National Cancer Prevention Policy - Tobacco Control Supersite

National Cancer Prevention Policy 

2007–09

National Cancer Prevention Policy 

2007–09

The Cancer Council Australia Member Organisations 

The Cancer Council ACT 

159 Maribyrnong Ave 

Kaleen Australian Capital Territory 2617 

T: (02) 6262 2222 

F: (02) 6262 2223 

www.actcancer.org 

The Cancer Council NSW 

153 Dowling Street 

Woolloomooloo New South Wales 2011 

T: (02) 9334 1900 

F: (02) 9358 1452 

www.cancercouncil.com.au 

The Cancer Council Northern Territory 

Casi House, Unit 1−3/25 Vanderlin Drive 

Casuarina Northern Territory 0810 

T: (08) 8927 4888 

F: (08) 8927 4990 

www.cancercouncilnt.com.au 

The Cancer Council Queensland 

553 Gregory Terrace 

Fortitude Valley Queensland 4006 

T: (07) 3258 2200 

F: (07) 3257 1306 

www.qldcancer.com.au 

The Cancer Council Australia is Australia’s peak national non-government cancer organisation. Its members 

are the leading state and territory cancer councils, working together to undertake and fund cancer research, 

prevent and control cancer, and provide information and support to people affected by cancer. 

Citation: The Cancer Council Australia 2007. National Cancer Prevention Policy 2007−09. NSW: The Cancer 

Council Australia. 

Copies available from: 

The Cancer Council Australia, Level 5, Medical 

Foundation Building, 92−4 Parramatta Road, 

Camperdown NSW 2050 

T: (02) 9036 3100 

F: (02) 9036 3101 

www.cancer.org.au 

ISBN 0 947283 88 9 

Published May 2007 

The Cancer Council South Australia 

202 Greenhill Road 

Eastwood South Australia 5063 

T: (08) 8291 4111 

F: (08) 8291 4122 

www.cancersa.org.au 

The Cancer Council Tasmania 

140 Bathurst Street 

Hobart Tasmania 7000 

T: (03) 6233 2030 

F: (03) 6233 2123 

www.cancertas.org.au 

The Cancer Council Victoria 

1 Rathdowne Street 

Carlton Victoria 3053 

T: (03) 9635 5000 

F: (03) 9635 5270 

www.cancervic.org.au 

The Cancer Council Western Australia 

46 Ventnor Avenue 

West Perth Western Australia 6005 

T: (08) 9212 4333 

F: (08) 9212 4334 

www.cancerwa.asn.au 

Prepared by the Publications Unit, The Cancer Council Victoria. 

This publication may be freely photocopied and distributed, providing the publisher is acknowledged. 

Main cover photo and ‘Screening’ photo page 121 by Brian Gilkes; page 175 ‘Immunisation’ photo by Kate 

Morris 

Thanks to the Australian Institute of Health and Welfare for permission to reproduce Figures 1.1 and 2.1 from 

Australian Institute of Health and Welfare & National Breast Cancer Centre 2006. Breast Cancer in Australia: 

an overview, 2006. Canberra: AIHW.

C o n t e n t s 

Abbreviations 6 

The National Cancer Prevention Policy 8 

References 10 

Section One: Preventable risk factors 

Tobacco 12 

Introduction 12 

The link between tobacco and cancer 13 

The impact 13 

The challenge 15 

Effective interventions 20 

The policy context 26 

Aims 34 

References 37 

Ultraviolet radiation 41 


The link between ultraviolet radiation and cancer 41 

The impact 43 




Aims 47 

References 49 

Nutrition 52 


The link between nutrition and cancer 52 

The impact 57 




Aims 64 

References 66 

Physical activity 71 


How physical activity is measured 72 

The link between physical activity and cancer 73 

The impact 74 




Aims 81 

References 82 

C o n t e n t s

Overweight and obesity 86 


The link between overweight and obesity and cancer 87 

The impact 89 




Aims 99 

References 102 

Alcohol 107 


The link between alcohol and cancer 107 

How the amount of disease caused by alcohol is estimated 110 

The impact 111 




Aims 116 


Section Two: Screening to detect cancer early 

Principles of screening 122 

Breast cancer 126 

Breast cancer in Australia 126 

Can breast cancer be prevented? 127 

Tests and programs for breast cancer 128 


Potential benefits and adverse effects of breast cancer screening 132 

Who should be screened? 132 

Aims 133 


Cervical cancer 138 

Cervical cancer in Australia 138 

Can cervical cancer be prevented? 138 

Screening tests and programs for cervical cancer 139 


Potential benefits and adverse effects of cervical cancer screening 141 


Aims 143 


Bowel (colorectal) cancer 145 

Bowel cancer in Australia 145 

Can bowel cancer be prevented? 145 

Tests and programs for bowel cancer 147 


Potential benefits and adverse effects of bowel cancer screening 153 


Aims 154 

References 156

Melanoma 161 

Melanoma in Australia 161 

Can melanoma be prevented? 161 

Screening tests for melanoma 161 

Rationale for screening for melanoma 162 

Would screening be of benefit at this stage? 163 

Aims 163 


Prostate cancer 165 

Prostate cancer in Australia 165 

Can prostate cancer be prevented? 166 

Tests for prostate cancer 166 


Potential benefits and adverse effects of prostate cancer screening 170 

Aims 171 


Section Three: Immunisation 

Human papilloma virus 176 

The link between HPV infection and cancer 176 





Aims 181 


Hepatitis B 186 


The link between hepatitis B infection and cancer 189 





Aims 197 


List of contributors 202 

Index 206 

C o n t e n t s

A b b r e v i a t i o n s 

AACR Australasian Association of Cancer Registries 

ABS Australian Bureau of Statistics 

ACCC Australian Competition and Consumer Commission 

ACN Australian Cancer Network 

AHRQ Agency for Healthcare Research and Quality 

AHTAC Australian Health Technology Advisory Committee 

AICR American Institute of Cancer Research 

AIHW Australian Institute of Health and Welfare 

BCC basal cell carcinoma 

BMI body mass index 

BRCA breast cancer (associated gene) 

BSE breast self-examination 

CBE clinical breast examination 

CDHAC Commonwealth Department of Health and Aged Care 

CDHS California Department of Health Services 

CDCP Centers for Disease Control and Prevention 

CFMDCY Committee on Food Marketing and the Diets of Children and Youth 

CGHFBC Collaborative Group on Hormonal Factors in Breast Cancer 

COAG Council of Australian Governments 

COSA Clinical Oncological Society of Australia 

CTFPHC Canadian Task Force on Preventive Health Care 

DHA Department of Health and Ageing (Australian Government) 

DHAC Department of Health and Aged Care 

DHS Department of Human Services (Victorian Government) 

DRE digital rectal examination 

FAP familial adenomatous polyposis 

FOBT faecal occult blood test 

GP general practitioner 

HNPCC hereditary non-polyposis colorectal cancer 

HPV human papilloma virus 

HRT hormone replacement therapy 

IARC International Agency for Research on Cancer 

MCDS Ministerial Council on Drug Safety 

MSAC Medical Services Advisory Committee 

National Cancer Prevention Policy 2007 – 09

NEACA National Expert Advisory Committee on Alcohol 

NACCHO National Aboriginal Community Controlled Health Organisation 

NATSI Working Party National Aboriginal and Torres Strait Islander Working Party 

NCCI National Cancer Control Initiative 

NCSG National Cancer Strategies Group 

NCSP National Cervical Screening Program 

NHMRC National Health and Medical Research Council 

NMSC non-melanoma skin cancer 

NOTF National Obesity Task Force 

NPHP National Public Health Partnership 

PPV positive predictive value 

PSA prostate-specific antigen 

RACGP Royal Australian College of General Practitioners 

SIGNAL Strategic Inter-Governmental Nutrition Alliance 

TCCA The Cancer Council Australia 

TRUS transrectal ultrasound 

UICC International Union Against Cancer 

USDHHS US Department of Health and Human Services 

USDHW US Department of Health 

UKFSSTI UK Flexible Sigmoidoscopy Screening Trial Investigators 

USPSTF US Preventive Services Task Force 

UV ultraviolet 

VCCR Victorian Cervical Cytology Registry 

VCTC VicHealth Centre for Tobacco Control 

WCRF World Cancer Research Fund 

WHO World Health Organization 

National Cancer Prevention Policy 2007 – 09 

A b b r e v i a t i o n s

T h e N a t i o n a l C a n c e r 

P r e v e n t i o n P o l i c y 

Australia faces an unprecedented cancer control challenge. 

Two years ago, the Australian Institute of Health and Welfare predicted that cancer 

incidence would increase by 31% between 2002 and 2011. This means we can expect 

more than 115,000 new cancer cases in 2011 (AIHW, AACR, NCSG & McDermid 2005). 

More recently, the Australian Burden of Disease Study showed cancer had overtaken 

cardiovascular disease as the nation’s biggest disease burden (Begg et al. in press). 

Linking cancer incidence to population ageing—an accurate predictor of future trends— 

implies an even greater overall increase in cancer incidence in the years after 2011, as the 

percentage of Australians aged 65 and over is projected to double by 2051. 

The problem will be compounded by a relatively smaller workforce able to support 

Australia’s inflated cancer patient base. On current trends, Australia’s obesity epidemic 

will also place an unprecedented burden on future cancer services. And people living with 

cancer will, quite rightly, have heightened expectations about the nation’s capacity to care 

for them, as gradual developments in cancer treatment continue. 

The future would be considerably less daunting, however, if we could reach our 

potential to reduce cancer incidence through prevention and identify more cancers and 

precancerous conditions early, using measures already shown to be effective. 

The latest AIHW data shows that around a third of cancer deaths in Australia are attributed 

to known avoidable risk factors. Many of the thousands of people who are successfully 

treated for cancer could also avoid, reduce or delay the distress of the cancer experience 

through appropriate prevention and early detection measures. 

Yet as new research reconfirms that cancer is the disease Australians fear more than 

any other (Cameron et al. 2006), we continue to fall well short of our capacity to prevent 

cancer. Moreover, many of our missed opportunities to prevent cancer also contribute 

significantly to the overall community cost of chronic disease in Australia: five of the six 

key modifiable cancer risk factors—smoking, poor diet, physical inactivity, overweight/ 

obesity and alcohol misuse—are all major risk factors for cardiovascular disease, while a 

number are also linked to diabetes, depression and asthma (see table below). 

Table A.1 Risk factors for chronic disease 

Disease Poor 

diet 

Heart disease 

Stroke 

Cancer 

Depression 

Diabetes 

Asthma 

Source: Adapted from AIHW 2002 

Physical 

inactivity 

Tobacco 

use 


Alcohol 

misuse 

Overweight 

and 

obesity 

High 

blood 

pressure 

High 

cholesterol

The Cancer Council Australia’s National Cancer Prevention Policy 2007–09 aims to provide 

a blueprint for optimal cancer prevention and early detection in Australia for 2007–09, 

drawing on the latest evidence and exploring the impact, risk factors, policy context and 

effective interventions. It also provides an opportunity to reflect on the 2004–06 period. 

In terms of immediate potential to reduce cancer death, the most significant individual 

measure was the Australian Government’s commitment to phase in a population-based 

bowel cancer screening program by 2008–09. We publicly welcomed this initiative as an 

election commitment in 2004 and the subsequent budget allocation in 2005–06. However, 

as 2007 begins, the program’s phase-in remains at an embryonic stage, and public 

information is limited on how federal and state/territory governments will work together 

to ensure it is built around a rigorous, quality-assured framework. The Cancer Council and 

its allies will continue to call for the Australian Government to work with all jurisdictions to 

deliver a program that is available to all Australians over 50 and adheres to the principles of 

best practice summarised in the bowel cancer screening chapter. 

In the area of primary prevention, the Cancer Council welcomes the tobacco control 

progress made in all jurisdictions, particularly the restrictions on smoking in public places, 

which will reduce cancer risk among smokers and non-smokers. But, as explored in the 

tobacco chapter, a great deal more needs to be done before smoking loses its status as the 

cause of the most preventable cancer deaths in Australia. 

Another key development was the discovery by a team led by Cancer Council Australia 

Vice-President Professor Ian Frazer of a vaccine for the human papilloma virus, which 

causes cervical cancer. The vaccine’s significance has motivated a new section on 

immunisation, which also examines hepatitis vaccination for preventing liver cancer. See 

the human papilloma virus and hepatitis B chapters in the immunisation section of the online 

edition of the National Cancer Prevention Policy 2007–09 (published in mid-2007 at www. 

cancer.org.au). 

HPV immunisation should be particularly effective in developing countries where cervical 

cancer is prevalent due to the absence of population-based Pap screening. In Australia, 

however, the vaccine’s introduction must not confuse the public about the importance of a 

Pap screen program which has delivered the world’s lowest cervical cancer mortality rates 

and which remains essential for women in target age groups. The vaccine also exemplifies 

the need to develop policy in response to new evidence and emerging issues. So, too, 

does the Pap screen program itself, with indications that an increase in screening interval, 

from two to three years, warrants consideration in view of the latest evidence. 

We welcomed the Government’s commitment to a national skin cancer awareness 

campaign, designed to reduce the impact of Australia’s most economically expensive 

cancer and the cause of more than 1500 deaths a year. There is a strong case for an 

ongoing commitment to such a campaign. Meanwhile, new evidence that excessive sun 

avoidance may cause vitamin D deficiency and increase autoimmune disease risk in some 

people again shows the importance of incorporating all the latest evidence into effective 

policy, as discussed in the skin cancer chapter. 

Obesity/overweight, nutrition, physical activity and alcohol are explored with renewed 

vigour. While we are gradually winning the battle against preventable disease on some 

fronts, the obesity epidemic threatens a reversal of the long-standing trend of future 

generations’ life expectancy exceeding that of their parents. Unless steps are taken now 

to reduce obesity, particularly among children, bowel and postmenopausal breast cancer 

rates may increase significantly beyond what is predicted as part of population ageing. 

One positive trend amid this concern is a growing recognition of general practitioners (GPs) 

as a pivotal part of chronic disease prevention. General practitioner groups have sought to 


P r e v e n t i o n p o l i c y

increase their understanding of managing disease risk and, in January 2006, the Council 

of Australian Governments announced a number of chronic disease prevention measures 

involving GPs. We focus on the role of GPs in cancer prevention on a chapter-by-chapter 

basis. 

The range of issues covered in the National Cancer Prevention Policy 2007–09 reflects the 

diversity of evidence-based expertise among the external authors and the members of our 

Public Health Committee, listed towards the end of this book. My thanks to them all, in 

particular the Chair of the Public Health Committee, Ms Dorothy Reading at The Cancer 

Council Victoria, who oversaw the document’s production. 

Cancer describes a complex range of malignancies. We all hope for a cancer-free future, 

for a cure for the disease that claims more Australian lives than any other cause. The 

evidence suggests that, rather than a single, miracle cure, reducing the impact of cancer 

will be the result of numerous separate developments targeting individual cancers. 

Moreover, the evidence shows that the greatest potential gains for reducing cancer 

incidence and mortality in Australia are in primary prevention and early detection, using 

knowledge we already possess and which is articulated in the National Cancer Prevention 

Policy 2007–09. 

Mrs Judith Roberts AO 

President, The Cancer Council Australia 

References 

Australian Institute of Health and Welfare (AIHW) 2002. Chronic diseases and associated risk factors in 

Australia, 2001. Canberra: AIHW. 

Australian Institute of Health and Welfare (AIHW), Australasian Association of Cancer Registries (AACR), 

National Cancer Strategies Group (NCSG) & McDermid I 2005. Cancer incidence projections, Australia 2002 to 

2011. Canberra: AIHW, AACR & NCSG. 

Begg S, Vos T, Goss J, Barker B, Stevenson C, Stanley L & Lopez AD (in press). The burden of disease and 

injury in Australia, 2003. Canberra: AIHW & Brisbane: University of Queensland. 

Cameron M, Sambell N, Wakefield M, Hill D 2006. Population change in most feared illnesses and perceived 

steps to reduce cancer risk. Presentation at Behavioural Research in Cancer Control Conference, Brisbane 

2006. 

10 Section One: Preventable risk factors

Section One: 

Preventable risk factors 


11 

P r e v e n t i o n p o l i c y

T o b a c c o 

Introduction 

12 Section One: Preventable risk factors 

Every day, around 43 Australians die from illnesses 

caused by smoking, equivalent to over 15,500 deaths 

every year. Unless action is taken now, Australians 

will continue to die from illnesses caused by smoking 

that could have been prevented. 

In Australia, cigarette smoking became widespread in the 20th century. At that time, 

tobacco was used by many societies, some of which had used it for many centuries; 

however, development of the manufactured cigarette in the late 19th century resulted 

in increased prevalence and consumption (Winstanley, Woodward & Walker 1995). In 

Australia, by the time of the First World War, tobacco smoking had become popular, 

particularly the smoking of manufactured cigarettes. By the end of the Second World War, 

the earliest date for which Australian data are available, 72% of men and 26% of women 

were smokers (Winstanley, Woodward & Walker 1995). 

Since the 1970s, various bodies, including the International Union Against Cancer and 

more recently the World Health Assembly (the governing body of the World Health 

Organization), have taken action in recognition of the rising number of deaths caused by 

tobacco use. The first ever public health treaty on tobacco that outlines comprehensive 

tobacco control strategies, the Framework Convention on Tobacco Control, was passed 

by the World Health Assembly in May 2003. By January 2007, 143 member states of the 

World Health Organization were party to the convention, representing over 90% of the 

world’s population and making it one of the most extensive and rapidly implemented 

pieces of international law in history (WHO 2006). 

Australia was one of the first nations to become active in tobacco control, having used a 

range of measures, including advertising restrictions, public information, price increases, 

and controls on smoking in public places, which have contributed to a significant reduction 

in the prevalence of smoking since the mid-1970s. Tobacco control remains one of the best 

investments governments can make to enhance the health and economic well-being of all 

Australians. While progress has been achieved in reducing the prevalence of smoking and 

protecting people from the harms of second-hand smoke, smoking continues to contribute 

to one of the highest levels of disease burden attributable to a preventable cause. Tobacco 

control must remain a high public policy priority, yet tobacco control initiatives are underfunded 

in the context of their demonstrated human and economic effectiveness. At the 

same time, efforts to reduce smoking prevalence are undermined by the tobacco industry, 

which continues to mislead, deceive and conceal the carnage caused by its deadly and 

addictive product, continues to pursue marketing strategies leading to high youth uptake, 

and obstructs measures designed to help reduce harm from smoking and exposure to 

second-hand smoke.

The link between tobacco and cancer 

Pathologists and other medical practitioners first observed a rise in the incidence of lung 

cancer in the 1920s and 1930s. Research published in 1950 confirmed that tobacco 

smoking was a cause of death and disease, and reports by the Royal College of Physicians 

in London in 1962 and the US Surgeon General in 1964 resulted in acknowledgment by 

some governments that smoking was a cause of disease (Winstanley, Woodward & Walker 

1995). In a 2004 review the US Surgeon General concluded that there was sufficient 

evidence to infer a causal relationship between smoking and cancer at the following sites: 

bladder, cervix, kidney, larynx, lung, oesophagus, oral cavity and pharynx, pancreas and 

stomach; and between smoking and acute myeloid leukaemia. 

There is well-documented evidence of the health effects of exposure to second-hand 

smoke or ‘passive smoking’. In 1986 a major conclusion of a report by the US Surgeon 

General was that involuntary smoking is a cause of disease, including lung cancer, in 

healthy non-smokers. This conclusion was supported by reviews published in the same 

year by the US National Research Council, the International Agency for Research on 

Cancer, and the Australian National Health and Medical Research Council (USDHHS 2006; 

Winstanley, Woodward & Walker 1995). In 1992 a US Environmental Protection Agency 

report classified cigarette smoke as a class A carcinogen and concluded that exposure 

to second-hand smoke causes lung cancer (USDHHS 2006). The 2006 report of the 

US Surgeon General on involuntary exposure to tobacco smoke reviews evidence that 

reaffirms and strengthens the findings of the 1986 report, concluding that exposure to 

second-hand smoke causes lung cancer and also that there is no risk-free level of exposure 

to second-hand smoke (see later in this chapter for data on the incidence of cancer and 

mortality caused by smoking in Australia). 

The impact 

In Australia, tobacco smoking kills more than 15,500 Australians each year (Begg et al. in 

press). As shown in the Figure 1.1 each year more Australians are killed by tobacco than 

by breast cancer, AIDS, traffic and other accidents, murders and suicides combined (AIHW 

2006; Begg et al. in press). 


13 

T o b a c c o

Figure 1.1 Number of Australians who died in 2004 because of smoking compared with selected other 

causes 

Causes of death 

Falls 

Drowning 

Transportation accidents 

Other accidents 

Suicide 

Homicide 

Breast cancer (females) 

AIDS 

Smoking* 

197 

168 

116 

1,558 

1,689 

1,335 

2,098 

2,614 

* Note that the estimate for deaths attributable to smoking is based on data for 2003. 

Sources: AIHW 2006; Begg et al. in press 


15,511 

The Australian Burden of Disease Study quantifies the contribution to health status of 

mortality, disability, impairment, illness and injury arising from tobacco smoking and other 

risk factors. The study found that tobacco is one of the leading risk factors for disease, 

being responsible for 7.8% of the total burden of disease in Australia. Only high body mass 

creates a greater burden of disease (8.6%) (Begg et al. in press). 

Most smokers begin smoking when they are young, and many remain addicted to smoking 

for life (Winstanley, Woodward & Walker 1995). As a consequence of their addiction, in 

Australia one in two lifetime smokers will die from diseases caused by tobacco, and more 

than 22% of these deaths are in people aged under 65 years (AIHW 1998). 

Tobacco smoking increases the risk of cardiovascular disease, lung disease and cancer, 

as well as a number of other conditions (USDHHS 2004). Many of the diseases caused 

by smoking are chronic and disabling, and it has been estimated that in the US, for every 

premature death caused by smoking in a given year, there were at least 20 smokers living 

with a smoking-related disease (USDHHS 2004). Table 1.1 lists the cancers caused by 

smoking. 

Tobacco smoking is a leading cause of cancer, and was estimated to have directly caused 

10,592 new cases of cancer (12% of all new cases of cancer) and 7,820 deaths (21.5% 

of cancer deaths) in Australia in 2001. Between 1991 and 2001, the incidence rate for 

men of cancers attributable to smoking fell by an average of 1.4% per year, while the rate 

for women rose by 0.7% per year. These differences are attributable to differences in the 

prevalence of smoking among Australian men and women over the past 30 years and the 

time lag between exposure to carcinogens and diagnosis of cancer (AIHW & AACR 2004).

Table 1.1 Cancer site and percentage of new cancers attributable to smoking in Australia in 2001 

Site Males (%) Females (%) 

Lung 89 70 

Larynx 69 60 

Oral cancers 52 42 

Renal (kidney) pelvis 51 43 

Oesophagus 50 41 

Anus 39 29 

Bladder 38 28 

Vulva – 32 

Cervix – 19 

Penis 21 – 

Pancreas 23 16 

Kidney 17 12 

Stomach 12 8 

Colon/rectum 12 12 

Sources AIHW & AACR 2004; Chao et al. 2000; USDHHS 2004 

The economic consequences of tobacco use in Australia have been examined, with the 

total social costs in 1998−99 having been estimated at $21 billion (Collins & Lapsley 

2002). It has also been estimated that the health system costs for lung cancer (85% of 

which is attributable to tobacco smoking) amounted to $107 million in 1993−94 (Mathers 

et al. 1998). Smoking causes very high levels of ill health and premature death among 

Aboriginal and Torres Strait Islander peoples, which adds to the social costs among these 

communities (Briggs, Lindorff & Ivers 2003). In Australia in 2001–02, smoking accounted 

for more than 291,000 hospital episodes per year, at a cost of $682 million (Hurley 2006). 

The challenge 

Adults 

The prevalence of smoking among Australian adults has been measured by a number 

of different surveys: the National Drug Strategy Household Survey conducted by the 

Australian Institute of Health and Welfare (AIHW 2005); Smoking and Health Surveys 

conducted by The Cancer Council Victoria (White, Hill et al. 2003); National Health Surveys 

(ABS 2006); and National Aboriginal and Torres Strait Islander Surveys conducted by the 

Australian Bureau of Statistics (ABS 1994). Consistent trends have been observed, despite 

minor variations in methods between the surveys, so trends over time rather than specific 

figures are important foci for policy development (White, Hill et al. 2003). 

In 2004 in Australia, 17.4% of people aged 14 years or older were daily smokers, with 

a further 3.9% of the population reporting weekly or less than weekly smoking (AIHW 

2005). The recent decline in the number of daily smokers among men (18.6%) and women 


15 

T o b a c c o

(16.3%) continues the trends observed over the last 25 years (White, Hill et al. 2003; AIHW 

2005). 

It has been noted that those smokers who regard themselves as ‘occasional’ or ‘social 

smokers’ may make up 29% of all smokers. This segment of smokers holds different 

attitudes towards smoking and quitting from other smokers, which has implications for 

campaigns and messages for this group of smokers (Morley et al. 2006). 

There are specific populations for which smoking rates remain significantly higher than 

average, including populations that are socio-economically disadvantaged, Aboriginal and 

Torres Strait Islander peoples and male Australians born overseas in particular countries. 

Socio-economically disadvantaged populations 

The prevalence of smoking in Australia in 2001 among lower blue collar workers (36%) 

remained higher than among upper white collar workers (16%), despite the significant 

declines in all occupational groups since 1980 observed in surveys of people aged 18 years 

or older by The Cancer Council Victoria (White, Hill et al. 2003). 

Aboriginal and Torres Strait Islander peoples 

The prevalence of smoking remains very high among Aboriginal and Torres Strait Islander 

peoples. The National Aboriginal and Torres Strait Islander health survey of 2004–05 

indicated that the prevalence of smoking in people aged 18 years and over has remained 

unchanged at 50% since 1995 (ABS 1994); however, the smoking rates among some 

remote Aboriginal and Torres Strait Islander communities are much higher (Ivers 2001). 

After adjusting for age differences, in 2004 Aboriginal and Torres Strait Islander people 

aged 18 years and over were more than twice as likely as non-Indigenous Australians to 

be smokers (AIHW 2006). A 2002 survey reported a smoking prevalence of 59% among 

Aboriginal health workers in New South Wales (Mark et al. 2005). 

Potential contributors to the higher prevalence of smoking among Aboriginal and Torres 

Strait Islander peoples include (Briggs, Lindorff & Ivers 2003; AGDHA 2005): 

• 

• 

• 

• 

• 

the effects of historical colonisation and dispossession (disruption and erosion of 

language and culture, creation of unhealthy living and social conditions, devaluation of 

cultural responses to health problems, general subordination due to racism) 

socio-economic disadvantage (the roles of lower levels of education, lower levels of 

employment and lower weekly income) 

cultural beliefs and strong links to a traditional lifestyle (recognition of homelands, 

believing in the important role of elders, and English not being a first language have 

been linked to higher prevalence of tobacco use) 

enjoyment and addiction (similar to their roles in the maintenance of smoking among 

non-Indigenous people) 

social contexts and pressures (role of smoking in becoming accepted as part of the 

social group, roles of boredom, stress and anxiety). 

A lack of knowledge on the health effects of tobacco does not appear to be a major factor 

in the higher prevalence of smoking among Aboriginal and Torres Strait Islander peoples 

(Briggs, Lindorff & Ivers 2003). 


Australians born in particular countries 

Smoking rates among Australians born in Australia and in other countries were measured 

in the National Health Survey 2004–05 for people aged 18 years and over (ABS 2006). 

The overall prevalence among men was 24.2%, but smoking was more prevalent among 

men born in North Africa and the Middle East (31.9%) and among men born in South East 

Asia (28.6%). For women born in Oceania (excluding Australia) the prevalence was 26.3%, 

compared with an overall prevalence among women of 18.4% (ABS 2006). 

Teenagers 

Among secondary students (Table 1.2), rates of smoking decreased in the late 1980s, and 

then remained relatively stable in the 1990s (Hill, White & Letcher 1999). Among older 

students (those aged 16–17 years), the significant decrease among males and females 

between 1999 and 2002 was the first seen in this age group since 1990 (White & Hayman 

2004). Among students aged 12–15 years, the prevalence of smoking also declined 

between 1996 and 2005. 

Table 1.2 Trends in rates of smoking among Australian secondary school children between 1984 and 

2005: proportion (%) of students who smoked in the last seven days (age adjusted) 

Year Girls 

12–15 years 

Boys 

12–15 years 

Girls 

16–17 years 

Boys 

16−17 years 

1984 20 19 32 28 

1987 14 13 30 26 

1990 14 13 28 24 

1993 16 15 29 28 

1996 16 16 32 28 

1999 16 15 29 30 

2002 12 10 25 21 

2005 7 7 17 16 

Sources: Hill, White & Letcher 1999; White & Hayman 2004; White & Hayman 2006 

Note that young people who had left school were not included in the national surveys on which this table is based. 

There were an estimated 4.3 million ex-smokers among the 16.4 million Australians aged 

14 and over in 2004 (AIHW 2005). However, there were still an estimated 2.9 million 

Australians who smoked on a daily basis in 2004 (AIHW 2005). 

Other challenges 

The prevention of more than 17,000 premature deaths in 1998 in Australia can be 

attributed to a range of successful tobacco control measures that delivered declines in 

smoking from the early 1970s (DHA 2003). However, with almost one in five Australians 

continuing to smoke, the nation faces a significant challenge to further reduce smoking 

rates and avert major social and economic costs to the community. 

Compounding the need to further reduce smoking rates is an expected increase in overall 

cancer incidence rates in Australia of around 30% over the next five to 10 years as a result 

of population ageing. This trend is likely to continue as the population ages. Reducing 

smoking prevalence now would lead to significantly fewer overall cancer diagnoses 


1 

T o b a c c o

in the longer-term future, when healthcare services in Australia are likely to be under 

unprecedented pressure owing to demographic change. 

Despite the progress made in Australia to date, significant challenges to achieving 

continued reductions in tobacco-related harm remain. These challenges include the 

disproportionate burden of harm among disadvantaged populations, attitudes that 

undermine effective tobacco control, the influence of the tobacco industry, and a 

reluctance from governments at all levels to take measures to reduce tobacco use 

commensurate with the economic and social damage caused by smoking. 

Disproportionate tobacco burden 

As documented elsewhere in this chapter, socially disadvantaged population groups 

bear a disproportionately high tobacco burden in Australia. Evidence increasingly shows 

that, as well as causing a growing inequity in health status, smoking among these 

groups contributes to a cycle of poverty and disadvantage. Recent research on financial 

deprivation and smoking has shown that disadvantaged smokers experience financial 

hardship as a result of tobacco use, and are more likely to want to quit smoking, but less 

likely to succeed in quitting (Siahpush, Heller & Singh 2005). 

Attitudes that undermine effective tobacco control 

Resistance to progressive tobacco control can be based on a set of attitudes that are 

clearly unsupported by evidence or are based on facile excuses for inaction, yet some of 

which are nonetheless cited by social commentators and policy makers to discourage 

efforts to reduce the tobacco burden. An important part of ‘de-normalising’ a habit that 

causes the extent of preventable death and disease documented in this chapter is to 

counter, using evidence, the inaccurate framing of tobacco issues cited as a justification for 

tobacco control complacency. Some of the salient catchphrases used to argue against an 

increased commitment to tobacco control can be readily debunked in view of the evidence 

as follows. 

‘We have done everything possible to control tobacco, apart from banning tobacco 

altogether.’ 

This view is contradicted by the evidence, which shows that a comprehensive policy 

commitment and sustained campaign funding are highly effective in reducing smoking 

rates. In California, which introduced comprehensive tobacco control measures in 1988, 

smoking rates have decreased by approximately 38%, from 22.7% to 14% (CDHS 2006). 

Jurisdictions such as Canada now have daily smoking rates as low as 13.5% (Canadian 

Tobacco Use Monitoring Survey 2006). There is every reason to believe that, with 

appropriate measures, smoking rates in Australia could be reduced to less than 5%. None 

of the required measures would involve banning tobacco products. 

‘Australia is doing OK already’ or ‘Australia is doing better than anyone else.’ 

While Australia should be acknowledged as a world leader in tobacco control policy given 

its reforms over the past three decades, more than 17% of Australians still smoke every 

day: which corresponds to almost one in five people incurring a 50% risk of dying as a 

result of smoking, half of them in middle age. Despite substantial reductions in smoking 

rates over the past 30 years, tobacco use remains one of the leading preventable causes 

of disease. Over 15,500 Australians die from smoking-caused diseases each year, and lung 

cancer rates in women continue to rise. 


‘It’s a legal product.’ 

Tobacco is a commercial and regulatory anomaly. Smoking causes a higher disease burden 

than the combined use or misuse of all other ‘legal products’ that are rigorously regulated 

for safety reasons, including over-the-counter drugs, prescription medicines, pesticides, 

alcohol and motor vehicles. On the basis of demonstrated harm, tobacco products are 

also under-regulated in comparison with government treatment of other environmental 

carcinogens and hazardous consumer products. 

‘Smoking provides economic benefits to government and society in general.’ 

Evidence indicates the opposite: tobacco control is one of the best investments 

governments can make. Independent economic analyses clearly demonstrate that smoking 

has a high net social and economic cost to the community. Similar analysis has also shown 

that a reduction in smoking rates would not harm the economy. There is also objective 

evidence for a strong return on investment in tobacco control. The most recent Department 

of Health and Ageing analysis on this issue found that every $1 spent on tobacco control 

yields $2 in savings, and the consultancy firm Applied Economics concludes that tobacco 

control yields better gains than any other public health program expenditure, with a benefit 

to cost ratio of 50:1 (Applied Economics 2003). 

‘Smoking is an adult choice.’ 

The vast majority of smokers start smoking while in adolescence, becoming addicted 

before they are mature enough to make an adult decision and fully understand the 

consequences of nicotine addiction and the harms of smoking (Schofield et al. 1998; 

Winstanley, Woodward & Walker 1995). Almost all smokers also say that they regret 

starting smoking (Fong et al. 2004). Evidence also shows that most adult smokers are not 

fully aware of the dangers of smoking, with a recent survey finding that while two-thirds 

identified lung cancer as smoking-related, only one-quarter knew that smoking caused 

heart disease and fewer than 10% understood the risk of emphysema, stroke and vascular 

problems (Quit Victoria 2006). Around 90% of smokers report regretting ever having 

started (Fong et al. 2004). 

‘Tobacco control is part of a nanny state.’ 

The argument that government action to reduce smoking rates is restricting personal 

freedoms with risk-averse, patronising public policy is debunked by the evidence outlined 

against the five arguments discussed above. In addition, most tobacco control measures 

are designed to support decisions that people are already making. Every year, 30% to 40% 

of smokers attempt to quit, but only one in 10 attempts to quit is successful. Tobacco 

control measures reduce relapse rates and help intending quitters to break their addiction. 

Measures are mainly about removing inducements to smoke or providing information, 

support and encouragement to quit. 

Governments also have a responsibility to protect non-smokers from the increasingly 

evident harms of environmental tobacco smoke and to reduce the economic burden, borne 

by the wider community, imposed by smoking. The restrictions on smokers imposed over 

recent years have attracted overwhelming community support (VCTC 2002). 

Tobacco industry influence 

While coordinated efforts to reduce the disease burden of tobacco have made Australia a 

challenging market for the tobacco industry compared with nations where there are fewer 

controls, almost one in five Australians continues to smoke, with Australian households 

spending more than $10 billion on tobacco products per year (ABS 2005). 


1 

T o b a c c o

Tobacco products are among the top 10 best-selling items for a range of retailers, including 

supermarket chains, grocery stores, petrol stations and newsagents. The tobacco industry 

in Australia was estimated to be worth $6.2 billion in 2002 (VCTC n.d.), with 52 brands of 

cigarettes available for sale in June 2003 (Australian Retail Tobacconist 2003). Therefore, 

tobacco companies are very well-resourced to counter attempts to reduce smoking rates; 

the industry continues to exploit loopholes in tobacco control regulations and to engage 

high-powered legal firms when called to account in the courts. The tobacco industry 

continues to try to court policy-makers and to adopt a stance of legitimacy and good 

corporate citizenship, despite a proven record of deceptive conduct. 

Effective interventions 

Comprehensive tobacco control strategies, if sufficiently funded, work to reduce tobacco 

consumption among both adults and teenage smokers (VCTC 2002). This conclusion is 

based on studies from the World Health Organization (WHO 1998) and the US Centers 

for Disease Control and Prevention (CDCP 1999; CDCP 2000; CDCP 2001), and a review 

carried out for the World Bank (Jha & Chaloupka 1999). 

In Australia over the last 30 years an estimated $8.6 billion has been saved through deaths 

avoided and declines in illness and disability due to reduced tobacco use (DHA 2003). It 

is estimated that $2 has been saved on health care for each $1 spent on tobacco control 

programs to date, with total economic benefits exceeding expenditure by at least 50 to 

1. Specific strategies include increasing the prices of tobacco products and changing 

social attitudes to smoking through regulation and hard-hitting media campaigns. The 

precise impact of any specific strategy has been difficult to assess, as many have been 

implemented simultaneously or partially, or in an ad hoc way without comprehensive 

evaluation (Chapman 1993). Moreover, all have been opposed and undermined by tobacco 

industry activity. 

Pivotal to a strategic and coordinated approach to smoking reduction in Australia is the 

willingness of governments to commit to, and seek to attain, specific smoking prevalence 

targets. Targets can only be achieved if adequate resources are committed to tobacco 

control measures in the long term. Evidence shows that it is feasible to achieve a decline of 

1% per annum in the prevalence of smoking if tobacco control measures are well-funded 

and implemented (CDCP 2001). The speed of the decline depends on government action in 

ensuring adequate spending levels as well as appropriate regulation. 

The Cancer Council encourages the Australian Government to set targets for smoking 

prevalence for Australian adults, children and disadvantaged groups, and to allocate 

adequate funds for comprehensive tobacco control programs to achieve these targets. In 

order to further reduce the unacceptable burden of smoking in Australia, governments and 

other institutions involved in public policy will need to build on the demonstrated success 

of tobacco control strategies employed in Australia over the past three decades. Priorities 

for further action are outlined below. 

Continual innovation in tobacco control is required to keep pace with changes in the 

smoking-related environment. For example, a growing evidence base showing the 

increasing extent of disease linked with smoking demonstrates the need for tobacco 

control programs that are commensurate with the burden smoking imposes on the 

community. Accumulated evidence showing which approaches to tobacco control are the 

most effective should inform government policy. Policy-makers must also be able to react 

quickly to the tobacco industry’s attempts to exploit loopholes in measures designed to 

reduce smoking rates. There are a number of other examples showing the need for flexible, 


progressive solutions, as well as evidence that indicates where public policy for tobacco 

control in Australia is inadequate. 

All jurisdictional governments in Australia have committed, in principle, to the following 

general approaches to tobacco control, as each priority is to some extent incorporated into 

the National Tobacco Strategy. However, implementation of the strategy has been gradual, 

and the funding commitment is not sufficient to convert policy into effective practice. The 

re-establishment of a multi-jurisdictional advisory body drawing on independent expertise 

from outside the bureaucracies, such as the former Ministerial Tobacco Advisory Group, 

would help to guide the implementation of the National Tobacco Strategy. 

