PM2.5, PM2.5-related air pollutants, health hazards and impacts on respiratory and cardiovascular disorders and diseases: systematic review and meta-analysis

Abstract

The objective of the study is to perform a critical review, exploration, and strong summary of the relationships between personal and ambient concentrations of mainly particulate matter with diameter of 2.5µm or less with the measures of cardiopulmonary health. A comprehensive search was carried out in mainstream bibliographic databases or Medical Subject Headings, including Scien Direct, PubMed, Scopus, and ISI Web of Science. The search was applied to the articles that were published between 2017 and early 2019. Needed article information was extracted from each article by: direct information including journal (research article, review article, meeting abstract, conference abstract, correspondence, author index, editorial board meeting abstract, discussion), book chapter, title, authors, abstract, full text documents of candidate studies, publishing year. Study period, Research (study) method used, types of air pollutants variables studied; Types of organ system disorder or disease studied The conclusions made about the health hazards, impacts on humans or animal models, novel therapeutics, and economic loss. With strict literature search and screening processes, it yielded 140 articles (2017=45; 2018=61; and early 2019=34 articles) from 3,968 articles of initial literature database (1952-early 2019). The main compositions of air pollutants are PM, particularly PM2.5 and PM10, O3, CO, SO2, and NOx. Exposure to O3 is frequently associated with respiratory tract inflammation, whereas exposure to PM, CO, No2, and SO2 is related to pulmonary edema, respiratory and cardiovascular hospitalizations, and cardiopulmonary mortality. Any compromise to endothelial cells, the key components of lung barrier integrity contributes to vascular leakage and inflammation. Endothelial cells could be the target of PM exposure. The various effects on various disease entities contribute to hypothesize that Melatonin might protect the lung integrity against PM2.5-induced acute lung injury. Bufei Huoxue (BFHX) could reduce secretory immunoglobulin A (sIgA) and collagen fibers deposition in lung, thus, improved pulmonary function. In conclusion, identification of various crucial signaling pathway involving PM-induced cardiopulmonary disorders and diseases may assist in the development of effective therapeutics, including clean energy use, clean industrialization, proper agriculture, high land use diversity, and proper urbanization for reduction of the air pollution.