486 results on '"Joel D. Kaufman"'
Search Results
2. Associations of residential green space with internalizing and externalizing behavior in early childhood
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Marnie F. Hazlehurst, Anjum Hajat, Pooja S. Tandon, Adam A. Szpiro, Joel D. Kaufman, Frances A. Tylavsky, Marion E. Hare, Sheela Sathyanarayana, Christine T. Loftus, Kaja Z. LeWinn, Nicole R. Bush, and Catherine J. Karr
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Child mental health ,Internalizing ,Externalizing ,Built environment ,Green space ,Industrial medicine. Industrial hygiene ,RC963-969 ,Public aspects of medicine ,RA1-1270 - Abstract
Abstract Background Green space exposures may promote child mental health and well-being across multiple domains and stages of development. The aim of this study was to investigate associations between residential green space exposures and child mental and behavioral health at age 4–6 years. Methods Children’s internalizing and externalizing behaviors in the Conditions Affecting Neurocognitive Development and Learning in Early Childhood (CANDLE) cohort in Shelby County, Tennessee, were parent-reported on the Child Behavior Checklist (CBCL). We examined three exposures—residential surrounding greenness calculated as the Normalized Difference Vegetation Index (NDVI), tree cover, and park proximity—averaged across the residential history for the year prior to outcome assessment. Linear regression models were adjusted for individual, household, and neighborhood-level confounders across multiple domains. Effect modification by neighborhood socioeconomic conditions was explored using multiplicative interaction terms. Results Children were on average 4.2 years (range 3.8-6.0) at outcome assessment. Among CANDLE mothers, 65% self-identified as Black, 29% as White, and 6% as another or multiple races; 41% had at least a college degree. Higher residential surrounding greenness was associated with lower internalizing behavior scores (-0.66 per 0.1 unit higher NDVI; 95% CI: -1.26, -0.07) in fully-adjusted models. The association between tree cover and internalizing behavior was in the hypothesized direction but confidence intervals included the null (-0.29 per 10% higher tree cover; 95% CI: -0.62, 0.04). No associations were observed between park proximity and internalizing behavior. We did not find any associations with externalizing behaviors or the attention problems subscale. Estimates were larger in neighborhoods with lower socioeconomic opportunity, but interaction terms were not statistically significant. Conclusions Our findings add to the accumulating evidence of the importance of residential green space for the prevention of internalizing problems among young children. This research suggests the prioritization of urban green spaces as a resource for child mental health.
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- 2024
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3. Correction: Associations of residential green space with internalizing and externalizing behavior in early childhood
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Marnie F. Hazlehurst, Anjum Hajat, Pooja S. Tandon, Adam A. Szpiro, Joel D. Kaufman, Frances A. Tylavsky, Marion E. Hare, Sheela Sathyanarayana, Christine T. Loftus, Kaja Z. LeWinn, Nicole R. Bush, and Catherine J. Karr
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Industrial medicine. Industrial hygiene ,RC963-969 ,Public aspects of medicine ,RA1-1270 - Published
- 2024
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4. Long-term exposure to ambient fine particulate matter and risk of liver cancer in the NIH-AARP Diet and Health Study
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Xiuqi Ma, Jared A. Fisher, Katherine A. McGlynn, Linda M. Liao, Vasilis Vasiliou, Ning Sun, Joel D. Kaufman, Debra T. Silverman, and Rena R. Jones
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Air pollution ,Liver cancer ,Hepatocellular carcinoma ,Particulate matter ,PM2.5 ,Environmental sciences ,GE1-350 - Abstract
Background: Fine particulate matter (PM2.5) exposure has been associated with liver cancer incidence and mortality in a limited number of studies. We sought to evaluate this relationship for the first time in a U.S. cohort with historical exposure assessment. Methods: We used spatiotemporal prediction models to estimate annual average historical PM2.5 concentrations (1980–2015) at residential addresses of 499,729 participants in the NIH-AARP Diet and Health Study, a cohort in 6 states (California, Florida, Louisiana, New Jersey, North Carolina, and Pennsylvania) and 2 metropolitan areas (Atlanta, Georgia, and Detroit, Michigan) enrolled in 1995–1996 and followed up through 2017. We used a time-varying Cox model to estimate the association for liver cancer and the predominant histologic type, hepatocellular carcinoma (HCC), per 5 µg/m3 increase in estimated outdoor PM2.5 levels, incorporating a 5-year average, lagged 10 years prior to cancer diagnosis and adjusting for age, sex, race/ethnicity, education level and catchment state. We also evaluated PM2.5 interactions with hypothesized effect modifiers. Results: We observed a non-significantly increased risk of liver cancer associated with estimated PM2.5 exposure (Hazard ratio [HR] = 1.05 [0.96–1.14], N = 1,625); associations were slightly stronger for HCC, (84 % of cases; HR = 1.08 [0.98–1.18]). Participants aged 70 or older at enrollment had an increased risk of liver cancer versus other age groups (HR = 1.50 [1.01–2.23]); p-interaction = 0.01) and risk was elevated among participants who did not exercise (HR = 1.81 [1.22–2.70]; p-interaction = 0.01). We found no evidence of effect modification by sex, smoking status, body mass index, diabetes status, or alcohol consumption (p-interaction > 0.05). Conclusions: Our findings in this large cohort suggest that residential ambient PM2.5 levels may be associated with liver cancer risk. Further exploration of the variation in associations by age and physical activity are important areas for future research.
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- 2024
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5. Traffic-related air pollution and dementia incidence in the Adult Changes in Thought Study
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Magali N. Blanco, Rachel M. Shaffer, Ge Li, Sara D. Adar, Marco Carone, Adam A. Szpiro, Joel D. Kaufman, Timothy V. Larson, Anjum Hajat, Eric B. Larson, Paul K. Crane, and Lianne Sheppard
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Ultrafine particles (UFP) ,Black carbon (BC) ,Nitrogen dioxide (NO2) traffic-related air pollution ,Alzheimer’s Disease (AD) and related dementias (ADRD) ,Cohort ,Environmental sciences ,GE1-350 - Abstract
Background: While epidemiologic evidence links higher levels of exposure to fine particulate matter (PM2.5) to decreased cognitive function, fewer studies have investigated links with traffic-related air pollution (TRAP), and none have examined ultrafine particles (UFP, ≤100 nm) and late-life dementia incidence. Objective: To evaluate associations between TRAP exposures (UFP, black carbon [BC], and nitrogen dioxide [NO2]) and late-life dementia incidence. Methods: We ascertained dementia incidence in the Seattle-based Adult Changes in Thought (ACT) prospective cohort study (beginning in 1994) and assessed ten-year average TRAP exposures for each participant based on prediction models derived from an extensive mobile monitoring campaign. We applied Cox proportional hazards models to investigate TRAP exposure and dementia incidence using age as the time axis and further adjusting for sex, self-reported race, calendar year, education, socioeconomic status, PM2.5, and APOE genotype. We ran sensitivity analyses where we did not adjust for PM2.5 and other sensitivity and secondary analyses where we adjusted for multiple pollutants, applied alternative exposure models (including total and size-specific UFP), modified the adjustment covariates, used calendar year as the time axis, assessed different exposure periods, dementia subtypes, and others. Results: We identified 1,041 incident all-cause dementia cases in 4,283 participants over 37,102 person-years of follow-up. We did not find evidence of a greater hazard of late-life dementia incidence with elevated levels of long-term TRAP exposures. The estimated hazard ratio of all-cause dementia was 0.98 (95 % CI: 0.92–1.05) for every 2000 pt/cm3 increment in UFP, 0.95 (0.89–1.01) for every 100 ng/m3 increment in BC, and 0.96 (0.91–1.02) for every 2 ppb increment in NO2. These findings were consistent across sensitivity and secondary analyses. Discussion: We did not find evidence of a greater hazard of late-life dementia risk with elevated long-term TRAP exposures in this population-based prospective cohort study.
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- 2024
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6. Air pollution and epigenetic aging among Black and White women in the US
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Sarah H. Koenigsberg, Che-Jung Chang, Jennifer Ish, Zongli Xu, Jacob K. Kresovich, Kaitlyn G. Lawrence, Joel D. Kaufman, Dale P. Sandler, Jack A. Taylor, and Alexandra J. White
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Air pollution ,DNA methylation ,Particulate matter ,Epigenetic age ,Epigenome-wide association study ,Environmental sciences ,GE1-350 - Abstract
Background: DNA methylation-based measures of biological aging have been associated with air pollution and may link pollutant exposures to aging-related health outcomes. However, evidence is inconsistent and there is little information for Black women. Objective: We examined associations of ambient particulate matter
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- 2023
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7. Air pollution and fecundability in a North American preconception cohort study
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Amelia K. Wesselink, Perry Hystad, Kipruto Kirwa, Joel D. Kaufman, Mary D. Willis, Tanran R. Wang, Adam A. Szpiro, Jonathan I. Levy, David A. Savitz, Kenneth J. Rothman, Elizabeth E. Hatch, and Lauren A. Wise
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Air pollution ,Fertility ,Time to pregnancy ,Preconception cohort ,Environmental sciences ,GE1-350 - Abstract
Background: Animal and epidemiologic studies indicate that air pollution may adversely affect fertility. However, the level of evidence is limited and specific pollutants driving the association are inconsistent across studies. Methods: We used data from a web-based preconception cohort study of pregnancy planners enrolled during 2013–2019 (Pregnancy Study Online; PRESTO). Eligible participants self-identified as female, were aged 21–45 years, resided in the United States (U.S.) or Canada, and were trying to conceive without fertility treatments. Participants completed a baseline questionnaire and bi-monthly follow-up questionnaires until conception or 12 months. We analyzed data from 8,747 participants (U.S.: 7,304; Canada: 1,443) who had been trying to conceive for
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- 2023
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8. The association of long-term exposure to criteria air pollutants, fine particulate matter components, and airborne trace metals with late-life brain amyloid burden in the Atherosclerosis Risk in Communities (ARIC) study
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Erin E. Bennett, Ziwei Song, Katie M. Lynch, Chelsea Liu, Emma K. Stapp, Xiaohui Xu, Eun Sug Park, Qi Ying, Richard L. Smith, James D. Stewart, Eric A. Whitsel, Thomas H. Mosley, Dean F. Wong, Duanping Liao, Jeff D. Yanosky, Adam A. Szpiro, Joel D. Kaufman, Rebecca F. Gottesman, and Melinda C. Power
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Environmental sciences ,GE1-350 - Abstract
Background: Studies suggest associations between long-term ambient air pollution exposure and outcomes related to Alzheimer’s disease (AD). Whether a link exists between pollutants and brain amyloid accumulation, a biomarker of AD, is unclear. We assessed whether long-term air pollutant exposures are associated with late-life brain amyloid deposition in Atherosclerosis Risk in Communities (ARIC) study participants. Methods: We used a chemical transport model with data fusion to estimate ambient concentrations of PM2.5 and its components, NO2, NOx, O3 (24-hour and 8-hour), CO, and airborne trace metals. We linked concentrations to geocoded participant addresses and calculated 10-year mean exposures (2002 to 2011). Brain amyloid deposition was measured using florbetapir amyloid positron emission tomography (PET) scans in 346 participants without dementia in 2012–2014, and we defined amyloid positivity as a global cortical standardized uptake value ratio ≥ the sample median of 1.2. We used logistic regression models to quantify the association between amyloid positivity and each air pollutant, adjusting for putative confounders. In sensitivity analyses, we considered whether use of alternate air pollution estimation approaches impacted findings for PM2.5, NO2, NOx, and 24-hour O3. Results: At PET imaging, eligible participants (N = 318) had a mean age of 78 years, 56% were female, 43% were Black, and 27% had mild cognitive impairment. We did not find evidence of associations between long-term exposure to any pollutant and brain amyloid positivity in adjusted models. Findings were materially unchanged in sensitivity analyses using alternate air pollution estimation approaches for PM2.5, NO2, NOx, and 24-hour O3. Conclusions: Air pollution may impact cognition and dementia independent of amyloid accumulation, though whether air pollution influences AD pathogenesis later in the disease course or at higher exposure levels deserves further consideration.
