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Measures as amended, taking into account amendments up to National Environment Protection (Assessment of Site Contamination) Amendment Measure 2013 (No. 1)
Administered by: Agriculture, Water and the Environment
Registered 03 Jun 2013
Start Date 16 May 2013

Commonwealth Coat of Arms

National Environment Protection (Assessment of Site Contamination) Measure 1999

as amended

made under section 14(1) of the

National Environment Protection Council Act 1994 (Cwlth), the National Environment Protection Council (New South Wales) Act 1995 (NSW), the National Environment Protection Council (Victoria) Act 1995 (Vic), the National Environment Protection Council (Queensland) Act 1994 (Qld), the National Environment Protection Council (Western Australia) Act 1996 (WA), the National Environment Protection Council (South Australia) Act 1995 (SA), the National Environment Protection Council (Tasmania) Act 1995 (Tas), the National Environment Protection Council Act 1994 (ACT) and the National Environment Protection Council (Northern Territory) Act 1994 (NT)

Compilation start date:                     16 May 2013

Includes amendments up to:            National Environment Protection (Assessment of Site Contamination) Amendment Measure 2013 (No. 1)

This compilation has been split into 22 volumes

Volume 1:       sections 1–6, Schedules A and B

Volume 2:       Schedule B1

Volume 3:       Schedule B2

Volume 4:       Schedule B3

Volume 5:       Schedule B4

Volume 6:       Schedule B5a

Volume 7:       Schedule B5b

Volume 8:       Schedule B5c

Volume 9:       Schedule B6

Volume 10:     Schedule B7 - Appendix 1

Volume 11:     Schedule B7 - Appendix 2

Volume 12:     Schedule B7 - Appendix 3

Volume 13:     Schedule B7 - Appendix 4

Volume 14:     Schedule B7 - Appendix 5

Volume 15:     Schedule B7 - Appendix 6

Volume 16:     Schedule B7 - Appendix B

Volume 17:     Schedule B7 - Appendix C

Volume 18:     Schedule B7 - Appendix D

Volume 19:     Schedule B7

Volume 20:     Schedule B8

Volume 21:     Schedule B9

Volume 22:     Endnotes

 

Each volume has its own contents

 

 

 

About this compilation

The compiled instrument

This is a compilation of the National Environment Protection (Assessment of Site Contamination) Measure 1999 as amended and in force on 16 May 2013. It includes any amendment affecting the compiled instrument to that date.

This compilation was prepared on 22 May 2013.

The notes at the end of this compilation (the endnotes) include information about amending Acts and instruments and the amendment history of each amended provision.

Uncommenced provisions and amendments

If a provision of the compiled instrument is affected by an uncommenced amendment, the text of the uncommenced amendment is set out in the endnotes.

Application, saving and transitional provisions for amendments

If the operation of an amendment is affected by an application, saving or transitional provision, the provision is identified in the endnotes.

Modifications

If a provision of the compiled instrument is affected by a textual modification that is in force, the text of the modifying provision is set out in the endnotes.

Provisions ceasing to have effect

If a provision of the compiled instrument has expired or otherwise ceased to have effect in accordance with a provision of the instrument, details of the provision are set out in the endnotes.

 

 

  

  

  


 

National Environment Protection (Assessment of Site Contamination) Measure 1999 National Environment Protection (Assessment of Site Contamination) Measure 1999 National Environment Protection (Assessment of Site Contamination) Measure 1999 National Environment Protection (Assessment of Site Contamination) Measure 1999 National Environment Protection (Assessment of Site Contamination) Measure 1999 National Environment Protection (Assessment of Site Contamination) Measure 1999 National Environment Protection (Assessment of Site Contamination) Measure 1999 National Environment Protection (Assessment of Site Contamination) Measure 1999 National Environment Protection (Assessment of Site Contamination) Measure 1999 National Environment Protection (Assessment of Site Contamination) Measure 1999 National Environment Protection (Assessment of

Schedule B7

APPENDIX A1

The Derivation of HILs
for Metals and Inorganics


Contents
The Derivation of HILs for Metals and Inorganics
                                                                                       Page

