Vol. 118, No. 8 NewsOpen AccessBringing the Bugs Back In: Environmental Health Research Model Combines Toxicology and Infectious Disease Harvey Black Harvey Black Search for more papers by this author Published:1 August 2010https://doi.org/10.1289/ehp.118-a353bCited by:1AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit Although pathogens are known to modify the effects of toxicants, U.S. environmental health research currently focuses on physical agents and chemical toxicants—a focus that limits the field by ignoring the interaction between pathogens and toxic agents [EHP118(8):1165–1172; Feingold et al.]. These authors present a conceptual paradigm that integrates infectious disease and toxicologic environmental health research, promotes cross-disciplinary education and communication, and elucidates a fuller body of environmental health risk factors.Chemical toxicity often involves relatively direct effects of exposures on health outcomes, but infectious disease transmission typically is more complex, depending on factors such as dynamic environmental and ecologic systems, patterns of contact among populations, and host immune status. But interactions between pathogens and toxicants are undeniable. For instance, hepatitis B virus and aflatoxin individually increase the risk of liver cancer, but combined exposure to both agents increases risk far more than would be expected based on effects of the two risk factors in isolation. And in the case of cervical cancer, although infection with human papillomavirus is believed to be necessary for the cancer to occur, smoking may act as a cofactor and increase the risk the cancer will occur in someone infected with the virus.The authors identify multiple points between initial exposure and clinical disease at which toxicant–pathogen interactions can occur. They also describe approaches common to both areas of research. Both focus on upstream interventions to prevent disease by preventing exposure. Both areas also focus on spatial context (i.e., proximity to toxic or pathogenic agents) and quantitative modeling to estimate exposure, and both use biomarkers to study exposure, susceptibility, and disease.Fostering collaborations between researchers in these fields can lead to a better understanding of complex exposures and resulting diseases. “Classic reductionist thinking in toxicology focuses on ‘one toxicant, one outcome’ research,” the authors write. In contrast, they conclude, “If basic research is to increase our ability to predict the consequences of exposure to environmental chemicals, we must embrace nonreductionist thinking and design experimental models that emulate human experience.”Pathogen–toxicant interactions may influence the progression from exposure to disease at multiple points.FiguresReferencesRelatedDetailsCited by Mishra P, Bhargava A, Pathak N, Desikan P, Maudar K, Varshney S, Shrivastava R and Jain A Molecular surveillance of hepatitis and tuberculosis infections in a cohort exposed to methyl isocyanate, International Journal of Occupational Medicine and Environmental Health, 10.2478/s13382-011-0006-2, 24:1 Vol. 118, No. 8 August 2010Metrics About Article Metrics Publication History Originally published1 August 2010Published in print1 August 2010 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.