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Poor air quality from industrial activities and the recent wildfires is a looming health risk for us all. Here are evidence-based strategies for removing toxic compounds from your body and mitigating the health risks of air pollution.
Besides the tragic loss of life and property, casualties to wildlife, and devastation to nature wrought by the recent wildfires, a toll to human health will be an inevitable consequence. Without taking into account the recent impact of these natural disasters, air pollution already claims more than two million lives per year (1).
Particulate Matter Emission from Forest Fires
Especially troubling is the particulate matter content of air pollution, which is connected to a litany of adverse health outcomes (2). Airborne particulate matter, which “consists of a heterogeneous mixture of solid and liquid particles suspended in air that varies continuously in size and chemical composition in space and time,” is more dangerous than both ground-level ozone and carbon monoxide (3). Among the constituents of particulate matter are biological components such as cell fragments and endotoxin, crustal material, heavy metals, particle-bound water, sulfates, nitrates, organic and elemental carbon, and dangerous combustion byproducts called polycyclic aromatic hydrocarbons such as naphthalene and benzo(a)pyrene (3, 4).
Anthropogenic, or manmade sources, such as construction sites, cooking, vehicle exhaust, agricultural or industrial byproducts, road erosion, mining operations, and combustion of solid-fuels including coal, oil, gasoline, biomass, and lignite can generate particulate matter (5, 6, 7, 8). However, particulate matter production can also emerge from natural sources such as sea spray, vegetation, volcanoes, dust storms, windblown soil, and most relevant to recent current events: forest fires (9).
Size Matters: PM-2.5 in Airborne Pollution Poses Massive Health Risks
The Environmental Protection Agency (EPA) classified particulate matter into ultra-fine (PM-0.1), fine (PM-2.5), and coarse (PM-10) based on its aerodynamic diameter in micrometers, which in turn influences its dissemination in the atmosphere and respiratory penetrance when inhaled by a living organism (10). For comparison, the average human hair and particle of fine beach sand have diameters of 70 and 90 micrometers, respectively (11). Fine particulate matter, which can be either directly released into the air or converted from gaseous precursors, poses monumental risks to health due to its suspension in air for weeks to months and its ability to be transported hundreds or thousands of kilometers (12).
The nasal cilia and mucus filter coarse particulates, and the coarse particulates that do settle in the trachea or bronchi of the respiratory passages are expelled via sneezing and coughing reflexes (13). However, the smaller particulates tend to lodge in the respiratory tract at increased rates, depositing deep within sites of gaseous exchange such as the respiratory bronchioles and the alveoli of the lungs, and ultimately translocate into tissue and circulation (14, 15).
At a mechanistic level, tissue damage to airways and inflammation can occur due to transition metals present in particulate matter, which induce production of electron-stealing, tissue-damaging reactive oxygen species (ROS) (3). Similarly, transition metals such as iron elicit genotoxic effects, damaging cellular genetic material (16). Disruption of cell membrane integrity is a consequence of the elemental components of particulate matter, which can lead to pulmonary fibrosis (17).
Particulate matter-mediated induction of pro-inflammatory cytokines, or intercellular signaling molecules which can elicit systemic inflammation, is implicated in cardiovascular disease (18). PM-2.5 alters vascular endothelial cells membranes, promoting permeability and consequent development of atherosclerotic lesions (19). Furthermore, PM-2.5 induces cardiac hypoxia, or oxygen deprivation, which can modify the function of vascular endothelial cell membranes and lead to plaque deposition (20). Specifically, “translocation of PM-2.5 from the lung…directly into the blood exacerbates the progression of atherosclerosis by initiating acute inflammatory responses” (19).
In addition, oxidative stress and inflammation caused by particulate matter may promote apoptosis, or programmed cell death (3). Lipopolysaccharide from gram-negative bacteria present in particulate matter can induce pathologic intestinal permeability, the precursor to autoimmune disease, as well as generate a milieu of metabolic endotoxemia which favors the development of airway dysfunction, obesity, metabolic syndrome, atherogenesis, and cardiovascular disease (21, 22).
