Microplastics in freshly fallen snow: How may it adversely impact human health and exacerbate the COVID-19 crisis?

Liaquat, Ayesha; Kashif, Aleena; Rathi, Sushma; Raza, Alishba

doi:10.1016/j.amsu.2022.104276

Cited by 4 publications

(1 citation statement)

References 12 publications

(23 reference statements)

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“…Considerable speculation regarding the health impacts of MP inhalation remains (Fiorito et al, 2022;Liaquat et al, 2022;Perera et al, 2023;Yang et al, 2022), with limited compelling in vivo data from humans and animal models. However, an emerging theme from such studies, including the current report, is that MPs can dysregulate and/or promote inflammatory processes in specific disease settings (Chen et al, 2023;Liu et al, 2022;Luo et al, 2022;Rawle et al, 2022;Taş et al, 2023;Yan et al, 2022c).…”

Section: Discussionmentioning

confidence: 99%

Microplastics dysregulate innate immunity in the SARS-CoV-2 infected lung

Bishop,

Yan,

Nguyen

et al. 2023

Preprint

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Global microplastic (MP) pollution is now well recognized, with humans and animals consuming and inhaling MPs on a daily basis. Herein we described the effects of azide-free, 1 µm polystyrene MP beads co-delivered into lungs with a SARS-CoV-2 omicron BA.5 inoculum using a mouse model of mild COVID-19. Lung virus titres and viral RNA levels were not significantly affected by MPs, with overt clinical or histopathological changes also not observed. However, RNA-Seq of infected lungs revealed that MP exposure suppressed innate immune responses at 2 days post infection (dpi) and increased pro-inflammatory signatures at 6 dpi. The cytokine profile at 6 dpi showed a significant correlation with the ‘cytokine release syndrome’ signature seen in some severe COVID-19 patients. This study adds to a growing body of literature suggesting that MPs can dysregulate inflammation in specific disease settings.Graphical AbstractHIGHLIGHTSA single inoculation of microplastics dysregulated SARS-CoV-2 lung inflammationAt the peak of SARS-CoV-2 infection microplastics decreased early innate responsesLater post infection microplastics promoted a “cytokine release syndrome” signatureA key mechanism may involve the inhibition of the phagocytosis of infected cellsAzide-free microplastics were used, with no elevated ROS responses identifiedPostulated mechanisms whereby microplastics might decrease the proinflammatory responses 2 days after SARS-CoV-2 infection, yet promote the proinflammatory ‘cytokine release syndrome’ signature at 6 days post infection.

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