Impact of Long-Term Exposures to Ambient PM2.5 and Ozone on ARDS Risk for Older Adults in the United States

Rhee, Jongeun; Dominici, Francesca; Zanobetti, Antonella; Schwartz, Joel; Wang, Yun; Di, Qian; Balmes, John R.; Christiani, David C.

doi:10.1016/j.chest.2019.03.017

Cited by 56 publications

(37 citation statements)

References 37 publications

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“…It has been associated with increased respiratory morbidity and mortality ( Liu et al, 2019 ), especially in susceptible people, due to cardiorespiratory events, including asthma, chronic obstructive pulmonary disease, and thrombosis ( Li et al, 2008 ; Rhee et al, 2019 ). In vitro and in vivo studies highlighted its role in the exacerbation of respiratory viral infections ( Becker and Soukup, 1999 ).…”

Section: Particulate Matter and Covid-19mentioning

confidence: 99%

The role of air pollution (PM and NO2) in COVID-19 spread and lethality: A systematic review

Copat

Cristaldi

Fiore

et al. 2020

Environmental Research

312

240

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A new coronavirus (SARS-CoV-2) has determined a pneumonia outbreak in China (Wuhan, Hubei Province) in December 2019, called COVID-19 disease. In addition to the person-to person transmission dynamic of the novel respiratory virus, it has been recently studied the role of environmental factors in accelerate SARS-CoV-2 spread and its lethality. The time being, air pollution has been identified as the largest environmental cause of disease and premature death in the world. It affects body's immunity, making people more vulnerable to pathogens. The hypothesis that air pollution, resulting from a combination of factors such as meteorological data, level of industrialization as well as regional topography, can acts both as a carrier of the infection and as a worsening factor of the health impact of COVID-19 disease, has been raised recently. With this review, we want to provide an update state of art relating the role of air pollution, in particular PM 2.5 , PM 10 and NO 2 , in COVID-19 spread and lethality. The Authors, who first investigated this association, often used different research methods or not all include confounding factors whenever possible. In addition, to date incidence data are underestimated in all countries and to a lesser extent also mortality data. For this reason, the cases included in the reviewed studies cannot be considered conclusive. Although it determines important limitations for direct comparison of results, and more studies are needed to strengthen scientific evidences and support firm conclusions, major findings are consistent, highlighting the important contribution of PM 2.5 and NO 2 as triggering of the COVID-19 spread and lethality, and with a less extent also PM 10 , although the potential effect of airborne virus exposure it has not been still demonstrated.

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Section: Particulate Matter and Covid-19mentioning

confidence: 99%

The role of air pollution (PM and NO2) in COVID-19 spread and lethality: A systematic review

Copat

Cristaldi

Fiore

et al. 2020

Environmental Research

312

240

View full text Add to dashboard Cite

show abstract

“…In particular, the observed aberrant inflammatory response-the so-called "cytokine storm" -occurring during COVID-19 infection is still not clear. In this uncertainty, chronic exposure to particulate matter (PM), ozone, and other pollutants is known to affect respiratory function, and recently, environmental pollution has been associated to ARDS (8)(9)(10)(11), which is one of the features of SARS-CoV-2 infection. Furthermore, environmental pollution, mostly PM, is 2 Available online at: https://www.istat.it/it/commercio-estero?comunicati.…”

Section: Air Pollution and Covid-19: The Italian Experiencementioning

confidence: 99%

The “Elderly” Lesson in a “Stressful” Life: Italian Holistic Approach to Increase COVID-19 Prevention and Awareness

et al. 2020

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It's a frightening time due to COVID-19, but the great elderly/centenarians, apparently with more frailty, seem to have a better response to the pandemic. "The South Italy" lifestyle seems an "effective strategy" promoting the well-being embedded in a holistic solution: healthy diet, less exposure to PM10 pollution, protected environment, and moderate physical activity. The European FP7 Project RISTOMED results, since 2010, have shown that dietary intervention improved a heathy status in the elderly people. Based on the RISTOMED results, in addition to sociocultural and environmental factors, the authors suggest an integrated approach for resilience to COVID-19. Such an approach during the next months could make the difference for the success of any government progress policy to fight COVID-19, finalizing long-term well-being and successful aging.

