2010 Progress Report: Project 3 -- Inhalation Exposure Assessment of San Joaquin Valley Aerosol

EPA Grant Number: R832414C003
Subproject: this is subproject number 003 , established and managed by the Center Director under grant R832414
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).

Center: San Joaquin Valley Aerosol Health Effects Research Center (SAHERC)
Center Director: Wexler, Anthony S.
Title: Project 3 -- Inhalation Exposure Assessment of San Joaquin Valley Aerosol
Investigators: Pinkerton, Kent E. , Bonham, Ann , Kleeman, Michael J.
Current Investigators: Pinkerton, Kent E. , Kleeman, Michael J.
Institution: University of California - Davis
EPA Project Officer: Chung, Serena
Project Period: October 1, 2005 through September 30, 2010 (Extended to September 30, 2011)
Project Period Covered by this Report: July 1, 2009 through June 30,2010
RFA: Particulate Matter Research Centers (2004) RFA Text |  Recipients Lists
Research Category: Health Effects , Air

Objective:

Epidemiological evidence suggests that the association between cardiac mortality and PM10 concentrations changes between the summer and winter months in the San Joaquin Valley (SJV). This shift likely is caused by seasonal variation in the size and composition distribution of airborne particles. This project will perform inhalation exposure and particle characterization studies at rural and urban locations in different seasons to quantify the features of the airborne particles that are associated with adverse health effects.

Progress Summary:

1. Differences in particle concentration, size distribution, and composition that occur as a function of season and location in the San Joaquin Valley (SJV) result in different health outcomes; these outcomes can be detected during inhalation exposure experiments.

Eight field measurement and exposure studies in the San Joaquin Valley have been completed: at an urban site located in Fresno, CA (500 East Shaw Avenue), for the summer and winter seasons in 2006, 2007, 2008 and 2009, and at a rural site located at Westside, CA, in 2007 and 2008.  Fine/ultrafine ambient particles were collected and concentrated on-site using a Versatile Aerosol Concentrator Enhancement System (VACES). Concentrated ambient particles (CAPs) samples collected during each exposure were analyzed for chemical composition.

Size and composition analysis of airborne particulate matter samples collected during each experiment reveals that OC was the dominant PM1.8 species during the summer and NO32- was the dominant species in the wintertime. Total number concentrations were larger during the summer sampling events. Fresh ~0.1 µm particles were emitted directly from combustion sources at the Fresno site from 9 am – 12 pm each day while number concentrations at Westside were dominated by nucleation events that ultimately produced particles in the 0.2 – 0.3 µm size range. Most PM1.8 and PM 0.1 metal concentrations were greater during the summer events than the winter events for both sampling sites. PM1.8 Br, Cu, K, P, Sn, Sb, S, and Zn concentrations were greater at the urban Fresno site than the rural Westside site with most of these species having size distribution peaks in the 0.1 – 1 µm range. The urban site exhibited enrichment (12% - 17%) of As and Se in PM0.1 relative to PM1.8 while the rural site exhibited enrichment (11% - 30%) of K, Fe, Rb, and Ca in the PM0.1 size fraction.

The seasonal trends in size distribution and composition described above suggest the deposition efficiency of key PM components (Mg, Al, S, V, Mn, Fe, Ni, Ba, SO42-, Na+, and Ca2+) in the human respiratory system is larger during the summer than during the winter months at Fresno.  This pattern matches apparent increase in toxicity of PM2.5 during the summer months as detected by independent epidemiological studies (Franklin et al. 2008).

Figure 1: Average total deposition efficiency in all regions of the respiratory tract comparing component deposition and PM1.8 total mass concentrations using least squares method. Units are (µg of each component deposited per µg PM1.8 total mass inhaled).  Error bars are 95% CI.

The results of these exposure studies are complete and peer-reviewed journal articles are in preparation documenting the results. 

2 & 3. The increased toxicity of airborne particles in the SJV is associated with increased concentrations of ultrafine carbon particles and associated with increased concentrations of accumulation mode ammonium/nitrate/sulfate particles.

The size and composition distribution of the airborne PM measured in the SJV was a function of season and location.  Nitrate was present in far greater quantities during the winter season, causing changes to the size distribution of other primary components due to condensational growth.  The timing of the experiments did not yield an event with high PM0.1­ OC concentrations.

