Impacts of number lines and circle visual displays on caregivers' fraction understanding.

Playful fraction picture books, together with math instructional content called "back matter," may promote fraction learning, which is crucial because fractions are difficult and often disliked content. However, open questions remain regarding how different types of back matter may affect caregivers' ability to use fraction picture books as a teaching tool. The current study offers a novel investigation into how back matter affects caregivers' (N = 160) fraction understanding (i.e., equivalence and arithmetic) and subjective beliefs about math using a pretest/posttest design. We contrasted existing back matter text with research-informed back matter text crossed with either circle area or number line visual displays. Caregivers' performance improved from pretest to posttest in the Researcher-Generated + Circles condition (fraction equivalence) and in the Existing + Circles, Researcher-Generated + Circles, and Researcher-Generated + Number Lines conditions (fraction arithmetic). In addition, caregivers were aware of their learning; they predicted improvements in their fraction arithmetic performance over time. These findings suggest that brief interventions, such as back matter in children's picture books, may improve adults' fraction understanding.

Effect measure modification of the association between short-term exposures to PM2.5 and hospitalizations by longs-term PM2.5 exposure among a cohort of people with Chronic Obstructive Pulmonary Disease (COPD) in North Carolina, 2002-2015.

BACKGROUND: Approximately nine million adults in the United States are living with chronic obstructive pulmonary disease (COPD), and positive associations between short-term air pollution exposure and increased risk of COPD hospitalizations in older adults are consistently reported. We examined the association between short-term PM2.5 exposure and hospitalizations and assessed if there is modification by long-term exposure in a cohort of individuals with COPD. METHODS: In a time-referent case-crossover design, we used a cohort of randomly selected individuals with electronic health records from the University of North Carolina Healthcare System, restricted to patients with a medical encounter coded with a COPD diagnosis from 2004-2016 (n = 520), and estimated ambient PM2.5 concentrations from an ensemble model. Odds ratios and 95% confidence intervals (OR (95%CI)) were estimated with conditional logistic regression for respiratory-related, cardiovascular (CVD), and all-cause hospitalizations. Exposures examined were 0-2 and 0-3 day lags of PM2.5 concentration, adjusting for daily census-tract temperature and humidity, and models were stratified by long-term (annual average) PM2.5 concentration at the median value. RESULTS: We observed generally null or low-magnitude negative associations with short-term PM2.5 exposure and respiratory-related (OR per 5 µg/m3 increase in 3-day lag PM2.5: 0.971 (0.885, 1.066)), CVD (2-day lag: 0.976 (0.900, 1.058) and all-cause (3 day lag: 1.003 (0.927, 1.086)) hospitalizations. Associations between short-term PM2.5 exposure and hospitalizations were higher among patients residing in areas with higher levels of annual PM2.5 concentrations (OR per 5 µg/m3 in 3-day lag PM2.5 for all-cause hospitalizations: 1.066 (0.958, 1.185)) than those in areas with lower annual PM2.5 concentrations (OR per 5 µg/m3 in 3-day lag PM2.5 for all-cause hospitalizations: 0.914 (0.804, 1.039)). CONCLUISONS: Differences in associations demonstrate that people in areas with higher annual PM2.5 exposure may be associated with higher risk of hospitalization during short-term increases in PM2.5 exposure.

Associations between source-apportioned PM2.5 and 30-day readmissions in heart failure patients.

BACKGROUND: Air pollution exposure is a significant risk factor for morbidity and mortality, especially for those with pre-existing chronic disease. Previous studies highlighted the risks that long-term particulate matter exposure has for readmissions. However, few studies have evaluated source and component specific associations particularly among vulnerable patient populations. OBJECTIVES: Use electronic health records from 5556 heart failure (HF) patients diagnosed between July 5, 2004 and December 31, 2010 that were part of the EPA CARES resource in conjunction with modeled source-specific fine particulate matter (PM2.5) to estimate the association between exposure to source and component apportioned PM2.5 at the time of HF diagnosis and 30-day readmissions. METHODS: We used zero-inflated mixed effects Poisson models with a random intercept for zip code to model associations while adjusting for age at diagnosis, year of diagnosis, race, sex, smoking status, and neighborhood socioeconomic status. We undertook several sensitivity analyses to explore the impact of geocoding precision and other factors on associations and expressed associations per interquartile range increase in exposures. RESULTS: We observed associations between 30-day readmissions and an interquartile range increase in gasoline- (16.9% increase; 95% confidence interval = 4.8%, 30.4%) and diesel-derived PM2.5 (9.9% increase; 95% confidence interval = 1.7%, 18.7%), and the secondary organic carbon component of PM2.5 (SOC; 20.4% increase; 95% confidence interval = 8.3%, 33.9%). Associations were stable in sensitivity analyses, and most consistently observed among Black study participants, those in lower income areas, and those diagnosed with HF at an earlier age. Concentration-response curves indicated a linear association for diesel and SOC. While there was some non-linearity in the gasoline concentration-response curve, only the linear component was associated with 30-day readmissions. DISCUSSION: There appear to be source specific associations between PM2.5 and 30-day readmissions particularly for traffic-related sources, potentially indicating unique toxicity of some sources for readmission risks that should be further explored.

