— July 10, 2026 · PFOA and Cancer: Kidney, Testicular, Thyroid and Pancreatic Findings in 32,050 Mid-Ohio Valley Residents and Workers

Table of Contents

1. At a Glance
2. What Was Done
3. What Was Found, Number by Number
4. How PFOA Behaves in the Body
5. How It Fits With Earlier Research
6. What It Cannot Show
7. What Agencies Have Said
8. Since Then: The Companion Mortality Study
9. What Remains Unknown
10. Sources and Primary Documents
11. Key Research Papers
12. Connections

At a Glance

• Paper — Hofmann JN, Tan Y, Barry V, et al. “Perfluorooctanoic acid and cancer incidence: an updated investigation of a cohort in the mid-Ohio Valley.” Environment International 214:110405 (August 2026 issue), published online July 10, 2026. Open access.
• Who — the Division of Cancer Epidemiology and Genetics of the US National Cancer Institute (NCI), Emory University’s Rollins School of Public Health, Mercer School of Medicine and a research data-services contractor. The authors declare no competing interests.
• Design — observational cohort of highly exposed adults, with modelled yearly serum PFOA from 1952 to 2020 summed into a cumulative exposure for each person, and cancer diagnoses through 2020.
• Size — 32,050 participants: 28,398 community members and 3,652 workers.
• What is new — about ten more years of follow-up on average than the earlier analysis, and linkage to a national system that matches study participants against cancer registries across the country.
• Kidney cancer — community members aged 60 or younger, highest exposure group: hazard ratio 1.82 (1.02 to 3.26), trend p = 0.03. Localized (early-stage) kidney cancer, highest group: 1.72 (1.01 to 2.95), trend p = 0.17.
• Testicular cancer — community members, highest exposure group: hazard ratio 3.62 (1.03 to 12.7), trend p = 0.12.
• Thyroid and pancreatic cancer — positive associations (thyroid particularly in women, pancreatic in older participants); among workers, hazard ratios of 1.79 (1.07 to 2.97) for thyroid and 1.70 (1.08 to 2.67) for pancreatic cancer per one-unit step in log-scale cumulative exposure.
• Evidence type — association in a single highly exposed population; it cannot by itself prove that PFOA caused these cancers.

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What Was Done

The community

The study population grew out of the C8 Health Project (“C8” is an older name for PFOA). Over 13 months in 2005 and 2006, 69,030 people from six contaminated water districts in Ohio and West Virginia gave blood samples and health information. Their geometric mean serum PFOA was 32.91 ng/mL, which the project’s 2009 report described as “500% higher than previously reported for a representative American population.” The research team’s companion paper puts the 2005–2006 mean and median at 82.9 and 28.2 ng/mL, against a mean of 4 ng/mL in US adults generally in the same years.

Between 2008 and 2011, adults from that project and workers from the plant were interviewed about their health, homes, jobs and habits, and the diseases they reported were checked against medical records and registries. That cohort was 32,254 people (28,541 community members and 3,713 workers), with participation of 81.5% among community members and 72.9% among workers. The 2026 analysis uses 32,050 of them.

Estimating each person’s exposure

Nobody in the valley had their blood tested every year, so the researchers reconstructed exposure. An earlier modelling study combined the plant’s historical PFOA emissions, how the chemical moves through air, soil and groundwater, each person’s home addresses over time, maps of the public water networks, and a model of how the body absorbs and clears PFOA. For 45,276 community participants, the model’s predicted median serum level for 2005–2006 was 14.2 ppb against an observed 24.3 ppb (rank correlation 0.67); in 1,074 people who had lived and worked in the same water district for five years and reported how much tap water they drank, the figures were 32.2 and 40.0 ppb (correlation 0.82).

For workers, the companion paper describes a job-exposure matrix built from 2,125 historical serum measurements and each person’s work history. The combined estimates for 2005–2006 correlated at 0.71 with 30,303 measured serum levels. The model starts in 1952, the year after the plant’s first PFOA emissions according to the companion paper, and treats exposure as having stopped in 2008, after water filtration was installed and emissions were reduced, with levels then declining each year.

Each person’s yearly estimates are added together into a cumulative serum PFOA figure, which reflects both how high the level was and for how long. That cumulative figure is the exposure measure in the 2026 analysis.

