Environmental Toxins, Atherosclerosis, Mast Cells And Hypercoagulability: A Complex Interplay

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Environmental

Toxins, Atherosclerosis, Mast Cells, and Hypercoagulability:

A C o m p l e x I n t e r p l a y

Cardiovascular disease (CVD), including heart attacks, strokes, and atherosclerosis, remains the leading cause of death worldwide, accounting for approximately 17.9 million deaths annually worldwide, making up about 32% of all global deaths (WHO, 2021). While genetics, diet, and lifestyle are well-known contributors, an often-overlooked factor is environmental toxicants. These harmful substances pervasive in air, water, food, and household products play a critical role in damaging cardiovascular health.

Let’s explore how environmental toxins contribute to the progression of atherosclerosis, the role of mast cells in inflammation and vascular health, and how hypercoagulability adds to the risk of heart attacks and strokes.

More importantly, we will explore actionable steps to mitigate exposure and supplements to support cardiovascular and overall health.

Understanding these risks isn’t just for those already at risk of heart disease; it’s for anyone who wants to protect their health and longevity. We can do this!

Take the "Toxic Burden Quiz"

Use this quiz to assess your potential exposure to harmful environmental toxins.

For each "Yes," give yourself one point.

Do you live near a busy road, industrial area, or airport?

1. Do you regularly eat non-organic produce or high-mercury fish (e.g., tuna)?

2. Have you experienced mold exposure in your home or workplace?

5.

3. Do you drink unfiltered tap water or use plastic containers for food storage? 4. Do you often use scented products, aerosols, or chemical cleaners at home?

Scoring:

1.

0-1: Low risk. Keep maintaining good habits.

2-3: Moderate risk. Time to start reducing exposures! 2.

4-5: High risk. Take action today to protect your health 3.

Read on to learn how you can protect yourself and your health!

The Silent Killer: Understanding Atherosclerosis

Atherosclerosis is a condition where fatty deposits (plaques) build up on the inner walls of arteries, narrowing them and restricting blood flow. These plaques form due to oxidative stress, inflammation, and lipid accumulation within the arterial walls. Over time, they can rupture, causing life-threatening blood clots, which we know as heart attacks and strokes.

Role of Environmental Toxins in Atherosclerosis

Your blood vessels are lined with a thin layer of cells called the endothelium, which keeps them flexible and smooth, allowing blood to flow freely.

Environmental toxins damage the endothelium—the thin layer of cells lining the arteries through oxidative stress and inflammation. Think of oxidative stress as rust forming inside your pipes: it weakens the structure and creates a breeding ground for further damage.

This damage triggers an immune response, sending white blood cells to “repair” the injury. Over time, fats, cholesterol, and cellular debris stick to these sites, forming plaques that narrow the arteries. This process, known as atherosclerosis, increases the risk of heart attack, strokes and vascular dysfunction.

Even though we may not be able to tell, we are constantly exposed to environmental toxins. They exist in our food, our water, and the air we breathe. Additionally, we are exposed to multiple toxins simultaneously, which amplifies their harmful effects. Information is power, so join me to learn more about some of the culprits and what you can do to protect yourself and your loved ones.

Air Pollution: A Silent Killer

Particulate matter (PM2.5), tiny particles from vehicle emissions, industrial activities, and wildfires, is particularly harmful. When inhaled, PM2.5 travels from the lungs into the blood, triggering inflammation that damages the endothelium. Ultimately, much of the air we breathe could be delivering microscopic toxins into your bloodstream.

Fine particulate matter (PM 2.5) levels are consistently above recommended limits in many urban areas. WHO data indicates that 90% of the global population breathes air exceeding PM 2.5 safety levels, significantly elevating CVD risk, as much as 20–30% higher risk of cardiovascular events like heart attacks. High pollution exposure accounts for an estimated 15-20% of all CVD cases worldwide, with the American Heart Association attributing over 50,000 CVD-related deaths annually to air pollution in the United States alone.

PM 2.5 promotes inflammation, endothelial dysfunction, and lipid oxidation, leading to atherosclerosis.

There are many other chemicals that may be in the air that we breathe that are linked to cardiovascular disease. For example, many of the electronic equipment in our homes such as our computers and our televisions are made up of plastics. Over time these plastics break down into microplastics and nanoplastics and reside in the dust in our homes. We breathe this in!

