About

Miatta Buxton, PhD, MPH, is an Assistant Research Scientist in Epidemiology and an Adjunct Lecturer at the University of Michigan School of Public Health. Her research interests focus on environmental and other influences on maternal and child health, including risk factors such as lower reproductive tract infections, environmental pollution, and nutrition, which contribute to adverse pregnancy outcomes. She specifically investigates the relationships among environmental, dietary factors, and preterm birth, exploring the mechanistic pathways and how these associations may be modified. Dr. Buxton's work also includes understanding patterns of inflammation in normal pregnancy and utilizing novel approaches such as precision health methodologies to identify determinants of preterm birth and measures for risk assessment. Her long-term goals involve advancing a research program that explores the causes of preterm birth and developing community intervention programs aimed at reducing its impact. She has conducted research using data from a Mexico-based cohort to study longitudinal evaluation of systemic inflammation among adolescents prior to the childbearing period. In collaboration with investigators from Michigan State University and Harvard Brigham and Women's Hospital, her projects investigate the associations between dietary inflammatory potential and placental inflammation. Dr. Buxton holds a PhD and MPH from the University of Michigan and a BA from Queens College, New York.

Research topics

• Medicine
• Biology
• Internal medicine
• Family medicine
• Social psychology
• Demography
• Psychology
• Environmental health
• Obstetrics
• Immunology

Selected publications

• Wildfire-Specific Fine Particulate Matter and Preterm Birth in the U.S. ECHO-Wide Cohort

  SSRN Electronic Journal · 2025-01-01

  preprintOpen access
  PublisherDOI

• Wildfire-specific fine particulate matter and preterm birth: a US ECHO Cohort analysis

  The Lancet Planetary Health · 2025-11-05 · 3 citations

  articleOpen access

  BACKGROUND: exposure intensity, duration, and timing. METHODS: exposure with preterm birth (delivery before 37 weeks of gestation) were analysed by adjusted pooled logistic regression in the nationwide ECHO sample and in the US West census region. Associations between smoke days in gestational weeks 0-35 and preterm birth were evaluated by logistic regression in the national sample. FINDINGS: or greater. INTERPRETATION: exposure in the western USA, with findings suggesting an exposure-response relationship for increasing exposure intensity and duration. Preterm birth was also associated with exposure to smoke days in mid-to-late pregnancy at the national level. For practice and policy, these findings support the need for public health interventions aimed at reducing exposure to wildfire smoke during pregnancy. FUNDING: ECHO Program, US National Institutes of Health Office of the Director.

  PublisherDOI

• Pre- and postnatal exposure to PM2.5 and NO2 and blood pressure in children: Results from the ECHO Cohort

  Environmental Research · 2025-12-23

  articleOpen access

  BACKGROUND: There is growing interest in understanding the link between early life exposures to ambient air pollution and childhood blood pressure; however, existing findings, largely from single site/cohort studies, are inconclusive. METHODS: (per 10-ppb) exposures with blood pressure outcomes were estimated using linear and Poisson regressions adjusted for sociodemographic, lifestyle, temporal, and spatial confounders. RESULTS: with both SBP (β: -2.42, 95 %CI: -4.70, -0.14) and DBP (β: -1.94, 95 %CI: -3.81, -0.08) percentiles were suggested. CONCLUSION: and blood pressure was counterintuitive and warrants further investigation.

  PublisherDOI

• Effects of PM10 Airborne Particles from Different Regions of a Megacity on In Vitro Secretion of Cytokines by a Monocyte Line during Different Seasons

  Toxics · 2024-02-15 · 3 citations

  articleOpen access

  Several epidemiological studies have demonstrated that particulate matter (PM) in air pollution can be involved in the genesis or aggravation of different cardiovascular, respiratory, perinatal, and cancer diseases. This study assessed the in vitro effects of PM10 on the secretion of cytokines by a human monocytic cell line (THP-1). We compared the chemotactic, pro-inflammatory, and anti-inflammatory cytokines induced by PM10 collected for two years during three different seasons in five different Mexico City locations. MIP-1α, IP-10, MCP-1, TNF-α, and VEGF were the main secretion products after stimulation with 80 μg/mL of PM10 for 24 h. The THP-1 cells showed a differential response to PM10 obtained in the different sites of Mexico City. The PM10 from the north and the central city areas induced a higher pro-inflammatory cytokine response than those from the south. Seasonal pro-inflammatory cytokine secretion always exceeded anti-inflammatory secretion. The rainy-season-derived particles caused the lowest pro-inflammatory effects. We concluded that toxicological assessment of airborne particles provides evidence supporting their potential role in the chronic exacerbation of local or systemic inflammatory responses that may worsen the evolution of some chronic diseases.

  PublisherOA PDFDOI

• Grandmother’s PM10 Exposure and Preterm Birth among their Grandchildren in Black and White Families in South Carolina, United States

  ISEE Conference Abstracts · 2024-07-31

  articleOpen access1st authorCorresponding
  PublisherDOI

• Effects of PM10 Airborne Particles from Different Regions and Seasons of a Megacity on In-Vitro Secretion of Cytokines by a Monocyte Line.

