Abstract

Carbon fibres (CF) are synthetic fibres which are used commercially for their thermal resistance, excellent electrical conductivity, flexibility and high tensile strength. The dimensions of most of the carbon fibre types currently available fall outside the respirable range, having nominal diameters from 5 to 10 μm. The pitch-based experimental fibres used in this study (1–4 fim diameter) have the potential to cause toxic pulmonary effects. Groups of male Crl:CD® BR rats were exposed to aerosols of pitch or polyacrylonitrile (PAN)-based carbon fibres at target concentrations of 50 or 100 mgm−3 for periods ranging from 1 to 5 days. Following the exposure period, cells and fluids from sham and carbon fibre-exposed animals were recovered by bronchoalveolar lavage (BAL). Alkaline phosphatase, lactate dehydrogenase (LDH) and protein values were measured in BAL fluids at several time points post-exposure. Alveolar macrophages were evaluated for viability and functional capacity. The lungs of additional exposed animals were processed for histopathological analysis. A 5-day exposure to respirable pitch carbon fibres at design concentrations of 50 and 120 mg m−3 (fibre concentrations at 47 and 62 fibres cm−3 of air) produced dose-dependent, transient inflammatory responses in the lungs of exposed rats, manifested by increased numbers of neutrophils. In addition, significant increases in LDH, protein or alkaline phosphatase levels were measured in BAL fluids at early post-exposure time periods but were reversible within 10 days after exposure. No significant differences were measured in the morphology or in vitro phagocytic capacities of macrophages recovered from sham or pitch-based carbon fibre-exposed rats. Results from cell labelling studies in rats exposed to pitch-based carbon fibres for 5 days demonstrated an increased turnover of lung parenchymal cells at 10 days or 1 month after exposure but no increases in cell turnover were measured in the airways at any time post-exposure. The lungs of additional exposed animals were processed for histopathology at 1 or 3 months after a 5-day exposure. Pigment-laden alveolar macrophages as well as minimal Type II epithelial cell hyperplasia was observed primarily at the junctions of terminal bronchioles and alveolar ducts. An additional group of rats was exposed for 1 day (i.e. 6 h) to a sample of polyacrilonitrile (PAN)-based carbon fibres (fibre diameter = 4.4 μm; MMAD = 9 μm). These materials were used as negative controls since the physical dimensions of these fibres fell outside the respirable range. Exposures to the PAN-based fibres produced no cellular, cytotoxic or alveolar-capillary membrane permeability changes at any time post-exposure. The results of this study demonstrate that the pulmonary toxicity of respirable, pitch-based carbon fibres is substantially different from well-known fibrogenic agents such as crystalline silica and asbestos.

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