Part 2B: Health Risk Assessment - RW CORKERY...ABN: 46 114 162 597 Part 2B: Health Risk Assessment...

ABN: 46 114 162 597

Part 2B:

Health Risk Assessment

Prepared for: R.W. Corkery & Co. Pty Limited 1st Floor, 12 Dangar Road PO Box 239 BROOKLYN NSW 2083

Tel: (02) 9985 8511 Email: [email protected]

On behalf of: Gloucester Resources Limited Level 37, Riverside Centre

123 Eagle Street BRISBANE QLD 4000

Tel: (07) 3006 1830 Fax: (07) 3006 1840 Email: [email protected]

Prepared by: Pacific Environment Limited

Suite 1, Level 1 146 Arthur Street

NORTH SYDNEY NSW 2060

Tel: (02) 9870 0900 Fax: (02) 9870 0999 Email: [email protected] Ref No: 7210

June 2016

GLOUCESTER RESOURCES LIMITED SPECIALIST CONSULTANT STUDIES

Amended Rocky Hill Coal Project Part 2B: Health Risk Assessment

Report No. 806/14

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This Copyright is included for the protection of this document

COPYRIGHT

© Pacific Environment Limited, 2016 and

© Gloucester Resources Limited, 2016

All intellectual property and copyright reserved.

Apart from any fair dealing for the purpose of private study, research, criticism or review, as permitted under the Copyright Act, 1968, no part of this report may be reproduced, transmitted, stored in a retrieval system or adapted in any form or by any means (electronic, mechanical, photocopying, recording or otherwise) without written permission. Enquiries should be addressed to Pacific Environment Limited.

SPECIALIST CONSULTANT STUDIES GLOUCESTER RESOURCES LIMITED

Part 2B: Health Risk Assessment Amended Rocky Hill Coal Project

Report No. 806/14

CONTENTS Page

2B-3

GLOSSARY OF COMMONLY USED TERMS AND ACRONYMS ..................................................... 2B-5

DEFINITION OF TERMS...................................................................................................................... 2B-6

DEFINITION OF TERMS (CONT’D) .................................................................................................... 2B-7

EXECUTIVE SUMMARY...................................................................................................................... 2B-9

1. INTRODUCTION ...................................................................................................................... 2B-13

1.1 SCOPE OF WORK .......................................................................................................2B-13

1.2 BACKGROUND ............................................................................................................2B-13

1.3 OVERVIEW OF THE AMENDED PROJECT ...............................................................2B-15

2. METHODOLOGY ..................................................................................................................... 2B-20

2.1 WHAT IS A RISK ASSESSMENT? ..............................................................................2B-20

2.2 OVERALL APPROACH ................................................................................................2B-21

3. COMMUNITY PROFILE ........................................................................................................... 2B-22

3.1 SURROUNDING AREA AND POPULATION ..............................................................2B-22

3.2 POPULATION PROFILE ..............................................................................................2B-22

3.3 RESIDENCES AND SENSITIVE RECEIVERS ............................................................2B-24

3.4 COMMUNITY CONCERNS ..........................................................................................2B-24

4. OVERVIEW OF AIR QUALITY ASSESSMENT ...................................................................... 2B-25

4.1 EXISTING AIR QUALITY .............................................................................................2B-25

4.2 AIR QUALITY ASSESSMENT SCENARIOS ...............................................................2B-25

4.3 AIR QUALITY ASSESSMENT OUTCOMES ...............................................................2B-26

5. HEALTH RISK ASSESSMENT ............................................................................................... 2B-27

5.1 IDENTIFICATION OF EMISSIONS OF HAZARDOUS POLLUTANTS .......................2B-27

5.2 ASSESSMENT OF PARTICULATE MATTER .............................................................2B-28

5.2.1 Hazard Assessment ........................................................................................2B-28

5.2.2 Exposure Assessment .....................................................................................2B-40

5.2.3 Risk Characterisation ......................................................................................2B-41

5.2.4 Conclusion .......................................................................................................2B-46

5.3 ASSESSMENT OF NITROGEN DIOXIDE ...................................................................2B-46

5.3.1 Hazard Assesment ..........................................................................................2B-46

5.3.2 Exposure Assessment .....................................................................................2B-49

5.3.3 Risk Characterisation ......................................................................................2B-51

5.3.4 Conclusion .......................................................................................................2B-54

5.4 ASSESSMENT OF DIESEL .........................................................................................2B-54

6. LIMITATIONS .......................................................................................................................... 2B-56

7. CONCLUSIONS ....................................................................................................................... 2B-57

8. REFERENCES ......................................................................................................................... 2B-60



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APPENDICES

Appendix 1 Key Differences between the Health Risk Assessment for the 2013 Project and Amended Project ............................................................................................................ 2B-67

FIGURES

Figure 1.1 Locality Plan ................................................................................................................... 2B-14

Figure 1.2 Amended Site Layout ..................................................................................................... 2B-16

Figure 1.3 Amended Mine Area Layout ........................................................................................... 2B-17

Figure 1.4 Private Haul Road .......................................................................................................... 2B-19

Figure 3.1 Resource Company and Privately Owned Residences in the Vicinity of the Site ......... 2B-23

Figure 5.1 The Severity and Frequency of an Adverse Health Impact as a Result of Ambient Air Pollution Exposure (Source: WHO, 2001) ..................................................................... 2B-27

TABLES

Table 3.1 Population Age Profile Used in Analysis ........................................................................ 2B-22

Table 3.2 Community Concerns and Relevant Sections of the HRA ............................................. 2B-24

Table 5.1 NSW Impact Assessment Criteria for PM ...................................................................... 2B-29

Table 5.2 Concentration-Response Functions for PM2.5 based on Jalaludin and Cowie (2012) ... 2B-38

Table 5.3 Concentration-Response Functions for PM10 based on Jalaludin and Cowie (2012) .... 2B-39

Table 5.4 Maximum Predicted Project-only 24-hour Average Concentrations at the Most

Affected Receiver/residence (g/m3) ............................................................................. 2B-40

Table 5.5 Predicted Annual Average Concentrations at the Most Affected Receiver/Residence

(g/m3) ............................................................................................................................ 2B-41

Table 5.6 Baseline Health Incidence Rate per 100,000 used in Risk Calculations ....................... 2B-42

Table 5.7 Predicted Number of Attributable Cases Due to PM2.5 Exposure per 100,000: Gloucester State Suburb ................................................................................................ 2B-44

Table 5.8 Predicted Number of Attributable Cases Due to PM10 Exposure per 100,000: Gloucester State Suburb ................................................................................................ 2B-44

Table 5.9 Predicted Number of Attributable Cases Due to PM2.5 Exposure per 100,000: Faulkland State Suburb (Forbesdale Estate) ................................................................. 2B-45

Table 5.10 Predicted Number of Attributable Cases Due to PM10 Exposure per 100,000: Faulkland State Suburb (Forbesdale Estate) ................................................................. 2B-45

Table 5.11 Summary of National and International Criteria Established Relating to Short-term and Long-term Exposure to NO2 .................................................................................... 2B-49

Table 5.12 Cumulative maximum 1-hour and annual average NO2 concentrations (g/m3) ........... 2B-51

Table 5.13 Short-term and long-term HQs for Potential NO2 concentrations .................................. 2B-52

Table 5.14 Maximum Project-only 24-hour and Annual Average PM10 Concentrations at Private

Receivers/Residences (g/m3) ....................................................................................... 2B-53

Table 5.15 Short-term and long-term HQs for PM10 concentrations ................................................ 2B-53

Table 5.16 Short-term and long-term HIs for PM10 and NO2 concentrations ................................... 2B-54



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GLOSSARY OF COMMONLY USED TERMS AND ACRONYMS

ABS Australian Bureau of Statistics

ACS American Cancer Society

CHPP Coal Handling and Preparation Plant

COPD Chronic Obstructive Pulmonary Disease

CRF Concentration Response Function

DA Development Application

DPE Department of Planning and Environment

EIS Environmental Impact Statement

EPHC Environment Protection and Heritage Council

FEV Forced Expiratory Volume

GLCs Ground Level Concentrations

GMR Greater Metropolitan Region

GP General Practitioner

HI Hazard Index

HQ Hazard Quotient

HRA Health Risk Assessment

LOAEL Lowest Observed Adverse Effect Levels

NEPM AAQM National Environment Protection (Ambient Air Quality) Measure

NO Nitric Oxide

NO2 Nitrogen Dioxide

NOAEL No Observed Adverse Effect Level

NOx Oxides of Nitrogen

NSW New South Wales

OEHHA Office of Environmental Health Hazard Assessment

PM Particulate Matter

PM10 Particulate Matter less than 10 micrometres in aerodynamic diameter

PM2.5 Particulate Matter less than 2.5 micrometres in aerodynamic diameter

PPB Part per Billion

PPM Parts per Million

SMC Stratford Mining Complex

UFPs Ultrafine Particles

US EPA United States Environmental Protection Agency

WHO World Health Organisation



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DEFINITION OF TERMS

Term Definition

Air dispersion modelling Mathematical simulation of how air pollutants disperse in the ambient atmosphere.

Baseline health incidence

This is an estimate of the incidence rate (number of cases of the health effect per year, usually per 10,000 or 100,000 general population) in the assessment location corresponding to baseline pollutant levels in that location

Beta (β) coefficient The beta value is a measure of how strongly each predictor variable influences the criterion (dependent) variable. The beta is measured in units of standard deviation.

Ambient air quality The state of quality and chemical characteristics of air as it exists in the environment.

Concentration Response Function

A Concentration Response Function (CRF) (reported by epidemiological studies) is the empirically estimated relationship between the concentration of PM and the observed health endpoints of interest (for example, hospital admissions for asthma) in a population.

Carbon monoxide (CO) Carbon Monoxide (CO) is a toxic, colourless, odourless gas produced by burning any fuel.

Emissions Release of pollutants to air

Epidemiological studies These are studies that examine the patterns, causes, and effects of health and disease conditions in defined populations. Epidemiological information is used to plan and evaluate strategies to prevent illness

Exposure Assessment This identifies the groups of people who may be exposed to hazardous pollutants and provides an estimate as to the potential exposure concentrations.

Hazard Assessment Identifies hazards and health endpoints associated with exposure to hazardous pollutants and provides a review of the current understanding of the toxicity and risk relationship of the exposure of humans to the hazards.

Hazard Index A Hazard Index (HI) is the sum of the Hazard Quotients (HQs) for all pathways with similar toxic effects, assuming the health effects are additive

Hazard Quotient A Hazard Quotient (HQ) which is the ratio of predicted concentrations to the ambient air quality criterion

Health Risk Assessment (HRA)

A Health Risk Assessment (HRA) is an analysis that uses information about potentially hazardous pollutants to estimate a theoretical level of risk for people who might be exposed to defined levels of these pollutants. The information comes from scientific studies and measurement data of air emissions.

Lowest Observed Adverse Effect Level (LOAEL)

The lowest tested dose of a substance that has been reported to have no harmful (adverse) health effects on people or animals.

Nitrogen Dioxide (NO2) Nitrogen dioxide (NO2) is a reddish-brown gas. It is a lung irritant and is present in the highest concentrations among other oxides of nitrogen in ambient air. Nitric oxide (NO) and NO2 are collectively known as NOx.

No Observed Adverse Effect Level (NOAEL)

The highest tested dose of a substance that has been reported to have no harmful (adverse) health effects on people or animals.

NOx Oxides of nitrogen (NOx) is a generic term for mono-nitrogen oxides (NO and NO2). The oxides of nitrogen are predominantly (greater than 90%) nitric oxide (NO).

Particulate Matter (PM) Particulate Matter (PM) is a complex mixture of extremely small particles made up of a number of components, including acids (such as nitrates and sulphates), organic chemicals, metals, and soil or dust particles.



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DEFINITION OF TERMS (CONT’D)

Term Definition

PM10 Particulate Matter less than 10 micrometres in aerodynamic diameter

PM2.5 Particulate Matter less than 2.5 micrometres in aerodynamic diameter

Risk Characterisation This provides the qualitative/quantitative evaluation of potential risks to human health. The characterisation of risk is based on the review of the dose-response relationship and the assessment of the magnitude of exposure.

Sensitive receiver/ residence locations

Locations where vulnerable members of the community gather e.g. hospitals, schools



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EXECUTIVE SUMMARY

Gloucester Resources Limited (the Applicant) proposes to develop and operate an open cut

coal mine, approximately 3.5km to 7km southeast of the Gloucester urban area and

approximately 120km north of Newcastle, New South Wales (NSW) in the Gloucester Basin.

The Applicant contracted Pacific Environment Limited (then Toxikos Propriety Limited) to

update the Health Risk Assessment (HRA) undertaken for the 2013 Project using the air

quality modelling outcomes for the amended Project. The applied HRA methodology was

consistent with the protocols and guidelines recommended by the Australian enHealth Council

(enHealth, 2012a). This HRA addresses likely impacts on community health from exposure to

air emissions from the “amended Rocky Hill Coal Project” (“the amended Project”), considering

the direct health effects from acute (short-term) and chronic (long-term) exposures. Ground

Level Concentrations (GLCs) of key air quality metrics were predicted at discrete locations

around the Site using air dispersion modelling conducted by Pacific Environment (detailed

within the standalone Air Quality Impact Assessment – Part 2A of the Specialist Consultant

Studies Compendium). The emissions of concern addressed in the assessment were

Particulate Matter (PM), diesel exhaust (from activities associated with open cut coal mining)

and nitrogen dioxide (NO2) (resulting from blasting).

The exposure assessment used estimates of the total potential cumulative exposure

(i.e. background plus modelled PM2.5 and PM10 increment from the amended Project) on an

annual and daily basis at the most affected private receivers/residences (receiver 6 in

Gloucester and receiver 18 in Forbesdale) on the worst day of each modelled year. By using

the modelled predictions at the most affected private receivers/residences to represent

exposure across the populations of the respective state suburbs, the overall community

exposure is over estimated and the resulting HRA should be considered conservative. The air

quality impact assessment for the amended Project (Pacific Environment, 2016) presents the

dispersion modelling predictions for maximum 24-hour and annual average PM2.5 and PM10

GLCs at a total of 160 non-resource related assessment locations i.e. 157 privately-owned

receivers/residences in the vicinity of the Site and 3 sensitive receiver locations with the

Gloucester township. For both PM2.5 and PM10, the full dataset based on the 160 assessment

locations in conjunction with background were examined as part of the HRA.

The health endpoints assessed for PM2.5 and PM10 were short- and long-term mortality and

daily hospitalisations. The general approach used to calculate the risks to health has drawn

upon estimates determined to be relevant to the Australian context in order to determine the

impact of PM2.5 and PM10 on health in relation to the known health indicators for NSW. This

involved estimating the change in the incidence of a health outcome resulting from a given

change in PM2.5 and PM10 concentrations. Concentration-Response Functions (CRFs) for each

of the health endpoints were sourced from the review conducted by Jalaludin and Cowie 2012.