1                             Arsenic                                                             1

1.1             General                                                                                        1

1.2             Previous HIL                                                                               1

1.3             Significance of Exposure Pathways                                          1

1.3.1                Oral Bioavailability                                                         1

1.3.2                Dermal Absorption                                                          3

1.3.3                Inhalation of Dust                                                            3

1.3.4                Plant Uptake                                                                    3

1.3.5                Intakes from Other Sources – Background                    3

1.4             Identification of Toxicity Reference Values                             4

1.4.1                Classification                                                                    4

1.4.2                Review of Oral Information                                            4

1.4.3                Assessment of End Points – Oral Exposures                   6

1.4.3.1                 Existing Oral Dose-Response Approaches - Australia     6

1.4.3.2                 Oral Dose-Response Approaches - International                6

1.4.4                Inhalation Values                                                             8

1.4.5                Recommendation                                                             8

1.5             Calculated HILs                                                                          9

1.6             References                                                                                 11

2                             Beryllium                                                       14

2.1             General                                                                                      14

2.2             Previous HIL                                                                             14

2.3             Significance of Exposure Pathways                                        14

2.3.1                Oral Bioavailability                                                       15

2.3.2                Dermal absorption                                                         15

2.3.3                Inhalation of Dust                                                          15

2.3.4                Plant Uptake                                                                  15

2.3.5                Intakes from Other Sources – Background                  15

2.4             Identification of Toxicity Reference Values                           16

2.4.1                Classification                                                                  16

2.4.2                Review of Available Values/Information                      16

2.4.3                Recommendation                                                           17

2.5             Calculated HILs                                                                        18

2.6             References                                                                                 19

3                             Boron                                                             20

3.1             General                                                                                      20

3.2             Previous HIL                                                                             20

3.3             Significance of Exposure Pathways                                        20

3.3.1                Oral Bioavailability                                                       21

3.3.2                Dermal absorption                                                         21

3.3.3                Inhalation of Dust                                                          21

3.3.4                Plant Uptake                                                                  21

3.3.5                Intakes from Other Sources – Background                  22

3.4             Identification of Toxicity Reference Values                           22

3.4.1                Classification                                                                  22

3.4.2                Review of Available Values/Information                      22

3.4.3                Recommendation                                                           23

3.5             Calculated HILs                                                                        23

3.6             References                                                                                 24

4                             Cadmium                                                      25

4.1             General                                                                                      25

4.2             Previous HIL                                                                             25

4.3             Significance of Exposure Pathways                                        26

4.3.1                Oral Bioavailability                                                       26

4.3.2                Dermal absorption                                                         26

4.3.3                Inhalation of Dust                                                          26

4.3.4                Plant Uptake                                                                  26

4.3.5                Intakes from Other Sources – Background                  27

4.4             Identification of Toxicity Reference Values                           27

4.4.1                Classification                                                                  27

4.4.2                Review of Available Values/Information                      27

4.4.3                Oral (and Dermal) Intakes                                            28

4.4.4                Inhalation Exposures                                                     29

4.4.5                Recommendation                                                           30

4.5             Calculated HILs                                                                        30

4.6             References                                                                                 31

5                             Chromium VI                                                33

5.1             General                                                                                      33

5.2             Previous HIL                                                                             33

5.3             Significance of Exposure Pathways                                        34

5.3.1                Oral Bioavailability                                                       34

5.3.2                Dermal absorption                                                         34

5.3.3                Inhalation of Dust                                                          34

5.3.4                Plant Uptake                                                                  34

5.3.5                Intakes from Other Sources – Background                  35

5.4             Identification of Toxicity Reference Values                           35

5.4.1                Classification                                                                  35

5.4.2                Review of Available Values/Information                      35

5.4.2.1                 Oral Intakes                                                                                 35

5.4.2.2                 Inhalation Exposures                                                                36

5.4.3                Recommendation                                                           37

5.5             Calculated HILs                                                                        38

5.6             References                                                                                 39

6                             Cobalt                                                            41

6.1             General                                                                                      41

6.2             Previous HIL                                                                             41

6.3             Significance of Exposure Pathways                                        42

6.3.1                Oral Bioavailability                                                       42

6.3.2                Dermal absorption                                                         42

6.3.3                Inhalation of Dust                                                          42

6.3.4                Plant Uptake                                                                  42

6.3.5                Intakes from Other Sources – Background                  42

6.4             Identification of Toxicity Reference Values                           43

6.4.1                Classification                                                                  43

6.4.2                Review of Available Values/Information                      43

6.4.3                Recommendation                                                           44

6.5             Calculated HILs                                                                        44

6.6             References                                                                                 45

7                             Copper                                                           46

7.1             General                                                                                      46

7.2             Previous HIL                                                                             46

7.3             Significance of Exposure Pathways                                        46

7.3.1                Oral Bioavailability                                                       47

7.3.2                Dermal absorption                                                         47

7.3.3                Inhalation of Dust                                                          47

7.3.4                Plant Uptake                                                                  47

7.3.5                Intakes from Other Sources – Background                  48

7.4             Identification of Toxicity Reference Values                           48

7.4.1                Classification                                                                  48

7.4.2                Review of Available Values/Information                      48

7.4.3                Recommendation                                                           50

7.5             Calculated HILs                                                                        50

7.6             References                                                                                 51

8                             Lead                                                               53

8.1             General                                                                                      53

8.2             Previous HIL                                                                             53

8.3             Significance of Exposure Pathways                                        54

8.3.1                Oral Bioavailability                                                       54

8.3.2                Dermal absorption                                                         55

8.3.3                Inhalation of Dust                                                          55

8.3.4                Plant Uptake                                                                  55

8.3.5                Intakes from Other Sources – Background                  55

8.4             Identification of Toxicity Reference Values                           56

8.4.1                Classification                                                                  56

8.4.2                Review of Available Values/Information                      56

8.5             Calculated HILs                                                                        58

8.5.1                HILs                                                                               58

8.6             References                                                                                 59

9                             Manganese                                                    61

9.1             General                                                                                      61

9.2             Previous HIL                                                                             61

9.3             Significance of Exposure Pathways                                        61

9.3.1                Oral Bioavailability                                                       61

9.3.2                Dermal absorption                                                         62

9.3.3                Inhalation of Dust                                                          62

9.3.4                Plant Uptake                                                                  62

9.3.5                Intakes from Other Sources – Background                  62

9.4             Identification of Toxicity Reference Values                           63

9.4.1                Classification                                                                  63

9.4.2                Review of Available Values/Information                      63

9.4.3                Recommendation                                                           65

9.5             Calculated HILs                                                                        65

9.6             References                                                                                 66

10                          Mercury                                                         67

10.1          General                                                                                      67

10.2          Previous HIL                                                                             67

10.3          Significance of Exposure Pathways                                        68

10.3.1             Oral Bioavailability                                                       68

10.3.2             Dermal absorption                                                         68

10.3.3             Inhalation of Dust                                                          69

10.3.4             Plant Uptake                                                                  69

10.3.5             Intakes from Other Sources – Background                  69

10.4          Identification of Toxicity Reference Values                           70

10.4.1             Classification                                                                  70

10.4.2             Review of Available Values/Information                      70

10.4.2.1               Inorganic Mercury                                                                    70

10.4.2.2               Methyl Mercury                                                                         72

10.4.3             Recommendation                                                           73

10.5          Calculated HILs                                                                        74

10.5.1             Inorganic Mercury                                                        74

10.5.2             Methyl Mercury                                                             74

10.6          References                                                                                 76

11                          Nickel                                                             78

11.1          General                                                                                      78

11.2          Previous HIL                                                                             78

11.3          Significance of Exposure Pathways                                        78

11.3.1             Oral Bioavailability                                                       78

11.3.2             Dermal absorption                                                         79

11.3.3             Inhalation of Dust                                                          79

11.3.4             Plant Uptake                                                                  79

11.3.5             Intakes from Other Sources – Background                  80

11.4          Identification of Toxicity Reference Values                           80

11.4.1             Classification                                                                  80

11.4.2             Review of Available Values/Information                      80

11.4.2.1               Oral                                                                                               81

11.4.2.2               Inhalation                                                                                     81

11.4.2.3               Identified TRVs                                                                          83

11.4.3             Recommendation                                                           84

11.5          Calculated HILs                                                                        84

11.6          References                                                                                 85

12                          Selenium                                                        87

12.1          General                                                                                      87

12.2          Previous HIL                                                                             87

12.3          Significance of Exposure Pathways                                        87

12.3.1             Oral Bioavailability                                                       87

12.3.2             Dermal absorption                                                         87

12.3.3             Inhalation of Dust                                                          87

12.3.4             Plant Uptake                                                                  88

12.3.5             Intakes from Other Sources – Background                  88

12.4          Identification of Toxicity Reference Values                           88

12.4.1             Classification                                                                  88

12.4.2             Review of Available Values/Information                      89

12.4.3             Recommendation                                                           91

12.5          Calculated HILs                                                                        91

12.6          References                                                                                 92

13                          Zinc                                                                93

13.1          General                                                                                      93

13.2          Previous HIL                                                                             93

13.3          Significance of Exposure Pathways                                        93

13.3.1             Oral Bioavailability                                                       94

13.3.2             Dermal absorption                                                         94

13.3.3             Inhalation of Dust                                                          94

13.3.4             Plant Uptake                                                                  94

13.3.5             Intakes from Other Sources – Background                  95

13.4          Identification of Toxicity Reference Values                           96

13.4.1             Classification                                                                  96

13.4.2             Review of Available Values/Information                      96

13.4.3             Recommendation                                                           98

13.5          Calculated HILs                                                                        98

13.6          References                                                                                 99

14                          Cyanide (free)                                              101

14.1          General                                                                                    101

14.2          Previous HIL                                                                           101

14.3          Significance of Exposure Pathways                                      102

14.3.1             Oral Bioavailability                                                     102

14.3.2             Dermal absorption                                                       102

14.3.3             Inhalation of Dust                                                        102

14.3.4             Inhalation of HCN Gas                                                102

14.3.5             Plant Uptake                                                                102

14.3.6             Intakes from Other Sources – Background                103

14.4          Identification of Toxicity Reference Values                         103

14.4.1             Classification                                                                103

14.4.2             Review of Available Values/Information                    103

14.4.3             Recommendation                                                         106

14.5          Calculated HILs                                                                      106

14.6          References                                                                               108

15                          Shortened forms                                          110

 

 


1                  Arsenic

1.1              General

Several comprehensive reviews of arsenic in the environment and its toxicity to humans are available and should be consulted for more detailed information not presented in this summary (ATSDR 2007; NRC 2001; WHO 2001; and EA 2009a). The following provides a summary of the key aspects of arsenic that are relevant to the derivation of a soil health investigation level (HIL).

 

Arsenic is a metalloid that can exist in four valence states (-3, 0, +3 and +5) and forms a steel grey, brittle solid in elemental form (ATSDR 2007). Under reducing conditions, arsenite (As III) is the dominant form and, in well oxygenated environments, arsenate (As V) predominates (WHO 2000). Arsenic is the 20th most commonly occurring element in the Earth’s crust, occurring at an average concentration of 3.4 ppm (ATSDR 2007).

1.2              Previous HIL

The derivation of the HIL (HIL A = 100 mg/kg) for arsenic is presented by Langley (1991). In summary, the previous HIL was derived on the basis of the following:

·         Intakes of arsenic from other sources were estimated, with dietary intakes considered most significant for the general population. Intakes based on data from the 1987 and 1990 Australian Market Basket Surveys were estimated to be 6.7 µg/kg/week for a 2-year-old child. This was approximated to contribute up to 50% of the provisional tolerable weekly intake (PTWI) considered.

·         A PTWI of 15 µg/kg/week referenced from the World Health Organization (WHO) was adopted as the toxicity reference value.

·         Ingestion of both soil and dust was considered assuming 100% is bioavailable and is absorbed.

·         Dermal absorption was considered to be low with 1% of arsenic compounds absorbed in 24 hours;

·         Inhalation of arsenic in dust, both outdoors and indoors, has been considered.

·         The total absorption of arsenic, based on 100 mg/kg in soil, for a young child was calculated to be 11.4 µg/day, approximately 40% of the adopted toxicity reference value.

1.3              Significance of Exposure Pathways

Ingestion of soil and dust is considered the most significant pathway of exposure for inorganics in soil. The consideration of bioavailability and inclusion of other exposure pathways in the derivation of a soil HIL has been further reviewed, as noted below.

1.3.1        Oral Bioavailability

Most international jurisdictions have adopted a default value of 100% oral bioavailability in the derivation of investigation levels, allowing site-specific bioavailability to then be considered in further assessment. It is also understood that review of arsenic bioavailability in Australia (Ng et al. 2009) has not identified a default value.

 

As a note, some default bioavailability values have been adopted in the USA (based on reviews of state-specific data) as follows:

·         Region 8 (US EPA 2009) recommends a default of 0.5 (50%), noting that where concentrations are near a level of concern, site-specific bioavailability data is recommended.

·         Region 10 (US EPA 2000) recommends a default of 0.8 (80%) for soil at smelter sites, 0.6 (60%) for soil at mine sites and 1 (100%) for all other sites.

·         Texas recommends a default of 0.78 (78%).

While it may not be sufficiently conservative to apply a low value as adopted by the Australian Pesticides and Veterinary Medicines Authority (APVMA) (25%), some consideration of a conservative default in Australia is presented. It is noted that bioavailability is complex; however, based on relative bioavailability data available for Australian sites (presented in Ng et al. 2009; Juhasz et al. 2003), upper values were in the range of approximately 50-70% with most significantly lower than these values, and a few studies reporting upper limit values that are higher (up to 97%). Juhasz et al. (2003) suggested a worst-case value of 50% could be considered. When considering long-term exposures from soil it is overly conservative to consider the maximum bioavailability value from one particular study, as exposures will be averaged over accessible soil/dust. Hence it would be reasonable to consider a conservative value of 70% bioavailability as a reasonable upper estimate that adequately addresses arsenic that may be derived from mine sites, smelters, railway corridors and other areas where herbicides/pesticides have been used.

