Neighborhood Environment and DNA Methylation: Implications for Cardiovascular Disease Risk.

Exposure to chronic stress such as living in disadvantaged neighborhoods has been related to cardiovascular disease (CVD). Chronic stress may increase the risk for CVD by increasing levels of systemic inflammation (e.g., higher levels of pro-inflammatory cytokines). Differential DNA methylation of inflammation-related candidate genes is also related to higher risk for CVD. Thus, the purpose of this review was to examine the association of neighborhood disadvantage with DNA methylation. A search of literature was conducted using Scopus, CINAHL, PubMed, Medline, and Embase databases. The keywords neighborhood, neighborhood disorder, neighborhood crime, neighborhood violence, neighborhood safety, built environment, and housing vacancy were combined with the keywords DNA methylation and epigenetics. Five studies were included in this review (n = 3 adult blood samples and n = 2 fetal blood samples). Four of the five studies reported an association of neighborhood socioeconomic status, social environment, and crime with either global or gene-specific DNA methylation. Only two studies examined the association of neighborhood disadvantage with inflammation-related candidate genes. One of these studies found a significant association of neighborhood socioeconomic disadvantage and social environment with DNA methylation in inflammation-related candidate genes. Thus, data are limited on the association between neighborhood disadvantage and DNA methylation of inflammation-related candidate genes, as well as genes in other potential mechanistic pathways including psychosocial stress, toxin response, and adiposity. Future studies should examine these associations and the potential epigenetic mechanisms by which neighborhood disadvantage increases the risk for CVD.

Alteration of fertility endpoints in adult male F-344 rats by subchronic exposure to inhaled benzo(a)pyrene.

The objective of this study was to evaluate the reproductive risk associated with exposure of adult male Fisher-344 rats to inhaled benzo(a)pyrene (BaP). Rats were assigned randomly to a treatment or control group. Treatment consisted of sub-chronic exposure of rats via inhalation to 75microgBaP/m(3), 4h daily for 60 days, while control animals were unexposed (UNC). Blood samples were collected immediately after the cessation of exposures (time 0) and subsequently at 24, 48, and 72h, to assess the effect of bioavailable BaP on plasma testosterone and luteinizing hormone (LH) concentrations. Rats were sacrificed after the last blood collection. Testes were harvested, weighed and prepared for histology and morphometric analysis, and cauda epididymides were isolated for the determination of progressive motility and density of stored spermatozoa. BaP exposure reduced testis weight compared with UNC (mean+/-SE; 2.01+/-0.11 versus 3.04+/-0.16g; P<0.025), and caused significant reductions in the components of the steroidogenic and spermatogenic compartments of the testis. Progressive motility and mean density of stored spermatozoa were reduced (P<0.05). Plasma testosterone concentrations were decreased by two-thirds in BaP-exposed rats throughout the time periods studied compared with those of their UNC counterparts (P<0.05), concomitant with increased concentrations of LH in BaP-exposed rats (P<0.05). These data suggest that sub-chronic exposure to inhaled BaP contribute to reduced testicular and epididymal function in exposed rats.