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Characterization of Urban Atmospheres during Inhalation Exposure Studies in Detroit and Grand Rapids, Michigan

Gerald J. Keeler1
Masako Morishita1
James G. Wagner2
Jack R. Harkema2

1 Air Quality Laboratory, The University of Michigan, Ann Arbor, Michigan 48109, USA
2 Pathobiology and Diagnostic Investigation, Michigan State University, East Lansing, Michigan 48824, USA

Correspondence: Address correspondence to: Gerald J. Keeler, 109 South Observatory, The University of Michigan, Ann Arbor, MI 48109-2029; e-mail:jkeeler{at}umich.edu


   Abstract
Top
 Abstract
Introduction
 Materials And Methods
 Results
 Discussion
 References
 
An inhalation exposure study for particulate matter (PM) investigates links between exposure and observed changes in respiratory function by evaluating the interactions of chemical and physical properties of the PM with physiological mechanisms. Laboratory studies are useful in this regard, but provide limited information because of the difficulty in reproducing real atmospheric PM compositions and processes. To better understand the types of particles to which people are actually exposed in their daily lives, and the human health risks for source-specific PM, a real world assessment of the source-to-receptor pathways for ambient PM is vital. This was accomplished using a unique mobile air research laboratory (AirCARE1) which enables inhalation exposure studies in real-world settings. The overall goal of this study was to determine the effects of concentrated air particulates (CAPs) from 2 different urban atmospheres in Michigan on the lungs of ovalbumin-sensitized rats concurrently challenged with the allergen. Our work demonstrated that short-term (8 hours) exposure to ambient fine particulate matter (aerodynamic diameter ≤ 2.5 µm; PM2.5) concentrated from 2 different urban atmospheres in Michigan induced distinct allergic responses in the lungs of rats. This paper presents detailed characterization of CAPs and their sources in an effort to define possible associations between the observed health effects and source-specific ambient PM2.5.

Key Words: PM2.5 • CAPs (concentrated ambient particulates) • inhalation exposure • complex mixtures


   Introduction
Top
 Abstract
 Introduction
Materials And Methods
 Results
 Discussion
 References
 
Particulate matter (PM) in ambient air is a complex mixture of pollutants that varies in chemical composition and size distribution, as well as in space and time as a result of the dynamic interactions among source type, source strength, sinks, and meteorology. In order to understand atmospheric properties of PM, human exposure, and ultimately its health effects, continuous and comprehensive monitoring of the physicochemical characteristics of PM and its co-pollutants is essential.

Several toxicological studies have employed a particle concentrator for concentrating respirable particles from ambient air for delivery to a controlled environment chamber to conduct inhalation studies (Sioutas et al., 1995; Clarke et al., 2000; Godleski et al., 2000; Saldiva et al., 2002; Daigle et al., 2003; Harkema et al., 2004). These inhalation exposure studies utilized concentrated ambient particles (CAPs), generated from actual atmospheric particles, to understand the linkages between characteristics of PM, the resulting toxicity and the underlying mechanisms.

Our investigation has attempted to assess complete the source-receptor-health continuum of anthropogenic particles from a variety of high-temperature combustion sources in complex urban air sheds such as Detroit. Our research employed detailed characterization of ambient PM concurrent with inhalation toxicology studies using animal models and CAPs. The detailed characterization of ambient PM2.5 is essential for identification of PM2.5 sources by using receptor modeling and subsequently for developing emissions control strategies.

AirCARE1, a mobile air research laboratory, was moved to 2 different urban air sheds for inhalation toxicology studies. The first location is a southwest Detroit community where impacts of several local combustion sources are strong in addition to transported pollution. The second is a Grand Rapids community where the PM mixture is characterized by a large contribution from transported, aged pollution from regional sources.

The study presented here was designed to determine the effects of CAPs from 2 different urban atmospheres in Michigan on the lungs of ovalbumin-sensitized rats concurrently challenged with the allergen. The results showed disparate biological effects between the 2 sites despite very similar mass concentration of CAPs. This paper focuses on presenting detailed characterization of CAPs and their sources in an effort to define possible associations between the observed health effects and source-specific ambient PM2.5.


