Appendix 22 – Health Impact Assessment

Residual Waste to Energy Facility, Laverton North: Health Impact Assessment Prepared for: Recovered Energy Australia

21 June 2019

Document History and Status

Report Reference RE/19/WER001 Revision B - Final Date 21 June 2019

Previous Revisions A – Draft issued on 12 June 2019

Limitations

Environmental Risk Sciences has prepared this report for the use of Recovered Energy Australia in accordance with the usual care and thoroughness of the consulting profession. It is based on generally accepted practices and standards at the time it was prepared. No other warranty, expressed or implied, is made as to the professional advice included in this report.

It is prepared in accordance with the scope of work and for the purpose outlined in the Section 1 of this report.

The methodology adopted, and sources of information used are outlined in this report. Environmental Risk Sciences has made no independent verification of this information beyond the agreed scope of works and assumes no responsibility for any inaccuracies or omissions. No indications were found that information contained in the reports provided for use in this assessment was false.

This report was prepared between April and June 2019 and is based on the information provided and reviewed at that time. Environmental Risk Sciences disclaims responsibility for any changes that may have occurred after this time.

This report should be read in full. No responsibility is accepted for use of any part of this report in any other context or for any other purpose or by third parties. This report does not purport to give legal advice. Legal advice can only be given by qualified legal practitioners.

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Table of Contents

Executive Summary ...... ES-1 Section 1. Introduction ...... 1 1.1 Background ...... 1 1.2 Objectives ...... 1 1.3 Approach and scope of works ...... 1 1.4 Definitions ...... 3 1.5 Available information ...... 4 Section 2. Project description ...... 5 2.1 Site description and location ...... 5 2.2 Project description ...... 6 Section 3. Community profile ...... 7 3.1 General ...... 7 3.2 Land uses ...... 7 3.3 Population ...... 7 3.4 Population health ...... 8 Section 4. Community engagement ...... 11 Section 5. Assessment of health impacts: Air emissions ...... 12 5.1 Approach ...... 12 5.2 Modelled air impacts ...... 12 5.3 Conceptual site model ...... 14 5.4 Inhalation exposures ...... 17 General...... 17 Particulates ...... 17 All other pollutants ...... 18 5.5 Multiple pathway exposures ...... 22 General...... 22 Assessment approach ...... 22 Calculated risks ...... 23 5.6 Odour ...... 23 5.7 Uncertainties...... 24 5.8 Outcomes of health impact assessment ...... 26 Section 6. Health impacts: Noise ...... 27 6.1 Approach ...... 27 6.2 Summary of noise assessment ...... 28 General...... 28 Site noise assessment ...... 28 6.3 Health impacts associated with noise ...... 28 6.4 Outcomes of health impact assessment: noise ...... 30

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Section 7. Health impact assessment: Water, economics, transport, hazardous waste, community and social aspects ...... 31 7.1 Approach ...... 31 7.2 Overview and assessment of issues ...... 31 Section 8. Summary of HIA Outcomes ...... 34 Section 9. References ...... 37

Appendices

Appendix A Calculation of risks from PM2.5 Appendix B Methodology and assumptions Appendix C Risk calculations

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Glossary of Terms and Abbreviations

Term Definition ABS Australian Bureau of Statistics Acute exposure Contact with a substance that occurs once or for only a short time (up to 14 days) Absorption The process of taking in. For a person or an animal, absorption is the process of a substance getting into the body through the eyes, skin, stomach, intestines, or lungs Adverse health effect A change in body function or cell structure that might lead to disease or health problems ATSDR Agency for Toxic Substances and Disease Register AAQ Ambient air quality ANZECC Australia and New Zealand Environment and Conservation Council Background level An average or expected amount of a substance or material in a specific environment, or typical amounts of substances that occur naturally in an environment. Biodegradation Decomposition or breakdown of a substance through the action of micro- organisms (such as bacteria or fungi) or other natural physical processes (such as sunlight). Body burden The total amount of a substance in the body. Some substances build up in the body because they are stored in fat or bone or because they leave the body very slowly. Carcinogen A substance that causes cancer. CCME Canadian Council of Ministers of the Environment Chronic exposure Contact with a substance or stressor that occurs over a long time (more than one year) [compare with acute exposure and intermediate duration exposure]. CO Carbon monoxide DECCW NSW Department of Environment, Climate Change and Water DEFRA Department for Environment, Food & Rural Affairs DEH Australian Department of Environment and Heritage Dose The amount of a substance to which a person is exposed over some time period. Dose is a measurement of exposure. Dose is often expressed as milligram (amount) per kilogram (a measure of body weight) per day (a measure of time) when people eat or drink contaminated water, food, or soil. In general, the greater the dose, the greater the likelihood of an effect. An ‘exposure dose’ is how much of a substance is encountered in the environment. An ‘absorbed dose’ is the amount of a substance that actually got into the body through the eyes, skin, stomach, intestines, or lungs. Exposure Contact with a substance by swallowing, breathing, or touching the skin or eyes. Also includes contact with a stressor such as noise or vibration. Exposure may be short term [acute exposure], of intermediate duration, or long term [chronic exposure]. Exposure assessment The process of finding out how people come into contact with a hazardous substance, how often and for how long they are in contact with the substance, and how much of the substance they are in contact with.

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Term Definition Exposure pathway The route a substance takes from its source (where it began) to its endpoint (where it ends), and how people can come into contact with (or get exposed) to it. An exposure pathway has five parts: a source of contamination (such as chemical substance leakage into the subsurface); an environmental media and transport mechanism (such as movement through groundwater); a point of exposure (such as a private well); a route of exposure (eating, drinking, breathing, or touching), and a receptor population (people potentially or actually exposed). When all five parts are present, the exposure pathway is termed a completed exposure pathway. Genotoxic carcinogen These are carcinogens that have the potential to result in genetic (DNA) damage (gene mutation, gene amplification, chromosomal rearrangement). Where this occurs, the damage may be sufficient to result in the initiation of cancer at some time during a lifetime. Guideline value Guideline value is a concentration in soil, sediment, water, biota or air (established by relevant regulatory authorities such as the NSW Department of Environment and Conservation (DEC) or institutions such as the National Health and Medical Research Council (NHMRC), Australia and New Zealand Environment and Conservation Council (ANZECC) and World Health Organization (WHO)), that is used to identify conditions below which no adverse effects, nuisance or indirect health effects are expected. The derivation of a guideline value utilises relevant studies on animals or humans and relevant factors to account for inter and intra-species variations and uncertainty factors. Separate guidelines may be identified for protection of human health and the environment. Dependent on the source, guidelines would have different names, such as investigation level, trigger value and ambient guideline. HI Hazard Index IARC International Agency for Research on Cancer Inhalation The act of breathing. A hazardous substance can enter the body this way [see route of exposure]. Intermediate exposure Contact with a substance that occurs for more than 14 days and less than a Duration year [compare with acute exposure and chronic exposure]. LGA Local Government Area LOR Limit of Reporting Metabolism The conversion or breakdown of a substance from one form to another by a living organism. NEPC National Environment Protection Council NEPM National Environment Protection Measure NHMRC National Health and Medical Research Council NO2 Nitrogen dioxide NOx Nitrogen oxides NSW New South Wales NSW EPA NSW Environment Protection Authority OEH NSW Office of Environment and Heritage OEHHA Office of Environmental Health Hazard Assessment, California Environment Protection Agency (Cal EPA) PM Particulate matter PM2.5 Particulate matter of aerodynamic diameter 2.5 µm and less PM10 Particulate matter of aerodynamic diameter 10 µm and less Point of exposure The place where someone can come into contact with a substance present in the environment [see exposure pathway]. Population A group or number of people living within a specified area or sharing similar characteristics (such as occupation or age).

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Term Definition Receptor population People who could come into contact with hazardous substances [see exposure pathway]. Risk The probability that something would cause injury or harm. Route of exposure The way people come into contact with a hazardous substance. Three routes of exposure are breathing [inhalation], eating or drinking [ingestion], or contact with the skin [dermal contact]. SEIFA Socio-Economic Index for Areas SO2 Sulfur dioxide TCEQ Texas Commission on Environmental Quality Toxicity The degree of danger posed by a substance to human, animal or plant life. Toxicity data Characterisation or quantitative value estimated (by recognised authorities) for each individual chemical substance for relevant exposure pathway (inhalation, oral or dermal), with special emphasis on dose-response characteristics. The data are based on based on available toxicity studies relevant to humans and/or animals and relevant safety factors. Toxicological profile An assessment that examines, summarises, and interprets information about a hazardous substance to determine harmful levels of exposure and associated health effects. A toxicological profile also identifies significant gaps in knowledge on the substance and describes areas where further research is needed. Toxicology The study of the harmful effects of substances on humans or animals. TSP Total suspended particulates UK United Kingdom US United States USEPA United States Environmental Protection Agency WHO World Health Organization µg/m3 Micrograms per cubic metre

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Executive Summary Environmental Risk Sciences Pty Ltd (enRiskS) has been engaged by Recovered Energy Australia (REA) with a proposal to undertake a Health Impact Assessment (HIA) for a Residual Waste to Energy (WtE) Project at 24 Alex Fraser Drive in Laverton North, 18 km to the west of the Melbourne CBD in Victoria (the “site”).

The WtE Project relates to the use of waste separated from the general waste stream (from Melbourne local municipal areas), converting this to electricity using a gasification technology to generate steam.

The HIA has been undertaken to evaluate potential impacts and benefits of the proposed project to community health and wellbeing. The assessment has been prepared on the basis of existing information on the operation of the proposed facility and specialist studies that relate to impacts to air quality, noise, odour, waste management, transport.

Based on the assessment undertaken the following has been concluded:

◼ Air emissions: Where the facility is operating under normal operating conditions there are no risks to the health of workers in adjacent industrial areas or residents in the surrounding community. Even where upset operating conditions are considered, there are no risks to the health of workers in adjacent industrial areas or residents in the surrounding community. ◼ Odours: There are no odour impacts from the proposed facility for residents in the surrounding community. There is the low potential for odours to be noticeable on the southern site boundary, which would not affect local industry. ◼ Noise: There are no noise impacts from the proposed facility that would impact ion the health of the community. ◼ Water: There are no water impacts that would affect the health of the community. ◼ Transport: There are no impacts on community health and safety. ◼ Safety: There are no safety or hazard risks that would affect the local community. ◼ Employment: The project has some benefits to health in terms of employment, with these benefits to be enhanced through encouraging employment from local areas at the facility. ◼ Social: The project has the potential to provide enhancing feelings of wellbeing for aspects such as sustainability.

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Section 1. Introduction 1.1 Background Environmental Risk Sciences Pty Ltd (enRiskS) has been engaged by Recovered Energy Australia (REA) with a proposal to undertake a Health Impact Assessment (HIA) for a Residual Waste to Energy (WtE) Project at 24 Alex Fraser Drive in Laverton North, 18 km to the west of the Melbourne CBD in Victoria (the “site”).

The WtE Project relates to the use of waste separated from the general waste stream (from Melbourne local municipal areas), converting this to electricity using a gasification technology to generate steam.

It is understood that a Works Approval Application (WAA) has been submitted for the proposed project, which included a number of key specialist studies to support the application. EPA Victoria has subsequently requested that a HIA be completed for the project. In addition, the EPA provided a scope of what the HIA needs to address.

1.2 Objectives The objective of the HIA presented in this report is to assess potential impacts to community health in relation to the operation of a proposed WtE facility in Laverton North.

The focus of the HIA relates to impacts on community health. The HIA has not addressed any worker health and safety risks relevant to the operation of the facility.

1.3 Approach and scope of works The HIA has been undertaken in accordance with the following guidance (and associated references as relevant):

◼ Environment Protection Act 1970 (EP Act); ◼ enHealth, 2017. Health Impact Assessment Guidelines (enHealth 2017); ◼ enHealth, 2012. Environmental Health Risk Assessment: Guidelines for Assessing Human Health Risks from Environmental Hazards (enHealth 2012a); ◼ enHealth, 2012. Australian Exposure Factor Guidance – Guidelines for Assessing Human Health Risks from Environmental Hazards (enHealth 2012b); and ◼ Harris, P., Harris-Roxas, B., Harris, E. & Kemp, L., Health Impact Assessment: A Practical Guide, Centre for Health Equity Training, Research and Evaluation (CHETRE). Part of the UNSW Research Centre for Primary Health Care and Equity. University of New South Wales, Sydney, 2007 (Harris 2007).

While the conduct of the HIA does not involve any additional air quality modelling, as that has been completed by others for the WAA, the HIA does draw on the air quality modelling undertaken and provides an assessment of health impacts. Where the air modelling aspects are considered, the following guidance will be considered (where relevant):

◼ State Environment Protection Policy (Air Quality Management) No. S240, Gazette 21/12/2001 (SEPP AQM)

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◼ EPA Victoria 2013. Publication 1551 – Guidance Notes for Using the Regulatory Air Model AERMOD in Victoria (Publication 1551) The above guidance for the conduct of HIA requires the consideration of impacts that relate to a wider definition of health and well-being within the community. Health and health inequalities are affected by a wide range of factors, as illustrated below. These factors may be affected by a specific project in different ways. In some cases, the changes will result in negative impacts on health (and hence the HIA needs to determine what these impacts are and how they can be minimised) or positive impacts or benefits (and it is important that the HIA identify these and determine if these benefits can be enhanced).

Figure 1: Wider determinants of health, as presented by Harris et al (2007)

HIA has been undertaken as a desk-top assessment, based on information available from other available specialist studies that relate to impacts to air quality, noise, odour, waste management, transport. Where relevant the HIA has identified where any additional mitigation may be required and areas where measures may be considered to enhance positive health impacts (benefits) of the project.

To address the above scope of works the HIA has presented the following:

◼ Identification of the community of concern – this is the location and characteristics of the population surrounding the site (Section 3). ◼ Assessment of health impacts from air emissions – this is a quantitative assessment of potential community health impacts from changes in air quality as a result of the operation of the facility (Section 5). ◼ Assessment of health impacts from changes in noise – this is a qualitative assessment of potential community health impacts from changes in noise as a result of the operation of the facility (Section 6). ◼ Assessment of other health impacts relevant to the operation of the facility, including odour, waste management issues such as fire hazards, and changes in traffic. The benefits of the project will also be presented (where relevant to health) (Section 7). ◼ Uncertainty and sensitivity assessment (Section 5.7)

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◼ Conclusions (Section 8)

1.4 Definitions For the conduct of the HIA the following definitions are relevant and should be considered when reading this report.

Health: The World Health Organisation defines health as “a (dynamic) state of complete physical, mental and social wellbeing and not merely the absence of disease or infirmity”.

Hence the assessment of health should include both the traditional/medical definition that focuses on illness and disease as well as the more broad social definition that includes the general health and wellbeing of a population.

Health Hazard: These are aspects of a Project, or specific activities that present a hazard or source of negative risk to health or well-being.

In relation to the HIA these hazards may be associated with specific aspects of the proposed development/construction or operational activities, incidents or circumstances that have the potential to directly affect health. In addition, some activities may have a flow-on effect that results in some effect on health. Hence health hazards may be identified on the basis of the potential for both direct and indirect effects on health.

Health Outcomes: These are the effects of the activity on health. These outcomes can be negative (such as injury, disease or disadvantage), or positive (such as good quality of life, physical and mental wellbeing, reduction in injury, diseases or disadvantage).

It is noted that where health effects are considered these are also associated with a time or duration with some effects being experienced for a short period of time (acute) and other for a long period of time (chronic). The terminology relevant to acute and chronic effects is most often applied to the assessment of negative/adverse effects as these are typically the focus of technical evaluations of various aspects of the project.

Likelihood: This refers to how likely it is that an effect or health outcome will be experienced. It is often referred to as the probability of an impact occurring.

Risk: This is the chance of something happening that will have an impact on objectives. In relation to the proposed project and the conduct of the HIA, the concept of risk more specifically relates to the chance that some aspect of the project will result in a reduction or improvement in the health and/or well-being of the local community. The assessment of risk has been undertaken on a quantitative basis for air, water and noise emissions and a qualitative basis for all other impacts. This is in line with the methods and levels of evidence currently available to assess risk.

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Equity:

Equity relates to the potential for the project to lead to impacts that are differentially distributed in the surrounding population. Population groups may be advantaged or disadvantaged based on age, gender, socioeconomic status, geographic location, cultural background, aboriginality, and current health status and existing disability.

1.5 Available information In relation to the proposed project, the HIA has been undertaken on the basis of existing information which is available in the following reports:

◼ Edge 2019, Air Quality Impact Assessment (AQIA). Report dated June 2019 ◼ REA 2019, Works Approval Application (WAA), Laverton North, Residual Municipal Solid Waste Gasification to Energy. Report dated January 2019. Including appendices referenced and utilised in the HIA: o One Mile Grid 2018, Traffic Impact Assessment, Renewable Energy Generation Facility. Appendix 12 of WAA, dated 14 May 2018 o Edge 2018, Noise Sensitivity Analysis Assessment. Appendix 16 of the WAA, dated December 2018 o Preliminary Hazard Analysis (PHA), Appendix 19 of the WAA.

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Section 2. Project description 2.1 Site description and location The site is located within an industrial precinct located 15 kilometres west of Melbourne at 24 Alex Fraser Drive, Laverton North (refer to Figure 1). The surrounding area is predominantly industrial with the closest residential dwelling residing at a distance of 1.8 kilometres south from the site and the prison receptor approximately 1.3 kilometres west of the site. The site, and adjacent properties are zoned industrial zone 2 (IN2) within the Wyndham Planning Scheme.

Figure 1: Site location and setting

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2.2 Project description The project is a municipal solid waste gasification to energy facility, with municipal solid waste (MSW) used to provide steam and heat to local industry and 15 megawatts (MW) power to the national grid.

The fuel source is approximately 600 tonnes per day of residual household waste and residual waste from sorting facilities. The facility will not accept hazardous waste or prescribed industrial waste.

The waste will go through a two-stage process which includes (as shown in the figure below):

1. gasification in a high temperature and low oxygen environment (within the gasification chamber). This means that rather than combust, the waste is decomposed rapidly to produce a gas similar to natural gas, called syngas. 2. combustion of the syngas at a high temperature in a separate oxidation chamber. Heat recovered from the combustion of the syngas will be directed to a boiler system which converts the heat into super-heated steam which is then used to drive a steam turbine and generator to produce electricity.

Flue gas exiting the combustion chamber is treated using an acid scrubber (to remove acid gases and sulfur dioxide), activated carbon (to remove organic compounds) and particle filters prior to discharge to air via a stack. In addition, a SCNR will be used to remove oxides of nitrogen.

Figure 2: Diagram of proposed gasification WtE process

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Section 3. Community profile 3.1 General This section provides an overview of the community potentially impacted by the proposed project. It is noted that the key focus of this assessment is the local community surrounding the site.

3.2 Land uses The site is located in an industrial area of Laverton North, with the closest residential areas located 1.3 kilometres to the west (prison) and 1.8 kilometres to the south and southwest (refer to Figure 1) are low density urban residential properties within the suburb of Williams Landing and Laverton. Other, new residential properties are being constructed further west (more than 2.5 km) in the suburb of Trugania. All these areas sit within the City of Wyndham and Hobsons Bay City Council local government areas (LGAs)

These residential areas are low-density properties where there is sufficient garden area for the growing of some fruit and vegetables.

Within the City of Wyndham and Hobsons Bay City Council area chickens may be kept, however farm animals (which include horses, sheep, pigs, goats and cattle) are not permitted in residential areas1.

Based on the above, there is the potential for residential areas surrounding the site to include some homegrown fruit and vegetables and keep chickens for eggs. However other livestock raised for meat or milk are precluded.

3.3 Population Table 1 presents a summary of the populations in Williams Landing, Laverton and Laverton North (based on 2016 Census and 2016 Socio-Economic data from the Australian Bureau of Statistics) in comparison to Victoria and Australian populations.

1 https://www.wyndham.vic.gov.au/sites/default/files/2016-06/Keeping%20Pets%20in%20Wyndham.pdf https://www.hobsonsbay.vic.gov.au/Services/Pets-Animals/Animal-Pet-Permits?BestBetMatch=chicken|d13b95b2-5146- 4b00-9e3e-a80c73739a64|4f05f368-ecaa-4a93-b749-7ad6c4867c1f|en-AU

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Table 1: Summary of populations surrounding the proposed project site (ABS Census 2016)

Indicator Suburb or Statistical Area Victoria Australia Laverton North Williams Landing Laverton Total population 73 6646 4915 5926624 23401892 Population 0 - 4 years 0 13.3% (884) 7.1% (350) 6.3% (371220) 6.3% (1464779) Population 5 - 19 years 4.1% (3) 17.8% (1182) 14.4% (709) 18.0% 18.5% (1066042) (4321427) Population 20 - 64 years 75.3% (55) 66.9% (4448) 69.2% (3402) 60.2% 59.6% (3566775) (13938918) Population 65 years and 21.9% (16) 2.4% (150) 9.4% (463) 15.6% 15.7% over (922598) (3676758) Median age 52 31 31 37 38 Household size 1.2 3.3 2.7 2.6 2.6 Unemployment NA 8.6% 10.7% 6.6% 6.9% Tertiary education NA 23.2% 29% 23.5% 22% SEIFA IRSAD 635 1090 912 -- -- SEIFA rank 1 5 1 -- -- SEIFA IRSD 610 1075 908 -- -- SEIFA rank 1 5 1 -- -- Indigenous NA 0.2% 1.1% 0.8% 2.8% Born overseas NA 61.4% 58.1% 28.4% 26.3% NA as population size in Laverton North is too small for this information to be presented by the ABS SEIFA IRSAD = index of socioeconomic advantage and disadvantage, rank relates to rank in Australia that ranges from 1 = most disadvantaged to 5 = most advantaged SEIFA IRSD = index of socioeconomic disadvantage, rank relates to rank in Australia that ranges from 1 = most disadvantaged to 5 = least disadvantaged Shading relates to comparison against Victoria: lower than; greater than (note these comparisons not used for Laverton North as the population is too small to be meaningful)

Based on the population data available and presented in Table 1, the community surrounding the site (in general), has a higher proportion of working aged individuals (and children aged 0-4 years in Williams Landing), with higher levels of unemployment and proportion of the population that is born overseas. These suburbs have a lower proportion of people aged 65 years and older (and children aged 5-19 years in Laverton) reflecting the greater proportion of people of a working age. These suburbs show very distinctly different indexes for socioeconomic advantage and disadvantage, with Williams Landing being most advantaged (compared to the Victorian population) and Laverton (and Laverton North) being most disadvantaged (compared with the Victorian population).

