Evaluating Soil Contamination Risks in Residential Properties: A Bristol Case Study

1. Living at home – toorisky? Dealing with uncertainty in HHRA

2. Outline • Objectives • Methodology • Results • Discussion of results • Conclusions

3. Objectives • Part IIA style investigation of a residential property in Bristol • Objectives: • Understand the risks posed to residents from contaminants in soil (specifically PAHs) • Determine whether those risks pose significant possibility of significant harm • Assess the need for further assessment to more accurately assess risk • Assess the need for risk mitigation

4. Property • Terraced house built c.1900 on greenfield site • Located adjacent to a park • Small, mostly hard covered front garden • Small (5 x 7 m) rear garden with some parts used for growing vegetables

5. Sampling strategy Flower Beds Decking Grass 5.3 m House Paving 7 m

6. Sampling strategy HA3 HA4 HA2 HA1 HA5 DS1 + PM10 monitoring Composite sample HA6 • Samples analysed by ALcontrol Laboratories for PAHs and SOM HA7 (dup)

7. Fieldwork • Best practice sampling protocols followed • Using suitably qualified and experienced field staff

8. Analytical results

9. GQRA • Compared concentrations of PAHs with LQM/CIEH 2nd edition GAC for residential land-use • Concentrations of PAHs < GAC with exception of BaP • Mean concentration of BaP in surface soil samples = 1.2 mg/kg • So now what?

10. DQRA • Exceedence of GAC means further assessment required • DQRA moves from the use of GAC based on generic assumptions to SSAC based on site specific assumptions • Uncertainty analysis is also an important element of DQRA • Identify site specific adjustments that will produce a more realistic estimation of risks: • Changes to conceptual model? • Changes to models used? • Changes to input parameters? • Use of statistics? • Changes to input parameters - focus on principle risk driving pathways

11. Pathway contributions • Pathway contributions to total exposure and risk for generic residential scenario (0 to 6 yr female child) Inhalation of dust important contributor to risk

12. CLEA parameters * Contaminant specific

13. Exposure via soil/dust ingestion • Generic assumptions: • Child eats average of 100 mg soil per day 365 days per year • Female child of average body weight • Site specific assumptions • I have two boys, no girls yet • Big one is skinny, little one is not • Both eat soil indoors and out • Do they eat 36.5 grams soil per year? • Does it all come from garden?

14. Exposure via dust inhalation • Generic assumptions: • Soil derived PM10 indoors >> soil derived PM10 outdoors • Indoor PM10 from soil = outdoor PM10 derived from soil + (DL x TF) • PM10outdoor_soil = 0.425 ug/m3 • Indoor dust loading (DL) = 50 ug/m3 • Soil to dust transport factor (TF) = 0.5 Critical parameters

15. Indoor dust loading • PM10 indoors = 30 to 40 ug/m3 • Further monitoring required to give average daily PM10 indoors • CLEA generic DL = 50 ug/m3

16. Soil to dust transport factor • What proportion of PM10 is likely to be from garden soil? • 2 lines of evidence: • PAH analysis of dust from hoover bag vs soil analysis • Average [BaP] in surface soil = 1.2 mg/kg • [BaP] in dust = 1.0 mg/kg • PAH profile in dust similar to garden soil • SOM analysis of dust from hoover bag vs soil analysis • Average SOM in surface soil = 13% • SOM in dust = 32% • If we assume that dust composed of soil (13% SOM) + skin/food (100% SOM), TF = 0.8 – higher than CLEA generic assumption!

17. Results of DQRA • Exposure frequencies and gender made specific to my children • Average (as opposed to upper 95th %ile) dermal adherence factors used • TF increased from 0.5 to 0.8 • SSAC for BaP = 1.28 mg/kg • [BaP] in surface soil = 0.65 to 1.6 mg/kg • Average [BaP] in surface soil = 1.2 mg/kg • UCL 95 [BaP] = 1.57 mg/kg

18. Discussion of results • DQRA shows that best (most realistic) estimate of ADE:HCV ratio for my children = 0.92 • ADE:HCV ratio < 1 indicate minimal or negligible risk • However, there is uncertainty in the 0.92 number • Uncertainties in representative exposure concentration, soil ingestion rate etc, mean that actual ADE:HCV ratio could differ from 0.92 • May be more meaningful to say that ADE:HCV ratio is likely to be somewhere between 0.5 to 1.5

19. Discussion of results • Even if ADE:HCV ratio = 1.5 – is this a problem? • Dust inhalation biggest contributor to risk (57%) • How does dust inhalation pathway compare to background inhalation exposure? • Exposure to BaP via inhalation of soil derived dust = 20% of background exposure to BaP via inhalation (assuming average UK urban air conc of BaP of 0.21 ng/m3) • Thus remediation of garden soil will not cause significant reduction in overall inhalation risk • Soil/dust ingestion contributes 40% of risk • HCVoral for BaP based on WHO drinking water standard which is based on dose-response data for forestomach tumours in mice. • High degree of uncertainty in trying to extrapolate the dose-response to humans • WHO DWS incorporates safety factors to account for this uncertainty and ensure that DWS is protective • As a result of these safety factors an ADE:HCV ratio of 1.5 is unlikely to constitute SPOSH

20. Conclusions • Risk assessment is meaningless without consideration of uncertainties • Generic parameters in CLEA model appear a reasonable basis for Part IIA assessments but: • site specific adjustments should be made where possible • uncertainties should be recognised and made transparent in risk assessment report • This amateur research work has identified a need for further research: • Exposure from inhalation of indoor dust • Soil and dust ingestion rates • Further guidance required on: • Significance of exceedence in the context of uncertainties involved in derivation of HCV

21. Acknowledgements • Many thanks to www.firthconsultants.co.uk