 

Roberts et al. (2002) showed monkey absorption of arsenic from pesticide-treated soil and cattle dip soil is 10.7-24.7%. In August 2001, the US EPA Health Effects Division’s Hazard Identification Assessment Review Committee (HIARC) evaluated the toxicology database for inorganic arsenic and established toxicological end points for incidental residential and commercial/industrial exposure risk assessments (US EPA 2001). As a key component of that assessment, HIARC established the appropriate relative bioavailability of arsenic in soil versus arsenic in water. For purposes of health risk assessment, US EPA evaluated a number of studies of relative bioavailability of arsenic (US EPA 2001). After careful consideration of data reported in the various bioavailability studies, US EPA determined that the monkey was considered an appropriate study model for humans due to its similarity in excretion and gastrointestinal absorption characteristics (US EPA 2001). The US EPA identified the comprehensive monkey study conducted by Roberts et al. (2002) as the study of choice. This study was conducted on behalf of the Florida Department of Environmental Protection (DEP) in order to specifically establish a gastrointestinal absorption efficiency factor for arsenic in soil that could be applied to soil risk assessments. The Roberts et al. (2002) study identified the maximum of the arithmetic mean value of 24.7% (for five animals and for relative bioavailability for each of five soil types) as a ‘conservative, upper bound case for any particular soil type’. While the maximum individual value reported in the study was 32.4%, the authors did not recommend this value for use as a reasonable maximum exposure (RME) value for risk assessment on the basis that ‘only under highly specific, rare circumstances is the maximum value for a particular parameter used in environmental characterisation, exposure assessment and risk assessment’ (Roberts et al. 2002). The US EPA agreed with the Florida DEP and selected 25% as an RME value for relative bioavailability for health risk assessments of arsenic in soil (US EPA 2001) and both agencies currently endorse the value of 25%. While the Roberts et al. (2002) study used five soil types typical of Florida soils, another monkey study (using a difference species) was conducted by Freeman et al. (1995) using soil near a smelter in Anaconda, Montana. The mean absolute percentage bioavailabilities, based on urinary excretion data, were 68, 19, and 14% for the gavage (soluble sodium arsenate in oral solution), house dust, and soil treatments, respectively. The values for house dust and soil are consistent with those reported by Roberts et al. (2002) for soil.

 

Available data from Bendigo in Victoria suggests that the bioavailability of arsenic in soil derived from mine tailings in this region commonly ranges from 10-20% and is generally less than 30%. The value of 25% that is adopted by the US EPA would be appropriate in these areas.

 

With consideration of the above, a range of 25-70% bioavailability may be appropriate for the assessment of arsenic in soil. The range of bioavailabilities considered would need to be based on suitable data in relation to source and site-specific bioavailability (where lower bioavailability values were considered appropriate).

1.3.2        Dermal Absorption

Review of dermal absorption by the New Zealand Ministry for the Environment (MfE 2011) has noted that ‘despite the fact that skin cancer is a primary toxicological effect of concern as a result of exposure to arsenic, dermal absorption of arsenic is generally considered to be negligible. US EPA (2004) guidance uses a dermal absorption factor of 3% based on Wester et al. (1993), who examined the dermal uptake of arsenic in solution. However, recent studies on the dermal absorption of soil-absorbed arsenic in rhesus monkeys indicate that the mean dermal absorption is 0.5%, i.e. negligible (Lowney et al. 2007)’.

 

On the basis of the above, a dermal absorption value of 0.5% has been considered in the derivation of an HIL for arsenic in soil.

1.3.3        Inhalation of Dust

Arsenic is not volatile and inhalation exposures associated with particulates outdoors and indoors are expected to be of less significance than ingestion of soil. While likely to be negligible, potential inhalation exposures associated with dust have been considered in the HIL derived.

1.3.4        Plant Uptake

In the review of arsenic presented by Langley (1991), a study by Merry et al. (1986) was cited which involved evaluation of the uptake of arsenic by radishes and silverbeets in soil with concentrations ranging from 26-260 ppm. The study showed ‘no concentrations that exceeded currently accepted health limits for human consumption’ Langley (1991). Langley (1991) also noted that plant growth was likely to be affected before plant concentrations were substantially elevated.

Further review of plant uptake of arsenic is presented by the UK Environment Agency (EA 2009b). This review considered studies that are based on the uptake of arsenic into green vegetables, root vegetables, tuber vegetables, herbaceous fruit, shrub fruit and tree fruit. The review provides recommendations as to relevant soil-to-plant uptake factors that are relevant for these types of produce. The recommendations from this review have been considered in the derivation of a residential HIL A and are summarised below for the range of crops considered:

 

Produce Group

Plant Uptake Factors (mg/kg produce fresh weight per mg/kg soil) (EA 2009b)

Green vegetables

0.00043

Root vegetables

0.0004

Tuber vegetables

0.00023

Tree fruit

0.0011

 

It is noted that the inclusion of home-grown produce in the calculations presented for HIL A results in some double counting of intakes from fruit and vegetable produce (also included in background intakes). To address this in the derivation of HIL A, half the intake estimated to be derived from home-grown produce is assumed to be already accounted for in the total background intake (noted below).

1.3.5        Intakes from Other Sources – Background

The most recent Australian Total Diet Survey (ATDS) that addresses arsenic in food was published by FSANZ in 2011 (FSANZ 2011). Based on data presented in this report, dietary intake of arsenic for children aged 2-5 years ranges from a mean of 1.2 µg/kg/day to a 90th percentile of 2.8 µg/kg/day. These intakes are based on total arsenic in produce, rather than inorganic arsenic.

 

Review of background intakes from food, water, air, soil and contact with play equipment, based on available Australian data presented by APVMA (2005), suggests background intakes of inorganic arsenic by young children may average 0.62 µg/kg/day. Further review of inorganic arsenic intakes by the Joint FAO/WHO Expert Committee on Food Additives (WHO 2011a) indicated that for populations not located in areas of arsenic-contaminated groundwater, intakes by young children ranged from 0.14-1.39 µg/kg/day. On the basis of the range of intake estimations available, a reasonable estimation of 50% of the oral toxicity reference value (TRV) from sources other than soil has been assumed. It is noted that the inclusion of home-grown produce in the calculations presented for HIL A results in some double counting of intakes from fruit and vegetable produce (addressed when assessing intakes from home-grown produce).

 

Intakes from inhalation exposures are low (around 0.0017 µg/kg/day (APVMA 2005)), comprising <1% of the inhalation TRV adopted.

1.4              Identification of Toxicity Reference Values

With respect to arsenic toxicity and the identification of appropriate toxicity reference values, a number of issues need to be considered. These include:

·         the relevance of non-threshold carcinogenic values for the assessment of oral exposures

·         identification of an appropriate oral toxicity value

·         identification of an appropriate approach and value for inhalation exposures.

These are discussed below.

1.4.1        Classification

The International Agency for Research on Cancer (IARC) has classified arsenic and inorganic arsenic compounds as Group 1 -  ‘carcinogenic to humans’ (IARC 2012).

1.4.2        Review of Oral Information

Arsenic is a known human carcinogen, based on human epidemiological studies that show skin and internal cancers (in particular, bladder, liver and lung) associated with chronic exposures to arsenic in drinking water. The research available on arsenic carcinogenicity is dominated by epidemiological studies (which have limitations) rather than animal studies. This differs from carcinogenic assessments undertaken on many other chemicals. The principal reason for the lack of animal studies is because arsenic has not been shown to cause cancer in rodents (the most common species used in animal tests), due to interspecies differences between rodents and humans.

 

Review of arsenic by IARC (2012) has concluded the following:

·         For inorganic arsenic and its metabolites, the evidence points to weak or non-existent direct mutagenesis (genotoxicity), which is seen only at highly cytotoxic concentrations.

·         Long-term, low-dose exposures to inorganic arsenic (more relevant to human exposure) is likely to cause increased mutagenesis as a secondary effect of genomic instability. While the mechanism of action (MOA) is not fully understood, it is suggested by IARC (2012) that it may be mediated by increased levels of reactive oxygen species, as well as co-mutagenesis with other agents. The major underlying mechanisms observed at low concentrations include the rapid induction of oxidative DNA damage and DNA-repair inhibition, and slower changes in DNA-methylation patterns, aneuploidy, and gene amplification.

·         Inhibition of DNA repair leads to co-carcinogenicity.

 Revision to the WHO guidelines on drinking water (WHO 2011b) adopted a practical value based on the analytical limit of reporting rather than based on a dose-response approach. The oral slope factor derived by the US has not been used to derive a guideline, as the slope factor is noted by WHO as likely to be an overestimate.

 

US EPA reviews have retained the use of a non-threshold approach, based on sufficient supporting evidence associated with increased rates of bladder and lung cancer (for inhalation exposures (US EPA 2001)). The US EPA approach adopted follows a review by the NRC (2001) which concluded that ‘ internal cancers are more appropriate as  end points for risk assessment than non-melanoma skin cancers’. Slope factors relevant for the assessment of these end points range from 0.4-23 (mg/kg/day)-1. The use of a non-threshold approach (slope factor), however, is more by default by following the US EPA Carcinogenic Guidelines (US EPA 2005), as there remains uncertainty on the carcinogenic MOA for arsenic (Sams et al. 2007). Further research is required to define and review the MOA prior to the US revising the dose-response approach currently adopted. Inherent in the current US approach (where a non-threshold slope factor is derived) are some key uncertainties that likely result in an overestimate of risk (Boyce et al. 2008), which include (SAB 2005, Brown 2007, Lamm & Kruse 2005 and Chu & Crawford-Brown 2006):

·         the choice of the cancer end point

·         the choice of the mathematical model used to estimate risk (shape of the dose-response curve at low doses) as there is no clear biological basis for extrapolation-

·         the assumptions used to estimate exposure from studies (primarily epidemiological studies).

Review of recent studies presented by Boyce et al. (2008) has indicated that, for carcinogenic effects associated with arsenic exposure, a linear (or non-threshold) dose-response is not supported (also note discussion by Clewell et al. 2007). This is based on the following:

·         Epidemiological studies (worldwide) that have repeatedly demonstrated that cancers associated with inorganic arsenic ingestion are observed only in populations exposed to arsenic concentrations in drinking water that are greater than 150 μg/L. In the US, exposures to concentrations in drinking water have only been associated with carcinogenic effects where mean concentrations are greater than 190 µg/L (Schoen et al. 2004).