The Cancer Council Australia outlines the major areas where reform is required below. 

Rejection of tobacco industry donations by all political parties, while not explored as 

a specific tobacco control measure below, would also be a significant step in ‘denormalising’ 

smoking and challenging the legitimacy of the tobacco industry. 

Recommended funding 

Despite the well-documented successes of comprehensive strategies to address tobacco 

use and the resultant savings in public finances (DHA 2003), government funding of 

tobacco control in Australia is well below optimal. The US Centers for Disease Control 

has developed best practice guidelines for the implementation of comprehensive tobacco 

control programs (CDCP 1999). These guidelines draw on evidence-based analyses of 

programs implemented in California, Massachusetts and other US states. The guidelines 

outline nine program components and estimate a range of annual costs. For a state 

with a population under three million people the cost would be US$7–20 per capita, for 

populations between three and seven million the cost would be US$6–17 per capita, 

and for populations over seven million (e.g. Australia-wide) the cost would be US$5–16 

(A$7–21). Recommendations from the VicHealth Centre for Tobacco Control on how 

comprehensive tobacco control programs should be implemented in Australia, based on 

the Centers for Disease Control best practice guidelines (CDCP 1999), are summarised in 

Table 1.3 (VCTC 2003). 

Table 1.3 Recommended levels of funding for tobacco control programs (Australian dollars, 2003) 

Component A$ million 

Community programs 23.25 

Chronic disease programs 1.15 

School programs 1.65 

Enforcement 12.25 

Statewide programs 13.07 

Counter marketing 64.00 

Cessation programs 59.35 

Subtotal 174.69 

Surveillance and evaluation 8.00 

Administration and management 11.80 

Total 194.49 

Source: VCTC 2003 


21 

T o b a c c o

In 2007, given estimated costs of $200 million and an Australian population of 20.7 million, 

the recommended tobacco control measures would cost around A$10 per head. The Better 

Health for All Australians Initiative from the Council of Australian Governments (federal, 

state and territory governments) provides an opportunity to meet the recommended levels 

of investment for tobacco control with its stated intent to: ‘promote healthy lifestyles; 

support early detection of lifestyles risks and chronic disease through a new Well Person’s 

Health Check (available nationally to people around 45 years old with one or more 

identifiable risks that lead to chronic disease); and support lifestyle and risk modification 

through referral to services that assist people wanting to make changes to their lifestyle, 

for example, give up smoking’ (COAG 2006). Disappointingly, the initial round of funding in 

2006 did not include additional funding for tobacco control initiatives, limiting its impact on 

cost-effective approaches to health improvement. The Cancer Council and its allies working 

across all nine jurisdictions in Australia will continue to encourage government to fund 

evidence-based tobacco control programs on the basis of their potential to deliver optimal 

social and economic gains to the community. 

Social marketing campaigns 

The National Tobacco Campaign of the late 1990s (‘Every Cigarette Is Doing You Damage’) 

was the first coordinated, multimedia anti-smoking campaign that was run on a national 

basis and supported by related activities in jurisdictions (e.g. state Quit programs etc.). 

An independent economic evaluation of the campaign, based on a rigorous analysis, 

calculated that the $7.1 million invested in the program by the Australian Government in 

1997 yielded full cost offsets to the whole economy of $24.2 million, meaning that the 

campaign paid for itself three times over. Direct savings to the Australian Government 

alone were calculated to be $10.9 million within the year of its implementation (DHA 2000). 

Yet the campaign has not been run on a national basis for more than seven years, despite 

the clear economic benefits and potential for larger long-term returns. Moreover, evidence 

shows that without recurrent commitment to widely accessible information about the risks 

of tobacco use, declines in smoking rates can stall or are at risk of reversing. 

Based on the success of the National Tobacco Campaign, and adjusting for inflation, 

there is a clear economic case for committing $11 million on a recurrent basis to a new, 

evidence-based social marketing campaign. Such a campaign would have a major impact 

on bringing smoking rates closer to a feasible 5% of the Australian population and add to 

the success of other tobacco control measures. 

Elimination of tobacco promotion 

When responding to the Government’s review of the Tobacco Advertising Prohibition Act, 

The Cancer Council Australia and allies presented evidence of tobacco industry activity that 

contradicted the spirit of the Act and, in some cases, represented potential breaches. On 

the basis of that evidence, the Cancer Council put forward a number of recommendations 

for amending the Act. However, these were not adopted, and the review committee 

concluded that no amendments would be made to the Act. An evidence-based case 

remains, however, for amending the Act to enact and enforce the following additional 

restrictions on tobacco promotion. Recommended measures include: 

• 

• 

amend the definition of ‘tobacco advertisement’ to include the use of imagery that 

associates smoking with a desirable lifestyle, and expand the definition of ‘tobacco 

product’ to include cigar and cigarette cases (including the slips introduced to conceal 

graphic warnings on cigarette packets) 

prohibit all advertising and display at the point of sale 


• 

• 

• 

• 

• 

• 

• 

• 

• 

• 

• 

• 

address smoking in films: for example, classify films with positive depictions of 

smoking, and run anti-smoking advertisements before cinema screenings of such films 

prohibit the giving of free samples, gifts and other promotional offers aimed at boosting 

tobacco sales 

prohibit ‘mobile retailing’: sales of tobacco products should be restricted to places that 

operate as shops, and shops only, at all times 

prohibit vending machines 

require all tobacco products to be sold only in prescribed generic packaging that does 

not have any colours or branding or information other than that prescribed by regulation 

regulate Internet advertising and sales, direct mail/sending of catalogues, and mail order 

make it an offence to encourage/employ someone else to run a tobacco advertisement 

in breach of the Act 

remove exemptions for tobacco advertisements on international flights in and out of 

Australia 

prohibit marketing outside Australia by Australian companies that would be illegal in 

Australia 

prohibit false or misleading statements by manufacturers about the addictiveness or 

health effects of smoking or exposure to smoke 

require tobacco manufacturers to report on all promotional activities and expenditure 

and on sales volume 

tighten provisions relating to magazines imported from countries with fewer restrictions 

on tobacco advertising in periodicals. 

There are a number of other recommended amendments, indicating both the extent 

to which the Act is limited in achieving its stated aims and the scope for the tobacco 

industry to continue to promote its products. The effectiveness of the Tobacco Advertising 

Prohibition Act is also limited by the relatively small penalties associated with breaches, 

particularly in light of the potential revenues associated with recruiting new smokers 

through illegal marketing strategies. 

While a strengthened Tobacco Advertising Prohibition Act would be the appropriate 

legislative instrument to further restrict tobacco promotion as described, it is unlikely 

that government would call for another general review of the Act in the near future, thus 

other approaches to achieve similar results should be considered. For example, direct 

approaches to supermarket chains to remove tobacco products from sight have the 

potential to further ‘de-normalise’ smoking and assist quitters who are at higher risk of 

relapse when cigarettes are in plain view and more readily accessible. In the meantime, 

The Cancer Council Australia will continue to make the case for incremental amendments 

to the Act to phase in the tighter measures described above. 

Australia also needs to ensure that the protocols of the World Health Organization 

Framework Convention on Tobacco Control, which was ratified here in 2004, are observed 

in the domestic environment, in particular for eliminating loopholes allowing for tobacco 

industry sponsorship of sporting events. 

Product regulation 

As discussed later in this chapter, tobacco products are a regulatory anomaly in view of 

the burden that their unregulated availability imposes on the community. All government 

jurisdictions in Australia have agreed to the principle of reducing smoking rates through 


23 

T o b a c c o

improved regulation, by collectively endorsing the National Tobacco Strategy (see later in 

this chapter). However, the slow progress of implementation has increased the urgency of 

tobacco regulation priorities, which include: 

• 

• 

• 

• 

• 

• 

imposing penalties for misleading statements (see recommended amendments to the 

Tobacco Advertising Prohibition Act) 

banning additives that aid palatability and addictiveness 

making reduced ignition propensity cigarettes (shown to significantly reduce fire risk) 

mandatory 

banning filter venting 

making detailed information on the content of all tobacco products publicly available 

(possibly on a public domain website) 

imposing a ‘polluter pays’ requirement/levy on industry. 

Real price increases 

As articulated in the National Tobacco Strategy (see later in this chapter), imposing price 

increases on tobacco products through taxation has been shown to directly reduce 

smoking rates, and is therefore endorsed as evidence-based tobacco control policy. 

Government revenue derived from increased tobacco tax should fund additional smoking 

cessation services, to help ensure that people on lower incomes, who already bear a 

disproportionate tobacco burden, are better supported to quit smoking. 

Accountability 

Litigation is an increasingly effective way to help make the tobacco industry accountable 

for the death and disease caused by its products and to obtain funds to support tobacco 

control measures (Advocacy Institute 2005). The achievements of litigation include 

(Daynard 2003): 

• 

• 

• 

• 

disclosure of documents that demonstrate the intent of the tobacco industry to target 

children; deliberately mislead scientists, politicians, and customers about the lethal 

and addictive nature of their products; and to conspire with smugglers and money 

launderers around the world 

verdicts against tobacco companies in tobacco cases in the US, made possible by 

the above-mentioned documents, involving punitive damages of millions or billions of 

dollars have added to the industry’s confusion and loss of legitimacy and, in the US, the 

increasing possibility of bankruptcy further weakens the industry’s position politically 

and in the financial community 

the first stirrings of responsible behaviour by tobacco companies (Philip Morris now 

concedes on its website that cigarette smoking is addictive and causes lung cancer and 

other diseases) 

media coverage and public discussions about tobacco lawsuits, which educate the 

community about addiction and disease caused by smoking. 

In Australia the Australian Competition and Consumer Commission has had some success 

in enforcing the law against the tobacco industry with respect to its deceptive practices, 

with the industry agreeing to court-enforceable undertakings to remove ‘light’ and ‘mild’ 

brands from sale and pay for corrective advertising. The industry also promptly withdrew 

‘split packs’ (see elsewhere in this chapter), which represented a breach of packaging 

regulations, following prompt action from the commission. However, the wealthy tobacco 

industry is a formidable legal opponent, and the Australian Competition and Consumer 


Commission lacks sufficient funds to effectively bring the industry to account. The 

Australian Government should adequately fund the Australian Competition and Consumer 

Commission to take on the tobacco industry. 

Access to smoking cessation aids 

The Cancer Council Australia recommends improved access to smoking cessation aids 

to an extent commensurate with the damage caused by smoking and the percentage of 

smokers who would like to quit. Implementation of the other measures articulated in this 

section would also require an increase in the availability of smoking aids to help ensure an 

optimal return on investment in initiatives such as social marketing campaigns. A range 

of products and services needs to be available to support intending quitters, such as 

counselling, information and education, and nicotine replacement and pharmacological 

products. 

Improved tobacco control policy requires: 

• 

• 

• 

• 

• 

• 

promotion of tobacco-dependence treatment as an integral component of cost-effective 

health care 

increased government funding of the delivery and promotion of non-drug smoking 

cessation support services, including Quitlines 

increased funding for programs to educate and prompt healthcare providers to identify 

and advise patients who smoke to quit, and to refer them to appropriate support 

services 

implementation of subsidy and access arrangements for pharmacological interventions, 

to help ensure that treatment is equitable and cost-effective 

tailoring of cessation support services for disadvantaged and high-risk groups, such as 

Aboriginal and Torres Strait Islander people 

introduction of a Medicare rebate for general practitioners to counsel patients about 

smoking cessation or for referral to the Quitline or other effective services. 

Smoke-free environments 

The restrictions on smoking in public places that gained momentum in the mid-to-late 

1980s with bans on smoking in Australian workplaces and domestic flights have extended 

to a number of environments, with evidence showing a significant decrease in the health 

risks encountered due to second-hand smoke. Smoke-free environments also help to 

‘de-normalise’ smoking and encourage smokers to quit. While all Australian jurisdictions 

have adopted some bans on smoking in public places, the pace of reform varies, and 

opportunities for significant improvement remain. In order for restrictions to reach their 

potential to adequately protect all individuals from the dangers of second-hand smoke, 

tightening of laws is required in all jurisdictions, with evidence-based recommendations to: 

• 

• 

• 

• 

eliminate the loopholes/exemptions exploited by pubs and clubs 

eliminate ‘high-roller’ room exemptions (e.g. in casinos, where wealthy patrons are 

permitted to smoke in enclosed spaces despite the risks to staff) 

ban smoking in outdoor dining areas 

create smoke-free campuses/higher learning institutions. 

There is also a clear case for banning smoking in cars carrying children and pregnant 

women. 


25 

T o b a c c o

Tobacco control strategy for Aboriginal and Torres Strait Islander peoples 

The prevalence of smoking among Aborigines and Torres Strait Islanders is around 50%, 

more than 2½ times the smoking rate of non-Indigenous Australians. Evidence shows 

that smoking among Aborigines and Torres Strait Islander people is a significant cause of 

increased cancer mortality and other chronic disease. Indigenous Australians are more 

than twice as likely to die within five years of a cancer diagnosis as non-Indigenous cancer 

patients, in large part because of the poor prognosis of cancers caused by smoking 

(Condon et al. 2005). 

The cycle of poverty and disadvantage exacerbated by smoking (discussed elsewhere 

in this chapter) is particularly acute among Aborigines and Torres Strait Islander people. 

Despite the importance of smoking in the crisis in Indigenous health, efforts to address the 

issue have been substantially under-funded. Yet evidence shows that measures to reduce 

tobacco use, such as information, education and nicotine replacement therapy, can work 

in Indigenous communities if adequately funded and promoted in a culturally appropriate 

framework (Briggs, Lindorff & Ivers 2003; Ivers 2004). A tailored approach to tobacco 

control for Indigenous people, developed in consultation with Indigenous health groups 

such as the National Aboriginal Community Controlled Health Organisation, is essential 

to improving the inequity in health outcomes between Indigenous and non-Indigenous 

Australians and for breaking the cycle of poverty, poor preventive health and disease. 

The policy context 

Brief history of tobacco control policy in Australia 

Australia’s tobacco control record over the past three decades has been relatively good. 

However, governments were initially slow to respond to the evidence demonstrating the 

dangers of smoking, and evidence-based tobacco control measures continue to be subject 

to delays and insufficient funding across jurisdictions, despite historical evidence showing 

the benefits of a strategic approach to reducing smoking rates. 

Health authorities in Australia first called for formal government action to reduce tobacco 

use in the early 1960s, following international research that demonstrated the serious 

health risks associated with smoking. In 1962, health promotion organisations endorsed a 

report recommending restrictions on tobacco advertising and the introduction of a public 

health education campaign. While it took a decade for government to respond to calls for 

tobacco control measures, male smoking rates fell as the news media informed the public 

of the dangers of smoking. 

The first significant government action, in 1972, was mandatory placement of health 

warnings on cigarette packages. From 1973 to 1976, broadcast advertising of cigarettes 

was phased out. These two national measures coincided with a major decline in smoking 

rates, a trend that has continued, in step with other measures aimed at reducing tobacco 

use. 

In the 1980s, establishment of preventive health care as a public policy issue, evidence that 

smoking was the largest cause of preventable death and disease, and a shift in community 

attitudes to smoking, encouraged governments to do more to reduce the tobacco 

burden. Passive smoking became a prominent issue in the 1980s because of research 

demonstrating the dangers of exposure. The Australian Government legislated to eliminate 

smoking from federal workplaces in 1986 and from domestic aircraft in 1987. 


State and territory governments, with varying levels of commitment and delay, have 

subsequently introduced restrictions on smoking in public places that are subject to 

jurisdictional legislation, such as public transport, taxis, and enclosed public places (e.g. 

shopping centres, restaurants and theatres and, in some states, pubs and bars). The 

Australian Government also banned tobacco advertising in the print media in 1989. In 

1992, federal parliament passed the Tobacco Advertising Prohibition Act, phasing out most 

remaining forms of tobacco advertising by 1995. 

Other key tobacco control measures have been excises on tobacco products (deterring 

purchase and providing revenue towards the tobacco disease burden) and social marketing 

campaigns aimed at raising public awareness of the dangers of smoking. 

A milestone social marketing initiative was the Australian Government’s National Tobacco 

Campaign run in 1997 and 1998. A government-commissioned independent evaluation of 

the campaign found that investment in the first six months of the campaign alone returned 

more than double in savings via reduced healthcare costs and life-years saved. Despite this 

success, and recommendations from the evaluation team to re-run the campaign, there 

has been no coordinated national social marketing campaign aimed at reducing smoking 

rates on this scale since then. Because of its success, the campaign has been adapted for 

use in other countries. 

Figure 1.2 Adult per capita consumption of tobacco products in Australia 

Annual amount of toacco dutied per adult over 15 years (kg) 

4.0 

3.5 

3.0 

2.5 

2.0 

1.5 

1.0 

0.5 

Introduction of 

manufactured 

cigarettes in 

Australia 

Depression 

Uptake by 

women 

Second 

World War 

0.0 

1903 07 11 15 19 23 27 31 35 39 43 47 51 55 59 63 67 71 75 79 83 87 91 95 

YEAR 

Source: Compiled by Michelle Scollo, VicHealth Centre for Tobacco Control 

Early research on 

the health effects 

of smoking 

Report of the US 

Surgeon General 

Broadcast tobacco 

advertising phased 

out 


Commencement of 

Quit campaigns 

Introduction of 

workplace smoking 

bans 

New health 

warnings 

2 

T o b a c c o

Australian National Tobacco Strategy 2004–200 

Current national and inter-jurisdictional tobacco control policy is articulated in the 

Australian National Tobacco Strategy 2004–2009. The strategy sets out the intentions 

of federal, state and territory governments to work together and collaborate with nongovernment 

agencies on a long-term, comprehensive, evidence-based and coordinated 

national plan ‘to significantly improve health and to reduce the social costs caused by, and 

the inequity exacerbated by, tobacco in all its forms’ (MCDS 2004). 

The Cancer Council endorses the objectives of the National Tobacco Strategy, which are, 

across all social groups: 

• 

• 

• 

• 

to prevent uptake of smoking 

to encourage and assist as many smokers as possible to quit as soon as possible 

to eliminate harmful exposure to tobacco smoke among non-smokers 

where feasible, to reduce harm associated with continuing use of and dependence on 

tobacco and nicotine. 

The National Tobacco Strategy identifies the following areas for action: 

• 

• 

• 

• 

• 

• 

• 

• 

regulation of tobacco 

» 

» 

» 

» 

» 

» 

promotion 

place of sale 

price (through tobacco tax) 

place of use 

packaging 

products 

promotion of Quit and Smokefree messages 

cessation services and treatment 

community support and education 

» 

» 

informing the community 

preventing smoking uptake by children 

addressing social and cultural determinants of health 

tailoring initiatives for disadvantaged groups 

research, evaluation, monitoring and surveillance 

workforce development. 

Regulation of tobacco promotion 

Comprehensive bans on cigarette advertising and promotion were shown to reduce 

consumption, but more limited partial bans were found have little or no effect in data from 

1970 to 1992 from 22 high-income countries (Jha & Chaloupka 1999). Econometric studies 

in high-income countries suggest that comprehensive bans on promotion reduce demand 

for tobacco by around 7% (CDCP 1999). When governments ban tobacco advertising in 

one medium, the tobacco industry will substitute advertising in other media with little or 

no effect on overall marketing expenditure (Jha & Chaloupka 1999). In Australia, tobacco 

promotion still occurs at point of sale and on packaging. Research suggests that such 

advertising increases positive feelings about cigarette brands (MCDS 2004). 


Regulation of place of sale 

Regulation of the supply of tobacco products should ensure that they are available to 

adults, but are not highly visible and are not sold to children. Laws banning sales to minors 

are more effective if the penalties are substantial and the laws are vigorously enforced so 

that the probability and cost of being caught outweighs the benefit of continuing illegal 

sales (MCDS 2004). Reductions in cigarette consumption by young people, however, have 

not always followed increasing sales restrictions. In Australia, the proportion of 12–17-yearolds 

who report buying their own cigarettes has declined since 1996, but there has been 

a corresponding increase in reports of obtaining cigarettes by having someone else buy 

them (White & Hayman 2004). 

Regulation of price through tobacco tax 

‘Real’ price increases (where increases are not matched by greater earning capacity, 

and affordability decreases) can depress demand for cigarettes (Jha & Chaloupka 1999). 

Higher prices (usually resulting from taxation increases) induce some smokers to quit, 

prevent other people from starting (CDCP 2000), reduce the number of ex-smokers who 

relapse, and reduce consumption among continuing smokers. A price rise of 10% on a 

pack of cigarettes would be expected to reduce demand by about 4%, but efforts to set an 

‘economically optimal’ tax level have produced a wide range of estimates (Jha & Chaloupka 

1999). However, effective taxation policy must ensure that increases are real, well 

publicised, and occur as often as necessary to maintain effective price rises. It is important 

that taxation effects are not insulated or absorbed by economies in manufacturing or 

tobacco companies’ pricing policies (Winstanley, Woodward & Walker 1995). 

Increasing the price of tobacco products will decrease consumption more in low than in 

high-income groups. However, tax increases can cause financial stress for people on low 

incomes who continue to smoke. Support for price increases will be more likely if there is 

increased investment in supporting people on low incomes to quit (MCDS 2004). 

Regulation of place of use 

Restrictions on smoking in public places and workplaces will obviously benefit nonsmokers. 

Importantly, smokers in workplaces with total bans on smoking are also likely 

to reduce the amount they smoke and increase their chances of successfully quitting 

(Fichtenberg & Glantz 2002). There is a high level of public support for restricting smoking 

in public places in Australia (AIHW 2005). 

Regulation of packaging 

Tobacco product packaging allows information on the product to be communicated to 

consumers. Since March 2006 cigarette packages in Australia have been required to carry 

colour graphic and text warnings on 30% of the front of the pack and 90% of the back of 

the pack. Information on a national Quit website and Quitline number appears on the back 

of the pack (DHA 2006). Tobacco products in Australia will no longer carry information 

about ‘yield’ of components (e.g. nicotine and tar) following concerns that consumers 

did not understand this information and acknowledgment that the labelling systems 

were based on flawed testing (MCDS 2004). Use of descriptors such as ‘light’ and ‘mild’ 

has also ceased after the Australian Competition and Consumer Commission found that 

the claimed relative health benefits of low yield cigarettes were misleading and likely to 

breach the Trade Practices Act (ACCC 2005). However, there is still potential for smokers 

to be misled, with continued use of colours and descriptors implying comparative health 

benefits, and the mechanism by which deception occurs has not been addressed (King & 

Borland 2005). 


2 

T o b a c c o

Regulation of products 

Possible regulations could be requirements for ‘fire safe’ or reduced ignition propensity 

cigarettes (which automatically extinguish when they are not being smoked), and 

measures to reduce the addictiveness and palatability of products. A policy is needed ‘to 

coordinate regulation of tobacco products and products designed to replace tobacco, in 

ways that combine to reduce overall population harm’ (MCDS 2004). 

Promotion of Quit and Smokefree messages 

Long-term, high-intensity counter-advertising campaigns can reduce consumption 

when part of a multi-component program (Jamrozik 2004). Such campaigns also 

effectively reduce initiation of tobacco use, in combination with other interventions such 

as price increases and school and community programs (CDCP 2000). The National 

Tobacco Campaign initiated in 1997 (‘Every Cigarette Is Doing You Damage’) involved 

advertisements on television, on radio, in newspapers, and on bus billboards (CDHAC 

2004). In a survey conducted to evaluate a 2004 campaign, 48% of smokers reported that 

the campaign messages provided encouragement to quit (CDHAC 2004). 

Cessation services and treatment 

Many people are able to overcome their dependence on tobacco and stop smoking, 

although people commonly have multiple attempts before succeeding (MCDS 2004). In 

Australia in 2004, 26% of people aged 14 and over described themselves as ex-smokers 

(AIHW 2005). The Cochrane Collaboration Methods have found the following interventions 

aimed at improving rates of quitting to be effective: brief advice from doctors; nicotine 

replacement therapy (via chewing gum, transdermal patch, nasal spray, inhaler, or 

tablet); the antidepressant drug bupropion (Zyban); tailored self-help materials; telephone 

counselling; and individual or group counselling (Cochrane Library 2006). However, 

pharmacotherapies are sometimes not used properly, reducing their efficacy, and clinical 

trial results are not always replicated when cessation aids are used in the real world. 

Resources to encourage and assist doctors to provide cessation advice include the 

Guidelines for prevention activities in general practice (the ‘red book’) and the SNAP guide 

on smoking, nutrition, alcohol and physical activity as population health risk factors 

(RACGP 2005; RACGP 2004). A study on the application of SNAP in general practice noted 

that while verbal advice on smoking cessation advice is reported as being provided ‘very 

often’ by 68% of general practitioners, other studies indicate that only 0.6% of patient 

encounters involve cessation advice (Amoroso, Hobbs & Harris 2005). 

The National Tobacco Strategy recommends an integrated strategy for cessation services 

that would enable coordination of policy and spending by programs covering public health, 

medical and pharmaceutical benefits, medical education, development of general practice 

and continuing education of virtually all health professionals (MCDS 2004). 

Informing the community 

Counter-advertising or negative messages about smoking from governments and health 

promotion organisations have been found to reduce consumption consistently according 

to studies from Australia, North America, Europe and Israel (CDHAC 1999). In general, 

the impact is greatest and most sustained when there is low general awareness of the 

health risks of smoking (Jha & Chaloupka 1999). In Australia, there is a high level of public 

knowledge of illnesses associated with passive smoking, although more could be done to 

update the community on new research (VCTC 2002a). 


Preventing smoking uptake by children 

A recent Australian review of youth tobacco prevention (DHA 2005) notes that prevention 

of tobacco uptake is a critical component of any comprehensive tobacco control strategy. 

Such efforts have largely focused on young people, given that smoking initiation is most 

likely to occur before 18 years of age. Theoretically, prevention or ‘early intervention’ 

initiatives represent a better long-term solution than cessation initiatives, given the 

addictive properties of nicotine. However, effective prevention strategies have remained 

largely elusive (DHA 2005). 

High-profile campaigns to reset community norms about smoking and help adult rolemodels 

to quit can also greatly reduce smoking by children (MCDS 2004). Focusing efforts 

on adult smokers is supported by research that demonstrates that mortality can be better 

reduced by focusing on current smokers and near-term health problems (Levy, Cummings 

& Hyland 2000; Peto et al. 2000). Parental and sibling smoking is a well-established risk 

factor for smoking in adolescents (USDHW 1979). When parents who smoke quit before 

their children begin smoking, the risk of their children taking up smoking is significantly 

reduced (Farkas et al. 1999). 

Adolescents (15–17 years) and people aged 18 to 39 years had similar responses to the 

Australian National Tobacco Campaign (White, Tan et al. 2003), suggesting that an adult 

approach is more effective with adolescents than a campaign specifically targeting them 

(Wakefield, Miller & Roberts 1999). Adolescents showed high campaign awareness 

regardless of smoking status, and many felt it was relevant to them, including almost 50% 

of non-smokers. In addition, 85% thought that the campaign made smoking seem less 

cool and around one-third felt it had discouraged some friends from taking up smoking 

(White, Tan et al. 2003). 

There is little evidence that school-based programs are effective in the long term in 

preventing uptake of smoking. A review by the Cochrane Collaboration identified 23 highquality 

randomised controlled trials of school-based programs to prevent children who 

had never smoked becoming smokers (Cochrane Library 2006). The interventions included 

information-giving, social influence approaches (representing the majority of studies), 

social skills training, and community interventions. There is little evidence that information 

alone is effective. Although half of the best quality studies in this group found short-term 

effects, the highest quality and longest trial (the Hutchinson Smoking Prevention Project) 

found no long-term effects from 65 lessons over eight years (Cochrane Library 2006). 

Addressing social and cultural determinants of health 

Investing in programs that strengthen community and cultural resources (e.g. programs to 

reduce the chance of educational failure, family conflict, loss of cultural identity and mental 

health problems) may well reduce uptake by young people of smoking (MCDS 2004). Such 

investment is crucial in Aboriginal and Torres Strait Islander and other very disadvantaged 

communities. 

Tailoring initiatives for disadvantaged groups 

Several social groups in Australia suffer a particularly high burden of tobacco-related death 

and disease (MCDS 2004): 

• 

• 

• 

Australian Aboriginal and Torres Strait Islander peoples 

people suffering severe and disabling mental illness 

people who are institutionalised, including those in custodial settings 


31 

T o b a c c o

• 

• 

parents/carers and children living in disadvantaged areas 

immigrants who left their home countries at a time when the dangers of smoking were 

not well understood. 

Australian Aboriginal and Torres Strait Islander peoples 

In 2004, 50% of Aboriginal and Torres Strait Islander people aged 18 years and over were 

current smokers, the same level reported in 1995. During the same period the prevalence 

of current smoking (daily, weekly and occasional) among all Australians fell from 27% to 

21% (ABS 1994). 

An audit by the Centre for Excellence in Indigenous Tobacco Control produced the 

following recommendations to improve and strengthen Indigenous tobacco control 

(Adams & Briggs 2005): 

• 

• 

• 

• 

• 

• 

• 

• 

• 

• 

Improve representation of Indigenous people on boards, advisory groups and in 

partnerships for tobacco control. 

Each state and territory should establish a process to ensure Indigenous tobacco control 

initiatives are sustainable and consistent. 

Tobacco control training for Aboriginal health workers should be supported through 

accredited training delivery. 

Professional development training in Indigenous tobacco control should be available. 

Organisations that fund tobacco control research should direct a proportion of their 

funding to Indigenous tobacco control research. 

Tobacco control research should include Indigenous people. 

Improve accountability of tobacco control organisations to provide services to 

Indigenous people. 

Develop an Indigenous tobacco control strategy. 

Provide a more consistent approach to tobacco control education for young Indigenous 

people in schools. 

Improve access to nicotine replacement therapies. 

Initiatives for other disadvantaged groups 

Projects targeting people with mental illness, people in custodial settings, people in 

disadvantaged areas, and people with limited English skills operate in some state and 

territory jurisdictions (MCDS 2004). 

Research, evaluation, monitoring and surveillance 

The National Drug Strategy Household Survey, which is conducted every three years, 

provides comparative data for adult smoking prevalence, but only limited data is currently 

available for Aboriginal and Torres Strait Islander peoples and particular cultural groups 

(AIHW 2005). Australia’s regular, standardised three-yearly surveys of student smoking are 

a valuable resource, providing reliable data about changes in children’s smoking behaviour 

since 1984 (White & Hayman 2004). Annual evaluation of the National Tobacco Campaign 

has provided data about smoking knowledge, attitudes and intentions, and Australia is 

also contributing to the International Tobacco Control Policy Evaluation Study to provide 

information on how tobacco control policies affect smoking cessation (MCDS 2004). 


Workforce development 

Recruitment and training 

Given the focus on policy and regulation, the National Tobacco Strategy has identified a 

need to attract more people from legal, economic, public policy and scientific disciplines 

to crucial research and policy jobs. In addition, the importance of the public receiving 

accurate information about the health risks of smoking and the effectiveness of various 

treatments, policies and programs requires more people skilled in media relations. 

Continuing education 

As well as the behavioural aspects of smoking, people working in tobacco control need 

to better understand the toxicology and epidemiology of tobacco use and the social, 

economic and legal aspects of tobacco control. Training for health professionals must 

also be addressed as part of a comprehensive policy to treat tobacco dependence. To this 

end, the Australian National Training Authority has endorsed two units of competency in 

smoking cessation as part of the national population health training package. 

Access to crucial information 

Short term strategies endorsed in the National Tobacco Strategy are to: 

• 

• 

• 

• 

better synthesise information about developments internationally 

facilitate access to relevant research evidence 

facilitate sharing of ideas and resources between states and territories 

support biennial Australasian tobacco control conferences. 

Framework Convention on Tobacco Control 

In 2004 the Australian Government ratified the World Health Organization Framework 

Convention on Tobacco Control. The objective of the convention was to protect present 

and future generations from the health, social, environmental and economic consequences 

of smoking and exposure to tobacco smoke. Countries that ratify the convention 

undertake to implement a range of measures relating to tobacco price and tax increases; 

tobacco advertising and sponsorship; regulation of tobacco products; tobacco product 

disclosure; packaging and labelling; education, communication, training and public 

awareness; cessation measures; illicit trade; sales to minors; support for economically 

viable alternatives; liability issues; and scientific and technical cooperation and exchange of 

information (WHO 2004). 

Tobacco Advertising Prohibition Act 

The Tobacco Advertising Prohibition Act was passed in 1992 to, according to section 3 

of the Act, ‘limit the exposure of the public to messages and images that may persuade 

them to start smoking, continue smoking, or use, or continue using, tobacco products’; 

and ‘to improve public health’. Evidence shows that the Act has worked effectively as a 

legislative instrument to limit the exposure of the Australian public to tobacco advertising 

through traditional mass media forms of marketing. However, a growing evidence base 

also shows that the Act has been ineffective in limiting exposure through other channels of 

communication, to which the tobacco industry has increasingly been turning since the Act 

was introduced. 

In August 2003, the Australian Department of Health and Ageing published an issues paper 

as part of the Government’s review of the Tobacco Advertising Prohibition Act, inviting 

submissions to seek ‘community views on the relevance of the Act’. The Cancer Council 


33 

T o b a c c o

Australia in partnership with a number of other health promotion organisations, prepared 

a detailed submission documenting why the Act needed amendment to help eliminate the 

many ‘guerrilla’ and ‘under the radar’ marketing strategies used by the tobacco industry 

to sustain a lucrative market base in Australia. Evidence was presented, in the submission 

and at hearings, of strategies that circumvented and contradicted the objectives of the 

Act, such as event and venue promotions; point-of-sale marketing; direct marketing and 

the use of databases; premiums and value-added promotions; vending machines; internet 

marketing; international magazines; ‘buzz’ marketing; sporting and cultural events; and the 

promotion of smoking by broadcasters, publishers, film-makers, etc. 

Despite the extent of this evidence, supported by separate submissions from health 

promotion bodies such as the Royal Australian College of General Practitioners, in April 

2005 the Australian Government announced that the Tobacco Advertising Prohibition Act 

would not be amended, as the review found it to be working well in its current form and 

that any gains derived from amendment would be ‘insignificant’. The Cancer Council 

and its allies will continue to collect evidence on the tobacco industry’s exploitation of 

loopholes in the Act. While a general review of the Act is unlikely in the near future, 

opportunities may exist for one-off amendments. 

Trade Practices Act 

The Trade Practices Act (Consumer Product Information Standard) 1974 is the legislative 

instrument under which graphic warnings on tobacco packaging were approved by federal 

parliament in 2004 and phased in from March 2006. Further amendments to the Act may 

facilitate the elimination of tobacco industry innovations such as slips to conceal graphic 

smoking warnings on tobacco products and ‘split packs’ enabling people with limited 

funds, such as children, to pool their money and break cigarette packets in half. In fact, 

prompt court action from the Australian Competition and Consumer Commission forced 

the withdrawal of ‘split packs’ less than three weeks after their appearance in October 

2006. While this was an encouraging outcome, the introduction of the packs demonstrates 

the tobacco industry’s capacity to creatively exploit new markets, a capacity that evidence 

shows would be reduced through tighter packaging regulations under the Trade Practices 

Act and an updated and more rigorous Tobacco Advertising Prohibition Act. 

Tobacco control: a blue chip investment in public health 

Developed by the VicHealth Centre for Tobacco Control and The Cancer Council 

Victoria, Tobacco control: a blue chip investment in public health details a comprehensive 

framework for tobacco control investment based on analysis of the evidence. It makes 

recommendations for action by federal, state and territory governments and nongovernment 

organisations. 

Aims 

The Cancer Council endorses the objectives of the National Tobacco Strategy, which are to: 

• 

• 

• 

• 

prevent the uptake of smoking 

encourage and assist as many smokers as possible to quit as soon as possible 

eliminate harmful exposure to tobacco smoke among non-smokers 

where feasible, reduce the harm associated with continuing use of, and dependence on, 

tobacco and nicotine. 


What needs to be achieved How The Cancer Council Australia and its members (the state and 

territory cancer councils) will do this 

Funding for tobacco control 

activities at a level that is 

commensurate with the 

scale of the harms caused, 

and sufficient to achieve 

specific declines in the 

prevalence of smoking 

Informing and reminding 

smokers about the harms 

of smoking, and motivating 

them to quit smoking 

Eliminating the promotion 

and marketing of tobacco 

Regulating tobacco products 

to protect the public interest 

Encourage the Australian Government to set targets for smoking 

prevalence for Australian adults, children and among disadvantaged 

groups 

Encourage the Australian Government to allocate adequate funds for 

comprehensive tobacco control programs to achieve these targets 

Continue to develop proposals for funding sources and/or economic 

assessments to assist in obtaining the required level of tobacco control 

funding 

Advocate for the development and implementation of a well-funded and 

evaluated social marketing campaign 

Participate in national collaboration on the delivery of social marketing 

campaigns 

Urge the Australian, state and territory governments to eliminate 

loopholes in the current legislation and address the remaining avenues of 

promotion and marketing of tobacco, with a particular focus on: 

• images that portray smoking as desirable, in movies and other popular 

culture 

• vending machines and mobile retailing of tobacco 

• marketing through pack design 

• Internet advertising and sales display of tobacco products in retail 

settings 

• sale of devices designed to conceal health warnings 

Continue to identify, document and report any examples of promotion 

and marketing of tobacco and its effect on attitudes, knowledge and 

behaviour of smokers or those at risk of taking up smoking 

Urge the Australian, state and territory governments to regulate tobacco 

products to protect the public and smokers, by: 

• introducing stronger mechanisms to prevent false or misleading claims 

by the tobacco industry about its products 

• banning the use of additives in cigarettes that aid palatability and 

addictiveness 

• requiring that all cigarettes in Australia meet standards for reduced fire 

risk 

• banning filter venting as part of cigarette design 

• 

requiring that tobacco companies publish detailed information about 

the contents, emissions and design features of all tobacco products 

Encourage the Australian, state and territory governments to adopt 

licensing schemes to regulate the retailing of tobacco products 

Continue to identify, document and report problems that arise from the 

absence of regulation of tobacco products, and the harms caused to 

smokers as a result 

Together with public health groups, examine options and opportunities 

for improved regulation of tobacco products 


35 

T o b a c c o



Further real increases in the 

price of tobacco products 

Strengthening existing 

accountability mechanisms 

to hold tobacco companies 

to account for the effects of 

their unlawful conduct 

Improvements in access to 

cessation support 

Protection of people from 

involuntary exposure to 

second-hand smoke and 

increasing the number of 

smoke-free public places 


Encourage the Australian Government to increase the excise on tobacco 

products at least in line with increases in average weekly earnings 

Encourage the Australian Government to ban the sale of duty-free 

cigarettes in Australia 

Encourage governments to step up measures to prevent evasion of excise 

and customs duty on tobacco 

Publicly expose examples of the unlawful conduct of tobacco companies, 

and demonstrate the ongoing effects of that conduct 

Encourage litigation against tobacco companies where this is in the 

public interest 

Encourage the Australian, state and territory governments to provide 

resources and powers to bodies charged with enforcing accountability by 

the tobacco industry, including the Australian Competition and Consumer 

Commission and state/territory heath authorities 

Promote tobacco-dependence treatment as an integral component of 

cost-effective health care 

Work with governments and other parties to: 

• increase funding for Quit services, to meet need 

• implement subsidy and access arrangements for pharmacological 

assistance for those most in need 

• increase the incidence of primary health-care providers referring 

patients for cessation advice and assistance 

Facilitate the development and use of effective tailored and targeted 

support programs for high-risk groups, including Indigenous Australians 

Urge state and territory governments to enact strong measures to create 

smoke-free environments with a particular focus on: 

• ensuring that legislation in relation to smoke-free pubs and clubs 

eliminates exposure to second-hand smoke 

• ending the exemptions to smoke-free legislation currently provided to 

high-roller rooms and other selected gambling venues 

• outdoor dining areas 

• addressing the need for cars carrying children and pregnant women to 

be smoke-free 

• 

health facilities and campuses 

Collaborate with the higher education sector and individual institutions 

to encourage smoke-free campuses 

Continue to conduct research to demonstrate the importance of smokefree 

environments in protecting health, assisting smokers to quit, and 

changing public attitudes towards smoking



Development of targeted 

tobacco control strategies 

for Indigenous Australians 

and others at high risk 

Timely implementation of 

Australia’s obligations under 

the Framework Convention 

on Tobacco Control 

Effective implementation 

and further development 

of the Framework 

Convention on Tobacco 

Control internationally and 

regionally 

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Encourage and support the development of a national tailored tobacco 

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National Aboriginal Community Controlled Health Organisation and other 

Indigenous health groups 

Encourage governments to provide adequate funding and other 

resources for the implementation of a tailored tobacco control strategy 

for Indigenous Australians 

Continue to identify, document and report on tailored tobacco control 

interventions for disadvantaged groups 

Monitor, and report on, progress of implementation of Framework 

Convention on Tobacco Control measures in Australia 

Support Framework Convention on Tobacco Control implementation in 

developing countries in the Western Pacific region 

Encourage the Australian Government to play a leading role in the further 

development of the Framework Convention on Tobacco Control, including 

developing guidelines, protocols and compliance monitoring 

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U l t r a v i o l e t r a d i a t i o n 

Introduction 

Melanoma incidence now exceeds lung cancer 

incidence. Skin cancer is, in financial terms, the 

most costly burden to the health system. 

