Protecting Yourself from the Damaging Effects of Air Pollution
Share this post
How to keep your cells healthy in the face of particulate matter pollution in the air
The more populated our world becomes, the more the by-products of development, consumerism, and transportation become an issue. Many of the effects are obvious: we can’t avoid seeing supermarkets popping up where there once were trees, new shiny apartments where there used to be convenience stores, and commutes that are twice as long when we go to work.
Air pollution is a major issue that remains “unseen”, making it easy to neglect. Yet medical providers and the general public alike are aware of the increase in conditions related to air pollution, including allergies and asthma,,,, heart disease, diabetes, autoimmunity, and even early aging.,,,
When it comes to air pollution, smaller size particles (less than or equal to 2.5 micrometers, known as PM2.5) penetrate more deeply into the lungs, thereby causing oxidative stress and pro-inflammatory effects., Ultrafine particulates that are smaller than 100 nanometers (PM0.1) are potentially even more problematic because they are able to travel from the lungs into the circulation, making them far more toxic and immunogenic than their larger counterparts., 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 such as mercury, and endotoxin from mold cell walls.
Exposure to fine or ultrafine air pollution particles also alters the blood-brain barrier integrity and generates oxidative stress, neuroinflammation, and an autoimmune response directed at the tissues and cells in the brain.
After passing into the bloodstream, the ultrafine PM0.1 particles can then penetrate the cells, induce cellular swelling, and damage the mitochondria (the energy-producing organelles within human cells).,, Glutathione, an important antioxidant in the cells, is used in the body’s efforts to remove the damaging particles and balance the oxidative stress induced by this damage. Over time, however, the body’s glutathione levels run low, and the damage roars on.
Exposure to fine or ultrafine air pollution particles also alters the blood-brain barrier integrity and generates oxidative stress, neuroinflammation, and an autoimmune response directed at the tissues and cells in the brain. , This has even been seen in children and young adults, and is characterized by accumulation of amyloid-beta and alpha-synuclein in the brain, proteins associated with Alzheimer’s and Parkinson’s disease.
Additionally, air pollution exposure increases blood pressure and capillary permeability (the “leakiness” of blood vessels). Exacerbations in patients with Alzheimer’s and Parkinson’s disease as well as relapses in patients with multiple sclerosis have been associated with air pollution, likely due to some of these mechanisms.,
What can we do to protect our cells and the brain?
As discussed in the previous article pertaining to air pollution, dietary supplements that increase nuclear factor erythroid 2 (NF-E2)-related factor (Nrf2) may be of benefit in enhancing glutathione production to help combat the effects of air pollution. Substances that induce Nrf2 include gingko biloba, green tea polyphenols, and lipoic acid.,, These natural products may be of particular benefit to the elderly population, as even without exposure to excessive air pollution, the ability of the body to upregulate Nrf2 and the body’s glutathione levels both decline with age.,
In many cases, the cellular damage caused by particulate matter exceeds the body’s ability to generate the level of antioxidants and other components that are necessary for mitochondrial, cellular, and membrane repair.
In many cases, the cellular damage caused by particulate matter exceeds the body’s ability to generate the level of antioxidants and other components that are necessary for mitochondrial, cellular, and membrane repair. Because intracellular glutathione is depleted with exposure to air pollution, explicit strategies for increasing cellular glutathione levels should be considered. Many substances – such as some of the other antioxidants, selenium, and N-acetylcysteine – can support glutathione production, but the most direct means is by supplementing glutathione directly through acetyl-glutathione or via liposomal delivery, both of which have been shown to significantly raise intracellular glutathione.,
Supporting mitochondrial function and repair
Substances targeting mitochondrial function and repair are of utmost value, because the mitochondria are the focal point of damage associated with the ultrafine particles. Nutrients such as coenzyme Q10 (CoQ10), lipoic acid, tocotrienols, acetyl-L-carnitine, and resveratrol, act to decrease mitochondrial oxidative damage and support cellular repair pathways.,,, CoQ10, lipoic acid, resveratrol, and tocotrienols each play a role in calming neuroinflammation, and reduce activation of the immune system responders in the brain., Many of these supplemental nutrients have also been studied in neurodegenerative conditions such as Parkinson’s disease, Alzheimer’s, and multiple sclerosis, each of which can be further compromised by air pollution.,,
Nutrients such as coenzyme Q10 (CoQ10), lipoic acid, tocotrienols, acetyl-L-carnitine, and resveratrol, act to decrease mitochondrial oxidative damage and support cellular repair pathways.
