Particle and Fibre Toxicology最新文献

{"title":"Concentration-dependent increase in symptoms due to diesel exhaust in a controlled human exposure study.","authors":"Juma Orach,&nbsp;Christopher Francis Rider,&nbsp;Agnes Che Yan Yuen,&nbsp;Christopher Carlsten","doi":"10.1186/s12989-022-00506-6","DOIUrl":"https://doi.org/10.1186/s12989-022-00506-6","url":null,"abstract":"<p><strong>Background: </strong>Traffic-related air pollution (TRAP) exposure causes adverse effects on wellbeing and quality of life, which can be studied non-invasively using self-reported symptoms. However, little is known about the effects of different TRAP concentrations on symptoms following controlled exposures, where acute responses can be studied with limited confounding. We investigated the concentration-response relationship between diesel exhaust (DE) exposure, as a model TRAP, and self-reported symptoms.</p><p><strong>Methods: </strong>We recruited 17 healthy non-smokers into a double-blind crossover study where they were exposed to filtered air (FA) and DE standardized to 20, 50, 150 µg/m³ PM_2.5 for 4 h, with a ≥ 4-week washout between exposures. Immediately before, and at 4 h and 24 h from the beginning of the exposure, we administered visual analog scale (VAS) questionnaires and grouped responses into chest, constitutional, eye, neurological, and nasal categories. Additionally, we assessed how the symptom response was related to exposure perception and airway function.</p><p><strong>Results: </strong>An increase in DE concentration raised total (β ± standard error = 0.05 ± 0.03, P = 0.04), constitutional (0.01 ± 0.01, P = 0.03) and eye (0.02 ± 0.01, P = 0.05) symptoms at 4 h, modified by perception of temperature, noise, and anxiety. These symptoms were also correlated with airway inflammation. Compared to FA, symptoms were significantly increased at 150 µg/m³ for the total (8.45 ± 3.92, P = 0.04) and eye (3.18 ± 1.55, P = 0.05) categories, with trends towards higher values in the constitutional (1.49 ± 0.86, P = 0.09) and nasal (1.71 ± 0.96, P = 0.08) categories.</p><p><strong>Conclusion: </strong>DE exposure induced a concentration-dependent increase in symptoms, primarily in the eyes and body, that was modified by environmental perception. These observations emphasize the inflammatory and sensory effects of TRAP, with a potential threshold below 150 µg/m³ PM_2.5. We demonstrate VAS questionnaires as a useful tool for health monitoring and provide insight into the TRAP concentration-response at exposure levels relevant to public health policy.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":null,"pages":null},"PeriodicalIF":10.0,"publicationDate":"2022-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9685897/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40702855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pro-thrombotic changes associated with exposure to ambient ultrafine particles in patients with chronic obstructive pulmonary disease: roles of lipid peroxidation and systemic inflammation.","authors":"Teng Wang,&nbsp;Xi Chen,&nbsp;Haonan Li,&nbsp;Wu Chen,&nbsp;Yifan Xu,&nbsp;Yuan Yao,&nbsp;Hanxiyue Zhang,&nbsp;Yiqun Han,&nbsp;Lina Zhang,&nbsp;Chengli Que,&nbsp;Jicheng Gong,&nbsp;Xinghua Qiu,&nbsp;Tong Zhu","doi":"10.1186/s12989-022-00503-9","DOIUrl":"https://doi.org/10.1186/s12989-022-00503-9","url":null,"abstract":"<p><strong>Background: </strong>Exposure to particulate matter air pollution is associated with an increased risk of cardiovascular mortality in patients with chronic obstructive pulmonary disease (COPD), but the underlying mechanisms are not yet understood. Enhanced platelet and pro-thrombotic activity in COPD patients may explain their increased cardiovascular risk. We aim to explore whether short-term exposure to ambient particulate matter is associated with pro-thrombotic changes in adults with and without COPD, and investigate the underlying biological mechanisms in a longitudinal panel study. Serum concentration of thromboxane (Tx)B2 was measured to reflect platelet and pro-thrombotic activity. Lipoxygenase-mediated lipid peroxidation products (hydroxyeicosatetraenoic acids [HETEs]) and inflammatory biomarkers (interleukins [ILs], monocyte chemoattractant protein-1 [MCP-1], tumour necrosis factor alpha [TNF-α], and macrophage inflammatory proteins [MIPs]) were measured as potential mediating determinants of particle-associated pro-thrombotic changes.