Finding the cancers

The 2026 update extended cancer follow-up by about ten years on average, through 2020, and linked the cohort to the Virtual Pooled Registry–Cancer Linkage System, a system the NCI created with the North American Association of Central Cancer Registries that links a research cohort with central cancer registries across the country in one streamlined process. The authors describe the aim as better characterising cancers of prior interest (kidney and testicular) and exploring others. Hazard ratios were estimated with Cox proportional hazards models adjusted for potential confounding factors.

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What Was Found, Number by Number

A hazard ratio compares the rate of a cancer in a more exposed group with the rate in a less exposed reference group; 1.0 means no difference. The abstract reports two kinds. “HR_Q4” compares the top of four exposure groups (quartiles) with the reference group. “HR_cont” is the change in rate for each one-unit step on the natural-logarithm scale of cumulative exposure, a scale on which each step stands for multiplying exposure, not adding to it. The 95% confidence interval is the range of values compatible with the data; an interval that starts just above 1.0 marks a finding at the edge of statistical significance.

Kidney cancer

• Whole study population: a positive association (the abstract gives no single overall figure).
• Community members aged 60 or younger, highest exposure quartile: HR 1.82 (95% CI 1.02 to 3.26); test for trend across quartiles p = 0.03.
• Localized kidney cancer (disease that had not spread at diagnosis), highest quartile: HR 1.72 (1.01 to 2.95); trend p = 0.17.

When the International Agency for Research on Cancer classified PFOA in 2023, it named renal cell carcinoma, a form of kidney cancer, as one of two cancers with limited evidence in humans. The authors write that the kidney association was “most pronounced” in younger community members and in localized disease.

Testicular cancer

• Community members, highest exposure quartile: HR 3.62 (95% CI 1.03 to 12.7); trend p = 0.12.

Testicular cancer is uncommon (the 2013 analysis of this cohort had 17 cases), and an interval this wide, from barely above 1 to more than 12, is typical of small numbers. The trend test did not reach the usual 0.05 threshold.

Thyroid cancer (new in this analysis)

• Positive associations, “particularly among female participants.”
• Among the more highly exposed workers: HR_cont 1.79 (95% CI 1.07 to 2.97) per one-unit step in log cumulative exposure.

Pancreatic cancer (new in this analysis)

• Positive associations “among older participants.”
• Among the more highly exposed workers: HR_cont 1.70 (95% CI 1.08 to 2.67) per one-unit step in log cumulative exposure.

The authors write that the exposure-response relationships for both thyroid and pancreatic cancer were “strongest among the more highly exposed workers.”

Other cancers, as the team describes them elsewhere

The same researchers’ companion mortality paper, which cites this incidence study, says it “also found a positive association with aggressive brain cancer,” “a borderline positive association with aggressive bladder cancer,” and “an excess of pancreatic cancer, again in older cohort members (>72 years).” Those statements come from the companion paper; the incidence paper’s abstract does not give figures for brain or bladder cancer.

What the abstract does not report

The abstract does not list the number of cases for each cancer, the confounders adjusted for, the hazard ratio for thyroid cancer in women, the age-specific figure for pancreatic cancer, or the exact definition of the reference group. Those details are in the full paper and are not reconstructed here.

The authors’ conclusion

“Our findings in this high PFOA-exposed cohort provide additional epidemiologic evidence of increased kidney and testicular cancer risk, as well as new evidence of associations with thyroid and pancreatic cancers. These findings have important implications regarding our understanding of the carcinogenic potential of PFOA and the cancer burden related to this ubiquitous environmental contaminant.”

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How PFOA Behaves in the Body

A chemical that stays

PFOA belongs to the per- and polyfluoroalkyl substances (PFAS), which the International Agency for Research on Cancer (IARC) notes are “sometimes called ‘forever chemicals’ because they do not degrade easily.” In the body it is cleared slowly. After two water districts in this valley began granular activated carbon filtration in 2007, serum PFOA in 200 residents fell by about 26% a year (95% CI 25% to 28%), consistent with a median half-life of 2.3 years. In Ronneby, Sweden, after contaminated municipal water was replaced at the end of 2013, the estimated PFOA half-life was 2.7 years (2.5 to 2.9). The companion paper cites the US Agency for Toxic Substances and Disease Registry (ATSDR) for a half-life of approximately 2 to 4 years.