Figure 2: Relative MOUDI size distributions of individual species. Concentrations are normalized to values in the parenthesis. Dashed lines represent summer while solid represent winter.

Biologic responses to particle aspiration. To better understand the importance of particle mass and composition, mice were administered 50 ug of H2O-extracted ambient PM2.5 from the summer and winter seasons of Fresno and Westside by intratracheal microspray. Each field sample had been lyophilized and resuspended in PBS. Mice were euthanized 24 hours following instillation, and pulmonary and systemic inflammatory markers were measured.

Biologic Samples Collected:

  • Bronchoalveolar Lavage (BAL)
    • Inflammation
      • Total Cells
      • Cell Differential
    • Cytotoxicity
      • Cell Viability
      • Total Protein
      • LDH
  • Blood
    • Inflammation
      • CBC count
  • Lung Tissue
    • Inflammation
      • Histology

Findings:

There was a statistically significant elevation of total cells recruited to the lungs following instillation of a 50 ug dose of PM from Westside Winter only (Figure 3). All other PM suspensions elicited responses similar to PBS control values. Additionally, th enumber of neutrophils recruited for the Westside Summer and Winter samples demonstrated a trend towards an elevation from PBS controls (Figure 4). No significant differences were observed for changes in cell viability (Figure 5) or weight across all samples.

Figure 3:

*p value < 0.02 One way ANOVA compared to PBS Control with Fishers LSD post test

Figure 4

Figure 5

4. The health effects of San Joaquin Valley aerosol can be directly related to the emissions source of the fine and ultrafine particles.

The size-resolved source contributions to airborne particulate matter at Fresno and Westside have been determined during the first four exposure periods.  Diesel engines accounted for the majority of the PM0.1 and PM1.8 EC at both the urban and rural sampling locations in both the summer and winter seasons.  Meat cooking accounted for 33-67% and diesel engines accounted for 15-21% of the PM0.1 OC at Fresno.  Meat cooking accounted for 22-26% of the PM0.1 OC at the rural Westside location, while diesel engines accounted for 8-9%.  Wood burning contributions to PM0.1 OC increased to as much as 12% of PM0.1 OC during the wintertime.  The modest contribution of wood smoke reflects the success of emissions control programs over the past decade.  In contrast to PM0.1 , PM1.8 OC had a higher fraction of unidentified source contributions (68-85%) suggesting that this material is composed of secondary organic aerosol (SOA) or primary organic aerosol (POA) that has been processed by atmospheric chemical reactions.  Meat cooking was the largest identified source of PM1.8 organic carbon (OC) at the Fresno site (12-13%) while diesel engines were the largest identified PM1.8 OC source at the rural site (5-8%).  Wood burning contributions to PM1.8 OC increased during the winter time at both sites (6-9%) but were relatively small during the summertime (~1%).

Figure 6: Source contributions estimates to PM0.1 OC.

Progressive PM exposure study. To better understand the effects of progressive exposure to ambient particles of the SJV, we exposed mice to CAPs for consecutive days (three, six, nine or twelve) at the Fresno site to investigate the acute cardiopulmonary response with increasing duration of exposure to CAPs. Mice were euthanized 24 hours post-exposure and pulmonary and blood samples were collected for analysis. CAPs exposure concentrations were approximately 150 ug/m3 for the first nine days of exposure and were slightly reduced afterwards due to changes in atmospheric mixing heights and wind patterns. 

Biologic Samples Collected:

  • Bronchoalveolar Lavage (BAL)
    • Inflammation
      • Total Cells
      • Cell Differential
    • Cytotoxicity
      • Cell Viability
      • Total Protein
      • LDH
  • Lung Tissue
    • Inflammation
      • Cytokines
      • Chemokines
  • Blood
    • Inflammation
      • CBC count

The inflammatory cell profile within the lungs demonstrated a duration-dependent pattern of total leukocyte recruitment with a significant elevation in mice exposed for six days followed by a significant reduction back to day-matched control values at the end of 12 days of exposure. Cellular differential analysis showed a duration-dependent increase in neutrophils that gradually elevated with increasing exposure duration and peaked significantly in mice by the end of 12 days of exposure. Circulating inflammatory cells and platelets were also elevated at six days, but had decreased to control levels following twelve days of exposure.