The indicators outlined in Table 1 generally reflect the vulnerability of the population, its ability to adapt to environmental stresses, and are important to highlight from an equity point of view. The project will be implemented within a community may has some increased susceptibility to impacts from the project (should these be of significance).

3.4 Population health The health of the community is influenced by a complex range of interactive factors including age, socio-economic status, social capital, behaviours, beliefs and lifestyle, life experiences, country of origin, genetic predisposition and access to health and social care. The health indicators available and reviewed in this report (Table 2) generally reflect a wide range of these factors.

The population adjacent to the proposed site is relatively small and health data is not available that specifically relates to this population. However, it is assumed that the health of the local community is consistent with that reported in the larger LGAs of Wyndham and Hobsons Bay.

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Table 2 presents a summary of the general population health considered relevant to the area. The table presents available information on health-related behaviours (i.e. key factors related to lifestyle and behaviours known to be of importance to health) and indicators for the burden of disease within the community compared to Victoria. It is noted that in relation to health behaviours the Victorian Population Health Surveys only collect data on adults. Hence there is no data available that is considered current and relevant to children.

Table 2: Summary of health indicators/data

Health indicator/data Wyndham LGA Hobsons Bay LGA Victoria Health behaviours Adults - compliance with fruit 43.5% (37.5% - 49.6%) 53.6% (44.8% - 62.3%) 47.8% (46.6% - 49.0%) consumption guidelines (2014)1 Adults - compliance with vegetable 3.4% (2.0% - 5.5%) 7.1% (3.6% - 13.5%) 6.4% (5.9% - 6.8%) consumption guidelines (2014)1 Adults - increased lifetime risk of alcohol 51.7% (46.3% - 57.2%) 60.1% (51.9% - 67.8%) 59.2% (58.0% - 60.3%) related harm (2014) 1 Adults - body weight (preobese or 58.9% (51.7% - 63.8%) 51.6% (42.9% - 60.3%) 50.0 % (48.5% - obese) (2014) 1 52.4%) Adults – insufficient physical activity 55.1% (48.9% - 61.0%) 48.5% (40.5% - 53.1%) 50.4% (49.2% - 51.5%) (2014) 1 Current smoker (2014) 1 13.1% (9.7% - 17.4%) 11.8% (8.3% - 16.5%) 13.1% (12.3% - 14.0%) Adults – self-reported health status as 25.8% (20.9% - 31.3%) 17.5% (13.3% - 22.8%) 20.3% (19.4% - 21.3%) ‘Fair/poor’ (2014) 1 Burden of disease Morbidity - cardiovascular disease 2896.3* 2428.4* 2229.4* hospitalisations (2016/17)3 Morbidity – respiratory disease 1998.2* 1846.3* 1913.4* hospitalisations (2016/17)3 Mortality – all causes (2016)2 589.6* 513.9* 553.9* (Australia) Children (school entrant) – prevalence of 8.7% 9.5% 12.2% asthma (2016)4 * Rate per 100,000 population (age-standardised) 1 Data from Victorian Population Health Survey 2014 (Department of Health and Human Services 2016) (noting that this is the most recent survey where data is available for LGAs) 2 Data from Mortality Over Regions and Time (MORT) books, LGAs, 2012-2016 3 Age standardised ratio - data relevant to the years 2016-2017 from the Social Health Atlas of Australia, Victoria (as published February 2019), http://phidu.torrens.edu.au/social-health-atlases/data#social-health-atlases-of-australia-local-government- areas 4 Data available from School Entrant Health Questionnaire, 2017 https://www.education.vic.gov.au/about/research/Pages/reportdatahealth.aspx Shading relates to comparison against Victoria: statistic/data suggestive of a potential higher vulnerability within the population to health stressors

statistic/data suggestive of a potential lower vulnerability within the population to health stressors

statistics/data different to that of Victoria, but this indicator is not a clear determinant of only higher or lower vulnerability to health stressors

In general, the key indicators of health for the population in the Wyndham and Hobsons Bay LGAs are somewhat similar to those for Victoria, with adult rates of overweight and obesity and adequate consumption of vegetables in the Wyndham LGA suggesting a population that is potential more vulnerable to health stressors. However the population indicators for Hobsons Bay LGA for vegetable intakes and Wyndham for long-term risk alcohol consumption suggests lower vulnerability. Higher rates of cardiovascular disease and lower rates of respiratory disease and prevalence of childhood asthma are also noted.

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This data, along with data presented in Table 1, suggest the population in the areas surrounding the site may not be more sensitive (in terms of health) to impacts derived from the proposed WtE facility.

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Section 4. Community engagement Section 4 of the WAA provides information on the community engagement activities undertaken in relation to the project as well details in relation to the Community Engagement Plan (CEP). The community consultation works undertaken have included consultation with a range of stakeholders including neighbours, state government, Wyndham City Council, Statutory and regulatory agencies/authorities, community groups, broader industry and environmental groups and the local media.

The CEP includes a wide range of activities and methods for community engagement, as well as the activities (including all meetings) conducted to date. A summary of the issues raised by stakeholders as part of the community engagement process are listed in Section 4 of the WAA. No specific health issues were raised, however issues relating more generally to aspects such as pollution, noise and odour, all of which are addressed in the HIA form a community health perspective.

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Section 5. Assessment of health impacts: Air emissions 5.1 Approach This section presents a review of impacts on health associated with predicted air emissions, relevant to the operation of the facility. The assessment presented has relied on the Edge (2019) AQIA.

The characterisation of risk follows the general principles outlined in the enHealth document Environmental Health Risk Assessment: Guidelines for Assessing Human Health Risks from Environmental Hazards (enHealth 2012a).

5.2 Modelled air impacts To predict the concentration of emissions from the proposed WtE facility, a study area was defined (Figure 3) and predicted emissions from the stack were modelled using the AEROMOD air dispersion model, which is the Victorian EPA regulatory dispersion model. This model uses air emissions estimates (as noted above), plant design (for example stack location and height), local terrain and meteorological data to predict the ground level concentrations and deposition of pollutants within a defined study area, and more specifically at the residential receptor locations.

The modelling undertaken predicted concentrations and deposition rates over a grid covering an area of 4 km x 4 km, with a 50 m spacing. In addition, three sensitive receptors were included (refer to Figure 3):

◼ 2 residential receptors CDR1 and CDR2, which are the closest residential properties to the site, and; ◼ 1 prison receptor CDR3 located approximately 1.3 km to the west.

These three receptors have been considered to represent the closest and most sensitive residential receptors in the HIA.

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Figure 3: Modelling domain and sensitive receptor locations (Edge 2019)

Emissions from the facility were based on data provided from reference plants as discussed by Edge (2019). Based on the available emissions data, the AQIA has presented the following scenarios:

◼ Normal operating conditions – based on average emissions concentrations, representing steady-state operating conditions for the proposed facility; and ◼ Upset conditions – based on the maximum emissions concentrations.

The emissions evaluated in the AQIA has also considered the Industrial Emissions Directive (IED) limits.

The emissions considered in the AQIA relate to oxides of nitrogen (NOx), sulfur dioxide (SO2), carbon monoxide (CO), particulates as PM10 and PM2.5, hydrogen fluotride (HF), hydrogen chloride (HCl), fluoride, metals (lead, mercury, cadmium, antimony, arsenic, chromium, copper, manganese, nickel) and dioxins and furans. In addition, to address Victorian EPA Schedule A compounds, representative compounds of beryllium (and beryllium compounds) and diphenylmethane diisocyanate (MDI) and toluene diisocyanate (TDI) were also modelled, based on assumed emission rates, not from any measurement that shows that these compounds are, or likely

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to be present in the emissions or any measured emission rates. Hence inclusion of these compounds, particularly MDI and TDI in the AQIA is considered conservative. For the HIA, beryllium has been evaluated as well as MDI (assuming 100% of MDI and TDI is present as PDI) with this compound only relevant to be evaluated for inhalation exposures (due to its very short half life in air). For chromium, it is assumed that the total chromium reported comprises 10% chromium VI. In addition, it was assumed that 100% of NOx was present in the atmosphere as NO2.

Background, or existing pollutant concentrations were obtained from the EPA Victoria air monitoring station at Altona North.

The maximum predicted impacts over the whole grid (which are representative of commercial/industrial areas close to the site) and at the closest residential receptors have been used in the HIA. The modelling undertaken by Edge (2019) provided 1 hour average and annual average air concentrations for use in the HIA, as well as deposition rates for pollutants present in a particulate form.

Odour was also assessed in the AQIA, based on receiving 200,000 tonnes per annum with deliveries anytime between 6am and 6pm, 7 days per week. The receival area is within the facility building which has a roller door. It was assumed that the roller door would be open for 30 minutes of every hour for 24 hours of the day to account for truck movements.

5.3 Conceptual site model Understanding how a community member may come into contact with pollutants released in air emissions from the proposed WtE facility is a vital step in assessing potential health risk from these emissions. A conceptual site model provides a holistic view of these exposures, outlining the ways a community may come in contact with these pollutants.

There are three main ways a community member may be exposed to a chemical substance emitted from the WtE facility:

• inhalation (breathing it in) • ingestion (eating or drinking it) or • dermally (absorbing it through the skin).

For some of the emissions from the proposed WtE facility, inhalation is considered the only route of exposure. This is due to the substance’s chemical properties, which make the other pathways inconsequential. In this instance, gases such as NO2, SO2, HCl, HF and CO as well as fine particulate matter as particulates less than 10 micrometres (PM10) and particulate matter less than

2.5 micrometres (PM2.5) that are so small they remain suspended in air could be considered in this class (i.e. inhalation only exposure pathway). The composition of the fine particulates, comprising metals and organics are also important from a inhalation perspective.

Other emissions may be inhaled, but also may be deposited on the ground. These emissions can then be ingested either directly through incidental consumption of soil/dust or indirectly through food grown or raised in the soil (fruit, vegetables and eggs – which may be present in urban yards). Skin contact with the soil is also possible. Therefore, it is important with these emissions that all three exposure pathways are considered. In this instance, metals and organics that are bound to the

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heavier particulate matter that may fall out and deposit onto the ground could be considered in this class.

Table 3 lists the substances considered in the WtE emissions and the exposure pathway/s of potential concern. Figure 4 provides a diagrammatical representation of the community exposures to emissions from the WtW facility (conceptual site model).

Table 3: Substances and routes of exposure

Substance Route of exposure Nitrogen dioxide (NO2) Sulfur dioxide (SO2) Hydrogen chloride (HCl) Inhalation only as these are gases Hydrogen fluoride (HF) Carbon monoxide (CO) Diphenylmethane Inhalation only as this compound likely to be present as vapour and has a very short diisocyanate (MDI) half-life in air PM10 Inhalation only as these particulates are very small and will remain suspended in air. It is noted that other exposure pathways have also been assessed for the individual PM2.5 chemical substances bound to these particles. These other pathways relate to the individual chemical substances, rather than the physical size of the particulates.

Antimony Arsenic Beryllium Inhalation of these pollutants adhered to fine particulates Cadmium Ingestion and dermal contact with these pollutants deposited to soil Chromium Ingestion of produce grown in soil potentially impacted by these pollutants (i.e. Copper homegrown fruit and vegetables and eggs – where the pollutants can be taken Lead up/bioaccumulated into plants and animals). Manganese As the area surrounding the site is a low-density urban area, the raising of livestock Mercury for meat or milk is not permitted and has not been assessed. Nickel Dioxins & furans

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Figure 4: Conceptual site model (illustrative only)

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5.4 Inhalation exposures General For all the pollutants released to air from the proposed facility, whether present as a gas or as particulates, there is the potential for the community to be exposed via inhalation. Assessment of potential health impacts relevant to inhalation exposures for these pollutants is discussed further below.

Particulates The assessment of potential health impacts associated with exposure to particulate matter, based on the size of the particulate matter, rather than composition, has been undertaken and presented

Edge (2019). The assessment has focused on fine particulates, as both PM10 and PM2.5, which are small enough to reach deep into the lungs. PM2.5 in particular, have been linked with, and shown to be causal, for a wide range of health effects (USEPA 2012, 2018; WHO 2013). These health effects were considered in the derivation of the NEPM air guideline for PM10 and PM2.5 (NEPC 2016).

The NEPM criteria relate to total exposures to PM10 and PM2.5, that is background or existing levels as well as the additional impact from the proposed facility.

Table 4 provides a summary of the contribution of the project to the total PM10 and PM2.5 concentrations, and the NEPM air criteria. This table shows that the maximum PM10 and PM2.5 derived from the facility makes a negligible contribution to existing concentrations and only makes up a very small fraction of the NEPM guideline. The total concentration (background pus project) remains less than the NEPM guideline. Note that 24-hour average background concentrations were not identified for PM10 or PM2.5 by Edge (2019).

Table 4: PM10 and PM2.5 impacts from the project – maximum residential receptor

3 3 Parameter PM2.5 (µg/m ) PM10 (µg/m ) 24-hour average Annual average 24-hour average Annual average Guideline (NEPM 2016) 25 8 50 30 Background NA 7 NA 21 Normal operating conditions Contribution from project 0.345 0.0215 0.345 0.0215 Total (background plus -- 7 -- 21 project) % contribution of project to 1.4% 0.27% 0.7% 0.07% NEPM % contribution of project to -- 0.31% -- 0.1% background Upset operating conditions Contribution from project 0.86 0.054 0.86 0.054 Total (background plus -- 7 -- 21 project) % contribution of project to 3.4% 0.7% 1.7% 0.2% NEPM % contribution of project to -- 0.8% -- 0.26% background

In addition to the analysis presented above, it is possible to also estimate the incremental individual risk associated with the change in PM2.5 from the facility. This calculation has been undertaken on

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the basis of the most significant health indicator, namely mortality, for which changes in PM2.5 have been identified to have a causal relationship. It is noted that the relationship for PM10 not as strong, hence the focus is on exposures to PM2.5. The health indicator also captures a wide range of other health effects associated with PM2.5.

The calculation has considered the baseline mortality rate for Wyndham LGA of 589.6 per 100,000 for 2016 (all ages and all causes) (refer to Table 2), along with the exposure-response relationship relevant to assessing all-cause mortality for PM2.5. Further details and calculations are presented in Appendix A. These calculations assume that someone is present at the location of maximum increase in PM2.5 from the facility for 24 hours a day, every day of the year.

3 For a maximum annual increase of PM2.5 of 0.054 µg/m for upset conditions in residential areas, this results in a maximum individual risk of 2 x 10-6. This risk level is considered to be low and below the mortality risk criteria outlined by NEPM (NEPC 2011).

On the basis of the above, changes in PM2.5 (and PM10) derived from the project are considered to have a negligible impact on the health of the community.

All other pollutants For all other pollutants, inhalation exposures have considered both short-term/acute exposures as well as chronic exposures.

Acute exposures

The assessment of acute exposures is based on comparing the maximum predicted 1-hour average concentration with health-based criteria relevant to an acute or short-term exposure, also based on a 1-hour average exposure time. The ratio of the maximum predicted concentration to the acute guideline is termed a hazard index (HI).

For this assessment, the maximum predicted 1-hour average concentration from all receptors (noting that the maximum will be in the commercial/industrial area) has been considered. This has been done to address acute inhalation exposures that may occur in all areas, including industrial areas, and this will be conservative for residential areas. Table 5 presents a summary of the relevant health-based guideline, the predicted maximum 1-hour average concentration and the calculated HI for each pollutant.

The assessment of exposures to nitrogen dioxide (NO2) and sulfur dioxide (SO2) has utilised the NEPM guidelines that are protective of health. Risks associated with these pollutants are not considered to be additive. However, potential exposures to all other gases and chemical substances attached to fine particulates have been assumed to be additive and the total HI (the sum of all individual HI’s) is also presented.

Risks associated with acute exposures are considered to be acceptable where the individual and total HI’s are less than or equal to 1. Based on the assessment presented in Table 5, all the individual and total HI’s are less than 1.

On this basis there are no acute risk issues of concern in relation to inhalation exposures.

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Table 5: Review of acute exposures and risks (maximum receptor anywhere)

Air Concentration (mg/m3) Calculated HI Pollutants Acute air Maximum - Maximum - Maximum - Maximum guideline (1- Normal Upset Normal - Upset hour average) (mg/m3) NEPM pollutants 1 Nitrogen dioxide (NO2) 0.22 1.2E-02 4.3E-02 0.056 0.2 1 Sulfur dioxide (SO2) 0.5 6.5E-03 1.3E-02 0.013 0.026 Other pollutants Hydrogen chloride (HCl) 0.662 2.5E-04 1.6E-03 0.00038 0.0023 Hydrogen fluoride (HF) 0.062 2.3E-05 2.3E-05 0.00038 0.00038 Cadmium 0.00542 7.9E-08 2.0E-07 0.000015 0.000037 Beryllium 0.00234 2.3E-07 2.3E-07 0.00010 0.00010 Mercury 0.00063 4.8E-07 2.0E-06 0.00080 0.0033 Antimony 1.54 7.4E-07 2.2E-06 0.00000049 0.0000015 Arsenic 0.0032 2.4E-05 7.4E-05 0.0080 0.025 Lead 0.154 1.2E-05 2.4E-05 0.000080 0.00016 Chromium (Cr VI assumed) 0.00132 9.0E-07 4.8E-06 0.00069 0.0037 Copper 0.13 1.3E-06 3.3E-06 0.000013 0.000033 Manganese 0.00912 1.9E-06 5.5E-06 0.00021 0.00060 Nickel 0.00112 4.1E-06 1.8E-05 0.0037 0.016 Dioxins and furans 0.000134 1.1E-11 2.3E-11 0.000000085 0.00000018 MDI and TDI 0.0123 1.4E-05 1.4E-05 0.0012 0.0012 Total HI (other pollutants) 0.016 0.053 Target (acceptable HI) ≤ 1 ≤ 1 References for health-based acute air guidelines (1-hour average): 1 = NEPM health based guideline (NEPC 2016) 2 = Guideline available from the Texas Commission on Environmental Quality (TCEQ), https://www.tceq.texas.gov/toxicology/dsd/final.html 3 = Guideline available from California Office of Environmental Health Hazard Assessment (OEHHA) https://oehha.ca.gov/air/general- info/oehha-acute-8-hour-and-chronic-reference-exposure-level-rel-summary 4 = Guideline available from the USEPA as Protective Action Criteria (PAC), where the most conservative value has been adopted https://www.energy.gov/ehss/protective-action-criteria-pac-aegls-erpgs-teels-rev-29-chemicals-concern-may-2016

Chronic exposures

For the assessment of chronic exposures, all the pollutants evaluated have a threshold guideline value that enables the predicted annual average concentration to be compared with a health based, or acceptable, guideline. For the assessment of chronic effects, the assessment has also considered potential intakes of these chemical substances from other sources, i.e. background intakes. As a result, the HI is calculated as follows:

Exposure Concentration HI= (Health based criteria or Tolerable Concentration (TC))x(100%-Background)

Where: Exposure concentration = concentration in air relevant to the exposure period – annual average (mg/m3) Health based criteria or TC = health-based threshold protective of all health effects for the community (mg/m3) Background = proportion of the TC that may be derived from other sources/exposures such as water, soil or products (%)

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For this assessment, both the maximum concentration predicted in a commercial industrial area, and the residential receptors have been considered.

For residents, it is assumed that they are home 24 hours per day for 365 days of the year, where normal operating conditions occur for 360 days and upset conditions occur for 5 days of the year.

For industrial workers, it is assumed that they are at work for 8 hours per day for 240 days of the year, where normal operating conditions occur for 235 days and upset conditions occur for 5 days of the year.

Appendix B presents the relevant health-based criteria values adopted in these calculations, along with assumptions adopted quantification of inhalation exposures. Appendix C presents the calculations undertaken for residential and industrial inhalation exposures.

Table 6 presents the calculated individual HI relevant to the assessment of chronic inhalation exposures. The table presents the calculations relevant to the maximum residential receptors, where the maximum predicted annual average concentration has been utilised.

The assessment of exposures to NO2 and SO2 has utilised the NEPM guidelines that are protective of health. Risks associated with these pollutants are not considered to be additive. However, potential exposures to all other gases and chemical substances attached to fine particulates have been assumed to be additive and the total HI (the sum of all individual HI’s) is also presented.

Risks associated with chronic exposures are considered to be negligible (or acceptable) where the individual and total HI’s are less than or equal to 1.

Based on the assessment presented in Table 6, all the individual and total HI’s for the maximum inhalation exposures that may occur in industrial areas and the closest residential receptors are less than 1.

On this basis, there are no chronic risk issues of concern in relation to inhalation exposures. This would include exposure in future industrial premises that may be constructed close to the facility.

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Table 6: Calculated chronic risks for inhalation exposures*

Pollutants Maximum calculated HI – Maximum calculated HI Industrial areas – Residential areas NEPM pollutants Nitrogen dioxide (NO2) 0.048 0.0023 Sulfur dioxide (SO2) 0.027 0.0013 Other pollutants Hydrogen chloride (HCl) 0.0022 0.000099 Hydrogen fluoride (HF) 0.00016 0.0000079 Cadmium 0.0016 0.000075 Beryllium 0.0011 0.000054 Mercury 0.00022 0.000010 Antimony 0.00030 0.000014 Arsenic 0.0019 0.000093 Lead 0.0020 0.000091 Chromium (Cr VI assumed) 0.00076 0.000035 Copper 0.00000022 0.000000010 Manganese 0.0013 0.000060 Nickel 0.021 0.00098 Dioxin 0.00023 0.000011 MDI 0.00080 0.000038

Total HI (other pollutants) 0.034 0.0016 Negligible risk ≤1 * Refer to Appendices B and C for detail on health based criteria and risk calculations

Carbon monoxide

It is noted that for the assessment of carbon monoxide, the NEPM air guideline relates to an 8 hour average concentration rather than an annual average. Guidelines are available in Australia from NEPC (NEPC 2016) that are based on the protection of adverse health effects associated with carbon monoxide. The air guidelines currently available from NEPC are consistent with health based guidelines currently available from the WHO (2005) and the USEPA (20112, specifically listed to be protective of exposures by sensitive populations including asthmatics, children and the elderly). On this basis, the current NEPC guidelines are considered appropriate for the assessment of potential health impacts associated with the project.