In examining the increased risk in the population as a consequence of the amended Project

(based on annual mortality rates, all causes) due to the increased long-term exposure to PM2.5

and PM10 concentrations as a result of cumulative and project-only exposure, it is noted that

the number of attributable health outcomes would be well below 1 in 100,000. The predicted

number of attributable cases are therefore considered to be “sufficiently small and to be of no

cause for concern” (NEPM AAQM). Shorter term exposures to PM2.5 and PM10 are also

considered not to pose an unacceptable risk as the predicted number of attributable cases due

to daily mortality (all cause all ages and cardiovascular disease all ages are less than 1 in

orders of magnitude lower than that due to long-term exposure.



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The critical health outcomes from acute and chronic exposure to NO2 include respiratory

disease and associated symptoms, and associated changes in lung function. The NSW EPA

impact assessment criteria, which are protective of these health outcomes in sensitive

subpopulations, have been used to determine the potential for acute effects (246µg/m3) and

chronic effects (62µg/m3) in association with exposure to NO2 from the amended Project. As

NO2 emissions for the selected receivers/residences were less than the Australian air quality

criterion, it is considered unlikely that the blast emissions would cause direct acute and/or

chronic health effects.

The calculated HQs for blast NO2 emissions for the worst affected private receivers/residences

are all less than 1, therefore it is unlikely the cumulative NO2 emissions i.e. blasting, diesel

powered equipment and background monitoring data, would cause direct short-term and/or

long-term health effects. The calculated HIs for short-term cumulative blast and fuel

combustion associated NO2 and PM10 were slightly greater than unity (greater than 1) at three

of the four worst affected private receivers/residences. All the long-term HIs were less than

unity (less than 1). As such there is only a potential for short-term health effects due to

exposure from cumulative blast and fuel combustion associated NO2 and PM10. Given the

conservative approach to predicting NO2 emissions, it is considered appropriate that potential

short-term effects can be mitigated by the use of measures known to minimise fume

generation blast design, product selection and quality, blast crew education, on bench

practices and, and blasting under wind conditions that favour dispersion of pollutants. Each of

these measures would be identified in a Blast Fume Management Strategy appended to the

Blast Management Plan for the amended Project in order to prevent the modelled NO2

concentrations occurring that were utilised in this assessment.

Diesel exhaust particles are primarily PM2.5 (including a considerable component of ultrafine

particles, PM0.1) (WIMR-CAR, 2015). The organic fraction of diesel exhaust particulate matter

contains compounds such as aldehydes, alkanes and alkenes, aliphatic hydrocarbons,

polycyclic aromatic hydrocarbons and their derivatives. These substances are considered toxic

air contaminants and some of them are genotoxic and carcinogenic. Overall diesel exhaust

particles are considered to be carcinogenic (OEHHA, 2001). Therefore, it has been considered

appropriate to further assess the carcinogenic inhalation risk using the project-only PM2.5 –

diesel concentration i.e. the highest annual average PM2.5 – diesel concentration combined

with background monitoring data (receiver/residence 18 in Year 10).

This concentration was applied across the whole population i.e. Gloucester State Suburb and

Faulkland State Suburb (Forbesdale Estate) providing a conservative estimate of the potential

cancer risk. This PM2.5 – diesel concentration was then multiplied by the cancer unit risk factor

i.e. 0.000034 μg/m3, derived by the World Health Organisation (WHO) and an adjustment

factor (0.25). The resultant risk, 0.31 in 100,000 / 3.1 in 1,000,000, is within the acceptable

cancer risk range, i.e. 1 in 100,000 to 1 in 1,000,000 generally accepted by NSW, national and

international authorities, for airborne contaminants. In addition, it should be noted that real-time

monitoring of PM2.5 and PM10 particulates, reactive management of all particle emissions, and

regular maintenance of diesel vehicles and machinery on site, would reduce the exposure of

the community to diesel particles and further reduce potential risks to health.

There are inherent uncertainties in the methods used to estimate emissions and

concentrations and limitations on how accurately the impacts of the amended Project can be

estimated in future years. As such, in order to minimise the risk of under estimation throughout

the HRA, conservatism has been applied where possible. The modelling data used to inform



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this HRA used worst case assumptions and therefore it is expected that actual ground level

concentrations would be lower during the normal operation of the amended Project. The

modelled predictions at the most affected private receivers/residences were used to represent

exposure across the populations of the respective state suburbs and consequently the overall

community exposure was over estimated. The PM2.5 and PM10 exposure assessment evaluates

the potential of the emissions to cause direct effects on individuals who may be exposed either

on a short-term, infrequent basis or long-term basis, i.e. assuming 24 hours per day for each

day of the year for 70 years. This exposure scenario is highly unlikely especially since the life

of the mine is estimated to be up to 21 years.

The applied exposure assessment method for PM2.5 and PM10 is typically reserved for

populations of greater than 25,000 because there are important challenges in translating

methods intended for large populations to those for addressing risk in smaller populations.

Nevertheless, when taken together with the modelling predictions, the uncertainties err on the

side of safety. The predicted NO2 emissions due to blasting considered a range of

meteorological conditions, including unrealistic scenarios of blasting during unfavourable

conditions and assuming a worst case Level 4 fume category, which over-estimated the peak

concentrations of NO2 at the selected private receivers/residences. The PM2.5 – diesel

exposure assessment used PM2.5 – diesel modelled predictions based on the highest diesel

consumption for any of the mining years, from a mine operation year (Year 7) predicted to

have the highest predicted PM2.5 concentration.

In consideration of the community concerns raised, it is important to note that health issues in

relation to exposure to PM - total, cumulative NO2 and PM2.5 – diesel from the amended Project

have been outlined and the associated potential for acute or chronic effects assessed. The

exposure assessments have used both standards adopted by all Australian jurisdictions and

exposure response functions relevant to the Australian population (where relevant) to estimate

likelihood of unacceptable risk. Susceptible/ vulnerable groups within adjacent communities

have been taken into consideration and a range of health end points assessed, i.e. short- and

long-term mortality and daily hospitalisations. Overall it is concluded that air emissions from

the amended Rocky Hill Coal Project present little likelihood of causing adverse health effects

to exposed individuals in the vicinity of the Site.



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1. I N T RO D U C TI ON

1.1 SCOPE OF WORK

Gloucester Resources Limited (the Applicant) proposes to develop and operate an open cut

coal mine, approximately 3.5km to 7km southeast of the Gloucester urban area, approximately

120km north of Newcastle, New South Wales (NSW) in the Gloucester Basin (Figure 1.1).

The Applicant contracted Pacific Environment Limited (then Toxikos Propriety Limited) to

update the Health Risk Assessment (HRA) undertaken for the 2013 Project using the air

quality modelling outcomes for the “amended Rocky Hill Coal Project” (“the amended Project”).

The applied HRA methodology was consistent with the protocols and guidelines recommended

by the Australian enHealth Council (enHealth, 2012a). This HRA addresses likely impacts on

community health from exposure to air emissions from the amended Project, considering the

direct health effects from acute (short-term) and chronic (long-term) exposures. It evaluates

the potential of the emissions to cause direct effects on individuals who may be exposed either

on a short-term, infrequent basis or long-term basis, i.e. assuming 24 hours per day for each

day of the year for 70 years. Thus, from the aspect of long-term exposure assumptions, the

HRA is conservative (i.e. errs on the side of safety), as the life of the mine is estimated to be

up to 21 years.

Ground Level Concentrations (GLCs) of key air quality metrics were predicted at discrete

locations around the Site using air dispersion modelling conducted by Pacific Environment

(detailed within the standalone Air Quality Impact Assessment – Part 2A of the Specialist

Consultant Studies Compendium). The emissions of concern addressed in the HRA

assessment were Particulate Matter (PM), diesel exhaust (from activities associated with open

cut coal mining) and nitrogen dioxide (NO2) (resulting from blasting activities and fuel

combustion).

The HRA has been facilitated by provision of spreadsheet results from the dispersion

modelling undertaken by Pacific Environment Limited (presented within the Air Quality Impact

Assessment – Part 2A of the Specialist Consultant Studies Compendium). These modelled

outputs contain predicted Ground Level Concentrations (GLCs) of individual pollutants at a

total of 160 non-resource related assessment locations i.e. 157 privately-owned

receivers/residences in the vicinity of the Site and 3 sensitive receiver locations with the

Gloucester township.

1.2 BACKGROUND

In August 2013, Gloucester Resources Limited (“the Applicant”) submitted a Development

Application (No. SSD 5156) for the Rocky Hill Coal Project (the 2013 Project) which was

supported by an Environmental Impact Statement (EIS) prepared by R.W. Corkery & Co. Pty

Limited on behalf of the Applicant. The 2013 Project comprised the development of an open-

cut coal mine to produce up to 2.5 million tonnes per annum (Mtpa) of run-of-mine (ROM) coal,

a coal handling and preparation plant (CHPP), an overland conveyor and a rail load-out facility.

The 2013 Project also anticipated up to 1.75Mtpa of product coal would be transported by rail

to the Port of Newcastle for export. The Mine Area for the 2013 and amended Project is

situated 3.5km to 7.0km southeast of the Gloucester urban area within the former Gloucester

Local Government Area, in New South Wales (NSW).



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Figure 1.1 Locality Plan



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In June 2015, the Applicant submitted a request that the NSW Department of Planning and

Environment (DPE) to place the determination of its development application on hold as it was

in negotiations regarding a potential commercial arrangement with the owner of the Stratford

Mining Complex, Yancoal Australia Limited (Yancoal). In December 2015, the Applicant and

Yancoal formally advised DPE that a commercial agreement had been reached between the

two companies whereby sized ROM coal would be transported from the Rocky Hill Mine Area

to the Stratford Mining Complex via a private haul road and processed in the Stratford CHPP

before being loaded onto rail for transportation to the Port of Newcastle. Hence the amended

Project will no longer require its own CHPP, overland conveyor, rail loop or train loader.

1.3 OVERVIEW OF THE AMENDED PROJECT

The proposed amended Rocky Hill Coal Project comprises three principal components (see

Figure 1.2).

1. The “Mine Area” incorporating three contiguous open cut pits, a run-of-mine

(ROM) pad with a breaker station and sized coal bin, amenity barriers,

overburden emplacements and an administration area with site offices,

amenities, workshop, water treatment plant and ancillary facilities.

2. The “private haul road”, a 4.4km sealed road to be used for the transportation of

sized coal from the Rocky Hill Mine Area to the Stratford Mining Complex for

washing and despatch to the Port of Newcastle. The private haul road extends

from the southern boundary of the Rocky Hill Mine Area to the northern boundary

of the Stratford Mining Complex, owned by Stratford Coal Pty Limited.

3. Two “power line corridors” incorporating a re-located 132kV power line and a new

low voltage (11kV or as nominated by Essential Energy) power line external to

the Rocky Hill Mine Area.

Each of these components is located in an area referred to as “the Site”.

Figure 1.3 displays the conceptual layout of the Mine Area, including the following major

components.

The Mine Area entrance off McKinleys Lane, approximately 50m south of the

intersection with Waukivory Road.

An administration area, incorporating site offices, amenities, workshop, water

treatment plant and ancillary facilities. The administration area is located on land

off McKinleys Lane and would be accessed by a private road, referred to as the

Mine Area access road, which would be aligned generally parallel to and

immediately east of McKinleys Lane.

Three contiguous open cut pits (Avon, Bowen Road and Main) varying in depth

from approximately 80m to 220m. Though based on current planning, the open

cut pit depths nominated are approximate only given the steeply dipping nature of

the coal seams, the extent of geological knowledge, and the potential effects of

changes in controlling economic factors. The ultimate depths of development in

each open cut pit would reflect the optimisation of coal quality, the outcomes of

detailed planning as coal extraction progresses and market factors.



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Figure 1.2 Amended Site Layout



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Figure 1.3 Amended Mine Area Layout



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A series of interim and long-term amenity barriers to visually screen areas of

activity and/or to provide for noise mitigation. The upper surfaces of the barriers

would either mimic the existing underlying landform or provide a variable

comparatively natural appearance. The barriers would either be stand-alone

structures (i.e. the western and northern amenity barrier) or comprise the western

faces of the permanent overburden emplacement as it is progressively

developed, i.e. interim amenity barriers.

A consolidated in-pit overburden emplacement and permanent out-of-pit

overburden emplacement extending to the west of the open cut pits. An interim

overburden emplacement which would be located to the north of the permanent

overburden emplacement but would be removed at the cessation of coal

extraction to provide some of the backfill for the final void in the Main Pit.

A ROM pad and associated breaker station comprising a feed conveyor, rotary

breaker, a sized coal conveyor and a nominal 500t capacity overhead sized coal

bin from which 60t nominal capacity road-registered trucks would be loaded. The

ROM pad would have a capacity to store approximately 80 000t of coal awaiting

processing through the breaker station, i.e. sufficient capacity for approximately

two weeks production at the maximum scheduled production rate.

A 5km section of re-located 132kV power line and a new 11kV power line

providing power for the on-site operations. The remaining sections of the re-

located 132kV power line and the 11kV power line lie external to the Mine Area

within the defined power line corridors.

Figure 1.4 displays the 4.4km private haul road comprising a minimum 7m seal on a 10m

formation extending between the sized coal bin and the boundary of ML1733, the northern

extent of the Stratford Mining Complex. The private haul road would link with a section of new

road to be constructed within ML1733 and then into the existing on-site haul road system

within the Stratford Mining Complex.

In light of this amendment, the Applicant has re-designed the open cut pits and mine

sequencing to focus on the production of metallurgical coal and is not proceeding with the

construction and operation of the on-site CHPP, overland conveyor, rail loop and rail load-out

facility.



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Figure 1.4 Private Haul Road



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2. M ET H O DO LO GY

2.1 WHAT IS A RISK ASSESSMENT?

Health is defined by the World Health Organization (WHO) as a state of complete physical,

mental and social well-being and not merely the absence of disease or infirmity (WHO, 1948).

Well-being is broadly described as an individual’s self-assessment of their state of happiness,

healthiness and prosperity. It relates to the quality of life and one’s ability to enjoy it. There are

many social and economic factors that impinge upon well-being.

The following are examples of determinants of health well-being (enHealth 2012a, NHC 2004):

Social and cultural factors (e.g. social support, participation, access to cultural

resources).

Economic factors (e.g. income levels, access to employment).

Environmental factors (e.g. land use, air quality).

Population-based services (e.g. health and disability services, leisure services).

Individual/behavioural factors (e.g. physical activity, smoking).

Biological factors (e.g. biological age).

According to enHealth (2012a), all developments have a potential impact on health. Some

would have positive health impacts by providing jobs, attracting health services to an area, and

improving overall economic well-being of a community, etc. Other developments may have

negative impacts such as increased risk of disease, social disruption, increased noise etc.

