Prose narrative derived directly from the COI audit table (Völkel, Teeguarden, LaKind and related review/panel literature), with superscripted numerical footnotes keyed to a citation table.

Overview

The audit table captures a recurring pattern in the BPA literature: a small number of high‑influence papers and reviews are repeatedly used to support broad conclusions about internal dose (“free BPA” in serum), toxicokinetics (rapid first‑pass conjugation after oral intake), and population exposure (intake back‑calculated from urinary biomonitoring). Where these nodes shape public-facing reassurance or regulatory modeling, conflicts of interest matter—not as proof of incorrect science, but as an interpretive context that can affect framing, choice of comparisons, sensitivity analyses, and how uncertainty is communicated. The narrative below follows the table’s structure and preserves each entry’s disclosed funding/affiliations, its role in debate, and the recurring criticisms noted in COI discussions.

Across the studies summarized here, the main scientific claims fall into three categories. First are arguments that reported serum “free BPA” is frequently attributable to contamination rather than true circulating levels.^1,6 Second are controlled human toxicokinetic studies supporting extensive first‑pass metabolism after oral ingestion (with low systemic free BPA).^3,5 Third are biomonitoring-to-intake translations that conclude typical population intakes are low relative to prevailing guidance values.^4,7 The COI signals in the table cluster most clearly around industry trade-group sponsorship of key “low exposure/contamination” narratives, particularly via the ACC Polycarbonate/BPA Global Group (Global Alliance).¹²

A. Contamination control and the “free BPA in serum” dispute

Dekant & Völkel’s 2008 biomonitoring review is frequently cited to argue that many published reports of “free BPA” in serum are implausible given known metabolism and are more consistent with contamination introduced during collection, processing, or analysis.¹ In policy debates, the review’s influence is amplified because it provides a concise narrative: rapid conjugation should leave little unconjugated BPA in blood after oral exposure, so unexpectedly high serum values are treated as a red flag for artefact.¹ The COI relevance highlighted in the table is that the review disclosed partial support from the Polycarbonate/BPA Global Group under the ACC—an industry trade association representing manufacturers and stakeholders with a direct interest in BPA risk framing.¹² As a result, the paper is often treated as both a scientific position and an industry‑adjacent position within the broader controversy.⁹

Teeguarden et al. (2013) reinforces this contamination-centered skepticism from a different funding posture. In that Food and Chemical Toxicology review, the authors argue that many “typical” serum BPA concentrations reported in the literature appear inconsistent with established toxicokinetics, and they emphasize contamination control as essential for credible serum measurements.⁶ The audit table notes that this review reported U.S. EPA STAR grant support and stated no competing financial interests, making it a methodological ally of contamination skepticism without an industry sponsorship signal in the funding statement.⁶

Teeguarden et al. (2015) adds controlled human data in the same argumentative direction. In a soup‑ingestion design, the study reports extensive first‑pass metabolism over 24 hours and presents evidence against meaningful sublingual absorption under that scenario—an important point because “sublingual bypass” is sometimes invoked to reconcile high serum BPA reports with rapid hepatic conjugation.⁵ The table flags COI concerns because the 2015 study acknowledges funding from the ACC Polycarbonate/BPA Global Group (and describes FDA support for certain laboratory activities). Although the authors declared no competing interests, the trade-group grant source is regularly cited in COI discussions because the study’s conclusions are strategically relevant to the serum‑BPA controversy.^5,12 In short, the contamination/low‑free‑BPA thesis is supported by both industry‑funded and non‑industry‑funded sources in this set, but the table’s purpose is to keep the sponsorship context visible when the thesis is used as a broad dismissal of contrary biomonitoring findings.

B. Oral first-pass metabolism and “low bioavailability” as a regulatory backbone

Völkel et al. (2002) is repeatedly treated as cornerstone human PK evidence for the “low bioavailability” model: after low oral doses, BPA is rapidly metabolized (primarily to conjugates) with low measurable free BPA in circulation.³ The audit table lists the study’s support as described in its disclosures (German Environment Agency support; with related institutional equipment support described in later disclosures). The COI signal here is not industry funding per se, but the study’s downstream policy role: it is often used to justify modeling assumptions that treat oral BPA exposure as efficiently neutralized by first‑pass conjugation.³ The table also notes limitations that recur in critiques—small cohorts and the possibility that an oral‑dose paradigm may not capture all real‑world exposure routes or sources of variability in internal dose.

