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.

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.

Associations between neighborhood socioeconomic cluster and hypertension, diabetes, myocardial infarction, and coronary artery disease within a cohort of cardiac catheterization patients.

BACKGROUND: Neighborhood-level socioeconomic status (SES) is associated with health outcomes, including cardiovascular disease and diabetes, but these associations are rarely studied across large, diverse populations. METHODS: We used Ward's Hierarchical clustering to define eight neighborhood clusters across North Carolina using 11 census-based indicators of SES, race, housing, and urbanicity and assigned 6992 cardiac catheterization patients at Duke University Hospital from 2001 to 2010 to clusters. We examined associations between clusters and coronary artery disease index > 23 (CAD), history of myocardial infarction, hypertension, and diabetes using logistic regression adjusted for age, race, sex, body mass index, region of North Carolina, distance to Duke University Hospital, and smoking status. RESULTS: Four clusters were urban, three rural, and one suburban higher-middle-SES (referent). We observed greater odds of myocardial infarction in all six clusters with lower or middle-SES. Odds of CAD were elevated in the rural cluster that was low-SES and plurality Black (OR 1.16, 95% CI 0.94-1.43) and in the rural cluster that was majority American Indian (OR 1.31, 95% CI 0.91-1.90). Odds of diabetes and hypertension were elevated in two urban and one rural low- and lower-middle SES clusters with large Black populations. CONCLUSIONS: We observed higher prevalence of cardiovascular disease and diabetes in neighborhoods that were predominantly rural, low-SES, and non-White, highlighting the importance of public health and healthcare system outreach into these communities to promote cardiometabolic health and prevent and manage hypertension, diabetes and coronary artery disease.

Air pollution dispersion from biomass stoves to neighboring homes in Mirpur, Dhaka, Bangladesh.

BACKGROUND: Indoor air pollution, including fine particulate matter (PM2.5) and carbon monoxide (CO), is a major risk factor for pneumonia and other respiratory diseases. Biomass-burning cookstoves are major contributors to PM2.5 and CO concentrations. However, high concentrations of PM2.5 (> 1000 µg/m3) have been observed in homes in Dhaka, Bangladesh that do not burn biomass. We described dispersion of PM2.5 and CO from biomass burning into nearby homes in a low-income urban area of Dhaka, Bangladesh. METHODS: We recruited 10 clusters of homes, each with one biomass-burning (index) home, and 3-4 neighboring homes that used cleaner fuels with no other major sources of PM2.5 or CO. We administered a questionnaire and recorded physical features of all homes. Over 24 h, we recorded PM2.5 and CO concentrations inside each home, near each stove, and outside one neighbor home per cluster. During 8 of these 24 h, we conducted observations for pollutant-generating activities such as cooking. For each monitor, we calculated geometric mean PM2.5 concentrations at 5-6 am (baseline), during biomass burning times, during non-cooking times, and over 24 h. We used linear regressions to describe associations between monitor location and PM2.5 and CO concentrations. RESULTS: We recruited a total of 44 homes across the 10 clusters. Geometric mean PM2.5 and CO concentrations for all monitors were lowest at baseline and highest during biomass burning. During biomass burning, linear regression showed a decreasing trend of geometric mean PM2.5 and CO concentrations from the biomass stove (326.3 µg/m3, 12.3 ppm), to index home (322.7 µg/m3, 11.2 ppm), neighbor homes sharing a wall with the index home (278.4 µg/m3, 3.6 ppm), outdoors (154.2 µg/m3, 0.7 ppm), then neighbor homes that do not share a wall with the index home (83.1 µg/m3,0.2 ppm) (p = 0.03 for PM2.5, p = 0.006 for CO). CONCLUSION: Biomass burning in one home can be a source of indoor air pollution for several homes. The impact of biomass burning on PM2.5 or CO is greatest in homes that share a wall with the biomass-burning home. Eliminating biomass burning in one home may improve air quality for several households in a community.

Effects of smoke-free air law on acute myocardial infarction hospitalization in Indianapolis and Marion County, Indiana.

