Air pollution and particulate matter (PM) are classified as carcinogenic to humans.
Pollutants evidence for public health concern include coarse (PM10) and fine (PM2.5)
particles. However, ultrafine particles (PM0.1) are assumed to be more toxic than
larger particles, but data are still needed to better understand their mechanism of
action. In this context, the aim of our work was to investigate the in vitro and in
vivo genotoxic potential of fine (PM2.5-018) and quasi ultra-fine (PM0.18) particles
from an urban-industrial area (Dunkirk, France) by using comet, micronucleus and/or
gene mutation assays. In vitro assessment was performed with 2 lung immortalized cell
lines (BEAS-2B and NCI-H292) and primary normal human bronchial epithelial cells (NHBE)
grown at the air-liquid interface or in submerged conditions (5 µg PM/cm2). For in
vivo assessment, tests were performed after acute (24 h, 100 µg PM/animal), subacute
(1 month, 10 µg PM/animal) and subchronic (3 months, 10 µg PM/animal) intranasal exposure
of BALB/c mice. In vitro, our results show that PM2.5-018 and PM0.18 induced primary
DNA damage but no chromosomal aberrations in immortalized cells. Negative results
were noted in primary cells for both endpoints. In vivo assays revealed that PM2.5-018
and PM0.18 induced no significant increases in DNA primary damage, chromosomal aberrations
or gene mutations, whatever the duration of exposure. This investigation provides
initial answers regarding the in vitro and in vivo genotoxic mode of action of PM2.5-018
and PM0.18 at moderate doses and highlights the need to develop standardized specific
methodologies for assessing the genotoxicity of PM. Moreover, other mechanisms possibly
implicated in pulmonary carcinogenesis, e.g. epigenetics, should be investigated.