The public has recently raised concerns regarding potential human health and environmental risks associated with tire crumb constituents in the artificial turf of football fields. The aim of the present study was to develop an environmental analysis drawing a comparison between artificial turf football fields and urban areas relative to concentrations of particles (PM10 and PM2.5) and related polycyclic aromatic hydrocarbons (PAHs), aromatic hydrocarbons (BTXs), and mutagenicity of organic extracts from PM10 and PM2.5. No significant differences were found between PM10 concentrations at an urban site and on a turf football field, both during warm and in cold seasons, either with or without on-field activity. PM2.5 concentrations were significantly greater at the urban site in the cold season as was the ratio of PM2.5 to PM10. BTXs were significantly greater at urban sites than on turf football fields on both on warm and cold days. The ratio of toluene to benzene (T/B ratio) was always comparable with that of normal urban conditions. The concentration of PAHs on the monitored football fields was comparable with urban levels during the two different sampling periods, and the contribution of PAHs released from the granular material was negligible. PM10 organic extract mutagenicity for artificial turf football fields was greater, whereas PM2.5 organic extract mutagenicity was lower, compared with the urban site studied. However, both organic extract mutagenicity values were comparable with the organic extract mutagenicity reported in the literature for urban sites. On the basis of environmental monitoring, artificial turf football fields present no more exposure risks than the rest of the city.

Many studies have pointed out a correlation between airborne PM quantitative exposure and health effects. The aim of this research is the investigation of the role of the PM 2.5 chemical fraction in the DNA damage induction in human cells (A549). Air samples (PM 2.5 ) were collected in different sites (urban, industrial and highway) using a high-volume sampler. Organic and water-soluble extracts of PM 2.5 were tested on A549 cells to evaluate genotoxic and oxidative damage using the Comet assay without and with formamido-pyrimidine-glycosylase (Fpg). Organic and water extracts were analysed for determination of PAHs by GC-MS methods and metals by the ICP-MS technique respectively. The PM 2.5 organic extract of all the samples caused a significant dose-dependent increase of the A549 DNA damage. The genotoxic effect was related to IPA PM 2.5 content and the highest effect was observed for the motorway site sample (65.03 CL/10m3 ) while the oxidative damage was observed in PM 2.5 water extract of the industrial and motorway sites. The extent of the oxidative damage seems to be related to the type and concentration of metals present in these samples. The results of this study emphasize the importance of evaluating the PM chemical composition for the biological effect determination. This concern highlights the need for considering its qualitative composition in addition to its size and air concentration for PM health effect evaluation and exposure management.