·         Mechanistic information on how arsenic affects the cellular processes associate with carcinogenicity. This includes consideration that arsenic and its metabolites may modify DNA function through more indirect mechanisms such as inhibition of DNA repair, induction of dysfunctional cell division, perturbation of DNA methylation patterns, modulation of signal transduction pathways (leading to changes in transcriptional controls and the over-stimulation of growth factors), and generation of oxidative stress (ATSDR 2007 and IARC 2012) and that evidence for the indirect mechanisms for genotoxicity identified in in vitro studies have nearly all been at concentrations that are cytotoxic (Klein et al. 2007).

Hence the default approach adopted by the US EPA in adopting a non-threshold approach to the assessment of the carcinogenic effects associated with arsenic exposure is not well supported by the available data. This is consistent with the most recent Australian review available (APVMA 2005). The review conducted considered current information on arsenic carcinogenicity and genotoxicity which noted the following:

 

‘Although exposure to high concentrations of inorganic arsenic results in tumour formation and chromosomal damage (clastogenic effect), the mechanism by which these tumours develop does not appear to involve mutagenesis. Arsenic appears to act on the chromosomes and acts as a tumour promoter rather than as an initiator ’. ‘Furthermore, the epidemiological evidence from occupational exposure studies indicates that arsenic acts at a later stage in the development of cancer, as noted with the increased risk of lung cancer mortality with increasing age of initial exposure, independent of time after exposure ’ ‘Hence arsenic appears to behave like a carcinogen which exhibits a threshold effect. This would also be conceptually consistent with the notion that humans have ingested food and water containing arsenic over millennia and so the presence of a threshold seems likely. Nevertheless the mechanism by which tumour formation develops following arsenic exposure has been and still continues to be a source of intensive scientific investigation.’

 

On the basis of the above the use of a threshold dose-response approach for the assessment of carcinogenic effects associated with arsenic exposure is considered appropriate and has been adopted in the derivation of soil HILs.

 

The review of arsenic by the New Zealand Ministry for the Environment (MfE 2011) noted that, while there is general consensus that arsenic is likely to act indirectly on DNA in a sub-linear or threshold manner, it is considered that there is insufficient data available to determine a ‘well-defined non-linear dose-response’. For this reason the derivation of the New Zealand soil guideline values has adopted a non-threshold (linear) approach for arsenic (i.e. adopting a default non-threshold approach similar to that adopted by default by the US EPA). This differs from the approach adopted in Australia.

1.4.3        Assessment of End Points – Oral Exposures

1.4.3.1       Existing Oral Dose-Response Approaches - Australia

Arsenic intakes (oral) have been considered in Australia in the derivation of the current HIL (Langley 1991) and the Australian Drinking Water Guidelines (ADWG) (NHMRC 2011). The following can be noted from these guidelines:

·         The derivation of the HIL for arsenic is dated (Langley 1991) and considers all intakes of arsenic on the basis of a threshold PTWI established by WHO in 1983, and reconfirmed in 1988 (WHO 1989). The PTWI adopted is 15 μg/kg/week. In setting the PTWI it was noted that there is ‘a narrow margin between the PTWI and intakes reported to have toxic effects in epidemiological studies’ (WHO 1989). The PTWI was withdrawn by JECFA (WHO 2011a) following further review (refer to discussion below).

·         The previous ADWG (NHMRC 2004) derived criteria of 7 μg/L for inorganic arsenic in drinking water, based on the former WHO PTWI (noted above) converted to a daily intake (provisional maximum tolerable daily intake) of 2 μg/kg/day. The current ADWG (NHMRC 2011) has adopted a guideline of 10 μg/L based on a ‘practicable achievable’ approach supported by contemporary epidemiological studies in which elevated cancer risks and other adverse effects are not demonstrable at arsenic concentrations around 10 µg/L. It is noted that this level is equivalent to an adult (70 kg) intake of 0.28 μg/kg/day.

A review of arsenic toxicity was conducted by APVMA (2005) where a threshold approach was considered appropriate (noted above). A threshold value of 3 μg/kg/day was derived by the Australian and New Zealand Food Authority (ANZFA, now Food Standards Australia New Zealand (FSANZ)) in 1999, and considered in the APVMA (2005) review. The review considered that skin cancers appear to be the most sensitive indicator of carcinogenicity of inorganic arsenic in humans and, based on epidemiological studies, a threshold of 2.9 μg/kg/day (rounded to 3 μg/kg/day) can be obtained. This threshold is the value adopted as a provisional tolerable daily intake (PTDI) by FSANZ (FSANZ 2003), similar to the former PTWI available from WHO (noted above). This approach has been considered by APVMA for all intakes of arsenic (oral, dermal and inhalation). The evaluation has not been further updated.

1.4.3.2       Oral Dose-Response Approaches - International

Evaluation of arsenic by JECFA (WHO 2011a) considered the available epidemiological data in relation to the increased incidence of lung cancer and urinary tract cancer associated with exposure to arsenic in water and food. Using the data associated with these end points, JECFA derived a benchmark dose lower confidence limit for a 0.5% increased incidence (BMDL0.5) of lung cancer (most sensitive  end point) of 3 μg/kg/day (ranging from 2-7 μg/kg/day). Uncertainties associated with the assumptions associated with total exposure, extrapolation of the BMDL0.5 and influences of the existing health status of the population were identified. Given the uncertainties and that the BMDL0.5 was essentially equal to the PTWI (WHO 1989), the PTWI was withdrawn. No alternative threshold values were suggested by JECFA, as the application of the BMDL needs to be addressed on a regulatory level, including when establishing guideline levels.

 

The review conducted by JECFA is generally consistent with that conducted by the European Food Safety Authority (EFSA) Panel on Contaminants in the Food Chain (CONTAM) (EFSA 2010). The review concluded that the PTWI was ‘no longer appropriate as data is available that shows inorganic arsenic causes cancer of the lung and bladder in addition to skin, and that the range of adverse effects had been reported at exposures lower than those reviewed by the JECFA’ in establishing the PTWI. Modelling conducted by EFSA considered the available epidemiological studies and selected a benchmark response (lower limits) of 1% extra risk (BMDL01). BMDL01 range from 0.3-8 μg/kg/day for cancers of the lung, bladder and skin. The CONTAM Panel (EFSA 2010) concluded that the overall range of BMDL01 values of 0.3-8 μg/kg/day should be used for the risk characterisation of inorganic arsenic rather than a single reference point, primarily due to the number of uncertainties associated with the possible dose-response relationships considered. On this basis it would not be appropriate to consider just one value in the range presented.

 

The derivation of a soil HIL requires the identification of an appropriate TRV, rather than a wide range of values, that is considered adequately protective of the population potentially exposed. The determination of an appropriate TRV for arsenic in soil in Australia has therefore considered the following:

·         The studies considered in the derivation of the different ranges of BMDL values (WHO 2011a and EFSA 2010) are based on drinking water studies. No studies considered are derived from other sources including soil. There are uncertainties inherent in the epidemiological studies considered by WHO (2011a) and EFSA (2010). These uncertainties include limitations or absence of information on levels of individual exposure or arsenic intake (from drinking water), limited quantification of arsenic intakes from other sources including food, size of the studies (variable) and the assumption that arsenic intake is the single cause of all  end points identified.

·         The drinking water studies are primarily associated with populations that have poorer nutritional status (i.e. Taiwan and Bangladesh). Studies (as summarised by EFSA 2010) have shown that populations with poor nutrition (and health status) are more susceptible to the prevalence and severity of arsenic-related health effects.

·         The largest of the studies conducted was within rural Asian populations, which differ from Australian populations with respect to generic lifestyle factors.

In view of the above, consideration of the lower end of the range of BMDL values available from WHO (2011a) and EFSA (2010) is not considered appropriate for the Australian population.

 

Based on the above considerations, a TRV of 2 µg/kg/day has been adopted in the derivation of a soil HIL. The TRV has been selected on the basis of the following:

·         The TRV is the lower end of the range derived from JECFA (WHO 2011a), and also lies within, but is not at the lower end of, the range presented by EFSA (2010).

·         The value is within the range of no observable adverse effect levels (NOAELs) identified by RIVM (2001), US EPA (US EPA 1998) and ATSDR (2007) that are associated with non-carcinogenic effects (and derived from drinking water studies in Taiwan and Bangladesh) of 0.8-8 µg/kg/day. Consistent with the approach discussed above in relation to the range of TRVs relevant to a cancer  end point, it is not considered appropriate that the most conservative end of this range is adopted for the Australian population.

Due to the level of uncertainty in relation to determining a single TRV for the assessment of arsenic exposures, the oral TRV used for the derivation of the soil HIL has not been considered to be a definitive value (refer to the calculations presented below). In addition, the approach adopted is based on developing science that should be reviewed in line with further developments in both science and policy.

1.4.4        Inhalation Values

Less data is available with respect to inhalation exposures to arsenic, though trivalent arsenic has been shown to be carcinogenic via inhalation exposures (with lung cancer as the end point). Review of the relevant mechanisms for carcinogenicity by RIVM (2001) suggests that the mechanism for arsenic carcinogenicity is the same regardless of the route of exposure. Hence a threshold is also considered relevant for the assessment of inhalation exposures. This is consistent with the approach adopted in the derivation of the previous arsenic HIL (Langley 1991) and in the review undertaken by APVMA (2005). While NEPC and APVMA adopted the oral PTWI as relevant for all routes of exposure, RIVM (2001) has derived an inhalation-specific threshold value. The RIVM (2001) review identified that the critical effect associated with chronic inhalation exposures in humans is lung cancer. The lowest observable adverse effect concentration (LOAEC) for trivalent arsenic associated with these effects is 10 μg/m3 (based on the review by ATSDR 2007). Applying an uncertainty factor of 10 to address variability in human susceptibility, a tolerable concentration (TC) in air of 1 μg/m3 was derived.

