Estimates of potential childhood lead exposure from

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Environmental Research 156 (2017) 781–790

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Estimates of potential childhood lead exposure from contaminated soil using the US EPA IEUBK Model in Sydney, Australia

MARK



Mark A.S. Laidlawa, , Shaike M. Mohmmadb, Brian L. Gulsonc, Mark P. Taylord, Louise J. Kristensene, Gavin Birchb a

Centre for Environmental Sustainability and Remediation (EnSuRe), School of Science, RMIT University, PO Box 71, Bundoora, Victoria, Australia - 3083 Environmental Geology Group, School of Geosciences, Sydney University, Sydney, NSW 2006, Australia c Department of Environmental Sciences, Faculty of Science and Engineering, Macquarie University, Sydney, NSW 2109, Australia d Department of Environmental Sciences, Faculty of Science and Engineering, Macquarie University, Sydney, NSW 2109, Australia e Department of Chemistry and Biochemistry, University of California, San Diego, La Jolla, CA 92093, USA b

A R T I C L E I N F O

A B S T R A C T

Keywords: Sydney Blood Lead Soil Toxicity Australia

Surface soils in portions of the Sydney (New South Wales, Australia) urban area are contaminated with lead (Pb) primarily from past use of Pb in gasoline, the deterioration of exterior lead-based paints, and industrial activities. Surface soil samples (n=341) were collected from a depth of 0–2.5 cm at a density of approximately one sample per square kilometre within the Sydney estuary catchment and analysed for lead. The bioaccessibility of soil Pb was analysed in 18 samples. The blood lead level (BLL) of a hypothetical 24 month old child was predicted at soil sampling sites in residential and open land use using the United States Environmental Protection Agency (US EPA) Integrated Exposure Uptake and Biokinetic (IEUBK) model. Other environmental exposures used the Australian National Environmental Protection Measure (NEPM) default values. The IEUBK model predicted a geometric mean BLL of 2.0 ± 2.1 µg/dL using measured soil lead bioavailability measurements (bioavailability =34%) and 2.4 ± 2.8 µg/dL using the Australian NEPM default assumption (bioavailability =50%). Assuming children were present and residing at the sampling locations, the IEUBK model incorporating soil Pb bioavailability predicted that 5.6% of the children at the sampling locations could potentially have BLLs exceeding 5 µg/dL and 2.1% potentially could have BLLs exceeding 10 µg/dL. These estimations are consistent with BLLs previously measured in children in Sydney.

1. Introduction 1.1. Soil investigations in the Sydney area Environmental contamination of air, dust and soils in Australia is derived from a range of industrial sources, which peaked in the 1970s and declined thereafter (Kristensen et al., 2017). The largest anthropogenic source of Pb emissions was Australian motor vehicles using petrol containing tetramethyl and tetraethyl Pb additives from 1932 to 2002 (Kristensen, 2015). Atmospheric emissions of Pb to the entire Australian continent from leaded petrol were calculated to total 240,510 t over seven decades of use, attaining a maximum of 7869 t in 1974 (Kristensen, 2015). Kristensen (2015) calculated that approximately 68,000 t of lead were emitted into the atmosphere from leaded petrol in the state of New South Wales (NSW) between 1958 and 2002. From 1980 to 2001 leaded gasoline contributed approximately 90% to



Pb in Sydney air (Chiaradia et al., 1997). Other sources of environmental lead include Australian paint, which were up to 50% Pb by volume before the 1950s, thereafter several mandated reductions reduced the allowable concentration to 0.1% (by weight) in 1997 (AGFOEE, 2017). Rouillon et al. (2017) showed that soil around houses in Sydney with painted exteriors built before 1970 were markedly more contaminated than non-painted houses and houses that were built from the 1970s onwards. The Pb from past petrol lead emissions, industrial sources and the deterioration of exterior lead-based paints have been deposited and concentrated in surface soils and urban areas of Australia (Gulson et al., 1995a; Olszowy et al., 1995; Laidlaw and Taylor, 2011; Harvey et al., 2017; Rouillon et al., 2017; Kristensen et al., 2017). Birch et al. (2011) systematically sampled soil Pb concentrations in surface soils (0–2.5 cm) at 491 locations across the Sydney estuary catchment (480 km2; Fig. 1). One soil sample was collected in each 1 km2 grid and sampling sites (one per grid square) were selected

Corresponding author. E-mail addresses: [email protected] (M.A.S. Laidlaw), [email protected] (S.M. Mohmmad), [email protected] (B.L. Gulson), [email protected] (M.P. Taylor), [email protected] (L.J. Kristensen), [email protected] (G. Birch). http://dx.doi.org/10.1016/j.envres.2017.04.040 Received 17 March 2017; Received in revised form 28 April 2017; Accepted 29 April 2017 Available online 09 May 2017 0013-9351/ © 2017 Elsevier Inc. All rights reserved.

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Fig. 1. Temporal blood lead levels for Sydney children (data from Table 1) plotted against NSW petrol lead emissions data (figure from Kristensen et al., 2017).

300 mg/kg soil lead guideline for residential homes and 15% of homes contained soil lead > 1000 mg/kg. High soil Pb concentrations were located within the following areas: City of Sydney (including the CBD), Leichhardt (located 0.5 to 2 km west of the CBD) and Marrickville (approximately 3.75 km southwest of the CBD) (located approximately 3.75 km southwest of the CBD), which exhibited mean soil Pb concentrations of 883 mg/kg, 960 mg/kg and 689 mg/kg, respectively.

randomly for the dominant land use type in each square. The results indicated that soil concentrations in the < 2 mm grain size fraction had an arithmetic mean and median Pb concentration of 194 mg/kg and 60 mg/kg, respectively. Spatial patterns indicated that the inner city suburbs were most contaminated with concentrations decreasing with distance from the city centre (see also Rouillon et al., 2017). Olszowy etal. (1995) analysed 80 surface soil samples from residential properties in Sydney and found that about 40% of soil samples exceeded the National Environmental Protection Council (NEPM) residential soil Pb guideline of 300 mg/kg (NEPM, 2013a). In Balmain, an inner Sydney suburb located 2.5 km north-west of the Sydney central business district (CBD), a soil Pb survey of 41 samples found 68% of residential housing samples exceeded the residential soil Pb guideline (Royal Prince Alfred Hospital and Central and Southern Sydney Area Health Service, 1988). In Glebe, a suburb located approximately 1 km west of Sydney CBD, Markus and McBratney (1996) collected 219 surface soil samples and found that 50% of Pb concentrations exceeded the residential soil Pb guideline. Cattle et al. (2002) reported that 41% of 807 surface soil samples in Glebe and Camperdown (located immediately west of Glebe) exceeded the residential soil Pb guideline. At 24 inner Sydney suburban homes, Fett et al. (1992) observed a median and mean ‘play’ area soil Pb concentration of 380 mg/kg and 627 mg/kg, respectively with 54% of the soil samples exceeding the residential soil Pb guideline. In 18 of the same inner Sydney homes, Fett et al. (1992) observed median and mean ‘sink’ (garden) soil Pb concentrations of 1237 mg/kg and 1944 mg/kg (range 123 to 5407 mg/kg), respectively. Lead concentrations ranged from 37 to 2660 mg/kg in bulk soil samples from 8 houses in the same inner Sydney suburbs investigated by Fett et al. (1992) and up to 3130 mg/kg (Gulson et al., 1995a). Skinner et al. (1993) collected seven soil samples at a depth of 0–5 cm from Bradfield Park (beneath the Harbour Bridge) and three samples at distances up to 350 m from the park. Four sites were sampled farther north at distances of 50–300 m from the major arterial Warringah Freeway in North Sydney. The median values for the two areas were 708 mg/kg (range 19 to 1451 mg/kg) and 637 mg/kg (range 216 to 1269 mg/kg), respectively. Gulson and Ray (1997) measured Pb in surface soil from playground areas, sandpits and along the eaves line in six day care centres from inner Sydney suburbs and compared these data with vacuum cleaner dust, long-term dust accumulation using petri dishes and paint lead. They found Pb levels below the Australian NEPM guidelines of 300 mg/ kg in five of the six soil samples, although in one case the sandpit soil had been recently replaced. Most recently, the Rouillon et al. (2017) study of Sydney gardens (as opposed to public spaces) showed that 40% of the 203 homes sampled contained soil that exceeded the NEPM