Many developments would have both positive and negative aspects. It should be understood

that the potential influence of the amended Project on local area economic factors, social

disruption and other such factors are not addressed in this document. These matters are

addressed as part of the Social Impact Assessment and Economic Impact Assessment (Parts

14 and 15 of the Specialist Consultant Studies Compendium). Air quality is one of the many

parameters influencing well-being. This HRA seeks to evaluate what the likelihood is for direct

health effects when exposures to air emissions from the amended Project occur.

A health risk assessment is an analysis that uses information about potentially hazardous

pollutants to estimate a theoretical level of risk for people who might be exposed to defined

levels of these pollutants.

Risk assessments are often conducted by considering possible or theoretical community

exposures based on the outcomes of air dispersion modelling. Conservative safety margins

are built into a risk assessment analysis to ensure protection of the public. Therefore, people

would not necessarily become unwell even if they are exposed to pollutants at higher

concentration levels than those estimated by the risk assessment. During a risk assessment

analysis, the most vulnerable people (e.g. children, the sick and elderly) are carefully

considered to make sure that all members of the public would be protected.



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The risk assessment helps answer the following common questions for people who might be

exposed to hazardous pollutants in the environment, in this case components of the air

emissions from the amended Project.

Under what circumstances might I, my family and neighbours be exposed to

hazardous pollutants from the amended Project?

Is it possible we might be exposed to hazardous pollutants at levels higher than

those determined to be safe?

If the levels of hazardous pollutants are higher than regulatory standards, what

are the health effects that might occur?

The HRA is a useful tool for estimating the likelihood and severity of risks to human health,

safety and the environment and for informing decisions about how to manage those risks. It is

a document that assembles and synthesizes scientific information to determine whether a

potential hazard exists and/or the extent of possible risk to human health.

Although this report describes certain technical aspects of the risk assessment, it does not

address the processes of risk management and risk communication.

2.2 OVERALL APPROACH

The methodology adopted in the conduct of this HRA is consistent with the protocols and

guidelines recommended by the enHealth Council. These are detailed in the document

“Environmental Health Risk Assessment: Guidelines for assessing human health risks from

environmental hazards” (enHealth, 2012a).

The development of a formalised HRA has resulted in the process being categorised into

distinct stages. Some of the key factors and questions that are taken into consideration at each

of these stages include the following.

1. Hazard Assessment

Identifies hazards and health endpoints associated with exposure to hazardous

pollutants and provides a review of the current understanding of the toxicity and

risk relationship of the exposure of humans to the hazards.

2. Exposure Assessment

This task identifies the groups of people who may be exposed to hazardous

pollutants and provides an estimate as to the potential exposure concentrations.

3. Risk Characterisation

This task provides the qualitative/quantitative evaluation of potential risks to

human health. The characterisation of risk is based on the review of the dose-

response relationship and the assessment of the magnitude of exposure.



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3. C OM M U NI TY PR O FI L E

This section discusses the community adjacent to the Site of the amended Project that may

potentially be affected by emissions over its lifetime. Figure 1.1 illustrates the location of the

amended Project and the potentially affected communities.

3.1 SURROUNDING AREA AND POPULATION

The Site is located approximately 120km north of Newcastle in the Gloucester Basin. The

amended Project is located in a rural area characterised by cattle (beef and dairy) grazing on

native and improved pastures, with intervening areas of remnant bushland. Other land uses in

the local area include rural residential, the existing Stratford Mining Complex (SMC) to the

south, residential development in Gloucester and other townships such as Stratford,

Barrington, Craven, estates such as Forbesdale and areas of National Park/Nature Reserve.

There are a number of privately-owned and resource company-owned residences in the

vicinity of the Site, as shown on Figure 3.1, with resource company-owned residences

comprising those owned by GRL, Yancoal, AGL or associated companies. Properties under a

purchase option to the Applicant subject to the receipt of development consent and/or a mining

lease are also identified as resource company-owned.

3.2 POPULATION PROFILE

The composition of the population in Gloucester, as defined by the State Suburb boundaries,

was reviewed. The State suburb of Gloucester includes the township of Gloucester as well as

the Avon River and Thunderbolt residential estates (Figure 1.1). There is no statistical

breakdown only covering the Forbesdale Estate area (Figure 1.1), therefore, given it is wholly

located within the Faulkland State Suburb, Faulkland State Suburb data has been used to

assess the health issues in the Forbesdale Estate. The population statistics considered for this

assessment are available from the Australian Bureau of Statistics (ABS) website for the

census year 2011 and are summarised in Table 3.1.

Table 3.1

Population Age Profile Used in Analysis

Age Group

Number of individuals

Gloucester State Suburb Faulkland State Suburb

(Forbesdale Estate)

All ages 2878 241

65+ years 799 57

30+ years 2017 176

15-64 years 1607 151

0-14 years 472 33

Source: ABS data 2011



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Figure 3.1 Resource Company and Privately Owned Residences in the Vicinity of the Site



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3.3 RESIDENCES AND SENSITIVE RECEIVERS

The HRA considers locations where maximum impacts of the amended Project may occur as

well as the adjacent locations where people live, i.e. Gloucester (including the Thunderbolt and

Avon River Estates) and Forbesdale. A total of 157 private receivers/residences, where people

reside and 3 sensitive receiver locations, where people gather were assessed. The

receivers/residences therefore captured the sensitive members in the communities, i.e. the

very young (0-14 years) and the elderly (65+years).

3.4 COMMUNITY CONCERNS

As part of the approval process, the Applicant initially lodged an Environmental Impact

Statement (EIS) for the 2013 Project to the (then) Department of Planning and Infrastructure

(DP&I). DP&I sought public comment on the EIS between 28 August 2013 and

28 October 2013. The concerns raised through this process were captured within the formal

response to submissions on the EIS for the 2013 Project, with the relevant sections of the HRA

for the amended Project addressing these as identified in Table 3.2.

Table 3.2

Community Concerns and Relevant Sections of the HRA

Concern Section

General health issues from air pollution 5.2 - 5.4

The potential for asthma impacts on children within 5km of the mine 5.2 - 5.4

Potential impacts of PM2.5 and PM10 to the susceptible/ vulnerable groups within adjacent communities

5.2

The range of health effects considered for the adjacent communities 5.2.1.4

Health effect due to diesel emissions 5.4

Use of appropriately stringent criteria in the assessment 5.2.1, 5.3.1 & 5.4



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4. O VE RVI E W O F AI R Q U AL I T Y AS S E S SM E N T

A brief overview of the Air Quality Assessment is provided in the following subsections. Further

detail regarding the existing air quality environment, modelling methodology and modelling

outcome is provided within the Air Quality Assessment – Part 2A of the Specialist Consultant

Studies Compendium.

4.1 EXISTING AIR QUALITY

In July 2010, an air quality monitoring program was established to determine the baseline air

quality and meteorological conditions in the vicinity of the Mine Area. The monitoring network

consists of eight dust deposition gauges measuring dust deposition rates over the period of

one month, two Tapered Element Oscillating Microbalance (TEOMs) measuring continuous

PM10 and PM2.5 concentrations for 24-hour periods, two high volume air samplers (HVASs)

measuring PM10 concentrations for 24 hours periods on a one day in six run cycle and a

meteorological monitoring station. Prevailing winds at the Site are from the south and

northeast on an annual basis, and are similar but slightly different to winds measured at the

Stratford Mining Complex meteorological station, approximately 7km south of the Mine Area.

A review of the air quality monitoring data indicates that ambient air quality in the Stroud-

Gloucester Valley is generally good and well below the relevant ambient air quality criteria.

4.2 AIR QUALITY ASSESSMENT SCENARIOS

Mining operations would involve the sequential activities of vegetation clearing, soil stripping,

overburden/interburden removal, coal recovery, breaking of coal to <120mm, transportation of

sized coal via the private haul road, and progressive rehabilitation of the Mine Area. Four

operational scenarios were therefore chosen for quantitative air quality dispersion modelling.

These years, along with their rationale for selection, are provided below and were further

assessed in the Air Quality Assessment with the outcomes of the modelling used in this HRA.

1. Year 1: Representative of the development of the open cut pit and the western

and northern amenity barrier. Minimal ROM coal production and

operations restricted to day time only.

2. Year 4: Representative of operations at the commencement of day and evening

operations and ramping up of overburden and ROM coal production.

3. Year 7: Representative of operations at maximum overburden production, 80%

of maximum coal production and a wide geographic spread of activities

across the Mine Area.

4. Year 10: Representative of operations at maximum overburden production and

95% of maximum coal production but with mining activities occurring at

depth and overburden emplacement predominantly occurring in-pit.



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4.3 AIR QUALITY ASSESSMENT OUTCOMES

The modelling indicates that no private receivers/residences are predicted to experience 24-

hour average PM10 or PM2.5 levels above the criterion of 50 μg/m3 and 25 μg/m3 respectively

across all mining years. There are no private receivers/residences that are predicted to

experience annual average PM10, PM2.5, TSP or dust deposition above the assessment criteria,

either from the amended Project alone or cumulatively.



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5. H E ALT H R I S K AS S E S SM E N T

5.1 IDENTIFICATION OF EMISSIONS OF HAZARDOUS POLLUTANTS

Open cut mines, such as that proposed in the amended Project, mine coal using open cut

methods, predominately using haul trucks and hydraulic excavators. Emissions may occur

during the six distinct stages of the mining process i.e. land preparation, blasting, overburden

removal, coal recovery, coal processing and transport off site, and mined land rehabilitation. In

consideration of these activities, the main pollutants would be particulate matter (PM) and

oxides of nitrogen (NOx). Fugitive PM would be emitted at every stage of the mining process.

PM is typically characterised in terms of its size fractions, with common metrics for health

assessment being PM less than 10 micrometres in aerodynamic diameter (PM10) and PM less

than 2.5 micrometres in aerodynamic diameter (PM2.5). NOx would most likely be emitted

during the blasting phase of the mining process, and would comprise both nitric oxide (NO)

and nitrogen dioxide (NO2). From the point of view of impacts on human health and frequency

of exposure, it is PM which is of greatest concern.

The adverse health effects resulting from exposure to ambient pollutants, such as PM and

NO2, range from the relatively mild sub-clinical effects such as throat irritation, to clinical effects

of reduction in lung function or increased medication usage, through to seeking medical

attention from a General Practitioner (GP), emergency department attendances, hospital

admission and premature mortality due to various diseases. Figure 5.1 illustrates the

relationship between the frequency of an adverse health outcome and its severity. Mortality

and hospital admissions are often studied in relation to ambient air pollutants, since they are

clearly defined health outcomes that have a measurable impact on the community. Further

discussion on the health endpoints of concern with respect to PM and NOX are provided in

Section 5.2.1 and Section 5.3.1.

Figure 5.1 The Severity and Frequency of an Adverse Health Impact as a Result of Ambient Air Pollution Exposure (Source: WHO, 2001)

Premature mortality

Hospital admissions

Emergency room visits

GP visits

Restricted activity/reduced performance Medication use

Symptoms

Impaired pulmonary functions

Subtle effects

Proportion of population affected

Severity of health impacts



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5.2 ASSESSMENT OF PARTICULATE MATTER

5.2.1 Hazard Assessment

5.2.1.1 Types of Particulate Matter and Assessment Criteria

Particulate Matter (PM) is an air-suspended mixture of solid and liquid particles that vary in

number, size, shape, surface area, chemical composition, solubility and origin. PM is classified

by aerodynamic diameter, as size is a critical determinant of the likelihood and site of

deposition within the respiratory tract.

1. PM10 includes all inhalable particles less than 10 µm aerodynamic diameter.

These are sufficiently small to penetrate to the thoracic region. Coarse particles

consist of those between PM2.5 and PM10 (i.e. PM2.5-10) and sometimes may be

referred to as ‘thoracic’ particles.

2. PM2.5 (fine particles) includes those inhalable particles less than 2.5 µm

aerodynamic diameter. These have a high probability of deposition in the smaller

conducting airways and alveoli.

3. PM10 includes coarse, fine and ultrafine particles (< 0.1 μm).

4. PM2.5 includes fine and ultrafine particles (< 0.1 μm).

Both natural (e.g. crustal dust eroded from the earth’s surface) and anthropogenic processes

(e.g. mining, quarrying, wood fires) contribute to the atmospheric load of PM. The human

contribution to ambient PM in urban regions often exceeds the contribution from natural

sources and results in higher ambient PM concentrations compared to non-urban background

sites which receive lower contributions of PM generated by human activities. It has been

estimated that in 2008 in the Greater Metropolitan Region (GMR) of NSW (incorporating the

greater Sydney, Newcastle and Wollongong areas), the majority of PM emissions (>70%) were

of anthropogenic origin (Hime et al 2015). Coal mining in the GMR is estimated to contribute

~45% of the PM emissions i.e. 42.5% PM10 and 22.6% of PM2.5, via associated activities such

as coal extraction, transfer & loading of coal, removal of overburden and wheel generated dust

(NSW EPA 2012; WIMR-CAR 2015, Katestone 2011).

The generated dust can come from either disturbance of soil (e.g. land preparation and wheel

generated emissions from haul trucks), or coal dust (excavators digging soil and stockpiling the

coal). Coal dust is a fine powdered form of coal that is created during its mining, processing

and transportation. Most of the coal dust emissions are in the coarse particle fraction (PM2.5-10)

rather than PM2.5. However the amount of dust generated during mining and coal processing

depends on weather conditions, local geology, mining/processing activity, and methods of dust

suppression (Hime et al 2015).

All particles, irrespective of their origin, appear to cause adverse health impacts. In recent

years, a significant amount of research has focused on the health effects of particles and an

increasing body of literature reports associations between PM and adverse health effects. A

range of health effects have been found for both PM10 and PM2.5, with the majority of the

information coming from population-based epidemiological studies.



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Table 5.1 presents a summary of the established NSW EPA impact assessment criteria (other

than PM2.5 which is drawn from NEPM 2016).

Table 5.1

NSW Impact Assessment Criteria for PM

Pollutant Averaging

period Criteria (µg/ m

3) Reference

PM2.5 24-hour 25 NEPM (2016)

Annual 8 NEPM (2016)

PM10 24-hour 50* NSW DEC (2005)

Annual 30 NSW DEC (2005)

*one exceptional exceedance

5.2.1.2 Coal Dust

Health consequences of significant coal dust exposure have been suspected ever since an

increase in the prevalence of pneumoconiosis became evident among coal workers in South

Wales in the 1930s (Heppleston 1992). There are many occupational exposure studies on coal

mine workers that have shown an association between coal dust exposure and

pneumoconiosis, chronic bronchitis, emphysema and loss of lung function (Heppleston 1992,

Wouters et al. 1994, Petsonk et al. 2013). Data indicate a dose-response relationship between

coal dust inhalation and the incidence and severity of pneumoconiosis as well as the

development of emphysema and chronic bronchitis (Finkelman et al. 2002, Cohen et al. 2009).

