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- Lepistö, Teemu, et al.
(författare)
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Particle lung deposited surface area (LDSAal) size distributions in different urban environments and geographical regions : Towards understanding of the PM2.5 dose–response
- 2023
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Ingår i: Environment International. - : Elsevier. - 0160-4120 .- 1873-6750. ; 180
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Tidskriftsartikel (refereegranskat)abstract
- Recent studies indicate that monitoring only fine particulate matter (PM2.5) may not be enough to understand and tackle the health risk caused by particulate pollution. Health effects per unit PM2.5 seem to increase in countries with low PM2.5, but also near local pollution sources (e.g., traffic) within cities. The aim of this study is to understand the differences in the characteristics of lung-depositing particles in different geographical regions and urban environments. Particle lung deposited surface area (LDSAal) concentrations and size distributions, along with PM2.5, were compared with ambient measurement data from Finland, Germany, Czechia, Chile, and India, covering traffic sites, residential areas, airports, shipping, and industrial sites. In Finland (low PM2.5), LDSAal size distributions depended significantly on the urban environment and were mainly attributable to ultrafine particles (<100 nm). In Central Europe (moderate PM2.5), LDSAal was also dependent on the urban environment, but furthermore heavily influenced by the regional aerosol. In Chile and India (high PM2.5), LDSAal was mostly contributed by the regional aerosol despite that the measurements were done at busy traffic sites. The results indicate that the characteristics of lung-depositing particles vary significantly both within cities and between geographical regions. In addition, ratio between LDSAal and PM2.5 depended notably on the environment and the country, suggesting that LDSAal exposure per unit PM2.5 may be multiple times higher in areas having low PM2.5 compared to areas with continuously high PM2.5. These findings may partly explain why PM2.5 seems more toxic near local pollution sources and in areas with low PM2.5. Furthermore, performance of a typical sensor based LDSAal measurement is discussed and a new LDSAal2.5 notation indicating deposition region and particle size range is introduced. Overall, the study emphasizes the need for country-specific emission mitigation strategies, and the potential of LDSAal concentration as a health-relevant pollution metric.
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- Martikainen, Maria-Viola, et al.
(författare)
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TUBE project: Transport-derived ultrafines and the brain effects
- 2022
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Ingår i: International Journal of Environmental Research and Public Health. - : MDPI. - 1661-7827 .- 1660-4601. ; 19:1
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Tidskriftsartikel (refereegranskat)abstract
- The adverse effects of air pollutants on the respiratory and cardiovascular systems are unquestionable. However, in recent years, indications of effects beyond these organ systems have become more evident. Traffic-related air pollution has been linked with neurological diseases, exacerbated cognitive dysfunction, and Alzheimer’s disease. However, the exact air pollutant compositions and exposure scenarios leading to these adverse health effects are not known. Although several components of air pollution may be at play, recent experimental studies point to a key role of ultrafine particles (UFPs). While the importance of UFPs has been recognized, almost nothing is known about the smallest fraction of UFPs, and only >23 nm emissions are regulated in the EU. Moreover, the role of the semivolatile fraction of the emissions has been neglected. The Transport-Derived Ultrafines and the Brain Effects (TUBE) project will increase knowledge on harmful ultrafine air pollutants, as well as semivolatile compounds related to adverse health effects. By including all the major current combustion and emission control technologies, the TUBE project aims to provide new information on the adverse health effects of current traffic, as well as information for decision makers to develop more effective emission legislation. Most importantly, the TUBE project will include adverse health effects beyond the respiratory system; TUBE will assess how air pollution affects the brain and how air pollution particles might be removed from the brain. The purpose of this report is to describe the TUBE project, its background, and its goals.
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- Muala, Ala, et al.
(författare)
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Acute exposure to wood smoke from incomplete combustion - indications of cytotoxicity
- 2015
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Ingår i: Particle and Fibre Toxicology. - : Springer Science and Business Media LLC. - 1743-8977. ; 12
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Tidskriftsartikel (refereegranskat)abstract
- Background: Smoke from combustion of biomass fuels is a major risk factor for respiratory disease, but the underlying mechanisms are poorly understood. The aim of this study was to determine whether exposure to wood smoke from incomplete combustion would elicit airway inflammation in humans. Methods: Fourteen healthy subjects underwent controlled exposures on two separate occasions to filtered air and wood smoke from incomplete combustion with PM1 concentration at 314 mu g/m(3) for 3 h in a chamber. Bronchoscopy with bronchial wash (BW), bronchoalveolar lavage (BAL) and endobronchial mucosal biopsies was performed after 24 h. Differential cell counts and soluble components were analyzed, with biopsies stained for inflammatory markers using immunohistochemistry. In parallel experiments, the toxicity of the particulate matter (PM) generated during the chamber exposures was investigated in vitro using the RAW264.7 macrophage cell line. Results: Significant reductions in macrophage, neutrophil and lymphocyte numbers were observed in BW (p < 0.01, < 0.05, < 0.05, respectively) following the wood smoke exposure, with a reduction in lymphocytes numbers in BAL fluid (< 0.01. This unexpected cellular response was accompanied by decreased levels of sICAM-1, MPO and MMP-9 (p < 0.05, < 0.05 and < 0.01). In contrast, significant increases in submucosal and epithelial CD3+ cells, epithelial CD8+ cells and submucosal mast cells (p < 0.01, < 0.05, < 0.05 and < 0.05, respectively), were observed after wood smoke exposure. The in vitro data demonstrated that wood smoke particles generated under these incomplete combustion conditions induced cell death and DNA damage, with only minor inflammatory responses. Conclusions: Short-term exposure to sooty PAH rich wood smoke did not induce an acute neutrophilic inflammation, a classic hallmark of air pollution exposure in humans. While minor proinflammatory lymphocytic and mast cells effects were observed in the bronchial biopsies, significant reductions in BW and BAL cells and soluble components were noted. This unexpected observation, combined with the in vitro data, suggests that wood smoke particles from incomplete combustion could be potentially cytotoxic. Additional research is required to establish the mechanism of this dramatic reduction in airway leukocytes and to clarify how this acute response contributes to the adverse health effects attributed to wood smoke exposure.