BACKGROUND: A comprehensive smoke-free air law was enacted on June 1, 2012 in most of Marion County, Indiana, including all of the City of Indianapolis. We evaluated changes in acute myocardial infarction (AMI) admission rates in Indianapolis and Marion County before compared to after the law. METHODS: We collected AMI admissions from five Marion County hospitals between May 2007 and December 2014. We used Poisson regression to evaluate the overall effects of the law on monthly AMI hospitalizations, adjusting for month, seasonality, meteorology, air pollution, and hospital utilization. We tested the interactions between the law and AMI risk factors on monthly AMI admission rates to identify subpopulations for which the effects might be stronger. RESULTS: Monthly AMI admissions declined 20% (95% CI 14-25%) in Marion County and 25% (95% CI 20-29%) in Indianapolis after the law was implemented. We observed decreases among never (21%, 95% CI 13-29%), former (28%, 95% CI 21-34%), and current smokers (26%, 95% CI 11-38%); Medicaid beneficiaries (19%, 95% CI 9-29%) and non-beneficiaries (26%, 95% CI 20-31%). We observed decreases among those with a history of diabetes (Yes: 22%, 95% CI 14-29%; No: 25%, 95% CI 18-31%), congestive heart failure (Yes: 23%, 95% CI 16-30%; No: 24%, 95% CI 17-31%), and hypertension (Yes: 23%, 95% CI 17-28%: No: 26%, 95% CI 15-36%). CONCLUSIONS: We observed decreases in AMI admissions comparable with previous studies. We identified subpopulations who benefitted from the law, such as former and current smokers, and those without comorbidities such as congestive heart failure and hypertension.

Household-level risk factors for secondary influenza-like illness in a rural area of Bangladesh.

OBJECTIVE: To describe household-level risk factors for secondary influenza-like illness (ILI), an important public health concern in the low-income population of Bangladesh. METHODS: Secondary analysis of control participants in a randomised controlled trial evaluating the effect of handwashing to prevent household ILI transmission. We recruited index-case patients with ILI - fever (<5 years); fever, cough or sore throat (≥5 years) - from health facilities, collected information on household factors and conducted syndromic surveillance among household contacts for 10 days after resolution of index-case patients' symptoms. We evaluated the associations between household factors at baseline and secondary ILI among household contacts using negative binomial regression, accounting for clustering by household. RESULTS: Our sample was 1491 household contacts of 184 index-case patients. Seventy-one percentage reported that smoking occurred in their home, 27% shared a latrine with one other household and 36% shared a latrine with >1 other household. A total of 114 household contacts (7.6%) had symptoms of ILI during follow-up. Smoking in the home (RRadj 1.9, 95% CI: 1.2, 3.0) and sharing a latrine with one household (RRadj 2.1, 95% CI: 1.2, 3.6) or >1 household (RRadj 3.1, 95% CI: 1.8-5.2) were independently associated with increased risk of secondary ILI. CONCLUSION: Tobacco use in homes could increase respiratory illness in Bangladesh. The mechanism between use of shared latrines and household ILI transmission is not clear. It is possible that respiratory pathogens could be transmitted through faecal contact or contaminated fomites in shared latrines.

Residential distance to major roadways and cardiac structure in African Americans: cross-sectional results from the Jackson Heart Study.

BACKGROUND: Heart failure (HF) is a significant source of morbidity and mortality among African Americans. Ambient air pollution, including from traffic, is associated with HF, but the mechanisms remain unknown. The objectives of this study were to estimate the cross-sectional associations between residential distance to major roadways with markers of cardiac structure: left ventricular (LV) mass index, LV end-diastolic diameter, LV end-systolic diameter, and LV hypertrophy among African Americans. METHODS: We studied baseline participants of the Jackson Heart Study (recruited 2000-2004), a prospective cohort of cardiovascular disease (CVD) among African Americans living in Jackson, Mississippi, USA. All cardiac measures were assessed from echocardiograms. We assessed the associations between residential distance to roads and cardiac structure indicators using multivariable linear regression or multivariable logistic regression, adjusting for potential confounders. RESULTS: Among 4826 participants, residential distance to road was <150 m for 103 participants, 150-299 m for 158, 300-999 for 1156, and ≥1000 m for 3409. Those who lived <150 m from a major road had mean 1.2 mm (95% CI 0.2, 2.1) greater LV diameter at end-systole compared to those who lived ≥1000 m. We did not observe statistically significant associations between distance to roads and LV mass index, LV end-diastolic diameter, or LV hypertrophy. Results did not materially change after additional adjustment for hypertension and diabetes or exclusion of those with CVD at baseline; results strengthened when modeling distance to A1 roads (such as interstate highways) as the exposure of interest. CONCLUSIONS: We found that residential distance to roads may be associated with LV end-systolic diameter, a marker of systolic dysfunction, in this cohort of African Americans, suggesting a potential mechanism by which exposure to traffic pollution increases the risk of HF.