Völkel, Kiranoglu & Fromme (2008) complements this framework with biomonitoring in urine. By measuring free and total BPA in human urine and using those data to assess daily uptake, the paper concludes that daily exposure is low and below guidance values.⁴ In the audit table, this study is noted as having later declarations indicating no external funding and being conducted within a public health authority context (Bavarian Health and Food Safety Authority).⁴ The key interpretive point is methodological: biomonitoring-to-intake back‑calculations depend strongly on PK assumptions (excretion fractions, timing, and steady‑state approximations). Thus, even absent a clear COI signal, the study’s influence in risk characterization makes its assumptions and uncertainty framing part of the critical-reading burden.

C. Urinary biomonitoring and intake estimation: where assumptions and COI intersect

LaKind & Naiman (2011) is a central population-intake paper because it back‑calculates daily BPA intake from NHANES urinary biomonitoring (2005–2006) and reports low average intakes.⁷ The audit table flags explicit COI relevance: the paper’s disclosures include consulting relationships spanning government and industry contexts, and the work is described as supported by the Polycarbonate/BPA Global Group.^7,12 Because this study is frequently cited to argue that exposures fall below regulatory thresholds, the funding and consulting disclosures are consequential: they sit at the interface between a technical modeling exercise (intake estimation from urine) and a public health narrative (population exposure is “low”).⁷ The table’s critique emphasis is that the numerical intake estimates are sensitive to assumptions about excretion fractions and the episodic, short‑lived nature of BPA exposure, meaning that “low intake” conclusions can be fragile to model structure and sampling design.

LaKind et al. (2019) broadens the focus from a single-country intake estimate to how national biomonitoring data are interpreted across multiple countries, using BPA as a case study. The paper is often used in methodological debates about cross‑country comparisons and interpretation pitfalls for short‑lived chemical biomarkers.⁸ The COI significance in the audit table is primarily contextual: the author affiliation includes LaKind Associates (private consulting), and readers are encouraged to consult the paper’s own disclosure section and interpretive framing in light of the broader consulting role reflected across related BPA publications.⁸

D. Consensus reviews and declared interests: the Hengstler panel as an archetype

Hengstler et al. (2011), published in Critical Reviews in Toxicology, exemplifies how panel‑style reviews can consolidate contested evidence into a posture of reassurance. The panel argued (as assessed at that time) that BPA was unlikely to pose significant risk at prevailing exposures.² The audit table highlights explicit declared interests: the panel included an employee of Bayer; the declaration noted that Völkel reported prior support from the BPA Global Group; and the declaration referenced industry sponsorship connected to a guest author’s participation.^2,12 Because such reviews are repeatedly cited in regulatory and media contexts, the declared interests matter: they provide a concrete basis for readers to scrutinize how uncertainties are weighted and which studies are treated as authoritative when competing lines of evidence exist.⁹

The table also notes that later regulatory positions diverged, underscoring that apparent “consensus” can shift. EFSA’s April 2023 re‑evaluation adopted a much lower tolerable daily intake for BPA, while the U.S. FDA’s public position around the same period maintained that BPA is safe for currently approved food‑contact uses at current exposure levels.^10,11 This divergence is not itself evidence of COI, but it is relevant to COI interpretation: it demonstrates that different institutions can legitimately reach different risk conclusions based on endpoint selection, evidentiary weighting, and evolving standards—making it even more important to track how funding and declared interests intersect with the most policy‑leveraged claims in the literature.

Interpretive synthesis: what the COI pattern does—and does not—prove

The COI signals captured in the audit table do not establish that any particular dataset is invalid. Instead, they identify where financially interested parties intersect with the most consequential narrative pivots in BPA disputes: whether serum “free BPA” findings should be treated as artefact; whether oral exposure is effectively neutralized by first‑pass metabolism; and whether population intakes inferred from urine are reliably “low.”^1,3,5,7,12 When industry trade-group sponsorship aligns with conclusions that down‑weight internal exposure or risk, a prudent reader does not dismiss the science outright—but does demand clearer documentation of methods, contamination controls, sensitivity analyses, and uncertainty framing, and gives added attention to independent replication and triangulation across study designs.

