPD (Blanchette et al., 2012). In the US, the impact of COPD in women has continued to increase such that the annual number of COPD-related deaths in females now exceeds that of males (Mehari & Gillum, 2015), with the trend stronger in specific states (Edwards et al., 2005). In females, smoking appears to result in greater lung function decline compared to males and even after adjusting for the amount of smoking, females exhibit greater risk of hospitalization for COPD (Prescott et al., 1997). Females also appear to be at increased risk of developing adult-onset asthma, developing more severe asthma (Melgert et al., 2007) and are more likely to be hospitalized for asthma compared to men (Lin et al., 2013). Of note, the proportion of females with COPD who lack a history of smoking is 3–4 fold higher than the proportion of males (Terzikhan et al., 2016). Thus, other inhaled exposures such as air pollution may contribute to these trends (Eisner et al., 2010; Liu et al., 2016; Schikowski et al., 2014; To et al., 2016). For example, heavy exposure to traffic-related air pollution is associated with lower forced expiratory lung capacity, especially in women (Carlsen et al., 2015). Increased emergency room visits (Malig et al., 2016) and hospital admissions (Ghanbari Ghozikali et al. 2016) for COPD are associated with chronic exposure to higher concentrations of the oxidant pollutant, ozone. Additional factors contributing to sex differences in COPD prevalence, progression and mortality include genetic predisposition (Raghavan & Jain, 2016), sex steroid signaling (Sathish et al., 2015) and sociocultural factors (Pinkerton et al., 2015). A large body of literature suggests that the pathogenesis of COPD involves systemic and distal airspace oxidant/anti-oxidant imbalances (Bernardo et al., 2015; Maury et al., 2015; Zinellu et al., 2016) which in some manner accelerate aging processes within the lung (Choudhury & MacNee, 2016). In healthy people, age and sex influence pro/antioxidant status (Kowalska & Milnerowicz, 2016). In the elderly, greater risk of developing COPD is associated with reduced vitamin C (ascorbic acid) and vitamin E (alpha-tocopherol) serum levels (Rodriguez-Rodriguez et al., 2016). Maury et al. (2015) reported that nearly 90% of COPD patients have a systemic antioxidant imbalance based on decreases in serum ascorbic acid, glutathione and glutathione peroxidase — while female COPD patients also show evidence of increased lipid peroxidation.

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