Spacer Devices
Hans Bisgaard, Chris O’Callaghan, Gerald C. Smaldone in Drug Delivery to the Lung, 2001
It seems obvious that manufacturers of spacer devices should use only nonelectrostatic materials in the future. Certainly, it is not satisfactory to require the patient to remember a certain priming procedure, which is likely to jeopardize compliance. Metal is an obvious, robust, and safe choice for a nonelectrostatic spacer (24,34), since it carries no charge no matter how it is handled and requires no chemical treatment. Alternatively a nonelectrostatic plastic material (carbon black) has been produced by mixing a conductive material into the plastic during the moulding procedure; other nonelectrostatic materials may be developed in the future. Key Points:Electrostatic charges in plastic spacers cause a clinically significant reduction of lung dose.Possible priming procedures for available plastic spacers should be studied with respect to stability, toxicity, drug interactions, and impact on patient compliance.Only nonelectrostatic devices should be used in the future.
Outdoor Emissions
William J. Rea, Kalpana D. Patel in Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
Another hypothesis builds on the premise that the particles themselves may stimulate innate immunity in the brain. Pattern recognition receptors are present in the brain's resident innate immune cells, microglia, and identify large pathogen-associated molecular patterns, such as charge and protein aggregates.248 Studies examining the toxic effects of nanometer-sized carbon (carbon black, a model of PM missing adsorbed compounds) confirm that inhalation of carbon black alone is known to cause inflammation,249 suggesting that something inherent in the particle may be culpable. Indeed, UFPM exposure in mice induces the production of pro-inflammatory cytokines (ILa-β, TNF-α, and INF-γ) in the OBs of exposed animals.248 Work by Veronesi et al.250 reports that the inflammatory response to PM in both respiratory epithelial cells110,250 and microglia251 (brain macrophages) relates to physiochemical features of the particles, such as surface charge. Thus, PM itself may indeed be a proinflammatory stimulus once it reaches the brain.
Nanoparticles in the Gastrointestinal Tract
Shayne C. Gad in Toxicology of the Gastrointestinal Tract, 2018
Exposure to nanosized carbon black (CB) particles may increase the risk of cardiovascular diseases by endothelial dysfunction, particularly in susceptible subjects with metabolic syndrome [64]. Vasomotor dysfunction in aorta from obese and lean Zucker rats was investigated after oral exposure to nanosized carbon black (CB). Rats were exposed to 1 or 10 weekly doses of 0, 0.064, 0.64 or 6.4 mg/kg bodyweight and sacrificed 24 hours or 13 weeks later. The exposure to 10 doses of 0.064 or 0.64 mg/kg reduced the acetylcholine-induced vasorelaxation in the lean and obese rats. The half maximal effect concentration values increased by twofold (95% CI: 1.1–3.5-fold) and fourfold (95% CI: 2.3–6.9-fold) in the rats exposed to 0.064 and 0.64 mg/kg compared with the controls, respectively. The rats exposed to 10 doses of 0.64 mg/kg had also 20% (95% CI: 10%–29%) lower maximal effect value compared with the controls. However, the nitroglycerin-induced vasorelaxation and phenylephrine-induced vasocontraction were not affected in rats exposed to CB. The endothelial dysfunction was not observed in rats sacrificed 13 weeks after the last CB exposure. There was unaltered expression of Chrm3, Nos3, Nos2, Ccl2, and Hmox1 in aorta tissue of CB-exposed rats. In conclusion, repeated oral exposure to CB was associated with endothelial dysfunction in rats, further aggravating the effect of metabolic syndrome [64].