   Materials And Methods
Top
 Abstract
 Introduction
 Materials And Methods
Results
 Discussion
 References
 
Site Description
Each 8-hour exposure study in Detroit and Grand Rapids, MI was conducted on 29 July 2002 and 11 August 2003, respectively. Figure 1 is a map of Michigan showing the location of the two sampling sites and major point emission sources for PM2.5 (EPA, 1999a). Furthermore, an enlarged map of metropolitan Detroit shows some of major industries in Wayne County that were ranked as one of top 15 PM2.5 point sources in 1999 (EPA, 1999a). In Detroit, the densest industrial activity in the city is located in southwest area and includes iron-steel manufacturing, coke ovens, chemical plants, refineries, sewage sludge incineration, and coal-fired utilities (Keeler et al., 2002). In addition, southwest Detroit experiences heavy motor vehicle traffic, both passenger car and diesel truck traffic, due to its proximity to major interstates and the entrance to the Ambassador Bridge.


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  		Figure 1 A map of Michigan showing the location of the 2 sampling sites (asterisks: left-Grand Rapids and right-Detroit) and major emission sources for PM2.5 (EPA Facility Map, 1999).

 
Relative to Detroit, western Michigan frequently experiences elevated levels of transported secondary air pollutants that are generated from precursor emission sources in Illinois, Indiana, Ohio, Wisconsin, and Canada. These pollutants are transported and chemically react as they move across Lake Michigan or move from Ohio River Valley into Michigan. Our second sampling location was located in Grand Rapids, which is Michigan’s second largest city.

Inhalation Exposure Studies
Mobile Air Research Laboratory
AirCARE 1 was designed and constructed collaboratively by Michigan State University and the University of Michigan to conduct air pollution health effects studies (Harkema et al., 2004). The inhalation exposure lab contains a fine particle concentrator and 2 reinforced stainless steel Hinners-type whole-body inhalation chambers. These 2 chambers have a volume of 0.32 m3 and hold a single level of 16 rats. One chamber was used for CAPs exposure while the second chamber was used for a clean air control group, with HEPA-filtered clean air at the same flow rate as the CAPs exposed group of animals. The fine particle concentrator is a 3-stage aerosol concentrator that utilizes the technology of virtual impactors to increase the concentration of particles (size range 0.1–2.5 µm) by an approximate factor of 30 (Sioutas et al., 1997).

Animals
For each 8-hour exposure study, 32 male brown Norway rats (Charles River, Portage, MI), 10–12 weeks of age, were randomly assigned to 1 of 4 experimental groups (n = 8/group). Rats were free of pathogens and respiratory disease, and used in accordance with guidelines set forth by the Institutional Animal Care and Use Committee at Michigan State University. Exposure details are described in Harkema et al. (2004). Briefly, rats were housed in polycarbonate, shoebox style animal cages with filter lids and had free access to food and water. During the inhalation portion of the study, rats were transferred on-site to the AirCARE1 and housed individually in rack-mounted stainless steel wire cages in Hazleton chambers (HC-100, Lab Products, Maywood, NJ), and transferred to Hinners exposure chambers during CAPs inhalation exposures.

Allergen Sensitization/Challenge Protocol
Rats were sensitized and challenged with saline vehicle or to chicken albumin (ovalbumin; OVA; Sigma Chemical Co., St. Louis, MO) by intranasal (IN) instillation of OVA (0% or 0.5% in saline, 150 µl/nasal passage) for 3 consecutive days. Rats were instilled IN while under light anesthesia (4% halothane in oxygen). This airway sensitization and challenge protocol does not use an adjuvant, and produces allergic airway disease which we have characterized with pathological endpoints of secretory cell metaplasia, mucus hypersecretion and inflammatory cell recruitment 24 hours after the exposure period (Wagner et al., 2002).

CAPs Inhalation Exposure
Approximately 30–40 minutes after each intranasal challenge with OVA, rats were placed into exposure chambers and exposed to CAPs or filtered air for 8 hours, from 7:30 AM–3:30 PM. Rats were challenged with allergen and exposed to CAPs and by this regimen for 3 consecutive days.

