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Size and Dynamic of particles in the lung and other tissues. Large particles can be deposited in upper airways through sedimentation or impaction while in the lower airways Brownian diffusion can deposit them in the alveoli. Ultrafine particles can translocate to blood-circulating and be deposited in the liver, spleen or brain, although they might also penetrate through trans-synaptic mechanisms.
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Urban air pollution is a serious worldwide problem due to its impact on human health. In the past sixty years, growing evidence established a correlation between exposure to air pollutants and the developing of severe respiratory diseases. Recently Particulate matter (PM) is drawing more public attention to various aspects including historical back...
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Citations
... The World Health Organization has declared that atmospheric particulate matter (PM) is responsible for 4.2 million premature deaths every year (World Health Organization, 2018), thus confirming atmospheric pollution to be a threat to global public health. Epidemiological researchers have found that prolonged exposure to PM can result in multiple negative effects on health, including respiratory ailments such as lung cancer (Clark et al., 2010;Zhou et al., 2015;Falcon-Rodriguez et al., 2016;Raaschou-Nielsen et al., 2016), cardiovascular mortality (Burnett et al., 2018), and more adverse consequences in newborns (Lee et al., 2013;Klepac et al., 2018). ...
Open-pit mines are an important source of atmospheric particulate matter (PM) owing to the constant earth-moving and crushing. The well-known association between high PM concentrations and adverse health effects has made the permanent control of fugitive emissions from mines a public health concern. Nevertheless, the large size of these mines renders this task difficult and expensive to perform with regulatory apparatuses; subsequently, the mining industry requires other technologies with a suitable quality/price ratio. In this study, a novel methodology for the space–time monitoring of PM concentrations in open-pit mines using mobile low-cost sensors (LCSs) is proposed. The study was carried out in the renowned mine of Riotinto for three years (2019–2021). It included a detailed calibration of the mobile LCSs that fulfilled the European/US standards. Time tendency diagrams determined the maximum PM concentrations emitted (≈1600μg PM 10/m³) and also the seasonal variations. The spatial distribution also revealed the main sources of PM within the mine, which were the mining pit, mineral processing plant, spoil heap of fine materials, and main mining tracks. Finally, the integration of these data together with meteorological information allowed the discovery of the routes of escape of fugitive emissions from the mine toward nearby populations: toward W-SW, with concentrations primarily ranging between 50–100 μg PM10/m³ and 20–50 μg PM2.5/m³. The results of this research are important as mobile LCSs seem to solve the issue of fugitive emissions monitoring in mining ambiances and will aid the exploitations to become more environmentally friendly.
... Epidemiological studies have reported strong associations between air pollution and the arise of chronic-degenerative diseases. From these studies, it has been demonstrated that particulate matter (PM) released into the environment by vehicles and industries increases the incidence of multiple respiratory diseases, such as asthma, chronic obstructive pulmonary disease, and, in the long term, cancer [1][2][3][4]. On the other hand, toxicological studies have described the biological mechanisms altered by PM in numerous models and how these cellular alterations contribute to uncontrolled cell proliferation and, thus, carcinogenesis [5][6][7][8]. ...
In cells, oxidative stress is an imbalance between the production/accumulation of oxidants and the ability of the antioxidant system to detoxify these reactive products. Reactive oxygen species (ROS), cause multiple cellular damages through their interaction with biomolecules such as lipids, proteins, and DNA. Genotoxic damage caused by oxidative stress has become relevant since it can lead to mutation and play a central role in malignant transformation. The evidence describes chronic oxidative stress as an important factor implicated in all stages of the multistep carcinogenic process: initiation, promotion, and progression. In recent years, ambient air pollution by particulate matter (PM) has been cataloged as a cancer risk factor, increasing the incidence of different types of tumors. Epidemiological and toxicological evidence shows how PM-induced oxidative stress could mediate multiple events oriented to carcinogenesis, such as proliferative signaling, evasion of growth suppressors, resistance to cell death, induction of angiogenesis, and activation of invasion/metastasis pathways. In this review, we summarize the findings regarding the involvement of oxidative and genotoxic mechanisms generated by PM in malignant cell transformation. We also discuss the importance of new approaches oriented to studying the development of tumors associated with PM with more accuracy, pursuing the goal of weighing the impact of oxidative stress and genotoxicity as one of the main mechanisms associated with its carcinogenic potential.
