About

Andrew Davis is an assistant professor in the Department of Sociology and Anthropology at NC State University. His research focuses on topics related to politics, culture, crime and punishment, violence, human rights, and law, often with a global perspective. He examines states, organizations, and other actors from a macro perspective to understand the factors that influence consequential behaviors. His methodological approaches include advanced statistical regression techniques, network analysis, and computational text analysis. His work has been published in a variety of peer-reviewed journals across disciplinary subfields, such as Social Problems, Law & Society Review, Justice Quarterly, the British Journal of Sociology, British Journal of Criminology, Social Science Research, Poetics, Punishment and Society, and the International Journal of Comparative Sociology. He has received awards from the American Sociological Association's Section on Human Rights and Section on Peace, War, & Social Conflict, as well as from the American Society of Criminology's Division on International Criminology. Currently, he serves as Co-Editor of Social Currents, the official journal of the Southern Sociological Society. His teaching and research interests include Political Sociology, Law & Society, Crime & Punishment, Global Sociology, Culture, Human Rights, Pandemic Politics, and Methods.

Research topics

• Biology
• Computational biology
• Genetics
• Bioinformatics
• Computer Science
• Medicine
• Chemistry
• Pharmacology
• Pathology
• Ecology
• Psychiatry
• Database
• Internal medicine

Selected publications

• Linking chemical data from the Comparative Toxicogenomics Database with adverse outcome pathways from the AOP-Wiki: a mechanistic data-oriented approach to help inform environmental health

  F1000Research · 2025-11-17 · 1 citations

  articleOpen access1st authorCorresponding

  <ns7:p>Background Chemicals can perturb gene functions to affect chronic human diseases, and a significant amount of biological knowledge involved in environmental health is available in public databases. Combining information across resources can assist in the discovery of novel testable hypotheses related to how chemical exposures influence human diseases, such as autism. Methods The Comparative Toxicogenomics Database (CTD) is a public resource that provides curated content for chemicals, genes, phenotypes, diseases, and exposures. The AOP-Wiki is a repository of adverse outcome pathways (AOPs) that provide defined biological frameworks describing disease processes. Here, we intersect CTD toxicogenomic content with the AOP-Wiki to identify environmental chemicals that could potentially modulate key steps in autism. Results We identify numerous chemical stressors that intersect with the individual events of the autism AOP, including bisphenol compounds, per/polyfluoroalkyl substances, pesticides, metals, and air pollutants, suggesting a wide range of environmental factors that could synergize to potentially affect autism. By integrating additional CTD curated content for three autism-associated chemicals (bisphenol A, particulate matter, and valproic acid), we discover other mechanisms, including specific genes (e.g., SLC1A1, GSTP1, CNTNAP2) and phenotypes (e.g., lipid metabolism, inflammatory response, social behavior) that can be used to help refine or expand this AOP or create an entirely new pathway for autism. Furthermore, related diseases are identified to build interconnected networks, mechanistically linking autism to fatty liver disease, intellectual disability, and cancer. Conclusions We demonstrate the value of integrating content from different resources to address environmental health questions related to autism etiology and co-morbidities. Importantly, our methodology is easily adapted for any AOP in the AOP-Wiki to identify potential environmental influences on the disease process and help support or refine AOPs. This analysis underscores the importance of standardizing public databases to make them efficiently interoperable for enhanced shared utility across the numerous bioknowledge digital landscapes.</ns7:p>

  PublisherOA PDFDOI

• Integrating AI-powered text mining from PubTator into the manual curation workflow at the Comparative Toxicogenomics Database

  Database · 2025-01-01 · 32 citations

  articleOpen access

  The Comparative Toxicogenomics Database (CTD) is a manually curated knowledge- and discovery-base that seeks to advance understanding about the relationship between environmental exposures and human health. CTD's manual curation process extracts from the biomedical literature molecular relationships between chemicals/drugs, genes/proteins, phenotypes, diseases, anatomical terms, and species. These relationships are organized in a highly systematic way in order to make them not only informative but also scientifically computational, enabling inferential hypotheses to be formed to address gaps in understanding. Integral to CTD's functionality is the use of structured, hierarchical ontologies and controlled vocabularies to describe these molecular relationships. Normalizing text (i.e. translating raw text from the literature into these controlled vocabularies) can be a time-consuming process for biocurators. To facilitate the normalization process and improve the efficiency with which our scientists curate the literature, CTD evaluated and integrated into the curation process PubTator 3.0, a state-of-the-art, AI-powered resource which extracts and normalizes from the literature many of the key biomedical concepts CTD curates. Here, we describe CTD's long-standing history with Natural Language Processing (NLP), how this history helped form our objectives for NLP integration, the evaluation of PubTator against our objectives, and the integration of PubTator into CTD's curation workflow. Database URL: https://ctdbase.org.