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- 2023
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9. Black carbon content in airway macrophages is associated with increased severe exacerbations and worse COPD morbidity in SPIROMICS
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Vickram Tejwani, Han Woo, Chen Liu, Anna K. Tillery, Amanda J. Gassett, Richard E. Kanner, Eric A. Hoffman, Fernando J. Martinez, Prescott G. Woodruff, R. Graham Barr, Ashraf Fawzy, Kirsten Koehler, Jeffrey L. Curtis, Christine M. Freeman, Christopher B. Cooper, Alejandro P. Comellas, Cheryl Pirozzi, Robert Paine, Donald Tashkin, Jerry A. Krishnan, Coralynn Sack, Nirupama Putcha, Laura M. Paulin, Marina Zusman, Joel D. Kaufman, Neil E. Alexis, and Nadia N. Hansel
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Macrophage ,Black carbon ,COPD ,Diseases of the respiratory system ,RC705-779 - Abstract
Abstract Background Airway macrophages (AM), crucial for the immune response in chronic obstructive pulmonary disease (COPD), are exposed to environmental particulate matter (PM), which they retain in their cytoplasm as black carbon (BC). However, whether AM BC accurately reflects environmental PM2.5 exposure, and can serve as a biomarker of COPD outcomes, is unknown. Methods We analyzed induced sputum from participants at 7 of 12 sites SPIROMICS sites for AM BC content, which we related to exposures and to lung function and respiratory outcomes. Models were adjusted for batch (first vs. second), age, race (white vs. non-white), income (
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- 2022
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10. Air pollution and plasma amyloid beta in a cohort of older adults: Evidence from the Ginkgo Evaluation of Memory study
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Anjum Hajat, Christina Park, Claire Adam, Annette L. Fitzpatrick, Sindana D. Ilango, Cindy Leary, Tanya Libby, Oscar Lopez, Erin O. Semmens, and Joel D. Kaufman
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Air pollution ,Alzheimer’s disease ,Dementia ,Biomarkers ,Amyloid beta ,Aging ,Environmental sciences ,GE1-350 - Abstract
Air pollution has been linked to Alzheimer’s disease and related dementias (ADRD), but the mechanisms connecting air pollution to ADRD have not been firmly established. Air pollution may cause oxidative stress and neuroinflammation and contribute to the deposition of amyloid beta (Aβ) in the brain. We examined the association between fine particulate matter
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- 2023
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11. Neighborhood greenspace exposure as a protective factor in dementia risk among U.S. adults 75 years or older: a cohort study
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Erik D. Slawsky, Anjum Hajat, Isaac C. Rhew, Helen Russette, Erin O. Semmens, Joel D. Kaufman, Cindy S. Leary, and Annette L. Fitzpatrick
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Dementia ,Greenspace ,NDVI ,Residential exposures ,Alzheimer’s disease ,Industrial medicine. Industrial hygiene ,RC963-969 ,Public aspects of medicine ,RA1-1270 - Abstract
Highlights Residential greenspace exposure was found to be associated with moderate cognitive health benefit for older U.S. adults. Dementia subtypes may be differentially impacted by exposure to residential greenspace. Combining multiple greenspace measures may better capture a holistic picture of exposure to greenspace compared to one measure alone.
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- 2022
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12. Neighborhood greenspace and risk of type 2 diabetes in a prospective cohort: the Multi-Ethncity Study of Atherosclerosis
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Annie Doubleday, Catherine J. Knott, Marnie F. Hazlehurst, Alain G. Bertoni, Joel D. Kaufman, and Anjum Hajat
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Neighborhood greenspace ,Environmental epidemiology ,Type 2 diabetes ,Industrial medicine. Industrial hygiene ,RC963-969 ,Public aspects of medicine ,RA1-1270 - Abstract
Abstract Background Neighborhood greenspaces provide opportunities for increased physical activity and social interaction, and thus may reduce the risk of Type 2 diabetes. However, there is little robust research on greenspace and diabetes. In this study, we examine the longitudinal association between neighborhood greenspace and incident diabetes in the Multi-Ethnic Study of Atherosclerosis. Methods A prospective cohort study (N = 6814; 2000-2018) was conducted to examine the association between greenspace, measured as annual and high vegetation season median greenness determined by satellite (Normalized Difference Vegetation Index) within 1000 m of participant homes, and incident diabetes assessed at clinician visits, defined as a fasting glucose level of at least 126 mg/dL, use of insulin or use of hypoglycemic medication, controlling for covariates in stages. Five thousand five hundred seventy-four participants free of prevalent diabetes at baseline were included in our analysis. Results Over the study period, 886 (15.9%) participants developed diabetes. Adjusting for individual characteristics, individual and neighborhood-scale SES, additional neighborhood factors, and diabetes risk factors, we found a 21% decrease in the risk of developing diabetes per IQR increase in greenspace (HR: 0.79; 95% CI: 0.63, 0.99). Conclusions Overall, neighborhood greenspace provides a protective influence in the development of diabetes, suggesting that neighborhood-level urban planning that supports access to greenspace--along with healthy behaviors--may aid in diabetes prevention. Additional research is needed to better understand how an area’s greenness influences diabetes risk, how to better characterize greenspace exposure and usage, and future studies should focus on robust adjustment for neighborhood-level confounders.
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- 2022
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13. Prenatal exposure to particulate matter and placental gene expression
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Daniel A. Enquobahrie, James MacDonald, Michael Hussey, Theo K. Bammler, Christine T. Loftus, Alison G. Paquette, Nora Byington, Carmen J. Marsit, Adam Szpiro, Joel D. Kaufman, Kaja Z. LeWinn, Nicole R. Bush, Frances Tylavsky, Catherine J. Karr, and Sheela Sathyanarayana
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Air pollution ,Fine particulate matter ,PM2.5 ,Pregnancy ,Placenta ,Gene expression ,Environmental sciences ,GE1-350 - Abstract
Background: While strong evidence supports adverse maternal and offspring consequences of air pollution, mechanisms that involve the placenta, a key part of the intrauterine environment, are largely unknown. Previous studies of air pollution and placental gene expression were small candidate gene studies that rarely considered prenatal windows of exposure or the potential role of offspring sex. We examined overall and sex-specific associations of prenatal exposure to fine particulate matter (PM2.5) with genome-wide placental gene expression. Methods: Participants with placenta samples, collected at birth, and childhood health outcomes from CANDLE (Memphis, TN) (n = 776) and GAPPS (Seattle, WA) (n = 205) cohorts of the ECHO-PATHWAYS Consortium were included in this study. PM2.5 exposures during trimesters 1, 2, 3, and the first and last months of pregnancy, were estimated using a spatiotemporal model. Cohort-specific linear adjusted models were fit for each exposure window and expression of >11,000 protein coding genes from paired end RNA sequencing data. Models with interaction terms were used to examine PM2.5-offspring sex interactions. False discovery rate (FDR
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- 2022
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14. Disparities in access to food and chronic obstructive pulmonary disease (COPD)-related outcomes: a cross-sectional analysis
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Eric Moughames, Han Woo, Panagis Galiatsatos, Karina Romero-Rivero, Sarath Raju, Vickram Tejwani, Eric A. Hoffman, Alejandro P. Comellas, Victor E. Ortega, Trisha Parekh, Jerry A. Krishnan, Michael B. Drummond, David Couper, Russell G. Buhr, Robert Paine, Joel D. Kaufman, Laura M. Paulin, Nirupama Putcha, and Nadia N. Hansel
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Food ,Access ,Food desert ,Disparities ,COPD ,Respiratory ,Diseases of the respiratory system ,RC705-779 - Abstract
Abstract Background Millions of Americans are living in food deserts in the United States, however the role of the local food environment on COPD has not been studied. The aim of this study is to determine the association between food deserts and COPD-related outcomes. Method In this cross-sectional analysis we linked data collected from SPIROMICS (SubPopulations and InteRmediate Outcome Measures in COPD Study) between 2010 and 2015 and food desert data, defined as an underserved area that lacks access to affordable healthy foods, from the Food Access Research Atlas. COPD outcomes include percentage of predicted forced expiratory volume in one second (FEV1%), St. George’s Respiratory Questionnaire (SGRQ), COPD Assessment Test (CAT), 6-min walk distance test (6MWD), exacerbations, and air trapping. We used generalized linear mixed models to evaluate the association between living in food deserts and respiratory outcomes, adjusting for age, gender, race, education, income, marital status, BMI, smoking status, pack years, and urban status Results Among 2713 participants, 22% lived in food deserts. Participants living in food deserts were less likely to be white and more likely to have a lower income than those who did not live in food deserts. In the adjusted model controlling for demographics and individual income, living in food deserts was associated lower FEV1% (β = – 2.51, P = 0.046), higher air trapping (β = 2.47, P = 0.008), worse SGRQ (β = 3.48, P = 0.001) and CAT (β = 1.20, P = 0.003) scores, and 56% greater odds of severe exacerbations (P = 0.004). Results were consistent when looking at food access alone, regardless of whether participants lived in low income areas. Conclusions Findings suggest an independent association between food desert and food access alone with COPD outcomes. Health program planning may benefit from addressing disparities in access to food.
