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- Quaternary mixtures of TiO2NP, CeO2NP, arsenic, and mercury potentiate A549, HepG2 and SH-SY5Y cells cytotoxicityPublication . Rosário, Fernanda; Costa, Carla; Teixeira, João; Reis, Ana TeresaIntroduction: Nanoparticles (NP) released to the environment interact with pre-existing contaminants, potentially leading to cytotoxicity and raising concerns regarding human safety to co- exposure to multiple chemicals. This work assesses and compares viability of A549, HepG2 and SH-SY5Y cells after short (24h; WST-1 assay) and long-term (7 days; clonogenic assay) exposure to single and quaternary mixtures of: titanium dioxide nanoparticles (TiO2NP) 0.75; 75 mg/L; cerium oxide nanoparticles (CeO2NP) 0.1; 10 μg/L; arsenic (As) 0.01; 0.75; 2.5 mg/L; and mercury (Hg) 0.5; 10; 20 mg/L. Mixtures were divided in four groups: low, mid-low, mid- high and high.
- Genotoxicity and Gene Expression in the Rat Lung Tissue following Instillation and Inhalation of Different Variants of Amorphous Silica Nanomaterials (aSiO2 NM)Publication . Brandão, Fátima; Costa, Carla; Bessa, Maria João; Dumortier, Elise; Debacq-Chainiaux, Florence; Hubaux, Roland; Salmon, Michel; Laloy, Julie; Stan, Miruna S.; Hermenean, Anca; Gharbia, Sami; Dinischiotu, Anca; Bannuscher, Anne; Hellack, Bryan; Haase, Andrea; Fraga, Sónia; Teixeira, JoãoSeveral reports on amorphous silica nanomaterial (aSiO2 NM) toxicity have been questioning their safety. Herein, we investigated the in vivo pulmonary toxicity of four variants of aSiO2 NM: SiO2_15_Unmod, SiO2_15_Amino, SiO2_7 and SiO2_40. We focused on alterations in lung DNA and protein integrity, and gene expression following single intratracheal instillation in rats. Additionally, a short-term inhalation study (STIS) was carried out for SiO2_7, using TiO2_NM105 as a benchmark NM. In the instillation study, a significant but slight increase in oxidative DNA damage in rats exposed to the highest instilled dose (0.36 mg/rat) of SiO2_15_Amino was observed in the recovery (R) group. Exposure to SiO2_7 or SiO2_40 markedly increased oxidative DNA lesions in rat lung cells of the exposure (E) group at every tested dose. This damage seems to be repaired, since no changes compared to controls were observed in the R groups. In STIS, a significant increase in DNA strand breaks of the lung cells exposed to 0.5 mg/m3 of SiO2_7 or 50 mg/m3 of TiO2_NM105 was observed in both groups. The detected gene expression changes suggest that oxidative stress and/or inflammation pathways are likely implicated in the induction of (oxidative) DNA damage. Overall, all tested aSiO2 NM were not associated with marked in vivo toxicity following instillation or STIS. The genotoxicity findings for SiO2_7 from instillation and STIS are concordant; however, changes in STIS animals were more permanent/difficult to revert.
- Comparative assessment of the acute toxicity of commonly used metal nanoparticles in two in vitro models of human barriersPublication . Pires, J.; Moreira, L.; Teixeira, João; Fraga, SóniaMetal nanoparticles (M-NP) have application in several areas such as industry, environment, agriculture, and biomedicine. Consequently, human exposure to these nanosized materials is increasing, which raises serious concerns regarding their safety to the human health and the environment. Biological barriers are important lines of defence to xenobiotics, thus expected targets for M-NP. The present study investigated the in vitro toxicity of different types of M-NP in two cell models of biological barriers: human intestinal (Caco-2) and trophoblastic (BeWo clone b30) epithelial cells. Cells were exposed for 24 h to varied concentrations (0.8-48 µg/cm2) of M NP of different chemical composition (Au, Ag, TiO2), primary size (10, 30 and 60 nm), capping (citrate, PEG) and crystal structure (rutile, anatase) and toxicity assessed by determining changes in cell morphology, metabolic activity, plasma membrane integrity, generation of intracellular reactive oxygen species (ROS) and intracellular ATP levels. Our data show that the potential toxicity of the tested M-NPs is similar for both cell lines with AgNPs > AuNPs > TiO2NPs, being the effects more visible at higher concentrations. The influence of the size in the cytotoxic-induced effects was more evident for AgNP than for AuNP, with the smaller NP causing more toxicity, being the BeWo cells more sensitive to these M-NP. In addition, PEG-capping effectively attenuated AuNP-induced toxicity both in Caco-2 and BeWo cells. Only cells exposed to AgNP exhibited significant increased levels of ROS. Thus, our data support that the physicochemical properties of the nanomaterials, in this particular case of M-NP, is an important determinant of their cytotoxicity and that intestinal and trophoblastic cells exhibit different sensitivity to the tested M-NP. Future studies would be useful to further explore the effects of M-NP in the human barriers