The Correlation Between PM-2.5 and Disease
Cardiovascular disorders, including acute coronary syndrome, hypertension, venous thrombosis (blood clots), arrhythmia, stroke, exacerbation of congestive heart failure, increased rates of heart attacks, and aberrations in cholesterol profiles, can manifest from PM-2.5 exposure (3, 23, 24, 25, 26). Increases in PM-2.5 are associated with increased carotid intimal-media thickness, a measure of cardiovascular risk and marker for the accumulation of atheromas, or abnormal masses of fatty material in the arterial wall (27). Decreased tone of the anti-inflammatory ‘rest and digest’ parasympathetic arm of the nervous system, as exhibited by depressed heart rate variability, is also associated with exposure to PM-2.5 (28).
Particulate matter is likewise correlated with adult diabetes, even after accounting for other risk factors such as ethnicity and obesity (29). PM-2.5 is also associated with reduced lung function, elevated respiratory-related mortality, and increased hospital admissions for pneumonia, asthma, and chronic obstructive pulmonary disease (COPD) (11, 24, 30). In fact, at a global level, particulate matter is responsible for approximately 5% of deaths due to lung cancer and 3% of cardiopulmonary deaths (31). PM-2.5 in particular reduces lifespan by an estimated 8.6 months (32). This is not withstanding the financial toll incurred by particulate matter, which cost China and the United States $106.5 billion and $29 billion, respectively, in one year alone (3).
Optimize Phase II Detoxification to Protect Yourself
In the first phase of hepatic detoxification, toxins undergo chemical modifications such as oxidation, reduction, or hydrolysis, and are therefore rendered even more reactive with the potential to wreak havoc. The second phase, thus, is essential in order to render phase I metabolites more hydrophilic, or water-soluble, so that they can be excreted. Sulfation, acetylation, glucuronidation, and glutathione conjugation are examples of phase II processes whereby the phase I intermediate is attached to a conjugating agent by a transferase enzyme, in order for the toxicant to be eliminated from the body.
Genetic polymorphisms, as well as liver congestion due to over-burdening of the detoxification systems, can create a bottleneck where phase I outpaces phase II, which leads to an accumulation of free radicals that deplete the body of the master endogenous antioxidant, glutathione (33). Signaling is then directed down pathways that activate mitogen activated protein kinase (MAPK) and nuclear factor kappa beta (NFkB), which leads to a pro-inflammatory cascade (34).
In order to promote removal of harmful substances from the body, it is essential to ensure phase II detoxification is running unimpeded. As a fundamental endogenous defense system against oxidative stress, phase II enzymes scavenge reactive oxygen species, metabolize foreign compounds, and have demonstrated protective effects against xenobiotics including ozone, tobacco smoke, and diesel exhaust particles (35, 36, 37).
As noted by Fahey and colleagues, “Induction of phase 2 detoxication enzymes [e.g., glutathione transferases, epoxide hydrolase, NAD(P)H: quinone reductase, and glucuronosyltransferases] is a powerful strategy for achieving protection against carcinogenesis, mutagenesis, and other forms of toxicity of electrophiles and reactive forms of oxygen” (33). Researchers propose that induction of phase II enzymes may represent a powerful strategy to combat the oxidative stress resulting from oxidant pollutants (37).
Eat More Cruciferous Vegetables
Some of the cruciferous vegetables, belonging to the Brassicaceae or mustard family, include arugula, broccoli, Brussel sprouts, red, green, Chinese, and savoy cabbage, cauliflower, chard, collard greens, radish, rapini, rutabaga, turnip and turnip greens, wasabi, and watercress.
Sulforaphane, an isothiocyanate compound enriched in all cruciferous or Brassica vegetables, but particularly concentrated in broccoli sprouts, is the most potent inducer of phase II enzymes yet identified (33, 37). In fact, “3-day-old sprouts of cultivars of certain crucifers including broccoli and cauliflower contain 10-100 times higher levels of glucoraphanin (the glucosinolate of sulforaphane) than do the corresponding mature plants” (33, p. 10367).