The NEPM guideline level of carbon monoxide of nine parts per million (ppm) by volume (or 10 mg/m3) over an 8-hour period was considered to provide protection (for both acute and chronic health effects) for most members of the population. An additional 1.5-fold uncertainty factor to protect more susceptible groups in the population was included in the development of the guideline.

For this project, the maximum concentration of carbon monoxide over an 8 hour average is estimated to be 0.026 mg/m3 (all receptors) during normal operating conditions and 0.05 mg/m3 (all

2 Most recent review of the Primary National Ambient Air Quality Standards for Carbon Monoxide published by the USEPA in the Federal Register Volume 76, No. 169, 2011, available from: http://www.gpo.gov/fdsys/pkg/FR-2011-08- 31/html/2011-21359.htm

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receptors) during upset conditions. These concentrations are 0.026% to 0.5% of the NEPM criteria. On this basis the operation of the facility is not expected to significantly contribute to ambient levels of CO, and there are no health risk issues of concern in relation to these emissions.

5.5 Multiple pathway exposures General Where pollutants may be bound to particulates, are persistent in the environment and have the potential to bioaccumulate in plants or animals, it is relevant to also assess potential exposures that may occur as a result of particulates depositing to the environment where a range of other exposures may then occur. These include:

◼ Incidental ingestion and dermal contact with soil (and dust indoors that is derived from outdoor soil or deposited particulates); ◼ Ingestion of homegrown fruit and vegetables where particulates may deposit onto the plants and is also present in the soil where the plants are grown, and where pollutants bound to these particles are taken up into these plants; ◼ Ingestion of eggs where particulates may deposit onto the ground and be present in soil (which the pasture/feed grows in and animals also ingest when feeding), and the pollutants bound to these particles are taken up into the eggs.

The above exposures are chronic or long-term exposures.

Assessment approach In relation to these exposures, such exposures will only occur on urban residential properties where people live and where some homegrown produce may be present.

To evaluate these pathways a dust deposition rate is required. This has been provided by Edge (2019), for normal and upset operating conditions. As the multiple pathway exposures are only relevant in the residential areas, the maximum deposition rates for the residential receptors has been utilised in the HIA.

The calculation of risks posed by multiple pathway exposures only relates to pollutants that are bound to the particulates, not to pollutants only present as vapours or gases.

Appendix B includes the equations and assumptions adopted for the assessment of potential exposures via these exposure pathways, with the calculation of risk for each of these exposure pathways presented in Appendix C.

For the pollutants considered in this assessment, the risk calculations undertaken relate to a threshold HI. As discussed in Section 5.4.3, the following criteria have been adopted for determining when risks, as a HI, are considered to be negligible or acceptable.

◼ HI: the individual and total HI, where calculated as the sum over all relevant exposure pathways and pollutants ≤ 1 = negligible/acceptable risk to human health

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Calculated risks Table 7 presents the calculated risks associated with these multiple pathway exposures relevant to both adults and children. These risks have been calculated on the basis of the maximum predicted deposition rate for all of the residential receptors, assuming that normal operating conditions occur for 360 days of the year and upset operating conditions occur for 5 days of the year. The table presents the total HI for each exposure pathway, calculated as the sum over all the pollutants evaluated. The table also includes the calculated HI associated with inhalation exposures, as these exposures are additive to the other exposure pathways for the residential properties.

Depending on the use of the off-site residential properties, the types of exposures that may occur are likely to vary. For this assessment, a number of scenarios have been considered where a range of different exposures may occur. The sum of risks associated with these multiple exposures is presented in Table 7.

Table 7: Summary of risks for multiple pathway exposures

Calculated HI Exposure pathway Adults Children Individual exposure pathways Inhalation (I) 0.0016 0.0016 Soil ingestion (SI) 0.0000023 0.000021 Soil dermal contact (SD) 0.00000079 0.0000016 Ingestion of homegrown fruit and vegetables (F&V) 0.0000018 0.0000043 Ingestion of homegrown eggs (E) 0.000000013 0.00000026 Multiple pathways (i.e. combined exposure pathways) I + SI + SD 0.0016 0.0016 I + SI + SD + F&V 0.0016 0.0016 I + SI + SD + E 0.0016 0.0016 I + SI + SD + F&V + E 0.0016 0.0016

Negligible risk ≤1 ≤1 Refer to Appendix C for detailed risk calculations for each exposure pathway

Review of Table 7 indicates that all calculated risks associated with each individual exposure pathway as well as a combination of multiple exposure pathways, remain below the target risk levels considered representative of negligible risks. The multiple pathway exposures do not significantly contribute to the total risk.

On the basis of the assessment undertaken there are no chronic risk issues of concern in relation to multiple pathway exposures that may be relevant to the residential use of the surrounding areas.

5.6 Odour Predominate odour emissions that may occur from the WtE facility will be as a result of fugitive emissions from the receival area and refuse pit. To counter this, the receival area and refuse pit will be equipped with automatic roller doors that will open and close quickly as trucks enter and leave the refuse area to minimise fugitive odour escaping the building. Further, the receival area and refuse pit will be held under negative air pressure to minimise fugitive emissions from the doors and creating the ability to control emissions. It is expected that air from these areas will be used as combustion air in the WtE combustion chamber.

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Assessment of odorous emissions from the operation of the facility has been undertaken by Edge (2019). This assessment determined that odours predicted at sensitive receptors are below the relevant Design Criteria for odour.

For the receptors located on the site boundary, all odours are predicted to be below the odour criteria with the exception of the southern boundary receptor (SB6) which is closest to the waste drop-off point. The odour predicted at this location is 1.2 odour units (OU) which just exceeds the criteria of 1 OU. Review of these impacts by Edge (2019) determined that it is unlikely that odour will impact the community.

5.7 Uncertainties The characterisation of potential health risks related to exposures to emissions to air from the proposed WtE facility has utilised data from the air quality modelling as well as a number of assumptions. The following presents further discussion on these data and parameters, the level of uncertainty in these values and whether changes in these values will change the outcome of the assessment presented.

Air modelling

The modelling of air emissions has been undertaken by Edge (2019) using a regulatory approved model, which utilises meteorological and terrain data for the local area. The emissions data used in the assessment was based on measured emissions from reference facilities. It is noted that the reference facilities did not include treatment specific for nitrogen emissions. The proposed facility will include additional flue gas treatment to remove NOx. Hence the estimates of NOx emissions based on data from the reference facilities is conservative and will have overestimated inhalation risks. It has also been assumed that all NOx emissions will be NO2, which is also conservative and will overestimate actual exposures to NO2. In addition to the assessment pf NO2, the modelling of emissions such as arsenic is also considered to be conservative.

Inhalation exposures

Industrial workers:

For this scenario it is assumed that workers are exposed to the maximum predicted concentrations (anywhere within the grid receptors modelled) for 8 hours a day for 240 days of the year (where 235 days are normal operating conditions and 5 days upset conditions).

If workers are present at this location for longer, say 12 hours per day, the calculated HI will increase slightly from 0.034 to 0.05.

If upset conditions occur more often than 5 working days in each year, the calculated HI will increase. If it is assumed that upset conditions occur for 20 days in the working year, and normal conditions occurred for 220 days per year, the HI increases from 0.034 to 0.039.

These changes are very small, with risks remaining very low. Hence changing these assumptions does not change the outcomes of the assessment presented for industrial workers.

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Residential exposures:

It is assumed that residents are home 24 hours per day, every day of the year for as long as they live at their home. This is overly conservative as most people attend childcare, school, work or other activities and holidays away from the home. As a result, the risks calculated for inhalation exposures will be an overestimate for residents. The calculation, however is relevant for exposures that may occur for residents at the prison, where they will be present 24 hours per day for 365 days of the year.

If upset conditions occur more often than 5 working days in each year, the calculated HI will increase. If it is assumed that upset conditions occur for 20 days, and normal conditions occurred for 345 days per year, the HI increases from 0.0016 to 0.0018. If upset conditions occur for 100 days of the year, then the HI increases to 0.0027.

These changes are very small, with risks remaining very low. Hence changing these assumptions does not change the outcomes of the assessment presented for residents.

Multi-pathway exposures

These have been calculated on the basis of modelled dust deposition rates. It is noted that due to the use of a particulate filter the deposition rate is estimated to be very low. For the assessment of exposures in residential areas, the maximum deposition rate for all three closest residential receptors for both normal operating conditions and upset conditions has been adopted, assuming this occurs every year.

The quantification of potential intakes via ingestion of soil, fruit and vegetables and eggs, and dermal contact with soil, has adopted a number of assumptions relating to how the dust mixes in with soil, how much accumulates in fruit and vegetables and eggs, and how people may be exposed. These assumptions have used conservative models and uptake factors that are likely to overestimate the accumulation of pollutants in soil, fruit and vegetables and eggs. In addition, default exposure parameters have been adopted assuming exposures occur all day every day, which is conservative.

Overall the approach taken will have overestimated actual exposures and risks. Changes in the assumptions to those more representative of actual exposures will result in lower levels of risk, rather than higher levels of risk.

It is noted that for multi-pathway exposures, intakes would need to increase by more than 30,000 fold to be considered to be of concern to health. Variation in assumptions adopted for the characterisation of these exposures will never result in changes that are this significant. On this basis there is no need to further evaluate changes in assumptions used in the multi-pathway exposure assessment.

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5.8 Outcomes of health impact assessment Table 8 presents a summary of the outcomes of the assessment undertaken in relation to the impacts of changes in air quality, associated with the proposed project, on community health.

Table 8: Summary of health impacts – air quality

Impacts associated with air emissions Benefits There are no benefits to the off-site community in relation to air emissions of this type Impacts Based on the available data and information in relation to emissions to air from the proposed facility, potential impacts on the health of the community have been assessed. The impact assessment has concluded the following: ◼ There are no acute inhalation exposure risks of concern ◼ There are no chronic inhalation exposure risks of concern ◼ There are no chronic risks of concern from exposure to pollutants from the facility via soil or ingestion of home-grown produce The design of the facility, specifically the receival area and refuse tip, will ensure that there are no significant fugitive odour emissions from the site. Mitigation The proper operation and maintenance, and monitoring (including continuous monitoring), of the facility and pollution control/flue gas equipment.

Management measures have been identified to minimise odours, which include ◼ MSW collected in closed vehicles (compactor trucks); ◼ Unloading of MSW in an entirely enclosed building; ◼ Automated roller door for truck access to receival area; ◼ Automated doors at tipping point from receival area to refuse pit, which open and close with proximity switches which minimise odour transmission from the refuse pit to the waste receival area; and ◼ Receival area and refuse pit under negative pressure as air is drawn from these areas to supply the gasifier and the secondary combustion chamber

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Section 6. Health impacts: Noise 6.1 Approach This section presents a review and further assessment of impacts on health associated with noise, relevant to the operation of the facility. The assessment presented has relied on the information provided by Edge (2018).

The site is located within an Industrial 2 Zone (IZ2) and surrounded by industrial premises. The nearest sensitive receptors to the proposed facility are residential premises in the Honey Hush Caravan Park located approximately 1.4 km to the south, residential homes located approximately 1.8 km to the south and the prison located approximately 1.6 km to the west. The noise assessment specifically focused on noise from the facility and impacts on these sensitive receptors, shown in Figure 5.

Figure 5: Location of noise sensitive receptors (Edge 2018)

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6.2 Summary of noise assessment General The noise assessment was based on criteria outlined in the guideline – State Environmental protection Policy (Control of Noise from Commerce, Industry and Trade), number N-1 (SEPP N-1). This guideline provides a process for assessing noise impacts from commercial, industrial or trade noise that may affect a noise sensitive area (NSA). From this guideline ambient background noise levels (based on measured noise levels) and Noise Limits are determined for the NSAs.

Site noise assessment Noise impact from the project was estimated by noise associated with WtE facility equipment, along with likely truck movements within the facility. Noise generation from the equipment was estimated from a noise database of common plant equipment, design details sourced from published material on similar WtE facilities as well as industry recognised data sources. The entire processing area and plant are located within an enclosure (or building) which provides a significant reduction in noise. The site was estimated to have 120 truck movements per day, most likely during the day time hours but noting that some waste may be delivered at any time (day or night).

Noise from the proposed facility were modelled by Edge (2018) using the Environmental Noise Model (ENM), with noise levels predicted during three different meteorological conditions that include a breeze in the direction of the sensitive receivers, calm conditions and a breeze away from and/or perpendicular to the sensitive receivers.

Based on the noise modelling presented noise levels at the sensitive receivers are not impacted by noise from the facility and are in compliance with the SEPP N-1 noise limits, including under the scenario where there is a light breeze assisting in the propagation of noise.

6.3 Health impacts associated with noise Environmental noise has been identified (enHealth 2018; I-INCE 2011; WHO 2011) as a growing concern in urban areas because it has negative effects on quality of life and well-being and it has the potential for causing harmful physiological health effects. With increasingly urbanised societies impacts of noise on communities have the potential to increase over time.

Sound is a natural phenomenon that only becomes noise when it has some undesirable effect on people or animals. Unlike chemical pollution, noise energy does not accumulate either in the body or in the environment, but it can have both short-term and long-term adverse effects on people. These health effects include (WHO 1999b, 2011):

◼ Sleep disturbance (sleep fragmentation that can affect psychomotor performance, memory consolidation, creativity, risk-taking behaviour and risk of accidents) ◼ Annoyance ◼ Hearing impairment ◼ Interference with speech and other daily activities ◼ Impacts on children’s school performance (through effects on memory and concentration) ◼ Impacts on cardiovascular health.

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Other effects for which evidence of health impacts exists, but for which the evidence is weaker, include:

◼ Effects on mental health (usually in the form of exacerbation of existing issues for vulnerable populations rather than direct effects) ◼ Tinnitus (which can also result in sleep disturbance, anxiety, depression, communication and listening problems, frustration, irritability, inability to work, reduced efficiency and a restricted participation in social life) ◼ Cognitive impairment in children (including deficits in long term memory and reading comprehension) ◼ Some evidence of indirect effects such as impacts on the immune system.

Within a community the severity of the health effects of exposure to noise and the number of people who may be affected are schematically illustrated in Figure 6.

Figure 6: Schematic of severity of health effects of exposure to noise and the number of people affected (WHO 2011)

Often, annoyance is the major consideration because it reflects the community’s dislike of noise and their concerns about the full range of potential negative effects, and it affects the greatest number of people in the population.

There are many possible reasons for noise annoyance in different situations. Noise can interfere with communication or other desired activities. Noise can contribute to sleep disturbance, which can obviously be very annoying and has the potential to lead to long-term health effects. Sometimes noise is just perceived as being inappropriate in a particular setting without there being any objectively measurable effect at all. In this respect, the context in which sound becomes noise can be more important than the sound level itself.

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Different individuals have different sensitivities to types of noise and this reflects differences in expectations and attitudes more than it reflects any differences in underlying auditory physiology. A noise level that is perceived as reasonable by one person in one context (for example in their kitchen when preparing a meal) may be considered completely unacceptable by that same person in another context (for example in their bedroom when they are trying to sleep). In this case the annoyance relates, in part, to the intrusion from the noise. Similarly, a noise level, which is considered to be completely unacceptable by one person, may be of little consequence to another even if they are in essentially the same room. In this case, the annoyance depends almost entirely on the personal preferences, lifestyles and attitudes of the listeners concerned.

In relation to this project, potential noise impacts have been assessed against criteria developed by the World Health Organization (WHO 1999b, 2009) that have been established on the basis of the relationship between noise and health impacts, where annoyance and sleep disturbance are of most significance. The predicted noise impacts are those that would be outside of a dwelling. These predicted impacts are all below the World Health Organization guideline values that are protective of adverse health effects.

Based on the available information and the assessment presented by Edge (2019), the potential for noise impacts to result in adverse health impacts at the closest noise sensitive receptors is considered to be negligible.

6.4 Outcomes of health impact assessment: noise Table 9 presents a summary of the outcomes of the assessment undertaken in relation to the impacts of changes in noise, associated with the proposed project, on community health.

Table 9: Summary of health impacts - noise

Health impacts associated with noise emissions Benefits There are no benefits to the off-site community in relation to noise emissions Impacts Based on the noise assessment completed by Edge (2018) there are no noise impacts predicted at the closest sensitive receptors, hence risks to community health are considered to be negligible. It is noted that there is a significant distance between the facility and the closest noise sensitive receptor (1.4 to 1.8 km) which is sufficient to mitigate noise impacts from the proposed facility, even under conditions with a light breeze that propagates noise in the direction of the receptors. Mitigation Noise mitigation measures as outlined by Edge (2018) are proposed to be implemented, which is appropriate. It is also expected that noise levels will be measured at the commissioning of the facility. In relation to the enclosure proposed, this is designed such that machinery noise is not discernible above background 100 metres from the building. Edge (2018) also conclude that noise impacts are further assessed once the facility has been commissioned if noise measurements vary significantly from the modelled impacts.

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Section 7. Health impact assessment: Water, economics, transport, hazardous waste, community and social aspects 7.1 Approach Health impacts associated with other aspects of the proposed project, including wastewater, economics, transport, pestilence, community and social aspects have been addressed in this section. The assessment presented has relied on information provided in various sections and appendices of the WAA. The assessment has been undertaken as a qualitative evaluation, to identify benefits and impacts associated with the project.

7.2 Overview and assessment of issues Water

The use and discharge of water is described in Section 9 of the WAA. The section indicates that the amount of water to be used is expected to be approximately 104 ML per year, with 2.7 ML of this water captured from roof runoff. The rest of the water is sourced from the mains water supply (42%), water from municipal solid waste (MSW) (28%) and from water generated within the gasifier (by the reaction of hydrogen and oxygen) (29%). Water entering the facility will be processes through a water treatment plant. The use of mains water has been minimised.

Based on the proposed process where there are various water losses (steam and via the stack) and the reuse of leachate back into the gasifier, no wastewater treatment is required and do wastewater is expected to be discharged. In addition, no trade waste is expected.

As no wastewater is to be discharged form the facility, there is no potential for the community to be exposed to this water at any point.

On this basis no further, detailed assessment of water discharges from the proposed EtW facility is required.

Project benefits

Benefits of the proposed project are outlined in Section 1 of the WAA. These benefits include:

◼ 400 jobs during construction and 40 full time jobs during operation ◼ Localised electricity generation (which can support local industry and community) and increased energy security ◼ Improved environmental waste management outcomes ◼ Localised waste management operation which will reduce waste haulage distances ◼ Reduction in net greenhouse gas emissions.

In relation to the above, the most significant health outcomes in the community are expected to be benefits associated with job creation. While there is evidence to support that finding employment has health benefits, most studies are related to the negative impacts of unemployment. It would seem reasonable that if unemployment has a range of negative effects then finding employment would have positive effects. Health outcomes from unemployment include increases in the risk of

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illness and premature death and there are impacts on a range of mental health issues (anxiety, stress etc.) and social aspects of life (lower self-esteem, feelings of insecurity etc.). Finding employment is expected to be associated with improvements in these aspects of health and wellbeing. This is especially important for the local community where there may be some areas that are mode susceptible to negative health impacts of unemployment (Section 3). The local areas also have higher than average unemployment.

Therefore, improvements in health and wellbeing in the local community can be enhanced by encouraging local employment at the facility.

Transport

An assessment of the proposed traffic generation and traffic impacts of the proposed WtE facility has been undertaken by One Mile Grid (2018).

The assessment identified that the traffic volumes generated by the proposed project are relatively low and expected to be easily accommodated by the existing road network. In addition, the proposed project includes car parking onsite as well as bicycle parking which will encourage active communing.

Increased traffic congestion has the potential to decrease road safety and increase levels of stress and anxiety in the community. The assessment concluded that no significant reduction in travel times are expected on the existing roads. Based on current information, the health impacts from increased traffic are considered to be negligible.

The inclusion of bicycle storage has the potential to encourage active commuting for site employees. Active commuting has a number of health benefits for workers and should be encouraged where possible. The use of active transport can be further encouraged by ensuring appropriate showering facilities are available.

Discovery and disposal of hazardous waste

It is inevitable that during operations the discovery of hazardous waste will occur. Hazardous waste includes smoke alarms, batteries (household, car, phone, laptop and rechargeable) and light bulbs. As outlined in Section 6 of the WAA, the facility will accept only non-hazardous MSW from contracted Councils and MRFs. These contracts will include clauses which define the types of waste that will be accepted, and waste that will not be accepted at the facility. Random compliance audits will be conducted on waste supplied from transfer stations of MRF’s.

Hazards

A Preliminary Hazard Analysis (PHA) has been undertaken, and is available in Appendix 19 of the WAA. In addition and Environmental Risk Assessment is presented in Appendix 4 and Section 5 of the WAA. In relation to safety risk issues that are relevant to the off-site community the PHA has considered and addressed the following:

◼ Generation and leakage of hazardous gases from the MSW feed pit leachate collection tank (methane). The facility will include a number of management measures to mitigate risks of explosion from these areas, including the use of negative pressures and forced ventilation.

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◼ Release of syngas from the gasifier and other faults that may result in gases, dust, fires and explosions – these hazards are principally restricted to employees within the facility and a number of mitigation measures have been identified to minimise these risks. No risks for the off-site community have been identified.

Community and Social

There are a range of benefits the overall project offers to the community (discussed above). In addition, other benefits of the project relate to feelings of wellbeing in relation to sustainability and the reuse of residual waste for the local generation of electricity. The benefits of residual waste to energy facilities in Melbourne’s west has been the subject of more recent community discussion3, with broad support for waste to energy as an alternative to landfill, but there are concerns for having large facilities that only burden some parts of the population. A facility that is relatively small scale that addresses local waste and energy issues is preferred.

Given the location of the facility within an existing industrial area, situated at least 1.5 km from the nearest residential receptor, the facility is not expected to change the existing visual landscape, or change any existing uses of residential areas.

As outlined in Sections 5 and 6 there are no impacts on the off-site community in relation to changes in air quality, odour or noise that would adversely affect the health of the off-site community, provided appropriate migration measures are undertaken. Hence there are no equity issues that require further consideration in relation to the distribution of health-related impacts in the off-site residential areas.

