Lauren H. Wyatt
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Lauren H. Wyatt has a total of 66 co-authors. Here are the top co-authors by number of shared publications:
- Ana Grohovac Rappold
U.S. Environmental Protection Agency
6 shared publications - Cavin K. Ward-Caviness
Center for Public Health and Environmental Assessment, US Environmental Protection Agency, Chapel Hill, USA
4 shared publications David Diaz-Sanchez
US Environmental Protection Agency Center for Public Health and Environmental Assessment, Research Triangle Park, North Carolina, USA
3 shared publications- Heileen Hsu-Kim
Duke University
3 shared publications - Joel Newman Meyer
Duke University
3 shared publications Joshua Moyer
Center for Public Health and Environmental Assessment, US Environmental Protection Agency, Chapel Hill, NC, USA
3 shared publications
Latest Publications
- 5 April 2023
- Published by Elsevier in Environmental Research
- Vol. 228, 115839
Associations between source-apportioned PM2.5 and 30-day readmissions in heart failure patients
- 5 April 2023
- Published by Elsevier in Environmental Research
- Vol. 228, 115839
Associations between source-apportioned PM2.5 and 30-day readmissions in heart failure patients
- Open Access
- 12 January 2023
- Published by Elsevier in Environmental Pollution
- Vol. 320, 121085
Long-term exposure to ambient O3 and PM2.5 is associated with reduced cognitive performance in young adults: A retrospective longitudinal repeated measures study in adults aged 18–90 years
- 12 January 2023
- Published by Elsevier in Environmental Pollution
- Vol. 320, 121085
Open AccessLong-term exposure to ambient O3 and PM2.5 is associated with reduced cognitive performance in young adults: A retrospective longitudinal repeated measures study in adults aged 18–90 years
- Open Access
- 24 June 2022
- Published by BMJ in Open Heart
- Vol. 9 (1) , e001891
Associations between short-term exposure to PM2.5 and cardiomyocyte injury in myocardial infarction survivors in North Carolina
Objective: Short-term ambient fine particulate matter (PM2.5) is associated with adverse cardiovascular events including myocardial infarction (MI). However, few studies have examined associations between PM2.5 and subclinical cardiomyocyte damage outside of overt cardiovascular events. Here we evaluate the impact of daily PM2.5 on cardiac troponin I, a cardiomyocyte specific biomarker of cellular damage. Methods: We conducted a retrospective cohort study of 2924 patients identified using electronic health records from the University of North Carolina Healthcare System who had a recorded MI between 2004 and 2016. Troponin I measurements were available from 2014 to 2016, and were required to be at least 1 week away from a clinically diagnosed MI. Daily ambient PM2.5 concentrations were estimated at 1 km resolution and assigned to patient residence. Associations between log-transformed troponin I and daily PM2.5 were evaluated using distributed lag linear mixed effects models adjusted for patient demographics, socioeconomic status and meteorology. Results: A 10 µg/m3 elevation in PM2.5 3 days before troponin I measurement was associated with 0.06 ng/mL higher troponin I (95% CI=0.004 to 0.12). In stratified models, this association was strongest in patients that were men, white and living in less urban areas. Similar associations were observed when using 2-day rolling averages and were consistently strongest when using the average exposure over the 5 days prior to troponin I measurement. Conclusions: Daily elevations in PM2.5 were associated with damage to cardiomyocytes, outside of the occurrence of an MI. Poor air quality may cause persistent damage to the cardiovascular system leading to increased risk of cardiovascular disease and adverse cardiovascular events.
- 24 June 2022
- Published by BMJ in Open Heart
- Vol. 9 (1) , e001891
Open AccessAssociations between short-term exposure to PM2.5 and cardiomyocyte injury in myocardial infarction survivors in North Carolina
Objective: Short-term ambient fine particulate matter (PM2.5) is associated with adverse cardiovascular events including myocardial infarction (MI). However, few studies have examined associations between PM2.5 and subclinical cardiomyocyte damage outside of overt cardiovascular events. Here we evaluate the impact of daily PM2.5 on cardiac troponin I, a cardiomyocyte specific biomarker of cellular damage. Methods: We conducted a retrospective cohort study of 2924 patients identified using electronic health records from the University of North Carolina Healthcare System who had a recorded MI between 2004 and 2016. Troponin I measurements were available from 2014 to 2016, and were required to be at least 1 week away from a clinically diagnosed MI. Daily ambient PM2.5 concentrations were estimated at 1 km resolution and assigned to patient residence. Associations between log-transformed troponin I and daily PM2.5 were evaluated using distributed lag linear mixed effects models adjusted for patient demographics, socioeconomic status and meteorology. Results: A 10 µg/m3 elevation in PM2.5 3 days before troponin I measurement was associated with 0.06 ng/mL higher troponin I (95% CI=0.004 to 0.12). In stratified models, this association was strongest in patients that were men, white and living in less urban areas. Similar associations were observed when using 2-day rolling averages and were consistently strongest when using the average exposure over the 5 days prior to troponin I measurement. Conclusions: Daily elevations in PM2.5 were associated with damage to cardiomyocytes, outside of the occurrence of an MI. Poor air quality may cause persistent damage to the cardiovascular system leading to increased risk of cardiovascular disease and adverse cardiovascular events.
