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em DigitalCommons@The Texas Medical Center


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Outdoor environmental risk factors for asthma have been extensively researched, even though the majority of a person's daily activity occurs indoors. There is limited evidence linking personal exposure concentrations of ozone, pollen, mold, temperature, and humidity to childhood asthma. ^ The current study consisted of a secondary, more complex analysis of the data from the Houston Air Toxics and Asthma in Children (ATAC) Study to further investigate the association of personal ozone exposure on asthma outcome variability among middle school children with asthma. The ATAC Study primarily investigated the association between selected oxygenated air toxics and indicators of asthma variability (PEFR, FEV1, asthma symptoms, and rescue medication usage) among 30 labile and persistent Houston middle-school children with diagnosed asthma. This panel study used a repeated measurements design of four separate 10-day sampling periods that extended over a 20 month period. The secondary analysis included aggregate regression models that were constructed with two different estimates of ozone exposure (daily maximum hourly outdoor concentration and daily maximum hourly personal exposure), with three different estimates of personal environmental temperature and humidity exposures (daily average, intraday difference, and interday difference), and for thee different time periods [same day of exposure (lag 0), one day after initial exposure (lag 1), and two days after initial exposure (lag 2)]. ^ Overall, the models using daily maximum hourly personal ozone exposures in combination with intraday and interday personal temperature and humidity differences produced more significant plausible associations than models using daily maximum hourly personal ozone exposures with personal average temperature and humidity exposures. Significant associations were identified between daily maximum hourly personal ozone exposure and clinical indicators of asthma variability. The increasing effect on rescue medication usage from daily maximum hourly personal ozone exposure were identified as soon as the same day of exposure (lag 0; p=0.0072), and the same effects were delayed until the second next day (lag 2; p= 0.0026). The increasing effect on asthma symptoms were identified on the second next day after initial exposure (lag 2; p= 0.0024). There was a consistent inverse relationship between personal relative humidity exposure and indicators of asthma variability. Decreasing effects on daily FEV1 variability from personal relative humidity exposure were identified on the same day of exposure (lag 0; p= 0.034), increasing effects on morning PEFR were identified on the next day after initial exposure (lag 1; p= 0.0001), and decreasing effects on overnight PEFR variability were identified on the second next day after the initial exposure (lag 2; p= 0.007). With the conclusion of this research, there are opportunities for future similar studies in the preventive management of asthma in children living in high-ozone areas.^