About

Dana C Dolinoy, PhD, MSc, is the NSF International Chair of Environmental Health Sciences and a Professor at the University of Michigan School of Public Health, specializing in environmental health sciences and nutritional sciences. Her research has a broad focus on genomics and toxicology, with specific interest in epigenetic research, including environmental epigenomics and the developmental origins of health and disease. She integrates the work of toxicologists, epidemiologists, and bioinformaticians to characterize the effects of environmental factors on the epigenome and develops precision environmental epigenomics tools for toxicological research and therapeutic applications, particularly related to metabolic syndrome, neurodevelopmental disorders, and cancer. Dr. Dolinoy serves as the Director of the University of Michigan NIEHS P30 Core Center, 'Lifestage Environmental Exposures and Diseases' (M-LEEaD), and as Faculty Director of the Michigan Medical Center's Epigenomics Core. Her commitment to environmental and nutritional epigenomics research emphasizes the impact of environmental insults during sensitive life stages that influence adult disease risk. Her research projects include advancing understanding of perinatal exposures on the epigenome and health risks, utilizing human and mouse models, and longitudinal birth cohort samples. She is also a member of the NIEHS TaRGET II Consortia and MPI of a project investigating the effects of preconception weight loss on birth outcomes. Her work aims to promote translational research to better understand how environmental exposures influence disease risk through epigenetic mechanisms.

Research topics

• Biology
• Genetics
• Medicine
• Physiology
• Internal medicine
• Endocrinology
• Chemistry
• Immunology
• Computer Science
• Ecology
• Cell biology
• Environmental health
• Biochemistry
• Risk analysis (engineering)
• Data science
• Bioinformatics
• Obstetrics
• Computational biology
• Environmental chemistry
• Evolutionary biology

Selected publications

• Circadian gene expression in adolescents: Associations with concurrent circadian disruption and subsequent changes in cardiometabolic risk measures

  Sleep Medicine · 2026-02-05

  articleOpen access

  OBJECTIVES: Circadian disruption has been linked to adverse metabolic health. Adolescents are particularly susceptible to circadian disruptors, such as delayed sleep onset and social jetlag, which may have sex-specific effects. However, evidence linking these disruptors with circadian gene expression and subsequent cardiometabolic risk remains limited. METHODS: Our study included 203 adolescents (53% females, median age 13.6 years) from the ELEMENT cohort in Mexico City. Sleep was assessed via 7-day wrist actigraphy. A fasting venipuncture blood sample was collected between 8:00 a.m. and 12:00 p.m. RNA was isolated from blood leukocytes and sequenced to determine the relative expression of genes. We conducted differential gene expression analysis for 12 core clock genes in relation to sleep midpoint and social jetlag, adjusting for sleep duration and other potential confounders. We further evaluated how circadian gene expression associated with changes in adiposity, glucose metabolism, blood pressure, and lipid profiles over two years using linear regression. RESULTS: Later sleep midpoint (per 1-h increase) was associated with reduced mid-morning expression of four circadian genes: RORA (log2 fold change [LFC]: -0.190; P value: 0.001), RORC (LFC: -0.147; P value: 0.039), CLOCK (LFC: -0.141; P value: 0.019), and NR1D2 (LFC: -0.093; P value: 0.029). Additionally, expression levels of several clock genes (CRY1, NR1D2, BMAL1, and PER1-3) were associated with changes in metabolic biomarkers over two years in sex-specific patterns. For instance, NR1D2 showed a negative association with fasting glucose among females (β: -0.0012; P value: 0.020), while demonstrating positive associations with LDL cholesterol (β: 0.0023; P value: 0.002) and total cholesterol (β: 0.0016; P value: 0.028) among males. CONCLUSIONS: Expression of core clock genes was linked to circadian disruption and changes in cardiometabolic risk factors in a sex-specific manner among adolescents. Our findings provide novel insights into potential biological mechanisms underlying associations of circadian disruption with cardiometabolic health.

