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The COVID Wildfire Link

The COVID Wildfire Link

Wildfires increase risk of serious reactions to COVID. Guest author Dr. Lyn Patrick explains what you can do about it.

Content from the following article was previously published by the author as a Blog Series at: https://www.environmentalhealthsymposium.com/blog

Smoke from wildfires blanketing the West Coast in the last two years have caused some of the planet’s worst air quality, with smoke reaching the East Coast and  Europe. 

The EPA PM 2.5 AQI (Air Quality Index) in Portland, Eugene OR and Vancouver British Columbia reached over 700 last year, according to PurpleAir, a network of local indoor and outdoor air sensors purchased and used by individuals throughout the U.S. and uploaded to a national map in real time. 

This would make them the most polluted cities in the world for that period. And as the EPA AQI only goes to 500, the EPA is clear that recommendations for readings above 500 is to “remain in a room or building with filtered air”.   

The live PurpleAir map screenshot of Northern California taken at 10:30 am on August 25th 2021, shows multiple readings in N. California over 150. According to the EPA, for readings between 151-200: “everyone may experience health effects if exposed for more than 24 hours, members of sensitive groups may experience more serious health effects.”  

When the air quality index rises over 400 the EPA is clear: “Health warnings of emergency conditions if exposed for 24 hours. The entire population is more likely to be affected.” An emergency condition includes the following: acute respiratory distress, myocardial infarction and stroke.  

Last year, according to the World AQI tracking data, San Francisco (AQI of 108) has about the same level of polluted air as Beijing (122) but more polluted than Shanghai (88) or Wuhan (91).  

 And, on Sept. 9th, 2020 the I-5 corridor in Oregon had air quality index (AQI) readings that hit 599 on the  EPA’s map  for the state, and approximately 700 in some locations on the crowd-sourced  PurpleAir  monitoring site. Again, the EPA AQI scale only reaches 500, so the effects of these high levels of exposure have are unknown. 

An NPR analysis of  U.S. Environmental Protection Agency air quality data  found that nearly 50 million people in California, Oregon and Washington live in counties that experienced at least one day of “unhealthy” or worse air quality during wildfire season in 2020. That’s 1 in 7 Americans, an increase of more than 9 million people compared with 2018, the worst previous year. Demographics for those considered “sensitive” to air pollution make up about 30 percent of the U.S. population: children under 18, adults over 65, women who are pregnant and those with medical conditions including heart or lung disease, COPD, asthma, diabetes or compromised immune systems.    

Unfortunately, wildfire smoke contains more than particulate matter. Burning trees and bushes give off solvents (benzene, formaldehyde, toluene, xylene), harmful gases like ozone, nitrogen and sulfur dioxide, carbon monoxide and respiratory irritants like acrolein. The further the smoke drifts, the more ozone is created when the gases in the smoke are exposed to sunlight and nitrous oxide. Ozone is a serious lung toxicant, contributing to damage that can cause COPD in both adults and children. 

Woodsmoke also contains arsenicmercury, and PAH (polycyclic aromatic hydrocarbons) -all known carcinogens and DNA-damaging toxicants.  

Wildfire smoke, also known as carbon black, appears to cause glutathione depletion in macrophages and monocytes and also causes massive amounts of ROS (reactive oxygen species aka free radicals) which not surprisingly, also contributes to lower levels of glutathione. These ROS (particularly hydroxyl radicals) have been identified as the culprit in wood smoke-related lung injury in animals.

recent study on wildfire smoke exposure was conducted in Seeley Lake, MT (outside of Missoula) where residents experienced an average AQI of 220.9 μg/m3 for 6 weeks in the summer of 2017. Follow-up in 2018 and 2019 showed that the residents (specifically those over 65) had a significant decrease in lung function (FEV1/FVC ratio: forced expiratory volume /forced vital capacity). More than twice the number of participants fell below the lower limit of normal than would have been expected one year following the wildfire event (10.2% in 2017 to 45.9% in 2018). This decrease in lung function remained two years post exposure in 34% of the tested population.  