3 http://www.cesarmelhem.com.au/waste-to-energy-consultations-in-the-west/

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Section 8. Summary of HIA Outcomes Based on the evaluations presented in Section 5 to 7, a range of outcomes (both positive and negative) have been assessed in relation to health impacts relevant to the off-site community. Where negative impacts have been identified, these are considered to be negligible in terms of community health.

These outcomes, along with measures that could be implemented to enhance or mitigate the identified health impacts, are summarised in Table 10.

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Table 10: Summary of HIA outcomes and enhancement/mitigation measures

Health Reference in Potential Health Impact Identified (positive or Types of measures that could be implemented to Aspect/Issue HIA Impacts Considered negative and significance) enhance positive impacts or mitigate negative impacts

Air quality – Section 5.4 Range of health effects All exposures: Negative but negligible The proper operation and maintenance, and monitoring, of the Inhalation associated with exposure More specifically: pollution control/flue gas equipment. exposures to pollutants released to air ◼ No acute risk issues of concern from the proposed facility ◼ No chronic risk issues of concern ◼ Particulate exposures are negligible Air quality – Section 5.5 Range of health effects All exposures: Negative but negligible The proper operation and maintenance, and monitoring, of the Multiple pathway associated with exposure More specifically: pollution control/flue gas equipment. exposures to pollutants released to air ◼ No chronic risk issues of concern from the proposed facility, for multiple pathway exposures that may then deposit and accumulate in soil, homegrown fruit and vegetables and other homegrown produce (eggs) Odour Section 5.6 Annoyance, stress, anxiety Not significant and negligible The proper operation of the refuse receival area as proposed to ensure fugitive odour emissions are effectively managed. Noise Section 6 Sleep disturbance, Modelled noise impacts: negligible Mitigation measures as proposed to be implemented. Monitoring annoyance, children’s noise impacts at residential receivers of noise at commissioning to be undertaken, with review against school performance and and hence negligible potential for health the noise modelling, cardiovascular health impacts Economic Section 7 Reduction in anxiety, Positive improvements in health and The identified positive outcomes in the local community can be Environment stress and feelings of wellbeing enhanced by encouraging employment of people who live within insecurity the local community

Traffic and Section 7 Injury or death, stress and Negligible NA transport anxiety. Discovery and Section 7 Possible injury if incorrectly Negative but minimal Appropriate management of contractors delivering waste disposal of disposed of through the use of contracts (with Waste Acceptance Criteria) hazardous waste and auditing of waste materials Hazardous events Section 7 Injury Negative but minimal. Negligible for the Management and monitoring of all processes in the facility as off-site residential areas proposed.

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Health Reference in Potential Health Impact Identified (positive or Types of measures that could be implemented to Aspect/Issue HIA Impacts Considered negative and significance) enhance positive impacts or mitigate negative impacts

Community and Section 7 Wellbeing, changes in Positive outcomes enhancing feelings of These health impacts relate to community perceptions and trust. social levels of stress and anxiety wellbeing for aspects such as sustainability It is therefore important that the positive impacts associated with the project are enhanced within the local community and community consultation is continued. It is important that an effective communication/ community consultation program is maintained throughout the construction, commissioning and operational phases of the project.

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Section 9. References Australian Bureau of Statistics, 2016. Selected characteristics retrieved from QuickStats, TableBuilder and DataPacks. www.abs.gov.au. Accessed December 2019.

ATSDR 2012a, Toxicological Profile for Vanadium, Agency for Toxic Substances and Disease Registry.

ATSDR 2012b, Toxicological Profile for Manganese, US Department of Health and Human Services, Agency for Toxic Substances and Disease Registry. .

ATSDR 2012c, Toxicological Profile for Chromium, Agency for Toxic Substances and Disease Registry, United States Department of Health and Human Services, Atlanta, Georgia, USA. viewed 2015, .

Baars, AJ, Theelen, RMC, Janssen, PJCM, Hesse, JM, Apeldorn, MEv, Meijerink, MCM, Verdam, L & Zeilmaker, MJ 2001, Re-evaluation of human-toxicological maximum permissible risk levels, RIVM.

CRC CARE 2011, Health screening levels for petroleum hydrocarbons in soil and groundwater. Part 1: Technical development document, CRC for Contamination Assessment and Remediation of the Environment, CRC CARE Technical Report no. 10, Adelaide. .

DEH 2005, National Dioxins Program, Technical Report No. 12, Human Health Risk Assessment of Dioxins in Australia, Office of Chemical Safety, Australian Government Department of the Environment and Heritage.

Department of Health and Human Services 2016, Victorian Population Health Survey 2014: Health and wellbeing,chronic conditions, screening and eye health, State Government of Victoria, Melbourne. enHealth 2012a, Environmental Health Risk Assessment, Guidelines for assessing human health risks from environmental hazards, Commonwealth of Australia, Canberra. . enHealth 2012b, Australian Exposure Factors Guide, Commonwealth of Australia, Canberra. . enHealth 2017, Health Impact Assessment Guidelines, enHealth. enHealth 2018, The health effects of environmental noise, Commonwealth Department of Health, Canberra.

EPHC 2005, National Dioxins Program - National Action Plan for Addressing Dioxins in Australia, Environment Protection and Heritage Council.

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.

EPHC 2010, Expansion of the multi-city mortality and morbidity study, Final Report, Environment Protection and Heritage Council.

FSANZ 2017, Supporting Document 2 Assessment of potential dietary exposure to perfluorooctane sulfonate (PFOS), perfluorooctanoic acid (PFOA) and perfluorohexane sulfonate (PFHxS) occurring in foods sampled from contaminated sites, Food Standards Australia and New Zealand, Commonwealth Department of Health. .

Harris, P, Harris-Roxas, B., Harris, E. & Kemp, L. 2007, Health Impact Assessment: A Practical Guide, Centre for Health Equity Training, Research and Evaluation (CHETRE). Part of the UNSW Research Centre for Primary Health Care and Equity. University of New South Wales.

I-INCE 2011, Guidelines for Community Noise Impact Assessment and Mitigation, I-INCE Publication Number: 11-1, International Institute of Noise Control Engineering (I-INCE) Technical Study Group on Community Noise: Environmental Noise Impact Assessment and Mitigation.

Jalaudin, B & Cowie, C 2012, Health Risk Assessment - Preliminary Work to Identify Concentration- Response Functions for Selected Ambient Air Pollutants, Woolcock Institute of Medical Research. .

Krewski, D, Jerrett, M, Burnett, RT, Ma, R, Hughes, E, Shi, Y, Turner, MC, Pope, CA, 3rd, Thurston, G, Calle, EE, Thun, MJ, Beckerman, B, DeLuca, P, Finkelstein, N, Ito, K, Moore, DK, Newbold, KB, Ramsay, T, Ross, Z, Shin, H & Tempalski, B 2009, 'Extended follow-up and spatial analysis of the American Cancer Society study linking particulate air pollution and mortality', Research report, no. 140, May, pp. 5-114; discussion 15-36.

NEPC 1999 amended 2013a, Schedule B4, Guideline on Health Risk Assessment Methodology, National Environment Protection (Assessment of Site Contamination) Measure, National Environment Protection Council. .

NEPC 1999 amended 2013b, Schedule B7, Guideline on Health-Based Investigation Levels, National Environment Protection (Assessment of Site Contamination) Measure, National Environment Protection Council. .

NEPC 2011, Methodology for setting air quality standards in Australia Part A, National Environment Protection Council, Adelaide.

NEPC 2016, National Environment Protection (Ambient Air Quality) Measure, Federal Register of Legislative Instruments F2016C00215.

NHMRC 1999, Toxicity Assessment for Carcinogenic Soil Contaminants, National Health and Medical Research Council.

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NHMRC 2002, Dioxins: Recommendation for a Tolerable Monthly Intake for Australians, National Health and Medical Research Council and Therapeutic Goods Administration.

NHMRC 2011 updated 2018, Australian Drinking Water Guidelines 6, Version 3.5 Updated August 2018, National Water Quality Management Strategy, National Health and Medical Research Council, National Resource Management Ministerial Council, Canberra.

OEHHA 2003, The Air Toxics Hot Spots Program Guidance Manual for Preparation of Health Risk Assessments, Office of Environmental Health Hazard Assessment, California Environmental Protection Agency.

OEHHA 2012, Air Toxics Hot Spots Program, Risk Assessment Guidelines, Technical Support Document, Exposure Assessment and Stochastic Analysis, Office of Environmental Health Hazard Assessment, California Environmental Protection Agency.

OEHHA 2015, Air Toxics Hot Spots Program, Risk Assessment Guidelines, Guidance Manual for Preparation of Health Risk Assessments, Air, Community, and Environmental Research Branch, Office of Environmental Health Hazard Assessment, California Environmental Protection Agency.

Ostro, B, Broadwin, R, Green, S, Feng, WY & Lipsett, M 2006, 'Fine particulate air pollution and mortality in nine California counties: results from CALFINE', Environmental health perspectives, vol. 114, no. 1, Jan, pp. 29-33.

Pope, IC, Burnett, RT, Thun, MJ & et al. 2002, 'Lung cancer, cardiopulmonary mortality, and long- term exposure to fine particulate air pollution', JAMA, vol. 287, no. 9, pp. 1132-41.

RAIS The Risk Assessment Information System, Department of Energy's (DOE's) Oak Ridge Operations Office (ORO).

SAHC 1998, The Health Risk Assessment and Management of Contaminated Sites, Proceedings of the Fourth National Workshop on the Assessment of Site Contamination.

Stevens, B 1991, '2,3,7,8-Tetrachlorobenzo-p-Dioxin in the Agricultural Food Chain: Potential Impact of MSW Incineration on Human Health', in HA Hattemer-Frey & T Curtis (eds), Health Effects of Municipal Waste Incineration, CRC Press.

TCEQ 2014, Development Support Document, Ammonia, Texas Commission on Environmental Quality.

TCEQ 2015a, Hydrogen Chloride, Development Support Document, Texas Commission on Environmental Quality.

TCEQ 2015b, Hydrogen Fluoride and Other Soluble Inorganic Fluorides, Texas Commission on Environmental Quality.

UK EA 2009, Contaminants of soil: updated collation of toxicological data and intake values for humans, Nickel. viewed May 2009, .

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USEPA 1989, Risk Assessment Guidance for Superfund, Volume I, Human Health Evaluation Manual (Part A), Office of Emergency and Remedial Response, United States Environmental Protection Agency, Washington.

USEPA 2004, Risk Assessment Guidance for Superfund, Volume I: Human Health Evaluation Manual, (Part E, Supplemental Guidance for Dermal Risk Assessment), United States Environmental Protection Agency, Washington, D.C.

USEPA 2005, Human Health Risk Assessment Protocol for Hazardous Waste Combustion Facilities, Office of Solid Waste and Emergency Response, US Environmental Protection Agency. .

USEPA 2009, Risk Assessment Guidance for Superfund, Volume I: Human Health Evaluation Manual, (Part F, Supplemental Guidance for Inhalation Risk Assessment), United States Environmental Protection Agency, Washington, D.C.

USEPA 2012, Provisional Assessment of Recent Studies on Health Effects of Particulate Matter Exposure, National Center for Environmental Assessment RTP Division, Office of Research and Development, U.S. Environmental Protection Agency.

USEPA 2018, Integrated Science Assessment for Particulate Matter (External Review Draft), EPA/600/R-18/179, National Center for Environmental Assessment―RTP Division, Office of Research and Development, U.S. Environmental Protection Agency.

USEPA IRIS Integrated Risk Information System (IRIS), United States Environmental Protection Agency. van Vlaardingen, PLA, Posthumus, R & Posthuma-Doodeman, CJAM 2005, Environmental Risk Limits for Nine Trace Elements, National Institute for Public Health and the Environment, RIVM.

WHO 1999a, Manganese and its Compounds. Concise International Chemicals Assessment Document 12, United Nations Environment Programme, the International Labour Organisation, and the World Health Organization. .

WHO 1999b, Guidelines for Community Noise, World Health Organisation, Geneva.

WHO 2000a, Diphenylmethane Diisocyanate (MDI), Concise International Chemical Assessment Document 27, United Nations Environment Programme, the International Labour Organization, and the World Health Organization. .

WHO 2000b, Air Quality Guidelines for Europe, Second Edition, Copenhagen. .

WHO 2003, Elemental Mercury and Inorganic Mercury Compounds: Human Health Aspects, World Health Organization, Geneva.

WHO 2006a, Health risks or particulate matter from long-range transboundary air pollution, World Health Organisation Regional Office for Europe.

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WHO 2006b, Cobalt and Inorganic Cobalt Compounds. Concise International Chemical Assessment Document No. 69. .

WHO 2009, Night Noise Guidelines for Europe World Health Organisation Regional Office for Europe.

WHO 2011, Burden of disease from environmental noise, Quantification of healthy life years lost in Europe, World Health Organisation and JRC European Commission.

WHO 2013, Health Effects of Particulate Matter, Policy implications for countries in eastern Europe, Caucasus and central Asia, WHO Regional Office for Europe.

WHO 2017, Guidelines for Drinking Water Quality, Fourth Edition incorporating the First Addendum, World Health Organisation. .

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Appendix A Calculation of risks from PM2.5

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Calculation of risk: PM2.5

A quantitative assessment of risk for these endpoints uses a mathematical relationship between an exposure concentration (ie concentration in air) and a response (namely a health effect). This relationship is termed an exposure-response relationship and is relevant to the range of health effects (or endpoints) identified as relevant (to the nature of the emissions assessed) and robust (as identified in the main document). An exposure-response relationship can have a threshold, where there is a safe level of exposure, below which there are no adverse effects; or the relationship can have no threshold (and is regarded as linear) where there is some potential for adverse effects at any level of exposure.

In relation to the health effects associated with exposure to particulate matter, no threshold has been identified. Non-threshold exposure-response relationships have been identified for the health endpoints considered in this assessment.

Risk calculations relevant to exposures to PM2.5 by the community have been undertaken utilising concentration-response functions relevant to the most significant health effect associated with exposure to PM2.5, namely mortality (all cause).

The assessment of potential risks associated with exposure to particulate matter involves the calculation of a relative risk (RR). For the purpose of this assessment the shape of the exposure- response function used to calculate the relative risk is assumed to be linear4. The calculation of a relative risk based on the change in relative risk exposure concentration from baseline/existing (ie based on incremental impacts from the project) can be calculated on the basis of the following equation (Ostro 2004):

Equation 1 RR = exp[β(X-X0)] Where: X-X0 = the change in particulate matter concentration to which the population is exposed (µg/m3) β = regression/slope coefficient, or the slope of the exposure-response function which can also be expressed as the per cent change in response per 1 µg/m3 increase in particulate matter exposure.

Based on this equation, where the published studies have derived relative risk values that are associated with a 10 micrograms per cubic metre increase in exposure, the β coefficient can be calculated using the following equation:

4 Some reviews have identified that a log-linear exposure-response function may be more relevant for some of the health endpoints considered in this assessment. Review of outcomes where a log-linear exposure-response function has been adopted (Ostro 2004) for PM2.5 identified that the log-linear relationship calculated slightly higher relative risks compared with the linear relationship within the range 10–30 micrograms per cubic metre,(relevant for evaluating potential impacts associated with air quality goals or guidelines) but lower relative risks below and above this range. For this assessment

(where impacts from a particular project are being evaluated) the impacts assessed relate to concentrations of PM2.5 that are well below 10 micrograms per cubic metre and hence use of the linear relationship is expected to provide a more conservative estimate of relative risk.

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ln (RR)  = Equation 2 10 Where: RR = relative risk for the relevant health endpoint as published (µg/m3) 10 = increase in particulate matter concentration associated with the RR (where the RR is associated with a 10 µg/m3 increase in concentration).

The assessment of health impacts for a particular population associated with exposure to particulate matter has been undertaken utilising the methodology presented by the WHO (Ostro 2004)5 where the exposure-response relationships identified have been directly considered on the basis of the approach outlined below.

An additional risk can be calculated as:

Equation 3 Risk=β x ∆X x B Where: β = slope coefficient relevant to the per cent change in response to a 1 µg/m3 change in exposure ΔX = change (increment) in exposure concentration in µg/m3 relevant to the project at the point of exposure B = baseline incidence of a given health effect per person (eg annual mortality rate)

The calculation of the incremental individual risk for relevant health endpoints associated with exposure to particulate matter as outlined by the WHO (Ostro 2004) has considered the following four elements:

◼ Estimates of the changes in particulate matter exposure levels (ie incremental impacts) due to the project for the relevant modelled scenarios – these have been modelled for the proposed project, with the maximum change in residential areas addressed. For this

assessment the change in PM2.5 relates to the change in annual average air concentrations and the value considered in this assessment is 0.054 µg/m3

◼ Baseline incidence of the key health endpoints that are relevant to the population exposed – the assessment undertaken has considered the baseline mortality data relevant to the

5 For regional guidance, such as that provided for Europe by the WHO WHO 2006a, Health risks or particulate matter from long-range transboundary air pollution regional background incidence data for relevant health endpoints are combined with exposure-response functions to present an impact function, which is expressed as the number/change in incidence/new cases per 100,000 population exposed per microgram per cubic metre change in particulate matter exposure. These impact functions are simpler to use than the approach adopted in this assessment, however in utilising this approach it is assumed that the baseline incidence of the health effects is consistent throughout the whole population (as used in the studies) and is specifically applicable to the sub-population group being evaluated. For the assessment of exposures in the areas evaluated surrounding the project it is more relevant to utilise local data in relation to baseline incidence rather than assume that the population is similar to that in Europe (where these relationships are derived).

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Wyndham LGA in 2016 (refer to Table 2), which is 589.6 per 100,000 (all ages, all causes). This is 0.005896 per person.

◼ Exposure-response relationships expressed as a percentage change in health endpoint per microgram per cubic metre change in particulate matter exposure, where a relative risk (RR) is determined (refer to Equation 1). The concentration response function used in this report is that recommended in a NEPC published report (Jalaudin & Cowie 2012). It was derived from a study in the United States which examined the health outcomes of hundreds of thousands of people living in cities all over the United States. These people were exposed to

all different concentrations of PM2.5 (Pope et al. 2002). The study found a relative risk (RR) 3 of all-cause mortality of 1.06 per 10µg/m change in PM2.5, and that this risk relationship was 3 in the form of an exponential function. Based on a RR of 1.06 per 10µg/m change in PM2.5, this results in a β = 0.0058. It is noted that the exposure response relationship established in this study was re-affirmed in a follow-up study (that included approximately 500,000 participants in the US) (Krewski et al. 2009) and is consistent with findings from California (Ostro et al. 2006). The relationship is also more conservative than a study undertaken in Australia and New Zealand (EPHC 2010).

The above approach (while presented slightly differently) is consistent with that presented in Australia (Burgers & Walsh 2002), US (OEHHA 2002; USEPA 2005b, 2010) and Europe (Martuzzi et al. 2002; Sjoberg et al. 2009).

Based on the calculations undertaken the calculated incremental individual risk:

Risk=β x ∆X x B = 0.0058 x 0.054 x 0.005896 = 2 x 10-6

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Appendix B Methodology and assumptions

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B1 Introduction

This appendix presents the methodology and assumptions adopted in the calculation of risk related to the assessment of chronic risks via inhalation or other pathways that may occur following deposition of chemical substances that are persistent.

B2 Chronic toxicity reference values

Approach

The quantitative assessment of potential risks to human health for any substance requires the consideration of the health end-points and where carcinogenicity is identified; the mechanism of action needs to be understood. This will determine whether the chemical substance is considered a threshold or non-threshold chemical substance. A threshold chemical has a concentration below which health effects are not considered to occur. A non-threshold chemical substance is believed to theoretically cause health effects at any concentration, and it is the level of health risk posed by the concentration of the chemical substance that is assessed. The following paragraphs provide further context around these concepts.

For chemical substances that are not carcinogenic, a threshold exists below which there are no adverse effects (for all relevant end-points). The threshold typically adopted in risk calculations (a tolerable daily intake [TDI] or tolerable concentration [TC]) is based on the lowest no observed adverse effect level (NOAEL), typically from animal or human (e.g. occupational) studies, and the application of a number of safety or uncertainty factors. Intakes/exposures lower than the TDI/TC is considered safe, or not associated with an adverse health risk (NHMRC 1999).

Where the chemical substance has the potential for carcinogenic effects the mechanism of action needs to be understood as this defines the way that the dose-response is assessed. Carcinogenic effects are associated with multi-step and multi-mechanism processes that may include genetic damage, altering gene expression and stimulating proliferation of transformed cells. Some carcinogens have the potential to result in genetic (DNA) damage (gene mutation, gene amplification, chromosomal rearrangement) and are termed genotoxic carcinogens. For these carcinogens it is assumed that any exposure may result in one mutation or one DNA damage event that is considered sufficient to initiate the process for the development of cancer sometime during a lifetime (NHMRC 1999). Hence no safe-dose or threshold is assumed and assessment of exposure is based on a linear non-threshold approach using slope factors or unit risk values.

For other (non-genotoxic) carcinogens, while some form of genetic damage (or altered cell growth) is still necessary for cancer to develop, it is not the primary mode of action for these chemical substances. For these chemical substances carcinogenic effects are associated with indirect mechanisms (that do not directly interact with genetic material) where a threshold is believed to exist.

In the case of particulate matter (PM10 or PM2.5), current health evidence has not been able to find a concentration below which health impacts do not exist. Thus, the quantification of risk for PM2.5 follows a non-threshold approach as described in Appendix A.

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Values adopted

Chronic toxicity reference values (TRVs) associated with inhalation, ingestion and dermal exposures have been adopted from credible peer-reviewed sources as detailed in the NEPM (NEPC 1999 amended 2013a) and enHealth (enHealth 2012a).

For the gaseous pollutants considered in this assessment, only inhalation TRVs have been adopted. For inorganics as well as dioxins, TRVs relevant to all exposure pathways have been adopted. Background intakes of these pollutants have been estimated on the basis of existing available information as noted.

The assessment of chronic exposures has considered pollutants that are listed under the NEPM

(NEPC 2016), namely NO2 and SO2, where the assessment requires comparison of the total intake (background plus the project) to the NEPM air criteria, relevant to an annual average. This has been undertaken separately to the other pollutants, and these pollutants have only been assessed on the basis of inhalation exposures.

