A critical review of assays for hazardous components of air pollution

Abstract

Increased mortality and diverse morbidities are globally associated with exposure to ambient air pollution (AAP), cigarette smoke (CS), and household air pollution (HAP). The AAP-CS-HAP aerosols present heterogeneous particulate matter (PM) of diverse chemical and physical characteristics. Some epidemiological models have assumed the same health hazards by PM weight for AAP, CS, and HAP regardless of the composition. While others have recognized that biological activities and toxicity will vary with components, we focus particularly on oxidation because of its major role in assay outcomes. Our review of PM assays considers misinterpretations of some chemical measures used for oxidative activity. Overall, there is low consistency across chemical and cell-based assays for oxidative and inflammatory activity. We also note gaps in understanding how much airborne PM of various sizes enter cells and organs. For CS, the body burden per cigarette may be much below current assumptions. Synergies shown for health hazards of AAP and CS suggest crosstalk in detoxification pathways mediated by AHR, NF-κB, and Nrf2. These complex genomic and biochemical interactions frustrate resolution of the toxicity of specific AAP components. We propose further strategies based on targeted gene expression based on cell-type differences.

Impact of Obesity and Ozone on the Association Between Particulate Air Pollution and Cardiovascular Disease and Stroke Mortality Among US Adults

“…4,5 Although considerable effort has been directed at controlling and monitoring ambient concentrations of PM for the past 30 years, and these efforts have been largely successful, levels of air pollution in larger US cities still occasionally exceed by an order of magnitude the recommended safe levels of PM 2.5 pollution. 6 Worldwide, it has been suggested that particulate air pollution is responsible for >3 million deaths every year. 5,7 PM 2.5 can be deposited in the upper and lower airways, and because of its small size, it can reach more deeply into the lungs and circulation.…”

The State of Air Pollution with PM2.5 in the City of Targu Jiu

“…Unlike other pollutants, PM is a mixture of particles, coming from different sources and having different sizes, different compositions and different properties. The sizes of particulate matter are identified by the aerodynamic diameter in micrometers such as PM 10 , PM 2.5 , and PM 0.1 [16]. The larger size classes are those that include all smaller PM [16].…”

“…The sizes of particulate matter are identified by the aerodynamic diameter in micrometers such as PM 10 , PM 2.5 , and PM 0.1 [16]. The larger size classes are those that include all smaller PM [16]. The larger size classes PM 10 and PM 2.5 are considered less toxic and they are trapped into the upper airways, while the PM 0.1 and smaller (ultrafine) are even more toxic than PM 2.5 [16].…”

“…The larger size classes are those that include all smaller PM [16]. The larger size classes PM 10 and PM 2.5 are considered less toxic and they are trapped into the upper airways, while the PM 0.1 and smaller (ultrafine) are even more toxic than PM 2.5 [16]. Epidemiologic studies generally reveal robust associations of health hazards with the level ofPM 2.5 into ambient air [16].…”

“…The larger size classes PM 10 and PM 2.5 are considered less toxic and they are trapped into the upper airways, while the PM 0.1 and smaller (ultrafine) are even more toxic than PM 2.5 [16]. Epidemiologic studies generally reveal robust associations of health hazards with the level ofPM 2.5 into ambient air [16]. The main diseases associated with PM air pollution are: cancer of lung, neurodegeneration cognitive decline including dementia, Alzheimer's disease, and Parkinson's disease in elderly population, chronic bronchitis, cardiac arrhythmias, cardiovascular decline and mortality, brain damage [17][18][19].…”