  PublisherDOI

• Epigenetic age acceleration in adolescence: cross-sectional associations with dietary intake and prospective associations with cardiometabolic risk indicators in a Mexico City cohort

  Nutrition Metabolism and Cardiovascular Diseases · 2026-01-23

  articleOpen access

  BACKGROUND AND AIMS: To examine the cross-sectional relationship between dietary intake and epigenetic age acceleration, as well as the prospective relationship between epigenetic age acceleration and cardiometabolic parameters measured two years later. METHODS AND RESULTS: ), fasting insulin (β = 0.86 μIU/mL), and insulin resistance (β = 0.21). Skin-Blood acceleration was associated with decreased HDL in males, and PedBE acceleration was associated with triglycerides in both sexes, though in opposing directions. CONCLUSION: Adolescent diet was not strongly associated with baseline epigenetic age acceleration. However, epigenetic age acceleration was associated prospectively with fat distribution and insulin resistance.

  PublisherDOI

• Perinatal Lead (Pb) Exposure Increases Mouse Embryonic Weight and Alters Neuronal Gene Expression

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-09-20

  preprintOpen access

  ABSTRACT Acute and chronic exposure to lead (Pb) during pregnancy is linked to adverse health outcomes, including delayed neurodevelopment in offspring. However, the pathways by which Pb exposure influences long-term health remain poorly understood. To address this, we measured the effects of perinatal Pb exposure on gene expression including imprinted genes, X-linked genes, and sexually dimorphic genes. Female mice were given control or Pb acetate dosed (32 ppm) drinking water two weeks prior to timed mating until embryonic day (E)10–12, upon which whole embryos were collected, weighed, and sexed at E13–15. From a subset of embryo heads ( n ≥9 per sex per group), we extracted and sequenced RNA. We used linear regression to assess Pb impacts on embryonic weight and gene expression across all mice and stratified by sex. Among the differentially expressed genes, we identified significantly enriched pathways. Pb-exposed embryos weighed more than controls ( p =0.007), across both sexes. Collectively, we identified 2,920 differentially expressed genes (FDR<0.05), including 31 imprinted genes and 120 X-linked genes upon Pb exposure. Pb exposure altered expression in gene pathways related to neuronal structure and function as well as sexually dimorphic genes (44 for females; 76 for males). These findings highlight perinatal Pb-linked alterations that may drive later-life health outcomes.

  PublisherDOI

• Interaction of mercury exposure and DNA methylation with sustained attention in children in a novel analysis of epigenetic susceptibility

  Current Zoology · 2025-01-01 · 1 citations

  articleOpen access

  Abstract The etiology of attention-deficit/hyperactivity disorder (ADHD) remains poorly understood, despite it being one of the most common neurodevelopmental disorders worldwide. Past research suggests methylmercury exposure and DNA methylation (DNAm) levels are each associated with ADHD in children, yet whether they interact to affect ADHD is unknown. Leveraging data from a longitudinal cohort of children in Mexico, this novel epigenetic–environment interaction study identified significant interactions between childhood mercury exposure (measured at 6–12 years of age) and adolescent blood leukocyte DNAm in their association with sustained attention [quantified via the Conners continuous performance test, 3rd edition (CPT3)] measured on average 5.6 ± 0.99 years later. Using adjusted linear regression, we assessed associations between hair and urine mercury concentrations and CPT3 scores reflecting inattention, impulsivity, vigilance, and sustained attention (N = 399). We then tested the interaction between mercury and DNAm at loci previously associated with the CPT3 outcomes (N = 374). Significant associations between mercury and CPT3 differed in magnitude and direction depending on the mercury biomarker and CPT3 variable. These associations often differed by gender. For example, urine mercury was positively associated with vigilance scores in males [β = 1.31(SE = 0.65), P = .045] but not in females [β = −0.20 (SE = 0.81), P = .80). In all children, three significant mercury–DNAm interactions were identified for either inattention or vigilance outcomes. Among females, 155 significant interaction terms were identified for the inattention models. In males, three significant interactions were identified for the impulsivity model. Overall, results suggest in some cases DNAm can influence the association between mercury exposure and ADHD-like symptoms.

