Emissions from plastic incineration induce inflammation, oxidative stress, and impaired bioenergetics in primary human respiratory epithelial cells

Inhalation exposure to plastic incineration emissions (PIEs) is a problem of increasing human relevance, as plastic production and waste creation have drastically increased since mainstream integration during the 20th century. We investigated the effects of PIEs on human nasal epithelial cells (HNEC...

Full description

Saved in:

Bibliographic Details
Published in:	Toxicological sciences Vol. 199; no. 2; pp. 301 - 315
Main Authors:	Rogers, Keith, WaMaina, Elisa, Barber, Andrew, Masood, Syed, Love, Charlotte, Kim, Yong Ho, Gilmour, M Ian, Jaspers, Ilona
Format:	Journal Article
Language:	English
Published:	United States 28-05-2024
Subjects:	Air Pollutants - toxicity Cells, Cultured Cytochrome P-450 CYP1A1 - genetics Cytochrome P-450 CYP1A1 - metabolism Cytochrome P-450 CYP1B1 - genetics Cytochrome P-450 CYP1B1 - metabolism Cytokines - metabolism Energy Metabolism - drug effects Epithelial Cells - drug effects Epithelial Cells - metabolism Female Glutathione - metabolism Humans Incineration Inflammation - chemically induced Inflammation - metabolism Inhalation Exposure - adverse effects Male Mitochondria - drug effects Mitochondria - metabolism Oxidative Stress - drug effects Plastics - toxicity Respiratory Mucosa - drug effects Respiratory Mucosa - metabolism Smoke - adverse effects flaming plastic incineration emissions (PIEs) human nasal epithelial cells (HNECs) smoldering in vitro
Online Access:	Get full text
Tags:	Add Tag No Tags, Be the first to tag this record!

Description
Summary:	Inhalation exposure to plastic incineration emissions (PIEs) is a problem of increasing human relevance, as plastic production and waste creation have drastically increased since mainstream integration during the 20th century. We investigated the effects of PIEs on human nasal epithelial cells (HNECs) to understand if such exposures cause damage and dysfunction to respiratory epithelia. Primary HNECs from male and female donors were cultured at air-liquid interface (ALI), and 16HBE cells were cultured on coverslips. Smoke condensates were generated from incineration of plastic at flaming (640°C) and smoldering (500°C) temperatures, and cells were subsequently exposed to these materials at 5-50 μg/cm2 concentrations. HNECs were assessed for mitochondrial dysfunction and 16HBE cells for glutathione oxidation in real-time analyses. HNEC culture supernatants and total RNA were collected at 4-h postexposure for cytokine and gene expression analysis, and results show that PIEs can acutely induce inflammation, oxidative stress, and mitochondrial dysfunction in HNECs, and that incineration temperature modifies biological responses. Specifically, condensates from flaming and smoldering PIEs significantly increased HNEC secretion of cytokines IL-8, IL-1β, and IL-13, as well as expression of xenobiotic metabolism pathways and genes such as CYP1A1 and CYP1B1 at 5 and 20 μg/cm2 concentrations. Only 50 μg/cm2 flaming PIEs significantly increased glutathione oxidation in 16HBEs, and decreased respiration and ATP production in HNEC mitochondria. Impact Statement: Our data reveal the impact of incineration temperatures on biological outcomes associated with PIE exposures, emphasizing the importance of temperature as a factor when evaluating respiratory disease associated with PIEs exposure.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1096-6080 1096-0929
DOI:	10.1093/toxsci/kfae038