Though occupational exposure to coal dust can cause serious, sometimes fatal, respiratory

disease, the effects of occupational exposure cannot be directly extrapolated to the effects of

non-occupational exposures in the general community. Occupational exposure is often

substantially greater than community exposure due to the proximity of workers to the emission

source and the dispersion of coal dust in the atmosphere (Hime et al 2015).

No Australian studies have specifically examined the health effect of non-occupational

exposures to coal dust, however, there have been studies of the health of coal mining

communities. These studies report higher rates of respiratory disease, cardiovascular disease

and increased presentations to hospital emergency departments for asthma (NSW Health

2010a, NSW Health 2010b). None of these investigations included air pollution data in the

analyses, therefore, it is not clear whether any differences in health outcomes in areas

surrounding coal mining activity, compared to populations elsewhere, are the result of

exposure to locally emitted PM. Furthermore, the health data from these studies were not

adjusted for other possible causes of chronic disease such as rates of smoking and dietary

habits, making it problematic to assign any observed poor health outcomes to the

environmental health effects of coal mining. Given the limitations to the research to date, there

is insufficient evidence that reported adverse health outcomes in Australian communities

surrounding coal mining operations are related to exposure to coal dust. However,

observations of higher rates of respiratory and cardiovascular outcomes in some coal mining

areas warrant further investigation to determine associations between health outcomes

(adjusted for known causes of disease) and exposure to PM derived from coal mining activities

(NSW Health 2010a; NSW Health 2010b; WIMR-CAR 2015). Given the foregoing, the

following sections describe the hazardous effects of PM.



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5.2.1.3 Health Effects of Particulate Matter

The health effects of particles linked to ambient exposures have been well studied and

reviewed by international agencies (NEPM, 2010; US EPA, 2004, 2009, 2012; WHO, 2006,

2013; OEHHA, 2000). In recent years, a large amount of research has focussed on the health

effects of particles and an increasing body of literature reports associations between particles

and adverse health effects. Effects have been found for both PM10 and PM2.5 and, to a lesser

extent, ultrafine particles (UFPs). Most information comes from population-based

epidemiological studies that find increases in daily mortality, as well as morbidity outcomes

such as increases in hospital admissions and emergency room attendances, and exacerbation

of asthma to be associated with daily changes in ambient particle levels. There has been an

increasing focus on the link between exposure to particles and cardiovascular outcomes. In

addition to studies on the various size metrics for particles, research has also investigated the

role of particle composition in the observed health effects (US EPA, 2009, 2012; WHO, 2013).

The evidence on the health effects of particles comes from several major lines of scientific

investigation: characterisation of inhaled particles; consideration of the deposition and

clearance of particles in the respiratory tract and the doses delivered to the upper and lower

airway and the alveoli; animal and cellular studies of toxicity; studies involving inhalation of

particles by human volunteers; and population-based epidemiological studies. The findings of

these different lines of investigation are complementary and each has well-identified strengths

and limitations. While the findings of epidemiological studies have been given the greatest

weight in setting standards for airborne particles, studies on human volunteers (clinical studies)

can provide information on exposure–response relationships for short-term, transient effects in

healthy and potentially susceptible individuals. Studies of this design, involving both healthy

persons and adults with chronic diseases, have been carried out using exposure to

concentrated ambient particles (US EPA, 2009).

There is substantial new evidence from time series studies of daily mortality, particularly from

multi-city studies that span Europe and North America (US EPA, 2012, 2009; WHO, 2013) and

also Australia (NEPM, 2010). Several studies conducted in Australia also show adverse effects

of both PM10 and PM2.5 on mortality and morbidity outcomes (Simpson et al., 2005a, b; Barnett

et al., 2005) similar to those observed in overseas studies. The effects observed in the

Australian studies appear to be higher than those observed in the US and Europe but

comparable to the results of Canadian studies. The epidemiological evidence is supported by

an increasingly strong foundation of toxicological research. Various mechanisms have been

proposed by which particles may cause and/or exacerbate short-term and chronic diseases.

Inflammation due to the production of reactive oxygen species is emerging as a central

mechanism.

PM2.5

The health effects of PM2.5 have been extensively studied and reviewed in recent years (WHO,

2013; US EPA, 2012, 2009; NEPM 2010). There is a large database that supports a causal

association between exposure to PM2.5 and a range of both short-term and long-term mortality

and morbidity outcomes. In 2013, a large European cohort study investigated the association

of exposure to PM2.5 with cause-specific mortality in adults included in the Rome Longitudinal

Study. The authors found that long-term exposure to PM2.5 is linked to increases in accidental

mortality associated with ischaemic heart diseases, cardiovascular diseases and lung cancer

(Cesaroni et al., 2013).



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Short-term Health Effects of PM2.5

In recent years, there has been a substantive increase in studies showing associations

between particles and cardiovascular effects. Epidemiological studies that examined the

association between PM10, PM2.5 and mortality have provided strong evidence for particle-

related cardiovascular effects. Multi-city studies have found consistent, positive associations

between short-term exposure to PM2.5 and cardiovascular mortality ranging from 0.47 to 0.85%

in study locations with mean1 24-hour average PM2.5 concentrations above 12.8μg/m3. These

associations were reported at short lags (0-1 days). Although examinations of potential

confounders of the PM2.5-cardiovascular mortality relationship are limited, the observed

associations are supported by PM10-mortality studies, which found that particle risk estimates

remained robust to the inclusion of co-pollutants in models. Although the overall effect

estimates reported in the multi-city studies are consistently positive, it should be noted that a

large degree of variability exists between cities when examining city-specific effect estimates

potentially due to differences between cities and regional differences in PM2.5 composition.

An evaluation of the epidemiological literature indicates consistent positive associations

between short-term exposure to PM2.5 and all-cause, cardiovascular- and respiratory-related

mortality. The evaluation of multi-city studies found that risk estimates for all-cause (non-

accidental) mortality ranged from 0.29% to 1.21% per 10μg/m3 increase in 24-hour average

PM2.5 at lags of 1 and 0–1 days. These consistent effects were observed in study locations with

mean 24-hour average PM2.5 concentrations as low as 13μg/m3. Cardiovascular-related

mortality risk estimates were found to be similar to those for all-cause mortality whereas, the

risk estimates for respiratory-related mortality were consistently larger: 1.01–2.2% using the

same lag periods and averaging indices (US EPA, 2009).

Examinations of potential confounders of the PM2.5-respiratory mortality relationship are

limited, however, the observed associations are supported by PM10-mortality studies, which

found that particle risk estimates remained robust to the inclusion of co-pollutants in models

(Ostro et al. 2006, Franklin et al., 2008).

A large body of evidence from studies of the effect of PM2.5 on hospital admissions and

emergency department visits for cardiovascular diseases has shown that associations with

PM2.5 are consistently positive, with the majority of studies reporting increases in hospital

admissions or emergency department visits ranging from a 0.5% to 3.4% per 10μg/m3 increase

in PM2.5 (Bell et al., 2008, Dominici et al., 2006). The results of these studies provide support

for associations between short-term PM2.5 exposure and increased risk of cardiovascular

hospital admissions in areas with mean concentrations ranging from 7 to 18μg/m3.

A number of studies have found consistent associations between PM2.5 and hospital

admissions and emergency department visits for respiratory disease, with effect estimates in

the range of ~1% to 4% per 10μg/m3 increase in PM2.5. These associations have been

observed in areas with mean 24-hour PM2.5 concentrations between 6.1 and 22μg/m3. Further

studies have focused on increasingly specific disease endpoints such as asthma, Chronic

Obstructive Pulmonary Disease (COPD) and respiratory infection. The strongest evidence of

an association comes from large multicity studies of COPD, respiratory tract infection and all

respiratory diseases among Medicare recipients (65+ years old) (Dominici et al., 2006; Bell et

al., 2008). Studies of children have also found evidence of an effect of PM2.5 on hospital

admissions for all respiratory diseases, including asthma and respiratory infection (Peel et al.,

2005)

1 In this context, mean represents the arithmetic mean of 24-h average PM concentrations.



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Controlled human exposure studies in adults demonstrating increased markers of pulmonary

inflammation following diesel exhaust and other traffic-related exposures, oxidative responses

to diesel exhaust and wood smoke, and exacerbations of allergic responses and allergic

sensitization following exposure to diesel exhaust particles add further support for these effects

(US EPA, 2009). Some controlled human exposure studies have reported small decrements in

various measures of pulmonary function following controlled exposures to PM2.5. Numerous

toxicological studies demonstrating a wide range of responses provide biological plausibility for

the associations between PM2.5 and respiratory morbidity observed in epidemiological studies.

Altered pulmonary function, mild pulmonary inflammation and injury, oxidative responses,

airway hyper responsiveness in allergic and non-allergic animals, exacerbations of allergic

responses and increased susceptibility to infections were observed in a large number of

studies involving exposure to concentrated ambient particles, diesel exhaust, other traffic-

related particles and wood smoke. The numerous and wide range of respiratory responses

observed in both the human clinical and toxicological studies provide biological plausibility for

an association between short-term exposure to PM2.5 and respiratory morbidity. The US EPA,

(2009) concluded that the consistent and coherent results found in the epidemiological, human

clinical, and toxicological literature provide sufficient evidence that a causal relationship is

likely to exist between short-term exposures to ambient concentrations of PM2.5 and respiratory

morbidity.

Epidemiological studies of asthmatic children have found increases in respiratory symptoms

and asthma medication use associated with higher PM2.5 or PM10 concentrations. Associations

with respiratory symptoms and medication use are less consistent among asthmatic adults,

and there is no evidence to suggest an association between respiratory symptoms with PM2.5

among healthy individuals (US EPA, 2009). In addition, respiratory symptoms have not been

reported following controlled exposures to PM2.5 among healthy or health-compromised adults.

Several new controlled human exposure studies report traffic or diesel-induced increases in

markers of inflammation in airway lavage fluid (fluid used to rinse the airways) from healthy

adults. There is also additional evidence in support of a pulmonary oxidative response to diesel

exhaust in humans. Preliminary findings indicate little to no pulmonary injury in humans

following controlled exposures to fine urban traffic particles or diesel exhaust, in contrast to a

number of toxicological studies demonstrating injury with concentrated ambient particles or

diesel exhaust.

Long-term Health Effects of PM2.5

The earlier studies on the long-term effects of PM2.5 on mortality – the Six Cities Study

(Dockery et al., 1993) and the American Cancer Society (ACS) study (Pope et al., 2002) –

have been pivotal in the development of air quality standards and guidelines worldwide. These

studies have been updated several times with systemic increases in the number of years of

analysis and deaths that were followed in these cohorts and in the statistical approaches used

in the analysis (Laden et al., 2006; Krewski et al., 2009). These reanalyses continue to find a

consistent, statistically significant association between long-term exposure to PM2.5 and the risk

of mortality. The magnitude of the effects estimate (the mortality effect per unit of exposure)

remains consistent with that of the original study (WHO, 2013). Using the 51 cities from the

ACS study, Pope et al., (2009) reported that reductions in PM2.5 across the metropolitan

regions between 1980 and 2000 were strongly associated with increases in life expectancy

after correcting for other risk factors.



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A large number of new prospective cohort studies from Asia, Canada, Europe and the US

have been reported since 2005 (summarised in WHO, 2013). These studies provide additional

evidence of the effects of long-term exposure to PM2.5 on mortality. These effects have been

observed at lower concentrations than previously studied and there is still no evidence of a

threshold below which adverse effects do not occur. These studies have been undertaken in

areas that cover a variety of environmental settings, PM mixtures, baseline health conditions,

socioeconomic settings and personal characteristics. Given the consistency in the findings of

these studies, WHO (2013) and US EPA (2012; 2009) have determined that it is appropriate to

extrapolate the findings of these studies to other regions. The risk of ischemic heart disease

has particularly strong associations with PM2.5.

Hoek et al (2013) conducted a systematic review of the literature on the long-term effects of air

pollution on all cause, cardiovascular and respiratory mortality. Where more than 5 studies

were identified, a meta-analysis was conducted to obtain an overall effects estimate for each

outcome. The authors identified a number of cohort studies conducted in various parts of the

world that found associations between PM2.5 and PM10 and all cause, cardiovascular and

respiratory mortality. The effects estimates identified per 10μg/m3 increase in annual average

PM2.5 were 6% all cause, 11% cardiovascular and 3% respiratory mortality. For PM10, a 3.5%

increase in all-cause mortality per 10μg/m3 increase in annual average PM10 was found. There

was significant heterogeneity in the effects estimates from individual studies which was

thought to be due to differences in particle composition, indoor exposures as well as

population and baseline health status of the exposed populations.

Recent studies have also shown the effects of long-term exposure to PM2.5 on diseases other

than cardiovascular and respiratory diseases (WHO, 2013). Evidence suggests effects on

diabetes, neurological development in children and neurological disorders in adults (Ruckerl et

al., 2011). Epidemiological studies in Germany (Kramer et al., 2010) and Denmark (Anderson

et al., 2012; Raaschou-Nielsen et al., 2013) have all found strong associations between

exposure to PM2.5 and diabetes. These findings have been supported by mechanistic studies

(WHO, 2013).

The effects of PM2.5 on birth outcomes have been studied in a number of cohort studies

(Brauer et al., 2007; Gehring et al., 2010; MacIntyre et al., 2011; Morgenstern et al., 2007).

Evidence is accumulating for PM2.5 effects on low birth weight and infant mortality, especially

due to respiratory causes during the post-neonatal period. The mean PM2.5 concentrations

during the study periods ranged from 5.3 to 27.4μg/m3 with effects becoming more precise and

consistently positive in locations with mean PM2.5 concentrations of 15μg/m3 and above (US

EPA, 2009). Exposure to PM2.5 was usually associated with greater reductions in birth weight

than exposure to PM10. The evidence from a few studies that investigated PM10 effects on

foetal growth, which reported similar decrements in birthweight, provide consistency for the

PM2.5 associations observed and strengthen the interpretation that particle exposure may be

causally related to reductions in birth weight.

In summary, the potential health effects of PM2.5 are as follows:

Short-term:

1. Cardiovascular and respiratory mortality,

2. All cause cardiovascular effects e.g. Ischaemic heart diseases and respiratory

effects e.g. Asthma,

3. Hospital admissions and emergency department visits due to cardiovascular and

respiratory disease



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Long-term

1. Accidental mortality associated with ischaemic heart diseases, cardiovascular

diseases and lung cancer

2. Other disease including diabetes, neurological development in children and

neurological disorders in adults

3. Birth outcomes including low birth weight and infant mortality

4. All cause, cardiovascular and respiratory mortality

PM10

Short-term Health Effects of PM10

Most of the evidence of an association between short-term exposure to particles and adverse

health outcomes comes from time-series epidemiological studies looking at daily increases in

mortality and hospital admissions and emergency room attendances linked to ambient particle

concentrations. In addition, the results of panel studies and controlled exposure studies add

further evidence for the association between short-term exposure to particles and adverse

health effects. The results of recent reviews and studies relevant to PM10 are summarised

below.