... The ultrafine particles are capable of translocation through blood circulation to distal organs and tissues, such as liver tissue for detoxification. 24 Particles deposited in the respiratory tract in sufficient amounts can induce pulmonary inflammation. Controlled human and animal exposure studies have demonstrated increased markers for pulmonary inflammation following exposure to a variety of different particles. ...
Background: There is accumulating evidence that roadside pollution is detrimental to health. Traffic police personnel are exposed to roadside pollution due to the nature of their job and are at risk of adverse health outcomes. Objective: This study aims to compare the risk of adverse respiratory symptoms in different categories of traffic police including traffic constables, sergeants, and inspectors. Methods: The study population consisted of 369 randomly selected traffic police personnel from the city of Chittagong in Bangladesh. Information on their occupation and respiratory health symptoms were collected. The health outcomes were coughing, coughing sputum, coughing up blood, shortness of breathing, wheezing, and chest pain Result: The risk of coughing [adjusted Odds Ratio (AOR) = 4.469, 95% CI=1.265-15.793], coughing sputum [AOR= 3.687, 95% CI= 1.004 -13.540], coughing up blood [AOR=1.040, 95% CI=0.227-6.162], shortness of breathing [AOR=3.937, 95% CI=1.069-14.500], wheezing [AOR= 2.464, 95% CI= 0.613-9.906] and chest pain with deep breathing [AOR=2.163,95% CI= 0.560-8.349] was higher in traffic constables compared to inspectors. In sergeants odds increased for coughing up blood [AOR=1.102, 95% CI= 0.283-4.286] and wheezing [AOR=1.260, 95% CI= 0.304-5.229]. Conclusion: There was a substantial difference in the risk of studied respiratory symptoms between different categories of traffic police jobs. Targeted occupational health interventions are recommended.
... With advancements in technology, the exposure to airborne microparticles such as PM in daily life has been increasing. Microparticles including nanoplastic can form as a result of industrial processes, with other sources including traffic or road construction [23][24][25][26]. Fragments and fibres are the most commonly found forms of plastic in different environments worldwide [27]. ...
Background:
Polypropylene (PP) is used in various products such as disposable containers, spoons, and automobile parts. The disposable masks used for COVID-19 prevention mainly comprise PP, and the disposal of such masks is concerning because of the potential environmental pollution. Recent reports have suggested that weathered PP microparticles can be inhaled, however, the inhalation toxicology of PP microparticles is poorly understood.
Results:
Inflammatory cell numbers, reactive oxygen species (ROS) production, and the levels of inflammatory cytokines and chemokines in PP-instilled mice (2.5 or 5 mg/kg) increased significantly compared to with those in the control. Histopathological analysis of the lung tissue of PP-stimulated mice revealed lung injuries, including the infiltration of inflammatory cells into the perivascular/parenchymal space, alveolar epithelial hyperplasia, and foamy macrophage aggregates. The in vitro study indicated that PP stimulation causes mitochondrial dysfunction including mitochondrial depolarization and decreased adenosine triphosphate (ATP) levels. PP stimulation led to cytotoxicity, ROS production, increase of inflammatory cytokines, and cell deaths in A549 cells. The results showed that PP stimulation increased the p-p38 and p-NF-κB protein levels both in vivo and in vitro, while p-ERK and p-JNK remained unchanged. Interestingly, the cytotoxicity that was induced by PP exposure was regulated by p38 and ROS inhibition in A549 cells.