- Short term associations of ambient nitrogen dioxide with daily total, cardiovascular, and respiratory mortality: multilocation analysis in 398 citiesPublication . Meng, Xia; Liu, Cong; Chen, Renjie; Sera, Francesco; Vicedo-Cabrera, Ana Maria; Milojevic, Ai; Guo, Yuming; Tong, Shilu; Coelho, Micheline de Sousa Zanotti Staglior; Saldiva, Paulo Hilario Nascimento; Lavigne, Eric; Correa, Patricia Matus; Ortega, Nicolas Valdes; Osorio Garcia, Samuel; Kyselý, Jan; Urban, Aleš; Orru, Hans; Maasikmets, Marek; Jaakkola, Jouni J.K.; Ryti, Niilo; Huber, Veronika; Schneider, Alexandra; Katsouyanni, Klea; Analitis, Antonis; Hashizume, Masahiro; Honda, Yasushi; Ng, Chris Fook Sheng; Nunes, Baltazar; Teixeira, João Paulo; Holobaca, Iulian Horia; Fratianni, Simona; Kim, Ho; Tobias, Aurelio; Íñiguez, Carmen; Forsberg, Bertil; Åström, Christofer; Ragettli, Martina S.; Guo, Yue-Liang Leon; Pan, Shih-Chun; Li, Shanshan; Bell, Michelle L.; Zanobetti, Antonella; Schwartz, Joel; Wu, Tangchun; Gasparrini, Antonio; Kan, HaidongObjective: To evaluate the short term associations between nitrogen dioxide (NO2) and total, cardiovascular, and respiratory mortality across multiple countries/regions worldwide, using a uniform analytical protocol. Design: Two stage, time series approach, with overdispersed generalised linear models and multilevel meta-analysis. Setting: 398 cities in 22 low to high income countries/regions. Main outcome measures: Daily deaths from total (62.8 million), cardiovascular (19.7 million), and respiratory (5.5 million) causes between 1973 and 2018. Results: On average, a 10 μg/m3 increase in NO2 concentration on lag 1 day (previous day) was associated with 0.46% (95% confidence interval 0.36% to 0.57%), 0.37% (0.22% to 0.51%), and 0.47% (0.21% to 0.72%) increases in total, cardiovascular, and respiratory mortality, respectively. These associations remained robust after adjusting for co-pollutants (particulate matter with aerodynamic diameter ≤10 μm or ≤2.5 μm (PM10 and PM2.5, respectively), ozone, sulfur dioxide, and carbon monoxide). The pooled concentration-response curves for all three causes were almost linear without discernible thresholds. The proportion of deaths attributable to NO2 concentration above the counterfactual zero level was 1.23% (95% confidence interval 0.96% to 1.51%) across the 398 cities. Conclusions: This multilocation study provides key evidence on the independent and linear associations between short term exposure to NO2 and increased risk of total, cardiovascular, and respiratory mortality, suggesting that health benefits would be achieved by tightening the guidelines and regulatory limits of NO2.
- Effects of Hot Nights on Mortality in Southern EuropePublication . Royé, Dominic; Sera, Francesco; Tobías, Aurelio; Lowe, Rachel; Gasparrini, Antonio; Pascal, Mathilde; de’Donato, Francesca; Nunes, Baltazar; Teixeira, João PauloBackground: There is strong evidence concerning the impact of heat stress on mortality, particularly from high temperatures. However, few studies to our knowledge emphasize the importance of hot nights, which may prevent necessary nocturnal rest. Objectives: In this study, we use hot-night duration and excess to predict daily cause-specific mortality in summer, using multiple cities across Southern Europe. Methods: We fitted time series regression models to summer cause-specific mortality, including natural, respiratory, and cardiovascular causes, in 11 cities across four countries. We included a distributed lag nonlinear model with lags up to 7 days for hot night duration and excess adjusted by daily mean temperature. We summarized city-specific associations as overall-cumulative exposure-response curves at the country level using meta-analysis. Results: We found positive but generally nonlinear associations between relative risk (RR) of cause-specific mortality and duration and excess of hot nights. RR of duration associated with nonaccidental mortality in Portugal was 1.29 (95% confidence interval [CI] = 1.07, 1.54); other associations were imprecise, but we also found positive city-specific estimates for Rome and Madrid. Risk of hot-night excess ranged from 1.12 (95% CI = 1.05, 1.20) for France to 1.37 (95% CI = 1.26, 1.48) for Portugal. Risk estimates for excess were consistently higher than for duration. Conclusions: This study provides new evidence that, over a wider range of locations, hot night indices are strongly associated with cause-specific deaths. Modeling the impact of thermal characteristics during summer nights on mortality could improve decisionmaking for preventive public health strategies.