Substance use disorder is a growing public health challenge in the United States. People who use drugs may be more vulnerable to ambient heat due to the effects of drugs on thermoregulation and their risk environment. There have been limited population-based studies of ambient temperature and drug-related morbidity. We examined short-term associations between daily ambient temperature and emergency department (ED) visits for use or overdose of amphetamine, cocaine and opioids in California during the period 2005 to 2019. Daily ZIP code-level maximum, mean, and minimum temperature exposures were derived from 1-km data Daymet products. A time-stratified case-crossover design was used to estimate cumulative non-linear associations of daily temperature for lag days 0 to 3. Stratified analyses by patient sex, race, and ethnicity were also conducted. The study included over 3.4 million drug-related ED visits. We found positive associations between daily temperature and ED visits for all outcomes examined. An increase in daily mean temperature from the 50th to the 95th percentile was associated with ED visits for amphetamine use (OR = 1.072, 95% CI: 1.058, 1.086), cocaine use (OR = 1.044, 95% CI: 1.021, 1.068 and opioid use (OR = 1.041, 95% CI: 1.025, 1.057). Stronger positive associations were also observed for overdose: amphetamine overdose (OR = 1.150, 95% CI: 1.085, 1.218), cocaine overdose (OR = 1.159, 95% CI: 1.053, 1.276), and opioid overdose (OR = 1.079, 95% CI: 1.054, 1.106). In summary, people who use stimulants and opioids may be a subpopulation sensitive to short-term higher ambient temperature. Mitigating heat exposure can be considered in harm reduction strategies in response to the substance use epidemic and global climate change.
by
Stefanie Ebelt;
L. Baxter;
H.S. Erickson;
L.R.F. Henneman;
S. Lange;
T.J. Luben;
M. Neidell;
A.M. Rule;
A.G. Russell;
J. Wendt Hess;
C.J. Burns;
J.S. LaKind;
J.E. Goodman
Air pollution accountability studies examine the relationship(s) between an intervention, regulation, or event and the resulting downstream impacts, if any, on emissions, exposure, and/or health. The sequence of events has been schematically described as an accountability chain. Here, we update the existing framework to capture real-life complexities and to highlight important factors that fall outside the linear chain. This new “accountability web” is intended to convey the intricacies associated with conducting an accountability study to various audiences, including researchers, policy makers, and stakeholders. We also identify data considerations for planning and completing a robust accountability study, including those relevant to novel and innovative air pollution and exposure data. Finally, we present a series of recommendations for the accountability research community that can serve as a guide for the next generation of accountability studies.
Background:
Compared to many environmental risk factors, the relationship between pollen and asthma is understudied, including how associations may differ by pollen type and between subgroups, and how associations may be changing over time.
Objectives:
We evaluated the association between ambient pollen concentrations and emergency department (ED) visits for asthma and wheeze in Atlanta, Georgia during 1993–2018. We estimated overall associations for 13 individual pollen taxa, as well as associations by decade, race, age (5–17, 18–64, 65+), and insurance status (Medicaid vs non-Medicaid).
Methods:
Speciated pollen data were acquired from Atlanta Allergy & Asthma, a nationally certified pollen counting station. ED visit data were obtained from individual hospitals and from the Georgia Hospital Association. We performed time-series analyses using quasi-Poisson distributed lag models, with primary analyses assessing 3-day (lag 0–2 days) pollen levels. Models controlled for day of week, holidays, air temperature, month, year, and month-by-year interactions.
Results:
From 1993 to 2018, there were 686,259 ED visits for asthma and wheeze in the dataset, and the number of ED visits increased over time. We observed positive associations of asthma and wheeze ED visits with nine of the 13 pollen taxa: trees (maple, birch, pine, oak, willow, sycamore, and mulberry), two weeds (nettle and pigweed), and grasses. Rate ratios indicated 1–8% increases in asthma and wheeze ED visits per standard deviation increases in pollen. In general, we observed stronger associations in the earliest period (1993–2000), in younger people, and in Black patients; however, results varied by pollen taxa.
Conclusions:
Some, but not all, types of pollen are associated with increased ED visits for asthma/wheeze. Associations are generally higher in Black and younger patients and appear to have decreased over time.
Background:
Air pollution has been associated with cognitive function in the elderly. Previous studies have not evaluated the simultaneous effect of neighborhood-level socioeconomic status (N-SES), which can be an essential source of bias.
Objectives:
We explored N-SES as a confounder and effect modifier in a cross-sectional study of air pollution and subjective cognitive function.
