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U.S. biomedical research has tilted heavily toward genetic traits and late-stage disease treatments, leaving nonheritable and environmental drivers of disease dramatically underfunded. Given the mounting evidence that environmental exposures contribute equally—or in many cases more—to disease onset as compared to genetics, a rebalance in funding is desperately needed.
The burden of disease attributable to environmental exposures is substantial: one in five deaths worldwide is attributed to air pollution alone, with pollutants such as PM2.5 and NO2 having strong connections to Alzheimer's disease, type 2 diabetes, NAFLD/NASH, and some cancers (Burnett et al., 2018; The Lancet Commission on Pollution and Health). Lead exposure accounts for an estimated five million cardiovascular deaths globally each year (Lanphear et al., 2018). Endocrine disruptors like BPA, phthalates, and PFAS interfere with metabolic and reproductive axes, contributing to diabetes, infertility, and hormone-sensitive cancers (Gore et al., 2015; Trasande, 2019). Solvents and pesticides, including trichloroethylene, are implicated in Parkinson's disease, ALS, and malignancies (Goldman, 2014). Metals such as cadmium and manganese exacerbate neurodegenerative and reproductive risks (ATSDR).
Yet funding allocations favor studies on mechanisms related to the disease and its treatments over environmental factors that contribute to onset. For Parkinson's Disease, $12.5M of $253M in grants are dedicated to environmental exposures, despite twin studies showing only 30-40% of PD risk can be explained by polygenic risk factors. Despite the established relationship between lung cancer and smoking, 10-20% of lung cancer patients have no family history and never smoked—and rates of non-smoking lung cancer are increasing. The NIH has invested only $8.3M of $492M into chemical exposures of lung cancer in FY2024 (See Figure 1). These are examples of a structural blind spot, with the world's largest public funder of biomedical research investing billions in treating disease, while spending comparatively little to predict and prevent harm upstream.
A historic funding gap impedes progress at the intersection of biotech and environmental toxicants research. Some public agencies have had limited budget increases in recent decades, and examining pollutants as agents of disease has been largely outside their purview. The EPA's strategy for protecting human health focuses on regulating chemical exposures. The NSF is largely focused on basic science well outside the realm of application to protecting populations from disease. Meanwhile, the NIH has had massive budget increases in the past half-century, yet the bulk is designated to research on downstream treatments of disease to support fields ripe for commercialization. Federal dollars have largely dictated where private dollars follow, with public funding often matched several-fold by private sector investment.
Tracing trends in federal appropriations for the NIH budget over the past 50 years reveals how urgency influences government funding. The NCI funding surged first in the 1970s due to the National Cancer Act launching the "War on Cancer," then again in the late 1990s–early 2000s as part of the bipartisan push to double the NIH budget amid rising scientific opportunity and advocacy. NHLBI's funding has been well established since the 1970s to address cardiovascular, lung, and blood diseases—the nation's leading causes of death.
NIAID gained traction in the 1990s due to the AIDS epidemic, but received the largest funding increase in the history of any institute after September 11, 2001 to bolster defense against chemical, biological, radiological, or nuclear (CBRN) threats. The FY2003 President's budget contained $4 billion for NIAID—a $1.5 billion (57%) increase over the 2002 allocation, described as "the largest single increase for an Institute in the history of the NIH" (OJP, 2002). This reflected the priority of developing rapid-response capabilities, including Dr. Fauci's vision of "bug to drug in 24 hours"—the ability to identify treatments for genetically engineered bioagents within a day (Homeland Security Archives, 2003).
The National Institute on Aging gained traction after the National Alzheimer's Project Act passed in 2011, and NIA became the major focal point for Alzheimer's Disease funding in 2016 after federal spending caps were lifted. This influx came partly from hopes that the human genome would unlock many cures—a lesson for current initiatives to avoid overpromising single-paradigm solutions (Hayden, 2022). By 2018, the Alzheimer's research field had experienced a funding surge that attracted researchers from across disciplines (Begley, 2019). These patterns of research dollar influxes reflect public pressure, underlying shifts in disease burden, policy changes, and chemical defense priorities.
Unlike some institutes, the National Institute of Environmental Health Sciences has not seen the same dramatic funding uptick over the past half-century, as pollution has not been prioritized as a factor of U.S. morbidity and mortality, public policy, or biodefense initiatives. Yet there is copious evidence that chemical pollutants—pesticides, endocrine disruptors, PFAS, heavy metals—are drivers of common conditions including cardiovascular disease, metabolic disorders, reproductive disorders, and neurodegenerative disease.
To incorporate environmental factors into translational research, the academic environmental health field must orient away from the outdated single exposure–single effect framework. Epidemiology has leaned heavily on the 1:1 chemical:disease ratio carved out by occupational health and industrial hygiene studies. Chronic, higher-level exposures in work settings led to simple linear regression models of dose-response and well-defined adverse outcome pathways. Yet for environmental exposures in unmonitored conditions (e.g., during early life), more sophisticated real-world models must account for multi-target outcomes of cumulative exposures and the stochastic effects of environmental pollutants on human biology (Wild, 2021).
NIEHS holds great potential to inform other institutes on scientific approaches and strategic directions if ample resources were allocated to researching cellular damage and molecular-level targets of effects caused by environmental pollutants. Integration of exposure-related mechanistic studies could span well-funded areas across NIH institutes. According to the NIH's Research, Condition, and Disease Categories (RCDC) dashboard, large tranches of public dollars are already designated to focus areas well-aligned with a new environmental health strategy. The nexus of environmental health and biotech could be situated under umbrellas designated to clinical research (~$19B), biotechnology/bioengineering (>$15B combined), genetics (~$12B), and prevention (~$12B).
Federal agencies have already endorsed and adopted biotechnology approaches. The NIH's Exposome NEXUS initiative represents a collaboration across institutes to study how environmental exposures throughout life contribute to health and disease, integrating 'omics technologies, wearable sensors, and advanced data science. The EPA has invested in high-throughput toxicology screening (ToxCast/Tox21) to assess chemical hazards using computational and in vitro methods. The NSF supports fundamental research in biosensors, environmental monitoring technologies, and data science that underpins exposure assessment.
Expansion of this work could have profound implications for population health. By systematically integrating exposure science into the biotech toolkit—identifying exposure-induced molecular targets, biomarkers of early cellular stress, and pathways of resilience—environmental health research could move from observational correlations to actionable, target-driven biology. This shift would not only expand the universe of druggable targets, but also enable new classes of preventive and protective interventions aligned with the translational incentives of the biotech ecosystem.
The Impact Model included in this application illustrates the potential scale of this opportunity: by addressing the pollution-attributable fraction of common diseases, we can project the healthcare costs avoided, the investment required, and the number of people who could benefit from curative or preventive interventions. Environmental health initiatives riding alongside the epicenter of U.S. biotech and clinical research could develop new addressable molecular targets to build resilience against cellular harm—transforming environmental health from a regulatory concern into a therapeutic frontier.