Mortality

The epidemiological literature indicates consistent positive associations between short-term

exposure to PM10 and all-cause mortality. The results of multicity studies report an approximate

0.12% to 0.81% increase in all-cause mortality per 10μg/m3 increase in PM10 with 24-hour

average PM10 concentrations ranging from 13 to 53.2μg/m3. Consistent positive associations

have also been found between PM10 and respiratory and cardiovascular-related mortality.

Studies conducted in Australia have found similar results with a 0.2% (-0.8% to 1.2%) increase

in all-cause mortality per 10μg/m3 increase in 24-hour average PM10 (Simpson et al., 2005a).

Morbidity

The majority of recent evidence for an association between short-term exposure to PM10 and

cardiovascular health effects is derived from epidemiological studies of hospital admissions

and emergency department visits. Although some regional heterogeneity is evident in the

single-city effect estimates, consistent increases in hospital admissions and emergency

department visits for cardiovascular diseases, have been observed across studies, with the

majority of estimates ranging from 0.5% to 1.0% per 10μg/m3 increase in PM10 (WHO, 2013). A

detailed examination of specific cardiovascular health outcomes has suggested that ischemic

heart disease and chronic heart failure are responsible for the majority of particle-related

cardiovascular disease hospital admissions, however, one large multicity study provides

evidence of an association between PM10 and ischemic stroke (US EPA, 2009). Overall, the

literature provides consistent evidence for associations between short-term exposure to PM10

and increased risk of cardiovascular hospital admissions and emergency department visits in

cities with mean 24-hour average concentrations ranging from 16.8 to 48μg/m3.

Epidemiological studies that examined the association between short-term exposure to PM10

and respiratory morbidity found consistent positive effects in asthmatic children and adults, but

no evidence of an association in healthy individuals in both Australian and overseas studies.

The majority of the studies that examined the association between PM10 and respiratory



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symptoms and medication use found an increased risk ranging from ~1.0 to 1.75 for cough,

phlegm, difficulty breathing, and bronchodilator use in asthmatic children in cities with mean

24-hour average concentrations ranging from 16.8 to 64.5μg/m3. Positive, but less consistent

effects for respiratory symptoms and medication use were observed in asthmatic adults. An

evaluation of respiratory emergency department visits and hospital admission studies found

consistent positive associations at ambient PM10 concentrations ranging from 13.3 to

60.8μg/m3 among asthmatic children (~ 2% increase) and older adults with chronic obstructive

pulmonary disease (COPD) (~ 0 to 3% increase). Although no toxicological or human clinical

studies have examined the effect of short-term exposure to PM10 on respiratory morbidity, the

consistent epidemiological evidence alone was sufficient for the US EPA (2009) to conclude

that a causal relationship is likely to exist between short-term exposure to ambient

concentrations of PM10 and respiratory morbidity.

Long-term Health Effects of PM10

Most studies investigating the effects of long-term exposure to air pollution have focussed on

PM2.5. However there are some that have investigated the effects of PM10.

Mortality

Chen et al 2005 reported a positive association between PM2.5-10 and PM10 exposure and

coronary heart disease mortality which has been found to be more prevalent in females than

males. In addition, Gehring et al., 2006 has found that there is an association between

cardiopulmonary mortality and PM10 exposure.

Morbidity

Children may be at greater risk from long-term exposures to particles or other air pollutants

because the growth and development of the respiratory system may be permanently affected

by early environmental insults. Several studies have examined this and overall the evidence of

particle effects of morbidity in relation to long-term exposures is not as consistent as for

mortality. Overall, there is evidence of a particle-related effect on chronic morbidity, as

measured by chronic respiratory symptoms and lung function. However, it is not possible,

based on current evidence, to identify which size fractions or specific constituents are likely to

be most influential (US EPA, 2009; OEHHA, 2001).

In summary, the health effects of PM10 are as follows:

Short-term:

1. All-cause mortality,

2. Respiratory morbidity in asthmatics,

3. Hospital admissions and emergency department visits due to cardiovascular

health effects such as ischemic heart disease and chronic heart failure.

Long-term:

1. Respiratory morbidity, and

2. Coronary heart disease and cardiopulmonary mortality.



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5.2.1.4 Health effects and Concentration-response Relationships

Studies have demonstrated that for a wide range of PM concentrations, including

concentrations below current assessment criteria, there are measurable associations between

incremental increases in particle concentration and adverse health effects. That is, no

threshold has been identified for particles and any increase in concentration may affect health.

As such, it can be deduced that ambient guidelines do not lead to complete protection against

adverse health effects of PM.

However, the results of epidemiological studies can be used to make quantitative estimates

concerning the health effects of air pollution on a population. A Concentration Response

Function (CRF) (reported by epidemiological studies) is the empirically estimated relationship

between the concentration of PM and the observed health endpoints of interest (for example,

hospital admissions for asthma) in a population. There is a dose-response relationship with PM

and many health outcomes where the health risk increases with exposure to both PM10 and

PM2.5.

Epidemiological studies estimating health outcomes in the population are often not available

for a particular location, or the available results from local studies may not be considered as

robust as the combined results of epidemiological studies from other locations/populations.

Because the uncertainty in the precision of the risk estimate from an epidemiological study

decreases with increasing sample size (for example, the population in the study), combining

results from several studies may yield more robust estimates of effect (e.g., meta-analysis). At

present, Australian studies, in particular studies involving mining and extractive industries, are

currently considered insufficient to reliably establish specific Australian concentration-response

relationships for relevant health outcomes and PM exposures. Therefore, overseas data has

been used to quantify health effects in this health risk assessment. Additionally, in line with

WHO advice, all particles should be treated as equally harmful irrespective of source and

chemical composition.

In order to generate sufficient data to adequately characterise the concentration-response

relationship for compounds present in air, meta-analytic point estimates rather than estimates

from one single study can enhance the value of the available information and deal with

potential heterogeneity between studies. As a result, cities with large populations provide the

best data upon which to study and characterise the concentration-response relationship for

compounds present in air. Similarly, multi-city studies can also produce even more reliable

effect estimates as the sample size is much larger than those in single city studies. While, the

results are based on compounds and exposures typical to an urban setting and not those of a

rural, mine-based setting, they nevertheless provide the best information upon which to

characterise the concentration-response.

Over the last few decades, there has been a substantial amount of research that has added to

the evidence that breathing PM is harmful to human health. Various lines of research have

helped connect some of the important gaps in our knowledge. Different studies using

alternative time series approaches and case crossover designs continue to observe

reasonably consistent associations between morbidity and mortality outcomes and daily

changes in PM. The associations are observed, not only in many single-city studies, but also in

various large multicity studies (Pope and Dockery, 2006). The evidence of long-term health

effects has been strengthened by various reanalyses and extended analyses of the Harvard

Six Cities study (Dockery et al. 1993), ACS cohorts (Pope et al. 1995) and by results from

several other independent studies of long-term PM exposure.



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The PM-mortality effect estimates from the studies of long-term exposure are substantially

larger than those from the short-term time series or case-crossover studies that evaluate daily

changes in exposure. Overall, the results suggest that PM health effects are dependent on

both exposure concentrations and length of exposure and that the short-term studies only

capture a small amount of the overall health effects of PM exposure. Long-term repeated

exposures have larger, more persistent cumulative effects than short-term transient exposures.

It is important to note that the observed association between PM and health outcomes is

statistical. As such, particles are not the primary cause of the observed increase in mortality,

but are one of many environmental and other risk factors. The statistical associations have

been revised downwards based on a review of the statistical methods used, but the

association remains (HEI, 2003).

The specific health effects (or endpoints) evaluated in this assessment are outlined below:

1. Annual mortality all cause 30+ years

2. Cardiopulmonary mortality 30+ years

3. Ischaemic Heart Disease 30+ years

4. Lung Cancer mortality 30+ years

5. Daily mortality all causes all ages

6. Daily mortality cardiovascular disease all ages

7. Hospital admissions respiratory disease 65+

8. Hospital admissions cardiac disease 65+

9. Hospital admissions pneumonia and bronchitis 65+

10. Hospital admissions cardiovascular disease 65+ years

11. Hospital admissions respiratory disease 15-64 years

12. Emergency department visits (asthma) 1-14 years

The CRFs chosen for this risk assessment were taken from the review conducted by Jalaludin

and Cowie 2012, who recommended CRFs to be used for HRAs in the Australian context.

Jalaludin and Cowie 2012 presented functional forms of the CRFs as reported in

epidemiological studies (relative risks, odds ratios, percentage incidence/ prevalence). It was

therefore necessary to convert these into standardised estimates i.e. beta (β) coefficients, for

the purpose of risk characterisation using the following equation:

Table 5.2 and Table 5.3 present a summary of the health endpoints, concentration response

functions used and associated β coefficient relevant to the relative risk calculation.



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Table 5.2

Concentration-Response Functions for PM2.5 based on Jalaludin and Cowie (2012)

Health Endpoint CRF Adopted β coefficient for

1µg/m3 increase in PM

Reference

Annual mortality all cause 30+ years 6% (4-8%) per 10 μg/m3 5.82e-3

(Krewski, Jerrett et al. 2009) (US EPA 2010)

Cardiopulmonary mortality 30+ years 14% (11-17%) per 10 μg/m3 1.31e-2


Ischaemic Heart Disease 30+ years 24% (19-28%) per 10 μg/m3 2.15e-2


Lung Cancer mortality 30+ years 14% (6-12.3%) per 10 μg/m3 1.31e-2


Daily mortality all causes all ages 0.9% (0.2-1.6%) per 3.78 μg/m3

2.37e-3 (EPHC 2005)

Daily mortality cardiovascular disease all ages 1.5% (0.7-2.3%) per 3.78 μg/m3 3.94e-3 (EPHC 2005)

Hospital admissions respiratory disease 65+ 1.6% (0.9-2.3%) increase per 3.78 μg/m3 4.20e-3 (EPHC 2005)

Hospital admissions cardiac disease 65+ 1.9% (1.0-2.7%) increase per 3.78 μg/m3 4.97e-3 (EPHC 2005)

Hospital admissions pneumonia and bronchitis 65+ 2.0% (0.8-3.2%) per 3.78 μg/m3 5.24e-3 (EPHC 2005)

Hospital admissions cardiovascular disease 65+ years 1.3% (0.6-2.0) increase per 3.78 μg/m3 3.42e-3 (EPHC 2005)

Hospital admissions respiratory disease 15-64 years 1.1% (0.0-2.1%) increase per 3.78 μg/m3 2.89e-3 (EPHC 2005)

Emergency department visits (asthma) 1-14 years 1.4% (0.9-1.8%) increase per 9.4 μg/m3 1.48e-3 (Jalaludin, Khalaj et al. 2008)



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Table 5.3

Concentration-Response Functions for PM10 based on Jalaludin and Cowie (2012)

Health Endpoint CRF Adopted β coefficient for 1µg/m

3 increase in PM

Reference

Annual mortality all cause 30+ years 0.386% (0.295-0.477%) per 1 μg/m3 3.85e-3 (Pope, Thun et al. 1995)

Daily mortality cardiovascular disease all ages 1.3% (0.4-2.3%) per 10 μg/m3 1.29e-3 (Morgan, Sheppeard et al. 2010)

#

Hospital admissions respiratory disease 65+ 1.8% (0.6-3.0%) per 7.53 μg/m3 2.37e-3 (EPHC 2005)

Hospital admissions cardiac disease 65+ 1.04% (0.02- 2.07%) per 10 μg/m

3

(all ages = larger CRF) 1.035e-3 (Morgan, Sheppeard et al. 2010)

#

Hospital admissions pneumonia and bronchitis 65+ 1.4% (0.5-2.2%) per 7.53 μg/m3 1.85e-3 (EPHC 2005)

Hospital admissions respiratory disease 15-64 years 1.22% (0.41 to 2.03%) per 10 μg/m

3


#

Emergency department visits (asthma) 1-14 years 1.04% (0.02- 2.07%) per 10 μg/m

3


#

Annual mortality all cause 30+ years 0.386% (0.295-0.477%) per 1 μg/m3 3.85e-3 (Pope, Thun et al. 1995)

# In instances where there was no effect reported in Australian 4-cities meta-analysis (Environment Protection and Heritage Council 2005), the CRF recommendation for a sensitivity analysis was

used i.e. (Morgan, Sheppeard et al. 2010).



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5.2.2 Exposure Assessment

The exposure assessment outlined below estimates the total cumulative exposure

(i.e. background plus modelled PM10 and PM2.5 increment from the amended Project) on an

annual and daily basis at the most affected private receivers/residences (receiver 6 in

Gloucester and receiver 18 in Forbesdale) on the worst day of each modelled year. By using

the modelled predictions at the most affected private receivers/residences to represent

exposure across the populations of the respective state suburbs, the overall community

exposure is over estimated and the resulting HRA would be considered conservative.

The air quality impact assessment for the amended Project (Pacific Environment, 2016)

presents the dispersion modelling predictions for maximum 24-hour and annual average PM2.5

and PM10 GLCs at a total of 160 non-resource related assessment locations. For both PM2.5

and PM10, the full dataset based on the 160 assessment locations in conjunction with

background were examined as part of the HRA.

An assessment of cumulative 24-hour average PM2.5 and PM10 impacts was conducted at the

five most impacted private receivers/residences i.e. receiver 6, 18, 19A and 23 and 36, via the

frequency distribution. For PM2.5, there were no predicted exceedances of 25µg/m3 as a result

of the amended Project-only however there was an increased probability at receiver 6, 18, 23

and 36 that cumulative 24-hour PM2.5 concentrations would result in two additional days of

average 24-hour PM2.5 concentrations over the Australian air quality criterion of 25µg/m3.

Similarly the PM10 assessment found no predicted exceedances of 50µg/m3 as a result of the

amended Project-only however there was an increased probability at receiver 6, 18 and 23 that

cumulative 24-hour PM10 concentrations would result in less than one additional day of

average 24-hour PM10 concentrations over the Australian air quality criterion of 50µg/m3.

Table 5.4 and Table 5.5 outline the modelled 24 hour project-only contributions of the

amended Project and annual average and cumulative concentrations (the background plus the

amended Project increment) respectively. These values were used in the risk calculations to

estimate the potential increase in base incidence due to attributable PM2.5 and PM10

concentrations.

Table 5.4

Maximum Predicted Project-only 24-hour Average Concentrations at the Most Affected

Receiver/residence (g/m3)

Gloucester State Suburb (Receiver 6)

Faulkland State Suburb (Forbesdale Estate) (Receiver 18)

PM2.5 PM10 PM2.5 PM10

Year 1 0.75 3.39 1.32 5.42

Year 4 3.58 19.70 2.75 16.60

Year 7 6.32 35.35 3.98 24.30

Year 10 3.48 21.03 4.60 24.91

Source: Pacific Environment (2016) – Tables 9.5 and 9.6.