And microplastics are not just in the air. Microplastics are found in 94% of tap water samples in the United States and 72% of European samples. Their role as emerging contaminants in vascular disease is linked to chronic inflammation. Microplastics promote oxidative stress, a known contributor to atherosclerosis. Laboratory models have shown that microplastic exposure leads to up to a 15% increase in inflammatory markers like IL-6, TNF-α, and C-reactive protein. Reducing plastic pollution and developing advanced water filtration systems could mitigate health risks. Public health measures aimed at decreasing plastic exposure could potentially reduce vascular inflammation-related risks by up to 10%.

Microplastic ingestion has been estimated at 74,000-121,000 particles per person annually through food and water, with potential chronic vascular effects that require further investigation.

Toxic Heavy Metals: The Heart’s Worst Enemy

Heavy metals like lead, cadmium, mercury, and arsenic are some of the most studied toxins linked to heart disease. These metals don’t break down in the environment, meaning they persist in the air, soil, and water for decades.

Lead is commonly found in old paint, lead pipes and was previously used in gasoline until its use was banned in the 1970s in paint and gas. Many people born before lead use was banned were exposed and sometimes that lead deposited in the bones in place of calcium and other bone minerals. As people age and start to lose minerals from bone, developing low bone density, the lead can leach out of the bones also and get deposited in the soft tissues, causing more problems. Many older folks who have lost bone may be developing hypertension and cardiovascular disease due to their unsuspecting lead burden from their bones!

Another often overlooked source of lead besides pipes is the lead used in firearms. I find that indoor gun enthusiasts or professionals who use guns such as police officers are often contaminated with lead from the bullet casings. A good test for lead is a whole blood lead level. If it is >1, there is an exposure that needs to be investigated and removed.

Cadmium, another toxic metal, is very common in tobacco smoke and in non-organic fertilizers. Cadmium is also a byproduct of industrial processes that gets stored in the kidneys and liver. Often the toxic effects spill over into the cardiovascular system. Research shows cadmium exposure increases the risk of atherosclerosis and coronary artery disease. Avoiding cigarette smoke and consuming foods rich in zinc can help block cadmium absorption.

Exposure to the toxic metal, arsenic, correlates with increased incidence of ischemic heart disease. Mercury, often found in fish like tuna and swordfish, interferes with the body’s antioxidant defenses, increasing oxidative stress. Consuming smaller fish like salmon or using supplements like selenium can reduce mercury’s impact. Some studies show that mercury exposure is NOT correlated with cardiovascular disease, although it has many health effects.

Persistent Organic Pollutants (POPs)

POPS cover a large category of environmental chemicals including older, banned toxicants like Polychlorinated Biphenyls (PCBs) and DDT, which is a chlorinated pesticide. A number of flame retardants often fall in this category as well. The challenge with these toxicants is that they are fat soluble and are called persistent because they are both persistent in the environment and our bodies. They are found in highest concentrations in fatty foods such as butter and fatty animal products.

POPs such as PCBs and dioxins are linked to increased cardiovascular risk by affecting lipid profiles and promoting atherosclerosis. People with high PCB levels show a 20% increase in low-density lipoprotein (LDL) cholesterol and triglycerides, a 20-30% increase in the prevalence of carotid artery plaques and up to a 70% increased risk of myocardial infarction.

Because POPs are fat soluble, they are transported by lipoproteins and accumulate in adipose tissue, leading to chronic inflammation, lipid oxidation, and arterial plaque formation. Regulatory measures limiting exposure to POPs, combined with public health policies to reduce the use of these chemicals, could decrease the cardiovascular burden. Reducing POP exposure can lead to a 30-40% decrease in CVD risk over time in affected populations.

Endocrine-Disrupting Chemicals

There are a couple of non-persistent chemicals known best for the endocrine disrupting effects, such as Bisphenols and phthalates that both have adverse effects on the cardiovascular system. Bisphenol A (BPA) is associated with increased blood pressure and endothelial dysfunction. Phthalates are linked to hypertension and atherosclerosis.

Mycotoxins

Mycotoxins are the metabolites of certain species of molds that grow in water damaged buildings. The mycotoxins are part of the mold’s arsenal in their war against other molds, and humans (and sadly, our pets) are the innocent bystanders in the mold wars.

Mycotoxins are often inhaled but can also be ingested, and these cause tremendous oxidative stress and inflammation both of which can contribute to atherosclerosis in susceptible people. Not all molds create mycotoxins which can lead to atherosclerosis, but Aspergillus and Stachybotrys mold species commonly are found in water damaged buildings and Dr Wolfson has found that the presence of these organisms and their metabolites can lead to cardiovascular disease.