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- 2021
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15. Epigenome-wide analysis of long-term air pollution exposure and DNA methylation in monocytes: results from the Multi-Ethnic Study of Atherosclerosis
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Gloria C. Chi, Yongmei Liu, James W. MacDonald, Lindsay M. Reynolds, Daniel A. Enquobahrie, Annette L. Fitzpatrick, Kathleen F. Kerr, Matthew J. Budoff, Su-In Lee, David Siscovick, and Joel D. Kaufman
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air pollution ,fine particulate matter ,oxides of nitrogen ,dna methylation ,gene expression ,Genetics ,QH426-470 - Abstract
Air pollution might affect atherosclerosis through DNA methylation changes in cells crucial to atherosclerosis, such as monocytes. We conducted an epigenome-wide study of DNA methylation in CD14+ monocytes and long-term ambient air pollution exposure in adults participating in the Multi-Ethnic Study of Atherosclerosis (MESA). We also assessed the association between differentially methylated signals and cis-gene expression. Using spatiotemporal models, one-year average concentrations of outdoor fine particulate matter (PM2.5) and oxides of nitrogen (NOX) were estimated at participants’ homes. We assessed DNA methylation and gene expression using Illumina 450k and HumanHT-12 v4 Expression BeadChips, respectively (n = 1,207). We used bump hunting and site-specific approaches to identify differentially methylated signals (false discovery rate of 0.05) and used linear models to assess associations between differentially methylated signals and cis-gene expression. Four differentially methylated regions (DMRs) located on chromosomes 5, 6, 7, and 16 (within or near SDHAP3, ZFP57, HOXA5, and PRM1, respectively) were associated with PM2.5. The DMRs on chromosomes 5 and 6 also associated with NOX. The DMR on chromosome 5 had the smallest p-value for both PM2.5 (p = 1.4×10−6) and NOX (p = 7.7×10−6). Three differentially methylated CpGs were identified for PM2.5, and cg05926640 (near TOMM20) had the smallest p-value (p = 5.6×10−8). NOX significantly associated with cg11756214 within ZNF347 (p = 5.6×10−8). Several differentially methylated signals were also associated with cis-gene expression. The DMR located on chromosome 7 was associated with the expression of HOXA5, HOXA9, and HOXA10. The DMRs located on chromosomes 5 and 16 were associated with expression of MRPL36 and DEXI, respectively. The CpG cg05926640 was associated with expression of ARID4B, IRF2BP2, and TOMM20. We identified differential DNA methylation in monocytes associated with long-term air pollution exposure. Methylation signals associated with gene expression might help explain how air pollution contributes to cardiovascular disease.
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- 2022
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16. Publicly available low-cost sensor measurements for PM2.5 exposure modeling: Guidance for monitor deployment and data selection
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Jianzhao Bi, Nancy Carmona, Magali N. Blanco, Amanda J. Gassett, Edmund Seto, Adam A. Szpiro, Timothy V. Larson, Paul D. Sampson, Joel D. Kaufman, and Lianne Sheppard
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PurpleAir ,High-resolution ,Exposure assessment ,Fine particulate matter ,Model validation ,Environmental sciences ,GE1-350 - Abstract
High-resolution, high-quality exposure modeling is critical for assessing the health effects of ambient PM2.5 in epidemiological studies. Using sparse regulatory PM2.5 measurements as principal model inputs may result in two issues in exposure prediction: (1) they may affect the models’ accuracy in predicting PM2.5 spatial distribution; (2) the internal validation based on these measurements may not reliably reflect the model performance at locations of interest (e.g., a cohort’s residential locations). In this study, we used the PM2.5 measurements from a publicly available commercial low-cost PM2.5 network, PurpleAir, with an external validation dataset at the residential locations of a representative sample of participants from the Adult Changes in Thought - Air Pollution (ACT-AP) study, to improve the accuracy of exposure prediction at the cohort participant locations. We also proposed a metric based on principal component analysis (PCA) - the PCA distance - to assess the similarity between monitor and cohort locations to guide monitor deployment and data selection. The analysis was based on a spatiotemporal modeling framework with 51 “gold-standard” monitors and 58 PurpleAir monitors for model development, as well as 105 home monitors at the cohort locations for model validation, in the Puget Sound region of Washington State from June 2017 to March 2019. After including calibrated PurpleAir measurements as part of the dependent variable, the external spatiotemporal validation R2 and root-mean-square error, RMSE, for two-week concentration averages improved from 0.84 and 2.22 μg/m3 to 0.92 and 1.63 μg/m3, respectively. The external spatial validation R2 and RMSE for long-term averages over the modeling period improved from 0.72 and 1.01 μg/m3 to 0.79 and 0.88 μg/m3, respectively. The exposure predictions incorporating PurpleAir measurements demonstrated sharper urban-suburban concentration gradients. The PurpleAir monitors with shorter PCA distances improved the model’s prediction accuracy more substantially than the monitors with longer PCA distances, supporting the use of this similarity metric.
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- 2022
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17. WHO Air Quality Guidelines 2021–Aiming for Healthier Air for all: A Joint Statement by Medical, Public Health, Scientific Societies and Patient Representative Organisations
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Barbara Hoffmann, Hanna Boogaard, Audrey de Nazelle, Zorana J. Andersen, Michael Abramson, Michael Brauer, Bert Brunekreef, Francesco Forastiere, Wei Huang, Haidong Kan, Joel D. Kaufman, Klea Katsouyanni, Michal Krzyzanowski, Nino Kuenzli, Francine Laden, Mark Nieuwenhuijsen, Adetoun Mustapha, Pippa Powell, Mary Rice, Aina Roca-Barceló, Charlotte J. Roscoe, Agnes Soares, Kurt Straif, and George Thurston
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air pollution ,WHO Air Quality Guidelines ,health effects ,policy implications ,average population exposure ,Public aspects of medicine ,RA1-1270 - Published
- 2021
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18. Correction to: Neighborhood greenspace and risk of type 2 diabetes in a prospective cohort: the Multi-Ethnic Study of Atherosclerosis
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Annie Doubleday, Catherine J. Knott, Marnie F. Hazlehurst, Alain G. Bertoni, Joel D. Kaufman, and Anjum Hajat
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Industrial medicine. Industrial hygiene ,RC963-969 ,Public aspects of medicine ,RA1-1270 - Published
- 2022
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19. Long-term exposure to ambient air pollution, APOE-ε4 status, and cognitive decline in a cohort of older adults in northern Manhattan
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Erin R. Kulick, Mitchell S.V. Elkind, Amelia K. Boehme, Nina R. Joyce, Nicole Schupf, Joel D. Kaufman, Richard Mayeux, Jennifer J. Manly, and Gregory A. Wellenius
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Environmental sciences ,GE1-350 - Abstract
Background: There is mounting evidence that long-term exposure to air pollution is related to accelerated cognitive decline in aging populations. Factors that influence individual susceptibility remain largely unknown, but may involve the apolipoprotein E genotype E4 (APOE-ε4) allele. Objectives: We assessed whether the association between long-term exposure to ambient air pollution and cognitive decline differed by APOE-ε4 status and cognitive risk factors. Methods: The Washington Heights Inwood Community Aging Project (WHICAP) is a prospective study of aging and dementia. Neuropsychological testing and medical examinations occur every 18–24 months. We used mixed-effects models to evaluate whether the association between markers of ambient air pollution (nitrogen dioxide [NO2]), fine [PM2.5], and coarse [PM10] particulate matter) and the rate of decline in global and domain-specific cognition differed across strata defined by APOE-ε4 genotypes and cognitive risk factors, adjusting for sociodemographic factors and temporal trends. Results: Among 4821 participants with an average of 6 years follow-up, higher concentrations of ambient air pollution were associated with more rapid cognitive decline. This association was more pronounced among APOE-ε4 carriers (p
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- 2020
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20. Biomass Fuel Use and Cardiac Function in Nepali Women
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Jasleen Tiwana, Catherine Benziger, Laura Hooper, Karl Pope, Vijay Alurkar, Ramchandra Kafle, Tula R. Sijali, John R. Balmes, Joel D. Kaufman, and Michael N. Bates
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household air pollution ,echocardiography ,cardiovascular changes ,Diseases of the circulatory (Cardiovascular) system ,RC666-701 ,Public aspects of medicine ,RA1-1270 - Abstract
Background: Exposure to household air pollution (HAP) from cooking with biomass fuel affects billions of people. We hypothesized that HAP from woodsmoke, compared to other household fuels, was associated with adverse cardiovascular outcomes, of which there have been few studies. Methods: A cross-sectional study was completed in 299 females aged 40–70 years in Kaski District, Nepal, during 2017–18. All participants underwent a standard 12-lead ECG, ankle and brachial systolic blood pressure measurement, and 2D color and Doppler echocardiography. Current stove type was confirmed by inspection. Blood pressure, height, and weight were measured using a standardized protocol. Hypertension was defined as ≥140/90 mmHg or prior diagnosis. Hemoglobin A1c (HbA1c) was obtained, with diabetes mellitus defined as a prior diagnosis or HbA1C ≥ 6.5%. We used adjusted linear and logistic multivariable regressions to examine the relationship of stove type with cardiac structure and function. Results: The majority of women primarily used liquified petroleum gas (LPG) stoves (65%), while 12% used biogas, and 23% used wood-burning cook-stoves. Prevalence of major cardiovascular risk factors was 35% with hypertension, 19% with diabetes mellitus, and 15% current smokers. After adjustment, compared to LPG, wood stove use was associated with increased indexed left atrial volume (β = 3.15, 95% CI 1.22 to 5.09) and increased indexed left ventricular end diastolic volume (β = 7.97, 95% CI 3.11 to 12.83). There was no association between stove type and systemic hypertension, left ventricular mass, systolic dysfunction, diastolic dysfunction, pulmonary hypertension, abnormal ankle-brachial index, or clinically significant ECG abnormalities. Conclusion: Biomass fuel use was associated with increased indexed left atrial volume and increased indexed left ventricular diastolic volume in Nepali women, suggesting subclinical adverse cardiac remodeling from HAP in this cross-sectional study. We did not find evidence of an association with hypertension or typical cardiac sequelae of hypertension. Future studies to confirm these results are needed.
