The longitudinal effect of arsenic on DNA methylation and blood pressure in pediatric populations

The National Institute of Environmental Health Sciences awarded Trustees of Boston University $100,228 on November 13, 2026, under the Environmental Health program (CFDA 93.113) to investigate the longitudinal effect of arsenic on DNA methylation and blood pressure in pediatric populations.

The research leverages secondary data from the Bangladesh Environmental Research in Children's Health (BIRCH) cohort, which enrolled participants aged 5–7 years and followed them into adolescence. The study will examine arsenic exposure assessed through toenail clippings and spot urine samples, blood pressure measurements, and whole blood epigenome-wide DNA methylation data collected at two time points (ages 5–7 years and 12–14 years). The investigator will employ linear regression models to assess associations between early childhood arsenic exposure and longitudinal blood pressure changes between early childhood and adolescence, and to evaluate the relationship between arsenic exposure and changes in DNA methylation during the same period. Dr. Maria Argos serves as primary sponsor, with mentorship committee support in arsenic and cardiovascular epidemiology, biostatistical methods, and epigenetic analyses.

The award is classified as a Project Grant, an assistance type supporting research by a named principal investigator. Performance of work occurs in Roxbury, Massachusetts. The period of performance runs from November 13, 2026, through August 31, 2028.

Abstract

Cardiovascular disease (CVD) is the leading cause of death in the united states and many communities globally. Arsenic is a toxic metalloid found in drinking water worldwide, and exposure to this element has been associated with an increased risk of CVD, potentially through increased blood pressure. One possible mechanism underlying the association between arsenic exposure and blood pressure is the alteration of DNA methylation, which affects gene transcription. However, few studies have interrogated this mechanism, particularly in early life. To enhance our understanding of the role of arsenic exposure on cardiovascular endpoints, the proposed study leverages secondary data from the bangladesh environmental research in children's health (birch) cohort, which enrolled participants aged 5-7 years and has followed them into adolescence. The proposed research will leverage existing data on arsenic exposure assessed in toenail clippings and spot urine samples, blood pressure measurements, and whole blood epigenome-wide DNA methylation data available from two time points (ages 5-7 years and 12-14 years). Under the supervision of DR. Maria argos (primary sponsor) and my mentorship committee, with expertise in arsenic and cardiovascular epidemiology, biostatistical methods, and epigenetic analyses, i propose to explore the association between arsenic exposure in early childhood and longitudinal blood pressure changes between early childhood and adolescence. I will also evaluate the relationship between arsenic exposure and changes in DNA methylation between early childhood and adolescence. These represent critical life stages for epigenetic programming due to them being periods of rapid growth and development. Linear regression models will be employed to assess the associations between arsenic exposure and longitudinal change in blood pressure (aim 1) and longitudinal change of DNA methylation at individual CPG loci in an epigenome-wide analysis (aim 2). In conducting these analyses, i will expand existing knowledge and develop new skills and experience in biostatistical methods and the analysis of epigenetic data. I will enhance my training through external workshops, additional coursework, and direct mentorship from my sponsor and mentorship team. The proposed study addresses several research gaps, including contributing knowledge on early-life impacts of arsenic exposure and underlying mechanisms of toxicity. The results of the proposed analyses may help to inform future research on later-life cardiovascular health and support the inclusion of environmental health as a factor in reducing the public health burden of CVD. The proposed study is also well-aligned with the niehs strategic goals, including strengthening mechanistic biology and toxicology research as we seek to contribute novel data from a human study evaluating DNA methylation as a mechanism of arsenic toxicity.