Long-term exposure to ambient O3 and PM2.5 is associated with reduced cognitive performance in young adults: A retrospective longitudinal repeated measures study in adults aged 18-90 years.

A growing body of evidence indicates that exposure to air pollution affects cognitive performance; however, few studies have assessed this in the context of repeated measures within a large group of individuals or in a population with a large age range. In this study, we evaluated the associations between long-term exposure to fine particulate matter (PM2.5) and ozone (O3) in large cohort of adults aged 18-90 years. The study cohort included 29,091 Lumosity users in the contiguous US who completed 20 repetitions of the Lost in Migration game between 2017 and 2018. Game scores reflect the ability to filter information and avoid distracting information. Long-term air pollution data included ambient PM2.5 and O3 averaged for the 365-day period before each gameplay date. Generalized linear models were used to examine the associations between long-term PM2.5 and O3 and game score percentile. Co-pollutant models were adjusted for meteorology, time trend, age, gender, device, education, local socioeconomic factors, and urbanicity. Results represent the change in attention game score percentile per 1 µg/m3 increase in PM2.5 or 0.01 ppm increase in O3. In the entire cohort, a -0.10 (95% CI: -0.16, -0.04) change in score percentile was associated with PM2.5, while no significant association was observed with O3. Modification of these associations by age was observed for both PM2.5 and O3, with stronger associations observed in younger users. In users aged 18-29, a -0.25 (-0.45, -0.05) change in score percentile was associated with PM2.5, while no associations were observed in other age groups. With O3, there was a -2.92 (-4.63, -1.19) and -2.81 (-4.29, -1.25) change in score percentile for users aged 18-29 and 30-39, respectively. We observed that elevated long-term PM2.5 and O3 were associated with decreased focus scores in young adults, but follow-up research is necessary to further illuminate these associations.

Associations between short-term exposure to PM2.5 and cardiomyocyte injury in myocardial infarction survivors in North Carolina.

OBJECTIVE: Short-term ambient fine particulate matter (PM2.5) is associated with adverse cardiovascular events including myocardial infarction (MI). However, few studies have examined associations between PM2.5 and subclinical cardiomyocyte damage outside of overt cardiovascular events. Here we evaluate the impact of daily PM2.5 on cardiac troponin I, a cardiomyocyte specific biomarker of cellular damage. METHODS: We conducted a retrospective cohort study of 2924 patients identified using electronic health records from the University of North Carolina Healthcare System who had a recorded MI between 2004 and 2016. Troponin I measurements were available from 2014 to 2016, and were required to be at least 1 week away from a clinically diagnosed MI. Daily ambient PM2.5 concentrations were estimated at 1 km resolution and assigned to patient residence. Associations between log-transformed troponin I and daily PM2.5 were evaluated using distributed lag linear mixed effects models adjusted for patient demographics, socioeconomic status and meteorology. RESULTS: A 10 µg/m3 elevation in PM2.5 3 days before troponin I measurement was associated with 0.06 ng/mL higher troponin I (95% CI=0.004 to 0.12). In stratified models, this association was strongest in patients that were men, white and living in less urban areas. Similar associations were observed when using 2-day rolling averages and were consistently strongest when using the average exposure over the 5 days prior to troponin I measurement. CONCLUSIONS: Daily elevations in PM2.5 were associated with damage to cardiomyocytes, outside of the occurrence of an MI. Poor air quality may cause persistent damage to the cardiovascular system leading to increased risk of cardiovascular disease and adverse cardiovascular events.

Short-Term Exposure to Wildfire Smoke and PM2.5 and Cognitive Performance in a Brain-Training Game: A Longitudinal Study of U.S. Adults.

BACKGROUND: There is increasing evidence that long-term exposure to fine particulate matter [PM ≤2.5µm in aerodynamic diameter (PM2.5)] may adversely impact cognitive performance. Wildfire smoke is one of the biggest sources of PM2.5 and concentrations are likely to increase under climate change. However, little is known about how short-term exposure impacts cognitive function. OBJECTIVES: We aimed to evaluate the associations between daily and subdaily (hourly) PM2.5 and wildfire smoke exposure and cognitive performance in adults. METHODS: Scores from 20 plays of an attention-oriented brain-training game were obtained for 10,228 adults in the United States (U.S.). We estimated daily and hourly PM2.5 exposure through a data fusion of observations from multiple monitoring networks. Daily smoke exposure in the western U.S. was obtained from satellite-derived estimates of smoke plume density. We used a longitudinal repeated measures design with linear mixed effects models to test for associations between short-term exposure and attention score. Results were also stratified by age, gender, user behavior, and region. RESULTS: Daily and subdaily PM2.5 were negatively associated with attention score. A 10 µg/m3 increase in PM2.5 in the 3 h prior to gameplay was associated with a 21.0 [95% confidence interval (CI): 3.3, 38.7]-point decrease in score. PM2.5 exposure over 20 plays accounted for an estimated average 3.7% (95% CI: 0.7%, 6.7%) reduction in final score. Associations were more pronounced in the wildfire-impacted western U.S. Medium and heavy smoke density were also negatively associated with score. Heavy smoke density the day prior to gameplay was associated with a 117.0 (95% CI: 1.7, 232.3)-point decrease in score relative to no smoke. Although differences between subgroups were not statistically significant, associations were most pronounced for younger (18-29 y), older (≥70y), habitual, and male users. DISCUSSION: Our results indicate that PM2.5 and wildfire smoke were associated with reduced attention in adults within hours and days of exposure, but further research is needed to elucidate these relationships. https://doi.org/10.1289/EHP10498.

