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Abstract Wildfires cause elevated air pollution that can be detrimental to human health. However, health impact assessments associated with emissions from wildfire events are subject to uncertainty arising from different sources. Here, we quantify and compare major uncertainties in mortality and morbidity outcomes of exposure to fine particulate matter (PM_2.5) pollution estimated for a series of wildfires in the Southeastern U.S. We present an approach to compare uncertainty in estimated health impacts specifically due to two driving factors, wildfire‐related smoke PM_2.5fields and variability in concentration‐response parameters from epidemiologic studies of ambient and smoke PM_2.5. This analysis, focused on the 2016 Southeastern wildfires, suggests that emissions from these fires had public health consequences in North Carolina. Using several methods based on publicly available monitor data and atmospheric models to represent wildfire‐attributable PM_2.5, we estimate impacts on several health outcomes and quantify associated uncertainty. Multiple concentration‐response parameters derived from studies of ambient and wildfire‐specific PM_2.5are used to assess health‐related uncertainty. Results show large variability and uncertainty in wildfire impact estimates, with comparable uncertainties due to the smoke pollution fields and health response parameters for some outcomes, but substantially larger health‐related uncertainty for several outcomes. Consideration of these uncertainties can support efforts to improve estimates of wildfire impacts and inform fire‐related decision‐making. 

Genetic screens in Drosophila melanogaster have long been used to identify genes found in a variety of developmental, cellular, and behavioral processes. Here we describe the characterization and mapping of a mutation identified in a conditional screen for genetic regulators of cell growth and cell division. Within a Flp/FRT system, mutant G.3.2 results in a reduction of mutant tissue and a rough eye phenotype. We find that G.3.2 maps to the gene cnk, providing further support that cnk is a critical gene in Drosophila eye development. This mutant was characterized, mapped and sequenced by undergraduate students within the Fly-CURE consortium.