Data on the effect of in utero exposure to polycyclic aromatic hydrocarbons on genome-wide patterns of DNA methylation in lung tissues.
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ABSTRACT:
SUBMITTER: Fish TJ
PROVIDER: S-EPMC5491394 | biostudies-literature | 2017 Aug
REPOSITORIES: biostudies-literature
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Data on the effect of in utero exposure to polycyclic aromatic hydrocarbons on genome-wide patterns of DNA methylation in lung tissues.
Fish Trevor J TJ Benninghoff Abby D AD
Data in brief 20170621
Data in this article depict patterns of methylation in lung tissues obtained from the offspring of B6129SF1/J dams and 129S1/SvImJ sires exposed <i>in utero</i> to benzo[<i>a</i>]pyrene (BaP) or dibenzo[<i>def,p</i>]chrysene (DBC) as compared to non-exposed offspring. Genome-wide methylation of lung tumors in adult offspring was determined using methylated DNA immunoprecipitation (MeDIP) with the NimbleGen mouse DNA methylation CpG island array. This data article refers to the research article " ...[more]
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Project description:Polycyclic aromatic hydrocarbons (PAHs) comprise an important class of environmental pollutants that are known to cause lung cancer in animals and are suspected lung carcinogens in humans. Moreover, evidence from cell-based studies points to PAHs as modulators of the epigenome. The objective of this work was to assess patterns of genome-wide DNA methylation in lung tissues of adult offspring initiated in utero with the transplacental PAH carcinogens dibenzo [def,p]chrysene (DBC) or benzo [a]pyrene (BaP). Genome-wide methylation patterns for normal (not exposed), normal adjacent and lung tumor tissues obtained from adult offspring were determined using methylated DNA immunoprecipitation (MeDIP) with the NimbleGen mouse DNA methylation CpG island array. Lung tumor incidence in 45-week old mice initiated with BaP was 32%, much lower than that of the DBC-exposed offspring at 96%. Also, male offspring appeared more susceptible to BaP as compared to females. Distinct patterns of DNA methylation were associated with non-exposed, normal adjacent and adenocarcinoma lung tissues, as determined by principal components, hierarchical clustering and gene ontology analyses. From these methylation profiles, a set of genes of interest was identified that includes potential important targets for epigenetic modification during the process of lung tumorigenesis in animals exposed to environmental PAHs.
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Project description:BackgroundAging is related to an increased risk of morbidity and mortality and is affected by environmental factors. Exposure to polycyclic aromatic hydrocarbons (PAHs) is associated with adverse health outcomes; but the association of such exposure with DNA methylation aging, a novel aging marker, is unclear.ObjectivesOur aim was to investigate the association of PAH exposure with methylation aging.MethodsWe trained and validated a methylation age predictor suitable for Chinese populations using whole blood methylation data in 989 Chinese and 160 Caucasians. We defined two aging indicators: δage, as methylation age minus chronological age; and aging rate, the ratio of methylation to chronological age. The association of PAH exposure with aging indicators was evaluated using linear regressions in three panels of healthy Chinese participants (N=539, among the aforementioned 989 Chinese participants) whose exposure levels were assessed by 10 urinary monohydroxy-PAH metabolites.ResultsWe developed a methylation age predictor providing accurate predictions in both Chinese individuals and Caucasian persons (R=0.94-0.96, RMSE=3.8-4.3). Among the 10 urinary metabolites that we measured, 1-hydroxypyrene and 9-hydroxyphenanthrene were associated with methylation aging independently of other OH-PAHs and risk factors; 1-unit increase in 1-hydroxypyrene was associated with a 0.53-y increase in Δage [95% confidence interval (CI): 0.18, 0.88; false discovery rate (FDR) FDR=0.004] and 1.17% increase in aging rate (95% CI: 0.36, 1.98; FDR=0.02), whereas for 9-hydroxyphenanthrene, the increase was 0.54-y for Δage (95% CI: 0.17, 0.91; FDR=0.004), and 1.15% for aging rate (95% CI: 0.31, 1.99; FDR=0.02). The association direction was consistent across the three Chinese panels with the association magnitude correlating with the panels' exposure levels; the association was validated by methylation data of purified leukocytes. Several cytosine-phosphoguanines, including those located on FHL2 and ELOVL2, were found associated with both aging indicators and monohydroxy-PAH levels.ConclusionsWe developed a methylation age predictor specific for Chinese populations but also accurate for Caucasian populations. Our findings suggest that exposure to PAHs may be associated with an adverse impact on human aging and epigenetic alterations in Chinese populations. https://doi.org/10.1289/EHP2773.
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Project description:Polycyclic aromatic hydrocarbons degraders Raw sequence reads
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Project description:BackgroundThere is fast-growing epidemiologic evidence of the effects of environmental chemicals on respiratory health. Polycyclic aromatic hydrocarbons (PAHs) have been linked with airway obstruction common in asthma and/or asthma exacerbation, and chronic bronchitis and emphysema.ObjectivesA systematic review of the association between exposure to PAHs and obstructive lung diseases is not yet available. The present systematic review aims to evaluate the evidence available in epidemiological studies that have associated PAHs with obstructive lung diseases such as asthma, chronic bronchitis, emphysema.MethodsWe performed a systematic literature search on PubMed, Google Scholar, and Scopus databases using relevant keywords and guided by predesigned eligibility criteria.ResultsFrom the total of 30 articles reviewed, 16 articles examined the link between PAHs and lung function in both adults and children. Twelve articles investigated the association between PAHs and asthma, asthma biomarkers, and/or asthma symptoms in children. Two articles studied the relationship between PAHs and fractional exhaled nitric oxide (FeNO), a biomarker of airway inflammation and the relationship between PAHs and obstructive lung diseases and infections, respectively. One study assessed exposure to daily ambient PAHs and cough occurrence.DiscussionTwenty-seven studies found an association between PAHs and asthma and reduced lung function. In children it is reinforced by studies on prenatal and postnatal exposure, whereas in adults, reductions in lung function tests marked by low forced expiratory volume in 1 second, (FEV1), forced vital capacity (FVC), and forced expiratory flow (FEF25-75%) were the major health outcomes. Some studies recorded contrasting results: insignificant and/or no association between the two variables of interest. The studies reviewed had limitations ranging from small sample size, to the use of cross-sectional rather than longitudinal study design.ConclusionsThe literature reviewed in the present study largely suggest positive correlations between PAHs and obstructive lung diseases marked mainly by asthma and reduced respiratory function. This review was registered with PROSPERO (Registration no: CRD42020212894).Competing interestsThe authors declare no competing financial interests.