Effects of short-term ambient PM2.5 exposure on cardiovascular disease incidence and mortality among U.S. hemodialysis patients: a retrospective cohort study.

BACKGROUND: Ambient PM2.5 is a ubiquitous air pollutant with demonstrated adverse health impacts in population. Hemodialysis patients are a highly vulnerable population and may be particularly susceptible to the effects of PM2.5 exposure. This study examines associations between short-term PM2.5 exposure and cardiovascular disease (CVD) and mortality among patients receiving maintenance in-center hemodialysis. METHODS: Using the United State Renal Data System (USRDS) registry, we enumerated a cohort of all US adult kidney failure patients who initiated in-center hemodialysis between 1/1/2011 and 12/31/2016. Daily ambient PM2.5 exposure estimates were assigned to cohort members based on the ZIP code of the dialysis clinic. CVD incidence and mortality were ascertained through 2016 based on USRDS records. Discrete time hazards regression was used to estimate the association between lagged PM2.5 exposure and CVD incidence, CVD-specific mortality, and all-cause mortality 1 t adjusting for temperature, humidity, day of the week, season, age at baseline, race, employment status, and geographic region. Effect measure modification was assessed for age, sex, race, and comorbidities. RESULTS: Among 314,079 hemodialysis patients, a 10 µg/m3 increase in the average lag 0-1 daily PM2.5 exposure was associated with CVD incidence (HR: 1.03 (95% CI: 1.02, 1.04)), CVD mortality (1.05 (95% CI: 1.03, 1.08)), and all-cause mortality (1.04 (95% CI: 1.03, 1.06)). The association was larger for people who initiated dialysis at an older age, while minimal evidence of effect modification was observed across levels of sex, race, or baseline comorbidities. CONCLUSIONS: Short-term ambient PM2.5 exposure was positively associated with incident CVD events and mortality among patients receiving in-center hemodialysis. Older patients appeared to be more susceptible to PM2.5-associated CVD events than younger hemodialysis patients.

Short-term PM2.5 exposure and early-readmission risk: a retrospective cohort study in North Carolina heart failure patients.

BACKGROUND: Short-term changes in ambient fine particulate matter (PM2.5) increase the risk for unplanned hospital readmissions. However, this association has not been fully evaluated for high-risk patients or examined to determine if the readmission risk differs based on time since discharge. Here we investigate the relation between ambient PM2.5 and 30-day readmission risk in heart failure (HF) patients using daily time windows and examine how this risk varies with respect to time following discharge. METHODS: We performed a retrospective cohort study of 17,674 patients with a recorded HF diagnosis between 2004 and 2016. The cohort was identified using the EPA CARES electronic health record resource. The association between ambient daily PM2.5 (µg/m3) concentration and 30-day readmissions was evaluated using time-dependent Cox proportional hazard models. PM2.5 associated readmission risk was examined throughout the 30-day readmission period and for early readmissions (1-3 days post-discharge). Models for 30-day readmissions included a parametric continuous function to estimate the daily PM2.5 associated readmission hazard. Fine-resolution ambient PM2.5 data were assigned to patient residential address and hazard ratios are expressed per 10 µg/m3 of PM2.5. Secondary analyses examined potential effect modification based on the time after a HF diagnosis, urbanicity, medication prescription, comorbidities, and type of HF. RESULTS: The hazard of a PM2.5-related readmission within 3 days of discharge was 1.33 (95% CI 1.18-1.51). This PM2.5 readmission hazard was slightly elevated in patients residing in non-urban areas (1.43, 95%CI 1.22-1.67) and for HF patients without a beta-blocker prescription prior to the readmission (1.35; 95% CI 1.19-1.53). CONCLUSION: Our findings add to the evidence indicating substantial air quality-related health risks in individuals with underlying cardiovascular disease. Hospital readmissions are key metrics for patients and providers alike. As a potentially modifiable risk factor, air pollution-related interventions may be enacted that might assist in reducing costly and burdensome unplanned readmissions.