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Table 5.5

Predicted Annual Average Concentrations at the Most Affected Receiver/Residence (g/m3)

Gloucester State Suburb (Receiver 6)

Forbesdale State Suburb (Receiver 18)

PM2.5 PM10 PM2.5 PM10

Project-only

Year 1 0.05 0.26 0.17 0.79

Year 4 0.26 1.40 0.52 3.39

Year 7 0.42 2.29 0.75 4.94

Year 10 0.19 1.05 0.83 4.95

Cumulative

Year 1 4.70 9.44 4.95 10.6

Year 4 4.90 10.6 5.28 13.3

Year 7 5.06 11.5 5.51 14.8

Year 10 4.82 10.2 5.55 14.5


5.2.3 Risk Characterisation

The NEPM AAQM considers an additional risk of ‘1 per 100,000’ for adverse health outcomes

to be sufficiently small and to be of no cause for concern. The recent enHealth update on

environmental risk assessment has not prescribed a target risk level. Rather, it has noted that

any target risk level does not:

“… imply certainty that one person will get the disease if there are at least one

million people exposed. It is simply a way of expressing risk, as a numerical

expression of the likelihood of an event occurring under the defined conditions of

exposure, based on extrapolation of dose–response data.”

As such, it is important to note that the risk values provided based on the CRFs for PM

represent only probabilities, and not defined health outcomes.

5.2.3.1 Baseline Health Statistics

Baseline health incidence data was not available for the local areas i.e. Gloucester and

Faulkland State Suburbs, however, data was available for Tamworth, Newcastle and Sydney.

The data from Tamworth has been used in the calculations given that the local environment of

Tamworth is more similar to the local area under assessment, than Newcastle and Sydney.

Table 5.6 summarises the baseline health statistics used in the risk calculations.



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Table 5.6

Baseline Health Incidence Rate per 100,000 used in Risk Calculations

Health Endpoint

Baseline Health Incidence Rate per 100,000

(Tamworth) - 2010

MORTALITY

All causes 30+ years 353

All cause (non-trauma) 30+ years 27

Cardiopulmonary disease 30+ years 164

Ischaemic Heart Disease 30+ years 66

Lung Cancer mortality 30+ years 16

All cause all ages -

All cause (non-trauma) all ages 350

Cardiovascular all ages 136

HOSPITAL ADMISSIONS

Respiratory disease 65+ years 297

Cardiac disease 65+ years 542

Pneumonia and bronchitis 65+ years 96

Cardiovascular disease 65+ years 747

Respiratory disease 15-64 years 299

Emergency department visits (asthma) 258

5.2.3.2 Risk Calculations

The general approach used to calculate the risks to health has drawn upon internationally

recognised estimates of the impact of PM on health in relation to the known health indicators

for NSW. It involves estimating the change in the incidence of a health outcome resulting from

a given change in PM concentrations. The CRFs provide an estimate of the relationship

between the health endpoint of interest and PM concentrations. The baseline health effect

incidence rate provides the number of cases of the health effect per year, usually per 100,000

of the general population.

The risk factors in Table 5.2 and Table 5.3 have been used to estimate the risks associated

with exposure to the particulate emissions both from the amended Project alone and

cumulatively. Baseline Health incidence statistics were obtained from the NSW Health website

(http://www.healthstats.nsw.gov.au).

The equation used to calculate the number of cases attributable to exposure to a contaminant

per 100,000 is as follows:

http://www.healthstats.nsw.gov.au/



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For example Year 7, PM2.5 cumulative modelled output for Gloucester

The number of attributable cases based on annual mortality rates for all causes (30+ years)

was calculated as follows:

= 0.210

Where:

Adopted β coefficient for 1µg/m3 increase in PM = 0.00582 (Table 5.2)

PM2.5 cumulative modelled output = 5.06 g/m3 (Table 5.5)

Baseline incidence rate per 100,000 = 353 (Table 5.6)

Population of Gloucester aged 30+ = 2017 (Table 3.1)

The resultant increase in base incidence for annual mortality all causes 30+ years was

calculated as follows:

= 0.05%

Where:

Number of attributable cases = 0.210 (Table 5.7)

Baseline incidence rate per 100,000 = 353 (Table 5.6)

Table 5.7 to Table 5.10 show the predicted number of attributable health effects for PM2.5 and

PM10 arising from the amended Project for each of these communities.

The average PM2.5 and PM10 concentrations that were used for both Gloucester and

Forbesdale in the calculations are shown in Table 5.4 and Table 5.5. These were the

maximum concentrations predicted within the state suburbs for each year assessed. These

were extrapolated across the whole community to take a conservative approach. For the

assessment of long-term mortality, the annual average concentrations were used in the

calculations. For the short-term effects, the predicted 24-hour average concentrations for the

same locations were used and extrapolated across the relevant populations. These values

were used to calculate the daily mortality health endpoints.



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Table 5.7

Predicted Number of Attributable Cases Due to PM2.5 Exposure per 100,000: Gloucester State Suburb

Health Endpoint

Gloucester

Y1 Y4 Y7 Y10

Annual mortality all cause 30+ years 0.20 0.20 0.21 0.20

Cardiopulmonary mortality 30+ years 0.21 0.21 0.22 0.21

Ischaemic Heart Disease 30+ years 0.14 0.14 0.15 0.14

Lung Cancer mortality 30+ years 0.02 0.02 0.02 0.02

Daily mortality all causes all ages 0.00 0.00 0.00 0.00

Daily mortality cardiovascular disease all ages 0.00 0.00 0.00 0.00

Hospital admissions respiratory disease 65+ years 0.05 0.05 0.05 0.05

Hospital admissions cardiac disease 65+ years 0.10 0.11 0.11 0.11

Hospital admissions pneumonia and bronchitis 65+ years 0.02 0.02 0.02 0.02

Hospital admissions cardiovascular disease 65+ years 0.01 0.10 0.10 0.10

Hospital admissions respiratory disease 15-64 years 0.07 0.07 0.07 0.07

Emergency department visits (asthma) 1-14 years 0.01 0.01 0.01 0.01

Table 5.8

Predicted Number of Attributable Cases Due to PM10 Exposure per 100,000: Gloucester State Suburb

Health Endpoint

Gloucester

Y1 Y4 Y7 Y10











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Table 5.9

Predicted Number of Attributable Cases Due to PM2.5 Exposure per 100,000: Faulkland State Suburb (Forbesdale Estate)

Health Endpoint

Faulkland State Suburb (Forbesdale Estate)

Y1 Y4 Y7 Y10


Cardiopulmonary mortality 30+ years 0.02 0.02 0.02 0.02

Ischaemic Heart Disease 30+ years 0.01 0.01 0.01 0.01

Lung Cancer mortality 30+ years 0.00 0.00 0.00 0.00






Hospital admissions cardiovascular disease 65+ years 0.01 0.01 0.01 0.01



Table 5.10

Predicted Number of Attributable Cases Due to PM10 Exposure per 100,000: Faulkland State Suburb (Forbesdale Estate)

Health Endpoint

Faulkland State Suburb (Forbesdale Estate)

Y1 Y4 Y7 Y10









In examining the increased risk in the population (based on annual mortality rates, all causes)

due to the worst case annual average increased long-term exposure to PM2.5 and PM10 as a

result of the amended Project and cumulative exposure, it was noted that the resultant

increase in base incidence in Gloucester State Suburb and Faulkland State Suburb

(Forbesdale Estate) would be less than 1 in 100,000 therefore considered to be “sufficiently

small and to be of no cause for concern” (NEPM AAQM).

Shorter term exposures to PM2.5 and PM10 are also considered not to pose an unacceptable

risk as the predicted number of attributable cases due to daily mortality (all cause all ages and

cardiovascular disease all ages are less than 1 in orders of magnitude lower than that due to

long-term exposure.



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5.2.4 Conclusion

The analysis provides estimates of the increase in annual and daily mortality due to cumulative

and project-only emissions from the amended Project at the private receivers/residences 6 and

18, i.e. the most affected private receivers/residences in each of the Gloucester and Faulkland

State Suburbs in each modelled year. In addition, estimates are provided on the increase in

daily hospital admissions that could be expected from the most exposed individual due to

maximum predicted impacts from the amended Project. In examining the increased risk in the

population (based on annual mortality rates, all causes) due to the increased long-term

exposure to PM2.5 and PM10 concentrations as a result of cumulative and project-only

exposure, it is noted that the number of attributable health outcomes would be well below 1 in

100,000 therefore considered to be “sufficiently small and to be of no cause for concern”

(NEPM AAQM).

In examining the four most impacted private receivers/residences via the frequency

distribution, it was noted that, based on the air modelling, the cumulative maximum 24 hour

average PM2.5 concentrations showed less than two additional days over the 25µg/m3 criterion

than would occur anyway due to background in the absence of the amended Project.

Cumulative 24 hour PM10 concentrations showed that there was an increased probability that

Residences 6 and 18 would experience less than one additional day of average 24 hour PM10

concentrations of the 50µg/m3 criterion than would occur anyway in the absence of the

amended Project.

Considering the context of these risk assessment results, it should be noted that the dispersion

modelling results are estimates only and the predicted annual average concentration for PM2.5

and PM10 represent a very low concentration and are subject to significant conservatism. It is

also important to note that PM2.5 and PM10 exposure alone does not result in mortality, but is

one of many factors that can combine to contribute to a premature mortality in susceptible

populations (e.g., elderly, persons with breathing problems – COPD, etc.).

Shorter term exposures to PM2.5 and PM10 are also considered not to pose an unacceptable

risk as the predicted number of attributable cases due to daily mortality (all cause all ages and

cardiovascular disease all ages are less than 1 in orders of magnitude lower than that due to

long-term exposure.

Based on the above discussion, it is considered unlikely that an unacceptable risk due to PM

exposure would result from the amended Project.

5.3 ASSESSMENT OF NITROGEN DIOXIDE

5.3.1 Hazard Assesment

Blasting activities and fuel combustion (i.e. motor vehicles and industry) within the Site have

the potential to result in emissions of oxides of nitrogen (NOX). NOX comprises both nitric oxide

(NO) and nitrogen dioxide (NO2).

In recent years, the health effects of NO2 linked to ambient exposures have been well studied

and reviewed by international agencies (US EPA, 2008; WHO, 2006; OEHHA 1999). The main

short-term health outcomes identified in epidemiology studies are increased respiratory



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disease and symptoms. The evidence for the long-term effects of long-term exposure to NO2 is

limited. As with short-term exposure, the critical health outcomes with long-term exposure

include respiratory disease and associated symptoms, and associated changes in lung

function. Individuals with asthma and other chronic lung disease and cardiovascular diseases

are recognised as being particularly vulnerable. Other susceptible populations include infants,

children and the elderly (>65 years of age) (NEPM 2010).

Only very high concentrations of NO2 (approximately 2,000μg/m3 (~1,050 ppb)) affect

breathing in healthy people. However, small changes in lung function (< 5%) and changes in

airway responsiveness have been reported in several studies of sensitive asthmatics or the

elderly exposed to concentrations as low as 375-575μg/m3 (~200-300 ppb) over a period of 20

minutes to 4 hours (Bauer et al., 1986; Bylin et al., 1988; Roger et al., 1985; Morrow et al.,

1992; Strand et al., 1996, 1997, Streeton 1997). These levels represent a clear lowest-

observed-effect level (LOEL) for NO2 based on increased responsiveness in mild asthmatics to

bronchoconstrictors or in subjects with chronic obstructive pulmonary disease (COPD). It is

noted that the study by Bauer et al., (1986) did not find a significant change in pulmonary

function when asthmatics were exposed to 560μg/m3 NO2 when resting, with decreases

recorded only after the subjects exercised. Similarly, testing asthmatics the day after exposure

to 490μg/m3 NO2 did not decrease lung function before allergen challenge (Strand et al.,

1997), noting that the effects of NO2 exposure are transient in nature.

The identification of an obvious No Observed Adverse Effect Level (NOAEL) is less clear, but it

is suggested to be around 200μg/m3 (approximately 100 ppb). Studies have shown that effects

can be detected in mild asthmatics after short-term exposure (20 minutes to 4 hours in

duration) to 488-500μg/m3 (260-240 ppb) NO2 who are subsequently exposed to an inhalation

challenge (Strand et al., 1996, 1997; Kraft et al., 2005). However, in a study where mild

asthmatic subjects were exposed for 1hour to 200μg/m3 (~100 ppb) NO2 and then immediately

exposed to a house dust mite challenge, the late asthmatic response (as tested using Forced

Expiratory Volume in one second; FEV1) was found to be greater than when compared to air

(NO2 -7.76% vs. Air -2.85%), but the results were not found to be significant (Tunnicliffe et al.,

1994). The current air guideline for short-term exposure to NO2 in the NEPM is 246µg/m3 (0.12

ppm) measured as a 1hour average.

According to Streeton (1997), there is an increasing body of evidence to suggest that longer

term (years) ambient exposure to significantly lower concentrations of NO2, of the order of 40

to 80 ppb (approx. 75-150μg/m3) during early and middle childhood years can lead to the

development of recurrent upper and lower respiratory tract symptoms, such as recurrent

‘colds’, a productive cough, and an increased incidence of respiratory infection with resultant

absenteeism from school.

Similarly, more recent studies of self-reported asthmatic individuals living in homes with flue-

less gas heaters have shown significant effects of NO2 exposures to those aged ≤ 14 years,

with chest tightness, breathlessness on exertion and asthma attacks experienced either the

same day or with one-day lag (Smith et al., 2000). The range of median indoor levels of NO2

measured by positional passive samplers in homes during this study were indicated to be

between 0 to 147 ppb (0 to 277μg/m3) with time weighted average levels measured by

personal passive sampler of 0 to 1 760 ppb (0 to 3 300μg/m3). Subsequent investigations with

flue-less space heaters in primary schools indicated that over the 12 week winter heating

period, asthma symptoms were significantly higher in children exposed to gas combustion

products, with mean NO2 levels of 47.0 ppb (88μg/m3) versus children in schools where a

replacement intervention programme had removed or replaced the flue-less gas heaters,

leading to a mean NO2 level of 15.5 ppb (29.3μg/m3) (Pilotto et al., 2004).



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Streeton 1997 also found that NO2 was demonstrated to potentiate the effects of exposure to

other known irritants such as ozone, sulfur dioxide and respirable particles (DoH 1993). NO2

interaction with respirable particles is relevant to this HRA, however, the understanding of this

interaction is limited.