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- 2020
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21. Rice Intake, Arsenic Exposure, and Subclinical Cardiovascular Disease Among US Adults in MESA
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Marisa H. Sobel, Tiffany R. Sanchez, Miranda R. Jones, Joel D. Kaufman, Kevin A. Francesconi, Michael J. Blaha, Dhananjay Vaidya, Daichi Shimbo, Walter Gossler, Mary V. Gamble, Jeanine M. Genkinger, and Ana Navas‐Acien
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arsenic ,cardiovascular disease ,inflammation ,rice ,Diseases of the circulatory (Cardiovascular) system ,RC666-701 - Abstract
Background Arsenic‐related cardiovascular effects at exposure levels below the US Environmental Protection Agency's standard of 10 μg/L are unclear. For these populations, food, especially rice, is a major source of exposure. We investigated associations of rice intake, a marker of arsenic exposure, with subclinical cardiovascular disease (CVD) markers in a multiethnic population. Methods and Results Between 2000 and 2002, MESA (Multi‐Ethnic Study of Atherosclerosis) enrolled 6814 adults without clinical CVD. We included 5050 participants with baseline data on rice intake and markers of 3 CVD domains: inflammation (hsCRP [high‐sensitivity C‐reactive protein], interleukin‐6, and fibrinogen), vascular function (aortic distensibility, carotid distensibility, and brachial flow‐mediated dilation), and subclinical atherosclerosis at 3 vascular sites (carotid intima‐media thickness, coronary artery calcification, and ankle‐brachial index). We also evaluated endothelial‐related biomarkers previously associated with arsenic. Rice intake was assessed by food frequency questionnaire. Urinary arsenic was measured in 310 participants. A total of 13% of participants consumed ≥1 serving of rice/day. Compared with individuals consuming
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- 2020
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22. Calibration of low-cost particulate matter sensors: Model development for a multi-city epidemiological study
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Marina Zusman, Cooper S. Schumacher, Amanda J. Gassett, Elizabeth W. Spalt, Elena Austin, Timothy V. Larson, Graeme Carvlin, Edmund Seto, Joel D. Kaufman, and Lianne Sheppard
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Environmental sciences ,GE1-350 - Abstract
Low-cost air monitoring sensors are an appealing tool for assessing pollutants in environmental studies. Portable low-cost sensors hold promise to expand temporal and spatial coverage of air quality information. However, researchers have reported challenges in these sensors′ operational quality. We evaluated the performance characteristics of two widely used sensors, the Plantower PMS A003 and Shinyei PPD42NS, for measuring fine particulate matter compared to reference methods, and developed regional calibration models for the Los Angeles, Chicago, New York, Baltimore, Minneapolis-St. Paul, Winston-Salem and Seattle metropolitan areas. Duplicate Plantower PMS A003 sensors demonstrated a high level of precision (averaged Pearson′s r = 0.99), and compared with regulatory instruments, showed good accuracy (cross-validated R2 = 0.96, RMSE = 1.15 µg/m3 for daily averaged PM2.5 estimates in the Seattle region). Shinyei PPD42NS sensor results had lower precision (Pearson′s r = 0.84) and accuracy (cross-validated R2 = 0.40, RMSE = 4.49 µg/m3). Region-specific Plantower PMS A003 models, calibrated with regulatory instruments and adjusted for temperature and relative humidity, demonstrated acceptable performance metrics for daily average measurements in the other six regions (R2 = 0.74–0.95, RMSE = 2.46–0.84 µg/m3). Applying the Seattle model to the other regions resulted in decreased performance (R2 = 0.67–0.84, RMSE = 3.41–1.67 µg/m3), likely due to differences in meteorological conditions and particle sources. We describe an approach to metropolitan region-specific calibration models for low-cost sensors that can be used with caution for exposure measurement in epidemiological studies. Keywords: Low-cost monitors (LCM), Calibration, Air pollution, Fine particulate matter, Multicenter study design, Air quality system network (AQS)
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- 2020
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23. Air pollution, particulate matter composition and methylation-based biologic age
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Alexandra J. White, Jacob K. Kresovich, Joshua P. Keller, Zongli Xu, Joel D. Kaufman, Clarice R. Weinberg, Jack A. Taylor, and Dale P. Sandler
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Environmental sciences ,GE1-350 - Abstract
Background: Epigenetic age, as defined by DNA methylation, may be influenced by air pollution exposure. Objective: To evaluate the relationship between NO2, particulate matter (PM), PM components and accelerated epigenetic age. Methods: In a sample of non-Hispanic white women living in the contiguous U.S. (n = 2747), we estimated residential exposure to PM2.5, PM10 and NO2 using a model incorporating land-use regression and kriging. Predictive k-means was used to assign participants to clusters representing different PM2.5 component profiles. We measured DNA methylation (DNAm) in blood using the Illumina's Infinium HumanMethylation450 BeadChip and calculated DNAm age using the Hannum, Horvath and Levine epigenetic clocks. Age acceleration was defined based on residuals after regressing DNAm age on chronological age. We estimated associations between interquartile range (IQR) increases in pollutants and age acceleration using linear regression. For PM2.5, we stratified by cluster membership. We examined epigenome-wide associations using robust linear regression models corrected with false discovery rate q-values. Results: NO2 was inversely associated with age acceleration using the Hannum clock (β = −0.24, 95% CI: −0.47, −0.02). No associations were observed for PM10. For PM2.5, the association with age acceleration varied by PM2.5 component cluster. For example, with the Levine clock, an IQR increase in PM2.5 was associated with an over 6-year age acceleration in a cluster that has relatively high fractions of crustal elements relative to overall PM2.5 (β = 6.57, 95% CI: 2.68, 10.47), and an almost 2-year acceleration in a cluster characterized by relatively low sulfur fractions (β = 1.88, 95% CI: 0.51, 3.25). In a cluster distinguished by lower relative nitrate concentrations, PM2.5 was inversely associated with age acceleration (β = −1.33, 95% CI: −2.43, −0.23). Across the epigenome, NO2 was associated with methylation at 2 CpG sites. Conclusion: Air pollution was associated with epigenetic age, a marker of mortality and disease risk, among certain PM2.5 component profiles. Keywords: Breast cancer, Air pollution, Particulate matter, Clustering, Mixtures
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- 2019
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24. The cross-sectional and longitudinal association between air pollution and salivary cortisol: Evidence from the Multi-Ethnic Study of Atherosclerosis
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Anjum Hajat, Marnie F. Hazlehurst, Sherita Hill Golden, Sharon Stein Merkin, Teresa Seeman, Adam A. Szpiro, Joel D. Kaufman, and Ana Diez Roux
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Environmental sciences ,GE1-350 - Abstract
Background: Cortisol, a stress hormone released by the activation of the hypothalamic-pituitary-adrenal (HPA) axis, is critical to the body's adaptive response to physiological and psychological stress. Cortisol has also been implicated in the health effects of air pollution through the activation of the sympathetic nervous system. This study evaluates the cross-sectional and longitudinal association between several air pollutants and salivary cortisol. Methods: We used data from the Multi-Ethnic Study of Atherosclerosis (MESA), a cohort of 45–85 years old participants from six US cities. Salivary cortisol was evaluated at two time points between 2004 and 2006 and then again from 2010 to 2012. Cortisol samples were taken several times per day on two or three consecutive days. Particulate matter
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- 2019
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25. Exposure to ambient air pollution and calcification of the mitral annulus and aortic valve: the multi-ethnic study of atherosclerosis (MESA)
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Martin Tibuakuu, Miranda R. Jones, Ana Navas-Acien, Di Zhao, Eliseo Guallar, Amanda J. Gassett, Lianne Sheppard, Matthew J. Budoff, Joel D. Kaufman, and Erin D. Michos
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Air pollution ,Valvular calcification ,Aortic valve calcification ,Mitral annulus calcification ,Epidemiology ,Prevention ,Industrial medicine. Industrial hygiene ,RC963-969 ,Public aspects of medicine ,RA1-1270 - Abstract
Abstract Background Long-term exposure to high ambient air pollution has been associated with coronary artery calcium (CAC), a marker of cardiovascular disease (CVD). Calcifications of left-sided heart valves are also markers of CVD risk. We investigated whether air pollution was associated with valvular calcification and its progression. Methods We studied 6253 MESA participants aged 45–84 years who underwent two cardiac CT scans 2.5 years apart to quantify aortic valve calcium (AVC) and mitral annular calcium (MAC). CAC was included for the same timeframe for comparison with AVC/MAC. Ambient particulate matter
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- 2017
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26. Explaining racial/ethnic differences in all-cause mortality in the Multi-Ethnic Study of Atherosclerosis (MESA): Substantive complexity and hazardous working conditions as mediating factors
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Kaori Fujishiro, Anjum Hajat, Paul A. Landsbergis, John D. Meyer, Pamela J. Schreiner, and Joel D. Kaufman
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Public aspects of medicine ,RA1-1270 ,Social sciences (General) ,H1-99 - Abstract
Research on racial/ethnic health disparities and socioeconomic position has not fully considered occupation. However, because occupations are racially patterned, certain occupational characteristics may explain racial/ethnic difference in health. This study examines the role of occupational characteristics in racial/ethnic disparities in all-cause mortality. Data are from a U.S. community-based cohort study (n=6342, median follow-up: 12.2 years), in which 893 deaths (14.1%) occurred. We estimated mortality hazard ratios (HRs) for African Americans, Hispanics, and Chinese Americans compared with whites. We also estimated the proportion of the HR mediated by each of two occupational characteristics, substantive complexity of work (e.g., problem solving, inductive/deductive reasoning on the job) and hazardous conditions (e.g., noise, extreme temperature, chemicals), derived from the Occupational Information Network database (O*NET). Analyses were adjusted for age, sex, nativity, working status at baseline, and study sites. African Americans had a higher rate of all-cause death (HR 1.41; 95% confidence interval [CI]: 1.19–1.66) than whites. Chinese-American ethnicity was protective (HR 0.59, CI: 0.40–0.85); Hispanic ethnicity was not significantly different from whites (HR 0.88; CI: 0.67–1.17). Substantive complexity of work mediated 30% of the higher rate of death for African Americans compared with whites. For other groups, mediation was not significant. Hazardous conditions did not significantly mediate mortality in any racial/ethnic group. Lower levels of substantive complexity of work mediate a substantial part of the health disadvantage in African Americans. This job characteristic may be an important factor in explaining racial health disparities.
