Differential expression of pro-inflammatory and oxidative stress mediators induced by nitrogen dioxide and ozone in primary human bronchial epithelial cells

NO2 and O3 are ubiquitous air toxicants capable of inducing lung damage to the respiratory epithelium. Due to their oxidizing capabilities, these pollutants have been proposed to target specific biological pathways, but few publications have compared the pathways activated

Ozone exposure is associated with acute changes in inflammation, fibrinolysis, and endothelial cell function in coronary artery disease patients

Air pollution is a major risk factor for cardiovascular disease, of which ozone is a major contributor. Several studies have found associations between ozone and cardiovascular morbidity, but the results have been inconclusive. We investigated associations between ozone and changes across biological pathways associated with cardiovascular disease

A novel approach for measuring residential socioeconomic factors associated with cardiovascular and metabolic health

Individual-level characteristics, including socioeconomic status, have been associated with poor metabolic and cardiovascular health; however, residential area-level characteristics may also independently contribute to health status. In the current study, we used hierarchical clustering to aggregate 444 US Census block groups in Durham, Orange, and Wake Counties, NC, USA into six homogeneous clusters of similar characteristics based on 12 demographic factors. We assigned 2254 cardiac catheterization patients to these clusters based on residence at first catheterization. After controlling for individual age, sex, smoking status, and race, there were elevated odds of patients being obese (odds ratio (OR) = 1.92, 95% confidence intervals (CI) = 1.39, 2.67), and having diabetes (OR = 2.19, 95% CI = 1.57, 3.04), congestive heart failure (OR = 1.99, 95% CI = 1.39, 2.83), and hypertension (OR = 2.05, 95% CI = 1.38, 3.11) in a cluster that was urban, impoverished, and unemployed, compared with a cluster that was urban with a low percentage of people that were impoverished or unemployed. Our findings demonstrate the feasibility of applying hierarchical clustering to an assessment of area-level characteristics and that living in impoverished, urban residential clusters may have an adverse impact on health

Repeated measures of inflammation, blood pressure, and heart rate variability associated with traffic exposures in healthy adults

Abstract Background Previous human exposure studies of traffic-related air pollutants have demonstrated adverse health effects in human populations by comparing areas of high and low traffic, but few studies have utilized microenvironmental monitoring of pollutants at multiple traffic locations while looking at a vast array of health endpoints in the same population. We evaluated inflammatory markers, heart rate variability (HRV), blood pressure, exhaled nitric oxide, and lung function in healthy participants after exposures to varying mixtures of traffic pollutants. Methods A repeated-measures, crossover study design was used in which 23 healthy, non-smoking adults had clinical cardiopulmonary and systemic inflammatory measurements taken prior to, immediately after, and 24 hours after intermittent walking for two hours in the summer months along three diverse roadways having unique emission characteristics. Measurements of PM2.5, PM10, black carbon (BC), elemental carbon (EC), and organic carbon (OC) were collected. Mixed effect models were used to assess changes in health effects associated with these specific pollutant classes. Results Minimal associations were observed with lung function measurements and the pollutants measured. Small decreases in BP measurements and rMSSD, and increases in IL-1β and the low frequency to high frequency ratio measured in HRV, were observed with increasing concentrations of PM2.5 EC. Conclusions Small, acute changes in cardiovascular and inflammation-related effects of microenvironmental exposures to traffic-related air pollution were observed in a group of healthy young adults. The associations were most profound with the diesel-source EC

Differential expression of pro-inflammatory and oxidative stress mediators induced by nitrogen dioxide and ozone in primary human bronchial epithelial cells

CONTEXT: NO(2) and O(3) are ubiquitous air toxicants capable of inducing lung damage to the respiratory epithelium. Due to their oxidizing capabilities, these pollutants have been proposed to target specific biological pathways, but few publications have compared the pathways activated. OBJECTIVE: This work will test the premise that NO(2) and O(3) induce toxicity by activating similar cellular pathways. METHODS: Primary human bronchial epithelial cells (HBECs, n = 3 donors) were exposed for 2 hours at an air-liquid interface to 3 ppm NO(2), 0.75 ppm O(3), or filtered air and harvested 1 hr post-exposure. To give an overview of pathways that may be influenced by each exposure, gene expression was measured using PCR arrays for toxicity and oxidative stress. Based on the results, genes were selected to quantify whether expression changes were changed in a dose- and time-response manner using NO(2) (1, 2, 3, or 5 ppm), O(3) (0.25, 0.50, 0.75, or 1.00 ppm), or filtered air and harvesting 0, 1, 4 and 24 hrs post-exposure. RESULTS: Using the arrays, genes related to oxidative stress were highly induced with NO(2) while expression of pro-inflammatory and vascular function genes were found subsequent to O(3). NO(2) elicited the greatest HMOX1 response, whereas O(3) more greatly induced IL-6, IL-8, and PTGS2 expression. Additionally, O(3) elicited a greater response 1 hr post-exposure and NO(2) produced a maximal response after 4 hrs. CONCLUSION: We have demonstrated that these two oxidant gases stimulate differing mechanistic responses in vitro and these responses occur at dissimilar times

