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BACKGROUND: Recent studies have reported the association between air pollution exposure and reduced kidney function. However, it is unclear whether air pollution is associated with an increased risk of acute kidney injury (AKI). OBJECTIVES: To address this gap in knowledge, we investigated the effect estimates of long-term exposures to fine particulate matter [PM ≤ 2.5 μm in aerodynamic diameter (PM2.5)], nitrogen dioxide (NO2), and ozone (O3) on the risk of first hospital admission for AKI using nationwide Medicare data. METHODS: This nationwide population-based longitudinal cohort study included 61,300,754 beneficiaries enrolled in Medicare Part A fee-for-service (FFS) who were ≥65 years of age and resided in the continental United States from the years 2000 through 2016. We applied Cox-equivalent Poisson models to estimate the association between air pollution and first hospital admission for AKI. RESULTS: Exposure to PM2.5, NO2, and O3 was associated with increased risk for first hospital admission for AKI, with hazard ratios (HRs) of 1.17 (95% CI: 1.16, 1.19) for a 5-μg/m³ increase in PM2.5, 1.12 (95% CI: 1.11, 1.13) for a 10-ppb increase in NO2, and 1.03 (95% CI: 1.02, 1.04) for a 10-ppb increase in summer-period O3 (June to September). The associations persisted at annual exposures lower than the current National Ambient Air Quality Standard. DISCUSSION: This study found an association between exposures to air pollution and the risk of the first hospital admission with AKI, and this association persisted even at low concentrations of air pollution. Our findings provide beneficial implications for public health policies and air pollution guidelines to alleviate health care expenditures and the disease burden attributable to AKI. [ABSTRACT FROM AUTHOR]

BACKGROUND: Studies across the globe generally reported increased mortality risks associated with particulate matter with aerodynamic diameter ≤2.5 μm (PM2.5) exposure with large heterogeneity in the magnitude of reported associations and the shape of concentration-response functions (CRFs). We aimed to evaluate the impact of key study design factors (including confounders, applied exposure model, population age, and outcome definition) on PM2.5 effect estimates by harmonizing analyses on three previously published large studies in Canada [Mortality-Air Pollution Associations in Low Exposure Environments (MAPLE), 1991-2016], the United States (Medicare, 2000-2016), and Europe [Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), 2000-2016] as much as possible. METHODS: We harmonized the study populations to individuals 65+ years of age, applied the same satellite-derived PM2.5 exposure estimates, and selected the same sets of potential confounders and the same outcome. We evaluated whether differences in previously published effect estimates across cohorts were reduced after harmonization among these factors. Additional analyses were conducted to assess the influence of key design features on estimated risks, including adjusted covariates and exposure assessment method. A combined CRF was assessed with meta-analysis based on the extended shape-constrained health impact function (eSCHIF). RESULTS: More than 81 million participants were included, contributing 692 million person-years of follow-up. Hazard ratios and 95% confidence intervals (CIs) for all-cause mortality associated with a 5-μg/m³ increase in PM2.5 were 1.039 (1.032, 1.046) in MAPLE, 1.025 (1.021, 1.029) in Medicare, and 1.041 (1.014, 1.069) in ELAPSE. Applying a harmonized analytical approach marginally reduced difference in the observed associations across the three studies. Magnitude of the association was affected by the adjusted covariates, exposure assessment methodology, age of the population, and marginally by outcome definition. Shape of the CRFs differed across cohorts but generally showed associations down to the lowest observed PM2.5 levels. A common CRF suggested a monotonically increased risk down to the lowest exposure level. [ABSTRACT FROM AUTHOR]

Southern corn rust (Puccinia polysora Underw.) is a major tropical disease that can lead to severe yield losses in the tropics. Occasionally it becomes of concern in temperate regions, as in 2010. We summarize 45 yr of research on the occurrence, genetic basis, and breeding of general resistance. Trials were conducted in Colombia, Hawaii, Nigeria, the Philippines, Texas, and Thailand. Temperate maize proved uniformly susceptible. No racially specific monogenes were effective. Resistance varied continuously among tropical inbreds and many of these showed stable intermediate tolerance. Two diallel populations revealed high correlations of inbred values with hybrid array means and slight heterosis for resistance. Narrow-sense heritabilities were 51% and 66%, and mean square ratios for general to specific combining ability (GCA:SCA) were 7.8 and 10.7 to 1. Generation mean analyses were performed on six sets of families. Mean and additive effects were significant across families, while significant nonadditive effects were rare. Heritability values ranged from 19% to 49%. A set of recombinant lines segregated a primary susceptibility locus on chromosome 6. Studies of 137 near-isogenic inbred lines (NILs) of resistant tropical inbred Hi27 revealed a dominant susceptibility quantitative trait locus (QTL) in the NIL for dwarf-1 locus, but linkage could not be confirmed. Premature senescence was associated with rust infections in many NILs, emphasizing the ubiquity of modifying genes. No correlation existed between resistance to southern and common rusts. Resistant tropical inbreds and populations were bred to serve as sources for future improvement. [ABSTRACT FROM AUTHOR]