Introduction: Cigarette smoking has been associated with adverse health outcomes for mothers and children and is a major contributor to heart disease. Although cigarette smoking is known to affect the epigenome, few studies have been done in African American populations. In this study, we investigated the association between cigarette smoking and DNA methylation (DNAm) among African Americans from the Intergenerational Impact of Genetic and Psychological Factors on Blood Pressure Study (InterGEN), and the Genetic Epidemiology Network of Arteriopathy (GENOA). Methods: The InterGEN study aims to examine the effects of genetic and psychological factors on blood pressure among African American women and their children. Current cigarette smoking was assessed at baseline. DNAm of saliva was assessed using the 850K EPIC Illumina BeadChip for Epigenome-Wide Association analyses. A replication study was conducted among 1100 participants in the GENOA study using the same BeadChip. Results: After controlling for age, body mass index, population structure and cell composition, 26 epigenome-wide significant sites (FDR q < 0.05) were identified, including the AHRR and PHF14 genes associated with atherosclerosis and lung disease, respectively. Six novel CpG sites were discovered in the InterGEN sample and replicated in the GENOA sample. Genes mapped include RARA, FSIP1, ALPP, PIK3R5, KIAA0087, and MGAT3, which were largely associated with cancer development. Conclusion: We observed significant epigenetic associations between smoking and disease-associated genes (e.g., cardiovascular disease, lung cancer). Six novel CpG sites were identified and replicated across saliva and blood samples.

Gene expression may be an important biological mediator in associations between social factors and health. However, previous studies were limited by small sample sizes and use of differing cell types with heterogeneous expression patterns. We use a large population-based cohort with gene expression measured solely in monocytes to investigate associations between seven social factors and expression of genes previously found to be sensitive to social factors. We employ three methodological approaches: 1) omnibus test for the entire gene set (Global ANCOVA), 2) assessment of each association individually (linear regression), and 3) machine learning method that performs variable selection with correlated predictors (elastic net). In global analyses, significant associations with the a priori defined socially sensitive gene set were detected for major or lifetime discrimination and chronic burden (p = 0.019 and p = 0.047, respectively). Marginally significant associations were detected for loneliness and adult socioeconomic status (p = 0.066, p = 0.093, respectively). No associations were significant in linear regression analyses after accounting for multiple testing. However, a small percentage of gene expressions (up to 11%) were associated with at least one social factor using elastic net. The Global ANCOVA and elastic net findings suggest that a small percentage of genes may be “socially sensitive,” (i.e. demonstrate differential expression by social factor), yet single gene approaches such as linear regression may be ill powered to capture this relationship. Future research should further investigate the biological mechanisms through which social factors act to influence gene expression and how systemic changes in gene expression affect overall health.

Background: Exposure to psychosocial stress and employment of high effort coping strategies have been identified as risk factors that may partially explain the high prevalence of hypertension among African Americans. One biological mechanism through which stress and coping may affect risk of hypertension is via epigenetic modifications (e.g., DNA methylation) in blood pressure-related genes; however, this area remains understudied in African Americans. Methods: We used data from the ongoing Intergenerational Blood Pressure Study, a longitudinal study designed to investigate factors that contribute to hypertension risk in African American women (n = 120) and their young children, to investigate the association between stress overload, problem-solving coping, avoidance coping, and social support coping with DNA methylation in 25 candidate genes related to blood pressure. Multivariable linear regression and multilevel modeling were used to conduct methylation site-level and gene-level analyses, respectively. Results: In site-level analyses, stress overload, problem-solving coping, social support coping, and avoidance coping were associated with 47, 63, 66, and 61 sites, respectively, at p < 0.05. However, no associations were statistically significant after multiple testing correction. There were also no significant associations in gene-level analyses. Conclusions: As human social epigenomics is an emerging, evolving area of research, there is much to be learned from studies with statistically significant findings as well as studies with null findings. Factors such as characteristics of the social stressor, source of DNA, and synchronization of exposure and outcome are likely important considerations as we move the field forward.

Background: Unfair treatment such as discrimination and racism contribute to depression and perceived stress in African Americans. Although studies have examined how responding to such treatment is associated with ameliorating depressive symptoms and levels of perceived stress, most do not focus on African Americans. The purpose of this study is to assess how talking to others in response to unfair treatment is associated with self-reported depressive symptoms and perceived stress levels in African Americans. Methods: A sample from the 2010–2013 Minority Health Genomics and Translational Research Bio-Repository Database was used and consisted of 376 African American adults aged 30–55 years old residing in the southern region of the United States. Linear regression models were used to assess the association between talking to others following unfair treatment, compared to keeping it to oneself, on self-reported depressive symptoms and perceived stress. The predictor variable was based on the question “If you have been treated unfairly, do you usually talk to people about it or keep it to yourself?”. Results: Talking to someone after being treated unfairly was inversely associated with perceived stress ( $$\beta$$β : -3.62, SE: 1.14, p ≤ 0.05) and depressive symptoms ( $$\beta$$β : -3.62, SE: 1.14, p ≤ 0.05). Conclusions: African Americans who talked to others in response to unfair treatment had lower depressive symptoms and perceived stress than those who kept it to themselves. More outreach to African Americans regarding the importance of talk in response to exposure to unfair treatment is needed as a potential coping mechanism.