1.2. Previous BLL studies in the Sydney area Most of the available BLL data collected from children in the Sydney area are from years of high petrol lead emissions, when exposures were considerably higher than in more recent times, and methods of sample collection and analysis were more variable. Assessment of historic petrol lead emissions and opportunistic studies of BLLs in Sydney show that BLLs in Sydney have declined substantially following the gradual phasing out of Pb in petrol between the 1970s and 2002 (Kristensen, 2015; Table 1 and Fig. 1). Until about 1998, blood lead surveys of Sydney's children indicated that average BLLs were above the current 5 µg/dL reference level (NHMRC, 2015). The sample sizes of the opportunistic blood lead studies of children in Sydney and other localities in Australia have been small compared with those undertaken in the United States where universal screening is implemented in some communities (CEH, 1998). The US Centres for Disease Control and Prevention (CDC) recommends that children at high risk of exposure be sampled at the ages of 12 and 24 months or at ages between 36 and 72 months if they have not previously been screened (CDC, 2000). For example, in the city of Detroit (USA) between 2001 and 2009, the Michigan Department of Community Health (MDCH) measured BLLs in 367,839 children (Zahran et al., 2013b). The only Australia-wide investigation into sources of lead and childhood BLLs was carried out in 1995 (Donovan, 1996). The geometric mean BLL of children sampled in the Donovan (1996) study was 5.05 µg/dL (n=1572), which was half of the Australian guideline of 10 µg/dL at the time. The effect of removing lead additives from Australian gasoline is evidenced by the relationship in Fig. 1, which showed the two were strongly correlated (r =0.96, p < 0.01, simple linear regression) (Kristensen et al., 2017). 1.3. Reviews of the health effects of lead exposure Several comprehensive reviews of Pb have been undertaken in recent years and include those by the United States National Toxicology Program (NTP, 2012), CDC (2004), WHO (WHO, 2010) and the Australian National Health and Medical Research Council (NHMRC, 782

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Table 1 Blood lead levels from studies conducted in Sydney. Year

References

Number of Samples (children)

Mean (µg/dL)

1974 1974 1975 1981 1983 1984 1990 1991 1993 1999 2000 2002–2006

Garnys et al. (1979) Mencel and Thorp (1976) Garnys et al. (1979) McBride et al. (1982) Cooney et al. (1989) Cooney et al. (1989) Young et al. (1992) Fett et al. (1992) Cowie et al. (1997) NSW Health (2002) Gulson et al. (2001) Gulson et al. (2014)

unknown 133 (adults) unknown 400 253 239 30 63 191 unknown 15 108

20.8 12.4 17 14 15.4 15.2 14.3 12 7.2 2.4 2.26 2.4a

a

Range (µg/dL)

2.7–51.1 2–29

5–30 8–14 2.8–15.7

2–3 year old children

2.3. Laboratory Techniques

2015). The CDC (2000) (2017b) and the WHO (2017) recently stated that there is no safe level for Pb. The Australian NHMRC (NHMRC, 2015) stated: ‘If a person has a blood lead level greater than 5 micrograms per decilitre, it is recommended that the source of exposure should be investigated and reduced, particularly if the person is a child or pregnant woman.’. This study examines the hazard that remains primarily from legacy use of lead paint and petrol additives used in the Sydney metropolitan environments. The specific risk for a 24 month aged child is assessed using the United States Environmental Protection Agency (US EPA) Integrated Exposure Uptake and Biokinetic (IEUBK) model. The aim of this study is to:

Soil samples were oven dried at 60 °C and sieved to < 250 µm using nylon mesh. Approximately 0.5 g of sample was weighed and oven dried at 105 o C overnight until dry, after which the sample was reweighed and placed in an evaporating basin. Samples were digested using nitric acid to decompose organic matter and hydrochloric acid to complete the digestion process. Digested samples were then filtered and analysed by ICP-OES (US EPA method 200.8 and 6010 C) by a certified laboratory (Environmental Services, SGS, Australia Pty Ltd., NSW, Australia) with results reported on a dry-weight basis. 2.4. QA/QC

(a) ascertain the likely impact from legacy contamination held in urban soils by applying the IEUBK model to predict BLLs of children aged 24-month old in the Sydney catchment (b) compare modelled BLLs with most recently measured BLL data (c) display the spatial patterns of predicted BLLs.

Precision, expressed as the mean Relative Percentage Difference (RPD) of duplicates (n=32), was 8.1% and ranged between 1% and 26% for individual analyses (RPD=Original Result-Replicate Result x Mean/100). Analytical accuracy was determined using Laboratory Control Samples (LCS) and matrix spikes (MS) and expressed as Percentage Recovery (PR). Mean PR for LCS was 98.7% and ranged between 93% and 106% for individual analyses (n=22). Mean PR for the matrix spikes was 88.3%, ranging from 78% to 100% for individual analyses (n=12). Laboratory Control Sample results were evaluated against the concentration of PR analytes spiked into the control during sample preparation, whereas MS results were evaluated against concentrations of analytes spiked into a field sub-sample during sample preparation. Procedural Blanks (PB) (n=22) were less than the laboratory's Limit of Reporting (< 1 mg/kg).

2. Methods 2.1. Field methods Samples were originally collected from across the Sydney estuary (Port Jackson) catchment at a resolution of one sample per 1 km2, collected from a depth of 0–2.5 cm (Birch et al., 2011). Samples were taken from the dominant land use type in each sample grid square. Land uses were classified as commercial, residential, industrial, park land, main road verge and special use (government and institutional areas such as schools and hospitals). Samples were collected as a composite of four subsamples within 1 m2 to reduce small-scale spatial variability (SSSV) using 6 cm diameter stainless steel rings, inserted into the soil to a depth of 2.5 cm and the contents collected with a plastic spatula. Samples were sieved on site to < 2 mm using nylon mesh to remove debris and organic fragments and the material placed into acid-free plastic bags, which were refrigerated at 4 °C until analysis.

