Pulmonary Retention of Particulate Matter is Associated with Airway Inflammation in Allergic Rats Exposed to Air Pollution in Urban Detroit

Abstract

A collaborative research study was conducted in order to improve our understanding of the source-to-receptor pathway for ambient fine particulate matter (aerodynamic diameter < or = 2.5 mu m; PM2.5) and subsequently to investigate the identity and sources of toxic components in PM2.5 responsible for adverse health effects in allergic humans. This research used a Harvard fine particle concentrator to expose Brown Norway rats, with and without ovalbumin-induced allergic airway disease, to concentrated air particles (CAPs) generated from ambient air in an urban Detroit community where the pediatric asthma rate was three times higher than the national average. Rats were exposed to CAPs during the exposure periods in July (mean = 676 microg/m3) and September (313 microg/m3) of 2000. Twenty-four hours after exposures lung lobes were either lavaged with saline to determine cellularity and protein in bronchoalveolar lavage fluid (BALF), or removed for analysis by inductively coupled plasma-mass spectrometry (ICP-MS) to detect ambient PM2.5-derived trace element retention. PM2.5 trace elements of anthropogenic origin, lanthanum (La), vanadium (V), manganese (Mn), and sulfur (S), were recovered from the lung tissues of CAPs-exposed rats. Recovery of those pulmonary anthropogenic particles was further increased in rats with allergic airways. In addition, eosinophils and protein in BALF were increased only in allergic animals exposed to CAPs. These results demonstrate preferential retention in allergic airways of air particulates derived from identified local combustion sources after a short-term exposure. Our findings suggest that the enhancement of allergic airway responses by exposure to PM2.5 is mediated in part by increased pulmonary deposition and localization of potentially toxic elements in urban air.

Air Pollution, Lipids and Atherosclerosis

“…However, while some studies have shown that inhaled ultrafi ne carbon particles (Andre et al 2006 ) or CAPs (Lei et al 2004 ) can also lead to increased infl ammatory cell counts in the BALF or increased infl ammatory cytokines (Kampfrath et al 2011 ), others have shown no effects on either BALF cell counts, histology or lung pro-infl ammatory gene expression (Gunnison and Chen 2005 ;Ito et al 2008 ;Heidenfelder et al 2009 ). These different responses could be due to the variability in CAPs composition or length of exposures (Saldiva et al 2002 ;Morishita et al 2004 ). Consistent with the latter, we have observed that DE for 2 weeks (Yin et al 2013 ) or CAPs for 5 weeks (Araujo et al 2008 ) did not result in the development of obvious pulmonary infl ammation (Araujo et al 2008 ;Yin et al 2013 ), but clearly led to lipid and pro-atherogenic effects, respectively.…”

Adjuvant effect of zymosan after pulmonary treatment in a mouse ovalbumin allergy model

“…Previously, our group has shown that pulmonary exposure to particulate zymosan increased lung neutrophil influx, LDH activity, and alveolar macrophage activation [26]. Others have shown that different lung pro-inflammatory agents, such residual oil fly ash [31,32], diesel exhaust particles [33], ambient particulate matter [34,35], and house dust mites [36] have adjuvant effects in animal respiratory allergy models.…”

The Applicability of Plasma‐Based Techniques to Biological Monitoring

“…Moss was used as well for similar purposes [76]. Pulmonary retention of particulate matter in the lung tissues of exposed rats was used both as evidence for the transport of particles and specific effects (allergic reactions) of toxic substances on organisms [77]. Bioaccessibility of trace metals originating from urban particulate matter was assessed in a worst case scenario to evaluate the uptake and thus the hazardous potential of these metals via gastric juice.…”