Conclusions:
These results suggest that PP stimulation may contribute to inflammation pathogenesis via the p38 phosphorylation-mediated NF-κB pathway as a result of mitochondrial damage.
... Depending on its size, PM has the potential of causing health problems in the respiratory tract. According to the United States Environmental Protection Agency (EPA), small particles with an aerodynamic diameter less than 10 μm (PM 10 ) can be deposited in deeper airways and, in some cases, incorporated to the bloodstream [3]. PM 10 contains inorganic, organic, and biological compounds, originating from natural and anthropogenic activities, and is considered the inhalable fraction [4,5] with a complex mixture of elemental carbon, metals (lead, iron, vanadium, nickel, copper, platinum, among others), ions (sulfates and nitrates), biological components (endotoxins, pollen, fungi), and organic compounds, including Polycyclic Aromatic Hydrocarbons (PAH), dioxins and aromatic amines [6][7][8]. ...
Background
Particulate matter with an aerodynamic size ≤ 10 μm (PM10) is a risk factor for lung cancer development, mainly because some components are highly toxic. Polycyclic aromatic hydrocarbons (PAHs) are present in PM10, such as benzo[a]pyrene (BaP), which is a well-known genotoxic and carcinogenic compound to humans, capable of activating AP-1 transcription factor family genes through the Aryl Hydrocarbon Receptor (AhR). Because effects of BaP include metalloprotease 9 (MMP-9) activation, cell invasion, and other pathways related to carcinogenesis, we aimed to demonstrate that PM10 (10 µg/cm²) exposure induces the activation of AP-1 family members as well as cell invasion in lung epithelial cells, through AhR pathway.
Methods and results
The role of the AhR gene in cells exposed to PM10 (10 µg/cm²) and BaP (1µM) for 48 h was evaluated using AhR-targeted interference siRNA. Then, the AP-1 family members (c-Jun, Jun B, Jun D, Fos B, C-Fos, and Fra-1), the levels/activity of MMP-9, and cell invasion were analyzed. We found that PM10 increased AhR levels and promoted its nuclear localization in A549 treated cells. Also, PM10 and BaP deregulated the activity of AP-1 family members. Moreover, PM10 upregulated the secretion and activity of MMP-9 through AhR, while BaP had no effect. Finally, we found that cell invasion in A549 cells exposed to PM10 and BaP is modulated by AhR.
Conclusion
Our results demonstrated that PM10 exposure induces upregulation of the c-Jun, Jun B, and Fra-1 activity, the expression/activity of MMP-9, and the cell invasion in lung epithelial cells, effects mediated through the AhR. Also, the Fos B and C-Fos activity were downregulated. In addition, the effects induced by PM10 exposure were like those induced by BaP, which highlights the potentially toxic effects of the PM10 mixture in lung epithelial cells.
... Induction of CYP1A1 and NQO-1 is crucial for the degradation of harmful toxicants, including PAHs and quinones 37 . However, persistent AhR activation and subsequent oncogene activation can also lead to the increase of carcinogenic metabolite-induced DNA damage and the unbalanced promotion of cell proliferation 1,7,10 . EGCG exposure was reported to cause inconsistent regulation of Nrf2, HO-1, and NQO-1 expression in different cell types 38,39 . ...
