Genomic Signatures for Pesticide Exposure in Latino Farmworkers
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE30335 | GEO | 2019/12/31
REPOSITORIES: GEO
Similar Datasets
Project description:Genomic Signatures for Pesticide Exposure in Latino Farmworkers
| PRJNA143623 | ENA
Project description:Prenatal environmental conditions may influence disease risk in later life. We previously found a gene-environment interaction between the paraoxonase 1 (PON1) Q192R genotype and prenatal pesticide exposure leading to a cardio-metabolic risk profile at school age. However, the molecular mechanisms involved have not yet been resolved. It has been hypothesized that epigenetics might be involved. The aim of the present study was to investigate whether DNA methylation patterns in blood cells were related to prenatal pesticide exposure level, PON1 Q192R genotype, and associated metabolic effects observed in the children. Whole blood DNA methylation patterns in 48 children (6-11 years of age), whose mothers were occupationally unexposed or exposed to pesticides early in pregnancy, were determined by Illumina 450K methylation arrays. A specific methylation profile was observed in prenatally pesticide exposed children carrying the PON1 192R allele. Differentially methylated genes were enriched in several neuroendocrine signaling pathways including dopamine-DARPP32 feedback (appetite, reward pathways), corticotrophin releasing hormone signalling, nNOS, neuregulin signalling, mTOR signalling and type II diabetes mellitus signalling suggesting a possible link with the metabolic effects observed in these children. Furthermore, we were able to identify possible candidate genes which mediate the effect between pesticide exposure, leptin levels, delta BMI Z-score, and body fat percentage. In conclusion, DNA methylation may be an underlying mechanism explaining cardio-metabolic health outcomes in children that are prenatally exposed to pesticides and carrier of the PON1 192R allele.
2017-05-01 | GSE90117 | GEO
Project description:Consumers are exposed through food intake to a cocktail of pesticides at low doses. Epidemiological evidence suggested a link between pesticide exposure and the development of the metabolic syndrome. We used a mouse model to mimic consumer exposure and assessed the metabolic consequences of a chronic dietary exposure to a cocktail of 6 commonly used pesticides (boscalid, captan, chlorpyrifos, thiofanate, thiacloprid and ziram) at non-toxic doses (acceptable daily intake ADI). One year of exposure induced body weight and adiposity gain, hepatic steatosis and glucose intolerance in males. Females did not display significant changes in body weight but displayed fasted hyperglycemia and perturbations of gut-microbiota related urinary metabolites. Exposure of mice invalidated for the constitutive androstane receptor (CAR) demonstrated that this nuclear receptor was involved in the observed sexual dimorphic response to pesticide exposure. These results demonstrate for the first time that chronic dietary exposure to a pesticide cocktail at the ADI levels induces metabolic perturbations favouring obesity and diabetic state and raise the questions of the relevance of the ADI levels of individual pesticides when present in mixture.
2018-07-05 | GSE101405 | GEO
Project description:Environmental compounds including fungicides, plastics, pesticides, dioxin and hydrocarbons can promote the epigenetic transgenerational inheritance of adult-onset disease in future generation progeny following ancestral exposure during the critical period of fetal gonadal sex determination. This study examined the actions of the pesticide methoxychlor to promote the epigenetic transgenerational inheritance of adult-onset disease and associated differential DNA methylation regions (i.e. epimutations) in sperm. Gestating F0 generation female rats were transiently exposed to methoxychlor during fetal gonadal development (gestation days 8 to 14) and then adult-onset disease was evaluated in adult F1 and F3 (great-grand offspring) generation progeny for control (vehicle exposed) and methoxychlor lineage offspring. There were increases in the incidence of kidney disease, ovary disease, and obesity in the methoxychlor lineage animals. In females and males the incidence of disease increased in both the F1 and the F3 generations and the incidence of multiple disease increased in the F3 generation. There was increased disease incidence in F4 generation reverse outcross (female) offspring indicating disease transmission was primarily transmitted through the female germline. Analysis of the F3 generation sperm epigenome of the methoxychlor lineage males identified differentially DNA methylated regions (DMR) termed epimutations in a genome-wide gene promoters analysis. These epimutations were found to be methoxychlor exposure specific in comparison with other exposure specific sperm epimutation signatures. Observations indicate that the pesticide methoxychlor has the potential to promote the epigenetic transgenerational inheritance of disease and the sperm epimutations appear to provide exposure specific epigenetic biomarkers for transgenerational disease and ancestral environmental exposures. Methylated sperm DNA was isolated from rats ancestrally exposed to methoxychlor. Three independent samples from each treatment group were obtained. Differential DNA methylation between treatment groups was determined using Nimblegen microarrays. Treated samples were paired with control samples and hybridized together on arrays, resulting in three arrays for the treatment.