Table B1 presents the TRVs adopted for the assessment of chronic health effects associated with exposure to the other pollutants considered in this assessment.

Table B1: Summary of chronic TRVs adopted for pollutants – threshold effects

Pollutant Inhalation Oral/dermal GI Dermal Background TRV TRV absorption absorption* intakes (as (mg/m3) (mg/kg/day) factor* percentage of TRV) Hydrogen chloride (HCl) 0.026 T NA (gaseous pollutant) 0% Hydrogen fluoride (HF) 0.029 T NA (gaseous pollutant) 0% Cadmium 0.000005 W 0.0008 W 100% 0 60% Beryllium 0.00002 W, U 0.002 W, U 100% 0.001 10% Mercury (as inorganic and 0.0002 W 0.0006 W 7% 0.001 40% elemental) Antimony 0.0002 U 0.00086 NH 15% 0 0% Arsenic 0.001 D 0.002 N 100% 0.005 50% Lead 0.0005 N 0.0035 NH 100% 0 50% Chromium (Cr VI assumed) 0.0001 U 0.001 A 100% 0 10% Copper 0.49 R 0.14 W 100% 0 60% Manganese 0.00015 W 0.14 A 100% 0 50% Nickel 0.00002 E 0.012 W 100% 0.005 60% Dioxins and furans 8.05E-09 R 2.3E-09 NH 100% 0.03 54% MDI 0.0006 W, U NA (likely present as vapour and has short 0% half-life in air)

Notes for Table B1: * GI factor and dermal absorption values adopted from RAIS (accessed in 2018) (RAIS) ** Background intakes relate to intakes from inhalation, drinking water and food products. The values adopted based on information provided in the ASC-NEPM (NEPC 1999 amended 2013b) and relevant sources as noted for the TRVs. Gaseous pollutant background intakes are not known and hence for this assessment they have been assumed to be negligible R = No inhalation-specific TRV available, hence inhalation exposures assessed on the basis of route-extrapolation from the oral TRV, as per USEPA guidance (USEPA 2009) A = TRV available from ATSDR, relevant to chronic intakes (ATSDR 2012a, 2012b, 2012c) D = TRV available from RIVM (Baars et al. 2001; van Vlaardingen, Posthumus & Posthuma-Doodeman 2005) E = TRV available from the UK Environment Agency (UK EA 2009) N = Inhalation guideline adopted for lead from the NEPM (NEPC 2016), and arsenic oral/dermal value as adopted in ASC- NEPM (NEPC 1999 amended 2013b).

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NH = Dioxin value (and background intakes, which includes natural soil) adopted from NHMRC (NHMRC 2002) and Environment Australia (DEH 2005; EPHC 2005), and antimony and lead value consistent with that adopted by NHMRC to assess intakes in drinking water (NHMRC 2011 updated 2018) T = TRV available from TCEQ, relevant to chronic inhalation exposures (and HI=1) (TCEQ 2014, 2015a, 2015b) U = TRV available from the USEPA IRIS (current database) (USEPA IRIS) W = TRV available from the WHO, relevant to chronic inhalation exposures (WHO 1999a, 2000b, 2000a, 2006b, 2017), noting inhalation value adopted for mercury is for elemental mercury (WHO 2003)

B3 Quantification of inhalation exposure

Intakes via inhalation has been assessed on the basis of the inhalation guidance available from the USEPA and recommended for use in the ASC NEPM and enHealth (enHealth 2012a; NEPC 1999 amended 2013b; USEPA 2009).

This guidance requires the calculation of an exposure concentration which is based on the concentration in air and the time/duration spent in the area of impact. It is not dependent on age or body weight. The following equation outlines the calculation of an inhalation exposure concentration, and Table B2 provides details on the assumptions adopted in this assessment:

ET•EF•ED Exposure Concentration=C • (mg/m3) a AT

Table B2: Inhalation exposure assumptions

Parameter Value adopted Basis Ca Concentration of chemical Modelled from facility, adopting the Calculations undertaken on the substance in air (mg/m3) maximum predicted anywhere (all grid basis of the maximum predicted receptors) and the maximum from all impacts discrete receptors ET Exposure time (dependant Industrial workers: 8 hours/day Assume someone is exposed at on activity) (hours/day) Residents: 24 hours/day the maximum location all day, EF Exposure frequency Industrial workers: 240 days/year every day of the year, and (days/year) Residents: 365 days/year workers are exposed every work day ED Exposure duration (years) Industrial workers: 30 years Duration of work and residency as Residents: 35 years per enHealth (enHealth 2012b) AT Averaging time (hours) Threshold = ED x 365 days/year x 24 As per enHealth (enHealth 2012a) hours/day guidance Non-threshold = 70 years x 365 days/year x 24 hours/day

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B4 Multiple pathway exposures

B4.1 Ingestion and dermal absorption

Chemical substances that are deposited on the ground have the potential to be ingested either directly through accidental consumption of dirt or indirectly through food grown or raised in the soil (fruit and vegetables and eggs) that is subsequently consumed.

The assessment of the potential ingestion of chemical substances has been undertaken using the approach presented by enHealth and the USEPA (enHealth 2012a; USEPA 1989). This approach is presented in the following equation, and parameters adopted in this assessment are presented in Table B3:

IRM•FI•B•CF•EF•ED Daily Chemical Intake =C • (mg/kg/day) Ingestion M BW•AT

Chemical substances that are deposited on the ground have the potential to be absorbed through the skin when skin comes in contact with soil or dust.

The assessment of the potential dermal absorption of chemical substances has been generally undertaken using the approach presented by the USEPA (USEPA 1989, 2004). The USEPA define a simple approach to the evaluation of dermal absorption associated with soil contact. This is presented in the following equation and parameters adopted in this assessment are presented in Table B3:

SA•AF•ABSd•CF•EF•ED Daily Chemical Intake =C • (mg/kg/day) Dermal M BW•AT

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Table B3: Ingestion and dermal exposure assumptions

Parameter Value adopted Basis Young children Adults CM Concentration of chemical Modelled based on deposition of Calculations undertaken on the basis substance in media or particulates to soil, adopting the of the maximum predicted impacts relevance (soil, fruit and maximum from all residential relevant to areas where multi-pathway vegetables or eggs) receptors exposures may occur (mg/kg)

IRM Ingestion rate of media Soil (mg/day) 100 mg/day 50 mg/day Ingestion rate of outdoor soil and dust (tracked or deposited indoors) as per enHealth (enHealth 2012b) Fruit and vegetables 0.28 kg/day 0.4 kg/day Total fruit and vegetable intakes per (kg/day) 85% from 73% from day as per ASC NEPM (NEPC 1999 aboveground aboveground amended 2013b) crops crops 16% from root 27% from root crops crops Eggs (kg/day) 0.006 kg/day 0.014 kg/day Ingestion rate of eggs per day as per enHealth (enHealth 2012b), also consistent with P90 intakes from FSANZ (FSANZ 2017) FI Fraction of media ingested derived from impacted media, or fraction of produce consumed each day derived from the property Soil 100% 100% Assume all soil contact occurs on the one property Fruit and vegetables 35% 35% Rate assumed for rural area (higher than the default of 10% for urban areas) Eggs 200% 200% Assume higher intake of home- produced eggs in rural areas (SAHC 1998) B Bioavailability or absorption 100% 100% Conservative assumption of chemical substance via ingestion SA Surface area of body 2700 6300 Exposed skin surface area relevant to exposed to soil per day adults as per ASC NEPM (NEPC (cm2/day) 1999 amended 2013b) AF Adherence factor, amount 0.5 0.5 Default (conservative) value from of soil that adheres to the ASC NEPM (NEPC 1999 amended skin per unit area which 2013b) depends on soil properties and area of body (mg/cm2 per event) ABSd Dermal absorption fraction Chemical specific Refer to Tables B1 and B2 (unitless) CF Conversion factor Soil 1x10-6 to convert mg to kg Conversion of units relevant to soil ingestion and dermal contact Produce 1 No units conversion required for these calculations BW Body weight 70 15 As per enHealth (enHealth 2012b) and ASC NEPM (NEPC 1999 amended 2013b) EF Exposure frequency 365 365 Assume residents exposed every day (days/year) ED Exposure duration (years) 6 years 29 Duration of residency as per enHealth (enHealth 2012b) and split between young children and adults as per ASC NEPM (NEPC 1999 amended 2013b)

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Parameter Value adopted Basis Young children Adults AT Averaging time (days) Threshold = ED x 365 days/year As per enHealth (enHealth 2012a) Non-threshold = 70 years x 365 guidance days/year

B4.2 Calculation of concentrations in various media

Potential Concentrations in Soil

The potential accumulation of persistent and bioaccumulative chemical substances in soil, which may be the result of deposition from a number of air emissions source, can be estimated using a soil accumulation model (OEHHA 2015; Stevens 1991).

The concentration in soil, which may be the result of deposition following emission of persistent chemical substances, can be calculated using the following equation, with assumptions adopted in this assessment presented in Table B4.

DR•[1-e-k•t] C = •1000 (mg/kg) s d•ρ•k

Table B4: Assumptions adopted to estimate soil concentrations

Parameter Value adopted Basis Surface soil* Agricultural soil* DR Particle deposition rate for Adopted maximum deposition rate for Relevant to areas where multi- accidental release discrete receptors pathway exposures may occur (mg/m2/year) k Chemical-specific soil-loss Calculated Calculated constant (1/year) = ln(2)/T0.5 T0.5 Chemical half-life in soil Chemical Chemical specific Default values adopted for (years) specific pollutants considered as per OEHHA (2015) t Accumulation time (years) 70 years 70 years Default value (OEHHA 2015) d Soil mixing depth (m) 0.01 m 0.15 m Default values (OEHHA 2015)  Soil bulk-density (g/m3) 1600000 1600000 Default for fill material (CRC CARE 2011) 1000 Conversion from g to kg Default conversion of units * Surface soil values adopted for the assessment of direct contact exposures. All other exposures including produce and meat/milk intakes utilise soil concentrations calculated for agricultural intakes (OEHHA 2015)

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Homegrown fruit and vegetables

Plants may become contaminated with persistent chemical substances via deposition directly onto the plant outer surface and following uptake via the root system. Both mechanisms have been assessed.

The potential concentration of persistent chemical substances that may be present within the plant following atmospheric deposition can be estimated using the following equation (Stevens 1991), with the parameters and assumptions adopted outlined in Table B5:

DR•F•[1-e-k•t] C = (mg/kg plant – wet weight) p Y•k

The potential uptake of persistent chemical substances into edible crops via the roots can be estimated using the following equation (OEHHA 2015; USEPA 2005), with the parameters and assumptions adopted outlined in Table B5:

Crp=Cs•RUF (mg/kg plant – wet weight)

Table B5: Assumptions adopted to estimate concentration in fruit and vegetables

Parameter Value adopted Basis DR Particle deposition rate for Adopted maximum Relevant to areas where multi-pathway accidental release (mg/m2/day) deposition rate for discrete exposures may occur receptors F Fraction for the surface area of plant 0.051 Relevant to aboveground exposed (unitless) crops as per Stevens (1991) and OEHHA (OEHHA 2012) k Chemical-specific loss constant for calculated particles on plants (1/days) = ln(2)/T0.5 T0.5 Chemical half-life on plant (day) 14 days Weathering of particulates on plant surfaces does occur and in the absence of measured data, it is generally assumed that organics deposited onto the outer portion of plant surfaces have a weathering half life of 14 days (Stevens, 1991) t Deposition time or length of growing 70 days Relevant to aboveground crops based season (days) on the value relevant to tomatoes, consistent with the value adopted by Stevens (1991) Y Crop yield (kg/m2) 2 kg/m2 Value for aboveground crops (OEHHA 2015) Cs Concentration of pollutant in soil Calculated value for Calculated as described above and (mg/kg) agricultural soil assumptions in Table B4 RUF Root uptake factor (unitless) Chemical specific value Root uptake factors from RAIS (RAIS) adopted (soil to wet weight of plant)

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Eggs

The concentration of bioaccumulative pollutants in animal products is calculated on the basis of the intakes of these pollutants by the animal (chicken) and the transfer of these pollutants to the edible produce. The approach adopted in this assessment has involved calculation of intakes from pasture, assumed to be grown on the property, and soil.

The concentration (CP) calculated in eggs is calculated using the following equation (OEHHA 2015), with parameters and assumptions adopted presented in Table B6:

C푃=(FI x IR퐶 x C + IR푆 x Cs x B) x TF푃

Table B6: Assumptions adopted to estimate concentration in animal produce

Parameter Value adopted Basis FI Fraction of grain/crop ingested 100% Assume all pasture/crops ingested by animals each day derived by chickens and cows are grown on from the property (unitless) the property IRC Ingestion rate of pasture/crops by each animal considered (kg/day) Chickens 0.12 kg/day Ingestion rate from OEHHA (2015) C Concentration of pollutant in Assume equal to that Calculated as described above with crops consumed by animals calculated in assumptions in Table B5 (mg/kg) aboveground produce IRS Ingestion rate of soil by animals each day (kg/day) Chickens 0.0024 kg/day Based on data from OEHHA 2015 (2% total produce intakes from soil) Cs Concentration of pollutant in soil Calculated value for Calculated as described above and (mg/kg) agricultural soil assumptions in Table B5 B Bioavailability of soil ingested 100% Conservative assumption (unitless) TFP Transfer factor for the produce of interest Eggs Chemical specific Transfer factors adopted from OEHHA (2015), with the exception of chromium where the value was derived from an earlier OEHHA (OEHHA 2003) evaluation and the value for antimony has been calculated from a fat transfer factor as per OEHHA (OEHHA 2012)

All calculations relevant to the estimation of pollutant concentrations in soil, fruit and vegetables as well as animal products are presented in Appendix C.

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Appendix C Risk calculations

Residual Waste to Energy Facility, Laverton North: Health Impact Assessment Ref: RE/19/WER001-B

Inhalation exposures

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Inhalation - gases and fine particulates ET •FI •EF •ED InhalationExposureConc = C • (mg/m3) V a AT

Parameters Relevant to Quantification of Community Exposures - Commercial/industrial Exposure Time at Home (ET, hr/day) 8 Workers present for 8 hours per day as per enHealth (2012) Fraction Inhaled from Source (FI, unitless) 1 Assume workers at the same location each day Dust lung retention factor (unitless) 0.375 Percentage of respirable dust that is small enough to reach and be retained in the lungs (NEPM 1999 amended 2013) - NA for gasses Exposure Frequency - normal conditions (EF, days/yr) 235 Days at work (normal conditions), as per NEPM (1999 amended 2013) Exposure Frequency - upset conditions (EFu, days/yr) 5 Assume upset conditions may occur over work 5 days in any one year Exposure Duration (ED, years) 30 As per NEPM (1999 amended 2013) Averaging Time - NonThreshold (Atc, hours) 613200 US EPA 2009 Averaging Time - Threshold (Atn, hours) 262800 US EPA 2009

Normal operating conditions Toxicity Data Concentration Daily Exposure Calculated Risk Inhalation Chronic TC Background Chronic TC Allowable Estimated Inhalation Inhalation Exposure Non- % Total Chronic Hazard % Total Total HI (normal Unit Risk Air Intake (% for Assessment (TC- Concentration in Air - Exposure Concentration - Threshold Risk Quotient HI and upset) Chronic TC) Background) Maximum anywhere Concentration - Threshold Risk Key Chemical (Ca) NonThreshold (mg/m 3)-1 (mg/m 3) (mg/m 3) (mg/m 3) (mg/m 3) (mg/m3) (unitless) (unitless) (unitless) Nitrogen dioxide (NO2) 0.0E+00 5.6E-02 0% 5.6E-02 1.2E-02 1.1E-03 2.5E-03 -- 0.044 0.048 Sulfur dioxide (SO2) 0.0E+00 5.0E-02 0% 5.0E-02 6.1E-03 5.6E-04 1.3E-03 -- 0.026 0.027 Hydrogen chloride (HCl) 0.0E+00 2.6E-02 0% 2.6E-02 2.3E-04 2.1E-05 5.0E-05 -- 0.0019 6% 0.0022 Hydrogen fluoride (HF) 0.0E+00 2.9E-02 0% 2.9E-02 2.2E-05 2.0E-06 4.7E-06 -- 0.00016 1% 0.00016 Cadmium 0.0E+00 5.0E-06 20% 4.0E-06 7.4E-08 2.6E-09 6.0E-09 -- 0.0015 5% 0.0016 Beryllium 0.0E+00 2.0E-05 20% 1.6E-05 2.2E-07 7.6E-09 1.8E-08 -- 0.0011 4% 0.0011 Mercury 0.0E+00 2.0E-04 10% 1.8E-04 4.5E-07 1.6E-08 3.6E-08 -- 0.00020 1% 0.00022 Antimony 0.0E+00 2.0E-04 0% 2.0E-04 7.0E-07 2.4E-08 5.6E-08 -- 0.00028 1% 0.00030 Arsenic 0.0E+00 1.0E-03 0% 1.0E-03 2.3E-05 7.8E-07 1.8E-06 -- 0.0018 6% 0.0019 Lead 0.0E+00 5.0E-04 0% 5.0E-04 1.2E-05 4.0E-07 9.4E-07 -- 0.0019 6% 0.0020 Chromium (Cr VI assumed) 0.0E+00 1.0E-04 0% 1.0E-04 8.5E-07 2.9E-08 6.8E-08 -- 0.00068 2% 0.00076 Copper 0.0E+00 4.9E-01 0% 4.9E-01 1.3E-06 4.5E-08 1.0E-07 -- 0.00000021 0% 0.00000022 Manganese 0.0E+00 1.5E-04 20% 1.2E-04 1.8E-06 6.1E-08 1.4E-07 -- 0.0012 4% 0.0013 Nickel 0.0E+00 2.0E-05 20% 1.6E-05 3.8E-06 1.3E-07 3.1E-07 -- 0.019 62% 0.021 Dioxins and furans 0.0E+00 8.1E-09 54% 3.7E-09 1.0E-11 3.6E-13 8.3E-13 -- 0.00022 1% 0.00023 MDI 0.0E+00 6.0E-04 0% 6.0E-04 2.2E-06 2.0E-07 4.7E-07 -- 0.00079 3% 0.00080 TOTAL 0.0E+00 0.031 0.034

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Upset operating conditions Toxicity Data Concentration Daily Exposure Calculated Risk Inhalation Chronic TC Background Chronic TC Allowable Estimated Inhalation Inhalation Exposure Non- % Total Chronic Hazard % Total Unit Risk Air Intake (% for Assessment (TC- Concentration in Air - Exposure Concentration - Threshold Risk Quotient HI Chronic TC) Background) Maximum receptors Concentration - Threshold Risk Key Chemical (Ca) NonThreshold (mg/m3)-1 (mg/m3) (mg/m3) (mg/m3) (mg/m3) (mg/m3) (unitless) (unitless) Nitrogen dioxide (NO2) 0.0E+00 5.6E-02 0% 5.6E-02 4.1E-02 7.9E-05 1.9E-04 -- 0.0033 Sulfur dioxide (SO2) 0.0E+00 5.0E-02 0% 5.0E-02 1.2E-02 2.4E-05 5.7E-05 -- 0.0011 Hydrogen chloride (HCl) 0.0E+00 2.6E-02 0% 2.6E-02 1.5E-03 2.9E-06 6.7E-06 -- 0.00026 10% Hydrogen fluoride (HF) 0.0E+00 2.9E-02 0% 2.9E-02 2.2E-05 4.3E-08 1.0E-07 -- 0.0000034 0% Cadmium 0.0E+00 5.0E-06 20% 4.0E-06 1.9E-07 1.4E-10 3.3E-10 -- 0.000081 3% Beryllium 0.0E+00 2.0E-05 20% 1.6E-05 2.2E-07 1.6E-10 3.8E-10 -- 0.000024 1% Mercury 0.0E+00 2.0E-04 10% 1.8E-04 1.9E-06 1.4E-09 3.3E-09 -- 0.000018 1% Antimony 0.0E+00 2.0E-04 0% 2.0E-04 2.1E-06 1.5E-09 3.6E-09 -- 0.000018 1% Arsenic 0.0E+00 1.0E-03 0% 1.0E-03 7.0E-05 5.1E-08 1.2E-07 -- 0.00012 5% Lead 0.0E+00 5.0E-04 0% 5.0E-04 2.2E-05 1.6E-08 3.8E-08 -- 0.000075 3% Chromium (Cr VI assumed) 0.0E+00 1.0E-04 0% 1.0E-04 4.5E-06 3.3E-09 7.7E-09 -- 0.000077 3% Copper 0.0E+00 4.9E-01 0% 4.9E-01 3.2E-06 2.3E-09 5.5E-09 -- 0.000000011 0% Manganese 0.0E+00 1.5E-04 20% 1.2E-04 5.2E-06 3.8E-09 8.9E-09 -- 0.000074 3% Nickel 0.0E+00 2.0E-05 20% 1.6E-05 1.7E-05 1.2E-08 2.9E-08 -- 0.0018 70% Dioxins and furans 0.0E+00 8.1E-09 54% 3.7E-09 2.2E-11 1.6E-14 3.8E-14 -- 0.000010 0% MDI 0.0E+00 6.0E-04 0% 6.0E-04 2.2E-06 4.3E-09 1.0E-08 -- 0.000017 1%

TOTAL 0.0E+00 0.0026

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Inhalation - gases and fine particulates ET •FI •EF •ED InhalationExposureConc = C • (mg/m3) V a AT

Parameters Relevant to Quantification of Community Exposures - Residents Exposure Time at Home (ET, hr/day) 24 Assume residents at home or on property 24 hours per day Fraction Inhaled from Source (FI, unitless) 1 Assume resident at the same property Dust lung retention factor (unitless) 0.375 Percentage of respirable dust that is small enough to reach and be retained in the lungs (NEPM 1999 amended 2013) - NA for gasses Exposure Frequency - normal conditions (EF, days/yr) 360 Days at home (normal conditions), as per NEPM (1999 amended 2013) Exposure Frequency - upset conditions (EFu, days/yr) 5 Assume upset conditions may occur over 5 days in any one year Exposure Duration (ED, years) 35 As per NEPM (1999 amended 2013) Averaging Time - NonThreshold (Atc, hours) 613200 US EPA 2009 Averaging Time - Threshold (Atn, hours) 306600 US EPA 2009