  PublisherDOI

• Transforming environmental health datasets from the comparative toxicogenomics database into chord diagrams to visualize molecular mechanisms

  Frontiers in Toxicology · 2024-07-22 · 16 citations

  articleOpen accessCorresponding

  In environmental health, the specific molecular mechanisms connecting a chemical exposure to an adverse endpoint are often unknown, reflecting knowledge gaps. At the public Comparative Toxicogenomics Database (CTD; https://ctdbase.org/), we integrate manually curated, literature-based interactions from CTD to compute four-unit blocks of information organized as a potential step-wise molecular mechanism, known as "CGPD-tetramers," wherein a chemical interacts with a gene product to trigger a phenotype which can be linked to a disease. These computationally derived datasets can be used to fill the gaps and offer testable mechanistic information. Users can generate CGPD-tetramers for any combination of chemical, gene, phenotype, and/or disease of interest at CTD; however, such queries typically result in the generation of thousands of CGPD-tetramers. Here, we describe a novel approach to transform these large datasets into user-friendly chord diagrams using R. This visualization process is straightforward, simple to implement, and accessible to inexperienced users that have never used R before. Combining CGPD-tetramers into a single chord diagram helps identify potential key chemicals, genes, phenotypes, and diseases. This visualization allows users to more readily analyze computational datasets that can fill the exposure knowledge gaps in the environmental health continuum.

  PublisherOA PDFDOI

• Comparative Toxicogenomics Database’s 20th anniversary: update 2025

  Nucleic Acids Research · 2024-10-10 · 181 citations

  articleOpen access1st authorCorresponding

  For 20 years, the Comparative Toxicogenomics Database (CTD; https://ctdbase.org) has provided high-quality, literature-based curated content describing how environmental chemicals affect human health. Today, CTD includes over 94 million toxicogenomic connections relating chemicals, genes/proteins, phenotypes, anatomical terms, diseases, comparative species, pathways and exposures. In this 20th year anniversary update, we reflect on CTD's remarkable growth and provide an overview of the increased data content and new features, including enhancements to the curation workflow (e.g. new exposure curation tool and expanded use of natural language processing), added functionality (e.g. improvements to CTD Tetramers and Pathway View tools) and significant upgrades to software and infrastructure. Linking lab-based core curation with real-world human exposure curation via the use of controlled vocabularies facilitates analysis of content across the entire environmental health continuum, from molecular toxicological mechanisms to the population level, and vice versa. The 'prototype database' originally described in 2004 has evolved into a premier, sophisticated, highly cited and well-engineered knowledgebase and discoverybase that is utilized by scientists worldwide to design testable hypotheses about environmental health.

  PublisherDOI

• Comparative Toxicogenomics Database: A tool to investigate the effects of environmental exposures on the etiology of Alzheimer’s disease

  Alzheimer s & Dementia · 2023-12-01

  articleOpen accessSenior author

  Abstract Background Most human diseases involve interactions between genetic and environmental factors. Although the environment is implicated in most chronic diseases, the etiology and mechanisms of action underlying these diseases remain unclear. It is estimated that more than 80,000 chemicals are currently used in commerce, challenging elucidation about chemical mechanisms‐of‐action and prioritization of environmental health research. Integration of diverse data is required to understand environment‐disease associations, mechanisms of chemical action, toxicity prediction and development of effective therapeutic interventions. Method The Comparative Toxicogenomics Database (CTD; http://ctdbase.org ) was launched publicly to address an unmet need for a public data resource dedicated exclusively to advancing understanding about environment‐disease connections. CTD provides a combination of richly annotated data describing chemical‐gene‐phenotype‐disease interactions, exposure information, and novel analysis tools that enable user‐driven discoveries about environmental influences on human health. Results Currently, CTD provides &gt;2.5 million manually curated relationships for 16,800 chemicals; 52,000 genes/proteins; 5,500 phenotypes; and 7,200 diseases. The value of CTD has been specifically leveraged for a range of chronic and neurological diseases, including Alzheimer’s disease. Conclusion There is growing evidence of environmental influences on the etiology of a range of neuropsychiatric syndromes. This presentation will provide an overview of CTD content and functionality and how it can be used to explore environmental influences on the etiology and underlying mechanisms of Alzheimer’s disease and other disorders.