2014-05-30 | E-GEOD-58091 | biostudies-arrayexpress
Project description:Environmental compounds are known to promote epigenetic transgenerational inheritance of disease. The current study was designed to determine if a M-bM-^@M-^\pesticide mixtureM-bM-^@M-^] (pesticide permethrin and insect repellent N,N-Diethyl-meta-toluamide, DEET) promotes epigenetic transgenerational inheritance of disease and associated DNA methylation epimutations in sperm. Gestating F0 generation female rats were exposed during fetal gonadal sex determination and the incidence of disease evaluated in F1 and F3 generations. There were significant increases in the incidence of total diseases in animals from pesticide lineage F1 and F3 generation animals. Pubertal abnormalities, testis disease, and ovarian disease (primordial follicle loss and polycystic ovarian disease) were increased in F3 generation animals. Analysis of the pesticide lineage F3 generation sperm epigenome identified 363 differential DNA methylation regions (DMR) termed epimutations. Observations demonstrate that a pesticide mixture (permethrin and DEET) can promote epigenetic transgenerational inheritance of adult onset disease and potential sperm epigenetic biomarkers for ancestral environmental exposures. Methylated sperm DNA was isolated from rats ancestrally exposed to pesticides (Pip). Three independent samples from the treatment group were obtained. Differential DNA methylation between treatment groups was determined using Nimblegen microarrays. Treated samples were paired with control samples and hybridized together on arrays (Pip1/Cip1, Pip2/Cip2, and Pip3/Cip3), resulting in three arrays for the treatment.
2014-07-22 | E-GEOD-59554 | biostudies-arrayexpress
Project description:The effect of benzene exposure on peripheral blood mononuclear cell (PBMC) gene expression was examined in a population of shoe-factory workers with well-characterized occupational exposures to benzene. We compared data from two microarray platforms (Illumina and Affymetrix). Keywords: occupational exposure
2009-05-11 | GSE9569 | GEO
Project description:Hispanic/Latino populations possess a complex genetic structure that reflects recent admixture among and potentially ancient substructure within Native American, European, and West African source populations. Here, we quantify genome-wide patterns of SNP and haplotype variation among 100 individuals with ancestry from Ecuador, Colombia, Puerto Rico, and the Dominican Republic genotyped using Illumina technology. To investigate variations of continental ancestry between different Hispanic/Latino groups (using self-reported country-specific identification of individual, both parents, and all four grandparents) and within them from healthy controls represented in the New York Health Project Biorepository. Genotyped on the Illumina 610-Quad, which is identical to HumanHap550-v3 SNPs plus an additional ~60,000 SNPs for CNV, no CNV data is provided or was analyzed.