Based upon a review of the literature, Streeton (1997) considered short-term ambient

exposures to 200 to 300 ppb (375 to 565μg/m3) NO2 and long-term exposures between 40 to

80 ppb (75 to 150μg/m3) capable of causing recurrent upper and lower respiratory tract

symptoms, an increased incidence of respiratory infection and onset of symptoms in mild

asthmatics. Streeton (1997) considered these effects as the Lowest Observed Adverse Effect

Levels (LOAEL), and has suggested that a safety factor of 50% of the LOAEL need apply to

account for susceptible people within the population, therefore establishing a short-term

exposure guideline in the range 100 to 150 ppb (188 to 282μg/m3) as a 1hour average and a

long-term exposure guideline between 20 to 40 ppb (37.6 to 75.2μg/m3) for longer term

exposures as an annual average.

The WHO (1997, 2000a) took a different approach to reach a similar conclusion. Similar to

Streeton (1997), the WHO noted the epidemiological studies suggesting human health effects

associated with long-term NO2 exposures. However, the WHO (1997) have stated that this is

supported by animal toxicological findings showing increased susceptibility to respiratory

infections and impairment of host defences as a result of sub chronic or chronic exposures to

NO2 concentrations near ambient concentrations (i.e. 20 to 60μg/m3; 11 to 32 ppb). On the

basis of a background level of 15μg/m3 (8 ppb) as determined in Finland during the 1980s

(Jaakkola et al., 1991) and the fact that significant adverse health effects occur with an

additional concentration of 28.2μg/m3 (15 ppb) or more, which is an estimate of an increased

risk of about 20% for respiratory symptoms and disease (Hasselblad et al., 1992; WHO, 1997),

an annual guideline value of 40μg/m3 (22 ppb) was derived by the WHO (1997). The WHO

considers the guideline value would be protective of most serious effects. The fact that a no-

effect level for sub chronic or chronic NO2 exposure concentrations has not yet been

determined was emphasised.

Since their publication, both the NEPM AAQM and the WHO air quality guidelines for particles,

ozone, nitrogen dioxide and sulfur dioxide have been subject to review (NEPM, 2010; WHO,

2006). In both instances, review of the guidelines considered newly available information from

various locations around the world, including Australia. The WHO concluded that the scientific

literature has not accumulated sufficient evidence to justify revising the existing NO2

guidelines. According to NEPM AAQM (2010), available epidemiological information indicates

increased hospital admissions and emergency department attendance for respiratory

symptoms, particularly in asthmatics and children, following short-term exposure to ambient

concentrations. However, the available information remains under consideration by the NEPM

AAQM and no changes to the standards have been made at this point in time (NEPM 2010).

In summary:

Concentrations of NO2 of around 2,000μg/m3 (~1,000 ppb) are needed to affect

respiration of healthy people based on short-term exposure (less than 24 hours).

The low effect level of NO2 for increased bronchial reactivity in sensitive

asthmatics is 375 to 575μg/m3 (~200 to 300 ppb) for exposures from 20 minutes

up to 4 hours.



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The no effect level for increased bronchial reactivity based on short-term

exposure is ~376μg/m3.

The increased bronchial reactivity may remain for up to 10 hours after cessation

of NO2 exposure.

Table 5.11 presents a summary of guideline values established relating to short-term exposure

to NO2. For the estimation of risks, the NEPM (1998) AAQ has been used.

Table 5.11

Summary of National and International Criteria Established Relating to Short-term and Long-term Exposure to NO2

Guideline Averaging period

Derivation Reference µg / m

3 ppb

246 120 1 hour

The Australian National Environmental Protection Council ambient air quality standard. It is based on a LOAEL of 0.2 to 0.3 ppm derived from statistical reviews of epidemiological data suggesting an increased incidence of lower respiratory tract symptoms in children and aggravation of asthma. A safety factor of 0.5 to protect susceptible people (i.e. asthmatic children) was applied to the LOAEL.

NEPM (1998), Streeton (1997)

62 30 Annual

The Australian National Environmental Protection Council ambient air quality standard. It is based on a LOAEL of 0.04 to 0.08 ppm derived from statistical reviews of epidemiological data suggesting development of recurrent upper and lower respiratory tract symptoms and an increased incidence of respiratory infection with resultant absenteeism from school in children. A safety factor of 0.5 to protect susceptible people (i.e. asthmatic children) was applied to the LOAEL.

NEPM (1998), Streeton (1997)

The Australian NEPM AAQ criteria, which are protective of health outcomes in sensitive

subpopulations, are used to determine the potential for short-term effects (246µg/m3) and long-

term effects (62µg/m3) in association with exposure to NO2 from the amended Project.

5.3.2 Exposure Assessment

The cumulative air dispersion modelling conducted by Pacific Environment (2016) provided

probability estimates for the predicted concentrations of NO2 resulting from blasting, diesel

combustion and existing background levels at four selected private receivers/residences.

Concentrations of NO2 in the air from blasting and, to a lesser extent, diesel combustion, are

not constant: the concentrations are anticipated to vary according to the direction and strength

of the wind, time of day, and how far away a receiver/residence is from the blast and operating

equipment. Other factors known to contribute to blast fume generation include geology and

influence of controls in terms of explosive selection, quality, blast design and on bench

practices.



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The mine plans for Year 4 and Year 7 were chosen for modelling of blasting as these years

represent the periods when blasting impacts are expected to be greatest (i.e. when pits are

largest and therefore closest to private receivers/residences). The modelling assumed a

possible 2190 hours per year when blasting could occur (6 hours a day, 365 days a year). In

reality, blasting would only occur to a maximum of four events per week and a maximum of

120 per year, when meteorological conditions are favourable. As outlined in Section 11 of the

Air Quality Assessment, the initial NO2 concentration in the blast plumes were based on the

Rating 4 Fume Category which would typically appear as an orange / red plume. However, an

ACARP monitoring study that assessed emissions from blasting from open cut coal mines over

18 months and 500 blasts determined that 73% of blasts had a Rating 0 Fume Category, i.e.

little to no NO2 was produced (Day et.al, 2013). Given that a visible orange / red plume from a

blast is considered to be a reportable incident and based on the ACARP monitoring study, the

likelihood of a Rating 4 Fume Category is very low. Furthermore, measures to minimise or

avoid imperfect blasts and blasting in unfavourable conditions would be implemented and

addressed in a Blast Management Plan.

The modelling for diesel combustion was based on the highest diesel consumption for any of

the mining years (Year 10) but has been applied to mine operation year (Year 7) which is

predicted to have the highest PM concentrations. Private receivers/residences 6, 18, 19A and

23 were chosen for the assessment as they represented the highest potential impacts and

provided spatial variety around the Site. In addition these private receivers/residences were

consistent with those chosen for Monte Carlo analysis. In capturing a range of meteorological

conditions, including unrealistic scenarios of blasting during unfavourable conditions and

assuming a worst case Rating 4 Fume Category, this also over-estimates the peak

concentrations of NO2 at the selected private receivers/residences resulting in a conservative

assessment of potential exposure.

To factor a person’s behaviour (i.e. average daily movements) into a risk assessment is quite

challenging, and is rarely done. Instead, an assumption is made that, throughout their entire

life, a person is in a situation where they could be exposed to the highest concentrations

predicted to occur by the dispersion modelling. This assumption adds conservatism

(i.e. safety) into the risk assessment. Based on this assumption, whether or not a person is

affected by a pollutant compound in air requires them to be present at the location at the same

time the high concentration occurs. However, people do not spend all their time in one spot, for

example an average adult only spends approximately 1.5 hours outdoors per day. Given that

people also move around during the time they spend outdoors, the chance of being present in

the unlikely event that NO2 concentrations are elevated may also be quite low.

Table 5.12 provides the cumulative predicted concentrations for 1 hour average NO2 at the

four private receivers/residences based on the above conservative assumptions. The

cumulative predicted concentrations consisted of NO2 from blasting, diesel powered equipment

and background monitoring data from the closest EPA monitoring station Wallsend EPA

monitoring station2.

Annual NO2 concentrations were determined by averaging the 1 hour time series NO2

concentrations at the private receivers/residences for the assessment years (Pacific

Environment 2016).

2 Source: Pacific Environment (2016) – Section 11.5



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Table 5.12

Cumulative maximum 1-hour and annual average NO2 concentrations (g/m3)

Receiver 6 Receiver 18 Receiver 19A Receiver 23

1-hour maximum concentration

Year 4 138 186 160 138

Year 7 143 187 160 139

Annual maximum concentration

Year 4 24 25 23 23

Year 7 25 26 24 24


5.3.3 Risk Characterisation

Streeton (1997) provides the most scientifically defensible information with respect to the

potential for both short-term and long-term effects in association with exposure to NO2. As a

result, the NSW EPA impact assessment criteria which are protective of health outcomes in

sensitive subpopulations are used to determine the potential for short-term effects (246µg/m3)

and long-term effects (62µg/m3) in association with exposure to NO2 from the amended

Project. For assessing the potential short-term and long-term health impacts of NO2, the

predicted cumulative concentrations are presented in Table 5.12 are compared to individual

health-based ambient air quality criteria generated to protect public health. This comparison is

performed by calculating a Hazard Quotient (HQ) which is the ratio of predicted concentrations

to the ambient air quality criterion. A Hazard Index (HI) is the sum of the HQs for all pathways

with similar toxic effects, assuming the health effects are additive”, and is evaluated as follows:

1. HIs of less than or equal to one means that all the maximum predicted

concentrations are below the health based air guideline value and there are no

additive health impacts of concern.

2. HIs of greater than one means that there is the potential for adverse health

effects

The HQ is calculated using the simple equation below.

HQ = Predicted concentration/Health based air guideline value

An example of the calculation is shown below:

For example short-term HQ at receiver 6 in year 4

HQ = 0.49

Where:

Predicted Concentration = 120 g/m3 (Table 5.12)

Health based air guideline value = 246 g/m3 (Table 5.11)



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An ‘unacceptable’ risk, as defined by regulatory standards and requirements, is often

determined as the exposure being larger than the air quality criterion used to calculate the

HQs/HIs, i.e. the HQs/HIs >1. This definition of unacceptable risk does not equate with

imminent adverse health effects or even high risk of adverse health effects. It simply means

that the health guideline level has been exceeded.

Notwithstanding their use in this risk assessment, HQs/HIs are relatively blunt tools used to

assist in characterising and prioritising risks. Care must be taken as to the level of importance

that is placed on the numerical value of the HQs/HIs. HQs/HIs should not be used in isolation

of other pertinent data such as mechanistic information on the toxic mode of action and

knowledge of the conservatism incorporated into the exposure assessment and the toxicity

values.

The general rule of thumb for interpreting HQs/HIs is that, values less than 1 present no cause

for concern and values greater than 1 but less than 10 generally also do not represent cause

for concern because of the inherent conservatism embedded in the exposure portions of a risk

assessment. However, it is usual to examine, and perhaps refine, the level of conservatism

that has been assumed in the exposure assumptions. HQs/HIs that are around 10 or greater

present some concern regarding possible health risks, and in these circumstances it is usual to

evaluate the extent to which the “safety margins” in the health guideline value used to compare

estimated exposures may have been eroded in order to gauge whether concern is warranted.

It is common that the risk assessment needs to be refined using site-specific exposure

information or additional analytical data when HQs/HIs are greater than unity (greater than 1).

5.3.3.1 Risk Calculations

Table 5.13 shows the short-term and long-term HQs for the representative of predicted

concentrations of cumulative NO2 at the four modelled private receivers/residences. All the

HQs are less than unity (less than 1) indicating short-term health effects are very unlikely.

Table 5.13

Short-term and long-term HQs for Potential NO2 concentrations


1 hour maximum concentration

Year 4 0.56 0.76 0.65 0.56

Year 7 0.58 0.76 0.65 0.57

Annual Maximum concentration

Year 4 0.39 0.40 0.37 0.37

Year 7 0.40 0.42 0.39 0.39

It is noted that NO2 and PM10 potentially have additive effects (Streeton, 1997). As such, a

summary of the PM10 emissions (all operations) is presented in Table 5.14 and an assessment

was conducted for the HQ of PM10 and the HI for PM10 and NO2 as presented in Table 5.15

and Table 5.16.



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Table 5.14

Maximum Project-only 24-hour and Annual Average PM10 Concentrations at Private

Receivers/Residences (g/m3)


24 hour maximum concentration

Year 4 18.81 16.60 10.36 19.70

Year 7 35.35 24.30 15.12 32.45

Annual maximum concentration

Year 4 1.40 3.39 2.09 1.16

Year 7 2.28 4.94 3.03 1.76


An example of the HQ calculation is shown below:

For example short-term HQ at receiver 6 in Year 4

HQ = 0.38

Where:

Predicted Concentration = 18.8 g/m3 (Table 5.14)

Health based air guideline value = 50 g/m3 (Table 5.1)

Table 5.15

Short-term and long-term HQs for PM10 concentrations


Short-term

Year 4 0.38 0.33 0.21 0.39

Year 7 0.71 0.49 0.30 0.65

Long-term

Year 4 0.05 0.11 0.07 0.04

Year 7 0.08 0.16 0.10 0.06

Table 5.16 shows the short-term and long-term HIs for the representative of predicted

concentrations of NO2 and PM10 from the four modelled private receivers/residences

associated with blast and fuel combustion emissions.



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Table 5.16

Short-term and long-term HIs for PM10 and NO2 concentrations


Short-term

Year 4 0.94 1.09 0.86 0.95

Year 7 1.29 1.25 0.95 1.22

Long-term

Year 4 0.44 0.51 0.44 0.41

Year 7 0.48 0.58 0.49 0.45

Four of the short-term HIs were slightly above unity however it should be noted that these

values were based on conservative predictions (See Section 5.3.2). It is therefore considered

appropriate that potential short-term effects can be mitigated by the use of measures known to

minimise fume generation blast design, product selection and quality, blast crew education, on

bench practices, and blasting under wind conditions that favour dispersion of pollutants. Each

of these measures would be identified in a Blast Fume Management Strategy appended to the

Blast Management Plan for the amended Project in order to prevent the modelled NO2

concentrations (orange / red plumes) occurring that were utilised in this assessment.

All of the long-term HIs were found to be less than unity (less than 1). Therefore the cumulative

PM10 and NO2 emissions do not present a long-term health concern.

5.3.4 Conclusion

Because all of HQs for cumulative NO2 emissions for the worst affected private

receivers/residences are all less than or approximately 1, it is very unlikely the emissions

would cause direct short-term and/or long-term health effects. The calculated HIs for

cumulative blast and fuel combustion associated NO2 and PM10 were slightly greater than unity

(greater than 1) at three of the four worst affected private receivers/residences. All the long-

term HIs were less than unity (less than 1). As such there is only a potential for short-term

health effects due to exposure from cumulative blast and fuel combustion associated NO2 and

PM10. Given the conservative approach to predicting NO2 emissions, it is considered

appropriate that potential short-term effects can be mitigated by the use of measures known to

minimise fume generation blast design, product selection and quality, blast crew education, on

bench practices and, and blasting under wind conditions that favour dispersion of pollutants.