  PublisherOA PDFDOI

• Establishing a prospective cohort to examine the impact of medication for opioid use disorder in pregnancy

  American Journal of Obstetrics & Gynecology MFM · 2025-12-11

  articleOpen access

  OBJECTIVE: To describe the design and initial findings of a prospective cohort study examining the impact of opioid treatment during pregnancy on maternal and infant outcomes. STUDY DESIGN: A multi-site prospective cohort study of 127 pregnancies (including 3 sets of twins), comprising 86 individuals with medication for opioid use disorder exposure and 41 matched controls. Data collection included structured clinical interviews, medical record abstraction, and biospecimen sampling from maternal and neonatal sources. RESULTS: The cohort is predominantly non-Hispanic White and multiparous. Among opioid-exposed participants, mood disorders, nicotine use, and hepatitis C were common. Over 80% of opioid-exposed infants developed neonatal withdrawal, with nearly half experiencing severe symptoms. CONCLUSIONS: High rates of co-occurring conditions were observed among pregnant individuals receiving medication for opioid use disorder. Most opioid-exposed neonates developed neonatal withdrawal. This cohort provides a rich clinical resource for investigating the effects of prenatal opioid exposure on maternal and infant health.

  PublisherDOI

• Environmentally Relevant Lead Exposure Alters Cell Morphology and Expression of Neural Hallmarks During SH-SY5Y Neuronal Differentiation

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-02-21 · 1 citations

  preprintOpen access

  Lead (Pb) continues to be a public health burden, in the US and around the world, and yet the effects of historical and current exposure levels on neurogenesis are not fully understood. Here we examine the effects of a range of environmentally relevant Pb concentrations (0.16μM, 1.26μM, and 10μM Pb) relative to control on neural differentiation in the SH-SY5Y cell model. Pb exposure began on Day 5 and continued throughout differentiation at Day 18. We assessed morphological measures related to neurogenesis at several time points during this process, including the expression of proteins key in neural differentiation (β-tubulin III and GAP43), cell number and size, as well as the development of neurites. The bulk of detectable changes occurred with 10μM Pb exposure, most notably that of β-tubulin III and GAP43 expression. Effects with the 0.16μM and 1.26μM Pb exposure conditions increased as differentiation progressed, with significant reductions in cell and nuclear size as well as the number and length of neural projections by Day 18. Best benchmark concentration (BMC) analysis revealed many of these metrics to be susceptible to levels of Pb at or below historically relevant levels. This work highlights the disruption of neurite formation and protein expression as potential new mechanisms by which environmentally relevant Pb exposure impacts neurogenesis and morphology and perturb cognitive health throughout the life course.

  PublisherOA PDFDOI

• 0299 Sleep Timing and Social Jet Lag Are Associated with Circadian Gene Expression: A Cross-sectional Study in Mexico City Adolescents

  SLEEP · 2025-05-01

  articleOpen access

  Abstract Introduction Circadian disruption has been linked to adverse metabolic health, potentially mediated through altered expression of circadian genes. Adolescents are particularly susceptible to circadian disruptors, such as delayed sleep onset and social jetlag. This study of adolescents during peri-puberty investigated associations between circadian disruption and circadian gene expression, independent of sleep duration, and potential sex differences in the associations. Methods The analytic sample included 203 adolescents (96 boys, 107 girls) from the ELEMENT longitudinal cohort in Mexico City. Sleep was assessed via 7-day wrist actigraphy, and a fasted blood sample was collected during a study visit between 8:00 AM and 12:00 PM. Sleep midpoint was calculated as the midpoint between bed and wake times, and social jetlag as the difference in sleep midpoint on weekends versus weekdays. RNA was isolated from blood leukocytes, and RNA sequencing was performed to determine the relative expression of genes. We conducted differential gene expression analysis, in relation to weekday sleep midpoint and social jetlag, for 12 core clock genes using the DESeq2 package (R), adjusting for sleep duration and other potential confounders. A Bonferroni-corrected statistical significance (0.05/12 genes) was considered. Results Participants had a median age of 14 years (interquartile range: 12–16). Later sleep midpoint (per 1-hour increase) was associated with reduced mid-morning expression of four circadian genes: RORA (log2 fold change [LFC]: -0.190; P value: 0.001), RORC (LFC: -0.147; P value: 0.039), CLOCK (LFC: -0.141; P value: 0.019), and NR1D2 (LFC: -0.093; P value: 0.029). In sex-stratified analysis, later sleep midpoint was significantly associated with lower RORA expression in girls only (LFC: -0.255; P value: 0.002). Greater social jetlag was linked to increased expression of PER1 (LFC: 0.275; P value: 0.017) in girls, but no associations were found in boys or the combined sample. The associations with RORA met a more stringent Bonferroni-corrected statistical significance (P< 0.004). Conclusion Later weekday sleep midpoint and greater social jetlag were associated with altered expression of some core clock genes collected in mid-morning, particularly among adolescent females. Future studies are needed to evaluate the potential impact of differential clock gene expression, especially for RORA, on cardiometabolic health. Support (if any) K01HL151673

