Biological effects of inhaled hydraulic fracturing sand dust in rats
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA623605 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11504900_1.fastq.gz | Fastqsanger.gz | |||
| SRR11504900_2.fastq.gz | Fastqsanger.gz | |||
| SRR11504901_1.fastq.gz | Fastqsanger.gz | |||
| SRR11504901_2.fastq.gz | Fastqsanger.gz | |||
| SRR11504902_1.fastq.gz | Fastqsanger.gz |
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Project description:The pulmonary inflammatory response to inhalation exposure to fracking sand dust (FSD) was investigated in a rat model. Adult male Sprague-Dawley rats were exposed by whole-body inhalation to air or an aerosol of FSD at concentrations of 10 or 30 mg/m3, 6 hours/day for 4 days. The control and FSD-exposed rats were euthanized at post-exposure time intervals of 1, 7 or 27days and pulmonary inflammatory, cytotoxic and oxidant responses were determined. Deposition of FSD particles was detected in the lungs of all the FSD-exposed rats. Analysis of bronchoalveolar lavage parameters of toxicity, oxidant generation, and inflammation did not reveal any significant persistent pulmonary toxicity in the FSD- exposed rats. Similarly, the lung histology of the FSD-exposed rats showed only minimal changes in influx of macrophages following the exposure. Determination of global gene expression profiles detected significant differential expressions of only six and five genes in the 10 mg/m3, 1 day post-exposure, and the 30 mg/m3, 7-day post-exposure FSD groups, respectively. Taken together, data obtained from the present study demonstrated that FSD inhalation exposure resulted in minimal/no toxicity or gene expression changes in the lungs of the rats.
2020-10-01 | GSE148255 | GEO
Project description:Hydraulic fracturing ("fracking") is a process used to enhance retrieval of gas from subterranean natural gas-laden rock by fracturing it under pressure. Sand used to stabilize fissures and facilitate gas flow creates a potential occupational hazard from respirable fracking sand dust (FSD). As studies of the immunotoxicity of FSD are lacking, the effects of whole-body inhalation (6 h/d for 4 d) of a FSD, i.e., FSD 8, was investigated at 1, 7, and 27 d post-exposure in rats. Exposure to 10 mg/m3 FSD 8 resulted in decreased lung-associated lymph node (LLN) cellularity, total B-cells, CD4+ T-cells, CD8+ T-cells and total natural killer (NK) cells at 7-d post exposure. The frequency of CD4+ T-cells decreased while the frequency of B-cells increased (7 and 27 d) in the LLN. In contrast, increases in LLN cellularity and increases in total CD4+ and CD8+ T-cells were observed in rats following 30 mg/m3 FSD 8 at 1 d post-exposure. Increases in the frequency and number of CD4+ T-cells and NK cells were observed in bronchial alveolar lavage fluid at 7-d post-exposure (10 mg/m3) along with an increase in total CD4+ T-cells, CD11b + cells, and NK cells at 1-day post-exposure (30 mg/m3). Increases in the numbers of B-cells and CD8+ T-cells were observed in the spleen at 1-day post 30 mg/m3 FSD 8 exposure. In addition, NK cell activity was suppressed at 1 d (30 mg/m3) and 27 d post-exposure (10 mg/m3). No change in the IgM response to sheep red blood cells was observed. The findings indicate that FSD 8 caused alterations in cellularity, phenotypic subsets, and impairment of immune function.
