TY - JOUR

T1 - Systematic review on primary and secondary genotoxicity of carbon black nanoparticles in mammalian cells and animals

AU - Di Ianni, Emilio

AU - Jacobsen, Nicklas Raun

AU - Vogel, Ulla Birgitte

AU - Moller, Peter

PY - 2022

Y1 - 2022

N2 - Carbon black exposure causes oxidative stress, inflammation and genotoxicity. The objective of this systematic review was to assess the contributions of primary (i.e. direct formation of DNA damage) and secondary genotoxicity (i.e., DNA lesions produced indirectly by inflammation) to the overall level of DNA damage by carbon black. The database is dominated by studies that have measured DNA damage by the comet assay. Cell culture studies indicate a genotoxic action of carbon black, which might be mediated by oxidative stress. Many in vivo studies originate from one laboratory that has investigated the genotoxic effects of Printex 90 in mice by intratracheal instillation. Meta-analysis and pooled analysis of these results demonstrate that Printex 90 exposure is associated with a slightly increased level of DNA strand breaks in bronchoalveolar lavage cells and lung tissue. Other types of genotoxic damage have not been investigated as thoroughly as DNA strand breaks, although there is evidence to suggest that carbon black exposure might increase the mutation frequency and cytogenetic endpoints. Stratification of studies according to concurrent inflammation and DNA damage does not indicate that carbon black exposure gives rise to secondary genotoxicity. Even substantial pulmonary inflammation is at best only associated with a weak genotoxic response in lung tissue. In conclusion, the review indicates that nanosized carbon black is a weak genotoxic agent and this effect is more likely to originate from a primary genotoxic mechanism of action, mediated by e.g., oxidative stress, than inflammation-driven (secondary) genotoxicity.

AB - Carbon black exposure causes oxidative stress, inflammation and genotoxicity. The objective of this systematic review was to assess the contributions of primary (i.e. direct formation of DNA damage) and secondary genotoxicity (i.e., DNA lesions produced indirectly by inflammation) to the overall level of DNA damage by carbon black. The database is dominated by studies that have measured DNA damage by the comet assay. Cell culture studies indicate a genotoxic action of carbon black, which might be mediated by oxidative stress. Many in vivo studies originate from one laboratory that has investigated the genotoxic effects of Printex 90 in mice by intratracheal instillation. Meta-analysis and pooled analysis of these results demonstrate that Printex 90 exposure is associated with a slightly increased level of DNA strand breaks in bronchoalveolar lavage cells and lung tissue. Other types of genotoxic damage have not been investigated as thoroughly as DNA strand breaks, although there is evidence to suggest that carbon black exposure might increase the mutation frequency and cytogenetic endpoints. Stratification of studies according to concurrent inflammation and DNA damage does not indicate that carbon black exposure gives rise to secondary genotoxicity. Even substantial pulmonary inflammation is at best only associated with a weak genotoxic response in lung tissue. In conclusion, the review indicates that nanosized carbon black is a weak genotoxic agent and this effect is more likely to originate from a primary genotoxic mechanism of action, mediated by e.g., oxidative stress, than inflammation-driven (secondary) genotoxicity.

KW - Carbon black

KW - Genotoxicity

KW - Nanoparticles

KW - Oxidative DNA damage

KW - Secondary genotoxicity

KW - Systematic review

KW - OXIDATIVELY DAMAGED DNA

KW - DIESEL EXHAUST PARTICLES

KW - COMET ASSAY

KW - STRAND BREAKS

KW - PULMONARY INFLAMMATION

KW - SUBCHRONIC INHALATION

KW - LUNG INFLAMMATION

KW - EXPOSURE

KW - RATS

KW - RESPONSES

U2 - 10.1016/j.mrrev.2022.108441

DO - 10.1016/j.mrrev.2022.108441

M3 - Review

C2 - 36007825

VL - 790

JO - Mutation Research - Reviews

JF - Mutation Research - Reviews

SN - 1383-5742

M1 - 108441

ER -