48 Effect of atmospheric conditions on clinical, physiological, and biologic parameters of asthma

Monday, 29 September 2014
Salon I (Embassy Suites Cleveland - Rockside)
Haseena Rajeevan, Yale University, New Haven, CT; and X. Yan, W. Sessa, R. Scatena, and G. Chupp

Asthma is a complex heterogeneous disease that is driven by genetic susceptibility and environmental factors [1, 2]. Published literature has established that changes in atmospheric conditions such as temperature, relative humidity and barometric pressure affect disease activity [3, 4]. Meanwhile, the effects of these fluctuations on the molecular signals associated with asthma are unknown. Therefore, this study explored the effect that atmospheric changes have on molecular signals that has been measured in the sputum and circulation of individuals with asthma. The atmospheric variables were retrieved from National Climatic Data Center (NCDC), which performs measurements at eight airport weather stations around the state of Connecticut. Our research team at the Yale Center for Asthma and Airway Diseases (YCAAD) has been accumulating data on clinical phenotype and gene expression in the airway from individuals with asthma that reside in the state of Connecticut. Patients were clustered by the weather stations associated with their zip codes. Difference in temperature (T), relative humidity (RH), and barometric pressure (BP) between day of the visit of the individual to the clinic (T0, RH0, BP0), one day (T1, RH1, BP1), and two days (T2, RH2, BP2) prior were selected as the atmospheric variables. Weather parameters were correlated with the clinical, physiological, and biologic parameters of asthma. The atmospheric conditions that influenced the most number of disease phenotypes were the barometric pressure and temperature values one day prior to the visit date. Correlation results indicate that clinical phenotypes such as shortness of breath (r=- 0.207, p = 0.020), chest tightness (r=- 0.202, p = 0.024), and social activity (r=- 0.214, p = 0.017), were negatively correlated with barometric pressure one day prior to the visit. Lung function variables post FEV1 (r= 0.164, p = 0.033), and pre FEV1(r= 0.154, p = 0.047), were positively associated with the temperature value one day prior to the individuals visit. The sputum NOGO (Neurite outgrowth inhibitory protein) levels were significantly correlated with T0 (r= 0.217, p = 0.016), T1 (r= 0.208, p = 0.021), and T2 (r= 0.233, p = 0.010); temperature values on the visit day, one day prior and two days prior respectively. The number of disease parameters influenced by the change in temperature (T0-T1 and T1-T2), barometric pressure (BP0-BP1, BP1-BP2), and relative humidity (RH0-RH1 and RH1-RH2) were low compared to the atmospheric conditions one day prior to the visit. Conclusions: Above mentioned preliminary correlation studies suggest association of atmospheric conditions days before and on the day of the visit with clinical and molecular signals of asthma. The presence of statistically significant association of temperature values with sputum NOGO levels and the lack of significant association with serum NOGO levels need further investigation. In addition, the association of atmospheric conditions on the gene expression in the circulation and airway in asthma will be investigated to better understand the role of environmental conditions in the progression of the disease. References: 1. Duffy, D.L., et al., Genetics of asthma and hay fever in Australian twins. Am Rev Respir Dis, 1990. 142(6 Pt 1): p. 1351-8. 2. Palmer, L.J., et al., Independent inheritance of serum immunoglobulin E concentrations and airway responsiveness. Am J Respir Crit Care Med, 2000. 161(6): p. 1836-43. 3. Mireku, N., et al., Changes in weather and the effects on pediatric asthma exacerbations. Ann Allergy Asthma Immunol, 2009. 103(3): p. 220-4. 4. Beard, J.D., et al., Winter temperature inversions and emergency department visits for asthma in Salt Lake County, Utah, 2003-2008. Environ Health Perspect, 2012. 120(10): p. 1385-90. This abstract is funded by: R01HL118346-02
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