2.5. Bioaccessibility Analysis Soil Pb bioaccessibility was measured in 18 surface soils from the Sydney area by the US EPA National Exposure Research Laboratory using their in vitro bioaccessibility (IVBA) assay for Pb in soil (US EPA, 2012). The soil samples were selected to ensure that a range of total soil Pb concentrations was assessed. The IVBA assay considers the gastric phase alone and is highly correlated with in vivo tests for Pb relative bioavailability (RBA). The RBA is calculated using the following relationship:

2.2. Grain Size

RBA = 0.878 × IVBA − 0.028

Originally, 491 surface soil samples were collected and analysed for the concentration of several metals in the < 2 mm grain size fraction as was reported in Birch et al. (2011). In this study, 341 of the original 491 surface soil samples that could be classified as residential or open space land uses were re-analysed for soil lead concentrations in the < 250 µm grain size fraction. The < 250 µm grain size fraction is used in the IEUBK model because it is most likely to adhere to children's hands (or other objects that a child may put in its mouth) and be subsequently ingested (US EPA, 2000).

where the RBA and IVBA are expressed as fractions, and the RBA is standardised against Pb acetate (US EPA, 2012). Applying the calculated RBA for the 18 test soils analysed and applying an absolute bioavailability (ABA) of soluble Pb in water and food of 50% (US EPA, 1999), the Pb ABA in the test soils was determined using the following equation:

ABA = RBA × 0.5 783

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2.6. Software Used to Predict Children's Blood Lead Levels

Table 2 Summary of soil lead concentrations from across the Sydney estuary catchment area.

The US EPA IEUBK model is an empirically-derived model that calculates an estimate of children's BLLs using environmental input variables of lead in soil, house dust, air, water, and diet (US EPA, 2016); version IEUBK win v1.1 build 11 was used to predict BLLs in Sydney (US EPA, 2016). 2.7. Children's Blood Lead Prediction Method Blood lead levels were predicted from soil samples collected in locations where land use was classified as residential or open space and not from industrial, or commercial land use areas. This reduced the number of samples from the original 491 collected to 341. The predicted BLL of a 24-month old child was selected in the IEUBK model as many studies have shown that peak BLLs in children occur in the 2 to 3 year age-range (e.g., US EPA, 2013). The input variables of air, water, diet used in the IEUBK model were sourced from Schedule B7 (Appendix C) of the 2013 amendment of the Australian National Environment Protection (Assessment of Site Contamination) Measure 1999 (NEPM, 2013b). The input variables were adjusted according to whether the soil samples were sourced from residential (HIL-A) or open space (HIL-C) land-use scenarios. Blood lead levels were calculated using two bioaccessibility scenarios: the Australian NEPM default model bioavailability specified in the NEPM (bioavailability of 50%) and the median Pb bioavailability determined from the 18 soil samples described above (bioavailability 34%). Blood lead levels were estimated in batch mode using measured soil lead concentrations (< 250 µm grain size fraction) for each location. A second BLL modelling scenario was also conducted. Median air lead levels (0.011 µg/m3) measured in Sydney at the Mascot monitoring station (ANSTO, 2017) between 2002 and 2006 and median water lead levels (1.3 µg/L) recently measured in Sydney and the state of NSW (Harvey et al., 2016) were used in the model to see if using measured data would change the predicted children's BLLs using the IEUBK model compared withusing NEPM default values for air (0.1 µg/m3) and water (0.7 µg/L) lead (NEPM, 2013b).

Statistic

Soil lead (< 250 µm size fraction; mg/kg; n =341)

Mean Geometric Mean Median Min 25th Percentile 75th Percentile 90th Percentile 95th Percentile Max

133 65 61 5 30 130 260 430 9400

Note - There was one soil lead sample with a concentration of 9400 mg/kg. This value was not used in the modelling of blood lead values because the IEUBK model does not accurately predict BLLs at soil lead concentrations > 3000 mg/kg.

highest adjacent to major traffic thoroughfares (Fig. 2). The area with the lowest soil Pb concentrations is located in the northern suburbs of the Sydney area where traffic volumes are lower. The soils sampled at most of the residential locations were sampled in the front gardens of the homes, where soil Pb may be more elevated from exposure to traffic compared to soil located in gardens (yards) at the rear of the homes, particularly under the drip lines of homes where soil lead concentrations are typically elevated due to the deterioration of exterior leadbased paint (see Rouillon et al., 2017). 3.4. Children's Blood Lead Levels in Sydney Predicted Using the US EPA IEUBK Model Assuming an absolute bioavailability of 34%, the IEUBK model predicts a geometric mean BLL of 2.0 ± 2.0 µg/dL with a range from 1.3 to 16.8 µg/dL (Table 3 and Fig. 3) with 5.6% of the predicted BLLs exceeding the NHMRC (2015) reference level for lead in blood of 5 µg/ dL and 2.1% exceeding 10 µg/dL. Assuming an absolute bioavailability of 50% (the NEPM default assumption) the IEUBK model predicts a geometric mean BLL of 2.4 ± 2.8 µg/dL with a range from 1.3 to 21.5 µg/dL (Table 3 and Fig. 4). Approximately 8.8% of the predicted BLLs exceed the NHMRC reference level of 5 µg/dL (NHMRC, 2015) and 2.3% exceed a BLL of 10 µg/dL, the former Australian guideline. No difference in BLL was observed using measured Sydney median ANSTO air lead data from 2002 to 2006 and recently collected water lead in NSW (Harvey et al., 2016) compared withusing default values from the NEPM (NEPM, 2013b). A summary of the statistics for the predicted BLLs for the 341 soil sample locations using the 34% and 50% absolute bioavailability scenarios is presented in Table 3. Summary BLL statistics with respect to cut-off levels of 0–2.5 µg/dL, > 2.5 µg/dL, > 5 µg/dL and > 10 µg/ dL in the two absolute bioavailability scenarios are presented in Table 3. Table 3 presents the BLLs predicted for the two soil lead bioavailability scenarios. This table indicates that BLLs are predicted to be more elevated if the NEPM default absolute bioavailability of 50% is used. This suggests that when predicting blood lead levels from soil, reliance on the NEPM default absolute bioavailability of 50% is likely to overpredict BLLs at higher soil Pb concentrations compared with bioavailability values estimated from soil samples collected in the field. Fig. 5 displays the spatial distributions of the predicted BLLs at the 341 soil sampling locations using the absolute bioavailability of 34%.

3. Results 3.1. Soil Lead Summary Statistics Summary statistics for the soil Pb concentrations in the < 250 µm grain size fractions in the residential and open space land use categories are presented in Table 2. Soil Pb concentrations in residential land use areas were substantially higher (mean =210 mg/kg; SD =694 mg/kg; geomean =85 mg/ kg) than open space land use categories (mean =71 mg/kg; SD=100 mg/kg; geomean =42 mg/kg). 3.2. Bioaccessibility and Bioavailability of Sydney's Soils Soil Pb bioaccessibility concentrations in the selected 18 samples from the Sydney urban area ranged from 135 mg/kg to 3727 mg/kg, with an arithmetic mean, standard deviation, median and geometric mean of 1076 mg/kg, 998 mg/kg, 700 mg/kg, and 718 mg/kg, respectively. The samples were selected to assess the bioaccessibility in soils with a range of soil Pb concentrations present across the Sydney area. The median bioaccessibility for these samples was 77 ± 11% with a range of 57–98% and absolute bioavailability was 34 ± 5% with a range of 25–43%.

4. Discussion

3.3. Spatial Patterns of Soil Lead Concentrations

4.1. Modelled Blood Lead Levels Compared with Measured Levels

As observed in many other studies over decades, including those from Australia (e.g. (De Silva et al., 2016)), soil Pb concentrations are

The most recent children's BLL study in Sydney is the 5-year longitudinal investigation of 108 children aged < 6 years old (at 784

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Fig. 2. Soil lead concentrations in the < 250 µm grain size in Sydney metropolitan area. Soil lead guidelines sources - CEPA, 2009; NEPM, 2013a.