Lead brownfields and birth defects in North Carolina 2003-2015: A cross-sectional case-control study.

BACKGROUND: Brownfields consist of abandoned and disused sites, spanning many former purposes. Brownfields represent a heterogenous yet ubiquitous exposure for many Americans, which may contain hazardous wastes and represent urban blight. Neonates and pregnant individuals are often sensitive to subtle environmental exposures. We evaluate if residential exposure to lead (Pb) brownfields is associated with birth defects. METHODS: Using North Carolina birth records from 2003 to 2015, we sampled 169,499 births within 10 km of a Pb brownfield with 3255 cardiovascular, central nervous, or external defects identified. Exposure was classified by binary specification of residing within 3 km of a Pb brownfield. We utilized multivariable logistic regression models adjusted for demographic covariates available from birth records and 2010 Census to estimate odds ratios (OR) and 95% confidence intervals (CI). Effect measure modification was assessed by inclusion of interaction terms and stratification for the potential modifiers of race/ethnicity and diabetes status. RESULTS: We observed positive associations between cardiovascular birth defects and residential proximity to Pb brownfields, OR (95%CI): 1.15 (1.04, 1.26), with suggestive positive associations for central nervous 1.16 (0.91, 1.47) and external defects 1.19 (0.88, 1.59). We did observe evidence of effect measure modification via likelihood ratio tests (LRT) for race/ethnicity for central nervous and external defect groups (LRT p values 0.08 and 0.02). We did observe modification by diabetes status for the cardiovascular group (LRT p value 0.08). CONCLUSIONS: Our results from this analysis indicate that residential proximity to Pb brownfields is associated with cardiovascular birth defects with suggestive associations for central nervous and external defects. In-depth analyses of individual defects and other contaminants or brownfield site functions may reveal additional novel associations.

Alcohol intake over the life course and breast cancer survival in Western New York exposures and breast cancer (WEB) study: quantity and intensity of intake.

Alcohol intake is a risk factor for breast cancer, but the association between alcohol and mortality among breast cancer survivors is poorly understood. We examined the association between alcohol intake from all sources, assessed by cognitive lifetime drinking history, and all-cause and breast cancer mortality among women with breast cancer (N = 1,097) who participated in a population-based case-control study. Vital status was ascertained through 2006 using the National Death Index. Using Cox proportional hazards models, we computed hazard ratios for all-cause and breast cancer mortality in association with alcohol intake. We examined lifetime volume and intensity (drinks per drinking day) of alcohol consumption as well as drinking status during various life periods. Analyses were stratified by menopausal status. After adjustment for total intake, postmenopausal women with consumption of four or more drinks per drinking day over their lifetimes were nearly three times more likely to die from any cause compared to abstainers (HR 2.94, 95 % CI 1.31, 6.62). There was a similar but non-significant association with breast cancer mortality (HR 2.68, 95 % CI 0.94, 7.67). Postmenopausal women who drank one drink or fewer per drinking day between menarche and first birth had a significantly decreased hazard of all-cause (HR 0.54, 95 % CI 0.31, 0.95) and breast cancer mortality (HR 0.27, 95 % CI 0.09, 0.77). Premenopausal breast cancer survival was not associated with drinking intensity. We observed no associations between drinking status or total volume of alcohol intake and breast cancer or all-cause mortality. High-intensity alcohol consumption may be associated with decreased survival in postmenopausal women with breast cancer. Low-intensity alcohol consumption between menarche and first birth may be inversely associated with all-cause and breast cancer mortality; this period may be critical for development of and survival from breast cancer. Intensity of alcohol intake may be a more important factor than absolute volume of intake on survival in women with breast cancer.

