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List of Chemical Substances
Published in T.S.S. Dikshith, and Safety, 2016
Various asbestos-induced illnesses are known from the industrial-medicine sector in which the size of the fibers plays a crucial role. Generally speaking, fibers with a diameter of <2 m and a length of >5 μm are considered to be hazardous to health (diameter:length = 1:3). Such a fiber size is capable of entering the lungs, accumulating and becoming encapsulated. Fibers have also been found to have a certain migration capability in the organism and the cell metabolism. Accumulation in the lungs causes sclerosis of the pulmonary alveoli, thereby impairing oxygen exchange. The inhalation of large quantities of fiber can cause asbestosis, which increases the risk of bronchial cancer. In particular, dusts <200 μm are highly toxic and are suspected of being a direct cause of tumors. Exposure to asbestos irritates the eyes and the respiratory tract. Direct penetration into damaged skin produces excessive hornification. Fibers in the lungs cause chronic bronchitis, irritation of the pleura and pleurisy. Distension of the lungs can result in lung cancer. Workplace exposure may produce periods of latency in the gastrointestinal tract lasting up to 40 years. To date, there are no known characteristic toxicology data (W, 1988).
Nanomaterials in the Work Environment
Published in Małgorzata Pośniak, Emerging Chemical Risks in the Work Environment, 2020
Lidia Zapór, Przemysław Oberbek
The lungs consist of bronchi and pulmonary alveoli (300–500 million), blood, and lymphatic vessels. Each alveolus is covered with lung capillaries, forming an extensive network of over 280 billion, which constitutes the gas exchange region with an area of 50–130 m2. The pulmonary alveoli walls are built from two types of epithelial cells, type I and II pneumocytes. Tight junctions between the epithelial cells along with the pulmonary surfactant, a mucous lining of the lung alveoli, act as an additional barrier for particle transport. Particles capable of crossing this barrier enter the circulatory system or are phagocyted by alveolar macrophages [Geiser 2010].
Emerging applications of microfluidic techniques for in vitro toxicity studies of atmospheric particulate matter
Published in Aerosol Science and Technology, 2021
Fobang Liu, Nga Lee Ng, Hang Lu
To date, most in vitro cellular assays are performed using two-dimensional (2D) monolayer cell culture method. However, 2D cell culture does not adequately reconstruct the natural three-dimensional (3D) cellular microenvironments in vivo, excluding the interactions with neighboring cells and extracellular matrix (ECM). It has been suggested in diverse research studies that 3D cell culture systems are better models than 2D cell culture systems due to improved simulation of in vivo situations such as cell morphology, cell population, cell-cell and cell-ECM interactions (Edmondson et al. 2014; Kasurinen et al. 2018; Ravi et al. 2015). Microfluidics has become a valuable technology to further increase the physiological relevance of 3D cell culture by enabling spatiotemporal control over fluids in micrometer-sized channels (Van Duinen et al. 2015). Some microfluidic 3D cell culture systems have been established for PM toxicity evaluation (Huh et al. 2010; Xu et al. 2020; Zhang et al. 2020; Zheng et al. 2019). In general, these systems consist of two tissue layers separated by a thin, porous, ECM-coated membrane, which mimics the alveolar-capillary interface. Human alveolar epithelial cells are cultured on the top side of the membrane, and human vascular endothelial cells are cultured on the opposite side of the membrane (Figure 5A-a and b). Zhang et al. (2020) developed a 3D coculture-based pulmonary alveolus microsystem and compared a variety of cellular responses between either microfluidic coculture and monoculture or on-chip and off-chip culture. Two highly toxic pollutants (i.e., nicotine and benzo[a]pyrene) that may exist in ambient PM, were exposed to cells and used for the comparative assessment. Two important conclusions emerged from the results: first, cellular responses from on-chip culture are more sensitive than off-chip culture; second, the coculture of the epithelium with the endothelium layer strengthens the chemical resistance of the pulmonary alveolus system to the exogenous pollutants (Figure 5A-c). These results point to the importance of creating complex in vitro tissue microenvironments to explore pollution-induced human pathology.