Methods:
We included 12,058 participants age 50+ years from the Emory Healthy Aging Study in Metro Atlanta using the Cognitive Function Instrument (CFI) score as our outcome, with higher scores representing worse subjective cognitive function. We estimated 9-year average ambient carbon monoxide (CO), nitrogen oxides (NOx), and fine particulate matter (PM2.5) concentrations at residential addresses using a fusion of dispersion and chemical transport models. We collected census-tract level N-SES indicators and created two composite measures via principal component analysis and k-means clustering. Associations between pollutants and CFI and effect modification by N-SES were estimated via linear regression models adjusted for age, education, race and N-SES.
Results:
N-SES confounded the association between air pollution and CFI, independent of individual characteristics. We found significant effect modifications by N-SES for the association between air pollution and CFI (p-values<0.001) suggesting that effects of air pollution differ depending on N-SES. Participants living in areas with low N-SES were most vulnerable to air pollution. In the lowest N-SES urban areas, interquartile range (IQR) increases in CO, NOx, and PM2.5 were associated with 5.4% (95%-confidence interval, −0.2,11.3), 4.9% (−0.4,10.4), and 9.8% (2.2,18.0) changes in CFI, respectively. In lowest N-SES suburban areas, IQR increases in CO, NOx, and PM2.5 were associated with higher changes in CFI, namely 13.0% (0.9,26.5), 13.0% (−0.1,27.8), and 17.3% (2.5,34.2), respectively.
Discussion:
N-SES is an important confounder and effect modifier in our study. This finding could have implications for studying health effects of air pollution and identifying susceptible populations.
Dust storms are increasing in frequency and correlate with adverse health outcomes but remain understudied in the United States (U.S.), partially due to the limited spatio‐temporal coverage, resolution, and accuracy of current data sets. In this work, dust‐related metrics from four public areal data products were compared to a monitor‐based “gold standard” dust data set. The data products included the National Weather Service (NWS) storm event database, the Modern‐Era Retrospective analysis for Research and Applications—Version 2, the EPA's Air QUAlity TimE Series (EQUATES) Project using the Community Multiscale Air Quality Modeling System (CMAQ), and the Copernicus Atmosphere Monitoring Service global reanalysis product. California, Nevada, Utah, and Arizona, which account for most dust storms reported in the U.S., were examined. Dichotomous and continuous metrics based on reported dust storms, particulate matter concentrations (PM10 and PM2.5), and aerosol‐type variables were extracted or derived from the data products. Associations between these metrics and a validated dust storm detection method utilizing Interagency Monitoring of Protected Visual Environments monitors were estimated via quasi‐binomial regression. In general, metrics from CAMS yielded the strongest associations with the “gold standard,” followed by the NWS storm database metric. Dust aerosol (0.9–20 μm) mixing ratio, vertically integrated mass of dust aerosol (9–20 μm), and dust aerosol optical depth at 550 nm from CAMS generated the highest standardized odds ratios among all metrics. Future work will apply machine‐learning methods to the best‐performing metrics to create a public dust storm database suitable for long‐term epidemiologic studies.
Background
Exposure to traffic pollution has been linked to numerous adverse health endpoints. Despite this, limited data examining traffic exposures during realistic commutes and acute response exists. Objectives: We conducted the Atlanta Commuters Exposures (ACE-1) Study, an extensive panel-based exposure and health study, to measure chemically-resolved in-vehicle exposures and corresponding changes in acute oxidative stress, lipid peroxidation, pulmonary and systemic inflammation and autonomic response.
Methods
We recruited 42 adults (21 with and 21 without asthma) to conduct two 2-h scripted highway commutes during morning rush hour in the metropolitan Atlanta area. A suite of in-vehicle particulate components were measured in the subjects’ private vehicles. Biomarker measurements were conducted before, during, and immediately after the commutes and in 3 hourly intervals after commutes.
Results
At measurement time points within 3 h after the commute, we observed mild to pronounced elevations relative to baseline in exhaled nitric oxide, C-reactive-protein, and exhaled malondialdehyde, indicative of pulmonary and systemic inflammation and oxidative stress initiation, as well as decreases relative to baseline levels in the time-domain heart-rate variability parameters, SDNN and rMSSD, indicative of autonomic dysfunction. We did not observe any detectable changes in lung function measurements (FEV1, FVC), the frequency-domain heart-rate variability parameter or other systemic biomarkers of vascular injury. Water soluble organic carbon was associated with changes in eNO at all post-commute time-points (p < 0.0001).
Conclusions
Our results point to measureable changes in pulmonary and autonomic biomarkers following a scripted 2-h highway commute.
Background: Mechanisms underlying the effects of traffic-related air pollution on people with asthma remain largely unknown, despite the abundance of observational and controlled studies reporting associations between traffic sources and asthma exacerbation and hospitalizations.
