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. 2011 Jun;119(6):778-83.
doi: 10.1289/ehp.1002543. Epub 2010 Dec 17.

Ambient PM2.5 exposure up-regulates the expression of costimulatory receptors on circulating monocytes in diabetic individuals

Alexandra Schneider  1 , Neil E Alexis, David Diaz-Sanchez, Lucas M Neas, Shirley Harder, Margaret C Herbst, Wayne E Cascio, John B Buse, Annette Peters, Robert B Devlin
Affiliations

Ambient PM2.5 exposure up-regulates the expression of costimulatory receptors on circulating monocytes in diabetic individuals

Alexandra Schneider et al. Environ Health Perspect. 2011 Jun.

Abstract

Background: Exposure of humans to air pollutants such as ozone and particulate matter (PM) may result in airway and systemic inflammation and altered immune function. One putative mechanism may be through modification of cell-surface costimulatory molecules.

Objectives: We examined whether changes in expression of costimulatory molecules on circulating cells are associated with ambient levels of fine PM [aerodynamic diameter ≤ 2.5 μm (PM2.5)] in a susceptible population of diabetic individuals.

Methods: Twenty subjects were studied for 4 consecutive days. Daily measurements of PM2.5 and meteorologic data were acquired on the rooftop of the exam site. Circulating cell-surface markers that mediate innate immune and inflammatory responses were assessed by flow cytometry on each day. Sensitivity analysis was conducted on glutathione S-transferase M1 (GSTM1) genotype, body mass index, and glycosylated hemoglobin A1c (HbA1c) levels to determine their role as effect modifiers. Data were analyzed using random effects models adjusting for season, weekday, and meteorology.

Results: We found significantly increased monocyte expression (mean fluorescent intensity) of CD80, CD40, CD86, HLA-DR, and CD23 per 10-μg/m3 increase in PM2.5 at 2- to 4-day lag times after exposure. These findings were significantly higher in obese individuals, in individuals with HbA1c > 7%, and in participants who were GSTM1 null.

Conclusions: Exposure to PM2.5 can enhance antigen-presenting cell phenotypes on circulating cells, which may have consequences in the development of allergic or autoimmune diseases. These effects are amplified in diabetic individuals with characteristics that are associated with insulin resistance or with oxidative stress.

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Figures

Figure 1
Figure 1
Procedure example. (A) Scatterplot of gated leukocyte populations based on forward (FSC) and side (SSC) light scatter properties: lymphocytes (red), monocytes (blue), neutrophils (green), and eosinophils (pink). (B and C) Quadrant plots showing monocytes in the control region using fluorescein isothiocyanate (FITC)– and phycoerythrin (PE)–labeled IgG1 as isotypic controls for CD80 versus CD40, respectively, showing > 80% CD40+ cells (C).
Figure 2
Figure 2
Effect estimates based on percentages of peripheral blood monocyte cellular activation markers (with 95% CIs) for immediate (lag 0) and delayed (lags 1–4) associations with PM2.5: IgE group (A), APC group parts 1 (B) and 2 (C), and cell migration group (D). Abbreviations: aff, affinity; rec, receptor.
Figure 3
Figure 3
Effect estimates based on MFI for peripheral blood monocyte cellular activation markers (with 95% CIs) for (lag 0) and delayed (lags 1–4) associations with PM2.5: IgE group (A), APC group parts 1 (B) and 2 (C), and cell migration group (D). Abbreviations: aff, affinity; rec, receptor.
Figure 4
Figure 4
Effect estimates based on percentages of neutrophil cellular activation markers (with 95% CIs) for immediate (lag 0) and delayed (lags 1–4) associations with PM2.5.
Figure 5
Figure 5
Effect estimates based on MFI for neutrophil cellular activation markers (with 95% CIs) for immediate (lag 0) and delayed (lags 1–4) associations with PM2.5.
Figure 6
Figure 6
CD40 monocyte effect modification estimates (with 95% CIs) based on MFI for immediate (lag 0) and delayed (lags 1–4) associations with PM2.5: BMI (A), HbA1c (B), and GSTM1 (C).
Figure 7
Figure 7
CD80 monocyte effect modification estimates (with 95% CIs) based on MFI for (lag 0) and delayed (lags 1–4) associations with PM2.5: BMI (A), HbA1c (B), and GSTM1 (C).
See this image and copyright information in PMC

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