Exposures to low-levels of fine particulate matter are associated with acute changes in heart rate variability, cardiac repolarization, and circulating blood lipids in coronary artery disease patients.

Exposure to air pollution is a major risk factor for cardiovascular disease, disease risk factors, and mortality. Specifically, particulate matter (PM), and to some extent ozone, are contributors to these effects. In addition, exposures to these pollutants may be especially dangerous for susceptible populations. In this repeated-visit panel study, cardiovascular markers were collected from thirteen male participants with stable coronary artery disease. For 0-4 days prior to the health measurement collections, daily concentrations of fine PM (PM2.5) and ozone were obtained from local central monitoring stations located near the participant's homes. Then, single (PM2.5) and two-pollutant (PM2.5 and ozone) models were used to assess whether there were short-term changes in cardiovascular health markers. Per interquartile range increase in PM2.5, there were decrements in several heart rate variability metrics, including the standard deviation of the normal-to-normal intervals (lag 3, -5.8%, 95% confidence interval (CI) = -11.5, 0.3) and root-mean squared of successive differences (five day moving average, -8.1%, 95% CI = -15.0, -0.7). In addition, increases in PM2.5 were also associated with changes in P complexity (lag 1, 4.4%, 95% CI = 0.5, 8.5), QRS complexity (lag 1, 4.9%, 95% CI = 1.4, 8.5), total cholesterol (five day moving average, -2.1%, 95% CI = -4.1, -0.1), and high-density lipoprotein cholesterol (lag 2, -1.6%, 95% CI = -3.1, -0.1). Comparisons to our previously published work on ozone were conducted. We found that ozone affected inflammation and endothelial function, whereas PM2.5 influenced heart rate variability, repolarization, and lipids. All the health changes from these two studies were found at concentrations below the United States Environmental Protection Agency's National Ambient Air Quality Standards. Our results imply clear differences in the cardiovascular outcomes observed with exposure to the two ubiquitous air pollutants PM2.5 and ozone; this observation suggests different mechanisms of toxicity for these exposures.

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

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. Supplementary Information: The online version contains supplementary material available at 10.1007/s44217-022-00023-w.

Air quality changes in New York City during the COVID-19 pandemic.

In December 2019, a new, severe coronavirus (COVID-19) appeared in Wuhan, China. Shortly after, the first COVID-19 case was confirmed in the United States. The emergence of this virus led many United States governors to enact executive orders in an effort to limit the person-to-person spread of the virus. One state that utilized such measures was New York, which contains New York City (NYC), the most populous city in the United States. Many reports have shown that due to the government-backed shutdowns, the air quality in major global cities improved. However, there has been only limited work on whether this same trend is seen throughout the United States, specifically within the densely populated NYC area. Thus, the focus of this study was to examine whether changes in air quality were observed in NYC resulting from New York State's COVID-19-associated shutdown measures. To do this, daily concentrations of fine particulate matter (PM2.5) and nitrogen dioxide (NO2) were obtained from 15 central monitoring stations throughout the five NYC boroughs for the first 17 weeks (January through May) of 2015-2020. Decreases in PM2.5 (36%) and NO2 (51%) concentrations were observed shortly after the shutdown took place; however, using a linear time lag model, when changes in these pollutant concentrations were compared to those measured during the same span of time in 2015-2019, no significant difference between the years was found. Therefore, we highlight the importance of considering temporal variability and long-term trends of pollutant concentrations when analyzing for short-term differences in air pollutant concentrations related to the COVID-19 shutdowns.

Neighborhood sociodemographic effects on the associations between long-term PM2.5 exposure and cardiovascular outcomes and diabetes.