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Project description:Assessing the potential carcinogenicity of human toxins represents an ongoing challenge. Chronic rodent bioassays predict human cancer risk with limited reliability, and are expensive and time-consuming. To identify alternative prediction methods, we evaluated a transcriptomics-based human in vitro model to classify carcinogens by their modes of action. The aim of this study was to determine the transcriptomic response and identify specific molecular signatures of polycyclic aromatic hydrocarbons (PAHs), which can be used as predictors of carcinogenicity of environmental toxins in human in vitro systems. We found that characteristic molecular signatures facilitate identification and prediction of carcinogens.
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Project description:BACKGROUND:Workers on coke oven plants may be exposed to potentially carcinogenic polycyclic aromatic hydrocarbons (PAHs), particularly during work on the ovens tops. Two cohorts, employees of National Smokeless Fuels (NSF) and the British Steel Corporation (BSC) totalling more than 6,600 British coke plant workers employed in 1967, had been followed up to mid-1987 for mortality. Previous analyses suggested an excess in lung cancer risk of around 25%, or less when compared with Social Class IV ('partly skilled').Analyses based on internal comparisons within the cohorts identified statistical associations with estimates of individual exposures, up to the start of follow-up, to benzene-soluble materials (BSM), widely used as a metric for mixtures of PAHs. Some associations were also found with times spent in certain coke ovens jobs with specific exposure scenarios, but results were not consistent across the two cohorts and limitations in the exposure estimates were noted. The present study was designed to reanalyse the existing data on lung cancer mortality, incorporating revised and improved exposure estimates to BSM and to benzo[a]pyrene (B[a]P), including increments during the follow-up and a lag for latency. METHODS:Mean annual average concentrations of both BSM and B[a]P were estimated by analysis of variance (ANOVA) from concentration measurements at all NSF and six BSC plants, and summarised by job and plant, with a temporal trend (for the BSM only). These were combined with subjects' work histories, to produce exposure estimates in each year of follow-up, with a 10-year lag to allow for latency. Exposures to BSM and to B[a]P were sufficiently uncorrelated to permit analysis in relation to each variable separately.Lung cancer death risks during the follow-up were analysed in relation to the estimated time-dependent exposures, both continuous and grouped, using Cox regression models, with adjustment for age. RESULTS:Changing the exposure estimates changed the estimated relative risks compared with earlier results, but the new analyses showed no significant trends with continuous measures of exposure to either BSM or B[a]P, nor with time spent on ovens tops. Analyses with grouped exposures showed mixed results. Across all BSC plants, the relative risk coefficient for working 5 or more years on ovens tops, where the exposures were highest, was 1.81, which was statistically significant. However, results for those with 0-5 years on ovens tops did not suggest a trend; the evidence for an underlying relationship was thus suggestive but not strong. CONCLUSIONS:The new results are in line with previous findings; they show some signs consistent with an effect of coke ovens work on lung cancer risk, especially on ovens tops, but the preponderant absence of significant results, and the inconsistencies between results for NSF and BSC, highlight how little evidence there is in these data of any effect.
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Project description:BackgroundIn recent times, there has been an increase in the incidence of type 2 diabetes mellitus (T2DM) particularly in children. Adipocyte dysfunction provide a critical link between obesity and insulin resistance resulting in diabetes outcome. Further, environmental chemical exposure during early years of life might be a significant contributing factor to the increase in the incidence of T2DM. This study tests the idea that exposure to environmental contaminants (2-aminoanthracene [2AA]) in utero will show effects in the adipose tissue (AT) that signify T2DM vulnerability. 2AA is a polycyclic aromatic hydrocarbon found in a variety of products.MethodsTo accomplish the study objective, pregnant dams were fed various amounts of 2AA adulterated diets from gestation through postnatal period. The neonates and older offspring were analyzed for diabetic-like genes in the ATs and analysis of serum glucose. Furthermore, weight monitoring, histopathology and immunohistochemical (IHC) staining for CD68 in AT, adipocyte size determination and adiponectin amounts in serum were undertaken.ResultsUp-regulation of adiponectin and interleukin-6 genes were noted in the pups and older rats. Combination of intrauterine 2AA toxicity with moderate high fat diet exhibited gene expression patterns similar to those of the neonates. Elevated serum glucose levels were noted in treated groups. IHC of the AT indicated no significant malformations; however, CD68+ cells were greater in the animals treated to 2AA. Similarly, mean sizes of the adipocytes were larger in treated and combined 2AA and moderate high fat animals. Adiponectin was reduced in 2AA groups.ConclusionFrom the preceding, it appears intrauterine 2AA disturbance, when combined with excess fat accumulation will lead to greater risk for the diabetic condition.
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Project description:Polycyclic aromatic hydrocarbons-Polluted Soil Metagenome
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