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- Nordin, Erik, et al.
(författare)
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Influence of ozone initiated processing on the toxicity of aerosol particles from small scale wood combustion
- 2015
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Ingår i: Atmospheric Environment. - : Elsevier BV. - 1352-2310 .- 1873-2844. ; 102, s. 282-289
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Tidskriftsartikel (refereegranskat)abstract
- Black carbon containing emissions from biomass combustion are being transformed in the atmosphere upon processing induced by tropospheric ozone and UV. The knowledge today is very limited on how atmospheric processing affects the toxicological properties of the emissions. The aim of this study was to investigate the influence of ozone initiated (dark) atmospheric processing on the physicochemical and toxicological properties of particulate emissions from wood combustion. Emissions from a conventional wood stove operated at two combustion conditions (nominal and hot air starved) were diluted and transferred to a chamber. Particulate matter (PM) was collected before and after ozone addition to the chamber using an impactor. Detailed chemical and physical characterization was performed on chamber air and collected PM. The collected PM was investigated toxicologically in vitro with a mouse macrophage model, endpoints included: cell cycle analysis, viability, inflammation and genotoxicity. The results suggest that changes in the organic fraction, including polycyclic aromatic hydrocarbons (PAHs) are the main driver for differences in obtained toxicological effects. Fresh hot air starved emissions containing a higher organic and PAH mass-fraction affected cell viability stronger than fresh emissions from nominal combustion. The PAH mass fractions decreased upon aging due to chemical degradation. Dark aging increased genotoxicity, reduced viability and reduced release of inflammatory markers. These differences were statistically significant for single doses and typically less pronounced. We hypothesize that the alterations in toxicity upon simulated dark aging in the atmosphere may be caused by reaction products that form when PAHs and other organic compounds react with ozone and nitrate radicals. (C) 2014 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/3.0/).
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- Wu, Qi-Zhen, et al.
(författare)
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Long-term exposure to major constituents of fine particulate matter and neurodegenerative diseases : a population-based survey in the Pearl River Delta Region, China
- 2024
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Ingår i: Journal of Hazardous Materials. - : Elsevier. - 0304-3894 .- 1873-3336. ; 470
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Tidskriftsartikel (refereegranskat)abstract
- Background: Exposure to PM2.5 has been linked to neurodegenerative diseases, with limited understanding of constituent-specific contributions.Objectives: To explore the associations between long-term exposure to PM2.5 constituents and neurodegenerative diseases.Methods: We recruited 148,274 individuals aged ≥ 60 from four cities in the Pearl River Delta region, China (2020 to 2021). We calculated twenty-year average air pollutant concentrations (PM2.5 mass, black carbon (BC), organic matter (OM), ammonium (NH4+), nitrate (NO3-) and sulfate (SO42-)) at the individuals' home addresses. Neurodegenerative diseases were determined by self-reported doctor-diagnosed Alzheimer's disease (AD) and Parkinson's disease (PD). Generalized linear mixed models were employed to explore associations between pollutants and neurodegenerative disease prevalence.Results: PM2.5 and all five constituents were significantly associated with a higher prevalence of AD and PD. The observed associations generally exhibited a non-linear pattern. For example, compared with the lowest quartile, higher quartiles of BC were associated with greater odds for AD prevalence (i.e., the adjusted odds ratios were 1.81; 95% CI, 1.45–2.27; 1.78; 95% CI, 1.37–2.32; and 1.99; 95% CI, 1.54–2.57 for the second, third, and fourth quartiles, respectively).Conclusions: Long-term exposure to PM2.5 and its constituents, particularly combustion-related BC, OM, and SO42-, was significantly associated with higher prevalence of AD and PD in Chinese individuals.Environmental implication: PM2.5 is a routinely regulated mixture of multiple hazardous constituents that can lead to diverse adverse health outcomes. However, current evidence on the specific contributions of PM2.5 constituents to health effects is scarce. This study firstly investigated the association between PM2.5 constituents and neurodegenerative diseases in the moderately to highly polluted Pearl River Delta region in China, and identified hazardous constituents within PM2.5 that have significant impacts. This study provides important implications for the development of targeted PM2.5 prevention and control policies to reduce specific hazardous PM2.5 constituents.
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