Skip to main content

Evaluating adverse effects of environmental agents in food: a brief critique of the US FDA’s criteria



In the US, the Food and Drug Administration (US FDA) is charged with protecting the safety of food from both pathogens and chemicals used in food production and food packaging. To protect the public in a transparent manner, the FDA needs to have an operational definition of what it considers to be an “adverse effect” so that it can take action against harmful agents. The FDA has recently published two statements where, for the first time, it defines the characteristics of an adverse effect that it uses to interpret toxicity studies.


In this brief review, we examine two recent actions by the FDA, a proposed rule regarding a color additive used in vegetarian burgers and a decision not to recall fish with high levels of scombrotoxin. We evaluated the FDA’s description of the criteria used to determine which outcomes should be considered adverse.


We describe three reasons why the FDA’s criteria for “adverse effects” is not public health protective. These include an unscientific requirement for a monotonic dose response, which conflates hazard assessment and dose response assessment while also ignoring evidence for non-linear and non-monotonic effects for many environmental agents; a requirement that the effect be observed in both sexes, which fails to acknowledge the many sex- and gender-specific effects on physiology, disease incidence and severity, and anatomy; and a requirement that the effects are irreversible, which does not acknowledge the role of exposure timing or appreciate transgenerational effects that have been demonstrated for environmental chemicals.


The FDA’s criteria for identifying adverse effects are inadequate because they are not science-based. Addressing this is important, because the acknowledgement of adverse effects is central to regulatory decisions and the protection of public health.

Peer Review reports

The US Food and Drug Administration (FDA) is charged with protecting the safety of the nation's foods [1] from pathogens, such as E. coli, as well as from chemicals used in the production of food and food packaging. Both chemicals and pathogens can cause adverse health effects, but the specific adverse effects of their exposures are very different. For example, the US Centers for Disease Control and Prevention (CDC) estimates that 48 million Americans will become ill each year from pathogens and “unspecified agents” causing acute foodborne illnesses [2]; of these, 3,000 people (about 0.1% of the American population) will die. In contrast, greater than 95% of Americans (hundreds of millions of people) are exposed every day to chemicals found in food, and exposures to these chemicals have been shown to increase the risk of chronic, rather than acute, health effects [3].

An agent has the potential to produce an adverse effect by virtue of its fundamental properties (e.g., it may be a carcinogen, a developmental toxicant, etc.). Thus, a central feature of “risk assessment” is the identification of an “adverse effect” caused by the hazard, and the “potency” of the hazard on that adverse effect. The adverse effect is a health “endpoint”, or measurement of something that a regulatory agency would consider to be important enough to regulate a chemical or pathogen to protect human health. For some pathogens, like specific strains of E. coli that cause death, the adverse effects of exposure are relatively straightforward. For other hazards, like chemicals such as phthalates or perfluoroalkyl and polyfluoroalkyl substances (PFAS) that are commonly found in food and food packaging [4, 5], exposures have been associated with increased incidence of various chronic diseases (or biomarkers of disease) [6,7,8]; in these cases, determining which measurable endpoints affected by environmental exposures are “adverse” is less simple [9, 10] but remains critical.

Until recently, the FDA has not provided an objective, transparent explanation of what the agency considers an “adverse effect”[11]. This is important because an observed effect must be considered adverse for it to be used in a regulatory decision; in other words, if there is no adverse effect, no risk is anticipated and no action will be taken by a regulatory agency. The opacity of what the FDA considers an adverse effect makes it difficult for the consuming public to know whether any risk assessment is sufficient to protect public health. In addition, identification of the most sensitive adverse effect is critical for public health protection [10]. For example, if an agent causes death at one dose, but contributes to the incidence of type 2 diabetes at a million-fold lower dose, it is not public health protective to regulate on the basis of the exposure that causes death.