Amplifying the levels of phase II enzymes with sulforaphane can inhibit diesel exhaust particle-stimulated production of inflammatory cytokines by airway epithelial cells (61). As a chemoprotective agent, sulforaphane also decreases the incidence, number, and rate of development of mammary tumors in rats treated with the carcinogenic chemical dimethylbenz(a)anthracene (33).
Proof of concept was provided by a twelve-week randomized clinical trial which evaluated the effects of a broccoli sprout-derived beverage on the urinary excretion of airborne pollutants in participants from the Yangtze River delta region of China notorious for air pollution (38). Based on increased appearance of glutathione-derived conjugates of the pollutants benzene and acrolein in the urine of those who received the broccoli sprout beverage, the researchers concluded, “intervention with broccoli sprouts enhances the detoxication of some airborne pollutants and may provide a frugal means to attenuate their associated long-term health risks” (38).
In a similar study, subjects recruited from the polluted Qidong, China, consumed either a glucoraphanin-rich or sulforaphane-rich broccoli sprout-derived beverage in a randomized cross-over clinical trial (39). Excretion of glutathione-derived conjugates of several pollutants, including acrolein, crotonaldehyde and benzene, were significantly increased compared to baseline (39). In other words, the broccoli sprout intervention enhanced phase II, glutathione-mediated elimination of toxic air pollutants.
Consume Botanical Agents that Enhance Phase II Detoxification
Cinnamaldehyde, the flavonoid that imparts a characteristic odor and flavor to cinnamon, causes the transcription factor called nuclear erythroid 2-related factor 2 (Nrf2) to translocate to the cell nucleus and bind to a sequence known as the antioxidant response element (ARE), which “regulates the expression of a large battery of genes involved in the cellular antioxidant and anti-inflammatory defense as well as mitochondrial protection” (40). Activation of ARE, in turn, stimulates glutathione production and induces expression of phase II enzymes to promote detoxification (40). Not only does this cinnamon compound have the chemopreventative potential to protect cells from the toxic effects of chemotherapy drugs, but it also may support the detoxification of air pollution.
Rooibos and Honeybush Teas
In addition, rooibos and honeybush teas have been demonstrated to significantly augment activity of phase II enzymes such as glutathione S-transferase, as well as increase the ratio of reduced to oxidized glutathione, both of which are important for limiting the damage done by heavy metals, free radicals, and lipid peroxides (41, 42). In this way, these natural agents may be able to confer protection against the oxidative damage and mutagenesis resulting from particulate matter exposure.
Another traditional herb, Indian holy basil, significantly increases levels of glutathione (GSH) and the antioxidant enzymes glutathione transferase (GST), glutathione peroxidase (GSPx), and glutathione reductase (GSRx), the catalysts which detoxify xenobiotic substrates, neutralize oxidative stress, and regenerate glutathione, respectively (43). Likewise, holy basil increases levels of superoxide dismutase (SOD), an enzyme which neutralizes cell-damaging reactive oxygen species (43). Holy basil also maintains levels of glutathione as well as all of the aforementioned enzymes in the face of gamma radiation and reduces the level of lipid peroxidation (oxidative deterioration of lipids) induced by radiation (43).
A powerhouse botanical which prevents glutathione depletion is curcumin, a yellow compound in turmeric root (44, 62). In a rat model, curcumin extract protected against liver injury after exposure to the toxic chemical carbon tetrachloride (CCl4) by improving levels of glutathione, superoxide dismutase, and glutathione peroxidase (44). As a result, damage to cell membranes, as indicated by lipid peroxidation, was reduced, and CCl4-mediated elevation in the liver enzyme AST was prevented (44). Curcumin has similarly been demonstrated to prevent mitochondrial dysfunction and reduce hepatoxicity induced by metals such as arsenic, lead, mercury, copper, chromium, and cadmium (45).