A slow clearance rate is why researchers in this community use a cumulative exposure measure. Years of drinking contaminated water build up a body burden that falls only gradually after the source is removed, so a single blood test at one point in time describes only part of a person’s history.

What the mechanism evidence shows

When IARC classified PFOA as carcinogenic to humans in 2023, it cited “strong mechanistic evidence (for epigenetic alterations and immunosuppression) in exposed humans,” and strong mechanistic evidence in human primary cells and experimental systems for those and “several other key characteristics of carcinogens.” Epigenetic alterations are changes in the chemical tags that switch genes on and off; immunosuppression is a weakening of the immune defences that help clear abnormal cells.

What animal studies show

The US Environmental Protection Agency (EPA), in its 2024 drinking-water rule, based its cancer classification of PFOA on “the evidence of kidney and testicular cancer in humans and Leydig cell tumors, pancreatic acinar cell tumors, and hepatocellular tumors in rats.” Leydig cells are hormone-making cells of the testis, acinar cells are the enzyme-making cells of the pancreas, and hepatocellular tumours arise in the liver. The pancreatic signal now reported in people therefore points to an organ where tumours had already been seen in rats. The 2013 analysis of this cohort also noted that no such hepatocellular, testicular or pancreatic tumours were found in male monkeys exposed to PFOA for 26 weeks.

The thyroid

The C8 Science Panel, which studied this community through 2012, reported a probable link between PFOA and (non-cancer) thyroid disease on July 30, 2012. In 2013 the cohort’s researchers wrote that they knew of “no reports of an association between PFOA and thyroid cancer from experimental studies of animals or observational studies of human populations.” How PFOA might act on thyroid tissue is not set out in the 2026 abstract. The site’s thyroid disorders page covers the gland and its common diseases.

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How It Fits With Earlier Research

The 2012 panel findings

On April 16, 2012, the C8 Science Panel reported “a probable link between exposure to C8 (also known as PFOA) and testicular cancer and kidney cancer but not any of the other cancers that were considered.” The panel defined a probable link as a connection that, on the available evidence, was more likely than not. Its other probable-link findings covered high cholesterol, ulcerative colitis, thyroid disease and pregnancy-induced hypertension.

The 2013 cancer analysis of the same cohort

Barry and colleagues followed the 32,254-person cohort with exposure estimated through 2011 and found 2,507 validated cancers of 21 types. For each one-unit step in log cumulative serum PFOA, the hazard ratio was 1.10 (0.98 to 1.24) for kidney cancer and 1.34 (1.00 to 1.79) for testicular cancer. Across exposure quartiles, kidney cancer hazard ratios rose 1.0, 1.23, 1.48 and 1.58 (trend p = 0.18) and testicular cancer 1.0, 1.04, 1.91 and 3.17 (trend p = 0.04).

The same paper’s full text shows how the two newer signals looked then. Thyroid cancer (86 cases) had a hazard ratio of 1.10 (0.95 to 1.26) per log unit, with the association “positive and significant” in plant workers but not community residents. Pancreatic cancer (24 cases) showed no association, 1.00 (0.78 to 1.29). The authors warned that because the cohort was “largely a survivor cohort,” results “must be interpreted with caution, especially for highly fatal cancers such as pancreatic and lung cancer.” Kidney cancer then rested on 105 cases and testicular cancer on 17.

A registry study of the wider area

Vieira and colleagues (2013) examined 7,869 Ohio and 17,238 West Virginia cancer cases diagnosed from 1996 to 2005. Kidney cancer was associated with the very high and high estimated serum categories (adjusted odds ratios 2.0, 1.0 to 3.9, 9 cases; and 2.0, 1.3 to 3.2, 22 cases). The highest estimate was for testicular cancer in the very high category (2.8, 0.8 to 9.2, 6 cases), which the authors called imprecise because of small numbers.

Beyond the valley

In the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial, a large US study of people with ordinary general-population exposure, each doubling of prediagnostic serum PFOA was associated with higher odds of renal cell carcinoma (odds ratio 1.71, 1.23 to 2.37), and the top versus bottom quartile with 2.63 (1.33 to 5.20), among 324 cases and 324 matched controls. A 2021 scoping review by two of the new paper’s authors concluded that “the cancer sites with the most evidence of an association with PFAS are testicular and kidney cancer,” while “overall, the evidence for an association between cancer and PFAS remains sparse.”

