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Article ; Online: A commentary on "Core content of the medical school surgical curriculum: Consensus report from the association of surgeons in training (ASIT)".

Brooker-Thompson, Chad

International journal of surgery (London, England)

2021 Volume 88, Page(s) 105927

MeSH term(s)	Consensus ; Curriculum ; Humans ; Schools, Medical ; Surgeons
Language	English
Publishing date	2021-03-20
Publishing country	England
Document type	Letter ; Comment
ZDB-ID	2212038-5
ISSN	1743-9159 ; 1743-9191
ISSN (online)	1743-9159
ISSN	1743-9191
DOI	10.1016/j.ijsu.2021.105927
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Article ; Online: A commentary on "Crisis management for surgical teams and their leaders, lessons from the COVID-19 pandemic; a structured approach to developing resilience or natural organisational responses".

Brooker-Thompson, Chad

International journal of surgery (London, England)

2021 Volume 95, Page(s) 106145

MeSH term(s)	COVID-19 ; Humans ; Pandemics ; SARS-CoV-2
Language	English
Publishing date	2021-10-22
Publishing country	England
Document type	Letter ; Comment
ZDB-ID	2212038-5
ISSN	1743-9159 ; 1743-9191
ISSN (online)	1743-9159
ISSN	1743-9191
DOI	10.1016/j.ijsu.2021.106145
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Article ; Online: Letter to "Chepelev et al. Establishing a quantitative framework for regulatory interpretation of genetic toxicity dose-response data: Margin of exposure case study of 48 compounds with both in vivo mutagenicity and carcinogenicity dose-response data".

Thompson, Chad M / Proctor, Deborah M / Harris, Mark A

Environmental and molecular mutagenesis

2023 Volume 64, Issue 4, Page(s) 259–260

MeSH term(s)	Mutagens/toxicity ; Mutagenesis ; Mutagenicity Tests ; Carcinogenicity Tests ; Carcinogens/toxicity
Chemical Substances	Mutagens ; Carcinogens
Language	English
Publishing date	2023-04-08
Publishing country	United States
Document type	Letter ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	639145-x
ISSN	1098-2280 ; 0893-6692
ISSN (online)	1098-2280
ISSN	0893-6692
DOI	10.1002/em.22537
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Article ; Online: Derivation of oral cancer slope factors for hexavalent chromium informed by pharmacokinetic models and in vivo genotoxicity data.

Thompson, Chad M / Kirman, Christopher / Harris, Mark A

Regulatory toxicology and pharmacology : RTP

2023 Volume 145, Page(s) 105521

Abstract: Hexavalent chromium [Cr(VI)] is present in drinking water from natural and anthropogenic sources at approximately 1 ppb. Several regulatory bodies have recently developed threshold-based safety criteria for Cr(VI) of 30-100 ppb based on evidence that ... ...

Abstract	Hexavalent chromium [Cr(VI)] is present in drinking water from natural and anthropogenic sources at approximately 1 ppb. Several regulatory bodies have recently developed threshold-based safety criteria for Cr(VI) of 30-100 ppb based on evidence that small intestine tumors in mice following exposure to ≥20,000 ppb are the result of a non-mutagenic mode of action (MOA). In contrast, U.S. EPA has recently concluded that Cr(VI) acts through a mutagenic MOA based, in part, on scoring numerous in vivo genotoxicity studies as having low confidence; and therefore derived a cancer slope factor (CSF) of 0.5 (mg/kg-day)
MeSH term(s)	Mice ; Animals ; Chromium/toxicity ; Intestinal Neoplasms/pathology ; Mouth Neoplasms ; Mutagenesis ; Mutagens/toxicity
Chemical Substances	chromium hexavalent ion (18540-29-9) ; Chromium (0R0008Q3JB) ; Mutagens
Language	English
Publishing date	2023-10-19
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	604672-1
ISSN	1096-0295 ; 0273-2300
ISSN (online)	1096-0295
ISSN	0273-2300
DOI	10.1016/j.yrtph.2023.105521
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Article: Commentary on New Formaldehyde Studies in Trp53 Haploinsufficient Mice: Further Support for Nonlinear Risks From Inhaled Formaldehyde.

