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Hazard-based regulation to curb environmental impacts on health

If CEPA was indeed protecting public health, we would expect declining diseases associated with anthropogenic exposures, rather than the opposite.

Yes, today children are exposed to lower levels of tobacco smoke, some old pesticides, and lead in drinking water, gasoline exhaust and paint. Unfortunately, endocrine-related obesity and metabolic syndrome, disorders of early development and sexual differentiation, and cancers in hormone-sensitive tissues (e.g., breast, prostate, thyroid) have not been prevented. This is as groups of chemicals (e.g., phthalates, bisphenols, flame retardants and some pesticides) remain in commerce, in water, food and products, in homes, schools and the workplace, and in the environment, for decades before being restricted or banned.

Endocrine disruption does not follow a classic dose-response, and can be perpetuated under risk-based management. Endocrine disrupting chemicals (EDCs) require actions based on their innate hazard. With many thousands of EDCs, classes of similar chemicals require group actions.

Single-chemical regulation does not work, and Canadian-led research highlights how aggregate effects of low dose mixtures of chemicals can cause cancer.1 This explains today’s increasing health conditions associated with altered signalling in hormone-driven endocrine systems. Examples include: disorders of sexual development and reproduction; obesity, metabolism and diabetes; neurological development and function; and some cancers. As well, intergenerational effects occur even when the genetic code is not mutated; rather, epigenetic changes that affect expression and suppression of particular genes, can alter susceptibility to dysfunction and disease. Higher prevalence is seen in racialized2 and more highly exposed populations.

Examples of adverse trends in public health linked to toxicants include:

  • Extensive basic research illuminating interacting mechanisms3 of chemicals in cellular signalling,4,5 gene expression (epi-genetic effects),6 metabolism (including oxidative stress), development and health as a result of environmental exposures and the microbiome,7,8 from pre-conception and across the life span.9 
  • Although historically exceedingly rare in children, prevalence of type 2 diabetes now exceeds that of type 1 diabetes in Canadian youth. In Manitoba, where rates are up to 20-fold higher than in some other areas of Canada, type 2 diabetes increased from 9 to 21 per 100,000 children <18 years of age between 2006 and 2011.10 Type 2 diabetes is also increasing rapidly in Ontario children.11 Potentially informing aetiology, a prospective nurses’ study report and review describes associations between plasma levels of persistent toxicants and diabetes, as well as interactions with weight changes (Fatty tissue is thought to be protective because it sequesters lipophilic toxicants, that are released into the bloodstream and other tissues during weight loss).12
  • Storage of toxic chemicals in fat, evident with increased blood levels of toxicants with weight loss, may underlie numerous adverse conditions.13,14,15 The “obesity paradox” where adipose tissue appears to be protective against disease has been noted for cancer (with cautions regarding analytical complexities),16 heart failure and mortality in patients with diabetes,17 and increasing population-adjusted rates of certain cancers, many of which are hormone-related;18
  • Obesity increases risks for about a dozen cancers.19,20 In Canada, smoking-related cancers are decreasing as smoking rates have fallen, but obesity- and endocrine-related cancers are increasing,18 although early detection and treatment can help to avert severe disease. Scientists recently found that SARS-CoV-2 can infect fat cells, thus predisposing obese patients to a more severe disease and worse outcomes with COVID-19;21
  • Male genital birth defects clustered in agricultural regions of Nova Scotia, in contrast with non-endocrine mediated congenital abnormalities that were not clustered;22
  • Lymphoid leukemia incidence rate in Manitoba children increased between 1984 and 2013, with variations by geographic area (suspected to be related to unidentified environmental agents);23
  • Autoimmune disease is increasing rapidly in developed countries.24 Canada ranks globally among the highest rates of inflammatory bowel disease in children, driven by increasing incidence in the youngest children of 6.5% annually;25
  • Inflammatory bowel disease predisposes to colorectal cancer, which is increasing 7% annually in Canadian adolescents and young adults26 (the similar rates are thought to be associated);
  • Neurological development can be impacted by many toxicants,27 such as metals lead,28 mercury 29 and manganese,30 and endocrine disruptors such as bisphenol-A (BPA),31 to name a few. Increases in prevalence and incidence of treated attention-deficit hyperactivity disorder (ADHD) were not uniform across Canadian provinces, suggesting non-uniform contributors to the condition;32
  • Recent research reviews life-changing biological impacts of volatile chemicals and the myriad of scented products in daily use.33


