Conclusion

Epidemiology studies show that under the worst-case exposure scenarios (which occurs in production, and exposure in the past was much worse, in comparison with today ), the lung dust burdens of miners exceeded those observed in rodent studies in which overloading of lung clearance has been observed (Morrow 1992). However, numerous epidemiology studies have failed to adequately demonstrate an increased risk of lung cancer due to occupational exposure coal dust.

Carbon black is not carcinogenic to mice (oral, skin or inhalation), hamsters (inhalation or intratracheal), guinea pigs (inhalation), rabbits (skin or inhalation), primates (skin or inhalation) or rats (oral). Only studies in rats conducted by inhalation and intratracheal administration have shown significant increases in benign and malignant lung tumours. This species-specific response by the rat to carbon black, not seen in any other laboratory species and which has not been reported in humans, strongly suggests that the results of the rat inhalation bioassay should not be considered directly relevant when assessing human risk. Therefore, carbon black should not be classified as carcinogenic to humans based on the rodent bioassay data (Rausch et al, 2004). So overload in rodent tests cannot be used as a predictive parameter for adverse human health effects, such as lung cancer.

The IARC evaluations of carbon black and titanium oxide (possibly carcinogenic to humans, group 2B; based on inadequate evidence for humans and sufficient evidence for animals; IARC, 2010) do not distinguish between the different species response to lung burden by rodents and humans as suggested by Rausch et al (2004), and seems to be over conservative in the precautionary approach that lung cancer may occur, although epidemiology and various animal tests do not support this causal relation.

Chronic particle exposure may cause adverse health effects other than lung cancer in humans, such as systemic inflammation and pneumoconiosis. However, further analyses of these data including toxicokinetic modelling to evaluate hypotheses about relationships between lifetime exposures, retained lung dust, overloading of lung clearance and disease development are recommended.