Supporting cellular membrane repair
The ongoing maintenance and repair of cellular membranes is also critical., The damage to cell membranes caused by air pollution is not temporary. It persists, waxing and waning with exposures and other events such as infection, in which more oxidative stress is generated. Membrane lipid replacement (MLR) is a strategy to support the body’s need for the phospholipids necessary to repair cellular membranes.
Ideally, MLR is accomplished with a blend of phospholipids including phosphatidylcholine (PC), phosphatidylinositol (PI), phosphatidylethanolamine (PE), phosphatidylserine (PS), and phosphatidylgycerol (PG), as each of these is abundant in cellular membranes. PC is the most prominent, comprising approximately 50% of cellular membrane lipids. When lipids such as these are taken in a supplement format, bound to an antioxidant carrier, they can be absorbed intact and are better able to reach their target tissues without degradation.,
In addition to the phospholipids that are essential for cellular membranes, substances such as vitamin E (particularly tocotrienols) and essential fatty acids also support membrane health and function.
In addition to the phospholipids that are essential for cellular membranes, substances such as vitamin E (particularly tocotrienols) and essential fatty acids also support membrane health and function. Vitamin E, a lipid-soluble vitamin and antioxidant, is one of the body’s main defences against oxidation of the cellular (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.,
The most important step in preventing health problems is to stop them before they occur – namely by limiting our exposure to particulate matter. Targeted nutritional support including fat-soluble antioxidants and glutathione, necessary components for cellular membrane repair, and essential fatty acids also can help to protect our cells from this often-progressive damage.
Click here to see References
 Khafaie MA, et al. Critical review of air pollution health effects with special concern on respiratory health. J Air Pollution Health. 2016 May 29;1(2):123-36.
 Bowatte G, et al. The influence of childhood traffic-related air pollution exposure on asthma, allergy and sensitization: a systematic review and a meta-analysis of birth cohort studies. Allergy. 2015 Mar;70(3):245-56.
 Orellano P, et al. Effect of outdoor air pollution on asthma exacerbations in children and adults: Systematic review and multilevel meta-analysis. PLoS One. 2017 Mar 20;12(3):e0174050.
 Kabashima K, et al. Linking air pollution to atopic dermatitis. Nat Immunol. 2016 Dec 16;18(1):5-6.
 Shah AS, et al. Global association of air pollution and heart failure: a systematic review and meta-analysis. Lancet. 2013 Sep 21;382(9897):1039-48.
 Liu C, et al. Associations between long-term exposure to ambient particulate air pollution and type 2 diabetes prevalence, blood glucose and glycosylated hemoglobin levels in China. Environ Int. 2016 Jul-Aug;92-93:416-21.
 Sun G, et al. Association between air pollution and the development of rheumatic disease: a systematic review. Int J Rheumatol. 2016;2016:5356307.
 Lee EY, et at. Traffic-related air pollution and telomere length in children and adolescents living in Fresno, CA: a pilot study. J Occup Environ Med. 2017 May;59(5):446-452.
 Mazzoli-Rocha F, et al. Roles of oxidative stress in signaling and inflammation induced by particulate matter. Cell Biol Toxicol. 2010 Oct;26(5):481-98.
 Negherbon JP, et al. Whole blood cytokine response to local traffic-related particulate matter in Peruvian children with and without asthma. Front Pharmacol. 2017 Mar 30;8:157.
 Stone V, et al. Air pollution, ultrafine and nanoparticle toxicology: cellular and molecular interactions. IEEE Trans Nanobioscience. 2007 Dec;6(4):331-40.
 Terzano C, et al. Air pollution ultrafine particles: toxicity beyond the lung. Eur Rev Med Pharmacol Sci. 2010 Oct;14(10):809-21.
 Rylander R. Endotoxin in the environment–exposure and effects. J Endotoxin Res. 2002;8(4):241-52.
 Xia T, et al. Quinones and aromatic chemical compounds in particulate matter induce mitochondrial dysfunction: implications for ultrafine particle toxicity. Environ Health Perspect. 2004 Oct;112(14):1347-58.
 Li N, et al. Ultrafine particulate pollutants induce oxidative stress and mitochondrial damage. Environ Health Perspect. 2003 Apr;111(4):455-60.