The principal cancer related to excess ultraviolet (UV) radiation is skin cancer. Australia has 

the highest rates of skin cancer in the world. Skin cancer includes cutaneous melanoma 

and non-melanoma skin cancers (NMSC), namely basal cell carcinoma (BCC) and 

squamous cell carcinoma (SCC). 

From as early as the 1950s and ‘60s, concern over high skin cancer rates led to limited 

community education campaigns programs in Victoria and Queensland. These aimed 

to raise public awareness about skin cancer and to increase health professionals’ early 

detection of skin cancer. 

Since the 1980s, more extensive public health programs aimed at preventing excessive 

exposure to UV radiation have been implemented across Australia by cancer organisations 

and government health services. The ‘Slip! Slop! Slap!’ and SunSmart slogans, developed 

in 1980 and 1987 by The Cancer Council Victoria, have been the themes of many 

campaigns and are well recognised by Australians in relation to sun protection. The focus 

of these skin cancer prevention programs has been on reducing the potential harm of skin 

cancer by decreasing exposure to UV radiation and increasing early detection and effective 

treatment. 

Despite the challenges of evaluating programs aimed at changing sun protection 

behaviour, evidence of the effectiveness and cost-efficiency of programs in Australia and 

overseas is accumulating. Research is increasingly linking public health programs that 

encourage behaviour change to reductions in incidence and mortality. 

In addition to this, in Australia, there is evidence that primary prevention programs aimed 

at reducing sunlight exposure may be affecting skin cancer rates (Staples et al. 2006) and 

that changes in adult behaviour have resulted in some reduction in skin cancer incidence 

(Slevin, Clarkson & English 2000). 

The link between ultraviolet radiation and cancer 

The major causative factor in the development of melanoma and NMSC is UV radiation 

exposure (Sun Protection Programs Working Party 1996; Armstrong 2004). Childhood sun 

exposure is clearly important. In addition, adult exposure appears to contribute. The exact 

exposure needed to develop various skin cancers is not entirely clear. It is likely that both 

cumulative and episodic exposures are important, particularly if they cause sunburn. 

Based on a review of recalled sun exposure by period of life in studies of melanoma, the 

relative risk of melanoma with a history of childhood sunburn is 1.8, while for sunburn in 

adulthood it is 1.5 (Whiteman, Whiteman & Green 2001). 


41 

U l t r a v i o l e t r a d i a t i o n

In adult life, recreational (intermittent) sun exposure appears to be the strongest 

determinant of melanoma risk followed by total lifetime sun exposure and occupational 

exposure. Fair skin, which tends to burn easily and tan poorly, is also an important risk 

factor for skin cancer (Sun Protection Programs Working Party 1996; English et al. 1997; 

Armstrong 2004). 

In relation to NMSC, there is evidence that childhood and recreational (that is intermittent 

and non-occupational) sun exposure is important in determining the risk of basal cell 

carcinoma, while cumulative sun exposure, latitude and occupational exposure are 

associated with squamous cell carcinoma (Sun Protection Programs Working Party 1996). 

The burden of disease depends on geographical location. Both BCC and SCC rates are 

around three times higher in latitudes closer to the equator (Staples, Marks & Giles 1998; 

NCCI 2003), where UV radiation is higher. 

Impact of ozone depletion 

Changes in the stratospheric ozone may also play a role in the incidence of skin cancer. 

The ozone layer acts as a barrier to UV radiation. Its depletion over the 20th century has 

resulted in higher incident radiation levels reaching the earth’s surface generally. The breakup 

of the Antarctic ozone layer has caused profound but localised ozone depletion over 

southern land masses (Armstrong 1996). 

International measures to protect the ozone layer are showing signs of impact; despite this, 

climate change is expected to affect future ozone levels, slowing recovery of the ozone 

layer (Severi & English 2004). Due to the large variations in UV radiation levels during the 

day, it is difficult to accurately assess what impact ozone depletion has had on overall skin 

cancer incidence rates. 

Solariums 

Artificial UV radiation sources are also hazardous and for this reason solarium use should 

be avoided. Recent epidemiological studies have raised the possibility of an association 

between solarium use and melanoma (Young 2004; Gallagher, Spinelli & Lee 2005), 

however, epidemiological results generally lack consistency. Limited data from long-term 

follow-up of patients with severe psoriasis raise the possibility of an increase in SCC and 

BCC rates associated with solarium use (Autier 2004). There is no current evidence that 

supports the view that exposure to UV radiation through solariums is ‘safe’ or that tanning 

in this way protects against skin cancer. 

Sunscreens 

There has been some debate about the role of sunscreens in skin cancer prevention, 

and the potential association of sunscreen use with melanoma risk. A review (Gallagher, 

Lee & Bajdik 2004) found mounting evidence that sunscreen can prevent SCC, but no 

evidence that it can prevent BCC. It has been suggested that people may use sunscreen 

in order to stay longer in the sun and thus may increase their risk of cutaneous melanoma 

(IARC 2000). However, Gallagher et al. caution that retrospective case–control studies of 

melanoma and sunscreen use should be interpreted with great care, because of subject 

recall problems and confounding effects (2004). 

Vitamin D 

There is good evidence that vitamin D is obtained through sun exposure. There is also 

increasing evidence that vitamin D may protect against certain types of cancers (Garland 

et al. 1985; Garland et al. 1989; Giovannucci et al. 2006; Boniol, Armstrong & Dore 2006) 


and can be beneficial in reducing the risk of osteoporosis. Therefore a balance is required 

between avoiding an increase in the risk of skin cancer and achieving enough UV radiation 

exposure to maintain adequate vitamin D levels. 

For people with fair skin, it has been estimated that adequate vitamin D levels (>50 nmol/l) 

can be achieved in summer by exposing the face, arms and hands or an equivalent surface 

area for as little as 10 to 15 minutes, either side of the peak UV periods, on most days of 

the week (Samanek et al. 2006). In winter, in the southern states of Australia, where UV 

radiation levels are less intense, vitamin D levels may be maintained by approximately 

two to three hours of sunlight exposure accumulated over a week to the face, arms and 

hands or equivalent surface area. In northern states, the amount of sunlight exposure 

required to maintain adequate vitamin D levels is significantly less than this. Most people 

would achieve sufficient levels of sunlight exposure with normal outdoor activities without 

needing to deliberately seek additional sun exposure (TCCA 2006). 

However, some people are at risk of vitamin D deficiency, for example, women with dark 

skin who wear veils (particularly in pregnancy) and elderly or disabled people in institutional 

care or who are housebound. These people may require dietary supplements (Marks et 

al. 1995; Nowson & Margerison 2002). In most situations, sun protection to prevent skin 

cancer is required during times when the UV Index is moderate or above (>3). At these 

levels, it is unlikely to put people at risk of vitamin D deficiency. 

The impact 

Skin cancer accounts for 81% of all new cases of cancer diagnosed in Australia each year 

(AIHW & AACR 2004). 

Melanoma and NMSC account for almost 47% of the cancers managed by general 

practitioners (AIHW & AACR 2004). 

Melanoma 

Excluding NMSC, in 2005 melanoma was estimated to be the third most common cancer 

diagnosed in Australian women (after breast cancer and colorectal cancer, and the third 

most common in Australian men (after prostate and colorectal cancer). Overall melanoma 

incidence now exceeds that of lung cancer (AIHW & AACR 2004). 

In Australia in 2005, 10,014 people were diagnosed with melanoma (5705 men and 4309 

women) (AIHW, AACR, NCSG & McDermid 2005). 

In Australia in 2005, there were 1273 deaths from melanoma (862 men and 411 women) 

(ABS 2007). 

Trends in incidence and mortality 

Melanoma is rare in populations of non-European origin (Severi & English 2004). 

In Australia the lifetime risk (to age 75 years) of developing melanoma is 1 in 24 for men 

and 1 in 33 for women. In 2005 the mean age of first diagnosis for melanoma was 61 years 

for men and 57 for women. Between 1991 and 2005 the incidence rate for melanoma 

increased on average 1.5% per year among men and 0.9% per year among women (AIHW, 

AACR, NCSG & McDermid 2005). 

Among younger age groups (< 25), the rate of new cases of melanoma (incidence) is 

stable (AIHW & AACR 2004). This is most probably due to a change in sun protection 


43 


ehaviours as a result of public education programs, although it may in part be related to a 

change in the racial mix in the Australian population. 

Mortality from melanoma rose steadily from 1931 to 1985 with annual rates of increase of 

6% in men and 3% in women (Giles & Thursfield 2001). 

Since 1990 the rate of death from melanoma in Australia has been relatively stable but 

remains twice as high for men compared to women. Mortality rates for men increased 

0.7% per year between 1991 and 2005 and mortality rates for women decreased by 0.4% 

per year between 1991 and 2005 (AIHW, AACR, NCSG & McDermid 2005; ABS 2007). 

Non-melanoma skin cancer (NMSC) 

NMSC is the most common cancer in Australia (AIHW & AACR 2004). 

Cases of NMSC are not reported routinely to cancer registries but data obtained from 

population surveys suggests that 374,000 Australians (equivalent to 1.8% of the 

population) are treated for NMSC each year (AIHW & AACR 2004; Staples et al. 2006). 

It has been estimated that in 2002 in Australia, 256,000 people were diagnosed with BCC 

and 118,000 people were diagnosed with SCC (NCCI 2003). 

In Australia in 2002, there were 407 deaths from NMSC (270 men and 137 females) (ABS 

2004). 

Trends in incidence and mortality 

In 2002 the cumulative risks of developing at least one NMSC to age 70 years were 70% 

for men and 58% for women. Incidence rates of NMSC have increased from 1985 to 2002. 

The increase has been greatest for people 60 years and older while rates for people under 

60 have stabilised (Staples et al. 2006). 

The rate of treatment (and therefore diagnosis) of new cases of SCC rose by 133% 

between 1985 and 2002 and was similar across the sexes. The rate of treatment (and 

therefore diagnosis) of new cases of BCC rose by 35% between 1985 and 2002 and was 

greater in men (42%) than in women (26%). NMSC rates for both SCC and BCC were 

higher in more northerly parts of Australia (NCCI 2003). 

Mortality from NMSC decreased overall between 1950 and 1994 but an increase in deaths 

among men was noted from the mid-1980s to the mid-1990s, a phenomenon thought to 

be related to the HIV/AIDS epidemic (Giles & Thursfield 2001). Mortality rates (2002) are 

now 1.6 per 100,000 for men and 0.5 per 100,000 for women (ABS 2004). 

NMSC is Australia’s most expensive cancer. More than $264 million (9% of the total costs 

of cancer) was spent on diagnosis and treatment in 2000–01 (Staples et al. 2006). 

The challenge 

Growth in the solarium industry 

One of our great challenges is to counter the growing influence of solariums as agencies 

that promote the desirability of a tan and potentially expose users to dangerous 

UV radiation. The number of solariums and their commercial profile have increased 

significantly over the last few years and competition in the industry has led to substantial 

publicity and marketing campaigns being waged by solarium operators. Solariums 


have been assertively marketed to the young as a health and beauty aid. The number of 

establishments in one city alone (Melbourne) increased by more than 650% over five years 

to the end of 2001 (Fox 2001). We need to continue to educate the public on the dangers 

of solariums and dispel the many solarium myths. 

Advocating for solarium regulation 

Regulation of the solarium industry also remains a challenge. In the face of a degree 

of apparent reluctance by all state and territory governments, and also the Australian 

Government, to regulate the solarium industry, there needs to be persistent efforts to 

maintain and increase industry standards. 

A study of 30 solarium centres in Melbourne during the 2003–04 summer demonstrated 

poor compliance by many operators with numerous aspects of the voluntary Australian 

Standard: 90% provided access to fair skinned customers and 52% of people aged 16 

years were able to buy solarium services without the parental consent the code requires 

(Dobbinson, Wakefield & Sambell 2006). 

Increases in the desirability of a tan 

Despite improving attitudes towards sun protection, there is worrying evidence that 

attitudes to tanning and sun protection behaviours are again changing. There are 

indications of a recent increase in the desirability of a tan. This is thought to have been 

influenced by the growth in the number and profile of commercial solariums and fashions 

that have emphasised skimpy clothing with maximum skin exposure. The absence of a 

substantial paid mass media campaign around skin cancer may also have played a role. 

Given the association between sun protection advertising and people’s attitudes and 

behaviours, there needs to be more investment in mass media campaigns to reverse these 

trends before they affect skin cancer incidence and mortality. 

Explaining the risks and benefits of UV radiation exposure 

New debates continue to emerge in relation to the health risks and benefits of UV radiation 

exposure in terms of vitamin D. Some of these debates have the potential to confuse 

Australians and contaminate the sun protection message. The SunSmart UV Alert is 

a useful tool that can help explain when people need to protect themselves from UV 

radiation and when protection is not essential. However, this initiative requires monitoring 

and further marketing to ensure that the public understands and responds appropriately. 

Upskilling GPs in the assessment, diagnosis and treatment of skin cancer 

We need to ensure that the knowledge and skills of GPs keeps pace with scientific 

developments in the detection and treatment of skin cancer. It is critical that GPs know 

how to respond when people ask for a skin cancer check in response to SunSmart 

messages that tell them to seek GP advice about any suspicious spot or lesion. 

Changing adolescents’ sun exposure patterns 

Adolescents generally adopt sun protection behaviours less frequently than adults and it 

is more challenging to achieve attitude and behaviour changes among teenagers (Arthey 

& Clarke 1995; Mermelstein & Riesenberg 1992; Dobbinson & Hill 2004). Adolescents 

spend more time in the sun than any other group. While they have been shown to have a 

high level of knowledge on the dangers of sun exposure, they engage in relatively few sun 

protection behaviours. We need effective interventions that address adolescents’ growing 

perception of sun-tanning as desirable. 


45 


Screening for melanoma 

There is insufficient Australian research to support a population melanoma screening 

program (refer to the chapter on melanoma for more information). 

Absence of a long-term coordinated national skin cancer control program 

For the first time the Australian Government has committed funds to a national approach, 

with $5.5 million being allocated to a social marketing approach delivered over the summer 

of 2006–07. However, despite achievements of over 20 years, Australia still lacks a longterm 

national skin cancer program. Cooperation continues to grow between the state 

cancer councils, but there is also considerable inconsistency in the funding available across 

states and territories to implement population-based skin cancer control campaigns. 


After more than 20 years of work, Australia is recognised as having the most extensive, 

comprehensive and longest-lasting skin cancer prevention programs in the world. Many 

have been based on and modified by extensive research and evaluation (Montague, 

Borland & Sinclair 2001). 

Skin cancer prevention programs delivered throughout Australia by the state and territory 

cancer councils have been formed through needs analysis and formative research that has 

guided the development of effective and appropriately targeted strategies. 

The Cancer Council Australia has a strong commitment to research that facilitates the 

development of evidence-based practice. Several state and territory cancer councils fund 

epidemiological and behavioural research that provides valuable expertise towards the 

development and evaluation of skin cancer prevention and early detection programs. 

In 2003, The Cancer Council Australia and its members initiated the inaugural national 

sun survey to determine attitudes, knowledge and behaviours of the community with a 

specific focus on sun protection behaviours and sunburn incidence of Australian children, 

adolescents and adults (TCCA, unpublished data). The results of this survey provide 

valuable evidence to guide the development of skin cancer prevention strategies. 

The health belief model (Egger, Spark & Donovan 2005) guides strategies that might 

influence people’s perceived risk, and ability to reduce this risk, within supportive 

environments, to motivate behavioural and attitudinal change. Once skin cancer prevention 

programs are implemented, evaluation determines the effectiveness of strategies and 

possible areas for improvement. 

Site-specific interventions targeting settings such as childcare centres, pre-schools, 

primary and secondary schools, outdoor recreation settings, workplaces and health care 

settings have been shown to help reduce exposure to UV radiation (Glanz, Saraiya & 

Briss 2004). Of all settings, school programs have been shown to be most effective for 

improving knowledge and attitudes and in some cases improving short-term behaviours. 

For skin cancer prevention programs to be most effective, they should adopt a multistrategic 

approach that enables a variety of priority groups to be targeted. Glanz, 

Saraiya and Briss (2004) recommend that programs use individual-directed strategies, 

environmental, policy and structural interventions, media campaigns and community-wide 

multi-component interventions. 


Buller and Borland (1999) concluded that comprehensive, community-wide programs can 

increase sun protection behaviours and reduce UV radiation exposure. These programs are 

more effective than smaller-scale interventions since they are delivered through multiple 

channels, creating repeated exposure to consistent sun protection messages. Overall, 

though more expensive, community-wide interventions may prove to be the most efficient 

and cost-effective way to achieve behaviour change. 

In addition, skin cancer prevention programs should embrace the recommendations of the 

Ottawa Charter (WHO 1986) in relation to public policy development, advocacy strategies, 

developing personal skills, reorientating health services and strengthening community 

action. 


Skin cancer prevention can be aided by regulating the solarium industry, effective shade 

design by local government, and advocacy and policy for sun protection behaviours in 

the workplace. Strategies that increase GPs’ skills in early detection of skin cancer and 

encourage people to seek early diagnosis and treatment should also be supported. 

Where possible, The Cancer Council Australia and its members seek to build strong 

partnerships with key stakeholders to support sound skin cancer prevention strategies. This 

collaborative approach allows the Cancer Council to access valuable advice and feedback 

from leading medical, policy and industry representatives, as well as consumers. 

Aims 

We encourage Australians to protect themselves throughout life against UV radiation, 

avoid unnecessary sun exposure and avoid exposure to other sources of UV radiation. Our 

aims are to: 

• 

• 

• 

• 

• 

change the attitudes, knowledge and skills of individuals, particularly young people, 

about skin cancer and sun protection 

develop strategies for the early detection and effective diagnosis of skin cancer 

achieve healthy settings, organisations, products, policies and practices that promote 

sun protection 

strengthen the community’s capacity for coordinated action on skin cancer prevention 

inform the design, implementation and evaluation of skin cancer prevention strategies. 



Positive changes in the 

attitudes of Australians 

towards sun protection with 

a particular emphasis on 

young people 

Encourage the Australian Department of Health and Ageing to develop 

and implement a well-evaluated, long-term and comprehensive national 

social marketing campaign for children and young people aged 17 to 25 

years 


4 




An increase in knowledge of 

the UV Index and application 

of the UV Index to sun 

protection behaviours 

An increased capacity to 

monitor behavioural trends 


monitor epidemiological 

trends 


know what works in relation 

to program delivery 

Protection of young people 

in caring and educational 

settings 

An increase in the amount of 

natural or constructed shade 

in public places 

Improved sun protection 

practices among outdoor 

workers 

An increase in the early 

identification of harmful skin 

lesions among older people, 

especially men over 50 years 


Ensure adequate public information dissemination of the UV Index 

through the media and other settings to reach population sub-groups 

involved in activities and situations identified at high risk for UV 

radiation exposure 

Provide training and information to news agencies to support the 

widespread use of the UV Index 

Every three years implement a national survey of sun protection along 

the lines of the Victorian Sun Survey, involving telephone interviews 

about sun-related experiences over the previous weekend, and details of 

temperature, cloud cover and UV radiation levels 

Implement the Primary Schools and Early Childhood Survey nationally 

every three years 

Conduct a survey of incidence of non-melanoma skin cancer every five 

years: the next survey is due in 2007 

Undertake specific research and evaluation studies to: 

• evaluate skin cancer control strategies 

• increase the likelihood of long-term Australian Government investment 

in skin cancer prevention 

• gather more evidence relating to the economic evaluation of skin 

cancer prevention 

• lead national and international understanding of what works in 

relation to skin cancer prevention 

Provide support for the implementation of sun protection policies 

and practices by all childcare and pre-school centres across Australia 

in conjunction with local, state and territory and Commonwealth 

governments 

Ensure state and territory governments adopt sun protection policies 

and practices in all Australian primary schools: in most states and 

territories this will involve continued development and extension of the 

National SunSmart Schools Program in all primary schools 

Determine effective strategies and support their implementation to 

improve sun protection practices of students in secondary schools 

across Australia 

Encourage the adoption of shade provision and construction policies 

and building design standards by relevant areas of local, state and 

territory and Commonwealth governments 

Encourage the inclusion of sun protection policies and practices in all 

relevant industrial agreements 

Ensure the incorporation of specific provisions for sun protection 

practices into existing and future state and territory and Commonwealth 

occupational health and safety legislation 

Coordinate public relations activity and promotional material to educate 

people over 50 years about the importance of early detection



The safer operation and 

promotion of solariums 

Increased knowledge of skin 

cancer prevention strategies 

among key professional 

groups 

Effective coordinated 

policy development and 

implementation 

Increased knowledge and 

skills of medical practitioners 

in the early detection and 

treatment of melanoma 

References 

Ultraviolet radiation 

Encourage state and territory governments to implement and monitor 

legislation to control solarium operation and promotion 

Monitor compliance by the solarium industry to the guidelines issued by 

the Australian Competition and Consumer Commission (ACCC) and the 

AS/NZS 2635:2002 standard for solaria, and draw any non-compliance 

with the Trade Practices Act to the ACCC’s attention 

Encourage tertiary institutions to include information on sun exposure 

and sun protection in relevant education of childcare workers and 

teachers, medical practitioners, nurses and health professionals 

Develop and maintain evidence-based policy positions about the 

relationship between ultraviolet radiation and cancer to complement the 

Australian policy context 

Ensure effective and coordinated policy development and 

implementation to ensure existing policies reflect the best available 

evidence 

Encourage professional associations to increase GP skills in diagnosis 

of early skin cancer in order to avoid missed lesions and reduce 

unnecessary lesion removal through accredited training programs 

Encourage state and Commonwealth governments to increase access 

for all Australians to diagnostic and treatment services, particularly 

Australians in rural and remote areas 

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depletion. Cancer Forum (special edition) 20(3): 152–7. 

Armstrong BK 2004. How sun exposure causes skin cancer. In Prevention of skin cancer, eds DJ Hill, JM 

Elwood & DR English. Dordrecht: Kluwer Academic Publishers. 

Arthey S & Clarke VA 1995. Suntanning and sun protection: a review of the psychological literature. Soc Sci 

Med 40(2): 265–74. 

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——— 2006. Year book Australia, 2006. Cat. no. 1301.0. 

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Autier P 2004. Issues about solaria. In Prevention of skin cancer, eds DJ Hill, JM Elwood & DR English. 

Dordrecht: Kluwer Academic Publishers. 

Boniol M, Armstrong BK & Dore JF 2006. Variation in incidence and fatality of melanoma by season of 

diagnosis in new South Wales, Australia. Cancer Epidemiol Biomarkers Prev 15(3): 524–6. 

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317–43. 

Dobbinson S & Hill DJ 2004. Patterns and causes of sun exposing and sun protecting behaviour. In 

Prevention of skin cancer, eds DJ Hill, JM Elwood & DR English. Dordrecht: Kluwer Academic Publishers. 

Dobbinson S, Wakefield M & Sambell N 2006. Access to commercial indoor tanning facilities by adults with 

highly sensitive skin and by under-age youth: compliance tests at solarium centres in Melbourne, Australia. 

Eur J Cancer Prev. 15(5): 424–30. 

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McGraw-Hill Australia Pty Ltd. 

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271–83. 

Fox R 2001. A study into the development of suntanning centres (solariums) in Melbourne 1992–2001. 

Melbourne: The Cancer Council Victoria. 

Gallagher RP, Lee TK & Bajdik CD 2004. Sunscreens: can they prevent skin cancer? In Prevention of skin 

cancer, eds DJ Hill, JM Elwood & DR English. Dordrecht: Kluwer Academic Publishers. 

Gallagher RP, Spinelli JJ & Lee TK 2005. Tanning beds, sunlamps, and risk of cutaneous malignant 

melanoma. Cancer Epidemiol Biomarkers Prev 14(3): 562–6. 

Garland C, Shekelle RB, Barrett-Connor E, Criqui MH, Rossof AH & Paul O 1985. Dietary vitamin D and 

calcium and risk of colorectal cancer: a 19-year prospective study in men. Lancet 1(8424): 307–9. 

Garland CF, Comstock GW, Garland FC, Helsing KJ, Shaw EK & Gorham ED 1989. Serum 25-hydroxyvitamin 

D and colon cancer: eight-year prospective study. Lancet 2(8673): 1176–8. 

Giles GG & Thursfield V 2001. Trends in cancer mortality, Australia 1910–1999. Melbourne: The Cancer Council 

Victoria. 

Giovannucci E, Liu Y, Rimm EB, Hollis BW, Fuchs CS, Stampfer MJ & Willett WC 2006. Prospective study of 

predictors of vitamin D status and cancer incidence and mortality in men. J Natl Cancer Inst 98(7): 451–9. 

Glanz K, Saraiya M & Briss P 2004. Impact of intervention strategies to reduce UVR exposure. In Prevention of 

skin cancer, eds DJ Hill, JM Elwood & DR English. Dordrecht: Kluwer Academic Publishers. 

International Agency for Research in Cancer (IARC) 2000. Do sunscreens prevent skin cancer? Lyon: World 

Health Organization. 

Marks R, Foley PA, Jolley D, Knight KR, Harrison J & Thompson SC 1995. The effect of regular sunscreen 

use on vitamin D levels in an Australian population. Results of a randomized controlled trial. Arch Dermatol 

131(4): 415–21. 

Mermelstein RJ & Riesenberg LA 1992. Changing knowledge and attitudes about skin cancer risk factors in 

adolescents. Health Psychol 11(6): 371–6. 

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and 20 years of population-based campaigning. Health Educ Behav 28(3): 290–305. 

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Melbourne: NCCI. 

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149–52. 


Samanek AJ, Croager EJ, Gies P, Milne E, Prince R, McMichael AJ, Lucas RM & Slevin T 2006. Estimates of 

beneficial and harmful sun exposure times during the year for major Australian population centres. Med J 

Aust 184(7): 338–41. 

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Hill, JM Elwood & DR English. Dordrecht: Kluwer Academic Publishers. 

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learned? Radiat Prot Dosimetry 91(1–3): 303–6. 

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in Australia 1985–1995: are primary prevention programs starting to have an effect? Int J Cancer 78(2): 

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51 


N u t r i t i o n 

Introduction 


In Australia, more than 6000 deaths from cancer 

each year may be attributed to three major risk 

factors: inadequate intake of vegetables and fruit, 

inadequate physical activity, and overweight and 

obesity. 

The importance of food in the prevention of cancer is becoming increasingly recognised. 

International variation in cancer rates, combined with the diversity of eating patterns 

around the world, is the first line of evidence that food and nutrition play a role in cancer 

aetiology. In the past few decades, case–control studies, large prospective cohort studies 

and the use of meta-analyses have provided good evidence to support this link. As well, 

potential mechanisms of action of specific nutrition components have been identified in 

experimental studies. 

The study of the influence of nutrition on cancer is a complex area of research. 

Contributing to the complexity are obtaining accurate records of what and how much a 

person eats, determining the separate and/or combined effects of different foods on cancer 

risk, and the long timeframes between dietary exposure and development of disease. 

Despite these challenges, there is accumulating evidence to show certain foods and 

nutrients can either increase or decrease cancer risk. There is also convincing evidence 

that maintaining a healthy body weight can help to reduce cancer risk, and a healthy 

diet combined with sufficient physical activity is key to maintaining a healthy body 

weight. The recommended eating patterns for reducing cancer risk are consistent with 

recommendations for the prevention of cardiovascular disease and type 2 diabetes. Diets 

that include vegetables, fruit, grains and cereals (preferably wholegrain), and are low in 

fat (particularly saturated fat), salt and energy, support the prevention of all three of these 

chronic diseases. 

The remainder of this chapter summarises current national recommendations and 

population trends concerning food and nutrition. It should be read with the chapters on 

physical activity and overweight and obesity. Alcohol, while an aspect of diet, is dealt with 

in a separate chapter. 

The link between nutrition and cancer 

In recent years there have been four major reviews of the epidemiological literature linking 

nutrition and cancer: 

• 

• 

World Cancer Research Fund and American Institute for Cancer Research: Food, 

nutrition and the prevention of cancer: a global perspective (WCRF & AICR 1997) 

Committee on the Medical Aspects of the Food Supply, UK Department of Health: 

Nutritional aspects of the development of cancer (the ‘COMA report’) (UK Department of 

Health 1998)

• 

• 

World Health Organization and Food and Agriculture Organization: Diet, nutrition and the 

prevention of chronic diseases (WHO & FAO 2003) 

International Agency for Research on Cancer: IARC handbooks of cancer prevention 

volume 8: fruit and vegetables (IARC 2003). 

The updated report from the World Cancer Research Fund is due for release at the end of 

2007. 

An overview of the findings from these reports, plus more recent evidence, is summarised 

below. 

Fruit and vegetables 

Fruit and vegetables are recommended, for their important role as a low-energy-dense 

source of nutrients (vitamins, minerals, phytochemicals and fibre) and for their contribution 

to weight management, as well as for their probable cancer-protective effect exerted 

through a range of bioactive constituents which are plausible anti-cancer agents. 

The evidence supporting a protective effect of fruit and vegetables is strongest in relation 

to cancers of the digestive tract. Ensuring an adequate intake of fruit and vegetables is 

likely to reduce the risk of cancers of the oral cavity, oesophagus, stomach, colorectum and 

lung (IARC 2003). 

Over the last 10 years there has been a shifting of the evidence relating to the cancer 

protectiveness of fruit and vegetables, as outlined in the table below. While earlier reviews, 

which mostly relied on the evidence from case–control studies, concluded that fruit and 

vegetable consumption convincingly reduces the risk of cancers of the gastrointestinal 

tract, more recent prospective studies have not found results to support this (Michels et 

al. 2000; Bingham et al. 2003). It is generally believed that fruit and vegetables may help to 

indirectly protect against cancer by helping to maintain a healthy body weight. 


53 

N u t r i t i o n

Table 1.4 Conclusions of the major nutrition and cancer reports regarding the cancer-protective effect of 

vegetables and fruit 

Organisation review Highest evidence Moderate evidence Lower evidence 

WCRF & AICR 1997 Convincing 

Mouth 

Pharynx 

Oesophagus 

Stomach 

Colon 

Rectum 

Lung 

UK COMA 1998 Strongly consistent 

Oesophagus 


Probable 

Larynx 

Pancreas 

Breast 

Bladder 

Moderate association 

Stomach 

Colon 

Rectum 

WHO & FAO 2003 Probable 

Oral cavity 

Oesophagus 

Stomach 

Colorectum 

IARC 2003 Probable 

Oesophagus (fruit & 

vegetables) 

Stomach (fruit) 

Lung (fruit) 

Colon-rectum 

(vegetables) 

Source: Dixon et al. 2004 

Possible 

Ovaries 

Cervix 

Endometrium 

Thyroid 

Liver 

Prostate 

Kidney 

Weak 

Breast cancer 

Possible 

Mouth (fruit & 

vegetables) 

Pharynx (fruit & 

vegetables) 

Colon-rectum (fruit) 

Larynx (fruit & 

vegetables) 

Kidney (fruit & 

vegetables) 

Bladder (fruit) 

Stomach (vegetables) 

Lung (vegetables) 

Ovary (vegetables)

Fruit and vegetables contain an array of protective nutrients and phytochemicals. Despite 

many attempts, research has not identified which specific component of fruit or vegetables 

provides a cancer-protective effect. A recent review by IARC (2004) suggests cruciferous 

vegetables may be important because they contain substantial amounts of glucosinolates, 

which are hydrolysed to isothiocyanates and indoles. Experimental studies have shown 

that these compounds inhibit carcinogenesis, however these results have only been 

partially corroborated by epidemiological studies. It is generally agreed that there is 

inadequate evidence to suggest that the consumption of cruciferous vegetables or any 

one particular type of fruit or vegetable reduces the risk of cancer—consuming a variety of 

fruits and vegetables appears to be the most beneficial (WCRF & AICR 1997; IARC 2004). 

Fibre 

The current weight of evidence suggests a diet high in fibre could reduce colorectal cancer 

risk. The European Prospective Intervention into Cancer (EPIC) cohort study confirmed 

previous findings that high intakes of dietary fibre reduced the risk of colorectal cancer 

(WCRF & AICR 1997; Bingham et al. 2003). Such diets are high in fibre from a range of 

sources including wholegrain cereals, fruits and vegetables. 

Meat 

Research suggests that high red meat consumption, and in particular processed meat 

consumption, is associated with an increase in colorectal cancer risk (Norat et al. 

2002; Sandhu, White & McPherson 2001). An Australian cohort study has identified an 

association between red meat and increased risk of rectal cancer (English et al. 2004). 

There has been some inconsistency in the evidence, which may be related to issues 

such as the definition of red meat or control of confounding factors such as other related 

aspects of diet (fat, low vegetable intake, etc.), but overall results, including findings from 

the EPIC cohort study (Norat et al. 2005), support a modest increase in risk. 

Some research suggests that eating burnt or charred meat may increase cancer risk; 

however, the evidence is not conclusive (Norat & Riboli 2001). 

Fish 

Experimental studies have shown that omega-3 fatty acids influence cancer development 

by lowering inflammation (Rose & Connolly 1999). Fish is a good dietary source of omega- 

3 fatty acids. Some epidemiological studies show that higher intakes of fish and/or omega- 

3 fatty acids may reduce the risk of developing colorectal cancer and hormone-dependent 

cancers such as breast and prostate cancer, but this research can only be described as 

suggestive not conclusive (Ralph et al. 2006). 

Dietary fat 

There has been a great deal of interest in the possible association between fat and cancer. 

The World Cancer Research Fund report concluded that total fat possibly increased risk of 

cancer of the lung, colon, rectum, breast and prostate (WCRF & AICR 1997), although the 

UK review did not find sufficient evidence to make any recommendations about fat and 

cancer (UK Department of Health 1998). 

Current evidence does not indicate a direct link between fat intake and cancer at any site 

(Kushi & Giovannucci 2002; Willett 1998). As foods high in fat have a high energy density, 

diets high in fat can contribute to obesity (NHMRC 2003a), and obesity is a risk factor for 

several cancers (IARC Working Group 2002). 


55 

N u t r i t i o n

It may be possible that different types of fat affect cancer differently, as some studies have 

suggested that omega-3 fatty acids may reduce the risk of developing colorectal, breast 

and prostate cancer (Ralph et al. 2006). 

Salt 

Diets high in salted foods have been linked to an increased risk of stomach cancer (WCRF 

& AICR 1997). The evidence for an increased incidence of stomach cancer in association 

with high-salt diets comes from countries where salting of foods (meats) is a common 

preserving method. Ecological research has shown that in countries where refrigeration is 

commonly used for storage of perishable forms of food, stomach cancer has a relatively 

low incidence (Cohen & Roe 1997; Roder 2002). 

Dietary supplements 

Certain foods that are rich in micronutrients and phytochemicals may play a role in 

cancer prevention. Micronutrients include vitamins (e.g. folate, beta-carotene, vitamins 

C and E) and minerals (e.g. selenium, calcium). Some biologically active substances or 

phytochemicals (e.g. lycopenes, indoles and allicin) have been investigated for cancer 

protective properties. 

Much of the evidence for dietary supplements is derived from experimental studies and 

not properly conducted clinical trials. However the results from the large-scale randomised 

controlled trials on the efficacy of dietary supplements to reduce the risk of cancer have 

been disappointing. For example, the Alpha-Tocopherol, Beta-Carotene Cancer (ATBC) 

Prevention Trial and Beta-Carotene and Retinol Efficacy Trial (CARET) both showed 

increased risk of certain cancers and mortality with supplementation (Bowen et al. 2003; 

Leppala et al. 2000; Smigel 1996). 

Any diet–cancer association is far more complex than simply supplementing the diet with 

micronutrients. Micronutrients ingested in supplement form are often pharmacologically 

active, and contain much higher doses than the level of micronutrients someone would 

receive in a typical diet. It seems to be the combination and interaction of nutrients and 

phytochemicals found together in whole foods that helps reduce the risk of chronic 

diseases (WCRF & AICR 1997). The use of supplements in place of a well-balanced diet is 

generally not recommended (WCRF & AICR 1997). However some randomised controlled 

trials of calcium supplements have shown some potential for lowering the risk of bowel 

polyps and cancer (Weingarten, Zalmanovici & Yaphe 2005). 

Selenium 

Some studies suggest that selenium may be inversely associated with prostate cancer 

and colorectal cancer, but most of this evidence comes from trials designed to answer 

questions about other types of cancer (Clark et al. 1996; Duffield-Lillico, Dalkin et al. 2003; 

Duffield-Lillico, Slate et al. 2003). The evidence of a protective role of selenium in other 

types of cancers is weak and inconsistent (Duffield-Lillico et al. 2002; WCRF & AICR 1997; 

WHO & FAO 2003). The true effects of selenium require confirmation in independent 

trials before new public health recommendations regarding selenium (either from dietary 

sources or as supplements) can be made (Combs 2005). The Selenium and Vitamin E 

Cancer Prevention Trial (SELECT) will determine if selenium supplements can protect 

against prostate cancer. However the results of this trial will not be available until 2012. 


