PMID- 17886059
OWN - NLM
STAT- MEDLINE
DCOM- 20071119
LR  - 20191026
IS  - 1091-7691 (Electronic)
IS  - 0895-8378 (Linking)
VI  - 19 Suppl 1
DP  - 2007
TI  - Inhalation of concentrated ambient particulate matter near a heavily trafficked 
      road stimulates antigen-induced airway responses in mice.
PG  - 117-26
AB  - 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.
FAU - Kleinman, Michael T
AU  - Kleinman MT
AD  - Department of Community and Environmental Medicine, University of California, 
      Irvine, California 92697-1825, USA. mtkleinm@uci.edu
FAU - Sioutas, Constantinos
AU  - Sioutas C
FAU - Froines, John R
AU  - Froines JR
FAU - Fanning, Elinor
AU  - Fanning E
FAU - Hamade, Ali
AU  - Hamade A
FAU - Mendez, Loyda
AU  - Mendez L
FAU - Meacher, Dianne
AU  - Meacher D
FAU - Oldham, Michael
AU  - Oldham M
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - England
TA  - Inhal Toxicol
JT  - Inhalation toxicology
JID - 8910739
RN  - 0 (Air Pollutants)
RN  - 0 (Antigens)
RN  - 0 (Particulate Matter)
RN  - 0 (Vehicle Emissions)
SB  - IM
MH  - Air Pollutants/analysis/toxicity
MH  - Animals
MH  - Antigens/*immunology
MH  - Asthma/chemically induced/immunology
MH  - Bronchoalveolar Lavage Fluid/*immunology
MH  - Inhalation Exposure/adverse effects/*analysis
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Particle Size
MH  - Particulate Matter/*analysis/toxicity
MH  - Vehicle Emissions/*analysis/toxicity
EDAT- 2007/10/04 09:00
MHDA- 2007/12/06 09:00
CRDT- 2007/10/04 09:00
PHST- 2007/10/04 09:00 [pubmed]
PHST- 2007/12/06 09:00 [medline]
PHST- 2007/10/04 09:00 [entrez]
AID - 782017124 [pii]
AID - 10.1080/08958370701495345 [doi]
PST - ppublish
SO  - Inhal Toxicol. 2007;19 Suppl 1:117-26. doi: 10.1080/08958370701495345.