About

Justin Colacino is an Associate Professor of Environmental Health Sciences and Nutritional Sciences at the University of Michigan, affiliated with the School of Public Health and the College of Literature, Science, and the Arts, as well as the School for Environment and Sustainability. His educational background includes a PhD in Environmental Health Sciences from the University of Michigan School of Public Health, an MA in Statistics from the University of Michigan, an MPH from the University of Texas School of Public Health, and a BS in Biochemistry from the University of Texas at Austin. His research focuses on environmental health, particularly the effects of environmental exposures such as pesticides, lead, and cadmium on human health and development. His work involves analyzing the biological impacts of these exposures, including their influence on stem cells, cancer development, and epigenetic modifications. Colacino has contributed to understanding racial disparities in chemical biomarker concentrations and the molecular mechanisms underlying environmental toxicants' effects on human tissues. His publications reflect a strong emphasis on the intersection of environmental exposures, molecular biology, and health outcomes.

Research topics

• Genetics
• Biology
• Immunology
• Medicine
• Internal medicine
• Environmental health
• Demography
• Biochemistry
• Gerontology
• Cell biology
• Computational biology
• Endocrinology
• Bioinformatics
• Pathology

Selected publications

• Exploring the Influence of Chemical Exposures in Breast Cancer Disparities: High-Throughput Transcriptomic Analysis in Normal Breast Cells from Diverse Donors

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-02-24

  articleOpen accessSenior authorCorresponding

  Abstract Racial disparities in the incidence of, and mortality from, aggressive breast cancers are a pressing public health issue. Many factors have been investigated in these inequities; however, the role of toxicant exposures is not well characterized. We and others have identified substantial inequities in chemical biomarker concentrations by race. The goal of this study was to test the hypothesis that exposure to these chemicals is linked to biological changes relevant to aggressive breast cancers, such as dysregulation of the Hallmarks of Cancer. We used high throughput transcriptomic profiling of normal primary human breast epithelial cells from diverse donors ( n=6 ) to test effects of 8 chemicals (cadmium, lead, arsenic, copper, PFNA, BPA, BPS, p,p’-DDE) with documented exposure disparities by race/ethnicity across 3 concentrations (100nM, 1µM, 10µM). Across chemicals, we identified that pathways related to cell cycle regulation and protein secretion were commonly affected. Through bioinformatic estimation of cell type proportions, we found that metals like lead and cadmium induced cell-type shifts, consistent with the dysregulated cellular plasticity cancer hallmark. Lead and arsenic response genes were enriched for genes associated with poor breast cancer survival in the Cancer Genome Atlas. Integrating concentration-response modeling and chemical biomonitoring data, BPA, p,p’-DDE, copper, and lead elicited expression changes at concentrations relevant to the US population. Finally, we identified substantial interindividual heterogeneity in response to organic compounds, but less so in metals. These findings highlight the value of high-throughput transcriptomics as a New Approach Methodology (NAM) in quantifying how common exposures may impact aggressive breast cancer associated biological processes.

  PublisherDOI

• NADPH-producing enzymes restrict the formation of pancreatic precancerous lesions

  Nature Metabolism · 2026-04-01 · 2 citations

  articleOpen access

  Acinar-to-ductal metaplasia (ADM) is a reversible cell state that facilitates pancreas repair following injury. Oncogenic KRAS mutations can progress ADM to pancreatic intraepithelial neoplasia (PanIN) and pancreatic ductal adenocarcinoma (PDAC). However, the metabolic alterations in these precancerous lesions are understudied. Here, we identify global changes in central carbon metabolism genes and metabolites during ADM formation. In particular, NRF2-target genes are significantly induced in ADM. Among these, we focus on genes encoding NADPH-producing enzymes glucose-6-phosphate dehydrogenase (G6PD) and malic enzyme 1 (ME1), which participate in the regulation of oxidative stress. In mouse models of pancreatic tumourigenesis, G6PD deficiency or Me1 loss increases reactive oxygen species and lipid peroxidation, which is accompanied by accelerated formation of ADM and PanIN lesions. Notably, Me1 loss, but not G6PD deficiency, promotes faster PDAC progression. We demonstrate that oxidative stress is required for ADM, as pharmacological antioxidant treatment attenuates ADM progression in vivo and ex vivo. Conversely, depleting the antioxidant glutathione promotes precancerous lesions in primary human acinar cells and in mice. Together, our findings shed light on metabolic reprogramming in the precancerous pancreas.