Dietary intakes of total and specific lignans are associated with clinical breast tumor characteristics.

Dietary lignans may affect breast cancer by modifying tumor characteristics likely to affect prognosis. We investigated usual dietary intakes of total and specific lignans with tumor characteristics in 683 women with breast cancer and 611 healthy women without breast cancer enrolled in the Data Bank and BioRepository at Roswell Park Cancer Institute (RPCI). Clinicopathologic data were abstracted from the RPCI breast cancer database. Dietary lignan intakes were calculated from FFQ. OR and 95% CI were estimated with logistic regression adjusting for potential confounders and stratified by menopausal status. Women in the highest compared to the lowest tertile of total lignan intakes had a 40-50% lower odds of breast cancer regardless of menopausal status and substantially reduced odds of an invasive tumor, especially among premenopausal women [OR 0.48 (95% CI 0.26-0.86)]. Lignan intakes were inversely associated with odds of grade 3 tumors among premenopausal women. Lignan intakes were inversely associated with risk of estrogen receptor (ER) negative (ER(-)) breast cancer among premenopausal women [OR 0.16 (95% CI 0.03-0.44)] and particularly triple negative tumors [ER(-), progesterone receptor negative, HER2 negative; OR 0.16 (95% CI 0.04-0.62)]. There were significant differences in the contribution to these effects by specific lignans, especially matairesinol and lariciresinol. In summary, in this case-control study of dietary lignan intakes and breast cancer, we found that higher lignan intakes were associated with lower risks of breast cancer with more favorable prognostic characteristics. Future investigations are warranted to explore the strong associations observed with ER(-) cancer in premenopausal women.

A cross-sectional study of brownfields and birth defects.

BACKGROUND: Brownfields are a multitude of abandoned and disused sites, spanning many former purposes. Brownfields represent a heterogenous yet ubiquitous exposure for many Americans, which may contain hazardous wastes and represent urban blight. Neonates and pregnant individuals are often sensitive to subtle environmental exposures. We evaluate whether residential brownfield exposure is associated with birth defects. METHODS: Using North Carolina birth records from 2003 to 2015, we sampled 753,195 births with 39,495 defects identified. We examined defect groups and 30 distinct phenotypes. Number of brownfields within 2,000 m of the residential address at birth was summed. We utilized mixed effects multivariable logistic regression models adjusted for demographic and environmental covariates available from birth records, 2010 Census, and EPA's Environmental Quality Index to estimate odds ratios (OR) and 95% confidence intervals (CI). RESULTS: We observed positive associations between cardiovascular and external defect groups (OR [95% CI]: 1.07 [1.02-1.13] and 1.17 [1.01-1.35], respectively) and any brownfield exposure. We also observed positive associations with atrial septal and ventricular septal defects (1.08 [1.01-1.16] and 1.15 [1.03-1.28], respectively), congenital cataracts (1.38 [0.98-1.96]), and an inverse association with gastroschisis (0.74 [0.58-0.94]). Effect estimates for several additional defects were positive, though we observed null associations for most group and individual defects. Additional analyses indicated an exposure-response relationship for several defects across levels of brownfield exposure. CONCLUSIONS: Our results indicate that residential proximity to brownfields is associated with birth defects, especially cardiovascular and external defects. In-depth analyses of individual defects and specific contaminants or brownfield sites may reveal additional novel 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.

Associations between air pollution indicators and prevalent and incident diabetes in an African American cohort, the Jackson Heart Study.