1.         Goodson WH, Lowe L, Gilbertson M, Carpenter DO. Testing the low dose mixtures hypothesis from the Halifax project. Reviews on Environmental Health. 2020 18;35(4):333–57.

2.         Waldron I. Environmental Racism in Canada. The Canadian Encyclopedia; 2022

3.         Androutsopoulos VP, Hernandez AF, Liesivuori J, Tsatsakis AM. A mechanistic overview of health associated effects of low levels of organochlorine and organophosphorous pesticides. Toxicology. 2013;307:89–94.

4.         Diamanti-Kandarakis E, Bourguignon JP, Giudice LC, Hauser R, Prins GS, Soto AM, et al. Endocrine-Disrupting Chemicals: An Endocrine Society Scientific Statement. Endocr Rev. 2009;30(4):293–342.

5.         Gore AC, Chappell VA, Fenton SE, Flaws JA, Nadal A, Prins GS, et al. EDC-2: The Endocrine Society’s Second Scientific Statement on Endocrine-Disrupting Chemicals. Endocrine Reviews. 2015 Dec;36(6):E1–150.

6.         Barouki R, Melén E, Herceg Z, Beckers J, Chen J, Karagas M, et al. Epigenetics as a mechanism linking developmental exposures to long-term toxicity. Environment International. 2018 May [cited 2018 Mar 6];114:77–86.

7.         National Academies of Sciences E. Environmental Chemicals, the Human Microbiome, and Health Risk: A Research Strategy. 2017

8.         Claus SP, Guillou H, Ellero-Simatos S. The gut microbiota: a major player in the toxicity of environmental pollutants? Biofilms and Microbiomes. 2016;2:16003. Available from:

9.         Lo CL, Zhou FC. Environmental Alterations of Epigenetics Prior to the Birth. Int Rev Neurobiol. 2014;115:1–49.

10.       Halipchuk J, Temple B, Dart A, Martin D, Sellers EAC. Prenatal, Obstetric and Perinatal Factors Associated with the Development of Childhood-Onset Type 2 Diabetes. Canadian Journal of Diabetes. 2017

11.       Nakhla M, Rahme E, Simard M, Guttmann A. Outcomes associated with a pediatric clinical diabetes network in Ontario: a population-based time-trend analysis. cmajo. 2017;5(3):E586–93.

12.       Zong G, Valvi D, Coull B, Göen T, Hu FB, Nielsen F, et al. Persistent organic pollutants and risk of type 2 diabetes: A prospective investigation among middle-aged women in Nurses’ Health Study II. Environment International. 2018

13.       Teixeira D, Pestana D, Santos C, Correia-Sá L, Marques C, Norberto S, et al. Inflammatory and Cardiometabolic Risk on Obesity: Role of Environmental Xenoestrogens. J Clin Endocrinol Metab. 2015;100(5):1792–801.

14.       Janesick AS, Blumberg B. Obesogens: an emerging threat to public health. American Journal of Obstetrics and Gynecology. 2016;214(5):559–65.

15.       van den Dungen MW, Murk AJ, Kok DE, Steegenga WT. Persistent organic pollutants alter DNA methylation during human adipocyte differentiation. Toxicology in Vitro. 2017;40:79–87.

16.       Curtis JP, Selter JG, Wang Y, Rathore SS, Jovin IS, Jadbabaie F, et al. The Obesity Paradox: Body Mass Index and Outcomes in Patients With Heart Failure. Arch Intern Med. 2005 Jan;165(1):55–61.

