The Effects of Ambient Particulate Matter on Human Alveolar Macrophage Oxidative and Inflammatory Responses

Abstract

Epidemiologic and occupational studies demonstrated that ambient particulate matter (PM) and diesel exhaust particles (DEP) exert deleterious effects on human cardiopulmonary health, including exacerbation of pre-existing lung disease and development of respiratory infections. The effects of ambient PM on lung cell responsiveness are poorly defined. Human alveolar macrophages (AM) were exposed to SRM 1649 (Washington, DC, urban dust; UD), SRM 2975 (forklift diesel exhaust particles; DEP), and fine or coarse ambient PM collected in Chapel Hill, NC, during the late fall (November) and early summer (June) of 2001-2002. AM were subsequently incubated with lipopolysaccharide (LPS), phorbol myristate acetate (PMA), or calcium ionophore A23817 for 6 or 24 h after PM exposure. UD and DEP markedly suppressed O2- release 24 h post-PM exposure. UD exposure significantly inhibited tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-8 release after exposure to 10 nanog/ml LPS. DEP significantly suppressed only TNF-alpha and IL-6 release. Suppressed cytokine release may also be produced by reduced cellular cytokine production. Data suggested that decreased cytokine release is not produced by the presence of benzo[a]pyrene (BaP), a polycyclic aromatic hydrocarbon. Comparison of TNF-alpha release after LPS, PMA, or A23817 revealed that suppressive effects of UD are LPS dependent, whereas inhibitory effects of DEP may work across multiple mechanistic pathways. November and June Chapel Hill PM exposure stimulated TNF-alpha and IL-8 release before LPS exposure. Fine and coarse November PM exposure markedly suppressed TNF-alpha release 6 h after LPS stimulation, but appeared to exert a stimulatory effect on IL-8 release 24 h after LPS exposure. June fine and coarse PM suppressed IL-8 release after LPS exposure. Data suggest that seasonal influences on PM composition affect AM inflammatory response before and after bacterial exposure. Overall, delayed or inhibited AM immune responses to LPS after PM exposure suggest human exposure to ambient PM may enhance pulmonary susceptibility to respiratory infections.

Performance Evaluation of AERMOD and ADMS-Urban for Total Suspended Particulate Matter Concentrations in Megacity Delhi

“…The poor air quality of the city in terms of particulate matter is attributed mainly to emissions from exhaust of motor vehicles, coal based thermal power plants and commercial and domestic use of solid and liquid fuels. Adverse impact of elevated levels of particulate matter in air on human health is evident in many earlier studies (Russel et al, 2009;Sawyer et al, 2010) which show a strong relationship of respiratory and cardiovascular morbidity as well as mortality with finer particles such as PM 10 (Jonathan et al, 2008;Samoli et al, 2008) and PM 2.5 (Chen et al, 2005;Cavallari et al, 2008). Mohan et al (2011) applied AERMOD for the exposure assessment for the year 2004 based on air quality predictions of total suspended particulate matter and found a significant decrease in mortality with reduction scenarios in particulate matter emissions.…”

Oxidative Stress, Inflammatory Biomarkers, and Toxicity in Mouse Lung and Liver after Inhalation Exposure to 100% Biodiesel or Petroleum Diesel Emissions

“…This article is not subject to U.S. copyright. Epidemiologic and occupational studies demonstrated that ambient particular matter (PM) and diesel exhaust particles exert deleterious effects on human health, including exacerbation of preexisting lung disease, increased incidence of respiratory infections, decrement in lung capacity, and enhanced risk of lung cancer (Sawyer et al, 2010;LaGier et al, 2013). According to the U.S. Environmental Protection Agency (EPA), elevated levels of airborne PM, nitrogen oxides, and sulfur oxides contribute to serious health problems in the United States, producing increased acute respiratory symptoms, chronic bronchitis, and aggravation of asthma, cardiovascular diseases, and premature mortality (Ghio et al, 2012).…”

Effects of Atmospheric Particles and Several Model Particles of Particulate Matter Components on Human Monocyte-Derived Macrophage Oxidative Responses

“…Although the amount of 3-NBA in the DEP sample was less than that in the MCC sample, the DEP sample included various other components, some of which could be common to DEP and PM. Sawyer et al indicated that urban dust and DEP suppressed superoxide release by normal human alveolar macrophages in response to phorbol-12,13-myristate acetate (PMA) stimulation [24]. Aam and Fonnum observed that the organic extract of DEP decreased the amount of ROS released by rat alveolar macrophages stimulated by PMA [25].…”