11 environmental triggers of Hashimoto’s

The number of people diagnosed with an underactive thyroid and Hashimoto’s has been on the constant increase since the 1950s, making it one of the most common autoimmune diseases, and the most common hormonal disorder of today [1,2].

In biological terms, such a rapid increase in the number of people with Hashimoto’s and underactive thyroid cannot be explained only by inherited changes within our genes, as it takes at least two generations in order to acquire and transfer gene mutations. Science has found that challenges imposed through our environment indeed can trigger Hashimoto’s [3,4].

We at BOOST want to better understand the impact of the environment and the food we eat on Hashimoto’s and the thyroid gland, and are conducting a scientific survey: we invite you to participate.

In the current scientific literature, several environmental causes are mentioned; 11 of them are listed below.

1. Changes in the cleanliness of our environment.

Evolutionarily speaking, we have spent a large portion of our human history fighting microorganisms that tried to invade our bodies. Our immune system co-evolved with our defence needs through tens of thousands of years, but in the past century our environment turned increasingly hygienic, and our immune system was suddenly left without an invader to fight against. As a result we started developing more allergies and autoimmune diseases [5,6].

2. An excess in dietary iodine,

which can exacerbate Hashimoto’s in people with genetic predisposition, but at the same time iodine helps people with Hashimoto’s to reduce the goiter (an enlargement of the thyroid gland) [7]. Iodine controls production of reactive oxygen species (ROS) in thyroid cells (for more info on this mechanism, please see lower section on “How does the environment trigger Hashimoto’s?” ).

3. Inadequate dietary selenium intake.

Several studies have addressed this topic with more or less success, but there are evidence that selenium in combination with inositol may be beneficial for people with an underactive thyroid, for at least reducing the level of antibodies targeting and destroying the thyroid gland [8,9]. There is one large study underway, which will hopefully confirm or defer the hypothesis [10].

4. Low vitamin D levels or insufficient sun exposure,

although it is not clear if the lower levels of vitamin D might be the part of the cause and the consequence of Hashimoto’s [11,12].

5. Certain anticancer or multiple sclerosis medications,

such as tyrosine kinase inhibitors, antibodies or interferon-α can induce Hashimoto’s and an underactive thyroid [13,14].

6. Repeated and/or chronic infections,

mostly with hepatitis C or a subset of herpesvirus, but also some bacterial infections. This causes ongoing inflammation, which activates many components of our immune system including the part responsible for the onset of autoimmunity [15,16].

7. Living in a vicinity of petrochemical complex,

such as oil refinery [17]. People living in the areas surrounding petrochemical complexes have higher risk of developing anti-thyroid antibodies, and Hashimoto’s.

8. Exposure to certain synthetic pesticides.

There is an increased chance of developing hypothyroidism (an underactive thyroid) if a person was exposed to any insecticides and fungicides, and specifically herbicide paraquat as well as the pesticide maneb/mancozeb [18].

The growth in synthetic pesticides production and use started in 1940s, with DDT being the most popular, and even secured its discoverer a Nobel prize. Only in the 1962 were potentially toxic effects outlined by Rachel Carson in the book “Silent Spring”. Until then food pre-treated with pesticides was considered harmless for the consumption. According to Stockholm Convention on Persistent Organic Pollutants, 9 out of 12 most dangerous and persistent pollutants are pesticides [19].

Pesticide exposure, even from before the person is born, causes increase of the size of thyroid gland (goiter) and the increase in the TPO antibodies, as well as signs of some other autoimmune diseases (including diabetes) [20].

9. Polychlorinated biphenyls (PCBs).

PCBs are a group of human-made chemicals. They started to be produced in the late 1920s and were widely used until the end of 1970s. They were banned or severely restricted in many countries because of environmental concerns. Since PCBs are chemically very stable, about 10% of those produced still remain in our environment today [21].

Before the ban, industries using PCBs were dumping them in water (lakes/rivers). That is the reason PCBs are found in food (mostly fish, meat, milk and eggs) [22] and human samples (blood, milk and fat). PCBs accumulated in mothers are transferred to the offspring through milk. PCBs are very soluble in fats, and can be stored in animal fat cells. Once PCBs enter the fat, they remain there, and this is how the body can accumulate PCBs over time. Although the main route of entry is through eating food containing PCBs, there are other routes: skin, when for example swimming in the water areas with high levels of PCBs, but the amount is generally considered not to be high and/or dangerous, unless repeated frequently. PCBs have been found throughout the world. PCBs can trick our body into mistaking them for hormones, and interrupt our hormonal balance, and they are believed to reduce the concentration of thyroid hormones in our bloodstream [23].

