Comparative study of the acute lung toxicity of pure cobalt powder and cobalt-tungsten carbide mixture in rat

Nanotoxicity: emerging concerns regarding nanomaterial safety and occupational hard metal (WC-Co) nanoparticle exposure

“…Early data concerning the effects of inhaled WC-Co dusts first emerged in the 1960s and continued through the 1980s, providing researchers the foundation to further explore the toxic effects of hard metal exposure using in vitro [71][72][73][74][75][76][77][78][79][80][81][82][83][84][85][86][87][88] and in vivo 72,[89][90][91][92][93][94][95][96] models. Although cobalt itself was originally considered the causative agent of HMLD, several studies demonstrated that this is not the case and the disease mainly develops due to the simultaneous presence of WC with Co. 71,74,[76][77][78][79]90,91 It is currently understood that the combination of WC-Co is more toxic than Co, W, or WC particles alone, both in vitro and in vivo, 71,72,74,78,79,81,85,90,91,93,94,…”

“…Although cobalt itself was originally considered the causative agent of HMLD, several studies demonstrated that this is not the case and the disease mainly develops due to the simultaneous presence of WC with Co. 71,74,[76][77][78][79]90,91 It is currently understood that the combination of WC-Co is more toxic than Co, W, or WC particles alone, both in vitro and in vivo, 71,72,74,78,79,81,85,90,91,93,94,[97][98][99] but the reason for this enhanced toxicity is still not well defined.…”

“…5,72,[89][90][91][92]94 As noted in Table 5, the in vivo studies examined the effects of WC-Co particles in the Table 5 Summary of in vivo wC-Co toxicity studies Single IT bolus at 0-500 μg per rat 24 h exposure A consistent lack of acute local pulmonary inflammation was observed in terms of the BAL fluid parameters examined in animals exposed to wC-Co NPs while significant acute pulmonary inflammation was observed in the CeO 2 NP group micron-size range, using the mass-per-body weight dosing scheme (ie, mg/kg or mg/g), although some variation in particle size was noted in most cases (overall, WC-Co size ranging from 0.1 to 6 μm). Specifically, micro-sized WC-Co particle exposure caused significant pulmonary inflammation in rats, marked by increased bronchoalveolar lavage (BAL) fluid parameters such as lactate dehydrogenase (LDH) and albumin content, compared to control animals, in as little as 24 h after delivery the of WC-Co IT bolus.…”

Characterization of exposures among cemented tungsten carbide workers. Part I: Size-fractionated exposures to airborne cobalt and tungsten particles

“…Using in vitro and in vivo models, researchers investigating the mechanistic basis of HMD (Lasfargues et al, 1992;Lison and Lauwerys, 1990, 1994, 1995Lison et al, , 1996Zanetti and Fubini, 1997;Keane et al, 2002;Mutti and Corradi, 2006;Moriyama et al, 2007) observed that a mechanical mixture of pure cobalt and tungsten carbide powders prepared in the laboratory and pre-sintered hard metal powder (mixture of cobalt, tungsten, and carbon) were more toxic than pure tungsten carbide or pure cobalt powder alone; the increased toxicity of the powder mixtures was attributed to the generation of free radicals via a localized reaction, that is, on a particle surface or between particle surfaces in contact, and not from the reaction of a solubilized component at the solid surface. Using powder concentrations of 22.5 mg/ml (which is high relative to observed mass concentrations in Table 1) and an electron spin resonance technique, Lison et al ( , 1996 proposed the following precise mechanism for HMD: when both cobalt metal (which is thermodynamically able to reduce ambient oxygen) particles and tungsten carbide (a good electron conductor) particles are associated, electrons provided by the cobalt metal are easily transferred to the surface of the carbide particles, where reduction of oxygen can occur at an increased rate, resulting in the generation of free radicals.…”

“…Workplace studies have identified cases of occupational asthma among CTC workers exposed to both cobalt and tungsten (Davison et al, 1983;Sprince et al 1988;Meyer-Bisch et al, 1989;Shirakawa et al, 1989;Kusaka et al, 1996) and diamond polishers exposed to cobalt alone (Gheysens et al, 1985). Cases of HMD have been reported among workers in all phases of CTC production (Bech et al, 1962;Coates and Watson, 1971;Sjo¨gren et al, 1980;Davison et al, 1983;Sprince et al, 1984Sprince et al, , 1988Meyer-Bisch et al, 1989;Cugell et al, 1990;Figueroa et al, 1992;Fischbein et al, 1992), which may be due to exposures to tungsten carbide particles in association with cobalt particles (Lasfargues et al, 1992(Lasfargues et al, , 1995Lison and Lauwerys, 1990, 1994, 1995Lison et al, , 1996. In humans, excess lung cancer has been observed among hard metal workers exposed to CTC dusts (Lasfargues et al, 1994;Moulin et al, 1998;Wild et al, 2000;Lison et al, 2001), but not among cobalt production workers exposed to cobalt alone (Moulin et al, 1993).…”