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Machine learning reveals that prolonged exposure to air pollution is associated with SARS-CoV-2 mortality and infectivity in Italy.

ABSTRACT: Air pollution can increase the risk of respiratory diseases, enhancing the susceptibility to viral and bacterial infections. Some studies suggest that small air particles facilitate the spread of viruses and also of the new coronavirus, besides the direct person-to-person contagion. However, the effects of the exposure to particulate matter and other contaminants on SARS-CoV-2 has been poorly explored. Here we examined the possible reasons why the new coronavirus differently impacted on Italian regional and provincial populations. With the help of artificial intelligence, we studied the importance of air pollution for mortality and positivity rates of the SARS-CoV-2 outbreak in Italy. We discovered that among several environmental, health, and socio-economic factors, air pollution and fine particulate matter (PM2.5), as its main component, resulted as the most important predictors of SARS-CoV-2 effects. We also found that the emissions from industries, farms, and road traffic - in order of importance - might be responsible for more than 70% of the deaths associated with SARS-CoV-2 nationwide. Given the major contribution played by air pollution (much more important than other health and socio-economic factors, as we discovered), we projected that, with an increase of 5-10% in air pollution, similar future pathogens may inflate the epidemic toll of Italy by 21-32% additional cases, whose 19-28% more positives and 4-14% more deaths. Our findings, demonstrating that fine-particulate (PM2.5) pollutant level is the most important factor to predict SARS-CoV-2 effects that would worsen even with a slight decrease of air quality, highlight that the imperative of productivity before health and environmental protection is, indeed, a short-term/small-minded resolution.

SUBMITTER: Cazzolla Gatti R

PROVIDER: S-EPMC7442434 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature

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Machine learning reveals that prolonged exposure to air pollution is associated with SARS-CoV-2 mortality and infectivity in Italy.

Cazzolla Gatti Roberto R Velichevskaya Alena A Tateo Andrea A Amoroso Nicola N Monaco Alfonso A

Environmental pollution (Barking, Essex : 1987) 20200821

Air pollution can increase the risk of respiratory diseases, enhancing the susceptibility to viral and bacterial infections. Some studies suggest that small air particles facilitate the spread of viruses and also of the new coronavirus, besides the direct person-to-person contagion. However, the effects of the exposure to particulate matter and other contaminants on SARS-CoV-2 has been poorly explored. Here we examined the possible reasons why the new coronavirus differently impacted on Italian ...[more]

PMID: 32882464

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Project description:Zinc (Zn) is a major elemental component of respirable ambient particulate matter (PM) detected often at alarming levels in urban air. Exposure to PM has been widely associated with increased cardiovascular morbidity and mortality, however, it is not known what components or sources of PM are causative. We recently demonstrated that long-term episodic inhalation of combustion PM, having similar amount of Zn found in urban PM, caused myocardial lesions in rats. We further demonstrated that a single pulmonary exposure to Zn at high concentration is associated with disturbances in cardiac mitochondrial function, ion channel regulation, calcium homeostasis, and cell signaling. Therefore, in this study we investigated the role of PM-associated Zn in cardiac injury using multiple exposure scenarios. Male Wistar-Kyoto (WKY) rats of 12-14 wks age were intratracheally exposed (once per wk x 8 or16 wks) to either (1) saline (control); (2) PM having no soluble Zn; (3) combustion PM suspension containing 14.5 ug/mg water-soluble Zn at high and (4) low dose levels, (5) the aqueous fraction of this suspension devoid of solid insoluble particulate fraction (14.5 ug/mg soluble Zn), or (6) Zn sulfate. Zn concentrations were identical in groups 3, 5 and 6. Pulmonary toxicity was apparent in all exposure groups when compared to saline as determined by recovery of cells in bronchoalveolar lavage fluid. Long-term exposure to PM with or without soluble Zn, or Zn sulfate caused distinct myocardial lesions characterized by subepicardial and randomly distributed myocardial inflammation, degeneration, and fibrosis. The lesion severity was higher in those groups receiving Zn PM. Because cardiac mitochondria are likely the primary target of inhaled metal or other absorbed PM components, we analyzed mitochondrial DNA damage using QPCR and found that all exposure groups except those exposed to PM without Zn caused variable degree of damage. Aconitase activity, sensitive to inhibition by oxidative stress was inhibited slightly but significantly in rats receiving zinc sulfate. Although modest, microarray (Affymetrix) analysis revealed expression changes in the heart reflective of effects on cell signaling, inflammation/oxidative stress, mitochondrial fatty acid metabolisms and cell cycle regulation in rats exposed to zinc sulfate. However, these changes were minimal following exposure to PM devoid of soluble metals. We demonstrate that episodic subchronic pulmonary exposure to zinc sulfate causes cardiac injury and mitochondrial DNA damage. Thus, water-soluble PM-associated zinc may be one of the PM components responsible for cardiovascular morbidity. Experiment Overall Design: Group 1 received Saline to serve as a control. Group 2 received Mount St. Helenâs ash, which does not contain any water-soluble zinc or other metals such that we can delineate any cardiac effect secondary to pulmonary deposition of these particles as these fine mode particles themselves are not likely to translocate to the heart. Group 3 received whole saline suspension of the same fugitive oil combustion particle sample used in the previous study, which contained insoluble components plus water-soluble zinc (Kodavanti et al., 2003; 14.5 ug/mg zinc) and also a small amount of water-soluble nickel (3.0 Âµg/mg). Elemental composition of this PM is comparable to Ottawa urban PM (Kodavanti et al., 2003). Group 4 also received same particle sample but at half the dose than group 3. Group 5 received saline-soluble or leachable fraction of PM-HD devoid of any solid material but contained soluble components including zinc and nickel. And, group 6 received zinc sulfate at concentration that was present in groups 3 or 5. This design allowed us to test if cardiac injury in rats was due to leached of zinc or solid particles. There were 4 replicates per treatment group.

