# Particulate matter exposure potentiates SARS-CoV-2 delta variant infection by suppressing epithelial antiviral responses

## TL;DR

Exposure to coarse particulate matter may worsen Delta variant SARS-CoV-2 infections by weakening the body's antiviral defenses in lung cells.

## Contribution

This study reveals a novel mechanism by which PM10 enhances Delta variant infection through suppressed antiviral responses.

## Key findings

- PM10 increased Delta variant infection by 13.7% and viral titers by 2.6-fold in Calu-3 cells.
- PM10 suppressed apoptosis and reduced pro-inflammatory cytokines like IFN-γ, IP-10, and TNF-α during Delta infection.
- The effect was specific to the Delta variant and not due to changes in ACE2 receptor expression or viral entry.

## Abstract

Airborne particulate matter (PM), particularly fine (PM2.5) and coarse (PM10) particles, is a major environmental health concern linked to increased respiratory morbidity and mortality. During the COVID-19 pandemic, epidemiological studies suggested that PM exposure may worsen SARS-CoV-2 infection outcomes; however, cellular mechanisms underlying this association remain incompletely understood. Here, we investigated how pre-exposure to PM2.5 and PM10 impacts SARS-CoV-2 infection dynamics in Calu-3 human epithelial cells.

Calu-3 cells were pre-exposed to PM for 72 h prior to infection with either the wild-type Wuhan strain or the more virulent Delta variant for additional 48 h. Viral infection, receptor expression, apoptosis and cytokine responses were assessed.

PM10, but not PM2.5, enhanced Delta variant infection, increasing the proportion of infected cells by 13.7% and viral titers by 2.6-fold compared with controls. This enhancement was not attributable to changes in ACE2 receptor expression or viral entry efficiency but instead impaired antiviral defenses. PM10 pre-exposure suppressed apoptosis and reduced the expression of pro-inflammatory cytokines including IFN-γ, IP-10, and TNF-α during Delta infection.

These findings suggest that PM10 compromise epithelial antiviral response by dampening apoptotic cell clearance and inflammatory responses, thereby creating a cellular condition more permissive to viral replication. Our study provides a mechanistic basis by which particulate air pollution may amplify SARS-CoV-2 pathogenicity in a variant-specific manner. These results underscore further validation in physiologically relevant systems and highlight the potential public health implications of air pollution during viral pandemics.