Air pollution is a pervasive and often ignored factor in the aging process. Airborne ultra-fine (nanoparticles) pollution particles are microscopic and pose special dangers to health. Researchers agree that ultra-fine air pollution particles are a major threat in negative health consequences in humans. (1) While being very detrimental to the lungs, long-term exposure to ultra-fine particles also damages the cardiovascular system, contributes to atherosclerosis plaque formation and may lead to degenerative brain diseases - including Alzheimer's disease. These very small particles are able to travel deep into lung tissue and into the blood stream. As a result, there are significant increases in systemic oxidative stress, inflammation with increased DNA damage and mutagenicity. (2-6) Telomere length, which is an indicator of biological aging, becomes shorter in people living in air pollution areas. Shorter telomeres is associated with accelerated aging.(7-8)
Neuroinflammation. Especially alarming is the effect of ultra-fine particles on the brain. Airborne nano-sized particulate matter migrates through the lungs into the bloodstream and eventually into the brain. Longtime exposure to ultra-fine air pollutants leads to chronic brain inflammation which leads to neurodegenerative diseases. Epidemiological research has linked ultra-fine air particulate matter as a significant environmental factor involved in Alzheimer's Disease and Parkinson's Disease.(2)
Ultra-fine pollutant particles are produced by high heat sources including automobiles, trucks, airplane exhaust and factories and play a significant role in health and longevity. Urban areas, transit routes (highways and roads) and airports are major sources of pollutants but the suburbs are not immune. Such pollutants are so small that most people are unaware that they are inhaling toxic pollutants. Airborne fine particulate matter is a major component of air pollution.
Sources of ultra-fine particle pollutants:
(1) City / Urban Areas Particulate Matter. Urban areas create a confluence of major activity which generate ultra-fine air pollution. In studies involving six China urban areas, ultra-fine particulate matter (PM), including polycyclic aromatic hydrocarbon (PAH), were analyzed. The particulate matter was determined as having cytotoxicty to the bronchial cells of the lungs.(9) Substantial sources of outdoor PAHs in particulate pollution include cars and trucks.
(2) Highways / roadways. high volumes of traffic on highways are significant sources of ultra-fine particulate matter and PAH which is then distributed to surrounding areas and runoff into water ways. People living close to major roadways have increased health risks due increased air pollution exposure. Road paving and asphalt manufacturing are also major sources.
(3) Indoor sources. Burning of biofuels including coal and wood create dangerous levels of emissions. Also emissions from cigarette smoke.
(4) Diesel exhaust - classified as a group 1 carcinogen. Shown to cause lung and possibly bladder cancer.Contains nitric oxide and fine particulate matter.
(5) Airports / Aircraft turbine engines - these aircraft engines produce significant levels of hazardous ultra-fine air pollutants (including benzene and formaldehyde) at both in flight and ground levels. In fact, air quality impacts areas extend far from the airports. The LA times reports that communities as far as 10 miles from LAX airport are exposed to unsafe levels of air pollutants from aircraft engine exhaust.(10)
SULFORAPHANE - Sulforaphane is a potent activator of phase 2 detoxification in the body. In a study in high air pollution areas in China, sulforaphane beverages were shown to signifcantly increase metabolism and excretion of hazardous air pollutants benzene and acrolein in participants.(11) Further studies indicate that through activation of Nrf2, sulforaphane enhances protection against airborne toxin carcinogens and carcinogenesis. (12) Sulforaphane also protects against oxidant effects of diesel emission by invoking an over expression of antioxidant enzymes.(13)
N-ACETYL-CYSTEINE - Offers protection against air pollution induced inflammation. Includes specific mitigation against formaldehyde induced lung damage. Formaldehyde is a major emission toxin from airplane exhaust.(14)
(1) Chen R, et al. Beyond PM2.5: The role of ultrafine particles on adverse health effects of air pollution. Biochim Biophys Acta. 2016 Dec
(2) Heusinkveld HJ, et al. Neurodegenerative and neurological disorders by small inhaled particles. Neurotoxicology. 2016 Sep
(3) Valavanidis A, et al. Airborne particulate matter and human health: toxicological assessment and importance of size and composition of particles for oxidative damage and carcinogenic mechanisms. Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2008 Oct-DecBottom of Form
(4) Pope CA, et al. Exposure to Fine Particulate Air Pollution Is Associated with Endothelial Injury and Systemic Inflammation. Circ Res. 2016 Oct 25
(5) Bai Y, et al. Fine particulate matter air pollution and atherosclerosis: Mechanistic insights. Biochim Biophys Acta. 2016 Dec
(6) Risom L, et al. Oxidative stress-induced DNA damage by particulate air pollution. Mutat Res. 2005 Dec 30
(7) Martens Ds, et al. Air Pollution Stress and the Aging Phenotype: The Telomere Connection. Curr Environ Health Rep. 2016 Sep
(8) Ward-Caviness CK, et al. Long-term exposure to air pollution is associated with biological aging. Oncotarget 2016 Oct 25
(9) Yang L, et al. Pro-inflammatory response and oxidative stress induced by specific components in ambient particulate matter in human bronchial epithelial cells. Environ Toxicol. 2016 Aug
(10) Ridgeway L. New concerns raised about air pollution at LAX. May 30, 2014
(11) Egnar PA, et al. Rapid and sustainable detoxication of airborne pollutants by broccoli sprout beverage: results of a randomized clinical trial in China.
(12) Kensler TW, et al. Keap1-nrf2 signaling: a target for cancer prevention by sulforaphane. Top Curr Chem. 2013.
(13) Wan J, et al. Antioxidant enzyme induction: a new protective approach against the adverse effects of diesel exhaust particles. Inhal Toxicol 2007.
(14) Wang M, et al. N-acetylcysteine: A promising drug against formaldehyde-induced damage in lung epithelial cells. Med Hypotheses. 2014 Nov