</p><p><strong>Results: </strong>53 COPD and 82 non-COPD individuals were followed-up on a maximum of four visits conducted from August 2016 to September 2017 in Beijing, China. Compared to non-COPD individuals, the association between exposure to ambient ultrafine particles (UFPs) during the 3-8 days preceding clinical visits and the TxB2 serum concentration was significantly stronger in COPD patients. For example, a 10³/cm³ increase in the 6-day average UFP level was associated with a 25.4% increase in the TxB2 level in the COPD group but only an 11.2% increase in the non-COPD group. The association in the COPD group remained robust after adjustment for the levels of fine particulate matter and gaseous pollutants. Compared to the non-COPD group, the COPD group also showed greater increases in the serum concentrations of 12-HETE (16.6% vs. 6.5%) and 15-HETE (9.3% vs. 4.5%) per 10³/cm³ increase in the 6-day UFP average. The two lipid peroxidation products mediated 35% and 33% of the UFP-associated increase in the TxB2 level of COPD patients. UFP exposure was also associated with the increased levels of IL-8, MCP-1, MIP-1α, MIP-1β, TNF-α, and IL-1β in COPD patients, but these inflammatory biomarkers did not mediate the TxB2 increase.</p><p><strong>Conclusions: </strong>Short-term exposure to ambient UFPs was associated with a greater pro-thrombotic change among patients with COPD, at least partially driven by lipoxygenase-mediated pathways following exposure. Trial registration ChiCTR1900023692 . Date of registration June 7, 2019, i.e. retrospectively registered.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":null,"pages":null},"PeriodicalIF":10.0,"publicationDate":"2022-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9590143/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10858823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dimethylarginine dimethylaminohydrolase 1 protects PM_2.5 exposure-induced lung injury in mice by repressing inflammation and oxidative stress.","authors":"Junling Gao,&nbsp;Tong Lei,&nbsp;Hongyun Wang,&nbsp;Kai Luo,&nbsp;Yuanli Wang,&nbsp;Bingqing Cui,&nbsp;Zhuoran Yu,&nbsp;Xiaoqi Hu,&nbsp;Fang Zhang,&nbsp;Yingjie Chen,&nbsp;Wenjun Ding,&nbsp;Zhongbing Lu","doi":"10.1186/s12989-022-00505-7","DOIUrl":"https://doi.org/10.1186/s12989-022-00505-7","url":null,"abstract":"<p><strong>Background: </strong>Airborne fine particulate matter with aerodynamic diameter ≤ 2.5 μm (PM_2.5) pollution is associated with the prevalence of respiratory diseases, including asthma, bronchitis and chronic obstructive pulmonary disease. In patients with those diseases, circulating asymmetric dimethylarginine (ADMA) levels are increased, which contributes to airway nitric oxide deficiency, oxidative stress and inflammation. Overexpression of dimethylarginine dimethylaminohydrolase 1 (DDAH1), an enzyme degrading ADMA, exerts protective effects in animal models. However, the impact of DDAH1/ADMA on PM_2.5-induced lung injury has not been investigated.</p><p><strong>Methods: </strong>Ddah1^-/- and DDAH1-transgenic mice, as well as their respective wild-type (WT) littermates, were exposed to either filtered air or airborne PM_2.5 (mean daily concentration ~ 50 µg/m³) for 6 months through a whole-body exposure system. Mice were also acutely exposed to 10 mg/kg PM_2.5 and/or exogenous ADMA (2 mg/kg) via intratracheal instillation every other day for 2 weeks. Inflammatory response, oxidative stress and related gene expressions in the lungs were examined. In addition, RAW264.7 cells were exposed to PM_2.5 and/or ADMA and the changes in intracellular oxidative stress and inflammatory response were determined.