To distinguish the influences of fuel type and truck speed on chemical composition and sub-toxic effects of particulates (PM 2.5 ) from engine emissions, biomarkers—interleukin-6 (IL-6), cytochrome P450 (CYP) 1A1, heme oxygenase (HO)-1, and NADPH-quinone oxidoreductase (NQO)-1—were studied in A549 human lung cells. Fuel type and truck speed preferentially affected the quantity and ion/polycyclic aromatic hydrocarbon (PAH) composition of PM 2.5 , respectively. Under idling operation, phenanthrene was the most abundant PAH. At high speed, more than 50% of the PAHs had high molecular weight (HMW), of which benzo[ a ]pyrene (B[a]P), benzo[ ghi ]perylene (B[ghi]P), and indeno[1,2,3- cd ]pyrene (I[cd]P) were the main PAHs. B[a]P, B[ghi]P, and I[cd]P caused potent induction of IL-6, CYP1A1, and NQO-1, whereas phenanthrene mildly induced CYP1A1. Based on the PAH-mediated induction, the predicted increases in biomarkers were positively correlated with the measured increases. HMW-PAHs contribute to the biomarker induction by PM 2.5 , at high speed, which was reduced by co-exposure to epigallocatechin-3-gallate.
... The size of PM plays an essential role in determining the deposition site in the lungs. [17] Our subgroup analysis showed that PM 2.5 may have a more significant effect on asthma and COPD hospitalization than PM 10. These findings may be because while the coarse fraction (PM 2.5-10 ) can penetrate the airways, the fine fraction (PM 1-2.5 ) may be deposited in the lungs, particularly in the alveoli, and may pass into systemic circulation. ...
We investigated the effects of particulate matter (PM) factors on hospitalization rates for asthma and chronic obstructive pulmonary disease (COPD). We obtained data on pollutants—PM10, PM2.5—in Seoul, South Korea. We also investigated data for asthma and COPD exacerbation that required hospitalization from 2006 to 2016. We used a time-stratified case-crossover design and generalized additive models with log transformation to assess adjusted risk, and conditional logistic regression was performed to analyze these data. Our study showed that PM10 and PM2.5, on different best lag days, were associated with increased risks of COPD or asthma hospitalization. The odds ratios (ORs) for each per-unit increase in PM10 and PM2.5 were higher in patients with male asthma (PM10: OR, 1.012; 95% confidence interval [CI], 1.008–1.016 and PM2.5: OR, 1.015; 95% CI, 1008–1.023), preschool asthma (PM10: OR, 1.015; 95% CI, 1.006–1.015 and PM2.5: OR, 1.015; 95% CI, 1.009–1.024), male COPD (PM10: OR, 1.012; 95% CI, 1.005–1.019 and PM2.5: OR, 1.013; 95% CI, 1.000–1.026), and senior COPD (PM10: OR, 1.016; 95% CI, 1.008–1.024 and PM2.5: OR, 1.022; 95% CI, 1.007–1.036). Increasing PM levels increased hospitalizations for asthma and COPD. Additionally, the consequences may be different according to age and sex, and PM2.5 may have a more significant effect on airway disease patients than PM10.
... Because PM 2.5 can penetrate into the alveoli by bypassing physiological barrier in the respiratory system, the lungs are the primary organs affected by PM 2. 5 . In a molecular toxicological aspect, PM 2.5 contains various toxicants, such as polyaromatic hydrocarbons (PAHs), heavy metals, sulfate, and endotoxin [4]. These toxicants alter vascular permeability and trigger oxidative stress-mediated inflammation [5,6]. ...
Chronic exposure of particulate matter of less than 2.5 μm (PM2.5) has been considered as one of the major etiologies for various respiratory diseases. Adenophora stricta Miq. is a medicinal herb that has been used for treating respiratory diseases in East Asia. The present study investigated the effect of A. stricta root extract (AsE) on PM2.5-induced lung injury in mice. Oral administration of 100–400 mg/kg AsE for 10 days significantly reduced the PM2.5-mediated increase in relative lung weight, but there was no difference in body weight with AsE administration. In addition, AsE dose-dependently decreased congested region of the lung tissue, prevented apoptosis and matrix degradation, and alleviated mucus stasis induced by PM2.5. Moreover, cytological analysis of bronchioalveolar lavage fluid revealed that AsE significantly inhibited the infiltration of immune cells into the lungs. Consistently, AsE also decreased expression of proinflammatory cytokines and chemokines in lung tissue. Furthermore, AsE administration blocked reactive oxygen species production and lipid peroxidation through attenuating the PM2.5-dependent reduction of antioxidant defense system in the lungs. Therefore, A. stricta root would be a promising candidate for protecting lung tissue from air pollution such as PM2.5.