 Li Ning, et al. Comparison of the pro-oxidative and proinflammatory effects of organic diesel exhaust particle chemicals in bronchial epithelial cells and macrophages. J Immunol. 2002 Oct 15;169(8):4531-4541.
 Jayaraj RL, et al. Outdoor ambient air pollution and neurodegenerative diseases: the neuroinflammation hypothesis. Curr Environ Health Rep. 2017 Jun;4(2):166-179.
 Calderón-Garcidueñas L, et al. Air pollution and children: neural and tight junction antibodies and combustion metals, the role of barrier breakdown and brain immunity in neurodegeneration. J Alzheimers Dis. 2015;43(3):1039-58.
 Calderón-Garcidueñas L, et al. Long-term air pollution exposure is associated with neuroinflammation, an altered innate immune response, disruption of the blood-brain barrier, ultrafine particulate deposition, and accumulation of amyloid beta-42 and alpha-synuclein in children and young adults. Toxicol Pathol. 2008 Feb;36(2):289-310.
 Wright JC, Ding Y. Pathophysiological effects of particulate matter air pollution on the central nervous system. Environmental Disease. 2016 Jul 1;1(3):85.
 Babadjouni RM, et al. Clinical effects of air pollution on the central nervous system; a review. J Clin Neurosci. 2017 May 18. pii: S0967-5868(17)30228-X
 Vojinović S, et al. Disease relapses in multiple sclerosis can be influenced by air pollution and climate seasonal conditions. Vojnosanit Pregl. 2015 Jan;72(1):44-9.
 Liu XP, et al. Extract of Ginkgo biloba induces phase 2 genes through Keap1-Nrf2-ARE signaling pathway. Life Sci. 2007 Apr 3;80(17):1586-91.
 Na HK, Surh YJ. Modulation of Nrf2-mediated antioxidant and detoxifying enzyme induction by the green tea polyphenol EGCG. Food Chem Toxicol. 2008 Apr;46(4):1271-8.
 Suh JH, et al. Decline in transcriptional activity of Nrf2 causes age-related loss of glutathione synthesis, which is reversible with lipoic acid. Proc Natl Acad Sci U S A. 2004 Mar 9;101(10):3381-6.
 Zhang H, et al. Nrf2-regulated phase II enzymes are induced by chronic ambient nanoparticle exposure in young mice with age-related impairments. Free Radic Biol Med. 2012 May 1;52(9):2038-46.
 Lang CA, et al. Low blood glutathione levels in healthy aging adults. J Lab Clin Med. 1992 Nov;120(5):720-5.
 Okun JG, et al. S-Acetylglutathione normalizes intracellular glutathione content in cultured fibroblasts from patients with glutathione synthetase deficiency. J Inherit Metab Dis. 2004;27(6):783-6.
 Zeevalk GD, et al. Liposomal-glutathione provides maintenance of intracellular glutathione and neuroprotection in mesencephalic neuronal cells. Neurochem Res. 2010 Oct;35(10):1575-87.
 Sridharan V, et al. A tocotrienol-enriched formulation protects against radiation-induced changes in cardiac mitochondria without modifying late cardiac function or structure. Radiat Res. 2015 Mar;183(3):357-66.
 Lagouge M, et al. Resveratrol improves mitochondrial function and protects against metabolic disease by activating SIRT1 and PGC-1alpha. Cell. 2006 Dec 15;127(6):1109-22.
 Liu J. The effects and mechanisms of mitochondrial nutrient alpha-lipoic acid on improving age-associated mitochondrial and cognitive dysfunction: an overview. Neurochem Res. 2008 Jan;33(1):194-203.
 Hagen TM, et al. Acetyl-L-carnitine fed to old rats partially restores mitochondrial function and ambulatory activity. Proc Natl Acad Sci U S A. 1998 Aug 4;95(16):9562-6.
 Tan SW, et al. Inhibitory effects of palm α-, γ- and δ-tocotrienol on lipopolysaccharide-induced nitric oxide production in BV2 microglia. Cell Immunol. 2011;271(2):205-9.
 Zhang F, et al. Anti-inflammatory activities of resveratrol in the brain: role of resveratrol in microglial activation. Eur J Pharmacol. 2010 Jun 25;636(1-3):1-7.
