ArticleInhalation toxicology2013
Adverse effects of wood smoke PM(2.5) exposure on macrophage functions.
Article in Inhalation toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- A State of the Science Review of Wildfire-Specific Fine Particulate Matter Data Sources, Methods, and Models.Environmental health perspectives · 2025Pooled it
- Wood Smoke Exposure Alters Human Inflammatory Responses to Viral Infection in a Sex-Specific Manner. A Randomized, Placebo-controlled Study.American journal of respiratory and critical care medicine · 2019Trial
- Early Environments, Lasting Effects: Air Pollution, Microbes, and Respiratory Infection Risk in Children.Pediatric pulmonology · 2026Review
- Temporal variation in markers of immune signaling and wound repair in primary human airway epithelial cells following acute versus repeated woodsmoke condensate exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Ovarian hormone deficiency enhances wood smoke-induced immune dysfunction via transcriptomic and metabolic alterations.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Effects of urban PM2.5 on primary sinonasal epithelial cells in individuals with chronic rhinosinusitis.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Ovarian hormone deficiency enhances wood smoke-induced immune dysfunction via transcriptomic and metabolic alterations.bioRxiv : the preprint server for biology · 2026Article
- Environmental Exposures and the Microbiome: Where There Is Smoke, Is There Fire?American journal of respiratory and critical care medicine · 2025Article
- Human Sputum Microbiome Composition and Sputum Inflammatory Cell Profiles Are Altered with Controlled Wood Smoke Exposure as a Model for Wildfire Smoke.American journal of respiratory and critical care medicine · 2025Article
- Air Pollution and Global Pediatric Pneumococcal Disease.Open forum infectious diseases · 2025Review
- Gestational exposure to particulate matter from urban wildfires is associated with changes in circulating oxylipins but not flame retardants 7 to 13 months post-exposure.Environment international · 2025Article
- Respiratory Health Impacts from Natural Disasters and Other Extreme Weather Events: The Role of Environmental Stressors on Asthma and Allergies.Current allergy and asthma reports · 2025Review
- Spatial Discrimination Limit Analysis of Macrophage Phagocytosis Between Target Antigens and Non-Target Objects Using Microcapillary Manipulation Assay.Micromachines · 2024Article
- A mouse model of wildfire smoke-induced health effects: sex differences in acute and sustained effects of inhalation exposures.Inhalation toxicology · 2024Article
- Impact of Wildfires on Cardiovascular Health.Circulation research · 2024Review
- Immunology in COPD and the use of combustible cigarettes and heated tobacco products.European journal of medical research · 2023Review
- Prolonged smoldering Douglas fir smoke inhalation augments respiratory resistances, stiffens the aorta, and curbs ejection fraction in hypercholesterolemic mice.The Science of the total environment · 2023Article
- On-Chip Free-Flow Measurement Revealed Possible Depletion of Macrophages by Indigestible PM2.5 within a Few Hours by the Fastest Intervals of Serial Phagocytosis.Micromachines · 2023Article
- Physicochemical and toxicological properties of wood smoke particulate matter as a function of wood species and combustion condition.Journal of hazardous materials · 2023Article
- Chloroform Fraction of Prasiola japonica Ethanolic Extract Alleviates UPM 1648a-Induced Lung Injury by Suppressing NF-κB SignalingFoods (Basel, Switzerland) · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Epidemiological studies have shown a correlation between chronic biomass smoke exposure and increased respiratory infection. Pulmonary macrophages are instrumental in both the innate and the adaptive immune responses to respiratory infection. In the present study, in vitro systems were utilized where alveolar macrophages (AM) and bone marrow-derived macrophages (BMdM) were exposed to concentrated wood smoke-derived particulate matter (WS-PM) and mice were exposed in vivo to either concentrated WS-PM or inhaled WS. In vivo studies demonstrated that WS-exposed mice inoculated with Streptococcus pneumoniae had a higher bacterial load 24 h post-exposure, and corresponding AM were found to have decreased lymphocyte activation activity. Additionally, while classic markers of inflammation (cellular infiltration, total protein, neutrophils) were not affected, there were changes in pulmonary macrophages populations, including significant decreases in macrophages expressing markers of activation in WS-exposed mice. The lymphocyte activation activity of WS-PM-exposed AM was significantly suppressed, but the phagocytic activity appeared unchanged. In an effort to determine a pathway for WS-induced suppression, RelB activation, assessed by nuclear translocation, was observed in AM exposed to either inhaled WS or instilled WS-PM. Finally, an analysis of WS-PM fractions determined the presence of 4-5 polycyclic aromatic hydrocarbons (PAHs), and preliminary work suggests a potential role for these PAHs to alter macrophage functions. These studies show a decreased ability of WS-exposed pulmonary macrophages to effectively mount a defense against infection, the effect lasts at least a week post-exposure, and appears to be mediated via RelB activation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.