10. Bisphenol-A (BPA),

a chemical produced in massive amounts in the production of polycarbonate plastics, epoxy resins that coat food cans and in dental sealants. BPA is also used in production of flame retardants [24].

BPA can bind to the thyroid hormone receptors, which are virtually present on all the cells in human body, and are necessary for thyroid hormone action, and by that block the thyroid hormone function. It is also shown that the TPO antibody levels increased with increased BPA exposure [22]. One explanation for that might be in an individual’s exposure to BPA even before birth. Research in animals has shown that maternal BPA exposure is causing the increased inflammation in the offspring [25, 26].

BPA gets into our bodies mostly through diet; air and water are other possible sources.

BPA from the protective internal epoxy resin coating, tableware, food storage containers, water or other beverage bottles can contaminate foods and drinks. It is especially dangerous to expose BPA-containing product to high temperature (e.g. microwaving the food inside polycarbonate food container).

11. Irradiation (either accidental or for medical purposes).

Radiotherapy (irradiation for medical purposes) started in the mid 1930s, and is one of the common approaches to treat cancers. Radiotherapy to the head and neck region can destroy the thyroid gland and cause hypothyroidism. About 3 in 10 people receiving radiotherapy develop hypothyroidism, usually within the first five years [27].

Nuclear medicine imaging techniques use iodine radioisotope 131I-iodine, which accumulates in the thyroid gland. Depending on the amount, as 131I-iodine decays, it may cause damage to the thyroid gland function. 131I-iodine is also present as a byproduct after nuclear disasters (such as Fukushima) [28].

Irradiation causes thyroid injury, damaging blood vessels, cells and causing auto-immune reaction. Total dose as well as the size of the irradiated area are the most important factors associated with the risk of developing hypothyroidism [29].

How does the environment trigger Hashimoto’s?

Environmental impact on Hashimoto’s is rapid, and can cause the onset of Hashimoto’s within months or years. One mechanism is that our genetic susceptibilities are triggered by the environment. One example comes from reactive oxygen species (ROS), chemical molecules containing oxygen 30. ROS are a normal byproduct of cellular metabolism, but in high amounts they can cause tissue damage.

One of the most abundant ROS in our bodies is hydrogen peroxide (H2O2). Hydrogen peroxide is produced within thyroid cells and is necessary for our body to make thyroid hormones. However in order to maintain the balance and prevent cellular damage, thyroid cells contain antioxidant which blocks peroxide and protect the cells from peroxide-caused oxidative damage.

In people genetically susceptible to Hashimoto’s certain environmental triggers, might change the peroxide — antioxidants balance, where the increasing amount of peroxide causes activation of molecules responsible for triggering Hashimoto’s [30]. These environmental triggers might be an increase in the iodine intake or activated immune system in response to bacteria, in that case large amounts of hydrogen peroxide will be produced by our own cells to fight the infection [31].

Environmental changes are too fast and are not caused by acquired mutations in our genes. However, there is a change in our immune system that is dependent on the way the information coming from our genes is processed. This is epigenetics, and epigenetic changes to how our genetic code is read are responsible for a rapid onset of a disease. Epigenetic effects are not coded in our DNA, but we can still inherit them from our predecessors and transfer them to our genetic offspring.

Epigenetic changes are one of several proposed mechanisms through which our environment impacts on autoimmune disease development, and so far one of the most plausible ones. Epigenetic changes are most likely induced through infection and inflammation [32–35].


Although there is growing evidence, the research is still not 100% conclusive nor is it decided on the full spectrum of environmental effects and the rate of their contribution to Hashimoto’s.

Hashimoto’s has been medically a long neglected condition, and although there are indications that the number of diagnosed people is on a rapid increase, it is important to note that the disease was not a main focus of diagnosis until very recently, hence this might be a result of an increase in the awareness rather than in the onset of the disease.

Environment clearly plays a role, and it is advisable to avoid the pollutants listed above, but also to be aware that this is not a complete list.


If you want to know more about the most common foods as a trigger of Hashimoto’s, participate in our survey. We will publish anonymized results on our blog and you can see how you compare to other Hashimoto’s patients.


