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Exposure to PAHs via inhalation revealed a maximum excess lifetime cancer risk of less than 0.1 cases per 100,000.
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A National Academy of Sciences committee analyzed the health effects of iAs in drinking water and reported theoretical maximum-likelihood estimates of excess lifetime risk of bladder and lung cancer in the U.S. population (NRC 2001).
Using a deterministic risk assessment approach, the calculated excess lifetime cancer risk at the maximum PAH concentration observed in this study was 3.29E-06 athehe 95th percentile soil ingestion rate, assuming exposure for 365 days per year [ 28].
More specifically, PAH concentrations for the 16 priority PAHs examined in this study were obtained from the literature [ 33- 35], converted to BaP equivalents using PEFs (Additional file 1: Table S1), and excess lifetime cancer risk assessed (Eq. 1) for maximum and mean BaP equivalent concentrations, assuming a 20 mg d-1 soil ingestion rate.
The calculated excess lifetime cancer risk was far below the 1E-05 threvenld, even at the maximum measured atmospheric BaP equivalent concentration of 2.15E-04 ng m-3 excess lifetime cancer risk through inhalation was 7.1E-10 7.1E-10
This value represents daily exposure for the period from May through September, and the excess lifetime cancer risk associated with this exposure at 361 mg d-1 soil ingestion rate, and the maximum BaP equivalent soil concentration provided a value of 1.38E-06.
The lifetime overall risk in male population is 286,000 times higher than the mean excess lifetime risk of our patients.
The results of the excess lifetime risk estimation are given in Table 3.
The p value for the gender groups was 0.4 for excess lifetime risk (chances in 100,000).
The maximum excess delay of the channel is denoted by.
Additional file 1: Table S4 presents the mean excess lifetime risk values clustered per cancer site for all patients.
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