Ginger, Resveratrol, and Quercetin
Along similar lines, ginger rhizome protects against liver fibrosis induced by the toxin CCl4 by significantly increasing glutathione and superoxide dismutase (46). In this study, ginger also significantly decreased levels of the mutagenic and carcinogenic compound malondialdehyde, indicating that ginger suppressed CCl4-mediated damage to lipids (46). Resveratrol, on the other hand, from foods such as grapes, blueberries, and cranberries, increases expression of the antioxidant enzymes superoxide dismutase and glutathione peroxidase in a concentration-dependent manner, which accounts for the vascular protective effects of this phytonutrient (47). In another in vitro study, both resveratrol and quercetin (a flavonoid found in plant foods such as apples and onions) increased levels of glutathione and antioxidant defense enzymes including superoxide dismutase, glutathione transferase, and glutathione peroxidase, as well as adiponectin, an anti-inflammatory signaling molecule secreted by fat cells (48).
Increase Antioxidant Supplementation
Emissions of particulate matter are associated with excess generation of reactive oxygen species (ROS), agents which perpetuate pathology and require antioxidants for neutralization (49). In South Brazil subjects exposed to particulate matter from a coal electric-power plant, surrogate markers for oxidative stress including byproducts of lipid degradation called thiobarbituric acid reactive substances (TBARS) and protein carbonyls (PC), reflecting oxidative damage to proteins, were elevated (49). Levels of endogenous antioxidants, including reduced glutathione (GSH) and vitamin E, were also compromised in those exposed to coal combustion (49).
All of these biomarkers normalized after daily supplementation with 500 mg vitamin C and 800 mg vitamin E, indicating that, “The antioxidant intervention was able to confer a protective effect of vitamins C and E against the oxidative insult associated with airborne contamination derived from coal burning of an electric-power plant” (49, p. 175).
Consume More of the Most Antioxidant-Rich Foods
In addition to targeted supplementation under the guidance of a licensed physician, increasing consumption of colorful plant foods is a therapeutic strategy to increase antioxidant intake. Phytochemicals, or bioactive constituents derived from plants, can be classified as antioxidants due to their participation in redox reactions where electrons are exchanged (50). Not only do plant antioxidants defend against reactive oxygen and nitrogen species, but they also favorably modulate gene expression and promote cell maintenance, repair of genetic material, and longevity (51, 52, 53).
Berries have high antioxidant potential due to active phytochemical constituents including lignans, phenolic acids, stibenoids, tannins, and flavonoids such as anthocyanidins (54). Ranking highest in antioxidant capacity are dried varieties of amla (Indian gooseberry), dog rose, and bilberries, but fresh black currants, blackberries, cranberries, crowberries, goji berries, strawberries, and zebeck (red sour berries) also rank high (50). In an analysis of 581 fruits and vegetables, artichokes, green and red chili peppers, lemon skin, curly kale, and okra flour, as well as dried varieties of apples, plums, and apricots, were classified as antioxidant-rich (50).
Although herbs and spices make up a small proportion of a meal, they also represent a potent source of antioxidants. Researchers state, “Sorted by antioxidant content, clove has the highest mean antioxidant value, followed by peppermint, allspice, cinnamon, oregano, thyme, sage, rosemary, saffron and estragon, all dried and ground” (50). Traditional botanical medicines are also reservoirs of antioxidants, which explains their therapeutic properties. Half of the plant medicine products analyzed ranked in the 90th percentile or higher for antioxidant capacity (50).
Beverages worthy of inclusion for boosting antioxidant levels are unprocessed tea powders, tea leaves, and coffee beans. The antioxidant content in coffee is attributable to heterocyclic and volatile aromatic compounds, caffeine, and polyphenols, whereas monomer catechins such as epigallocatechin gallate (EGCG) and polymerized catechin such as theaflavin and thearubigen predominate in green tea and black tea, respectively (50). Chocolate is likewise a prominent source of antioxidants, with antioxidant content correlating directly with percentage cocoa (50).