- 1 June 2022
- Published by American Chemical Society (ACS) in Environmental Health Perspectives
- Vol. 130 (6) , 67005
Short-Term Exposure to Wildfire Smoke and PM2.5 and Cognitive Performance in a Brain-Training Game: A Longitudinal Study of U.S. Adults
Environmental Health Perspectives is an Open Access journal published by the National Institute of Environmental Health Sciences. Environmental Health Perspectives is an Open Access journal published by the National Institute of Environmental Health Sciences.
- 1 June 2022
- Published by American Chemical Society (ACS) in Environmental Health Perspectives
- Vol. 130 (6) , 67005
Short-Term Exposure to Wildfire Smoke and PM2.5 and Cognitive Performance in a Brain-Training Game: A Longitudinal Study of U.S. Adults
Environmental Health Perspectives is an Open Access journal published by the National Institute of Environmental Health Sciences. Environmental Health Perspectives is an Open Access journal published by the National Institute of Environmental Health Sciences.
- 7 March 2022
- Published by Elsevier in American Heart Journal
- Vol. 248, 130-138
Short-term PM2.5 exposure and early-readmission risk: a retrospective cohort study in North Carolina heart failure patients
- 7 March 2022
- Published by Elsevier in American Heart Journal
- Vol. 248, 130-138
Short-term PM2.5 exposure and early-readmission risk: a retrospective cohort study in North Carolina heart failure patients
- Open Access
- 23 August 2021
- Published by Environmental Health Perspectives in ISEE Conference Abstracts
- Vol. 2021 (1)
Short-Term PM2.5 Exposure Impacts Cognitive Performance: A Longitudinal Repeated Measures Study of the Western US 2017-2018
Environmental Health Perspectives is an Open Access journal published by the National Institute of Environmental Health Sciences. Environmental Health Perspectives is an Open Access journal published by the National Institute of Environmental Health Sciences.
- 23 August 2021
- Published by Environmental Health Perspectives in ISEE Conference Abstracts
- Vol. 2021 (1)
Open AccessShort-Term PM2.5 Exposure Impacts Cognitive Performance: A Longitudinal Repeated Measures Study of the Western US 2017-2018
Environmental Health Perspectives is an Open Access journal published by the National Institute of Environmental Health Sciences. Environmental Health Perspectives is an Open Access journal published by the National Institute of Environmental Health Sciences.
- Open Access
Association of short-term exposure to ambient PM 2.5 with hospital admissions and 30-day readmissions in end-stage renal disease patients: population-based retrospective cohort study
Objectives: To examine the effect of short-term exposure to ambient fine particulate matter (PM 2.5 ) on all-cause, cardiovascular and respiratory-related hospital admissions and readmissions among patients receiving outpatient haemodialysis. Design: Retrospective cohort study. Setting: Inpatient hospitalisation claims identified from the US Renal Data System in 530 US counties. Participants: All patients receiving in-centre haemodialysis between 2008 and 2014. Primary and secondary outcome measures: Risk of all-cause, cardiovascular and respiratory-related hospital admissions and 30-day all-cause and cause-specific readmission following an all-cause, cardiovascular, and respiratory-related discharges. Readmission risk was evaluated for early (1–7 days postdischarge) and late (8–30 days postdischarge) readmission time periods. Relative risk is expressed per 10 μg/m 3 of PM 2.5 . Results: Same-day ambient PM 2.5 was associated with increased hospital admission risk for cardiovascular causes (0.9%, 95% CI 0.2 to 1.7). Greater PM 2.5 -related associations were observed with 30-day readmission risk. Early-readmission risk was increased by 1.6%–1.8% following all-cause (1.6%, 95% CI 0.6% to 2.6%), cardiovascular (1.8%, 95% CI 0.4% to 3.2%) and respiratory (1.8%, 95% CI 0.4% to 3.2%) discharges; while late-readmission risk increased by 1.2%–1.3% following all-cause and cardiovascular discharges. PM 2.5 -related associations with readmission risk were greatest for certain cause-specific readmissions ranging 4.0%–6.5% for dysrhythmia and conduction disorder, heart failure, chronic obstructive pulmonary disease, other non-cardiac chest pain or respiratory syndrome and pneumonia. Following all-cause discharges, the cause-specific early-readmission risk was increased by 6.5% (95% CI 3.5% to 9.6%) for pneumonia, 4.8% (95% CI 2.3% to 7.4%) for dysrhythmia and conduction disorder, 3.7% (95% CI 1.4% to 6.0%) for heart failure and 2.7% (95% CI 1.2% to 4.2%) for other non-cardiac chest pain or respiratory syndrome-related causes. Conclusions: Daily ambient PM 2.5 was associated with an increased risk of cardiovascular admissions and 30-day readmissions following cardiopulmonary-related discharges in a vulnerable end-stage renal disease population. In the first week following discharge, greater PM 2.5 -related risk of rehospitalisation was identified for some diagnoses.
