Ship Emissions Weaken Antiviral Defenses

SHIP emissions rich in ultrafine particles triggered lung inflammation and weakened antiviral defenses in laboratory models.

Ship Emissions Contain Metal-Rich Ultrafine Particles

Researchers examined the composition and biological effects of size-separated particulate matter collected from several locations across a busy mixed-use port. Sampling sites represented cruise and container terminals, road freight, metal recycling, research docks, and an urban background location.

Ultrafine particulate matter collected near the cruise terminal during the summer shipping season contained substantially higher concentrations of vanadium, nickel, and cobalt than samples from the background site. The enrichment was most pronounced among particles measuring less than 100 nanometers.

The distribution of these metals, differences between summer and winter samples, wind direction, and the presence of cruise ships at nearby berths indicated that heavy fuel oil combustion was the likely source. Vanadium and nickel are established markers of heavy fuel oil, while cobalt emerged as a possible additional marker of desulfurized fuel combustion.

Ship Emissions Trigger Lung Inflammation

When bronchial epithelial cells were exposed to cruise ship ultrafine particulate matter, they released higher levels of several inflammatory mediators, including interleukin-8, interleukin-6, tumor necrosis factor-alpha, and interleukin-1 beta.

Gene expression analysis identified 925 upregulated genes and 412 downregulated genes following exposure. The changes indicated activation of broad inflammatory pathways, including tumor necrosis factor signaling through nuclear factor kappa B.

At the same time, ship emissions suppressed genes involved in innate antiviral defenses. Responses associated with interferon-alpha and interferon-gamma signaling were reduced, suggesting that exposed respiratory cells could become less capable of controlling respiratory infections.

Vanadium Facilitates Viral Replication

Vanadium reproduced key effects of the cruise ship particles, including inflammatory signaling and suppression of interferon-stimulated genes. Nickel and cobalt did not produce comparable responses.

In primary bronchial epithelial cells, vanadium exposure increased replication of human rhinovirus-16. Separate experiments also showed a concentration-dependent increase in SARS-CoV-2 replication, reaching almost five times the level observed in virus-only controls.

The findings were generated in cell-based models using particulate matter concentrations considerably higher than expected real-world lung deposition. The results therefore demonstrate biological plausibility rather than directly measuring clinical outcomes or population-level risk.

Nevertheless, the simultaneous induction of inflammation and impairment of antiviral defenses suggests that metal-rich ultrafine ship emissions may have disproportionate respiratory effects. Further research is needed to characterize acute and chronic exposure among populations living near ports and heavily traveled shipping routes.

Reference
Easton NHC et al. Ultrafine particulate matter emitted from ships drives inflammation and susceptibility to viral infection. Environ Int. 2026;214:110381.

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