Tissue Collection and Analysis
Twenty-four hours after the last allergen challenge/CAPs exposure, rats were anesthetized with sodium pentobarbital and euthanized by exsanguinations. A midline laporatomy performed, the trachea cannulated, and the heart and lung removed enbloc. The left lung lobes were lavaged twice with 4 ml aliquots of saline and bronchoalveolar lavage fluid (BALF) was pooled and total cell numbers enumerated using a hemocytometer. BALF was spun in a centrifuge and cell free BALF was analyzed for total protein content by the bicinchoninic acid method (BCA kit, Pierce, Rockford, IL). Data is expressed as mean ± SEM with criterion for significance set at p ≤ 0.05.

Measurements of CAPs
CAPs samples were collected for the duration of each eight-hour exposure period. The output flow from the third stage of the concentrator was approximately 50 LPM with 15 LPM used for characterization measurements and the remaining 35 LPM of flow administered to the animal exposure chambers. The mass of CAPs was determined by placing 47-mm Teflon filters (PTFE, Gelman, Ann Arbor, MI) in Teflon/Teflon-coated aluminum filter packs attached to the back of the animal exposure chamber at flow rates of 3 LPM. Annular denuder/filter packs were employed to collect the acidic gaseous species and inorganic fine particulate ions including sulfate, nitrate ammonium. A detailed description of the annular denuder sampling system was provided previously (Keeler et al., 1991). The volume of air drawn through each particulate sampling train was determined using a calibrated dry test meter (DTM) (Schlumberger, Owenton, KY). The DTMs were calibrated against a primary calibration standard spirometer (Warren E. Collins, Inc., Boston, MA). Furthermore, a calibrated rotameter (Matheson Inc., Montgomeryville, PA) was used to check the flow rate at the beginning and end of each sampling period. A TEOM 1400a (Rupprecht and Patashnick Inc., Albany, NY) was placed inline to continuously measure the CAPs concentration during the eight-hour exposure periods.

Urban Ambient Aerosol and Gaseous Pollutant Measurements
Size-segregated aerosol sampling was performed with integrated samplers including a six-stage micro-orifice impactors (MOIs) and PM2.5 cyclone samplers. The volume of air drawn through each particulate sampling train was determined using calibrated DTMs as described. Scanning mobility particle sizer (TSI, model 3936) system was operated to measure 5-min average concentrations of sub-micrometer aerosols. In addition, gaseous air pollutants were measured continuously including ozone (O3), sulfur dioxide (SO2), nitrogen oxides (NOx) and carbon monoxide (CO). Meteorological parameters including temperature, relative humidity, precipitation, wind speed and direction were monitored continuously to assess the day-to-day variability in local transport pathways and source influences.

Analytical Methods
Sample handling, processing, and analysis took place in a Class 100 ultra-clean laboratory at the University of Michigan Air Quality Laboratory, designed for ultra-trace element analysis with an emphasis on low-level environmental determinations.

Gravimetric Analysis
Gravimetric analysis was performed using a microbalance (MT-5 Mettler Toledo, Columbus, OH) in a temperature/humidity-controlled clean laboratory as described in Federal Reference Method (Code of Federal Regulations, EPA 1999b). Measurements including field blanks, filter-lot blanks, replicate analyses, and externally certified standard weights were incorporated into all gravimetric analyses for quality assurance and quality control purposes.

Organic and Elemental Carbon
PM samples collected on quartz filters were maintained at temperatures at –40°C after sampling and were analyzed for carbonaceous aerosols by a thermal-optical analyzer (Sunset Labs, Forest Grove, OR).

Major Ions and Acid Aerosol
After sampling, the annual denuders and filter packs were disassembled in an ammonia-free hood and Teflon filters and carbonate-coated backup filters were extracted in Milli-Q ultrapure water. Extracts were then analyzed for anions and cations for gaseous species and major ions by ion chromatography (Model DX-600, DIONEX, Sunnyvale, CA).

Trace Element Analysis
After completion of gravimetric analysis, Teflon sample filters were placed in 15 mL centrifuge tubes and were wetted with 150 µl of ethanol before extraction in 10 ml of 10% HNO3. The extraction solution was then sonicated for 48-hours in an ultrasonic bath, and then allowed to passively acid-digest for two-week duration. Sample extracts were then analyzed for a trace elements using high-resolution inductively coupled plasma-mass spectrometry (ICP-MS) (ELEMENT2, Thermo Finnigan, San Jose, CA).