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- 2017
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27. Deployment, Calibration, and Cross-Validation of Low-Cost Electrochemical Sensors for Carbon Monoxide, Nitrogen Oxides, and Ozone for an Epidemiological Study
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Christopher Zuidema, Cooper S. Schumacher, Elena Austin, Graeme Carvlin, Timothy V. Larson, Elizabeth W. Spalt, Marina Zusman, Amanda J. Gassett, Edmund Seto, Joel D. Kaufman, and Lianne Sheppard
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low-cost sensors ,sensor network ,hazardous gases ,air pollution ,exposure assessment ,environmental epidemiology ,Chemical technology ,TP1-1185 - Abstract
We designed and built a network of monitors for ambient air pollution equipped with low-cost gas sensors to be used to supplement regulatory agency monitoring for exposure assessment within a large epidemiological study. This paper describes the development of a series of hourly and daily field calibration models for Alphasense sensors for carbon monoxide (CO; CO-B4), nitric oxide (NO; NO-B4), nitrogen dioxide (NO2; NO2-B43F), and oxidizing gases (OX-B431)—which refers to ozone (O3) and NO2. The monitor network was deployed in the Puget Sound region of Washington, USA, from May 2017 to March 2019. Monitors were rotated throughout the region, including at two Puget Sound Clean Air Agency monitoring sites for calibration purposes, and over 100 residences, including the homes of epidemiological study participants, with the goal of improving long-term pollutant exposure predictions at participant locations. Calibration models improved when accounting for individual sensor performance, ambient temperature and humidity, and concentrations of co-pollutants as measured by other low-cost sensors in the monitors. Predictions from the final daily models for CO and NO performed the best considering agreement with regulatory monitors in cross-validated root-mean-square error (RMSE) and R2 measures (CO: RMSE = 18 ppb, R2 = 0.97; NO: RMSE = 2 ppb, R2 = 0.97). Performance measures for NO2 and O3 were somewhat lower (NO2: RMSE = 3 ppb, R2 = 0.79; O3: RMSE = 4 ppb, R2 = 0.81). These high levels of calibration performance add confidence that low-cost sensor measurements collected at the homes of epidemiological study participants can be integrated into spatiotemporal models of pollutant concentrations, improving exposure assessment for epidemiological inference.
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- 2021
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28. Blood monocyte transcriptome and epigenome analyses reveal loci associated with human atherosclerosis
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Yongmei Liu, Lindsay M. Reynolds, Jingzhong Ding, Li Hou, Kurt Lohman, Tracey Young, Wei Cui, Zhiqing Huang, Carole Grenier, Ma Wan, Hendrik G. Stunnenberg, David Siscovick, Lifang Hou, Bruce M. Psaty, Stephen S. Rich, Jerome I. Rotter, Joel D. Kaufman, Gregory L. Burke, Susan Murphy, David R. Jacobs, Wendy Post, Ina Hoeschele, Douglas A. Bell, David Herrington, John S. Parks, Russell P. Tracy, Charles E. McCall, and James H. Stein
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Science - Abstract
The molecular mechanisms mediating the impact of environmental factors in atherosclerosis are unclear. Here, the authors examine CD14+ blood monocyte’s transcriptome and epigenome signatures to find differential methylation and expression of ARID5B to be associated with human atherosclerosis.
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- 2017
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29. Genome-wide association study of subclinical interstitial lung disease in MESA
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Ani Manichaikul, Xin-Qun Wang, Li Sun, Josée Dupuis, Alain C. Borczuk, Jennifer N. Nguyen, Ganesh Raghu, Eric A. Hoffman, Suna Onengut-Gumuscu, Emily A. Farber, Joel D. Kaufman, Dan Rabinowitz, Karen D. Hinckley Stukovsky, Steven M. Kawut, Gary M. Hunninghake, George R. Washko, George T. O’Connor, Stephen S. Rich, R. Graham Barr, and David J. Lederer
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Interstitial lung disease ,Genetics ,Genome-wide association study ,Epidemiology ,Diseases of the respiratory system ,RC705-779 - Abstract
Abstract Background We conducted a genome-wide association study (GWAS) of subclinical interstitial lung disease (ILD), defined as high attenuation areas (HAA) on CT, in the population-based Multi-Ethnic Study of Atherosclerosis Study. Methods We measured the percentage of high attenuation areas (HAA) in the lung fields on cardiac CT scan defined as voxels with CT attenuation values between -600 and -250 HU. Genetic analyses were performed in MESA combined across race/ethnic groups: non-Hispanic White (n = 2,434), African American (n = 2,470), Hispanic (n = 2,065) and Chinese (n = 702), as well as stratified by race/ethnicity. Results Among 7,671 participants, regions at genome-wide significance were identified for basilar peel-core ratio of HAA in FLJ35282 downstream of ANRIL (rs7852363, P = 2.1x10−9) and within introns of SNAI3-AS1 (rs140142658, P = 9.6x10−9) and D21S2088E (rs3079677, P = 2.3x10−8). Within race/ethnic groups, 18 additional loci were identified at genome-wide significance, including genes related to development (FOXP4), cell adhesion (ALCAM) and glycosylation (GNPDA2, GYPC, GFPT1 and FUT10). Among these loci, SNP rs6844387 near GNPDA2 demonstrated nominal evidence of replication in analysis of n = 1,959 participants from the Framingham Heart Study (P = 0.029). FOXP4 region SNP rs2894439 demonstrated evidence of validation in analysis of n = 228 White ILD cases from the Columbia ILD Study compared to race/ethnicity-matched controls from MESA (one-sided P = 0.007). In lung tissue from 15 adults with idiopathic pulmonary fibrosis compared to 15 adults without lung disease. ANRIL (P = 0.001), ALCAM (P = 0.03) and FOXP4 (P = 0.046) were differentially expressed. Conclusions Our results suggest novel roles for protein glycosylation and cell cycle disinhibition by long non-coding RNA in the pathogenesis of ILD.
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- 2017
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30. Carotid Artery Echolucency, Texture Features, and Incident Cardiovascular Disease Events: The MESA Study
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Carol C. Mitchell, Claudia E. Korcarz, Adam D. Gepner, Rebecca Nye, Rebekah L. Young, Mika Matsuzaki, Wendy S. Post, Joel D. Kaufman, Robyn L. McClelland, and James H. Stein
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cardiovascular events ,carotid artery ,texture features ,ultrasound ,Diseases of the circulatory (Cardiovascular) system ,RC666-701 - Abstract
Background We hypothesized that measures of common carotid artery echolucency and grayscale texture features were associated with cardiovascular disease (CVD) risk factors and could predict CVD events. Methods and Results Using a case‐cohort design, we measured common carotid artery ultrasound images from 1788 participants in Exam 1 of the MESA study (Multi‐Ethnic Study of Atherosclerosis) to derive 4 grayscale features: grayscale median, entropy, gray level difference statistic‐contrast, and spatial gray level dependence matrices‐angular second moment. CVD risk factor associations were determined by linear regression. Cox proportional hazard models with inverse selection probability weighting and adjustments for age, sex, race/ethnicity, CVD risk factors, and C‐reactive protein were used to determine if standardized values for grayscale median, entropy, gray level difference statistic‐contrast, and spatial gray level dependence matrices‐angular second moment could predict incident coronary heart disease, stroke, and total CVD events over a median 13 years follow‐up. Participants were mean (SD) 63.1 (10.3) years of age, 52.6% female, 32.1% white, 27.8% black, 23.3% Hispanic, and 16.8% Chinese. There were 283 coronary heart disease, 120 stroke, and 416 CVD events. Several associations of grayscale features with CVD risk factors were identified. In fully adjusted models, higher gray level difference statistic‐contrast was associated with a lower risk of incident coronary heart disease (hazard ratio 0.82, 95% CI 0.71–0.94, padj=0.005) and CVD events (hazard ratio 0.87, 95% CI 0.77–0.98, padj=0.018); higher spatial gray level dependence matrices‐angular second moment was associated with a higher risk of CVD events (hazard ratio 1.09, 95% CI 1.00–1.19, padj=0.044). Conclusions Gray level difference statistic‐contrast and spatial gray level dependence matrices‐angular second moment predicted CVD events independent of risk factors, indicating their potential use as biomarkers to assess future CVD risk.
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- 2019
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31. Secondhand Smoke Exposure and Subclinical Cardiovascular Disease: The Multi‐Ethnic Study of Atherosclerosis
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Miranda R. Jones, Hoda S. Magid, Mahmoud Al‐Rifai, John W. McEvoy, Joel D. Kaufman, Karen D. Hinckley Stukovsky, Moyses Szklo, Joseph Polak, Gregory L. Burke, Wendy S. Post, Michael J. Blaha, and Ana Navas‐Acien
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ankle‐brachial index ,atherosclerosis ,carotid intima‐media thickness ,coronary artery calcium ,inflammation ,peripheral artery disease ,Diseases of the circulatory (Cardiovascular) system ,RC666-701 - Abstract
BackgroundFew studies have evaluated the association between secondhand smoke (SHS) and subclinical cardiovascular disease among ethnically diverse populations. This study assesses the impact of SHS on inflammation and atherosclerosis (carotid intima‐media thickness, coronary artery calcification, and peripheral arterial disease). Methods and ResultsWe examined 5032 nonsmoking adults aged 45 to 84 years without prior cardiovascular disease participating in the Multi‐Ethnic Study of Atherosclerosis (MESA) from 2000 to 2002. SHS exposure was determined by self‐report, and urinary cotinine was measured in a representative subset (n=2893). The multi‐adjusted geometric mean ratios (95% CIs) for high‐sensitivity C‐reactive protein and interleukin‐6 comparing 407 participants with SHS ≥12 h/wk versus 3035 unexposed participants were 1.13 (1.02–1.26) and 1.04 (0.98–1.11), respectively. The multi‐adjusted geometric mean ratio for carotid intima‐media thickness was 1.02 (0.97–1.07). Fibrinogen and coronary artery calcification were not associated with SHS. The prevalence of peripheral arterial disease (ankle‐brachial index ≤0.9 or ≥1.4) was associated with detectable urinary cotinine (odds ratio, 2.10; 95% CI, 1.09–4.04) but not with self‐reported SHS. Urinary cotinine was not associated with inflammation or carotid intima‐media thickness. ConclusionsDespite limited exposure assessment, this study supports the association of SHS exposure with inflammation and peripheral arterial disease.
