Rachel Miller, MD
- PROFESSOR | Medicine, Clinical Immunology
- PROFESSOR | Environmental Medicine & Public Health
Specialties:Allergy and Immunology, Pulmonary Medicine (Lung)
Research Topics:Allergy, Environmental Health, Epigenetics
Endowed Chair, The Dr. David and Dorothy Merksamer Professor of Medicine (Allergy and Immunology)
Dr. Miller is board certified in Pulmonary Disease and Allergy and Immunology and a Fellow at the American Academy of Allergy Asthma and Immunology. She joined the faculty at Mount Sinai after a long tenure at Columbia where she served as Director of the Allergy and Immunology Fellowship program, Director of Adult Allergy, and Director of the Division of Pediatric Allergy, Immunology and Rheumatology. At Mount Sinai, she is the Chief of the Division of Clinical Immunology and Merksamer Professor in Immunology and continues her work as the Deputy Editor of The Journal of Allergy and Clinical Immunology.
Her research concentrates on the mechanisms for the onset of asthma. One large research focus involves establishing and studying a birth cohort from Northern Manhattan (Columbia Center for Children’s Environmental Health), determining the importance of environmental allergens, traffic-related pollutants, and phthalate and bisphenol A exposure to the onset of allergies, asthma, and allergic immune responses. A major emphasis is on the role of prenatal and early postnatal exposure on later pediatric and adolescent asthma risk. Additional areas of research include identifying novel genetic by environment interactions important to the onset of asthma. She also has established several mouse models examining the importance of prenatal and postnatal environmental exposures on risk for asthma and other complex diseases. More recent initiatives have been to build a program in environmental epigenetics and asthma by studying DNA methylation in cell, mouse and human systems for which she is now internationally recognized. At Sinai, she is leading efforts to build a new registry of patients undergoing immune modulation and assessing immunological signals that may correlate with disease activity and remission.
American Board of Allergy & Immunology
- Allergic Asthma
- Allergic Cough
- Allergic Rhinitis
- Allergy Injections
- Allergy Testing
- Drug Allergy/Reactions
- Food Allergy
- Immune Deficiency (non-HIV)
- Pollen Allergy
- Pulmonary Function Tests
MD, New York University School of Medicine
Residency, Internal Medicine, Columbia University Medical Center
Fellowship, Pulmonary & Critical Care, Columbia Presbyterian Medical Center
Fellowship, Allergy & Immunology, Columbia University Medical Center
I. Leonard Bernstein, MD FAAAAI Memorial Lectureship at the AAAAI/ACAAI Joint Congress
AAAAI Foundation and Sheldon L. Spector, MD FAAAAI Memorial Lectureship at the AAAAI/ACAAI Joint Congress for delivering the talk “Epigenetic Changes Ascribed to Pollutant Exposures”
Thomas A. Neff Lecturer at the Thomas L. Petty Aspen Lung Conference, 60th Annual Meeting,
Samberg Scholar in Children’s Health
Florence and Herbert Irving Clinical Research Career Award
Eve Flechner Award in Internal Medicine
Mitochondrial DNA biomarkers to assess responses to changes in personal environmental exposures in pediatric urban asthma
We are interrogating novel biomarkers that capture responses to multiple environmental stressors, and are highly sensitive to the dynamics of dysregulation, on lung function and airway inflammation. Mitochondrial (mt) DNA lacks protective histones and possesses diminished DNA repair mechanisms, rendering it more susceptible than the nuclear genome to damage by reactive oxygen species (ROS), interrupting redox homeostasis, and causing inflammation. Our group and others have shown that exposure to air pollution and allergens increases intracellular levels of ROS in mitochondria. The ensuing mtDNA damage increases its quantity or content. Urban exposures also may alter methylation at key mitochondrial replication and transcriptional control regions. Asthmatics may be more susceptible. Mitochondrial DNA damage can reverse, possibly more readily than other plasma biomarkers of oxidative stress. Our objective is to elucidate the dynamic interplay between reductions in multiple inflammatory urban exposures, attributable changes in mtDNA content and methylation, and improvements in pediatric asthma outcomes over time. We intend to capture the pivotal role of novel mt biomarkers in measuring the dynamic biological responses following induction and remediation of oxidative damage, triggered by a child's changing personal environment. Results could direct more effective personalized biomarker-guided therapy or intervention, including environmental remediation, pathway inhibitors, or dietary interventions, for children with persistent asthma, and for all children exposed to an urban environment.
Children's Respiratory Research Workgroup (CREW) consortium
We have teamed up with investigators that lead 12 asthma birth cohorts across the U.S. to establish the Children's Respiratory Research Workgroup (CREW) consortium. CREW proposes to identify specific types of childhood asthma, develop an understanding of what early life environmental influences cause these different types of asthma and when, and identify targets for future efforts aimed at preventing childhood asthma. CREW will include data from a large number of children (over 9,000 at birth, 6,000-7,000 who are still being followed, and at least 5,667 expected to enroll in CREW) and their families, with broad diversity in terms of ethnicity, family characteristics, neighborhoods and geographic locations. One of the primary goals of CREW is to put together sets of data and samples of participating cohorts to identify phenotypes of childhood asthma (i.e. specific subtypes of asthma that can be distinguished by clinical features such as natural history, triggers, exacerbation frequency, concurrent allergies, lung function, sex, etc). As we obtain mechanistic insights about personal and early life risk factors, we will connect asthma phenotypes with underlying causes and pathogenic mechanisms to define endotypes of childhood asthma. CREW is itself a "cohort" funded as part of the NIH Environmental Influences on Child Health Outcomes (ECHO) program. As such, in addition to sharing data and samples among CREW investigators, CREW cohort data will also be shared with the larger ECHO program.
Air pollution exposure and complex diseases-mouse models
We also have established several mouse models examining the importance of prenatal and postnatal environmental exposures on risk for asthma and other complex diseases that include obesity and neurocognitive dysfunction. More recent research focuses on the mechanistic effects of prenatal and pregnancy-associated polycyclic aromatic hydrocarbon exposure on breast cancer risk in mice.