   Results
Top
 Abstract
 Introduction
 Materials And Methods
 Results
Discussion
 References
 
CAPs-Induced Pulmonary Inflammation
Exposure nonallergic rats to CAPs had no effect on airway inflammatory markers of total protein and total cells recovered in bronchoalveolar lavage (BAL) fluid (Figures 2A and 2B). Sensitization and challenge of rats with OVA-induced inflammatory and allergic airway responses as indicated by significant increases of BAL protein and cellularity. These allergic airway responses were attenuated by exposure to Grand Rapids CAPs. By comparison, exposure of allergic rats to Detroit CAPs produced a consistent, yet nonsignificant trend toward increased protein and total cells compared to allergic rats exposed to filtered air. As a result, more detailed comparisons of the physicochemical composition of CAPs and source identification were pursued in order to identify critical differences in air quality for these 2 exposure periods that might explain the disparate biological effects.


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  		Figure 2 Effects of CAPs exposure in Detroit and Grand Rapids on (A) protein and (B) cell content of bronchoalveolar lavage fluid from rats with normal or allergic airways. Lavage was collected as described in Materials and Methods. Data are expressed as mean ± SEM; a= Significantly different from similarly exposed animals with normal airways. b = Significantly different from respective group exposed to filtered air. p < 0.05.

 
Physical and Chemical Characterization of CAPs
CAPs Mass Concentration
During the exposure periods, the concentrator performance was examined carefully for each exposure period to make sure that the CAPs to which the laboratory animals were exposed in the inhalation chamber reflected a complicated mixture of ambient PM2.5, and the evaluation of the concentrator performance was described in detail (Lawrence et al., 2004; Keeler et al., 2005). The average mass concentration of CAPs during the 8-hour exposure period in Detroit and Grand Rapids were 542 µg/m3 and 519 µg/m3, respectively. Although the mass concentrations of CAPs were very similar, detailed physical and chemical characterizations of CAPs between the Detroit and Grand Rapids sampling sites revealed significant differences as expected.

CAPs Size Distribution
Figure 3 illustrates comparison of mass size distributions of CAPs (<0.18, 0.18–0.6, 0.6–1, 1–2.5, 2.5–5, 5 <µm) from the micro-orifice impactor that was placed after the concentrator’s second stage during the exposure period. The most distinct difference between the 2 sites was that the ultrafine particle (particles with aerodynamic diameters da <0.1 µm) mass concentration in Detroit was more than twice as high as what we measured in Grand Rapids. Specifically, the smallest fraction (<0.18 µm) and the second smallest fraction (0.6 > 0.18 µm) measured in Detroit were 3.4 and 2.1 times higher than those in Grand Rapids.


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  		Figure 3 Size distribution of CAPs during 8-hour exposure studies in Detroit (29 July 2002) and in Grand Rapids (11 August 2003).

 
CAPs Chemical Composition
Figure 4 illustrates a comparison of major chemical composition of the CAPs measured during the 8-hour inhalation exposure periods in Detroit and Grand Rapids. The major chemical composition in Detroit was dominated by sulfates, whereas Grand Rapids had major contributions from organic carbon. Table 1 shows total and elemental mass concentrations of CAPs during 8-hour exposure periods in Detroit and Grand Rapids. Elemental concentrations of the 2 sites also revealed distinct differences. The concentrations of La, Pb, V, and Se in Detroit were 1.8, 2.2, 3.5, and 2.3 times higher, respectively, than those in Grand Rapids. In contrast, the concentrations of Ba, Ca, Mn, and Cu in Grand Rapids were 3.6, 1.5, 2.2, and 3.6 times higher, respectively than those in Detroit.


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  		Figure 4 Average major chemical composition of CAPs during 8-hour exposure studies in Detroit (29 July 2002) and in Grand Rapids (11 August 2003).

 

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  		Table 1 Total and elemental mass concentrations of CAPs during 8-hour exposure periods in Detroit and Grand Rapids.