Using personas and the ADKAR framework to evaluate a network designed to facilitate sustained change toward active learning in the undergraduate classroom

Abstract One promising practice for increasing active learning in undergraduate science education is the use of a mentoring network. The Promoting Active Learning and Mentoring (PALM) Network was launched with practitioners from several professional societies and disciplines to make changes in their teaching based on evidence-based practices and to encourage the members to reflect deeply on their teaching experiences. Members of the Network interviewed seven previous Fellows, 1 to 6 years after completing their fellowship, to better understand the value of the Network and how these interactions impacted their ability to sustain change toward more active teaching practices. The interviews resulted in the creation of three personas that reflect the kinds of educators who engaged with the Network: Neil the Novice, Issa the Isolated, and Etta the Expert. Key themes emerged from the interviews about how interactions with the PALM Network sustained change toward evidence-based teaching practices allowing the members to readily adapt to the online learning environment during the COVID-19 pandemic. Understanding how the personas intersect with the ADKAR model contributes to a better understanding of how mentoring networks facilitate transformative change toward active learning and can inform additional professional development programs

In vitro and in vivo toxicity of urban and rural particulate matter from California

Particulate matter (PM) varies in chemical composition and mass concentration based on location, source, and particle size. This study sought to evaluate the in vitro and in vivo toxicity of coarse (PM10-2.5) and fine (PM25) PM samples collected at 5 diverse sites within California. Coarse and fine PM samples were collected simultaneously at 2 rural and 3 urban sites within California during the summer. A human pulmonary microvascular endothelial cell line (HPMEC-ST1.6R) was exposed to PM suspensions (50 μg/mL) and analyzed for reactive oxygen species (ROS) after 5 hours of treatment. In addition, FVB/N mice were exposed by oropharyngeal aspiration to 50 μg PM, and lavage fluid was collected 24 hrs post-exposure and analyzed for total protein and %PMNs. Correlations between trace metal concentrations, endotoxin, and biological endpoints were calculated, and the effect of particle size range, locale (urban vs. rural), and location was determined. Absolute principal factor analysis was used to identify pollution sources of PM from elemental tracers of those sources. Ambient PM elicited an ROS and pro-inflammatory-related response in the cell and mouse models, respectively. These responses were dependent on particle size, locale, and location. Trace elements associated with soil and traffic markers were most strongly linked to the adverse effects in vitro and in vivo. Particle size, location, source, and composition of PM collected at 5 locations in California affected the ROS response in human pulmonary endothelial cells and the inflammatory response in mice

Ozone exposure is associated with acute changes in inflammation, fibrinolysis, and endothelial cell function in coronary artery disease patients

Abstract Background Air pollution is a major risk factor for cardiovascular disease, of which ozone is a major contributor. Several studies have found associations between ozone and cardiovascular morbidity, but the results have been inconclusive. We investigated associations between ozone and changes across biological pathways associated with cardiovascular disease. Methods Using a panel study design, 13 participants with coronary artery disease were assessed for markers of systemic inflammation, heart rate variability and repolarization, lipids, blood pressure, and endothelial function. Daily measurements of ozone and particulate matter (PM2.5) were obtained from central monitoring stations. Single (ozone) and two-pollutant (ozone and PM2.5) models were used to assess percent changes in measurements per interquartile ranges of pollutants. Results Per interquartile increase in ozone, changes in tissue plasminogen factor (6.6%, 95% confidence intervals (CI) = 0.4, 13.2), plasminogen activator inhibitor-1 (40.5%, 95% CI = 8.7, 81.6), neutrophils (8.7% 95% CI = 1.5, 16.4), monocytes (10.2%, 95% CI = 1.0, 20.1), interleukin-6 (15.9%, 95% CI = 3.6, 29.6), large-artery elasticity index (−19.5%, 95% CI = −34.0, −1.7), and the baseline diameter of the brachial artery (−2.5%, 95% CI = −5.0, 0.1) were observed. These associations were robust in the two-pollutant model. Conclusions We observed alterations across several pathways associated with cardiovascular disease in 13 coronary artery disease patients following ozone exposures, independent of PM2.5. The results support the biological plausibility of ozone-induced cardiovascular effects. The effects were found at concentrations below the EPA National Ambient Air Quality Standards for both ozone and PM2.5