The impact 

On a global basis and at current rates, appropriate nutrition and physical activity may 

prevent three to four million cases of cancer every year (WCRF & AICR 1997). In Australia, 

more than 6000 deaths from cancer each year may be attributed to three major risk factors: 

inadequate intake of vegetables and fruit, inadequate physical activity, and overweight and 

obesity (Mathers, Vos & Stevenson 1999). These risk factors, through their contribution 

to development of cancer alone, are estimated to contribute 3.8% of the total burden of 

disease and injury in Australia. Inadequate vegetable and fruit intake has been estimated 

to cause 11% of the total cancer burden (Mathers, Vos & Stevenson 1999) and 1.4% of the 

total burden of disease in Australia (AIHW 2006). 

In Australia, the direct cost of poor diet to the Australian health care system (that is 

hospitals, medical expenses, allied health professional services, pharmaceutical expenses 

and nursing homes) has been estimated to be in the order of $1.5 billion per year. This 

increases to $2.2 billion when indirect costs such as low productivity are included (Lester 

1994; Mathers, Vos & Stevenson 1999). 

Costs associated with some diet-related cancer have been estimated at $61 million 

(1989−90 figures) in direct costs, and $132 million in indirect costs (Crowley et al. 1992). 

Increasing average vegetable consumption by one serve/day has been estimated to save 

$24.4 million per year from the cost of colorectal, breast, lung and prostate cancers, 

and increasing average fruit consumption by one serve/day could save $8.6 million per 

year from the costs of breast and lung cancers (Marks et al. 2001). This same report also 

estimated that consuming more than one serve of red meat per day accounted for $8.6 

million of the total health system cost for colorectal cancer (Marks et al. 2001). Increasing 

fruit and vegetable consumption by one serve a day per person would result in direct 

health care savings of $180 million a year (Marks et al. 2001). These figures are based on 

consumption patterns from the 1995 National Nutrition Survey and a meta-analysis of the 

diet–cancer relationship conducted in 2001, and therefore may not truly reflect the current 

situation. 

The challenge 

A number of surveys have documented that Australians have below-optimum eating 

habits to protect them against overweight, obesity and cancer risk (and other chronic 

diseases such as cardiovascular disease and diabetes). The 1983, 1985 and 1995 National 

Nutrition Surveys (ABS & CDHAC 1997) and the Australian Bureau of Statistics’ Apparent 

Consumption of Foodstuffs and Nutrients (ABS 2000) data provide an indication of dietary 

intakes in Australia. State-based dietary surveys have also been conducted, for example in 

Western Australia (Miller & Kose 1996; Hands et al. 2004), Victoria (CSIRO 1993; Catford 

2002), and New South Wales (Bauman et al. 2003) 

Currently the Australian population does not consume the recommended levels of most 

key dietary items, such as vegetables, fruit and wholegrain cereals. Recent trends are 

shown in the table below. Over the last 20 years it appears that wholegrain cereal food 

intake has increased, but it is still not at recommended levels. Fat intake has reduced, but 

is still not low enough, particularly saturated fats. Consumption of vegetables and fruit is 

too low, particularly among children. 


5 

N u t r i t i o n

Table 1.5 Current trends in consumption and the proportion of the population not consuming 

recommended levels of specific foods related to cancer risk 

Dietary factor 

related to 

cancer risk 

Vegetable 

intake 

NHMRC 

recommended levels 

of consumption 

(NHMRC 2003 a & b) 

Adults: average of 5 

serves per day 

Children and 

adolescents: minimum 

of 2 to 4 serves a day 

depending on age 

(CDHFS 1998) 

Fruit intake Adults: average of 2 


Children and 

adolescents: between 

1 and 3 serves a day 


Cereal, bread, 

pasta intake 

Adult men: 5−12 


Adult women: 4−9 


Children and 

adolescents: 3−11 

serves per day, 


Meat intake Moderate serve of 

meat: 65−100 g of 

cooked red meat, 3−4 

times a week (CDHFS 

1998) 

Children and 

adolescents 

½–1 serve per day 


(CDHRS 1998) 


Trend in consumption Proportion NOT meeting 

minimum levels of 

consumption in 1995 

Decline in consumption 

in both adults and 

children 1983−95 (Cook, 

Rutishauser & Seelig 

2001) 

Decline in consumption 

in both adults and 



2001) 

Slight decline in adults 

eating cereal foods on 

day of survey 1983−95 

(Cook, Rutishauser & 

Seelig 2001) 

No significant change in 



2001) BUT significant 

increase in mean intake 

of less healthy cerealbased 

products (e.g. 

cakes, pies, biscuits) 

1985−95 

No change in adult 

men, declined in 

women 1983−95 (Cook, 


2001) 

Slight rise in children’s 

mean intake 1983−95 

(Cook, Rutishauser & 

Seelig 2001) 

Adults: 2 in 3 did not meet the 

recommended daily intake for 

vegetables (Magarey, McKean & 

Daniels 2006) 

Children: 2 in 3 did not meet the 

recommended daily intake for 

vegetables (Magarey, Daniels & 

Smith 2001) 

Adults: 2 in 3 did not meet 

the recommended daily intake 

for fruit (Magarey, McKean & 

Daniels 2006) 

Children: More than half did not 

meet the recommended daily 

intake for fruit (Magarey, Daniels 

& Smith 2001) 

Adults: 2 in 3 men and 4 

in 5 women did not meet 

recommended levels on day of 

survey (NHMRC 2003a) 

5% of men and 4% of women did 

not eat a cereal product on the 

day of the survey (McLennan & 

Podger 1998) 

Children:

Dietary factor 

related to 

cancer risk 

Dietary fat 

intake 

NHMRC 

recommended levels 

of consumption 

(NHMRC 2003 a & b) 

Adults: total fat about 

30% of total energy 

intake: maximum of 


intake from saturated 

fat 

Children and 

adolescents: total 

fat about 30−50% of 

total energy intake 

(depending on age). 

Over 5 years saturated 

fat at maximum of 


intake 

Salt intake Maximum level of 

2300 mg/day: this 

includes sodium in 

food as well as that 

added in cooking or 

consumption 

Sugar intake < 10% of energy. This 

includes all sugars 

added to foods by the 

manufacturer, cook or 

consumer, plus sugars 

naturally present in 

honey, syrups and fruit 

juices (WHO & FAO 

2003) 

Trend in consumption Proportion NOT meeting 

minimum levels of 

consumption in 1995 

Adults: significant 

decline (a positive trend) 

in mean intake of total 

fats 1983−95 (Cook, 


2001) 

Children: no significant 

change in total fat 

intake 1983−95 (Cook, 


2001) 

No national trend data 

available 

No national trend data 

available 

Adults & children: mean total 

fat intake and saturated fat 

intake on day of survey slightly 

exceeded recommended levels 

(McLennan & Podger 1998; 

Marks et al. 2001) 

Adults: 1993 national data 

indicate mean sodium intake 

higher than recommended levels 

(Baghurst et al. 1996) 

Children: no data available 

(NHMRC 2003b) 

Adults: no data available 

Children: Mean daily intake 

ranged from 7–15% of energy 

in girls and 8–14% of energy in 

boys (Somerset 2003) 

Table adapted from data presented in Body weight, nutrition, alcohol and physical activity: key messages for The Cancer 

Council Australia by Dixon et al. 2004. The interested reader is referred to this document for greater detail. 

Specific population groups 

Certain population groups have significantly poorer nutrition and are at higher risk of 

nutrition-related disease, principally cardiovascular disease and type 2 diabetes (AIHW 

2006). The clustering of poor nutrition (both under- and over-nutrition) with smoking, 

physical inactivity, lower levels of education and income, and low socio-economic status 

signal the need to develop effective interventions targeting these population groups. 

Aboriginal and Torres Strait Islander people are particularly at risk, along with residents 

in remote areas of Australia and those living on low incomes (SIGNAL 2001; Woods, 

Swinburn & Burns 2003). This clustering presents a complex challenge for addressing 

nutrition related issues (NATSI Working Party 2001). 


There is mounting evidence about the nature of effective nutrition interventions. Overall the 

findings from the literature suggest that diet-related interventions can be effective when 

they are multi-focused and sustainable and involve individual and structural change and 


5 

N u t r i t i o n

key stakeholders (Sorensen et al. 1998; Syme 1997; Gill, King & Webb 2005; Thomas et al. 

2004; Sahay et al. 2006). 

This section focuses on interventions that aim to increase consumption of specific foods 

such as vegetables and fruit and that support dietary modification or healthy eating 

generally. 

Educational interventions focus on changing knowledge, attitudes, skills or the behaviour 

of individuals. Environmental interventions create opportunities or remove barriers for 

groups of people. With environmental interventions, the emphasis to change health 

behaviour moves from the individual to the society that facilitates the unhealthy behaviour. 

In the case of nutrition, educational interventions attempt to influence the individual 

demand for certain foods such as soft drinks or high fat food. Environmental interventions 

attempt to influence the supply of food (e.g. removing soft drinks from vending machines, 

increasing fruit and vegetable choices at school canteens or cafeterias). 

The US Agency for Healthcare Research and Quality reviewed 92 studies of behavioural 

interventions to promote dietary change considered relevant to cancer risk (AHRQ 2000). 

In summary, behavioural interventions to increase the intake of fruits and vegetables and 

to decrease intake of total fat and saturated fat were assessed as successful, although 

child- and adult-focused interventions varied in efficacy. Interventions were more 

effective in increasing fruit intake among children and vegetable intake among adults, 

and more successful at reducing total fat intake of children rather than adults. In contrast, 

interventions with children were less successful than with adults at reducing saturated fat 

intake. 

Another review, which focused on behavioural interventions to modify fruit and vegetable 

intake, found that more than three-quarters of the identified studies reported significant 

increases in fruit and vegetable intake, with an average increase of 0.6 servings/day 

(Ammerman et al. 2002). Interventions appeared to be more successful at positively 

changing dietary behaviour among populations at risk of diseases than among general 

healthy populations. Goal setting and the use of small groups seemed to be particularly 

promising strategies (Ammerman et al. 2002). Elements of effective interventions include 

theoretical basis, family involvement, participatory planning and implementation models, 

clear messages, and adequate training and ongoing support for health professionals (Sahay 

et al. 2006; Ammerman et al. 2002) 

A review of environmental interventions to improve nutrition in children and young people 

found that multi-component interventions including an education and environmental 

component directed at improving nutrition were most effective, and that children’s 

nutritional intake can be modified when their food source is modified (Thomas et al. 2004). 

For primary school and high school students, multifaceted interventions (school curricula, 

mass media, parent mailings, cafeteria changes) over at least eight to 10 weeks show the 

most promise for altering food intake (Thomas et al. 2004). Educational messages targeted 

to behaviour change (as opposed to knowledge acquisition) and to specific behaviours 

(increase fruit intake, reduce fat intake as opposed to general nutritional changes) are more 

successful in changing food behaviours (Thomas et al. 2004). 

Reviews of population-based diet interventions have emphasised the need to address 

policies that promote structural change and include community involvement in identifying 

priorities and interventions (Sorensen et al. 1998; Syme 1997; Gill, King & Webb 2005; 

Thomas et al. 2004). Less successful interventions fail to address theories and mediating 

variables in behaviour change (AHRQ 2000). 

Further work needs to be done on the cost-effectiveness of interventions. 


National and statewide nutrition promotions 

Examples of comprehensive approaches to cancer prevention through modification of diet 

and/or physical activity are limited. In 1991, the US National Cancer Institute launched 

the 5-a-Day for Better Health Program, a national, population-based nutrition initiative 

to prevent cancer (Heimendinger et al. 1996). The program was a partnership between 

the National Cancer Institute and the vegetable and fruit industry and had multi-strategy, 

multi-setting, multi-level and intersectoral components. Evaluation results indicate that 

the campaign raised public awareness that vegetables and fruit help reduce cancer risk, 

increased vegetable consumption and created an ongoing partnership between health and 

agribusiness (Foerster et al. 1995). 

In Australia, there have been several statewide campaigns aimed at promoting increased 

consumption of vegetables and fruit (e.g. the ‘Go for 2&5’ campaign, Western Australia 

2001–2003; Fruit ‘ n’ Veg with Every Meal, Western Australia 1989–93 and South Australia 

1990–91; 2 fruit and 5 Vegetables Every Day, Western Australia 1989–93 and Victoria 

1992–95; and Eat Well, Tasmania 1997), although these campaigns did not have a specific 

cancer prevention focus. 

Such campaigns use social marketing strategies to increase public awareness of 

dietary recommendations for fruit and vegetable consumption and ultimately increase 

consumption. Where available, evaluation shows these campaigns succeeded in promoting 

increased awareness, improved public attitudes to fruit and vegetable consumption, and 

increased knowledge of the recommended number of serves of fruit and vegetables. 

Campaigns sustained for a number of years (e.g. Victoria and Western Australia) increased 

reported vegetable and fruit consumption (Dixon et al. 1998; Ejlak, Seal & van Vaetzen 

1998; Miller, Pollard & Paterson 1996; Nutrition & Physical Activity Branch 2005). The ‘Go 

for 2&5’ campaign in Western Australia resulted in behavioural changes and in the period 

2000 to 2003, fruit intake among WA adults increased from 1.6 serves to 2.1 serves while 

vegetable intake increased from 2.6 serves to 2.9 serves (Nutrition & Physical Activity 

Branch 2005) 

Thus, while the evidence is not sufficiently long term, there is general acceptance that a 

comprehensive public health program can encourage healthy eating. Such an approach 

should encompass education and training, personal health services, mass media, 

community action, organisational development, environmental support and economic and 

regulatory measures. 

Specific cancer prevention interventions 

There have been some cancer prevention intervention trials that have examined the 

effectiveness of various dietary changes to prevent cancer or cancer precursors (such 

as adenomatous polyps). Generally the results from large-scale randomised controlled 

trials on the efficacy of dietary supplements to reduce the risk of cancer have been 

disappointing. For example, the Alpha-Tocopherol, Beta-Carotene Cancer (ATBC) Prevention 

Trial and Beta-Carotene and Retinol Efficacy Trial (CARET) both showed increased risk of 

lung cancer and mortality (Bowen et al. 2003; Leppala et al. 2000; Smigel 1996). 

The Cochrane Database of Systematic Reviews have concluded that a daily intake of 1 g 

of dietary calcium may have a moderate protective effect on the development of colorectal 

adenomatous polyps, although this result is only based on two well conducted randomised 

controlled trails (Weingarten, Zalmanovici & Yaphe 2005). Dietary interventions to increase 

fibre have not shown a statistically significant reduction in the risk of colorectal cancer 

(Asano & McLeod 2002). 


1 

N u t r i t i o n

A large scale randomised controlled trial, the Women’s Health Initiative, randomised 

women to a very low fat diet intervention or a usual fat diet (Prentice et al. 2006). Women 

on the low fat diet had a 9% lower incidence of breast cancer compared with the control 

group, but this result was not statistically significant. However in sub-group analyses, 

breast cancer rates were reduced by 22% among women who started with the highest 

fat intake (>37% energy from fat) and reduced their fat the most (to 24% after one year) 

(Stein 2006). Interestingly, there was suggestive evidence that the low fat diet had a more 

protective effect against oestrogen receptor positive breast cancer. Despite the lack of an 

apparent effect on colorectal cancer, adenomas were significantly reduced among the low 

fat diet group (Stein 2006). 

In terms of dietary interventions for cancer survivors, there are only a few successful trials 

that suggest that there is hopeful progress in this area. A systematic review of 59 diet 

interventions for cancer patients and survivors (mostly with breast cancer) found nonstatistically 

significant improvements in overall survival and survival from cancer (Davies 

et al. 2006). Most of the included studies in the review were too small and only provided 

limited data. A large randomised controlled trial, known as the Women’s Intervention in 

Nutrition Study, found that the intervention group who decreased their dietary fat intake 

had a lower risk of recurrence of breast cancer (Chlebowski et al. 2005). 

General practice 

The role of general practice in chronic disease prevention is potentially important, given 

that 86% of the population have at least one visit to the general practitioner every year 

(RACGP 2005). 

A review of primary care interventions found that moderate- or high-intensity counselling 

interventions, including the use of interactive health communication tools, can reduce 

consumption of saturated fat and increase intake of fruit and vegetables. Brief counselling 

of unselected patients by primary care providers appears to produce small changes in 

dietary behaviour, but its effect on health outcomes is unclear (Pignone et al. 2003; Steptoe 

et al. 2003). 

The Royal Australian College of General Practitioners has produced three significant 

publications relating to the role of general practice and nutrition. The first, Guidelines for 

preventive activities in general practice (the ‘red book’) (RACGP 2005), focuses on the 

role of the GP within the consultation, recommending that all adult patients should be 

advised to follow the National Health and Medical Research Council’s Dietary guidelines for 

Australian adults. (Nutrition advice for children should be based on the National Health and 

Medical Research Council’s Dietary guidelines for children and adolescents in Australia.) 

Nutrition advice should be given at two-yearly intervals for adults and on every visit for 

children. Their more specific publication: SNAP: A population health guide to behavioural 

risk factors in general practice (RACGP 2004) provides more extensive information and 

recommendations regarding healthy nutrition (among other common lifestyle risk factors), 

focusing on a patient education and behaviour modification approach based upon the 

5As (ask, assess, advise, assist, arrange). Lastly, their publication Putting prevention into 

practice: guidelines for the implementation of prevention in the general practice setting (the 

‘green book’) (RACGP 2006) assists in developing systems in general practice to support 

prevention activities at the practice and consultation levels. 

In further support of the GP’s role in promoting good nutrition and obesity prevention, 

the Commonwealth Department of Health and Ageing, in the 2003/04 budget, funded 

the Lifestyle Prescriptions program (commonly known as Lifescripts). Lifescripts is 

being implemented through local divisions of general practice, promoting risk factor 

management in general practice and primary health care services. Lifestyle prescriptions 


are tools for GPs to use when providing lifestyle advice to patients. Advice may be about 

quitting smoking, increasing physical activity, eating a healthier diet, maintaining healthy 

weight, reducing alcohol consumption, or a combination of these. 


Commonwealth, state and territory governments are becoming increasingly aware of the 

importance of healthy eating in the face of increasing trends to overweight and obesity 

among younger and adult Australians. This has resulted in a number of national strategic 

agendas including: 

• 

• 

• 

• 

Healthy weight 2008, Australia’s future. The national action agenda for children and 

young people and their families (NOTF 2003). 

The Eat Well Australia approach under the SIGNAL National Public Health Partnership 

(now disbanded), which developed two key action plans: An agenda for action for 

public health nutrition 2000–2010 (SIGNAL 2001), which seeks to set the agenda for 

and reflect national and state action on nutrition; and the National Aboriginal and Torres 

Strait Islander nutrition strategy and action plan 2000–2010 (SIGNAL 2001), which sets 

a framework for action to respond to the significant diet-related illness experienced by 

these Australians. 

The Food Standards Code: food standards and regulation fall under the domain of 

the statutory authority Food Standards Australia New Zealand. This authority has 

responsibility for setting standards for the production and sale of food in Australia, 

including food labelling issues such as nutrition and health claims. 

Children’s Television Standards: in Australia, food marketing operates under a system 

of co-regulation, with the Australian Communications and Media Authority having 

responsibility for the Children’s Television Standards, which has some regulations 

for limiting television food advertising to children. The Advertising Standards Bureau 

administers the industry Codes of Practice developed by Free TV Australia and the 

Australian Association of National Advertisers, which add very little to the statutory 

regulations. 

Several state and territory governments have taken steps to mirror or complement the 

Eat Well Australia approach, and there is clearly greater recognition of the importance of 

having a focus on healthy eating and physical activity as part of obesity and associated 

disease prevention (DHS 1997; Northern Territory Government 2001; Queensland Public 

Health Forum 2002; NSW Health 2002). 

The key challenge now is to move beyond framework development and strategy setting 

into comprehensive program implementation. 

Two key documents frame the international policy context around nutrition and cancer 

prevention: 

• 

The World Health Organization Global strategy on diet, physical activity and health 

was developed through a series of consultations with stakeholders in response to a 

request from Member States at the 2002 World Health Assembly. This preventionbased 

strategy aims to ‘reduce the risk of chronic non-communicable diseases across 

populations by addressing two of the main risk factors, diet and physical activity, 

through comprehensive, multi-sectoral interventions’ (WHO 2004). 


3 

N u t r i t i o n

• 

The International Union Against Cancer’s Evidence-based cancer prevention: strategies 

for NGOs highlights the need for policy and legislation as part of a multifaceted 

approach to improve the nutritional health of populations and individuals (UICC 2004). 

Existing recommendations 

In general, diet and nutrition recommendations to reduce cancer risk are consistent with 

the recommendations of Australian Government health authorities about healthy eating 

patterns. The Cancer Council Australia endorses the National Health and Medical Research 

Council Dietary guidelines for Australian adults (NHMRC 2003a), for older Australians 

(NHMRC 1999), and for children and adolescents (NHMRC 2003b) and concurs with the 

levels of intake of specific food groups recommended by the Australian guide to healthy 

eating (CDHFS 1998) and Nutrient reference values (NHMRC 2005). 

The Cancer Council also acknowledges that its healthy eating recommendations are 

consistent with those of other chronic disease prevention groups, such as the National 

Heart Foundation (NHF 2002), with the exception that current research suggests that 

limiting alcohol consumption would help prevent cancer. 

Aims 

Our aims are to encourage the Australian population to: 

• 

• 

• 

consume nutritionally adequate and varied diets based primarily on foods of plant origin 

such as vegetables, fruit, pulses and wholegrain cereals, as well as lean meats, fish and 

low fat dairy products 

ensure children have a nutritionally adequate and varied diet along similar lines with 

appropriate moderation to suit different age groups 

maintain a healthy body weight through a balance of food intake and physical activity. 

The Cancer Council believes that a national and related state-based comprehensive public 

health program is required. Such a program would have an overweight and obesity 

focus that would incorporate healthy eating and physical activity with a chronic disease 

prevention focus encompassing cancer, diabetes and cardiovascular disease. This would 

require collaboration between key organisations in the government, non-government, 

medical, education, consumer, media and commercial sectors. 



Increased awareness of the 

link between nutrition and 

cancer among the general 

public and key health 

professional groups 





Monitor and clarify best evidence on the relationship between nutrition 

and cancer causation 

Ensure key messages are promoted to the public and relevant 

health professionals in publications, presentations, programs, media 

statements and where opportunities arise 

Promote and/or develop complementary primary health resources, 

specifically for general practice, to improve evidence-based 

interventions by health professionals 


relationship between nutrition and cancer to complement the 



implementation




that promote healthy eating 


monitor epidemiological trends 



More supportive environments 

that assist people to make 

healthy food choices 

An increased capacity to know 

what works in relation to 

program delivery 

Advocate for nationwide social marketing campaigns, that promote 

healthy eating across the life course, which are coordinated, 

sustainable and far reaching, 

Encourage the Australian, state and territory Governments to commit to 

long-term investment in promoting healthy eating 

Support and deliver effective community interventions at a local and 

state level to address healthy eating 

Support and conduct high quality epidemiological research further 

clarifying the relationship between nutrition and cancer 

Support and conduct high-quality behavioural research further 

clarifying the barriers and enabling factors for people to adopt healthy 

eating 

Work towards a better understanding of the determinants of the 

obesogenic environment, to inform policy development 

Encourage the Australian Government to fund a comprehensive 

National Nutrition and Physical Activity Survey of both children and 

adults, which is conducted, as a minimum on a regular five-year basis 

Encourage the Australian Government to address the broader social 

and environmental determinants of poor nutrition, in particular: 

• call for a ban of television food advertising to children 

• develop effective regulatory systems for decreasing the level of food 

marketing to children (including television food advertising and other 

forms of food marketing) 

• improved access to healthy food choices for people who are socially 

or geographically disadvantaged 

• develop effective regulatory systems for communicating accurate 

nutrition and health information on food labels 

• improve health literacy for reading food labels 

Continue to support and promote the Parents Jury 

Participate on the Coalition on Food Advertising to Children 

Coordinate public health responses to relevant food regulatory issues, 

including changes to food labelling, through participation on the 

Coalition on a Healthy Australian Food Supply 


• evaluate healthy eating interventions 

• gather more evidence relating to the economic evaluation of cancer 

prevention 

• lead national understanding of what works in relation to cancer 

prevention 

• identify barriers and enabling factors for implementation of these 

recommendations in general practice and other health settings 

Note: Refer also to the action plans of the physical activity and obesity chapters when considering promotion of nutrition. 


5 

N u t r i t i o n

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P h y s i c a l a c t i v i t y 

Introduction 

Less than half of the Australian adult population 

achieves the current recommended levels of 150 

minutes a week of moderate-intensity physical 

activity and less than one-third achieves the higher 

level of 60 minutes a day estimated to reduce colon 

cancer risk (Cerin et al. 2005). 

The study of physical inactivity as a risk factor for chronic disease commenced in the 1950s 

and focused on the epidemic of cardiovascular disease in Western countries. A pivotal 

review highlighted the public health benefits of regular physical activity (Pate et al. 1995). 

This was followed by the US Surgeon General’s report, Physical activity and health, which 

summarised the scientific evidence for the health benefits of physical activity (USDHHS 

1996). More recently an Australian review has confirmed the dose–response relationship 

between physical activity and better health outcomes, specifically all-cause mortality, 

cardiovascular disease, stroke, some cancers, type 2 diabetes, depression and obesity 

(Bull, Bauman et al. 2004). In addition to the reduction in chronic disease risk, it is clear 

that physical activity provides age-specific benefits over a person’s life (Bull, Bauman et al. 

2004). 

Research on the link between levels of physical activity and specific cancers began during 

the 1980s but has increased rapidly over the last decade. Not surprisingly, the most 

commonly occurring cancers in men (prostate, lung, colorectal) and in women (breast, 

lung, colorectal) have been the subject of most published epidemiological studies. Recent 

reviews of physical activity and cancer have identified several hundred relevant studies 

(Friedenreich & Orenstein 2002; IARC Working Group 2002; Lee 2003; McTiernan 2003; 

Bull, Bauman et al. 2004; Gotay 2005). However, the majority of studies are observational 

rather than interventional (McTiernan 2003). More intervention studies are required to 

determine the optimal physical activity ‘dose’ for cancer prevention (McTiernan 2003). 

The strongest evidence is for two of the most common cancers: breast cancer and colon 

cancer. It is also suggested that regular physical activity is associated with a reduction in 

all-cancer morbidity and mortality (Bull, Bauman et al. 2004); however this is likely to be 

due to the effect of exercise on breast and colon cancer. Whether physical activity reduces 

the risk of other cancers, including rectal, endometrial, prostate, testicular, kidney and lung 

cancer, remains less certain due to limited and inconclusive data (IARC Working Group 

2002; Lee 2003). This remains an active area of research internationally. 

Physical activity (along with nutrition) contributes to weight control by contributing to 

energy balance. Overweight and obesity have been associated with an increased risk of 

several cancers. It is clear that physical activity protects against cancer independently 

of its contribution to weight control. Overweight and obesity and physical inactivity are 

independent risk factors for cancer (Thune & Furberg 2001; Friedenreich & Orenstein 2002; 

IARC Working Group 2002; McTiernan et al. 2003). 

More recently, physical activity and physical fitness have been shown to be beneficial to 

cancer patients. Despite being a relatively new area of research, physical activity before, 

during and after treatment is consistently showing a positive association with cancer 

outcomes (Courneya 2003). 


1 

P h y s i c a l a c t i v i t y

How physical activity is measured 

Understanding the ‘dose’ required 

The epidemiological research investigating the contribution of physical inactivity to 

chronic disease, including cancers, is complicated by the complexities of physical activity 

assessment protocols in population-based research (Shephard 2003). 

Physical activity is often classified by type. The type, or mode, of physical activity relates 

to the specific activity being performed (AIHW 2003). Broadly speaking, the three types of 

physical activity are aerobic, resistance and flexibility. Many activities cross more than one 

type, for example gymnastics has an aerobic, flexibility and resistance component (Whaley 

2006). 

Aerobic activities are assessed in terms of energy expenditure, which is a function of 

intensity, duration and frequency of activity. Intensity is a measure of how hard an activity 

is, duration is the time spent doing the activity and frequency is how many times, usually in 

a week, the activity is done (AIHW 2003). 

In research, energy expenditure is often calculated in metabolic equivalents (METs). MET 

values are multiples of the resting metabolic rate (RMR), that is, 1 MET is the energy used 

when sitting quietly. One MET is equivalent to an oxygen uptake of 3.5 mL.kg-1.min-1 or to 

a caloric value of 1 kcal.kg-1.hr-1 (4.184 kilojoules per kilogram per hour) (Ainsworth et al. 

2000). 

Table 1.6 Examples of activities and MET intensities 

METs Activity Examples 

1.0 Inactivity, quiet Sitting quietly and watching television 

3.5 Walking Walking for pleasure 

8.0 Bicycling Bicycling, 19–24 km/h, leisure, moderate 

8.0 Water activities Swimming, crawl, slow (50 m/min), moderate or light 

effort 

12.5 Running Running, 12 km/h (5 min/km) 

Source: Ainsworth et al. 2000 

More commonly the frequency, intensity and duration of physical activity are expressed 

separately, or frequency and duration are aggregated to give a total time (in minutes) per 

week. Activities are grouped according to intensity, for ease of use. 

• 

• 

Vigorous-intensity activity makes a person short of breath or ‘puff and pant’ (i.e. 7-9 

METs). 

Moderate-intensity activity is when it is still possible to hold a conversation (i.e. 3-4 

METs). 

• 

Walking includes for recreation, transport or exercise. 

(Ainsworth et al. 2000) 

Total activity time per week is used to assess whether an individual has completed 

sufficient physical activity for a health benefit (see next table). To account for the greater 

intensity, time spent in vigorous-intensity activity is weighted by a factor of two (that is, 

doubled) when calculating the total activity time per week. 


Table 1.7 Definitions of sufficient and insufficient physical activity and sedentary 

Term Definition 

Sufficient The accumulation of at least 150 minutes of activity over one week in at 

least five sessions. 

Insufficient The accumulation of some activity but less than 150 minutes of activity 

per week. 

Sedentary No activity reported over the week. 

Source: AIHW 2003 

Recall of participation is a known difficulty in the assessment of physical activity. Vigorous 

intensity activity is generally reported better than moderate intensity activity (Slattery and 

Jacobs 1995). Misclassification of moderate intensity activities would decrease the ability 

to detect a real association (IARC Working Group 2002). 

The link between physical activity and cancer 

The role of physical activity in the prevention of specific cancers continues to be an 

active area of research and review (Lee 2003; McTiernan 2003; Roberts & Barnard 2005; 

Warburton, Nicol & Bredin 2006). 

For the 2002 World Health Report, the World Health Organization systematically reviewed 

the evidence on breast and colon cancer (WHO 2002; Bull, Armstrong et al. 2004). In 

the same year, the International Agency for Research on Cancer (IARC) published its 

report, Weight control and physical activity, which included a comprehensive review of the 

epidemiological evidence relating to all cancers (IARC Working Group 2002). In 2003, The 

Cancer Council commissioned a review of the epidemiological literature linking physical 

activity and specific cancers (Bauman, Habibullah & Holford 2003), which is summarised 

in Getting Australia active II (Bull, Bauman et al. 2004). In the same year, Lee reviewed the 

epidemiological evidence for the major cancer sites: breast, colon, rectum, prostate and 

lung. Overall the findings are consistent: colon cancer and breast cancer risk decrease with 

increasing levels of physical activity (IARC Working Group 2002; Lee 2003; Slattery et al. 

1997). 

All the reviews have used similar criteria to assess the research design and population 

studied: number and characteristics of cancer cases; definition and measurement of 

physical activity; estimated time between physical activity exposure and cancer outcome; 

and estimated effect size, expressed as an adjusted odds ratio or relative risk (RR). 

For colon cancer there is consensus that the risk reduction for physically active men and 

women is around 30% to 40% (RR 0.6–0.7), compared with inactive people (IARC Working 

Group 2002; Lee 2003; Slattery et al. 1997). By contrast, the evidence for rectal cancer is 

inconsistent, with most studies not able to detect a significant difference or reporting a 

weak association (Lee 2003; Slattery et al. 1997). There is a dose–response relationship 

between physical activity and colon cancer, with optimal protection proffered by 3.5 to 4 

hours of vigorous physical activity or 7 to 35 hours of moderate physical activity each week 

(Slattery et al. 1997). There remains no clear agreement on the biological mechanism(s) for 

the protective effect (Westerlind 2003; Slattery et al. 1997). Current suggestions include 

a reduction in gastrointestinal transit time, improvements in immune function, hormone 

modulation (insulin, sex hormones and insulin-like growth factor), a reduction in free 

radicals and prostaglandin modulation (Westerlind 2003; Slattery et al. 1997). 


3 


There is consistent epidemiological agreement that physically active women have about a 

20% to 30% reduction in breast cancer risk (RR 0.7–0.8) compared with inactive women 

(IARC Working Group 2002; Lee 2003). Unlike colon cancer, there is not specific detail on 

the optimal dose of physical activity for breast cancer, although it appears that 30 to 60 

minutes per day of moderate to vigorous exercise is required to reduce risk. Again there 

is evidence of a dose–response relationship: breast cancer risk decreases with increasing 

levels of physical activity (Lee 2003). Risk reduction has been reported for both pre- and 

post-menopausal women. However it is still unclear which time period(s) in a woman’s 

lifespan are most important for physical activity in the development of breast cancer (IARC 

Working Group 2002). Like colon cancer, the biological mechanism(s) are not clear. Similar 

mechanisms have been postulated, with greater emphasis on oestrogen metabolism (IARC 

Working Group 2002; Lee 2003; Westerlind 2003). 

There is no consistent evidence of an association between physical activity and other 

specific cancers. Endometrial, prostate, testicular, ovarian and lung cancers have been 

the subject of the most attention. Although some studies show an association between 

physical activity and lung cancer, it is possible that this relationship is confounded by 

smoking and/or other lung diseases (IARC Working Group 2002; Lee 2003). 

Many questions remain unanswered in this comparatively new area of cancer research. 

It appears that more intense and more frequent and longer duration of activity may 

generally provide more protection (Bauman, Habibullah & Holford 2003). Further research 

is required into the dose–response relationship between physical activity and cancer and 

specific cancer sites; the type, frequency, intensity and duration of physical activity; and 

the biological mechanisms influencing cancer development (Lee 2003; UICC 2004; Gotay 

2005; Roberts & Barnard 2005). 

The impact 

The population attributable risk (PAR) is often used to assess the relative public health 

importance of a risk factor. PAR is a function of the prevalence and strength of the 

association between the risk factor and the disease outcome. In the case of physical 

inactivity it represents the proportion of cases (for example colon cancer) that could be 

prevented if exposure to the risk factor were eliminated, that is, 100% of the population 

achieving sufficient physical activity (Bauman 1998; Stephenson et al. 2000). The PAR for 

physical inactivity has been estimated for two types of cancer, colon cancer and breast 

cancer, as the strongest epidemiological evidence relates to these cancers. 

Table 1.8 Estimates of population attributable risk (PAR) for physical activity and cancer 

Author Year Breast cancer Colon cancer 

Mezzetti et al. 1998 10.6% 

Stephenson et al.* 2000 9% 19% 

WHO 2002 10% 16% 

IARC 2002 11% 13–14% 

Slattery 2004 12–14% 

* Estimate for the Australian population 

Sources: Mezzetti et al. 1998; Stephenson et al. 2000; IARC Working Group 2002; WHO 2002; Smith 2004; Slattery 2004 


Broadly speaking, there is agreement between the various estimates. It is likely however 

that these underestimate the true PAR. Variation in measurement and definition of physical 

activity between studies and the unaccounted-for contribution of physical inactivity to 

weight gain are all sources of potential error (IARC Working Group 2002). 

In broad terms, therefore, it follows that increasing physical activity could prevent up to 

1165 colon cancer and 1297 breast cancer cases annually (AIHW & AACR 2004). 

The challenge 

Australia has had three national physical activity surveys: in 1997, 1999 and 2000. The 

results from the three surveys (see figure below) are of concern, with a discernable 

downward trend in the proportion of the population reporting sufficient physical activity. 

In 2000, just over half of the adult population (56.8%) achieved the current recommended 

levels of 150 minutes per week while the proportion of Australians reporting no physical 

activity (sedentary) increased (13.4% in 1997 to 15.3% in 2000) (Bauman, Ford & 

Armstrong 2001). 

Figure 1.3 Trends in proportion of Australian adults meeting recommended levels of physical activity 

Percentage 

70 

60 

50 

40 

30 

20 

10 

0 

Men 

63 61 

1997 

62 

Women Total 

60 

54 

57 58 

56 

1999 2000 

YEAR 

Source: Bauman, Ford & Armstrong 2001 

There has not been a national physical activity survey since 2000 so it is not possible to 

make an accurate assessment of the current population physical activity level in Australia. 

A number of states have conducted surveys during the intervening period based on the 

same instrument, the Active Australia questionnaire. Data from these state-based surveys 

show that the downward trend in physical activity has most likely continued. 

The data from the 2000 national physical activity survey were re-analysed against three 

criteria for achieving sufficient physical activity (Cerin et al. 2005) (refer to figure 1.4 

below): 

• 

National physical activity guidelines for adults: accrual of ≥150 minutes of at least 

moderate-intensity activity through five or more sessions in the previous week (DHAC 

1999). 

57 


5 


• 

• 

Moderate-intensity physical activity to reduce colon cancer risk: accrual of ≥420 

minutes of at least moderate-intensity activity in the previous week (Slattery et al. 1997). 

Vigorous physical activity to reduce colon cancer risk: accrual of ≥210 minutes of 

vigorous activity in the previous week (Slattery et al. 1997). 

Figure 1.4 Proportion of the population achieving three criteria for sufficient activity 

Percentage 

50 

40 

30 

20 

10 

0 

150 min/wk 

Source: Cerin et al. 2005 

MEN WOMEN 

GENDER 


420 min/wk (moderate) 210 min/wk (vigorous) 

The application of different criteria to the data from the 2000 national physical activity 

survey highlights that the prevalence of meeting physical activity criteria for colon cancer 

prevention is low and much lower than that related to the more generic physical activity 

recommendations. Less than half of the population (46%) achieves the recommended 

≥150 minutes of at least moderate-intensity activity through five or more sessions in a 

week and only 26% meet the colon cancer criteria (Cerin et al. 2005). The same review 

also examined the socio-demographic factors associated with achievement of the physical 

activity criteria. Across each of the three criteria, physical activity is higher in males than 

females, decreases with age and increases with educational attainment (Cerin et al. 2005). 


There is potential to promote higher levels of participation in physical activity in the 

Australian population. Several recent reviews and reports have examined the evidence on 

effectiveness, key characteristics and best strategies for a population-based approach to 

promoting physical activity (Kahn et al. 2002; Bull, Bellew et al. 2004; NPHP 2005). 