Histogram of Predicted Blood Lead Levels: Bioavailability = 34%

Table 3 Summary statistics of IEUBK model predicted blood lead levels for a 24-month old child.

250

Average Median Geomean Standard Dev. Min Max 25th Percentile 75th Percentile 90th Percentile 95th Percentile Blood lead ranges (µg/dL) 0–2.5 > 2.5 >5 > 10

34% Absolute Bioavailability

50% Absolute Bioavailability

2.4 1.7 2.0 2.1 1.3 16.8 1.5 2.4 3.7 5.2 1.3–16.8

2.9 2.0 2.4 2.8 1.3 21.5 1.8 3.6 5.6 8.2 1.3–21.5

76.8% 23.2% 5.6% 2.1%

65.7% 34.3% 8.8% 2.3%

Sample numbers

Blood Lead Level (µg/dL)

200 150 100 50 0

Blood lead level (µg/dL) Fig. 3. Histogram of predicted blood lead levels using a lead bioavailability value of 34%.

completion) in which venous blood and environmental samples were collected at 6 monthly intervals from 2002–2006 (Gulson et al., 2014). The children were distributed relatively evenly throughout the Greater Sydney area. The geometric mean BLL at 2–3 years of age was 2.4 ± 2.1 µg/dL (n=169) (Gulson et al., 2014), consistent with the modelled geometric mean BLLs of 2.0 ± 2.1 µg/dL (34% bioavailability) and 2.4 ± 2.8 µg/dL (50% bioavailability) shown here in Table 3.

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Sample numbers

Histogram of Predicted Blood Lead Levels: Bioavailability = 50%

concentrations and ABA estimates for 53 topsoil samples. They determined a mean bioaccessibility of Pb in surface soil of 61%. In 2012, the measured geometric mean BLL level of Broken Hill children was 5.4 μg/dL, with 20.2% of those children having BLLs exceeding 10 μg/dL (Lesjak et al., 2013). IEUBK modelling using a mean surface soil bioaccessibility values of 61% (mean Pb concentration of 724 mg/ kg) predicted that Broken Hill children had a geometric mean BLL of 7.4 μg/dL, with 50% of the children having BLLs greater than 5 μg/dL and 23% of the children expected to have BLLs exceeding 10 μg/dL (Yang and Cattle, 2015). Thus, the IEUBK model appeared to overestimate the predicted geometric mean blood lead levels, but was reasonably accurate with respect to the percentage of children with blood lead levels > 5 and 10 μg/dL.

200 180 160 140 120 100 80 60 40 20 0

Blood lead level (µg/dL) Fig. 4. Histogram of predicted blood lead levels using the NEPM default value for lead bioavailability of 50%.

4.3. Temporal and Spatial Association between Soil Lead and Blood Lead Levels

4.2. IEUBK Model Validity

Many environmental studies have demonstrated that surface soil Pb concentrations and resuspended soil Pb dust are associated with children's BLLs. For example, Zahran et al. (2013a) concluded that Pb levels from 5467 surface soil samples explained 77% of the variation in 55,551 children's BLLs in New Orleans, Louisiana (USA). Mielke et al. (1997) and Bickel (2010) found similar results in New Orleans and Detroit, respectively. Zahran et al. (2013b) evaluated atmospheric concentrations of soil and Pb aerosols, and BBLs in 367,839 children (ages 0–10) in Detroit, Michigan (USA) from 2001 to 2009 to test a hypothesized soil to air to dust to child pathway of contemporary Pb risk. This study established that children's BLLs were strongly asso-

An important question is whether the IEUBK model can accurately predict children's blood lead levels. Multiple studies have used the IEUBK model by comparing predicted BLLs with observed BLLs for a given soil lead distribution but most of these were for contaminated mining and smelting sites in the US. The IEUBK model was independently calibrated and empirically validated for BLLs below 30 μg/dL in the United States (Hogan et al., 1998; Bowers and Mattuck, 2001; Pounds and Leggett, 1998). With respect to Australian examples of the use of the IEUBK model, Yang and Cattle (2015) predicted children's BLLs in three areas of the lead mining town of Broken Hill using soil Pb

Fig. 5. Spatial distributions of the predicted BLLs at the 341 soil sampling locations, calculated using the conservative 34% absolute bioavailability scenario.

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larly within 100 m of major thoroughfares (Chamberlain et al., 1978). Birch et al. (2011) created a contour plot of soil Pb concentrations for their 491 samples in the < 2 mm grain size fraction from the Sydney estuary catchment area. The contour plot shows the spatial pattern of soil Pb concentrations is associated with the major traffic corridors, suggesting leaded petrol is one of the main sources of lead in surface soils of the Sydney metropolitan area. The contour plot also displays a ‘bulls-eye’ pattern with soil lead concentrations highest in the inner city areas and decreasing with distance towards the suburban and rural areas, which is consistent with the source being derived from leaded gasoline emissions and older areas with homes coated with exterior lead based paint (Rouillon et al., 2017). Laidlaw et al. (2014) found Pb isotopic ratios in soil samples from four urban locations in Sydney were similar to those in petrol samples and air filters collected in Sydney when lead was used in petrol (Chiaradia et al., 1997). However, in an earlier study using higher precision Pb isotopic measurements of 8 houses from inner Sydney suburbs, Gulson et al. (1995a), (1995b) found that Pb from exterior paint was the most significant contributor to BLLs in children. Another potential source of lead in inner-city Sydney soils is from old industrial sites and emissions. The long history of industry has left behind legacy hotspots of various metals (Markus and McBratney, 1996). Additional sources of soil lead contamination in inner-city Sydney soils include the application of lead-based paint to buildings and structures (Gulson et al., 2016).

ciated with atmospheric dust. Several studies in NSW (Australia) have also shown an association between soil Pb concentrations and BLLs. In Sydney, Fett et al. (1992) found that BLLs were correlated significantly with concentrations of Pb in yard soil (r =0.555, p=0.026) and play area soil (r =0.492, p=0.016). Young et al. (1992) also observed that soil Pb levels were significantly correlated with BLLs near the Southern Copper smelter south of Sydney. Lead isotopic and lead concentration measurements were obtained for children from 24 dwellings in the Donovan (1996) Australia-wide study whose BLLs were ≥15 μg/dL in an attempt to determine the source(s) of their elevated blood lead (Gulson et al., 2013). Results indicated correlations between isotopic ratios in blood and dust wipes (r =0.52, 95% CI 0.19- 0.74), blood and soil (r =0.33, 95% CI −0.05–0.62), and blood and paint (r =0.56, 95% CI 0.09–0.83). Furthermore, there was a strong isotopic correlation of Pb in soils and house dust (r =0.53, 95% CI 0.20–0.75) indicative of a common source(s) for lead in soil and house dust. In Sydney between 2001 and 2004 Gulson and colleagues (Gulson et al., 2006, 2014) undertook comprehensive blood and environmental sampling in 108 houses involving more than 7000 samples. The environmental samples included handwipes (interior and after exterior playing), 6-day duplicate diet, drinking water, interior house and day care dust fall accumulation using petri dishes, exterior dust fall accumulation, exterior dust sweepings, paint, soil and urban air. Using a path modelling approach, mixed model analyses for a fully adjusted model showed the strongest associations for BLL were with interior house dust and soil, although the predictor variables only explained 9% of the variance for lead. The strongest pathways for environmental samples were from soil to dust sweepings to interior dust and then to blood lead, but not from soil directly to BLL. This suggests that while soil is a robust indicator in studies with adequate sample numbers, dust lead may actually be more reliable because exposures are likely to be more direct, especially in children of 24-months age or less.