The FDA has recently written two decisions in which it defined the general characteristics it considers as an “adverse effect”. These declarations raise serious concern about how the agency defines and identifies adverse outcomes so that it can set total daily exposure limits that are health protective. In the first, the FDA was responding to objections raised by the Center for Food Safety on the agency’s proposed final rule regarding a color additive used in vegetarian burgers to make them appear more like ground beef [12]. The FDA wrote: “For an observed effect to be toxicologically relevant (i.e., potentially adverse), a clear dose–response should be seen (e.g., increasing the dose of a test substance causes an increase in the observed effect in the test subjects), and the observed effect should occur in both sexes of test species” [12] [emphasis added]. In the second example, the FDA investigated poisoning by scombrotoxin, which occurs when fish are not properly refrigerated and high levels of histamine are produced [13]. The FDA declined to pursue a mandatory recall of affected fish because “scombrotoxin fish poisoning causes temporary or medically reversible adverse health consequences” such as nausea, diarrhea, blurred vision, and respiratory distress [emphasis added] [14]. The public would likely question whether these outcomes would be considered inconsequential, and there is no further justification for why a medically treatable outcome should be ignored by a regulatory agency charged with protecting the public’s health. Furthermore, in some cases, individuals exposed to scrombotoxin can experience life-threatening anaphylactic reactions or cardiovascular conditions requiring hospitalization, especially if these individuals have other conditions that increase their medical vulnerability [15].

These actions by the FDA provide an explicit description of the criteria used by the agency to determine which outcomes, induced by chemicals, agents, or pathogens in food, are considered adverse. They shed light on a process that has been criticized for its lack of transparency both by the regulated and scientific communities [16]. But with this transparency comes a stunning realization that FDA is not basing its risk assessments on a logical footing. Rather, there are several well-established scientific observations that require rejection of these criteria because they are neither health protective nor adequate. These observations are:

  1. 1)

    Requiring a “clear dose response” where “increasing the dose of a test substance causes an increase in the observed effect” (e.g., monotonicity). This is problematic for two reasons. The first is pragmatic: it conflates the dose response evaluation with hazard identification itself, which are two separate and independent steps in a risk assessment. In other words, with the FDA’s current approach, a chemical or agent will not be identified as a hazard unless it is considered a potential risk. The second problem is scientific: in defining a “clear dose response” as a monotonic relationship between exposure and effect, the FDA ignores well-known non-monotonic relationships that can exist between dose and effect for a range of substances including environmental chemicals, pharmaceuticals, hormones, vitamins, and essential nutrients [17, 18]. The FDA’s own data on pharmaceuticals recognizes that low doses can induce undesirable effects that are opposite to those observed at higher doses. An example comes from Lupron, a drug that acts as an agonist for the Gonadotropin Releasing Hormone (GnRH) receptor which is used for the treatment of numerous hormone-mediated diseases including prostate cancer, endometriosis, female infertility, polycystic ovarian syndrome, and uterine fibroids. When a patient with a disease like endometriosis is first administered Lupron, the lower circulating concentrations can increase the adverse symptoms associated with endometriosis including ectopic growth of uterine tissue [19], whereas continued exposure producing higher circulating levels of Lupron is used to manage the disease [20]. Similarly, when breast cancer patients first start taking the drug tamoxifen, low serum concentrations can increase bone and tumor pain as well as localized tumor flare (i.e., growth) whereas at higher serum concentrations, tumor growth is inhibited [21, 22].

    A related issue is that the FDA has dismissed the presence of non-monotonic dose responses for chemicals found in food. For example, after stakeholders claimed that “FDA does not recognize that some substances have a greater adverse effect at low doses than at medium doses, which is one example of what is referred to as a nonmonotonic dose–response relationship”, the FDA responded in a November 2022 report from the US Government Accountability Office [23] that “they have reviewed the scientific literature but found that the available studies do not support concerns about health effects associated with nonmonotonic dose–response relationships.”

  2. 2)

    Requiring that the effect is observed in both sexes. This is problematic because it does not acknowledge that males and females are physiologically and anatomically different, and therefore provides no guidance for how the FDA might consider adverse effects that occur in the gonads or primary/secondary sex organs and other tissues that exhibit sex-specific responses. It fails to recognize that disease incidence, course of progression, and severity differ between males and females for a number of conditions including cardiovascular diseases, autoimmune diseases, neurological and psychiatric disorders, asthma, and some cancers [24, 25]. Males and females also experience pain differently [26], have differences in the sizes of different brain regions as well as the age at which brain volume reaches its peak [27], and differences in their gut microbiota, with implications for disease susceptibility [28]. Finally, although females have long been excluded from many clinical trials, there is strong evidence for sex differences in the metabolism of hormones, drugs, and other chemicals [29, 30].