Be active Australia: a framework for health sector action for physical activity (NPHP 2005) 

is the current strategic framework for population-based physical activity promotion in 

Australia. The strategic focus of this framework contains three areas: settings, overarching 

strategies and population groups. The action areas are summarised below: 

1. Settings 

• Community environments and organisations 

• 

Health services

• 

• 

• 

Childcare and out of school hours care 

Schools 

Workplaces 

2. Overarching strategies 

• 

• 

• 

• 

Communication 

Workforce capacity 

Evidence, research, monitoring and evaluation 

Strategic management and coordination 

3. Priority populations 

• Aboriginal and Torres Strait Islander peoples 

• 

Populations with special needs 

Be active Australia is underpinned by Getting Australia active II, a major review of physical 

activity interventions across different settings and approaches and for different populations 

(Bull, Bauman et al. 2004). 

Settings 

Community environments and organisations 

The influence of the environment on physical activity has been the subject of increased 

attention for the past decade. It is commonly accepted that the built environment provides 

opportunities (and barriers) to physical activity and can facilitate incidental physical activity. 

Unfortunately there is a paucity of evidence on the relative contribution of the environment 

to physical activity behaviour and there are limited data on the specific environmental 

attributes that increase physical activity (McCormack et al. 2004; Giles-Corti 2006). 

Environmental improvements require collaboration with and commitment from sectors 

outside of health, such as transport and urban planning. The health sector has a role in 

education, workforce development and advocacy, as well as contributing to the evidence 

base (Giles-Corti 2006). 

Health services 

Health services, particularly primary health care, are an important setting for individual 

physical activity interventions. There is little evidence on the effectiveness of populationbased 

physical activity promotion in health services. Health professionals, in particular 

general practitioners (GPs) are an accessible, credible source of information for patients 

(RACGP 2004). Approximately 85% of Australians visit a GP in any given year (Britt et al. 

2005). 

Brief interventions for physical activity behaviour change, often based on the transtheoretical 

or stages of change model, are recommended for use in general practice 

(RACGP 2005). Verbal advice, written materials (such as pamphlets and booklets) and 

exercise prescriptions can produce short-term increases in physical activity (Smith 

2004). The nature and degree of change is not unexpected given the relatively brief 

counselling that patients receive. This could potentially be improved by involving other 

health professionals (for example, practice nurses), either in partnership with GPs or 

independently, to reinforce health messages and provide more follow-up with patients 



to help them achieve greater and more sustained behavioural changes to their habitual 

physical activity behaviours (Smith 2004; Brown 2006). 

A number of electronic and paper-based resources are available to assist general practice 

to work with patients to improve physical activity, including: 

• 

• 

• 

• 

• 

SNAP: A population health guide to behavioural risk factors in general practice (RACGP 

2004) 

Lifestyle prescriptions (‘Lifescripts’) (DHA 2005) 

Guidelines for preventive activities in general practice (‘the red book’) (RACGP 2005) 

Putting prevention into practice: guidelines for the implementation of prevention activities 

in the general practice setting (‘the green book’) (RACGP 2006a) 

National guide to a preventive health assessment in Aboriginal and Torres Strait Islander 

peoples (NACCHO 2005). 

Childcare and out of school hours care 

There is very little published research on the effectiveness of physical activity interventions 

in the childcare setting (Timperio, Salmon & Ball 2004); however health promotion 

programs targeting childcare centres have proven to be very popular. The demand for 

SunSmart Centres and Start Right Eat Right (in Western Australia) suggests that childcare 

is a setting very receptive to health promotion interventions. 

The majority of out-of-school-hours interventions published were conducted on primaryschool-aged 

children in the US, either as after school, summer camp or family-based 

interventions. Programs that involved parents were the most effective. Out-of-school-hours 

care is a setting that offers considerable promise, but more evidence is needed in an 

Australian context and for adolescents (Timperio, Salmon & Ball 2004). 

Schools 

Schools are frequently identified as an important setting for health promotion. Successful 

school-based health promotion can simultaneously improve education and health (WHO 

1997). School-based physical activity interventions can be classified into three types: 

curriculum-based strategies, environmental change strategies and policy-based strategies 

(Timperio, Salmon & Ball 2004). The most successful interventions incorporated a wholeof-school 

approach: that is, curriculum-, environmental- and policy-based strategies 

(CDCP 1999). Health promotion in schools requires cooperation and collaboration with the 

education sector, consistent with the health promoting schools framework (WHO 1997; 

NPHP 2005). 

Workplaces 

Workplace health promotion presents enormous potential to access large numbers of 

people at once and improve the health and productivity of the workforce. Up to now, 

however, there has been limited evidence supporting the effectiveness of workplace 

health promotion programs (Marshall 2004). Workplaces, like other physical and social 

environments, provide opportunities and barriers to physical activity. Non-specific 

programs and policies that promote incidental physical activity appear to be more 

successful and sustainable than individualised or targeted programs in the workplace 

(Marshall 2004). 


Strategies 

Communication 

Communication and community education include mass media (social marketing), printed 

material, websites, telephone interventions and community education (Marshall, Owen 

& Bauman 2004; NPHP 2005). Overall, mass media successfully raise awareness of 

physical activity, measured through recall, but have modest effects on behaviour. Individual 

campaigns have reported more success in changing behaviour (Marshall, Owen & Bauman 

2004). Interventions using print materials have shown some success in changing physical 

activity behaviour in the short term, whereas telephone- and Internet-based interventions 

have demonstrated limited success (Marshall, Owen & Bauman 2004). 

Workforce capacity 

Physical activity promotion is one priority among a range of conflicting and complementary 

prevention activities for health professionals (RACGP 2006a; RACGP 2006b). The capacity 

of the workforce is limited by the number of health professionals and the time available 

to them. All health professionals, not just GPs or those trained in exercise science, should 

play a role in increasing physical activity (Brown 2006). Opportunities exist to develop 

training packages, both informal and formal, for health (and other) professionals in primary 

prevention, specifically physical activity (NPHP 2005). Complementary resources (posters, 

pamphlets or brochures) and online support would add value and support for those who 

undertake training. 

Evidence, research, monitoring and evaluation 

There are no national data on the current level of physical activity for Australians. The 

most recent data were collected, and reported, in 2000. Since 2000, individual states 

and territories have undertaken a range of monitoring and surveillance activities, without 

national coordination. Better national coordination of the available data would allow a more 

accurate assessment of population physical activity trends over time and evaluation of the 

impact of national interventions. 

Evidence continues to accumulate to support the protective role of physical activity in 

health. Despite this there are specific research areas with conflicting or insufficient data, 

including the role of physical activity in cancer prevention beyond breast cancer and colon 

cancer and the optimal amount and type of physical activity for weight loss and disease 

prevention. 

It is clear that there is still a need for more well-designed research to evaluate which 

interventions work best, particularly those tailored to specific population groups and/or 

settings. The research identifies areas of promise and ‘best bets’, but considerable work 

remains to implement and test these approaches on a larger scale in the Australian 

context. 

Strategic management and coordination 

Successful action on physical activity requires strategic leadership and commitment at a 

national level as well as a coordinated approach at national, state, territory and local levels, 

with good communication between all stakeholders, including the non-government sector 

(NPHP 2005). The development of a national framework, Be active Australia, is the first 

step to underpinning good public health practice (Bull, Bellew et al. 2004). The absence of 

mandated accountability and adequate resourcing at a national level limits the opportunity 

for successful implementation of the framework (Bull, Bellew et al. 2004). 



Populations 


The review of interventions with Aboriginal and Torres Strait Islander peoples found very 

little published evaluation, despite an increase in the number and diversity of programs in 

these communities (Shilton & Brown 2004). There remains a need for much more effort in 

this area, in relation to measurement and interventions in urban as well as rural and remote 

communities (NACCHO 2005). 

Populations with special needs 

Populations with special needs are those Australians who face additional barriers to 

being physically active. It includes people with a chronic condition, including cancer 

(NPHP 2005). The number of cancer survivors (including people living with cancer) in 

Australia continues to increase. People who have survived cancer are at increased risk of 

many chronic diseases and may have to contend with disability associated with cancer 

treatment. Population-based physical activity strategies may not be suitable; rather, small 

group or individual interventions would be more appropriate for these groups (NPHP 2005). 


Policies, reports and strategic plans have been produced by most state and territory 

governments, providing direction for improvement in physical activity levels in Australia. 

The Cancer Council strongly supports the work of other chronic disease prevention 

agencies and institutions in the promotion of physical activity. 

The National physical activity guidelines for Australians (DHAC 1999) includes these 

recommendations: 

• 

• 

• 

• 

Think of movement as an opportunity, not an inconvenience. 

Be active every day in as many ways as you can. 

Put together at least 30 minutes of moderate-intensity physical activity on most, 

preferably all, days. 

If you can, also enjoy some regular, vigorous exercise for extra health and fitness. 

Australia’s physical activity recommendations for 5–12 year olds and Australia’s physical 

activity recommendations for 12–18 year olds (DHA 2004a; DHA 2004b) recommend that: 

• 

• 

Children need at least 60 minutes (and up to several hours) of moderate to vigorous 

physical activity every day. 

Children should not spend more than two hours a day using electronic media for 

entertainment (e.g. computer games, TV, Internet), particularly during daylight hours. 

This is a recommended minimum level of activity for children, youth and adults. Higher 

levels are likely to give greater benefits. 

Colon cancer and breast cancer risk reduces with increasing levels of physical activity. The 

optimal risk reduction for colon cancer is achieved at 3.5 to 4 hours of vigorous physical 

activity or 7 to 35 hours of moderate physical activity each week (Slattery et al. 1997). The 

American Cancer Society recommends that 45 to 60 minutes of moderate to vigorous 

activity on at least five days of the week is preferable (Kushi et al. 2006). 


Aims 

The Cancer Council Australia recognises the strength of evidence for physical activity in 

the prevention of breast and colon cancer and in the reduction of risk for other diseases, 

particularly cardiovascular disease and diabetes. 

The body of evidence on health benefits of physical activity has led to general public health 

recommendations for adults to have 30 minutes of regular, moderate-intensity physical 

activity on most days of the week (DHAC 1999). To date, there is insufficient evidence to 

support the development of separate public health advice for the prevention of different 

illnesses, thus The Cancer Council endorses the recommendations that have been put 

forward in a consistent fashion by federal, state and territory bodies and other agencies. 

The Cancer Council’s aims are to encourage the Australian population throughout life to: 

• 

• 

• 

maintain at least a minimum level of physical activity: for adults at least 30 minutes of 

moderate-intensity activity on most days of the week, for children and adolescents at 

least 60 minutes 

participate in physical activity of longer duration and higher intensity, to further reduce 

colon cancer risk, where possible across the lifespan (consistent with the National 

physical activity guidelines for Australians) 

maintain a healthy body weight through a balance of food intake and physical activity. 



Increased awareness of 

the link between physical 

inactivity and cancer among 

the general public and key 

health professionals 





that promote physical activity 



trends 

Monitor and clarify best evidence on the relationship between physical 

inactivity and cancer causation 

Ensure key messages are promoted to the public and relevant health 

professionals in publications, presentations, programs, media statements 

and where opportunities arise 


specifically for general practice, to improve evidence-based interventions 

by health professionals 


relationship between physical inactivity and cancer to complement the 




Advocate for nationwide social marketing campaigns that promote 

physical activity across the life course which are coordinated, 

sustainable and far-reaching 

Encourage the Australian, state and territory governments to commit to 

long-term investment to increase the awareness of the health benefits of 

physical activity and promote increased participation 

Support and deliver effective community interventions at a local, state 

and national level to address physical inactivity 


clarifying the relationship between physical inactivity and cancer 


1 




More supportive 

environments that assist 

people to be more physically 

active 





Support and conduct high quality behavioural research further clarifying 

the barriers and enabling factors for participation in physical activity 



Encourage the Australian Government to fund a comprehensive National 

Nutrition and Physical Activity Survey of children and adults, which is 

conducted, as a minimum on a regular five-year basis 

Encourage the Australian Government to address the broader social 

and environmental determinants of physical inactivity and sedentary 

lifestyles 



• evaluate physical activity interventions 


prevention 


prevention 



Note: Refer also to the action plans of the nutrition and obesity chapters when considering promotion of physical activity. 

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5 


O v e r w e i g h t a n d 

o b e s i t y 

Introduction 

Obesity is associated with increased risk of cancer of 

the colon, breast (post-menopause), endometrium, 

kidney, oesophagus and gall bladder. Levels of 

overweight and obesity in Australia continue to be a 

major health concern. Of particular concern is the 

latest estimate that one in four children is overweight 

or obese. 

Rising rates of overweight and obesity have been described as reaching epidemic 

proportions in the developed nations and causing concern in developing nations. Australia 

is no exception. Over the last 30 years, rates of overweight and obesity among adults and, 

even more worrying, among children, have risen and the rise is accelerating. 

Overweight and obesity are a major public health issue: they are an established cause 

of morbidity and mortality and are one of the largest risk factors for chronic diseases in 

Western countries, particularly increasing the risk of diabetes, cardiovascular disease and 

some cancers (WHO & FAO 2003). 

There are several ways to measure disease risk associated with overweight and obesity, 

including body mass index (BMI) and waist circumference. 

BMI is the most commonly used and internationally accepted measure to assess 

overweight and obesity (NHMRC 2003a). This is calculated by dividing a person’s 

weight (in kilograms) by their height (in metres squared). According to the World Health 

Organization’s definitions, adults: 

• 

• 

• 

• 

with a BMI under 18.5 kg/m2 are classified as underweight 

with a BMI of >18.5 to 25 to 30 kg/m2 or higher are classified as obese (WHO & FAO 2003). 

As BMI increases from a healthy weight to overweight or obesity, the risk of ill health rises. 

Individuals who are obese have a 50% to 100% increased chance of premature death from 

all causes compared to individuals with a BMI in the healthy range (WHO 2000). 

It should be noted, however, that these classifications are not suitable for children and 

adolescents due to age-related growth patterns, and BMI-for-age percentile charts, 

developed by the Centers for Disease Control and Prevention, should be used to assess 

overweight and obesity in children. The National Health and Medical Research Council 

defines the following cut-offs for children and adolescents: 

• 

• 

BMI above the 85th percentile is indicative of overweight 

BMI above the 95th percentile is indicative of obesity (NHMRC 2003b). 


The specific cut-off measurements of BMI may not be suitable for all ethnic groups, who 

may have equivalent levels of risk at a lower BMI (e.g. Asians) or higher BMI (e.g. Pacific 

Islanders or Polynesians). 

Measurement of waist circumference may be a simpler valid alternative to BMI for health 

promotion (Han et al. 1996). 

Waist circumference may also a good predictor of cancer risk. The exact relationship 

between increased abdominal fat and increased cancer risk is currently unclear. Significant 

increased risk appears to occur when the waist circumference is greater than 102 cm for 

men and 88 cm for women (NHMRC 2003c). 

Emerging epidemiological data highlight the importance of acting on obesity as a matter 

of considerable importance and urgency. The increasing trends to overweight and obesity 

among young Australians are particularly worrying. There is mounting evidence of links 

between childhood eating behaviour, physical activity trends and obesity, and of their 

association with long-term chronic conditions, including some cancers, diabetes and 

cardiovascular disease (Dietz 1998; Freedman et al. 1999; WHO 2000; Dunstan et al. 2000; 

Ebbeling, Pawlak & Ludwig 2002). 

More children and adolescents are displaying the markers of adult chronic diseases, such 

as cardiovascular disease, type 2 diabetes and fatty liver disease (Booth et al. 2006). 

Obesity essentially results from an imbalance between declining energy expenditure due to 

physical inactivity and high energy in the diet. High consumption of energy dense/nutrient 

poor foods (excess calories from high sugar or fat foods) is the main determinant of the 

obesity epidemic (WHO & FAO 2003). 

These trends imply a pattern of rising health costs for governments as well as for 

individuals and the community in which they live (Booth et al. 2001). 

The link between overweight and obesity and cancer 

Obesity (BMI >30 kg/m2) is associated with increased risk of cancer at several sites; the 

evidence is clear for cancers of the colon, breast (post-menopause), endometrium, kidney, 

oesophagus and gall bladder (IARC Working Group 2002). Overweight (BMI of >25 to 

Table 1.9 Proportion of cancer attributable to overweight and obesity and associated factors 

Type of cancer Proportion 

of incidence 

attributable to 

overweight or 

obesity 


Aspects of the association between overweight or obesity 

and cancer 

Colon cancer 11% Association seems greater in men than women 

Risk not dependent on whether person has been overweight 

in early adulthood or later in life 

Some evidence that association in women may be increased 

by menopausal status and hormone replacement therapy 

(HRT) use in the obese (Slattery et al. 2003) 

Post-menopausal 

breast cancer 

Endometrial 

cancer 

9% Increase in risk of 30% in women with a BMI ≥28 kg/m2 

compared to those with a BMI of 25 kg/m2 have a two- to three-fold 

increase in risk 

Limited evidence suggests risk is similar in pre- and postmenopausal 

women 

Kidney cancer 25% Individuals with a BMI of ≥30 kg/m2 have a two- to three-fold 

increase in risk compared to those below 25 kg/m2 

The effect is similar in men and women 

Oesophageal 

adenocarcinoma 

Gall bladder 

cancer 

Source: Bergstrom et al. 2001, based on figures from Europe 

37% Strong association between being overweight and 

adenocarcinomas of the lower oesophagus and the gastric 

cardia, with a two-fold increase in risk in individuals with a 

BMI of >25 kg/m2 

24% Limited evidence available but there is a suggestion of almost 

a two-fold risk, especially in women 

There is also emerging evidence that obesity is associated with increased risk of cancers 

of the pancreas and liver, and multiple myeloma and non-Hodgkin lymphoma (Calle et al. 

2003). 

It is interesting to note that overweight and obesity are risks factors for some of the most 

common cancers in Australia, such as colon and breast cancer. With the rising rates of 

obesity in Australia, there is concern that this will translate into an increased incidence of 

some of the less common cancers associated with obesity. 

Up to now we have known that excess body weight increases cancer risk, but there has 

been a dearth of evidence to suggest whether losing weight would lower cancer risk. 

Recent evidence indicates that weight loss in those who are overweight lowers breast 

cancer risk (Eliassen et al. 2006). 

Most of the evidence associating body weight with cancer is derived from case–control 

and cohort studies. However there has been one large scale randomised controlled 

trial, the Women’s Health Initiative, which randomised women to a very low fat diet 

intervention or a usual fat diet (Prentice et al. 2006). Unfortunately the Women’s Health 

Initiative was not designed to address weight loss, with the intervention group only losing

0.4 kg more weight than the control group. While women on the low fat diet had a 9% 

lower incidence of breast cancer compared with the control group, this result was not 

statistically significant. However in sub-group analyses, breast cancer rates were reduced 

by 22% among women who started with the highest fat intake (>37% energy from fat) and 

reduced their fat the most (to 24% after one year) (Stein 2006). 

Interestingly, there was suggestive evidence that the low fat diet had a more protective 

effect against oestrogen receptor-positive breast cancer. Despite the lack of an apparent 

effect on colorectal cancer, adenomas were significantly reduced among the low fat diet 

group (Stein 2006). 

As well as a healthy body weight being associated with preventing cancer, it is also 

associated with preventing cancer recurrence and improving survival for people diagnosed 

with cancer (Brown et al. 2003). There is a reasonable level of evidence that weight 

management and physical activity positively impacts on quality of life, cancer recurrence 

and overall survival for cancer survivors (Brown et al. 2003). Randomised controlled trials, 

such as the Women’s Intervention in Nutrition Study, have shown encouraging results of 

the effectiveness of nutrition and physical activity interventions in improving outcomes for 

cancer survivors (Chlebowski et al. 2005). 

The impact 

Obesity and its underlying factors of excess energy intake and physical inactivity contribute 

substantially to the overall Australian ‘burden of disease’, that is, the overall health 

problems based on mortality and disability. 

For the first time in Australia, overweight and obesity has overtaken tobacco as the risk 

factor responsible for the most significant burden of disease: 8.6% compared with 7.8% 

for tobacco (AIHW 2006). Overweight and obesity accounted for 8.8% of the disease 

burden for males and 8.3% for females. Even though the burden from tobacco is only 

slightly lower than the burden from obesity, it is likely that the obesity burden will continue 

to increase, whereas the tobacco impact is declining due to the decreases in smoking 

prevalence over the last 40 years. 

In Australia, 3% of all cancer deaths have been attributed to a BMI of >25 kg/m2 (Mathers, 

Vos & Stevenson 1999). More recent estimates from America suggest that overweight 

and obesity may account for 14% of cancer deaths in men and 20% in women (Calle et al. 

2003). 

US studies have suggested that the effects of obesity on quality of life and on health care 

costs are equivalent to 20 years of ageing (Sturm 2002), and that obesity is associated with 

at least as much morbidity as poverty, smoking or drinking (Sturm & Wells 2001). 

Nationally, the direct costs of obesity represent a significant proportion of the health care 

budget and there is great potential savings from reducing the problem. International 

studies on the economic costs of excess body weight, including data from Australia, have 

shown that, conservatively, between 2% and 7% of total health care costs may be directly 

attributable to overweight and/or obesity (WHO 2002). In Australia in 2003 it was estimated 

to equate to about $1.2 billion per year (WHO 2002). Studies of indirect costs of work 

workforce participation have shown increased rates of long-term sick leave and premature 

disability leading to loss of productivity (WHO 2002). 

A recent Australian report estimated that the total financial cost of obesity in 2005 was 

$3.7 billion (Access Economics 2006). The total health costs from cancer due to obesity 


O v e r w e i g h t & o b e s i t y

were $107.3 million in 2005, with 79% of the costs related to bowel and breast cancers. 

Given the social and psychological consequences of obesity, intangible costs such as 

impaired quality of life are significant, with estimates for obesity-related cancers at $218 

million (Access Economics 2006). 

Importantly, the escalating cost of health care of an obesity-related disorder, such as 

diabetes, has been calculated as almost doubling over time with normal progression of 

the disease (Bennett, Magnus & Gibson 2004). This suggests that the economic burden 

is not only significant, but is likely to get worse even if there is no further growth in the 

prevalence of obesity. Overseas studies have also found that those who are obese attain 

lower levels of occupational prestige and lower incomes than non-obese people (Bennett, 

Magnus & Gibson 2004). In addition, other studies have found that obese people as a 

group receive more sickness and unemployment benefits than people with a healthy body 

weight (Bennett, Magnus & Gibson 2004). Indirect costs, which are far greater than direct 

costs, include workdays lost, doctor visits, disability pensions and premature mortality, all 

of which increase as people go from a healthy weight to overweight or obesity (Wolf & 

Colditz 1996). 

The challenge 

In the 10-year period from 1985 to 1995, the level of combined overweight/obesity in 

Australian children more than doubled, while the level of obesity tripled in all age groups 

and for both sexes (Cameron et al. 2003). 

Adults 

There is a lack of recent national data on the levels of overweight and obesity in Australian 

adults, as the last National Nutrition Survey was conducted in 1995. 

The Australian Diabetes, Obesity and Lifestyle Study in 1999−2000 found that the 

prevalence of overweight and obesity combined was almost 60% among Australian adults 

aged 25 years and over (Cameron et al. 2003). The rate for males was 67% and for females 

52%. The prevalence of being overweight was 39%. For adult males it was 48% and for 

adult females 30%. The prevalence of obesity was 21% or more than double the rate 

observed 15 years earlier: 19% of adult males and 22% of adult females were obese. 

According to the five-year follow-up of the Australian Diabetes, Obesity and Lifestyle Study, 

more than 600 adults progress from being overweight to being obese every day (i.e. more 

than 200,000 annually) (Barr et al. 2006). 

The 1995 National Nutrition Survey found that the proportion of overweight and/or obesity 

increases with age for both males and females (Marks et al. 2001). Adult men seem to 

increase their weight rapidly between the ages of 25 and 40 years, while the weight of 

women changes most markedly during the menopausal years (45 to 55). Among people 

aged 19 to 24 years, one in three males and one in four females are overweight or obese. 

Among people aged 45 to 64 years, this rises to three out of four males and almost two out 

of three females. 

Research has confirmed that weight increases are not just a result of ageing. Younger 

people are gaining weight faster than previous generations and weight gain is accelerating 

as modern life influences weight patterns. More people are entering adulthood weighing 

more. Data shows that those born later in the 20th century (Generation X) will gain weight 

as they age at a faster rate than their parents did (Allman-Farinelli et al. 2006a & 2006b). 

This is believed to be a result of the increasing obesogenic environment (see description 

later in this chapter). 


Children 

Figure 1.5 Prevalence of overweight and obesity in children aged 7–11 years 

Percentage 

35 

30 

25 

20 

15 

10 

5 

0 

BOYS GIRLS 

OBESE 

OVERWEIGHT 

1985 1995 2003 1985 1995 2003 

Sources: Magarey, Daniels & Boulton 2001; Sangiorski et al. in press 

YEAR 

OBESE 

OVERWEIGHT 

The most recent data on the levels of overweight and obesity in Australian children comes 

from the 2004 NSW Schools Physical Activity and Nutrition Survey (SPANS), which 

surveyed 5500 children from 5 to 16 years of age (Bauman et al. 2003). 

In 2004, almost a quarter of children and young people from kindergarten to Year 10 (aged 

five to 16 years) were overweight or obese (25% of boys and 23% of girls) (Bauman et al. 

2003). Children aged nine to 12 had some of the highest rates (32% in Year 6 boys and 

30% in Year 4 girls). Children from lower socio-economic areas and boys from Middle 

Eastern backgrounds were more likely to be overweight or obese (Bauman et al. 2003). 

Overweight and obesity is far more common than it used to be. The proportion of school 

children who are overweight or obese has increased markedly over the past 20 years. It 

appears that in boys, the trend towards being overweight or obese is accelerating (Bauman 

et al. 2003). In girls the trend is not accelerating, but is still of concern (Bauman et al. 

2003). 

A study looking at weight changes among Australian children over three decades found 

that between 1985 and 1997, the combined prevalence of overweight and obesity doubled, 

and that of obesity trebled among young Australians. The increase over the previous 16 

years was far smaller (Booth et al. 2001). In 1985 the prevalence of overweight and obesity 

in boys was 11% and 12% in girls, with 1.4% of boys and 1.2% of girls being obese. Only 

10 years later, depending upon age, 14% to 26% of boys and 19% to 24% of girls were 

overweight or obese. The prevalence of obesity was 2% to 7% in boys and 4% to 6% in 

girls (Baur 2001; Magarey, Daniels & Boulton 2001). 

Overall there was a statistically significant increase in children’s mean energy intake 

between 1983 and 1995. For boys, there was an increase of 1400 kJ per day; for girls, 

there was an increase of 900 kJ per day. These increases are much greater than those seen 

in adults (Cook, Rutishauser & Seelig 2001). The increase in energy intake was derived 

from an increase in foods high in refined sugars, such as soft drinks and confectionery 

(Cook, Rutishauser & Seelig 2001). 


1 


Obese children have a 25% to 50% chance of progression to adult obesity, and this may 

be as high as 78% in older obese adolescents (Must & Strauss 1999). This significant risk 

confirms the importance of preventive action. 

Specific population groups 

The problem of overweight and obesity is so large and widespread throughout the 

community that it is difficult to identify any particular group that is not profoundly affected 

by the problem. However there are certain groups in the Australian community that bear a 

disproportionate burden of this condition. 

Data suggest that among Aboriginal Australians and Torres Strait Islanders, overweight 

and obesity affect 60% of men and 58% of women (ABS 1995 National Health Survey 

results, cited in NHMRC 1997; NATSI Working Party 2001). The prevalence of obesity in 

males is 25% and in females 28%, compared with an overall population prevalence of 

obesity of 18%. Differences in the level of overweight and obesity between Aboriginal and 

non-Aboriginal men and women are most pronounced in the younger age groups. High 

levels of obesity are found even among the youngest age groups of Aboriginal men and 

women and they continue to increase throughout life, up to the sixth decade. However, the 

association between overweight and obesity and diseases such as diabetes, cardiovascular 

disease and cancers in these communities remains unclear (Guest et al. 1993; Leonard et 

al. 2002; Wang & Hoy 2002). 

The level of overweight and obesity is higher (up to two to three times) among people 

of Southern European and Middle Eastern ethnic origin, when compared to those of 

British descent (NSW Health 2003). In contrast, those born in South East Asia had 

substantially lower levels of overweight, although care must be taken in interpreting 

these figures as the classification system may underestimate overweight in Asian people 

(Bennett & Magnus 1994; Bennett 1995; Mathers 1994; NSW Health 2003). 

A low social status and low level of education are associated with a higher level of 

overweight and obesity, although the effect is more obvious in women and is not as strong 

as the relationship between social status and other illnesses (NSW Health 2003). Around 

53% of women in the lowest socio-economic group were overweight, compared with 44% 

of women in the highest socio-economic group. In addition, 24% of women in the lowest 

socio-economic group were obese compared with only 14% of those in the highest group. 

There was no significant difference in the number of overweight or obese men in the 

highest when compared to the lowest socio-economic groups. 

Some data suggest that rural and remote communities have higher levels of overweight 

and obesity (NSW Health 2003). The issue of access to appropriate foods and opportunities 

to engage in appropriate physical activity are likely to be major contributing factors to these 

differentials in rural and remote communities. 

The clustering of factors such as low levels of education, low income and food insecurity, 

and their association with overweight and obesity levels, requires complex and sensitive 

interventions. 



Table 1.10 lists the key physical activity and eating behaviours that need to be increased or 

decreased to prevent overweight and obesity. 

Most individual studies have been conducted in a very narrow range of settings and relied 

heavily on education approaches to small sections of the community. Very few studies 

have dealt with environmental, structural or policy change or were conducted on a truly 

community-wide basis (Campbell et al. 2005; Reilly et al. 2002; Ebbeling, Pawlak & Ludwig 

2002; WHO & FAO 2003; Gill, King & Webb 2005; Summerbell et al. 2003). 

Overall the literature states that for an intervention to be effective, initiatives should be 

long-lasting, multi-faceted and sustainable, and should target the whole environment 

and be behaviourally focused (Campbell et al. 2005; Reilly et al. 2002; Ebbeling, Pawlak & 

Ludwig 2002; WHO & FAO 2003; Gill, King & Webb 2005; Summerbell et al. 2003). 

Some researchers have proposed a life-course approach to cancer prevention (Uauy & 

Solomons 2005). This should start before conception, be followed through childhood and 

continue through all stages of the life course, as described in the figure below. Mothers 

should start pregnancy with a healthy weight and avoid excessive or low weight gain 

during pregnancy. Infant and children’s growth should be regularly assessed to ensure 

children to do not gain weight excessively. 

Figure 1.6 The life course approach to cancer prevention 

DEVELOPMENT OF CANCER 

FETAL LIFE INFANCY & CHILDHOOD ADOLESCENCE ADULT LIFE OLDER AGES 

Mother’s 

nutrition 

Fetal growth 

Birth weight 

Carcinogen 

exposure 

Source: Uauy & Solomons 2005 

Breast feeding 

Infections/PEM 

Micronutrients 

Contaminants 

(air, food, water) 

Growth rate 

Stature 

Behaviours 


Food choice 

Obesity 

Carcinogen exposure 

Smoking 

Contaminants 

(air, food, water) 

Timing of puberty 

Obesity 


Inactivity 

(exercise & sedentariness) 


AGE 

Pregnancy & lactation 

Established adult risky behaviours 

Diet & physical activity 


Alcohol 


ACCUMULATED RISK 

GENETIC SUSCEPTIBILITY TO CANCER 

There is general agreement that efforts should be heavily oriented towards prevention 

interventions in children because of the greater likelihood of success at a younger age. 

More effort needs to be directed at creating environmental and policy changes that will 

support the adoption of behaviours conducive to weight control, rather than simply relying 

on education approaches. 


3 


Table 1.10 Summary of the strengths of the evidence on factors that might protect or promote against 

weight gain and obesity 

Evidence Decreases risk Increases risk 

Convincing Regular physical activity 

High dietary fibre intake 

Probable Home and school 

environment that supports 

healthy food choices for 

children 

Possible Low glycaemic index foods 

Breastfeeding 

Insufficient Increased eating frequency Alcohol 

* Energy dense foods are high in fat/sugar and energy. 

Source: WHO & FAO 2003 


High intake of energy dense foods* 

Sedentary lifestyles 

Heavy marketing of energy-dense foods and fast 

food outlets 

Sugar-sweetened soft drinks and juices 

Adverse social and economic conditions in 

developed countries 

Large portion sizes 

High proportion of food prepared outside of home 

Rigid restraint/ periodic disinhibition of eating 

patterns 

Obesogenic environment 

In the past, the usual environment throughout much of Australia enforced a reasonable 

degree of physical activity and limited food choice. Today there is access to a wide 

variety of cheap, energy dense/nutrient poor foods that are marketed powerfully and the 

population is encouraged, directly or indirectly, to avoid expending energy through physical 

activity. This has led researchers to describe the environment as ‘obesogenic‘ in that it 

inhibits appropriate dietary and physical activity patterns and encourages energy imbalance 

(Gebel et al. 2005). 

The next table summarises the best options to prevent weight gain based on a framework 

for a broad portfolio of actions for tackling weight gain prevention (Gill, King & Webb 

2005). This framework considers the level of potential health gain and level of uncertainty 

of risk associated with different interventions, and adopts the concept of assessing the 

level of ‘promise’ to judge the worth of interventions.

Table 1.11 Best options to prevent weight gain 

Target setting Activities 

Best options for families Reduce time spent watching TV and other sedentary behaviours 

Best options for early 

childhood care 

Improve parental knowledge and skills through early childhood care facilities 

Enhance food service policies in early childhood care facilities 

Enhance policies in early childcare facilities to promote physical activity 

Best options for schools Establish a network of health promoting schools: 

• policy on food and drinks 

• school physical environment 

• physical activity opportunities 

• health education curricula 

• programs for out of school hours care 

Best options for active 

neighbourhoods 

Best options for 

workplaces 

Best options for primary 

care 

Best options for industry 

/ food supply 

Best options for media / 

marketing 

Best options for support 

structures 

Source: Gill, King & Webb 2005 

Active transport 

Safe space for exercise facilities 

Improve access to food options for families 

Increase options for incidental physical activity 

Reduce passive work environments 

Improve workplace food service options 

Improve skills and knowledge of health workers 

Work with local suppliers to reduce fat in common foods 

Introduce taxation measures and subsidies to make healthy food options 

cheaper 

Develop a simplified food labelling system indicating energy and fat content 

Reduce exposure of children to food advertising 

Implement social marketing strategies to support improvement of parents as 

healthy role models 

Improve monitoring of weight and fitness status 

Implement ‘whole of community’ demonstration projects 

Individual behaviour change 

What research there is has generally focused on individual behaviour change with little 

attention to organisational and environmental change. There is a lack of research on the 

efficacy of different approaches to high risk, hard-to-reach, low income, and culturally and 

linguistically diverse populations that appear to experience higher rates of overweight and 

obesity. 

Some short-term intense programs are reported as being effective in terms of weight loss, 

but there are doubts about sustainability (Huon, Wardle & Szatto 1999; Gortmaker et al. 

1999; Sahota et al. 2001). Researchers (Ebbeling, Pawlak & Ludwig 2002) suggest that 

these interventions have tended to focus on highly motivated families through specialist 

clinics, and that, on the whole, there is little evidence that treatment interventions are 


5 


more than moderately effective. The relatively small short-term weight losses are generally 

reversed in the long term. 

Schools and workplaces 

Most prevention interventions targeting children and adults have been implemented in 

schools and workplaces and have adopted health education and/or behaviour modification 

strategies. With a few exceptions, these have largely been shown to be ineffective. 

School-based interventions to reduce soft drink intake among children have shown 

potential to be effective in preventing excess energy intake and overweight (James 

et al. 2004; Ebbeling et al. 2006). Other interventions that show the greatest potential 

for reducing obesity in children are those that reduce sedentary behaviours at home 

(particularly hours spent viewing TV), and promote physical activity—both in and out of 

school hours—as well as improved diet. 

Many states in Australia have introduced policy guidelines for school canteens, to address 

the need for healthier choices to be available at schools. 

Obesity prevention interventions that have tended to fail have been those that addressed 

either diet only or physical activity only, that relied primarily on education strategies without 

considering environmental influences, or that focused on activities and behaviours that 

only occur in limited settings, such as school hours (Ebbeling, Pawlak & Ludwig 2002; 

Reilly et al. 2002; Micucci, Thomas & Vohra 2002). One of the challenges in tackling 

childhood obesity is the difficulty in engaging and reaching parents. Schools can be a 

delivery site for interventions but must consider options to reach the whole family. 

Policy 

Although evidence is sparse on the effectiveness of environmental change interventions, 

particularly policy and regulatory interventions, they have been proposed as an essential 

strategy for combating the obesity epidemic. 

There is limited evidence about the effectiveness of economic intervention, such as taxes, 

price policies and incentives, in containing or reducing food consumption, particularly 

energy dense foods (Goodman & Anise 2006). However, modelling analyses drawing upon 

actual market data to track how food purchasing responds to changes in prices suggest 

that a combination of increased prices (in the form of taxes) for such nutrients as fat, 

saturated fat and sugar and subsidies on high fibre foods could reduce the consumption of 

the taxed nutrients as well as total energy intake. 

A small body of evidence indicates that reducing the price of fruit, vegetables and other 

healthy snacks at the point of purchase (vending machines, cafeterias and supermarkets) 

increase their consumption (Anderson et al. 2001; Buscher, Martin & Crocker 2001; French, 

Jeffery et al. 1997; French, Story et al. 1997; French et al. 2001; Jeffery et al. 1994; Kristal 

et al. 1997). 

Although economic measures were an important strategy in tobacco control, there is a 

risk that economic policy interventions involving increases in food prices would negatively 

impact on low socio-economic groups. Therefore they would need to be carefully 

assessed before being implemented. Taxation of soft drinks has been proposed as a 

potential strategy, particularly because of the success of taxation of alcoholic drinks in 

lowering alcohol consumption. Reduction in intake of soft drinks is associated with obesity 

reduction (James et al. 2004; Ebbeling et al. 2006). Soft drinks are a single dietary item that 

generally provides little nutrition apart from sugar and energy. 

More effective regulation around food marketing has been proposed as an important and 

cost-effective strategy for addressing childhood obesity (DHS 2006). Children require 


special consideration with respect to advertising, as they are less able than adults to 

understand fully the intent of advertising or its persuasive techniques, and are thus less 

able to judge the advertisements critically. The excessive level of food advertising on 

Australian televisions contributes to an obesogenic environment (Chapman, Nicholas 

& Supramaniam 2006; Neville, Thomas & Bauman 2005). Systematic literature reviews 

indicate that food advertising contributes to poor food choices, poor overall diet and thus 

increased weight gain and obesity (CFMDCY 2005; Hastings et al. 2003). 