2010-04-07 | E-GEOD-21248 | biostudies-arrayexpress
Project description:Epigenetics presents a dynamic approach to assess complex individual variation in obesity susceptibility. However, few studies have examined epigenetic patterns in preschool-age children, despite the relevance of this developmental stage to trajectories of weight gain, because of difficulties obtaining blood tissue samples. This proof of principle study examined DNA methylation in 92 saliva samples, comparing Latino preschool children of normal weight mothers (Body Mass Index [BMI] <27 kg/m2 and WC <90 cm) to children of obese mothers (BMI >30 kg/m2 and WC >100 cm). We hypothesized that salivary DNA methylation patterns in Latino preschool age children born of normal weight vs obese weight mothers would be: 1) associated with maternal BMI phenotype in continuous linear regression analysis; 2) saliva could demonstrate epigenetic variation across individuals; and 3) preschool child saliva would be differentially methylated when comparing those children with obese versus normal weight mothers. One hundred and nineteen CpG sites were significantly (p-value <1.56 X 10-5, p-value adjusted <.05) associated with maternal BMI in linear regression models controlling for child’s age, gender, and BMI. Of these 119 CpG sites, 41 were found within the transcription start site, 5’ UTR, 3’ UTR, or another regulatory region outside of the gene body. Saliva, a practical human tissue to obtain in naturalistic settings and in pediatric populations, was confirmed to be a viable medium for genome-wide epigenetic testing with maternal weight. Although not identical to results yielded from other human tissue types (i.e., cord blood samples), saliva findings indicate potential epigenetic differences in Latino preschool children at risk for pediatric obesity.
2016-02-25 | GSE72556 | GEO
Project description:Environmental compounds are known to promote epigenetic transgenerational inheritance of disease. The current study was designed to determine if a “pesticide mixture” (pesticide permethrin and insect repellent N,N-Diethyl-meta-toluamide, DEET) promotes epigenetic transgenerational inheritance of disease and associated DNA methylation epimutations in sperm. Gestating F0 generation female rats were exposed during fetal gonadal sex determination and the incidence of disease evaluated in F1 and F3 generations. There were significant increases in the incidence of total diseases in animals from pesticide lineage F1 and F3 generation animals. Pubertal abnormalities, testis disease, and ovarian disease (primordial follicle loss and polycystic ovarian disease) were increased in F3 generation animals. Analysis of the pesticide lineage F3 generation sperm epigenome identified 363 differential DNA methylation regions (DMR) termed epimutations. Observations demonstrate that a pesticide mixture (permethrin and DEET) can promote epigenetic transgenerational inheritance of adult onset disease and potential sperm epigenetic biomarkers for ancestral environmental exposures.
2014-07-22 | GSE59554 | GEO
Project description:Environmental compounds including fungicides, plastics, pesticides, dioxin and hydrocarbons can promote the epigenetic transgenerational inheritance of adult-onset disease in future generation progeny following ancestral exposure during the critical period of fetal gonadal sex determination. This study examined the actions of the pesticide methoxychlor to promote the epigenetic transgenerational inheritance of adult-onset disease and associated differential DNA methylation regions (i.e. epimutations) in sperm. Gestating F0 generation female rats were transiently exposed to methoxychlor during fetal gonadal development (gestation days 8 to 14) and then adult-onset disease was evaluated in adult F1 and F3 (great-grand offspring) generation progeny for control (vehicle exposed) and methoxychlor lineage offspring. There were increases in the incidence of kidney disease, ovary disease, and obesity in the methoxychlor lineage animals. In females and males the incidence of disease increased in both the F1 and the F3 generations and the incidence of multiple disease increased in the F3 generation. There was increased disease incidence in F4 generation reverse outcross (female) offspring indicating disease transmission was primarily transmitted through the female germline. Analysis of the F3 generation sperm epigenome of the methoxychlor lineage males identified differentially DNA methylated regions (DMR) termed epimutations in a genome-wide gene promoters analysis. These epimutations were found to be methoxychlor exposure specific in comparison with other exposure specific sperm epimutation signatures. Observations indicate that the pesticide methoxychlor has the potential to promote the epigenetic transgenerational inheritance of disease and the sperm epimutations appear to provide exposure specific epigenetic biomarkers for transgenerational disease and ancestral environmental exposures.
2014-05-30 | GSE58091 | GEO