The study authors concluded that the period of 6 weeks of exposure of AIQ around 220 had long lasting effects. Although the median age in this study was 63 (so more likely to have respiratory problems), the decline in lung function was greater than expected for that age group.  

FEV1 values are used to determine whether lung function is declining at a normal rate based on age. According to the Mayo Clinic, the expected annual decline in pulmonary function in FEV1 is 30 mL for males and 25 mL for women. The Seeley Lake cohort (specifically those without woodstoves) saw a decline in their FEV1 from 289.3 to 189.7 mL = 100 mL over a one year period of time, 3-4 times the expected decline.  

Another study revealed that after severe fire seasons influenza was three to five times worse during the traditional flu season of fall and winter. This study identified that after four bad fire years, including 2017, the number of annual flu cases in Montana jumped from the typical 3,000 to around 12,000, far above any historical fluctuation.

The following section of this article includes the link between exposure to PM2.5, lung damage, and systemic inflammation. Please follow this deep dive into pathophysiology as it is crucial to understand the link between PM2.5 exposure and Covid-19 vulnerability. If you want to skip the science go to the end of the article for recommendations on protection.

PM2.5 (or smaller) in fire smoke and air pollution have been linked with endothelial dysfunction, systemic inflammatory and oxidative stress responses and the progression of atherosclerosis. And chronic exposure to PM2.5 leads to chronic pulmonary inflammation and sets the stage for chronic obstructive pulmonary disease, which affects 12–16 million people in the United States and is the third-leading cause of death. 

Alveolar macrophages, think of them as the waste removal service of the body, process inhaled particulate matter—everything from “soot” (PM 10) to fine (PM 2.5 μm or less) and ultrafine (0.1 μm or less) particles.  

Alveolar macrophages function normally to surround these particles—which include metal (lead, iron, etc.) nanoparticles and PAH (polycyclic aromatic hydrocarbons) and to evacuate them from the lungs via the lymphatic circulation. As a result of contact between these particles (PM 2.5 in particular)  and the lung lining, phospholipids in the lung tissue are oxidized and  stimulate the activation of the alveolar macrophages generating reactive oxygen species (ROS)

In response to big particles of wildfire smoke (PM10) the lungs produce tumor necrosis-factor (TNF), interleukin 6 (IL-6),  and cyclo-oxygenase 2 (COX-2) -all mediators of inflammation that upregulate oxidant stress. This innate immune response results in the elevation of other mediators of inflammation, including the production of nuclear factor (NF)-κB and interleukin (IL)-1β

Even though the mechanism responsible for this damage starts with local macrophage activation, it initiates a cellular inflammatory response throughout the body, specifically in the sensitive endothelial lining of the circulatory system. 

This response is like an alarm that rings throughout the body and effects the entire vascular system, causing inflammation and potential formation of both microthrombi and emboli. 

This is one of the mechanisms for particulate matter exposure in air pollution that leads to cardiovascular disease. In animal models, exposure to PM2.5 leads to decreased prothrombin and partial thromboplastin times (decreased plasma clotting times), increased levels of fibrinogen, and increased activity of factor II, VIII, and X

The animals that could not produce IL-6 were protected from the prothrombotic effect of particulate matter exposure, indicating that IL-6 is an important mediator in the inflammatory response.  This systemic response includes not just an upregulation of IL-6, but more oxidative stress, activation of Toll-Like Receptor4 and activation of NADPH oxidase (NOX)dependent pathways. In addition to causing vascular injury, this series of inflammatory events has also been shown to cause acute lung injury and is the same mechanism in H5N1, SARS, and some features of COVID-19.  

