Keeping Your Cells Healthy in the Setting of Damage from Air Pollution Particulate Matter
Dr Carrie Decker ND and Michael Ash DO, ND, RNT explore the role of natural agents in assisting the bodys healing capacity from damage linked to particulates. In a recent article, mechanisms by which the particulate matter (PM) found in air pollution may be detrimental to health were discussed, as well as how specific antioxidants, cell membrane specific lipids and some of the B vitamins may offset this damage. Here, we dive deeper into these potential issues and the importance of supporting the body in the process of ongoing cellular repair and detoxification.
The more populated our world becomes, the more the by-products of development, consumerism, and transportation become an issue. Some of these things we can’t avoid seeing such as supermarkets popping up where there once were trees, and piles of waste and rubbish growing outside the new apartments down the street. Air pollution also is an issue, but for many it is easy to neglect as it remains “unseen.” Yet medical providers, and even many of the general public, are well aware of the increases in related conditions such as allergies and asthma. Although there are many potential contributors to their propagation and air pollution is undeniably a contributing factor.,,, The impact of air pollution on our health does not stop with classic diseases of atopy and respiratory disease, it has association with heart disease, diabetes, autoimmunity, and even telomere length and aging.,,,
As a brief review on the substances in air which contribute to the biological responses, smaller size particles (less than or equal to 2.5 micrometers, known as PM2.5) are the more significant contributors to air pollution-related conditions than the large, 10 micrometer (PM10) particles. This is because particles that are smaller in size are able to penetrate more deeply into the lungs. Ultrafine particulate matter, with sizes of less than 100 nanometers (PM0.1) are potentially even more problematic because they are able to translocate from the respiratory epithelium into circulation, contributing even more than the larger particles to systemic effects.  And the problem does not stop there, as other than particulate matter, other air pollutants include carbon monoxide (CO), sulphur dioxide (SO(2)), nitrogen oxides (NOx), volatile organic compounds (VOCs), ozone (O(3)), heavy metals, and endotoxin from mould cell walls.
In order to dive deeper into the topic here, we must pick a course. For today, we will go smaller, as the potential impacts of air pollution on our health systemically is an issue of concern for all. One of the mechanisms by which the very fine PM2.5 and PM0.1 substances impact health is by causing oxidative stress and proinflammatory effects. We often think about this in terms of cytokines and immune activation, which definitely is part of the issue with air pollution particles of all sizes. But how does air pollution impact us on a cellular level, and what can be done to overcome this?
The ultrafine PM0.1 nanoparticles are a high level of concern, as at a nanoscale size, many of these substances are far more toxic and immunogenic than their larger counterparts.  Commonly these airborne nanoparticle substances include titanium dioxide, carbon black and polystyrene. Some studies have looked at these more closely, however there is a broad range of substances and even variants of these (surface characteristics, typical shape) which exist. These particles pass into the bloodstream, and into the cells, inducing swelling and damage in the mitochondria via the quinones and other redox-active compounds associated with them. The PM0.1 substances also accumulate in the mitochondria, leading to a decrease in the mitochondrial membrane potential, superoxide production, and ATP leakage and associated depletion., In efforts to remove the damaging particles and balance the oxidative stress generated by mitochondrial damage, intracellular glutathione is depleted. While low levels of oxidative stress activate the defence mechanisms in the cell via inducing transcription of nuclear factor erythroid 2-related factor (Nrf2), at higher levels oxidative damage surpasses antioxidant defences and is cytotoxic. The cellular damage and death that is created in this situation is why these ultrafine particles may be the most damaging. This has been observed at a cellular level in in vitro assays with several different cell lines including macrophages and bronchial epithelial tissue.