4.5. Paint as a Potential Contributor of Highly Elevated BLLs Lead-based paints have been associated with elevated BLLs in Queensland. For example, between 2000 and 2011 > 50% of Queensland's non-occupational blood lead exposures were linked to the removal of Pb-based paint (Queensland Health, 2003, 2011). Unfortunately, as noted by Rouillon et al. (2017), equivalent information about the environmental sources of Pb exposure data for NSW are not available because NSW Health had incomplete entries on blood Pb exposures cases. As identified above, using high precision lead isotopic tracing Gulson et al. (1995a), (1995b) demonstrated that paint was a major contributor to BLLs for a small number of children in inner Sydney. Furthermore, elevated BLLs in 8% of the children from the longitudinal study in Sydney could be traced to renovations involving leaded paint and/or very close proximity to highly trafficked thoroughfares (Gulson et al., 2014). In Victoria, Australia, recent data on nonoccupation BLLs in the adult Victorian population support the contention that old Pb-based paint remains an ever-present risk of exposure in adults from home renovation and restoration (Kelsall et al., 2013). This implies that children residing in homes with Pb-based paint subject to renovation would be at risk of exposure.

4.4. Sources of Pb in Sydney's Surface Soil Exterior Pb paint appears to be a major contributor to soil Pb contamination in the older inner city areas of Sydney. Prior to 1970, lead-based paints ranging between 1% and 50% Pb by weight, were used on the exterior of many older homes in urban areas of Australia (Gulson et al., 1995a; AGDOEE, 2017; Rouillon et al., 2017). Soil samples collected along the drip line adjacent to homes are partially representative of contributions from exterior lead-based paint, which has flaked and combined with soil immediately adjacent to the house. In addition, Pb particles emitted from petrol have also contributed to soil lead concentrations in soils adjacent to homes (Linton et al., 1980; Mielke et al., 1983). Rouillon et al.’s (2017) study findings in Sydney garden soils are consistent with the accumulation of Pb in soils from these sources. The Rouillon et al. (2017) study analysed 410 soil samples from 203 homes within a pre-defined area consisting of 22 local government areas (LGAs) from the Sydney Metropolitan Area. Their results returned mean Pb concentrations of 413 mg/kg in the front yard, 707 mg/kg in the drip line beside the house, 226 mg/kg in the back yard and 301 mg/kg in the vegetable gardens. A large volume of Pb was emitted from the use of leaded petrol in Sydney. Kristensen, p 198) (2015) stated that ‘Fallout rates from leaded petrol [previously] averaged 1 µg/cm2/day in metropolitan Sydney with rates rising to 5 µg/cm2/day in the inner city area [Davies (1980)]. This equates to roughly 700 t/year of lead in the CBD region of Sydney, approximately 20–30% of lead emitted in NSW during the peak period of leaded petrol use. With roughly 50–60% of leaded petrol consumed in metropolitan Sydney, it is possible that another 700 t during peak emissions was deposited in Sydney outside the CBD…’. Furthermore, over the period 1980 to 2001 Pb from gasoline contributed approximately 90% of the lead to Sydney's air (Chiaradia et al., 1997), which would have been the major contributor to surface soil contamination in locations, particu-

4.6. NSW Regulatory Guidelines Currently, The NSW regulatory guidelines state that there is no duty to report ‘widespread diffuse urban pollution that is not attributed to a specific industrial, commercial or agricultural activity’ (NSW EPA, 2015). Therefore, because residential soil Pb contamination in Sydney is generally considered ‘diffuse’, the owner is not required to report soil Pb contamination under s 60 of the Contaminated Land Management Act 1997 (NSW) even if soil Pb levels exceed the NEPM trigger value for residential soil lead of 300 mg/kg. Therefore, even if the property is sold or rented, the new occupiers of the home are unlikely to be aware of the contamination or even that there is a potential risk of contaminated based upon the age of the house or their residential location. However, if soil Pb contamination exceeding regulatory guidelines was found at an industrial, commercial or agricultural site, it is likely that that the contamination would be reported to the NSW EPA because a polluter or owner would have a duty to identify the contamination because it could be attributable ‘to a specific industrial, 787

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are typically higher than the surrounding environment. The other deficiency in this study is the lack of data for house dust, usually collected in the past by vacuum cleaning. House dust is recognised as probably the most significant contributor to BLLs in children (e.g. Lanphear et al., 1998). Where data for house dust are lacking, the IEUBK uses the soil value to estimate a dust value but this may or may not be consistent with levels present in a dwelling.

commercial or agricultural activity’ (NSW EPA, 2015). Records of sites notified to the NSW are publicly available (NSW EPA, 2017a) as are records of notices that have been served on owners of lots of contaminated land (NSW EPA 2017b). As noted in a recent review of the NSW EPA's management of contaminated sites, it would be prudent to ensure that local government councils across NSW are ‘appropriately making notations of contamination of land on certificates issued under s 149 of the Environmental Planning and Assessment Act 1979 (NSW)’ (Taylor and Cosenza, 2016, p. 252). Section 149 certificates are issued to vendors on purchase of homes and provide an opportunity to inform vendors of the presence or possibility of contamination affecting the land that councils may be aware of. In contrast to Australia, The United States has introduced legislation to ensure that homeowners or rentors of properties are informed about Pb-based paint hazards (US-HUD, 2017) and failure to comply is subject to significant penalties (e.g. Harrington, 2012). Furthermore, there is no single contaminated land database in either of the two most populated states of Australia, NSW and Victoria, further restricting informed consent about the nature of land or its potential legacy for users, owners or vendors (Taylor and Cosenza, 2016).

6. Recommendations Higher density soil sampling (4–8 samples/km2) is recommended in the Sydney areas with older housing, industrial areas and where elevated soil lead levels have been previously observed. It is noted that high density sampling in suburbs such as Glebe (Markus and McBrantney, 1996) and Iron Cove (Snowdon and Birch (2004)) have demonstrated that soil lead levels exceeding regulatory guidelines can be widespread in some suburbs of the Sydney area. It is recommended that this study be replicated in all the major cities of Australia to gain a better understanding of the potential health hazards that exposure to lead in soil may pose to children. Knowledge of contamination could be used to instigate interventions, as recommended by Laidlaw et al. (2017). The above study design could also be replicated internationally where soil lead levels are elevated and there is an absence of BLL data among the populace, or to better understand the potential contribution of soil Pb to BLLs. Furthermore, it is recommended that homeowners, or their environmental consultant, collect multiple soil samples for analysis in their homes.

