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The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

Toxicological information

Acute Toxicity: inhalation

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Administrative data

Endpoint:
acute toxicity: inhalation
Type of information:
experimental study
Adequacy of study:
supporting study
Study period:
No data
Reliability:
2 (reliable with restrictions)
Rationale for reliability incl. deficiencies:
other: Non-GLP compliant, non-guideline experimental investigation. Study published in scientific, peer reviewed journal.

Data source

Reference
Reference Type:
publication
Title:
Acute pulmonary and systemic effects of inhaled coal fly ash in rats: comparison to ambient environmental particles.
Author:
Smith K R, Veranth J M, Kodavanti U P, et al.
Year:
2006
Bibliographic source:
Toxicol Sci. 93(2):390-9.

Materials and methods

Principles of method if other than guideline:
The effect of CFA on pulmonary and systemic inflammation and injury was measured in male Sprague-Dawley rats exposed to filtered air or CFA for 4 h/day for 3 days.
GLP compliance:
no
Test type:
other: in vivo

Test material

Constituent 1
Reference substance name:
Coal fly ash
EC Number:
924-417-0
IUPAC Name:
Coal fly ash
Details on test material:
The particulate material used for inhalation was derived from a bulk sample of fly ash collected by air pollution control equipment on a 400-MW power plant burning bituminous coal from multiple mines in the Wasatch Plateau, UT, USA, coal field. Size-fractionated material, enriched in 0.4- to 2-um sized particles, was extracted from the bulk fly ash by mechanical resuspension and aerodynamic separation. The capture efficiency of typical coal power plant air pollution control equipment is at a minimum for the size range of CFA particles used in the current study, but is still > 90%. Extracting particles in the minimum efficiency size range from captured power plant fly ash produces an aerosol similar to the emitted particles.

Test animals

Species:
rat
Strain:
Sprague-Dawley
Sex:
male
Details on test animals or test system and environmental conditions:
Forty-eight male Sprague-Dawley rats, 8 weeks of age (260– 270 g) and free of respiratory pathogens or disease, were purchased from Harlan (San Diego, CA). Prior to CFA exposure, animals were acclimated to nose-only exposure tubes for 5 days (2, 3, 4, 4, 4 h, on days 1–5, respectively). Animals were handled in accordance with standards established by the U.S. Animal Welfare Acts as set forth in the National Institutes of Health guidelines (Institute of Laboratory Animal Resources (1996) as well as the Animal Care and Use committee of the University of California, Davis. Rats were housed in plastic cages with TEK-Chip pelleted paper bedding (Harlan Teklad, Madison, WI) and maintained on a 12-h light/12-h dark cycle. All animals had access to water and Laboratory Rodent Diet 5001 (LabDiet, Brentwood, MO) ad libitum except during each daily acclimation or exposure period.

Administration / exposure

Route of administration:
inhalation: aerosol
Type of inhalation exposure:
nose only
Vehicle:
other: filtered air
Details on inhalation exposure:
CFA was aerosolized using a belt feeder and fluidized bed system (Figure 1). PM2.5 size-fractionated particles were premixed with 100- to 200-um-diameter glass beads and loaded into a dust feed for delivery to a vibrating fluidized bed system for aerosolization of both CFA and glass beads. The aerosol subsequently passed through a cyclone separator to remove the glass beads, while the CFA remained aerosolized passing through a krypton-85 source (to reduce particle agglomeration) to the nose-only inhalation system.
Analytical verification of test atmosphere concentrations:
yes
Remarks:
Particle concentration during exposure was monitored by a continuous-reading, light-scattering, dust concentration monitor and filter connected to the exposure chamber. A Grimm Series 1.108 Aerosol Spectrometer (GRIMM Aerosol Technik GmbH, Douglasville, G
Duration of exposure:
3 d
Remarks on duration:
4h per day for 3 days
Concentrations:
1400 ug/m3
No. of animals per sex per dose:
5 – 6 per time point per group
Control animals:
yes
Details on study design:
Rats were exposed to filtered air or aerosolized CFA in a nose-only exposure system for 4 h/day for 3 days and examined 18 or 36 h after the last exposure to CFA. These necropsy times were selected to measure acute responses and to approximate the 1- to 3-day lag time between increases in PM concentration and human effects commonly observed in epidemiology studies.
Statistics:
All numerical data were calculated as the mean and standard deviation. Comparisons between animals exposed to CFA and filtered air were made by Student’s t-test or, where appropriate, by analysis of variance followed by Fisher’s protected least significant difference posttest. Comparisons were considered significant if a value of p < 0.05 was observed. Statistical analysis was performed with StatView 5.0.1 (SAS Institute, Inc., Cary, NC).

Results and discussion

Mortality:
No effects
Clinical signs:
other: No data
Body weight:
No data
Gross pathology:
No data
Other findings:
Total number of neutrophils in bronchoalveolar lavage fluid (BALF) following exposure to CFA was significantly increased along with significantly elevated blood neutrophils. Exposure to CFA caused slight increases in macrophage inflammatory protein-2, and marked increases in transferrin in BALF. Interleukin-1beta and total antioxidant potential in lung tissues were also increased in rats exposed to CFA. Histological examination of lung tissue demonstrated focal alveolar septal thickening and increased cellularity in select alveoli immediately beyond terminal bronchioles. These responses are consistent with the ability of CFA to induce mild neutrophilic inflammation in the lung and blood following short-term exposure at levels that could be occupationally relevant.

Any other information on results incl. tables

Exposure to CFA caused slight increases in macrophage inflammatory protein-2, and marked increases in transferrin in BALF. Interleukin-1beta and total antioxidant potential in lung tissues were also increased in rats exposed to CFA. Histological examination of lung tissue demonstrated focal alveolar septal thickening and increased cellularity in select alveoli immediately beyond terminal bronchioles.

Applicant's summary and conclusion

Interpretation of results:
other: no data
Remarks:
Criteria used for interpretation of results: other: no data
Conclusions:
When comparing the effects of CFA with those of concentrated ambient particles, CFA does not appear to have greater potency to cause pulmonary alterations.
Executive summary:

The effect of CFA on pulmonary and systemic inflammation and injury was measured in male Sprague-Dawley rats exposed to filtered air or CFA for 4 h/day for 3 days. The average concentration of CFA particulate matter less than 2.5 microm (PM(2.5)) was 1400 microg/m(3), of which 600 microg/m(3) was PM(1). Animals were examined 18 and 36 h postexposure. Chemical analysis of CFA detected silicon, calcium, aluminum, and iron as major components. Total number of neutrophils in bronchoalveolar lavage fluid (BALF) following exposure to CFA was significantly increased along with significantly elevated blood neutrophils. Exposure to CFA caused slight increases in macrophage inflammatory protein-2, and marked increases in transferrin in BALF. Interleukin-1beta and total antioxidant potential in lung tissues were also increased in rats exposed to CFA. Histological examination of lung tissue demonstrated focal alveolar septal thickening and increased cellularity in select alveoli immediately beyond terminal bronchioles. These responses are consistent with the ability of CFA to induce mild neutrophilic inflammation in the lung and blood following short-term exposure at levels that could be occupationally relevant. However, when comparing the effects of CFA with those of concentrated ambient particles, CFA does not appear to have greater potency to cause pulmonary alterations.