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Private wells often lack centralized oversight, drinking water quality standards, and consistent testing methodologies. For lead in well water, the lack of standardized data collection methods can impact reported measurements, which can misinform health risks. Here, we conducted a targeted community science testing of 1143 wells across 17 counties in North Carolina (USA) and compared results to state testing data primarily associated with new well construction compiled in the NCWELL database. The goal of our study was to explore the impacts of sampling methodology and household representation on estimated lead exposures and subsequent health risks. At the household scale, we illustrated how sampling and analytical techniques impact lead measurements. The community science testing first draw samples (characterizing drinking water) had a 90th percentile lead value of 12.8μg l⁻¹while the NCWELL database flushed samples (characterizing groundwater) had a value below the reporting level of 5μg l⁻¹. As lead was associated with the corrosion of premise plumbing, flushing prior to collection substantially reduced lead concentrations. At the community scale, we examined how the lack of representation based on household demographics and well construction characteristics impacted the knowledge of lead and blood lead level (BLL) occurrence. When simulating representative demographics of the well populations, we observed that the 90th percentile lead level could differ by up to 6μg l⁻¹, resulting in communities being above the USEPA action level. This translated to a 1.0–1.3μg dl⁻¹difference in predicted geometric mean BLL among infants consuming reconstituted formula. Further, inclusion of less common well construction types also increased lead in water occurrence. Overall, under- and overestimations of lead concentrations associated with differences in sampling techniques and sample representation can misinform conclusions about risks of elevated BLLs associated with drinking water from private wells which may hinder investigations of waterborne lead exposure.

 

Hydroxyl radical (·OH)-initiated oxidation of isoprene, the most abundant nonmethane hydrocarbon in the atmosphere, is responsible for substantial amounts of secondary organic aerosol (SOA) within ambient fine particles. Fine particulate 2-methyltetrol sulfate diastereoisomers (2-MTSs) are abundant SOA products formed via acid-catalyzed multiphase chemistry of isoprene-derived epoxydiols with inorganic sulfate aerosols under low-nitric oxide conditions. We recently demonstrated that heterogeneous ·OH oxidation of particulate 2-MTSs leads to the particle-phase formation of multifunctional organosulfates (OSs). However, it remains uncertain if atmospheric chemical aging of particulate 2-MTSs induces toxic effects within human lung cells. We show that inhibitory concentration-50 (IC50) values decreased from exposure to fine particulate 2-MTSs that were heterogeneously aged for 0 to 22 days by ·OH, indicating increased particulate toxicity in BEAS-2B lung cells. Lung cells further exhibited concentration-dependent modulation of oxidative stress- and inflammatory-related gene expression. Principal component analysis was carried out on the chemical mixtures and revealed positive correlations between exposure to aged multifunctional OSs and altered expression of targeted genes. Exposure to particulate 2-MTSs alone was associated with an altered expression of antireactive oxygen species (ROS)-related genes (NQO-1, SOD-2, and CAT) indicative of a response to ROS in the cells. Increased aging of particulate 2-MTSs by ·OH exposure was associated with an increased expression of glutathione pathway related genes (GCLM and GCLC) and an anti-inflammatory gene (IL-10).