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Welcome to PSR's Environmental Health Policy Institute, where we ask questions -- then we ask the experts to answer them. Join us as physicians, health professionals, and environmental health experts share their ideas, inspiration, and analysis about toxic chemicals and environmental health policy.

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Particulate Matter: Well-documented Cause of Chronic Disease, Premature Death

By Brian Moench, MD

In response to: Particulate Matter: Widespread and Deadly

Environmental regulation has emerged as a key difference between the two major political parties and has become a prominent stroke in the different portraits painted by political candidates of this country's future.  Physicians should have a central role in this debate because the medical and toxicological research has become overwhelming in establishing that environmental protection is public health protection. 

Air pollution in particular plays a much larger role in longevity and multiple chronic diseases than was recognized even ten years ago.  As advocates for our patients and for the health of the public at large, physicians should be become familiar with the research and be willing to step forward in defense of public policy that steers our nation toward pollution mitigation.

Of the multiple components of typical urban air pollution, particulate matter is considered the most toxic of the high-volume pollutants and has been the most heavily researched.  The signature physiologic and pathologic consequence of particulate air pollution is essentially the same as cigarette smoke:  a low-grade arterial inflammation, arteriolar narrowing, and vascular prothrombotic changes.  (1,2, 3, 4, 5, 6) As with cigarette smoke, the effect can be almost immediate (7) and chronic exposure to even low concentrations of pollution are associated with significant arteriolar narrowing (8).   Even in young healthy adults, air pollution increases biomarkers of inflammation and thrombosis (5).

These vascular changes cause average blood pressure to increase -- as soon as minutes after exposure (9) -- and therefore all organs are affected, especially those with the highest metabolic rate or the most tenuous blood supply, i.e. the heart, lungs, brain, and the placenta.  Rates of heart attack and stroke increase with air pollution and are the primary cause for increased community mortality rates (10,11,12,13, 14, 15).  Those rates increase within hours after exposure and stay elevated for as long as 30 days after the exposure has ended.

Particulate pollution exacerbates virtually all pulmonary diseases and likely plays a causative role in reactive airways disease.  It is associated with increased rates of hospitalization and death from respiratory diseases from neonates to the elderly (20, 21, 22, 23).   Particulate pollution permanently inhibits lung growth in children, preventing them from achieving their full adult lung capacity (24, 25).  Brief exposure to either ozone or particulate matter reduces lung function even in young healthy adults and the reduction can last for a week after the pollution exposure is over (26, 27).

Particulate pollution causes morphologic changes in the placenta, inhibiting blood transfer to the fetus (28).  Pregnant women exposed to more air pollution have multiple adverse pregnancy outcomes including higher blood pressure, higher rates of pre- eclampsia, intrauterine growth retardation, premature births, low birth weight syndrome and neonates with smaller head circumference (29, 30, 31, 32, 33).   Air pollution is associated with higher rates of birth defects, including neural tube and cardiac birth defects (34).

The systemic inflammation caused by particulate pollution also affects the brain. Air pollution components reach the brain not only through the vascular system, but translocate via the nasal mucosa, along axons of the olfactory and trigeminal nerves into the central nervous system (CNS), allowing deep penetration into the parenchyma and brain stem (35, 36).  Furthermore, many of the compounds adsorbed to particulate matter, like heavy metals, are neurotoxic.  Through this mechanism, particulate pollution causes CNS oxidative stress, neuroinflammation, neuronal damage, cortical stress measured by EEG, enhancement of Alzheimer type-abnormal filamentous proteins, BBB changes, and cerebrovascular damage.   Many of these changes can be found in children and young adults.   Greater air pollution exposure is associated with lower intelligence, poorer motor function, attention deficits and behavioral problems in children, decreased cognition in adults, higher rates of strokes, multiple sclerosis, autism, Parkinson's and other neurodegenerative diseases (37, 38, 39, 40, 41, 42, 43, 44).

By triggering the inflammatory cascade, particulate pollution causes systemic oxidative stress, cytotoxicity, and can penetrate cellular structures, including the cell nucleus, causing chemically mediated epigenetic changes to chromosomal function.  This genotoxicity may represent air pollution's greatest impact on public health.  Pregnant women exposed to more air pollution give birth to babies with significantly more chromosomal aberrations and epigenetic changes which can be passed on to multiple subsequent generations (45, 46, 47, 48, 49, 50, 51).

When exposure even to brief episodes of pollution occurs at critical stages in the development of the human embryo, it can result in increased likelihood of multiple chronic diseases, including those of the heart, lungs, immune system and brain and even obesity, diabetes and cancer (52, 53, 54, 55, 56).  Exposure to intermittent air pollution is associated with sperm DNA damage (57) and consequent increase in the rates of male infertility, miscarriages and other adverse reproductive outcomes.  Children living near petrochemical industries are exposed to high PAH levels which appear to be particularly capable of provoking DNA damage.  Industrial pollution is even more genotoxic than traffic pollution.   Air pollution also shortens the telomeres on chromosomes, thereby accelerating the aging process (58).

In May 2010, the American Heart Association published guidelines based on hundreds of epidemiologic studies offering a quantitative assessment of particulate pollution's mortality impact (16).  For every 1 ug/m3 increase in PM2.5 (particulate matter less than 2.5 microns in size), community mortality rates from all causes increase about 1%.  Research since then suggests that the number should be closer to 1.4% (17). That means that the air pollution in a typical urban setting, where most Americans live, increases the mortality rate between 10 and 14%.   Concomitantly, average life expectancy has improved by about five months from just  20 years worth of reduced particulate pollution, thanks to implementation of the Clean Air Act (18).

Mortality plotted against particulate pollution concentrations shows no safe threshold, even at levels well below EPA national ambient air quality standards (NAAQS).  Furthermore this curve is not linear (19).  The steepest part of the curve is at low doses, i.e. small reductions in air pollution have even greater public health benefit when the concentrations are already low. 

Medical research does not support the concept of a safe level of particulate air pollution any more than it does a safe level of cigarette smoke and for much the same reason.  It is indeed regrettable that science-based public health protection has become politicized.  The antipathy towards strengthening environmental regulations seems to be merely a capitulation to the profit demands of industry and cannot be justified by anyone who self-identifies as a medical scientist.  Physicians should advocate for public health and environmental policy that reflects the science.   Our patients, our families, our children, and our pregnant mothers deserve to breathe air as clean as realistically possible.

References

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