Air Pollutants – Are They Truly a Health Issue?

Reading Time: 11 minutes

biomolecules-05-01399-g001-1024Dr Carrie Decker ND explores some of the mechanisms linked to airpollution and human health. The action of taking a deep breath in and slowly exhaling is an experience we can likely all attest to as being restorative, balancing, and calming. Even much better so if this experience can be in a place where we are held by nature such as a forest with trees towering around us or at the oceanside with the sand between our toes. We take it for granted that the very action of breathing is a positive health-promoting activity, and how can it not be? Everyone, even the very little child, is aware that we cannot hold our breath far beyond a minute without the need for the refreshing blast of a new gulp of oxygen. It is our very nature to breathe, and now we even have evidence from studies surrounding meditation and controlled breathing techniques that further our knowledge that yes, taking time to breathe, will positively impact our health.[1],[2] Additionally, we also can thank science for showing us that the experience of breathing in natural settings also is truly more restorative than in an urban environment.[3],[4]

But what if you were told this very experience of breathing may have negative impacts on your health? A claim that many regard dubiously, often the same individuals who prefer to look to evidence stating there is no difference between organic and non-organic foods, and that water quality is not an issue of concern.  Others of us may accept this fact as reasonable, be it from personal experience living in or traveling to a region with increased traffic and industry, or from having health issues such as asthma where factors such as air quality may be more often noticed. Regardless whether we do or do not want to accept this, the data weighs in showing us that air quality is a significant issue of concern, and it does have impacts on our health.[5],[6]

The particulate matter (PM) found in air has variable effects on health depending on size. When air quality is evaluated, the two size thresholds which are evaluated are 2.5 micrometers (referred to as PM2.5) and 10 micrometers (referred to as PM10). It is the smaller size particles, PM2.5, that actually are more dangerous from a health perspective as they are able to be inhaled into the lungs more deeply, however the larger particles, PM10, also have negative impacts on health.[7],[8] Even smaller particulate matter, known as ultrafine particulates, also exist and are on the size range of 100 nanometers, or PM0.1.[9] In addition to the PM found in air, other air pollutants include carbon monoxide (CO), sulfur dioxide (SO(2)), nitrogen oxides (NOx), volatile organic compounds (VOCs), ozone (O(3)), and heavy metals. Many studies that look at the impacts of unique air pollutants or PM on health, however it is the combined effect of these many things that leads to overall increases in diseases such as chronic respiratory and heart disease, lung cancer, acute respiratory infections, chronic bronchitis, stroke, or asthmatic attacks and premature mortality.[10],[11] It is estimated that 3.3 million premature deaths per year occur worldwide due to outdoor air pollution, mostly associated with PM2.5 exposure. This includes emissions from residential energy use, traffic and power generation, and agriculture with the most significant factors varying by region. And the changing climate and increasing temperatures are only making things worse, and have been estimated to contribute to an additional 290 deaths a year associated with air pollution exposure in the US between 1994 – 2012.[12]PMsizes_350

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.[13] This activates a number of redox-responsive signalling pathways that also impact the expression of genes.[14] Additionally, the ultrafine PM0.1 particles are capable of translocation from the respiratory epithelium to circulation, resulting in distribution throughout the body with potential effects on coagulation, autonomic nervous system function, and even potential neurotoxic consequences.9 The ultrafine PM0.1 particles, and even some of the slightly larger particles have been shown to localize in mitochondria, inducing major structural damage, as well as deplete intracellular levels of glutathione.[15] The very young and the elderly seem to be most susceptible to the negative impacts of air pollution. In the very young this may be due to an immature immune system and because they inhale a higher volume of air per body weight than adults,[16] while in the elderly, a reduced capability of responding with upregulation of Nrf2-regulated phase II genes may be to blame.[17]

One way to address the issue is to minimize exposure. There are various websites devoted to providing information about air quality. One which shows the air quality in various major cities and regions of the UK as well as other countries can be found at the link http://aqicn.org/map/. A city of interest can be searched, and the current level as well as data from the past 48 hours is displayed for factors including PM10, PM2.5, ozone, NO(2), SO(2), and CO.  Temperature, humidity, and wind patterns affect the movement of air and are also tracked here, as these factors also will impact daily and hourly pollutant levels. As there are times when the levels are lower, using this data to inform when activities involving increased respiration such as exercise occur would be prudent. Exercise actually has been shown to increase the pro-thrombotic effect of air pollutant exposure.[18]