Open AccessAssociation of short-term exposure to ambient PM 2.5 with hospital admissions and 30-day readmissions in end-stage renal disease patients: population-based retrospective cohort study
Objectives: To examine the effect of short-term exposure to ambient fine particulate matter (PM 2.5 ) on all-cause, cardiovascular and respiratory-related hospital admissions and readmissions among patients receiving outpatient haemodialysis. Design: Retrospective cohort study. Setting: Inpatient hospitalisation claims identified from the US Renal Data System in 530 US counties. Participants: All patients receiving in-centre haemodialysis between 2008 and 2014. Primary and secondary outcome measures: Risk of all-cause, cardiovascular and respiratory-related hospital admissions and 30-day all-cause and cause-specific readmission following an all-cause, cardiovascular, and respiratory-related discharges. Readmission risk was evaluated for early (1–7 days postdischarge) and late (8–30 days postdischarge) readmission time periods. Relative risk is expressed per 10 μg/m 3 of PM 2.5 . Results: Same-day ambient PM 2.5 was associated with increased hospital admission risk for cardiovascular causes (0.9%, 95% CI 0.2 to 1.7). Greater PM 2.5 -related associations were observed with 30-day readmission risk. Early-readmission risk was increased by 1.6%–1.8% following all-cause (1.6%, 95% CI 0.6% to 2.6%), cardiovascular (1.8%, 95% CI 0.4% to 3.2%) and respiratory (1.8%, 95% CI 0.4% to 3.2%) discharges; while late-readmission risk increased by 1.2%–1.3% following all-cause and cardiovascular discharges. PM 2.5 -related associations with readmission risk were greatest for certain cause-specific readmissions ranging 4.0%–6.5% for dysrhythmia and conduction disorder, heart failure, chronic obstructive pulmonary disease, other non-cardiac chest pain or respiratory syndrome and pneumonia. Following all-cause discharges, the cause-specific early-readmission risk was increased by 6.5% (95% CI 3.5% to 9.6%) for pneumonia, 4.8% (95% CI 2.3% to 7.4%) for dysrhythmia and conduction disorder, 3.7% (95% CI 1.4% to 6.0%) for heart failure and 2.7% (95% CI 1.2% to 4.2%) for other non-cardiac chest pain or respiratory syndrome-related causes. Conclusions: Daily ambient PM 2.5 was associated with an increased risk of cardiovascular admissions and 30-day readmissions following cardiopulmonary-related discharges in a vulnerable end-stage renal disease population. In the first week following discharge, greater PM 2.5 -related risk of rehospitalisation was identified for some diagnoses.