Normal operating conditions Toxicity Data Concentration Daily Exposure Calculated Risk Inhalation Chronic TC Background Chronic TC Allowable Estimated Inhalation Inhalation Exposure Non- % Total Chronic Hazard % Total Total HI Unit Risk Air Intake (% for Assessment (TC- Concentration in Air - Exposure Concentration - Threshold Risk Quotient HI (normal and Chronic TC) Background) Maximum anywhere Concentration - Threshold Risk upset) Key Chemical (Ca) NonThreshold (mg/m 3)-1 (mg/m 3) (mg/m3) (mg/m 3) (mg/m 3) (mg/m3) (unitless) (unitless) (unitless) Nitrogen dioxide (NO2) 0.0E+00 5.6E-02 0% 5.6E-02 1.2E-04 6.0E-05 1.2E-04 -- 0.0021 0.0023 Sulfur dioxide (SO2) 0.0E+00 5.0E-02 0% 5.0E-02 6.4E-05 3.2E-05 6.3E-05 -- 0.0013 0.0013 Hydrogen chloride (HCl) 0.0E+00 2.6E-02 0% 2.6E-02 2.4E-06 1.2E-06 2.4E-06 -- 0.000091 6% 0.000099 Hydrogen fluoride (HF) 0.0E+00 2.9E-02 0% 2.9E-02 2.3E-07 1.1E-07 2.3E-07 -- 0.0000078 1% 0.0000079 Cadmium 0.0E+00 5.0E-06 20% 4.0E-06 7.8E-10 1.4E-10 2.9E-10 -- 0.000072 5% 0.000075 Beryllium 0.0E+00 2.0E-05 20% 1.6E-05 2.3E-09 4.3E-10 8.5E-10 -- 0.000053 4% 0.000054 Mercury 0.0E+00 2.0E-04 10% 1.8E-04 4.7E-09 8.7E-10 1.7E-09 -- 0.000010 1% 0.000010 Antimony 0.0E+00 2.0E-04 0% 2.0E-04 7.3E-09 1.4E-09 2.7E-09 -- 0.000014 1% 0.000014 Arsenic 0.0E+00 1.0E-03 0% 1.0E-03 2.4E-07 4.4E-08 8.9E-08 -- 0.000089 6% 0.000093 Lead 0.0E+00 5.0E-04 0% 5.0E-04 1.2E-07 2.2E-08 4.4E-08 -- 0.000089 6% 0.000091 Chromium (Cr VI assumed) 0.0E+00 1.0E-04 0% 1.0E-04 8.9E-09 1.6E-09 3.3E-09 -- 0.000033 2% 0.000035 Copper 0.0E+00 4.9E-01 0% 4.9E-01 1.3E-08 2.4E-09 4.8E-09 -- 0.000000010 0% 0.000000010 Manganese 0.0E+00 1.5E-04 20% 1.2E-04 1.9E-08 3.4E-09 6.9E-09 -- 0.000057 4% 0.000060 Nickel 0.0E+00 2.0E-05 20% 1.6E-05 4.0E-08 7.4E-09 1.5E-08 -- 0.00092 62% 0.00098 Dioxins and furans 0.0E+00 8.1E-09 54% 3.7E-09 1.1E-13 2.0E-14 4.1E-14 -- 0.000011 1% 0.000011 MDI 0.0E+00 6.0E-04 0% 6.0E-04 2.3E-08 1.1E-08 2.2E-08 -- 0.000037 3% 0.000038

TOTAL 0.0E+00 0.0015 0.0016

Residual Waste to Energy Facility, Laverton North: Health Impact Assessment C-4 | P a g e Ref: F/18/CRS001- A

Upset operating conditions Toxicity Data Concentration Daily Exposure Calculated Risk Inhalation Chronic TC Background Chronic TC Allowable Estimated Inhalation Inhalation Exposure Non- % Total Chronic Hazard % Total Unit Risk Air Intake (% for Assessment (TC- Concentration in Air - Exposure Concentration - Threshold Risk Quotient HI Chronic TC) Background) Maximum receptors Concentration - Threshold Risk Key Chemical (Ca) NonThreshold (mg/m3)-1 (mg/m3) (mg/m3) (mg/m3) (mg/m3) (mg/m3) (unitless) (unitless) Nitrogen dioxide (NO2) 0.0E+00 5.6E-02 0% 5.6E-02 4.2E-04 2.9E-06 5.8E-06 -- 0.00010 Sulfur dioxide (SO2) 0.0E+00 5.0E-02 0% 5.0E-02 1.3E-04 8.9E-07 1.8E-06 -- 0.000036 Hydrogen chloride (HCl) 0.0E+00 2.6E-02 0% 2.6E-02 1.5E-05 1.0E-07 2.1E-07 -- 0.0000079 10% Hydrogen fluoride (HF) 0.0E+00 2.9E-02 0% 2.9E-02 2.3E-07 1.6E-09 3.2E-09 -- 0.00000011 0% Cadmium 0.0E+00 5.0E-06 20% 4.0E-06 2.0E-09 5.1E-12 1.0E-11 -- 0.0000026 3% Beryllium 0.0E+00 2.0E-05 20% 1.6E-05 2.3E-09 5.9E-12 1.2E-11 -- 0.00000074 1% Mercury 0.0E+00 2.0E-04 10% 1.8E-04 2.0E-08 5.1E-11 1.0E-10 -- 0.00000057 1% Antimony 0.0E+00 2.0E-04 0% 2.0E-04 2.2E-08 5.7E-11 1.1E-10 -- 0.00000057 1% Arsenic 0.0E+00 1.0E-03 0% 1.0E-03 7.3E-07 1.9E-09 3.8E-09 -- 0.0000038 5% Lead 0.0E+00 5.0E-04 0% 5.0E-04 2.3E-07 5.9E-10 1.2E-09 -- 0.0000024 3% Chromium (Cr VI assumed) 0.0E+00 1.0E-04 0% 1.0E-04 4.7E-08 1.2E-10 2.4E-10 -- 0.0000024 3% Copper 0.0E+00 4.9E-01 0% 4.9E-01 3.3E-08 8.5E-11 1.7E-10 -- 0.00000000035 0% Manganese 0.0E+00 1.5E-04 20% 1.2E-04 5.4E-08 1.4E-10 2.8E-10 -- 0.0000023 3% Nickel 0.0E+00 2.0E-05 20% 1.6E-05 1.8E-07 4.6E-10 9.2E-10 -- 0.000058 71% Dioxins and furans 0.0E+00 8.1E-09 54% 3.7E-09 2.3E-13 5.9E-16 1.2E-15 -- 0.00000032 0% MDI 0.0E+00 6.0E-04 0% 6.0E-04 2.3E-08 1.6E-10 3.1E-10 -- 0.00000052 1%

TOTAL 0.0E+00 0.000082

Residual Waste to Energy Facility, Laverton North: Health Impact Assessment C-5 | P a g e Ref: F/18/CRS001- A

Soil exposures

Residual Waste to Energy Facility, Laverton North: Health Impact Assessment C-6 | P a g e Ref: F/18/CRS001- A

Calculation of Concentrations in Soil

DR • 1− e −k•t C =  •1000 (mg/kg) ref: Stevens B. (1991) s d •  • k where: DR= Particle deposition rate (mg/m2/year) K = Chemical-specific soil-loss constant (1/year) = ln(2)/T0.5 T0.5 = Chemical half-life in soil (years) t = Accumulation time (years) d = Soil mixing depth (m) ρ = Soil bulk-density (g/m3) 1000 = Conversion from g to kg

Depth (for Surface (for agricultural General Parameters direct contact) pathways) Soil bulk density (p) g/m3 1600000 1600000 Default for fill materials General mixing depth (d) m 0.01 0.15 As per OEHHA (2015) guidance Duration of deposition (T) years 70 70 As per OEHHA (2015) guidance

Chemical-specific Inputs and calculations - maximum receptors (normal) Surface Agricultural Chemical Half-life in Loss constant Deposition Concentration in Concentration soil (K) Rate (DR) Soil in Soil years per year mg/m2/year mg/kg mg/kg Cadmium 273973 2.5E-06 1.4E-06 6.3E-06 4.2E-07 Beryllium 273973 2.5E-06 4.4E-06 1.9E-05 1.3E-06 Mercury 273973 2.5E-06 9.0E-06 4.0E-05 2.6E-06 Antimony 273973 2.5E-06 1.4E-05 6.1E-05 4.1E-06 Arsenic 273973 2.5E-06 4.5E-04 2.0E-03 1.3E-04 Lead 273973 2.5E-06 2.4E-04 1.0E-03 6.9E-05 Chromium (Cr VI assumed) 273973 2.5E-06 1.7E-05 7.5E-05 5.0E-06 Copper 273973 2.5E-06 2.5E-05 1.1E-04 7.4E-06 Manganese 273973 2.5E-06 3.6E-05 1.6E-04 1.0E-05 Nickel 273973 2.5E-06 7.7E-05 3.4E-04 2.2E-05 Dioxins and furans 0.069 2.0E-10 1.8E-10 1.2E-11

Half-life in soil: dioxin loss constant from Lowe et al (1991) and half-life for remainder from OEHHA (2015)

Chemical-specific Inputs and calculations - maximum receptors (upset) Surface Agricultural Chemical Half-life in Loss constant Deposition Concentration in Concentration soil (K) Rate (DR) Soil in Soil years per year mg/m2/year mg/kg mg/kg Cadmium 273973 2.5E-06 3.8E-06 1.7E-05 1.1E-06 Beryllium 273973 2.5E-06 4.4E-06 1.9E-05 1.3E-06 Mercury 273973 2.5E-06 3.8E-05 1.7E-04 1.1E-05 Antimony 273973 2.5E-06 4.2E-05 1.8E-04 1.2E-05 Arsenic 273973 2.5E-06 1.4E-03 6.3E-03 4.2E-04 Lead 273973 2.5E-06 4.4E-04 1.9E-03 1.3E-04 Chromium (Cr VI assumed) 273973 2.5E-06 9.0E-05 3.9E-04 2.6E-05 Copper 273973 2.5E-06 6.4E-05 2.8E-04 1.9E-05 Manganese 273973 2.5E-06 1.0E-04 4.6E-04 3.0E-05 Nickel 273973 2.5E-06 3.6E-04 1.6E-03 1.0E-04 Dioxins and furans 0.069 4.4E-10 4.0E-10 2.6E-11

Half-life in soil: dioxin loss constant from Lowe et al (1991) and half-life for remainder from OEHHA (2015)

Residual Waste to Energy Facility, Laverton North: Health Impact Assessment C-7 | P a g e Ref: F/18/CRS001- A

Exposure to Chemicals via Incidental Ingestion of Soil IR • FI •CF • B • EF • ED Daily Chemical Intake = C • S (mg/kg/day) IS S BW • AT

Parameters Relevant to Quantification of Exposure by Adults Ingestion Rate (IRs, mg/day) 50 As per NEPM 2013 Fraction Ingested from Source (FI, unitless) 100% All of daily soil intake occurs from site Exposure Frequency (EF, days/year) 360 Days at home (normal conditions), as per NEPM (1999 amended 2013) Exposure Frequency - upset (EFu, days/yr) 5 Assume upset conditions may occur over 5 days in any one year Exposure Duration (ED, years) 29 Time at one residence as adult as per enHealth 2002 and NEPM 1999 Body Weight (BW, kg) 70 For male and females combined (enHealth 2012) Conversion Factor (CF) 1.00E-06 conversion from mg to kg Averaging Time - NonThreshold (Atc, days) 25550 USEPA 1989 and CSMS 1996 Averaging Time - Threshold (Atn, days) 10585 USEPA 1989 and CSMS 1996

Maximum - All receptors (normal operationg conditions)

Toxicity Data Daily Intake Calculated Risk Non-Threshold Threshold Background TDI Allowable for Soil NonThreshold Threshold Non-Threshold % Total Chronic Hazard % Total Slope Factor TDI Intake (% TDI) Assessment (TDI- Concentration Risk Risk Quotient HI Key Chemical Background) Bioavailability (mg/kg-day)-1 (mg/kg/day) (mg/kg/day) (%) (mg/kg) (mg/kg/day) (mg/kg/day) (unitless) (unitless) Cadmium 8.0E-04 60% 3.2E-04 100% 6.3E-06 1.8E-12 4.4E-12 -- 1.4E-08 1% Beryllium 2.0E-03 20% 1.6E-03 100% 1.9E-05 5.6E-12 1.4E-11 -- 8.5E-09 0% Mercury 6.0E-04 40% 3.6E-04 100% 4.0E-05 1.2E-11 2.8E-11 -- 7.7E-08 4% Antimony 8.6E-04 8.6E-04 100% 6.1E-05 1.8E-11 4.3E-11 -- 5.0E-08 2% Arsenic 2.0E-03 50% 1.0E-03 100% 2.0E-03 5.8E-10 1.4E-09 -- 1.4E-06 64% Lead 3.5E-03 50% 1.8E-03 100% 1.0E-03 3.0E-10 7.2E-10 -- 4.1E-07 19% Chromium (Cr VI assumed) 1.0E-03 10% 9.0E-04 100% 7.5E-05 2.2E-11 5.3E-11 -- 5.9E-08 3% Copper 1.4E-01 60% 5.6E-02 100% 1.1E-04 3.2E-11 7.8E-11 -- 1.4E-09 0% Manganese 1.4E-01 50% 7.0E-02 100% 1.6E-04 4.6E-11 1.1E-10 -- 1.6E-09 0% Nickel 1.2E-02 60% 4.8E-03 100% 3.4E-04 9.8E-11 2.4E-10 -- 4.9E-08 2% Dioxins and furans 2.3E-09 54% 1.1E-09 100% 1.8E-10 5.3E-17 1.3E-16 -- 1.2E-07 6%

TOTAL 2.2E-6

Maximum - All receptors (upset operating conditions)

Toxicity Data Daily Intake Calculated Risk Non-Threshold Threshold Background TDI Allowable for Soil NonThreshold Threshold Non-Threshold % Total Chronic Hazard % Total Slope Factor TDI Intake (% TDI) Assessment (TDI- Concentration Risk Risk Quotient HI Key Chemical Background) Bioavailability (mg/kg-day)-1 (mg/kg/day) (mg/kg/day) (%) (mg/kg) (mg/kg/day) (mg/kg/day) (unitless) (unitless) Cadmium 8.0E-04 60% 3.2E-04 100% 1.7E-05 6.8E-14 1.6E-13 -- 5.1E-10 1% Beryllium 2.0E-03 20% 1.6E-03 100% 1.9E-05 7.9E-14 1.9E-13 -- 1.2E-10 0% Mercury 6.0E-04 40% 3.6E-04 100% 1.7E-04 6.8E-13 1.6E-12 -- 4.6E-09 5% Antimony 8.6E-04 8.6E-04 100% 1.8E-04 7.4E-13 1.8E-12 -- 2.1E-09 2% Arsenic 2.0E-03 50% 1.0E-03 100% 6.3E-03 2.6E-11 6.2E-11 -- 6.2E-08 68% Lead 3.5E-03 50% 1.8E-03 100% 1.9E-03 7.9E-12 1.9E-11 -- 1.1E-08 12% Chromium (Cr VI assumed) 1.0E-03 10% 9.0E-04 100% 3.9E-04 1.6E-12 3.9E-12 -- 4.3E-09 5% Copper 1.4E-01 60% 5.6E-02 100% 2.8E-04 1.1E-12 2.7E-12 -- 4.9E-11 0% Manganese 1.4E-01 50% 7.0E-02 100% 4.6E-04 1.9E-12 4.5E-12 -- 6.4E-11 0% Nickel 1.2E-02 60% 4.8E-03 100% 1.6E-03 6.4E-12 1.5E-11 -- 3.2E-09 4% Dioxins and furans 2.3E-09 54% 1.1E-09 100% 4.0E-10 1.6E-18 3.9E-18 -- 3.7E-09 4% TOTAL 9.1E-08 Residual Waste to Energy Facility, Laverton North: Health Impact Assessment C-8 | P a g e Ref: F/18/CRS001- A

Exposure to Chemicals via Incidental Ingestion of Soil IR • FI •CF • B • EF • ED Daily Chemical Intake = C • S (mg/kg/day) IS S BW • AT

Parameters Relevant to Quantification of Exposure by Young Children Ingestion Rate (IRs, mg/day) 100 Assumed daily soil ingestion rate for young children, enHealth (2012) Fraction Ingested from Source (FI, unitless) 100% All of daily soil intake occurs from site Exposure Frequency (EF, days/year) 360 Days at home (normal conditions), as per NEPM (1999 amended 2013) Exposure Frequency - upset (EFu, days/yr) 5 Assume upset conditions may occur over 5 days in any one year Exposure Duration (ED, years) 6 Duration as young child Body Weight (BW, kg) 15 Representative weight as per NEPM (2013) Conversion Factor (CF) 1.00E-06 conversion from mg to kg Averaging Time - NonThreshold (Atc, days) 25550 USEPA 1989 and CSMS 1996 Averaging Time - Threshold (Atn, days) 2190 USEPA 1989 and CSMS 1996

Maximum - All receptors (normal operationg conditions)

Toxicity Data Daily Intake Calculated Risk Non-Threshold Threshold Background TDI Allowable for Soil NonThreshold Threshold Non-Threshold % Total Chronic Hazard % Total Slope Factor TDI Intake (% TDI) Assessment (TDI- Concentration Risk Risk Quotient HI Key Chemical Background) Bioavailability (mg/kg-day)-1 (mg/kg/day) (mg/kg/day) (%) (mg/kg) (mg/kg/day) (mg/kg/day) (unitless) (unitless) Cadmium 8.0E-04 60% 3.2E-04 100% 6.3E-06 3.6E-12 4.1E-11 -- 1.3E-07 1% Beryllium 2.0E-03 20% 1.6E-03 100% 1.9E-05 1.1E-11 1.3E-10 -- 7.9E-08 0% Mercury 6.0E-04 40% 3.6E-04 100% 4.0E-05 2.2E-11 2.6E-10 -- 7.2E-07 4% Antimony 8.6E-04 8.6E-04 100% 6.1E-05 3.5E-11 4.0E-10 -- 4.7E-07 2% Arsenic 2.0E-03 50% 1.0E-03 100% 2.0E-03 1.1E-09 1.3E-08 -- 1.3E-05 64% Lead 3.5E-03 50% 1.8E-03 100% 1.0E-03 5.8E-10 6.8E-09 -- 3.9E-06 19% Chromium (Cr VI assumed) 1.0E-03 10% 9.0E-04 100% 7.5E-05 4.2E-11 4.9E-10 -- 5.5E-07 3% Copper 1.4E-01 60% 5.6E-02 100% 1.1E-04 6.2E-11 7.3E-10 -- 1.3E-08 0% Manganese 1.4E-01 50% 7.0E-02 100% 1.6E-04 8.9E-11 1.0E-09 -- 1.5E-08 0% Nickel 1.2E-02 60% 4.8E-03 100% 3.4E-04 1.9E-10 2.2E-09 -- 4.6E-07 2% Dioxins and furans 2.3E-09 54% 1.1E-09 100% 1.8E-10 1.0E-16 1.2E-15 -- 1.1E-06 6%

TOTAL 2.0E-5

Maximum - All receptors (upset operating conditions)

Toxicity Data Daily Intake Calculated Risk Non-Threshold Threshold Background TDI Allowable for Soil NonThreshold Threshold Non-Threshold % Total Chronic Hazard % Total Slope Factor TDI Intake (% TDI) Assessment (TDI- Concentration Risk Risk Quotient HI Key Chemical Background) Bioavailability (mg/kg-day)-1 (mg/kg/day) (mg/kg/day) (%) (mg/kg) (mg/kg/day) (mg/kg/day) (unitless) (unitless) Cadmium 8.0E-04 60% 3.2E-04 100% 1.7E-05 1.3E-13 1.5E-12 -- 4.8E-09 1% Beryllium 2.0E-03 20% 1.6E-03 100% 1.9E-05 1.5E-13 1.8E-12 -- 1.1E-09 0% Mercury 6.0E-04 40% 3.6E-04 100% 1.7E-04 1.3E-12 1.5E-11 -- 4.3E-08 5% Antimony 8.6E-04 8.6E-04 100% 1.8E-04 1.4E-12 1.7E-11 -- 2.0E-08 2% Arsenic 2.0E-03 50% 1.0E-03 100% 6.3E-03 4.9E-11 5.8E-10 -- 5.8E-07 68% Lead 3.5E-03 50% 1.8E-03 100% 1.9E-03 1.5E-11 1.8E-10 -- 1.0E-07 12% Chromium (Cr VI assumed) 1.0E-03 10% 9.0E-04 100% 3.9E-04 3.1E-12 3.6E-11 -- 4.0E-08 5% Copper 1.4E-01 60% 5.6E-02 100% 2.8E-04 2.2E-12 2.5E-11 -- 4.5E-10 0% Manganese 1.4E-01 50% 7.0E-02 100% 4.6E-04 3.6E-12 4.2E-11 -- 6.0E-10 0% Nickel 1.2E-02 60% 4.8E-03 100% 1.6E-03 1.2E-11 1.4E-10 -- 3.0E-08 4% Dioxins and furans 2.3E-09 54% 1.1E-09 100% 4.0E-10 3.1E-18 3.6E-17 -- 3.4E-08 4% TOTAL 8.5E-07 Residual Waste to Energy Facility, Laverton North: Health Impact Assessment C-9 | P a g e Ref: F/18/CRS001- A

Dermal Exposure to Chemicals via Contact with Soil

SA • AF • FE • ABS •CF • EF • ED Daily Chemical Intake = C • S (mg/kg/day) DS S BW • AT

Parameters Relevant to Quantification of Exposure by Adults Surface Area (SAs, cm2) 6300 Exposed skin surface area for adults as per NEPM (2013) Adherence Factor (AF, mg/cm2) 0.5 Default as per NEPM (2013) Fraction of Day Exposed 1 Assume skin is washed after 24 hours Conversion Factor (CF) 1.E-06 Conversion of units Dermal absorption (ABS, unitless) Chemical-specific (as below) Exposure Frequency (EF, days/year) 360 Days at home (normal conditions), as per NEPM (1999 amended 2013) Exposure Frequency - upset (EFu, days/yr) 5 Assume upset conditions may occur over 5 days in any one year Exposure Duration (ED, years) 29 Time at one residence as adult as per enHealth 2002 and NEPM 1999 Body Weight (BW, kg) 70 For male and females combined (enHealth 2012) Averaging Time - NonThreshold (Atc, days) 25550 USEPA 1989 and CSMS 1996 Averaging Time - Threshold (Atn, days) 10585 USEPA 1989 and CSMS 1996

