## Materials and Methods
### Risk Analysis
In the case of direct ingestion and dermal contact, the non-carcinogenic Hazard Quotient HQ (i.e., HQ\({}_{\text{ingesion}}\) and HQ\({}_{\text{dermal}}\)) was calculated by dividing the chronic daily intake by the corresponding reference dose (RfD, mg/kg/day) [53; 51], defined as the maximum daily exposure to a toxic agent that would not produce any appreciable deleterious effect on human health:  
\[\text{HQ}=\frac{\text{CDI}}{\text{RfD}}\]  
For the dust inhalation pathway, HQ\({}_{\text{inhalation}}\) was calculated by dividing the exposure concentration (EC, mg/m\({}^{3}\)) by the reference toxicity concentration value (RfC, mg/m\({}^{3}\)), which represents an estimate of continuous inhalation exposure without appreciable risk of deleterious effects during a lifetime [54]:  
\[\text{HQ}=\frac{\text{EC}}{\text{RfC}}\]  
where RfC was set to 1.5 \(\times\) 10\({}^{-5}\) mg/m\({}^{3}\)[51] and EC was estimated starting from the predicted concentration in air (mg/m\({}^{3}\)) as exposure metrics, rather than inhalation intake of a contaminant in air based on the inhalation rate and an average body weight, according to:  
\[\text{EC}=\frac{\text{C}_{\text{POE}}\times\text{ET}\times\text{EF}\times \text{ED}}{\text{AT}}\]  
Here, ET represents the exposure time (24 h/day, suitable for a residential area), AT is given by ED \(\times\) 365 day/yr \(\times\) 24 h/day and C\({}_{\text{POE}}\) is the concentration in air at the exposure point (mg/m\({}^{3}\)), calculated by means of the transport model related to the dust inhalation pathway as defined by the ASTM standard [46; 55]. The total non-carcinogenic risk for a single substance defines a screening level individual Hazard Index (HI\({}_{\text{i}}\)) as:  
\[\text{HI}_{\text{i}}=\text{HQ}_{\text{ingesion}}+\text{HQ}_{\text{dermal}}+\text{HQ}_{\text{inhalation}}\]  
An HI\({}_{\text{i}}\) value less than unity indicates that the risk is acceptable [53]. For each pathway, the carcinogenic risk (R) is defined as the incremental probability of an individual developing cancer over a lifetime resulting from exposure to the potential carcinogens [53] and is directly related to the intake:  
\[\text{R}=\text{CDI}\times\text{SF}\]  
where the slope factor (SF) (defined as the risk generated by a lifetime average amount of one mg/kg/day of carcinogen) is the contaminant specific toxicity reference value [51], which converts the estimated daily intake averaged over a lifetime of exposure directly into the incremental risk for an individual of developing cancer. The carcinogenic risk for soil due to direct exposure was calculated using an age-adjusted factor, namely a time-weighted average of these parameters for receptors exposed for an extended period of time (e.g., 30 years) from childhood through adulthood [48; 56]. The excess cancer risk for a receptor exposed via the inhalation pathway was estimated using [54]:  
\[\mathrm{R}=\mathrm{IUR}\times\mathrm{EC}\]  
where IUR represents the Inhalation Unit Risk, defined as an estimate of the increased cancer risk from inhalation exposure to a given concentration (1 \(\mathrm{\SIUnitSymbolMicro g}\)/m\({}^{3}\)) for a lifetime [51]; EC is the exposure concentration averaged over a lifetime of 70 years (AT = 70 years \(\times\) 365 days/year \(\times\) 24 h/day). The carcinogenic risk \(\mathrm{R_{i}}\) for a single substance is represented by the sum of the contributions due to each exposure route. The permissible limits are \(10^{-6}\) and \(10^{-4}\) for a single carcinogenic element and multi-element carcinogens, respectively. In particular, a risk value for arsenic lower than \(10^{-6}\) (one-in-a-million individual excess cancer risk) can be considered acceptable [47; 48; 57]. The maximum allowed concentration of contaminants in soil considered to be protective of human health (soil screening levels--SSLs, according to US EPA guidelines) was obtained by following the Risk Based Corrective Action procedure [46; 47].