 
Sources of CAPs
In an effort to identify differences in air quality that might explain the disparate biological effects, a next step was to figure out the nature of PM2.5 emission sources at each site from the measured ambient and CAPs chemical concentration data. Receptor modeling has been widely used to apportion the measured aerosol of chemical concentration at a sampling site to their sources (Hopke, 1991; Kim et al., 2001). A Positive Matrix Factorization (PMF) receptor model (Paatero and Tapper, 1994) was used to determine the major emission sources that contributed to ambient PM2.5 levels in southwest Detroit, and the results have been described in detail (Morishita et al., 2006). Although describing detailed results from the PMF analysis is not the scope of this paper, the PMF results indicated that 6 major sources including coal/secondary sulfate aerosol, motor vehicle/urban road dust, municipal waste incinerators, oil combustion/refineries, sewage sludge incinerators, and iron/steel manufacturing contributed to the observed ambient PM2.5 mass in southwest Detroit during the summer campaigns. These sources accounted for most of ambient PM2.5 measured in the southwest Detroit community during the exposure period on 29 July 2002 (Figure 5).


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  		Figure 5 Average major source contributions to ambient PM2.5 during the 8-hour exposure period in SW Detroit on 29 July 2002.

 
Meteorological data also supported our findings of the receptor modeling. Winds in Detroit were predominantly from the southwest during the 8-hour exposure period. Southwesterly winds in Detroit placed our exposure site directly downwind from several major point sources such as refineries, power plants, and steel industries (Figures 1 and 6). These data confirm the likely scenario that the study site was impacted by emissions from the identifiable local industrial sources during the Detroit exposure period.


Figure 60350015
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  		Figure 6 Frequency distribution of wind direction during 8-hour exposure studies in Detroit (left: 29 July 2002) and in Grand Rapids (11 August 2003) (rings are drawn at 10% intervals; wind flow is from the directions shown) (UAI Group, Inc. Roseworks software).

 
Although the receptor modeling for the Grand Rapids site has not been completed due to insufficient sample size, continuous pollutant measurements and characterization of CAPs and meteorological parameters have still enabled source identification. Figure 7 shows the temporal variation of ultrafine particle number, CO, NOx, and SO2 concentrations measured at the Grand Rapids site. The elevated ultrafine number, CO, NOx, and SO2 levels observed about 0800 EDT was likely to be the result of the morning rush hour traffic. In the early morning, the boundary layer depth is generally shallow due to the nocturnal inversion layer causing pollutants to be trapped closer to the ground. Dominant wind direction at the Grand Rapids site during the 8-hour exposure period was predominantly from the north. Northern winds placed our exposure site directly downwind from heavily trafficked roads in Grand Rapids, which also supports impacts from the morning rush hour traffic. As surface heating increased shortly after sunrise, the nocturnal inversion layer broke up due to intense vertical mixing, allowing the pollutants to disperse. Later in the day no other significant peaks in the ultrafine number and gaseous pollutant concentrations were observed.


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  		Figure 7 Time-series plot of air pollutant concentrations in Grand Rapids on 11 August 2003.

 

   Discussion
Top
 Abstract
 Introduction
 Materials And Methods
 Results
 Discussion
References
 
Despite similar mass concentrations in CAPs in Detroit and Grand Rapids (542 vs 519 µg/m3), we document disparate effects of allergic responses in laboratory animals during the 2 exposures. In Grand Rapids, CAPs clearly blunted airway allergic responses, whereas in Detroit these same endpoints were unaffected and even showed a mild, albeit insignificant, increase in response to CAPs exposure. Other parameters of allergic responses in these animals, such as eosinophils and mucous cell metaplasia were significantly enhanced by Detroit CAPs, but inhibited by Grand Rapids CAPs (Wagner et al., 2006). Because these divergent responses were independent of CAPs mass, then some specific chemical characteristics of the exposure aerosols are responsible for the enhancement (Detroit) vs. inhibition (Grand Rapids) that we have documented. As described in detail here, 2 readily distinguished markers between the exposures are sulfate (Detroit) and OC (Grand Rapids).