</p><p><strong>Results: </strong>Ddah1^-/- mice developed more severe lung injury than WT mice after long-term PM_2.5 exposure, which was associated with greater induction of pulmonary oxidative stress and inflammation. In the lungs of PM_2.5-exposed mice, Ddah1 deficiency increased protein expression of p-p65, iNOS and Bax, and decreased protein expression of Bcl-2, SOD1 and peroxiredoxin 4. Conversely, DDAH1 overexpression significantly alleviated lung injury, attenuated pulmonary oxidative stress and inflammation, and exerted opposite effects on those proteins in PM_2.5-exposed mice. In addition, exogenous ADMA administration could mimic the effect of Ddah1 deficiency on PM_2.5-induced lung injury, oxidative stress and inflammation. In PM_2.5-exposed macrophages, ADMA aggravated the inflammatory response and oxidative stress in an iNOS-dependent manner.</p><p><strong>Conclusion: </strong>Our data revealed that DDAH1 has a marked protective effect on long-term PM_2.5 exposure-induced lung injury.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":null,"pages":null},"PeriodicalIF":10.0,"publicationDate":"2022-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9569114/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33511562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Toxicokinetic study following intratracheal instillation or oral gavage of two [⁷Be]-tagged carbon black samples.","authors":"Otto Creutzenberg,&nbsp;Volker Hammann,&nbsp;Stefanie Wolf,&nbsp;Jürgen Daul,&nbsp;Yufanyi Ngiewih,&nbsp;Ishrat Chaudhuri,&nbsp;Len Levy","doi":"10.1186/s12989-022-00504-8","DOIUrl":"https://doi.org/10.1186/s12989-022-00504-8","url":null,"abstract":"<p><strong>Background: </strong>The toxicokinetic behaviour of nanostructured particles following pulmonary or oral deposition is of great scientific interest. In this toxicokinetic study, following the general principles of OECD TG 417, the systemic availability of carbon black, a nanostructured material consisting of agglomerated aggregates was characterised.</p><p><strong>Methods: </strong>Each of two grades of beryllium-7 labelled carbon black (Monarch® 1000, oxidized and Printex® 90; untreated) was administered either intratracheally or orally to adult rats. Independent of route, rats received a single dose of approximately 0.3 mg radiolabelled carbon black. A total of 12 rats were treated per grade and per exposure route: 4 females each for feces/urine/organs and serial blood kinetics; 4 males for organs. At necropsy, the complete suite of organs was analysed for females, but only the lungs, liver, kidney, reproductive organs for males.</p><p><strong>Results: </strong>In the pulmonarily exposed animals, ⁷Be-Monarch® 1000 and ⁷Be-Printex® 90 was detected in feces in the first 3 days after treatment at significant levels, i.e. 17.6% and 8.2%, respectively. In urine, small percentages of 6.7% and 0.4% were observed, respectively. In blood, radioactivity, representative of carbon black was within the background noise of the measurement method. At necropsy, 20 days post-instillation, both test items were practically exclusively found in lungs (75.1% and 91.0%, respectively) and in very small amounts (approximately 0.5%) in the lung-associated lymph nodes (LALN). In the other organs/tissues the test item was not detectable. BAL analyses indicated that carbon black particles were completely engulfed by alveolar macrophages. In orally exposed animals, 98% (⁷Be-Monarch® 1000) and 99% (⁷Be-Printex® 90) of the measured radioactivity was detected in feces. Excretion was complete within the first 3 days following treatment. 1.3% and 0.5% of measured activity was attributable to urine in animals that received ⁷Be-Monarch® 1000 and ⁷Be-Printex® 90, respectively. Radioactivity was absent in blood and other organs and tissues.</p><p><strong>Conclusion: </strong>Radioactivity, representative of carbon black, was not detected beyond the experimentally defined limit of quantitation systemically after deposition in lungs or stomach in rats. Under these experimental conditions, the two CB samples were not shown to translocate beyond the lung or the GI tract into the blood compartment.