Those fries really are toxic and it’s not because of the fat! It’s the chemical acrolein…

Acrolein, found in cigarette smoke, overheated cooking oils, and certain foods (like wine), is a potent environmental toxicant linked to atherosclerosis. Cigarette smoke contains around 100-200 micrograms of acrolein per cigarette, a major risk factor for those exposed chronically. French fries and potato chips are also significant sources. The mechanism by which acrolein causes issues is via oxidative stress, inflammation, and endothelial cell dysfunction, which are key in promoting plaque buildup in arteries. In studies, acrolein exposure accelerated atherosclerotic progression by 30% in animal models.

Reducing exposure to acrolein could have substantial impacts on cardiovascular risk reduction, especially for smokers and individuals exposed to high levels of air pollution. Smoking cessation can lower cardiovascular risk by 30% within two years, further reduced with time.

The Environmental Toxins Driving

Cardiovascular Risks

Environmental toxins come from various sources and impact

cardiovascular health through different mechanisms.

Here's a detailed look:

Toxin Source Mechanism

Lead (Pb)

Cadmium (Cd)

Mercury (Hg)

Persistent Organic Pollutants (POPs)

Fine Particulate Matter (PM2.5)

Microplastics

Mycotoxins

Paint, pipes, contaminated water

Tobacco smoke, industrial byproducts

Large fish (tuna, swordfish), dental amalgams

Industrial chemicals, pesticides

Air pollution (vehicle emissions, wildfires)

Degraded plastics in water, food

Mold (Aspergillus, Stachybotrys)

Induces oxidative stress, damages endothelium

Promotes calcification, oxidative stress

Impairs antioxidant defenses

Endocrine disruption, systemic inflammation

Systemic inflammation, oxidative damage

Vascular inflammation, oxidative stress

Endothelial damage, oxidative stress

Cardiovascular Impact

Hypertension, atherosclerosis

Coronary artery disease, arterial stiffness

Myocardial infarction, endothelial dysfunction

Plaque formation, lipid abnormalities

Increased heart attack and stroke risk

Emerging cardiovascular risks

Atherosclerosis, systemic inflammation

Mast Cells: The Inflammatory Link to Cardiovascular Disease

Mast cells, integral components of the immune system, play significant roles in cardiovascular health, the development of atherosclerosis, and the risk of cardiac diseases. Mast cells are immune cells that release histamine, cytokines, and proteases during allergic and immune responses. Emerging research highlights their role in atherosclerosis. When activated by toxins, mast cells exacerbate inflammation, destabilize plaques, and increase the risk of plaque rupture. Although not everyone may have a condition called Mast Cell Activation Syndrome with abnormal and hypersensitive mast cells, the presence of environmental toxicants trigger mast cells to release mediators in anyone who is exposed. Understanding mast cell response to environmental chemicals makes it easier to see how mast cells may be intimately involved in contributing to cardiovascular diseases.

1. Release of Inflammatory Mediators:

Histamine Release: Mast cells release histamine, which can cause vasodilation, increase vascular permeability, which worsens endothelial damage, and contributes to inflammatory responses within the cardiovascular system. SpringerLink

Cytokine Production: Activated mast cells produce pro-inflammatory cytokines such as TNF-α and IL-6, which can promote endothelial dysfunction and atherogenesis.

2. Promotion of Atherosclerosis:

Lipid Accumulation: Mast cell-derived proteases can degrade extracellular matrix components, facilitating the infiltration of lipids into the arterial wall and promoting plaque formation.

Plaque Instability: Enzymes like tryptase and chymase released by mast cells can degrade fibrous caps of atherosclerotic plaques, increasing the risk of plaque rupture and subsequent cardiovascular events.

3. Enzymes degrade fibrous cap

Protease Activity: Degrades the fibrous cap of plaques, making them prone to rupture.

4. Induction of Coronary Artery Spasm:

Kounis Syndrome: Mast cell activation can lead to coronary artery spasm, known as Kounis syndrome, resulting in chest pain and myocardial infarction.

5. Modulation of Vascular Tone:

Vasodilation and Vasoconstriction: Histamine and other mediators can cause both vasodilation and vasoconstriction, affecting blood pressure and contributing to conditions like hypertension.