  3. 3)

    Requiring that adverse effects be irreversible. This is problematic for two reasons. First: it assumes that exposures are transient. Yet, if the inducing agent is found in foods consumed daily, effects that would not seem severe if they were only induced once (like a headache or diarrhea), could occur more often. This is certainly the case for many chemicals used in food production and packaging (e.g., bisphenols, phthalates, perchlorate) which are found in the vast majority of human urine samples despite relatively short residence time in humans, documenting chronic exposures [31]. Second: the FDA’s reasoning assumed that all individuals are equally vulnerable (e.g., that they would only fall victim to the less serious outcomes like nausea, diarrhea, and blurred vision). With scombrotoxin fish poisoning, it is clear that some individuals are more vulnerable to its effects; in fact, while the dosage of scombrotoxin considered toxic is 1 mg/g fish consumed, many individuals will not have disease responses after exposure to these high doses, whereas other individuals will have reactions after exposures as low as 0.05 mg/g fish [32]. The presumption that all individuals are equally vulnerable is never evidence-based or justifiable. With hormones, hormonally active agents, and teratogens, the effects of even low doses can have permanent effects on embryos, fetuses and/or neonates when exposures occur during vulnerable periods of development, whereas exposures in adults produce effects that are often reversible once exposures cease [33,34,35]. FDA scientists acknowledged in a peer-reviewed journal article that they understand this basic fact [36]. This very brief analysis of FDA’s recent operational definition of adverse effects demonstrates that these are not scientifically defensible criteria to identify a hazard or characterize the risk posed by these agents. This analysis also indicates that a clear operational definition of an adverse effect is needed to support health-protective actions by the agency.

How are adverse effects defined by other regulatory agencies? The US EPA characterizes an adverse effect as any “biochemical change, functional impairment, or pathologic lesion that affects the performance of the whole organism, or reduces an organism’s ability to respond to an additional environmental challenge” [37]. Other international regulatory agencies use the definition put forth by the Organization for Economic Co-operation and Development (OECD): “a change in morphology, physiology, growth, development or lifespan of an organism which results in impairment of functional capacity or impairment of capacity to compensate for additional stress or increase in susceptibility to the harmful effects of other environmental influences” [38]. Thus, defining an “adverse effect” has not prevented other agencies from identifying hazards, or understanding never-before-seen health effects as they arise, and FDA should be similarly transparent and science-based.

There are many steps that the FDA, and other regulatory agencies, must take to improve chemical safety assessments and risk assessments to protect the public from hazardous agents in food. These include identifying the most sensitive, disease-relevant outcomes measurable in experimental studies [39]; changing practices with regard to the reliance on historical controls, which are often used to dismiss effects of environmental chemicals [40]; abolishing the use of “experts” hired by the chemical manufacturer, and thus relying on individuals with financial conflicts of interest to declare food chemicals “generally recognized as safe”, even in the absence of toxicity data [41]; and implementing strategies to consider the cumulative effects of chemicals, i.e., where multiple chemicals affect common outcomes or the same chemical is present in many products [42]. There is also a need for the FDA to be transparent in the agency’s decision-making processes, publish guidelines for how the agency will assess data and deal with data gaps, and develop improved techniques to systematically review the available literature and use all data in decision-making processes.

It is also clear that the FDA uses very different approaches to evaluate safety of chemicals depending on how they are intended to be used: non-monotonicity is understood in the context of drugs (e.g., Lupron and tamoxifen), but dismissed in the context of food chemicals; outcomes that would be considered adverse “side effects” requiring disclosure to patient administered drugs (e.g., nausea, diarrhea, blurred vision, and respiratory distress) are not automatically considered adverse if induced by food chemicals. This disconnect between the two sides of this federal agency argues against their claim of decision-making that is objective and based on science.