All advertising during children’s programs is prohibited in Sweden (since 1991), Norway 

(since 1992) and Quebec Canada (since 1980) (Hawkes 2004). In all three cases, the ban is 

enforced by a government agency. Children in Quebec who are not exposed to television 

food advertising, have significantly less overweight and obesity than the Canadian average 

(Shields 2006). A study showed a significantly positive correlation between the number of 

television food advertisements and the incidence of children’s overweight across countries 

(Lobstein & Dibb 2005). Sweden had the lowest number of food advertisements in this 

study and the lowest prevalence of overweight, whereas Australia and the US did not fare 

so well (Lobstein & Dibb 2005). The high levels of unhealthy food advertising are also a 

concern because of the potential to limit the effectiveness of social marketing campaigns 

for healthy foods and lifestyles (Hoek & Gendall 2006). 

Broad-based public health interventions 

Prevention interventions that have adopted a population, community-wide or even 

neighbourhood approach, and encompass environmental, legislative and regulatory 

change as well as education and behaviour modification strategies, are largely absent and 

effectiveness cannot be assessed. 

While we lack high-quality evidence on obesity interventions, there is growing knowledge 

about the efficacy of broad-based, comprehensive public health interventions in fields 

such as tobacco and skin cancer control, HIV/AIDS and road trauma reduction, increased 

immunisation rates, decreased coronary heart disease and increased physical activity 

(Hawe, Wise & Nutbeam 2001; DHA 2003; Bauman et al. 2002; Bauman et al. 2003; Gill, 

King & Webb 2005). The research suggests that effective public health interventions are 

sustained, research-based and multi-faceted, and tackle social, cultural, behavioural, 

organisational and environmental factors. 

Evidence of population-based obesity interventions is weak (because of a modest impact) 

or absent (they have not been tried and evaluated). The World Health Organization states: 

‘population education strategies will need a solid base of policy and environment-based 

changes to be effective in eventually reversing these trends’ (WHO & FAO 2003). 

General practice 

Although to date there has been insufficient research to provide an evidence base for 

the role of the general practitioner (GP) in obesity prevention, their role at the forefront 

of providing primary care in Australia is recognised as having ‘enormous potential to 

encourage patients to take greater responsibility for their health, which includes changing 

lifestyle’ (RACGP 2006). 

Several initiatives over recent years have targeted GPs as a crucial point of intervention 

in obesity. In 2003 the National Health and Medical Research Council published two 

guidelines for GPs (Overweight and obesity in adults and Overweight and obesity in children 

and adolescents). The guidelines focus on the clinical management of overweight and 

obesity to be applied in the general practice consultation. 


publications. The first, Guidelines for preventive activities in general practice (the ‘red book’) 

(RACGP 2005) also focuses on the role of the GP within the consultation recommending 



a screening approach particularly for children and adolescents. SNAP: A population 

health guide to behavioural risk factors in general practice (RACGP 2004) provides more 

extensive information and recommendations regarding overweight and obesity (among 

other common lifestyle risk factors), focusing on a patient education and behaviour 

modification approach based upon the 5As (ask, assess, advise, assist, arrange). Lastly, 

Putting prevention into practice: guidelines for the implementation of prevention in the 

general practice setting (the ‘green book’) (RACGP 2006) assists in the development of 

systems within general practice to support prevention activities at the practice as well as 

the consultation level. 

In further support of the GP’s role in obesity prevention, the Commonwealth Department 

of Health and Ageing, in the 2003/04 budget, funded the Lifestyle Prescriptions program 

(commonly known as Lifescripts). Lifescripts is being implemented through local divisions 

of general practice, promoting risk factor management in general practice and primary 

health care services. Lifestyle prescriptions are tools for GPs to use when providing lifestyle 

advice to patients. Advice may be about quitting smoking, increasing physical activity, 

eating a healthier diet, maintaining healthy weight, reducing alcohol consumption, or a 

combination of these. 


In 2003, the National Obesity Taskforce, with representation from Commonwealth and 

state health jurisdictions, developed a four-year national action plan for tackling obesity, 

known as Healthy weight 2008: the national action agenda for children and young people 

and their families (NOTF 2003). The goals are to: 

• 

• 

• 

• 

• 

achieve healthier weight in children and young people 

increase the proportion of children and young people participating in and maintaining 

healthy eating and adequate physical activity 

strengthen the knowledge, skills, responsibility and resources of all people and 

communities to achieve optimal weight 

address social and environmental determinants of poor nutrition and physical inactivity 

focus action on giving children, young people and families the best possible chance of 

maintaining a healthy weight. 

A ministerial taskforce to coordinate an anti-obesity campaign was announced in July 

2006. It includes government, industry and community representation from the areas of 

health, communications, education, and sport. 

Healthy weight 2008 was preceded by Acting on Australia’s weight: a strategic plan for 

the prevention of overweight and obesity (NHMRC 1997), Eat well Australia: a strategic 

framework for public health nutrition, (SIGNAL 2001), and the National physical activity for 

health action plan (NPHP 2005). 

Many of the states and territories have developed frameworks and action plans similar to 

the Commonwealth initiative. The New South Wales and Victorian governments held child 

obesity summits in 2002 and Queensland held a summit in 2006 to focus attention and 

action on rising rates of overweight and obesity in young people. 

Internationally, the World Health Organization has adopted a Global Strategy on Diet, 

Physical Activity and Health, which was endorsed by the May 2004 World Health 

Assembly (WHO 2004). The International Union Against Cancer has developed a policy to 


address action on a range of cancer prevention issues including obesity, in Evidence-based 

cancer prevention: strategies for NGOs (UICC 2004). 

Other relevant food policy contexts include the regulatory systems for food safety and food 

marketing. Food standards and regulation fall under the domain of the statutory authority, 

Food Standards Australia New Zealand. This has responsibility for setting standards for the 

production and sale of food in Australia, including food labelling issues such as nutrition 

and health claims. 

In Australia, food marketing operates under a system of co-regulation, with the Australian 

Communications and Media Authority having responsibility for the Children’s Television 

Standards, which include some regulations for limiting food advertising to children. The 

Advertising Standards Bureau administers the industry codes of practice developed by Free 

TV Australia and the Australian Association of National Advertisers, which add very little to 

the statutory regulations. 


The Cancer Council Australia supports the National Health and Medical Research Council 

recommendations in relation to body weight and the maintenance of a balance between 

energy intake (healthy eating) and energy output (physical activity). For adults, the 

guideline states, ‘Prevent weight gain: be physically active and eat according to your 

energy needs’ (NHMRC 2003c). For children, the guideline does not refer specifically to 

body weight, but reads, ‘Children and adolescents need sufficient nutritious foods to grow 

and develop normally. Growth should be checked regularly for young children. Physical 

activity is important for all children and adolescents’ (NHMRC 2003b). 

The Cancer Council recommends that adults maintain a healthy weight within a BMI 

range of 18.5–25 kg/m2. To achieve and maintain a healthy weight, The Cancer Council 

recommends regular physical activity and eating according to energy needs. Making fruit, 

vegetables, cereals and other low fat foods the basis of the diet may assist with achieving 

and maintaining healthy body weight. 

Aims 

Our aims are to encourage the Australian population to: 

• 

• 

• 

• 

maintain a healthy body weight throughout life by means of a balance of food intake 

and physical activity 

consume nutritionally adequate and varied diets based primarily on foods of plant origin 

such as vegetables, fruit, pulses and wholegrain cereals, as well as lean meats, fish and 

low fat dairy products 

adopt a physically active lifestyle 

ensure children have a nutritionally adequate and varied diet and adopt an active lifestyle 

appropriate to different age groups. 

We also aim to advocate for more supportive environments to make healthy choices easier 

choices. 






link between obesity and 



professional groups 





that promote healthy weight 

A reduction in rising rates of 

obesity in both children and 

adults 



trends 




Monitor and clarify best evidence on the relationship between obesity 






specifically for general practice, to improve evidence-based interventions 

by health professionals 


relationship between obesity and cancer to complement the Australian 

policy context 



Advocate for nationwide social marketing campaigns that promote 

a healthy body weight across the life course, which are coordinated, 

sustainable and far reaching 

Encourage the Australian Government to commit to long-term 

investment in promoting a healthy weight 

Support and deliver effective community interventions at a local and 

state level to address healthy weight 

Contribute to national developments on reducing obesity in Australia 

through collaboration and partnerships with major agencies 

Recognise the significant public health gains to be made in reducing 

rates of obesity in childhood 

Support and conduct high-quality epidemiological research further 

clarifying the relationship between obesity and cancer 

Support and conduct high-quality behavioural research further clarifying 

the barriers and enabling factors for people to adopt healthy eating and 

physical activity behaviours 



Encourage the Australian Government to fund a comprehensive National 

Nutrition and Physical Activity Survey of both children and adults, which 

is conducted as a minimum on a regular five-year basis



More supportive 

environments that assist 

people to make healthy 

food choices and provide 

opportunities to be physically 

active 




Encourage the Australian Government to address the broader social and 

environmental determinants of poor nutrition and sedentary lifestyles, in 

particular: 

• call for a ban of television food advertising to children 

• develop effective regulatory systems for decreasing the level of food 

marketing to children (including television food advertising and other 

forms of food marketing) 

• improved access to healthy food choices for people who are socially or 

geographically disadvantaged 

• develop effective regulatory systems for communicating accurate 

nutrition and health information on food labels 

• improve health literacy for reading food labels 

• improve physical environments to increase opportunities for physical 

activity 


Participate on the Coalition on Food Advertising to Children 

Coordinate public health responses to relevant food regulatory issues, 

including changes to food labelling, through participation on the 

Coalition on a Healthy Australian Food Supply 


• evaluate healthy weight interventions 


prevention 


prevention 



Note: Refer also to the action plans of the physical activity and nutrition chapters when considering promotion of healthy 

weight. 


101 


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A l c o h o l 

Introduction 

Alcohol is a known risk factor for cancer. There is no 

evidence to suggest that alcohol may be protective for 

any form of cancer. 

Alcoholic beverages have both nutritive and psychoactive properties. The history of 

alcohol use by humans can be traced back over thousands of years, where it has played 

an important role in the culture of a diverse range of communities throughout the world. 

Heavy drinking has been associated with Australian culture since the early days of 

European settlement (Room 1988). 

The National Health and Medical Research Council has established Alcohol guidelines for 

Australians based on a standard drink (i.e. 10 grams of ethanol). In order to avoid alcoholrelated 

harms in the short term, the guidelines recommend no more than six standard 

drinks for males and no more than four standard drinks for females during any single 

drinking occasion (NHMRC 2001). For individuals drinking more than this, the risk of injury 

or death due to short-term harms (e.g. road injury, violent assault, drowning, falls, alcoholic 

poisoning) increases significantly. Consumption in excess of these levels is categorised as 

either ‘risky’ or ‘high-risk’ depending on the amount drunk. 

In relation to long-term harms that can arise from ongoing excessive levels of consumption 

(e.g. alcoholic liver cirrhosis, a range of cancers, heart disease and stroke, dependence 

and psychosis) the National Health and Medical Research Council recommends that males 

drink no more than 28 standard drinks over a week and females no more than 14 standard 

drinks (NHMRC 2001). Drinkers who consume more than this are at risk of experiencing 

‘chronic’ alcohol-related disease and disability. Since chronic alcohol-related illness tends 

to develop over a lifetime of drinking, they occur most frequently among people over 45 

years of age (NHMRC 2001). 

The National Health and Medical Research Council alcohol guidelines reflect the fact that 

women are more susceptible to adverse effects of alcohol because they typically have a 

smaller body size and metabolise alcohol differently (NHMRC 2001). 

Information on the health burden attributable to alcohol in Australia largely comes from an 

examination of research into its health effects and estimation of the proportion of diseases 

(including cancer) attributable to alcohol e.g. (English et al. 1995; Ridolfo & Stevenson 

2001; Chikritzhs et al. 2003). 

The link between alcohol and cancer 

Alcohol is a known risk factor for cancer. In 1988 the International Agency for Research on 

Cancer classed alcohol as a Group 1 carcinogen (the highest IARC classification in humans) 

for cancers of the mouth, pharynx, larynx, oesophagus and liver (IARC 1988). 

Nearly 10 years later, the review by the World Cancer Research Fund and the American 

Institute of Cancer Research in 1997 concluded that there was convincing evidence 


10 

A l c o h o l

(the highest level of evidence in this report) that alcohol increases the risk of mouth, 

pharyngeal, laryngeal and oesophageal cancers (WCRF & AICR 1997). This review also 

found convincing evidence that alcohol increases the risk of primary liver cancer, probably 

by way of alcoholic cirrhosis. It found probable evidence that alcohol increases the risk of 

colorectal cancer and breast cancer, even at very low levels of consumption. The report 

states that risk is a function of the amount of alcohol consumed (WCRF & AICR 1997; IARC 

1988). 

More recently, the evidence for a significant relationship between alcohol and female 

breast cancer has grown, with a number of reviews concluding that the risk of breast 

cancer increases with increasing alcohol consumption. An international collaborative metaanalysis 

including 53 epidemiological studies concluded that the relative risk of breast 

cancer increased by 7.1% (95%CI 5.5−8.7%) for each additional 10 g of alcohol consumed 

daily (Hamajima et al. 2002). An Australian meta-analysis concurred with the international 

review, finding a significant dose–response relationship for the development of breast 

cancer, even at low levels of consumption, and increasing risk with increasing age (Ridolfo 

& Stevenson 2001). 

The most up to date and compelling review has just been released from IARC in 2007 and 

has confirmed that alcohol is a risk factor for the same cancers classified in 1988 and also 

for colorectal and breast cancer (IARC 2007). 

The table below summarises the current state of evidence showing an association between 

alcohol and specific cancer sites. There is convincing evidence that alcohol increases the 

risk of cancer of the mouth, pharynx, larynx, oesophagus, colon, rectum, breast and liver 

(WCRF & AICR 1997; IARC 1988; English et al. 1995; Single et al. 1999; Bagnardi et al. 

2001; Chapman 2003; Ridolfo & Stevenson 2001; IARC 2007). 

The overall evidence suggests that alcohol is not a risk factor for cancers of the prostate, 

pancreas and bladder (WCRF & AICR 1997; IARC 1988; English et al. 1995; Single et al. 

1999; Bagnardi et al. 2001; Chapman 2003; Ridolfo & Stevenson 2001; IARC 2007). For 

stomach, and lung cancer, the evidence is inconsistent or insufficient to conclude causality. 

For lung cancer, the studies generally do not adequately control for confounding from 

smoking. 

Excessive alcohol consumption carries a strong social stigma in many populations 

and most surveys which ask people about the amount of alcohol they consume may 

substantially underestimate true levels of consumption (2000). This could result in an 

underestimation of the actual carcinogenic effect of the habit and therefore alcohol is 

possibly a stronger risk factor than perceived (Stewart & Kleihaus 2003). 

Smoking and alcohol together have a synergistic effect on risk of cancers of the larynx, 

oropharynx and oesophagus (Jensen et al. 1996; Doll et al. 1999). This means the 

combined effects of smoking and alcohol greatly exceed the risk from either one of these 

factors alone. Alcohol and tobacco interact in a multiplicative way on the risk of cancers of 

the upper aero-digestive tract. For example, compared with the risk for non-smoking nondrinkers, 

the approximate relative risks for developing mouth and throat cancer are seven 

times greater for those who use tobacco, six times greater for those who use alcohol, and 

38 times greater for those who use both tobacco and alcohol (Blot 1992). 

This synergistic effect of alcohol and smoking has been estimated to be attributable 

for over 75% of cancers of the upper aero-digestive tract in developed countries (Blot 

1992). Alcohol has an independent effect on the risk of oral, pharyngeal, laryngeal and 

oesophageal cancers, but it is its synergistic effect with smoking that is most significant. 


There are also indications that alcohol and hepatitis B virus infection may exert a joint effect 

on cancer of the liver (Brechot, Nalpas & Feitelson 1996; Schiff 1997). Also of concern is 

the difference noted in liver cancer between Aboriginal Australians and the non-Aboriginal 

population; in a West Australian study the incidence and rate of deaths from liver cancer 

were 3.5 and 3.6 times higher for Aboriginal males than for non-Aboriginal males 

(Thompson & Irvine 2001). This highlights an important area for further investigation and 

action. 

In conclusion, the association between alcohol consumption and an increased risk of some 

cancers has been confirmed. There is a dose–response relationship in most studies after 

controlling for potential confounders such as tobacco smoking, and the relations appear to 

hold for women as well as men. The relationship is not a straight line, but shows upward 

curvature at higher drinking levels (Edwards et al. 1995). 

Table 1.12 Evidence of a link between alcohol and cancer 

Type of cancer Association between alcohol 

and cancer 

Level of evidence for causality 

Breast Increases risk Convincing 

Larynx Increases risk Convincing 

Liver Increases risk Convincing 

Mouth Increases risk Convincing 

Oesophagus Increases risk Convincing 

Pharynx Increases risk Convincing 

Colon/rectum Increases risk Convincing 

Lung Potential risk Insufficient 

Stomach Potential risk Insufficient 

Bladder Inconsistent and insufficient 

evidence of a relationship 

Pancreas Inconsistent and insufficient 


Prostate Inconsistent and insufficient 


Sources: Rehm et al. 2004; IARC 2007 

n/a 

n/a 

n/a 


10 

A l c o h o l

How the amount of disease caused by alcohol is 

estimated 

The amount of morbidity and mortality which is attributable to drinking alcohol in a 

population has typically been estimated using what may be referred to as the ‘populationattributable 

fraction method’. Since it is not possible to know about the drinking habits 

of all individuals who suffer from disease or injury, it is necessary to apply summary 

measures, based (in part) on collections of research studies, of the risk of developing or 

dying from a specific condition at various levels of consumption (i.e. relative risk or odds 

ratio) (Chikritzhs et al. 2002). 

There are two methodological frameworks for quantifying morbidity and mortality 

attributable to alcohol: 

• 

• 

The first method is based on the relative risk of death or disease among low-risk, risky 

and high-risk drinkers when compared to non-drinkers. 

The second method is based on a comparison between risky, high-risk drinkers and lowrisk 

drinkers and thus, unlike the first method, is not concerned with abstainers. 

In order to estimate the population-attributable fraction due to alcohol for any specific 

condition, in addition to condition-specific relative risk estimates, it is also necessary to 

have accurate information on the prevalence of alcohol consumption in the community 

of interest. Both the framework for estimating relative risks and estimates of drinking 

prevalence can dramatically influence the population -attributable fraction. The range of 

variability can be demonstrated by comparing population-attributable fraction estimates 

made by English and colleagues (English et al. 1995) versus those made by Ridolfo and 

Stevenson (2001) in a more recent publication (see Table 1.13 below). 

Ridolfo and Stevenson used non-drinkers as the reference group to estimate the 

contribution of low-risk, risky and high-risk alcohol consumption and applied drinking 

prevalence estimates from a 1998 national survey (Ridolfo & Stevenson 2001). English 

and colleagues used low-risk drinkers as the reference group and national consumption 

estimates from 1989/90: they were thereby confined to estimating morbidity and mortality 

due to risky and high-risk drinking only (English et al. 1995). As a direct result, population 

-attributable fractions due to alcohol for cancers—most of which include substantial risk 

at low levels of drinking when compared to abstinence—were relatively small compared 

to those estimated by Ridolfo and Stevenson. The rationale given for the English et al. 

approach was that it was consistent with the public health policy of minimising harm rather 

than achieving abstinence. Using low-risk drinkers as the reference group also avoids the 

need to incorporate protective effects of low level drinking on cardiovascular disease in 

mortality and morbidity estimates (Chikritzhs et al. 2002). It also avoids the difficulty of 

using as a reference group current abstainers, who may include both lifelong abstainers 

and ‘sick quitters’: those who stopped drinking when they developed health problems. 

In order to address the uncertainty and variability in relation to alcohol aetiologic 

fractions and subsequent mortality and morbidity estimates for Australia, a consortium 

of researchers attempted to establish a consensus position. They recommended that 

future estimates use abstainers as the reference group and that results be presented and 

disseminated in such a way that both the losses and savings in mortality and morbidity 

from each of the drinking levels could be distinguished—as opposed to a single estimate 

(Chikritzhs et al. 2002). This approach has subsequently been adopted by national costing 

studies and recent estimates of alcohol-attributable morbidity and mortality in Australia 

(e.g. Collins & Lapsley 2002; Chikritzhs et al. 2003) and is the most appropriate method for 

estimating the effect of alcohol-attributable cancers. 


Table 1.13 Cancer site and percentage attributable to alcohol 

Cancer site English et al. (1995) Ridolfo & Stevenson (2001) 

Males % Females % Males % Females % 

Breast − 3 − 12 

Larynx 21 13 51 46 

Liver 18 12 39 35 

Oesophagus 14 6 46 40 

Oropharynx 21 8 40 31 

The impact 

The harm caused by alcohol, such as the development of cancer and other illnesses and 

injuries, has been estimated at 4.9% of the total disease burden in Australia (Mathers, Vos 

& Stevenson 1999). At low to moderate intakes, alcohol consumption appears to reduce 

the risks of certain conditions, including ischaemic heart disease, stroke and gallstones. 

Taking into account these benefits, as well as the harms, alcohol is estimated to be 

associated with 2.2% of the total disease burden in Australia (Mathers, Vos & Stevenson 

1999). This demonstrates the importance of distinguishing between the effects of drinking 

that are low-risk, risky (where the risk of harm increases beyond any possible benefit) and 

high-risk (where there is substantial risk of serious harm) (NHMRC 2001). 

There is no evidence to suggest that alcohol may be protective for any form of 

cancer. Ridolfo and Stevenson estimated that in 1998, 1157 cancer deaths and 3171 

hospitalisations were attributable to any level of alcohol consumption (Ridolfo & Stevenson 

2001). The number of cancer deaths attributed to alcohol was greater than the combined 

total of all deaths attributed to any type of illicit drug (Ridolfo & Stevenson 2001). Over 

the years between 1992 and 2001, cancer was the third most common cause of alcoholattributable 

death, with only road crash injury and alcoholic liver cirrhosis accounting for 

greater numbers of premature deaths (Chikritzhs et al. 2003). 

Over half a million hospital episodes (577,269) were estimated to have been caused by 

risky or high-risk drinking in the years between 1993 and 2001 (Chikritzhs et al. 2003). 

Deaths caused by alcohol contribute substantially to potential years of life lost, which is 

a measure of the gap in years between age of death and the age before which death is 

considered premature. It has been estimated that about 17 years of life are prematurely lost 

for every death caused by risky and high-risk drinking in Australia. This is equivalent to over 

52,030 years of life lost every year from premature alcohol-attributable death (Chikritzhs et 

al. 2003). 

Undoubtedly, alcohol-attributable cancers represent a substantial proportion of the burden 

of disease and injury in Australia. The financial cost of disease, injury and crime caused 

by alcohol in this country has been estimated to be in excess of $7.6 billion. The exact 

proportion attributable to cancer is not clear (Collins & Lapsley 2002). 


111 

A l c o h o l

The challenge 

Adults 

Alcohol is a significant cause of drug-related harm and is one of the highest preventable 

causes of death and hospitalisation in Australia (NEACA 2001). According to the 2004 

National Drug Strategy Household Survey, some 9% of respondents aged 14 years or older 

drank alcohol daily, and 41% drank at least weekly (AIHW 2005). Thirty-three per cent of 

people drank less often but had drunk in the last 12 months. About 7% were ex-drinkers 

and about one in 10 people sampled had never had a full serve of alcohol (AIHW 2005). 

In 2004, about 21% of all those surveyed reportedly drank at risky or high-risk levels for 

short-term harm, compared to about 10% who were at risk of long-term harm. One in 10 

Australians surveyed reported drinking at levels considered risky or high risk for both short- 

and long-term harm in the previous 12 months. Males (24%) were more likely to have 

consumed alcohol in a risky or high-risk fashion for short-term harm than females (17%) 

(AIHW 2005). 

Substantial amounts of alcohol are consumed at levels above the National Health and 

Medical Research Council guidelines for short-term harm. In 2001, some 62% of all alcohol 

consumed by Australians aged 14 years and older was drunk during a single drinking 

session which exceeded low-risk levels for episodic drinking (e.g. binge drinking). For 

younger age groups (both males and females) this proportion was substantially higher and 

ranged between 78% and 85%. About 44% of all alcohol reported to have been drunk in 

2001 was consumed by people who were at risk or high risk of the long-term effects of 

drinking (e.g. various cancers) (Chikritzhs et al. 2003). 

Teenagers 

Experience with alcohol is common among secondary school students, with use increasing 

with age (White & Hayman 2006). By the age of 15 around 90% of students had tried 

alcohol, and by age 17, 70% of students had drunk alcohol in the month prior to the 

Australian School Students Alcohol and Drug (ASSAD) survey. The proportion of students 

drinking in the week prior to the survey increased with age, from around 16% of those 

aged 13 to about half of those aged 17 years. At age 13, about 2% of students reported 

having drunk beyond low-risk levels for short-term harms; by age 17 the proportion of 

students drinking at risky and high-risk levels for short-term harms increased to about 

21% (White & Hayman 2006). Analyses of national survey data has also shown that the 

proportion of females aged between 14 and 17 years who drank at risky/high-risk levels 

for long-term harms increased from 1% in 1998 to 9% in 2001. Among males of the same 

age, there was a small decline from 4.3% to 2.7% over the same years (Chikritzhs, Pascal & 

Jones 2004). 


Aboriginal and Torres Strait Islander Australians are more likely to abstain from alcohol 

than the general population, nevertheless, alcohol-related problems are of particular 

concern for these peoples. The most reliable national survey of Aboriginal and Torres Strait 

Islander drinking levels to date (Chikritzhs & Brady 2006) has estimated that about 51% of 

Indigenous Australians drink at risky or high-risk levels compared to about 11% among the 

non-Indigenous population (AIHW 1995). Deaths from alcohol-attributable conditions are 

about two and a half times greater for Aboriginal and Torres Strait Islander peoples when 

compared to the general population (Chikritzhs & Brady 2006) and males tend to have 

higher levels of consumption than females (AIHW 1995). The consumption of cheap cask 


wine is of particular concern for Aboriginal peoples living in rural and remote regions (Gray 

et al. 2000). 

Trends 

In general, from 1998 to 2001, the estimated proportion of the population consuming 

alcohol at risky/high-risk levels for chronic harm remained relatively stable among males 

and females of all ages, with an increase among girls aged 14 to 17 years and a small 

decline among young males being the main exceptions (Chikritzhs et al. 2003). 

Adult per capita pure alcohol (i.e. ethanol) consumption in Australia has remained relatively 

stable over the past decade and has most recently been estimated at about 9.0 litres, 

placing Australians in 22nd place in world rankings (WARC 2004). Beer consumption 

contributes to the bulk of all alcohol consumed in Australia, although there has been 

a substantial shift from regular to mid/low-strength beers since a tax saving for lower 

strength beers was introduced by the Australian Government. The market share of wine 

has increased dramatically since the 1960s but has remained relatively stable in recent 

years (World Drink Trends 2003). 


Public health policies on reducing alcohol consumption have a strong evidence base, 

which derives from research and interventions not necessarily directly related to cancer 

control. 

Work in various countries has demonstrated public health measures of proven 

effectiveness in the following areas: 

• 

• 

• 

• 

• 

• 

• 

retail price influences on alcohol consumption and taxation of alcohol as a prevention 

strategy 

access to alcohol and the effects of availability on consumption and alcohol-related 

problems 

restricting advertising and marketing of alcohol 

public safety and drinking within particular contexts such as driving or attendance at 

sporting venues 

community supported intervention programs which focus on enforcing laws in relation 

to legal minimum purchase age and drinking to intoxication 

giving information about alcohol through mass media campaigns and labelling 

individually directed interventions (e.g. brief intervention by general practitioners and 

treatment of alcohol dependence by pharmacotherapies or psychosocial interventions). 

Successful community-based interventions are typically those which are supported by the 

community itself, that are evidence-based and provided with adequate access to relevant 

expertise, infrastructure and human resources. A multi-component approach with a focus 

on reducing alcohol availability and increasing effective enforcement are fundamental to 

the success of community-based interventions (Loxley et al. 2004). 

The National Alcohol Strategy 2006 to 2009 is a plan for action, designed to reflect 

the National Drug Strategic Framework and developed through collaboration between 

governments, non-government organisations, industry partners and the broader Australian 

community. The goal of the National Alcohol Strategy is to prevent and minimise alcoholrelated 

harm to individuals, families and communities in the context of developing safer 


113 

A l c o h o l

and healthy drinking cultures in Australia. The National Alcohol Strategy has focused on 

four priority areas: intoxication, public safety and amenity, health impacts, and cultural 

place and availability (National Alcohol Strategy 2006). 


It is interesting to note that at the current time, Australia has two sets of alcohol 

recommendations produced by the National Health and Medical Research Council. 

The National Health and Medical Research Council considers the effects of alcohol on 

cancer in the Australian alcohol guidelines: health risks and benefits developed in 2001 

(NHMRC 2001). In these guidelines the National Health and Medical Research Council 

notes, ‘There is clear evidence to show that alcohol is associated with an increased risk 

of cancer overall and that it is a cause of cancer of the mouth, throat and oesophagus. 

In addition, the evidence suggests that it may also play a role in other specific cancers. 

In particular, further research is needed to clarify the possible role of alcohol in relation 

to breast cancer and bowel cancer’ (p. 74). The National Health and Medical Research 

Council emphasises that, ‘Unlike cardiovascular disease, there is no evidence that alcohol 

has any protective effect against cancer, at any level’ (p. 74). Also, in relation to heart 

disease, ‘The benefits of alcohol in preventing heart disease can be achieved with as little 

as half a standard drink per day … Similar benefits can also be gained from strategies such 

as regular exercise, giving up smoking and a healthy diet’ (pp. 68 & 69). 

Moreover, recent research suggests that the protective effect of alcohol on cardiovascular 

disease may have been exaggerated and many studies which have demonstrated an 

apparent increase in cardiovascular disease among non-drinkers have applied faulty 

methods and are subject to substantial measurement error (Fillmore et al. 2006). 

Thus, National Health and Medical Research Council Guideline 12 is also relevant: 

• 

• 

• 

• 

People who choose not to drink alcohol should not be urged to drink to gain 

any potential health benefit and should be supported in their decision not to 

drink. 

Guideline 1(a) states: To minimise risks and gain benefits in the longer term: 

Men should drink an average of no more than four standard drinks a day, and no more 

than 28 standard drinks per week 

Women should drink an average of no more than two standard drinks a day, and no 

more than 14 standard drinks per week. 

An Australian standard drink contains 10 g of alcohol (e.g. 425 ml light beer, 285 ml regular 

beer, 100 ml wine, 60 ml fortified wine, or 30 ml spirits or liqueurs). 

The National Health and Medical Research Council Dietary guidelines for Australian adults 

released in 2003 have set a lower recommended level of alcohol consumption based on 

the energy density of alcohol contributing to weight problems (NHMRC 2003). The dietary 

guidelines advise adults: 

Limit your alcohol intake if you choose to drink. 

Because of alcohol’s effect on both short- and long-term health, and because of 

the additional kilojoules it provides in the diets of a society with increasing rates 

of obesity, adults—if they drink at all—should limit their average daily intake of 

alcohol to no more than two standard drinks a day for men and one standard 

drink a day for women. 


The Cancer Council supports these lower recommendations for alcohol (as specified in the 

National Health and Medical Research Council Dietary guidelines for Australian adults) as 

drinking at these levels is both more appropriate for preventing obesity and decreasing the 

risk of all-cause mortality and cancer. The Cancer Council recommends that, to reduce the 

risk of cancer, alcohol consumption should be limited or avoided. For people who do drink 

alcohol, The Cancer Council recommends the following: 

• 

• 

For men—an average of no more than two standard drinks a day. 

For women—an average of no more than one standard drink a day. 

One of the primary aims of the National Alcohol Strategy is to improve health outcomes 

among all individuals and communities affected by alcohol. To achieve this objective in 

relation to cancer, The Cancer Council Australia and member cancer councils support 

the priority areas and actions outlined in the National Alcohol Strategy to reduce alcoholrelated 

harms and health consequences. 

The role of general practice 

The role of general practice in chronic disease prevention is potentially important, given 

that 86% of the population have at least one visit to their general practitioner (GP) every 

year (RACGP 2005). 

However, a review of primary care interventions in relation to alcohol gives mixed results. 

While there seemed to be evidence that GP intervention was effective (NHMRC 1996), 

this has become less clear in recent years. There still appears to be strong recognition of 

the potential for the GP to act as an intervention point (RACGP 2005; Loxley, Toumbourou 

& Stockwell 2005) and research is now tending to focusing on how to engage and 

train general practice to be more effective in providing alcohol advice (Funk et al. 2005; 

McCambridge et al. 2004). Certainly as a single point of intervention, evidence for efficacy 

is weakest. However as part of a multi-layered approach that includes policy, community 

and family interventions there is more potential for success in reducing at-risk levels of 

alcohol consumption (Holmwood 2002; Loxley, Toumbourou & Stockwell 2005). 


publications relating to the role of general practice and alcohol. The first, Guidelines for 

preventive activities in general practice (the ‘red book’) (RACGP 2005), focuses on the role 

of the GP within the consultation, recommending that all patients should be asked about 

the quantity and frequency of alcohol intake and number of alcohol-free days each week 

from 14 years of age and those with at-risk patterns of alcohol consumption should be 

offered brief advice to reduce their intake. Frequency of assessment varies depending on 

level of risk identified. All patients should be asked about frequency and intake every three 

years; those with an increased risk (such as people with high blood pressure, liver disease, 

pregnancy, etc.) should be asked and given brief advice every 12 months. Patients who 

report exceeding the recommended frequency and intake should be followed up monthly 

with a brief counselling intervention tailored to reduce alcohol consumption. Drug therapy 

is recommended for those patients who are physically or psychologically dependant 

or those with psychological, physical or social consequences of excessive alcohol 

consumption, and these patients should be followed up at each visit. 

Their more specific publication: SNAP: A population health guide to behavioural risk 

factors in general practice (RACGP 2004) provides more extensive information and 

recommendations regarding alcohol (among other common lifestyle risk factors), focusing 

on a patient education and behaviour modification approach based upon the 5As (ask, 

assess, advise, assist, arrange). Lastly, their publication Putting prevention into practice: 

guidelines for the implementation of prevention in the general practice setting (the ‘green 


115 

A l c o h o l

ook’) (RACGP 2006) assists in developing systems in general practice to support 

prevention activities at the practice and consultation levels. 

In further support of the GP’s role in promoting a healthy lifestyle and reducing harmful 

levels of alcohol, the Commonwealth Department of Health and Ageing, in the 2003/04 

budget, funded the Lifestyle Prescriptions program (commonly known as Lifescripts). 

Lifescripts is being implemented through local divisions of general practice, promoting 

risk factor management in general practice and primary health care services. Lifestyle 

prescriptions are tools for GPs to use when providing lifestyle advice to patients. Advice 

may be about quitting smoking, increasing physical activity, eating a healthier diet, 

maintaining healthy weight, reducing alcohol consumption, or a combination of these. 


There are a number of initiatives and evidence-based materials that point the way in policy 

directions on alcohol control in Australia. Some of the documents and programs that The 

Cancer Council supports and aims to complement are highlighted below. 

• 

• 

• 

The Dietary guidelines for Australian adults, released in 2003 (see discussion above) 

(NHMRC 2003). 

The National Alcohol Strategy 2006–2009: towards safer drinking cultures (National 

Alcohol Strategy 2006) 

The Australian alcohol guidelines: health risks and benefits (NHMRC 2001). The Cancer 

Council has developed a lower set of recommendations for safe drinking levels than 

what is recommended in these guidelines and supports a revision of these guidelines to 

better reflect the growing knowledge of the relationship between alcohol and cancer. 

Aims 

The Cancer Council’s aims are to: 

• 

• 

increase awareness of the link between alcohol consumption and cancer risk among 

health authorities, health professionals and the community 

encourage efforts to reduce alcohol consumption. 




link between alcohol and 



professionals 




Promote healthy policies 

in relation to alcohol 

consumption 


Monitor and clarify best evidence on the relationship between alcohol 


Ensure alcohol information in key messages is promoted to the public 

and relevant health professionals in publications, presentations, 

programs, media statements and where opportunities arise 


relationship between alcohol and cancer 



Identify, analyse and advocate for evidence-based policy initiatives to 

reduce alcohol consumption 

Act as a role model in the safe consumption of alcohol



trends 



References 

Alcohol 


clarifying the relationship between alcohol and cancer 

Support and conduct high-quality behavioural research to determine if 

increased knowledge about the link between alcohol and cancer will 

affect behaviour, and what sorts of messages should be communicated 

in any social marketing campaigns about responsible use of alcohol 

Conduct research to identify barriers and enabling factors for 

implementation of these recommendations in general practice and 

other health settings 

Australian Institute of Health and Welfare (AIHW) 2005. 2004 National Drug Strategy Household Survey: 

detailed findings. AIHW cat. no. PHE 66; Drug Statistics Series no. 16. Canberra: AIHW. 

Australian Institute of Health and Welfare (AIHW) 1995. National Drug Strategy Household Survey: urban 

Aboriginal and Torres Strait Islander Supplement 1994. Canberra: AIHW. 

Bagnardi V, Blangiardo M, La Vecchia VC & Corrao G 2001. A meta-analysis of alcohol drinking and cancer 

risk. Br J Cancer 85(11): 1700–5. 

Blot WJ 1992. Alcohol and cancer. Cancer Res 52(7 Suppl): S2119-23. 

Brechot C, Nalpas B & Feitelson MA 1996. Interactions between alcohol and hepatitis viruses in the liver. Clin 

Lab Med 16: 273–87. 

Chapman K 2003. Alcohol and cancer. Unpublished document prepared on behalf of The Cancer Council 

NSW. 

Chikritzhs T & Brady M 2006. Fact or fiction? A critique of the National Aboriginal and Torres Strait Islander 

Social Survey 2002. Drug Alcohol Rev 25(3): 277–87. 

Chikritzhs T, Catalano P, Stockwell T, Donath S, Ngo H, Young D & Matthews S 2003. Australian alcohol 

indicators, 1990–2001: patterns of alcohol use and related harms for Australian states and territories. Perth: 

National Drug Research Institute. 

Chikritzhs T, Pascal R & Jones P 2004. Under-age drinking and related harms in Australia. National Alcohol 

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Towards a standardised methodology for estimating alcohol-caused death, injury and illness in Australia. Aust 

N Z J Public Health 26(5): 443–50. 

Collins D & Lapsley H 2002. Counting the cost: estimates of the social costs of drug abuse in Australia in 

1998–9. National Drug Strategy Monograph Series no. 49. Canberra: Commonwealth Department of Health 

and Aged Care. 

Doll R, Forman D, La Vecchia C & Wouterson R 1999. Alcoholic beverages and cancers of the digestive tract 

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Edwards G, Anderson P, Babor T, Casswell S, Ferrence R, Giesbrexht N, Godfrey C, Holder H, Lemmens 

P, Makela K, Modanik L, Norstrom T, Osterberg E, Romelsko A, Room R, Simpura J & Skog O 1995. The 

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English DR, Holman CDJ, Milne E, Hulse GK, Codde JP, Bower CI, Corti B, de Klerk N, Knuiman MW, 

Kurinczuk JJ, Lewin GF & Ryan GA 1995. The quantification of drug-caused morbidity and mortality in Australia 

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Fillmore K, Stockwell T, Kerr W, Chikritzhs T & Bostrom A 2006. Moderate alcohol use and reduced mortality 

risk: systematic error in prospective studies. Addiction Res Theory 14(2): 101–32. 

