The flames that swept through Paradise moved at the speed of a “football field per second.” Visiting San Francisco (ironically, to hear my beautiful daughter present her environmental research at an academic meeting), I could avoid air quality in the “hazardous” range by at most 30% by staying indoors. But we could not hike together or have a café lunch without burning pain in our heads, skin, and lungs. Day after day, the air remained an ugly yellow-grey, thick with air pollution particles.
What is air pollution?
The particles that make up air pollution are organized by size, from ultrafine particles (UFPs) 1 micron in diameter to PM 2.5 and PM 10, which are 25 and 100 times larger, respectively. They share a similar structure: various (poly) circular (aromatic) hydrocarbons (PAHs) with a high surface charge bind to a core of organic carbon—the carbon naturally in the air—that attracts heavy me- tal ions and oxidative elements, which allows them to aggregate into the particles of various sizes (Figure).
Ultrafine particles and PM 2.5’s enter the brain by mechanisms that include vascular uptake and transport across the blood-brain barrier and retrograde neuronal transport similar to the herpes virus, along both pulmonary nerves that track to the vagal system and through the olfactory bulb. Ultrafine particles can penetrate the cell nucleus, causing both epigenetic changes and oxidatative damage.
Air pollution and children
Studies of the effects of these air pollution particles show dramatic effects across the lifespan, including impaired fetal growth in utero and smaller head circumference at birth, decreased scores for verbal and nonverbal intelligence, memory restriction, and poor performance on tests of visual reaction time, pursuit aiming, and others by ages 8 to 11 years.1,2
There are associations with a wide range of developmental disorders including autism, ADHD, learning disorders and other disorders of child behavior.3Frederica Perera and her colleagues studied infants born near high-polluting coal plants in Beijing, Krakow, and New York.4 Their work demonstrated that these babies had developmental delay, lower IQs, more anxiety, depression, and inattention, and reduced brain white matter, all of which correlated with levels of PAH-DNA.
In parallel to Perera’s work on the topic, Lilian Calderon-Garciduenes and colleagues,5 noting that dogs in Mexico City developed dementia-like behaviors at an early age, began a series of autopsy studies of children killed in traffic accidents in Mexico City and compared them with children who died in less polluted areas. Their findings indicate a wide variety of neuropathological changes similar to those seen in Alzheimer disease.
In a second study, her group found that compared with children from clean air environments children in Mexico City exhibit systemic and brain inflammation and low cerebrospinal fluid Aβ1-42 as well as the breakdown of nasal, olfactory, alveolar-capillary, duodenal, and blood-brain barriers.6 Volumetric and metabolic brain changes, attention and short-term memory deficits, and hallmarks of Alzheimer and Parkinson disease were also seen.
Using transmission electron microscopy, the researchers documented UFPs—strongly magnetic combustion-derived nanoparticles (CDNPs)—present in the neurons, glia, choroid plexus, and neurovascular units of young Mexico City residents compared with matched clean air controls. CDNPs were associated with pathology in mitochondria, endoplasmic reticulum, mitochondria-endoplasmic reticulum contacts (MERCs), axons, and dendrites. The researchers concluded that “exposed children and young adults need early neuroprotection and multidisciplinary prevention efforts to modify the course of Alzheimer disease at early stages.”
Dr Haase is Associate Professor of Psychiatry, University of Nevada School of Medicine at Reno, and Medical Director, Carson Tahoe Outpatient Behavioral Health.
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