scholarly journals Potential pathophysiological mechanisms of ultrafine particle toxic effects in humans

2008 ◽  
Vol 14 (1) ◽  
pp. 47-49 ◽  
Author(s):  
Jasmina Jovic-Stosic ◽  
Milena Jovasevic-Stojanovic

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, < 0.1 ?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. .

2018 ◽  
Vol 25 (8) ◽  
pp. 818-825 ◽  
Author(s):  
Simone Vidale ◽  
Carlo Campana

Air pollution has a great impact on health, representing one of the leading causes of death worldwide. Previous experimental and epidemiological studies suggested the role of pollutants as risk factors for cardiovascular diseases. For this reason, international guidelines included specific statements regarding the contribution of particulate matter exposure to increase the risk of these events. In this review, we summarise the main evidence concerning the mechanisms involved in the processes linking air pollutants to the development of cardiovascular diseases.


2019 ◽  
Vol 651 ◽  
pp. 1144-1153 ◽  
Author(s):  
Arthit Phosri ◽  
Kayo Ueda ◽  
Vera Ling Hui Phung ◽  
Benjawan Tawatsupa ◽  
Akiko Honda ◽  
...  

2018 ◽  
Vol 2018 (1) ◽  
Author(s):  
Nhung Thi Trang Nguyen ◽  
Christian Schindler ◽  
Dien Minh Tran ◽  
Chau Quy Ngo ◽  
Hoang Tu Le ◽  
...  

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Petter L Ljungman ◽  
Elissa H Wilker ◽  
Mary B Rice ◽  
Elena Austin ◽  
Joel Schwartz ◽  
...  

Background: Studies of ambient air pollution and microvascular function have shown conflicting results. Aim: We investigated whether the association between fine particle mass with diameter ≤2.5μm (PM 2.5 ) and microvascular function varies according to air pollution characteristics. Methods: We assessed baseline pulse amplitude and the ratio of fingertip pulse wave amplitude pre- and post- brachial artery occlusion (PAT ratio) in 1,365 participants of the Framingham Offspring and Third Generation Cohorts. We used K-means clustering to categorize mixtures of air pollutants into 5 distinct clusters of days with similar multi-pollutant profiles using elemental data and gases. We assessed the interaction between preceding day PM 2.5 and cluster adjusting for season, meteorology and covariates. Results: We observed differences in associations between PM 2.5 and baseline pulse amplitude by cluster (P=0.02 for interaction). On days with either low overall PM 2.5 levels but dominated by road and traffic dust and a high proportion of ultrafine particles (cluster 1) or high contributions of oil and wood combustion (cluster 5), higher PM 2.5 was associated with higher baseline pulse amplitude (see Figure). In contrast, on days with either a strong contribution of crustal materials, a mixture of fine and ultrafine particles, or agglomerated particles from regional sources (cluster 2, 3, and 4 respectively), PM 2.5 was not significantly associated with baseline pulse amplitude. We observed similar, non-significant associations between PM 2.5 and PAT ratio across the air pollution mixture clusters (P=0.14 for interaction). Conclusions: Air pollution mixtures with contributions from heating oil and wood combustion or traffic and road dust, both having high proportions of ultra-fine particles, were associated with altered microvascular tone. Our findings suggest that specific mixtures of particulate pollution may have distinct vascular consequences and support further studies of air pollution clusters to inform public policy. .


2013 ◽  
Vol 77 ◽  
pp. 968-973 ◽  
Author(s):  
Guang-Hui Dong ◽  
Zhengmin (Min) Qian ◽  
Jing Wang ◽  
Weiqing Chen ◽  
Wenjun Ma ◽  
...  

2021 ◽  
Vol 2021 (1) ◽  
Author(s):  
Suganthi Jaganathan ◽  
Jeroen De Bont ◽  
Marcus Dahlquist ◽  
Åsa Persson ◽  
Massimo Stafoggia ◽  
...  

2021 ◽  
pp. 181-194
Author(s):  
A.E. Nosov ◽  
◽  
A.S. Baydina ◽  
O.Yu. Ustinova ◽  
◽  
...  

Ambient air pollution causes approximately 3.3 million untimely deaths annually (2.1 deaths due to ischemic heart disease and 1.1 million deaths due to stroke). Mortality caused by ambient air pollution is higher than mortality due to such traditional risk factors as smoking, obesity, and elevated dextrose contents in blood. Relative risk of mortality amounts to 1.26 (95 % CI 1.08–1.47) in cities with the highest air pollution against those where air pollution is the lowest. Occupational exposure to various chemical air pollutants can cause more than 1 million untimely deaths all over the world but its contribution to prevalence of cardiovascular diseases has not been determined sufficiently. Aerogenic pollutants are quite variable in their chemical structure and include both particulate matter (PM for short) and gaseous matter. The American Heart Association and the European Society of Cardiology consider PM2.5 to be a risk factor causing cardiovascular diseases. This analytical review presents data on effects produced by aerogenic pollutants on development of cardio-metabolic pathology and population mortality due to vascular and metabolic diseases (arterial hypertension, atherosclerosis and ischemic heart disease, heart rhythm disturbances, and type 2 diabetes mellitus). There are also data on mechanisms of pathogenetic influence exerted by aerogenic pollutants on development of such diseases including generation of anti-inflammatory and oxidative mediators and their release into blood flow; developing imbalance in the autonomic nervous system with prevailing activity of the sympathetic nervous system and disrupted heart rate variability; direct introduction of aerogenic pollutants from the lungs into blood flow with developing direct toxic effects. We have also analyzed literature data on protective effects produced by reduction in ambient air pollution on prevalence of cardiovascular pathology.


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