The air we breathe might be more dangerous than we think...
2017 has been a year of hurricanes, floods and fires—Harvey, Irma, Jose, and rampant wildfires raging across the west and Canada, including Montana, Idaho, Oregon, California and Vancouver. We don’t think much about the air we breathe every moment of our waking and sleeping lives—until it morphs into 125 mph winds, or brings a haze of acrid smoke whose finest particles — particulate matter that's 2.5 microns or less in diameter — are not even visible to the naked eye. It is, however, those fine particles that are most dangerous, and can penetrate the lungs and enter the bloodstream, with harmful health effects.1,2,3
It is often what we cannot see in air that causes us trouble. All particulate matter can be detrimental to health—and it is all on the increase, with urban development and industrialization. The smaller the particulate matter (PM) in air, the more harmful it can be. The two size thresholds most commonly studied are 10 micrometers or less (referred to as PM10) and 2.5 micrometers or less (referred to as PM2.5). There is an even finer threshold of PM, known as ultrafine particulates, that is about 100 nanometers, or PM0.1. Regulations do not even exist for PM0.1, which are far smaller than the regulated PM10 and PM2.5 particle classes.4
Air pollution and smog are composed of high concentrations of PM2.5—which can carry toxins right past the nose hairs, accumulating by diffusion in the lungs, where they irritate and inflame the tissue and impair lung function.5 These fine particles are linked to mortality—a 1996 study found that PM2.5 is one of the leading causes of human non-accidental death.6 About 3.3 million premature deaths per year occur globally due to outdoor air pollution, linked mainly to PM2.5 exposure.7
The tiny size of PM allows them to penetrate vulnerable tissues: in fact, by moving from lung tissue into circulation, they can affect the ability of the blood to flow freely, the functioning of the autonomic nervous system, and even the health of cells themselves.8 They can cause oxidative stress and inflammation.9 Ultrafine PM0.1 particles can even penetrate and damage the mitochondria, the energy powerhouses within every cell, and also cause damage via oxidative stress to our DNA.10 They can damage the delicate membranes of the mitochondria, and deplete intracellular levels of our most important antioxidant, glutathione.11 A 2014 study found harmful ultrafine particles from takeoffs and landings at Los Angeles International Airport to be of much greater magnitude than previously believed—and possibly harming communities as far as ten miles away.12
PM sources are many. We are exposed to harmful particulates in everything from ocean spray and volcanic eruptions to wildfire smoke, combustion, automobile and airplane exhaust, photocopiers, tobacco smoke, vacuum cleaners, coal and biomass plant emissions, ozone, fresh paint, and airborne heavy metals brought down from the jet stream in storms, to name just a few. Aside from PM, there also is the fact that climate change and a warming planet are increasing the risks of airborne pathogens and toxins such as the fungus that causes Valley Fever13, the cyanotoxins from algae blooms,14,15 and molds arising from water-damaged buildings as flood events become more common.16 Pesticide exposure and drift is also an issue, both from agriculture and aerial spraying to combat pests such as mosquitoes.
Avoiding air pollution can be tough. One way to address the issue is to minimize exposure. Hepa air filters and whole house filtering systems can help filter out some of these particles. Air quality can vary widely by city, state, region, and season. Most states offer air monitoring data available on websites. Weather apps will also include air quality alerts. Outdoor activities can, and for many should, be minimized during times when there are higher levels of air pollution. Exercise actually has been shown to increase the pro-thrombotic effect of air pollutant exposure.17
Forest bathing—a term coined by the Japanese in the 1990’s—is an increasingly popular way to find fresher air and improve immune function. A 2011 study found that forest walks, as opposed to city walks, led to more significant reductions in blood pressure and stress hormones after just four hours.18 Trees remove air pollution by intercepting PM on the surface of their leaves. The leaves also help absorb gaseous pollutants.19
In this increasingly polluted world, lifestyle changes and avoidance of high exposure often is not enough, or simply not possible. In this setting, antioxidants or antioxidant-promoting strategies become necessary to help our bodies offset the negative health impacts of air pollution. Supplemental antioxidants such as glutathione and vitamin C help our body to combat the oxidative stress associated with air pollution,20 while additional support for our body’s endogenous production of glutathione with supplements like lipoic acid and diindolylmethane also are key.21,22
2 Dennekamp M, Straney LD, Erbas B et al. Forest Fire Smoke Exposures and Out-of-Hospital Cardiac Arrests in Melbourne, Australia: A Case-Crossover Study. Environ Health Perspect. 2015 Oct;123(10):959-64. View Full Paper
12 Hudda N, Gould T, Hartin K. Emissions from an international airport increase particle number concentrations 4-fold at 10 km downwind. Environ Sci Technol. 2014 Jun 17;48(12):6628-35. View Full Paper
14Banack SA, Caller T, Henegan P et al. Detection of Cyanotoxins, β-N-methylamino-l-alanine and Microcystins, from a Lake Surrounded by Cases of Amyotrophic Lateral Sclerosis Toxins (Basel) 2015 Feb; 7(2): 322–336 View Full Paper
21 Suh JH, Shenvi SV, Dixon BM, 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. View Full Paper
22 Ernst IM, Schuemann C, Wagner AE, Rimbach G. 3,3'-Diindolylmethane but not indole-3-carbinol activates Nrf2 and induces Nrf2 target gene expression in cultured murine fibroblasts. Free Radic Res. 2011 Aug;45(8):941-9. View Abstract