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Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
Odor identity, quality, and familiarity are mainly deciphered by the piriform cortex. Consciousness of smell is achieved by projections from the piriform cortex to the medial dorsal nucleus of the thalamus and to the orbitofrontal cortex, which the secondary olfactory cortex is part of.11 One sees the onset of odor supersensitivity, which may occur with pollutant, mold, or food sensitivity in this area.
Pollution characteristics, mechanism of toxicity and health effects of the ultrafine particles in the indoor environment: Current status and future perspectives
Published in Critical Reviews in Environmental Science and Technology, 2022
Muhammad Ubaid Ali, Siyi Lin, Balal Yousaf, Qumber Abbas, Mehr Ahmed Mujtaba Munir, Audil Rashid, Chunmiao Zheng, Xingxing Kuang, Ming Hung Wong
Long episode exposure to air pollutants may lead to direct translocation of UFPs into the central nervous system (CNS), where they can cause neuropathological effects through different pathways. However, the entry of UFPs might not lead directly into CNS, but it can exert negative impacts on CNS by generating soluble inflammatory mediators from primary entry systems and secondary deposition sites that lead to susceptibility for neuro-inflammation and neurodegeneration (Genc et al., 2012). A previous study revealed that after inhalation, the translocated UFPs can found in the brain within 4–24 h. The UFPs travel to the brain through the olfactory nerves from the nasal cavity. In animals, almost 20% of the UFPs deposited on olfactory mucosa were translocated to the olfactory bulb (Oberdörster et al., 2004). From the olfactory bulb, translocation may be through mitral cell axons that lead from the olfactory bulb to different parts of the brain such as the olfactory cortex, anterior olfactory nucleus, piriform cortex, hypothalamus and amygdala (Wang et al., 2007). In humans, the translocation pathways that can by-pass blood-brain barrier may more direct and the UFPs, not only translocate and effect neural tissue directly, but can also impact the autonomic function (Heusser et al., 2019; Tian et al., 2019). An increase in activity of the sympathetic nervous system was noticed due to a decrease in norepinephrine clearance after exposure to UFPs (Heusser et al., 2019). Small size and large surface areas enable UFPs to pass the barriers in the brain and lungs, and this ability explains the presence of UFPs in neurons and erythrocytes. As endothelial cells and erythrocytes are in close contact it can be a possible route for UFPs exchange between UFPs loaded erythrocytes and activated endothelial cells (Block & Caldero, 2009; Geiser et al., 2005).