Introduction: Exposure to PM2.5 air pollution and neighborhood-level sociodemographic characteristics are associated with cardiovascular disease and possibly diabetes. However, the joint effect of sociodemographics and PM2.5 on these outcomes is uncertain. Methods: We examined whether clusters of sociodemographic characteristics modified effects of long-term PM2.5 exposure on coronary artery disease (CAD), myocardial infarction (MI), hypertension, and diabetes. We used medical records data from 2192 cardiac catheterization patients residing in North Carolina and assigned to one of six previously-determined clusters. For each participant, we estimated annual PM2.5 exposure at their primary residence using a hybrid model with a 1 km2 resolution. We used logistic regression models adjusted for age, sex, body mass index, and smoking status, to assess cluster-specific associations with PM2.5 and to determine if there were interactions between cluster and PM2.5 on outcomes. Results: Compared to cluster 3 (OR 0.93, 95% CI 0.82-1.07; urban, low proportion of black individuals and high socioeconomic status), we observed greater associations between PM2.5 and hypertension in clusters 1 (OR 1.22, 95% CI 0.99-1.50, pint 0.03) and 2 (OR 1.64, 95% CI 1.16-2.32, pint 0.003), which were urban, high proportion of black individuals, and low socioeconomic status. PM2.5 was associated with MI (OR 1.29, 95% CI 1.16-1.42) but not diabetes, regardless of cluster and was associated with CAD in cluster 3 (OR 1.15, 95% CI 1.00, 1.31) and overall (OR 1.07, 95% CI 0.98, 1.17). Discussion: Areas of relative disadvantage have a stronger association between PM2.5 and hypertension compared to areas of relative advantage.

A simple, cost-effective, and novel method for determining the efficiency of industrial and commercial noise-canceling earmuffs.

CONTEXT: There are several ways to assess the noise reducing efficiency of earmuffs, but they usually involve using human participants and/or specialized equipment. OBJECTIVE: The current study was designed to develop a less labor-intensive, cost-effective, participant-free first-pass method for measuring the efficiency of earmuffs. METHODS: We evaluated the noise-cancelling ability of five different types of earmuffs (3M: Optime 98, Optime 105; iDEA USA V201; Tronsmart Encore S6; Bose QuietComfort 35) under laboratory and field conditions. We compared our results to the microphone-in-real-ear (MIRE) method. Lastly, a survey of college-aged students was also conducted to determine which earmuffs were the most comfortable and provided the best fit. RESULTS: Of the five earmuffs studied, the Optime 98 and Bose earmuffs were most effective at reducing noise levels in both the laboratory and field. These earmuffs also received the highest scores for comfort, fit, and perceived ability to reduce noise, with Bose being slightly more preferred than Optime 98. The MIRE method provided the same overall results as the laboratory and field tests. CONCLUSION: Our method for evaluating the noise-canceling ability of earmuffs could be used to supplement more complicated testing procedures as a first-pass method.

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

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.

Secondhand hookah smoke: an occupational hazard for hookah bar employees.

BACKGROUND: Despite the increasing popularity of hookah bars, there is a lack of research assessing the health effects of hookah smoke among employees. This study investigated indoor air quality in hookah bars and the health effects of secondhand hookah smoke on hookah bar workers. METHODS: Air samples were collected during the work shift of 10 workers in hookah bars in New York City (NYC). Air measurements of fine particulate matter (PM2.5), fine black carbon (BC2.5), carbon monoxide (CO), and nicotine were collected during each work shift. Blood pressure and heart rate, markers of active smoking and secondhand smoke exposure (exhaled CO and saliva cotinine levels), and selected inflammatory cytokines in blood (ineterleukin (IL)-1b, IL-6, IL-8, interferon γ (IFN-γ), tumour necrosis factor (TNF-α)) were assessed in workers immediately prior to and immediately after their work shift. RESULTS: The PM2.5 (gravimetric) and BC2.5 concentrations in indoor air varied greatly among the work shifts with mean levels of 363.8 µg/m3 and 2.2 µg/m3, respectively. The mean CO level was 12.9 ppm with a peak value of 22.5 ppm CO observed in one hookah bar. While heart rate was elevated by 6 bpm after occupational exposure, this change was not statistically significant. Levels of inflammatory cytokines in blood were all increased at postshift compared to preshift testing with IFN-Υ increasing from 0.85 (0.13) to 1.6 (0.25) (mean (standard error of the mean; SEM)) pg/mL (p<0.01). Exhaled CO levels were significantly elevated after the work shift with 2 of 10 workers having values >90 ppm exhaled CO. CONCLUSIONS: These results demonstrate that hookah bars have elevated concentrations of indoor air pollutants that appear to cause adverse health effects in employees. These data indicate the need for further research and a marked need for better air quality monitoring and policies in such establishments to improve the indoor air quality for workers and patrons.