Thompson, Chad M

Dose-response : a publication of International Hormesis Society

2018 Volume 16, Issue 2, Page(s) 1559325818777931

Language	English
Publishing date	2018-05-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2440820-7
ISSN	1559-3258 ; 1559-3258
ISSN (online)	1559-3258
ISSN	1559-3258
DOI	10.1177/1559325818777931
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Article ; Online: Assessment of the genotoxicity of tert-butyl alcohol in an in vivo thyroid comet assay.

Thompson, Chad M / Dewhurst, Nicole / Moundous, Dmitri / Borghoff, Susan J / Haws, Laurie C / Vasquez, Marie Z

Environmental and molecular mutagenesis

2024

Abstract: Chronic exposure to high (20,000 ppm) concentrations of tert-butyl alcohol (TBA) in drinking water, equivalent to ~2100 mg/kg bodyweight per day, is associated with slight increases in the incidence of thyroid follicular cell adenomas and carcinomas in ... ...

Abstract	Chronic exposure to high (20,000 ppm) concentrations of tert-butyl alcohol (TBA) in drinking water, equivalent to ~2100 mg/kg bodyweight per day, is associated with slight increases in the incidence of thyroid follicular cell adenomas and carcinomas in mice, with no other indications of carcinogenicity. In a recent toxicological review of TBA, the U.S. EPA determined that the genotoxic potential of TBA was inconclusive, largely based on non-standard studies such as in vitro comet assays. As such, the potential role of genotoxicity in the mode of action of thyroid tumors and therefore human relevance was considered uncertain. To address the potential role of genotoxicity in TBA-associated thyroid tumor formation, CD-1 mice were exposed up to a maximum tolerated dose of 1500 mg/kg-day via oral gavage for two consecutive days and DNA damage was assessed with the comet assay in the thyroid. Blood TBA levels were analyzed by headspace GC-MS to confirm systemic tissue exposure. At study termination, no significant increases (DNA breakage) or decreases (DNA crosslinks) in %DNA tail were observed in TBA exposed mice. In contrast, oral gavage of the positive control ethyl methanesulfonate significantly increased %DNA tail in the thyroid. These findings are consistent with most genotoxicity studies on TBA and provide mechanistic support for non-linear, threshold toxicity criteria for TBA. While the mode of action for the thyroid tumors remains unclear, linear low dose extrapolation methods for TBA appear more a matter of policy than science.
Language	English
Publishing date	2024-05-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	639145-x
ISSN	1098-2280 ; 0893-6692
ISSN (online)	1098-2280
ISSN	0893-6692
DOI	10.1002/em.22601
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Article ; Online: A putative adverse outcome network for neonatal mortality and lower birth weight in rodents: Applicability to per- and polyfluoroalkyl substances and relevance to human health.

Rogers, John M / Heintz, Melissa M / Thompson, Chad M / Haws, Laurie C

Birth defects research

2023 Volume 115, Issue 11, Page(s) 1011–1062

Abstract: Background: Some per- and poly-fluoroalkyl substances (PFAS) cause neonatal mortality and lower birth weight in rodents. We constructed an Adverse Outcome Pathway (AOP) network for neonatal mortality and lower birth weight in rodents, comprising three ... ...

Abstract	Background: Some per- and poly-fluoroalkyl substances (PFAS) cause neonatal mortality and lower birth weight in rodents. We constructed an Adverse Outcome Pathway (AOP) network for neonatal mortality and lower birth weight in rodents, comprising three putative AOPs. We then assessed strengths of the evidence for the AOPs and applicability to PFAS. Finally, we considered the relevance of this AOP network to human health. Methods: Literature searches targeted PFAS, peroxisome proliferator-activated receptor (PPAR) agonists, other nuclear receptors, relevant tissues, and developmental targets. We used reviews of established biology and described results of studies with prenatal PFAS exposure that assessed birth weight and neonatal survival. Molecular initiating events (MIEs) and key events (KEs) were proposed and strengths of KE relationships (KERs), applicability to PFAS, and human relevance were assessed. Results: Neonatal mortality has been observed in rodents following gestational exposure to most longer chain PFAS studied, often coincident with lower birth weight. In AOP 1, PPARα activation and PPARγ activation or downregulation are MIEs; placental insufficiency, fetal nutrient restriction, neonatal hepatic glycogen deficit, and hypoglycemia are KEs leading to neonatal mortality and lower birth weight. In AOP 2, constitutive androstane receptor (CAR) and pregnane X receptor (PXR) activation upregulates Phase II metabolism, lowering maternal circulating thyroid hormones. In AOP 3, disrupted pulmonary surfactant function and PPARγ downregulation cause neonatal airway collapse and mortality from respiratory failure. Conclusions: It is likely that different components of this AOP network will apply to different PFAS, largely determined by which nuclear receptors they activate. The MIEs and KEs in this AOP network can occur in humans, but differences in PPAR structure and function, and the timeline of liver and lung development, suggest that humans may be less susceptible to this AOP network. This putative AOP network elucidates knowledge gaps and research needed to better understand the developmental toxicity of PFAS.
MeSH term(s)	Infant, Newborn ; Animals ; Humans ; Pregnancy ; Female ; Birth Weight ; Rodentia ; PPAR gamma ; Placenta ; Infant Mortality ; Fluorocarbons/toxicity
Chemical Substances	PPAR gamma ; Fluorocarbons
Language	English
Publishing date	2023-05-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2104792-3
ISSN	2472-1727
ISSN (online)	2472-1727
DOI	10.1002/bdr2.2185
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Article ; Online: Crypt and Villus Transcriptomic Responses in Mouse Small Intestine Following Oral Exposure to Hexavalent Chromium.

