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Personal Fine Particulate Matter Constituents, Increased Systemic Inflammation, and the Role of DNA Hypomethylation.

ABSTRACT: Limited evidence is available on the effects of various fine particulate matter (PM2.5) components on inflammatory cytokines and DNA methylation. We examined whether 16 PM2.5 components are associated with changes in four blood biomarkers, that is, tumor necrosis factor-? (TNF-?), soluble cluster of differentiation 40 ligand (sCD40L), soluble intercellular adhesion molecule-1 (sICAM-1), and fibrinogen, as well as their corresponding DNA methylation levels in a panel of 36 healthy college students in Shanghai, China. We used linear mixed-effect models to evaluate the associations, with controls of potential confounders. We further conducted mediation analysis to evaluate the potential mediation effects of components on inflammatory markers through change in DNA methylation. We observed that several components were consistently associated with TNF-? and fibrinogen as well as their DNA hypomethylation. For example, an interquartile range increase in personal exposure to PM2.5-lead (Pb) was associated with 65.20% (95% CI: 37.07, 99.10) increase in TNF-? and 2.66 (95% CI: 37.07, 99.10) decrease in TNF-? methylation, 30.51% (95% CI: 0.72, 69.11) increase in fibrinogen and 1.25 (95% CI: 0.67, 1.83) decrease in F3 methylation. PM2.5 components were significantly associated with sICAM-1 methylation but not with sICAM-1 protein. DNA methylation mediated 19.89%-41.75% of the elevation in TNF-? expression by various PM2.5 constituents. Our findings provide clues that personal PM2.5 constituents exposure may contribute to increased systemic inflammation through DNA hypomethylation.

SUBMITTER: Lei X

PROVIDER: S-EPMC7092684 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature

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Personal Fine Particulate Matter Constituents, Increased Systemic Inflammation, and the Role of DNA Hypomethylation.

Lei Xiaoning X Chen Renjie R Wang Cuicui C Shi Jingjin J Zhao Zhuohui Z Li Weihua W Yan Beizhan B Chillrud Steve S Cai Jing J Kan Haidong H

Environmental science & technology 20190801 16

Limited evidence is available on the effects of various fine particulate matter (PM<sub>2.5</sub>) components on inflammatory cytokines and DNA methylation. We examined whether 16 PM<sub>2.5</sub> components are associated with changes in four blood biomarkers, that is, tumor necrosis factor-α (TNF-α), soluble cluster of differentiation 40 ligand (sCD40L), soluble intercellular adhesion molecule-1 (sICAM-1), and fibrinogen, as well as their corresponding DNA methylation levels in a panel of 36 h ...[more]

PMID: 31328512

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Project description:BackgroundNumerous studies have linked fine particles [? 2.5 µm in aerodynamic diameter (PM(2.5))] and health. Most studies focused on the total mass of the particles, although the chemical composition of the particles varies substantially. Which chemical components of fine particles that are the most harmful is not well understood, and research on the chemical composition of PM(2.5) and the components that are the most harmful is particularly limited in Asia.ObjectivesWe characterized PM(2.5) chemical composition and estimated the effects of cause-specific mortality of PM(2.5) mass and constituents in Seoul, Korea. We compared the chemical composition of particles to those of the eastern and western United States.MethodsWe examined temporal variability of PM(2.5) mass and its composition using hourly data. We applied an overdispersed Poisson generalized linear model, adjusting for time, day of week, temperature, and relative humidity to investigate the association between risk of mortality and PM(2.5) mass and its constituents in Seoul, Korea, for August 2008 through October 2009.ResultsPM(2.5) and chemical components exhibited temporal patterns by time of day and season. The chemical characteristics of Seoul's PM(2.5) were more similar to PM(2.5) found in the western United States than in the eastern United States. Seoul's PM(2.5) had lower sulfate (SO(4)) contributions and higher nitrate (NO(3)) contributions than that of the eastern United States, although overall PM(2.5) levels in Seoul were higher than in the United States. An interquartile range (IQR) increase in magnesium (Mg) (0.05 ?g/m³) was associated with a 1.4% increase (95% confidence interval: 0.2%, 2.6%) in total mortality on the following day. Several components that were among the largest contributors to PM(2.5) total mass--NO(3), SO(4), and ammonium (NH(4))--were moderately associated with same-day cardiovascular mortality at the p < 0.10 level. Other components with smaller mass contributions [Mg and chlorine (Cl)] exhibited moderate associations with respiratory mortality on the following day (p < 0.10).ConclusionsOur findings link PM(2.5) constituents with mortality and have implications for policy making on sources of PM(2.5) and on the relevance of PM(2.5) health studies from other areas to this region.