BACKGROUND: Diabetes is especially prevalent among African Americans. Prior studies suggest that long-term exposure to ambient air pollution may be associated with greater incidence of diabetes, but results remain heterogeneous. Few studies have included large numbers of African Americans. METHODS: We assessed diabetes status and concentrations of 1- and 3-year fine particulate matter (PM2.5) and ozone (O3) among African American participants of the Jackson Heart Study at visits 1 (2000-2004, N = 5128) and 2 (2005-2008, N = 2839). We used mixed-effect modified Poisson regression to estimate risk ratios (RRs) and 95% confidence intervals (CIs) of incidence of diabetes by visit 2 and prevalence ratios (PRs) of the association between air pollution exposure and prevalent diabetes at visits 1 and 2. We adjusted for potential confounding by patient characteristics, as well as inverse probability weights of diabetes at visit 2, accounting for clustering by census tract. RESULTS: We observed associations between incident diabetes and interquartile range increase in 1-year O3 (RR 1.34, 95% CI = 1.11, 1.61) and 3-year O3 (RR 0.88, 95% CI = 0.76, 1.02). We observed associations between prevalent diabetes and 1-year PM2.5 (PR 1.08, 95% CI = 1.00, 1.17), 1-year O3 (PR 1.18, 95% CI = 1.10, 1.27), and 3-year O3 (PR 0.95, 95% CI = 0.90, 1.01) at visit 2. CONCLUSIONS: Our results provide some evidence of positive associations between indicators of long-term PM2.5 and O3 exposure and diabetes. This study is particularly relevant to African Americans, who have higher prevalence of diabetes but relatively few studies of environmental pollution risk factors.

Long-Term Exposure to Particulate Air Pollution Is Associated With 30-Day Readmissions and Hospital Visits Among Patients With Heart Failure.

Background Long-term air pollution exposure is a significant risk factor for inpatient hospital admissions in the general population. However, we lack information on whether long-term air pollution exposure is a risk factor for hospital readmissions, particularly in individuals with elevated readmission rates. Methods and Results We determined the number of readmissions and total hospital visits (outpatient visits+emergency room visits+inpatient admissions) for 20 920 individuals with heart failure. We used quasi-Poisson regression models to associate annual average fine particulate matter at the date of heart failure diagnosis with the number of hospital visits and 30-day readmissions. We used inverse probability weights to balance the distribution of confounders and adjust for the competing risk of death. Models were adjusted for age, race, sex, smoking status, urbanicity, year of diagnosis, short-term fine particulate matter exposure, comorbid disease, and socioeconomic status. A 1-µg/m3 increase in fine particulate matter was associated with a 9.31% increase (95% CI, 7.85%-10.8%) in total hospital visits, a 4.35% increase (95% CI, 1.12%-7.68%) in inpatient admissions, and a 14.2% increase (95% CI, 8.41%-20.2%) in 30-day readmissions. Associations were robust to different modeling approaches. Conclusions These results highlight the potential for air pollution to play a role in hospital use, particularly hospital visits and readmissions. Given the elevated frequency of hospitalizations and readmissions among patients with heart failure, these results also represent an important insight into modifiable environmental risk factors that may improve outcomes and reduce hospital use among patients with heart failure.

Evaluation of PM2.5 air pollution sources and cardiovascular health.

Long-term air pollution exposure, notably fine particulate matter, is a global contributor to morbidity and mortality and a known risk factor for coronary artery disease (CAD) and myocardial infarctions (MI). Knowledge of impacts related to source-apportioned PM2.5 is limited. New modeling methods allow researchers to estimate source-specific long-term impacts on the prevalence of CAD and MI. The Catheterization Genetics (CATHGEN) cohort consists of patients who underwent a cardiac catheterization at Duke University Medical Center between 2002 and 2010. Severity of coronary blockage was determined by coronary angiography and converted into a binary indicator of clinical CAD. History of MI was extracted from medical records. Annual averages of source specific PM2.5 were estimated using an improved gas-constrained source apportionment model for North Carolina from 2002 to 2010. We tested six sources of PM2.5 mass for associations with CAD and MI using mixed effects multivariable logistic regression with a random intercept for county and multiple adjustments. PM2.5 fractions of ammonium bisulfate and ammonium nitrate were associated with increased prevalence of CAD (odds ratio [OR] 1.20; 95% CI = 1.11, 1.22 and OR 1.18; 95% CI = 1.05, 1.32, respectively). PM2.5 from ammonium bisulfate and ammonium nitrate were also associated with increased prevalence of MI (OR 1.20; 95% CI = 1.10, 1.29 and OR 1.35; 95% CI = 1.20, 1.53, respectively). Greater PM2.5 concentrations of ammonium bisulfate and ammonium nitrate are associated with greater MI and CAD prevalence. The association with bisulfate suggests aerosol acidity may play a role. Our findings suggest analyses of source specific PM2.5 mass can reveal novel associations.