 

Given the above, there is some basis for the assessment of inhalation exposures to arsenic to adopt an appropriate threshold value but the available epidemiological studies associated with exposures in copper smelters suggest a linear or non-threshold approach may be relevant. The WHO (2000) review of arsenic also suggested the use of a linear (non-threshold) approach to the assessment of inhalation exposures to arsenic. The assessment presented is limited and essentially adopts the US approach with no discussion or consideration of the relevance of the linear model adopted. The review by WHO (2001) with respect to inhalation exposures and lung cancer provides a more comprehensive review and assessment. The review presented identified that a linear dose-response relationship is supported by the occupational and epidemiological studies. The three key studies associated with copper smelters in Tacoma, Washington (USA), Anaconda, Montana (USA) and Ronnskar (Sweden) (as summarised by WHO 2001) demonstrate a statistically significant excess risk of lung cancer at cumulative exposure levels of approximately ³0.75 mg/m3 per year.

 

The relevance of inhalation values derived from studies near smelters to the assessment of contaminated arsenic in soil in areas away from smelters is not well founded. Hence it is recommended that a threshold approach is considered for the assessment of inhalation exposures associated with arsenic in soil. The threshold TC derived by RIVM (2001) of 1 μg/m3 is lower than the cumulative exposure value identified by WHO (2001) of 750 μg/m3.years as statistically associated with an increase in lung cancer. The values are considered reasonably comparable if the exposure occurs over a period of 40 years and appropriate uncertainty factors are applied to convert from a lowest observable adverse effect level (LOAEL) to a NOAEL. In addition the TC is consistent with the TC05 value derived by Health Canada (1993) associated with lung cancer in humans and an incremental lifetime risk of 1 in 100,000. The value adopted is lower than the recommended PTDI adopted for the assessment of oral intakes (when the TC is converted to a daily intake). Hence use of the RIVM TC has been considered appropriate and adequately protective of all health effects associated with inhalation exposures that may be derived from soil, including carcinogenicity.

1.4.5        Recommendation

On the basis of the discussion above the following toxicity reference values (TRVs) have been adopted for arsenic in the derivation of HILs:

Recommendations for Arsenic 
Oral TRV (TRVO) = 0.002 mg/kg/day for oral and dermal intakes (refer to discussion above)
Oral Bioavailability (BAO) = may vary from around 25-70% (with the value adopted dependent on the available site data to support the use of these values). Values of 100%, 70% and 25% reviewed as discussed below.
Inhalation TRV (TRVI) = 0.001 mg/m3 (RIVM 2001) 
Dermal absorption factor (DAF) = 0.005 (or 0.5%) (Lowney et al. 2007)
Background Intakes from other sources (as % of TRV):
BIO = 50% for oral and dermal
BIi = 0% for inhalation 
Uptake into home-grown produce addressed for HIL A.

 

1.5              Calculated HILs

The following comments relate to the derivation of an HIL A (the most sensitive exposure scenario) for arsenic:

·         Using the proposed oral TRV, and the exposure pathways/assumptions presented in this document, with 100% bioavailability, HIL A = 130 mg/kg. Given the uncertainties discussed above in relation to the identification of a relevant TRV, and uncertainties associated with the calculation of the HIL, the calculated value is considered to be essentially no different from the previous HIL of 100 mg/kg.

·         Using the proposed oral TRV, and the exposure pathways/assumptions presented in this document, with 70% bioavailability, HIL A = 180 mg/kg. Given the uncertainties discussed above in relation to the identification of a relevant TRV, and uncertainties associated with the calculation of the HIL, the calculated value is considered to be essentially no different from the previous HIL of 100 mg/kg.

·         Using the proposed oral TRV, and the exposure pathways/assumptions presented in this document, with 25% bioavailability, HIL A = 380 mg/kg.

·         With consideration of the uncertainties noted, it is not considered appropriate to modify the existing HIL A of 100 mg/kg (where arsenic bioaccessibility is within the range of 70-100%). 

 

On the basis of the above the following HILs have been derived for arsenic (refer to Appendix B for equations used to calculate the HILs and Appendix C for calculations):

HIL Scenario

HIL* (mg/kg)

Percentage Contribution from Exposure Pathways

Ingestion of Soil/Dust

Ingestion of Home-grown Produce

Dermal Absorption of Soil/Dust

Inhalation (dust)

Residential A

100

86

9

5

<1

Residential B

500

81

--

19

<1

Recreational C

300

90

--

10

<0.1

Commercial D

3000

72

--

28

<1

-- Pathway not included in derivation of HIL

* Value derived is based on consideration of the range of oral TRVs derived by JECFA (WHO 2011a) and EFSA (2010) and relevance of the key studies and derived ranges to the Australian population. The HILs are based on 70-100% bioavailabilitya more site specific bioavailability (such as 25%) may be considered where sufficiently justified.

 


 

1.6              References

APVMA 2005, The Reconsideration of Registrations of Arsenic Timber Treatment Products (CCA and Arsenic Trioxide) and their Associated Labels, Report of Review Findings and Regulatory Outcomes, Summary Report, Review Series 3, Australian Pesticides & Veterinary Medicines Authority, Canberra, Australia.

ATSDR 2007, Toxicological Profile for Arsenic, Agency for Toxic Substances and Disease Registry, US Department of Health and Human Services, Atlanta, USA.

Boyce, CP, Lewis, AS, Sax, SN, Eldan, M, Cohen, SM & Beck, BD 2008, ‘Probabilistic Analysis of Human Health Risks Associated with Background Concentrations of Inorganic Arsenic: Use of a Margin of Exposure Approach’, Human and Ecological Risk Assessment, vol. 14, pp. 1159-1201.

Brown, KG 2007, ‘How Credible are Cancer Risk Estimates from the S.W. Taiwan Database for Arsenic in Drinking Water’, Human and Ecological Risk Assessment, vol. 13, pp. 180-190.

Chu, H-A & Crawford-Brown, DJ 2006, ‘Inorganic Arsenic in Drinking Water and Bladder Cancer: A Meta-Analysis for Dose-Response Assessment’, International Journal of Environmental Research and Public Health, vol. 3, no. 4, pp. 316-322.

Clewell, HJ, Thomas, RS, Gentry, PR, Crump, KS, Kenyon, EM, El-Masri, HA & Yager, JW 2007, ‘Research toward the development of a biologically based dose response assessment for inorganic arsenic carcinogenicity: A progress report’, Toxicology and Applied Pharmacology, vol. 222, pp. 388-398.

EA 2009a, Soil Guideline Values for inorganic arsenic in Soil, Science Report SC050021/ arsenic SGV, Environment Agency, Bristol, UK.

EA 2009b, Supplementary information for the derivation of SGV for arsenic, Science Report SC050021, Environment Agency, Bristol, UK.

EFSA 2010, Scientific Opinion on Arsenic in Food, EFSA Panel on Contaminants in the Food Chain (CONTAM), European Food Safety Authority, Parma, Italy.

Freeman, GB, Schoof, RA, Ruby, MV, Davis, AO, Dill, JA, Liao, SC, Lapin, CA, & Bergstrom, PD, 1995, ‘Bioavailability of arsenic in soil and house dust impacted by smelter activities following oral administration in cynomolgus monkeys’, Toxicological Sciences, vol. 28, pp. 215-222.

FSANZ 2003, The 20th Australian Total Diet Survey. A total diet survey of pesticide residues and contaminants. Food Standards Australia and New Zealand.

FSANZ 2011, The 23rd Australian Total Diet Study, Food Standards Australia and New Zealand.

Health Canada 1993, Priority Substances List Assessment Report, Arsenic and its Compounds, Health Canada, 1993. Available from: http://www.hc-sc.gc.ca/ewh-semt/pubs/contaminants/psl1-lsp1/arsenic_comp/index-eng.php

IARC 2012, IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Volume 100. Part C: A Review of Human Carcinogens: Arsenic, Metals, Fibres, and Dusts, World Health Organization and International Agency for Research on Cancer. http://monographs.iarc.fr/ENG/Monographs/vol100C/mono100C-6.pdf.

Juhasz, A, Smith, E & Naidu, R 2003, Estimation of Human Bioavailability of Arsenic in Contaminated Soils, in Proceedings of the Fifth National Workshop on the Assessment of Site Contamination, Environmental Protection and Heritage Council.

Klein, CB, Leszczynska, J, Hickey, C & Rossman, TG 2007, ‘Further evidence against a direct genotoxic mode of action for arsenic-induced cancer’, Toxicology and Applied Pharmacology, vol. 222, pp. 289-297.

Lamm, SH & Kruse, MB 2005, ‘Arsenic Ingestion and Bladder Cancer Mortality—What Do the Dose-Response Relationships Suggest About Mechanism?’, Human and Ecological Risk Assessment: An International Journal, vol. 11, no. 2, pp. 433-450.

Langley, AJ 1991, Response Levels for Arsenic, in The Health Risk Assessment and Management of Contaminated Sites – Proceedings of a National Workshop on the Health Risk Assessment and Management of Contaminated Sites, El Saadi, O & Langley, A (Eds), South Australian Health Commission, Adelaide, Australia.

Lowney, YW, Wester, RC, Schoof, RA, Cushing, CA, Edwards, M & Ruby, M 2007, ‘Dermal absorption of arsenic from soils as measured in the rhesus monkey’, Toxicological Sciences, vol. 100, pp. 381-392.

