Publications by authors named "Carol A Trenga"

The physical and mental health impacts of wildfires are wide-ranging. We assessed associations between exposure to wildfire smoke and self-reported symptoms affecting mental health among adults living in Oregon. We linked by interview date and county of residence survey responses from 5807 adults who responded to the 2018 Behavioral Risk Factor Surveillance System's depression and anxiety module with smoke plume density, a proxy for wildfires and wildfire smoke exposure.

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Article Synopsis
  • Exposure to diesel exhaust (DE) leads to a significant decrease in the ratio of reduced to oxidized glutathione (GSH/GSSG) and a notable increase in IL-6 mRNA levels in healthy adults, indicating oxidative stress.
  • A study involving 19 nonsmoking adults demonstrated that inhaling DE negatively impacts antioxidant levels, but pre-exposure antioxidant supplementation did not significantly protect against these effects.
  • The results underscore that acute exposure to traffic-related air pollution can cause oxidative stress, which may contribute to cardiovascular and respiratory diseases, emphasizing the need for further research in this area.
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Rationale: Diesel exhaust inhalation, which is the model traffic-related air pollutant exposure, is associated with vascular dysfunction.

Objectives: To determine whether healthy subjects exposed to diesel exhaust exhibit acute vasoconstriction and whether this effect could be modified by the use of antioxidants or by common variants in the angiotensin II type 1 receptor (AGTR1) and other candidate genes.

Methods: In a genotype-stratified, double-blind, four-way crossover study, 21 healthy adult subjects were exposed at rest in a randomized, balanced order to diesel exhaust (200 μg/m(3) particulate matter with an aerodynamic diameter ≤ 2.

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Background: Traffic-related air pollution is associated with cardiovascular morbidity and mortality. Although the biological mechanisms are not well understood, oxidative stress may be a primary pathway. Subpopulations, such as individuals with metabolic syndrome (MeS), may be at increased risk of adverse effects associated with air pollution.

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Background: Traffic-related air pollution is consistently associated with cardiovascular morbidity and mortality. Recent human and animal studies suggest that exposure to air pollutants affects vascular function. Diesel exhaust (DE) is a major source of traffic-related air pollution.

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Objectives: Particulate matter (PM) air pollution is associated with alterations in cardiac conductance and sudden cardiac death in epidemiological studies. Traffic-related air pollutants, including diesel exhaust (DE) may be at least partly responsible for these effects. In this experimental study we assessed whether short-term exposure to DE would result in alterations in heart rate variability (HRV), a non-invasive measure of autonomic control of the heart.

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Ambient fine particulate matter has been associated with cardiovascular and other diseases in epidemiological studies, and diesel exhaust (DE) is a major source of urban fine particulate matter. Air pollution's cardiovascular effects have been attributed to oxidative stress and systemic inflammation, with resulting perturbation of vascular homeostasis. Peripheral leukocytes are involved in both inflammation and control of vascular homeostasis.

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Background: In order to establish a consistent method for brachial artery reactivity assessment, we analyzed commonly used approaches to the test and their effects on the magnitude and time-course of flow mediated dilation (FMD), and on test variability and repeatability. As a popular and noninvasive assessment of endothelial function, several different approaches have been employed to measure brachial artery reactivity with B-mode ultrasound. Despite some efforts, there remains a lack of defined normal values and large variability in measurement technique.

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Background: Ambient particulate matter (PM) is associated with cardiovascular morbidity and mortality. It has been proposed that PM induces a pro-thrombotic process, increasing the risk of cardiovascular events, with some support from epidemiological and laboratory-based models. Diesel exhaust is a major contributor to urban PM, and we conducted a controlled human exposure of diesel exhaust in healthy subjects.

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Background: The mechanism behind the triggering effect of fine particulate matter (PM) air pollution on cardiovascular events remains elusive. We postulated that elevated levels of PM would be associated with increased blood levels of inflammatory and thrombotic markers in elderly individuals. We also hypothesized that elevated PM would increase levels of cytokines in individuals with heart disease.

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Study Objective: To determine whether increased exposure to particulate matter air pollution (PM), measured with personal, residential, or central site monitoring, was associated with pulmonary function decrements in either adults with COPD or children with asthma.

Participants: We studied 57 adults with or without COPD and 17 children aged 6 to 13 years with physician-diagnosed asthma in Seattle during a 3-year panel study.

Study Design And Measurements: Indoor and outdoor PM measurements were made at subjects' homes.

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Background: Past studies of air pollution effects among sensitive subgroups have produced inconsistent results. Our objective was to determine relationships between various measures of air pollution and cardiorespiratory effects in older subjects.

Methods: We conducted a study that included repeated measurements of pulmonary function (arterial oxygen saturation) and cardiac function (heart rate and blood pressure) in a panel of 88 subjects (>57 years of age) in Seattle during the years 1999 to 2001.

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Most particulate matter (PM) health effects studies use outdoor (ambient) PM as a surrogate for personal exposure. However, people spend most of their time indoors exposed to a combination of indoor-generated particles and ambient particles that have infiltrated. Thus, it is important to investigate the differential health effects of indoor- and ambient-generated particles.

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