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- 2016
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32. Concentration of Smaller High‐Density Lipoprotein Particle (HDL‐P) Is Inversely Correlated With Carotid Intima Media Thickening After Confounder Adjustment: The Multi Ethnic Study of Atherosclerosis (MESA)
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Daniel Seung Kim, Yatong K. Li, Griffith A. Bell, Amber A. Burt, Tomas Vaisar, Patrick M. Hutchins, Clement E. Furlong, James D. Otvos, Joseph F. Polak, Martinson Kweku Arnan, Joel D. Kaufman, Robyn L. McClelland, W. T. Longstreth, and Gail P. Jarvik
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antioxidant ,carotid intima media thickening ,cerebrovascular disease ,high‐density lipoprotein cholesterol ,high‐density lipoprotein particle concentration ,paraoxonase 1 ,Diseases of the circulatory (Cardiovascular) system ,RC666-701 - Abstract
BackgroundRecent studies have failed to establish a causal relationship between high‐density lipoprotein cholesterol levels (HDL‐C) and cardiovascular disease (CVD), shifting focus to other HDL measures. We previously reported that smaller/denser HDL levels are protective against cerebrovascular disease. This study sought to determine which of small+medium HDL particle concentration (HDL‐P) or large HDL‐P was more strongly associated with carotid intima‐media thickening (cIMT) in an ethnically diverse cohort. Methods and ResultsIn cross‐sectional analyses of participants from the Multi Ethnic Study of Atherosclerosis (MESA), we evaluated the associations of nuclear magnetic resonance spectroscopy–measured small+medium versus large HDL‐P with cIMT measured in the common and internal carotid arteries, through linear regression. After adjustment for CVD confounders, low‐density lipoprotein cholesterol (LDL‐C), HDL‐C, and small+medium HDL‐P remained significantly and inversely associated with common (coefficient=−1.46 μm; P=0.00037; n=6512) and internal cIMT (coefficient=−3.82 μm; P=0.0051; n=6418) after Bonferroni correction for 4 independent tests (threshold for significance=0.0125; α=0.05/4). Large HDL‐P was significantly and inversely associated with both cIMT outcomes before HDL‐C adjustment; however, after adjustment for HDL‐C, the association of large HDL‐P with both common (coefficient=1.55 μm; P=0.30; n=6512) and internal cIMT (coefficient=4.84 μm; P=0.33; n=6418) was attenuated. In a separate sample of 126 men, small/medium HDL‐P was more strongly correlated with paraoxonase 1 activity (rp=0.32; P=0.00023) as compared to both total HDL‐P (rp=0.27; P=0.0024) and large HDL‐P (rp=0.02; P=0.41) measures. ConclusionsSmall+medium HDL‐P is significantly and inversely correlated with cIMT measurements. Correlation of small+medium HDL‐P with cardioprotective paraoxonase 1 activity may reflect a functional aspect of HDL responsible for this finding.
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- 2016
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33. Associations of prenatal exposure to NO2 and near roadway residence with placental gene expression
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Michael R. Hussey, Daniel A. Enquobahrie, Christine T. Loftus, James W. MacDonald, Theo K. Bammler, Alison G. Paquette, Carmen J. Marsit, Adam A. Szpiro, Joel D. Kaufman, Kaja Z. LeWinn, Nicole R. Bush, Frances Tylavsky, Qi Zhao, Catherine J. Karr, and Sheela Sathyanarayana
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Reproductive Medicine ,Obstetrics and Gynecology ,Developmental Biology - Published
- 2023
34. Associations Between Ambient Air Pollution and Cognitive Abilities from Midlife to Early Old Age: Modification by APOE Genotype
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Carol E. Franz, Daniel E. Gustavson, Jeremy A. Elman, Christine Fennema-Notestine, Donald J. Hagler Jr., Aaron Baraff, Xin M. Tu, Tsung-Chin Wu, Jaden De Anda, Asad Beck, Joel D. Kaufman, Nathan Whitsel, Caleb E. Finch, Jiu-Chiuan Chen, Michael J. Lyons, and William S. Kremen
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Psychiatry and Mental health ,Clinical Psychology ,General Neuroscience ,General Medicine ,Geriatrics and Gerontology - Abstract
Background: Fine particulate matter (PM2.5) and nitrogen dioxide (NO2) measures of ambient air pollution are associated with accelerated age-related cognitive impairment, and Alzheimer’s disease and related dementias (ADRD). Objective: We examined associations between air pollution, four cognitive factors, and the moderating role of apolipoprotein E (APOE) genotype in the understudied period of midlife. Methods: Participants were ∼1,100 men in the Vietnam Era Twin Study of Aging. Baseline cognitive assessments were from 2003 to 2007. Measures included past (1993–1999) and recent (3 years prior to baseline assessment) PM2.5 and NO2 exposure, in-person assessment of episodic memory, executive function, verbal fluency, and processing speed, and APOE genotype. Average baseline age was 56 years with a 12-year follow-up. Analyses adjusted for health and lifestyle covariates. Results: Performance in all cognitive domains declined from age 56 to 68. Higher PM2.5 exposures were associated with worse general verbal fluency. We found significant exposure-by-APOE genotype interactions for specific cognitive domains: PM2.5 with executive function and NO2 with episodic memory. Higher PM2.5 exposure was related to worse executive function in APOE ɛ4 carriers, but not in non-carriers. There were no associations with processing speed. Conclusion: These results indicate negative effects of ambient air pollution exposure on fluency alongside intriguing differential modifications of cognitive performance by APOE genotype. APOE ɛ4 carriers appeared more sensitive to environmental differences. The process by which air pollution and its interaction with genetic risk for ADRD affects risk for later life cognitive decline or progression to dementia may begin in midlife.
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- 2023
35. Role of Air Pollution in the Development of Asthma Among Children with a History of Bronchiolitis in Infancy
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Logan C Dearborn, Marnie F Hazlehurst, Christine T Loftus, Adam A Szpiro, Kecia N Carroll, Paul E Moore, Margaret A Adgent, Emily S Barrett, Ruby HN Nguyen, Sheela Sathyanarayana, Kaja Z LeWinn, Nicole R Bush, Joel D Kaufman, and Catherine J Karr
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Epidemiology - Published
- 2023
36. Multi-ancestry transcriptome-wide association analyses yield insights into tobacco use biology and drug repurposing
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Fang Chen, Xingyan Wang, Seon-Kyeong Jang, Bryan C. Quach, J. Dylan Weissenkampen, Chachrit Khunsriraksakul, Lina Yang, Renan Sauteraud, Christine M. Albert, Nicholette D. D. Allred, Donna K. Arnett, Allison E. Ashley-Koch, Kathleen C. Barnes, R. Graham Barr, Diane M. Becker, Lawrence F. Bielak, Joshua C. Bis, John Blangero, Meher Preethi Boorgula, Daniel I. Chasman, Sameer Chavan, Yii-Der I. Chen, Lee-Ming Chuang, Adolfo Correa, Joanne E. Curran, Sean P. David, Lisa de las Fuentes, Ranjan Deka, Ravindranath Duggirala, Jessica D. Faul, Melanie E. Garrett, Sina A. Gharib, Xiuqing Guo, Michael E. Hall, Nicola L. Hawley, Jiang He, Brian D. Hobbs, John E. Hokanson, Chao A. Hsiung, Shih-Jen Hwang, Thomas M. Hyde, Marguerite R. Irvin, Andrew E. Jaffe, Eric O. Johnson, Robert Kaplan, Sharon L. R. Kardia, Joel D. Kaufman, Tanika N. Kelly, Joel E. Kleinman, Charles Kooperberg, I-Te Lee, Daniel Levy, Sharon M. Lutz, Ani W. Manichaikul, Lisa W. Martin, Olivia Marx, Stephen T. McGarvey, Ryan L. Minster, Matthew Moll, Karine A. Moussa, Take Naseri, Kari E. North, Elizabeth C. Oelsner, Juan M. Peralta, Patricia A. Peyser, Bruce M. Psaty, Nicholas Rafaels, Laura M. Raffield, Muagututi’a Sefuiva Reupena, Stephen S. Rich, Jerome I. Rotter, David A. Schwartz, Aladdin H. Shadyab, Wayne H-H. Sheu, Mario Sims, Jennifer A. Smith, Xiao Sun, Kent D. Taylor, Marilyn J. Telen, Harold Watson, Daniel E. Weeks, David R. Weir, Lisa R. Yanek, Kendra A. Young, Kristin L. Young, Wei Zhao, Dana B. Hancock, Bibo Jiang, Scott Vrieze, and Dajiang J. Liu
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Tobacco Smoke and Health ,Human Genome ,Drug Repositioning ,Single Nucleotide ,Biological Sciences ,Medical and Health Sciences ,Brain Disorders ,Tobacco Use ,Substance Misuse ,Good Health and Well Being ,Tobacco ,Genetics ,Humans ,Genetic Predisposition to Disease ,Polymorphism ,Transcriptome ,Drug Abuse (NIDA only) ,Biology ,Genome-Wide Association Study ,Developmental Biology - Abstract
Most transcriptome-wide association studies (TWASs) so far focus on European ancestry and lack diversity. To overcome this limitation, we aggregated genome-wide association study (GWAS) summary statistics, whole-genome sequences and expression quantitative trait locus (eQTL) data from diverse ancestries. We developed a new approach, TESLA (multi-ancestry integrative study using an optimal linear combination of association statistics), to integrate an eQTL dataset with a multi-ancestry GWAS. By exploiting shared phenotypic effects between ancestries and accommodating potential effect heterogeneities, TESLA improves power over other TWAS methods. When applied to tobacco use phenotypes, TESLA identified 273 new genes, up to 55% more compared with alternative TWAS methods. These hits and subsequent fine mapping using TESLA point to target genes with biological relevance. In silico drug-repurposing analyses highlight several drugs with known efficacy, including dextromethorphan and galantamine, and new drugs such as muscle relaxants that may be repurposed for treating nicotine addiction.
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- 2023
37. Reproducibility of PTC1 and PTC2, indices of arterial compliance, from the radial artery waveform: The Multi-Ethnic Study of Atherosclerosis
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Lyndia C Brumback, Leah IB Andrews, David R Jacobs, Daniel Duprez, Elizabeth K Hom Thepaksorn, Joel D Kaufman, Julie Denenberg, and Matthew Allison
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Cardiology and Cardiovascular Medicine - Published
- 2023
38. Air pollution and dementia in older adults in the Ginkgo Evaluation of Memory Study
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Erin O, Semmens, Cindy S, Leary, Annette L, Fitzpatrick, Sindana D, Ilango, Christina, Park, Claire E, Adam, Steven T, DeKosky, Oscar, Lopez, Anjum, Hajat, and Joel D, Kaufman
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Psychiatry and Mental health ,Cellular and Molecular Neuroscience ,Developmental Neuroscience ,Epidemiology ,Health Policy ,Neurology (clinical) ,Geriatrics and Gerontology - Abstract
Growing evidence implicates air pollution as a risk factor for dementia, but prior work is limited by challenges in diagnostic accuracy and assessing exposures in the decades prior to disease development. We evaluated the impact of long-term fine particulate matter (PMA panel of neurologists adjudicated dementia cases based on extensive neuropsychological testing and magnetic resonance imaging. We applied validated fine-scale air pollutant models to reconstructed residential histories to assess exposures.An interquartile range increase in 20-year PMOur findings suggest that air pollutant exposures over decades contribute to dementia and that effects of current exposures may be experienced years into the future.
