Histone Methylation in Nickel-Smelting Industrial Workers

Ma, Li; Bai, Yana; Pu, Hongquan; Gou, Faxiang; Dai, Min; Wang, Hui; He, Jie; Zheng, Tongzhang; Cheng, Ning

doi:10.1371/journal.pone.0140339

Cited by 29 publications

(16 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In particular, modifications to histone H3 are one of the best-characterized in terms of identifying links to changes to gene expression (Henikoff and Shilatifard, 2011). Previous evidence has identified specific histone H3 modifications after exposure to organic chemical compounds (Baccarelli and Bollati, 2009; Bollati and Baccarelli, 2010; Hou et al, 2012b; Zhang et al, 2016) and heavy metals (Arita et al, 2012a, 2012b; Baccarelli and Bollati, 2009; Cantone et al, 2011; Chervona et al, 2012; Ma et al, 2015; Martinez-Zamudio and Ha, 2011; Sun et al, 2009; Zhou et al, 2008). However, few human studies have been conducted to evaluate the effects of ambienttraffic-derived PM on histoneH3 modifications.…”

Section: Introductionmentioning

confidence: 99%

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

Zheng

Sanchez-Guerra

Zhang

et al. 2017

Environmental Research

View full text Add to dashboard Cite

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.

show abstract

Section: Introductionmentioning

confidence: 99%

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

Zheng

Sanchez-Guerra

Zhang

et al. 2017

Environmental Research

View full text Add to dashboard Cite

show abstract

“…First, the histone markers were measured in whole blood samples reflecting a mixed cell population, which may limit our ability to understand the exact biological mechanism by specific blood cell type. Nonetheless, whole blood is easy to obtain and process – for this reason most human epigenetic studies use whole blood for epigenetic biomarker measurements, including histone modifications, in the hope of identifying blood-based, cost-effective disease biomarkers (Hou et al 2013, Hou et al 2014, Liu et al 2015, Ma et al 2015, Sanchez-Guerra et al 2015, Hou et al 2016, Zheng et al 2016, Zhang et al 2017). The rationale for our using mixed white blood cells is supported by the need to identify novel biomarkers of BP in easily obtainable blood samples.…”

Section: Discussionmentioning

confidence: 99%

Histone 3 modifications and blood pressure in the Beijing Truck Driver Air Pollution Study

et al. 2017

View full text Add to dashboard Cite

Context Histone modifications regulate gene expression; dysregulation has been linked with cardiovascular diseases. Associations between histone modification levels and blood pressure in humans are unclear. Objective We examine the relationship between global histone concentrations and various markers of blood pressure. Materials and methods Using the Beijing Truck Driver Air Pollution Study, we investigated global peripheral white blood cell histone modifications (H3K9ac, H3K9me3, H3K27me3, and H3K36me3) associations with pre- and post-work measurements of systolic (SBP) and diastolic (DBP) blood pressure, mean arterial pressure (MAP), and pulse pressure (PP) using multivariable mixed-effect models. Results H3K9ac was negatively associated with pre-work SBP and MAP; H3K9me3 was negatively associated with pre-work SBP, DBP, and MAP; and H3K27me3 was negatively associated with pre-work SBP. Among office workers, H3K9me3 was negatively associated with pre-work SBP, DBP, and MAP. Among truck drivers, H3K9ac and H3K27me were negatively associated with pre-work SBP, and H3K27me3 was positively associated with post-work PP. Discussion and conclusion Epigenome-wide H3K9ac, H3K9me3, and H3K27me3 were negatively associated with multiple pre-work blood pressure measures. These associations substantially changed during the day, suggesting an influence of daily activities. Blood-based histone modification biomarkers are potential candidates for studies requiring estimations of morning/pre-work blood pressure.

show abstract

“…Taken together, the totality of the evidence supports an indirect genotoxic and/or non-genotoxic MOA with thresholds for nickel carcinogenesis. [51] Apoptosis/Autophagy Increase [109,[112][113][114][115] Increase via increased expression of caspase 8 in workers [116] Histone modifications *Hypermethylation Positive at H3K9 [117,118] In workers at H3K4 [119][120][121] *Hyperphosphorylation Positive at H3S10 [122] *Hyperubiquitination…”

Section: Nickel Compounds' Genotoxic and Carcinogenic Mode Of Actionmentioning

confidence: 99%

Concise Review of Nickel Human Health Toxicology and Ecotoxicology

Buxton¹,

Garman²,

Heim³

et al. 2019

Inorganics

169

View full text Add to dashboard Cite

Nickel (Ni) metal and Ni compounds are widely used in applications like stainless steel, alloys, and batteries. Nickel is a naturally occurring element in water, soil, air, and living organisms, and is essential to microorganisms and plants. Thus, human and environmental nickel exposures are ubiquitous. Production and use of nickel and its compounds can, however, result in additional exposures to humans and the environment. Notable human health toxicity effects identified from human and/or animal studies include respiratory cancer, non-cancer toxicity effects following inhalation, dermatitis, and reproductive effects. These effects have thresholds, with indirect genotoxic and epigenetic events underlying the threshold mode of action for nickel carcinogenicity. Differences in human toxicity potencies/potentials of different nickel chemical forms are correlated with the bioavailability of the Ni2+ ion at target sites. Likewise, Ni2+ has been demonstrated to be the toxic chemical species in the environment, and models have been developed that account for the influence of abiotic factors on the bioavailability and toxicity of Ni2+ in different habitats. Emerging issues regarding the toxicity of nickel nanoforms and metal mixtures are briefly discussed. This review is unique in its covering of both human and environmental nickel toxicity data.

show abstract

Histone Methylation in Nickel-Smelting Industrial Workers

Cited by 29 publications

References 25 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

Histone 3 modifications and blood pressure in the Beijing Truck Driver Air Pollution Study

Concise Review of Nickel Human Health Toxicology and Ecotoxicology

Contact Info

Product

Resources

About