Ultrafine particulate pollutants induce oxidative stress and mitochondrial damage
Open accessAbstract
The objectives of this study were to determine whether differences in the size and composition of coarse (2.5-10 micro m), fine (< 2.5 microm), and ultrafine (< 0.1 microm) particulate matter (PM) are related to their uptake in macrophages and epithelial cells and their ability to induce oxidative stress. The premise for this study is the increasing awareness that various PM components induce pulmonary inflammation through the generation of oxidative stress. Coarse, fine, and ultrafine particles (UFPs) were collected by ambient particle concentrators in the Los Angeles basin in California and used to study their chemical composition in parallel with assays for generation of reactive oxygen species (ROS) and ability to induce oxidative stress in macrophages and epithelial cells. UFPs were most potent toward inducing cellular heme oxygenase-1 (HO-1) expression and depleting intracellular glutathione. HO-1 expression, a sensitive marker for oxidative stress, is directly correlated with the high organic carbon and polycyclic aromatic hydrocarbon (PAH) content of UFPs. The dithiothreitol (DTT) assay, a quantitative measure of in vitro ROS formation, was correlated with PAH content and HO-1 expression. UFPs also had the highest ROS activity in the DTT assay. Because the small size of UFPs allows better tissue penetration, we used electron microscopy to study subcellular localization. UFPs and, to a lesser extent, fine particles, localize in mitochondria, where they induce major structural damage. This may contribute to oxidative stress. Our studies demonstrate that the increased biological potency of UFPs is related to the content of redox cycling organic chemicals and their ability to damage mitochondria.
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Metals and organic constituents, like PAHs, adsorbed to PM2.5 and PM0.1 have high oxidative potential and ability to generate mitochondrial damage.
“Metals and organic constituents, like PAHs, adsorbed to PM2.5 and PM0.1 have high oxidative potential and ability to generate mitochondrial damage [141, 142].”
From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [141]
The Discussion (pp. 458–459) reports oxidative stress and mitochondrial damage from ultrafine particles, with lesser mitochondrial damage from fine particles. It links redox activity to organic carbon and PAH content and discusses a possible contribution from metals, but does not establish that the adsorbed metals and PAHs themselves cause the observed mitochondrial damage. (LLM, conf=0.84)
Experimental — accuracy not yet measuredOnce absorbed, ultrafine particles are able to induce oxidative stress and mitochondrial damage.
“Once absorbed, ultrafine particles are able to induce oxidative stress and mitochondrial damage [32].”
From Oxidative Stress and Ageing: The Influence of Environmental Pollution, Sunlight and Diet on Skin (2017) · cites this paper as [32]
Ultrafine particles are particularly harmful due to their ability to penetrate tissues more easily and localise in mitochondria.
“Ultrafine particles are particularly harmful due to their ability to penetrate tissues more easily and localise in the mitochondria [32].”
From Oxidative Stress and Ageing: The Influence of Environmental Pollution, Sunlight and Diet on Skin (2017) · cites this paper as [32]
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- Authors
- Li, N., Sioutas, C., Cho, A., Schmitz, D., Misra, C., Sempf, J., Wang, M., Oberley, T., Froines, J., & Nel, A.
- Affiliations
- University of California, Los Angeles (US)
- Department of Medicine, University of California, Los Angeles, California 90095, USA.
- Venue
- Environmental Health Perspectives
- Publisher
- American Chemical Society (ACS)
- Published
- 2003-04-01
- Volume
- 111
- Issue
- 4
- Pages
- 455-460
- ISSN
- 0091-6765 (ISSN-L)
- 1552-9924
- PMC
- PMC1241427
- OpenAlex
- W2056017024
- Cited by
- 2,097
- References
- 39
- Citations by year
- 2026: 34 · 2025: 64 · 2024: 71 · 2023: 64 · 2022: 64 · 2021: 112 · 2020: 98 · 2019: 118 · 2018: 118 · 2017: 115 · 2016: 112 · 2015: 125 · 2014: 93 · 2013: 97 · 2012: 117
- FWCI
- 43.23
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Environmental Health Perspectives (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- U.S. Environmental Protection Agency
- California Air Resources Board
- National Institute of Environmental Health Sciences (R01 ES10553, R01ES010553)
- 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
- ultrafine particles, PM2.5, coarse particles, oxidative stress, mitochondrial damage, reactive oxygen species, heme oxygenase-1, glutathione depletion, polycyclic aromatic hydrocarbons, macrophages, epithelial cells, lung inflammation, subcellular localization
- MeSH terms
- Aerosols, Air Pollutants, Animals, Biological Assay, Epithelial Cells, Heme Oxygenase (Decyclizing), Humans, Lung, Macrophages, Membrane Proteins, Mitochondria, Particle Size, Polycyclic Aromatic Hydrocarbons, Reactive Oxygen Species, Oxidative Stress, Mice, Heme Oxygenase-1
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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