Exposure to the fine or ultrafine air pollution particles has also been shown to alter the blood-brain barrier integrity, and with this generate oxidative stress, neuroinflammation, and an autoimmune response against neural tissues. This has been seen in children as well as young adults, and is also described by accumulation of amyloid-beta and alpha-synuclein in the brain, proteins associated with Alzheimer’s and Parkinson’s disease. With neuroinflammation there is increased levels of cytokines and oxidative stress in the brain, as well as activation of the microglia, the macrophages of the central nervous system (CNS). Additionally, exposure to air pollution has an effect of increasing blood pressure and capillary permeability, which also can lead to acute CNS events. Exacerbations in patients with Alzheimer’s and Parkinson’s disease as well as relapses in patients with multiple sclerosis have been also been associated with air pollution, likely due to some of these mechanisms.,
Because we truly are in the early stages of understanding the systemic and long-term health impacts of air pollution, particularly with respect to the ultrafine particles, we have to take from the things we have learned in dealing with other conditions of neuroinflammation, mitochondrial damage, and oxidative stress when approaching the prevention of air pollution-related damage.
As discussed in the previous article pertaining to this topic, supplementing with substances that promote the induction of Nrf2 may be of benefit in inducing the endogenous transcription of glutathione to help combat low levels of exposure to air pollution. Substances which induce Nrf2 include gingko biloba, green tea polyphenols, and lipoic acid.,, In an aging population, supplementation with these things may be beneficial even outside of exposure to excessive air pollution as the ability of the body to upregulate Nrf2 declines with age.
However, in many settings this may not be adequate, as the cellular damage exceeds the ability of the body to generate the level of antioxidants necessary for mitochondrial, cellular, and membrane repair. In effect the cell damage response system becomes tightly engaged in a feed forward cycle of activation. In this case, more intensive damage control is indicated. Because intracellular glutathione has been shown to be depleted with exposure to air pollution, explicit strategies for increasing cellular glutathione levels also should be considered. Although many substances such as some of the other antioxidants, selenium, and N-acetylcysteine can support glutathione production, the most direct means is supplementation of a format such as acetylglutathione or via liposomal delivery which both have been shown to significantly raise intracellular glutathione.,
Because the mitochondria are the focal point of localization and damage associated with the ultrafine particles, this must be an important focus of repair and support. Nutrients such as coenzyme Q10 (CoQ10), resveratrol, tocotrienols, acetyl-L-carnitine, and lipoic acid act to decrease mitochondrial oxidative damage, and support repair and function.,,, CoQ10, lipoic acid, resveratrol, and tocotrienols each play a role in regulating neuroinflammation, in part by reducing the damage associated with microglial activation. , Many of these things have been studied in neurodegenerative conditions such as Parkinson’s disease, Alzheimer’s and multiple sclerosis. ,,
The importance of membrane repair also cannot be neglected. In settings of oxidative stress, part of what contributes to cellular destruction and death is a loss of membrane integrity due to lipid peroxidation and permeabilisation in part due to altered purinergic signaling. This further contributes to damage as the membrane potential and gradient of electrolytes and other substances across the membrane cannot be maintained. This is not limited to the mitochondria but extends to the membranes of all cellular structures. Although the body has many mechanisms constantly in process to combat this damage and repair the cell, in settings of extensive damage this process also becomes inadequate.
Membrane lipid replacement (MLR) is a tool to support the body’s need for the phospholipids necessary to repair cellular membranes. Ideally MLR should be a blend of phospholipids including phosphatidylcholine (PC), phosphatidylinositol (PI), phosphatidylethanolamine (PE), phosphatidylserine (PS) and phosphatidylgycerol (PG) as each of these are abundant in cellular membranes, with PC being the most prominent comprising 50% of cellular membrane lipids. When lipids such as these are taken in a supplement format and bound to an antioxidant carrier in excess of the nominal amounts found in foods, they are absorbed intact via micelles, liposomes, or phospholipid globules, and are able to reach their final destinations of the cellular membranes without degradation.,
MLR should be considered as a long-term strategy for chronic diseases and toxin exposures such as this because the damages to cellular membranes and other structures are not temporary and continue, waxing and waning with exposures and other events such as infection in which more oxidative stress is generated. Additional substances such as vitamin E and essential fatty acids also support membrane health and function. Vitamin E, a lipid-soluble vitamin and antioxidant, is one of the main defences against oxidation of the body’s lipid membranes as it limits the waterfall effect that occurs with lipid peroxidation. Essential fatty acids simultaneously have an anti-inflammatory effect and support membrane health and fluidity.,
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