Project description:Zinc (Zn) is a major elemental component of respirable ambient particulate matter (PM) detected often at alarming levels in urban air. Exposure to PM has been widely associated with increased cardiovascular morbidity and mortality, however, it is not known what components or sources of PM are causative. We recently demonstrated that long-term episodic inhalation of combustion PM, having similar amount of Zn found in urban PM, caused myocardial lesions in rats. We further demonstrated that a single pulmonary exposure to Zn at high concentration is associated with disturbances in cardiac mitochondrial function, ion channel regulation, calcium homeostasis, and cell signaling. Therefore, in this study we investigated the role of PM-associated Zn in cardiac injury using multiple exposure scenarios. Male Wistar-Kyoto (WKY) rats of 12-14 wks age were intratracheally exposed (once per wk x 8 or16 wks) to either (1) saline (control); (2) PM having no soluble Zn; (3) combustion PM suspension containing 14.5 ug/mg water-soluble Zn at high and (4) low dose levels, (5) the aqueous fraction of this suspension devoid of solid insoluble particulate fraction (14.5 ug/mg soluble Zn), or (6) Zn sulfate. Zn concentrations were identical in groups 3, 5 and 6. Pulmonary toxicity was apparent in all exposure groups when compared to saline as determined by recovery of cells in bronchoalveolar lavage fluid. Long-term exposure to PM with or without soluble Zn, or Zn sulfate caused distinct myocardial lesions characterized by subepicardial and randomly distributed myocardial inflammation, degeneration, and fibrosis. The lesion severity was higher in those groups receiving Zn PM. Because cardiac mitochondria are likely the primary target of inhaled metal or other absorbed PM components, we analyzed mitochondrial DNA damage using QPCR and found that all exposure groups except those exposed to PM without Zn caused variable degree of damage. Aconitase activity, sensitive to inhibition by oxidative stress was inhibited slightly but significantly in rats receiving zinc sulfate. Although modest, microarray (Affymetrix) analysis revealed expression changes in the heart reflective of effects on cell signaling, inflammation/oxidative stress, mitochondrial fatty acid metabolisms and cell cycle regulation in rats exposed to zinc sulfate. However, these changes were minimal following exposure to PM devoid of soluble metals. We demonstrate that episodic subchronic pulmonary exposure to zinc sulfate causes cardiac injury and mitochondrial DNA damage. Thus, water-soluble PM-associated zinc may be one of the PM components responsible for cardiovascular morbidity. Keywords: Pulmonary exposure, Cardiac gene expression

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Machine learning reveals that prolonged exposure to air pollution is associated with SARS-CoV-2 mortality and infectivity in Italy.

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Machine learning reveals that prolonged exposure to air pollution is associated with SARS-CoV-2 mortality and infectivity in Italy.

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