As expected, the sulfate contribution in southwest Detroit was substantial during the summer months. During the exposure period in Detroit, the predominant southerly wind, associated with a high-pressure system over the Ohio valley, brought humid air masses and increased levels of the transported or secondary particles dominated by sulfate. In addition to secondary/transported sulfate, elevated anthropogenic metal concentrations including V, Pb, and Se, and meteorological conditions confirmed the likely scenario that the study site was impacted by emissions from the identifiable local industrial sources that were located several miles southwest of our exposure study location. These results from physical and chemical characterization of PM2.5 suggest that nearby emissions from an identified industrial complex in southwest Detroit was likely to have caused the observed trend of enhancement of allergic responses. These results are consistent with previous findings that metal composition of ambient PM2.5 is likely to have influenced the severity of allergic respiratory disease (Carter et al., 1997; Gavett et al., 2003; Morishita et al., 2004) and that specific metals particles such as V from combustion emission sources might be associated with the negative health impacts of ambient PM2.5 (Fernandez et al., 2003; Riley et al., 2003).

In contrast, the dominant wind direction during the 8-hour exposure period in Grand Rapids was northerly, which brought relatively clean air from the north since there are few major emission sources in the direction. Temporal variations of gaseous pollutants and ultrafine particle number concentration revealed strong impact from the traffic in the morning. These distinct differences in emission sources that have impacted the sites reflected on the elemental chemical composition of CAPs during the exposure period.

Another critical difference between the Detroit and Grand Rapids exposures is that the CAPs mass fraction of the ultrafine mode in Detroit exposure period was more than twice as high as the one in Grand Rapids. The result implicates impacts from local combustion sources in Detroit have stronger impacts than in Grand Rapids. Although the mass fraction of the ultrafine mode is negligible, this size range contains the highest number of ambient particles as well as the highest total surface area. An increasing number of toxicological and epidemiological studies has linked respiratory health effects and exposures to ultrafine particles (Oberdoerster et al., 1995; Peters et al., 1997). More specifically, several studies demonstrated a stronger association between health effects and exposures to ultrafine particles compared to accumulation mode or coarse particles (Peters et al., 1997; Spurny, 1998).

A recent study by Li et al. (2003) indicated that ultrafine PM induced more oxidative stress, compared to concurrently collected accumulation and coarse-mode PM. These distinct differences in physicochemical characteristics of PM between the 2 sites caused the distinct observed allergic responses. Although discussion of the detailed molecular and pathological responses is beyond scope of the study, our results provide a toxicological and atmospheric linkage to describe the potential adverse health effects of ambient PM2.5 in different urban communities.

Taken together, the studies described here enabled us to identify potential source-to-receptor pathways for PM2.5 and co-pollutants from local combustion sources in a southwest Detroit community, and from local traffic sources in Grand Rapids. These results support the concept that pulmonary injury is more closely associated with the physical and chemical composition, rather than mass concentration, of ambient PM2.5.

Future studies are in progress to assess the molecular and pathological responses to air particulates, and to determine source-specific toxicological responses from ambient PM2.5 exposures. Ongoing studies utilize higher time-resolved exposure methods to determine source-specific toxicological responses from ambient PM2.5, and to improve our apportionment of source emissions and inhalation exposure health effects. Further analysis of PM2.5 samples from additional cities with different levels of allergy and asthma will help clarify the relationship between the composition of PM2.5 and the prevalence and severity of allergic airways disease.


   Acknowledgments
 
The work presented here was funded by grants from the Michigan Life Sciences Corridor and Health Effects Institute. We gratefully acknowledge the field efforts of Jim Barres, Emily Christianson, Tim Dvonch, Lynne Gratz, Ali Kamal, Bian Liu, Sheryl Kennedy, Mary Lynam, Frank Marsik, Ed Timm, Fuyuen Yip, and Li-Hao Young. We also thank Ellen Snedeker of Maybury Elementary School for her support at the study location in Detroit and Calvin College for their support at the study location in Grand Rapids.


   References
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 Introduction
 Materials And Methods
 Results
 Discussion
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Toxicologic Pathology, Vol. 35, No. 1, 15-22 (2007)
DOI: 10.1080/01926230601132022
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B. L. Heidenfelder, D. M. Reif, J. R. Harkema, E. A. Cohen Hubal, E. E. Hudgens, L. A. Bramble, J. G. Wagner, M. Morishita, G. J. Keeler, S. W. Edwards, et al.
Comparative Microarray Analysis and Pulmonary Changes in Brown Norway Rats Exposed to Ovalbumin and Concentrated Air Particulates
Toxicol. Sci., March 1, 2009; 108(1): 207 - 221.
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