Include Healthy Fats and Oils
Even short-term exposure to PM-2.5 is associated with dysfunction in endothelial cells, or the thin layer of simple squamous cells that lines blood vessels and lymphatic vessels, interfacing between luminal contents and the vessel wall (55, 56). A disturbance in flow mediated dilation (FMD), or the capacity of a blood vessel to dilate with increased blood flow, reflects endothelial dysfunction, a key change in the development of atherosclerosis (57).
In middle-age volunteers, supplementation with three grams per day of olive oil for four weeks prior to exposure to concentrated ambient particulate (CAP) matter has been shown to prevent the reduction in FMD induced by particulate matter (58). Not only that, but this olive oil intervention blunted the adverse changes in blood markers associated with vasoconstriction (the narrowing of vessels) and fibrinolysis (the enzymatic break-down of blood clots) (58). The researchers suggest that dietary inclusion of olive oil may “prevent deleterious effects of CAP exposure on vascular function and might, therefore, represent a practical approach to reduce the mortality and morbidity of cardiovascular diseases associated with PM exposure” (58).
In another randomized, double-blinded, controlled study of healthy middle-aged participants by the same group, supplementation with three grams per day of fish oil, but not olive oil, prevented deleterious changes in lipids, cardiac rhythm, and heart rate variability resulting from exposure to particulate matter (23). A recent study also underscored how omega-3 fatty acids prevent systemic and pulmonary inflammation as well as oxidative stress induced by fine particulate matter, when administered either before or after exposure (59). The authors conclude, “Our findings demonstrate that elevating tissue omega-3 levels can prevent and treat fine particle-induced health problems and thereby present an immediate, practical solution for reducing the disease burden of air pollution” (59).
Therefore, it is prudent to incorporate high quality, extra virgin olive oil, as well as omega-3 fatty acids from wild-caught, low-mercury fatty fish such as salmon, mackerel, herring, or sardines. Omega-3s can also be obtained from pasture-raised eggs and grass-fed meat, the latter of which has been shown to predictably raise plasma and platelet long chain omega-3 polyunsaturated fatty acid status (60). Although supplementing with a professional-grade, molecularly distilled fish oil is a viable option with physician approval, consuming whole foods sources of omega-3s provides the added benefit of B vitamins, minerals, and amino acids, phospholipids, required for detoxification.
When used as part of a comprehensive regimen that incorporates an anti-inflammatory diet, stress management, exercise, and sleep optimization, these food, herb, and nutraceutical-based strategies can minimize the deleterious effects of exposure to air pollution, and optimize detoxification pathways to protect us from the onslaught of modern-day toxicant exposures.
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1. Shah, A.S.V. et al. (2013). Global association of air pollution and heart failure: a systematic review and meta-analysis. The Lancet, 382, 1039-1048.
2. Palacios, N. et al. (2017). Air Pollution and Risk of Parkinson's Disease in a Large Prospective Study of Men. Environmental Health Perspectives, 125(8), 087011. doi: 10.1289/EHP259.
3. Kim, K-H., Kabir, E., & Kabir, S. (2015). A review on the human health impact of airborne particulate matter. Environmental Internationl, 74, 136-43.
4. Cheung, K. et al. (2011). Spatial and temporal variation of chemical composition and mass closure of ambient coarse particulate matter (PM10–2.5) in the Los Angeles area. Atmosphere and Environment, 45, 2651-2662.
5. Juda-Rezler, K., Reizer, M., & Oudinet, J.P. (2011). Determination and analysis of PM10 source apportionment during episodes of air pollution in Central Eastern European urban areas. The Case of Wintertime, 45, 6557-6566.
6. Srimuruganandam, B., & Nagendra, S. (2012). Source characterization of PM10 and PM2.5 mass using a chemical mass balance model at urban roadside. Science of the Total Environment, 433, 8-19.
7. De-Kok, T.M.C.M., et al. (2006). Toxicological assessment of ambient and traffic-related particulate matter: a review of recent studies. Mutation Research, 2-3, 103-122.
