Extracellular histones mediate the effects of metal-rich air particles on blood coagulation

Cantone, Laura; Angelici, Laura; Bollati, Valentina; Bonzini, Matteo; Apostoli, Pietro; Tripodi, Armando; Bertazzi, Pier Alberto; Baccarelli, Andrea

doi:10.1016/j.envres.2014.03.029

Cited by 10 publications

(7 citation statements)

References 43 publications

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“…Cumulative exposure to inhaled nickel, arsenic, and iron have also identified associations with increased H3K9ac (Cantone et al, 2011). Moreover, H3K9ac mediates the effects of inhaled PM on blood coagulation (Cantone et al, 2014) suggesting that it may serve as a marker of air pollution-related cardiovascular outcomes, and if confirmed would provide public health officials and researchers with a useful exposure measurement and/or risk assessment tool. Conversely, we found no similar studies explaining a link between ambient air pollution exposure and H3K9me3.…”

Section: Discussionmentioning

confidence: 99%

Traffic-derived particulate matter exposure and histone H3 modification: A repeated measures study

Zheng

Sanchez-Guerra

Zhang

et al. 2017

Environmental Research

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Background Airborne particulate matter (PM) may induce epigenetic changes that potentially lead to chronic diseases. Histone modifications regulate gene expression by influencing chromatin structure that can change gene expression status. We evaluated whether traffic-derived PM exposure is associated with four types of environmentally inducible global histone H3 modifications. Methods The Beijing Truck Driver Air Pollution Study included 60 truck drivers and 60 office workers examined twice, 1–2 weeks apart, for ambient PM10 (both day-of and 14-day average exposures), personal PM2.5, black carbon (BC), and elemental components (potassium, sulfur, iron, silicon, aluminum, zinc, calcium, and titanium). For both PM10 measures, we obtained hourly ambient PM10 data for the study period from the Beijing Municipal Environmental Bureau’s 27 representatively distributed monitoring stations. We then calculated a 24 h average for each examination day and a moving average of ambient PM10 measured in the 14 days prior to each examination. Examinations measured global levels of H3 lysine 9 acetylation (H3K9ac), H3 lysine 9 tri-methylation (H3K9me3), H3 lysine 27 tri-methylation (H3K27me3), and H3 lysine 36 tri-methylation (H3K36me3) in blood leukocytes collected after work. We used adjusted linear mixed-effect models to examine percent changes in histone modifications per each μg/m3 increase in PM exposure. Results In all participants each μg/m3 increase in 14-day average ambient PM10 exposure was associated with lower H3K27me3 (β=−1.1%, 95% CI: −1.6, −0.6) and H3K36me3 levels (β=−0.8%, 95% CI: −1.4, −0.1). Occupation-stratified analyses showed associations between BC and both H3K9ac and H3K36me3 that were stronger in office workers (β=4.6%, 95% CI: 0.9, 8.4; and β=4.1%, 95% CI: 1.3; 7.0 respectively) than in truck drivers (β=0.1%, 95% CI: −1.3, 1.5; and β=0.9%, 95% CI: −0.9, 2.7, respectively; both pinteraction < 0.05). Sex-stratified analyses showed associations between examination-day PM10 and H3K9ac, and between BC and H3K9me3, were stronger in women (β=10.7%, 95% CI: 5.4, 16.2; and β=7.5%, 95% CI: 1.2, 14.2, respectively) than in men (β=1.4%, 95% CI: −0.9, 3.7; and β=0.9%, 95% CI: −0.9, 2.7, respectively; both pinteraction < 0.05). We observed no associations between personal PM2.5 or elemental components and histone modifications. Conclusions Our results suggest a possible role of global histone H3 modifications in effects of traffic-derived PM exposures, particularly BC exposure. Future studies should assess the roles of these modifications in human diseases and as potential mediators of air pollution-induced disease, in particular BC exposure.

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Section: Discussionmentioning

confidence: 99%

Traffic-derived particulate matter exposure and histone H3 modification: A repeated measures study

Zheng

Sanchez-Guerra

Zhang

et al. 2017

Environmental Research

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“…Changes in small non-coding RNAs have been found to be associated with inorganic arsenic [43] and ozone [44] exposures. Global changes in histone tail modifications have been shown to be associated with exposure to metals [45] and particulate matter [46,47].…”

Section: Epigenetic Modifications Are Environmentally Labilementioning

confidence: 99%

Epigenetic Signatures as Biomarkers of Exposure

Ladd‐Acosta

2015

Curr Envir Health Rpt

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To advance our knowledge of the influence of environmental exposures on human health and disease, robust studies are needed. However, for many exposures, robust studies are not feasible due to limitations with current ascertainment methods and/or study designs. Epigenetics, the study of mitotically heritable, reversible information that regulates critical cell processes, has gained much attention because it offers a potential mechanism to explain how exposures can influence cell states. Therefore, most studies have focused on epigenetics as a mechanism for disease. However, emerging evidence also suggests that epigenetic marks may also serve as biomarkers of exposure. Here, we highlight findings showing that the epigenome is labile to the environment and that these exposure-associated changes show long-term stability, are specific, are detectable in accessible tissues, can predict exposure status, and can be practically implemented, thus supporting the potential for epigenetic patterns to serve as robust measures of environmental exposure.

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“…Histone deacetylation is involved in the regulation of gene transcription under stress or pathological conditions [ 77 ]. In a study of workers in an Italian steel factory, Cantone and his colleagues observed that PM in the air is directly proportional to the extracellular plasma histone modification H3K9ac, and showed that histone modification mediates PM 2.5 to cause blood coagulation [ 78 ]. In addition, histone acetylation also plays an important role in PM 2.5 exposure-induced cardiac hypertrophy events.…”

Section: Introductionmentioning

confidence: 99%

The critical role of epigenetic mechanism in PM2.5-induced cardiovascular diseases

et al. 2021

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Cardiovascular disease (CVD) has become the leading cause of death worldwide, which seriously threatens human life and health. Epidemiological studies have confirmed the occurrence and development of CVD are closely related to air pollution. In particular, fine particulate matter (PM2.5) is recognized as an important environmental factor contributing to increased morbidity, mortality and hospitalization rates among adults and children. However, the underlying mechanism by which PM2.5 promotes CVD development remains unclear. With the development of epigenetics, recent studies have shown that PM2.5 exposure may induce or aggravate CVD through epigenetic changes. In order to better understand the potential mechanisms, this paper reviews the epigenetic changes of CVD caused by PM2.5. We summarized the epigenetic mechanisms of PM2.5 causing cardiovascular pathological damage and functional changes, mainly involving DNA methylation, non-coding RNA, histone modification and chromosome remodeling. It will provide important clues for exploring the biological mechanisms affecting cardiovascular health.

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Extracellular histones mediate the effects of metal-rich air particles on blood coagulation

Cited by 10 publications

References 43 publications

Traffic-derived particulate matter exposure and histone H3 modification: A repeated measures study

Traffic-derived particulate matter exposure and histone H3 modification: A repeated measures study

Epigenetic Signatures as Biomarkers of Exposure

The critical role of epigenetic mechanism in PM2.5-induced cardiovascular diseases

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