  PublisherOA PDFDOI

• CTD tetramers: a new online tool that computationally links curated chemicals, genes, phenotypes, and diseases to inform molecular mechanisms for environmental health

  Toxicological Sciences · 2023-07-21 · 83 citations

  articleOpen access1st authorCorresponding

  The molecular mechanisms connecting environmental exposures to adverse endpoints are often unknown, reflecting knowledge gaps. At the Comparative Toxicogenomics Database (CTD), we developed a bioinformatics approach that integrates manually curated, literature-based interactions from CTD to generate a "CGPD-tetramer": a 4-unit block of information organized as a step-wise molecular mechanism linking an initiating Chemical, an interacting Gene, a Phenotype, and a Disease outcome. Here, we describe a novel, user-friendly tool called CTD Tetramers that generates these evidence-based CGPD-tetramers for any curated chemical, gene, phenotype, or disease of interest. Tetramers offer potential solutions for the unknown underlying mechanisms and intermediary phenotypes connecting a chemical exposure to a disease. Additionally, multiple tetramers can be assembled to construct detailed modes-of-action for chemical-induced disease pathways. As well, tetramers can help inform environmental influences on adverse outcome pathways (AOPs). We demonstrate the tool's utility with relevant use cases for a variety of environmental chemicals (eg, perfluoroalkyl substances, bisphenol A), phenotypes (eg, apoptosis, spermatogenesis, inflammatory response), and diseases (eg, asthma, obesity, male infertility). Finally, we map AOP adverse outcome terms to corresponding CTD terms, allowing users to query for tetramers that can help augment AOP pathways with additional stressors, genes, and phenotypes, as well as formulate potential AOP disease networks (eg, liver cirrhosis and prostate cancer). This novel tool, as part of the complete suite of tools offered at CTD, provides users with computational datasets and their supporting evidence to potentially fill exposure knowledge gaps and develop testable hypotheses about environmental health.

  PublisherOA PDFDOI

• Comparative Toxicogenomics Database (CTD): update 2023

  Nucleic Acids Research · 2022 · 878 citations

  1st authorCorresponding
  • Computer Science
  • Biology
  • Computational biology

  The Comparative Toxicogenomics Database (CTD; http://ctdbase.org/) harmonizes cross-species heterogeneous data for chemical exposures and their biological repercussions by manually curating and interrelating chemical, gene, phenotype, anatomy, disease, taxa, and exposure content from the published literature. This curated information is integrated to generate inferences, providing potential molecular mediators to develop testable hypotheses and fill in knowledge gaps for environmental health. This dual nature, acting as both a knowledgebase and a discoverybase, makes CTD a unique resource for the scientific community. Here, we report a 20% increase in overall CTD content for 17 100 chemicals, 54 300 genes, 6100 phenotypes, 7270 diseases and 202 000 exposure statements. We also present CTD Tetramers, a novel tool that computationally generates four-unit information blocks connecting a chemical, gene, phenotype, and disease to construct potential molecular mechanistic pathways. Finally, we integrate terms for human biological media used in the CTD Exposure module to corresponding CTD Anatomy pages, allowing users to survey the chemical profiles for any tissue-of-interest and see how these environmental biomarkers are related to phenotypes for any anatomical site. These, and other webpage visual enhancements, continue to promote CTD as a practical, user-friendly, and innovative resource for finding information and generating testable hypotheses about environmental health.

  PublisherOA PDFDOI

• CTD anatomy: Analyzing chemical-induced phenotypes and exposures from an anatomical perspective, with implications for environmental health studies

  Current Research in Toxicology · 2021-01-01 · 33 citations

  articleOpen access1st authorCorresponding

  The Comparative Toxicogenomics Database (CTD) is a freely available public resource that curates and interrelates chemical, gene/protein, phenotype, disease, organism, and exposure data. CTD can be used to address toxicological mechanisms for environmental chemicals and facilitate the generation of testable hypotheses about how exposures affect human health. At CTD, manually curated interactions for chemical-induced phenotypes are enhanced with anatomy terms (tissues, fluids, and cell types) to describe the physiological system of the reported event. These same anatomy terms are used to annotate the human media (e.g., urine, hair, nail, blood, etc.) in which an environmental chemical was assayed for exposure. Currently, CTD uses more than 880 unique anatomy terms to contextualize over 255,000 chemical-phenotype interactions and 167,000 exposure statements. These annotations allow chemical-phenotype interactions and exposure data to be explored from a novel, anatomical perspective. Here, we describe CTD's anatomy curation process (including the construction of a controlled, interoperable vocabulary) and new anatomy webpages (that coalesce and organize the curated chemical-phenotype and exposure data sets). We also provide examples that demonstrate how this feature can be used to identify system- and cell-specific chemical-induced toxicities, help inform exposure data, prioritize phenotypes for environmental diseases, survey tissue and pregnancy exposomes, and facilitate data connections with external resources. Anatomy annotations advance understanding of environmental health by providing new ways to explore and survey chemical-induced events and exposure studies in the CTD framework.