Omega-3 fatty acids attenuate cardiovascular effects of short-term exposure to ambient air pollution.

BACKGROUND: Exposure to air pollution is associated with elevated cardiovascular risk. Evidence shows that omega-3 polyunsaturated fatty acids (omega-3 PUFA) may attenuate the adverse cardiovascular effects of exposure to fine particulate matter (PM2.5). However, it is unclear whether habitual dietary intake of omega-3 PUFA protects against the cardiovascular effects of short-term exposure to low-level ambient air pollution in healthy participants. In the present study, sixty-two adults with low or high dietary omega-3 PUFA intake were enrolled. Blood lipids, markers of vascular inflammation, coagulation and fibrinolysis, and heart rate variability (HRV) and repolarization were repeatedly assessed in 5 sessions separated by at least 7 days. This study was carried out in the Research Triangle area of North Carolina, USA between October 2016 and September 2019. Daily PM2.5 and maximum 8-h ozone (O3) concentrations were obtained from nearby air quality monitoring stations. Linear mixed-effects models were used to assess the associations between air pollutant concentrations and cardiovascular responses stratified by the omega-3 intake levels. RESULTS: The average concentrations of ambient PM2.5 and O3 were well below the U.S. National Ambient Air Quality Standards during the study period. Significant associations between exposure to PM2.5 and changes in total cholesterol, von Willebrand factor (vWF), tissue plasminogen activator, D-dimer, and very-low frequency HRV were observed in the low omega-3 group, but not in the high group. Similarly, O3-associated adverse changes in cardiovascular biomarkers (total cholesterol, high-density lipoprotein, serum amyloid A, soluable intracellular adhesion molecule 1, and vWF) were mainly observed in the low omega-3 group. Lag-time-dependent biphasic changes were observed for some biomarkers. CONCLUSIONS: This study demonstrates associations between short-term exposure to PM2.5 and O3, at concentrations below regulatory standard, and subclinical cardiovascular responses, and that dietary omega-3 PUFA consumption may provide protection against such cardiovascular effects in healthy adults.

The influence of dietary intake of omega-3 polyunsaturated fatty acids on the association between short-term exposure to ambient nitrogen dioxide and respiratory and cardiovascular outcomes among healthy adults.

BACKGROUND: Short-term exposure to ambient nitrogen dioxide (NO2) is associated with adverse respiratory and cardiovascular outcomes. Supplementation of omega-3 polyunsaturated fatty acids (PUFA) has shown protection against exposure to fine particulate matter. This study aims to investigate whether habitual omega-3 PUFA intake differentially modify the associations between respiratory and cardiovascular responses and short-term exposure to ambient NO2. METHODS: Sixty-two healthy participants were enrolled into low or high omega-3 groups based on their habitual omega-3 PUFA intake. Each participant was repeatedly assessed for lung function, blood lipids, markers of coagulation and fibrinolysis, vascular function, and heart rate variability (HRV) in up to five sessions, each separated by at least 7 days. This study was carried out in the Research Triangle area of North Carolina, USA between October 2016 and September 2019. Daily ambient NO2 concentrations were obtained from an area air quality monitoring station on the day of outcome assessment (Lag0), 4 days prior (Lag1-4), as well as 5-day moving average (5dMA). The associations between short-term exposure to NO2 and the measured indices were evaluated using linear mixed-effects models stratified by omega-3 levels and adjusted by covariates including relative humidity and temperature. RESULTS: The average concentration of ambient NO2 during the study periods was 5.3±3.8 ppb which was below the National Ambient Air Quality Standards (NAAQS). In the high omega-3 group, an interquartile range (IQR) increase in short-term NO2 concentrations was significantly associated with increased lung function [e.g. 1.2% (95%CI: 0.2%, 2.2%) in FVC at lag1, 2.6% (95%CI: 0.4%, 4.8%) in FEV1 at 5dMA], decreased blood lipids [e.g. -2.6% (95%CI: -4.4%, -0.9%) in total cholesterol at lag2, -3.1% (95%CI: -6.1%, 0.0%) in HDL at 5dMA, and -3.1% (95%CI: -5.5%, -0.7%) in LDL at lag2], improved vascular function [e.g. 8.9% (95%CI: 0.6%, 17.2%) increase in FMD and 43.1% (95%CI: -79.8%, -6.3%) decrease in endothelin-1 at 5dMA], and changed HRV parameters [e.g. -7.2% (95%CI: -13.6%, -0.8%) in HFn and 13.4% (95%CI: 0.2%, 28.3%) in LF/HF ratio at lag3]. In the low omega-3 group, an IQR increase in ambient NO2 was associated with elevations in coagulation markers (von Willebrand Factor, D-dimer) and a decrease in HRV (very-low frequency); however, null associations were observed between short-term NO2 exposure and changes in lung function, blood lipids, and vascular function. CONCLUSIONS: The results in this study imply that dietary omega-3 PUFA consumption may offer respiratory and vascular benefits in response to short-term exposure of healthy adults to NO2 levels below the NAAQS. TRIAL REGISTRATION: ClinicalTrials.gov ( NCT02921048 ).