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":null,"pages":null},"PeriodicalIF":10.0,"publicationDate":"2022-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9569049/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33513608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lung recovery from DNA damage induced by graphene oxide is dependent on size, dose and inflammation profile.","authors":"Luis Augusto Visani de Luna,&nbsp;Thomas Loret,&nbsp;Alexander Fordham,&nbsp;Atta Arshad,&nbsp;Matthew Drummond,&nbsp;Abbie Dodd,&nbsp;Neus Lozano,&nbsp;Kostas Kostarelos,&nbsp;Cyrill Bussy","doi":"10.1186/s12989-022-00502-w","DOIUrl":"https://doi.org/10.1186/s12989-022-00502-w","url":null,"abstract":"<p><strong>Background: </strong>A key aspect of any new material safety assessment is the evaluation of their in vivo genotoxicity. Graphene oxide (GO) has been studied for many promising applications, but there are remaining concerns about its safety profile, especially after inhalation. Herein we tested whether GO lateral dimension, comparing micrometric (LGO) and nanometric (USGO) GO sheets, has a role in the formation of DNA double strand breaks in mouse lungs. We used spatial resolution and differential cell type analysis to measure DNA damages in both epithelial and immune cells, after either single or repeated exposure.</p><p><strong>Results: </strong>GO induced DNA damages were size and dose dependent, in both exposure scenario. After single exposure to a high dose, both USGO and LGO induced significant DNA damage in the lung parenchyma, but only during the acute phase response (p < 0.05 for USGO; p < 0.01 for LGO). This was followed by a fast lung recovery at day 7 and 28 for both GOs. When evaluating the chronic impact of GO after repeated exposure, only a high dose of LGO induced long-term DNA damages in lung alveolar epithelia (at 84 days, p < 0.05). Regardless of size, low dose GO did not induce any significant DNA damage after repeated exposure. A multiparametric correlation analysis of our repeated exposure data revealed that transient or persistent inflammation and oxidative stress were associated to either recovery or persistent DNA damages. For USGO, recovery from DNA damage was correlated to efficient recovery from acute inflammation (i.e., significant secretion of SAA3, p < 0.001; infiltration of neutrophils, p < 0.01). In contrast, the persistence of LGO in lungs was associated to a long-lasting presence of multinucleated macrophages (up to 84 days, p < 0.05), an underlying inflammation (IL-1α secretion up to 28 days, p < 0.05) and the presence of persistent DNA damages at 84 days.</p><p><strong>Conclusions: </strong>Overall these results highlight the importance of the exposure scenario used. We showed that LGO was more genotoxic after repeated exposure than single exposure due to persistent lung inflammation. These findings are important in the context of human health risk assessment and toward establishing recommendations for a safe use of graphene based materials in the workplace.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":null,"pages":null},"PeriodicalIF":10.0,"publicationDate":"2022-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9490925/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40374060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel in-situ method to determine the respiratory tract deposition of carbonaceous particles reveals dangers of public commuting in highly polluted megacity.","authors":"Leizel Madueño,&nbsp;Simonas Kecorius,&nbsp;Jakob Löndahl,&nbsp;Jürgen Schnelle-Kreis,&nbsp;Alfred Wiedensohler,&nbsp;Mira Pöhlker","doi":"10.1186/s12989-022-00501-x","DOIUrl":"https://doi.org/10.1186/s12989-022-00501-x","url":null,"abstract":"<p><strong>Background: </strong>Exposure to air pollutants is one of the major environmental health risks faced by populations globally. Information about inhaled particle deposition dose is crucial in establishing the dose-response function for assessing health-related effects due to exposure to air pollution.</p><p><strong>Objective: </strong>This study aims to quantify the respiratory tract deposition (RTD) of equivalent black carbon (BC) particles in healthy young adults during a real-world commuting scenario, analyze factors affecting RTD of BC, and provide key parameters for the assessment of RTD.</p><p><strong>Methods: </strong>A novel in situ method was applied to experimentally determine the RTD of BC particles among subjects in the highly polluted megacity of Metro Manila, Philippines. Exposure measurements were made for 40 volunteers during public transport and walking.