5. Limitations There are multiple limitations that need to be considered when evaluating the data and results presented in this study. Our use of a single value for absolute bioavailability may have resulted in an underestimation of BLLs at some highly contaminated sites and the overestimation of BLL at some relatively clean sites. However, for the following reasons we contend that reliance on a single value for absolute bioavailability is not substantial. We assessed the range of absolute soil Pb bioavailabilities (15–43%) on the resulting modelled geometric mean BLL for the 341 soil sampling locations. The results of the modelling produced geometric mean BLLs of 1.86 ± 1.62 µg/dL, 2.0 ± 2.1 µg/dL, and 2.22 ± 2.47 when applying the minimum (25%), median (34%) and maximum (43%) values of absolute bioavailability, respectively. These values compare favourably with this study's calculated geomean BLLs of 2.0 ± 2.1 µg/dL (34% absolute bioavailability) and 2.4 ± 2.8 (50% absolute bioavailability) and those measured by Gulson et al. (2014) in 108 Sydney children in the mid 2000s of 2.4 ± 2.1 µg/dL (Table 1). Therefore, the results presented herein indicate that the ranges of soil Pb absolute bioavailability observed in Sydney do not substantially affect the predicted geometric mean BLLs in this study. Appleton et al. (2013) observed that on average, the Pb concentration in the < 250 µm grain size fraction is about 90% of the lead concentration of the < 2 mm grain size fraction. This should be understood when comparing the soil lead concentrations in this study with the soil lead guidelines. It must be stressed that the predictions of BLLs exceeding 5 µg/dL or 10 µg/dL are only representative of the BLLs calculated at the sampling points, and may not represent the actual percentages of children with BLLs exceeding these levels in the population. Even though the geometric mean predicted levels were consistent with those for a small cohort of young children, the calculated range from 1.3 to 16.8 µg/dL for the 34% bioavailability scenario is concerning and indicates the hazard posed by legacy contamination. The only way to precisely know the actual blood lead level distribution is to measure (preferably venous) blood samples from children. However, given the BLLs being reported in countries such as the US where the mean blood lead level of children aged 1–5 between 2013 and 2014 was approximately 0.8 µg/dL (Tsoi et al., 2016) sample collection and laboratory protocols to minimize contamination and stringent measurement procedures are paramount (e. g., Huang et al., 2016). The contribution to BLLs from interior, or exterior lead paint particles is not available in the IEUBK model, which could result in an underestimation of BLLs in some cases. The soil Pb levels and exposure for soil samples collected in this study may be biased high if the soil Pb samples were collected near roadside nature strips where soil Pb levels

7. Conclusions Prior to 2002 elevated BLLs in Sydney children had been largely attributed to petrol lead emissions (Kristensen, 2015) although small scale studies showed leaded paint to be more critical (Gulson et al., 1995a, 1995b). However, a substantial portion of the variation in children's BLLs appears to be attributable to lead-contaminated soil from two legacy sources: Pb used in petrol/gasoline and exterior lead-based paint. Contributions of children's BLL from interior Pb-based paints were not quantified in this study, however, Pb paint remains an important source of Pb exposure, particularly during home renovation, an activity being widely undertaken in many cities in Australia. Using soil Pb bioaccessibility analysed by the US EPA, the IEUBK exposure model predicted a geometric mean BLL of 2.0 ± 2.1 µg/dL (for a 24-month old child), with children's BLLs predicted to exceed the NHMRC reference level of 5 µg/dL for approximately 5.6% of the soil sampling locations. In the absence of children's BLLs, the IEUBK model may be an effective first step to predict the BLLs of children in urban areas where soils have been contaminated from legacy lead. Ultimately however, the only way to have high confidence in understanding actual exposures is to measure children's BLLs. The ultimate solution to the residential exposures from legacy contamination is to target the most contaminated areas where the risk is considered greatest and to remediate or cover contaminated soil (Laidlaw et al., 2017). To further maximise the effect of environmental remediation, it would also be necessary to permanently encapsulate exterior and interior lead-based paints, which would assist in limiting low-level lead toxicity from known sources in children that can cause potentially negative health outcomes. Acknowledgements Matthew Van and Marco Olmos conducted the soil sampling for this study and the results were originally published in Birch et al. (2011). Karen Bradham of the US EPA facilitated the soil lead bioaccessibility analysis. The US EPA National Exposure Research Laboratory performed the soil lead bioaccessibility analysis. Susan Spalinger of Terragraphics assisted with an independent assessment of the accuracy of the IEUBK calculations. 788

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Harvey, P.J., Handley, H.K., Taylor, M.P., 2016. Widespread copper and lead contamination of household drinking water, New South Wales, Australia. Environ. Res. 151, 275–285. Hogan, K., Marcus, A., Smith, R., White, P., 1998. Integrated exposure uptake biokinetic model for lead in children: empirical comparisons with epidemiologic data. Environ. Health Perspect. 106, 1557. Huang, S., Hu, H., Sánchez, B.N., Peterson, K.E., Ettinger, A.S., Lamadrid-Figueroa, H., Schnaas, L., Mercado-García, A., Wright, R.O., Basu, N., Cantonwine, D.E., 2016. Childhood blood lead levels and symptoms of attention deficit hyperactivity disorder (ADHD): a cross-sectional study of Mexican children. Environ. Health Perspect. 124, 868. Kelsall, L.M., de Gooyer, T.E., Carey, M., Vaughan, L., Ansari, Z., 2013. Blood lead levels in the adult Victorian population: results from the Victorian Health Monitor. Aust. N.Z. J. Public Health 37, 233–237. Kristensen, L.J., 2015. Quantification of atmospheric lead emissions from 70 years of leaded petrol consumption in Australia. Atmos. Environ. 111, 195–201. Kristensen, L.J., Taylor, M.P., Flegal, A.R., 2017. An odyssey of environmental pollution: the rise, fall and remobilisation of industrial lead in Australia. Appl. Geochem. http:// dx.doi.org/10.1016/j.apgeochem.2017.02.007. Laidlaw, M.A.S., Zahran, S., Pingitore, N., Clague, J., Devlin, G., Taylor, M.P., 2014. Identification of lead sources in residential environments: sydney Australia. Environ. Pollut. 184, 238–246. Laidlaw, M.A., Taylor, M.P., 2011. Potential for childhood lead poisoning in the inner cities of Australia due to exposure to lead in soil dust. Environ. Pollut. 159, 1–9. Laidlaw, M.A.S., Filippelli, G.M., Brown, S., Paz-Ferreiro, J., Reichman, S.M., Netherway, P., Truskewycz, A., Ball, A.S., Mielke, H.W., 2017. Case studies and evidence-based approaches to addressing urban soil lead contamination. Appl. Geochem. http://dx. doi.org/10.1016/j.apgeochem.2017.02.015. Lanphear, B.P., Matte, T.D., Rogers, J., Clickner, R.P., Dietz, B., et al., 1998. The contribution of lead-contaminated house dust and residential soil to children's blood lead levels. A pooled analysis of 12 epidemiologic studies. Environ. Res. 79, 51–68. Lesjak, M., Gough, N., Belshaw, D., Tall, J., Jones, T., 2013. Lead Health Report 2012. Children Less than 5 Years Old in Broken Hill. Population Health Unit, Western NSW & Far West Local Health Districts, Broken Hill, New South Wales. Available at: 〈http://docplayer.net/13037194-Lead-health-report-2012-children-less-than-5years-old-in-broken-hill.html〉 (accessed 9 February 2017). Linton, R.W., Natusch, D.F.S., Solomon, R.L., Evans, C.A., 1980. Physicochemical characterization of lead in urban dusts. A microanalytical approach to lead tracing. Environ. Sci. Technol. 14, 159–164. Markus, J.A., McBratney, A.B., 1996. An urban soil study: heavy metals in Glebe. Aust. Soil Res. 34 (3), 453–465. McBride, W.G., Black, B.P., English, B.J., 1982. Blood lead levels and behaviour of 400 preschool children. Med. J. Aust. 2, 26–29. Mencel, S.J., Thorp, R.H., 1976. A study of blood lead levels in residents of the Sydney area. Med. J. Aust. 1, 423–426. Mielke, H.W., Anderson, J.C., Berry, K.J., Mielke, P.W., Chaney, R.L., Leech, M., 1983. Lead concentrations in inner-city soils as a factor in the child lead problem. Am. J. Public Health 73, 1366–1369. National Health and Medical Research Council (NHMRC), 2015. NHMRC Statement: Evidence on the Effects of Lead on Human Health. 〈https://www.nhmrc.gov.au/ guidelines-publications/eh58〉 (accessed 9 February 2017). National Environment Protection (Assessment of Site Contamination) Measure, 2013a. National Environmental Protection Measure (Assessment of Site Contamination): Schedule B (7a) Guideline on Health-Based Investigation levels. 〈http://www.nepc. gov.au/system/files/resources/93ae0e77-e697-e494-656f-afaaf9fb4277/files/ schedule-b7-guideline-health-based-investigation-levels-updated-oct10.pdf〉 (accessed 9 February 2017). National Environment Protection (Assessment of Site Contamination) Measure (NEPM), 2013b. Blood Lead Model - IEUBK Modelling input parameters - child receptors. Schedule B7, Appendix C. 〈http://www.nepc.gov.au/system/files/resources/ 93ae0e77-e697-e494-656f-afaaf9fb4277/files/schedule-b7-appendix-c-blood-leadmodel-sep10.pdf〉 (accessed 9 February 2017). National Toxicology Program (NTP). NTP Monograph: Health Effects of Low-Level Lead. 2012. 〈https://ntp.niehs.nih.gov/pubhealth/hat/noms/lead/index.html〉 (accessed 9 February 2017). New South Wales Environmental Protection Authority, 2015. Guidel. Duty Report. Contam. Contam. Land Manag. Act. 1997. 〈http://www.epa.nsw.gov.au/resources/ clm/150164-report-land-contamination-guidelines.pdf〉 (accessed 14 February 2017). New South Wales Environmental Protection Authority, 2017a. List of NSW contaminated sites notified to EPA. Available at: 〈http://www.epa.nsw.gov.au/clm/publiclist.htm〉 (accessed 14 February 2017). New South Wales Environmental Protection Authority, 2017b. Search The Contaminated Land Record. Available at: 〈http://www.epa.nsw.gov.au/prclmapp/searchregister. aspx〉. (accessed 14 February 2017). New South Wales (NSW) Health, 2002. The Environment - Blood Lead in Children and Leaded Petrol Sales, Report of the New South Wales Chief Health Officer. NSW Department of Health, Sydney. Olszowy, H., Torr, P., Imray, P., 1995. Trace element concentrations in soils from Rural and Urban Areas of Australia. Contaminated sites series No. 4. (Department of Human Services and Health, Environment Protection Agency) South Australian Health Commission. Pounds, J.G., Leggett, R.W., 1998. The ICRP age-specific biokinetic model for lead: validations, empirical comparisons, and explorations. Environ. Health Perspect. 106, 1505. Queensland Health, 2003. Blood Lead Notifications in Queensland 2003. Queensland

