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Background  Current studies of environmental health suggest a link between air pollution components, such as particulate matter (PM), and various diseases. However, the specific genes and regulatory mechanisms implicated in PM-induced diseases remain largely unknown. Epigenetic systems such as covalent modification of histones in chromatin may mediate environmental factors in gene regulation. Investigating the relationships between PM exposure and histone modification status may help understand the mechanisms underlying environment-associated health conditions.    Methods  In this study, we obtained genome-wide profiles of H3K27ac (histone 3 lysine 27 acetylation), known to be an active gene regulatory histone modification marker, in blood samples collected from four Chinese individuals exposed to high or low PM 2.5  (particles with diameters up to 2.5 μm).    Results  The genome-wide chromatin immunoprecipitation sequencing (ChIP-Seq) data indicated a comprehensive differential H3K27ac landscape across the individual genomes, which was associated with high PM 2.5 . Moreover, a substantial number of these PM 2.5 -associated differential H3K27ac markers were in genes involved in immune cell activation, potentially linking these epigenetic changes with air pollution-induced immune and inflammatory responses.    Conclusions  Our study provides the first genome-wide characterization of H3K27ac profiles in individuals subjected to different exposure levels of PM 2.5 . Future systematic investigations of the relationships between air pollutants and histone modifications in large population samples are warranted to elucidate the contributions of histone modifications to environment-associated diseases.    Electronic supplementary material  The online version of this article (doi:10.1186/s12940-015-0052-5) contains supplementary material, which is available to authorized users.

Characterization of genome-wide H3K27ac profiles reveals a distinct PM2.5-associated histone modification signature