Association of short-term exposure to ambient PM2.5 with hospital admissions and 30-day readmissions in end-stage renal disease patients: population-based retrospective cohort study.

OBJECTIVES: To examine the effect of short-term exposure to ambient fine particulate matter (PM2.5) on all-cause, cardiovascular and respiratory-related hospital admissions and readmissions among patients receiving outpatient haemodialysis. DESIGN: Retrospective cohort study. SETTING: Inpatient hospitalisation claims identified from the US Renal Data System in 530 US counties. PARTICIPANTS: All patients receiving in-centre haemodialysis between 2008 and 2014. PRIMARY AND SECONDARY OUTCOME MEASURES: Risk of all-cause, cardiovascular and respiratory-related hospital admissions and 30-day all-cause and cause-specific readmission following an all-cause, cardiovascular, and respiratory-related discharges. Readmission risk was evaluated for early (1-7 days postdischarge) and late (8-30 days postdischarge) readmission time periods. Relative risk is expressed per 10 µg/m3 of PM2.5. RESULTS: Same-day ambient PM2.5 was associated with increased hospital admission risk for cardiovascular causes (0.9%, 95% CI 0.2 to 1.7). Greater PM2.5-related associations were observed with 30-day readmission risk. Early-readmission risk was increased by 1.6%-1.8% following all-cause (1.6%, 95% CI 0.6% to 2.6%), cardiovascular (1.8%, 95% CI 0.4% to 3.2%) and respiratory (1.8%, 95% CI 0.4% to 3.2%) discharges; while late-readmission risk increased by 1.2%-1.3% following all-cause and cardiovascular discharges. PM2.5-related associations with readmission risk were greatest for certain cause-specific readmissions ranging 4.0%-6.5% for dysrhythmia and conduction disorder, heart failure, chronic obstructive pulmonary disease, other non-cardiac chest pain or respiratory syndrome and pneumonia. Following all-cause discharges, the cause-specific early-readmission risk was increased by 6.5% (95% CI 3.5% to 9.6%) for pneumonia, 4.8% (95% CI 2.3% to 7.4%) for dysrhythmia and conduction disorder, 3.7% (95% CI 1.4% to 6.0%) for heart failure and 2.7% (95% CI 1.2% to 4.2%) for other non-cardiac chest pain or respiratory syndrome-related causes. CONCLUSIONS: Daily ambient PM2.5 was associated with an increased risk of cardiovascular admissions and 30-day readmissions following cardiopulmonary-related discharges in a vulnerable end-stage renal disease population. In the first week following discharge, greater PM2.5-related risk of rehospitalisation was identified for some diagnoses.

Low levels of fine particulate matter increase vascular damage and reduce pulmonary function in young healthy adults.

BACKGROUND: Fine particulate matter (PM2.5) related mild inflammation, altered autonomic control of cardiovascular function, and changes to cell function have been observed in controlled human exposure studies. METHODS: To measure the systemic and cardiopulmonary impacts of low-level PM exposure, we exposed 20 healthy, young volunteers to PM2.5, in the form of concentrated ambient particles (mean: 37.8 µg/m3, SD 6.5), and filtered air (mean: 2.1 µg/m3, SD 2.6). In this double-blind, crossover study the exposure order was randomized. During the 4 h exposure, volunteers (7 females and 13 males) underwent light intensity exercise to regulate ventilation rate. We measured pulmonary, cardiac, and hematologic end points before exposure, 1 h after exposure, and again 20 h after exposure. RESULTS: Low-level PM2.5 resulted in both pulmonary and extra-pulmonary changes characterized by alterations in systematic inflammation markers, cardiac repolarization, and decreased pulmonary function. A mean increase in PM2.5 concentration (37.8 µg/m3) significantly increased serum amyloid A (SAA), C-reactive protein (CRP), soluble intercellular adhesion molecule-1 (sICAM-1), and soluble vascular cell adhesion molecule-1 (sVCAM-1), 1 h after exposure by 8.7, 9.1, 10.7, and 6.6%, respectively, relative to the filtered air control. SAA remained significantly elevated (34.6%) 20 h after PM2.5 exposure which was accompanied by a 5.7% decrease in percent neutrophils. Decreased pulmonary function was observed 1 h after exposure through a 0.8 and 1.2% decrease in forced expiratory volume in 1 s (FEV1) and FEV1/ forced vital capacity (FEV1/FVC) respectively. Additionally, sex specific changes were observed in repolarization outcomes following PM2.5 exposure. In males, P-wave and QRS complex were increased by 15.4 and 5.4% 1 h after exposure. CONCLUSIONS: This study is the first controlled human exposure study to demonstrate biological effects in response to exposure to concentrated ambient air PM2.5 particles at levels near the PM2.5 US NAAQS standard. CLINICAL TRIAL REGISTRATION INFORMATION: clinicaltrials.gov ; Identifier: NCT03232086 . The study was registered retrospectively on July 25, 2017, prior to final data collection on October 25, 2017 and data analysis.

