Dataset Information

Ambient PM_2.5 exposure and rapid spread of COVID-19 in the United States.

ABSTRACT: It has been posited that populations being exposed to long-term air pollution are more susceptible to COVID-19. Evidence is emerging that long-term exposure to ambient PM_2.5 (particulate matter with aerodynamic diameter 2.5 ?m or less) associates with higher COVID-19 mortality rates, but whether it also associates with the speed at which the disease is capable of spreading in a population is unknown. Here, we establish the association between long-term exposure to ambient PM_2.5 in the United States (US) and COVID-19 basic reproduction ratio R₀- a dimensionless epidemic measure of the rapidity of disease spread through a population. We inferred state-level R₀ values using a state-of-the-art susceptible, exposed, infected, and recovered (SEIR) model initialized with COVID-19 epidemiological data corresponding to the period March 2-April 30. This period was characterized by a rapid surge in COVID-19 cases across the US states, implementation of strict social distancing measures, and a significant drop in outdoor air pollution. We find that an increase of 1 ?g/m³ in PM_2.5 levels below current national ambient air quality standards associates with an increase of 0.25 in R₀ (95% CI: 0.048-0.447). A 10% increase in secondary inorganic composition, sulfate-nitrate-ammonium, in PM_2.5 associates with ?10% increase in R₀ by 0.22 (95% CI: 0.083-0.352), and presence of black carbon (soot) in the ambient environment moderates this relationship. We considered several potential confounding factors in our analysis, including gaseous air pollutants and socio-economical and meteorological conditions. Our results underscore two policy implications - first, regulatory standards need to be better guided by exploring the concentration-response relationships near the lower end of the PM_2.5 air quality distribution; and second, pollution regulations need to be continually enforced for combustion emissions that largely determine secondary inorganic aerosol formation.

SUBMITTER: Chakrabarty RK

PROVIDER: S-EPMC7651233 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Ambient PM2.5 exposure and rapid spread of COVID-19 in the United States.

Chakrabarty Rajan K RK Beeler Payton P Liu Pai P Goswami Spondita S Harvey Richard D RD Pervez Shamsh S van Donkelaar Aaron A Martin Randall V RV

The Science of the total environment 20201109

It has been posited that populations being exposed to long-term air pollution are more susceptible to COVID-19. Evidence is emerging that long-term exposure to ambient PM2.5 (particulate matter with aerodynamic diameter 2.5 μm or less) associates with higher COVID-19 mortality rates, but whether it also associates with the speed at which the disease is capable of spreading in a population is unknown. Here, we establish the association between long-term exposure to ambient PM2.5</ ...[more]

PMID: 33250247

Similar Datasets

Project description:BackgroundStudies suggested that PM2.5 exposure could lead to adverse reproductive effects on male animals. However, the underlying mechanism is still not clear. Besides, animals in the majority of previous studies were exposed to PM2.5 through intratracheal instillation which should be improved. In addition, limited amount of research has been conducted in China where the PM2.5 concentration is higher and the PM2.5 components are different. The aim of this work is to explore the effects of concentrated ambient PM2.5 (CAP) on mice sperm quality and testosterone biosynthesis.MethodsA total of 12 male C57BL/6 mice were exposed to filtered air (FA) or CAP for 125 days using the Shanghai Meteorological and Environmental Animal Exposure System. The mice sperm concentration, sperm motility, DNA fragmentation index, high DNA stainability and plasma testosterone were analyzed. Testicular histology and sperm morphology were observed through optical microscope. Testosterone biosynthesis related gene expressions were analyzed using real-time PCR, including cytochrome P450 CHOL side-chain cleavage enzyme (P450scc), steroidogenic acute regulatory protein (StAR), 3β-hydroxysteroid dehydrogenase (3β HSD), 17β-hydroxysteroid dehydrogenase, cytochrome P450 aromatase (P450arom), estrogen receptor (ER), androgen receptor (AR) and follicle stimulating hormone receptor (FSHR).ResultsExposure to CAP resulted in disturbance of various stages of spermatogenesis and significant higher percentage of abnormal sperm (FA vs. CAP: 24.37% vs. 44.83%) in mice testis. CAP exposure significantly decreased sperm concentration (43.00 × 106 vs. 25.33 × 106) and motility (PR: 63.58% vs. 55.15%; PR + NP: 84.00% vs. 77.08%) in epididymis. Plasma testosterone concentration were significantly declined (0.28 ng/ml vs. 0.69 ng/ml) under CAP exposure. Notably, the levels of testosterone biosynthesis related genes, StAR, P450scc, P450arom, ER and FSHR were significantly decreased with CAP exposure.ConclusionConcentrated ambient PM2.5 exposure altered mice sperm concentration, motility and morphology, which might be mediated primarily by the decline in testosterone concentration and testosterone biosynthesis process.

Project description:BackgroundThe metabolomic signatures of short- and long-term exposure to PM2.5 have been reported and linked to inflammation and oxidative stress. However, little is known about the relative contribution of the specific PM2.5 species (hence sources) that drive these metabolomic signatures.ObjectivesWe aimed to determine the relative contribution of the different species of PM2.5 exposure to the perturbed metabolic pathways related to changes in the plasma metabolome.MethodsWe performed mass-spectrometry based metabolomic profiling of plasma samples among men from the Normative Aging Study to identify metabolic pathways associated with PM2.5 species. The exposure windows included short-term (one, seven-, and thirty-day moving average) and long-term (one year moving average). We used linear mixed-effect regression with subject-specific intercepts while simultaneously adjusting for PM2.5, NO2, O3, temperature, relative humidity, and covariates and correcting for multiple testing. We also used independent component analysis (ICA) to examine the relative contribution of patterns of PM2.5 species.ResultsBetween 2000 and 2016, 456 men provided 648 blood samples, in which 1158 metabolites were quantified. We chose 305 metabolites for the short-term and 288 metabolites for the long-term exposure in this analysis that were significantly associated (p-value < 0.01) with PM2.5 to include in our PM2.5 species analysis. On average, men were 75.0 years old and their body mass index was 27.7 kg/m2. Only 3% were current smokers. In the adjusted models, ultrafine particles (UFPs) were the most significant species of short-term PM2.5 exposure followed by nickel, vanadium, potassium, silicon, and aluminum. Black carbon, vanadium, zinc, nickel, iron, copper, and selenium were the significant species of long-term PM2.5 exposure. We identified several metabolic pathways perturbed with PM2.5 species including glycerophospholipid, sphingolipid, and glutathione. These pathways are involved in inflammation, oxidative stress, immunity, and nucleic acid damage and repair. Results were overlapped with the ICA.ConclusionsWe identified several significant perturbed plasma metabolites and metabolic pathways associated with exposure to PM2.5 species. These species are associated with traffic, fuel oil, and wood smoke. This is the largest study to report a metabolomic signature of PM2.5 species' exposure and the first to use ICA.

Dataset Information

Ambient PM_2.5 exposure and rapid spread of COVID-19 in the United States.

Publications

Ambient PM<sub>2.5</sub> exposure and rapid spread of COVID-19 in the United States.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets