Systemic Effects of short term inhalation of carbon at levels permitted by OSHA

Another laboratory study supports the observed cardiovascular toxicity of fine particles without other known toxicity. Carbon black is carcinogenic in the rat by inhalation. These exposure levels are about 1/3 of the OSHA limit for day in and day out exposure.

The condensed abstract notes:

…We hypothesized that inhaled ultrafine particles result in an inflammatory response which may stimulate systemic clotting factor release. … rats were exposed to either fine or ultrafine carbon black (CB) for 7 h. … total suspended particle concentrations were 1.66 mg/m(3) for ultrafine CB and 1.40 mg/m(3) for fine CB. Particle concentration of ultrafine particles was more than 10 times greater than that of fine particles… ultrafine CB caused an increase in total bronchoalveolar lavage (BAL) leukocytes… … Exposure to the ultrafine, but not fine, carbon was also associated with significant increases in the total numbers of blood leukocytes. … The data show that there is a small but consistent significant proinflammatory effect of this exposure to ultrafine particles that is greater than the effect of the same exposure to fine CB.

VVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVV

Toxicol Appl Pharmacol. 2004 Feb 15;195(1):35-44.

Pulmonary and systemic effects of short-term inhalation exposure to ultrafine carbon black particles.

Gilmour PS, Ziesenis A, Morrison ER, Vickers MA, Drost EM, Ford I, Karg E, Mossa C, Schroeppel A, Ferron GA, Heyder J, Greaves M, MacNee W, Donaldson K.

Edinburgh Lung and the Environment Group Initiative (ELEGI)/Colt Laboratory, The MRC Centre for Inflammation Research, Medical School, The University of Edinburgh, Edinburgh EH8 9AG, UK.

While environmental particles are associated with mortality and morbidity related to pulmonary and cardiovascular (CV) disease, the mechanisms involved in CV health effects are not known. Changes in systemic clotting factors have been associated with pulmonary inflammation. We hypothesized that inhaled ultrafine particles result in an inflammatory response which may stimulate systemic clotting factor release. Adult male Wistar rats were exposed to either fine or ultrafine carbon black (CB) for 7 h. The attained total suspended particle concentrations were 1.66 mg/m(3) for ultrafine CB and 1.40 mg/m(3) for fine CB. Particle concentration of ultrafine particles was more than 10 times greater than that of fine particles and the count median aerodynamic diameter averaged 114 nm for the ultrafine and 268 nm for the fine carbon particles. Data were collected immediately, 16 and 48 h following exposure. Only ultrafine CB caused an increase in total bronchoalveolar lavage (BAL) leukocytes, whereas both fine (2-fold) and ultrafine (4-fold) carbon particles caused an increase in BAL neutrophils at 16 h postexposure. Exposure to the ultrafine, but not fine, carbon was also associated with significant increases in the total numbers of blood leukocytes. Plasma fibrinogen, factor VII and von Willebrand factor (vWF) were unaffected by particle treatments as was plasma Trolox equivalent antioxidant status (TEAC). Macrophage inflammatory protein-2 mRNA was significantly increased in BAL cells 48 h following exposure to ultrafine CB. The data show that there is a small but consistent significant proinflammatory effect of this exposure to ultrafine particles that is greater than the effect of the same exposure to fine CB.