Funk M, Wutzke S, Kaner E, Anderson P, Pas L, McCormack R, Gual A, Barfod S, Saunders J, World Health 

Organisation Brief Study Group 2005. A multicountry controlled trial of strategies to promote dissemination 

and implementation of brief alcohol intervention in primary health care: findings of a World Health 

Organization collaborative study. J Stud Alcohol 66(3): 379–88. 

Gray D, Saggers S, Sputore B & Bourbon D 2000. What works? A review of evaluated alcohol misuse 

interventions among Aboriginal Australians. Addiction 95(1): 11–22. 

Hamajima N, Hirose K, Tajima K, et al. 2002. Alcohol, tobacco and breast cancer—collaborative reanalysis 

of individual data from 53 epidemiological studies, including 58,515 women with breast cancer and 95,067 

women without the disease. Br J Cancer 87(11): 1234–45. 

Holmwood C 2002. Alcohol-related problems in Australia: is there a role for general practice? MJA 177: 

102–3. 

International Agency for Research on Cancer (IARC) 2007. Carcinogenicity of alcoholic beverages, vol. 96 of 

IARC monographs. Lyon: IARC. 

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Jensen CM, Paine SL, McMichael AJ & Ewertz M 1996. Alcohol. In Cancer epidemiology and prevention. 

Second edition, eds D Schotterfeld & T Carroll. New York: Oxford University Press. 

Loxley W, Toumbourou J & Stockwell T 2005. A new integrated vision to how to prevent harmful drug use. 

MJA 182(2): 54–5. 

Loxley W, Toumbourou J, Stockwell T, Haines B, Scott K, Godfrey C, Waters E, Patton G, Fordham RJ, Gray D, 

Marshall J, Ryder D, Saggers S, Williams J, Sanci L (eds) 2004. The prevention of substance use, risk and harm 

in Australia: a review of the evidence. Canberra: National Drug Research Institute and Centre for Adolescent 

Health. 

Mathers C, Vos T & Stevenson C 1999. The burden of disease and injury in Australia. Australian Institute of 

Health and Welfare. 

McCambridge J, Platts S, Whooley D & Strang J 2004. Encouraging GP alcohol intervention: Pilot study of 

change-orientated reflective listening. Alcohol & Alcoholism 39(2): 146–9. 

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Canberra: Commonwealth Department of Health and Ageing. 

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2001 to 2003–04. Canberra: Commonwealth of Australia. 

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——— 2001. Australian alcohol guidelines: health risks and benefits. Canberra: NHMRC. 

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Rehm J, Room R, Monteiro M, Gmel G, Graham K, Rehn N, Sempos C T, Frick U, Jernigan D 2004. Alcohol 

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Room R 1988. The dialectic of drinking in Australian life: from the rum corps to the wine column. Aust Drug 

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the implementation of prevention in the general practice setting. Second edition. South Melbourne: RACGP. 

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Schiff ER 1997. Hepatitis C and alcohol. Hepatology 26(3) (1 Suppl): S39–42. 

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Stockwell T & Chikritzhs T (eds) 2000. International guide for monitoring alcohol consumption and alcoholrelated 

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Cancer Foundation of Western Australia. 

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11 

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Section Two: 

Screening to detect cancer early

P r i n c i p l e s o f 

s c r e e n i n g 

Screening refers to the application of a test to a population which has no overt signs or 

symptoms of the disease in question, to detect disease at a stage when treatment is more 

effective. The screening test is used to identify people who require further investigation to 

determine the presence or absence of disease and is not primarily a diagnostic test. 

The purpose of screening an asymptomatic individual is to detect early evidence of an 

abnormality or abnormalities such as pre-malignant changes (e.g. by Pap test) or early 

invasive malignancy (e.g. by mammography) in order to recommend preventive strategies 

or treatment that will provide a better health outcome than if the disease were diagnosed 

at a later stage. 

It is a commonly held belief among health professionals and the community that ‘early 

diagnosis’ of cancer is beneficial and therefore screening is bound to be effective. 

However, it cannot be assumed that each person who has a screen-detected abnormality 

or cancer within a screening program will benefit from that diagnosis. For example, it 

is now understood that a substantial proportion of early abnormalities on Pap tests (i.e. 

dyplastic changes) will regress without treatment. The potential benefits of organised 

population screening program for cancer must thus outweigh any potential harms that 

may result in the use of a screening test in people who are otherwise well (Miller 1996) 

and there must be strong evidence, preferably from randomised trials, that a screening 

program is effective in reducing mortality from cancer. 

Principles for the introduction of population screening 

The accepted criteria for the assessment of evidence on benefits, risks and costs of cancer 

screening are the principles adopted by the World Health Organization (Wilson & Jungner 

1968): 

• 

• 

• 

• 

• 

• 

• 

• 

• 

• 

the condition should be an important health problem 

there should be a recognisable latent or early symptomatic stage 

the natural history of the condition, including development from latent to declared 

disease, should be adequately understood 

there should be an accepted treatment for patients with recognised disease 

there should be a suitable test or examination that has a high level of accuracy 

the test should be acceptable to the population 

there should be an agreed policy on whom to treat as patients 

facilities for diagnosis and treatment should be available 

the cost of screening (including diagnosis and treatment of patients diagnosed) should 

be economically balanced in relation to possible expenditure on medical care as a 

whole, and 

screening should be a continuing process and not a ‘once and for all’ project. 

Recommendations for or against population screening interventions are influenced by 

the relative strength of the available scientific evidence in relation to these criteria. Most 

importantly, there should be sufficient direct evidence from well-conducted studies that 

122 Section Two: Screening to detect cancer early

early detection improves health outcomes, and that the benefits of screening outweigh any 

potential harms. 

Australia currently has three population screening programs for cancer which meet the 

World Health Organization criteria. Screening programs for breast, cervical and bowel 

cancer are discussed in the following chapters. Two further chapters examine the evidence 

for screening for prostate cancer and melanoma and conclude that, at this stage, there is 

insufficient evidence to recommend population screening. 

The condition 

For the disease to be amenable to screening, there must be a latent stage or ‘window’ 

during which it would be possible to detect the disease before it reaches an advanced 

stage. Most cancers are slow growing and many have a pre-invasive or precursor stage 

during which early treatment is successful in halting progression to invasive cancer. 

For example, pre-malignant lesions of the cervix can be detected by regular Pap tests. 

However, the sites of many cancers are not easily visualised and potential screening 

tests are insufficiently accurate, so that screening asymptomatic people is ineffective in 

detecting early disease. 

If detection of cancer at an early stage is possible, it is crucial that appropriate intervention 

at that time has the potential to alter the course of the disease. Ideally there should be 

strong evidence from well-conducted clinical trials that early treatment or intervention 

improves outcome. 

Estimation of benefit from early detection on health outcome may be influenced by leadtime 

bias and length-time bias. 

Lead-time bias refers to the apparent improvement in survival that is seen when screening 

advances the time of diagnosis without any change in the actual time of death. In this 

case, increased survival merely reflects a greater period of time that the individual is aware 

of the presence of cancer. 

Length-time bias refers to the tendency of screening to detect a disproportionate number 

of cases of slowly progressing cancer compared with more aggressive cases. Rapidly 

growing cancers may progress from being undetectable at the time of screening to 

symptomatic during the interval between screens and thus are less likely to be detected at 

screening or at an early stage. 

The screening test (from Miller 1 p. xiii) 

The screening test must be sufficiently accurate to detect the condition earlier than in the 

absence of screening. Accuracy is measured by considering sensitivity and specificity of 

the screening test. 

‘Sensitivity’ refers to the ability of a test to correctly identify people who have disease i.e. 

the proportion of people with the disease at the time of screening who have a positive 

screening test. A test with poor sensitivity will miss cases (persons with disease) and will 

produce a large number of false negative results (true cases will be told incorrectly that 

they are free of disease). 

‘Specificity’ describes the ability of the test to correctly identify people who do not have 

the disease. A test with poor specificity will result in a high rate of false positives (healthy 

persons will incorrectly test positive and may be subject to more invasive diagnostic 

testing). 


123 

P r i n c i p l e s o f s c r e e n i n g

Another useful characteristic of a screening test is the positive predictive value (PPV), 

which is the likelihood of having disease if the screening test is positive (i.e. true positive). 

The PPV depends on the sensitivity and specificity of the test, and whether the condition 

is common or rare in the population being screened. In the context of breast cancer 

screening, for example, the PPV represents the total number of cancers diagnosed 

as a proportion of women who have been recalled for further investigations after 

mammography screening. 

Finally, the screening test must be acceptable to the population and cause minimal 

discomfort, or participation in the screening program will be low. For example, many 

women find having a Pap test uncomfortable or embarrassing and are subsequently underscreened. 

Substantial resources are consequently required for educational campaigns 

to encourage women to undergo Pap tests. Pain on compression is reported by a small 

number of women undergoing mammographic screening . Resources are devoted to 

radiographer training to address this issue. 

Ethical issues in population screening: balance of benefits and harms 

‘ The ethical imperative with all medical interventions is to endeavour to ensure 

that potential benefits will outweigh harm. This is particularly so of screening. If a 

patient asks a doctor for help the doctor is obliged to do his or her best to help but … 

(if) ... the doctor initiates a screening program there is a presumption that this must 

benefit the patient’ (Fowler & Austoker 1997 p. 1585). 

It is very difficult to determine the benefit of screening for an individual. The distinction 

between benefits to the community and to individuals needs to be borne in mind when 

considering recommendations to participate in organised population screening programs. 

Participants in screening programs are ostensibly healthy people, so a program should, at 

the very least, be able to demonstrate evidence of an overall benefit to the community and 

a minimum of risk that certain individuals may be disadvantaged by the program (Miller 

1996). Not only is it important that information on the effectiveness of screening programs 

be available, it should also be disseminated widely. Regular monitoring and evaluation of 

screening programs is also vital to ensure that effectiveness is maintained and improved 

where possible. 

Potential harms from screening 

It is essential to recognise that an organised population approach to screening, which 

ultimately achieves a net health benefit to a community, can result in adverse outcomes for 

some individuals. 

There is a risk that people who receive false negative results may experience delays in 

diagnosis and treatment. Some may develop a false sense of security and ignore warning 

symptoms. Increasingly, false negative results can give rise to legal action by people whose 

cancers appear to have been missed. 

A false positive result can mean that people without the disease undergo follow-up testing 

that may be uncomfortable, expensive, and, in some cases, potentially harmful. Rarely, this 

can lead to unnecessary treatment. There may be psychological consequences such as 

anxiety for both the patient and their family. 

For example, a woman with a false positive mammogram undergoing surgical investigation 

(e.g. a fine needle biopsy) incurs costs such as anxiety, time lost to the procedure, and 

possible adverse effects of the surgery. A person undergoing a colonoscopy as a result of a 


false positive faecal occult blood test faces the possibility of a bowel perforation during the 

procedure. This risk might be as high as 1 in 1000 (Winawer et al. 1997). 

Informed consent 

As screening is initiated by ‘the health system’, individuals invited to participate must be 

informed, prior to any testing, of potential adverse effects as well as the potential benefits. 

There are concerns that false negative results can give rise to legal action by people whose 

cancers appear to have been missed. It is important that it is understood that screening 

for any disease is never 100% effective and a negative result does not ever constitute a 

guarantee that an individual is free of disease. This must be communicated effectively to 

the potential participants in a screening program to allow informed consideration of their 

involvement before any test is done. Communications must address differences in literacy 

and language competency to ensure that individuals are properly informed. 

Economic issues in screening 

Implementation of possible screening programs will be influenced by consideration of the 

equal distribution of limited resources across the whole community for maximum benefit. 

Resources allocated to a screening program will lower resources available for other health 

needs. 

Determining the costs of screening involves the costs of the test and subsequent 

diagnostic tests and the costs associated with any hazard of the test as well as the 

costs of over-treatment 

balanced against 

reduced costs of therapy for the primary condition, reduced costs associated with 

less expenditure on the treatment of the advanced disease, and the economic 

value of the additional years of life gained (Miller 1996 p. 1444). 

References 

Fowler G & Austoker J 1997. Screening. In Oxford textbook of public health, eds R Detels, WW Holland, J 

McEwan & GS Omenn. Third edition. New York: Oxford University Press. 

Miller AB 1996. Fundamental issues in screening for cancer. In Cancer epidemiology and prevention, eds D 

Schottenfeld & J Fraumeni. Second edition. New York: Oxford University Press. 

Wilson JMG & Jungner G 1968. Principles and practices of screening for disease. Public health paper. Geneva: 

World Health Organization. 

Winawer S, Fletcher R, Miller L et al. 1997. Colorectal cancer screening: clinical guidelines and rationale. 

Gastroenterol 112: 594–642. 


125 

P r i n c i p l e s o f s c r e e n i n g

B r e a s t c a n c e r 

Screening mammography is the only tool we have 

Breast cancer in Australia 

for early detection that has been shown to reduce 

population mortality from breast cancer. 

In 2005, breast cancer was estimated to be the most common cancer (apart from 

non-melanoma skin cancer) diagnosed in women in Australia, with 12,957 new cases 

diagnosed. It is estimated that this will increase to 14,818 new cases in 2011 (AIHW, 

AACR, NCSG & McDermid 2005). Breast cancer was also the most common cause of 

cancer death among Australian women in 2005, with 2,719 deaths recorded (ABS 2007). 

Between 1990 and 2005, the rate of deaths from breast cancer decreased by about 2% per 

year (ABS 2007; AIHW 2005). 

The risk of developing and dying from breast cancer increases with age. In 2005 

approximately 23% of women with breast cancer were aged under 50 years, 51% were 

aged between 50 and 69 years and 26% were aged 70 years and over. A woman has one 

chance in eight of being diagnosed with breast cancer before the age of 85 (AIHW, AACR, 

NCSG & McDermid 2005). 

Figure 2.1 Time trends in breast cancer age-specific incidence and mortality rates 

New cases per 100,000 women 

350 

300 

250 

200 

150 

100 

50 

0 

70+ years 

50–69 years 

All ages 

< 50 years 

Approximate commencement of the 

BreastScreen Australia Program 

1988 1990 1992 1994 1996 1998 2000 2002 

12 Section Two: Screening to detect cancer early 

Deaths per 100,000 women 

140 

120 

100 

INCIDENCE MORTALITY 

80 

70+ years 

60 

50–69 years 

Approximate commencement of the 

40 

20 

0 

BreastScreen Australia Program 

All ages 

1987, compared to 51.3 deaths per 100,000 women in 2004. A similar pattern of decline in 

mortality rates occurred in women aged 70 and over, while rates for women under 50 years 

remained consistently below 15 deaths per 100,000 women over the period 1987–2001 

(AIHW & NBCC 2006). 

Can breast cancer be prevented? 

Despite epidemiological evidence of possible risk factors for breast cancer, at this stage 

there is limited potential for prevention. Most risk factors are not readily amenable to 

change, while lifestyle-related factors that could potentially be modified are associated 

with only a small proportion of breast cancer risk. It is important to acknowledge that most 

of these risk factors are not established causes of disease, instead serving as surrogate 

markers to differentiate individuals at different levels of risk. 

Apart from being female, the strongest risk factor for breast cancer is age; in Australia in 

2005 the estimated rates of breast cancer varied from 1.5 per 100,000 in women aged 

20 to 24 years, to 7.4 per 100,000 in women aged 25 to 29 years, to 305.7 per 100,000 in 

women aged 80 to 84 years (AIHW, AACR, NCSG & McDermid 2005). 

Having a mother, sister or daughter and/or father, brother or son who has had breast 

cancer also increases the risk of breast cancer; the more first-degree relatives affected and 

the younger the age of diagnosis, the higher the breast cancer risk. Despite the strength of 

family history as a risk factor for breast cancer, inherited genetic susceptibility accounts for 

only about 5% of cases; for eight out of nine women who develop breast cancer, there is 

no strong family history of the disease (CGHFBC 2001). 

Two important genes have been identified that are associated with an inherited 

susceptibility to breast and ovarian cancer: BRCA1 and BRCA2). Variations in other genes 

have also been associated with breast cancer risk (Singletary 2003). 

Other risk factors that are not easily modified include early menarche, late menopause, and 

no children or a first child at 30 years or older (Singletary 2003; NBCC 2006). 

Breastfeeding is also associated with a reduction in the risk of breast cancer, with women’s 

risk decreasing by 4.3% for each year they breastfeed (CGHFBC 2002). 

Studies have demonstrated that use of hormone replacement therapy (HRT) is associated 

with an increased risk of breast cancer that increases with duration of therapy and age 

(Baber, O’Hara & Boyle 2003; Million Women Study Collaborators 2003; Gertig et al. 

2003; Rossouw et al. 2002). There is some suggestion that women taking HRT also 

have an increased risk of dying from breast cancer (Million Women Study Collaborators 

2003). A recent comprehensive Australian review suggests little or no increase in risk for 

oestrogen-alone HRT but an increased risk for combination HRT containing oestrogen and 

progesterone (NHMRC 2005). Based on the review and Australian incidence figures, it has 

been estimated that four additional breast cancers will be seen per 1000 women in their 

50s taking combination HRT for five years. The risk decreases with time after cessation of 

treatment. A reanalysis of more than 50 studies on oral contraceptives and breast cancer 

found a small increase in the risk of developing breast cancer, but this risk returned to 

normal within 10 years of discontinuing oral contraceptives (CGHFBC 1996). 

Modifiable lifestyle factors have also been shown to have various associations with breast 

cancer. There is convincing evidence that alcohol consumption of more than two standard 

drinks a day increases the risk of breast cancer (WCRF & AICR 1997; NBCC 2006). It has 

been estimated that in Australia, approximately 5% of breast cancers are attributable to 


12 

B r e a s t c a n c e r

alcohol consumption (NBCC 2006). There is evidence of a dose−response relationship with 

alcohol consumption, with the relative risk of breast cancer increasing by 7.1% for each 

additional 10 g per day of alcohol (CGHFBC 2002). (Refer also to the alcohol chapter.) 

Diet, physical activity and the maintenance of a healthy weight may play some role in 

protecting against breast cancer. Various reviews have found moderate to weak evidence 

of the cancer-protective effect of vegetables and fruit (WCRF & AICR 1997; UK Department 

of Health 1998). 

The World Health Organization estimates that 10% of breast cancer worldwide can be 

attributed to physical inactivity (WHO 2002). An Australian appraisal of the impact of 

physical inactivity suggests that the population-attributable risk for breast cancer is 9% 

(Stephenson et al. 2000). 

A number of reviews have concluded that there is now clear evidence that physical activity 

can protect against breast cancer (IARC Working Group 2002; Thune & Furberg 2001). The 

risk reduction is around 20% to 40%. The association has been reported for both pre- and 

postmenopausal women, but it is as yet unclear which time period(s) in a woman’s lifespan 

are most important for physical activity in the development of breast cancer (IARC Working 

Group 2002). 

Overweight and obesity in postmenopausal women are also associated with increased risk 

of breast cancer (Singletary 2003); there is an increase in risk of around 30% in women 

with a body mass index at or above 28 kg/m2 compared to those with a body mass index 

below 21 kg/m2 (Boyle et al. 2003). 

The potential for chemoprevention of breast cancer (in particular oestrogen receptor 

positive cancers)—through the use of selective oestrogen receptor modulators such 

as tamoxifen and raloxifene and, more recently, aromatase inhibitors—is undergoing 

investigation in randomised controlled trials. Evidence suggests that tamoxifen and 

raloxifene can reduce the risk of breast cancer by about 50%. However, as tamoxifen is 

associated with an increased risk of endometrial cancer, blood clots, uterine bleeding, 

hot flushes and other menopausal symptoms, the potential benefits of tamoxifen do 

not outweigh the potential risks in otherwise well women (Cuzick et al. 2003). The use 

of raloxifene appears to be associated with fewer side effects. None of these drugs is 

currently approved for prevention of breast cancer in Australia. 

Tests and programs for breast cancer 

Mammography 

Screening mammography is the best method available for detecting breast cancer early 

(IARC 2002). It is the only tool we have for early detection that has been shown to reduce 

population mortality from breast cancer. 

Research on the effectiveness of mammography screening for breast cancer has occurred 

through randomised controlled trials in North America and Europe. These trials have 

indicated that the natural history of breast cancer can be interrupted and mortality reduced 

through the detection of invasive disease when tumours are small and at an early stage. In 

addition, mammography in the context of an organised population screening program is 

effective in the detection of a large proportion of early tumours in asymptomatic women. 

The International Agency for Research on Cancer concluded that routine mammographic 

screening reduced risk of dying of breast cancer by 25% in women aged 50 to 69 years 

(IARC 2002). 


Breast self-examination 

Breast self-examination (BSE) as a method of early detection has come under considerable 

scrutiny. 

Evidence from meta-analyses (Kosters & Gotzsche 2003; Hackshaw & Paul 2003; 

Humphrey et al. 2002) and randomised controlled trials (Thomas et al. 2002; Semiglazov 

et al. 2003) shows that BSE does not result in a reduction in the size or stage of tumours 

at diagnosis or a decrease in mortality from breast cancer. Findings from a UK study that 

enrolled a cohort of women comparable to the Australian population demonstrated no 

impact of BSE on mortality after 16 years of follow-up (UK Trial of Early Detection of Breast 

Cancer Group 1999). 

Breast awareness 

In Australia, even with a fully established mammographic screening program, more than 

half of all breast cancers are found by a woman or her doctor after noticing a change in 

the breast. Although screen-detected breast cancers are typically smaller, the majority of 

non-screen-detected breast cancers are found at an early stage and treated conservatively 

(i.e. with surgery that removes as little of the breast as possible). This supports efforts to 

promote early detection beyond the mammographic screening program (RACGP 2005, 

2006a & 2006b). 

In the absence of proof that routine, systematic BSE reduces deaths from breast cancer 

across the population, the National Breast Cancer Centre and The Cancer Council Australia 

advocate a ‘breast awareness’ approach to encourage women to report new or unusual 

breast changes. This involves women being familiar with the normal look and feel of their 

breasts, so they may be better able to recognise an unusual change. 

Breast awareness encourages familiarity as part of general body awareness and health 

care. No specific technique or regularity is promoted, as there is no evidence of the 

effectiveness of any one approach. 

Because many breast cancers cannot be felt, the breast awareness approach should be 

seen as a supplement to—not a substitute for—regular mammograms in women within 

the target age range for mammographic screening. 

Clinical breast examination 

The effectiveness of clinical breast examination (CBE) as a screening method has also 

been questioned. The International Agency for Research on Cancer concluded that ‘there 

is inadequate evidence that screening with clinical breast examination, whether alone or 

in addition to screening mammography, can reduce mortality from breast cancer’ (IARC 

2002). 

The National Breast Cancer Centre’s position statement on the early detection of breast 

cancer (NBCC 2004) summarises the latest evidence. For asymptomatic women at average 

risk of breast cancer there is insufficient evidence to encourage CBE as a population 

screening tool. However, as there is no evidence to discourage the practice of CBE, 

individual women may wish to discuss their specific needs with their doctors. Those at 

high risk should discuss ongoing monitoring with their doctors. Options may include CBE. 


12 



The national breast cancer screening program, BreastScreen Australia, began in 1991 

(BreastScreen Australia 2004a). It is funded by the Australian Government (Giles & Amos 

2003) and co-funded and administered by state and territory governments. BreastScreen 

services operate under and are measured against the BreastScreen Australia National 

Accreditation Standards (BreastScreen Australia 2004a). The standards are used not only 

to drive quality improvement but also to balance the costs and benefits of the program 

to women in the target age group. It is a free service that targets asymptomatic women 

aged 50 to 69 years and is accessible to all women aged 40 years or above. Women in 

the target age range are sent reminders for repeat screens every two years. No doctor’s 

referral is required to attend screening, which is performed by two-view mammography. 

All mammograms are independently reviewed by two readers, with recall for further 

assessment of any abnormalities detected during film reading. The screening services 

are delivered through specialised units, either fixed or mobile, that operate as part 

of a designated BreastScreen Screening and Assessment Service, which carries out 

multidisciplinary assessment of screen-detected abnormalities. All procedures up to the 

definitive cytological or histological diagnosis of breast cancer are undertaken within 

BreastScreen Australia. 

Women in the target group are recruited through direct mail-outs based on the electoral 

roll, community education, advertising campaigns, brochures and health care providers 

(AIHW 1998). The Cancer Council supports recruitment of women through the activities of 

its state and territory cancer councils in community education, promotional literature and 

the Cancer Council Helpline. State and territory cancer councils also support BreastScreen 

Australia through professional education and by running cancer registries that monitor and 

evaluate the program in relation to cancer rates and mortality. 

BreastScreen Australia performance 

Participation rate 

Monitoring and evaluation are important for BreastScreen Australia. The most recent 

national data on breast cancer screening in Australia is in the BreastScreen Australia 

monitoring report 2003–04 (AIHW 2007). 

The total number of women screened by BreastScreen Australia over the two years 

2003–04 was 1,627,115, of whom 70.3% were in the target age group (50 to 69 years). The 

proportion of the target group screened (the participation rate) is at 55.6% (2003–04). 

There was some variation between participation rates in the states and territories, from a 

low of 44.4% in the Northern Territory to a high of 63.1% in South Australia. 

Table 2.1 Age-standardised participation by women aged 50–69 years in BreastScreen Australia 2003–04 

by states and territories 

Australia NSW Vic Qld WA SA Tas ACT NT 

Rate % 55.6 50.1 58.8 58.2 56.5 63.1 57.3 51.8 43.4 


The Australian Bureau of Statistics National Health Survey data show that 64% of 

Australian women report having a mammogram every two years (ABS 2002). While 

not all mammograms will be for cancer screening purposes, this figure suggests that 


a significant proportion of women are having mammograms outside the BreastScreen 

Australia program. This is of some concern to The Cancer Council because it means 

data are not recorded and the effects of screening for these women are not evaluated. 

If mammography screening is to be successful, it must be provided within an organised 

program that adheres to key standards of quality. 

Small invasive cancer detection rate 

This measures the rate of invasive breast cancers of 15 mm or less diagnosed in women 

attending BreastScreen Australia. It is expressed as the number of small cancers detected 

for every 10,000 women screened. In 2004, 64% of all invasive breast cancers among 

all women aged 40 or over were 15 mm or less. The age-standardised rate for the target 

group was 39.1 per 10,000 women for first-round screening and 26.8 per 10,000 women 

for subsequent rounds for women aged 40 years and over. 

Program sensitivity: interval cancer rate 

Program sensitivity is the proportion of invasive breast cancers that are detected by 

BreastScreen Australia out of all invasive cancers (interval cancers and screen-detected 

cancers) diagnosed in program-screened women during the screening interval. A low 

interval cancer rate suggests a successful program. An interval cancer is an invasive breast 

cancer that is diagnosed after a screening episode that detected no cancer and before the 

next scheduled screening episode. 

The age-standardised interval cancer rate for women in the target group 0–12 months after 

attending their first screen in 2000–02 was 9.6 per 10,000 following their first screen and 

10,1 per 10,000 following subsequent screens. 

Detection rate of ductal carcinoma in situ 

This indicator measures the rate of ductal carcinoma in situ (DCIS) diagnosed in women 

attending BreastScreen Australia. The ability to detect DCIS reflects good quality imaging 

and screen film reading. In 2004 the age-standardised DCIS detection rate for women in 

the target age group was 19.8 per 10,000 women and in subsequent rounds it was 10.4 

per 10,000 women. (For more on DCIS, see below.) 


The role of general practice in breast cancer screening is potentially important, given 

that 86% of the population have at least one visit with the general practitioner every year 

(RACGP 2005). 

General practitioners and general practice team members can contribute to promoting 

preventive health behaviours and identifying women at increased or high risk of developing 

breast cancer. Promoting breast awareness, mammography screening and individualised 

surveillance programs where appropriate are recognised activities of general practice 

as outlined in policy and guideline documents produced by Royal Australian College of 

General Practitioners (RACGP 2005, 2006a, 2006b). Findings from a national survey of well 

women indicated that GP recommendations to their female patients aged 50 to 69 to have 

a screening mammogram increased from 35% in 1995 to 62% in 2003. (Barratt et al. 1997; 

NBCC 2005) 


131 


Potential benefits and adverse effects of breast 

cancer screening 

Screening aims to detect a significant proportion of breast cancers that are small and 

of a low grade, enabling better health outcomes from earlier treatment (AIHW, AACR & 

NBCC 1999). Research has clearly demonstrated a significant benefit from population 

mammography screening for women in the target age group. It has been estimated that 

for every 1460 women screened, 13.5 biopsies and 7.4 breast cancers detected, one death 

from breast cancer is prevented (AIHW, BreastScreen Australia & NCSP 1999). Screening 

10,000 women in this age group is estimated to prevent approximately 10 to 20 deaths 

from breast cancer over 10 years (UK Trial of Early Detection of Breast Cancer Group 1999). 

Mortality benefits from the screening program, if they occur, will not be seen until five to 

10 years after a high participation rate is achieved. If 70% of Australian women in the target 

group participated in the screening program, death rates from breast cancer for women 

over 50 years offered screening would fall by approximately 25% to 30% (AHMAC 1990). 

Screening may reduce the trauma associated with treatment. Tumours diagnosed at an 

earlier stage and smaller size require less extensive surgery and chemotherapy. 

Potential adverse effects of screening 

Mammographic screening may have adverse psychological effects for some women. 

Of particular concern is increased anxiety experienced as a result of false negative and 

false positive results (see introduction to Section 2). The potential negative physical and 

psychological effects associated with a false positive test include anxiety induced by fear 

of being diagnosed with breast cancer, physical effects of the performance of invasive 

diagnostic procedures, diagnosis of non-lethal lesions, and exposure to radiation. 

DCIS (where the cancerous cells have not spread beyond the basement membrane of 

the breast ducts—described as non-invasive cancer) is often quoted as an example of an 

‘over-diagnosed’ breast condition. As recently pointed out by Professor David Roder: ‘The 

difficulty is that there is no way currently known to define in-situ lesions with any certainty 

as progressive or non-progressive. This definition cannot be made by looking under 

the microscope. The potential for over-diagnosis has arisen from statistical inferences, 

which are themselves based on assumptions. Differences in estimates are a function of 

differences in the assumptions made by researchers, much of which are uncertain and 

open to debate’ (GP review 2006). 

While the diagnosis and treatment of DCIS is still contested, and general reports suggest 

that women found through mammographic screening to have DCIS will be treated by 

surgery and/or radiotherapy without evidence of the benefits of treatment having been 

established (Rickard 1996), it should be noted that BreastScreen Victoria (2001) reports a 

steady decline in the proportion of women diagnosed with DCIS undergoing surgery. The 

issues about DCIS should not overwrite the effectiveness of the national breast cancer 

screening program in identifying invasive carcinoma of the breast. 

Who should be screened? 

Evidence of greatest benefit exists for the target age group (women aged 50 to 69 years). 

The Cancer Council recommends that all women in this age group have a mammogram 

every two years through BreastScreen Australia. Debate, however, is increasing around the 

benefit of extending screening to women in the decades either side of this age bracket. 


An Australian review of the benefits of screening women aged 40 to 49 years concluded 

that there is less benefit in screening these women. The benefit is greater for those at the 

older end of the age bracket, and for those with a strong family history of breast cancer. 

The benefit of screening women aged 40 to 49 years is estimated at approximately onethird 

of that of women aged 50 to 69 years (Irwig et al. 1997). BreastScreen Australia policy 

states: 

BreastScreen Australia selects women for screening on the basis of age alone. 

Women aged 40 years and above are eligible. Recruitment strategies will be targeted 

at women aged 50–69 years. The age for screening will be monitored and reviewed 

as new data becomes available (BreastScreen Australia 2004a). 

With increasing life expectancy, the value of screening women over 70 years has also 

come under investigation. Barratt et al. (2002) estimate that the benefit of screening 

women aged 70 to 79 years to be about 40% to 72% of that achieved in women aged 50 

to 69 years; this declines further with increasing age and when quality-of-life adjustment is 

made. They estimate that extending screening to women aged 70 to 79 years is relatively 

cost-effective and similar to the cost-effectiveness of extending screening to women aged 

40 to 49 years. The authors, however, also comment that the estimation of benefits, harms 

and costs would be improved with data—now lacking—from randomised trials in the 

appropriate age group. 

Aims 

The Cancer Council endorses the major aims of the BreastScreen Australia program (AIHW, 

BreastScreen & NCSP 1999): 

• 

• 

• 

• 

• 

• 

to ensure that the program is implemented in such a way that significant reductions can 

be achieved in morbidity and mortality attributable to breast cancer 

to maximise the early detection of breast cancer in the target population 

to ensure that screening for breast cancer in Australia is provided in dedicated 

accredited screening and assessment services as part of the BreastScreen Australia 

program 

to ensure equitable access for women aged 50–69 years to the program 

to ensure that services are acceptable and appropriate to the needs of the eligible 

population 

to achieve high standards of program management, service delivery, monitoring and 

evaluation and accountability (BreastScreen Australia 2004b). 


133 


What we want to achieve How The Cancer Council Australia and its members (the state and 


A 70% two-yearly 

participation rate in the 

national program by women 

in the target group (50–69 

years) and access on request 

to the program for women 

aged 40–49 years and 70 

years or more 

Referral to appropriate 

treatment services and 

collection of information 

about the outcome of 

treatment 

Sufficient workforce capacity 

to ensure the delivery of 

a best practice screening 

program to the target 

population (women 50–69) 

Timely evaluation of new 

technologies 

National evaluation of 

BreastScreen performance, 

capacity and policy issues 

by 2008 

134 National Section Two: Cancer Screening Prevention to detect Policy cancer 2004 – early 06 

Maintain and support education programs to raise awareness in the 

community and among health professionals to promote informed 

participation of women aged 50–69 years in breast cancer screening 

Advocate for government support, including adequate funding, to 

ensure targets for participation are met, while maintaining a focus on 

equity and access for women Priority should be given to maximising the 

participation of Australian Aboriginal and Torres Strait Islander women 

and women of culturally and linguistically diverse backgrounds 

Recognising that many women have mammograms outside 

BreastScreen, advocate for integration of screening of all asymptomatic 

women aged 50–69 years into the BreastScreen Australia program 

Recognising the importance of providing consistent high-quality care for 

women diagnosed with breast cancer in Australia: 

• support or advocate for examination of the extent to which women 

diagnosed in the screening program are being treated in accordance 

with the NHMRC Clinical practice guidelines for the management of 

early breast cancer (2001), Management of advanced breast cancer 

(2001) and Clinical Practice Guidelines for the Psychosocial Care of 

Adults with Cancer (2003) 

Recognising the importance of informed consumer involvement in 

all aspects of breast cancer screening, diagnosis and management, 

advocate for active roles for consumers within peak breast cancer 

bodies in Australia 

Recognising the implications in the short and longer term of radiography 

and radiology workforce constraints for BreastScreen Australia, 

advocate for increased funding to provide additional places for the 

training of radiographers and radiologists 

Monitor development of relevant new technologies, (such as digital 

mammography and MRI), advocate for rapid evaluation of their 

relevance for screening and adoption of those that are positively 

evaluated 

Support and contribute to national evaluation of the following areas: 

• reductions in breast cancer mortality due to screening, risks 

associated with screening, program governance and management, 

performance trends, accreditation system 

• workforce, new technologies and capacity issues 

• policy issues such as the appropriate target age range, screening 

interval, and screening of women at higher risk or those who present 

with symptoms

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Cancer 88(7): 1047–53. 

Humphrey LL, Helfand M, Chan BK & Woolf SH 2002. Breast cancer screening: a summary of the evidence 

for the U.S. Preventive Services Task Force. Ann Intern Med 137(5 Part 1): 347–60. 



activity eds H Vainio & F Bianchini. Lyon, France: IARC Press. 

International Agency for Research on Cancer (IARC) 2002. Handbooks of cancer prevention volume 7: breast 

cancer screening, eds H Vainio & F Bianchini. Lyon, France: IARC Press. 

Irwig L, Glasziou P, Barratt A & Salkeld G 1997. Review of the evidence about the value of mammographic 

screening in 40–49 year old women. Kings Cross, NSW: National Breast Cancer Centre. 

Kosters JP & Gotzsche PC 2003. Regular self-examination or clinical examination for early detection of breast 

cancer (Cochrane review). Cochrane Database of Systematic Reviews 2: CD003373. 

Million Women Study Collaborators 2003. Breast cancer and hormone replacement therapy in the Million 

Women Study. Lancet 362(9382): 419–27. 

National Breast Cancer Centre (NBCC) 2006. Report on the status of breast cancer risk factors. Unpublished 

report. 

——— 2005. National Breast Cancer Centre breast health technical report. Camperdown NSW: NBCC. 

——— 2004. Early detection of breast cancer: position statement. Camperdown NSW: NBCC. 

National Health and Medical Research Council (NHMRC) 2005. Hormone replacement therapy: a summary of 

the evidence. Canberra: NHMRC. 

Productivity Commission 2006. Report on government services 2006. Canberra: Australian Government 

Productivity Commission. 

Rickard M 1996. The increasing detection of DCIS: lessons for Australia. Kings Cross: National Breast Cancer 

Centre. 

Rossouw JE, Anderson GL, Prentice RL, LaCroix AZ, Kooperberg C, Stefanick ML, Jackson RD, Beresford 

SA, Howard BV, Johnson KC, Kotchen JM & Ockene J 2002. Risks and benefits of estrogen plus progestin in 

healthy postmenopausal women: principal results from the Women’s Health Initiative randomized controlled 

trial. JAMA 288(3): 321–33. 

Royal Australian College of General Practitioners (RACGP) 2006a. Putting prevention into practice: guidelines 

for the implementation of prevention in the general practice setting. Second edition. South Melbourne: RACGP. 

——— 2006b. The role of general practice in prevention and health promotion. Policy endorsed by the 48th 

RACGP Council, 18 May 2006. Melbourne: RACGP. 



13 National Section Two: Cancer Screening Prevention to detect Policy cancer 2004 – early 06

Semiglazov VF, Manikhas AG, Moiseenko VM, Protsenko SA, Kharikova RS, Seleznev IK, Popova RT, 

Migmanova NS, Orlov AA, Barash NI, Ivanova OA & Ivanov VG 2003. Results of a prospective randomized 

investigation [Russia (St Petersburg)/WHO] to evaluate the significance of self-examination for the early 

detection of breast cancer]. Vopr Onkol 49(4): 434–41. 

Singletary SE 2003. Rating the risk factors for breast cancer. Ann Surg 237(4): 474–82. 

Stephenson J, Bauman A, Armstrong T, Smith B & Bellew B 2000. The costs of illness attributable to physical 

inactivity in Australia. Canberra: Commonwealth Department of Health and Aged Care. 