  Preprints.org · 2024-01-26 · 2 citations

  preprintOpen access

  Several epidemiological studies have demonstrated that particulate matter (PM) in air pollution can be involved in the genesis or aggravation of different cardiovascular, respiratory, perinatal, and cancer diseases. This study assessed the in vitro effects of PM <10 μm in aerodynamic diameter (PM10) on the secretion of cytokines by a human monocytic cell line (THP-1). We compared the chemotactic, pro-inflammatory, and anti-inflammatory cytokines induced by PM10 collected for two years during three different seasons in five different Mexico City locations. MIP-1α, IP-10, MCP-1, TNF-α, and VEGF were the main secretion products after stimulation with 80 μg/mL of PM10 for 24 hours. The THP-1 cells showed a differential response to PM10 obtained in the different sites of Mexico City. The PM10 from the north and the central city areas induced a higher pro-inflammatory cytokine response than those from the south. Seasonal pro-inflammatory cytokine secretion always exceeded the anti-inflammatory one. The rainy season-derived particles caused the lowest pro-inflammatory effects. We concluded that toxicological assessment of airborne particles provides evidence supporting their potential role in chronic exacerbation of local or systemic inflammatory responses that may worsen the evolution of some chronic diseases.

  PublisherOA PDFDOI

• Elevated Exposure to Air Pollutants Accelerates Primary Glomerular Disease Progression

  Kidney International Reports · 2024-05-18 · 10 citations

  articleOpen access

  IntroductionEnvironmental contributors to kidney disease progression remain elusive. We explored how residential air pollution impacts disease progression in patients with primary glomerulopathies.MethodsNephrotic Syndrome Study Network (NEPTUNE) and CureGlomerulonephropathy (CureGN) participants with residential census tract data and ≥2 years of follow-up were included. Using Cox proportional hazards models, the associations per doubling in annual average baseline concentrations of total particulate matter with diameter ≤ 2.5 μm (PM2.5) and its components, black carbon, and sulfate, with time to ≥40% decline in estimated glomerular filtration rate (eGFR) or kidney failure were estimated. Serum tumor necrosis factor levels and kidney tissue transcriptomic inflammatory pathway activation scores were used as molecular markers of disease progression.ResultsPM2.5, black carbon, and sulfate exposures were comparable in NEPTUNE (n=228) and CureGN (n=697). In both cohorts, participants from areas with higher levels of pollutants had lower eGFR, were older and more likely self-reported racial and ethnic minorities. In a fully adjusted model combining both cohorts, kidney disease progression was associated with PM2.5 (adjusted HR 1.55 [95% CI:1.00, 2.38], p=0.0489) and black carbon (adjusted HR 1.43 [95% CI:0.98, 2.07], p=0.0608) exposure. Sulfate and PM2.5 exposure were positively correlated with serum tumor necrosis factor (TNF) (p=0.003) and interleukin-1β levels (p=0.03), respectively. Sulfate exposure was also directly associated with transcriptional activation of the TNF and JAK-STAT signaling pathways in kidneys (r=0.55-0.67, p-value <0.01).ConclusionElevated exposure to select air pollutants is associated with increased risk of disease progression and systemic inflammation in patients with primary glomerulopathies (word count: 248).

  PublisherOA PDFDOI

• The Impact of Exposure to Air Pollution on the Progression of Primary Glomerular Disease

  Journal of the American Society of Nephrology · 2023-11-01

  article
  PublisherDOI

• Structural racism, air pollution and the association with adverse birth outcomes in the United States: the value of examining intergenerational associations

  Frontiers in Epidemiology · 2023-06-22 · 3 citations

  reviewOpen access1st author

  Structurally racist policies and practices of the past are likely to be a driving factor in current day differences in exposure to air pollution and may contribute to observed racial and ethnic disparities in adverse birth outcomes in the United States (U.S.). Non-Hispanic Black women in the U.S. experience poorer health outcomes during pregnancy and throughout the life course compared to non-Hispanic White women. This disparity holds even among non-Hispanic Black women with higher socioeconomic status. Reasons for this finding remain unclear, but long-term environmental exposure, either historical exposure or both historical and ongoing exposure, may contribute. Structural racism likely contributes to differences in social and environmental exposures by race in the U.S. context, and these differences can affect health and wellbeing across multiple generations. In this paper, we briefly review current knowledge and recommendations on the study of race and structural racism in environmental epidemiology, specifically focused on air pollution. We describe a conceptual framework and opportunities to use existing historical data from multiple sources to evaluate multi-generational influences of air pollution and structurally racist policies on birth and other relevant health outcomes. Increased analysis of this kind of data is critical for our understanding of structural racism's impact on multiple factors, including environmental exposures and adverse health outcomes, and identifying how past policies can have enduring legacies in shaping health and well-being in the present day. The intended purpose of this manuscript is to provide an overview of the widespread reach of structural racism, its potential association with health disparities and a comprehensive approach in environmental health research that may be required to study and address these problems in the U.S. The collaborative and methodological approaches we highlight have the potential to identify modifiable factors that can lead to effective interventions for health equity.

  PublisherOA PDFDOI

• The pregnancy research on inflammation, nutrition, &amp; city environment: systematic analyses study (PRINCESA) cohort, 2009–2015

  European Journal of Epidemiology · 2023-08-29

  articleOpen access1st author
  PublisherOA PDFDOI

Frequent coauthors

• Felipe Vadillo‐Ortega

  Hospital Regional de Alta Especialidad del Bajío

  26 shared

• Marie S. O’Neill

  University of Michigan–Ann Arbor

  14 shared

• Marisol Castillo‐Castrejón

  University of Oklahoma Health Sciences Center

  9 shared

• Brisa N. Sánchez

  Drexel University

  9 shared

• Noemí Meraz‐Cruz

  National Institute of Genomic Medicine

  8 shared

• Carina J. Gronlund

  University of Michigan–Ann Arbor

  7 shared

• Álvaro Osornio-Vargas

  University of Alberta

  6 shared

• Betsy Foxman

  University of Michigan–Ann Arbor

  6 shared

Labs

• Miatta Buxton's LabPI