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 Anne Fairbrother.
[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cites procedural concerns including potential ghostwriting, undisclosed conflicts of interest, and omission of certain unpublished studies, invoking Committee on Publication Ethics guidelines despite lacking evidence of fraud or scientific flaws.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.
Discussions and applications of the policies and practices of the U.S. Environmental Protection Agency (USEPA) in ecological risk assessment will benefit from continued clarification of the concepts of assessment endpoints and of levels of biological organization. First, assessment endpoint entities and attributes can be defined at different levels of organization. Hence, an organism-level attribute, such as growth or survival, can be applied collectively to a population-level entity such as the brook trout in a stream. Second, assessment endpoints for ecological risk assessment are often mistakenly described as "individual level," which leads to the idea that such assessments are intended to protect individuals. Finally, populations play a more important role in risk assessments than is generally recognized. Organism-level attributes are used primarily for population-level assessments. In addition, the USEPA and other agencies already are basing management decisions on population or community entities and attributes such as production of fisheries, abundance of migratory bird populations, and aquatic community composition.
Sampling methods and results of a gene flow study are described that will be of interest to plant scientists, evolutionary biologists, ecologists, and stakeholders assessing the environmental safety of transgenic crops. This study documents gene flow on a landscape level from creeping bentgrass (Agrostis stolonifera L.), one of the first wind-pollinated, perennial, and highly outcrossing transgenic crops being developed for commercial use. Most of the gene flow occurred within 2 km in the direction of prevailing winds. The maximal gene flow distances observed were 21 km and 14 km in sentinel and resident plants, respectively, that were located in primarily nonagronomic habitats. The selectable marker used in these studies was the CP4 EPSPS gene derived from Agrobacterium spp. strain CP4 that encodes 5-enol-pyruvylshikimate-3-phosphate synthase and confers resistance to glyphosate herbicide. Evidence for gene flow to 75 of 138 sentinel plants of A. stolonifera and to 29 of 69 resident Agrostis plants was based on seedling progeny survival after spraying with glyphosate in greenhouse assays and positive TraitChek, PCR, and sequencing results. Additional studies are needed to determine whether introgression will occur and whether it will affect the ecological fitness of progeny or the structure of plant communities in which transgenic progeny may become established.
Published literature is investigated regarding the response of plants to various substances to determine the sensitivity of agricultural plants versus other species, the similarity of effects seen at different taxonomic levels, sensitivity of plants growing outdoors versus in a greenhouse, and the sensitivity of different measurement endpoints. We find that agricultural species are not consistently more or less sensitive to the herbicides tested than non-crop species. Genus and family taxonomic groupings may show similar responses among species, but this similarity quickly decreases as the comparison progress between orders and classes. Results from field and greenhouse studies are less in agreement between studies than data from the other topics. Shoot length will be affected at concentrations lower than for other vegetative endpoints for most species tested for inorganic substances, but for organic substances root and shoot mass were more sensitive. Overall, there is no one species or endpoint that is consistently the most sensitive for all species or all chemicals in all soils, and differences in bioavailability among compounds may confound comparison of test results. Therefore, species sensitivity distributions, adjusted for bioavailability when possible, should be considered in order to better evaluate effects to non-target terrestrial plants.
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Twenty mallards (Anas platyrhynchos) of both sexes were dosed by oral gavage with Heavi-Shot (H-S; Environ-Metal, Inc., Sweet Home, Oregon, USA) pellets, 20 with steel shot, and 10 with lead (Pb) pellets, all of equal size. All pellets were fired from a shotgun into an absorbent material, retrieved, and weighed prior to introduction into the ducks. Birds were fed whole kernel corn and grit and observed for signs of toxicity for 30 days following dosing. Hevi-Shot pellets lost an average of 6.2% of their mass and steel shot pellets lost 57% of their mass in the birds' gizzards. Almost all (90%) of the Pb shot dosed birds died before the end of the study, while no mortality was observed in the steel or H-S dosed groups. Even though total food consumption differed between the H-S and steel shot groups, mean bird weight change was not different. There were no significant morphologic or histopathologic abnormalities of the liver and kidney in the H-S and steel shot groups. Results indicated that mallards dosed orally with eight No. 4 H-S pellets were not adversely affected over a 30-day period, and that H-S provides another environmentally safe nontoxic shot for use in waterfowl hunting.
In this paper, we critically evaluate the statistical approaches and datasets previously used to derive chronic egg selenium thresholds for mallard ducks (laboratory data) and black-necked stilts (field data). These effect concentration thresholds of 3%, 10% (EC10), or 20% have been used by regulatory agencies to set avian protection criteria and site remediation goals, thus the need for careful assessment of the data. The present review indicates that the stilt field dataset used to establish a frequently cited chronic avian egg selenium threshold of 6 mg/kg dry weight lacks statistical robustness (r2 = 0.19-0.28 based on generalized linear models), suggesting that stilt embryo sensitivity to selenium is highly variable or that factors other than selenium are principally responsible for the increase in effects observed at the lower range of this dataset. Hockey stick regressions used with the stilt field dataset improve the statistical relationship (r2 = 0.90-0.97) but result in considerably higher egg selenium thresholds (EC10 = 21-31 mg/kg dry wt). Laboratory-derived (for mallards) and field-derived (for stilts) teratogenicity EC10 values are quite similar (16-24 mg/kg dry wt). Laboratory data regarding mallard egg inviability and duckling mortality data provide the most sensitive and statistically robust chronic threshold (EC10) with logit, probit, and hockey stick regressions fitted to laboratory data, resulting in mean egg selenium EC10 values of 12 to 15 mg/kg dry weight (r2 = 0.75-0.90).
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Methods for studying the avian immune system have matured during the past two decades, with laboratory studies predominating in earlier years and field studies being conducted only in the past decade. One application has been to determine the potential for environmental contaminants to produce immune suppression, while another research direction is looking at the evolutionary significance of a robust immune system, and the relationship between immune competence and fitness parameters. Laboratory studies of immunosuppression following exposure of birds to environmental contaminants have adapted conventional mammalian methods to the avian immune system, and both lines of research have developed field-deployable measures of immune function. This review describes the avian immune system with emphasis on how it differs from the better known mammalian system, reviews the literature on contaminant-induced immunosuppression, and discusses the work on evolutionary biology of avian immunocompetence. Evidence indicates that the field of avian immunology is technically robust, even for nontraditional species such as passerines, seabirds, raptors, and other free-ranging species. It is now possible to screen chemicals for immunotoxicological properties following the same tiered approach that has been established for mammals. Despite the increased capacity and interest in avian field studies, there has not yet been a reported study of measured immune suppression associated with an avian epizootic. It is more likely that the immune suppression in adult birds resulting from low-level chronic stress (e.g., crowding onto poor quality habitat, food reductions, or climate stress) and (or) environmental contaminants causes slow but consistent morbidity and mortality associated with multiple pathogens, rather than an acute epizootic with a single pathogen. Increased fitness costs associated with such stress may significantly alter genetic diversity and species survival over time.