These recent decisions from the FDA have demonstrated that the agency must be compelled to describe the criteria that are used to determine if an outcome is adverse, and those criteria must be scientifically justified. These criteria should also be subject to dynamic revisions as advances in scientific knowledge become available. Protecting the nation’s food supply is a big and important task; this task should be done consistently and correctly. To do so begins with a rational, transparent, consistent, and science-based definition of which health outcomes the FDA deems concerning enough to protect the public.

Availability of data and materials

Not applicable.


  1. Drexler M. Foodborne Illness: Who monitors our food?, vol. 21 Jan 2020. Waltham: Schuster Institute for Investigative Journalism at Brandeis University; 2011.

    Google Scholar 

  2. CDC. Estimates of Foodborne illness in the United States. 2018. Accessed 21 Jan 2020.

  3. Groh KJ, Backhaus T, Carney-Almroth B, Geueke B, Inostroza PA, Lennquist A, Leslie HA, Maffini M, Slunge D, Trasande L, et al. Overview of known plastic packaging-associated chemicals and their hazards. Sci Total Environ. 2019;651(Pt 2):3253–68.

    Article  CAS  Google Scholar 

  4. Muncke J, Andersson AM, Backhaus T, Boucher JM, Carney Almroth B, Castillo Castillo A, Chevrier J, Demeneix BA, Emmanuel JA, Fini JB, et al. Impacts of food contact chemicals on human health: a consensus statement. Environ Health. 2020;19(1):25.

    Article  Google Scholar 

  5. Geueke B, Groh KJ, Maffini MV, Martin OV, Boucher JM, Chiang YT, Gwosdz F, Jieh P, Kassotis CD, Łańska P et al. Systematic evidence on migrating and extractable food contact chemicals: Most chemicals detected in food contact materials are not listed for use. Crit Rev Food Sci Nutr 2022:1–11.

  6. Maffini MV, Geueke B, Groh K, Carney Almroth B, Muncke J. Role of epidemiology in risk assessment: a case study of five ortho-phthalates. Environ Health. 2021;20(1):114.

    Article  CAS  Google Scholar 

  7. Radke EG, Wright JM, Christensen K, Lin CJ, Goldstone AE, Lemeris C, Thayer KA. Epidemiology Evidence for Health Effects of 150 per- and Polyfluoroalkyl Substances: A Systematic Evidence Map. Environ Health Perspect. 2022;130(9):96003.

    Article  CAS  Google Scholar 

  8. Qi W, Clark JM, Timme-Laragy AR, Park Y. Per- and Polyfluoroalkyl Substances and Obesity, Type 2 Diabetes and Non-alcoholic Fatty Liver Disease: A Review of Epidemiologic Findings. Toxicol Environ Chem. 2020;102(1–4):1–36.

    Article  CAS  Google Scholar 

  9. Gore AC, Chappell VA, Fenton SE, Flaws JA, Nadal A, Prins GS, Toppari J, Zoeller RT. EDC-2: The Endocrine Society’s Second Scientific Statement on Endocrine-Disrupting Chemicals. Endocr Rev. 2015;36(6):E1-150.

    Article  CAS  Google Scholar 

  10. Woodruff TJ, Zeise L, Axelrad DA, Guyton KZ, Janssen S, Miller M, Miller GG, Schwartz JM, Alexeeff G, Anderson H, et al. Meeting report: moving upstream-evaluating adverse upstream end points for improved risk assessment and decision-making. Environ Health Perspect. 2008;116(11):1568–75.

    Article  Google Scholar 

  11. Zoeller RT, Bergman A, Becher G, Bjerregaard P, Bornman R, Brandt I, Iguchi T, Jobling S, Kidd KA, Kortenkamp A, et al. A path forward in the debate over health impacts of endocrine disrupting chemicals. Environ Health. 2014;13(1):118.

    Article  Google Scholar 

  12. US FDA: Listing of Color Additives Exempt From Certification; Soy Leghemoglobin. In., vol. 21 CFR 73. Federal Register; 2019: 69620–69626.