Merry, RH, Tiller, KG & Alston, AM 1986, ‘The effects of soil contamination with copper, lead and arsenic on the growth and composition of plants’, Plant and Soil, vol. 95, pp. 255-269.

Ng, JC, Juhasz, AL, Smith, E & Naidu, R 2009, Contaminant bioavailability and bioaccessibility. Part 2: Guidance for industry, CRC CARE Technical Report no. 14, CRC for Contamination Assessment and Remediation of the Environment, Adelaide, Australia.

NHMRC 2004, Australian Drinking Water Guidelines, National Water Quality Management Strategy, Australia. National Health and Medical Research Council and the Agriculture and Resource Management Council of Australia and New Zealand.

NHMRC 2011, National water quality management strategy. Australian drinking water guidelines, National Health and Medical Research Council, Australia.

NRC 2001, Arsenic in Drinking Water: 2001 Update, National Research Council, National Academy Press.

MfE 2011, Toxicological Intake Values for Priority Contaminants in Soil, New Zealand Ministry for the Environment, Wellington, New Zealand, http://www.mfe.govt.nz/publications/hazardous/toxicological-intake-values-for-priority-contaminants-in-soil/index.html.

RIVM 2001, Re-evaluation of human-toxicological maximum permissible risk levels, National Institute of Public Health and the Environment, (RIVM), Bilthoven, Netherlands. Available from: http://www.rivm.nl/bibliotheek/rapporten/711701025.html

Roberts, SM, Weimer, WR, Vinson, JRT, Munson, JW & Bergeron, RJ 2002, ‘Measurement of arsenic bioavailability in soil using a primate model’, Toxicological Sciences, vol. 67, pp. 303-310.

SAB 2005, Arsenic-Contaminated Soils, Questions and Discussion Materials, prepared for the Science Advisory Board, December 2005.

Sams, R II, Wolf, DC, Ramasamy, S, Ohanian, E, Chen, J & Lowit ,A 2007, ‘Workshop overview: Arsenic research and risk assessment’, Toxicology and Applied Pharmacology, vol. 222, pp. 245-251.

Schoen, A, Beck, B, Sharma, R & Dube, E 2004, ‘Arsenic Toxicity at Low Doses: Epidemiological and Model of Action Considerations’, Toxicology and Applied Pharmacology, vol. 198, Issue 3, pp. 253-267.

US EPA 2000, Guidance for Region 10 human health risk assessments regarding bioavailability of arsenic contaminated soil, United States Environmental Protection Agency, Washington, DC.

US EPA 2001, Inorganic Arsenic - Report of the Hazard Identification Assessment Review Committee, US EPA Health Effects Division, United States Environmental Protection Agency, Washington, DC. http://www.epa.gov/scipoly/sap/meetings/2001/october/inorganicarsenic.pdf

US EPA 2004, Risk assessment guidance for Superfund Vol. 1 Human Health Evaluation Manual (Part E, Supplemental guidance for dermal risk assessment), EPA/540/R-99/005. United States Environmental Protection Agency, Washington, DC.

US EPA 2005, Guidelines for Carcinogen Risk Assessment, Risk Assessment Forum, US EPA, EPA/630/P-03/001F, United States Environmental Protection Agency, Washington, DC.

US EPA 2009, Region 8 Recommendations for Quantifying the Bioavailability of Lead and Arsenic in Soil for Use in Human Health Risk Assessments, United States Environmental Protection Agency, Washington, DC. Online at: http://www.epa.gov/region8/r8risk/hh_rba.html#recs

US EPA 1998, Arsenic, inorganic (CASRN 7440-38-2),  Integrated Risk Information System, United States Environmental Protection Agency, Washington, DC.  Available from: http://www.epa.gov/iris/

Wester, RC, Maibach, HI, Bucks, DAW, Sedik, L, Melendres, J & Wade, M 1993, In vivo and in vitro percutaneous absorption and skin decontamination of arsenic from water and soil, Fundamental and Applied Toxicology, vol. 20, pp. 336–340.

WHO 1989, Arsenic, WHO Food Additives Series 24, Joint FAO/WHO Expert Committee on Food Additives, World Health Organization. Available from: http://www.inchem.org/documents/jecfa/jecmono/v024je08.htm.

WHO 2000, Air Quality Guidelines for Europe, 2nd Edn,  World Health Organization, Geneva.

WHO 2001, Arsenic and arsenic compounds, Environmental Health Criteria 224, World Health Organization.

WHO 2011a, Evaluation of certain contaminants in food: seventy-second report of the Joint FAO/WHO Expert Committee on Food Additives, WHO technical report series, no. 959, World Health Organization, Geneva.

WHO 2011b, Guidelines for drinking-water quality, 4th edition, World Health Organization, Geneva,  available from http://www.who.int/water_sanitation_health/dwq/chemicals/en/index.html.

 

 

2                  Beryllium

2.1              General

Several comprehensive reviews of beryllium in the environment and its toxicity to humans are available and should be consulted for more detailed information (ATSDR 2002; WHO 1993; WHO 2001). The following provides a summary of the key aspects of beryllium that are relevant to the derivation of a soil HIL.

 

Beryllium is a steel grey, brittle metal that is not found as the free metal in nature. There are approximately 45 mineralised forms of beryllium. The most important beryllium minerals in the world are beryl (3BeOAl2O36SiO2) and bertrandite (Be4Si2O7(OH)2) (ATSDR 2002). Beryllium is the lightest of all solids and chemically stable substances, with an unusually high melting point, specific heat, heat of fusion, and strength-to-weight ratio. Due to its high affinity for oxygen, a very stable surface film of beryllium oxide (BeO) is formed on the surface of metallic beryllium and beryllium alloys, providing high resistance to corrosion, water and cold oxidising acids (WHO 1993).

 

Occupational exposure to beryllium has been associated with acute and chronic lung diseases. The acute disease is normally associated with inhalation exposures to high levels of soluble beryllium salts (e.g. sulphate, chloride) and BeO, and may lead to chronic disease. The chronic disease is associated with long-term inhalation exposures to dust particles containing beryllium, has an immunological component and a latent period, which varies depending on the beryllium species. Dermatological effects may also occur on skin contact (Di Marco & Buckett 1996).

2.2              Previous HIL

The derivation of the previous HIL (HIL A = 20 mg/kg) for beryllium is presented by Di Marco & Buckett (1996). In summary, the HIL was derived on the basis of the following:

·         Intakes of beryllium from other sources were estimated with dietary intakes considered most significant for the general population. Based on the information available from Canada (considered more relevant than US data), background intakes of beryllium were assumed to be 0.65 µg/kg/day for preschoolers and 0.17 µg/kg/day for adults.

·         A provisional tolerable daily intake (PTDI) of 1 µg/kg/week based on the US EPA RfD of 5 µg/kg/day (derived from a NOEL of 0.54 mg/kg/day and an uncertainty factor of 100), however an additional uncertainty factor of 5 was considered more appropriate to address limitations with the critical study used (no other studies were available)

·         Ingestion of both soil and dust by an infant (2.5 years) has been considered assuming 1% is bioavailable.

·         Dermal absorption has been considered to be low with a conservative assumption of 0.1% considered.

·         Inhalation of beryllium in dust has been considered outdoors and indoors, assuming a dust concentration of 100 µg/m3 and outdoor dust contributes 75% to indoor dust.

·         Soil criteria derived on the basis of inhalation cancer risk values available from US EPA were calculated to be higher than the HIL of 20 mg/kg for infants (adopting a risk level of 10-5).

2.3              Significance of Exposure Pathways

Ingestion of soil and dust is considered the most significant pathway of exposure for inorganics in soil. The consideration of bioavailability and inclusion of other exposure pathways in the derivation of a soil HIL has been further reviewed, as noted below.

2.3.1        Oral Bioavailability

While oral bioavailability has been considered in the previous HIL, insufficient data is available to adequately define the bioavailability of beryllium in the range of contaminated sites that may need to be considered in Australia. On this basis, a default approach of assuming 100% oral bioavailability has been adopted in the derivation of an HIL. It is noted that a site-specific assessment of bioavailability can be undertaken where required.

2.3.2        Dermal absorption

In humans and animals sensitised to beryllium, contact with beryllium and its soluble and insoluble compounds can cause dermatitis and skin granulomas. In general, the more soluble the compound the greater the sensitising potential. Dermal effects usually occur on abraded skin. Dermal absorption of beryllium is assumed to be poor and would not likely cause further systemic effects. While it is noted that absorption through damaged/injured skin is expected to be higher, review of dermal absorption of beryllium (Deubner et al. 2001) noted that absorption through intact skin is considered negligible (<<1%). Hence the assumption of 0.1% dermal absorption considered in the previous HIL is considered appropriate. The value is consistent with the default presented by RAIS (2010).

 

It is noted that US EPA (2004) has recommended the use of a gastrointestinal absorption factor (GAF) of 0.7%, based on consideration of the rat study (with water) used in the derivation of the oral RfD. The GAF is used to modify the oral toxicity reference value to a dermal value in accordance with the US EPA (2004) guidance provided.

2.3.3        Inhalation of Dust

Beryllium is not volatile and inhalation exposures associated with particulates outdoors and indoors are expected to be of less significance than ingestion of soil. While likely to be negligible, potential inhalation exposures associated with dust have been considered in the HIL derived.

2.3.4        Plant Uptake

Limited data is available on the potential for the uptake of beryllium into plants, in particular,  edible fruit and vegetable crops. Review by ATSDR (2002) notes that in plants the uptake of beryllium appears to be restricted to the root system, with no significant translocation of beryllium to above-ground parts of the plant. Soluble forms of beryllium must be present for plant uptake to occur. In solution in the pH range of 6-8, beryllium is most commonly transformed to beryllium hydroxide, which has a very low solubility. Hence the potential for significant plant uptake is considered to be low.