Secondly, finding a region with trees actually has positive impacts on the exposure to these toxins. Trees remove air pollution by the interception of particulate matter on plant surfaces and the absorption of gaseous pollutants through the leaf stomata. Although computer stimulation data only shows this to improve overall air quality by less than 1% in the US, with amounts roughly equalling 17 million tonnes, greater health impacts were seen in urban areas.[19] Additionally, in heavily forested areas, one hour improvements were found to be as high as 16%. This study also only looked at things on a macro level, and it is known that trees also positively impact air pollutant levels by reducing air temperature, reduce wind speeds, and locally lead to less need for cooling and thereby reduce emissions from surrounding buildings.

A consideration for some, particularly those with conditions such as asthma or chronic obstructive pulmonary disease which may worsen with air pollutant exposure, is to wear a mask in regions with poor air quality. There are different mask designs and qualities of masks, and looking for one which both is effective for reduction of exposure to known pollutants (http://tinyurl.com/pdusk46) as well as one which is functional for exercise (http://tinyurl.com/lz8p58d) are both issues which are of concern to cyclists and runners who exercise in these areas.

Antioxidants or antioxidant-promoting strategies are one supplementation strategy for combating the negative health impacts of air pollutants. Nuclear factor erythroid 2 (NF-E2)-related factor (Nrf2) is a key transcription factor that may be an important protective factor against oxidative stresses induced by air pollution.[20] Ginkgo biloba has been shown to induce phase II detoxification enzymes via Nrf2 involved pathways.[21] Green tea polyphenols have also been shown to modulation Nrf2-mediated antioxidant and detoxifying enzyme transcription.[22] N-acetylcysteine has been shown to reduce air pollutant-induced increased airway responsiveness in individuals with airway hyper-reactivity, reducing the need for supplement bronchodilators.[23] And of course, because intracellular glutathione has been shown to be depleted with exposure to air pollution, direct strategies for increasing cellular glutathione levels also should be considered.

There are some supplement combinations which have specifically been studied in settings of air pollutant exposure.  A combination of B-vitamins (specifically 2.5 mg/d folic acid, 50 mg/d vitamin B6, and 1 mg/d vitamin B12) was shown to reduce increases in heart rate and white blood cell counts as well as improve decreases in heart rate variability which were induced by 2 hours of exposure to PM2.5 at a level of 250 μg/m3.[24] Additionally, the combination of the same B vitamins was shown to ameliorate PM2.5-associated reductions in mitochondrial DNA content as well as prevent methylation changes in genes involved with mitochondrial oxidative energy metabolism.[25] The improvements seen with the B vitamins may be in part explained by the hypomethylation of pro-inflammatory, pro-coagulant, and pro-vasoconstriction genes which occurs upon exposure to PM2.5 air pollution.[26] Finally, a multivitamin combination has been shown to improve immune function and health conditions which are worsened by exposure to air pollutants.[27]

In summary, it is important to consider strategies to reduce exposure to air pollutants as they do contribute to premature mortality, and for some, can also worsen or contribute to the development of chronic diseases. Lifestyle strategies for avoidance of exposure should be considered paramount, however supplemental therapies on an ongoing basis are a strategy to reduce the impact when exposure to higher levels of air pollutants do occur.

