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Particle and Fibre Toxicology

, 9:49

First Online: 12 December 2012Received: 15 September 2012Accepted: 09 December 2012

Abstract

BackgroundAmbient air pollution has been associated with activation of systemic inflammation and hypercoagulability and increased plasma homocysteine, but the chemical constituents behind the association are not well understood. We examined the relations of various chemical constituents of fine particles PM2.5 and biomarkers of inflammation, coagulation and homocysteine in the context of traffic-related air pollution.

MethodsA panel of 40 healthy college students underwent biweekly blood collection for 12 times before and after their relocation from a suburban campus to an urban campus with changing air pollution contents in Beijing. Blood samples were measured for circulatory biomarkers of high-sensitivity C reactive protein hs-CRP, tumor necrosis factor alpha TNF-α, fibrinogen, plasminogen activator inhibitor type 1 PAI-1, tissue-type plasminogen activator t-PA, von Willebrand factor vWF, soluble platelet selectin sP-selectin, and total homocysteine tHcy. Various air pollutants were measured in a central air-monitoring station in each campus and 32 PM2.5 chemical constituents were determined in the laboratory. We used three different mixed-effects models single-constituent model, constituent-PM2.5 joint model and constituent residual model controlling for potential confounders to estimate the effects of PM2.5 chemical constituents on circulatory biomarkers.

ResultsWe found consistent positive associations between the following biomarkers and PM2.5 chemical constituents across different models: TNF-α with secondary organic carbon, chloride, zinc, molybdenum and stannum; fibrinogen with magnesium, iron, titanium, cobalt and cadmium; PAI-1 with titanium, cobalt and manganese; t-PA with cadmium and selenium; vWF with aluminum. We also found consistent inverse associations of vWF with nitrate, chloride and sodium, and sP-selectin with manganese. Two positive associations of zinc with TNF-α and of cobalt with fibrinogen, and two inverse associations of nitrate with vWF, and of manganese with sP-selectin, were independent of the other constituents in two-constituent models using constituent residual data. We only found weak air pollution effects on hs-CRP and tHcy.

ConclusionsOur results provide clues for the potential roles that PM2.5 chemical constituents may play in the biological mechanisms through which air pollution may influence the cardiovascular system.

KeywordsAir pollution Chemical constituent Coagulation Inflammation Panel study Particulate matter AbbreviationsAlAluminum

BaBarium

BITBeijing Institute of Technology

BMIBody mass index

CdCadmium

CIConfidence interval

ClChloride

COCarbon monoxide

CoCobalt

ECElemental carbon

FFluoride

FeIron

hs-CRPhigh-sensitivity C reactive protein

IQRInterquartile range

MgMagnesium

MnManganese

NONitric oxide

NO2Nitrogen dioxide

NO3Nitrate

NOXNitrogen oxides

OCOrganic carbon

PAI-1Plasminogen activator inhibitor type 1

PbLead

PM2.5Particulate matter with aerodynamic diameter ≤2.5 μm

PM2.5–10Particulate matter with aerodynamic diameter between 2.5 and 10 μm

PM10Particulate matter with aerodynamic diameter ≤10 μm

SeSelenium

SO4Sulfate

sP-selectinSoluble platelet selectin

TiTitanium

TNF-αTumor necrosis factor alpha

tHcytotal homocysteine

t-PAtissue-type plasminogen activator

VVanadium

vWFvon Willebrand factor

ZnZinc.

Electronic supplementary materialThe online version of this article doi:10.1186-1743-8977-9-49 contains supplementary material, which is available to authorized users.

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Autor: Shaowei Wu - Furong Deng - Hongying Wei - Jing Huang - Hongyi Wang - Masayuki Shima - Xin Wang - Yu Qin - Chanjuan Zheng

Fuente: https://link.springer.com/







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