Inhalation of concentrated ambient particulate matter near a heavily trafficked road stimulates antigen-induced airway responses in mice.
Motor vehicle exhaust emissions are known to exacerbate asthma and other respiratory diseases. Several studies have demonstrated significant associations between living near highly trafficked roadways and increased incidence of asthma and increased severity of asthma-related symptoms, medication usage, and physician visits. This study tested the hypotheses that (1) exposure to particulate matter (PM) near a heavily trafficked Los Angeles freeway would enhance inflammatory and allergic responses in ovalbumin (OVA)-sensitized BALB/c mice compared to sensitized, clean air controls, and (2) there would be differences in response at two distances downwind of heavily traveled freeways because of greater toxicity of PM closest to the freeway. An ambient particle concentrator was used to expose ovalbumin (OVA)-treated BALB/c mice to purified air, to concentrated fine ambient particles, and to concentrated ultrafine airborne particles (CAPs) at 2 distances, 50 m and 150 m, downwind of a roadway that is impacted by emissions from both heavy-duty diesel and light duty gasoline vehicles. Tissues and biological fluids from the mice were analyzed after exposures for 5 days/wk in 2 consecutive weeks. The biomarkers of allergic or inflammatory responses that were assessed included cytokines released by Type 2 T-helper cells (interleukin [IL]-5 and IL-13), OVA-specific immunoglobulin E (IgE), OVA-specific immunoglobulin G1 (IgG1), and pulmonary infiltration of polymorphonuclear leukocytes and eosinophils. IL-5 and IgG1 were significantly increased in mice exposed to CAPs 50 m downwind of the road, compared to responses in mice exposed to purified air, providing evidence of allergic response. No significant increases in allergy-related responses were observed in mice exposed to CAPs 150 m downwind of the road. The biological responses at the 50-m site were significantly associated with organic and elemental carbon components of fine and ultrafine particles (p < or = .05). The primary source of these contaminants at the roadway sites was motor vehicle emissions, suggesting that particulate matter from motor vehicle fuel combustion could exert adjuvant effects and promote the development of allergic airway diseases.
Kleinman
Michael T
MT
Department of Community and Environmental Medicine, University of California, Irvine, California 92697-1825, USA. mtkleinm@uci.edu
Sioutas
Constantinos
C
Froines
John R
JR
Fanning
Elinor
E
Hamade
Ali
A
Mendez
Loyda
L
Meacher
Dianne
D
Oldham
Michael
M
D000393:Air Pollutants / Q000032:analysis / Q000633:toxicity; D000818:Animals; D000941:Antigens / Q000276:immunology*; D001249:Asthma / Q000139:chemically induced / Q000276:immunology; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology*; D019570:Inhalation Exposure / Q000009:adverse effects / Q000032:analysis*; D051379:Mice; D008807:Mice, Inbred BALB C; D010316:Particle Size; D052638:Particulate Matter / Q000032:analysis* / Q000633:toxicity; D001335:Vehicle Emissions / Q000032:analysis* / Q000633:toxicity
D000393:Air Pollutants; D000941:Antigens; D052638:Particulate Matter; D001335:Vehicle Emissions