8. Balakrishnan, K. et al. (2002). Daily average exposures to respirable particulate matter from combustion of biomass fuels in rural households of southern India. Environmental Health Perspectives, 110(11),1069-1075.
9. Misra, C. et al. (2001). Development and evaluation of a continuous coarse (PM10–PM2.5) particle monitor. Journal of the Air Waste Management Association, 51, 1309-1317.
10. Esworthy, R. (2013). Air quality: EPA's 2013 changes to the particulate matter (PM) standard. Congressional Research Service 7-5700, R42934, 6.
11. Guaita, R. et al. (2011). Short-term impact of particulate matter (PM2.5) on respiratory mortality in Madrid. International Journal of Environmental Health Research, 260-274.
12. Johansson, C., Norman, M., & Gidhagen, L. (2007). Spatial & temporal variations of PM10 and particle number concentrations in urban air. Environmental Monitoring Assessment, 127(1-3), 477-487.
13. Cadelis, G. et al. (2014). Short-term effects of the particulate pollutants contained in Saharan dust on the visits of children to the emergency department due to asthmatic conditions in Guadeloupe (French Archipelago of the Caribbean). PLoS ONE, 9(3), e91136.
14. Londahl, J. et al. (2006). A set-up for field studies of respiratory tract deposition of fine and ultrafine particles in humans. Journal of Aerosol Science, 9, 1152-1163.
15. Valavanidis, A., Fiotakis, K., & Vlachogianni, T. (2008). Airborne particulate matter and human health: toxicological assessment and importance of size and composition of particles for oxidative damage and carcinogenic mechanisms. Journal of Environmental Science, 26(4), 339-362.
16. Gilli, G. et al. (2007). Chemical characteristics and mutagenic activity 7 of PM10 in Torino, a Northern Italian City. Science of the Total Environment, 385, 97-107.
17. Osornio-Vargas, A.R. et al. (2011). In vitro biological effects of airborne PM2.5 and PM10 from a semi-desert city on the Mexico–US border. Chemosphere, 83, 618-626.
18. Araujo, J.A. (2011). Particulate air pollution, systemic oxidative stress, inflammation, and atherosclerosis. Air Quality and Atmospheric Health, 4(1), 79-93.
19. Dai, J. et al. (2016). Exposure to concentrated ambient fine particulate matter disrupts vascular endothelial cell barrier function via the IL-6/HIF-1α signaling pathway. FEBS Open Bio, 6, 720-728.
20. Rivero, D.H., et al. (2005). Acute cardiopulmonary alterations induced by fine particulate matter of Sao Paulo, Brazil. Toxicology Science, 85, 898-905.
21. Boutagy, N.E. et al. (2016). Metabolic endotoxemia with obesity: Is it real and is it relevant? Biochimie, 124, 11-20. doi: 10.1016/j.biochi.2015.06.020.
22. Pirie, R.S. et al. (2007). Inhaled endotoxin and organic dust particulates have synergistic proinflammatory effects in equine heaves (organic dust-induced asthma). Clinical and Experimental Allergy, 33(5), 676-683.
23. Tong, H. et al. (2012). Omega-3 fatty acid supplementation appears to attenuate particulate air pollution-induced cardiac effects and lipid changes in healthy middle-aged adults. Environmental Health Perspectives, 7(120), 952-957.
24. Gold, D.R. et al. (1999). Particulate and ozone pollutant effects on the respiratory function of children in southwest Mexico City. Epidemiology, 10, 8-16.
25. Sun, Q. et al. (2005). Long-term air pollution exposure and acceleration of atherosclerosis and vascular inflammation in an animal model. Journal of the American Medical Association, 294(23), 3003–3010.
26. Wang, C. et al. (2016). Personal exposure to fine particulate matter and blood pressure: A role of angiotensin converting enzyme and its DNA methylation. Environmental International, [Epub ahead of print]. doi: 10.1016/j.envint.2016.07.001.
27. Kunzli, N. et al. (2005). Ambient air pollution and atherosclerosis in Los Angeles. Environmental Health Perspectives, 113, 201-206.
