Pro-inflammatory effects of Dunkerque city air pollution particulate matter 2.5 in human epithelial lung cells (L132) in culture
Abstract
Exposure to urban airborne particulate matter (PM) has been associated with adverse health effects. The majority of research articles published on air pollution PM relate to PM10. However, increasing emphasis and stringent regulations have been placed on PM2.5. The mechanisms for PM-induced adverse health effects are not well understood, but inflammation seems to be of importance. We focused our attention also on the capacity of air pollution PM2.5 to induce cytotoxic and inflammatory responses in human epithelial lung cells (L132) in culture. Particulate matter was collected in Dunkerque, a French seaside city characterized by the proximity of industrial activity and heavy motor vehicle traffic. Size distribution results showed that the cumulative frequency of PM2.5 was 92.15% and their specific surface area was 1 m2 g(-1). Inorganic and organic chemicals usually associated with the natural environment but also so-called anthropogenic elements were found in PM, suggesting that much of the PM was derived from wind-borne dust from the industrial complex and the heavy diesel motor vehicle. We observed PM concentration-dependent cytotoxic effects in L132 cells (LC10 = 18.84 microg PM ml(-1); LC50 = 75.36 microg PM ml(-1)). We showed that exposure to Dunkerque City's PM2.5 induced significant increases (in a concentration- and time-dependent manner) in protein secretion and/or gene expression of inflammatory cytokines (i.e. TNF-alpha, IL-1beta, IL-8, GM-CSF, IL-6, TGF-beta1). We hypothesized also that the occurrence of the acute inflammatory response might rely on the capacity of such air pollutants to generate oxidative species, which have been implicated in the stringent regulation of the cytokine network. Hence, we suggest that the development of inflammatory effects that worsen over time stems from the cytotoxicity in Dunkerque City's PM2.5-exposed L132 cells in culture.
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PM2.5 can produce oxidative stress, in part because of lung inflammation.
“Subjects who develop COPD, an important cause of respiratory mortality, may have weakened antioxidant defenses (Rahman et al. 1996), and PM2.5 can produce oxidative stress, in part because of lung inflammation (Dagher et al. 2005; Zeka et al. 2006).”
From Differentiating the effects of fine and coarse particles on daily mortality in Shanghai, China (2007) · cites this paper as Dagher et al. 2005
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- Authors
- Dagher, Z., Garçon, G., Gosset, P., Ledoux, F., Surpateanu, G., Courcot, D., Aboukais, A., Puskaric, E., & Shirali, P.
- Affiliations
- Groupe Hospitalier de l'Institut Catholique de Lille (FR)
- Corresponding author
- Shirali, Pirouz
- Venue
- Journal of Applied Toxicology
- Publisher
- Wiley
- Published
- 2005-03
- Volume
- 25
- Issue
- 2
- Pages
- 166-175
- ISSN
- 0260-437X (ISSN-L)
- 1099-1263
- OpenAlex
- W2091733516
- Cited by
- 90
- References
- 54
- Citations by year
- 2026: 2 · 2025: 1 · 2023: 4 · 2022: 2 · 2021: 6 · 2020: 7 · 2019: 6 · 2018: 6 · 2017: 7 · 2016: 3 · 2015: 3 · 2014: 5 · 2013: 2 · 2012: 3
- FWCI
- 4.21
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Applied Toxicology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Littoral-Opale Coast
- Franco-British Interreg IIIA European Program
- Regional Council of Nord[sol ]Pas-de-Calais
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
- Physical Sciences › Earth and Planetary Sciences › Atmospheric Science › Atmospheric chemistry and aerosols
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Indoor Air Quality and Microbial Exposure
- Keywords
- PM2.5, urban air pollution, lung epithelial cells, L132 cells, cytotoxicity, inflammatory cytokines, oxidative stress, TNF-α, IL-1β, interleukin-8, GM-CSF, interleukin-6, TGF-β1, particle composition, Dunkirk
- MeSH terms
- Air Pollutants, Air Pollution, Cell Survival, Cells, Cultured, Cities, Culture Media, Epithelial Cells, France, Humans, Inflammation, Particle Size, Gene Expression, Cytokines
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