Platelet activation, upregulation of CD11b/CD18 expression on leukocytes and increase in circulating leukocyte-platelet aggregates in Indian women chronically exposed to biomass smoke

Author:

Ray M R1,Mukherjee S2,Roychoudhury S,Bhattacharya P,Banerjee M,Siddique S3,Chakraborty S2,Lahiri T3

Affiliation:

1. Experimental Hematology Unit, Chittaranjan National Cancer Institute, 37, SP Mukherjee Road, Kolkata 700 026, India

2. Experimental Hematology Unit, Chittaranjan National Cancer Institute, Kolkata 700 026, India

3. Department of Neuroendocrinology, Chittaranjan National Cancer Institute, Kolkata 700 026, India

Abstract

The majority of households in rural India still rely on unprocessed solid biomass for domestic energy. The aim of this study was to investigate whether chronic exposure to biomass smoke causes activation of leukocytes and the formation of leukocyte-platelet aggregates. We conducted flow cytometric analysis of β2 Mac-1 integrin (CD11b/CD18) expression on polymorphonuclear leukocytes (PMN) and monocytes, and P-selectin (CD62P) expression on the platelets of 165 women from eastern India, who cook solely with wood, dung and agricultural wastes, and 155 age- and socio-economic condition-matched control subjects, who used relatively cleaner fuel, liquefied petroleum gas (LPG). Leukocyte-platelet aggregates were defined as CD11b-positive PMN and monocytes co-expressing platelet-specific markers CD41 or CD62P. A significant increase in leukocyte-platelet aggregates was found in women who used biomass as cooking fuel. In addition, they showed increased surface expression of CD11b/CD18 in circulating PMN and monocytes and CD62P expression on platelets. The mean fluorescence intensity (MFI) of CD11b on the surface of circulating monocytes and PMN of biomass users increased by 50 and 68%, respectively. Similarly, a 62 and 48% increase in MFI was observed in CD18 expression on the surface of these cells in biomass users. The results show that chronic biomass smoke exposure activates circulating platelets, PMN and monocytes, and increases the number of leukocyte-platelet aggregates, which are considered a risk factor for thrombosis.

Publisher

SAGE Publications

Subject

Health, Toxicology and Mutagenesis,Toxicology,General Medicine

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