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- 2022
39. Ambient Air Pollution Exposure and Sleep Quality in COPD
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Mudiaga O. Sowho, Abigail L. Koch, Nirupama Putcha, Han Woo, Amanda Gassett, Laura M. Paulin, Kirsten Koehler, R. Graham Barr, Alejandro P. Comellas, Christopher B. Cooper, Igor Barjaktarevic, Michelle R. Zeidler, Martha E. Billings, Russell P. Bowler, MeiLan K. Han, Victor Kim, Robert Paine III, Trisha M. Parekh, Jerry A. Krishnan, Stephen P. Peters, Prescott G. Woodruff, Aaron M. Baugh, Joel D. Kaufman, David Couper, and Nadia N. Hansel
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Pulmonary and Respiratory Medicine ,Origianl Research - Abstract
Rationale: Ambient air pollution exposure is associated with respiratory morbidity among individuals with chronic obstructive pulmonary disease (COPD), particularly among those with concomitant obesity. Although people with COPD report high incidence of poor sleep quality, no studies have evaluated the association between air pollution exposure, obesity, and sleep disturbances in COPD. Methods: We analyzed data collected from current and former smokers with COPD enrolled in the Subpopulations and Intermediate Outcome Measures in COPD -Air Pollution ancillary study (SPIROMICS AIR). Socio-demographics and anthropometric measurements were collected, and 1-year mean historical ambient particulate matter (PM(2.5)) and ozone concentrations at participants’ residences were estimated by cohort-specific spatiotemporal modeling. Sleep quality was assessed with the Pittsburgh Sleep Quality Index (PSQI), and regression models were constructed to determine the association of 1-year PM(2.5 )(1Yr-PM(2.5)) and 1-year ozone (1Yr-ozone) with the PSQI score, and whether obesity modified the association. Results: In 1308 participants (age: 65.8±7.8 years, 42% women), results of regression analyses suggest that each 10µg/m(3) increase in 1Yr-PM(2.5 )was associated with a 2.1-point increase in PSQI (P=0.03). Obesity modified the association between 1Yr-PM(2.5) and PSQI (P=0.03). In obese and overweight participants, a 10µg/m(3) increase in 1Yr-PM(2.5) was associated with a higher PSQI (4.0 points, P
- Published
- 2023
40. Air Pollution and Breast Cancer: An Examination of Modification By Underlying Familial Breast Cancer Risk
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Nicole M. Niehoff, Mary Beth Terry, Deborah B. Bookwalter, Joel D. Kaufman, Katie M. O'Brien, Dale P. Sandler, and Alexandra J. White
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Adult ,Epidemiology ,Nitrogen Dioxide ,Breast Neoplasms ,Environmental Exposure ,Middle Aged ,United States ,Article ,Oncology ,Risk Factors ,Air Pollution ,Humans ,Female ,Prospective Studies - Abstract
Background: An increased familial risk of breast cancer may be due to both shared genetics and environment. Women with a breast cancer family history may have a higher prevalence of breast cancer–related gene variants and thus increased susceptibility to environmental exposures. We evaluated whether air pollutant and breast cancer associations varied by familial risk. Methods: Sister Study participants living in the contiguous United States at enrollment (2003–2009; N = 48,453), all of whom had at least one first-degree relative with breast cancer, were followed for breast cancer. Annual NO2 and PM2.5 concentrations were estimated at the enrollment addresses. We predicted 1-year familial breast cancer risk using the Breast and Ovarian Analysis of Disease Incidence and Carrier Estimation Algorithm (BOADICEA). Using Cox regression, we estimated HRs and 95% confidence intervals (CI) for associations between each pollutant dichotomized at the median and breast cancer with interaction terms to examine modification by BOADICEA score. Results: NO2 was associated with a higher breast cancer risk among those with BOADICEA score >90th percentile (HR, 1.28; 95% CI, 1.05–1.56) but not among those with BOADICEA score ≤90th percentile (HR, 0.98; 95% CI, 0.90–1.06; Pinteraction = 0.01). In contrast to NO2, associations between PM2.5 and breast cancer did not vary between individuals with BOADICEA score >90th percentile and ≤90th percentile (Pinteraction = 0.26). Conclusions: Our results provide additional evidence that air pollution may be implicated in breast cancer, particularly among women with a higher familial risk. Impact: Women at higher underlying breast cancer risk may benefit more from interventions to reduce exposure to NO2.
- Published
- 2021
41. Associations Between Air Pollution Exposure and Empirically Derived Profiles of Cognitive Performance in Older Women
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Mark A. Espeland, Keith F. Widaman, Gregory A. Wellenius, Stephen R. Rapp, Helena C. Chui, Susan M. Resnick, Andrew J. Petkus, Jiu-Chiuan Chen, Diana Younan, Joshua Millstein, Joel D. Kaufman, Daniel P. Beavers, Xinhui Wang, Tara L. Gruenewald, JoAnn E. Manson, Eric A. Whitsel, Margaret Gatz, and Zammit, Andrea
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Aging ,nitrogen dioxide ,Clinical Sciences ,Nitrogen Dioxide ,Neuropsychological Tests ,Basic Behavioral and Social Science ,Article ,Structural equation modeling ,Odds ,Cognitive aging ,Cognition ,Clinical Research ,Air Pollution ,Behavioral and Social Science ,latent class analysis ,Humans ,Medicine ,Effects of sleep deprivation on cognitive performance ,Neuropsychological assessment ,Episodic memory ,Aged ,particulate matter ,Air Pollutants ,Neurology & Neurosurgery ,medicine.diagnostic_test ,business.industry ,General Neuroscience ,Neurosciences ,Brain ,Environmental Exposure ,General Medicine ,Latent class model ,Confidence interval ,Psychiatry and Mental health ,Clinical Psychology ,Cognitive Sciences ,Female ,Particulate Matter ,women ,Geriatrics and Gerontology ,business ,Demography - Abstract
Background: Elucidating associations between exposures to ambient air pollutants and profiles of cognitive performance may provide insight into neurotoxic effects on the aging brain. Objective: We examined associations between empirically derived profiles of cognitive performance and residential concentrations of particulate matter of aerodynamic diameter
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- 2021
42. Long-Term Exposures to Urban Noise and Blood Pressure Levels and Control Among Older Adults
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Jennifer D'Souza, Jennifer Weuve, Joel D. Kaufman, Robert D. Brook, Sara D. Adar, and Denis A. Evans
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Aged, 80 and over ,Male ,medicine.medical_specialty ,Urban Population ,business.industry ,Blood Pressure ,Environmental Exposure ,Middle Aged ,Audiology ,Urban noise ,United States ,Article ,Term (time) ,Noise ,Blood pressure ,Hypertension ,Internal Medicine ,Humans ,Medicine ,Female ,business ,Aged - Abstract
Urban noise is a common environmental exposure that may increase the burden of hypertension in communities, yet it is largely unstudied in the United States, and it has not been studied in relation to blood pressure (BP) control. We investigated associations of urban noise with BP levels and control in the United States. We used repeated BP and medication data from Chicago-based participants of the Chicago Health and Aging Project (≥65 years) and MESA (Multi-Ethnic Study of Atherosclerosis; ≥45 years). Using a spatial prediction model with project-specific measurements, we estimated noise at participant homes. We imputed BP levels for those on medication and used mixed-effects models to evaluate associations with noise. Logistic regression was used for uncontrolled and apparent treatment-resistant hypertension. Models were run separately by cohort and altogether, all with adjustment for age, sex, sociodemographic factors, and other plausible sources of confounding. We evaluated 16 462 BP measurements from 6764 participants (6073 Chicago Health and Aging Project and 691 MESA) over an average of 4 years. For both cohorts, we found that greater levels of noise were associated with higher BP levels and greater risk of apparent treatment-resistant hypertension. In our pooled models, 10-dBA higher residential noise levels corresponded to 1.2 (95% CI, 0.1–2.2) and 1.1 mm Hg greater (95% CI, 0.6–1.7) systolic and diastolic BPs as well as a 20% increased odds of apparent treatment-resistant hypertension (odds ratio per 10 dBA: 1.2 [95% CI, 1.0–1.4], P =0.04). Urban noise may increase BP levels and complicate hypertension treatment in the United States.
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- 2021
43. Linking air pollution exposure to blood-based metabolic features in a community-based aging cohort
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Vrinda Kalia, Erin R. Kulick, Badri Vardarajan, Yian Gu, Jennifer J. Manly, Mitchell S.V. Elkind, Joel D. Kaufman, Dean P. Jones, Andrea A. Baccarelli, Richard P. Mayeux, Marianthi-Anna Kioumourtzoglou, and Gary W. Miller
- Abstract
Long-term exposure to air pollution has been associated with changes in levels of several metabolites measured in the peripheral blood. However, most work has been conducted in ethnically homogenous populations. We studied the relationship between the plasma metabolome and long-term exposure to three air pollutants: particulate matter (PM) less than 2.5 µm in aero diameter (PM2.5), PM less than 10 µm in aero diameter (PM10) and nitrogen dioxide (NO2) among 107 participants of the Washington Heights and Inwood Community Aging Project (WHICAP) in New York City. Plasma metabolomic profiles were generated using untargeted liquid chromatography coupled with high-resolution mass spectrometry. We estimated the association between each metabolic feature and predicted annual mean exposure to the air pollutants using three approaches: 1. A metabolome wide association study (MWAS) framework; 2. Feature selection using elastic net regression; and 3. A multivariate approach using partial least squares discriminant analysis. Additionally, we identified the pathways enriched by metabolic features associated with exposure through pathway analysis. The samples were collected from 1995 – 2015 and included non-Hispanic white, Caribbean Hispanic, and non-Hispanic Black older adults. Through the MWAS, we found 79 features associated with exposure to PM2.5(false discovery rate at 5%) but none associated with PM10or NO2. Pathway analysis revealed that PM2.5exposure was associated with altered amino acid metabolism, energy production, and oxidative stress response. Six features were found to be associated with PM2.5exposure through all three approaches, annotated as: cysteinylglycine disulfide, a diglyceride, and a dicarboxylic acid. Additionally, we found that the relationship between several features and PM2.5exposure was modified by diet and metabolic diseases. These signals, identified in a neighborhood-representative older population, could help understand the mechanisms through which PM2.5exposure can lead to altered metabolic outcomes in an older population.HIGHLIGHTSLong-term exposure to PM2.5is associated with altered plasma metabolic features in an aging populationThese associations are modified by a dementia diagnosis, history of diabetes, APOE-ε4 allele, and dietPathways related to energy production, amino acid metabolism, and redox homeostasis are associated with exposure to PM2.5GRAPHICAL ABSTRACT
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- 2022
44. Ambient Air Pollution and Stroke: An Updated Review
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Erin R. Kulick, Joel D. Kaufman, and Coralynn Sack
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Advanced and Specialized Nursing ,Neurology (clinical) ,Cardiology and Cardiovascular Medicine - Abstract
Despite recent advances in treatment and prevention, stroke remains a leading cause of morbidity and mortality. There is a critical need to identify novel modifiable risk factors for disease, including environmental agents. A body of evidence has accumulated suggesting that elevated levels of ambient air pollutants may not only trigger cerebrovascular events in susceptible people (short-term exposures) but also increase the risk of future events (long-term average exposures). This review assesses the updated evidence for both short and long-term exposure to ambient air pollution as a risk factor for stroke incidence and outcomes. It discusses the potential pathophysiologic mechanisms and makes recommendations to mitigate exposure on a personal and community level. The evidence indicates that reduction in air pollutant concentrations represent a significant population-level opportunity to reduce risk of cerebrovascular disease.
