Erratum: Retraction of the landmark glyphosate safety publication by Williams, Kroes and Munro (2000) should be reversed.
[This corrects the article on p. 1107 in vol. 25, PMID: 42517087.].
Biomedical subjects
Publications and source records attributed to Christopher J Borgert.
[This corrects the article on p. 1107 in vol. 25, PMID: 42517087.].
The decision by the co-Editor-in-Chief of Regulatory Toxicology and Pharmacology, Prof. Martin van den Berg, to retract the 2000 review article by Williams, Kroes, and Munro has elicited widespread criticism within the scientific community. Issued in late 2025, the retraction decision cites procedural concerns including potential ghostwriting, undisclosed conflicts of interest, and omission of certain unpublished studies, invoking Committee on Publication Ethics guidelines despite lacking evidence of fraud or scientific flaws. This editorial argues that the retraction decision involves editorial overreach and misapplication of the guidelines. The alleged omissions stemmed from proprietary data access limitations that were disclosed in the original paper. Subsequent reviews by several independent expert panels and regulatory authorities with access to all glyphosate data, including the studies cited by the retracting editor, reached similar conclusions. Claims of ghostwriting were previously investigated and found lacking, including a declaration by EFSA as to the clarity of the conflict disclosures. The retraction's timing, reliance on litigation documents, and apparent biases that were not disclosed in the retraction notice raise questions of ideological interference. Absent substantive rebuttals based on scientific merit rather than speculative claims of inappropriate authorship and data access, this retraction decision sets a dangerous precedent for retroactive censorship, potentially chilling beneficial industry-academic collaborations and eroding trust in the integrity of scientific publishing. With the strongest conviction, we assert that retracting a paper without scientific flaws isn't protection-it is censorship. We therefore call for the immediate reversal of this flawed and unjustified retraction to preserve trust in peer-reviewed literature.
The workshop objectives were to explore progress in implementing new, revised and alternative toxicological test methods across regulatory evaluation frameworks and decision-making programs in the United States, to identify barriers and to develop recommendations to further promote adoption of approaches that reduce, refine, or replace the use of animal methods. The workshop included sessions on: (1) current research, development, and validation of alternative methods within the U.S. federal government; (2) emerging alternative methodologies with potential applications to a broad spectrum of toxicity evaluation strategies; (3) tiered evaluation ("intelligent testing") strategies; and (4) identification of, and recommendations to address, critical barriers that affect adoption and use of new, revised alternative toxicological test methods by U.S. regulatory agencies. Through facilitated discussion, a list of barriers and recommendations were developed and grouped into categories of economic/financial, scientific/technical, and regulatory/policy. Overall, participants from all sectors collectively supported catalyzing actions to promote more meaningful and rapid progress for research to develop alternative methods focused for use in regulatory programs, accelerated lab investigations to validate such alternative methods and adoption of regulatory frameworks which embrace and incorporate these validated alternatives.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
This work describes the uptake of two organochlorine pesticides from slow-release pellets by largemouth bass and the utility of a blood plasma enzyme-linked immunosorbent assay (ELISA) method for exposure verification. We measured blood and tissue levels by gas chromatography/mass spectrometry and by a novel ELISA method, and present a critical comparison of the results.
Recent regulatory guidance for mixture risk assessments and for regulating pesticide chemicals recommends using information about the "mode" or "mechanism" of action of individual chemicals to predict dose response characteristics of mixtures. Dose addition is assumed for mixtures of chemicals that have similar mechanisms and response addition for those with dissimilar mechanisms. Three different sets of criteria have been formulated to guide the selection of an appropriate data set for characterizing a chemical's mode of action, but the sufficiency of those criteria to predict dose addition for a mixture has not been validated experimentally. Several examples from the pharmacological and toxicological literature challenge the premise that dose response characteristics of a mixture can be predicted from the modes of action of its components. Detoxification pathways may need to be understood before dose addition in the observable effect range can be extrapolated to mixture concentrations below the no observable effect levels of the mixture components. Because elucidating discreet mechanisms of action may be possible only for chemicals that exhibit a high degree of biological specificity and dose sensitivity, practical limitations on the approach must be defined. To reduce the large uncertainties inherent in the recommended approach, future research should be focused on defining the mechanistic features that predict dose additive toxicity in mixtures. A detailed characterization of pharmacodynamics, pharmacokinetics, and slope of dose response curves may be necessary to evaluate whether the toxicity of a mixture can be predicted by the mode of action of its component chemicals.
