Abstract P247: Multi-pollutant Mixtures and Digital Vascular Function in the Framingham Heart Study

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. .


Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 2640-2640 ◽  
Author(s):  
Marc Forestier ◽  
Linda Buechi ◽  
Corinna Hermann ◽  
Thomas Hartung ◽  
Juerg H. Beer

Abstract INTRODUCTION: Peaks of ambient air pollution with increased concentrations of particulate matter (i.e. PM2.5: Fine particles of < 2.5 μm diameter and UFP: Ultrafine particles of <0.1 μm diameter) easily reach levels of 100’000 particles/cm3 and are associated with increased cardiovascular morbidity and mortality. Especially the UFP-fraction rapidly crosses cellular membranes by non-phagocytotic mechanisms and is translocated into the circulation. The absorbed microparticles may affect the coagulation directly or indirectly via monocyte/macrophage activation. The data on prothrombotic and inflammatory effects are controversial, depending on the type, size and charge of particles and the experimental models chosen. HYPOTHESIS: We therefore hypothesized that typically sized particles differentially affect human platelets and coagulation either directly or indirectly by the proinflammatory response. METHODS AND RESULTS: Three microparticle sources were mixed with citrated human blood at concentrations of 5 and 50 μg/ml for one hour: a) PM2.5 polystyrene beads (PS) of 0.66 μm diameter. b) UFP ultrafine carbon black (ufCB, 14 nm, Printex), and c) residual oil fly ash (ROFA, with contents of Al, Zu, Cu-ions, and residual polyaromatic hydrocarbons). We calculated that >800 μg of microparticles may be absorbed by the human lung daily and thus a dose of appr. 5 μg/ml blood could be achieved easily. Platelet aggregation with ADP, collagen, arachidonate and ristocetin at different concentrations was not affected by any of the three types of microparticles and neither was PT, aPTT, fibrinogen, DDimer or soluble P-selectin. Direct microscopical observation did not show platelet aggregates, nor rosetting of platelets with leucocytes, nor mixed platelet aggregates with microparticles. PFA-100 CADP, however, was prolonged in the presence of PS beads from 85 ± 3 sec to 101 ± 6 (n = 3, p < 0.04); ROFA, on the other hand, shortened it by more than 20 sec to 78 ± 2 vs 110 ± 6 sec (n = 3, p < 0.05) and ufCB/UFP did not affect it. The standardized endogenous thrombin potential as measured by the thrombinoscope did not exhibit significant changes under the conditions chosen. Preliminary data of a highly standardized assay of cytokine release after 24 hours of stimulation with low dose LPS (1μg/ml blood) indicates a 2 - 3 fold increase of interferon, interleukine-1 and TNFa, but not of interleukine-8. CONCLUSION: Our data demonstrate a direct shortening effect on shear induced platelet aggregation (PFA-100) by ROFA and a prolongation by positively charged PS beads. None of the three particle types showed a direct effect in any of the other coagulation assays evaluated. The strong proinflammatory cytokine response to all three microparticle preparations is likely responsible for the procoagulant / prothrombotic effects which have been observed in experimental mouse and hamster models.





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. .



2020 ◽  
Author(s):  
Abdulrahman Jbaily ◽  
Xiaodan Zhou ◽  
Jie Liu ◽  
Ting-Hwan Lee ◽  
Stéphane Verguet ◽  
...  

Exposure to ambient air pollution contributes substantially to the global burden of disease, and in 2015, ambient exposure to PM2.5 (fine particles with a mass median aerodynamic diameter of less than 2.5 μm) was the fifth-ranking risk factor of mortality globally. We analyzed data from the US zip code tabulation areas (N=32047) for 2000-2016 and found strong evidence of inequalities in exposure to PM2.5 among both racial/ethnic and income groups. Most alarming, we found that these inequalities have been increasing over time. From 2010 to 2016 inequalities in the exposure to PM2.5 levels above 8 μg/m3 across racial/ethnic, and income groups increased by factors of 1.6 and 4.0 respectively. As shown in our powerful map visualizations, these results indicate that air pollution regulations must not only decrease PM2.5 concentration levels nationwide but also prioritize reducing environmental injustice across the US.



2020 ◽  
Vol 7 (1) ◽  
pp. e000549 ◽  
Author(s):  
Michael J Abramson ◽  
Claudia Wigmann ◽  
Hicran Altug ◽  
Tamara Schikowski

BackgroundAir pollution is a risk factor for chronic obstructive pulmonary disease (COPD). Fraction of exhaled nitric oxide (FeNO) could be a useful biomarker for health effects of air pollutants. However, there were limited data from older populations with higher prevalence of COPD and other inflammatory conditions.MethodsWe obtained data from the German Study on the influence of Air pollution on Lung function, Inflammation and Ageing. Spirometry and FeNO were measured by standard techniques. Air pollutant exposures were estimated following the European Study of Cohorts for Air Pollution Effects protocols, and ozone (O3) measured at the closest ground level monitoring station. Multiple linear regression models were fitted to FeNO with each pollutant separately and adjusted for potential confounders.ResultsIn 236 women (mean age 74.6 years), geometric mean FeNO was 15.2ppb. Almost a third (n=71, 30.1%) of the women had some chronic inflammatory respiratory condition. A higher FeNO concentration was associated with exposures to fine particles (PM2.5), PM2.5absorbance and respirable particles (PM10). There were no significant associations with PMcoarse, NO2, NOx, O3 or length of major roads within a 1 km buffer. Restricting the analysis to participants with a chronic inflammatory respiratory condition, with or without impaired lung function produced similar findings. Adjusting for diabetes did not materially alter the findings. There were no significant interactions between individual pollutants and asthma or current smoking.ConclusionsThis study adds to the evidence to reduce ambient PM2.5 concentrations as low as possible to protect the health of the general population.



2018 ◽  
Vol 24 (1) ◽  
Author(s):  
V. S. CHAUHAN ◽  
BHANUMATI SINGH ◽  
SHREE GANESH ◽  
JAMSHED ZAIDI

Studies on air pollution in large cities of India showed that ambient air pollution concentrations are at such levels where serious health effects are possible. This paper presents overview on the status of air quality index (AQI) of Jhansi city by using multivariate statistical techniques. This base line data can help governmental and non-governmental organizations for the management of air pollution.





Sign in / Sign up

Export Citation Format

Share Document