Browsing by Subject "PM2.5"

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    Artemisia pollen is the main vector for airborne endotoxin
    (Elsevier, 2018-08-09) Oteros, José; Bartusel, Elke; Alessandrini, Francesca; Núñez, Andrés; Moreno, Diego A.; Behrendt, Heidrun; Schmidt-Weber, Carsten; Traidl-Hoffmann, Claudia; Buters, Jeroen; Genética y Microbiología
    Background: Endotoxin (LPS) released from gram-negative bacteria causes strong immunologic and inflammatory effects and, when airborne, can contribute to respiratory conditions, such as allergic asthma. Objectives: We sought to identify the source of airborne endotoxin and the effect of this endotoxin on allergic sensitization. Methods: We determined LPS levels in outdoor air on a daily basis for 4 consecutive years in Munich (Germany) and Davos (Switzerland). Air was sampled as particulate matter (PM) greater than 10 μm (PM > 10) and PM between 2.5 and 10 μm. LPS levels were determined by using the recombinant Factor C assay. Results: More than 60% of the annual endotoxin exposure was detected in the PM > 10 fraction, showing that bacteria do not aerosolize as independent units or aggregates but adhered to large particles. In Munich 70% of annual exposure was detected between June 12th and August 28th. Multivariate modeling showed that endotoxin levels could be explained by phenological parameters (ie, plant growth). Indeed, days with high airborne endotoxin levels correlated well with the amount of Artemisia pollen in the air. Pollen collected from plants across Europe (100 locations) showed that the highest levels of endotoxin were detected on Artemisia vulgaris (mugwort) pollen, with little on other pollen. Microbiome analysis showed that LPS concentrations on mugwort pollen were related to the presence of Pseudomonas species and Pantoea species communities. In a mouse model of allergic disease, the presence of LPS on mugwort pollen was needed for allergic sensitization. Conclusions: The majority of airborne endotoxin stems from bacteria dispersed with pollen of only one plant: mugwort. This LPS was essential for inducing inflammation of the lung and allergic sensitization.
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    Histological and stereological insights into renal and adrenal changes in pregnant rats exposed to wood smoke-derived PM2.5
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Salinas, P.; Villarroel, F.; González Torres, C.; Lazcano, T.; Silva, J.; Maulen, A.; Rojas, E.
    Air pollution, particularly fine particulate matter (PM2.5), is a global health issue affecting millions. In southern Chile, firewood used for heating exacerbates pollution, especially in winter. This study examines the impact of wood smoke-derived PM2.5 on kidney and adrenal gland morphology in pregnant rats. It evaluates chronic PM2.5 exposure effects during pregestational and gestational periods in Sprague-Dawley rats. Pregnant rats were exposed to PM2.5 in Temuco, a city with high wood smoke pollution. Filtered and unfiltered air chambers simulated different exposure conditions. Histological and stereological analyses were conducted on rat kidneys and adrenal glands using systematic sampling and STEPanizer software. Findings showed significant changes in renal and adrenal morphology due to PM2.5 exposure. In the kidney, variations were observed in glomerular compaction, proximal convoluted tubules, and medullary rays. In the adrenal gland, the zona fasciculata showed decreased acidophilia and lipid content, reduced cytoplasmic homogeneity, and the appearance of empty spaces. These effects were more pronounced in rats exposed to unfiltered air during both pregestational and gestational periods. Wood smoke-derived PM2.5 exposure significantly impacts kidney and adrenal morphology in pregnant rats, emphasizing the need for strategies to reduce environmental pollutant exposure during critical developmental periods to protect maternal-fetal health.