6. Interaction with the Nervous System:

Sympathetic Nervous System Activation: Mast cell mediators can influence the release of norepinephrine, affecting heart rate and contributing to arrhythmias.

7. Contribution to Myocardial Injury:

Myocardial Infarction: Mast cell activation and degranulation can lead to myocardial injury through the release of proteases and inflammatory mediators, contributing to tissue damage during ischemic events.

8. Enhancement of Oxidative Stress:

Reactive Oxygen Species (ROS) Production: Mast cells can generate ROS, leading to oxidative stress, endothelial dysfunction, and progression of atherosclerosis.

9. Influence

on

Lipid Metabolism:

Altered Lipid Profiles: Mast cell mediators can affect lipid metabolism, potentially leading to dyslipidemia, a known risk factor for atherosclerosis.

Understanding these mechanisms highlights the complex role of mast cells in cardiovascular health and disease, emphasizing the need for targeted therapeutic strategies to mitigate their adverse effects. In reducing our exposures to environmental toxicants as much as able, we may still need to calm down mast cell reactivity as well, which is a complete topic in itself!

Hypercoagulability: When Blood Becomes Sticky

Up until now we have solely been discussing atherosclerosis and heart disease from the perspective of the blood vessels and in particular the endothelial lining of the blood vessels. It is critical to remember that it is the products in the blood that actually form the clots that lead to blockages in the blood vessels leading to a heart attack or a stroke.

Hypercoagulability refers to an increased tendency of blood to clot, which is closely linked to atherosclerosis and mast cell activation.

Environmental toxins and mast cell mediators promote excessive clot formation by:

Increasing Platelet Aggregation: Triggered by toxins like heavy metals.

1. Promoting Fibrin Deposition: Mast cell proteases activate clotting factors, leading to excessive fibrin buildup.

2. Inhibiting Fibrinolysis: Environmental toxins impair the body’s ability to break down clots.

3. This hypercoagulable state significantly raises the risk of strokes and heart attacks, particularly in individuals already at risk. There are a number of genetic risks for increased clotting that I have also seen contribute to CV risk. Some genetic clotting disorders are more associated with the development of pulmonary embolisms or deep vein thrombosis, but in my clinic, I have found that the gene plasminogen activator inhibitor -1 (PAI-1) is closely associated with a family history of cardiovascular or cerebrovascular disease. This gene means that people are less capable of breaking down clots. Therefore fibrous plaque ruptures, a clot is formed quickly and those with PAI-1 genetics can’t break it down quickly enough, leading to blockage and MI or stroke.

These genes can be tested for and addressed with proteolytic enzymes!

How to Minimize Exposure to Environmental Toxins

Now that you have a deep understanding of our chemical exposures, the good news is that by focusing on a few simple steps like clean air, clean water and clean food, and reducing plastic in our lives, we can improve our health substantially!

1. Air Quality:

Use HEPA air filters indoors.

Avoid outdoor activities during high-pollution days.

Consider getting an air quality meter like Air Knight 9-in-1 to monitor PM2.5, VOCs, temperature and humidity. Or an AtmoPro which is a portable air quality monitoring device.

2. Water Filtration:

Test city water sources and private wells for contaminants. Use tests like Tap Score.

Choose and install filters based on what the contaminants are in your water. If possible choose reverse osmosis, whole house filters if you are a homeowner. Under the sink filters in the kitchen work great, but don’t forget filters for your shower too!

3. Food Choices:

Choose organic produce to minimize pesticide exposure. Avoid high-mercury fish; opt for smaller fish like sardines or wild caught fish, like salmon, but eat sparingly. Choose organic animal products, like butter and cheese, to limit POPs.

4. Household Products:

Avoid plastics with any bisphenols. BPA free is still toxic as it is made with BPS or BPF which are equally toxic. Use glass or stainless steel containers.

Use non-toxic cleaning products and avoid scented aerosols.

Supplements to Support Cardiovascular Health and Detoxification

There are supplements that can support detoxification or temper the effects of toxins, stabilize mast cells, and reduce hypercoagulability.

Antioxidants for Oxidative Stress

Vitamin C (1,000-2,000 mg/day): Protects endothelial cells from oxidative damage.

Vitamin E (400-800 IU/day): Scavenges free radicals, reducing lipid oxidation.

Coenzyme Q10 (100-200 mg/day): Supports mitochondrial function and reduces oxidative stress.