Long-Term Air Pollution and Blood Pressure in an African American Cohort: the Jackson Heart Study.

INTRODUCTION: African Americans are disproportionately affected by high blood pressure, which may be associated with exposure to air pollutants, such as fine particulate matter and ozone. METHODS: Among African American Jackson Heart Study participants, this study examined associations between 1-year and 3-year mean fine particulate matter and ozone concentrations with prevalent and incident hypertension at Visits 1 (2000-2004, n=5,191) and 2 (2005-2008, n=4,105) using log binomial regression. Investigators examined associations with systolic blood pressure, diastolic blood pressure, pulse pressure, and mean arterial pressure using linear regression and hierarchical linear models, adjusting for sociodemographic, behavioral, and clinical characteristics. Analyses were conducted in 2017-2019. RESULTS: No associations were observed between fine particulate matter or ozone concentration and prevalent or incident hypertension. In linear models, an IQR increase in 1-year ozone concentration was associated with 0.67 mmHg higher systolic blood pressure (95% CI=0.27, 1.06), 0.42 mmHg higher diastolic blood pressure (95% CI=0.20, 0.63), and 0.50 mmHg higher mean arterial pressure (95% CI=0.26, 0.74). In hierarchical models, fine particulate matter was inversely associated with systolic blood pressure (-0.72, 95% CI= -1.31, -0.13), diastolic blood pressure (-0.69, 95% CI= -1.02, -0.36), and mean arterial pressure (-0.71, 95% CI= -1.08, -0.33). Attenuated associations were observed with 1-year concentrations and at Visit 1. CONCLUSIONS: Positive associations were observed between ozone and systolic blood pressure, diastolic blood pressure, and mean arterial pressure, and inverse associations between fine particulate matter and systolic blood pressure, diastolic blood pressure, and mean arterial pressure in an African American population with high (56%) prevalence of hypertension. Effect sizes were small and may not be clinically relevant.

Waterless Hand Cleansing with Chlorhexidine during the Neonatal Period by Mothers and Other Household Members: Findings from a Randomized Controlled Trial.

Observational data suggest maternal handwashing with soap prevents neonatal mortality. We tested the impact of a chlorhexidine-based waterless hand cleansing promotion on the behavior of mothers and other household members. In rural Bangladesh in 2014, we randomized consenting pregnant women to chlorhexidine provision and hand cleansing promotion or standard practices. We compared hand cleansing with chlorhexidine or handwashing with soap before baby care, among mothers and household members in the two groups, and measured chlorhexidine use in the intervention arm. Chlorhexidine was observed in the baby's sleep space in 97% of 130 intervention homes, versus soap in 59% of 128 control homes. Hand cleansing before baby care was observed 5.6 times more frequently among mothers in the intervention arm than in the controls (95% CI = 4.0-7.7). Hand cleansing was significantly more frequently observed in the intervention arm among women other than the mother (RR = 10.9) and girls (RR = 37.0). Men and boys in the intervention arm cleansed hands before 29% and 44% of baby care events, respectively, compared with 0% in the control arm. The median number of grams consumed during the neonatal period was 176 (IQR = 95-305 g), about 7.8 g/day (IQR = 4.2-13.8 g). Promotion of waterless chlorhexidine increased hand cleansing behavior among mothers and other household members. Discrepancy between observed use and measured chlorhexidine consumption suggested courtesy bias in structured observations. A waterless hand cleanser may represent one component of the multimodal strategies to prevent neonatal infections in low-resource settings.

Associations Between Long-Term Fine Particulate Matter Exposure and Mortality in Heart Failure Patients.

