War on Carcinogens: industry disputes human relevance of chemicals causing cancer in laboratory animals based on unproven hypotheses, using kidney tumors as an example

Our plain-English summary of War on Carcinogens: industry disputes human relevance of chemicals causing cancer in laboratory animals based on unproven hypotheses, using kidney tumors as an example, by R.L. Melnick, J.M. Ward, J. Huff (International Journal of Occupational and Environmental Health, 2013).

The study

• Authors: R.L. Melnick, J.M. Ward, J. Huff
• Journal: International Journal of Occupational and Environmental Health
• Published: 2013;19(4):255-60
• Type of article: Editorial
• Cited by: 7 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Evidence from studies in animals is essential for identifying chemicals likely to cause or contribute to many diseases in humans, including cancers. Yet, to avoid or delay the implementation of protective public health standards, the chemical industry typically denies cancer causation by agents they produce. The spurious arguments put forward to discount human relevance are often based on inadequately tested hypotheses or modes of action that fail to meet Bradford Hill criteria for causation. We term the industry attacks on the relevance of animal cancer findings as the "War on Carcinogens." Unfortunately, this tactic has been effective in preventing timely and appropriate health protective actions on many economically important yet carcinogenic chemicals, including: arsenic, asbestos, benzene, 1,3-butadiene, formaldehyde, methylene chloride, phthalates, tobacco usage, trichloroethylene [TCE], and others. Recent examples of the "War on Carcinogens" are chemicals causing kidney cancer in animals. Industry consultants argue that kidney tumor findings in rats with exacerbated chronic progressive nephropathy (CPN) are not relevant to humans exposed to these chemicals. We dispute and dismiss this unsubstantiated claim with data and facts, and divulge unprofessional actions from a leading toxicology journal.

In plain English

This article was a guest editorial, not a new study, and it reported no new data. The authors argued that industry has disputed whether cancers caused by chemicals in laboratory animals are relevant to people, a pattern they called the "War on Carcinogens". Asbestos was mentioned only in passing, as one such case. Their main example was a hypothesis promoted by Hard and colleagues: that chronic progressive nephropathy (CPN), an age-related rat kidney disease, explains chemically induced kidney cancers in male rats, and that kidney tumors caused by chemicals that also worsen CPN are not relevant to humans. The authors described their own earlier evaluation of National Toxicology Program studies in F344 rats. Among 43 studies with severe CPN in at least one dose group, only 21 chemicals showed some or clear evidence of kidney cancer. In the other 22 studies with severe CPN in male rats, the evidence was equivocal (5) or absent (17). The authors also described a dispute with the journal Toxicological Sciences over their reply to critics, and reprinted that withdrawn letter. The authors concluded that the CPN hypothesis lacked consistency and was unsupported by the data.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Guest editorial (commentary), including a reprinted letter to the editor; no new data
• Who was studied: Not a study population. The authors discussed their earlier evaluation of National Toxicology Program carcinogenicity studies in F344 rats with enhanced chronic progressive nephropathy (CPN).
• Exposure: Chemicals in NTP rat carcinogenicity studies that worsened CPN, including anthraquinone, benzofuran, tetrafluoroethylene, ethyl benzene and t-butyl alcohol. No asbestos exposure was studied; asbestos was only mentioned in the introduction.
• Main results:
  • In the authors' earlier evaluation, among 43 NTP studies in which at least one dose group had severe CPN, only 21 chemicals showed some or clear evidence of kidney carcinogenicity (about 50%).
  • In the 22 other studies with severe CPN in male rats, the evidence of kidney carcinogenic activity was equivocal in 5 and absent in 17.
  • For ethyl benzene, the authors noted that kidney tumors were also increased in female rats without severe CPN.
  • For t-butyl alcohol, the authors noted that female rats had worsened CPN of similar mean severity to male rats but no increase in kidney tumors.
  • The authors reported that the Editor-in-Chief of Toxicological Sciences initially rejected their letter replying to Hard et al. After a later review process, they withdrew the letter and published it in this journal instead.
• The authors' conclusion: The authors concluded that the hypothesis that high-severity CPN causes kidney cancer in rats lacks consistency and is unsupported by the data. In their view, it gives no basis for dismissing the human relevance of these kidney tumors.

Topics

Medical terms in this study, explained in our Lexicon: Causation, Bradford Hill Criteria, Carcinogenic.

Related studies

• Dangerous and cancer-causing properties of products and chemicals in the oil refining and petrochemical industry: Part V--Asbestos-caused cancers and exposure of workers in the oil refining industry — M.A. Mehlman (1991)
• Asbestos disease in maintenance workers of the chemical industry — R. Lilis, S. Daum, et al. (1979)
• Cancer incidence among asbestos-exposed chemical industry workers: an extended observation period — B. Hilt, A. Andersen, et al. (1991)
• Ban on asbestos diaphragms in the chlorine-related chemical industry and efforts toward a worldwide ban — F. Giannasi (2007)
• Regulation of priority carcinogens and reproductive or developmental toxicants — K. Hooper, J. LaDou, et al. (1992)
• After a Century of Research into Environmental Mutagens and Carcinogens, Where Do We Stand? — J.D. Vitorino, P.M. Costa (2023)

Browse more research in International Journal of Occupational and Environmental Health, or return to medical research.