  PublisherOA PDFDOI

• Plasticity of Epigenomic and Transcriptomic Aging Reveals Common Targets for Reprogramming by Environmental Exposures

  Research Square · 2025-09-19 · 1 citations

  preprintOpen access
  PublisherDOI

• Toxicogenomic Insights into Environmental Toxicant Exposures: The TaRGET II Resource

  Research Square · 2025-08-20

  preprintOpen access
  PublisherOA PDFDOI

• Sex-stratified piRNA expression analysis reveals shared functional impacts of perinatal lead (Pb) exposure in murine hearts

  Epigenetics · 2025-08-10 · 2 citations

  articleOpen accessSenior authorCorresponding

  The landscape of PIWI-interacting RNA (piRNA) expression in the heart is poorly understood, particularly regarding sex differences. Altered piRNA expression has been reported in cardiovascular disease (CVD), and although exposure to the metal lead (Pb) is strongly associated with CVD risk, no studies have investigated Pb's effects on cardiac piRNAs. This study aimed to characterize piRNA expression in the murine heart and assess sex-specific effects of human-relevant maternal Pb exposure on adult offspring cardiac piRNA expression. piRNAs were identified from whole mouse hearts using sodium periodate exclusion of small RNA and subsequent sequencing. Control mice expressed 18,956 piRNAs in combined-sex analysis; sex-specific analyses revealed 9,231 piRNAs in female hearts and 5,972 piRNAs in male hearts. Genomic mapping showed 28-41% aligned to introns, while 12-28% mapped to exons. Comparing control and Pb-exposed hearts, we found more potential Pb-induced expression changes in females (847) compared to males (187) (p-value < 0.05 and |logFC| > 1). These piRNAs were significantly enriched near genes involved in biological processes related to heart function and CVD development, including mitochondrial function, energy metabolism, and cardiac muscle structure (FDR < 0.05). Overall, we characterized combined and sex-stratified piRNA expression in both control and Pb-exposed murine hearts. In addition to providing a foundation for sex-specific piRNA expression in the heart, these findings suggest a novel epigenetic mechanism by which developmental Pb exposure may impact CVD risk later in life. Future studies will link these sex-specific molecular changes to Pb-induced alterations in cardiac function.

  PublisherDOI

Recent grants

• Environmental Epigenomics and Precision Environmental Health

  NIH · $6.1M · 2020–2028

• Integrated Health Sciences Core

  NIH · $33.1M · 2011–2027

• NIH Grant U2CES026553

  NIH · $19.0M · 2021

• Development of piRNAs for target-specific methylation

  NIH · $2.2M · 2015–2020

• NIH Grant R01ES017524

  NIH · $2.2M · 2016

Frequent coauthors

• Jaclyn M. Goodrich

  114 shared

• Karen E. Peterson

  University of Michigan–Ann Arbor

  76 shared

• Maureen A. Sartor

  University of Michigan–Ann Arbor

  63 shared

• Muna S. Nahar

  Menlo School

  57 shared

• Justin A. Colacino

  University of Michigan–Ann Arbor

  42 shared

• Christopher Faulk

  University of Minnesota

  41 shared

• Tamara R. Jones

  University of Michigan–Ann Arbor

  38 shared

• Martha María Téllez‐Rojo

  Instituto Nacional de Salud Pública

  38 shared

Labs

• Dolinoy LabPI

Awards & honors

• Director of the University of Michigan NIEHS P30 Core Center…
• Member of the NIEHS TaRGET II Consortia
• MPI of the NIDDK R01 project 'Maternal Metabolic and Molecul…