Evaluating the evidence on genotoxicity and reproductive toxicity of carbon black: a critical review
Published in Critical Reviews in Toxicology, 2018
Ishrat Chaudhuri, Claudia Fruijtier-Pölloth, Yufanyi Ngiewih, Len Levy
Carbon black [CAS. No. 1333-86-4] is elemental carbon in the form of particles that are produced industrially by the partial combustion or thermal decomposition of gaseous or liquid hydrocarbons under controlled conditions. Commercially available grades of carbon black differ in particle size, surface area, average aggregate mass, morphology, or structure. Potential health effects of carbon black have been investigated extensively in laboratory animal experiments and in epidemiological studies of carbon black production workers. The main health concerns associated with carbon black and other poorly soluble, low-toxicity (PSLT) particles are lung effects resulting from inhalation exposure. The International Agency for Research on Cancer (IARC 2010) proposed an overall mode of action for carbon black toxicity in rat lungs. Particle deposition above certain concentrations in the rat lungs may lead to a phenomenon known as “lung overload”, which in turn leads to sustained inflammation, production of reactive oxygen species (ROS), depletion of antioxidants and/or impairment of other defense mechanisms, cell proliferation, and gene mutations. These changes in the rat lung can lead to the induction of alveogenic tumors. Similar tumors have not been observed in mouse or hamster lungs.
Assessment of primary and inflammation-driven genotoxicity of carbon black nanoparticles in vitro and in vivo
Published in Nanotoxicology, 2022
Emilio Di Ianni, Peter Møller, Tanya Cholakova, Henrik Wolff, Nicklas Raun Jacobsen, Ulla Vogel
Carbon black (CB) consists of elemental carbon in the form of particles that are produced industrially by highly controlled partial combustion, or thermal decomposition, of gaseous or liquid hydrocarbons. CB particles are poorly soluble, and the commercially available grades of CB differ in particle size, surface area, average aggregate mass, content of poly-aromatic hydrocarbons (PAH), morphology, and structure (IARC 2010). Potential health effects of CB nanoparticles (CBNPs) have been investigated extensively in cell and laboratory animal experiments, as well as in epidemiological studies of CB production workers (Sorahan and Harrington 2007; Morfeld et al. 2016; Dell et al. 2015; Morfeld and McCunney 2007; Ramanakumar et al. 2008; Greene et al. 1979; Straif et al. 2000). CBNPs have been used as a benchmark material for in vivo toxicological evaluation of diesel exhaust particles and urban air particulate matter, and included as reference material (i.e. Printex 90) in studies of different nanomaterials (Saber, Jacobsen, et al. 2012; Wallin et al. 2017; Poulsen et al. 2017; Knudsen et al. 2019; Danielsen, Bendtsen et al. 2020; Barfod et al. 2020; Bengtson et al. 2017, Bendtsen et al. 2019, Bendtsen et al. 2020).
Organomodified nanoclays induce less inflammation, acute phase response, and genotoxicity than pristine nanoclays in mice lungs
Published in Nanotoxicology, 2020
Emilio Di Ianni, Peter Møller, Alicja Mortensen, Józef Szarek, Per Axel Clausen, Anne Thoustrup Saber, Ulla Vogel, Nicklas Raun Jacobsen
The objective of the present study was to evaluate how an organic surface modification of Bentonite clay modulates the toxic response in the murine lung. Prior to exposing mice, we assessed in vitro the cytotoxicity of four different ONC, as well as pure QAC, using mouse alveolar epithelial cells (FE1-MML), and compared these to unmodified Bentonite and carbon black. The preliminary in vitro screening and the physico-chemical characterization guided the selection of the ONC to be tested in mice. Mice were then exposed by single intratracheal instillation to two ONC and Bentonite. We have worked intensely on characterizing the carbon black material (Jacobsen et al. 2008; Høgsberg et al. 2013; Jacobsen and Clausen 2015) as well as the toxicity it causes. Carbon black has a high inflammogenicity and production of reactive oxygen species (ROS), leading to damage to the DNA and mutations (Jacobsen et al. 2007; Jacobsen et al. 2011). Here carbon black was included as benchmark material to allow comparisons with previously assessed materials (Bourdon et al. 2012; Saber et al. 2012; Poulsen, et al. 2013; Kyjovska et al. 2015; Modrzynska et al. 2018; Bendtsen et al. 2019; Hadrup et al. 2019, 2020; Danielsen et al. 2020). Inflammation, acute phase response, pro-fibrotic effects, local and systemic DNA damage, and liver morphology were analyzed 1, 3, and 28 days post-exposure.
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