  PublisherDOI

• Regulatory status of pesticide residues in cannabis: Implications to medical use in neurological diseases

  Current Research in Toxicology · 2021 · 21 citations

  • Medicine
  • Pharmacology
  • Biology

  Medical cannabis represents a potential route of pesticide exposure to susceptible populations. We compared the qualifying conditions for medical use and pesticide testing requirements of cannabis in 33 states and Washington, D.C. Movement disorders were the most common neurological category of qualifying conditions, including epilepsy, certain symptoms of multiple sclerosis, Parkinson's Disease, and any cause of symptoms leading to seizures or spasticity. Different approaches of pesticide regulation were implemented in cannabis and cannabis-derived products. Six states imposed the strictest U.S. EPA tolerances (i.e. maximum residue levels) for food commodities on up to 400 pesticidal active ingredients in cannabis, while pesticide testing was optional in three states. Dimethomorph showed the largest variation in action levels, ranging from 0.1 to 60 ppm in 5 states. We evaluated the potential connections between insecticides, cannabinoids, and seizure using the Comparative Toxicogenomics Database. Twenty-two insecticides, two cannabinoids, and 63 genes were associated with 674 computationally generated chemical-gene-phenotype-disease (CGPD) tetramer constructs. Notable functional clusters included oxidation-reduction process (183 CGPD-tetramers), synaptic signaling pathways (151), and neuropeptide hormone activity (46). Cholinergic, dopaminergic, and retrograde endocannabinoid signaling pathways were linked to 10 genetic variants of epilepsy patients. Further research is needed to assess human health risk of cannabinoids and pesticides in support of a national standard for cannabis pesticide regulations.

  PublisherDOI

• Predicting molecular mechanisms, pathways, and health outcomes induced by Juul e-cigarette aerosol chemicals using the Comparative Toxicogenomics Database

  Current Research in Toxicology · 2021 · 78 citations

  • Biology
  • Chemistry
  • Bioinformatics

  There is a critical need to understand the health risks associated with vaping e-cigarettes, which has reached epidemic levels among teens. Juul is currently the most popular type of e-cigarette on the market. Using the Comparative Toxicogenomics Database (CTD; http://ctdbase.org), a public resource that integrates chemical, gene, phenotype and disease data, we aimed to analyze the potential molecular mechanisms of eight chemicals detected in the aerosols generated by heating Juul e-cigarette pods: nicotine, acetaldehyde, formaldehyde, free radicals, crotonaldehyde, acetone, pyruvaldehyde, and particulate matter. Curated content in CTD, including chemical-gene, chemical-phenotype, and chemical-disease interactions, as well as associated phenotypes and pathway enrichment, were analyzed to help identify potential molecular mechanisms and diseases associated with vaping. Nicotine shows the most direct disease associations of these chemicals, followed by particulate matter and formaldehyde. Together, these chemicals show a direct marker or mechanistic relationship with 400 unique diseases in CTD, particularly in the categories of cardiovascular diseases, nervous system diseases, respiratory tract diseases, cancers, and mental disorders. We chose three respiratory tract diseases to investigate further, and found that in addition to cellular processes of apoptosis and cell proliferation, prioritized phenotypes underlying Juul-associated respiratory tract disease outcomes include response to oxidative stress, inflammatory response, and several cell signaling pathways (p38MAPK, NIK/NFkappaB, calcium-mediated).

  PublisherDOI

Recent grants

• Comparative Toxicogenomics Database (CTD)

  NIH · $10.5M · 2006–2022

Frequent coauthors

• John Mattingly

  North Carolina State University

  56 shared

• Thomas C. Wiegers

  North Carolina State University

  53 shared

• Daniela Sciaky

  North Carolina State University

  30 shared

• Robin J. Johnson

  North Central State College

  23 shared

• Jolene Wiegers

  North Carolina State University

  22 shared

• Michael C. Rosenstein

  Mount Desert Island Biological Laboratory

  14 shared

• Benjamin L. King

  University of Maine

  13 shared

• Cynthia Grondin

  North Carolina State University

  13 shared

Labs

• Research and EngagementPI

Education

• Ph.D., Political Science

  North Carolina State University

  2005

• M.A., Political Science

  University of North Carolina at Chapel Hill

  2000

• B.A., Political Science

  University of North Carolina at Chapel Hill

  1997