Objectives: To identify molecular pathways perturbed following traffic pollution exposures, we analyzed data as part of the Atlanta Commuters Exposure (ACE-2) study, a crossover panel of commuters with and without asthma.
Methods: We measured 27 air pollutants and conducted high-resolution metabolomics profiling on blood samples from 45 commuters before and after each exposure session. We evaluated metabolite and metabolic pathway perturbations using an untargeted metabolome-wide association study framework with pathway analyses and chemical annotation.
Results: Most of the measured pollutants were elevated in highway commutes (p < 0.05). From both negative and positive ionization modes, 17,586 and 9087 metabolic features were extracted from plasma, respectively. 494 and 220 unique features were associated with at least 3 of the 27 exposures, respectively (p < 0.05), after controlling confounders and false discovery rates. Pathway analysis indicated alteration of several inflammatory and oxidative stress related metabolic pathways, including leukotriene, vitamin E, cytochrome P450, and tryptophan metabolism. We identified and annotated 45 unique metabolites enriched in these pathways, including arginine, histidine, and methionine. Most of these metabolites were not only associated with multiple pollutants, but also differentially expressed between participants with and without asthma. The analysis indicated that these metabolites collectively participated in an interrelated molecular network centering on arginine metabolism, underlying the impact of traffic-related pollutants on individuals with asthma.
Conclusions: We detected numerous significant metabolic perturbations associated with in-vehicle exposures during commuting and validated metabolites that were closely linked to several inflammatory and redox pathways, elucidating the potential molecular mechanisms of traffic-related air pollution toxicity. These results support future studies of metabolic markers of traffic exposures and the corresponding molecular mechanisms.
Epidemiological studies have been critical for estimating associations between exposure to ambient particulate matter (PM) air pollution and adverse health outcomes. Because total PM mass is a temporally and spatially varying mixture of constituents with different physical and chemical properties, recent epidemiological studies have focused on PM constituents. Most studies have estimated associations between PM constituents and health using the same statistical methods as in studies of PM mass. However, these approaches may not be sufficient to address challenges specific to studies of PM constituents, namely assigning exposure, disentangling health effects, and handling measurement error. We reviewed large, population-based epidemiological studies of PM constituents and health and describe the statistical methods typically applied to address these challenges. Development of statistical methods that simultaneously address multiple challenges, for example, both disentangling health effects and handling measurement error, could improve estimation of associations between PM constituents and adverse health outcomes.
Background: The novel human coronavirus disease 2019 (COVID-19) pandemic has claimed more than 600,000 lives worldwide, causing tremendous public health, social, and economic damages. Although the risk factors of COVID-19 are still under investigation, environmental factors, such as urban air pollution, may play an important role in increasing population susceptibility to COVID-19 pathogenesis. Methods: We conducted a cross-sectional nationwide study using zero-inflated negative binomial models to estimate the association between long-term (2010–2016) county-level exposures to NO2, PM2.5, and O3 and county-level COVID-19 case-fatality and mortality rates in the United States. We used both single- and multi-pollutant models and controlled for spatial trends and a comprehensive set of potential confounders, including state-level test positive rate, county-level health care capacity, phase of epidemic, population mobility, population density, sociodemographics, socioeconomic status, race and ethnicity, behavioral risk factors, and meteorology. Results: From January 22, 2020, to July 17, 2020, 3,659,828 COVID-19 cases and 138,552 deaths were reported in 3,076 US counties, with an overall observed case-fatality rate of 3.8%. County-level average NO2 concentrations were positively associated with both COVID-19 case-fatality rate and mortality rate in single-, bi-, and tri-pollutant models. When adjusted for co-pollutants, per interquartile-range (IQR) increase in NO2 (4.6 ppb), COVID-19 case-fatality rate and mortality rate were associated with an increase of 11.3% (95% CI 4.9%–18.2%) and 16.2% (95% CI 8.7%–24.0%), respectively. We did not observe significant associations between COVID-19 case-fatality rate and long-term exposure to PM2.5 or O3, although per IQR increase in PM2.5 (2.6 μg/m3) was marginally associated, with a 14.9% (95% CI 0.0%–31.9%) increase in COVID-19 mortality rate when adjusted for co-pollutants. Discussion: Long-term exposure to NO2, which largely arises from urban combustion sources such as traffic, may enhance susceptibility to severe COVID-19 outcomes, independent of long-term PM2.5 and O3 exposure. The results support targeted public health actions to protect residents from COVID-19 in heavily polluted regions with historically high NO2 levels. Continuation of current efforts to lower traffic emissions and ambient air pollution may be an important component of reducing population-level risk of COVID-19 case fatality and mortality.