References

[1] Sharma P, et al. Rhythmic breathing: immunological, biochemical, and physiological effects on health. Adv Mind Body Med. 2015 Winter;29(1):18-25. View Abstract

[2] Lane JD, et al. Brief meditation training can improve perceived stress and negative mood. Altern Ther Health Med. 2007 Jan-Feb;13(1):38-44. View Abstract

[3] Gidlow CJ, et al. Where to put your best foot forward: Psycho-physiological responses to walking in natural and urban environments. J of Environ Psych. 2016 Mar 31;45:22-9. View Full Paper

[4] Kuo M. How might contact with nature promote human health? Promising mechanisms and a possible central pathway. Front Psychol. 2015 Aug 25;6:1093. View Full Paper

[5] Fuzzi S, et al. Particulate matter, air quality and climate: lessons learned and future needs. Atmos Chem Physics. 2015 Jul 24;15(14):8217-99. View Abstract

[6] Khafaie MA, Yajnik CS, Salvi SS, Ojha A. Critical review of air pollution health effects with special concern on respiratory health. J Air Pollution Health. 2016 May 29;1(2):123-36. View Abstract

[7] Ransom MR, Pope CA 3rd. Elementary school absences and PM10 pollution in Utah Valley. Environ Res. 1992 Aug;58(2):204-19. View Abstract

[8] Romieu I, et al. Multicity study of air pollution and mortality in Latin America (the ESCALA study). Res Rep Health Eff Inst. 2012 Oct;(171):5-86. View Abstract

[9] Terzano C, et al. Air pollution ultrafine particles: toxicity beyond the lung. Eur Rev Med Pharmacol Sci. 2010 Oct;14(10):809-21. View Abstract

[10] Kampa M, Castanas E. Human health effects of air pollution. Environ Pollut. 2008 Jan;151(2):362-7. View Abstract

[11] Lelieveld J, et al. The contribution of outdoor air pollution sources to premature mortality on a global scale. Nature. 2015 Sep 17;525(7569):367-71. View Abstract

[12] Jhun I, et al. The impact of weather changes on air quality and health in the United States in 1994-2012. Environ Res Lett. 2015 Aug;10(8). View Full Paper

[13] 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. View Abstract

[14] Shukla A, et al. Inhaled particulate matter causes expression of nuclear factor (NF)-kappaB-related genes and oxidant-dependent NF-kappaB activation in vitro. Am J Respir Cell Mol Biol. 2000 Aug;23(2):182-7. View Abstract

[15] Li N, et al. Ultrafine particulate pollutants induce oxidative stress and mitochondrial damage. Environ Health Perspect. 2003 Apr;111(4):455-60. View Full Paper

[16] Salvi S, et al. Health effects of ambient air pollution in children. Paediatr Respir Rev. 2007 Dec;8(4):275-80. View Abstract

[17] 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. View Full Paper

[18] Wauters A, et al.  Pro-thrombotic effect of exercise in a polluted environment: a P-selectin- and CD63-related platelet activation effect. Thromb Haemost. 2015 Jan;113(1):118-24. View Abstract

[19] Nowak DJ, et al. Tree and forest effects on air quality and human health in the United States. Environ Pollut. 2014 Oct;193:119-29. View Full Paper

[20] Li YJ, et al.  Nrf2 is a protective factor against oxidative stresses induced by diesel exhaust particle in allergic asthma. Oxid Med Cell Longev. 2013;2013:323607. View Abstract

[21] 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. View Abstract

[22] 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. View Abstract

[23] Carlsten C, et al.  Anti-oxidant N-acetylcysteine diminishes diesel exhaust-induced increased airway responsiveness in person with airway hyper-reactivity. Toxicol Sci. 2014 Jun;139(2):479-87. View Abstract

[24] Zhong J, et al. B-vitamin Supplementation Mitigates Effects of Fine Particles on Cardiac Autonomic Dysfunction and Inflammation: A Pilot Human Intervention Trial. Sci Rep. 2017 Apr 3;7:45322. View Full Paper

[25] Zhong J, et al. B vitamins attenuate the epigenetic effects of ambient fine particles in a pilot human intervention trial. Proc Natl Acad Sci U S A. 2017 Mar 28;114(13):3503-3508. View Abstract

[26] Chen R, et al. DNA hypomethylation and its mediation in the effects of fine particulate air pollution on cardiovascular biomarkers: A randomized crossover trial. Environ Int. 2016 Sep;94:614-9. View Abstract

[27] Haryanto B, et al. Multivitamin supplementation supports immune function and ameliorates conditions triggered by reduced air quality. Vitam. Miner. 2015;4:2376-1318. View Abstract

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