</p><p><strong>Results: </strong>The observed BC exposure concentration was up to 17-times higher than in developed regions. The deposition dose rate (DDR) of BC was up to 3 times higher during commute inside a public transport compared to walking (11.6 versus 4.4 μg hr^-1, respectively). This is twice higher than reported in similar studies. The average BC mass deposition fraction (DF) was found to be 43 ± 16%, which can in large be described by individual factors and does not depend on gender.</p><p><strong>Conclusions: </strong>Commuting by open-sided public transport, commonly used in developing regions, poses a significant health risk due to acquiring extremely high doses of carcinogenic traffic-related pollutants. There is an urgent need to drastically update air pollution mitigation strategies for reduction of dangerously high emissions of BC in urban setting in developing regions. The presented mobile measurement set-up to determine respiratory tract deposition dose is a practical and cost-effective tool that can be used to investigate respiratory deposition in challenging environments.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":null,"pages":null},"PeriodicalIF":10.0,"publicationDate":"2022-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9476571/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40361799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pulmonary dust foci as rat pneumoconiosis lesion induced by titanium dioxide nanoparticles in 13-week inhalation study.","authors":"Shotaro Yamano,&nbsp;Yuko Goto,&nbsp;Tomoki Takeda,&nbsp;Shigeyuki Hirai,&nbsp;Yusuke Furukawa,&nbsp;Yoshinori Kikuchi,&nbsp;Tatsuya Kasai,&nbsp;Kyohei Misumi,&nbsp;Masaaki Suzuki,&nbsp;Kenji Takanobu,&nbsp;Hideki Senoh,&nbsp;Misae Saito,&nbsp;Hitomi Kondo,&nbsp;Yumi Umeda","doi":"10.1186/s12989-022-00498-3","DOIUrl":"https://doi.org/10.1186/s12989-022-00498-3","url":null,"abstract":"<p><strong>Background: </strong>Most toxicological studies on titanium dioxide (TiO₂) particles to date have concentrated on carcinogenicity and acute toxicity, with few studies focusing of pneumoconiosis, which is a variety of airspace and interstitial lung diseases caused by particle-laden macrophages. The present study examined rat pulmonary lesions associated with pneumoconiosis after inhalation exposure to TiO₂ nanoparticles (NPs).</p><p><strong>Methods: </strong>Male and female F344 rats were exposed to 6.3, 12.5, 25, or 50 mg/m³ anatase type TiO₂ NPs for 6 h/day, 5 days/week for 13 weeks using a whole-body inhalation exposure system. After the last exposure the rats were euthanized and blood, bronchoalveolar lavage fluid, and all tissues including lungs and mediastinal lymph nodes were collected and subjected to biological and histopathological analyses.</p><p><strong>Results: </strong>Numerous milky white spots were present in the lungs after exposure to 25 and 50 mg/m³ TiO₂ NPs. Histopathological analysis revealed that the spots were alveolar lesions, characterized predominantly by the agglomeration of particle-laden macrophages and the presence of reactive alveolar epithelial type 2 cell (AEC2) hyperplasia. We defined this characteristic lesion as pulmonary dust foci (PDF). The PDF is an inflammatory niche, with decreased vascular endothelial cells in the interstitium, and proliferating AEC2 transformed into alveolar epithelial progenitor cells. In the present study, the AEC2 in the PDF had acquired DNA damage. Based on PDF induction, the lowest observed adverse effect concentration for pulmonary disorders in male and female rats was 12.5 mg/m³ and 6.3 mg/m³, respectively. The no observed adverse effect concentration for male rats was 6.3 mg/m³. There was a sex difference in lung lesion development, with females showing more pronounced lesion parameters than males.</p><p><strong>Conclusions: </strong>Inhalation exposure to TiO₂ NPs caused PDF, an air-space lesion which is an alveolar inflammatory niche containing particle-laden macrophages and proliferating AEC2. These PDFs histopathologically resemble some pneumoconiosis lesions (pulmonary siderosis and hard metal pneumoconiosis) in workers and lung disease in smokers, suggesting that PDFs caused by exposure to TiO₂ NPs in rats are an early pneumoconiosis lesion and may be a common alveolar reaction in mammals.