... With a maximum inhalation volume of 10,000 L, our lungs come into contact with significant quantities of dust every day (Gustafsson et al., 2018;Tsuda et al., 2013). Dust particles act as carriers for diverse semi-volatile organic and chemical compounds (Blanchard et al., 2014;Gupta et al., 2020;Melymuk et al., 2020;Neupane et al., 2020;Tofful et al., 2021), which increases adverse health impacts such as oxidative stress and inflammatory responses on humans (Falcon-Rodriguez et al., 2016). Human exposure to dust particles from the indoor atmosphere has received little attention. ...
This study is designed to determine the morphology, elemental composition, and identification of various minerals and functional groups in household dust in multiple locations in Dhanbad, India. Household dust samples were collected from different locations, and samples had been sieved for particle sizes of <75 μm for analysis. For indoor air quality, active PM sampling for each sampling site was done and concentrations of PM10, PM2.5, and PM1 were observed in the range of 31–137, 23–82, and 17–52 μg/m³, respectively. The morphology (FESEM) and elemental analysis (EDX) confirmed the existence of particles with different shapes and compositions in different households. Spherical shape and chain-like structures are indicative of coal combustion inside houses. In contrast, irregular-shaped structures with sharp-edged and sheet-like structures suggest mineral-rich crustal dust in LPG-based houses. Also, soot agglomerates were found in houses nearby roadside from outside vehicular emissions. Energy-dispersive X-ray spectroscopy (EDX) confirmed the relative distribution of elements varied between households and reported that C, O, Mg, Ca, Al, and Si were the primary elements in dust samples collected from various households. The Fourier Transform Infrared (FTIR) peaks for functional groups at various wavelengths such as –C–H, –CC, –CO, –C-X indicates coal dust and their combustion whereas –NH2, –NH4⁺, –R-SO3⁻ suggests the influence of walking, cleaning, and other household activities. X-ray diffraction (XRD) confirms that minerals such as calcite, vaterite, and quartz were found majorly in roadside houses whereas dolomite, quartz, and hematite were in other sites.
... Recent studies have found that airway inflammation might exert a critical role in PM 2.5 -related respiratory diseases, as inflammation was found to be associated with declined lung function (Falcon-Rodriguez et al. 2016). The possible mechanism might be related to the deposition of PM 2.5 in the human respiratory tract, lung-deposited surface area, and translocation of potential ultrafine particles from the lungs to the circulatory system (Yin et al. 2017). ...
Numerous studies focused on the association between lung function impairment and inflammation caused by fine particulate matter (PM2.5), but the causal relationships are difficult to clarify. In the current study, twenty healthy Chinese young adults who participated in 7 days of observation every four seasons were enrolled, and autoregression models (AM) and classification and regression trees (CART) in a machine learning framework were applied to analyze the association among PM2.5 exposure, inflammation, and lung function from a data structure perspective. There were strong cross-correlations between personal dose of PM2.5 (Dw) and lung functions (vital capacity (VC), forced vital capacity (FVC), etc.). These cross-correlation coefficients were associated with inflammatory indicators (uteroglobin (UG), serum amyloid (SAA), and fractional exhaled nitric oxide (FeNO)). CART reported that inflammatory indicators UG and SAA had the predictive ability of the directional association between Dw and FVC at 1-day lag and that high levels of UG and SAA predicted that PM2.5 exposure induced lung function decline. Consistently, lower lung function indicators at a 2-day lag after personal PM2.5 exposure predicted the high value of inflammatory indicator FeNO. Taken together, we applied machine learning algorithms to analyze repeated measurement data, finding that inflammation and lung function decline caused by PM2.5 could affect each other.