The average arteriole is between 0.3 mm and 10 microns (µm) in diameter, and ultrafine particulate matter (which makes up the bulk of PM2.5) includes everything with a diameter of 1.0 mm or less. Ultrafine particulate matter easily makes it way into the arterial system- not just in the lungs- but throughout the body and can be found embedded in the endothelial lining of arteries and arterioles, causing local and systemic inflammation. This is the mechanism through which particulate matter causes cardiovascular disease, where the presence of particulate matter in the linings of the vascular system directly triggers the inflammasome. 

The inflammasome complex is part of the innate immunity’s early warning system and allows us to mount a response to environmental pollutants or endogenous toxic substances (including those resulting from infections). There are 5 classes of inflammasomes found both inside the cell and on the cell membrane to cover every level of potential threat to the cell.  Inside the cell, the NLRP3 inflammasome – the most well characterized of all the proteins- can assemble into an active defense system when danger threatens the cell. 

Obviously, this is not a mistake- the inflammasome originally evolved to protect the body and this inflammatory response has a purpose: IL-1β induces fever and promotes T-cell survival, B-cell proliferation, and antibody production, and supports the migration of leukocytes to a site of infection and invasion. IL-18 can act with IL-12 to induce interferon-γ (IFNγ) production by activating T- and NK-cells. This is all an efficient way to mobilize innate immunity and is meant, over the short-term, to attack, disarm, kill, and eliminate pathogens and foreign invaders- engulfing foreign matter for export and eliminating particulate matter and toxicants through the lymphatic channels.  Exposure to PM2.5 is one of the things capable of causing lung inflammation via potent IL-1β secretion, as particulate matter in the lungs activates the NLRP3 inflammasome.

However, when chronically activated, the inflammasome promotes damaging responses found in what are now called “autoinflammatory” disease”: obesity, type2 diabetes,  rheumatoid arthritis, systemic lupus erythematosus, osteoarthritis, atherosclerosis, Alzheimer’s disease, Parkinson’s disease, and cancer. And as mentioned above, this list also includes asthma and COPD.  

This theory has been validated by a recent analysis by Harvard T H Chan School of Public Health which showed that there is strong evidence that wildfires have amplified the effect of PM2.5 on COVID-19 cases and deaths. They looked at 133 counties in three states (California, Washington, and Oregon) from March 15 to 1 December 16, 2020 (a total of 277 days) and saw a significant increase in Covid19 mortality related to wildfire smoke PM2.5 levels directly preceding the increased deaths.

Emerging evidence is beginning to show that PM2.5 from wildfire smoke may actually be more damaging to health than PM2.5 from other sources. The mechanism for this damage is the effect of wildfire smoke on the immune systems Th1/Th2 balance.

Air pollutants in PM2.5 particles stimulate pro-inflammatory immune responses across multiple classes of immune cells. PM2.5 can enhance T helper lymphocyte type 2 (Th2) and T helper lymphocyte type 17 (Th17) adaptive immune responses, as seen in allergy and asthma, and dysregulate anti-viral immune responses.

Although we originally understood that fatal infections with SARS-CoV2 were from acute respiratory distress and cytokine storm, it is now been shown that death is actually due to respiratory failure, stroke, myocardial injury, arrhythmias, coagulopathy, kidney failure, and secondary bacterial infections and that COVID-19–induced mortality and morbidity is due to an “immunological collapse” characterized by a loss of B and T cells in the spleen and secondary lymphoid organs.

To summarize, PM2.5 can induce inflammation,  increase risk for clotting and microthrombi, initiate immune dysfunction, and cause “autoinflammatory disease” and these are the reasons that air pollution may have a direct effect on increasing risk for Covid-19 infection.  

So, given the significantly increased respiratory, cardiac, and immune stress individuals are currently experiencing from wildfire smoke and the significant risk for damage to the lungs and vascular system, what affordable, safe interventions can be used prophylactically? As always, the first rule of toxicology is to remove the exposed individual from the environment or protect them from exposure, but with prolonged wildfire smoke exposure masking and indoor air filters may not be sufficient to protect vulnerable populations from exposure.