References Appleton, J.D., Cave, M.R., Palumbo-Roe, B., Wragg, J., 2013. Lead bioaccessibility in topsoils from lead mineralisation and urban domains, UK. Environ. Pollut. 178, 278–287. Australian Government Department of the Environment and Energy (AGFOEE), 2017. Lead in house paints. 〈http://www.environment.gov.au/protection/chemicalsmanagement/lead/lead-in-house-paint〉 (accessed 6 February 2017). Australian Nuclear Science and Technology Organisation (ANSTO), 2017. Fine particle pollution - coastal NSW. 〈http://www.ansto.gov.au/Resources/Localenvironment/ Atmosphericmonitoring/Fineparticlepollution/〉 (accessed 15 March 2017). Birch, G.F., Vanderhayden, M., Olmos, M., 2011. The nature and distribution of metals in soils of the Sydney estuary catchment, Australia. Water, Air, Soil Pollut. 216, 581–604. Bowers, T.S., Mattuck, R.L., 2001. Further comparisons of empirical and epidemiological data with predictions of the integrated exposure uptake biokinetic model for lead in children. Human. Ecol. Risk Assess. 7, 1699–1713. California Environmental Protection Agency (CEPA), 2009. Revised California Human Health Screening Levels For Lead. Available at: 〈http://oehha.ca.gov/media/ downloads/crnr/leadchhsl091709.pdf〉 (accessed 9 February 2017). Cattle, J.A., McBratney, A.B., Minasny, B., 2002. Kriging method evaluation for assessing the spatial distribution of urban soil lead contamination. J. Environ. Qual. 31, 1576–1588. Committee on Environmental Health (CEH), 1998. Screening for elevated blood lead levels. Pediatrics 101, 1072–1078. Centre for Disease Control (CDC), 2004. A Rev. Evid. Health Eff. Blood Lead. Lev. 10 µg/ dL Child. 〈https://www.cdc.gov/nceh/lead/ACCLPP/meetingMinutes/ lessThan10MtgMAR04.pdf〉 (accessed 1 March 2017). Centre for Disease Control (CDC), 2000. Recommendations for Blood Lead Screening of Young Children Enrolled in Medicaid: Targeting a Group at High Risk. MMWR Report 49(RR14); 1-13. Available at 〈https://www.cdc.gov/mmwr/preview/mmwrhtml/ rr4914a1.htm〉 (accessed 14 February 2017). Centre for Disease Control (CDC), 2017b. What Do Parents Need Know Prot. Their Child.? (Available at). 〈https://www.cdc.gov/nceh/lead/acclpp/blood_lead_levels.htm〉. Chamberlain, A.C., Heard, M.J., Little, P., Newton, D., Wells, A.C., Wiffen, R.D., 1978. Investig. into Lead. Mot. Veh (No. AERE-R9198 Monograph). Chiaradia, M., Gulson, B.L., James, M., Jameson, C.W., Johnson, D., 1997. Identification of secondary lead sources in the air of an urban environment. Atmos. Environ. 31, 3511–3521. Cooney, G.H., Bell, A., McBride, W., Carter, C., 1989. Low-Level Exposures to Lead: the Sydney Lead Study. Dev. Med. Child Neurol. 31, 640–649. Cowie, C., Black, D., Fraser, I., 1997. Blood lead levels in preschool children in eastern Sydney. Aust. N.Z. J. Public Health 21, 755–761. Davies, D.R.L., 1980. Lead in Petrol: toward a Cost Benefit Assessment. Centre for 458 Resource and Environmental Studies. Australian National University, Canberra. De Silva, S., Ball, A.S., Huynh, T., Reichman, S.M., 2016. Metal accumulation in roadside soil in Melbourne. Aust.: Eff. Road. age, Traffic Density Veh. Speed Environ. Pollut. 208, 102–109. Donovan, J., 1996. Lead in Australian children: report of the National Survey of Lead in Children. Australian Institute of Health and Welfare, Canberra. 〈https://www.lead. org.au/Lead_in_Australian_children.pdf〉 (accessed 7 February 2017). Fett, M.J., Mira, M., Smith, J., Alperstein, G., Causer, J., Brokenshire, T., Gulson, B., Cannata, S., 1992. Community prevalence survey of children's blood lead levels and environmental lead contamination in inner Sydney. Med. J. Aust. 157, 441–445. Garnys, V.P., Freeman, R., Smythe, L.E., 1979. Lead Burden of Sydney Schoolchildren. Department of Analytical Chemistry. University of New South Wales, Sydney. Gulson, B., Mizon, K., Korsch, M., Taylor, A., 2006. Changes in the lead isotopic composition of blood, diet and air in Australia over a decade: globalization and implications for future isotopic studies. Environ. Res. 100, 130–138. Gulson, B., Mizon, K., Taylor, A., Korsch, M., Stauber, J., Davis, J.M., Louie, H., Wu, M., Swan, H., 2006. Changes in manganese and lead in the environment and young children associated with the introduction of methylcyclopentadienyl manganese tricarbonyl in gasoline—preliminary results. Environ. Res. 100, 100–114. Gulson, B.L., Ray, J., 1997. Lead in dust and soil from day care centres. NSW Public Health Bull. 8, 94–96. Gulson, B.L., Davis, J.J., Bawden-Smith, J., 1995a. Paint as a source of recontamination of houses in urban environments and its role in maintaining elevated blood leads in children. Sci. Total Environ. 164, 221–235. Gulson, B.L., Davis, J.J., Mizon, K.J., Korsch, M.J., Bawden-Smith, J., 1995b. Sources of soil and dust and the use of dust fallout as a sampling medium. Sci. Total Environ. 166, 245–262. Gulson, B., Anderson, P., Taylor, A., 2013. Surface dust wipes are the best predictors of blood leads in young children with elevated blood lead levels. Environ. Res. 126, 171–178. Gulson, B., Mizon, K., Taylor, A., Korsch, M., Davis, J.M., Louie, H., Wu, M., Gomez, L., Antin, L., 2014. Pathways of Pb and Mn observed in a 5-year longitudinal investigation in young children and environmental measures from an urban setting. Environ. Pollut. 191, 38–49. Gulson, B., Chiaradia, M., Davis, J., O'Connor, G., 2016. Impact on the environment from steel bridge paint deterioration using lead isotopic tracing, paint compositions and soil deconstruction. Sci. Total Environ. 550, 69–72. Harrington, E., 2012. EPA Levies $40,000þ Fines on Landlords Who Fail to Provide ‘EPAapproved’ Pamphlets to Tenants. Available at: Available at: 〈http://www.cnsnews. com/news/article/epa-levies-40000-fines-landlords-who-fail-provide-epaapprovedpamphlets-tenants〉 (accessed 14 February 2017).

