Industrial Pollution's Link To Hypothyroidism: A Concern?

Industrial pollution is a major cause of concern for thyroid health. The thyroid is a small but vital endocrine gland that regulates cardiovascular and neurological function and supports immunity, metabolism, and energy levels. It is susceptible to damage from environmental toxins due to the chemical structure of the hormones it produces.

Industrial chemicals such as dioxin, perchlorate, perfluorinated chemicals, and polychlorinated biphenyls (PCBs) negatively affect thyroid function. Dioxin, a byproduct of manufacturing, reduces thyroid function by mimicking thyroid hormone structure and decreasing thyroxine (T4) levels. Perchlorate, used in airbags, batteries, and jet/rocket fuel, competes with iodine for uptake into the thyroid gland and reduces thyroid hormone production. PFCs, found in mattresses and detergents, disrupt thyroid function by either increasing or decreasing thyroid hormone production. PCBs, used in electrical equipment and adhesives, reduce the number of receptors available for triiodothyronine (T3) to bind to and decrease the amount of T4 circulating in the bloodstream.

Heavy metals such as aluminum, cadmium, lead, and mercury also damage the thyroid. Aluminum, found in deodorant and over-the-counter medications, oxidizes the thyroid and inhibits iodide uptake. Cadmium, released by mining and smelting, triggers thyroid enlargement and can induce thyroid cancer. Lead, found in old housing paint, some jewelry, and children's toys, has been linked to reduced thyroid function. Mercury, found in seafood and dental amalgams, lowers iodide uptake and prevents thyroid hormone production.

Pesticides, herbicides, and fungicides also weaken thyroid function and can cause hypothyroidism. These agricultural agents alter thyroid hormone gene expression, prevent the uptake of iodine, and promote thyroid hormone removal from the body.

The most common thyroid diseases, Hashimoto Thyroiditis and Graves' Disease, are autoimmune thyroid diseases (AITD) that affect the thyroid by recruiting antibodies to attack it. Research has found that AITD is caused by a combination of environmental toxicity and genetic predisposition.

Industrial chemicals and persistent organic pollutants (POPs)

Industrial chemicals are a major cause for concern when it comes to their impact on the environment and human health. They are toxic, man-made, hazardous chemicals that have been linked to a range of negative health effects, including thyroid problems. These chemicals, known as Persistent Organic Pollutants (POPs), are resistant to degradation and can persist in the environment for long periods, travelling through water and air, and accumulating in the fatty tissue of animals and humans.

POPs are a diverse group of compounds, with some being pesticides or insecticides, while others are solvents, pharmaceuticals, and industrial chemicals. They are often classified as possible human carcinogens and are toxic to living organisms. One of the key characteristics of POPs is their ability to bioaccumulate, which means they increase in concentration as they move up the food chain. This is particularly concerning as it results in higher levels of POPs in top predators, including humans, leading to a range of health issues.

The impact of POPs on thyroid function has been a growing area of research. A study linked the development of thyroid disorders, particularly in women, with living near a petrochemical complex. Polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers (PBDEs), and other brominated flame retardants are examples of industrial chemicals that contribute to hypothyroidism. These chemicals are easily inhaled and can be found in soft furnishings, building materials, electronics, and plastics.

The Stockholm Convention on Persistent Organic Pollutants, adopted in 2001, aims to address the global issue of POPs by reducing or eliminating their production, use, and release. As of 2024, 185 countries, including the European Union, have ratified the convention. This international effort recognises the potential human and environmental toxicity of POPs and their ability to bioaccumulate and biomagnify.

While progress has been made in reducing the use and release of POPs, the challenge of managing and removing them from the environment remains. Current studies are exploring ways to minimise POPs through photocatalytic oxidation reactions and adsorption techniques. Additionally, there is a growing focus on transitioning to safer alternatives and preventing the use of hazardous chemicals.

Inhalable toxins, such as flame retardants and pesticides

Several studies have found a link between exposure to air pollution and thyroid disorders such as hypothyroidism. Endocrine disruptors, or chemicals that interfere with the function of the endocrine system, are of particular concern. These include flame retardants and pesticides, which are commonly found in household products and can be inhaled or absorbed through the skin.

Flame retardants are chemicals that are applied to materials such as textiles, electrical equipment, and polyurethane foam to prevent or slow the spread of fire. Polybrominated diphenyl ethers (PBDEs) are a class of flame retardants that have been linked to thyroid issues. PBDEs are easily inhaled and can accumulate in the body, interfering with thyroid function. A study by NYU Langone researchers found that exposure to PBDEs was the greatest contributor to IQ loss among the endocrine disruptors studied, causing over 738,000 cases of intellectual disability.

Pesticides are chemicals used to kill pests such as insects, plants, or fungi. Organophosphates are commonly used as pesticides and have been linked to thyroid issues. Like PBDEs, organophosphates are toxic to the endocrine glands and can cause learning disabilities, autism, and behavioural issues when exposure occurs at a young age.

While the most toxic flame retardants and pesticides have been phased out in some countries, they have often been replaced with poorly studied alternatives that may also pose health risks. In addition, the minimal policies in place to regulate and eliminate these chemicals have been insufficient in protecting public health. As a result, exposure to flame retardants and pesticides continues, and there is a growing body of evidence suggesting that these chemicals are significant contributors to thyroid disorders.

To reduce exposure to these inhalable toxins, individuals can take steps such as avoiding the use of household products containing them, frequently opening windows to allow chemicals to escape, and eating certified organic produce.