1 Caturegli P, et al. Hashimoto’s thyroiditis: celebrating the centennial through the lens of the Johns Hopkins hospital surgical pathology records, 2013

2 Ott J, et al. The incidence of lymphocytic thyroid infiltration and Hashimoto’s thyroiditis increased in patients operated for benign goiter over a 31-year period, 2011

3 Brodin P, et al. Variation in the human immune system is largely driven by non-heritable influences, 2015

4 Brent GA. Environmental exposures and autoimmune thyroid disease, 2010

5 Chervonsky AV. Influence of microbial environment on autoimmunity, 2010

6 Kondrashova A, et al. The ‘Hygiene hypothesis’ and the sharp gradient in the incidence of autoimmune and allergic diseases between Russian Karelia and Finland, 2010

7 Aghini Lombardi F, et al. The effect of voluntary iodine prophylaxis in a small rural community: the Pescopagano survey 15 years later, 2013

8 van Zuuren EJ, et al. Selenium Supplementation for Hashimoto’s Thyroiditis: Summary of a Cochrane Systematic Review, 2014

9 Drutel A, et al. Selenium and the thyroid gland: more good news for clinicians, 2013

10 Winther, K. H. et al. The chronic autoimmune thyroiditis quality of life selenium trial (CATALYST): study protocol for a randomized controlled trial. Trials 15, 115, (2014).

11 Tamer, G. et al. Relative vitamin D insufficiency in Hashimoto’s thyroiditis. Thyroid 21, 891–896, (2011).

12 D’Aurizio, F. et al. Is vitamin D a player or not in the pathophysiology of autoimmune thyroid diseases? Autoimmun Rev 14, 363–369, (2015).

13 Torino, F. et al. Thyroid dysfunction as an unintended side effect of anticancer drugs. Thyroid 23, 1345–1366, (2013).

14 Daniels, G. H. et al. Alemtuzumab-related thyroid dysfunction in a phase 2 trial of patients with relapsing-remitting multiple sclerosis. J Clin Endocrinol Metab 99, 80–89, (2014).

15 Caselli, E. et al. Virologic and immunologic evidence supporting an association between HHV-6 and Hashimoto’s thyroiditis. PLoS Pathog 8, (2012).

16 Eschler, D. C. et al.Cutting edge: the etiology of autoimmune thyroid diseases. Clin Rev Allergy Immunol 41, 190–197, (2011).

17 de Freitas, C. U. et al. Can living in the surroundings of a petrochemical complex be a risk factor for autoimmune thyroid disease? Environ Res 110, 112–117, (2010).

18 Goldner, W. S. et al. Pesticide use and thyroid disease among women in the Agricultural Health Study. Am J Epidemiol 171, 455–464, (2010).

19 UNEP. Ridding the world of POPs: A guide to the Stockholm Convention on Persistent Organic Pollutants (2005).

20 Langer P. The impacts of organochlorines and other persistent pollutants on thyroid and metabolic health. Front Neuroendocrinol (2010).

21 Duntas, L. H. Environmental factors and autoimmune thyroiditis. Nat Clin Pract Endocrinol Metab 4, 454–460, (2008).

22 La Rocca, C. et al. From environment to food: the case of PCB. Ann Ist Super Sanita 42, 410–416 (2006).

23 Zoeller RT. Polychlorinated Biphenyls as Disruptors of Thyroid Hormone Action. PCBs: Recent Advances in Environmental Toxicology and Health Effects; (2001).

24 Diamanti-Kandarakis E, Bourguignon JP, Giudice LC, et al. Endocrine-disrupting chemicals: an Endocrine Society scientific statement. Endocr Rev,(2009).

25 O’Brien E. et al.Perinatal bisphenol A exposures increase production of pro-inflammatory mediators in bone marrow-derived mast cells of adult mice. J Immunotoxicol (2014).

26 Anderson O.S. et al. Epigenetic responses following maternal dietary exposure to physiologically relevant levels of bisphenol A. Environ Mol Mutagen (2012).

27 Anaya, J. M. et al.The Autoimmune Ecology. Front Immunol 7, 139, (2016).

28 Jereczek-Fossa B.A. et al. Radiotherapy-induced thyroid disorders. Cancer Treat Rev (2004).

29 Ohye H. et al. Dual oxidase, hydrogen peroxide and thyroid diseases. Exp Biol Med (Maywood), (2010).

30 Burek, C. L. et al. Autoimmune thyroiditis and ROS. Autoimmun Rev 7, 530–537, (2008).

31 Jonsson T.J. et al.Structure of the sulphiredoxin-peroxiredoxin complex reveals an essential repair embrace. Nature (2008)

32 Hewagama, A. et al. The genetics and epigenetics of autoimmune diseases. J Autoimmun 33, 3–11, (2009).

33 Farh, K. K. et al. Genetic and epigenetic fine mapping of causal autoimmune disease variants. Nature 518, 337–343, (2015).

34 Brooks, W. H. et al.Epigenetics and autoimmunity. J Autoimmun 34, J207–219, (2010).

35 Tomer, Y. Mechanisms of autoimmune thyroid diseases: from genetics to epigenetics. Annu Rev Pathol 9, 147–156, (2014).