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Particulate Air Pollution and Risk of Neuropsychiatric Outcomes
There is evidence that the impact of particle pollution on the brain, the portals of entry, the neural damage mechanisms, and ultimately the neurological and psychiatric outcomes statistically associated with exposures. PM pollution comes from natural and anthropogenic sources such as fossil fuel combustion, engineered nanoparticles (NP ≤ 100 nm), wildfires, and wood burning. We are all constantly exposed during normal daily activities to some level of particle pollution of various sizes—PM2.5 (≤2.5 µm), ultrafine PM (UFP ≤ 100 nm), or NPs. Inhalation, ingestion, and dermal absorption are key portals of entry.
We live surrounded by environmental hazards including toxic compounds in air, water, soil, and food. Pollution is ubiquitous and mostly unavoidable. Neurotoxic organic and inorganic compounds come from fossil fuel combustion, engineered nanoparticles, nanoplastics, and compounds resulting from disasters such as forest wildfires. We are constantly exposed to these environmental hazards, regardless of age, sex, or socioeconomic status. Some people are more vulnerable than others and the brain in development is a target. The complexities of our modern-day, fossil fuel-based society are a factor when we talk about central nervous system (CNS) effects and the role of specific pollutants.
Minding only criteria pollutants  does not give us the full picture of exposure risk because these six compounds are regulated primarily for meeting regional air quality standards, rather than explicitly for reducing chronic or acute exposures and causality of adverse health outcomes. Other policies and standards exist for limiting pollutant-specific near-source exposures. Furthermore, criteria pollutants measured in ambient air (ozone (O 3), particulate matter (PM), sulfur dioxide (SO 2), nitrogen dioxide (NO 2), carbon monoxide (CO), and lead (Pb)) are operationally defined. Comparisons of pollution burdens across regions and countries must begin by ensuring the application of identical measurement methods and analytical techniques, otherwise we risk comparing apples to oranges. In addition, PM and O 3 are not singular entities; rather, they are lumped parameters representing a family of source-dependent constituents and precursors that can vary greatly in space and time and in physicochemical and toxicological characteristics. For these reasons, it is extremely difficult to make comparisons of PM 2.5 pollution and health effects in, for example, Delhi versus New York City or Provo, Utah versus Metropolitan Mexico City. Moreover, the determinants of adverse health outcomes are numerous: the strength and nature of emission sources, exposure times, and cumulative exposures over a lifetime, age, morbidities, and occupational history are some of the most obvious. The cumulative effect of these and other factors will determine specific health outcomes and responses vary significantly by population in terms of genetics, nutrition, exercise patterns, and cultural factors. These arguments should be an alarm for the reader. The sophistication of instruments, methodologies, and models to characterize air pollutants, exposures, or the results and interpretation of a specific PM 2.5 study, for example, may not equate to ability to understand and compare results, not even within the same country, let alone across the globe. Thus, local capacity to understand emission sources, implement PM control measures, and establish clinical, laboratory, and pathology links becomes paramount.
There is strong evidence of causality between PM 2.5 air pollution exposure and cardiovascular morbidity and mortality . The 2021 WHO Global Air Quality Guidelines recommendation for annual PM 2.5 Air Quality Guideline Level is 5 µg/m 3, with four interim targets proposed as incremental steps in a progressive reduction of air pollution and intended for use in highly polluted areas . General practitioners, emergency room doctors, internists, neurologists, psychiatrists, pediatricians, cardiologists, infectologists (think COVID), and others see firsthand the morbidity and mortality effects of air pollution and need readily available information about how to interpret results across locations.
2. Portals of Entry to the Brain and Key Neural Damage Mechanisms
This entry is adapted from 10.3390/ijerph182111568
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