 

Based on the above, the uptake of beryllium into root crops only has been considered in the derivation of the HIL. Limited plant uptake data is available, hence the value presented by RAIS (2010) of 0.0025 mg/kg fresh produce per mg/kg soil has been considered.

 

It is noted that the inclusion of home-grown produce in the calculations presented for HIL A results in some double counting of intakes from fruit and vegetable produce (also included in background intakes). To address this in the derivation of HIL A, half the intake estimated to be derived from home-grown produce is assumed to be already accounted for in the total background intake (noted below).

2.3.5        Intakes from Other Sources – Background

Limited data is available from Australia with respect to levels of beryllium in drinking water or food. ATSDR (2002) report concentrations of beryllium in Australian rainwater tanks between 0.05 and 0.08 µg/L. Beryllium is not routinely tested in drinking water supplies in Australia. Beryllium was not detected in any air sample collected in New South Wales (DEC 2003). Hence intakes that may be derived from ambient air are considered negligible.

 

The ATSDR (2002) and WHO (2001) reviews have not provided an update of potential background exposures from that considered in derivation of the current HIL (Di Marco & Buckett 1996). There is no data available to suggest that the background intakes considered in the derivation of the current HIL are an underestimate and hence these intakes are recommended to be retained in the derivation of revised HILs. For pre-schoolers a background intake of 0.65 µg/kg/day has been adopted, which constitutes approximately 30% of the recommended TRV.

2.4              Identification of Toxicity Reference Values

2.4.1        Classification

IARC (2012) has classified beryllium and beryllium compounds as a Group 1 agent, which implies that it is considered carcinogenic to humans, though it is noted that the evidence of carcinogenicity applies to the inhalation route only.

2.4.2        Review of Available Values/Information

Available data with respect to carcinogenicity was reviewed by WHO (2001). The review provided is no different from that summarised by Di Marco & Buckett (1996). Beryllium and compounds are considered carcinogenic to humans with the most important  end point identified as lung cancer following inhalation exposures. WHO (2001) noted that the genotoxicity data for beryllium is mixed and it appears to be somewhat compound-dependent (NRC 2007). Although the bacterial assays have been largely negative, the mammalian test systems exposed to beryllium compounds have shown evidence of mutations, chromosomal aberrations, and cell transformations. ATSDR (2002) has considered beryllium compounds to be weakly genotoxic.

 

The mode of action for beryllium carcinogenicity is not well understood and the relevance of a non-threshold approach to the quantification of inhalation exposures is not clear. The following is noted by Di Marco & Buckett (1996) and is considered to remain relevant for the assessment of inhalation exposures:

‘Whilst lung cancer is the most important  end point, it is unlikely to be a concern for beryllium in soil. Acute beryllium lung disease appears to occur prior to the development of lung cancer and may play a role in its induction. In addition, this disease has only been reported after exposure to high levels of specific beryllium compounds in the workplace; conditions which are unlikely to be achieved on exposures to dust generated from beryllium contaminated soil.’

 

This is supported by a more recent review by Hollins et al. (2009) where it was concluded that ‘the increase in potential risk of lung cancer was observed among those exposed to very high levels of beryllium and that beryllium’s carcinogenic potential in humans at exposure levels that exist in modern industrial settings should be considered either inadequate or marginally suggestive’.

 

Further review of carcinogenic risk associated with inhalation exposures in the current HIL by Di Marco & Buckett (1996) indicated that a soil concentration that is protective of carcinogenic risk via inhalation at a level of 1 in 100,000 (more than 1000 mg/kg) was well in excess of the derived HIL (20 mg/kg). This is consistent with calculations that would be conducted using current exposure assumptions.

 

On the basis of the above it is recommended that a threshold approach be adopted for the derivation of an HIL for beryllium in soil.  The following are available from Level 1 Australian and International sources:

 


Source

Value

Basis/Comments

Australian

ADWG (NHMRC 2011)

TDI = 0.002 mg/kg/day

No quantitative evaluation is available in the previous ADWG (NHMRC 2004) due to lack of suitable oral data.

TDI presented in ADWG (NHMRC 2011) and is derived from the WHO (2001) evaluation as noted below.

International

WHO (2001)

TDI = 0.002 mg/kg/day

TC = 0.02 µg/m3

TDI derived on the same basis as the RfD derived by the US EPA (noted below).

TC based on the development of chronic beryllium disease in exposed workers, consistent with the study used by the US EPA (noted below).

Note that beryllium is included in the rolling revisions to the DWG. The current guidelines (WHO 2011) adopt the same TDI as noted in the WHO (2001) review.

ATSDR (2002)

Oral MRL = 0.002 mg/kg/day

Chronic oral MRL derived on the same basis as the US EPA (IRIS, 2010) evaluation below.

US EPA (IRIS 2012)

RfD = 0.002 mg/kg/day

RfC = 0.02 µg/m3

RfD based on a BMD of 0.46 mg/kg/day associated with a 10% increase in inflammatory lesions in the small intestines of male and female dogs (1976 study) and a 300-fold uncertainty factor.

RfC based on a LOAEL (HEC) of 0.0002 mg/kg/day associated with lung effects in a human study and a 10-fold uncertainty factor.

 

The available international sources reference the same key studies and have derived the same toxicity reference values.

No dermal-specific studies or data are available. For the presence of beryllium in soil it is considered appropriate to consider use of the available TDI for all oral and dermal pathways of exposure (taking into account the relevant gastrointestinal absorption factor noted above).

2.4.3        Recommendation

On the basis of the discussion above, the following toxicity reference values (TRVs) have been adopted for beryllium in the derivation of HILs:

Recommendation for Beryllium
Oral TRV (TRVO) = 0.002 mg/kg/day (WHO 2001) 
Dermal TRV (TRVD) = 0.000014 mg/kg/day (adjusted from the oral TRV on the basis of a GAF of 0.007 (US EPA 2004)
Inhalation TRV (TRVI) = 0.00002 mg/m3 (WHO 2001) 
Dermal absorption factor (DAF) = 0.001 (or 0.1%) (assumed relevant, also available from RAIS (2010))
Background Intakes from other sources (as % of TRV):
BIO = 30% for oral and dermal
BIi = 0% for inhalation. 
Uptake into home-grown produce addressed for HIL A.

2.5              Calculated HILs

On the basis of the above, the following HILs have been derived for beryllium (refer to Appendix B for equations used to calculate the HILs and Appendix C for calculations):

HIL Scenario

HIL (mg/kg)

Percentage Contribution from Exposure Pathways

Ingestion of Soil/Dust

Ingestion of Home-grown Produce

Dermal Absorption of Soil/Dust

Inhalation (dust)

Residential A

60

30

12

56

2

Residential B

90

11

--

86

3

Recreational C

90

20

--

79

1

Commercial D

500

8

--

88

4

-- Pathway not included in derivation of HIL


 

2.6              References

ATSDR 2002, Toxicological Profile for Beryllium, September 2002. Available from ATSDR website: http://www.atsdr.cdc.gov/toxfaqs/TF.asp?id=185&tid=33

DEC 2003, Ambient Air Quality Research Project (1996-2001), Internal working paper no. 4, Ambient concentrations of heavy metals in NSW, Department of Environment and Conservation (NSW).

Deubner, DC, Lowney, YW, Paustenbach, DJ & Warmerdam, J 2001, ‘Contribution of Incidental Exposure Pathways to Total Beryllium Exposures’, Applied Occupational and Environmental Hygiene, vol. 16(5), pp. 568–578.

Di Marco, PN & Buckett, KJ 1996, ‘Derivation of Health Investigation Levels for Beryllium and Beryllium Compounds’, presented in the proceedings of the Third National Workshop on the Health Risk Assessment and Management of Contaminated Sites, Contaminated Sites Monograph Series.

Hollins, DM, McKinley, MA, Williams, C, Fillos, D, Chapman, PS & Madi, AK 2009, ‘Beryllium and lung cancer: A weight of evidence evaluation of the toxicological and epidemiological literature’, Critical Reviews in Toxicology, vol. 39, No. s1, pp. 1-32.

IARC 2012, IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Volume 100. Part C: A Review of Human Carcinogens: Arsenic, Metals, Fibres, and Dusts, World Health Organization and International Agency for Research on Cancer. http://monographs.iarc.fr/ENG/Monographs/vol100C/mono100C-6.pdf.

NHMRC 2004 Australian Drinking Water Guidelines, National Water Quality Management Strategy. Australia: National Health and Medical Research Council and the Agriculture and Resource Management Council of Australia and New Zealand.

NRC 2007. Health Effects of Beryllium Exposure, A Literature Review, Committee on Beryllium Alloy Exposures, Committee on Toxicology, National Research Council of the National Academies.

RAIS 2010, Risk Assessment Information System, website and database maintained by the Oak Ridge Operations Office, available from: http://rais.ornl.gov/

US EPA (IRIS 2012). Data and information available from the Integrated Risk Information System, an online database, available from http://www.epa.gov/iris/.

US EPA 2004. Risk Assessment Guidance for Superfund, Volume I: Human Health Evaluation Manual (Part E, Supplemental Guidance for Dermal Risk Assessment), Final, EPA/540/R-99/005, OSWER 9285.7-02EP.

WHO 1993. Environmental Health Criteria 106 - Beryllium International Programme of Chemical Safety, World Health Organization, Geneva.

WHO 2001. Beryllium and Beryllium Compounds, Concise International Chemicals Assessment Document 32, World Health Organization, Geneva.