Project description:BACKGROUND:The link between PM2.5 exposure and adverse health outcomes is well documented from studies across the world. However, the reported effect estimates vary across studies, locations and constituents. We aimed to conduct a meta-analysis on associations between short-term exposure to PM2.5 constituents and mortality using city-specific estimates, and explore factors that may explain some of the observed heterogeneity. METHODS:We systematically reviewed epidemiological studies on particle constituents and mortality using PubMed and Web of Science databases up to July 2015.We included studies that examined the association between short-term exposure to PM2.5 constituents and all-cause, cardiovascular, and respiratory mortality, in the general adult population. Each study was summarized based on pre-specified study key parameters (e.g., location, time period, population, diagnostic classification standard), and we evaluated the risk of bias using the Office of Health Assessment and Translation (OHAT) Method for each included study. We extracted city-specific mortality risk estimates for each constituent and cause of mortality. For multi-city studies, we requested the city-specific risk estimates from the authors unless reported in the article. We performed random effects meta-analyses using city-specific estimates, and examined whether the effects vary across regions and city characteristics (PM2.5 concentration levels, air temperature, elevation, vegetation, size of elderly population, population density, and baseline mortality). RESULTS:We found a 0.89% (95% CI: 0.68, 1.10%) increase in all-cause, a 0.80% (95% CI: 0.41, 1.20%) increase in cardiovascular, and a 1.10% (95% CI: 0.59, 1.62%) increase in respiratory mortality per 10?g/m3 increase in PM2.5. Accounting for the downward bias induced by studies of single days, the all-cause mortality estimate increased to 1.01% (95% CI: 0.81, 1.20%). We found significant associations between mortality and several PM2.5 constituents. The most consistent and stronger associations were observed for elemental carbon (EC) and potassium (K). For most of the constituents, we observed high variability of effect estimates across cities. CONCLUSIONS:Our meta-analysis suggests that (a) combustion elements such as EC and K have a stronger association with mortality, (b) single lag studies underestimate effects, and (c) estimates of PM2.5 and constituents differ across regions. Accounting for PM mass in constituent's health models may lead to more stable and comparable effect estimates across different studies. SYSTEMATIC REVIEW REGISTRATION:PROSPERO: CRD42017055765.

Project description:BackgroundStudies have shown that nutritional supplements could reduce the adverse effects induced by air pollution. However, whether dietary patterns can modify the association of long-term exposure to fine particulate matter (PM2.5) and its constituents with hypertension defined by the 2017 ACC/AHA guideline has not been evaluated.MethodsWe included 47,501 Chinese adults from a nationwide cross-sectional study. PM2.5 and five constituents were estimated by satellite-based random forest models. Dietary approaches to stop hypertension (DASH) and alternative Mediterranean diet (AMED) scores were calculated for each participant. Interactions between dietary patterns and air pollution were examined by adding a multiplicative interaction term to logistic models.ResultsLong-term exposure to PM2.5 and its constituents was associated with an increased risk of hypertension and stage 1-2 hypertension. The DASH and AMED scores significantly modified these associations, as individuals with higher scores had a significantly lower risk of air pollution-related hypertension and stage 1-2 hypertension (P-interaction < 0.05), except for interaction between PM2.5, sulfate, nitrate, ammonium, and AMED score on stage 1 hypertension. For each IQR increase in PM2.5, participants with the lowest DASH and AMED quintiles had hypertension risk with ORs (95%CI) of 1.20 (1.10, 1.30) and 1.19 (1.09, 1.29), whereas those with the highest DASH and AMED quintiles had lower risks with 0.98 (0.91, 1.05) and 1.04 (0.97, 1.11). The stratified analysis found modification effect was more prominent in the < 65 years age group. Consuming more fresh vegetables, fruits, whole grains, and dairy would reduce the risk of hypertension caused by PM2.5 and its constituents.ConclusionsDietary patterns rich in antioxidants can reduce long-term exposure to PM2.5 and its constituents-induced hypertension defined by the 2017 ACC/AHA guideline, especially in young and middle-aged individuals. Compared to the Mediterranean diet, the DASH diet offers superior dietary guidance to prevent stage 1 hypertension caused by air pollution.

Project description:Fine particulate matter (PM2.5) released during the livestock industry endangers the respiratory health of animals. Our previous findings suggested that broilers exposed to PM2.5 exhibited lung inflammation and changes in the pulmonary microbiome. Therefore, this study was to investigate whether the pulmonary microbiota plays a causal role in the pathogenesis of PM2.5-induced lung inflammation. We first used antibiotics to establish a pulmonary microbiota intervention broiler model, which showed a significantly reduced total bacterial load in the lungs without affecting the microbiota composition or structure. Based on it, 45 AA broilers of similar body weight were randomly assigned to three groups: control (CON), PM2.5 (PM), and pulmonary microbiota intervention (ABX-PM). From 21 d of age, broilers in the ABX-PM group were intratracheally instilled with antibiotics once a day for 3 d. Meanwhile, broilers in the other two groups were simultaneously instilled with sterile saline. On 24 and 26 d of age, broilers in the PM and ABX-PM groups were intratracheally instilled with PM2.5 suspension to induce lung inflammation, and broilers in the CON group were simultaneously instilled with sterile saline. The lung histomorphology, inflammatory cytokines' expression levels, lung microbiome, and microbial growth conditions were analyzed to determine the effect of the pulmonary microbiota on PM2.5-induced lung inflammation. Broilers in the PM group showed lung histological injury, while broilers in the ABX-PM group had normal lung histomorphology. Furthermore, microbiota intervention significantly reduced mRNA expression levels of interleukin-1β, tumor necrosis factor-α, interleukin-6, interleukin-8, toll-like receptor 4 and nuclear factor kappa-B. PM2.5 induced significant changes in the β diversity and structure of the pulmonary microbiota in the PM group. However, no significant changes in microbiota structure were observed in the ABX-PM group. Moreover, the relative abundance of Enterococcus cecorum in the PM group was significantly higher than that in the CON and ABX-PM groups. And sterile bronchoalveolar lavage fluid from the PM group significantly promoted the growth of E. cecorum, indicating that PM2.5 altered the microbiota's growth condition. In conclusion, pulmonary microbiota can affect PM2.5-induced lung inflammation in broilers. PM2.5 can alter the bacterial growth environment and promote dysbiosis, potentially exacerbating inflammation.

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Personal Fine Particulate Matter Constituents, Increased Systemic Inflammation, and the Role of DNA Hypomethylation.

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Personal Fine Particulate Matter Constituents, Increased Systemic Inflammation, and the Role of DNA Hypomethylation.

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