For thyroid cancer the wider record is mixed. A 2024 systematic review and meta-analysis found results ranging “from significant positive to significant negative associations,” and its pooled estimates for PFOA and three other PFAS were not statistically significant; the reviewers described “limited knowledge and inconsistent results.” The 2026 thyroid finding therefore adds a signal from a highly exposed group to a literature that has not agreed.

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What It Cannot Show

• Cause and effect. The study measures associations. People with higher estimated exposure may differ in other ways, and adjustment for confounders reduces, but cannot remove, that possibility.
• Modelled, not measured, exposure. Yearly serum levels from 1952 onward are reconstructed. The model agrees reasonably well with blood tests taken in 2005–2006 (correlation 0.71 for the combined estimates), but individual histories carry error. The companion paper judges that this error is likely non-differential, which would tend to push results toward no effect rather than create false ones.
• Subgroups. The clearest kidney result is in community members aged 60 or younger, the testicular result in community members, the thyroid result particularly in women, and the strongest thyroid and pancreatic dose patterns in workers. Splitting data many ways raises the chance that some findings arise by chance.
• Small numbers and wide intervals. The testicular estimate spans 1.03 to 12.7, and two of the reported trend tests (p = 0.12 and 0.17) are above the conventional 0.05 threshold.
• A survivor cohort. Most participants were enrolled alive in 2005–2006. The 2013 analysis warned that this can hide cases among people who died earlier, especially for highly fatal cancers such as pancreatic cancer.
• Workers are a smaller group. The worker findings for thyroid and pancreatic cancer come from 3,652 of the 32,050 participants.
• A highly exposed population. Serum levels here were many times the national average, so the size of any risk at ordinary background exposure cannot be read directly from these results.
• This report rests on the abstract. Case counts, full tables and the authors’ own discussion of limitations were not available to this site, so none of them is reproduced here.

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What Agencies Have Said

International Agency for Research on Cancer (December 1, 2023)

A Working Group of 30 experts from 11 countries met in Lyon from November 7 to 14, 2023 and classified PFOA as carcinogenic to humans (Group 1) and PFOS as possibly carcinogenic to humans (Group 2B). For PFOA, the agency cited sufficient evidence in experimental animals and strong mechanistic evidence in exposed humans, and “limited evidence for cancer in humans (renal cell carcinoma and testicular cancer).” A summary appeared in The Lancet Oncology; two of the 2026 paper’s authors are among its authors. The agency also reported that “the general population is exposed mainly via food and drinking-water,” and that “at contaminated sites, drinking-water is the main exposure source for the general population.”

US Environmental Protection Agency (April 26, 2024)

The EPA’s final PFAS National Primary Drinking Water Regulation (89 FR 32532, docket EPA-HQ-OW-2022-0114, effective June 25, 2024) set the health-based goal for PFOA and PFOS at zero and the enforceable maximum contaminant level at 4.0 nanograms per litre (parts per trillion) for each. It also set limits of 10 ng/L for PFHxS, PFNA and HFPO-DA and a hazard index for mixtures. The rule required public water systems to comply with the limits by April 26, 2029. In the same rule the EPA designated PFOA and PFOS “Likely to Be Carcinogenic to Humans.” The companion paper notes that an earlier EPA recommendation had been 70 parts per trillion.

US Environmental Protection Agency (May 20, 2026)

On May 20, 2026, before the paper appeared, the EPA published two proposals. One (91 FR 29425, docket EPA-HQ-OW-2025-1742) would extend the compliance date for the PFOA and PFOS limits from April 26, 2029 to April 26, 2031 for water systems that submit a request; it concerns the deadline, not the 4.0 ng/L level. The other (91 FR 29413, docket EPA-HQ-OW-2025-0654) would rescind the limits for PFHxS, PFNA, HFPO-DA and the PFBS mixture, but not for PFOA or PFOS. The EPA held a public hearing on July 7, 2026, and comments on both were open until July 20, 2026.

