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Ultrafine particulate matter emitted from ships drives inflammation and susceptibility to viral infection

ABSTRACT: Exposure to ambient airborne particulate matter (PM) has been associated with almost 9 million premature deaths per year worldwide. Ports are essential infrastructure for trade and transport, with over 80% of the world’s international trade volume travelling by sea, yet there is little understanding of the potential health effects of PM from ships. Here, we studied the elemental and toxicological characteristics of size-fractionated PM collected at different areas of a busy European mixed-use port. We found that unregulated ultrafine PM, a PM size fraction <100 nm in aerodynamic diameter, originating from a cruise-ship source, was highly enriched compared to ultrafine PM from other sites in tracers of heavy fuel oil combustion (V and Ni), with Co identified as a novel tracer. In cell models of airway and alveolar epithelium, this cruise ship-associated ultrafine PM was markedly more pro-inflammatory than PM from other sites, while simultaneously reducing expression of a range of genes associated with the innate antiviral response. Investigation of the effects of the three metals found to be enriched in our cruise-ship ultrafine PM showed that these effects could be reproduced by vanadium exposure, which reduced interferon signalling and increased permissiveness to viral infection, facilitating replication of the respiratory viruses rhinovirus-16 and SARS-CoV-2. Our findings suggest that, despite a series of regulations introduced over the last 20 years, cruise ship-associated emissions of PM from heavy fuel oil combustion may exert disproportionate effects on health compared to PM from other sources. In particular, the effects manifest themselves through induction of a response with characteristics of a poor viral infection prognosis. More broadly, current regulations, which neglect PM source- and composition-related variations, and ultrafine PM in general, may need strengthening to better mitigate health effects resulting from exposure to PM.

ORGANISM(S): Homo sapiens

PROVIDER: GSE336628 | GEO | 2026/06/30

REPOSITORIES: GEO

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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.

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Ultrafine particulate matter emitted from ships drives inflammation and susceptibility to viral infection

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