Chappell, Grace A / Wolf, Jeffrey C / Thompson, Chad M

Toxicological sciences : an official journal of the Society of Toxicology

2022 Volume 186, Issue 1, Page(s) 43–57

Abstract: Oral exposure to hexavalent chromium (Cr(VI)) induces tumors in the mouse duodenum. Previous microarray-based transcriptomic analyses of homogenized mouse duodenal tissue have demonstrated Cr(VI)-induced alterations in various cellular pathways and ... ...

Abstract	Oral exposure to hexavalent chromium (Cr(VI)) induces tumors in the mouse duodenum. Previous microarray-based transcriptomic analyses of homogenized mouse duodenal tissue have demonstrated Cr(VI)-induced alterations in various cellular pathways and processes. However, X-ray fluorescence microscopy indicates that chromium localizes primarily to the duodenal villi following exposure to Cr(VI), suggesting that previous transcriptomic analyses of homogenized tissue provide an incomplete picture of transcriptomic responses in the duodenum. Herein, transcriptomic analyses were conducted separately on crypt and villus tissue from formalin-fixed paraffin-embedded transverse duodenal sections from the same study in which microarray-based analyses were previously conducted. A total of 28 groups (7 doses × 2 timepoints × 2 tissue compartments) were analyzed for differential gene expression, dose-response, and gene set enrichment. Tissue compartment isolation was confirmed by differences in expression of typical markers of crypt and villus compartments. Fewer than 21 genes were altered in the crypt compartment of mice exposed to 0.1-5 ppm Cr(VI) for 7 or 90 days, which increased to hundreds or thousands of genes at ≥20 ppm Cr(VI). Consistent with histological evidence for crypt proliferation, a significant, dose-dependent increase in genes that regulate mitotic cell cycle was prominent in the crypt, while subtle in the villus, when compared with samples from time-matched controls. Minimal transcriptomic evidence of DNA damage response in either the crypts or the villi is consistent with published in vivo genotoxicity data. These results are also discussed in the context of modes of action that have been proposed for Cr(VI)-induced small intestine tumors in mice.
MeSH term(s)	Animals ; Chromium/metabolism ; Chromium/toxicity ; Duodenum/metabolism ; Duodenum/pathology ; Intestinal Mucosa ; Mice ; Transcriptome
Chemical Substances	Chromium (0R0008Q3JB) ; chromium hexavalent ion (18540-29-9)
Language	English
Publishing date	2022-01-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	1420885-4
ISSN	1096-0929 ; 1096-6080
ISSN (online)	1096-0929
ISSN	1096-6080
DOI	10.1093/toxsci/kfab152
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Article ; Online: Evaluation of Transcriptomic Responses in Livers of Mice Exposed to the Short-Chain PFAS Compound HFPO-DA.

Heintz, Melissa M / Chappell, Grace A / Thompson, Chad M / Haws, Laurie C

Frontiers in toxicology

2022 Volume 4, Page(s) 937168

Abstract: HFPO-DA (ammonium 2,3,3,3-tetrafluoro-2-(heptafluoropropoxy)-propanoate; CASRN 62037-80-3) is a component of the GenX technology platform used as a polymerization aid in the manufacture of some types of fluoropolymers. The liver is the primary target of ... ...