Maximum - All receptors (normal operationg conditions)

Toxicity Data Daily Intake Calculated Risk Non-Threshold Threshold Background TDI Allowable for Dermal Soil Non- Threshold Non- % Total Chronic % Total Slope Factor TDI Intake (% TDI) Assessment (TDI- Absorption Concentration Threshold Threshold Risk Hazard HI Key Chemical Background) (ABS) Risk Quotient (mg/kg-day)-1 (mg/kg/day) (mg/kg/day) (mg/kg) (mg/kg/day) (mg/kg/day) (unitless) (unitless) Cadmium 8.0E-04 60% 3.2E-04 6.3E-06 -- -- Beryllium 2.0E-03 20% 1.6E-03 0.001 1.9E-05 3.5E-13 8.5E-13 -- 5.3E-10 0% Mercury 4.2E-05 40% 2.5E-05 0.001 4.0E-05 7.3E-13 1.8E-12 -- 7.0E-8 9% Antimony 1.3E-04 1.3E-04 6.1E-05 -- -- Arsenic 2.0E-03 50% 1.0E-03 0.005 2.0E-03 1.8E-10 4.4E-10 -- 4.4E-7 58% Lead 3.5E-03 50% 1.8E-03 1.0E-03 -- -- Chromium (Cr VI assumed) 1.0E-03 10% 9.0E-04 7.5E-05 -- -- Copper 1.4E-01 60% 5.6E-02 1.1E-04 -- -- Manganese 1.4E-01 50% 7.0E-02 1.6E-04 -- -- Nickel 1.2E-02 60% 4.8E-03 0.005 3.4E-04 3.1E-11 7.5E-11 -- 1.6E-8 2% Dioxins and furans 2.3E-09 54% 1.1E-09 0.03 1.8E-10 1.0E-16 2.4E-16 -- 2.3E-7 30%

TOTAL 7.5E-7

Maximum - All receptors (upset operating conditions)

Toxicity Data Daily Intake Calculated Risk Non-Threshold Threshold Background TDI Allowable for Dermal Soil Non- Threshold Non- % Total Chronic % Total Slope Factor TDI Intake (% TDI) Assessment (TDI- Absorption Concentration Threshold Threshold Risk Hazard HI Key Chemical Background) (ABS) Risk Quotient (mg/kg-day)-1 (mg/kg/day) (mg/kg/day) (mg/kg) (mg/kg/day) (mg/kg/day) (unitless) (unitless) Cadmium 8.0E-04 60% 3.2E-04 1.7E-05 -- -- Beryllium 2.0E-03 20% 1.6E-03 0.001 1.9E-05 5.0E-15 1.2E-14 -- 7.5E-12 0% Mercury 4.2E-05 40% 2.5E-05 0.001 1.7E-04 4.3E-14 1.0E-13 -- 4.1E-09 13% Antimony 1.3E-04 1.3E-04 1.8E-04 -- -- Arsenic 2.0E-03 50% 1.0E-03 0.005 6.3E-03 8.0E-12 1.9E-11 -- 1.9E-08 62% Lead 3.5E-03 50% 1.8E-03 1.9E-03 -- -- Chromium (Cr VI assumed) 1.0E-03 10% 9.0E-04 3.9E-04 -- -- Copper 1.4E-01 60% 5.6E-02 2.8E-04 -- -- Manganese 1.4E-01 50% 7.0E-02 4.6E-04 -- -- Nickel 1.2E-02 60% 4.8E-03 0.005 1.6E-03 2.0E-12 4.9E-12 -- 1.0E-09 3% Dioxins and furans 2.3E-09 54% 1.1E-09 0.03 4.0E-10 3.0E-18 7.3E-18 -- 6.9E-09 22% TOTAL 3.1E-08 Residual Waste to Energy Facility, Laverton North: Health Impact Assessment C-10 | P a g e Ref: F/18/CRS001- A

Dermal Exposure to Chemicals via Contact with Soil

SA • AF • FE • ABS •CF • EF • ED Daily Chemical Intake = C • S (mg/kg/day) DS S BW • AT

Parameters Relevant to Quantification of Exposure by Young Children Surface Area (SAs, cm2) 2700 Exposed skin surface area for young children as per NEPM (2013) Adherence Factor (AF, mg/cm2) 0.5 Default as per NEPM (2013) Fraction of Day Exposed 1 Assume skin is washed after 24 hours Conversion Factor (CF) 1.E-06 Conversion of units Dermal absorption (ABS, unitless) Chemical-specific (as below) Exposure Frequency (EF, days/year) 360 Days at home (normal conditions), as per NEPM (1999 amended 2013) Exposure Frequency - upset (EFu, days/yr) 5 Assume upset conditions may occur over 5 days in any one year Exposure Duration (ED, years) 6 Duration as young child Body Weight (BW, kg) 15 Representative weight as per NEPM (2013) Averaging Time - NonThreshold (Atc, days) 25550 USEPA 1989 and CSMS 1996 Averaging Time - Threshold (Atn, days) 2190 USEPA 1989 and CSMS 1996

Maximum - All receptors (normal operationg conditions)

Toxicity Data Daily Intake Calculated Risk Non-Threshold Threshold Background TDI Allowable for Dermal Soil Non- Threshold Non- % Total Chronic % Total Slope Factor TDI Intake (% TDI) Assessment (TDI- Absorption Concentration Threshold Threshold Risk Hazard HI Key Chemical Background) (ABS) Risk Quotient (mg/kg-day)-1 (mg/kg/day) (mg/kg/day) (mg/kg) (mg/kg/day) (mg/kg/day) (unitless) (unitless) Cadmium 8.0E-04 60% 3.2E-04 6.3E-06 -- -- Beryllium 2.0E-03 20% 1.6E-03 0.001 1.9E-05 1.5E-13 1.7E-12 -- 1.1E-9 0% Mercury 4.2E-05 40% 2.5E-05 0.001 4.0E-05 3.0E-13 3.5E-12 -- 1.4E-7 9% Antimony 1.3E-04 1.3E-04 6.1E-05 -- -- Arsenic 2.0E-03 50% 1.0E-03 0.005 2.0E-03 7.5E-11 8.8E-10 -- 8.8E-7 58% Lead 3.5E-03 50% 1.8E-03 1.0E-03 -- -- Chromium (Cr VI assumed) 1.0E-03 10% 9.0E-04 7.5E-05 -- -- Copper 1.4E-01 60% 5.6E-02 1.1E-04 -- -- Manganese 1.4E-01 50% 7.0E-02 1.6E-04 -- -- Nickel 1.2E-02 60% 4.8E-03 0.005 3.4E-04 1.3E-11 1.5E-10 -- 3.1E-8 2% Dioxins and furans 2.3E-09 54% 1.1E-09 0.03 1.8E-10 4.2E-17 4.9E-16 -- 4.6E-7 30%

TOTAL 1.5E-6

Maximum - All receptors (upset operating conditions)

Toxicity Data Daily Intake Calculated Risk Non-Threshold Threshold Background TDI Allowable for Dermal Soil Non- Threshold Non- % Total Chronic % Total Slope Factor TDI Intake (% TDI) Assessment (TDI- Absorption Concentration Threshold Threshold Risk Hazard HI Key Chemical Background) (ABS) Risk Quotient (mg/kg-day)-1 (mg/kg/day) (mg/kg/day) (mg/kg) (mg/kg/day) (mg/kg/day) (unitless) (unitless) Cadmium 8.0E-04 60% 3.2E-04 1.7E-05 -- -- Beryllium 2.0E-03 20% 1.6E-03 0.001 1.9E-05 2.1E-15 2.4E-14 -- 1.5E-11 0% Mercury 4.2E-05 40% 2.5E-05 0.001 1.7E-04 1.8E-14 2.1E-13 -- 8.2E-09 13% Antimony 1.3E-04 1.3E-04 1.8E-04 -- -- Arsenic 2.0E-03 50% 1.0E-03 0.005 6.3E-03 3.3E-12 3.9E-11 -- 3.9E-08 62% Lead 3.5E-03 50% 1.8E-03 1.9E-03 -- -- Chromium (Cr VI assumed) 1.0E-03 10% 9.0E-04 3.9E-04 -- -- Copper 1.4E-01 60% 5.6E-02 2.8E-04 -- -- Manganese 1.4E-01 50% 7.0E-02 4.6E-04 -- -- Nickel 1.2E-02 60% 4.8E-03 0.005 1.6E-03 8.3E-13 9.7E-12 -- 2.0E-09 3% Dioxins and furans 2.3E-09 54% 1.1E-09 0.03 4.0E-10 1.3E-18 1.5E-17 -- 1.4E-08 22% TOTAL 6.3E-08 Residual Waste to Energy Facility, Laverton North: Health Impact Assessment C-11 | P a g e Ref: F/18/CRS001- A

Homegrown fruit and vegetables

Residual Waste to Energy Facility, Laverton North: Health Impact Assessment C-12 | P a g e Ref: F/18/CRS001- A

Calculation of Concentrations in Plants ref: Stevens B. (1991)

Uptake Due to Deposition in Aboveground Crops Uptake via Roots from Soil

DR • F • 1− e−k •t  C = (mg/kg plant – wet weight) C rp = C s • RUF (mg/kg plant – wet weight) p Y • k where: where: DR= Particle deposition rate for accidental release (mg/m 2/day) Cs = Concentration of persistent chemical in soil assuming 15cm mixing depth F= Fraction for the surface area of plant (unitless) within gardens, calculated using Soil Equation for each chemical assessed (mg/kg) k= Chemical-specific soil-loss constant (1/years) = ln(2)/T0.5 RUF = Root uptake factor which differs for each Chemical (unitless)

T0.5= Chemical half-life as particulate on plant (days) t= Deposition time (days) Y= Crop yield (kg/m 2)

General Parameters Units Value Crop Edible crops Crop Yield (Y) kg/m2 2 Deposition Time (t) days 70 Plant Interception fraction (F) unitless 0.051

Chemical-specific Inputs and calculations - Maximum anywhere (normal conditions) Chemical Half-life in Loss constant Deposition Rate Aboveground Root Uptake Soil Below Ground

plant (T0.5) (k) (DR) Produce Factor (RUF) Concentration Produce Concentration (Cs) Concentration via Deposition days per day mg/m2/day mg/kg ww unitless mg/kg mg/kg ww Cadmium 14 0.05 3.9E-09 2.0E-09 0.125 4.2E-07 5.2E-08 Beryllium 14 0.05 1.2E-08 6.0E-09 0.0025 1.3E-06 3.2E-09 Mercury 14 0.05 2.5E-08 1.2E-08 0.225 2.6E-06 5.9E-07 Antimony 14 0.05 3.8E-08 1.9E-08 0.05 4.1E-06 2.0E-07 Arsenic 14 0.05 1.2E-06 6.2E-07 0.04 1.3E-04 5.3E-06 Lead 14 0.05 6.4E-07 3.2E-07 0.0113 6.9E-05 7.8E-07 Chromium (Cr VI assumed) 14 0.05 4.7E-08 2.3E-08 0.00188 5.0E-06 9.4E-09 Copper 14 0.05 6.9E-08 3.5E-08 0.1 7.4E-06 7.4E-07 Manganese 14 0.05 9.9E-08 4.9E-08 0.0625 1.0E-05 6.6E-07 Nickel 14 0.05 2.1E-07 1.0E-07 0.015 2.2E-05 3.4E-07 Dioxins and furans 14 0.05 5.6E-13 2.8E-13 0.000876 1.2E-11 1.1E-14

Root uptake factors from RAIS (soil to wet weight of plant)

Chemical-specific Inputs and calculations - Maximum anywhere (upset conditions) Chemical Half-life in Loss constant Deposition Rate Aboveground Root Uptake Soil Below Ground

plant (T0.5) (k) (DR) Produce Factor (RUF) Concentration Produce Concentration (Cs) Concentration via Deposition days per day mg/m2/day mg/kg ww unitless mg/kg mg/kg ww Cadmium 14 0.05 1.1E-08 5.2E-09 0.125 1.1E-06 1.4E-07 Beryllium 14 0.05 1.2E-08 6.1E-09 0.0025 1.3E-06 3.2E-09 Mercury 14 0.05 1.1E-07 5.2E-08 0.225 1.1E-05 2.5E-06 Antimony 14 0.05 1.2E-07 5.7E-08 0.05 1.2E-05 6.1E-07 Arsenic 14 0.05 3.9E-06 2.0E-06 0.04 4.2E-04 1.7E-05 Lead 14 0.05 1.2E-06 6.1E-07 0.0113 1.3E-04 1.5E-06 Chromium (Cr VI assumed) 14 0.05 2.5E-07 1.2E-07 0.00188 2.6E-05 4.9E-08 Copper 14 0.05 1.7E-07 8.7E-08 0.1 1.9E-05 1.9E-06 Manganese 14 0.05 2.9E-07 1.4E-07 0.0625 3.0E-05 1.9E-06 Nickel 14 0.05 9.9E-07 4.9E-07 0.015 1.0E-04 1.6E-06 Dioxins and furans 14 0.05 1.2E-12 6.1E-13 0.000876 2.6E-11 2.3E-14

Root uptake factors from RAIS (soil to wet weight of plant)

Residual Waste to Energy Facility, Laverton North: Health Impact Assessment C-13 | P a g e Ref: F/18/CRS001- A

Exposure to Chemicals via Ingestion of Homegrown Fruit and Vegetables

R x x x x x Rp x R x x x x (mg/kg/day) i i ke= x x B x R B x

Parameters Relevant to Quantification of Exposure by Adults Ingestion Rate of Produce (IRp) (kg/day) 0.4 Total fruit and vegetable consumption rate for adults as per NEPM (2013) Proportion of total intake from aboveground crops (%A) 73% Proportions as per NEPM (2013) Proportion of total intake from root crops (%R) 27% Proportions as per NEPM (2013) Fraction ingested that is homegrown (%) 10% Relevant to urban areas as per NEPM (2013) Matrix effect (unitless) 1 Assume chemicals ingested in produce is 100% bioavailable Exposure Frequency (EF, days/year) 360 Days at home (normal conditions), as per NEPM (1999 amended 2013) Exposure Frequency - upset (EFu, days/yr) 5 Assume upset conditions may occur over 5 days in any one year Exposure Duration (ED, years) 29 Time at one residence as adult as per enHealth 2002 and NEPM 1999 Body Weight (BW, kg) 70 For male and females combined (enHealth 2012) Averaging Time - NonThreshold (Atc, days) 25550 USEPA 1989 and CSMS 1996 Averaging Time - Threshold (Atn, days) 10585 USEPA 1989 and CSMS 1996

Maximum - All receptors (normal operationg conditions)

Toxicity Data Above ground Daily Intake Calculated Risk Non-Threshold Threshold Background TDI Allowable for Root crops NonThreshold Threshold Non-Threshold % Total Chronic Hazard % Total produce Slope Factor TDI Intake (% TDI) Assessment (TDI- concentrations Risk Risk Quotient HI Key Chemical Background) Bioavailability concentration (mg/kg-day)-1 (mg/kg/day) (mg/kg/day) (%) (mg/kg wet weight) (mg/kg wet weight) (mg/kg/day) (mg/kg/day) (unitless) (unitless) Cadmium 8.0E-04 60% 3.2E-04 100% 1.97E-09 5.25E-08 3.6E-12 8.8E-12 -- 2.7E-08 2% Beryllium 2.0E-03 20% 1.6E-03 100% 6.00E-09 3.20E-09 1.2E-12 3.0E-12 -- 1.8E-09 0% Mercury 6.0E-04 40% 3.6E-04 100% 1.24E-08 5.94E-07 4.0E-11 9.5E-11 -- 2.7E-07 16% Antimony 8.6E-04 8.6E-04 100% 1.92E-08 2.05E-07 1.6E-11 3.9E-11 -- 4.5E-08 3% Arsenic 2.0E-03 50% 1.0E-03 100% 6.18E-07 5.28E-06 4.4E-10 1.1E-09 -- 1.1E-06 63% Lead 3.5E-03 50% 1.8E-03 100% 3.22E-07 7.75E-07 1.0E-10 2.5E-10 -- 1.4E-07 8% Chromium (Cr VI assumed) 1.0E-03 10% 9.0E-04 100% 2.35E-08 9.41E-09 4.6E-12 1.1E-11 -- 1.2E-08 1% Copper 1.4E-01 60% 5.6E-02 100% 3.46E-08 7.38E-07 5.2E-11 1.3E-10 -- 2.3E-09 0% Manganese 1.4E-01 50% 7.0E-02 100% 4.92E-08 6.56E-07 5.0E-11 1.2E-10 -- 1.7E-09 0% Nickel 1.2E-02 60% 4.8E-03 100% 1.05E-07 3.36E-07 3.9E-11 9.4E-11 -- 2.0E-08 1% Dioxins and furans 2.3E-09 54% 1.1E-09 100% 2.79E-13 1.07E-14 4.8E-17 1.2E-16 -- 1.1E-07 7%

TOTAL 1.7E-06

Maximum - All receptors (upset operating conditions)

Toxicity Data Above ground Daily Intake Calculated Risk Non-Threshold Threshold Background TDI Allowable for Root crops NonThreshold Threshold Non-Threshold % Total Chronic Hazard % Total produce Slope Factor TDI Intake (% TDI) Assessment (TDI- concentrations Risk Risk Quotient HI Key Chemical Background) Bioavailability concentration (mg/kg-day)-1 (mg/kg/day) (mg/kg/day) (%) (mg/kg wet weight) (mg/kg wet weight) (mg/kg/day) (mg/kg/day) (unitless) (unitless) Cadmium 8.0E-04 60% 3.2E-04 100% 5.2E-09 1.4E-07 1.3E-13 3.3E-13 -- 1.0E-09 1% Beryllium 2.0E-03 20% 1.6E-03 100% 6.1E-09 3.2E-09 1.7E-14 4.2E-14 -- 2.6E-11 0% Mercury 6.0E-04 40% 3.6E-04 100% 5.2E-08 2.5E-06 2.3E-12 5.6E-12 -- 1.6E-08 21% Antimony 8.6E-04 8.6E-04 100% 5.7E-08 6.1E-07 6.7E-13 1.6E-12 -- 1.9E-09 3% Arsenic 2.0E-03 50% 1.0E-03 100% 2.0E-06 1.7E-05 1.9E-11 4.7E-11 -- 4.7E-08 63% Lead 3.5E-03 50% 1.8E-03 100% 6.1E-07 1.5E-06 2.7E-12 6.6E-12 -- 3.7E-09 5% Chromium (Cr VI assumed) 1.0E-03 10% 9.0E-04 100% 1.2E-07 4.9E-08 3.3E-13 8.1E-13 -- 9.0E-10 1% Copper 1.4E-01 60% 5.6E-02 100% 8.7E-08 1.9E-06 1.8E-12 4.4E-12 -- 7.9E-11 0% Manganese 1.4E-01 50% 7.0E-02 100% 1.4E-07 1.9E-06 2.0E-12 4.8E-12 -- 6.9E-11 0% Nickel 1.2E-02 60% 4.8E-03 100% 4.9E-07 1.6E-06 2.5E-12 6.1E-12 -- 1.3E-09 2% Dioxins and furans 2.3E-09 54% 1.1E-09 100% 6.1E-13 2.3E-14 1.5E-18 3.5E-18 -- 3.3E-09 4% TOTAL 7.5E-08 Residual Waste to Energy Facility, Laverton North: Health Impact Assessment C-14 | P a g e Ref: F/18/CRS001- A

Exposure to Chemicals via Ingestion of Homegrown Fruit and Vegetables

R x x x x x Rp x R x x x x (mg/kg/day) i i ke= x x B x R B x

Parameters Relevant to Quantification of Exposure by Young children Ingestion Rate of Produce (IRp) (kg/day) 0.28 Total fruit and vegetable consumption rate for children as per NEPM (2013) Proportion of total intake from aboveground crops (%A) 84% Proportions as per NEPM (2013) Proportion of total intake from root crops (%R) 16% Proportions as per NEPM (2013) Fraction ingested that is homegrown (%) 10% Relevant to urban areas as per NEPM (2013) Matrix effect (unitless) 1 Assume chemicals ingested in produce is 100% bioavailable Exposure Frequency (EF, days/year) 360 Days at home (normal conditions), as per NEPM (1999 amended 2013) Exposure Frequency - upset (EFu, days/yr) 5 Assume upset conditions may occur over 5 days in any one year Exposure Duration (ED, years) 6 Duration as young child Body Weight (BW, kg) 15 Representative weight as per NEPM (2013) Averaging Time - NonThreshold (Atc, days) 25550 USEPA 1989 and CSMS 1996 Averaging Time - Threshold (Atn, days) 2190 USEPA 1989 and CSMS 1996

Maximum - All receptors (normal operationg conditions)