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- 2022
45. Genetic subtypes of prediabetes, healthy lifestyle, and risk of type 2 diabetes: Prospective cohort study
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Yang Li, Guo-Chong Chen, Jee-Young Moon, Rhonda Arthur, Daniela Sotres-Alvarez, Martha L. Daviglus, Amber Pirzada, Josiemer Mattei, Krista M. Perreira, Jerome I. Rotter, Kent D. Taylor, Yii-Der Ida Chen, Sylvia Wassertheil-Smoller, Tao Wang, Thomas E. Rohan, Joel D. Kaufman, Robert Kaplan, and Qibin Qi
- Abstract
ObjectivesTo cluster participants with prediabetes with five type 2 diabetes (T2D)-related partitioned polygenetic risk scores (pPRSs) and examine the risk of incident diabetes and the benefit of adherence to healthy lifestyle across clusters.DesignProspective cohort studySettingHispanic Community Health Study/Study of Latinos (HCHS/SOL), US; UK Biobank (UKBB), UK.Participants7,227 US Hispanic/Latinos without diabetes from HCHS/SOL, including 3,677 participants with prediabetes. 400,149 non-Hispanic whites without diabetes from UKBB, including 16,284 participants with prediabetes.Main outcome measuresPrediabetes was defined by fasting plasma glucose (fasting glucose) between 100-125 mg/dL, 2-hour oral glucose tolerance test (OGTT 2h glucose) between 140-199 mg/dL, or hemoglobin A1c (HbA1c) between 5.7% and 6.5%. Diabetes was defined by fasting glucose levels ≥126 mg/dL, 2h glucose after OGTT ≥200 mg/dL, HbA1c ≥6.5%, current use of anti-diabetic medications, or medical record. Five pPRSs representing various pathways related to T2D were calculated based on 94 T2D-related genetic variants. Health lifestyle score was assessed with five modifiable risk factors, including body mass index (BMI), smoking, alcohol drinking, physical activity, and diet for T2D.ResultsUsing K-means consensus clustering on five pRPSs, six clusters of individuals with prediabetes were identified in HCHS/SOL, with each cluster presenting disparate patterns of pPRSs and different patterns of metabolic traits. Except cluster 3 which was not detected, the other five clusters were conformed in participants with prediabetes in UKBB, with each cluster showing the similar patterns of pPRSs to their corresponding cluster in HCHS/SOL. At baseline, proportion of impaired glucose tolerance (IGT)/impaired fasting glucose (IFG) and glycemic traits in HCHS/SOL (fasting glucose, OGTT 2h glucose, and HbA1c) were not significantly different across six clusters (P=0.13, P=0.62, P=0.35, P=0.96, respectively). In UKBB, random glucose and HbA1c at baseline did not show significant difference across five clusters (P=0.43, P=0.71, respectively). Although baseline glycemic traits were similar across clusters, cluster 6, which featured a very low proinsulin score, exhibited elevated risk of incident T2D in both cohorts (risk ratio [RR]=1.39, 95% confidence interval [95% CI]=[1.10, 1.76] vs. cluster 1 in HCHS/SOL; hazard ratio [HR]=1.29, 95% CI=[1.00, 1.69] vs. cluster 1 in UKBB; Combined RR/HR=1.34 [1.13, 1.60]). To explain the elevated risk of incident T2D in cluster 6, interactions between proinsulin score and other three pPRSs (Beta-cell score, Lipodystrophy-like score, Liver-lipid score) and sum score were detected (P for interaction=0.001, 0.04, 0.02 and 0.002, respectively). Cluster 5 showed an increased risk of incident T2D in UKBB (HR=1.35 [1.05, 1.75] vs. cluster 1) and in the combined analysis with HCHS/SOL (RR/HR=1.29 [1.08, 1.53]), although its risk of T2D was not significantly different from cluster 1 in HCHS/SOL (RR=1.23 [0.96, 1.57]). Inverse associations between the lifestyle score and risk of T2D were observed across different clusters, with a suggestively stronger association in Cluster 5 compared to Cluster 1, in both cohorts. Cluster 5 showed reduced risk of incident diabetes caused by healthy lifestyle score (RR=0.65 [0.47, 0.89], HR=0.71 [0.62, 0.81], respectively. Combined RR/HR=0.70 [0.62, 0.79]). Among individuals with a healthy lifestyle, those in Cluster 5 had a similar risk of T2D compared to those in Cluster 1 (combined RR/HR=1.03 [0.91-1.18], P>0.05).ConclusionsThis study identified genetic subtypes of prediabetes which differed in risk of progression to T2D, with two subtypes showing relatively high risk of T2D over time. Favorable relationship between healthy lifestyle and risk of T2D was observed, regardless of their genetic subtypes. Participants in one subtype with higher risk of T2D may realize extra benefits in terms of risk reduction from a healthy lifestyle.
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- 2022
46. Alzheimer’s Disease Related Neurodegeneration Partially Mediates Associations Between Air Pollution and Medial Temporal Lobe Atrophy in Older Women
- Author
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Andrew J. Petkus, Xinhui Wang, Lauren Salminen, Joshua Millstein, Daniel P. Beavers, Mark A. Espeland, Susan M. Resnick, Margaret Gatz, Meredith N Braskie, Paul M Thompson, Joel D. Kaufman, Diana Younan, and Jiu‐Chiuan Chen
- Subjects
Psychiatry and Mental health ,Cellular and Molecular Neuroscience ,Developmental Neuroscience ,Epidemiology ,Health Policy ,Neurology (clinical) ,Geriatrics and Gerontology - Published
- 2022
47. Association between late‐life air pollution exposure and medial temporal lobe atrophy in older women
- Author
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Xinhui Wang, Lauren Salminen, Andrew J. Petkus, Ira Driscoll, Joshua Millstein, Daniel P. Beavers, Mark A. Espeland, Meredith N Braskie, Paul M Thompson, Margaret Gatz, Helena C Chui, Susan M. Resnick, Joel D. Kaufman, Stephen R. Rapp, Sally A. Shumaker, Diana Younan, and Jiu‐Chiuan Chen
- Subjects
Psychiatry and Mental health ,Cellular and Molecular Neuroscience ,Developmental Neuroscience ,Epidemiology ,Health Policy ,Neurology (clinical) ,Geriatrics and Gerontology - Published
- 2022
48. Racial Segregation and Respiratory Outcomes among Urban Black Residents with and at Risk of Chronic Obstructive Pulmonary Disease
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Jerry A. Krishnan, Miranda R. Jones, Richard E. Kanner, Russell P. Bowler, Eric A. Hoffman, Nirupama Putcha, Nadia N. Hansel, Laura M. Paulin, Han Woo, Trisha M. Parekh, Victor E. Ortega, Panagis Galiatsatos, Gabriela R. Oates, MeiLan K. Han, Amanda J. Gassett, R. Graham Barr, Christopher B. Cooper, Joel D. Kaufman, Stephanie A. Christenson, Sarath Raju, Kassandra Allbright, D. Belz, Emily P. Brigham, Alejandro P. Comellas, C.O. Ejike, Fernando J. Martinez, and Gerard J. Criner
- Subjects
Adult ,Male ,Pulmonary and Respiratory Medicine ,medicine.medical_specialty ,Urban Population ,Pulmonary disease ,Critical Care and Intensive Care Medicine ,Health outcomes ,Pulmonary Disease, Chronic Obstructive ,Residence Characteristics ,Surveys and Questionnaires ,Humans ,Medicine ,Respiratory system ,Intensive care medicine ,Aged ,Aged, 80 and over ,COPD ,Social Segregation ,business.industry ,Editorials ,Health Status Disparities ,Middle Aged ,medicine.disease ,United States ,Health equity ,Black or African American ,Social Class ,Female ,business - Abstract
Rationale: Racial residential segregation has been associated with worse health outcomes, but the link with chronic obstructive pulmonary disease (COPD) morbidity has not been established.Objective...
- Published
- 2021
49. Within-City Variation in Ambient Carbon Monoxide Concentrations: Leveraging Low-Cost Monitors in a Spatiotemporal Modeling Framework
- Author
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Jianzhao Bi, Christopher Zuidema, David Clausen, Kipruto Kirwa, Michael T. Young, Amanda J. Gassett, Edmund Y. W. Seto, Paul D. Sampson, Timothy V. Larson, Adam A. Szpiro, Lianne Sheppard, and Joel D. Kaufman
- Subjects
Air Pollutants ,Carbon Monoxide ,Health, Toxicology and Mutagenesis ,Air Pollution ,Public Health, Environmental and Occupational Health ,Humans ,Particulate Matter ,Environmental Monitoring - Abstract
Based on human and animal experimental studies, exposure to ambient carbon monoxide (CO) may be associated with cardiovascular disease outcomes, but epidemiological evidence of this link is limited. The number and distribution of ground-level regulatory agency monitors are insufficient to characterize fine-scale variations in CO concentrations.To develop a daily, high-resolution ambient CO exposure prediction model at the city scale.We developed a CO prediction model in Baltimore, Maryland, based on a spatiotemporal statistical algorithm with regulatory agency monitoring data and measurements from calibrated low-cost gas monitors. We also evaluated the contribution of three novel parameters to model performance: high-resolution meteorological data, satellite remote sensing data, and copollutant (The CO model had spatial cross-validation (CV)The three novel parameters did not substantially improve model performance, suggesting that, on its own, our spatiotemporal modeling framework based on geographic features was reliable and robust. As low-cost air monitors become increasingly available, this approach to CO concentration modeling can be generalized to resource-restricted environments to facilitate comprehensive epidemiological research. https://doi.org/10.1289/EHP10889.
- Published
- 2022
50. Effects of Ambient Air Pollutants on Cardiac Structure and Function in ECHO-SOL
- Author
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Claire Leiser, Daniela Sotres-Alvarez, Elizabeth W. Spalt, Barry E. Hurwitz, Martha L. Daviglus, Gregory A. Talavera, Robert Kaplan, Bonnie E. Shook-Sa, Carlos J. Rodriguez, and Joel D. Kaufman
- Subjects
General Earth and Planetary Sciences ,General Environmental Science - Published
- 2022
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