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":null,"pages":null},"PeriodicalIF":10.0,"publicationDate":"2022-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9472424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33465801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A systematic quality evaluation and review of nanomaterial genotoxicity studies: a regulatory perspective.","authors":"Kirsi K Siivola,&nbsp;Michael J Burgum,&nbsp;Blanca Suárez-Merino,&nbsp;Martin J D Clift,&nbsp;Shareen H Doak,&nbsp;Julia Catalán","doi":"10.1186/s12989-022-00499-2","DOIUrl":"https://doi.org/10.1186/s12989-022-00499-2","url":null,"abstract":"<p><p>The number of publications in the field of nanogenotoxicology and the amount of genotoxicity data on nanomaterials (NMs) in several databases generated by European Union (EU) funded projects have increased during the last decade. In parallel, large research efforts have contributed to both our understanding of key physico-chemical (PC) parameters regarding NM characterization as well as the limitations of toxicological assays originally designed for soluble chemicals. Hence, it is becoming increasingly clear that not all of these data are reliable or relevant from the regulatory perspective. The aim of this systematic review is to investigate the extent of studies on genotoxicity of NMs that can be considered reliable and relevant by current standards and bring focus to what is needed for a study to be useful from the regulatory point of view. Due to the vast number of studies available, we chose to limit our search to two large groups, which have raised substantial interest in recent years: nanofibers (including nanotubes) and metal-containing nanoparticles. Focusing on peer-reviewed publications, we evaluated the completeness of PC characterization of the tested NMs, documentation of the model system, study design, and results according to the quality assessment approach developed in the EU FP-7 GUIDEnano project. Further, building on recently published recommendations for best practices in nanogenotoxicology research, we created a set of criteria that address assay-specific reliability and relevance for risk assessment purposes. Articles were then reviewed, the qualifying publications discussed, and the most common shortcomings in NM genotoxicity studies highlighted. Moreover, several EU projects under the FP7 and H2020 framework set the aim to collectively feed the information they produced into the eNanoMapper database. As a result, and over the years, the eNanoMapper database has been extended with data of various quality depending on the existing knowledge at the time of entry. These activities are highly relevant since negative results are often not published. Here, we have reviewed the NanoInformaTIX instance under the eNanoMapper database, which hosts data from nine EU initiatives. We evaluated the data quality and the feasibility of use of the data from a regulatory perspective for each experimental entry.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":null,"pages":null},"PeriodicalIF":10.0,"publicationDate":"2022-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9472411/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10442126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amine-modified nanoplastics promote the procoagulant activation of isolated human red blood cells and thrombus formation in rats.","authors":"Eun-Hye Kim,&nbsp;Sungbin Choi,&nbsp;Donghyun Kim,&nbsp;Han Jin Park,&nbsp;Yiying Bian,&nbsp;Sang Ho Choi,&nbsp;Han Young Chung,&nbsp;Ok-Nam Bae","doi":"10.1186/s12989-022-00500-y","DOIUrl":"https://doi.org/10.1186/s12989-022-00500-y","url":null,"abstract":"<p><strong>Background: </strong>Microplastics (MPs) and nanoplastics (NPs) formed from decomposed plastic are increasing environmental threats. Although MPs and NPs exposed through various routes enter the systemic circulation, the potential toxicity of those is largely unknown. We investigated whether polystyrene NPs (PS-NPs) promote the coagulation activity of red blood cells (RBCs).