Effects of simulated downwind coal combustion emissions on pre-existing allergic airway responses in mice.
BACKGROUND
Coal-fired power plant emissions can contribute a significant portion of the ambient air pollution in many parts of the world.


OBJECTIVE
We hypothesized that exposure to simulated downwind coal combustion emissions (SDCCE) may exacerbate pre-existing allergic airway responses.


METHODS
Mice were sensitized and challenged with ovalbumin (OVA). Parallel groups were sham-sensitized with saline. Mice were exposed 6 h/day for 3 days to air (control, C) or SDCCE containing particulate matter (PM) at low (L; 100 μg/m³), medium (M; 300 μg/m³), or high (H; 1000 μg/m³) concentrations, or to the H level with PM removed by filtration (high-filtered, HF). Immediately after SDCCE exposure, mice received another OVA challenge (pre-OVA protocol). In a second (post-OVA) protocol, mice were similarly sensitized but only challenged to OVA before air/SDCCE. Measurement of airway hyperresponsiveness (AHR), bronchoalveolar lavage (BAL), and blood collection were performed ~24 h after the last exposure.


RESULTS
SDCCE significantly increased BAL macrophages and eosinophils in OVA-sensitized mice from the post-OVA protocol. However, there was no effect of SDCCE on BAL macrophages or eosinophils in OVA-sensitized mice from the pre-OVA protocol. BAL neutrophils were elevated following SDCCE in both protocols in nonsensitized mice. These changes were not altered by filtering out the PM. In the post-OVA protocol, SDCCE decreased OVA-specific IgG₁ in OVA-sensitized mice but increased levels of total IgE, OVA-specific IgE and OVA-specific IgG₁ and IgG(2a) in non-sensitized animals. In the pre-OVA protocol, SDCCE increased OVA-specific IgE in both sensitized and non-sensitized animals. Additionally, BAL IL-4, IL-13, and IFN-γ levels were elevated in sensitized mice.


CONCLUSIONS
These results suggest that acute exposure to either the particulate or gaseous phase of SDCCE can exacerbate various features of allergic airway responses depending on the timing of exposure in relation to allergen challenge.
Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA. tbarrett@lrri.org
Edward G
EG
Barrett
Kimberly C
KC
Day
Andrew P
AP
Gigliotti
Matthew D
MD
Reed
Jacob D
JD
McDonald
Joe L
JL
Mauderly
Steven K
SK
Seilkop
D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D000906:Antibodies / Q000097:blood; D001985:Bronchial Provocation Tests; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D016085:Bronchoconstrictor Agents; D003031:Coal; D016207:Cytokines / Q000276:immunology; D004195:Disease Models, Animal; D004804:Eosinophils / Q000276:immunology; D008297:Male; D016210:Methacholine Chloride; D051379:Mice; D008807:Mice, Inbred BALB C; D009504:Neutrophils / Q000276:immunology; D010047:Ovalbumin; D052638:Particulate Matter / Q000633:toxicity*; D011014:Pneumonia / Q000139:chemically induced* / Q000276:immunology / Q000473:pathology; D011210:Power Plants; D012130:Respiratory Hypersensitivity / Q000139:chemically induced* / Q000276:immunology / Q000473:pathology
D000393:Air Pollutants; D000906:Antibodies; D016085:Bronchoconstrictor Agents; D003031:Coal; D016207:Cytokines; D052638:Particulate Matter; D016210:Methacholine Chloride; D010047:Ovalbumin