Research looking at plant extracts and nutrients may be strategies for addressing these inflammatory pathways and could aid in reducing potential ongoing damage from fire smoke and air pollution exposure. 

There are interventions that have been shown to assist with PM2.5 exposure:

  • B vitamins: 2.5 mg/d folic acid, 50 mg/d vitamin B6, and 1 mg/d vitamin B12 given for 4 weeks significantly reduced the inflammatory effects of PM2.5 on heart rate variability (90%), normalized heart rate, WBC count and lymphocyte count. (This study did not include testing for MTHFR or other single nucleotide polymorphisms in study participants so guidance for those with methylation snps would include methylfolate and methylB12)

Resveratrol has also been shown to protect lung epithelia against the effects of cigarette smoke by upregulating Nrf2 to promote glutathione production intracellularly. In animal models of inflammation resveratrol has been shown to be effective in upregulating SIRT1, and inhibiting NF-κB as a result.  

 Resveratrol, in animal models, has been shown to significantly alleviate asthma, inhibit mucus overproduction and down- regulate the inflammatory mediator TGF-β1.  

There are no extensive clinical studies using resveratrol in asthma, but it has been shown to have significant anti-inflammatory effects in cardiac disease. In a clinical study of 60 cardiac failure patients (half of them were given 100 mg. resveratrol daily for 3 months) the results were significant. Exercise capacity, ventilation parameters and quality of life improved dramatically in the resveratrol group. As importantly, markers of oxidative stress: IL-6 and IL-1 were significantly lowered in the patients on resveratrol.  

Resveratrol has also been shown to protect lung epithelial cells from damage by cigarette smoke exposure via the promotion of glutathione production intracellularly (where it counts).

Cardiac failure occurs in an environment of oxidative stress and resveratrol has been shown to have positive antioxidant effects in cardiac and vascular pathologies by increasing endothelial nitric oxide synthase (eNOS) activity as well as lowering levels of  TNF-α, IL-1β or IL-6 in other studies.

Meta-analyses of clinical trials with resveratrol assessing cardiometabolic risk and treatment for respiratory disease indicate that long-term dosing of moderate doses (450 mg. day) may be more beneficial than lower doses of 100 mg. day or infrequent dosing at higher doses of 1000 mg.

And although they lack clinical studies, there are many other flavonoid-based compounds that have been found to down-regulate the NLRP3 inflammasome and it’s downstream inflammatory markers: NFkB, TNF-a, IL-6, IL-1B and IL-18.  

Some are botanicals like:

And flavonoid components of many common foods: 

  • Dietary Components: 
  • b-hydroxybutyrate (induced by ketogenic diets, intermittent fasting, and exogenous use of b-hydroxybutyrate) was shown to suppress inflammasome formation in both fasted rats and rats given exogenous b-hydroxybutyrate. The mechanism here is an upregulation of cellular antioxidant production (superoxide dismutase, catalase) and a decrease in endoplasmic reticulum stress (caused by excessive reactive oxygen species). 

About the Author:

Lyn Patrick ND graduated from Bastyr University in 1984 and has held licenses in Arizona and Utah since then. She is a published author of numerous articles in peer-reviewed medical journals, a past Contributing Editor for the former Medline-indexed Alternative Medicine Review journal, and recently authored a chapter in the newly released textbook Clinical Environmental Medicine (Elsevier 2019). She speaks internationally on environmental medicine, nonalcoholic fatty liver disease, endocrine disruption, metal toxicology and other topics. She is currently Faculty for the Metabolic Medicine Institute Fellowship in collaboration with George Washington School of Medicine and Health Sciences.

She is also a founding partner and presenter at the Environmental Health Symposium, an annual international environmental medicine conference based in the United States. She is continuing to educate primary care providers through the EMEI (Environmental Medicine Education International)  Clinical Training in Environmental Medicine Course and EMEI Review podcasts at emeiglobal.com.

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