 Dumont M, et al. Coenzyme Q10 decreases amyloid pathology and improves behavior in a transgenic mouse model of Alzheimer’s disease. J Alzheimers Dis. 2011;27(1):211-23.
 Salinthone S, et al. Lipoic acid: a novel therapeutic approach for multiple sclerosis and other chronic inflammatory diseases of the CNS. Endocr Metab Immune Disord Drug Targets. 2008 Jun;8(2):132-42.
 Beal MF. Mitochondrial dysfunction and oxidative damage in Alzheimer’s and Parkinson’s diseases and coenzyme Q 10 as a potential treatment. J Bioen Biomemb. 2004 Aug 1;36(4):381-6.
 Gombault A, Baron L, Couillin I. ATP release and purinergic signaling in NLRP3 inflammasome activation. Front Immunol. 2013 Jan 8;3:414.
 van Meer G, Voelker DR, Feigenson GW. Membrane lipids: where they are and how they behave. Nat Rev Mol Cell Biol. 2008 Feb;9(2):112-24.
 Nicolson GL, Ash ME. Membrane Lipid Replacement for chronic illnesses, aging and cancer using oral glycerolphospholipid formulations with fructooligosaccharides to restore phospholipid function in cellular membranes, organelles, cells and tissues. Biochim Biophys Acta. 2017 Apr 18.
 Janmey PA Kinnunen PK. Biophysical properties of lipids and dynamic membranes. Trends Cell Biol. 2006 Oct;16(10):538-46.
 Zierenberg O, Grundy SM. Intestinal absorption of polyenephosphatidylcholine in man. J Lipid Res. 1982 Nov;23(8):1136-42.
 Dobbins WO 3rd. Morphologic aspects of lipid absorption. Am J Clin Nutr. 1969 Mar;22(3):257-65.
 Burton GW, Ingold KU. Autooxidation of biological molecules. 1. The antioxidant activity of vitamin E and related chain-breaking phenolic antioxidants in vitro. J Am Chem Soc 1981; 103: 6472-6477.
 Yates CM, et al. Pharmacology and therapeutics of omega-3 polyunsaturated fatty acids in chronic inflammatory disease. Pharmacol Ther. 2014 Mar;141(3):272-82.
 Maulucci G, et al. Fatty acid-related modulations of membrane fluidity in cells: detection and implications. Free Radic Res. 2016 Nov;50(sup1):S40-S50.
Share this post
Dr. Carrie Decker
Melatonin: Is It Really the Sedative We Think It Is?
Numerous clinical studies suggest otherwise, a look at their findings not related to sleep Since its discovery in 1958, we have learned much about the diverse functions of melatonin in animals, where it serves not only as a circadian rhythm regulator, but also as an antioxidant, immunoregulatory and anti-inflammatory molecule, hormone, metal chelator, and…
Pine Bark for Blood Vessels Big and Small, Part 2 of 2
A natural solution for erectile dysfunction, cold hands, and vision In Post 1 of 2, we explored the effects of maritime pine bark extract on blood pressure, hemorrhoids, and varicose veins. In this post we’ll zoom in on the extract’s effects on smaller blood vessels. Let’s take a closer look at the vascular diseases…
Do alkaline diets work? (Part 2 of 2)
Part 2 of 2: Managing Acid-Base Balance in the Body This post is part two of an exploration of acid-alkaline balance, its importance in health, and its response to dietary choices. Check out part 1 to learn about subclinical metabolic acidosis and the serious health conditions it may be associated with. Managing and measuring…
The Multivitamin Debate
What does science say about multivitamin and mineral supplementation? Dietary supplement use is common in the United States, with more than half of the population using such products.,,, Similarly, a majority of health professionals, including physicians and dieticians, use dietary supplements themselves and recommend them to patients.,, Among supplement users, multivitamin and mineral supplements…
How Harmful Is Air Pollution?
When breathing is a health risk, what can be done? Take a deep breath in. Slowly exhale. Deep, conscious breathing can be restorative, balancing, and calming. The experience is even better in nature – a forest with trees towering overhead, or by the ocean with the sand between our toes. We take it for…
Vitamin D: The Sunshine Vitamin
The role of vitamin D in autoimmunity and mood Vitamin D is known as the “sunshine vitamin” because it is generated within the skin upon exposure to ultraviolet B (UVB) rays, the rays responsible for suntans. Vitamin D is essential for strong bones, immunity, and many other bodily functions.,, In the absence of sun…