- Open Access
- 16 November 2020
- Published by Springer Nature in Particle and Fibre Toxicology
- Vol. 17 (1) , 1-12
Low levels of fine particulate matter increase vascular damage and reduce pulmonary function in young healthy adults
Background: Fine particulate matter (PM2.5) related mild inflammation, altered autonomic control of cardiovascular function, and changes to cell function have been observed in controlled human exposure studies. Methods: To measure the systemic and cardiopulmonary impacts of low-level PM exposure, we exposed 20 healthy, young volunteers to PM2.5, in the form of concentrated ambient particles (mean: 37.8 μg/m3, SD 6.5), and filtered air (mean: 2.1 μg/m3, SD 2.6). In this double-blind, crossover study the exposure order was randomized. During the 4 h exposure, volunteers (7 females and 13 males) underwent light intensity exercise to regulate ventilation rate. We measured pulmonary, cardiac, and hematologic end points before exposure, 1 h after exposure, and again 20 h after exposure. Results: Low-level PM2.5 resulted in both pulmonary and extra-pulmonary changes characterized by alterations in systematic inflammation markers, cardiac repolarization, and decreased pulmonary function. A mean increase in PM2.5 concentration (37.8 μg/m3) significantly increased serum amyloid A (SAA), C-reactive protein (CRP), soluble intercellular adhesion molecule-1 (sICAM-1), and soluble vascular cell adhesion molecule-1 (sVCAM-1), 1 h after exposure by 8.7, 9.1, 10.7, and 6.6%, respectively, relative to the filtered air control. SAA remained significantly elevated (34.6%) 20 h after PM2.5 exposure which was accompanied by a 5.7% decrease in percent neutrophils. Decreased pulmonary function was observed 1 h after exposure through a 0.8 and 1.2% decrease in forced expiratory volume in 1 s (FEV1) and FEV1/ forced vital capacity (FEV1/FVC) respectively. Additionally, sex specific changes were observed in repolarization outcomes following PM2.5 exposure. In males, P-wave and QRS complex were increased by 15.4 and 5.4% 1 h after exposure. Conclusions: This study is the first controlled human exposure study to demonstrate biological effects in response to exposure to concentrated ambient air PM2.5 particles at levels near the PM2.5 US NAAQS standard. Clinical trial registration information: clinicaltrials.gov; Identifier: NCT03232086. The study was registered retrospectively on July 25, 2017, prior to final data collection on October 25, 2017 and data analysis.
- 16 November 2020
- Published by Springer Nature in Particle and Fibre Toxicology
- Vol. 17 (1) , 1-12
Open AccessLow levels of fine particulate matter increase vascular damage and reduce pulmonary function in young healthy adults
Background: Fine particulate matter (PM2.5) related mild inflammation, altered autonomic control of cardiovascular function, and changes to cell function have been observed in controlled human exposure studies. Methods: To measure the systemic and cardiopulmonary impacts of low-level PM exposure, we exposed 20 healthy, young volunteers to PM2.5, in the form of concentrated ambient particles (mean: 37.8 μg/m3, SD 6.5), and filtered air (mean: 2.1 μg/m3, SD 2.6). In this double-blind, crossover study the exposure order was randomized. During the 4 h exposure, volunteers (7 females and 13 males) underwent light intensity exercise to regulate ventilation rate. We measured pulmonary, cardiac, and hematologic end points before exposure, 1 h after exposure, and again 20 h after exposure. Results: Low-level PM2.5 resulted in both pulmonary and extra-pulmonary changes characterized by alterations in systematic inflammation markers, cardiac repolarization, and decreased pulmonary function. A mean increase in PM2.5 concentration (37.8 μg/m3) significantly increased serum amyloid A (SAA), C-reactive protein (CRP), soluble intercellular adhesion molecule-1 (sICAM-1), and soluble vascular cell adhesion molecule-1 (sVCAM-1), 1 h after exposure by 8.7, 9.1, 10.7, and 6.6%, respectively, relative to the filtered air control. SAA remained significantly elevated (34.6%) 20 h after PM2.5 exposure which was accompanied by a 5.7% decrease in percent neutrophils. Decreased pulmonary function was observed 1 h after exposure through a 0.8 and 1.2% decrease in forced expiratory volume in 1 s (FEV1) and FEV1/ forced vital capacity (FEV1/FVC) respectively. Additionally, sex specific changes were observed in repolarization outcomes following PM2.5 exposure. In males, P-wave and QRS complex were increased by 15.4 and 5.4% 1 h after exposure. Conclusions: This study is the first controlled human exposure study to demonstrate biological effects in response to exposure to concentrated ambient air PM2.5 particles at levels near the PM2.5 US NAAQS standard. Clinical trial registration information: clinicaltrials.gov; Identifier: NCT03232086. The study was registered retrospectively on July 25, 2017, prior to final data collection on October 25, 2017 and data analysis.
- Open Access
- 1 June 2020
- Published by Elsevier in Data in Brief
- Vol. 30, 105318
Annual PM2.5 and cardiovascular mortality rate data: Trends modified by county socioeconomic status in 2,132 US counties
- 1 June 2020
- Published by Elsevier in Data in Brief
- Vol. 30, 105318
Open AccessAnnual PM2.5 and cardiovascular mortality rate data: Trends modified by county socioeconomic status in 2,132 US counties
- Open Access
- 1 March 2020
- Published by Elsevier in Environment International
- Vol. 136, 105430
The contribution of improved air quality to reduced cardiovascular mortality: Declines in socioeconomic differences over time
- 1 March 2020
- Published by Elsevier in Environment International
- Vol. 136, 105430
Open AccessThe contribution of improved air quality to reduced cardiovascular mortality: Declines in socioeconomic differences over time