  13. Scombrotoxin Poisoning and Decomposition.

  14. Outbreak Investigation of Scombrotoxin Fish Poisoning: Yellowfin/Ahi Tuna (November 2019).

  15. Tortorella V, Masciari P, Pezzi M, Mola A, Tiburzi SP, Zinzi MC, Scozzafava A, Verre M. Histamine poisoning from ingestion of fish or scombroid syndrome. Case Rep Emerg Med. 2014;2014:482531.

    Google Scholar 

  16. Maffini MV, Alger HM, Bongard ED, Neltner TG. Enhancing FDA’s evaluation of science to ensure chemicals added to human food are safe: workshop proceedings. Comp Rev Food Sci Food Safety. 2011;10(5):321–41.

    Article  Google Scholar 

  17. Vandenberg LN, Colborn T, Hayes TB, Heindel JJ, Jacobs DR Jr, Lee DH, Shioda T, Soto AM, vom Saal FS, Welshons WV, et al. Hormones and endocrine-disrupting chemicals: low-dose effects and nonmonotonic dose responses. Endocr Rev. 2012;33(3):378–455.

    Article  CAS  Google Scholar 

  18. Zoeller RT, Vandenberg LN. Assessing dose-response relationships for endocrine disrupting chemicals (EDCs): a focus on non-monotonicity. Environ Health. 2015;14(1):42.

    Article  Google Scholar 

  19. Hall LL, Malone JM, Ginsburg KA. Flare-up of endometriosis induced by gonadotropin-releasing hormone agonist leading to bowel obstruction. Fertil Steril. 1995;64(6):1204–6.

    Article  CAS  Google Scholar 

  20. US FDA. Full prescribing information: Lupron Depot 11.25 mg for management of endometriosis. 2018.

  21. US FDA: Full prescribing information: Soltamox (tamoxifen citrate) oral solution for management of estrogen-receptor positive breast cancer. 2018.

  22. Welshons WV, Thayer KA, Judy BM, Taylor JA, Curran EM, vom Saal FS. Large effects from small exposures: I. Mechanisms for endocrine-disrupting chemicals with estrogenic activity. Environ Health Perspect. 2003;111:994–1006.

    Article  CAS  Google Scholar 

  23. US Government Accountability Office. FOOD SAFETY: FDA Oversight of Substances Used in Manufacturing, Packaging, and Transporting Food Could Be Strengthened. 2022.

  24. Ober C, Loisel DA, Gilad Y. Sex-specific genetic architecture of human disease. Nat Rev Genet. 2008;9(12):911–22.

    Article  CAS  Google Scholar 

  25. Dorak MT, Karpuzoglu E. Gender differences in cancer susceptibility: an inadequately addressed issue. Front Genet. 2012;3:268.

    Article  Google Scholar 

  26. Pieretti S, Di Giannuario A, Di Giovannandrea R, Marzoli F, Piccaro G, Minosi P, Aloisi AM. Gender differences in pain and its relief. Ann Dell’ist Super Sanita. 2016;52(2):184–9.

    Google Scholar 

  27. Lenroot RK, Giedd JN. Sex differences in the adolescent brain. Brain Cogn. 2010;72(1):46–55.

    Article  Google Scholar 

  28. Krishnan KC, Mehrabian M, Lusis AJ. Sex differences in metabolism and cardiometabolic disorders. Curr Opin Lipidol. 2018;29(5):404.

    Article  Google Scholar 

  29. Barus R, Bergeron S, Chen Y, Gautier S. Sex differences: From preclinical pharmacology to clinical pharmacology. Therapie 2022.

  30. Zucker I, Prendergast BJ, Beery AK. Pervasive Neglect of Sex Differences in Biomedical Research. Cold Spring Harb Perspect Biol. 2022;14(4):a039156.

    CAS  Google Scholar 

  31. Przybyla J, Geldhof GJ, Smit E, Kile ML. A cross sectional study of urinary phthalates, phenols and perchlorate on thyroid hormones in US adults using structural equation models (NHANES 2007–2008). Environ Res. 2018;163:26–35.

    Article  CAS  Google Scholar 

  32. Bartholomew BA, Berry PR, Rodhouse JC, Gilbert RJ, Murray CK. Scombrotoxic fish poisoning in Britain: features of over 250 suspected incidents from 1976 to 1986. Epidemiol Infect. 1987;99(3):775–82.