Abstract	HFPO-DA (ammonium 2,3,3,3-tetrafluoro-2-(heptafluoropropoxy)-propanoate; CASRN 62037-80-3) is a component of the GenX technology platform used as a polymerization aid in the manufacture of some types of fluoropolymers. The liver is the primary target of toxicity for HFPO-DA in rodents and previous examination of hepatic transcriptomic responses in mice following oral exposure to HFPO-DA for 90 days showed induction of peroxisome proliferator-activated receptor signaling pathways, predominantly by PPARα, as well as increased gene expression of both peroxisomal and mitochondrial fatty acid metabolism. To further investigate the mechanism of liver toxicity, transcriptomic analysis was conducted on liver tissue from mice orally exposed to 0, 0.1, 0.5 or 5 mg/kg-bw/day HFPO-DA in a reproduction/developmental toxicity study. Hepatic gene expression changes demonstrated activation of the PPARα signaling pathway. Peroxisomal and mitochondrial fatty acid β-oxidation gene sets were enriched at lower HFPO-DA concentrations, and complement cascade, cell cycle and apoptosis related gene sets were enriched at higher HFPO-DA concentrations. These results support the reported histopathological findings in livers of mice from this study and indicate that the effects of HFPO-DA are mediated through rodent-specific PPARα signaling mechanisms regardless of reproductive status in mice.
Language	English
Publishing date	2022-06-27
Publishing country	Switzerland
Document type	Journal Article
ISSN	2673-3080
ISSN (online)	2673-3080
DOI	10.3389/ftox.2022.937168
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Article ; Online: Comparison of transcriptomic profiles between HFPO-DA and prototypical PPARα, PPARγ, and cytotoxic agents in mouse, rat, and pooled human hepatocytes.

Heintz, Melissa M / Klaren, William D / East, Alexander W / Haws, Laurie C / McGreal, Steven R / Campbell, Rebecca R / Thompson, Chad M

Toxicological sciences : an official journal of the Society of Toxicology

2024

Abstract: Like many per- or polyfluorinated alkyl substances (PFAS), toxicity studies with HFPO-DA (ammonium, 2,3,3,3-tetrafluoro-2-(heptafluoropropoxy)-propanoate), a short-chain PFAS used in the manufacture of some types of fluorinated polymers, indicate that ... ...

Abstract	Like many per- or polyfluorinated alkyl substances (PFAS), toxicity studies with HFPO-DA (ammonium, 2,3,3,3-tetrafluoro-2-(heptafluoropropoxy)-propanoate), a short-chain PFAS used in the manufacture of some types of fluorinated polymers, indicate that the liver is the primary target of toxicity in rodents following oral exposure. Although the current weight of evidence supports the PPARα mode of action (MOA) for liver effects in HFPO-DA-exposed mice, alternate MOAs have also been hypothesized including PPARγ or cytotoxicity. To further evaluate the MOA for HFPO-DA in rodent liver, transcriptomic analyses were conducted on samples from primary mouse, rat and pooled human hepatocytes treated for 12, 24 or 72 hours with various concentrations of HFPO-DA, or agonists of PPARα (GW7647), PPARγ (rosiglitazone), or cytotoxic agents (ie, acetaminophen or d-galactosamine). Concordance analyses of enriched pathways across chemicals within each species demonstrated greatest concordance between HFPO-DA and PPARα agonist GW7647-treated hepatocytes compared to the other chemicals evaluated. These findings were supported by benchmark concentration modeling and predicted upstream regulator results. In addition, transcriptomic analyses across species demonstrated a greater transcriptomic response in rodent hepatocytes treated with HFPO-DA or agonists of PPARα or PPARγ, indicating rodent hepatocytes are more sensitive to HFPO-DA or PPARα/γ agonist treatment. These results are consistent with previously published transcriptomic analyses and further support that liver effects in HFPO-DA-exposed rodents are mediated through rodent-specific PPARα signaling mechanisms as part of the MOA for PPARα activator-induced rodent hepatocarcinogenesis. Thus, effects observed in mouse liver are not appropriate endpoints for toxicity value development for HFPO-DA in human health risk assessment.
Language	English
Publishing date	2024-04-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	1420885-4
ISSN	1096-0929 ; 1096-6080
ISSN (online)	1096-0929
ISSN	1096-6080
DOI	10.1093/toxsci/kfae044
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