Potential Pathophysiological Mechanisms of Ultrafine Particle Toxic Effects in Humans
Апстракт
Epidemiological and clinical studies suggested the association of the particulate matter ambient air pollution and the increased morbidity and mortality, mainly from respiratory and cardiovascular diseases. The size of particles has great influence on their toxicity, because it determines the site in the respiratory tract where they deposit The most well established theory explaining the mechanisms behind the increased toxicity of ultrafine particles (UFP, LT 0.1 mu m) is that It has to do with the increased surface area and/or the combination with the increased number of particles, Biological effects of UFP are also determined by their shape and chemical composition, so it is not possible to estimate their toxicity in a general way. General hypothesis suggested that exposure to inhaled particles induces pulmonary alveolar inflammation as a basic pathophysiological event, triggering release of various proinflammatory cytokines. Chronic inflammation is a very important underlying mechan...ism in the genesis of atherosclerosis and cardiovascular diseases. UFP can freely move through the circulation, but their effects on the secondary organs are not known yet, so more studies on recognizing toxicological endpoints of UFP are needed Determination of UFP toxicity and the estimation of their internal and biologically active dose are necessary for the evidence based conclusions connecting air pollution by UFP and human diseases.
Кључне речи:
ultraflne particles / human health / pathophysiological mechanisms / chronic inflammation / respiratory disease / cardiovascular diseaseИзвор:
Chemical Industry and Chemical Engineering Quarterly / CICEQ, 2008, 14, 1, 47-49
DOI: 10.2298/CICEQ0801047J
ISSN: 1451-9372; 2217-7434
WoS: 000262251400008
Scopus: 2-s2.0-49649116169
Колекције
Институција/група
VinčaTY - JOUR AU - Jovic-Stosic, Jasmina AU - Jovašević-Stojanović, Milena PY - 2008 UR - https://vinar.vin.bg.ac.rs/handle/123456789/3612 AB - Epidemiological and clinical studies suggested the association of the particulate matter ambient air pollution and the increased morbidity and mortality, mainly from respiratory and cardiovascular diseases. The size of particles has great influence on their toxicity, because it determines the site in the respiratory tract where they deposit The most well established theory explaining the mechanisms behind the increased toxicity of ultrafine particles (UFP, LT 0.1 mu m) is that It has to do with the increased surface area and/or the combination with the increased number of particles, Biological effects of UFP are also determined by their shape and chemical composition, so it is not possible to estimate their toxicity in a general way. General hypothesis suggested that exposure to inhaled particles induces pulmonary alveolar inflammation as a basic pathophysiological event, triggering release of various proinflammatory cytokines. Chronic inflammation is a very important underlying mechanism in the genesis of atherosclerosis and cardiovascular diseases. UFP can freely move through the circulation, but their effects on the secondary organs are not known yet, so more studies on recognizing toxicological endpoints of UFP are needed Determination of UFP toxicity and the estimation of their internal and biologically active dose are necessary for the evidence based conclusions connecting air pollution by UFP and human diseases. T2 - Chemical Industry and Chemical Engineering Quarterly / CICEQ T1 - Potential Pathophysiological Mechanisms of Ultrafine Particle Toxic Effects in Humans VL - 14 IS - 1 SP - 47 EP - 49 DO - 10.2298/CICEQ0801047J ER -
@article{ author = "Jovic-Stosic, Jasmina and Jovašević-Stojanović, Milena", year = "2008", abstract = "Epidemiological and clinical studies suggested the association of the particulate matter ambient air pollution and the increased morbidity and mortality, mainly from respiratory and cardiovascular diseases. The size of particles has great influence on their toxicity, because it determines the site in the respiratory tract where they deposit The most well established theory explaining the mechanisms behind the increased toxicity of ultrafine particles (UFP, LT 0.1 mu m) is that It has to do with the increased surface area and/or the combination with the increased number of particles, Biological effects of UFP are also determined by their shape and chemical composition, so it is not possible to estimate their toxicity in a general way. General hypothesis suggested that exposure to inhaled particles induces pulmonary alveolar inflammation as a basic pathophysiological event, triggering release of various proinflammatory cytokines. Chronic inflammation is a very important underlying mechanism in the genesis of atherosclerosis and cardiovascular diseases. UFP can freely move through the circulation, but their effects on the secondary organs are not known yet, so more studies on recognizing toxicological endpoints of UFP are needed Determination of UFP toxicity and the estimation of their internal and biologically active dose are necessary for the evidence based conclusions connecting air pollution by UFP and human diseases.", journal = "Chemical Industry and Chemical Engineering Quarterly / CICEQ", title = "Potential Pathophysiological Mechanisms of Ultrafine Particle Toxic Effects in Humans", volume = "14", number = "1", pages = "47-49", doi = "10.2298/CICEQ0801047J" }
Jovic-Stosic, J.,& Jovašević-Stojanović, M.. (2008). Potential Pathophysiological Mechanisms of Ultrafine Particle Toxic Effects in Humans. in Chemical Industry and Chemical Engineering Quarterly / CICEQ, 14(1), 47-49. https://doi.org/10.2298/CICEQ0801047J
Jovic-Stosic J, Jovašević-Stojanović M. Potential Pathophysiological Mechanisms of Ultrafine Particle Toxic Effects in Humans. in Chemical Industry and Chemical Engineering Quarterly / CICEQ. 2008;14(1):47-49. doi:10.2298/CICEQ0801047J .
Jovic-Stosic, Jasmina, Jovašević-Stojanović, Milena, "Potential Pathophysiological Mechanisms of Ultrafine Particle Toxic Effects in Humans" in Chemical Industry and Chemical Engineering Quarterly / CICEQ, 14, no. 1 (2008):47-49, https://doi.org/10.2298/CICEQ0801047J . .