California wildfires of 2008: coarse and fine particulate matter toxicity

Abstract

Background: During the last week of June 2008, central and northern California experienced thousands of forest and brush fires, giving rise to a week of severe fire-related particulate air pollution throughout the region. California experienced PM(10-2.5) (particulate matter with mass median aerodynamic diameter > 2.5 mum to < 10 mum; coarse ) and PM(2.5) (particulate matter with mass median aerodynamic diameter < 2.5 mum; fine) concentrations greatly in excess of the air quality standards and among the highest values reported at these stations since data have been collected.

Objectives: These observations prompt a number of questions about the health impact of exposure to elevated levels of PM(10-2.5) and PM(2.5) and about the specific toxicity of PM arising from wildfires in this region.

Methods: Toxicity of PM(10-2.5) and PM(2.5) obtained during the time of peak concentrations of smoke in the air was determined with a mouse bioassay and compared with PM samples collected under normal conditions from the region during the month of June 2007.

Results: Concentrations of PM were not only higher during the wildfire episodes, but the PM was much more toxic to the lung on an equal weight basis than was PM collected from normal ambient air in the region. Toxicity was manifested as increased neutrophils and protein in lung lavage and by histologic indicators of increased cell influx and edema in the lung.

Conclusions: We conclude that the wildfire PM contains chemical components toxic to the lung, especially to alveolar macrophages, and they are more toxic to the lung than equal doses of PM collected from ambient air from the same region during a comparable season.

Keywords: PM10; PM2.5; air pollution; alveolar macrophage; lung inflammation; mouse; source-specific particulate matter.

Figure 1

Number (mean ± SE) of total cells (A) and macrophages (B) recovered in lung lavage fluid from mice intratracheally instilled with different doses of PM_10–2.5 (coarse) or PM_2.5 (fine) from the wildfire samples (PBS-instilled controls, 0 μg). Note difference in y-axis scale in A and B. *p <0.001 compared with control. **p < 0.01 compared with 25 or 50 μg.

Figure 2

(A) Percentage of neutrophils in the lung lavage fluid from mice instilled with the indicated amounts of PM_10–2.5 or PM_2.5 wildfire PM. All of the indicated values are significantly greater than PBS-instilled controls, which contained 0% polymorphonuclear leukocytes. (B) Number of macrophages in the lung lavage fluid of mice instilled with either 25 or 50 μg PM: comparison of wildfire PM and normal AA PM collected 1 year earlier from the same area. Values shown are mean ± SE. *p < 0.05 compared with either 25 or 50 μg wildfire PM samples.

Figure 3

Protein content of lung lavage fluid supernatant of mice instilled with the indicated amounts of wildfire PM_10–2.5 or PM_2.5. *p < 0.05 compared with control.

Figure 4

Representative lung sections from mice instilled 24 hr with 100 μg wildfire PM_10–2.5. (A) Whole lung; bar = 500 μm. Boxes indicate areas shown in higher magnification in (B) and (C). (B) Proximal lung with conducting airways; bar = 100 μm. (C) Distal lung with centriacinar region; bar = 100 μm. Arrows indicate typical areas with inflammatory cell infiltrates. Sections from control animals are shown in Figure 5.

Figure 5

Representative lung sections from control mice instilled 24 hr with 50 μL PBS solution. (A ) Whole lung (low magnification) showing airways, blood vessels, and parenchyma; bar = 500 μm. (B) Lung parenchyma (high magnification) showing thin delicate alveolar septal tissues; bar = 100 μm.

Figure 6

Representative lung sections from mice instilled 24 hr with 100 μg wildfire PM_2.5. (A ) Whole lung (low-magnification; bar = 500 μm); boxes indicate areas shown in higher magnification in (B) and (C). (B) Centriacinar lung region showing the prominent accumulation of numerous inflammatory cells within alveolar airspaces. (C) Distal alveolar region with a diffuse increase in septal cellularity and occasional inflammatory cells within the alveolar airspaces. Arrows indicate areas of inflammatory cell influx. Bar = 100 μm in (B) and (C).

Figure 7

Representative lung sections from mice instilled 24 hr with 10 μg wildfire PM_10–2.5. (A) Whole lung (low-magnification; bar = 500 μm); box indicates area shown in higher magnification in (B) and (C). (B) Centriacinar region with accumulations of inflammatory cells in the alveolar airspaces; arrow indicates area of cellular influx. (C) Distal alveolar region with subtle markings of pulmonary edema and increased abundance of alveolar macrophages. Bar = 100 μm in (B) and(C).