</p><p><strong>Results: </strong>We tested several types of PS-NPs using human RBCs and found that amine-modified 100 nm PS-NPs were the most potent. We measured the uptake of PS-NPs using flow cytometry and confocal microscopy. Electron microscopy revealed morphological changes of RBCs by PS-NPs. PS-NPs induced the externalization of phosphatidylserine, generation of microvesicles in RBCs, and perturbations in the intracellular microenvironment. PS-NPs increased the activity of scramblases responsible for phospholipid translocation in RBCs. PS-NPs modulated the functional interaction to adjacent tissues and coagulation cascade, enhancing RBC adhesion and thrombin generation. Our observations in human RBCs were consistent with those in isolated rat RBCs, showing no inter-species differences. In rat venous thrombosis models, the intravenous administration of PS-NPs enhanced thrombus formation.</p><p><strong>Conclusion: </strong>Amine-modified PS-NPs induce the prothrombotic activation of RBCs causing thrombus formation. We believe that our study will contribute to understanding the potential toxicity of amine-modified polystyrene particles in blood cells and cardiovascular systems.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":null,"pages":null},"PeriodicalIF":10.0,"publicationDate":"2022-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9472436/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40357109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic maternal exposure to titanium dioxide nanoparticles alters breathing in newborn offspring.","authors":"Eloïse Colnot,&nbsp;Laura Cardoit,&nbsp;Marie-Jeanne Cabirol,&nbsp;Lydia Roudier,&nbsp;Marie-Helene Delville,&nbsp;Anne Fayoux,&nbsp;Muriel Thoby-Brisson,&nbsp;Laurent Juvin,&nbsp;Didier Morin","doi":"10.1186/s12989-022-00497-4","DOIUrl":"https://doi.org/10.1186/s12989-022-00497-4","url":null,"abstract":"<p><strong>Background: </strong>Over the last two decades, nanotechnologies and the use of nanoparticles represent one of the greatest technological advances in many fields of human activity. Particles of titanium dioxide (TiO₂) are one of the nanomaterials most frequently found in everyday consumer products. But, due in particular to their extremely small size, TiO₂ nanoparticles (NPs) are prone to cross biological barriers and potentially lead to adverse health effects. The presence of TiO₂ NPs found in human placentae and in the infant meconium has indicated unequivocally the capacity for a materno-fetal transfer of this nanomaterial. Although chronic exposure to TiO₂ NPs during pregnancy is known to induce offspring cognitive deficits associated with neurotoxicity, the impact of a gestational exposure on a vital motor function such as respiration, whose functional emergence occurs during fetal development, remains unknown.</p><p><strong>Results: </strong>Using in vivo whole-body plethysmographic recordings from neonatal mice, we show that a chronic exposure to TiO₂ NPs during pregnancy alters the respiratory activity of offspring, characterized by an abnormally elevated rate of breathing. Correspondingly, using ex vivo electrophysiological recordings performed on isolated brainstem-spinal cord preparations of newborn mice and medullary slice preparations containing specific nuclei controlling breathing frequency, we show that the spontaneously generated respiratory-related rhythm is significantly and abnormally accelerated in animals prenatally exposed to TiO₂ NPs. Moreover, such a chronic prenatal exposure was found to impair the capacity of respiratory neural circuitry to effectively adjust breathing rates in response to excitatory environmental stimuli such as an increase in ambient temperature.</p><p><strong>Conclusions: </strong>Our findings thus demonstrate that a maternal exposure to TiO₂ NPs during pregnancy affects the normal development and operation of the respiratory centers in progeny.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":null,"pages":null},"PeriodicalIF":10.0,"publicationDate":"2022-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9386967/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40623691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}