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“…Lin H. et al has reported that short-term exposures to PM might be important triggers of ARDS in China [ 5 ]. Furthermore, Rhee J. et al has demonstrated that long-term exposures to ambient PM 2.5 and ozone increased ARDS risk for older adults in the United States [ 6 ]. To date, it has reported that exposures to air pollutant are associated with increased risk of ARDS [ 4 , 5 , 6 , 7 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, Rhee J. et al has demonstrated that long-term exposures to ambient PM 2.5 and ozone increased ARDS risk for older adults in the United States [ 6 ]. To date, it has reported that exposures to air pollutant are associated with increased risk of ARDS [ 4 , 5 , 6 , 7 , 8 ]. In addition, in an in vivo toxicological study, it was found that exposure to PM 2.5 including DEP increases susceptibility to lung infection by inducing dysfunction of immune cells [ 9 , 10 , 11 ].…”

Section: Introductionmentioning

confidence: 99%

Diesel Exhaust Particulates Enhances Susceptibility of LPS-Induced Acute Lung Injury through Upregulation of the IL-17 Cytokine-Derived TGF-β1/Collagen I Expression and Activation of NLRP3 Inflammasome Signaling in Mice

2021

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Diesel exhaust particulates (DEP) adversely affect the respiratory system and exacerbate lung diseases, resulting in high mortality rates. However, its pathogenesis is complicated, and the mechanisms involved are incompletely understood. We investigated the effects of DEP pre-exposure on lipopolysaccharide (LPS)-induced acute lung injury (ALI) and identified the roles of interleukin (IL)-17 in mice. Mice were divided into vehicle control, DEP, LPS, and DEP pre-exposed and LPS-instilled groups. Pre-exposure to DEP enhanced the number of total cells, neutrophils, and lymphocytes in the BAL fluid of LPS-instilled mice. Pre-exposure to DEP synergistically exacerbated pulmonary acute lung inflammation and granulomatous inflammation/pulmonary fibrosis, concomitant with the enhanced expression of inflammatory cytokines in the BAL fluid and of collagen I and TGF-β1 in the lungs of LPS-instilled mice. The number of TGF-β1-positive cells in the DEP pre-exposed and LPS-instilled group was higher than that in the LPS group. The expression of NLR family pyrin domain containing 3 (NLRP3) inflammasome components was markedly increased in the DEP pre-exposed and LPS-instilled group. IL-17 levels in the BAL fluid and IL-17-positive cells in the lungs were significantly increased by pre-exposure to DEP in the LPS-induced group compared to that in the DEP or LPS group. These results suggest that DEP predominantly contributes to fibrotic lung disease in LPS-related acute lung injury by upregulating IL-17 cytokine-mediated collagen I and TGF-β1 and, at least in part, by activating LPS-induced NLRP3 inflammasome signaling. The study should be useful in devising better strategies for prevention and management of ALI.

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Impact of Long-Term Exposures to Ambient PM2.5 and Ozone on ARDS Risk for Older Adults in the United States

Cited by 56 publications

References 37 publications

The role of air pollution (PM and NO2) in COVID-19 spread and lethality: A systematic review

The role of air pollution (PM and NO2) in COVID-19 spread and lethality: A systematic review

The “Elderly” Lesson in a “Stressful” Life: Italian Holistic Approach to Increase COVID-19 Prevention and Awareness

Diesel Exhaust Particulates Enhances Susceptibility of LPS-Induced Acute Lung Injury through Upregulation of the IL-17 Cytokine-Derived TGF-β1/Collagen I Expression and Activation of NLRP3 Inflammasome Signaling in Mice

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