WHO 2011, Guidelines for drinking-water quality, 4th edition, World Health Organization, Geneva, available from http://www.who.int/water_sanitation_health/dwq/chemicals/en/index.html.

 

 

3                  Boron

3.1              General

Several comprehensive reviews of boron in the environment and its toxicity to humans are available and should be consulted for more detailed information not presented in this summary (ATSDR 2010; WHO 1998; US EPA 2004b). The following provides a summary of the key aspects of boron that are relevant to the derivation of a soil HIL.

 

Boron is never found in its elemental form in nature. The most common boron-containing ores are alkali and alkaline earth borates, including borax (Na4B4O2.10H2O), kernite (Na2B4O7.4H2O), colemanite (Ca2B6O11.5H2O), and ulexite (NaCaB5O9.8H2O), and borosilicate minerals. Common boron-containing compounds used in commerce also include borax pentahydrate, boric acid and boron oxide (ATSDR 2010).

 

Boron and boron compounds are used in the production of products such as fibreglass, soaps, detergents, enamels, frits, glazes, fertilisers, herbicides and fire retardants. They are also used in industries such as metallurgy, chemical synthesis and in nuclear applications (ATSDR 2010).

 

The toxicological database is largest for boric acid and borax and most of the toxicological information for inorganic borates in animals and humans is derived from studies on boric acid and borax (Mangas 1998).

 

Boron is an essential micronutrient for most plants and there is evidence that it is also essential for animals, including humans (ATSDR 2010).

3.2              Previous HIL

The derivation of the previous HIL (HIL A = 3000 mg/kg) for boron is presented by Mangas (1998). In summary, the HIL was derived on the basis of the following:

·         Intakes of boron from other sources were estimated with dietary intakes considered most significant for the general population. Background intakes from dietary exposure (based on US data) and soil (background) were estimated to be 3.23 mg/day for an adult and 1.62 mg/day for infants (half the adult intake).

·         A provisional tolerable daily intake (PTDI) of 14 µg/day was derived for boron based on a NOAEL of 9.6 mg/kg, body weight of 70kg and an uncertainty factor of 48.

·         Ingestion of both soil and dust has been considered, assuming 100% is bioavailable and is absorbed.

·         Dermal absorption has been considered to be low, with a conservative assumption of 1% adopted.

·         Inhalation of boron in dust has been considered both outdoors and indoors, with 10% bioavailability of inhaled boron assumed and the amount of boron in indoor dust assumed to be 75% of that outdoors.

3.3              Significance of Exposure Pathways

Ingestion of soil and dust is considered the most significant pathway of exposure for inorganics in soil. The consideration of bioavailability and inclusion of other exposure pathways in the derivation of a soil HIL has been further reviewed as noted below.

3.3.1        Oral Bioavailability

While bioavailability (inhalation only) has been considered in the previous HIL, insufficient data is available to adequately define the bioavailability of boron. On this basis a default approach of assuming 100% oral (and inhalation) bioavailability has been adopted in the derivation of an HIL. It is noted that a site-specific assessment of bioavailability can be undertaken where required.

3.3.2        Dermal absorption

Dermal absorption of boron is considered to be low. While limited data is available, reviews by WHO (1998), ATSDR (2010) and US EPA (2004b) suggest the boron is not absorbed across intact skin. Review by MfE (2011) has also noted that dermal absorption is considered negligible and has not considered this pathway in the derivation of a soil guideline. It is noted that review of the derived HIL (based on 1% dermal absorption) contributes less than 5% of the HIL, and hence it is considered appropriate that, based on the available data, dermal absorption is not considered a significant pathway in the derivation of a soil HIL. This pathway has not been considered further.

3.3.3        Inhalation of Dust

Boron is not volatile and hence inhalation exposures associated with particulates outdoors and indoors are expected to be of less significance than ingestion of soil. While likely to be negligible, inhalation exposures have been considered in the HIL derived.

3.3.4        Plant Uptake

Review of plant uptake of boron by MfE (2011) has indicated that ‘it has not been possible to develop bioconcentration factors for boron. Reviewing the literature shows that boron uptake into plants is highly variable between species with no relationship with soil concentration or other soil parameters. Boron is an essential element for plant growth, but what may be optimal boron for one species may be toxic or insufficient for other species’. ‘Determining the significance of plant uptake of boron to human exposure is difficult, given the wide-ranging and overlapping concentrations that determine boron essentiality and toxicity in various species. Nonetheless, it appears that 300 mg/kg is a reasonable upper limit of non-toxic plant boron concentrations and thus can be used as the reasonable maximum amount of boron likely to be taken up in home-grown vegetables. Beyond that point vegetables are unlikely to be harvestable.’

 

The approach adopted by MfE (2011) in the derivation of a soil guideline for boron was to consider potential intakes associated with consumption of home-grown produce in soil concentrations that are not phytotoxic (300 mg/kg), as part of the overall intake from other sources. To obtain the additional background intake, a child’s produce consumption (0.048 kg DW[1]/day) was multiplied by 300 mg/kg and divided by the child body weight of 15.5 kg to obtain the maximum additional background daily intake for 100 % of produce being home-grown. For the consumption of 10% home-grown produce, this results in an additional intake of 0.09 mg/kg/day being considered.

 

It is noted that the inclusion of home-grown produce in the calculations presented for HIL A results in some double counting of intakes from fruit and vegetable produce (also included in background intakes). To address this in the derivation of HIL A, half the intake estimated to be derived from home-grown produce is assumed to be already accounted for in the total background intake (noted below). Hence background intakes that may be derived from all sources, including home-grown produce, are estimated to be 0.17 mg/kg/day.

3.3.5        Intakes from Other Sources – Background

No data is available on intakes of boron from sources other than soil in Australia. Hence the assessment of potential intakes from these sources has considered available international data.

 

Reviews of boron (WHO 1998 and ATSDR 2010) suggest that mean intakes of boron from the diet are approximately 1.2 mg/day for adults (and 0.85 mg/day for children), with intakes from consumer products approximately 0.1 mg/day (WHO 1998) and the contribution from air negligible. The total background intake presented by WHO (1998) is 1.9 mg/day. If this intake were assumed relevant for young children, it would comprise 0.13 mg/kg/day for young children. This is slightly higher than that estimated by MfE (2011), where intakes were estimated to be 0.08 mg/kg/day for young children (based on the same databut intakes from water were considered to be lower, based on the available water quality data from New Zealand). The higher value of 0.13 mg/kg/day has been adopted in the derivation of a soil HIL.

3.4              Identification of Toxicity Reference Values

3.4.1        Classification

The International Agency for Research on Cancer (IARC) has not evaluated boron due to inadequate data.

3.4.2        Review of Available Values/Information

Available studies on genotoxicity (US EPA 2004b and WHO 2009) were negative. This is consistent with the review presented by Mangas (1998). On the basis of the available information, it is recommended that a threshold approach be adopted for the derivation of an HIL for boron in soil.  The following are available from Level 1 Australian and International sources:

Source

Value

Basis/Comments

Australian

ADWG (NHMRC 2011)

TDI = 0.16 mg/kg/day

The ADWG (NHMRC 2011) derived a guideline for boron in drinking water on the basis of a TDI of 0.16 mg/kg/day, based on a NOAEL from a developmental rat study (Price et al. 1996) and an uncertainty factor of 60. 

International

WHO (1998)

TDI = 0.4 mg/kg/day

The WHO (1998) review derived a TDI of 0.4 mg/kg/day based on the same study considered in the ADWG (NHMRC 2011) and a different uncertainty factor of 25.

WHO DWG (2009)

TDI = 0.17 mg/kg/day

TDI adopted is consistent with that adopted in the ADWG (NHMRC 2011) and is based on a benchmark dose (BMD) derived from relevant developmental studies of 10.3 mg/kg/day and uncertainty factor of 60. The principal study (noted to be similar to Price et al. 1996) and evaluation is consistent with that presented in the US EPA review (note the US EPA rounded the TDI in its evaluation).

ATSDR (2010)

No evaluation available

 

US EPA (IRIS 2012)

RfD = 0.2 mg/kg/day

 

RfD (last reviewed in 2004) based on a BMD of 10.3 mg/kg/day associated with developmental effects in rats and an uncertainty factor of 66.

 

The ADI currently considered in the ADWG (NHMRC 2011) and by US EPA (2004b) and WHO (2011) are essentially the same value (from studies that have resulted in consistent evaluations), namely 0.2 mg/kg/day. This threshold value is therefore recommended for derivation of the HIL.

 

No inhalation specific studies or data are available. For the presence of boron in soil it is considered appropriate to consider use of the available TDI for all pathways of exposure.

3.4.3        Recommendation

On the basis of the discussion above, the following toxicity reference values (TRVs) have been adopted for boron in the derivation of HILs:

Recommendation for Boron
Oral TRV (TRVO) = 0.2 mg/kg/day (NHMRC 2011 and US EPA 2004b) for all routes of exposure
Inhalation TRV (TRVI) = 0.7 mg/m3 (based on the TRVO assuming body weight of 70 kg and inhalation of 20m3/day)
Dermal absorption factor (DAF) = negligible (0%)
Background intakes for the general population = 0.13 mg/kg/day = 65% of the oral TRV (adopted for HIL B, C and D)
Background intakes, including plant uptake = 0.17 mg/kg/day = 85% of oral TRV (adopted for HIL A)
Background intake assumed relevant for all pathways of exposure (BIO and BIi)

 

3.5              Calculated HILs

On the basis of the above, the following HILs have been derived for boron (refer to Appendix B for equations used to calculate the HILs and Appendix C for calculations):