US Food and Drug Administration (February 28, 2024)

The FDA announced that PFAS grease-proofing materials were no longer being sold for use in US food packaging; the site’s account is at PFAS grease-proofing leaves US food packaging.

On the new paper

No press release, news coverage or agency statement about this paper was found when this article was researched.

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Since Then: The Companion Mortality Study

August 30, 2026. The same team published a companion study in Environment International that followed the cohort for deaths through 2021, using the National Death Index. Among 32,081 participants there were 5,709 deaths, examined across 22 causes.

• Brain cancer deaths rose with log cumulative exposure: hazard ratio 1.25 (1.05 to 1.50).
• Bladder cancer showed a suggestive association that did not reach statistical significance: 1.17 (0.98 to 1.39).
• Pancreatic cancer deaths after age 72 rose with exposure: 1.23 (1.05 to 1.43).
• Kidney cancer deaths were few (31 as the underlying cause), and the trend was not statistically significant (p = 0.49).
• Exposure did not increase the all-cause death rate. Testicular and thyroid cancer could not be studied because few people die of them.

The authors wrote that “caution is warranted due to multiple comparisons.” The study was funded by the NCI Intramural Research Program, and its authors declared no competing interests. As of October 12, 2026, the Federal Register showed no final EPA action on either of the May 2026 drinking-water proposals.

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What Remains Unknown

• Whether the thyroid and pancreatic associations will appear in other highly exposed populations, and whether they reflect a causal effect.
• Why the kidney association was clearest in community members aged 60 or younger, and the thyroid association in women.
• How much of the worker findings reflects their higher exposures and how much reflects the smaller size of that group.
• What level of risk, if any, applies at the much lower PFOA levels found in the general population, although the screening-trial kidney study points to an association at ordinary levels.
• How PFOA might act on human thyroid and pancreatic tissue; the rat pancreatic tumours offer one lead, but no matching thyroid evidence was cited in 2013.
• The full set of results, case counts and stated limitations in the paper itself, which this report could not read.

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Sources and Primary Documents

Every figure attributed to the 2026 incidence study comes from its published abstract and its PubMed and Crossref records. Descriptions of the cohort’s exposure model and of other cancers come from the research team’s companion paper (full text read in PubMed Central) and from the earlier papers listed under Key Research Papers.

1. Hofmann JN, Tan Y, Barry V, Taylor A, Winquist A, Hyer M, et al. (2026). Perfluorooctanoic acid and cancer incidence: an updated investigation of a cohort in the mid-Ohio Valley. Environment International 214:110405. — doi:10.1016/j.envint.2026.110405 · PubMed PMID: 42442238
2. Tan Y, Hofmann JN, Barry V, Winquist A, Silverman DT, Steenland K (2026). Mortality study of a PFOA-exposed cohort in the mid-Ohio Valley. Environment International 215:110492. — doi:10.1016/j.envint.2026.110492 · PubMed PMID: 42691635
3. International Agency for Research on Cancer (December 1, 2023). IARC Monographs evaluate the carcinogenicity of perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS). — IARC news release
4. Environmental Protection Agency (April 26, 2024). PFAS National Primary Drinking Water Regulation. Final rule, 89 FR 32532, Docket EPA-HQ-OW-2022-0114. — Federal Register document 2024-07773
5. Environmental Protection Agency (May 20, 2026). Extending the Compliance Deadline for the PFOA and PFOS Maximum Contaminant Levels. Proposed rule, 91 FR 29425, Docket EPA-HQ-OW-2025-1742. — Federal Register document 2026-10086
6. Environmental Protection Agency (May 20, 2026). Rescission of Regulatory Determinations and Removal of Related Provisions for Four PFAS Substances. Proposed rule, 91 FR 29413, Docket EPA-HQ-OW-2025-0654. — Federal Register document 2026-10085
7. C8 Science Panel. Probable Link Reports (cancer report dated April 16, 2012). — C8 Science Panel probable link findings
8. North American Association of Central Cancer Registries. About the Virtual Pooled Registry Cancer Linkage System (VPR-CLS), coordinated by the association with funding from the National Cancer Institute. — NAACCR: About VPR-CLS

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Key Research Papers

Background papers on the cohort, its exposure model, earlier cancer findings, the 2023 classification and PFOA’s half-life. Each entry was checked against PubMed and Crossref before it was written down.