Background Environmental health risks for individuals with heart failure (HF) have been inadequately studied, as these individuals are not well represented in traditional cohort studies. To address this we studied associations between long-term air pollution exposure and mortality in HF patients. Methods and Results The study population was a hospital-based cohort of individuals diagnosed with HF between July 1, 2004 and December 31, 2016 compiled using electronic health records. Individuals were followed from 1 year after initial diagnosis until death or the end of the observation period (December 31, 2016). We used Cox proportional hazards models to evaluate the association of annual average fine particulate matter (PM2.5) exposure at the time of initial HF diagnosis with all-cause mortality, adjusted for age, race, sex, distance to the nearest air pollution monitor, and socioeconomic status indicators. Among 23 302 HF patients, a 1 µg/m3 increase in annual average PM2.5 was associated with an elevated risk of all-cause mortality (hazard ratio 1.13; 95% CI, 1.10-1.15). As compared with people with exposures below the current national PM2.5 exposure standard (12 µg/m3), those with elevated exposures experienced 0.84 (95% CI, 0.73-0.95) years of life lost over a 5-year period, an observation that persisted even for those residing in areas with PM2.5 concentrations below current standards. Conclusions Residential exposure to elevated concentrations of PM2.5 is a significant mortality risk factor for HF patients. Elevated PM2.5 exposures result in substantial years of life lost even at concentrations below current national standards.

Accelerated epigenetic age as a biomarker of cardiovascular sensitivity to traffic-related air pollution.

BACKGROUND: Accelerated epigenetic age has been proposed as a biomarker of increased aging, which may indicate disruptions in cellular and organ system homeostasis and thus contribute to sensitivity to environmental exposures. METHODS: Using 497 participants from the CATHGEN cohort, we evaluated whether accelerated epigenetic aging increases cardiovascular sensitivity to traffic-related air pollution (TRAP) exposure. We used residential proximity to major roadways and source apportioned air pollution models as measures of TRAP exposure, and chose peripheral arterial disease (PAD) and blood pressure as outcomes based on previous associations with TRAP. We used Horvath epigenetic age acceleration (AAD) and phenotypic age acceleration (PhenoAAD) as measures of age acceleration, and adjusted all models for chronological age, race, sex, smoking, and socioeconomic status. RESULTS: We observed significant interactions between TRAP and both AAD and PhenoAAD. Interactions indicated that increased epigenetic age acceleration elevated associations between proximity to roadways and PAD. Interactions were also observed between AAD and gasoline and diesel source apportioned PM2.5. CONCLUSION: Epigenetic age acceleration may be a biomarker of sensitivity to air pollution, particularly for TRAP in urban cohorts. This presents a novel means by which to understand sensitivity to air pollution and provides a molecular measure of environmental sensitivity.

Validation of a Dietary Questionnaire to Screen Omega-3 Fatty Acids Levels in Healthy Adults.

To facilitate a clinical observational study to identify healthy volunteers with low (defined as ≤4%) and high (defined as ≥5.5%) omega-3 indices, a dietary questionnaire to rapidly assess habitual dietary intake of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) was developed. This study aimed to determine the validity of this newly developed dietary questionnaire. One hundred and eight volunteers were included and were assessed for habitual dietary intake of EPA and DHA using the questionnaire. The United States Department of Agriculture food products database and nutrition fact label was referenced for calculation. Blood samples were collected for the analysis of fatty acids in whole blood specimens and to derive omega-3 indices. A linear correlation was observed between reported dietary consumption of EPA, DHA, EPA+DHA and the whole blood levels of EPA, DHA, and the omega-3 indices (r = 0.67, 0.62, 0.67, respectively, p < 0.001 for all). The findings also suggested that the questionnaire was substantially better at identifying volunteers with high omega-3 indices (sensitivity 89%, specificity 84%, and agreement 86%) compared to volunteers with low omega-3 indices (sensitivity 100%, specificity 66%, and agreement 42%). In conclusion, this newly developed questionnaire is an efficient tool for the assessment of omega-3 indices in study populations and is particularly effective in identifying individuals with high omega-3 indices.