Mortality in US Hemodialysis Patients Following Exposure to Wildfire Smoke.

BACKGROUND: Wildfires are increasingly a significant source of fine particulate matter (PM2.5), which has been linked to adverse health effects and increased mortality. ESKD patients are potentially susceptible to this environmental stressor. METHODS: We conducted a retrospective time-series analysis of the association between daily exposure to wildfire PM2.5 and mortality in 253 counties near a major wildfire between 2008 and 2012. Using quasi-Poisson regression models, we estimated rate ratios (RRs) for all-cause mortality on the day of exposure and up to 30 days following exposure, adjusted for background PM2.5, day of week, seasonality, and heat. We stratified the analysis by causes of death (cardiac, vascular, infectious, or other) and place of death (clinical or nonclinical setting) for differential PM2.5 exposure and outcome classification. RESULTS: We found 48,454 deaths matched to the 253 counties. A 10-µg/m3 increase in wildfire PM2.5 associated with a 4% increase in all-cause mortality on the same day (RR, 1.04; 95% confidence interval [95% CI], 1.01 to 1.07) and 7% increase cumulatively over 30 days following exposure (RR, 1.07; 95% CI, 1.01 to 1.12). Risk was elevated following exposure for deaths occurring in nonclinical settings (RR, 1.07; 95% CI, 1.02 to 1.12), suggesting modification of exposure by place of death. "Other" deaths (those not attributed to cardiac, vascular, or infectious causes) accounted for the largest portion of deaths and had a strong same-day effect (RR, 1.08; 95% CI, 1.03 to 1.12) and cumulative effect over the 30-day period. On days with a wildfire PM2.5 contribution >10 µg/m3, exposure accounted for 8.4% of mortality. CONCLUSIONS: Wildfire smoke exposure was positively associated with all-cause mortality among patients receiving in-center hemodialysis.

Annual PM2.5 and cardiovascular mortality rate data: Trends modified by county socioeconomic status in 2,132 US counties.

This article contains data on county-level socioeconomic status for 2132 US counties and each county's average annual cardiovascular mortality rate (CMR) and fine particulate matter (PM2.5) concentration for 21 years (1990-2010). County CMR, PM2.5, and socioeconomic data were obtained from the US National Center for Health Statistics, US Environmental Protection Agency's Community Multiscale Air Quality modeling system, and the US Census, respectively. Annual socioeconomic indices were created using seven county-level measures from the 1990, 2000, and 2010 US Census using factor analysis. Quintiles of this index were used to generate categories of county socioeconomic status. This national data set contains data for annual PM2.5 and CMR changes over a time-period when there was a significant reduction in US air pollutants (following the enactment of the 1970 Clean Air Act). These data are associated with the article "The contribution of improved air quality to reduced cardiovascular mortality: Declines in socioeconomic differences over time" [1]. Data are stored in a comma separated value format and can be downloaded from the USEPA ScienceHub data repository (https://doi.org/10.23719/1506014).

The contribution of improved air quality to reduced cardiovascular mortality: Declines in socioeconomic differences over time.

Major improvements in air quality since 1990, observed through reductions in fine particulate matter (PM2.5), have been associated with reduced cardiovascular mortality rates (CMR). However, it is not well understood whether the health benefit attributed to PM2.5 reductions has been similar across strata of socioeconomic deprivation (SED). Using mixed effect regression models, we estimated the PM2.5-related change in the CMR across 2,132 US counties in five SED strata between 1990 and 2010. The analysis included annual county CMR (deaths/100,000 person-year), annual county PM2.5 (µg/m3), and an index of county SED based on socioeconomic factors from the 1990 US Census. The contribution of PM2.5 reductions to decreased CMR varied by SED strata and over time. Yearly differences resulted from varying rates of PM2.5 reduction and because of the non-linear relationship between CMR and PM2.5 concentration. In early years, PM2.5-related CMR reductions were smallest in the most deprived counties compared to all other counties (range: 0.4-0.6 vs 0.7-1.6 fewer deaths/100,000 person-year), due to slower rates of PM2.5 reduction in these counties. However, in later years, PM2.5-related CMR reductions were highest counties with moderate to high deprivation, compared to counties with the least deprivation (range: 1.0-2.2 vs 0.5-0.9 fewer deaths/100,000 person-year) due to larger CMR reductions per decrease in PM2.5. We identified that CMR reductions related to air quality improvements have become more similar over time between socioeconomic strata.

Mercury Exposure and Poor Nutritional Status Reduce Response to Six Expanded Program on Immunization Vaccines in Children: An Observational Cohort Study of Communities Affected by Gold Mining in the Peruvian Amazon.