Inflammatory mediators measured in lung tissue had duration-dependent elevations in key pro-inflammatory cytokines involved in macrophage function and phagocytosis to include interferon gamma (IFN-g), and chemokines, such as neutrophil chemoattractant macrophage inflammatory protein (MIP-2), after only three days of exposure to CAPs. With increasing duration of exposure at 6 and 9 days of exposure, elevations in other pro-inflammatory chemokines (MIP-1a, MIP-1b, eotaxin), pro-inflammatory cytokines (TNF-α) and immune-mediated cytokines (IL-6, IL-10, IL-13) and growth factors (PDGF) were seen. However, a consistent reduction or attenuation of inflammatory mediator production was observed following 12 days of progressive exposure suggesting either influence of reduced ambient concentrations or a possible influence of tolerance to the inhalation of CAPs. 

In conclusion, significant pulmonary and systemic inflammation and lung cytotoxic and immune responses were observed throughout 12 days of exposure to concentrated ambient SJV PM with specific cytokines and chemokines being expressed in a time-dependent fashion. Nevertheless, inflammatory and cytotoxic responses observed in these studies cannot be solely predicted by particle chemical composition of the main players; carbons, nitrates, sulfates, ammonia, or transition metals or by the duration of exposure.

Future Activities:

Complete and submit for publication manuscripts describing all field studies completed in the SJV for the summer and winter seasons for urban and rural sites.


