Growth of Chlorella vulgaris and Chlamydomonas reinhardtii for biodiesel production and carbon dioxide capture

The growth of two strains of green microalgae, Chlorella vulgaris (UTEX 2714) and Chlamydomonas reinhardtii (UTEX 90) was tested in three types of media; Tris Acetate Phosphate (TAP), Bushnell Haas Broth (BHB), and Wright\u27s Cryptophytes (WC buffered with either glycylglycine or Tris-base). Also, initial medium pH is ranging from 4 to 10, light intensity ranging from 100 to 600 micromol photons/m 2s, and CO2 concentrations ranging from 0.038% (ambient) to 12%, were tested. WC medium at pH 8 buffered with glycylglycine sustained the highest yield and best buffering capacity for growth of both C. vulgaris and C. reinhardtii. A light intensity of 200 micromol photons m-2s-1 provided for both good growth and electron transport rate (ETR). Both C. vulgaris and C. reinhardtii produced highest final yields when grown with 6% CO2. Also, lipid content increased with increasing CO2 concentration. Myristoleic acid (C14:1), palmitic acid (C16:0), stearic acid (C18:0), oleic acid (C18:1n9), linoleic acid (C18:2), and docosahexaenoic acid (DHA) were found in higher content when C. vulgaris was grown on 12% CO2, while the content of palmitoleic acid (C16:1), elaidic acid (C18:1t9), vaccenic acid (C18:1n7) were similar among all CO 2 concentration tested. CO2 capture was explored using two approaches: consumption of known quantities of CO2 in sealed serum bottles, and consumption of CO2 flowing through immobilized algal beads. In both cases, fixation rate decreased with increasing CO2 concentration. CO2 consumption generally decreased over the five day experiment. The rate observed using immobilized algae was 20% of the maximum obtained in liquid culture, indicating the need to future optimize this novel method for CO2 capture

Integrated Transcriptomics, Metabolomics, and Lipidomics Profiling in Rat Lung, Blood, and Serum for Assessment of Laser Printer-Emitted Nanoparticle Inhalation Exposure-Induced Disease Risks

settings Open AccessArticle Integrated Transcriptomics, Metabolomics, and Lipidomics Profiling in Rat Lung, Blood, and Serum for Assessment of Laser Printer-Emitted Nanoparticle Inhalation Exposure-Induced Disease Risks by Nancy Lan Guo 1,*,Tuang Yeow Poh 2,Sandra Pirela 3,Mariana T. Farcas 4,Sanjay H. Chotirmall 2,Wai Kin Tham 5,Sunil S. Adav 5,Qing Ye 1,Yongyue Wei 6,Sipeng Shen 2,David C. Christiani 2,Kee Woei Ng 3,7,8,Treye Thomas 9,Yong Qian 4 andPhilip Demokritou 3 1 West Virginia University Cancer Institute/School of Public Health, West Virginia University, Morgantown, WV 26506, USA 2 Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore 308232, Singapore 3 Center for Nanotechnology and Nanotoxicology, Department of Environmental Health, T. H. Chan School of Public Health, Harvard University, Boston, MA 02115, USA 4 Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USA 5 Singapore Phenome Centre, Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore 636921, Singapore 6 Key Lab for Modern Toxicology, Department of Epidemiology and Biostatistics and Ministry of Education (MOE), School of Public Health, Nanjing Medical University, Nanjing 210029, China 7 School of Materials Science and Engineering, Nanyang Technological University, Singapore 639798, Singapore 8 Environmental Chemistry and Materials Centre, Nanyang Environment & Water Research Institute, Singapore 637141, Singapore 9 Office of Hazard Identification and Reduction, U.S. Consumer Product Safety Commission, Rockville, MD 20814, USA * Author to whom correspondence should be addressed. Int. J. Mol. Sci. 2019, 20(24), 6348; https://doi.org/10.3390/ijms20246348 Received: 2 December 2019 / Revised: 12 December 2019 / Accepted: 13 December 2019 / Published: 16 December 2019 (This article belongs to the Special Issue Advances in Nanostructured Materials between Pharmaceutics and Biomedicine) Download PDF Browse Figures Review Reports Cite This Paper Abstract Laser printer-emitted nanoparticles (PEPs) generated from toners during printing represent one of the most common types of life cycle released particulate matter from nano-enabled products. Toxicological assessment of PEPs is therefore important for occupational and consumer health protection. Our group recently reported exposure to PEPs induces adverse cardiovascular responses including hypertension and arrythmia via monitoring left ventricular pressure and electrocardiogram in rats. This study employed genome-wide mRNA and miRNA profiling in rat lung and blood integrated with metabolomics and lipidomics profiling in rat serum to identify biomarkers for assessing PEPs-induced disease risks. Whole-body inhalation of PEPs perturbed transcriptional activities associated with cardiovascular dysfunction, metabolic syndrome, and neural disorders at every observed time point in both rat lung and blood during the 21 days of exposure. Furthermore, the systematic analysis revealed PEPs-induced transcriptomic changes linking to other disease risks in rats, including diabetes, congenital defects, auto-recessive disorders, physical deformation, and carcinogenesis. The results were also confirmed with global metabolomics profiling in rat serum. Among the validated metabolites and lipids, linoleic acid, arachidonic acid, docosahexanoic acid, and histidine showed significant variation in PEPs-exposed rat serum. Overall, the identified PEPs-induced dysregulated genes, molecular pathways and functions, and miRNA-mediated transcriptional activities provide important insights into the disease mechanisms. The discovered important mRNAs, miRNAs, lipids and metabolites may serve as candidate biomarkers for future occupational and medical surveillance studies. To the best of our knowledge, this is the first study systematically integrating in vivo, transcriptomics, metabolomics, and lipidomics to assess PEPs inhalation exposure-induced disease risks using a rat model