Toxicity Data Above ground Daily Intake Calculated Risk Non-Threshold Threshold Background TDI Allowable for Root crops NonThreshold Threshold Non-Threshold % Total Chronic Hazard % Total produce Slope Factor TDI Intake (% TDI) Assessment (TDI- concentrations Risk Risk Quotient HI Key Chemical Background) Bioavailability concentration (mg/kg-day)-1 (mg/kg/day) (mg/kg/day) (%) (mg/kg wet weight) (mg/kg wet weight) (mg/kg/day) (mg/kg/day) (unitless) (unitless) Cadmium 8.0E-04 60% 3.2E-04 100% 1.97E-09 5.25E-08 1.6E-12 1.9E-11 -- 5.8E-08 1% Beryllium 2.0E-03 20% 1.6E-03 100% 6.00E-09 3.20E-09 8.8E-13 1.0E-11 -- 6.4E-09 0% Mercury 6.0E-04 40% 3.6E-04 100% 1.24E-08 5.94E-07 1.7E-11 1.9E-10 -- 5.4E-07 13% Antimony 8.6E-04 8.6E-04 100% 1.92E-08 2.05E-07 7.7E-12 9.0E-11 -- 1.0E-07 3% Arsenic 2.0E-03 50% 1.0E-03 100% 6.18E-07 5.28E-06 2.2E-10 2.5E-09 -- 2.5E-06 60% Lead 3.5E-03 50% 1.8E-03 100% 3.22E-07 7.75E-07 6.2E-11 7.3E-10 -- 4.1E-07 10% Chromium (Cr VI assumed) 1.0E-03 10% 9.0E-04 100% 2.35E-08 9.41E-09 3.3E-12 3.9E-11 -- 4.3E-08 1% Copper 1.4E-01 60% 5.6E-02 100% 3.46E-08 7.38E-07 2.3E-11 2.7E-10 -- 4.8E-09 0% Manganese 1.4E-01 50% 7.0E-02 100% 4.92E-08 6.56E-07 2.3E-11 2.7E-10 -- 3.8E-09 0% Nickel 1.2E-02 60% 4.8E-03 100% 1.05E-07 3.36E-07 2.2E-11 2.6E-10 -- 5.4E-08 1% Dioxins and furans 2.3E-09 54% 1.1E-09 100% 2.79E-13 1.07E-14 3.7E-17 4.3E-16 -- 4.1E-07 10%

TOTAL 4.2E-06

Maximum - All receptors (upset operating conditions)

Toxicity Data Above ground Daily Intake Calculated Risk Non-Threshold Threshold Background TDI Allowable for Root crops NonThreshold Threshold Non-Threshold % Total Chronic Hazard % Total produce Slope Factor TDI Intake (% TDI) Assessment (TDI- concentrations Risk Risk Quotient HI Key Chemical Background) Bioavailability concentration (mg/kg-day)-1 (mg/kg/day) (mg/kg/day) (%) (mg/kg wet weight) (mg/kg wet weight) (mg/kg/day) (mg/kg/day) (unitless) (unitless) Cadmium 8.0E-04 60% 3.2E-04 100% 5.2E-09 1.4E-07 5.9E-14 6.9E-13 -- 2.1E-09 1% Beryllium 2.0E-03 20% 1.6E-03 100% 6.1E-09 3.2E-09 1.2E-14 1.4E-13 -- 9.0E-11 0% Mercury 6.0E-04 40% 3.6E-04 100% 5.2E-08 2.5E-06 9.8E-13 1.1E-11 -- 3.2E-08 18% Antimony 8.6E-04 8.6E-04 100% 5.7E-08 6.1E-07 3.2E-13 3.7E-12 -- 4.3E-09 2% Arsenic 2.0E-03 50% 1.0E-03 100% 2.0E-06 1.7E-05 9.5E-12 1.1E-10 -- 1.1E-07 62% Lead 3.5E-03 50% 1.8E-03 100% 6.1E-07 1.5E-06 1.6E-12 1.9E-11 -- 1.1E-08 6% Chromium (Cr VI assumed) 1.0E-03 10% 9.0E-04 100% 1.2E-07 4.9E-08 2.4E-13 2.8E-12 -- 3.2E-09 2% Copper 1.4E-01 60% 5.6E-02 100% 8.7E-08 1.9E-06 8.1E-13 9.5E-12 -- 1.7E-10 0% Manganese 1.4E-01 50% 7.0E-02 100% 1.4E-07 1.9E-06 9.3E-13 1.1E-11 -- 1.6E-10 0% Nickel 1.2E-02 60% 4.8E-03 100% 4.9E-07 1.6E-06 1.5E-12 1.7E-11 -- 3.5E-09 2% Dioxins and furans 2.3E-09 54% 1.1E-09 100% 6.1E-13 2.3E-14 1.1E-18 1.3E-17 -- 1.2E-08 7% TOTAL 1.8E-07 Residual Waste to Energy Facility, Laverton North: Health Impact Assessment C-15 | P a g e Ref: F/18/CRS001- A

Ingestion of eggs

Residual Waste to Energy Facility, Laverton North: Health Impact Assessment C-16 | P a g e Ref: F/18/CRS001- A

Calculation of Concentrations in Eggs

Uptake in to chicken eggs

= x R x Rs x s x B x (mg/kg egg – wet weight)

where: FI = Fraction of pasture/crop ingested by chickens each day (unitless) IRc = Ingestion rate of pasture/crop by chicken each day (kg/day) C = Concentration of chemical in grain/crop eaten by chicken (mg/kg) IRs = Ingestion rate of soil by chickens each day (kg/day) Cs = Concentration in soil the chickens ingest (mg/kg) B = Bioavailability of soil ingested by chickens (%) TFE = Transfer factor from ingestion to eggs (day/kg)

General Parameters Units Value FI (fraction of crops ingested from property) 1 Assume 100% of crops consumed by chickens is grown in the same soil IRc (ingestion rate of crops) kg/day 0.12 Assumed ingestion rate from OEHHA 2015 (assume concentration the same as predicted for aboveground crops) IRs (ingestion rate of soil) kg/day 0.0024 Based on data from OEHHA 2015 (2% total produce intakes from soil) B (bioavailability) % 100%

Chemical-specific Inputs and calculations - Maximum anywhere (normal conditions) Chemical Concentration Soil Transfer factor to Egg in crops Concentration - eggs Concentration ingested by Agriculture (Cs) chickens mg/kg ww mg/kg day/kg mg/kg ww Cadmium 2.0E-09 4.2E-07 1.0E-02 1.2E-11 Beryllium 6.0E-09 1.3E-06 9.0E-02 3.4E-10 Mercury 1.2E-08 2.6E-06 8.0E-01 6.3E-09 Antimony 1.9E-08 4.1E-06 4.2E-04 5.1E-12 Arsenic 6.2E-07 1.3E-04 7.0E-02 2.7E-08 Lead 3.2E-07 6.9E-05 4.0E-02 8.1E-09 Chromium (Cr VI assumed) 2.3E-08 5.0E-06 9.2E-03 1.4E-10 OEHHA (2003) Copper 3.5E-08 7.4E-06 1.7E-01 3.7E-09 Manganese 4.9E-08 1.0E-05 1.7E-01 5.3E-09 Nickel 1.0E-07 2.2E-05 2.0E-02 1.3E-09 Dioxins and furans 2.8E-13 1.2E-11 1.0E+01 6.3E-13

Transfer factors from OEHHA 2015 unless otherwise noted

Chemical-specific Inputs and calculations - Maximum anywhere (upset conditions) Chemical Concentration Soil Transfer factor to Egg in crops Concentration - eggs Concentration ingested by Agriculture (Cs) chickens mg/kg ww mg/kg day/kg mg/kg ww Cadmium 5.2E-09 1.1E-06 1.0E-02 3.3E-11 Beryllium 6.1E-09 1.3E-06 9.0E-02 3.5E-10 Mercury 5.2E-08 1.1E-05 8.0E-01 2.7E-08 Antimony 5.7E-08 1.2E-05 4.2E-04 1.5E-11 Arsenic 2.0E-06 4.2E-04 7.0E-02 8.7E-08 Lead 6.1E-07 1.3E-04 4.0E-02 1.5E-08 Chromium (Cr VI assumed) 1.2E-07 2.6E-05 9.2E-03 7.2E-10 OEHHA (2003) Copper 8.7E-08 1.9E-05 1.7E-01 9.3E-09 Manganese 1.4E-07 3.0E-05 1.7E-01 1.5E-08 Nickel 4.9E-07 1.0E-04 2.0E-02 6.2E-09 Dioxins and furans 6.1E-13 2.6E-11 1.0E+01 1.4E-12

Transfer factors from OEHHA 2015 unless otherwise noted In the absense of chemical specific transfer factors the P95 value for all heavy metals has been adotped (Leeman et al 2007)

Residual Waste to Energy Facility, Laverton North: Health Impact Assessment C-17 | P a g e Ref: F/18/CRS001- A

Exposure to Chemicals via Ingestion of Eggs

R x x x x (mg/kg/day) i i ke= x B x

Parameters Relevant to Quantification of Exposure by Adults Ingestion Rate of Eggs (IRE) (kg/day) 0.014 Ingestion rate of eggs relevant for adults as per enHealth (2012) Fraction ingested that is homegrown (%) 100% Assume all eggs consumed in urban area are from backyard chickens Matrix effect (unitless) 1 Assume chemicals ingested in produce is 100% bioavailable Exposure Frequency (EF, days/year) 360 Days at home (normal conditions), as per NEPM (1999 amended 2013) Exposure Frequency - upset (EFu, days/yr) 5 Assume upset conditions may occur over 5 days in any one year Exposure Duration (ED, years) 29 Time at one residence as adult as per enHealth 2002 and NEPM 1999 Body Weight (BW, kg) 70 For male and females combined (enHealth 2012) Averaging Time - NonThreshold (Atc, days) 25550 USEPA 1989 and CSMS 1996 Averaging Time - Threshold (Atn, days) 10585 USEPA 1989 and CSMS 1996

Maximum - All receptors (normal operationg conditions)

Toxicity Data Daily Intake Calculated Risk Non-Threshold Threshold Background TDI Allowable for Egg NonThreshold Threshold Non-Threshold % Total Chronic Hazard % Total Slope Factor TDI Intake (% TDI) Assessment (TDI- concentration Risk Risk Quotient HI Key Chemical Background) Bioavailability (mg/kg-day)-1 (mg/kg/day) (mg/kg/day) (%) (mg/kg wet weight) (mg/kg/day) (mg/kg/day) (unitless) (unitless) Cadmium 8.0E-04 60% 3.2E-04 100% 1.24E-11 1.0E-15 2.5E-15 -- 7.7E-12 0% Beryllium 2.0E-03 20% 1.6E-03 100% 3.42E-10 2.8E-14 6.7E-14 -- 4.2E-11 0% Mercury 6.0E-04 40% 3.6E-04 100% 6.25E-09 5.1E-13 1.2E-12 -- 3.4E-09 3% Antimony 8.6E-04 8.6E-04 100% 5.11E-12 4.2E-16 1.0E-15 -- 1.2E-12 0% Arsenic 2.0E-03 50% 1.0E-03 100% 2.74E-08 2.2E-12 5.4E-12 -- 5.4E-09 4% Lead 3.5E-03 50% 1.8E-03 100% 8.13E-09 6.6E-13 1.6E-12 -- 9.2E-10 1% Chromium (Cr VI assumed) 1.0E-03 10% 9.0E-04 100% 1.36E-10 1.1E-14 2.7E-14 -- 3.0E-11 0% Copper 1.4E-01 60% 5.6E-02 100% 3.72E-09 3.0E-13 7.3E-13 -- 1.3E-11 0% Manganese 1.4E-01 50% 7.0E-02 100% 5.29E-09 4.3E-13 1.0E-12 -- 1.5E-11 0% Nickel 1.2E-02 60% 4.8E-03 100% 1.33E-09 1.1E-13 2.6E-13 -- 5.5E-11 0% Dioxins and furans 2.3E-09 54% 1.1E-09 100% 6.27E-13 5.1E-17 1.2E-16 -- 1.2E-07 92%

TOTAL 1.3E-07

Maximum - All receptors (upset operating conditions)

Toxicity Data Daily Intake Calculated Risk Non-Threshold Threshold Background TDI Allowable for Egg NonThreshold Threshold Non-Threshold % Total Chronic Hazard % Total Slope Factor TDI Intake (% TDI) Assessment (TDI- concentration Risk Risk Quotient HI Key Chemical Background) Bioavailability (mg/kg-day)-1 (mg/kg/day) (mg/kg/day) (%) (mg/kg wet weight) (mg/kg/day) (mg/kg/day) (unitless) (unitless) Cadmium 8.0E-04 60% 3.2E-04 100% 3.3E-11 3.8E-17 9.1E-17 -- 2.8E-13 0% Beryllium 2.0E-03 20% 1.6E-03 100% 3.5E-10 3.9E-16 9.5E-16 -- 5.9E-13 0% Mercury 6.0E-04 40% 3.6E-04 100% 2.7E-08 3.0E-14 7.3E-14 -- 2.0E-10 0% Antimony 8.6E-04 8.6E-04 100% 1.5E-11 1.7E-17 4.2E-17 -- 4.9E-14 0% Arsenic 2.0E-03 50% 1.0E-03 100% 8.7E-08 9.9E-14 2.4E-13 -- 2.4E-10 6% Lead 3.5E-03 50% 1.8E-03 100% 1.5E-08 1.7E-14 4.2E-14 -- 2.4E-11 1% Chromium (Cr VI assumed) 1.0E-03 10% 9.0E-04 100% 7.2E-10 8.1E-16 2.0E-15 -- 2.2E-12 0% Copper 1.4E-01 60% 5.6E-02 100% 9.3E-09 1.1E-14 2.6E-14 -- 4.6E-13 0% Manganese 1.4E-01 50% 7.0E-02 100% 1.5E-08 1.7E-14 4.2E-14 -- 6.0E-13 0% Nickel 1.2E-02 60% 4.8E-03 100% 6.2E-09 7.1E-15 1.7E-14 -- 3.6E-12 0% Dioxins and furans 2.3E-09 54% 1.1E-09 100% 1.4E-12 1.5E-18 3.7E-18 -- 3.5E-09 88% TOTAL 4.0E-09 Residual Waste to Energy Facility, Laverton North: Health Impact Assessment C-18 | P a g e Ref: F/18/CRS001- A

Exposure to Chemicals via Ingestion of Eggs

R x x x x (mg/kg/day) i i ke= x B x

Parameters Relevant to Quantification of Exposure by Young children Ingestion Rate of Eggs (IRE) (kg/day) 0.006 Ingestion rate of eggs relevant for young children as per enHealth (2012) Fraction ingested that is homegrown (%) 100% Assume all eggs consumed in urban area are from backyard chickens Matrix effect (unitless) 1 Assume chemicals ingested in produce is 100% bioavailable Exposure Frequency (EF, days/year) 360 Days at home (normal conditions), as per NEPM (1999 amended 2013) Exposure Frequency - upset (EFu, days/yr) 5 Assume upset conditions may occur over 5 days in any one year Exposure Duration (ED, years) 6 Duration as young child Body Weight (BW, kg) 15 Representative weight as per NEPM (2013) Averaging Time - NonThreshold (Atc, days) 25550 USEPA 1989 and CSMS 1996 Averaging Time - Threshold (Atn, days) 2190 USEPA 1989 and CSMS 1996

Maximum - All receptors (normal operationg conditions)

Toxicity Data Daily Intake Calculated Risk Non-Threshold Threshold Background TDI Allowable for Egg NonThreshold Threshold Non-Threshold % Total Chronic Hazard % Total Slope Factor TDI Intake (% TDI) Assessment (TDI- concentration Risk Risk Quotient HI Key Chemical Background) Bioavailability (mg/kg-day)-1 (mg/kg/day) (mg/kg/day) (%) (mg/kg wet weight) (mg/kg/day) (mg/kg/day) (unitless) (unitless) Cadmium 8.0E-04 60% 3.2E-04 100% 1.24E-11 4.2E-16 4.9E-15 -- 1.5E-11 0% Beryllium 2.0E-03 20% 1.6E-03 100% 3.42E-10 1.2E-14 1.3E-13 -- 8.4E-11 0% Mercury 6.0E-04 40% 3.6E-04 100% 6.25E-09 2.1E-13 2.5E-12 -- 6.9E-09 3% Antimony 8.6E-04 8.6E-04 100% 5.11E-12 1.7E-16 2.0E-15 -- 2.3E-12 0% Arsenic 2.0E-03 50% 1.0E-03 100% 2.74E-08 9.3E-13 1.1E-11 -- 1.1E-08 4% Lead 3.5E-03 50% 1.8E-03 100% 8.13E-09 2.7E-13 3.2E-12 -- 1.8E-09 1% Chromium (Cr VI assumed) 1.0E-03 10% 9.0E-04 100% 1.36E-10 4.6E-15 5.4E-14 -- 6.0E-11 0% Copper 1.4E-01 60% 5.6E-02 100% 3.72E-09 1.3E-13 1.5E-12 -- 2.6E-11 0% Manganese 1.4E-01 50% 7.0E-02 100% 5.29E-09 1.8E-13 2.1E-12 -- 3.0E-11 0% Nickel 1.2E-02 60% 4.8E-03 100% 1.33E-09 4.5E-14 5.2E-13 -- 1.1E-10 0% Dioxins and furans 2.3E-09 54% 1.1E-09 100% 6.27E-13 2.1E-17 2.5E-16 -- 2.3E-07 92%

TOTAL 2.5E-07

Maximum - All receptors (upset operating conditions)

Toxicity Data Daily Intake Calculated Risk Non-Threshold Threshold Background TDI Allowable for Egg NonThreshold Threshold Non-Threshold % Total Chronic Hazard % Total Slope Factor TDI Intake (% TDI) Assessment (TDI- concentration Risk Risk Quotient HI Key Chemical Background) Bioavailability (mg/kg-day)-1 (mg/kg/day) (mg/kg/day) (%) (mg/kg wet weight) (mg/kg/day) (mg/kg/day) (unitless) (unitless) Cadmium 8.0E-04 60% 3.2E-04 100% 3.3E-11 1.6E-17 1.8E-16 -- 5.7E-13 0% Beryllium 2.0E-03 20% 1.6E-03 100% 3.5E-10 1.6E-16 1.9E-15 -- 1.2E-12 0% Mercury 6.0E-04 40% 3.6E-04 100% 2.7E-08 1.2E-14 1.5E-13 -- 4.0E-10 0% Antimony 8.6E-04 8.6E-04 100% 1.5E-11 7.2E-18 8.4E-17 -- 9.7E-14 0% Arsenic 2.0E-03 50% 1.0E-03 100% 8.7E-08 4.1E-14 4.8E-13 -- 4.8E-10 6% Lead 3.5E-03 50% 1.8E-03 100% 1.5E-08 7.2E-15 8.4E-14 -- 4.8E-11 1% Chromium (Cr VI assumed) 1.0E-03 10% 9.0E-04 100% 7.2E-10 3.4E-16 3.9E-15 -- 4.4E-12 0% Copper 1.4E-01 60% 5.6E-02 100% 9.3E-09 4.4E-15 5.1E-14 -- 9.1E-13 0% Manganese 1.4E-01 50% 7.0E-02 100% 1.5E-08 7.2E-15 8.4E-14 -- 1.2E-12 0% Nickel 1.2E-02 60% 4.8E-03 100% 6.2E-09 2.9E-15 3.4E-14 -- 7.1E-12 0% Dioxins and furans 2.3E-09 54% 1.1E-09 100% 1.4E-12 6.4E-19 7.5E-18 -- 7.1E-09 88% TOTAL 8.0E-09 Residual Waste to Energy Facility, Laverton North: Health Impact Assessment C-19 | P a g e Ref: F/18/CRS001- A

Summary of risk

Residual Waste to Energy Facility, Laverton North: Health Impact Assessment C-20 | P a g e Ref: F/18/CRS001- A

Summary of Risks - Residential

Adults Exposure pathway Ingestion of Dermal home-grown contact with fruit and Ingestion of Sum over all Calculated HI for each CoPC Inhalation Ingestion of soil soil vegetables eggs pathways Hydrogen chloride (HCl) 9.9E-05 9.9E-05 Hydrogen fluoride (HF) 7.9E-06 7.9E-06 Cadmium 7.5E-05 1.4E-08 2.9E-08 8.0E-12 7.5E-05 Beryllium 5.4E-05 8.6E-09 5.4E-10 1.9E-09 4.3E-11 5.4E-05 Mercury 1.0E-05 8.2E-08 7.4E-08 2.8E-07 3.6E-09 1.1E-05 Antimony 1.4E-05 5.2E-08 4.7E-08 1.2E-12 1.4E-05 Arsenic 9.3E-05 1.5E-06 4.6E-07 1.1E-06 5.6E-09 9.6E-05 Lead 9.1E-05 4.3E-07 1.5E-07 9.4E-10 9.2E-05 Chromium (Cr VI assumed) 3.5E-05 6.3E-08 1.3E-08 3.2E-11 3.5E-05 Copper 1.0E-08 1.4E-09 2.3E-09 1.4E-11 1.4E-08 Manganese 6.0E-05 1.6E-09 1.8E-09 1.6E-11 6.0E-05 Nickel 9.8E-04 5.3E-08 1.7E-08 2.1E-08 5.8E-11 9.8E-04 Dioxins and furans 1.1E-05 1.3E-07 2.4E-07 1.1E-07 1.2E-07 1.2E-05 MDI 3.8E-05 3.8E-05 1.6E-03 2.3E-06 7.9E-07 1.8E-06 1.3E-07 1.5E-03

Young children Exposure pathway Ingestion of Dermal home-grown contact with fruit and Ingestion of Sum over all Calculated HI for each CoPC Inhalation Ingestion of soil soil vegetables eggs pathways Hydrogen chloride (HCl) 9.9E-05 9.9E-05 Hydrogen fluoride (HF) 7.9E-06 7.9E-06 Cadmium 7.5E-05 1.3E-07 6.0E-08 1.6E-11 7.5E-05 Beryllium 5.4E-05 8.0E-08 1.1E-09 6.5E-09 8.5E-11 5.4E-05 Mercury 1.0E-05 7.7E-07 1.5E-07 5.7E-07 7.3E-09 1.2E-05 Antimony 1.4E-05 4.9E-07 1.1E-07 2.4E-12 1.5E-05 Arsenic 9.3E-05 1.4E-05 9.2E-07 2.6E-06 1.1E-08 1.1E-04 Lead 9.1E-05 4.0E-06 4.3E-07 1.9E-09 9.6E-05 Chromium (Cr VI assumed) 3.5E-05 5.9E-07 4.7E-08 6.4E-11 3.6E-05 Copper 1.0E-08 1.3E-08 5.0E-09 2.7E-11 2.9E-08 Manganese 6.0E-05 1.5E-08 4.0E-09 3.1E-11 6.0E-05 Nickel 9.8E-04 4.9E-07 3.3E-08 5.8E-08 1.2E-10 9.8E-04 Dioxins and furans 1.1E-05 1.2E-06 4.7E-07 4.2E-07 2.4E-07 1.4E-05 MDI 3.8E-05 3.8E-05 1.6E-03 2.1E-05 1.6E-06 4.3E-06 2.6E-07 1.6E-03

Residual Waste to Energy Facility, Laverton North: Health Impact Assessment C-21 | P a g e Ref: F/18/CRS001- A