    Article  CAS  Google Scholar 

  33. Newbold RR. Developmental exposure to endocrine-disrupting chemicals programs for reproductive tract alterations and obesity later in life. Am J Clin Nutr. 2011;94(Suppl):1939S-1942S.

    Article  CAS  Google Scholar 

  34. Heindel JJ, Vandenberg LN. Developmental origins of health and disease: a paradigm for understanding disease cause and prevention. Curr Opin Pediatr. 2015;27(2):248–53.

    Article  CAS  Google Scholar 

  35. Diamanti-Kandarakis E, Bourguignon JP, Giudice LC, Hauser R, Prins GS, Soto AM, Zoeller RT, Gore AC. Endocrine-disrupting chemicals: an Endocrine Society scientific statement. Endocr Rev. 2009;30(4):293–342.

    Article  CAS  Google Scholar 

  36. Neal-Kluever A, Aungst J, Gu Y, Hatwell K, Muldoon-Jacobs K, Liem A, Ogungbesan A, Shackelford M. Infant toxicology: state of the science and considerations in evaluation of safety. Food Chem Toxicol. 2014;70:68–83.

    Article  CAS  Google Scholar 

  37. Integrated Risk Information Systems (IRIS) Glossary.

  38. (IPCS) IPoCS. IPCS risk assessment terminology. Geneva: World Health Organization; 2004.

    Google Scholar 

  39. Birnbaum LS, Bucher JR, Collman GW, Zeldin DC, Johnson AF, Schug TT, Heindel JJ. Consortium-based science: The NIEHS’s multipronged, collaborative approach to assessing the health effects of Bisphenol A. Environ Health Perspect. 2012;120(12):1640–4.

    Article  CAS  Google Scholar 

  40. Vandenberg LN, Prins GS, Patisaul HB, Zoeller RT. The Use and Misuse of Historical Controls in Regulatory Toxicology: Lessons from the CLARITY-BPA Study. Endocrinology. 2019.

    Article  Google Scholar 

  41. Neltner TG, Alger HM, O’Reilly JT, Krimsky S, Bero LA, Maffini MV. Conflicts of interest in approvals of additives to food determined to be generally recognized as safe: out of balance. JAMA Intern Med. 2013;173(22):2032–6.

    Article  Google Scholar 

  42. Maffini MV, Neltner TG. Brain drain: the cost of neglected responsibilities in evaluating cumulative effects of environmental chemicals. J Epidemiol Community Health. 2015;69(5):496–9.

    Article  Google Scholar 

Download references

Author information

Authors and Affiliations



LNV and RTZ wrote the first draft of the manuscript. GSP and LT provided critical edits and comments. All authors reviewed the manuscript. The author(s) read and approved the final manuscript.

Corresponding author

Correspondence to Laura N. Vandenberg.

Ethics declarations

Competing interests

LNV, RTZ, GSP and LT have received travel reimbursements from Universities, Governments, NGOs and Industry. All authors’ research has been funded by US government agencies. LNV has also received research funding from the University of Massachusetts Amherst, and NGOs including the Cornell Douglas Foundation, the Allen Family Foundation, and the Great Neck Breast Cancer Coalition. She is a scientific advisor to Sudoc LLC. RTZ’s research has been funded by government agencies in the US and EU and he serves as a scientific advisor to Sudoc LLC. GSP has received funding from the NIH and Department of Defense. LT acknowledges honoraria from Houghton Mifflin Harcourt, Audible, Paidos and Kobunsha; travel support from the Endocrine Society, WHO, UNEP, Japan Environment and Health Ministries and the American Academy of Pediatrics; as well as scientific advisory board activities for Ahimsa, Beautycounter, IS-Global and Footprint.

Additional information

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and Permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Vandenberg, L.N., Zoeller, R.T., Prins, G.S. et al. Evaluating adverse effects of environmental agents in food: a brief critique of the US FDA’s criteria. Environ Health 22, 38 (2023).

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI:


  • Hazard assessment
  • Pharmaceutical
  • Lupron
  • Gender difference
  • Transparency
  • Endocrine disrupting chemical