In vitro and in vivo toxicological evaluation of emissions from the fused filament fabrication three-dimensional printing

Fused filament fabrication (FFF), a three-dimensional (3-D) printing process, is an emerging technology that has recently gained wide popularity among both consumers and manufacturers. As filament is heated to above its glass transition temperature in a 3-D printer, a portion may undergo thermal decompostion, which releases ultrafine particles (UFP) and volatile organic compounds (VOCs) with potential adverse respiratory health effects are released into the air. This study\u27s central hypotheses is that emissions generated during 3-D printing are toxic and exposure to these emissions induces pulmonary and systemic adverse health effects. Considering that currently, limited understanding is available on the health impact of the FFF 3-D printer exposures, the overall goal of this research was to fill the knowledge gap by pursuing the following three studies. The aim of the first study was to assess acrylonitrile butadiene styrene (ABS) and polycarbonate (PC) filaments 3-D printer emissions-induced cell toxicity. In this study, the particles and vapors released during printing were collected directly into the cell culture medium and delivered to the small airway epithelial cells at six concentrations. At 24 h, various endpoints, such as cellular uptake, cell viability, cell membrane damage, ROS production, total antioxidant capacity, glutathione peroxidase levels in cell lysates, cell death mechanisms (apoptosis and necrosis), and cytokines and chemokines released in cell supernatants were measured. To analyze the data, mixed model regression analyses were performed on these endpoints using particle numbers as the independent variable. The regression lines illustrated a significant doseresponse relationship between a decrease in cell viability and the number of emitted particles, which correlated with a significant dose-dependent increase in the LDH activity, and all other endpoints evaluated. The aim of the second study was to assess pulmonary and systemic toxicity in rats following whole-body inhalation exposure to ABS filament 3-D printer emissions. In this study, male Sprague Dawley rats were exposed to filtered air or ABS emissions for 1, 4, 8, 15, or 30 days (4 h/day, 4 days/week). The average mass concentration and number of particulate generated during 4-h real-time printing of three desktop 3-D printers operating simultaneously was 240 µg/m3 and 8.84 x 10⁴ particles/m³. At the start of the exposure (day 1), a predominant pro-inflammatory response was seen in BALF, represented by an increase in IFN-γ and TNF-α Th1-type cytokines followed by a switch to an anti-inflammatory response by day 15 of exposure represented by a rise in IL-10 Th2-type cytokine. The Th1/Th2 switch could be responsible for the initial “delayed” influx of the alveolar macrophages and its peak occurrence at 15 days of exposure, which corresponded with a significant increase in blood monocytes and platelet counts. Other systemic changes noted were that initially (day 1), a significant increase in both hepatic and renal biomarkers was found; however, at day 15 of exposure, only renal biomarkers were increased. At the longest exposure duration (day 30), all the endpoints evaluated returned to the control levels. Neither pulmonary oxidative stress responses nor histopathological changes of the lungs and nasal passages were found among the treatments. The aim of the third study was to evaluate the pulmonary effects of FFF 3-D printer emissions using a relevant human ALI organotypic airway tissue model to mimic the respiratory behavior upon exposure. Primary normal, human-derived bronchial epithelial cells (NHBEs) were directly exposed for 4 h to ABS filament emissions. NHBEs epithelium integrity and differentiation changes, cytotoxicity, tissue injury, and inflammatory and immune system regulation markers were evaluated following exposure and 24 h after the end of the exposure. Overall, at the conditions applied, exposure of NHBEs to ABS emissions did not affect epithelium integrity, ciliation, mucus production, or induce cytotoxicity. At 24 h after the exposure, significant increases in IL-12p70, IFN-γ, TNF-α, IL-17A, VEGF, and MIP-1α were noted in the basal cell culture medium of ABS-exposed cells compared to chamber control cells. Overall, toxicological evaluation of FFF 3-D printer emissions was conducted in three different conditions, 1) traditional submerged culture of human small airway epithelial cells, 2) repeated whole-body inhalation exposure of rats to freshly generated aerosols, and 3) advanced human ALI organotypic airway tissue model. At the experimental conditions applied, in both in vitro models and in vivo, 3-D printer emissions produced minimal to moderate pulmonary toxicity. Furthermore, these findings were consistent with results observed in the physiologically relevant in vivo-like in vitro model cultured at ALI. In conclusion, these studies indicate that the FFF 3-D printer emissions could induce moderate toxicological effects. These studies are significant as they are amongst the first and comprehensive studies published to evaluate the pulmonary and systemic toxicity of 3-D printer emissions. Further studies are needed to establish a more broad exposure-dose-response relationships and integration of in vivo and in vitro responses

