Glyphosate links to cancers

Checked on February 3, 2026
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Executive summary

The question “Glyphosate links to cancers” has no single settled answer: a major cancer agency, IARC, classed glyphosate as “probably carcinogenic to humans” in 2015 based on limited human evidence and sufficient animal evidence [1], while regulators including the U.S. EPA and several national bodies have repeatedly concluded glyphosate is unlikely to cause cancer in humans [2]. Recent retractions, new animal bioassays, mechanistic reviews and epidemiologic meta-analyses have intensified debate ahead of regulatory reassessments expected in 2026 [3] [4] [5].

1. The evidence that supports a cancer link: epidemiology and meta-analyses

Multiple case‑control and pooled analyses have reported associations between glyphosate exposure and lymphoid cancers, particularly non‑Hodgkin lymphoma and other hematologic malignancies, with some meta‑analyses and occupational studies reporting elevated risks for highly exposed groups [6] [7] [8]. Community‑level and large observational studies have also linked frequent glyphosate use with higher risks of all cancers and site‑specific cancers such as colon, pancreatic and lung in some reports, although these are not uniformly replicated [9].

2. Animal studies and mechanistic plausibility

Long‑term rodent bioassays and systematic animal reviews document tumor increases and other carcinogenic signals in multiple organs after chronic glyphosate or glyphosate‑based herbicide exposure, providing biological plausibility for the epidemiologic signals [10] [11]. Mechanistic systematic reviews identify several “key characteristics” of carcinogens—genotoxicity, oxidative stress and other molecular events—strengthening the argument that glyphosate or formulated products could plausibly contribute to cancer pathways [12] [13].

3. The contrary evidence: major regulators and cohort studies

At the same time, long‑running cohort research such as the Agricultural Health Study has not found consistent associations between glyphosate exposure and overall cancer incidence across broad cohorts of licensed applicators, and major regulators including the EPA, EFSA and others have maintained glyphosate is unlikely to be carcinogenic in humans based on their weight‑of‑evidence evaluations [6] [2]. Key disagreements with IARC often hinge on which studies and data—especially unpublished industry studies of “technical” glyphosate versus real‑world formulated products—are prioritized in risk assessments [14].

4. Why different authorities reach different conclusions

The divergence rests on methodological choices: IARC classifies hazard (could glyphosate cause cancer under some conditions) and relied on published epidemiology, animal studies and mechanistic data to label glyphosate Group 2A [1], whereas regulatory agencies assess risk (likelihood at typical exposures) and have emphasized different datasets, including industry studies and exposure assessments, to judge human risk as low [14] [2]. Analysts also warn that commercial formulations include co‑formulants that can alter toxicity versus pure glyphosate tested in some regulatory studies, complicating comparisons [14].

5. Recent developments that change the context

Recent events have sharpened scrutiny: a high‑profile 2000 safety paper used in regulatory dossiers was retracted after litigation revealed undisclosed conflicts of interest, prompting calls for fresh regulatory re‑evaluations ahead of EPA deadlines in 2026 [3] [4]. New international rodent bioassays and institutional reports published since 2023–2025 claim replication of carcinogenic findings and reinforce IARC‑consistent concerns, while detection of glyphosate residues in playgrounds and environments has fueled public pressure even where exposure‑dose implications remain uncertain [5] [15].

6. Bottom line, uncertainties and what to watch next

The balance of evidence shows plausible mechanisms and animal evidence for carcinogenicity and epidemiologic signals—especially for hematologic cancers—in some exposed populations, but population‑level risk estimates remain contested because of inconsistent cohort findings, exposure assessment challenges, potential differences between pure glyphosate and commercial formulations, and disputed industry vs. independent data [12] [6] [14]. The unresolved questions that matter for public health are magnitude of risk at real‑world exposures, the role of co‑formulants, and the integrity of data used by regulators; upcoming EPA reassessments and independent long‑term studies deserve close attention [4] [13].

Want to dive deeper?
How did IARC and the U.S. EPA differ methodologically in their glyphosate assessments?
What evidence exists on glyphosate formulation co‑formulants changing toxicity compared with technical glyphosate?
Which recent animal bioassays replicate glyphosate carcinogenic findings and how were they designed?