No effect of acute exposure to coarse particulate matter air pollution in a rural location on high-density lipoprotein function - PubMed (original) (raw)

Randomized Controlled Trial

doi: 10.3109/08958378.2013.850761.

Hui-Yu Yang, Gajalakshmi Ramanathan, Fen Yin, Robert L Bard, Masako Morishita, J Timothy Dvonch, Lu Wang, Catherine Spino, Bhramar Mukherjee, Marcus A Badgeley, Alma Barajas-Espinosa, Qinghua Sun, Jack Harkema, Sanjay Rajagopalan, Jesus A Araujo, Robert D Brook

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Randomized Controlled Trial

No effect of acute exposure to coarse particulate matter air pollution in a rural location on high-density lipoprotein function

Andrei Maiseyeu et al. Inhal Toxicol. 2014 Jan.

Abstract

Context: High-density lipoprotein (HDL) particles perform numerous vascular-protective functions. Animal studies demonstrate that exposure to fine or ultrafine particulate matter (PM) can promote HDL dysfunction. However, the impact of PM on humans remains unknown.

Objective: We aimed to determine the effect of exposure to coarse concentrated ambient particles (CAP) on several metrics of HDL function in healthy humans.

Methods: Thirty-two adults (25.9 ± 6.6 years) were exposed to coarse CAP [76.2 ± 51.5 µg·m(-3)] in a rural location and filtered air (FA) for 2 h in a randomized double-blind crossover study. Venous blood collected 2- and 20-h post-exposures was measured for HDL-mediated efflux of [(3)H]-cholesterol from cells and 20-h exposures for HDL anti-oxidant capacity by a fluorescent assay and paraoxonase activity. The changes [median (first, third quartiles)] between exposures among 29 subjects with available results were compared by matched Wilcoxon tests.

Results: HDL-mediated cholesterol efflux capacity did not differ between exposures at either time point [16.60% (15.17, 19.19) 2-h post-CAP versus 17.56% (13.43, 20.98) post-FA, p = 0.768 and 14.90% (12.47, 19.15) 20-h post-CAP versus 17.75% (13.22, 23.95) post-FA, p = 0.216]. HOI [0.26 (0.24, 0.35) versus 0.28 (0.25, 0.40), p = 0.198] and paraoxonase activity [0.54 (0.39, 0.82) versus 0.60 μmol·min(-1 )ml plasma(-1) (0.40, 0.85), p = 0.137] did not differ 20-h post-CAP versus FA, respectively.

Conclusions: Brief inhalation of coarse PM from a rural location did not acutely impair several facets of HDL functionality. Whether coarse PM derived from urban sites, fine particles or longer term PM exposures can promote HDL dysfunction warrant future investigations.

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Figures

Figure 1

Figure 1. HDL-mediated cholesterol efflux activity results 2-hours (A, B [with cAMP added]) and 20-hours (C, D [with cAMP added]) post CAP versus FA exposures (n=29)

CAP, coarse concentrated ambient particles; FA, filtered air; cAMP, 0.3 mM 8-chloroadenosine 3′,5′-cyclic-monophosphate These experiments evaluated the ability of subjects’ HDL particles to cause efflux of H3-cholesterol from mouse macrophages. P values are calculated by paired Wilcoxon Signed Rank tests

Figure 1

Figure 1. HDL-mediated cholesterol efflux activity results 2-hours (A, B [with cAMP added]) and 20-hours (C, D [with cAMP added]) post CAP versus FA exposures (n=29)

CAP, coarse concentrated ambient particles; FA, filtered air; cAMP, 0.3 mM 8-chloroadenosine 3′,5′-cyclic-monophosphate These experiments evaluated the ability of subjects’ HDL particles to cause efflux of H3-cholesterol from mouse macrophages. P values are calculated by paired Wilcoxon Signed Rank tests

Figure 2

Figure 2. HDL oxidation index (A), adjusted HDL oxidation index (B), and PON activity 20 hours following CAP versus FA exposures (n=29)

CAP, coarse concentrated ambient particles; FA, filtered air; PON, paraoxonase HDL anti-oxidant capacity was assessed by a fluorescence assay that evaluated the ability of HDL to inhibit LDL oxidation, determined by dichlorofluorescein (DCF) fluorescence. PON activity was determined as the hydrolysis of paraoxon substrate (diethyl-_p_-nitrophenyl phosphate) to _p_-nitrophenol by PON-1 by spectrophotometry. P values are calculated by paired Wilcoxon Signed Rank tests

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