Conflict-Of-Interest-Audit of BPA Studies by Völkel, Teeguarden, and LaKind

This dossier summarizes key publications by three frequently cited BPA researchers (Völkel, Teeguarden, LaKind), with attention to their study claims, funding sources, conflicts of interest (COI), regulatory uptake, and critiques. It is intended as an audit-ready reference for evaluating the weight regulators (FDA vs. EFSA) place on these studies.

References (verified; superscript numbers in text)

1. Dekant, W., & Völkel, W. (2008). Human exposure to bisphenol A by biomonitoring: methods, results and assessment of environmental exposures. Toxicology and Applied Pharmacology, 228(1), 114–134. doi:10.1016/j.taap.2007.12.008 | PubMed — Accessed January 4, 2026.

2. Hengstler, J. G., et al. (2011). Critical evaluation of key evidence on the human health hazards of exposure to bisphenol A. Critical Reviews in Toxicology, 41(4), 263–291. doi:10.3109/10408444.2011.558487 | PMC full text — Accessed January 4, 2026.

3. Völkel, W., Colnot, T., Csanady, G. A., Filser, J. G., & Dekant, W. (2002). Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Chemical Research in Toxicology, 15(10), 1281–1287. doi:10.1021/tx025548t | PubMed — Accessed January 4, 2026.

4. Völkel, W., Kiranoglu, M., & Fromme, H. (2008). Determination of free and total bisphenol A in human urine to assess daily uptake as a basis for a valid risk assessment. Toxicology Letters, 179(3), 155–162. doi:10.1016/j.toxlet.2008.05.002 | PubMed — Accessed January 4, 2026.

5. Teeguarden, J. G., Twaddle, N. C., Churchwell, M. I., Yang, X., Fisher, J. W., Seryak, L. M., & Doerge, D. R. (2015). 24-hour human urine and serum profiles of bisphenol A: Evidence against sublingual absorption following ingestion in soup. Toxicology and Applied Pharmacology, 288(2), 131–142. doi:10.1016/j.taap.2015.01.009 | PubMed | CDC-hosted PDF — Accessed January 4, 2026.

6. Teeguarden, J. G., Hanson-Drury, S., Fisher, J. W., & Doerge, D. R. (2013). Are typical human serum BPA concentrations measurable and sufficient to be estrogenic in the general population? Food and Chemical Toxicology, 62, 949–963. doi:10.1016/j.fct.2013.08.001 — Accessed January 4, 2026.

7. LaKind, J. S., & Naiman, D. Q. (2011). Daily intake of bisphenol A and potential sources of exposure: 2005–2006 National Health and Nutrition Examination Survey. Journal of Exposure Science and Environmental Epidemiology, 21(3), 272–279. doi:10.1038/jes.2010.9 | PDF — Accessed January 4, 2026.

8. LaKind, J. S., Pollock, T., Naiman, D. Q., Kim, S., Nagasawa, A., & Clarke, J. (2019). Factors affecting interpretation of national biomonitoring data from multiple countries: Bisphenol A as a case study. Environmental Research, 173, 318–329. doi:10.1016/j.envres.2019.03.047 | PubMed — Accessed January 4, 2026.

9. Rust, S. (2011, April 28). Industry linked to study supporting safety of plastics chemical BPA. Center for Public Integrity. Article — Accessed January 4, 2026.

10. U.S. Food and Drug Administration. (2023, April 20). Bisphenol A (BPA): Use in food contact application. FDA page — Accessed January 4, 2026.

11. European Food Safety Authority. (n.d.). Bisphenol A (BPA) (topic page; notes April 2023 re-evaluation). EFSA topic page — Accessed January 4, 2026.

12. American Chemistry Council. (n.d.). Polycarbonate/Bisphenol A (BPA) Global Alliance. ACC page — Accessed January 4, 2026.