Two pollutant linear models were implemented for gestational exposures to explore potential confounding by co-pollutants.
Given limited resources, there are tradeoffs between number of exposures to explore and the accuracy and resolution with which they can be characterized.
First, we used the baseline exposure model and the most recent exposure model to explore the possible effect of follow-up time on the observed associations (Table 3).
Clearly, further research is needed, with better characterized exposure models, to explore this association in more detail.
However, due to the nature of CSOs, which are typically built in older urban areas, we are unable to define more comparable exposure regions to explore this association.
To the best of our knowledge, this study is the first of its kind to restrict exposure and to explore the dose response relationship between PM2.5 below the current U.S. EPA standards (12 μg/m of annual average PM2.5, 35 μg/m daily) and mortality.
We examine county-level prevalence of PTB in association with the EQI, as the EQI may reflect larger-scale exposure more appropriately than small scale or variable exposures, and to explore if there are drivers of county-level birth outcomes.
Given the laborious nature of chronic cigarette smoke-exposure protocols, many groups have used acute cigarette smoke-exposure protocols to explore the mediators and mechanisms that drive cigarette smoke-induced lung inflammation and damage.
In collecting this breadth of data, we will not only address our initial study question as to the disparity in asthma rates across the two regions but we hope to contribute information regarding differences between genetics and environmental exposures and to explore interactions between the two.