Each of these measures would be identified in a Blast Fume Management Strategy appended

to the Blast Management Plan for the amended Project in order to prevent the modelled NO2

concentrations occurring that were utilised in this assessment.

5.4 ASSESSMENT OF DIESEL


particles, PM0.1) (WIMR-CAR, 2015). These particulates consist mainly of aggregates of

spherical carbon particles coated with organic and inorganic substances, with the composition

of the particles being predominantly organic and inorganic carbon. The organic fraction of

diesel exhaust particulate matter contains compounds such as aldehydes, alkanes and



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alkenes, aliphatic hydrocarbons, polycyclic aromatic hydrocarbons and their derivatives. These

substances are considered toxic air contaminants and some of them are genotoxic and

carcinogenic. Overall diesel exhaust particles are considered to be carcinogenic (OEHHA,

2001).

Therefore, calculation of the carcinogenic inhalation risk due to PM2.5 – diesel has been

completed to enable an assessment of the cancer risk in the local community attributable to

the use of diesel within the Site. There is a precedent by NSW authorities i.e. NSW Health and

Office of Environment and Heritage (OEH) that the acceptable cancer risk range for airborne

contaminants is 1 in 100,000 to 1 in 1,000,000. The carcinogenic inhalation risk was therefore

calculated using project-only PM2.5 – diesel concentration i.e. the highest annual average PM2.5

– diesel concentration combined with background monitoring data from the closest EPA

monitoring station Wallsend EPA monitoring station3. This concentration was applied across

the whole population i.e. Gloucester State Suburb and Faulkland State Suburb (Forbesdale

Estate) providing a conservative estimate of the potential cancer risk. This PM2.5 – diesel

concentration was then multiplied by the cancer unit risk factor i.e. 0.000034 μg/m3, derived by

the World Health Organisation (WHO) and an adjustment factor (0.25). The adjustment factor

assumes that residents in the adjacent communities would be at home for 20 hours per day for

365 days of the year for the life of the mine i.e. 21 years. The adjustment factor was therefore

calculated as follows: (20/24 hours x 21/70 years) = 0.25.

The results of the PM2.5 – diesel emissions for the project-only at the 157 privately-owned

receivers/residences and 3 sensitive receiver locations show that the highest annual average

PM2.5 concentration was 0.37 μg/m3 at receiver/residence 18 in Year 104.

The carcinogenic inhalation risk calculation is shown below:

= 0.000003145 i.e. ~0.31 in 100,000/ 3.1 in 1,000,000

The resultant risk of 0.31 in 100,000 is within the acceptable cancer risk range, i.e. 1 in

100,000 to 1 in 1,000,000, generally accepted by NSW, national and international authorities

for airborne contaminants. In addition, it should be noted that real-time monitoring of PM2.5 and

PM10 particulates, reactive management of all particle emissions, and regular maintenance of

diesel vehicles and machinery on site, would reduce the exposure of the community to diesel

particles and further reduce potential risks to health.

3 Source: Pacific Environment (2016) – Section 11.5

4 Source: Pacific Environment (2016) – Table 12.4



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6. L I M I TAT I O N S

There are inherent uncertainties in the methods used to estimate emissions concentrations

and limitations on how accurately the impacts of the amended Project can be estimated in

future years. Conservatism has been applied where possible to minimise the risk of any

potential impacts being underestimated in the HRA. These are listed below:

1. Some of the applied concentration response functions (CRFs) were prescribed

for sensitive analysis in situations where a prescribed concentration response

function was not available. This is not unusual because the CRF is a value that is

usually derived from epidemiological studies of an exposed population and relies

on the population being large enough for the health effect to be discernible.

Furthermore multiple CRFs can exist depending on the potency of the

contaminant and the health effect under study. To overcome this, the best CRFs

were chosen with respect to the studied location and population.

2. The population statistics used for mortality were not normalised to account for

demographic differences between different cities and towns. In addition hospital

admissions data did not have any small count suppression for NSW data (public

and private data). Finally emergency department data was only available for

public hospitals. This is not unusual simply because it is not possible to measure

individuals attending private medical practices.



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7. C O N C L U SI O NS

This health risk assessment has estimated the risks of an increased incidence of selected

health outcomes due to increased exposures of PM - total, cumulative NO2 and PM2.5- diesel

as a consequence of the amended Project.

The exposure assessment used estimates of the total potential cumulative exposure

(i.e. background plus modelled PM2.5 and PM10 increment from the amended Project) on an

annual and daily basis at the most affected private receivers/residences (receiver 6 in the

Gloucester State Suburb and receiver 18 in the Faulkland State Suburb - Forbesdale) on the

worst day of each modelled year. By using the modelled predictions at the most affected

private receivers/residences to represent exposure across the populations of the respective

state suburbs, the overall community exposure is over estimated and the resulting HRA should

be considered conservative. The air quality impact assessment for the amended Project

(Pacific Environment, 2016) presents the dispersion modelling predictions for maximum 24-

hour and annual average PM2.5 and PM10 GLCs at a total of 160 non-resource related

assessment locations. For both PM2.5 and PM10, the full dataset based on the160 non-resource

related assessment locations in conjunction with background were examined as part of the

HRA.

The health endpoints assessed for PM2.5 and PM10 were short- and long-term mortality and

daily hospitalisations. The general approach used to calculate the risks to health has drawn

upon estimates determined to be relevant to the Australian context, to determine the impact of

PM2.5 and PM10 on health in relation to the known health indicators for NSW. This involved

estimating the change in the incidence of a health outcome resulting from a given change in

PM2.5 and PM10 concentrations. Concentration-response functions (CRFs) for each of the

health endpoints were sourced from the review conducted by Jalaludin and Cowie 2012. In

examining the increased risk in the population (based on annual mortality rates, all causes)

due to the increased long-term exposure to PM2.5 and PM10 concentrations as a result of

cumulative and project-only exposure, it is noted that the number of attributable health

outcomes would be well below 1 in 100,000. The predicted number of attributable cases are

therefore considered to be “sufficiently small and to be of no cause for concern” (NEPM

AAQM). Shorter term exposures to PM2.5 and PM10 are also considered not to pose an

unacceptable risk as the predicted number of attributable cases due to daily mortality (all

cause all ages and cardiovascular disease all ages are less than 1 in orders of magnitude

lower than that due to long-term exposure.

The critical health outcomes with acute and chronic exposure to NO2 include respiratory

disease and associated symptoms, and associated changes in lung function. The NSW EPA

impact assessment criteria, which are protective of these health outcomes in sensitive

subpopulations, have been used to determine the potential for acute effects (246µg/m3) and

chronic effects (62µg/m3) in association with exposure to NO2 from the amended Project. As

NO2 emissions for the selected receivers/residences were less than the Australian air quality

criterion, it is considered unlikely that the blast emissions would cause direct acute and/or

chronic health effects.

The calculated HQs for blast NO2 emissions for the worst affected private receivers/residences

are all less than 1, therefore it is unlikely the cumulative NO2 emissions i.e. blasting, diesel

powered equipment and background monitoring data, would cause direct short-term and/or

long-term health effects. The calculated HIs for cumulative blast and fuel combustion



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associated NO2 and PM10 were slightly greater than unity (greater than 1) at three of the four

worst affected private receivers/residences. All the long-term HIs were less than unity (less

than 1). As such there is only a potential for short-term health effects due to exposure from

cumulative blast and fuel combustion associated NO2 and PM10. Given the conservative

approach to predicting NO2 emissions, it is considered appropriate that potential short-term

effects can be mitigated by the use of measures known to minimise fume generation blast

design, product selection and quality, blast crew education, on bench practices and, and

blasting under wind conditions that favour dispersion of pollutants. Each of these measures

would be identified in a Blast Fume Management Strategy appended to the Blast Management

Plan for the amended Project in order to prevent the modelled NO2 concentrations occurring

that were utilised in this assessment.


particles, PM0.1) (WIMR-CAR, 2015). Calculation of the carcinogenic inhalation risk due to

PM2.5 – diesel enabled an assessment of the cancer risk in the local community attributable to

the use of diesel within the Site. The carcinogenic inhalation risk was therefore calculated

using project-only PM2.5 – diesel concentration i.e. the highest annual average PM2.5 – diesel

concentration combined with background monitoring data (receiver/residence 18 in Year 10).

This concentration was applied across the whole population i.e. Gloucester State Suburb and

Faulkland State Suburb (Forbesdale Estate) providing a conservative estimate of the potential

cancer risk. This PM2.5 – diesel concentration was then multiplied by the cancer unit risk factor

i.e. 0.000034 μg/m3, derived by the World Health Organisation (WHO) and an adjustment

factor (0.25). The resultant risk, 0.31 in 100,000, is within the acceptable cancer risk range, i.e.

1 in 100,000 to 1 in 1,000,000 generally accepted by NSW, national and international

authorities, for airborne contaminants. In addition, it should be noted that real-time monitoring

of PM2.5 and PM10 particulates, reactive management of all particle emissions, and regular

maintenance of diesel vehicles and machinery on site, would reduce the exposure of the

community to diesel particles and further reduce potential risks to health.

There are inherent uncertainties in the methods used to estimate emissions and

concentrations and limitations on how accurately the impacts of the amended Project can be

estimated in future years. Consequently, in order to minimise the risk of under estimation

throughout the HRA, conservatism has been applied where possible. The modelling data used

to inform this HRA used worst case assumptions and therefore it is expected that actual

ground level concentrations would be lower during the normal operation of the amended

Project. The modelled predictions at the most affected private receivers/residences were used

to represent exposure across the populations of the respective state suburbs with the result

that the overall community exposure was over estimated. This is further discussed in the

amended air quality assessment (Pacific Environment, 2016). The PM2.5 and PM10 exposure

assessment evaluates the potential of the emissions to cause direct effects on individuals who

may be exposed either on a short-term, infrequent basis or long-term basis, i.e. assuming 24

hours per day for each day of the year for 70 years. This exposure scenario is highly unlikely

especially since the life of the mine is estimated to be up to 21 years. The applied exposure

assessment method for PM2.5 and PM10 is typically reserved for populations of greater than

25,000 because there are important challenges in translating methods intended for large

populations to those for addressing risk in smaller populations. Nevertheless, when taken

together with the modelling predictions, the uncertainties err on the side of safety. The

predicted NO2 emissions due to blasting considered a range of meteorological conditions,

including unrealistic scenarios of blasting during unfavourable conditions as well as assuming

a worst case Level 4 fume category, which over-estimated the peak concentrations of NO2 at



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the selected private receivers/residences. This is further discussed in the amended air quality

assessment (Pacific Environment, 2016). The PM2.5 – diesel exposure assessment used PM2.5

– diesel modelled predictions based on the highest diesel consumption for any of the mining

years, from a mine operation year (Year 7) predicted to have the highest predicted PM2.5

concentration.

In consideration of the community concerns raised, it is important to note that health issues in

relation to exposure to PM - total, NO2 and PM2.5 – diesel from the amended Project have been

outlined and the associated potential for acute or chronic effects assessed. The exposure

assessments have used both standards adopted by all Australian jurisdictions and exposure

response functions relevant to the Australian population (where relevant) to estimate likelihood

of unacceptable risk. Susceptible/ vulnerable groups within adjacent communities have been

taken into consideration and a range of health end points assessed i.e. short- and long-term

mortality and daily hospitalisations. Overall it is concluded that air emissions from the amended

Rocky Hill Coal Project present little likelihood of causing adverse health effects to exposed

individuals in the vicinity of the Site.



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8. R E F E RE N C ES

Anderson GB, Krall JR, Peng RD, Bell ML (2012). Is the relation between ozone and mortality

confounded by chemical components of particulate matter? Analysis of 7 components

in 57 US communities. Am J Epidemiol. Oct 15;176(8):726-32

Barnett, A. G., Williams, G. M., Schwartz, J., Neller, A. H., Best, T. L., Petroeschevsky, A. L. &

Simpson, R. W. (2005). Air pollution and child respiratory health: a case-crossover

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APPENDIX 1

Key Differences between the Health Risk Assessment for the 2013 Project and

Amended Project

(Total number of pages including blank pages = 4)



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Key Differences between the Health Risk Assessment for the 2013 Project and Amended Project

Project Component 2013 Project Amended Project

Assessment Locations

The considered assessment locations included 150 privately-owned residences in the vicinity of the Site and 3 sensitive receiver locations within Gloucester township.

The considered assessment locations included 157 privately-owned residences in the vicinity of the Site and 3 sensitive receiver locations within Gloucester township.

Concentration Reference Factors

The source of the Concentration Reference Factors (CRFs) used in the exposure assessment was Anderson et al (2004).

The source of the CRFs used in the exposure assessment was changed to Jalaludin and Cowie (2012) because the latter study outlined recommended CRFs to be used for health risk assessments in the Australian context.

Baseline Health Statistics

The baseline health statistics used were based upon the Hunter New England Local Health District for 2009-2010 and daily hospital admissions for all of NSW in 2006-2007.

A total of four health endpoints were evaluated (i.e. long-term deaths, short-term deaths, hospitalisations due to cardiovascular and hospitalisations due to all respiratory disease).

The baseline health statistics used was for Tamworth given the local environment was more similar to the assessed communities i.e. State suburb of Gloucester and Faulkland State Suburb (Forbesdale Estate area).

The specific health endpoint evaluated in the exposure assessment was expanded to twelve health effects.

Blasting & Diesel Combustion

Blast fume assessed, however, no consideration of diesel combustion sources generating PM2.5 and NO2. No characterisation of risk for PM10.

Assessment of both blast fume and diesel combustion. The assessment of -diesel was conducted based upon the worst affected private residence during the year with the highest diesel consumption.

The potential additive effects of cumulative NO2 and PM10 were also considered as part of the Hazard Index calculation

Data Presentation The particulate matter and NO2

concentrations used in the exposure assessment were presented as percentiles.

The particulate matter and NO2

concentrations used in the exposure assessment are presented as maximum concentrations.

Health Risk Outcomes

From a health-risk perspective, the 2013 project assessed project-only particulate levels which resulted in an increase in base incidence in Gloucester State Suburb and Faulkland State Suburb (Forbesdale Estate) of less than 1 in 100,000, which is considered to be “sufficiently small and to be of no cause for concern” (NEPM AAQM).

From a health-risk perspective, the amended Project assessed cumulative particulate levels which resulted in an increase in base incidence in Gloucester State Suburb and Faulkland State Suburb (Forbesdale Estate) of less than 1 in 100,000, which is considered to be “sufficiently small and to be of no cause for concern” (NEPM AAQM). Whilst the changes in health risk are not directly comparable between the assessments, given the reductions in project-only particulate emissions, the overall health risk is likely to have similarly reduced.



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Part 2B: Health Risk Assessment - RW CORKERY...ABN: 46 114 162 597 Part 2B: Health Risk Assessment...

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