| S-EPMC7796771 | biostudies-literature
Project description:Pulmonary effects of inhaled diesel exhaust and fracking sand particles in rats
| PRJNA1011879 | ENA
Project description:Hydraulic fracturing creates fissures in subterranean rock to increase the flow and retrieval of natural gas. Sand ("proppant") in fracking fluid injected into the well bore maintains fissure patency. Fracking sand dust (FSD) is generated during manipulation of sand to prepare the fracking fluid. Containing respirable crystalline silica, FSD could pose hazards similar to those found in work sites where silica inhalation induces lung disease such as silicosis. This study was performed to evaluate the possible toxic effects following inhalation of a FSD (FSD 8) in the lung and airways. Rats were exposed (6 h/d × 4 d) to 10 or 30 mg/m3 of a FSD collected at a gas well, and measurements were performed 1, 7, 27 and, in one series of experiments, 90 d post-exposure. The following ventilatory and non-ventilatory parameters were measured in vivo and/or in vitro: 1) lung mechanics (respiratory system resistance and elastance, tissue damping, tissue elastance, Newtonian resistance and hysteresivity); 2) airway reactivity to inhaled methacholine (MCh); airway epithelium integrity (isolated, perfused trachea); airway efferent motor nerve activity (electric field stimulation in vitro); airway smooth muscle contractility; ion transport in intact and cultured epithelium; airway effector and sensory nerves; tracheal particle deposition; and neurogenic inflammation/vascular permeability. FSD 8 was without large effect on most parameters, and was not pro-inflammatory, as judged histologically and in cultured epithelial cells, but increased reactivity to inhaled MCh at some post-exposure time points and affected Na+ transport in airway epithelial cells.
| S-EPMC7736927 | biostudies-literature
Project description:The pulmonary response to inhalation exposure to diesel exhaust particles (DEP) and fracking sand particles (FSD) was investigated in a rat model. Healthy adult male Sprague-Dawley rats were exposed by whole-body inhalation to air (control) or an aerosol containing DEP at a concentration of 1.0 mg/m3 combined with FSD at concentrations of 30 mg/m3, 6 hours/day for 4 days. The control and DEP/FSD exposed rats were euthanized at post-exposure time intervals of 1, 7, or 27 days and pulmonary inflammatory, cytotoxic, and oxidant responses were determined. Analysis of bronchoalveolar lavage parameters of toxicity such as lactate dehydrogenase activity, oxidant generation, and inflammation revealed only minimal changes in pulmonary toxicity in the DEP/FSD-exposed rats, compared with the time-matched controls. The lung gene expression profiles showed only minimal changes in the DEP/FSD exposed rats compared with the controls. Specifically, there were a total of 6 genes significantly differentially expressed (fold change >1.5 and FDR p<0.05) only at the one-day post-exposure group. The data obtained from the present study demonstrated that DEP/FSD inhalation exposure, under the conditions employed in the present study, resulted in only minimal changes in lung toxicity and gene expression profile in the rats.
2024-12-01 | GSE242155 | GEO
Project description:Synergism of Iraqi Sand/Cigarette Smoke Co-Exposure in Rats. 24 samples are used.
2012-01-01 | GSE28804 | GEO
Project description:Hydraulic fracturing (fracking) is a process used to recover oil and gas from shale rock formation during unconventional drilling. Pressurized liquids containing water and sand (proppant) are used to fracture the oil- and natural gas-laden rock. The transportation and handling of proppant at well sites generate dust aerosols; thus, there is concern of worker exposure to such fracking sand dusts (FSD) by inhalation. FSD are generally composed of respirable crystalline silica and other minerals native to the geological source of the proppant material. Field investigations by NIOSH suggest that the levels of respirable crystalline silica at well sites can exceed the permissible exposure limits. Thus, from an occupational safety perspective, it is important to evaluate the potential toxicological effects of FSD, including any neurological risks. Here, we report that acute inhalation exposure of rats to one FSD, i.e., FSD 8, elicited neuroinflammation, altered the expression of blood brain barrier-related markers, and caused glial changes in the olfactory bulb, hippocampus and cerebellum. An intriguing observation was the persistent reduction of synaptophysin 1 and synaptotagmin 1 proteins in the cerebellum, indicative of synaptic disruption and/or injury. While our initial hazard identification studies suggest a likely neural risk, more research is necessary to determine if such molecular aberrations will progressively culminate in neuropathology/neurodegeneration leading to behavioral and/or functional deficits.