789

Environmental Research 156 (2017) 781–790

M.A.S. Laidlaw et al. Government, pp. 1e8. Available at: 〈https://www.health.qld.gov.au/ph/documents/ ehu/31751.pdf〉 (accessed 9 February 2017). Queensland Health, 2011. Non-Occupational Blood Lead Notifications in Queensland 2011. Queensland Government, pp. 1e6. Available at: 〈https://www.health.qld.gov. au/ph/documents/ehu/bl-notif-2011.pdf〉 (accessed 9 February 2017). Rouillon, M., Harvey, P.J., Kristensen, L.J., George, S.G., Taylor, M.P., 2017. VegeSafe: a community science program measuring soil-metal contamination, evaluating risk and providing advice for safe gardening. Environ. Pollut. 222, 557–566. http://dx.doi. org/10.1016/j.envpol.2016.11.024. Royal Prince Alfred Hospital and Central and Southern Sydney Area Health Service, 1988. Environmental lead investigation: an Interim report. Environ. Health Unit. Skinner, J., Baxter, R., Farnbach, E., Holt, D., 1993. Does lead paint from the Sydney harbour bridge cause significant pollution to areas nearby? New South Wales Public Health Bull. 4, 54–55. Snowdon, R., Birch, G.F., 2004. The nature and distribution of copper, lead, and zinc in soils of a highly urbanised sub-catchment (iron Cove) of Port Jackson, Sydney. Aust. J. Soil Res. 42, 329–338. Taylor, M.P., Cosenza, I.J., 2016. Review of the New South Wales Environment Protection Authority's Management of Contaminated Sites. Macquarie University, NSW, Australia, pp. 258. (Available at). 〈http://epa-inquiry.vic.gov.au/epa-inquiryreport〉 (accessed 14 July 2016). Tsoi, M.F., Cheung, C.L., Cheung, T.T., Cheung, B.M.Y., 2016. Continual Decrease in Blood Lead Level in Americans: United States National Health Nutrition and Examination Survey 1999–2014. Am. J. Med. 129, 1213–1218. United States Department of Housing and Urban Development (US-HUD), 2017. The lead disclosure rule. Healthy Homes and Lead Hazard Control. Available at: Available at: 〈https://www.epa.gov/lead/lead-renovation-repair-and-painting-program-rules〉, (accessed 14 February 2017). United States Environmental Protection Agency (US EPA), 2000. Short Sheet:TRW Recommendations For Sampling and Analysis of Soil at Lead (Pb) Sites. EPA #540-F-

00-010. Available at: http://www.itrcweb.org/ism−1/references/sssiev.pdf (accessed 14 February 2017). United States Environmental Protection Agency (US EPA), 1999. Short Sheet: IEUBK Model Bioavailability Variable. EPA #540-F-00-006. Available at: 〈https://www.epa. gov/superfund/lead-superfund-sites-guidance〉 (accessed 9 February 2017). United States Environmental Protection Agency (US EPA), 2012. Standard Operating Procedure for an In Vitro Bioaccessibility Assay for Lead in Soil. EPA 9200.2-86. Available at: 〈https://www.epa.gov/superfund/soil-bioavailability-superfund-sitesguidance〉 (accessed 9 February 2017). United States Environmental Protection Agency (US EPA), 2016. Lead at Superfund Sites: Software and Users' Manuals. 〈https://www.epa.gov/superfund/lead-superfundsites-software-and-users-manuals〉, (accessed 9 February 2017). World Health Organisation (WHO), 2010. Childhood Lead Poisoning. 〈http://www.who. int/ceh/publications/leadguidance.pdf〉 (accessed 3 March 2017). World Health Organisation (WHO), 2017. Lead poisoning and health. Available at: 〈http://www.who.int/mediacentre/factsheets/fs379/en/〉 (accessed 9 February 2017). Yang, K., Cattle, S.R., 2015. Bioaccessibility of lead in urban soil of broken Hill, Australia: a study based on in vitro digestion and the IEUBK model. Sci. Total Environ. 538, 922–933. Young, A.R.M., Bryant, E.A., Winchester, H.P.M., 1992. The wollongong lead study: an investigation of the blood lead levels of pre-school children and their relationship to soil lead levels. Aust. Geogr. 23, 121–133. Zahran, S., Mielke, H.W., McElmurry, S.P., Filippelli, G.M., Laidlaw, M.A., Taylor, M.P., 2013a. Determining the relative importance of soil sample locations to predict risk of child lead exposure. Environ. Int. 60, 7–14. Zahran, S., Laidlaw, M.A., McElmurry, S.P., Filippelli, G.M., Taylor, M., 2013b. Linking source and effect: resuspended soil lead, air lead, and children's blood lead levels in Detroit, Michigan. Environ. Sci. Technol. 47, 2839–2845.

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