p,p'-Dichlorodiphenyldichloroethylene (DDE) and methoxychlor were tested alone and in combination to assess the similarity of their actions on hormone synthesis in gonadal tissue from largemouth bass (Micropterus salmoides floridanus), a species whose reproductive fitness has relevance to ecosystem health in Florida (USA). Gonads were harvested from adult female bass (age, two to three years) during the peak reproductive season (January-May), minced, and incubated in culture medium with or without test agents for 48 h. Duplicates of each treatment were performed in each of three experiments using tissue from a different female. Both 17beta-estradiol and testosterone were measured in aliquots of culture medium by validated radioimmunoassay procedures. Dose-response relationships of individual agents were characterized over a 6-log concentration range (1 X 10(-2) to 1 X 10(4) ppb). Both DDE and methoxychlor, tested individually, produced a dose-dependent decrease in testosterone levels. 17beta-Estradiol levels were unaffected. Mixtures of the agents were tested at all concentration combinations of 0.01, 1, 100, and 10,000 ppb in culture medium. Statistical tests indicated that of 16 dose combinations tested, 15 were antagonistic, and only 1 was additive based on the Loewe additivity model of no interaction. These results imply that methoxychlor and DDE inhibit testosterone production by different mechanisms in bass ovaries.
The two primary sources of nutrition for infants are human milk and infant formula. Both contain an array of endogenous and exogenous chemicals that may act through many separate hormonal mechanisms. The safety of infant nutrition sources has been questioned based on the possibility that exogenous chemicals may exert adverse effects on nursing or formula-fed infants through estrogen-mediated mechanisms. In response to these and other concerns, the National Research Council recommended assessing the estrogenic potency of natural and anthropogenic hormonally active agents. Furthermore, the Endocrine Disruptor Screening and Testing Advisory Committee of the U.S. Environmental Protection Agency specifically recommended testing chemicals present in human milk as a representative mixture to which large segments of the population are exposed. To date, no clinical or epidemiologic evidence demonstrates that levels of chemicals currently found in human milk or infant formulas cause adverse effects in infants. Nonetheless, the question is sufficiently important to warrant a consideration of how best to evaluate potential estrogenic risks. We reviewed the types of data available for measuring estrogenic potency as well as methods for estimating health risks from mixtures of chemicals in infant nutrition sources that act via estrogenic mechanisms. We conclude that the science is insufficiently developed at this time to allow a credible assessment of health risks to infants based on estimates of estrogenic potency or on an understanding of toxicologic effects mediated by estrogenic mechanisms. However, clinical and epidemiologic data for infant nutrition sources may provide insights about risks of such substances in human milk and infant formulas.
This article describes issues related to the interpretation, presentation, and use of data from human milk surveillance and research studies. It is hoped that researchers conducting human milk studies in the future will consider these concepts when formulating study conclusions and presenting data. The key issues discussed are; (1) communication of information on human milk constituents to health care providers and the public; (2) complexities associated with assessing risks and benefits when comparing breast-feeding and formula-feeding; (3) use of human milk information for trends analysis and assessment of the efficacy of restrictions on use/release of chemicals in the environment; and (4) risk assessment and regulatory decision-making concepts regarding environmental chemicals in human milk. As researchers conduct surveillance and research involving human milk, it is of the utmost importance that the results of these studies are provided with information on risk and benefits that place the data in perspective, so that those involved in decision making regarding infant nutrition (e.g., expectant mothers, physicians, midwives, nurses, and lactation consultants) can appropriately interpret the research data.
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