Heavy metals, such as mercury and lead

Heavy metals such as mercury and lead are known environmental toxicants that can have adverse effects on human health, including the thyroid. Mercury and lead are often present in industrial activities and can be released into the environment through air emissions, water discharge, and waste disposal. Exposure to these heavy metals can occur through inhalation of contaminated air, ingestion of contaminated water or food, and direct skin contact.

Mercury is a toxic chemical that can interfere with thyroid function. It is similar in structure to iodine, which the thyroid needs to produce hormones. As a result, the thyroid can absorb and store mercury instead of iodine, leading to a decrease in the production of thyroid hormones. This disruption can cause hypothyroidism. Additionally, mercury can trigger autoimmune reactions and oxidative damage, which are linked to the development of thyroid cancer, autoimmune thyroiditis, and hypothyroidism. Studies have shown that the presence of mercury in the thyroid increases with age, and it is prevalent in over one-third of individuals aged 60 and above.

Lead exposure has also been associated with adverse effects on the thyroid. It can interfere with iodine uptake and disrupt thyroid hormone synthesis and metabolism. While the exact mechanism is not fully understood, lead exposure has been linked to reduced thyroid hormone levels and increased risk of hypothyroidism.

To reduce exposure to heavy metals like mercury and lead, it is important to limit consumption of high-mercury fish such as tuna and opt for low-mercury fish like salmon. Using water filtration systems and avoiding products with high levels of heavy metals, such as certain cosmetics and plastics, can also help reduce exposure. Additionally, reading product labels and being mindful of potential sources of heavy metals in the environment can help minimize exposure.

Electromagnetic fields (EMFs)

EMFs are a type of non-ionising radiation, which is frequently used in daily life. EMFs are emitted by mobile phones, base stations, and other electronic devices.

EMFs have been linked to several adverse health effects, including thyroid dysfunction. Hypothyroidism is the most reported abnormality associated with EMF exposure.

Several studies have investigated the impact of EMFs on thyroid function. The majority of these studies have focused on the effects of EMFs on thyroid hormones, specifically TSH, T3, and T4.

Animal Studies

Animal studies have shown that exposure to EMFs can lead to a decrease in TSH, T3, and T4 levels. For example, a study by Koyu et al. (2005) found that exposure to 900 MHz EMFs for 30 minutes per day, 5 days per week, for 4 weeks, resulted in significantly lower TSH, T3, and T4 levels in rats compared to a sham-exposed group.

Other animal studies have reported similar findings, with EMF exposure leading to decreased thyroid hormone levels and increased thyroid weight and volume.

Human Studies

Human studies have also found associations between EMF exposure and thyroid dysfunction. For instance, a study by Mortavazi et al. (2009) observed a higher TSH level, low mean T4, and normal T3 concentrations in mobile phone users compared to a control group.

Additionally, a systematic review and meta-analysis by Liu et al. (2023) found that exposure to PM2.5, PM10, NO2, SO2, and CO was associated with lower FT4 levels. The review also reported a link between PM2.5 exposure and hypothyroxinemia and high TSH levels.

Mechanisms

The exact mechanisms by which EMFs affect thyroid function are not yet fully understood. However, some proposed mechanisms include:

• EMFs may interfere with iodine uptake in the thyroid gland.
• EMFs may increase the pituitary gland temperature, leading to a rise in serum cortisol levels, which can inhibit the conversion of T4 to T3.
• EMFs may trigger a rise in ornithine carboxylase, which has been associated with glandular tumors.
• EMFs may induce caspase-dependent apoptotic pathways, leading to thyroid follicular cell apoptosis.

Susceptible Populations

Certain populations may be more susceptible to the effects of EMFs on thyroid function. For example, pregnant women, individuals with a family history of autoimmune thyroid disease, and those with existing thyroid autoantibodies may be at increased risk.

Additionally, individuals with iodine deficiency or excess may be more susceptible to the effects of EMFs on the thyroid.

Protective Measures

To reduce the potential impact of EMFs on thyroid function, the following protective measures can be considered:

• Maintain a regular and sufficient iodine intake, especially during pregnancy.
• Avoid exposure to known environmental toxicants and pollutants, such as PCBs, PBDEs, BPAs, pesticides, and heavy metals.
• Limit exposure to electronic devices, especially in the bedroom.
• Turn off Wi-Fi at night.
• Use EMF-protective products, such as cases and shields, for electronic devices.

Iodine deficiency

When the body does not have enough iodine, the thyroid gland has to work harder, and it can become swollen or enlarged, a condition known as a goiter. In some cases, the gland may not be able to produce enough thyroid hormones, leading to a condition called hypothyroidism.

Causes of iodine deficiency include consuming foods grown in iodine-poor soil and having a poor diet. Additionally, certain autoimmune conditions can lead to hypothyroidism in teenagers, especially those with a family history of autoimmune diseases such as Hashimoto's thyroiditis, type 1 diabetes, or Graves' disease.

Symptoms of iodine deficiency and related thyroid disorders can include swelling of the thyroid glands in the neck, weight gain, fatigue, weakness, feeling colder than usual, learning and memory difficulties, and heavy or irregular periods. In infants and youth, iodine deficiency may also cause delayed development of permanent teeth and slowed mental development.

To correct iodine deficiency, individuals may be advised to take iodine supplements, use iodized salt, or make dietary changes to include good sources of iodine, such as kelp and other sea vegetables.

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