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Occupational exposure to hexavalent chromium. Part I. Hazard assessment of non-cancer health effects.
Hessel, EVS, Staal, YCM, Piersma, AH, den Braver-Sewradj, SP, Ezendam, J
Regulatory toxicology and pharmacology : RTP. 2021;:105048
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Abstract
Hexavalent chromium (Cr(VI)) compounds have been studied extensively and several agencies have described their toxicological profile. In the past, personnel of the Dutch Ministry of Defence may have been exposed to Cr(VI) during maintenance activities. To investigate if this exposure may have caused irreversible adverse health effects, the Dutch National Institute for Public Health and the Environment (RIVM) summarized all available knowledge from previous evaluations. This information was complemented with a scoping review to retrieve new scientific literature. All scientific evidence was evaluated in workshops with external experts to come to an overview of irreversible adverse health effects that could be caused by occupational exposure to Cr(VI) compounds. This review focuses on non-cancer health effects. It was concluded that occupational exposure to Cr(VI) can cause perforation of the nasal septum by chromium ulcers, chronic lung diseases, including asthma, rhinitis, pulmonary fibrosis and COPD, skin ulcers and allergic contact dermatitis in humans. It is currently insufficiently clear if Cr(VI) can cause irreversible diseases due to disturbances of the immune system (other than allergic contact eczema, allergic asthma and rhinitis and chronic lung diseases) or adverse effects on fertility or prenatal development in humans.
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PBMC fixation and processing for Chromium single-cell RNA sequencing.
Chen, J, Cheung, F, Shi, R, Zhou, H, Lu, W, ,
Journal of translational medicine. 2018;(1):198
Abstract
BACKGROUND Interest in single-cell transcriptomic analysis is growing rapidly, especially for profiling rare or heterogeneous populations of cells. In almost all reported works investigators have used live cells, which introduces cell stress during preparation and hinders complex study designs. Recent studies have indicated that cells fixed by denaturing fixative can be used in single-cell sequencing, however they did not usually work with most types of primary cells including immune cells. METHODS The methanol-fixation and new processing method was introduced to preserve human peripheral blood mononuclear cells (PBMCs) for single-cell RNA sequencing (scRNA-Seq) analysis on 10× Chromium platform. RESULTS When methanol fixation protocol was broken up into three steps: fixation, storage and rehydration, we found that PBMC RNA was degraded during rehydration with PBS, not at cell fixation and up to 3-month storage steps. Resuspension but not rehydration in 3× saline sodium citrate (SSC) buffer instead of PBS preserved PBMC RNA integrity and prevented RNA leakage. Diluted SSC buffer did not interfere with full-length cDNA synthesis. The methanol-fixed PBMCs resuspended in 3× SSC were successfully implemented into 10× Chromium standard scRNA-seq workflows with no elevated low quality cells and cell doublets. The fixation process did not alter the single-cell transcriptional profiles and gene expression levels. Major subpopulations classified by marker genes could be identified in fixed PBMCs at a similar proportion as in live PBMCs. This new fixation processing protocol also worked in several other fixed primary cell types and cell lines as in live ones. CONCLUSIONS We expect that the methanol-based cell fixation procedure presented here will allow better and more effective batching schemes for a complex single cell experimental design with primary cells or tissues.
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A time-lapse approach to examine chromium and nickel effects on wound healing in vitro.
Perfetto, B, Stellavato, A, Melito, A, De Gregorio, V, Cammarota, M, Giuliano, M
Journal of immunotoxicology. 2012;(4):392-400
Abstract
Chromium and nickel cause allergic contact dermatitis, a common biological skin response to sensitizing agents. This study used a conventional in vitro wounding model to study the impact of sensitizing agents on the innate immune response of human keratinocytes. Experiments were designed to evaluate the involvement of specific Toll-like receptors and metalloproteinases as effectors molecules downstream, at a molecular level. Further, keratinocytes were co-cultured with monocytes (THP-1 cells) to reproduce an inductive stimulus on monocytes made by metals. Human keratinocytes (HaCat) were grown on plates covered with collagen type I, chemically treated, and then mechanically injured with a sterile pipette tip. Restoration of the monolayer integrity was monitored by time-lapse video microscopy. Effector gene expression was evaluated by real-time PCR. The presence of chromium significantly dropped the rate of wound closure, while nickel-induced hyper-proliferation ended in an acceleration of the healing process, an event that does not occur in vivo. This latter outcome led to considering nickel as an unsuitable example for use in the experimental model. Focusing solely on the chromium aspect of this study, RNA profiles of selected molecular markers were generated to ascertain if the detrimental stimulus from chromium was eliminated or persisted both in keratinocytes alone and/or during co-cultures of keratinocytes and monocytes. Monocytes accelerated the process of wound repair. This in vitro experimental model highlighted the involvement of innate immunity in response to chromium and might be useful for test molecules of therapeutic interest for the treatment of skin lesions. However, the experience with nickel reveals that there are limitations to the utility of this wound model system after all.
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A systematic comparison of the actual, potential, and theoretical health effects of cobalt and chromium exposures from industry and surgical implants.
Keegan, GM, Learmonth, ID, Case, CP
Critical reviews in toxicology. 2008;(8):645-74
Abstract
Humans are exposed to cobalt (Co) and chromium (Cr) from industry and surgical devices, most notably orthopedic joint replacements. This review compares the potential health effects of exposure to Co and Cr contaminants from these two different sources, both in the locally exposed tissues and at sites distant to the primary exposure. Surgical implantation results largely in exposures to ions, corrosion products, and particles of Co and Cr. Industrial exposures are predominantly to metal compounds and particles. Although there are large literatures on industrial and surgical exposures to these metals, there has yet to be a systematic comparison of the two to test whether more general lessons might be learned about the human toxicology of Co and Cr. Both industrial and surgical exposures cause inflammatory and other immune reactions in the directly exposed tissues. In the lung there is a well-established risk of cancer following long-term exposures to hexavalent Cr; however, the development of sarcoma in the connective tissues adjacent to implants in response to metal particles is rare. Both types of exposure are associated with changes in the peripheral blood, including evidence of oxidative stress, and altered numbers of circulating immune cells. There is dissemination of Co and Cr to sites distant to the orthopedic implant, but less is known about systemic dissemination of these metals away from the lung. The effects of industrial exposures in the reproductive, renal, and cardiac systems have been investigated, but this has yet to be explored after surgical exposures. The form of the metal (and associated elements) in both instances is key to the toxicological effects arising in the body and further characterization of debris released from devices is certainly recommended, as is the impact of nanotoxicology on the health and safety of workers and patients. Biomonitoring schemes currently used in industry could be translated, if required, into suitable programs for orthopedic out-patients. Cross-communication between experts in industrial and occupational medicine and regulatory agencies may be useful.