  PublisherDOI

• Author Correction: Intestinal non-canonical NFκB signaling shapes the local and systemic immune response

  Nature Communications · 2025-07-08

  erratumOpen access
  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 accessSenior author

  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

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

  Research Square · 2025-08-20

  preprintOpen access
  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

• RUNX2 promotes epigenetic WNT signaling in inflamed intestinal epithelial cells

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-11-17

  preprintOpen access

  Abstract Ulcerative colitis (UC) is characterized by chronic mucosal inflammation, recurrent epithelial injury, and impaired colonic mucosal wound healing. While WNT/β-catenin dysregulation has been reported in UC, the mechanisms of such abnormalities remain unclear. To investigate epithelial intrinsic alterations associated with UC, we performed single-nucleus RNA-seq (snRNA-seq) and ATAC-seq (snATAC-seq) multiomics on human primary colonic epithelial cells (colonoids) from healthy donors and patients with inactive or active UC. Colonoids were cultured in a 3D matrix recapitulating crypt base cells or grown as 2D monolayers in differentiation medium to recapitulate luminal epithelial cells. Colonoids from active UC had a unique cell population with elevated CTNNB1 and reduced APC expression. Chromatin profiling identified enrichment of RUNX2 motifs in this UC-associated cell population. Active UC colonoids exhibited reduced OLFM4 expression in 3D and the differentiation marker VIL1 in 2D, suggesting impaired self-renewal and maturation. RUNX2 inhibition using CADD522 reduced β-catenin levels in 3D colonoids and restored VIL1 expression and junctional β-catenin localization in 2D cultures. These findings reveal an intrinsic defect in epithelial renewal in UC, driven in part by RUNX2-dependent WNT dysregulation. Our study identifies RUNX2 as a transcriptional regulator of epithelial stem cell function and WNT signaling in the inflamed human colon. Graphical Abstract summary Single-nucleus RNA and ATAC sequencing of UC patient-derived colonoids reveals a RUNX2-associated WNT signature in active inflammation. Elevated β-catenin and reduced OLFM4 and VIL1 expression indicate impaired self-renewal and differentiation. Pharmacologic inhibition of RUNX2 restores epithelial maturation, identifying RUNX2 as a key regulator of epithelial dysfunction in UC.

  PublisherOA PDFDOI

• Exposome-wide association study of cognition among older adults in the National Health and Nutrition Examination Survey

  Exposome · 2025-01-01 · 10 citations

  articleOpen access

  Abstract Cognitive impairment among older adults is a growing public health challenge and environmental chemicals may be modifiable risk factors. A wide array of chemicals has not yet been tested for association with cognition in an environment-wide association framework. In the US National Health and Nutrition Examination Survey (NHANES) 1999-2000 and 2011-2014 cross-sectional cycles, cognition was assessed using the Digit Symbol Substitution Test (DSST, scores 0-117) among participants aged 60 years and older. Concentrations of environmental chemicals measured in blood or urine were log2 transformed and standardized. Chemicals with at least 50% of measures above the lower limit of detection were included (nchemicals = 147, nclasses=14). We tested for associations between chemical concentrations and cognition using parallel survey-weighted multivariable linear regression models adjusted for age, sex, race/ethnicity, education, smoking status, fish consumption, cycle year, urinary creatinine, and cotinine. Participants with at least one chemical measurement (n = 4982) were mean age 69.8 years, 55.0% female, 78.2% non-Hispanic White, and 77.0% at least high school educated. The mean DSST score was 50.4 (standard deviation (SD)=17.4). In adjusted analyses, 5 of 147 exposures were associated with DSST at P-value <.01. Notably, a SD increase in log2-scaled cotinine concentration was associated with 2.71 points lower DSST score (95% CI −3.69, −1.73). A SD increase in log2-scaled urinary tungsten concentration was associated with 1.34 points lower DSST score (95% CI −2.11, −0.56). Exposure to environmental chemicals, particularly metals and tobacco smoke, may be modifiable factors for cognition among older adults.

  PublisherDOI

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

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

  preprintOpen accessSenior author

  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

• Multiplex characterization of circulating tumor cells from ductal carcinoma in situ patients suggests early tumor dissemination

  Cancer Letters · 2025-04-17 · 3 citations

  article
  PublisherDOI

Recent grants

• Developmental Exposures, Stem Cell Reprogramming, and Breast Cancer Disparities

  NIH · $4.8M · 2018–2027

• Risk of Alzheimer's Disease and Related Dementias from Perinatal Lead Exposure: Brain Region and Cell Type Effects

  NIH · $3.7M · 2022–2026

Frequent coauthors

• Maureen A. Sartor

  University of Michigan–Ann Arbor

  50 shared

• Laura S. Rozek

  Georgetown University

  46 shared

• Dana C. Dolinoy

  42 shared

• Olivier Jolliet

  Technical University of Denmark

  34 shared

• Vy Nguyen

  32 shared

• Jin Niu

  Providence College

  30 shared

• Ya’acov Ritov

  30 shared

• Charlotte Brown

  30 shared