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    Impact of particulate matter on the incidence of atrial fibrillation and the risk of adverse clinical outcomes: a review
    (Elsevier, 2023-04-04) Mandaglio-Collados, Darío; López-Gálvez, Raquel; Ruiz Alcaraz, Antonio José; López-García, Cecilia; Roldán Schilling, Vanessa; Lip, Gregory Y.H.; Marín Ortuño, Francisco; Rivera Caravaca, José Miguel; Bioquímica y Biología Molecular B e Inmunología; Facultad de Biología
    Background. Atrial fibrillation (AF) is common and increases the risk of stroke and mortality. Previous studies have suggested that air pollution is an important risk factor for new-onset AF. Herein, we review the evidence regarding: 1) the association between exposure to particulate matter (PM) and new-onset AF, and 2) the risk of worse clinical outcomes in patients with pre-existent AF and their relation to PM exposure. Methods. A selection of studies between 2000 and 2023 linking PM exposure and AF was performed through searches in PubMed, Scopus, Web of Science, and Google Scholar. Results. 17 studies from different geographical areas demonstrated that exposure to PM was associated with an increased risk of new-onset AF, although the results were heterogeneous regarding the temporal pattern (short- or long-term) ultimately related to AF. Most of the studies concluded that the risk of new-onset AF increased between 2 %–18 % per 10 μg/m3 increment in PM2.5 or PM10 concentrations, whereas the incidence (percentage of change of incidence) increased between 0.29 %–2.95 % per 10 μg/m3 increment in PM2.5 or PM10. Evidence about the association between PM and adverse events in patients with pre-existent AF was scarce but 4 studies showed a higher risk of mortality and stroke (between 8 %–64 % in terms of hazard ratio) in patients with pre-existent AF when PM exposure was higher. Conclusions. Exposure to PM (both PM2.5 and PM10) is a risk factor for AF, and a risk factor for mortality and stroke in patients who already suffer from AF. Since the relationship between PM and AF is independent of the region of the world, PM should be considered as a global risk factor for both AF and worse clinical outcomes in AF patients. Specific measures to prevent air pollution exposure need to be adopted.
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    Melatonin inhibits the activation of microglia and cough sensitivity of guinea pigs exposed to PM2.5
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Zhang, Shu; Long, Li; Chai, Senlin; Lin, Mingtong; Lu, Hankun; Liu, Xuemei; He, Yaowei; Dong, Rong; Chen, Zhe; Biología Celular e Histología
    Objective. The study aimed to examine the impact of melatonin on mitigating brain inflammation and cough sensitivity resulting from exposure to particulate matter 2.5 (PM2.5). Methods. Guinea pigs were randomly assigned to the blank control group, normal saline group, PM2.5 exposure group, and PM2.5 exposure + melatonin group. The PM2.5 exposure and PM2.5 exposure + melatonin groups were given intranasal instillations of PM2.5 suspension twice daily for 28 consecutive days. Starting on day 21, the PM2.5 exposure + melatonin group was treated with an intraperitoneal injection of melatonin at 10 pm. Cough sensitivity to citric acid, microglia activation, IL-1β and TNF-α levels in the airway and dorsal vagal complex (DVC), and ultrastructural changes in neurons within the DVC were assessed. Results. The PM2.5 exposure group exhibited a significantly higher cough count to citric acid challenge (29.1±5.7 coughs) compared with the PM2.5 exposure + melatonin group (18.8±4.1 coughs), normal saline group (8.4±2.1 coughs), and blank control group (7.7±1.8 coughs). In addition, cough latency was shorter in the PM2.5 exposure group (26.9±6.5 seconds) than in the PM2.5 exposure + melatonin group (36.6±12.4 seconds), normal saline group (43.4±14.7 seconds), and blank control group (47.0±13.0 seconds). The PM2.5 exposure + melatonin group showed significantly reduced IL-1β (105.3±14.3 pg/ml) and TNF-α levels (113.0±23.5 pg/ml) in the DVC, as well as in the bronchoalveolar lavage fluid (IL-1β: 24.92±5.14 pg/ml, TNF-α: 12.72±3.99 pg/ml) compared with the PM2.5 exposure group (in the DVC: IL-1β: 132.7±17.6 pg/ml, TNF-α: 143.8±30.4 pg/ml; in the bronchoalveolar lavage fluid: IL-1β: 34.0±5.3 pg/ml; TNF-α: 15.8±0.8 pg/ml). Microglia in the DVC were less activated in the PM2.5 exposure + melatonin group (25.1±5.4) than in the PM2.5 exposure group (54.6±9.9). Furthermore, the PM2.5 exposure group exhibited an impaired blood-brain barrier in the DVC, which tended to alleviate the PM2.5 exposure + melatonin group. Conclusions. Exposure to PM2.5 induces airway inflammation, central facilitation, and heightened cough sensitivity in guinea pigs. Melatonin significantly inhibits microglia activation and reduces airway and DVC inflammation, which might contribute to attenuated cough hypersensit