1. Frisbee SJ, Brooks AP, Maher A, Flensborg P, Arnold S, Fletcher T, et al. (2009). The C8 health project: design, methods, and participants. Environmental Health Perspectives 117(12):1873-1882. — PubMed PMID: 20049206
2. Shin HM, Vieira VM, Ryan PB, Steenland K, Bartell SM (2011). Retrospective exposure estimation and predicted versus observed serum perfluorooctanoic acid concentrations for participants in the C8 Health Project. Environmental Health Perspectives 119(12):1760-1765. — PubMed PMID: 21813367
3. Winquist A, Lally C, Shin HM, Steenland K (2013). Design, methods, and population for a study of PFOA health effects among highly exposed mid-Ohio valley community residents and workers. Environmental Health Perspectives 121(8):893-899. — PubMed PMID: 23735518
4. Barry V, Winquist A, Steenland K (2013). Perfluorooctanoic acid (PFOA) exposures and incident cancers among adults living near a chemical plant. Environmental Health Perspectives 121(11-12):1313-1318. — PubMed PMID: 24007715
5. Vieira VM, Hoffman K, Shin HM, Weinberg JM, Webster TF, Fletcher T (2013). Perfluorooctanoic acid exposure and cancer outcomes in a contaminated community: a geographic analysis. Environmental Health Perspectives 121(3):318-323. — PubMed PMID: 23308854
6. Zahm S, Bonde JP, Chiu WA, Hoppin J, Kanno J, Abdallah M, et al. (2024). Carcinogenicity of perfluorooctanoic acid and perfluorooctanesulfonic acid. The Lancet Oncology 25(1):16-17. — PubMed PMID: 38043561
7. Shearer JJ, Callahan CL, Calafat AM, Huang WY, Jones RR, Sabbisetti VS, et al. (2021). Serum concentrations of per- and polyfluoroalkyl substances and risk of renal cell carcinoma. Journal of the National Cancer Institute 113(5):580-587. — PubMed PMID: 32944748
8. Steenland K, Winquist A (2021). PFAS and cancer, a scoping review of the epidemiologic evidence. Environmental Research 194:110690. — PubMed PMID: 33385391
9. van Gerwen M, Chung T, Monaghan M, Vermeulen R, Petrick L, Leung AM (2024). Per- and polyfluoroalkyl substances (PFAS) exposure and thyroid cancer: systematic review and meta-analysis. Toxicology Letters 399:52-58. — PubMed PMID: 39047923
10. Bartell SM, Calafat AM, Lyu C, Kato K, Ryan PB, Steenland K (2010). Rate of decline in serum PFOA concentrations after granular activated carbon filtration at two public water systems in Ohio and West Virginia. Environmental Health Perspectives 118(2):222-228. — PubMed PMID: 20123620
11. Li Y, Fletcher T, Mucs D, Scott K, Lindh CH, Tallving P, et al. (2018). Half-lives of PFOS, PFHxS and PFOA after end of exposure to contaminated drinking water. Occupational and Environmental Medicine 75(1):46-51. — PubMed PMID: 29133598

PubMed Topic Searches

1. PubMed: PFOA and kidney cancer
2. PubMed: PFOA and testicular cancer
3. PubMed: PFAS and thyroid cancer
4. PubMed: PFOA and pancreatic cancer
5. PubMed: The C8 Health Project

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Connections

• News Archive
• PFAS — the “forever chemicals” in water, food and blood
• PFAS Leaves US Food Packaging (2024) — the FDA’s grease-proofing phase-out
• Kidney Cancer — the cancer most consistently linked to PFOA in this community
• Renal Cell Carcinoma — the kidney cancer type IARC named for PFOA
• Testicular Cancer — the second cancer IARC named for PFOA
• Thyroid Cancer — one of the two new associations in the 2026 update
• Pancreatic Cancer — the other new association, also seen in rat studies
• Thyroid Disorders — non-cancer thyroid disease, a 2012 probable-link finding
• Tap-Water Disinfection Byproducts and Uterine Cancer — another July 2026 drinking-water cancer study
• Household Chemicals — everyday chemical exposures in the home
• Plastics and Packaging — the site’s category for PFAS, BPA and related chemicals
• Toxins — the site’s section on environmental and dietary toxins

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