GENERAL ASPECTS REGARDING THE PRESENT SITUATION OF AREAS AFFECTED BY SUBSIDENCE PRODUCED BY EXPLOITATION OF ROCK SALT BY DISSOLVING

The exploitation by dissolution has different characteristics compared to other types of exploitations, because these types of exploitations are exposed to uncontrolled dissolution phenomenon, which may occur in rapid subsidence and collapse, depending on the value of the hydraulic gradient. Study of areas affected by the exploitation of salt by dissolution was and is a constant concern of those in charge with the exploitation but has not been analysed in detail. The research was limited only to monitor the phenomena and to find solutions for eliminating the consequences than knowledge and removing the causes

Fibrillar vs crystalline nanocellulose pulmonary epithelial cell responses: Cytotoxicity or inflammation?

Nanocellulose (NC) is emerging as a highly promising nanomaterial for a wide range of applications. Moreover, many types of NC are produced, each exhibiting a slightly different shape, size, and chemistry. The main objective of this study was to compare cytotoxic effects of cellulose nanocrystals (CNC) and nanofibrillated cellulose (NCF). The human lung epithelial cells (A549) were exposed for 24 h and 72 h to five different NC particles to determine how variations in properties contribute to cellular outcomes, including cytotoxicity, oxidative stress, and cytokine secretion. Our results showed that NCF were more toxic compared to CNC particles with respect to cytotoxicity and oxidative stress responses. However, exposure to CNC caused an inflammatory response with significantly elevated inflammatory cytokines/chemokines compared to NCF. Interestingly, cellulose staining indicated that CNC particles, but not NCF, were taken up by the cells. Furthermore, clustering analysis of the inflammatory cytokines revealed a similarity of NCF to the carbon nanofibers response and CNC to the chitin, a known immune modulator and innate cell activator. Taken together, the present study has revealed distinct differences between fibrillar and crystalline nanocellulose and demonstrated that physicochemical properties of NC are critical in determining their toxicity

In Vitro Toxicity Evaluation of Lignin-(Un)coated Cellulose Based Nanomaterials on Human A549 and THP‑1 Cells

A significant amount of research toward commercial development of cellulose based nanomaterials (CNM) is now in progress with some potential applications. Using human A549 and THP-1 cells, we evaluated the biological responses of various CNMs, made out of similar material but with functional and morphological variations. While A549 cells displayed minimal or no cytotoxic responses following exposure to CNMs, THP-1 cells were more susceptible to cytotoxicity, cellular damage and inflammatory responses. Further analysis of these biological responses evaluated using hierarchical clustering approaches was effective in discriminating (dis)-similarities of various CNMs studied and identified potential inflammatory factors contributing to cytotoxicity. No correlation between cytotoxicity and surface properties of CNMs was found. This study clearly highlights that, in addition to the source and characteristics of CNMs, cell type-specific differences in the recognition/uptake of CNMs along with their inherent capability to respond to external stimuli are crucial for assessing the toxicity of CNMs