Journal Articles on this Report : 11 Displayed | Download in RIS Format

Other subproject views: All 28 publications 21 publications in selected types All 17 journal articles
Other center views: All 128 publications 71 publications in selected types All 64 journal articles
Type Citation Sub Project Document Sources
Journal Article Ham WA, Herner JD, Green PG, Kleeman MJ. Size distribution of health-relevant trace elements in airborne particulate matter during a severe winter stagnation event: implications for epidemiology and inhalation exposure studies. Aerosol Science and Technology 2010;44(9):753-765. R832414 (2010)
R832414C003 (2010)
R832414C003 (Final)
  • Full-text: Taylor Francis Online Full Text
    Exit
  • Abstract: informaworld
    Exit
  • Other: Taylor Francis Online Full Text PDF
    Exit
  • Journal Article Kleeman MJ, Riddle SG, Robert MA, Jakober CA, Fine PM, Hays MD, Schauer JJ, Hannigan MP. Source apportionment of fine (PM1.8) and ultrafine (PM0.1) airborne particulate matter during a severe winter pollution episode. Environmental Science & Technology 2009;43(2):272-279. R832414 (2010)
    R832414C003 (2009)
    R832414C003 (2010)
    R832414C003 (Final)
  • Abstract from PubMed
  • Abstract: Environmental Science & Technology
    Exit
  • Journal Article Madl AK, Pinkerton KE. Health effects of inhaled engineered and incidental nanoparticles. Critical Reviews in Toxicology 2009;39(8):629-658. R832414 (2010)
    R832414C003 (2009)
    R832414C003 (2010)
    R832414C003 (Final)
    R829215 (Final)
    R831714 (2005)
  • Abstract from PubMed
  • Abstract: Informa healthcare
    Exit
  • Journal Article Ngo MA, Pinkerton KE, Freeland S, Geller M, Ham W, Cliff S, Hopkins LE, Kleeman MJ, Kodavanti UP, Meharg E, Plummer L, Recendez JJ, Schenker MB, Sioutas C, Smiley-Jewell S, Haas C, Gutstein J, Wexler AS. Airborne particles in the San Joaquin Valley may affect human health. California Agriculture 2010;64(1):12-16. R832414 (2010)
    R832414C003 (2010)
    R832414C003 (Final)
    R826246 (Final)
    R832413 (Final)
    R832413C001 (2010)
    R832413C001 (Final)
  • Full-text: CaliforniaAgriculture-Full Text PDF
    Exit
  • Abstract: CaliforniaAgriculture-Abstract and Full Text HTML
    Exit
  • Journal Article Pham H, Bonham AC, Pinkerton KE, Chen CY. Central neuroplasticity and decreased heart rate variability after particulate matter exposure in mice. Environmental Health Perspectives 2009;117(9):1448-1453. R832414 (2010)
    R832414C003 (2009)
    R832414C003 (2010)
    R832414C003 (Final)
    R831918 (Final)
  • Full-text from PubMed
  • Abstract from PubMed
  • Associated PubMed link
  • Full-text: EHP
  • Abstract: EHP
  • Journal Article Ruehl CR, Ham WA, Kleeman MJ. Temperature-induced volatility of molecular markers in ambient airborne particulate matter. Atmospheric Chemistry and Physics 2011;11(1):67-76. R832414 (2010)
    R832414C003 (2010)
  • Full-text: Atmospheric Chemistry and Physics PDF
    Exit
  • Abstract: Atmospheric Chemistry and Physics
    Exit
  • Journal Article Schenker MB, Pinkerton KE, Mitchell D, Vallyathan V, Elvine-Kreis B, Green FHY. Pneumoconiosis from agricultural dust exposure among young California farmworkers. Environmental Health Perspectives 2009;117(6):988-994. R832414 (2010)
    R832414C003 (2009)
    R832414C003 (2010)
    R832414C003 (Final)
    R826246 (Final)
  • Full-text from PubMed
  • Abstract from PubMed
  • Associated PubMed link
  • Journal Article Sekizawa S-i, Joad JP, Pinkerton KE, Bonham AC. Secondhand tobacco smoke exposure differentially alters nucleus tractus solitarius neurons at two different ages in developing non-human primates. Toxicology and Applied Pharmacology 2010;242(2):199-208. R832414 (2010)
    R832414C003 (2010)
    R832414C003 (Final)
  • Abstract from PubMed
  • Full-text: Science Direct
    Exit
  • Abstract: Science Direct
    Exit
  • Other: Science Direct
    Exit
  • Journal Article Wegesser TC, Pinkerton KE, Last JA. California wildfires of 2008: coarse and fine particulate matter toxicity. Environmental Health Perspectives 2009;117(6):893-897. R832414 (2010)
    R832414C003 (2009)
    R832414C003 (2010)
    R832414C003 (Final)
  • Full-text from PubMed
  • Abstract from PubMed
  • Associated PubMed link
  • Full-text: EHP
  • Abstract: EHP
  • Journal Article Wilson DW, Aung HH, Lame MW, Plummer L, Pinkerton KE, Ham W, Kleeman M, Norris JW, Tablin F. Exposure of mice to concentrated ambient particulate matter results in platelet and systemic cytokine activation. Inhalation Toxicology 2010;22(4):267-276. R832414 (2010)
    R832414 (Final)
    R832414C002 (Final)
    R832414C003 (2010)
    R832414C003 (Final)
  • Abstract from PubMed
  • Abstract: Taylor&Francis-Abstract
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  • Journal Article Zhong C-Y, Zhou Y-M, Smith KR, Kennedy IM, Chen C-Y, Aust AE, Pinkerton KE. Oxidative injury in the lungs of neonatal rats following short-term exposure to ultrafine iron and soot particles. Journal of Toxicology and Environmental Health, Part A-Current Issues 2010;73(12):837-847. R832414 (2010)
    R832414C003 (2010)
    R832414C003 (Final)
    R829215 (Final)
  • Abstract from PubMed
  • Full-text: ResearchGate-Full Text PDF
    Exit
  • Abstract: Taylor&Francis-Abstract
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  • Supplemental Keywords:

    RFA, Health, Scientific Discipline, PHYSICAL ASPECTS, Air, particulate matter, Environmental Chemistry, Health Risk Assessment, Risk Assessments, Physical Processes, ambient aerosol, lung injury, long term exposure, lung disease, acute cardiovascular effects, airway disease, exposure, airborne particulate matter, San Joaquin Valley, cardiac arrest, human exposure, inhalation, ambient particle health effects, PM, concentrated air particles, cardiovascular disease, human health risk

    Progress and Final Reports:

    Original Abstract
  • 2006 Progress Report
  • 2007 Progress Report
  • 2008 Progress Report
  • 2009 Progress Report
  • Final Report

  • Main Center Abstract and Reports:

    R832414    San Joaquin Valley Aerosol Health Effects Research Center (SAHERC)

    Subprojects under this Center: (EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
    R832414C001 Project 1 -- Pulmonary Metabolic Response
    R832414C002 Endothelial Cell Responses to PM—In Vitro and In Vivo
    R832414C003 Project 3 -- Inhalation Exposure Assessment of San Joaquin Valley Aerosol
    R832414C004 Project 4 -- Transport and Fate Particles
    R832414C005 Project 5 -- Architecture Development and Particle Deposition