Epigenetics mediate environment :  gene effects on occupational sensitization.
OBJECTIVE
Epigenetics is the study of stable modifications of fixed genomes that direct which genes are expressed and which are silenced. Epigenetic changes are modulated by environmental exposures, making epigenetics the interface between genes and environment. This has particular relevance in understanding the effect of occupational exposures on the expression of allergic disease. The goal of this review is to describe how epigenetic changes affect transcription potential, and to examine more closely the effect of specific environmental and occupational exposures on epigenetic variations that alter allergy gene transcripts and the inflammatory milieu.


RESULTS
Gene transcription is activated when specific CpG sites are demethylated and histones are acetylated, and, conversely, silenced when sites are methylated and histones deacetylated. The development of Th1 and Th2 phenotypes, and expression of Treg cells, are now known to be modulated by epigenetic mechanisms. Workplace exposures such as tobacco smoke, particulates, diesel exhaust, polyaromatic hydrocarbons, ozone, and endotoxin, among others, suppress Treg development, and enhance expression of inflammatory cytokines and allergic phenotypes by epigenetic means.


CONCLUSIONS
Epigenetic manipulation to open and close transcription sites provides flexibility of gene expression in response to changing environmental cues. It may also be the window whereby allergic disease in the workplace can be reduced by targeted environmental interventions.
Division of Environmental and Occupational Health Sciences, Department of Medicine, National Jewish Health, Denver and Department of Environmental and Occupational Health, Colorado School of Public Health, Aurora, Colorado, USA. pachecok@njhealth.org
Karin A
KA
Pacheco
D000818:Animals; D001249:Asthma / Q000235:genetics / Q000276:immunology; D044127:Epigenesis, Genetic / Q000276:immunology*; D005260:Female; D051858:Forkhead Transcription Factors / Q000235:genetics; D006801:Humans; D006967:Hypersensitivity / Q000235:genetics / Q000276:immunology*; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D051379:Mice; D009784:Occupational Diseases / Q000235:genetics* / Q000276:immunology*; D016273:Occupational Exposure; D013601:T-Lymphocytes / Q000276:immunology; D014028:Tobacco Smoke Pollution / Q000009:adverse effects
C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; D014028:Tobacco Smoke Pollution