Exposing the Airway Surface to the Neonicotinoid Clothianidin Alters the Electrophysiological Properties of Human Airway Epithelia

TL;DR

Exposure to the insecticide clothianidin through the airway reduces the function of sodium channels in human airway cells, potentially affecting respiratory health.

Contribution

This study demonstrates that inhalation of clothianidin alters ion transport in human airway epithelia, highlighting a new route of exposure and potential health risk.

Findings

Acute exposure to clothianidin at 50 ppm or higher reduces sodium channel activity in airway epithelia.

Clothianidin exposure increases epithelial permeability without causing cell death, indicating compromised barrier integrity.

Abstract

The neonicotinoid
clothianidin is used indoors and outdoors
as
an insecticide and extensively as a seed coating in agriculture where
working solutions are prepared at 4000 ppm. Health effects of clothianidin
are often studied under the assumption that ingestion is the exposure
route, yet inhalation exposures are likely, given that clothianidin
is sprayed and dust is resuspended. We studied the effect of airway
exposure to clothianidin using human donor epithelia. Acute clothianidin
doses greater than 50 ppm applied to the apical (airway-facing) surface
resulted in decreased ion transport properties, specifically, decreased
activity of the surface sodium channel, ENaC. During a 6 h 500 ppm
clothianidin exposure, the permeability of airway epithelia to clothianidin
rose from ∼4.2 × 10–6 to ∼13.5
× 10–6 cm·s–1 without
an increase in cell death, indicating a loss of barrier integrity.
Respiratory precautions should be considered for those in proximity
to aerosol-generating clothianidin application.

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