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.

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

CONTEXT: 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. OBJECTIVE: This work will test the premise that NO2 and O3 induce toxicity by activating similar cellular pathways. METHODS: Primary human bronchial epithelial cells (HBECs, n = 3 donors) were exposed for 2 h at an air-liquid interface to 3 ppm NO2, 0.75 ppm O3, or filtered air and harvested 1 h 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 NO2 (1, 2, 3, or 5 ppm), O3 (0.25, 0.50, 0.75, or 1.00 ppm), or filtered air and harvesting 0, 1, 4 and 24 h post-exposure. RESULTS: Using the arrays, genes related to oxidative stress were highly induced with NO2 while expression of pro-inflammatory and vascular function genes was found subsequent to O3. NO2 elicited the greatest HMOX1 response, whereas O3 more greatly induced IL-6, IL-8 and PTGS2 expression. Additionally, O3 elicited a greater response 1 h post-exposure and NO2 produced a maximal response after 4 h. CONCLUSION: We have demonstrated that these two oxidant gases stimulate differing mechanistic responses in vitro and these responses occur at dissimilar times.

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.

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

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-1ß 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.

Noninvasive effects measurements for air pollution human studies: methods, analysis, and implications.

Human exposure studies, compared with cell and animal models, are heavily relied upon to study the associations between health effects in humans and air pollutant inhalation. Human studies vary in exposure methodology, with some work conducted in controlled settings, whereas other studies are conducted in ambient environments. Human studies can also vary in the health metrics explored, as there exists a myriad of health effect end points commonly measured. In this review, we compiled mini reviews of the most commonly used noninvasive health effect end points that are suitable for panel studies of air pollution, broken into cardiovascular end points, respiratory end points, and biomarkers of effect from biological specimens. Pertinent information regarding each health end point and the suggested methods for mobile collection in the field are assessed. In addition, the clinical implications for each health end point are summarized, along with the factors identified that can modify each measurement. Finally, the important research findings regarding each health end point and air pollutant exposures were reviewed. It appeared that most of the adverse health effects end points explored were found to positively correlate with pollutant levels, although differences in study design, pollutants measured, and study population were found to influence the magnitude of these effects. Thus, this review is intended to act as a guide for researchers interested in conducting human exposure studies of air pollutants while in the field, although there can be a wider application for using these end points in many epidemiological study designs.

The effect of particle size, location and season on the toxicity of urban and rural particulate matter.

Particulate matter (PM) varies in chemical composition and mass concentration based on a number of factors including location, season, source and particle size. The aim of this study was to evaluate the in vitro and in vivo toxicity of coarse and fine PM simultaneously collected at three rural and two urban sites within the metropolitan New York City (NYC) region during two seasons, and to assess how particle size and elemental composition affect toxicity. Human pulmonary microvascular endothelial (HPMEC-ST1.6R) and bronchial epithelial (BEAS-2B) cell lines were exposed to PM (50 µg/mL) and analyzed for reactive oxygen species (ROS). Mice (FVB/N) were exposed by oropharyngeal aspiration to 50 µg PM, and lavage fluid was analyzed for total protein and PMN influx. The ROS response was greater in the HPMEC-ST1.6R cell line compared to BEAS-2B cells, but the responses were significantly correlated (p < 0.01). The ROS response was affected by location, locale and the location:size interaction in both cell lines, and an additional association for size was observed from HPMEC-ST1.6R cells. Urban fine PM generated the highest ROS response. In the mouse model, inflammation was associated with particle size and by a season:size interaction, with coarse PM producing greater PMN inflammation. This study showed that the aerodynamic size, locale (i.e. urban versus rural), and site of PM samples affected the ROS response in pulmonary endothelial and epithelial cells and the inflammatory response in mice. Importantly, these responses were dependent upon the chemical composition of the PM samples.