28. Gold, D.R. et al. (2000). Ambient pollution and heart rate variability. Circulation, 101, 1267-1273.
29. Pearson, J.F. et al. (2010). Association between fine particulate matter and diabetes prevalence in the U.S. Diabetes Care, 33(10), 2196.
30. Halonen, J.I. et al. (2009). Particulate air pollution and acute cardiorespiratory hospital admissions and mortality among the elderly. Epidemiology, 20(1), 143-153. doi: 10.1097/EDE.0b013e31818c7237.
31. Fang, Y. et al. (2013). Air pollution and associated human mortality: the role of air pollutant emissions, climate change and methane concentration increases from the preindustrial period to present. Atmospheric Chemistry and Physics, 13, 1377-1394.
32. Krewsi, D. (2009). Evaluating the effects of ambient air pollution on life expectancy. New England Journal of Medicine, 360(4), 413-415.
33. Fahey, J.W., Zhang, Y., & Talalay, P. (1997). Broccoli sprouts: an exceptionally rich source of inducers of enzymes that protect against chemical carcinogens. Proceedings of the National Academy of Sciences (USA), 94, 10367-10372.
34. Li, N. et al. (2003). Particulate air pollutants and asthma. A paradigm for the role of oxidative stress in PM-induced adverse health effects. Clinical Immunology, 109, 250-265.
35. Scandalios, J.G. (2005). Oxidative stress: molecular perception and transduction of signals triggering antioxidant gene defenses. Brazilian Journal of Medical and Biological Research, 38, 995-1014.
36. Dhakshinamoorthy, S., Long II, D.J., & Jaiswal, A.K. (2000). Antioxidant regulation of genes encoding enzymes that detoxify xenobiotics and carcinogens. Current Topics in Cell Regulation, 36, 201-216.
37. Riedl, M.A., Saxon, A., & Diaz-Sanchez, D. (2009). Oral sulforaphane increases Phase II antioxidant enzymes in the human upper airway. Clinical Immunology, 130(3), 244-251.
38. Egner, P.A. et al. (2014). Rapid and sustainable detoxication of airborne pollutants by broccoli sprout beverage: results of a randomized clinical trial in China. Cancer Prevention and Research, 7(8), 813-823. doi: 10.1158/1940-6207.CAPR-14-0103.
39. Kensler, T.W. et al. (2012). Modulation of the metabolism of airborne pollutants by glucoraphanin-rich and sulforaphane-rich broccoli sprout beverages in Qidong, China. Carcinogenesis, 33(1), 101-107. doi: 10.1093/carcin/bgr229.
40. Petri, S., Körner, S., & Kiaei, M. (2012). Nrf2/ARE Signaling Pathway: Key Mediator in Oxidative Stress and Potential Therapeutic Target in ALS. Neurological Research International, 878030.
41. Pompella, A., & Corti, A. (2015). Editorial: the changing faces of glutathione, a cellular protagonist. Frontiers in Pharmacology, 6, 1-4.
42. Marnewick, J.L. et al. (2003). Modulation of hepatic drug metabolizing enzymes and oxidative status by rooibos (Aspalathus linearis) and Honeybush (Cyclopia intermedia), green and black (Camellia sinensis) teas in rats. Journal of Agriculture and Food Chemistry, 51(27), 8113-8119.
43. Devi, P.U., & Ganasoundari, A. (1999). Modulation of glutathione and antioxidant enzymes by Ocimum sanctum and its role in protection against radiation injury. Indian Journal of Experimental Biology, 37(3), 262-268.
44. Lee, G-H. et al. (2017). Protective effect of Curcuma longa L. extract on CCl4-induced acute hepatic stress. BMC Research Notes, 10(1), 77.
45. García-Niño, W.R., & Pedraza-Chaverrí, J. (2014). Protective effect of curcumin against heavy metals-induced liver damage. Food Chemistry and Toxicology, 69, 182-201. doi: 10.1016/j.fct.2014.04.016
46. Tarek, K. et al. (2011). Zingiber officinale acts as a nutraceutical agent against liver fibrosis. Nutrition and Metabolism, 8, 40. doi: 10.1186/1743-7075-8-40.