Background: Poor nutritional status combined with mercury exposure can generate adverse child health outcomes. Diet is a mediator of mercury exposure and evidence suggests that nutritional status modifies aspects of mercury toxicity. However, health impacts beyond the nervous system are poorly understood. This study evaluates antibody responses to six vaccines from the expanded program on immunization (EPI), including hepatitis B, Haemophilus influenzae type B, measles, pertussis, tetanus, and diphtheria in children with variable hair mercury and malnutrition indicators. Methods: An observational cohort study (n = 98) was conducted in native and non-native communities in Madre de Dios, Peru, a region with elevated mercury exposure from artisanal and small-scale gold mining. Adaptive immune responses in young (3⁻48 months) and older children (4⁻8 year olds) were evaluated by vaccine type (live attenuated, protein subunits, toxoids) to account for differences in response by antigen, and measured by total IgG concentration and antibody (IgG) concentrations of each EPI vaccine. Mercury was measured from hair samples and malnutrition determined using anthropometry and hemoglobin levels in blood. Generalized linear mixed models were used to evaluate associations with each antibody type. Results: Changes in child antibodies and protection levels were associated with malnutrition indicators, mercury exposure, and their interaction. Malnutrition was associated with decreased measles and diphtheria-specific IgG. A one-unit decrease in hemoglobin was associated with a 0.17 IU/mL (95% CI: 0.04⁻0.30) decline in measles-specific IgG in younger children and 2.56 (95% CI: 1.01⁻6.25) higher odds of being unprotected against diphtheria in older children. Associations between mercury exposure and immune responses were also dependent on child age. In younger children, one-unit increase in log10 child hair mercury content was associated with 0.68 IU/mL (95% CI: 0.18⁻1.17) higher pertussis and 0.79 IU/mL (95% CI: 0.18⁻1.70) higher diphtheria-specific IgG levels. In older children, child hair mercury content exceeding 1.2 µg/g was associated with 73.7 higher odds (95% CI: 2.7⁻1984.3) of being a non-responder against measles and hair mercury content exceeding 2.0 µg/g with 0.32 IU/mL (95% CI: 0.10⁻0.69) lower measles-specific antibodies. Log10 hair mercury significantly interacted with weight-for-height z-score, indicating a multiplicative effect of higher mercury and lower nutrition on measles response. Specifically, among older children with poor nutrition (WHZ = -1), log10 measles antibody is reduced from 1.40 to 0.43 for low (<1.2 µg/g) vs. high mercury exposure, whereas for children with good nutritional status (WHZ = 1), log10 measles antibody is minimally changed for low vs. high mercury exposure (0.72 vs. 0.81, respectively). Conclusions: Child immune response to EPI vaccines may be attenuated in regions with elevated mercury exposure risk and exacerbated by concurrent malnutrition.

Predictors of mitochondrial DNA copy number and damage in a mercury-exposed rural Peruvian population near artisanal and small-scale gold mining: An exploratory study.

Mitochondrial DNA (mtDNA) copy number (CN) and damage in circulating white blood cells have been proposed as effect biomarkers for pollutant exposures. Studies have shown that mercury accumulates in mitochondria and affects mitochondrial function and integrity; however, these data are derived largely from experiments in model systems, rather than human population studies that evaluate the potential utility of mitochondrial exposure biomarkers. We measured mtDNA CN and damage in white blood cells (WBCs) from 83 residents of nine communities in the Madre de Dios region of the Peruvian Amazon that vary in proximity to artisanal and small-scale gold mining. Prior research from this region reported high levels of mercury in fish and a significant association between food consumption and human total hair mercury level of residents. We observed that mtDNA CN and damage were both associated with consumption of fruit and vegetables, higher diversity of fruit consumed, residential location, and health characteristics, suggesting common environmental drivers. Surprisingly, we observed negative associations of mtDNA damage with both obesity and age. We did not observe any association between total hair mercury or, in contrast to previous results, age, with either mtDNA damage or CN. The results of this exploratory study highlight the importance of combining epidemiological and laboratory research in studying the effects of stressors on mitochondria, suggesting that future work should incorporate nutritional and social characteristics, and caution should be taken when applying conclusions from epidemiological studies conducted in the developed world to other regions, as results may not be easily translated. Environ. Mol. Mutagen. 60: 197-210, 2019. © 2018 Wiley Periodicals, Inc.

Spatial, Temporal, and Dietary Variables Associated with Elevated Mercury Exposure in Peruvian Riverine Communities Upstream and Downstream of Artisanal and Small-Scale Gold Mining.