17.       Tseng CH. Obesity paradox: Differential effects on cancer and noncancer mortality in patients with type 2 diabetes mellitus. Atherosclerosis. 2013;226(1):186–92.

18.       Canadian Cancer Society, Statistics Canada, Public Health Agency of Canada, Provincial/Territorial Cancer Registries. Canadian Cancer Statistics. 2017.

19.       National Cancer Institute. Obesity and Cancer. National Cancer Institute. 2017

20.       Gallagher EJ, LeRoith D. Obesity and Diabetes: The Increased Risk of Cancer and Cancer-Related Mortality. Physiological Reviews. 2015 Jul 1;95(3):727–48.

21.       Martínez-Colón GJ, Ratnasiri K, Chen H, Jiang S, Zanley E, Rustagi A, et al. SARS-CoV-2 infection drives an inflammatory response in human adipose tissue through infection of adipocytes and macrophages. Science Translational Medicine. 2022 Sep;0(0):eabm9151.

22.       Lane C, Boxall J, MacLellan D, Anderson PA, Dodds L, Romao RLP. A population-based study of prevalence trends and geospatial analysis of hypospadias and cryptorchidism compared with non-endocrine mediated congenital anomalies. J Pediatr Urol. 2017;13(3):284.e1-284.e7.

23.       Ye X, Torabi M, Lix LM, Mahmud SM. Time and spatial trends in lymphoid leukemia and lymphoma incidence and survival among children and adolescents in Manitoba, Canada: 1984-2013. PLOS ONE. 2017;12(4):e0175701.

24.       Lerner A, Jeremias P, Matthias T. The World Incidence and Prevalence of Autoimmune Diseases is Increasing. International Journal of Celiac Disease, International Journal of Celiac Disease. 2015;3(4):151–5.

25.       Benchimol EI, Bernstein CN, Bitton A, Carroll MW, Singh H, Otley AR, et al. Trends in Epidemiology of Pediatric Inflammatory Bowel Disease in Canada: Distributed Network Analysis of Multiple Population-Based Provincial Health Administrative Databases. Am J Gastroenterol. 2017;112(7):1120–34.

26.       Brenner DR, Heer E, Sutherland RL, Ruan Y, Tinmouth J, Heitman SJ, et al. National Trends in Colorectal Cancer Incidence Among Older and Younger Adults in Canada. JAMA Netw Open. 2019;2(7):e198090–e198090.

27.       Tran NQV, Miyake K. Neurodevelopmental Disorders and Environmental Toxicants: Epigenetics as an Underlying Mechanism. Int J Genomics. 2017

28.       Lanphear BP, Hornung R, Khoury J, Yolton K, Baghurst P, Bellinger DC, et al. Low-Level Environmental Lead Exposure and Children’s Intellectual Function: An International Pooled Analysis. Environ Health Perspect. 2005;113(7):894–9. Available from:

29.       Newland MC, Bailey JM. Behavior Science and Environmental Health Policy: Methylmercury as an Exemplar. Policy Insights from the Behavioral and Brain Sciences. 2017;4(1):96–103.

30.       Claus Henn B, Schnaas L, Ettinger AS, Schwartz J, Lamadrid-Figueroa H, Hernández-Avila M, et al. Associations of Early Childhood Manganese and Lead Coexposure with Neurodevelopment. Environmental Health Perspectives. 2011;120(1):126–31.

31.       Braun JM, Kalkbrenner AE, Calafat AM, Yolton K, Ye X, Dietrich KN, et al. Impact of Early-Life Bisphenol A Exposure on Behavior and Executive Function in Children. PEDIATRICS. 2011;128(5):873–82.

32.       Vasiliadis HM, Diallo FB, Rochette L, Smith M, Langille D, Lin E, et al. Temporal Trends in the Prevalence and Incidence of Diagnosed ADHD in Children and Young Adults between 1999 and 2012 in Canada: A Data Linkage Study. Can J Psychiatry. 2017;62(12):818–26.

33.       Patel S. Fragrance compounds: The wolves in sheep’s clothings. Medical Hypotheses. 2017;102:106–11.