47. Spanier, G. et al. (2008). Resveratrol reduces endothelial oxidative stress by modulating the gene expression of superoxide dismutase 1 (SOD1), glutathione peroxidase 1 (GPx1) and NADPH oxidase subunit (Nox4). Phytochemistry, 69(8), 1732-1738.
48. Yen, G-C. et al. (2011). Effects of polyphenolic compounds on tumor necrosis factor-α (TNF-α)-induced changes of adipokines and oxidative stress in 3T3-L1 adipocytes. Journal of Agriculture and Food Chemistry, 59(2), 546-551.
49. Possami, F.P. et al. (2010). Antioxidant intervention compensates oxidative stress in blood of subjects exposed to emissions from a coal electric-power plant in South Brazil. Environmental Toxicology and Pharmacology, 30(2), 175-180. doi: 10.1016/j.etap.2010.05.006.
50. Carlsen, M.H. et al. (2010). The total antioxidant content of more than 3100 foods, beverages, spices, herbs and supplements used worldwide. Nutrition Journal, 9(3), doi: 10.1186/1475-2891-9-3
51. Baur, J.A. et al. (2006). Resveratrol improves health and survival of mice on a high-calorie diet. Nature, 444, 337-342.
52. Astley, S.B. et al. (2004). Evidence that dietary supplementation with carotenoids and carotenoid-rich foods modulates the DNA damage: repair balance in human lymphocytes. British Journal of Nutrition, 91, 63-72. doi: 10.1079/BJN20031001.
53. Wood, J.G. et al. (2004). Sirtuin activators mimic caloric restriction and delay ageing in metazoans. Nature, 430, 686-689, doi: 10.1038/nature02789.
54. Kahkonen, M.P., Hopia, A.I, & Heinonen, M. (2001). Berry phenolics and their antioxidant activity. Journal of Agriculture and Food Chemistry, 49, 4076-4082.
55. Brook, R.D. et al. (2009). Insights into the mechanisms and mediators of the effects of air pollution exposure on blood pressure and vascular function in healthy humans. Hypertension, 54, 659–667.
56. Schneider, A. et al. (2008). Endothelial dysfunction: associations with exposure to ambient fine particles in diabetic individuals. Environmental Health Perspectives, 116, 1666-1674. doi: 10.1289/ehp.11666.
57. Kelm, M. (2002). Flow-mediated dilatation in human circulation: diagnostic and therapeutic aspects. American Journal of Physiology - Heart and Circulatory Physiology, 282(1), H1-H5.
58. Tong, H. et al. (2015). Dietary Supplementation with Olive Oil or Fish Oil and Vascular Effects of Concentrated Ambient Particulate Matter Exposure in Human Volunteers. Environmental Health Perspectives, 123(11). doi:10.1289/ehp.1408988
59. Li, X-Y. et al. (2017). Protection against fine particle-induced pulmonary and systemic inflammation by omega-3 polyunsaturated fatty acids. Biochemical et Biophysica Acta (BBA) - General Subjects, 18861(3), 577-584.
60. McAfee, A.J. (2011). Red meat from animals offered a grass diet increases plasma and platelet n-3 PUFA in healthy consumers. British Journal of Nutrition, 105(1), 80-90. doi: 10.1017/S0007114510003090.
61. Ritz, S.A., Wan, J., & Diaz-Sanchez, D. (2007). Sulforaphane-stimulated phase II enzyme induction inhibits cytokine production by airway epithelial cells stimulated with diesel extract. American Journal of Physiology, Lung Cellular and Molecular Physiology, 292, L33-L39.
62. Jagatha, B. et al. (2008). Curcumin treatment alleviates the effects of glutathione depletion in vitro and in vivo: therapeutic implications for Parkinson's disease explained via in silico studies. Free Radical Biology in Medicine, 44(5), 907-917.