Artisanal and small-scale gold mining (ASGM) is a primary contributor to global mercury and its rapid expansion raises concern for human exposure. Non-occupational exposure risks are presumed to be strongly tied to environmental contamination; however, the relationship between environmental and human mercury exposure, how exposure has changed over time, and risk factors beyond fish consumption are not well understood in ASGM settings. In Peruvian riverine communities (n = 12), where ASGM has increased 4-6 fold over the past decade, we provide a large-scale assessment of the connection between environmental and human mercury exposure by comparing total mercury contents in human hair (2-cm segment, n = 231) to locally caught fish tissue, analyzing temporal exposure in women of child bearing age (WCBA, 15-49 years, n = 46) over one year, and evaluating general mercury exposure risks including fish and non-fish dietary items through household surveys and linear mixed models. Calculations of an individual's oral reference dose using the total mercury content in locally-sourced fish underestimated the observed mercury exposure for individuals in many communities. This discrepancy was particularly evident in communities upstream of ASGM, where mercury levels in river fish, water, and sediment measurements from a previous study were low, yet hair mercury was chronically elevated. Hair from 86% of individuals and 77% of children exceeded a USEPA (U.S. Environmental Protection Agency) provisional level (1.2 µg/g) that could result in child developmental impairment. Chronically elevated mercury exposure was observed in the temporal analysis in WCBA. If the most recent exposure exceeded the USEPA level, there was a 97% probability that the individual exceeded that level 8-10 months of the previous year. Frequent household consumption of some fruits (tomato, banana) and grains (quinoa) was significantly associated with 29-75% reductions in hair mercury. Collectively, these data demonstrate that communities located hundreds of kilometers from ASGM are vulnerable to chronically elevated mercury exposure. Furthermore, unexpected associations with fish mercury contents and non-fish dietary intake highlight the need for more in-depth analyses of exposure regimes to identify the most vulnerable populations and to establish potential interventions.

Effects of methyl and inorganic mercury exposure on genome homeostasis and mitochondrial function in Caenorhabditis elegans.

Mercury toxicity mechanisms have the potential to induce DNA damage and disrupt cellular processes, like mitochondrial function. Proper mitochondrial function is important for cellular bioenergetics and immune signaling and function. Reported impacts of mercury on the nuclear genome (nDNA) are conflicting and inconclusive, and mitochondrial DNA (mtDNA) impacts are relatively unknown. In this study, we assessed genotoxic (mtDNA and nDNA), metabolic, and innate immune impacts of inorganic and organic mercury exposure in Caenorhabditis elegans. Genotoxic outcomes measured included DNA damage, DNA damage repair (nucleotide excision repair, NER; base excision repair, BER), and genomic copy number following MeHg and HgCl2 exposure alone and in combination with known DNA damage-inducing agents ultraviolet C radiation (UVC) and hydrogen peroxide (H2O2), which cause bulky DNA lesions and oxidative DNA damage, respectively. Following exposure to both MeHg and HgCl2, low-level DNA damage (∼0.25 lesions/10kb mtDNA and nDNA) was observed. Unexpectedly, a higher MeHg concentration reduced damage in both genomes compared to controls. However, this observation was likely the result of developmental delay. In co-exposure treatments, both mercury compounds increased initial DNA damage (mtDNA and nDNA) in combination with H2O2 exposure, but had no impact in combination with UVC exposure. Mercury exposure both increased and decreased DNA damage removal via BER. DNA repair after H2O2 exposure in mercury-exposed nematodes resulted in damage levels lower than measured in controls. Impacts to NER were not detected. mtDNA copy number was significantly decreased in the MeHg-UVC and MeHg-H2O2 co-exposure treatments. Mercury exposure had metabolic impacts (steady-state ATP levels) that differed between the compounds; HgCl2 exposure decreased these levels, while MeHg slightly increased levels or had no impact. Both mercury species reduced mRNA levels for immune signaling-related genes, but had mild or no effects on survival on pathogenic bacteria. Overall, mercury exposure disrupted mitochondrial endpoints in a mercury-compound dependent fashion.

Antagonistic Growth Effects of Mercury and Selenium in Caenorhabditis elegans Are Chemical-Species-Dependent and Do Not Depend on Internal Hg/Se Ratios.

The relationship between mercury (Hg) and selenium (Se) toxicity is complex, with coexposure reported to reduce, increase, and have no effect on toxicity. Different interactions may be related to chemical compound, but this has not been systematically examined. Our goal was to assess the interactive effects between the two elements on growth in the nematode Caenorhabditis elegans, focusing on inorganic and organic Hg (HgCl2 and MeHgCl) and Se (selenomethionine, sodium selenite, and sodium selenate) compounds. We utilized aqueous Hg/Se dosing molar ratios that were either above, below, or equal to 1 and measured the internal nematode total Hg and Se concentrations for the highest concentrations of each Se compound. Observed interactions were complicated, differed between Se and Hg compounds, and included greater-than-additive, additive, and less-than-additive growth impacts. Biologically significant interactions were only observed when the dosing Se solution concentration was 100-25,000 times greater than the dosing Hg concentration. Mitigation of growth impacts was not predictable on the basis of internal Hg/Se molar ratio; improved growth was observed at some internal Hg/Se molar ratios both above and below 1. These findings suggest that future assessments of the Hg and Se relationship should incorporate chemical compound into the evaluation.