Detoxification Support

Glutathione 500mg daily

N-Acetylcysteine (NAC) (500-1,000 mg/day): Boosts glutathione production for heavy metal detox.

Activated charcoal: (1-4 caps daily): Binds mycotoxins and other chemicals in the GI tract.

Bentonite clay (1-4 caps daily): Binds mycotoxins and other chemicals in the GI tract.

Chlorella (1-2 g/day): Binds to heavy metals for excretion.

Milk Thistle (150-300 mg/day): Enhances liver detox pathways

Mast Cell Stabilizers

Quercetin (500-1,000 mg/day): Reduces mast cell degranulation and inflammation.

Luteolin (50-100 mg/day): Potent flavonoid with anti-inflammatory properties.

Resveratrol (100-400mg): Inhibits mast cell degranulation and improves endothelial function

Vitamin D (1,000-4,000 IU/day): Modulates immune function, stabilizing mast cells.

Cardiovascular Protection

Omega-3 Fatty Acids (1-2 g/day): Reduces inflammation and supports heart health.

Phosphatidyl choline (1500-4000mg daily): Supports healthy cell membranes, removes toxins and may even clear calcifications.

Reduce Hypercoagulability

Lumbrokinase (20-40 mg/day): Improves blood flow by reducing clot formation.

Nattokinase (100-200 mg/day): Enhances fibrinolysis, breaking down clots.

Healthy Recipes for Cardiovascular Support

Eat a variety of fruits and vegetables. Choose healthy fats. LImit grains. Lean, organic, pasture raised meats.

Quercetin-Rich Salad

Ingredients: Spinach, apples, red onions, walnuts, and olive oil.

Benefits: High in quercetin and antioxidants to stabilize mast cells.

Turmeric Smoothie

Ingredients: Turmeric, almond milk, ginger, and honey.

Benefits: Anti-inflammatory properties for cardiovascular and immune health.

Why It Matters

Individuals with a family history of cardiovascular disease face compounded risks from environmental toxins. These toxicants trigger oxidative stress, inflammation, mast cell degranulation and clotting tendencies. However, understanding these risks and taking simple, actionable steps to minimize exposure and support detoxification, you can protect your heart health and overall wellbeing. Your heart and your health with thank you!

References

1. Chowdhury R, et al. Environmental toxic metal contaminants and cardiovascular risk. BMJ. 2018;362:k3310.

Brook RD, et al. Particulate matter air pollution and cardiovascular disease. Circulation. 2010;121(21):2331-2378.

2. Liu J, et al. Mast cells and atherosclerosis. Atherosclerosis. 2018;271:157-164.

3. Wright SL, et al. Microplastic ingestion and cardiovascular risks. Environmental Science & Technology. 2017;51(12):6634-6647.

4. Münzel T, et al. Environmental risk factors and cardiovascular diseases: a comprehensive expert review. Cardiovascular Research. 2022;118(14):2880–2902.

5. Asiwe JN, et al. Environmental toxicant-mediated cardiovascular diseases. Toxicol. Environ. Health Sci. 2024;16:1–19.

6. Hermans, M.A.W.; Roeters van Lennep, J.E.; van Daele, P.L.A.; Bot, I. Mast Cells in Cardiovascular Disease: From Bench to Bedside. Int. J. Mol. Sci. 2019, 20, 3395. https://doi.org/10.3390/ijms20143395

7. Hattori, Y., Hattori, K., Matsuda, N. (2016). Regulation of the Cardiovascular System by Histamine. In: Hattori, Y., Seifert, R. (eds) Histamine and Histamine Receptors in Health and Disease. Handbook of Experimental Pharmacology, vol 241. Springer, Cham. https://doi.org/10.1007/164 2016 15

8. https://tmsforacure.org/expert-information/mast-cells-heart-kounissyndrome-takotsubo-cardiomyopathy/

9. https://www.mastattack.org/2016/04/cardiovascular-manifestations-ofmast-cell-disease-part-1-of-5/ 10.

Thank you for downloading Environmental Toxins, Atherosclerosis, Mast Cells, and Hypercoagulability: A Complex Interplay! I’m Dr. Kelly McCann, founder of The Spring Center, where we focus on functional, integrative care to help you thrive.

Stay connected with me on Instagram @drkellymccann for expert tips on health and wellness. Explore my online store for carefully curated supplements and products to support your journey. If you’re ready to take the next step in your health, visit The Spring Center to learn more about becoming a new patient.

Let’s work together to unlock your healthiest self!

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