| S-EPMC7758814 | biostudies-literature
Project description:The pulmonary inflammatory response to inhalation exposure to a fracking sand dust (FSD 8) was investigated in a rat model. Adult male Sprague-Dawley rats were exposed by whole-body inhalation to air or an aerosol of a FSD, i.e., FSD 8, at concentrations of 10 or 30 mg/m3, 6 h/d for 4 d. The control and FSD 8-exposed rats were euthanized at post-exposure time intervals of 1, 7 or 27 d and pulmonary inflammatory, cytotoxic and oxidant responses were determined. Deposition of FSD 8 particles was detected in the lungs of all the FSD 8-exposed rats. Analysis of bronchoalveolar lavage parameters of toxicity, oxidant generation, and inflammation did not reveal any significant persistent pulmonary toxicity in the FSD 8-exposed rats. Similarly, the lung histology of the FSD 8-exposed rats showed only minimal changes in influx of macrophages following the exposure. Determination of global gene expression profiles detected statistically significant differential expressions of only six and five genes in the 10 mg/m3, 1-d post-exposure, and the 30 mg/m3, 7-d post-exposure FSD 8 groups, respectively. Taken together, data obtained from the present study demonstrated that FSD 8 inhalation exposure resulted in no statistically significant toxicity or gene expression changes in the lungs of the rats. In the absence of any information about its potential toxicity, a comprehensive rat animal model study (see Fedan, J.S., Toxicol Appl Pharmacol. 000, 000-000, 2020) has been designed to investigate the bioactivities of several FSDs in comparison to MIN-U-SIL® 5, a respirable α-quartz reference dust used in previous animal models of silicosis, in several organ systems.
| S-EPMC7748298 | biostudies-literature
Project description:Synergism of Iraqi Sand/Cigarette Smoke Co-Exposure in Rats. 24 samples are used. A total of 102 rats will be separated into six exposure groups: each group consisting of 17 male CD Sprague-Dawley rats, 10 to 15 weeks old. The six exposure groups were each exposed via two routes: 1. nose-only inhalation exposures --- air or cigarette smoke; 2. whole-body inhalation exposures -- air or manufactured silica sand or Iraqi sand. The nose only exposures were conducted 3 hours per day, 5 days per week for 6 weeks. During the last two weeks of the nose - only exposures, whole-body exposure were also conducted 18-19 hours per day, 7 days per week.
2012-01-01 | E-GEOD-28804 | biostudies-arrayexpress
Project description:Cultured murine macrophages (RAW 264.7) were used to investigate the effects of fracking sand dust (FSD) for its pro-inflammatory activity, in order to gain insight into the potential toxicity to workers associated with inhalation of FSD during hydraulic fracturing. While the role of respirable crystalline silica in the development of silicosis is well documented, nothing is known about the toxicity of inhaled FSD. The FSD (FSD 8) used in these studies was from an unconventional gas well drilling site. FSD 8was prepared as a 10 mg/ml stock solution in sterile PBS, vortexed for 15 s, and allowed to sit at room temperature for 30 min before applying the suspension to RAW 264.7cells. Compared to PBS controls, cellular viability was significantly decreased after a 24 h exposure to FSD. Intracellular reactive oxygen species (ROS) production and the production of IL-6, TNFα, and endothelin-1 (ET-1) were up-regulated as a result of the exposure, whereas the hydroxyl radical (.OH) was only detected in an acellular system. Immunofluorescent staining of cells against TNFα revealed that FSD 8 caused cellular blebbing, and engulfment of FSD 8 by macrophages was observed with enhanced dark-field microscopy. The observed changes in cellular viability, cellular morphology, free radical generation and cytokine production all confirm that FSD 8 is cytotoxic to RAW 264.7 cells and warrants future studies into the specific pathways and mechanisms by which these toxicities occur.
| S-EPMC7952011 | biostudies-literature