Thomas DB, Gao DL, Ray RM, Wang WW, Allison CJ, Chen FL, Porter P, Hu YW, Zhao GL, Pan LD, Li W, Wu 

C, Coriaty Z, Evans I, Lin MG, Stalsberg H & Self SG 2002. Randomized trial of breast self-examination in 

Shanghai: final results. J Natl Cancer Inst 94(19): 1445–57. 

Thune I & Furberg A 2001. Physical activity and cancer risk: dose-response and cancer, all sites and sitespecific. 

Med Sci Sports Exerc 33(Suppl): S530–50. 

UK Department of Health 1998. Nutritional aspects of the development of cancer. Report of the Working 

Group on Diet and Cancer of the Committee on Medical Aspects of Food and Nutrition Policy. Norwich, UK: 

The Stationery Office. 

UK Trial of Early Detection of Breast Cancer Group 1999. 16-year mortality from breast cancer in the UK Trial 

of Early Detection of Breast Cancer. Lancet 353: 1909–14. 

World Cancer Research Fund (WCRF) & American Institute for Cancer Research (AICR) 1997. Food, nutrition 

and the prevention of cancer: a global perspective. Washington, DC: AICR. 

World Health Organization (WHO) 2002. Risk to health 2002 world health report. Geneva: WHO. 


13 


C e r v i c a l c a n c e r 

In Australia, a vaccine that prevents the majority 

of cervical cancer is now available. The vaccine 

will have a profound impact on Australia’s cervical 

screening program, and in the future will influence 

changes to national policy. However, Pap tests will 

remain important in preventing cancer of the cervix. 

Cervical cancer in Australia 

In 2005 estimates, cancer of the cervix accounted for 610 new cancers in Australian 

women (AIHW, AACR, NCSG & McDermid 2005). The lifetime risk of a woman developing 

cervical cancer before the age of 75 years is 1 in 233 (AIHW, AACR, NCSG & McDermid 

2005). In Australia in 2004, cervical cancer accounted for 212 deaths (AIHW 2006). 

Between 1991 (when Australia’s National Cervical Screening Program commenced) and 

2005, the incidence of cervical cancer among women aged 20 to 69 halved from 17.2 per 

100,000 women to 7.3 in 2005 (AIHW, AACR, NCSG & McDermid 2005). The mortality 

rate has also declined from 4.0 in 1991 to 1.8 in 2004 (AIHW 2006), and is now among the 

lowest in the world (IARC 2002). 

Mortality data from 2001 to 2004 in Queensland, South Australia, Western Australia and 

the Northern Territory indicate that Indigenous women have a mortality rate attributable to 

cervical cancer of 9.9 per 100,000 women. This is more than four times the corresponding 

death rate of non-Indigenous women (2.1 per 100,000 women) (AIHW 2006). 

Can cervical cancer be prevented? 

The human papilloma virus (HPV) has been identified in 99.7% of cervical cancer 

specimens (Walboomers et al. 1999). While HPV is clearly necessary for the development 

of cervical cancer, it is certainly not sufficient (Walboomers et al. 1999). Worldwide, there 

are estimated to be 326 million adult women who are infected with HPV. This compares 

with approximately 450,000 new cases of cervical cancer worldwide each year (Bosch 

2000). Clearly cervical cancer is a very rare outcome of HPV infection. 

HPV is a sexually transmitted infection and almost all individuals become infected with 

HPV within two to five years of initiating sexual activity (Wright et al. 2006). HPV can 

be classified into high and low-risk types based on the strength of their association with 

cervical cancer. Co-factors that increase the risk of cervical cancer progressing in women 

who have a persistent high-risk HPV infection include exposure to tobacco smoke, more 

than five full-term pregnancies, the use of oral contraceptives for five years or more, 

immunosuppression, and presence of antibodies to Chlamydia trachomatis or to herpes 

simplex virus type 2 (IARC 2005). 


A vaccine to prevent HPV infection 

A vaccine designed to prevent two of the most common types of high-risk HPV (HPV 

16 and 18) is available in Australia, and from April 2007 was included on the National 

Immunisation Schedule. 

HPV types 16 and 18 are responsible for up to 70% of cervical cancers (Munoz et al. 

2003), and clinical trials have found the vaccine to be 100% effective (Wright et al. 2006). 

The vaccine is highly effective when given to females who are not already infected with 

the HPV types included in the vaccine. Therefore, it is recommended that the vaccine be 

administered prior to commencement of sexual activity (Wright et al. 2006). As the vaccine 

does not protect against all types of HPV that cause cervical cancer, vaccinated women 

should have regular Pap tests. 

In sexually active women, the most important measure to prevent cervical cancer is regular 

Pap tests. 

See the human papilloma virus chapter in the immunisation section of the online edition of 

the National Cancer Prevention Policy 2007–09 (published in June 2007 at www.cancer.org. 

au). 

Screening tests and programs for cervical cancer 

The Pap test 

Cervical cancer is one of the few cancers where screening can detect precancerous cell 

growth. These abnormalities can be treated, preventing the development of cancer. The 

Pap test (named after its developer, Dr George Papanicolaou) is the most widely used 

cancer screening test in the world (Eurogin 2003). Typically, cervical cancer takes 10 years 

or more to develop. Abnormalities detected by a Pap test can be monitored, or, if required, 

further investigated and early treatment initiated. 

Cervical screening with the Pap test began in British Columbia (Canada) in 1949. Although 

no randomised controlled trials evaluating screening have been conducted, a large number 

of observational studies have shown a strongly protective effect of screening (USPSTF 

1996). In particular, substantial declines in mortality and incidence of cervical cancer have 

been demonstrated after the introduction of screening programs. 

Other screening technologies 

In the past decade, a desire to improve the sensitivity of the Pap test and an increased 

understanding about the role of HPV has led to the development of new screening 

technologies. 

Liquid-based cytology 

Liquid-based cytology is a technique where the cervical cells collected on the sampling 

instruments are suspended in liquid. At the laboratory the liquid sample is filtered to 

remove unnecessary material such as blood, bacteria and other matter. The cells are then 

deposited as a single layer onto a slide, stained and examined under a microscope. 

As new technologies are evaluated for adoption, appropriate consideration must be given 

to how they will improve the cervical screening program in terms of sensitivity, specificity, 

cost-effectiveness and quality of life. An Australian Government review in Australia by 

the Medical Services Advisory Committee in 2002 concluded that there is insufficient 


13 

C e r v i c a l c a n c e r

evidence to suggest that liquid-based cytology is superior to the conventional Pap test, and 

recommended that public funding not be supported for this screening test in Australia at 

this time (MSAC 2002). Further research is ongoing into the use of this technology. 

HPV DNA testing 

Due to the relationship between persistent infection with high-risk types of HPV and 

the development of cervical cancer, testing for the presence of HPV DNA in cervical cell 

specimens has the potential to identify women at increased risk of developing cervical 

cancer. Commercially available HPV DNA testing kits can detect 13 high-risk types of HPV. 

Several countries have developed guidelines recognising the role of HPV testing as a 

primary screening test and in the management of abnormal cervical cell abnormalities (Cox 

& Cuzick 2006). The International Agency for Research on Cancer states that it is likely 

longer screening intervals could be achieved using HPV DNA testing as a screening test 

(IARC 2005). Currently in Australia, HPV DNA testing is recommended for use in women 

following treatment of a high-grade abnormality. The test is used to determine whether the 

virus has been cleared from the body (NCSP 2005). 

International studies continue to investigate the role of HPV DNA testing for triaging lowgrade 

cervical abnormalities and as a primary screening tool. 


In Australia, screening for cervical cancer was introduced on an ad hoc basis in the 1960s. 

Guidelines on cervical screening programs published in 1986 by the World Health 

Organization and the International Agency for Research on Cancer were used as a basis 

for a review of cervical screening in Australia. The review was conducted on behalf of 

Australian Health Ministers Advisory Council (AIHW, BreastScreen Australia & NCSP 1999). 

Following this review, cervical screening was organised into a structured program known 

today as the National Cervical Screening Program; this was implemented in 1991 as a joint 

initiative of the Australian, state and territory governments. 

State and territory cancer organisations have been involved in a coordinating role in the 

establishment of state Pap test registries and recruitment of women to the screening 

program. In some states and territories, cancer councils maintain an important role in 

cervical screening programs. 


The National Cervical Screening Program policy developed in 1991 provides guidelines for 

which women need screening and how often screening should occur. It states: 

1. 

2. 

Routine screening with Pap tests should be carried out every two years for women who 

have no symptoms. 

All women who have ever been sexually active should start having Pap tests between 

the ages of 18 and 20 years, or one or two years after beginning sex, whichever is later. 

In some cases, it may be appropriate to start screening before 18 years of age. 

3. 

Pap tests may cease at the age of 70 years for women who have had two normal Pap 

tests within the last five years. Women over 70 years who have never had a Pap test, 

or who request a Pap test, should be screened (Cervical Cancer Prevention Taskforce 

1991). 


It is anticipated that the introduction of the HPV vaccine will, in the future, influence 

changes to this national policy. 

Recent changes to guidelines 

Women with abnormal Pap test results should be managed in accordance with the 

National Health and Medical Research Council guidelines Screening to prevent cervical 

cancer: guidelines for the management of asymptomatic women with screen detected 

abnormalities (NCSP 2005). After extensive review, these guidelines were endorsed by the 

National Health and Medical Research Council in 2005 and came into effect in July 2006. 

Pap test quality 

One indicator of Pap test quality is the proportion of tests where an endocervical 

component is present. Presence of an endocervical component in 80% of Pap tests is 

generally considered acceptable. It is sometimes difficult to obtain the endocervical 

component when taking a Pap test in older women. There is some indication that the 

proportion of Pap tests lacking an endocervical component has increased over time. In 

Victoria, this has increased from 17.3% in 2000 to 22.1% in 2005 (VCCR 2006). 


In Australia, approximately 80% of Pap tests are taken by GPs (AIHW & AACR 2004) and 

therefore GPs play an important role in cervical screening in this country. GPs also play 

an important role in recruiting women who have never had a Pap test or are significantly 

under-screened. 

In November 2001, the Australian Government introduced a cervical screening Practice 

Incentive Payment to support general practices to enhance cervical cancer screening. 

The program has a number of components. Accredited practices receive a payment on 

registering for the scheme. GPs also receive a Special Incentive Payment when they 

perform a Pap test from unscreened and under-screened women aged between 20 and 

69 years. Finally, in order to encourage general practices to adopt a systematic approach 

to cervical screening, practices receive an outcomes payment when they reach a target 

screening rate (NCSP 2006). In May 2006, 91.7% of practices in Australia were signed on 

to participate in these activities (Medicare Australia 2006). 

Potential benefits and adverse effects of cervical 


Rationale 

It has been estimated that screening using the Pap test has the potential to reduce 

squamous cell carcinoma of the cervix by up to 90% (AIHW, BreastScreen Australia & 

NCSP 1999). 

In Australia, the age-standardised incidence rate for cervical cancer declined by an average 

of 6.2% each year between 1991 and 2001. Mortality rates have also fallen by an average 

of 5.2% per year since 1991 (AIHW & AACR 2004). These gains can be attributed, in part, 

to the success of the National Cervical Screening Program. 


141 


Potential adverse effects 

No screening test is 100% accurate. A Pap test every two years is about 90% accurate and 

is currently the best available protection against cervical cancer for women who have ever 

had sex. Like all screening tests, the Pap test is performed on asymptomatic women. False 

positive results as well as false negative results may occur. 

Even minor abnormalities can cause anxiety for some women. Women who receive false 

negative results may experience delays in diagnosis or treatment. False negative results 

may also create a false sense of security that may cause warning symptoms to be ignored. 


All women who have ever been sexually active should commence having Pap tests 

between the ages of 18 and 20 years, or within two years after beginning sex, whichever is 

later (Cervical Cancer Prevention Taskforce 1991). 

Who has been screened? 

Cervical cytology registers in Australia provide information on the majority of women who 

undergo screening, although an estimated 1% to 3% of women choose not to be included 

on the register (AIHW, BreastScreen Australia & NCSP 1999). In the two years between 

January 2003 and December 2004, the participation rate for cervical cancer screening in 

Australia was 60.7% for the target population of women aged 20 to 69 years (AIHW 2006). 

Table 2.2: Participation rates in the National Cervical Screening Program by age group, Australia 

2003−04 

Age group 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 

Percentage 47.8 58.1 62.8 63.8 64.3 65.9 64.0 66.6 57.2 49.6 


Participation in screening is highest in the age groups 30–34 to 55–59 but declines sharply 

after the age group of 55–59. The participation rate across the age groups 40–69 increased 

slightly in 2003–04 compared to 2001–02 (AIHW 2006). 

Australia’s two-yearly screening interval is conservative, with many countries 

recommending three years or more between tests. The International Agency for Research 

on Cancer recommend three-yearly screening for women aged 25 to 49 and five-yearly 

screening for women aged 50 to 64 (IARC 2005)—a recommendation that the NHS 

Cervical Screening Programme in the United Kingdom has recently adopted. Data from 

Victoria show that if participation in cervical screening is measured over a three-year time 

interval, then the participation rate in women aged 20 to 69 years is close to 80% (VCCR 

2006). 

Adherence to the recommended two-yearly screening interval is not optimal. Among 

women who received a negative Pap test report in February 2000, 26.2% were re-screened 

before two years had elapsed (AIHW 2006). Early re-screening increases the cost of the 

program and reduces cost-effectiveness. 


Recruitment 

Women in the target age group are recruited by a variety of initiatives determined mainly at 

the state/territory level. 

Recruitment strategies are implemented for particular population sub-groups, such as older 

women, Australian Aboriginal and Torres Strait Islander women and women from culturally 

diverse backgrounds (AIHW, BreastScreen Australia & NCSP 1999). 

Aims 

The Cancer Council aims to maximise participation in the cervical screening program of 

eligible women and contribute to improvements in the program. 



Maximum screening 

participation of eligible 

women 

Maximum vaccine uptake 

among eligible girls and 

young women and ensure 

screening messages remain 

visible 

Ongoing evaluation of the 

effectiveness and efficiency of 

the screening program, so as 

to inform policy and program 

development 

Promote and foster participation in cervical cancer screening, 

particularly among women in under-screened populations 

Collaborate with Indigenous communities to improve rates of cervical 

screening among Australian Aboriginal and Torres Strait Islander 

women 

Develop systems to ensure that data are collected on Indigenous status 

to enable evaluation of program effectiveness 

Work with all relevant health professionals to reduce early re-screening 

Work with all relevant health professionals and consumers to increase 

adherence to the updated guidelines: Screening to prevent cervical 

cancer: guidelines for the management of asymptomatic women with 

screen detected abnormalities (NCSP 2005) 

Promote participation in HPV immunisation programs to eligible girls 

and young women, with particular emphasis on population groups most 

at risk, such as Indigenous communities 

Work with all relevant health professionals and consumers to ensure 

women are aware that, vaccinated or not, Pap tests remain important in 

preventing cancer of the cervix 

Advocate for, and contribute expert advice to, the review of evidence in 

relation to: 

• a change in national policy following the introduction of the HPV 

vaccine 

• a change to the screening interval and age at first screen 

• investigation of new technologies 

• 

timely implementation of review findings 


143 


References 

Cervical cancer 

Australian Institute of Health and Welfare (AIHW) 2006. Cervical screening in Australia 2003–2004. AIHW cat. 

no. 28; Cancer Series no. 33. Canberra: AIHW. 






Australian Institute of Health and Welfare (AIHW), BreastScreen Australia & National Cervical Screening 

Program (NCSP) 1999. Breast and cervical cancer screening in Australia 1996–1997. Canberra: AIHW. 

Bosch F 2000. Clinical cancer and HPV: a worldwide perspective. In Proceedings of the Fourth International 

Multidisciplinary Congress: Eurogin 2000. Bologna: Italy. 

Cervical Cancer Prevention Taskforce 1991. Screening for the prevention of cervical cancer. Canberra: 

Department of Health, Housing and Community Services. 

Cox T & Cuzick J 2006. HPV DNA testing in cervical cancer screening: from evidence to policies. Gynecol 

Oncol 103(1): 8–11. 

Eurogin 2003. Conclusions: cervical cancer control, priorities and new directions. International charter. 1–22. 

International Agency for Research on Cancer (IARC) 2005. IARC handbooks on cancer prevention. Cervix 

cancer screening. Lyon, France: IARC. 

——— 2002. Globocan 2002. At http://www-dep.iarc.fr. Accessed 16 April 2007. 

Medical Services Advisory Committee (MSAC) 2002. Liquid based cytology for cervical screening. MSAC 

reference 12a. Canberra: Australian Government Department of Health and Ageing. 

Medicare Australia 2006. Medicare Australia statistical reporting: approved practices in the quarterly 

calculations by activity. Participation in the PIP. Through Medicare Australia / Health statistics / Statistical 

reporting / Divisions of general practice. Accessed 26 November 2006. 

Munoz N, Bosch FX, de Sanjose S, Herrero R, Castellsague X, Shah KV, Snijders PJ & Meijer CJ 2003. 

Epidemiologic classification of human papillomavirus types associated with cervical cancer. N Engl J Med 

348(6): 518–27. 

National Cervical Screening Program (NCSP) 2006. Information for health professionals. At http://www. 

cervicalscreen.health.gov.au/internet/screening/publishing.nsf/Content/professionals. Accessed 16 April 2007. 

——— 2005. Screening to prevent cervical cancer: guidelines for the management of asymptomatic women 

with screen detected abnormalities. Canberra, Commonwealth of Australia. 

National Health and Medical Research Council (NHMRC) 2005. Screening to prevent cervical cancer: 

guidelines for the management of asymptomatic women with screen detected abnormalities. Canberra: 

NHMRC. 

US Preventive Services Task Force (USPSTF) 1996. The guide to clinical preventive services, 2nd edition. 

Washington: US Department of Health and Human Services, Office of Disease Prevention and Health 

Promotion. 

Victorian Cervical Cytology Registry (VCCR) 2006. Statistical report 2005. Melbourne: VCCR. 

Walboomers JM, Jacobs MV, Manos MM, Bosch FX, Kummer JA, Shah KV, Snijders PJ, Peto J, Meijer CJ & 

Munoz N 1999. Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. J Pathol 

189(1): 12–19. 

Wright TC, Bosch FX, Franco EL, Cuzick J, Schiller JT, Garnett GP & Meheus A 2006. HPV vaccines and 

screening in the prevention of cervical cancer; conclusions from a 2006 workshop of international experts. 

Vaccine 24 (3 Suppl): S251–61. 


B o w e l ( c o l o r e c t a l ) 

c a n c e r 

Bowel cancer is the most common potentially fatal 

cancer in Australians and is expected to increase 

in incidence by more than 30% over the next five 

to 10 years as our population ages. Populationbased 

screening for bowel cancer, currently being 

introduced in Australia, can reduce mortality by 

30% to 40% in people screened. 

Bowel cancer in Australia 

Bowel cancer, also known as colorectal or large bowel cancer, is a major health problem 

in Australia. One in 18 men and one in 25 women is likely to develop the disease. In 2005, 

there were estimated to be 14,237 new cases of bowel cancer—7,765 in men and 6,472 

in women—representing 14.5% of all new cases of cancer (excluding non-melanoma skin 

cancer). The incidence rate rises steadily with advancing age and most cases occur after 

the age of 50. Between 1991 and 2005, age-adjusted rates of bowel cancer incidence 

remained steady in men and slowly increased in women. In the 10-year period 2001–11, 

the number of new cases of bowel cancer is projected to increase by about one-third 

(AIHW, AACR, NCSG & McDermid 2005). 

In 2005, there were 4171 deaths in Australia from bowel cancer: 2330 in men and 1641 

in women. Bowel cancer was the second most common cause of death from cancer over 

all, as well as being the third most common cause of death from cancer in men (after 

lung and prostate cancers) and the third most common in women (after breast and lung 

cancers) (ABS 2007). Between 1991 and 2005, the death rate for bowel cancer fell by 2.5% 

per annum for men and by 2.6% for women (ABS 2007; AIHW 2005). Despite the trend 

towards better survival, bowel cancer remains an important cause of premature death in 

Australia. 

In Indigenous communities, where incidence rates are believed to be under-recorded, 

bowel cancer is the third most common cancer affecting men and the fourth most 

common affecting women (ABS & AIHW 2005). The survival rate from bowel cancer 

is lower for Indigenous than non-Indigenous Australians (Condon et al. 2004). It is also 

recognised that Aboriginal people and Torres Strait Islanders often have co-morbidities that 

may hinder the effectiveness of cancer treatments (Valery et al. 2006). 

Can bowel cancer be prevented? 

Evidence shows that bowel cancer is associated with a number of modifiable and 

unmodifiable risk factors. 

Important risk factors that cannot be addressed through lifestyle or behavioural change 

include a personal history of bowel cancer, advanced adenoma, chronic inflammatory 

bowel disease or a strong family history of bowel cancer (ACN Revision Committee 


145 

B o w e l c a n c e r

2005). Two specific syndromes, which have a defined inherited genetic basis, are familial 

adenomatous polyposis (FAP) and hereditary non-polyposis colorectal cancer (HNPCC). 

HNPCC (also known as Lynch Syndrome) is also associated with an excess of cancers at 

other sites, including the endometrium and ovary. Clinical surveillance of individuals with 

these risk factors, as set out in The Cancer Council Australia’s Australian Cancer Network 

Clinical practice guidelines for the prevention, early detection and management of colorectal 

cancer, is recommended. 

Bowel cancer is also being increasingly linked to lifestyle and in recent decades, there has 

been considerable interest in identifying modifiable risk factors. 

The main focus of research into preventable risk factors associated with bowel cancer 

has been in relation to diet (including nutritional supplements), body weight and lifestyle 

factors such as physical activity, intake of aspirin and other non-steroidal anti-inflammatory 

drugs, and smoking (ACN Revision Committee 2005). A comprehensive overview of diet 

and cancer, published in 1997, estimated that changes in diet and physical activity could 

reduce the incidence of bowel cancer by 66% to 75% (WCRF & AICR 1997). (See the 

chapters on alcohol, nutrition, obesity and physical activity for more information.) 

Obesity, particularly central (around the waist) obesity, is an independent risk factor for 

bowel cancer and adenomas (IARC Working Group 2002; MacInnis et al. 2004). 

A number of studies have shown that smoking is a risk factor for bowel cancer and 

precancerous adenomas (Kune et al. 1992; Chao et al. 2000; Giovannucci 2001; Limburg et 

al. 2003; Anderson et al. 2003). The report from the Cancer Prevention Study II estimated 

that, in the US, approximately 12% of deaths from bowel cancer among both men and 

women were attributable to smoking (Chao et al. 2000). 

The review released from IARC in 2007 has confirmed that alcohol is a risk factor for the 

same cancers classified in 1988 and also for colorectal and breast cancer (IARC 2007). 

Aspirin has been shown to have potential in preventing bowel cancer (Sandler et al. 2003; 

Benamouzig et al. 2003; Chan et al. 2005). Findings from the Nurses’ Health Study and 

the Women’s Health Study indicate that the benefit is not evident until after more than a 

decade of regular aspirin consumption (Chan et al. 2005; Cook et al. 2005). Adverse effects 

of aspirin include acute upper gastrointestinal bleeding (Weil et al. 1995). After reviewing 

research into the effects of aspirin and non-steroidal anti-inflammatory drugs, the 

Australian Cancer Network stated that ‘it is reasonable to consider aspirin as prophylaxis 

in adenoma bearers’ but that ‘aspirin has not had broad scientific approval for use as a 

colorectal tumour chemo-preventive in individuals at average risk, because of uncertainties 

about the optimal dosage and duration of use, and adverse effects’ (ACN Revision 

Committee 2005). 

General practitioners and their teams have an important role in bowel cancer prevention. 

As they see 86% of the Australian population every year, they ‘have enormous potential to 

encourage patients to take greater responsibility for their health’ (RACGP 2006). Australian 

Doctor surveyed 1246 Australians in 2006, with 56% reporting they would act on advice 

from their GP in relation to lifestyle changes such as losing weight, quitting smoking and 

doing more exercise: all shown to reduce the risk of bowel cancer (Howe 2006). 

The Royal College of General Practitioners has published two key documents to support 

preventive work in general practice. The Guidelines for preventive activities in general 

practice (the ‘red book’) (RACGP 2005) is a guide listing who is most at risk, and 

evidence-based recommendations for screening or preventive care for a number of 

conditions including cancers. The other is Putting prevention into practice: guidelines for 

the implementation of prevention in the general practice setting (the ‘green book’) (RACGP 

2006). While there is evidence to show the benefits of GP preventive activities, there are 

many barriers, including the lack of time in typical general practice consultations. Solutions 


could focus on: how to use this time most effectively; the role of e-health measures such 

as follow-up, recall, and desktop prompts; non-GP measures such as practice nurse 

involvement; and non-clinical staff measures such as utilising waiting room opportunities. 

Tests and programs for bowel cancer 

Rationale 

Population-based screening provides an important opportunity to reduce bowel cancer 

mortality and morbidity. The combination of prevention measures, such as those outlined 

above, and population-based screening, has even greater potential to reduce the impact of 

bowel cancer in Australia. 

Research indicates that most bowel cancers develop from adenomatous polyps 

(adenomas); a small adenoma may grow into advanced cancer over an estimated 10 years. 

It should be recognised that it is common for middle-aged or elderly people to have one 

or more adenomas, most of which (estimated at around 19 out of 20) never progress to 

cancer. 

Adenomas are described as ‘advanced’ when certain features, such as larger size (10 

mm or more in diameter) are present. These features act as markers of greater likelihood 

of progression to cancer and greater risk for cancer elsewhere in the large bowel. Once 

cancer has developed, growth may occur gradually over 12 to 24 months or even longer. 

While the cancer remains confined to the bowel wall (stage A), surgical resection gives 

cure rates around 90% (ACN Revision Committee 2005). 

Most people with advanced adenomas and many with early stage cancer experience none 

of the symptoms that would alert them or their doctor to the presence of bowel cancer. For 

people diagnosed with bowel cancer, the pathological stage of development of the tumour 

at the time of diagnosis, as well as the treatments that follow, will affect their prognosis. 

Survival rates for bowel cancer are strongly related to stage, with five-year case survival 

rates found in South Australia (where statewide data is available) to be: 

• 

• 

• 

• 

88% for Stage A, when the cancer is contained within the bowel wall 

70% for Stage B, when the cancer has extended through the bowel wall, but with no 

lymph nodes affected 

43% for Stage C, when the cancer is present in the lymph nodes 

7% for Stage D, when the cancer cannot be removed by surgery or has spread to other 

areas of the body. 

There is an upward trend in these survival figures, due to a number of factors, including 

improvements in surgical technique and more widespread use of adjuvant chemotherapy 

and radiotherapy (ACN Revision Committee 2005). 

The two objectives of bowel cancer screening are 1) to prevent cancer by identifying and 

removing precancerous, advanced adenomas and 2) to diagnose and treat early stage, 

curable cancer. 

The evidence on screening for bowel cancer was reviewed in a report for the Australian 

Health Technology Advisory Committee (AHTAC 1997). The report concluded that the 

efficacy of screening based on the faecal occult blood test had been demonstrated, and 

that the best approach to mass screening of the Australian population required definition: 


14 


such as pilot studies to assess acceptance by the target population, feasibility and costeffectiveness. 

Guidelines for the prevention, early detection and management of bowel cancer, 

incorporating the Australian Health Technology Advisory Committee recommendations on 

screening, were developed by the Australian Cancer Network and endorsed by the National 

Health and Medical Research Council in 1999 (NHMRC, COSA & ACN 1999) and again in 

2005 (ACN Revision Committee 2005). 

Three screening tools for the early detection of bowel cancer are commonly available: 

the FOBT, sigmoidoscopy, and colonoscopy (ACN Revision Committee 2005). Two other 

tools—computerised tomographic (CT) colonography (also known as virtual colonoscopy) 

and faecal DNA testing—may have a future role in screening but are still undergoing 

evaluation (Van Dam et al. 2004; Cotton et al. 2004; Davies, Miller & Coleman 2005; 

Osborn & Ahlquist 2005). 

Faecal occult blood tests (FOBTs) 

Cancers in the large bowel have a tendency to produce low-grade bleeding (Macrae & 

St John 1982; St John et al. 1992). The detection of blood in small (often not visible) 

concentrations in the faeces provides the basis for use of FOBTs in screening for bowel 

cancer. 

With FOBTs, blood can be detected through the chemical or immunochemical properties 

of haem and haemoglobin. The chemical tests, most of which use guaiac-impregnated 

slides as the test system, depend on detection of the chemical activity of haem. Certain 

foods and medications have the potential to interfere with test results so dietary 

modification may be required—usually avoiding red meat and vitamin C supplements for 

several days. The immunochemical tests utilise antibodies to human globin and are not 

affected by diet or medications. (For further discussion of the properties of the tests refer 

to Young, Macrae & St John 1996; Young et al. 2002.) 

FOBTs are simple tests that can be done at home. Depending on the particular test, 

samples are collected from either two or three bowel actions. The samples are then 

sent to a laboratory for analysis to check for the presence of blood. As bleeding may 

be intermittent, the presence of blood in even one sample should be investigated by 

colonoscopy (see below). 

Bowel cancer will be identified in 5% to 10% of those with a positive FOBT, an adenoma 

will be identified in another 20% to 35%, and bleeding will be due to a non-neoplastic 

cause such as haemorrhoids in the remainder. However, as shown by FOBT-based 

randomised controlled trials and other large studies, the likelihood of finding bowel cancer 

is between 12 and 40 times greater in a person with a positive FOBT than in someone 

whose test shows no evidence of bleeding (Mandel et al. 1993; Mandel et al. 1999; 

Alexander & Weller 2003). 

A false negative result from the FOBT (i.e. no bleeding detected in a person who actually 

has bowel cancer or an advanced adenoma) may occur because of intermittent blood loss, 

uneven distribution of blood in the faeces or, in the case of chemical tests, because of 

intake of vitamin C supplements (Young, Macrae & St John 1996). The choice of FOBT also 

affects false negative rates, as different tests may have different thresholds for detection 

of blood, and therefore for cancer. The chemical test used in the European randomised 

controlled trials has a sensitivity for cancer of only 50% (Hardcastle et al. 1996; Kronborg et 

al. 1996) whereas many newer chemical and immunochemical tests have a sensitivity for 

cancer in the range 70% to 90% (Allison et al. 1996). 


Periodic testing is recommended, as a negative (i.e. normal) result does not rule out 

the possibility of future development of bowel cancer. Evidence from the European 

randomised controlled trials, which used a low-sensitivity test repeated two-yearly for 10 

years, suggests that this approach would lead to a reduction of 15% to 18% in mortality 

from bowel cancer among those offered screening (Hardcastle et al. 1996; Kronborg et 

al. 1996). The reduction in mortality was estimated to be 30% to 40% among those who 

actually performed the test (Jorgensen, Kronborg & Fenger 2002; Scholefield et al. 2002). 

Sigmoidoscopy 

Sigmoidoscopy involves tube examination of the rectum and the lower part of the colon 

(i.e. the section of large bowel closest to the anus). The sigmoidoscope may be rigid (best 

suited for examining the rectum) or flexible (reaching into the lower part but unable to 

examine the upper part of the colon). 

Flexible sigmoidoscopy allows examination of the area where 55% to 60% of bowel 

cancers and advanced adenomas occur (AHTAC 1997). When abnormalities are detected, 

a tissue sample (biopsy) can be collected for pathological examination. The sensitivity 

for detection of neoplastic lesions depends on the proficiency of the sigmoidoscopist. 

Adenoma detection rates were shown to vary considerably between examiners in 

several large studies (Atkin et al. 2004; Pinsky et al. 2005), highlighting the need for 

comprehensive training and the auditing of outcomes. In 2005, an international task force 

issued detailed recommendations to assist with quality improvement (Levin et al. 2005). 

Evidence from several case−control studies indicates that screening by flexible 

sigmoidoscopy should lead to a substantial reduction in the death rate from bowel cancer 

(Selby et al. 1992; Newcomb et al. 1992). Major randomised controlled trials using flexible 

sigmoidoscopy for screening are currently underway in the US, UK and Italy (Gohagan et 

al. 2000; UKSSTI 2002; Segnan et al. 2002). Progress results from the three trials show the 

screening procedure to be feasible, safe and well accepted (Weissfeld et al. 2005; Wardle, 

Miles & Atkin 2005; Segnan et al. 2002). 

The Australian Health Technology Advisory Committee report stated that the evidence 

is sufficient to warrant consideration of sigmoidoscopic screening as an alternative (or 

a complement) to FOBT screening, but noted that mortality data from the randomised 

controlled trials will not be available for several more years (AHTAC 1997). 

Colonoscopy 

A colonoscope is similar to a flexible sigmoidoscope but is much longer. Interest in using 

colonoscopy as a screening tool relates to its ability to detect a very high proportion 

of bowel cancers and advanced adenomas by examination of the entire length of the 

large bowel. It allows biopsies to be taken from any suspected abnormalities as well as 

enabling most adenomas and some polypoid cancers to be completely removed during the 

examination. 

Many studies have shown that colonoscopy has around 95% sensitivity for detection of 

cancer (Leaper et al. 2004; Robertson et al. 2005; Singh et al. 2006). The sensitivity for 

detection of adenomas varies according to their size and site within the large bowel (Rex 

et al. 1997). As with sigmoidoscopy, sensitivity for detection of lesions depends on the 

proficiency of the examiner, again highlighting the need for comprehensive training and 

the auditing of outcomes. In 2002, the US Multi-Society Task Force on Colorectal Cancer 

produced a detailed report on key performance indicators for colonoscopy (Rex et al. 

2002). 


14 


Colonoscopy is the recommended follow-up test for those with positive findings at FOBT 

or screening sigmoidoscopy. It is also recommended as the primary tool for cancer 

surveillance in people with an increased risk of bowel cancer. When it is not possible to 

examine the total length of the bowel by colonoscopy, a CT colonography or barium enema 

should be performed. 

The overall appropriateness of colonoscopy as the primary tool in population screening is 

much less certain. Acceptability of the procedure is limited by its invasive nature and the 

need for vigorous bowel preparation and sedation. The feasibility of providing colonoscopy 

for the five million Australians at average risk is also doubtful, given the high cost of the 

procedure, workforce and other logistic issues, and the required diversion of resources 

away from other health services. 

Of even greater importance, there is no high level evidence to support use of colonoscopy 

in population screening (ACN Revision Committee 2005). In 2001, the Canadian Task Force 

on Preventive Health Care stated that there was insufficient evidence to include or exclude 

colonoscopy as an initial screening test in people at average risk (CTFPHC 2001). Similarly, 

in 2002, the US Preventive Services Task Force was unable to find direct evidence that 

screening colonoscopy was effective in reducing the bowel cancer mortality rate (USPSTF 

2002). 


In 1999, in line with the Australian Health Technology Advisory Committee and the 

National Health and Medical Research Council recommendations, the National Cancer 

Control Initiative developed a proposal for a feasibility study for bowel cancer screening in 

the general population (NCCI 1999). The recommendations were formulated by an expert 

group that included representatives of the cancer councils. In response to this proposal, 

funds were set aside in the May 2000 federal budget to mount a four-year national 

feasibility study based on biennial screening using immunochemical FOBTs. 

The Population Screening Section of the Department of Health and Ageing then assumed 

responsibility for planning the National Bowel Cancer Screening Pilot Study. The Health 

Insurance Commission (known as Medicare Australia), cancer councils, and many other 

interested groups participated in the planning process. Three pilot sites—Mackay in 

Queensland, and defined suburbs in Adelaide and Melbourne—were chosen for the 

feasibility study, which was conducted between November 2002 and June 2004. The Pilot 

Evaluation Report concluded that a nationally coordinated bowel cancer screening program 

in Australia would be feasible, acceptable and cost effective (Healthcare Management 

Advisors 2005). 

In the 2005/06 federal budget, the Australian Government announced that it would provide 

$43.4 million over three years (including $7.8 million for the precursor pilot programs) to 

phase in a nationally coordinated, population-based bowel cancer screening program. 

The Department of Health and Ageing formed a new Bowel Cancer Screening Section to 

develop and coordinate the program. 

In August 2006 the Government confirmed that the National Bowel Cancer Screening 

Program would begin by inviting people who turn 55 or 65 years of age between 1 May 

2006 and 30 June 2008, and those who were invited to participate in the pilot, to complete 

an FOBT in their own home and return it by post to a laboratory for analysis. (Australia 

Post gave its approval.) Following consultation with state and territory governments, 

invitations to eligible participants would be issued on either a postcode or birth date basis 

and delivered through the mail. Nearly one million people were expected to be invited to 


participate in the initial phase; the first invitations were issued in Queensland on 7 August 

2006. 

A national bowel cancer screening register is set up within Medicare Australia. The 

register is responsible for issuing invitations and FOBTs, monitoring all data and arranging 

follow-up notifications for participants who receive positive FOBT results but do not have 

colonoscopies. It also runs the national Information Line. 

According to the Government, program implementation will be incremental and influenced 

by funding availability and healthcare system capacity, including colonoscopy and surgical 

services in each state and territory. The results of the first phase of National Bowel Cancer 

Screening Program are expected to be reviewed prior to the 2008/09 federal and state/ 

territory budgets. This review is expected to guide decisions about further implementation 

of the program. 

The Cancer Council fully supports and applauds the Australian Government’s introduction 

of a national bowel cancer screening program using faecal occult blood testing. As the 

program takes shape across Australia, the Cancer Council encourages all governments to 

ensure issues of access, quality and equity remain paramount. The availability of timely, 

high-quality colonoscopy following a positive FOBT will be an important issue affecting 

the success of the program, particularly in rural and remote areas where access may be 

limited. 

Appreciating the need for gradual implementation in the first instance, the Cancer Council 

encourages the Australian Government to make the necessary commitments, to ensure 

that the program becomes available to as many at-risk Australians as possible, in the 

shortest possible time. 

No upper age limit has been set for screening. Decisions about continued participation by 

the elderly are likely to be based on their personal preference and general state of health, 

and the perceived balance between benefits of screening and harms related to the followup 

investigations required in those with positive screening tests. 

Screening for people at increased risk of bowel cancer 

The Australian Health Technology Advisory Committee report on colorectal cancer 

screening noted that a national approach to population screening for people without 

symptoms would need to be complemented by a national policy for groups potentially 

at increased risk for bowel cancer: individuals with a family history of bowel cancer, or a 

personal history of bowel adenoma, bowel cancer or inflammatory bowel disease (AHTAC 

1997). GPs are well positioned to determine bowel cancer risk on the basis of family history 

and to instigate appropriate management, again consistent with guidelines (RACGP 2005; 

ACN Revision Committee 2005; McMurrick, Dorien & Shapiro 2006). 

The Australian Cancer Network Clinical practice guidelines for the prevention, early detection 

and management of colorectal cancer defines three categories of people in relation to risk 

for bowel cancer based on their family history of the disease. 

• 

• 

In the first category, people who have just one first-degree relative with bowel cancer 

are advised to have the same screening as those at average risk, provided their relative 

was diagnosed with cancer at or over the age of 55. 

The second category includes people with two or more first-degree relatives with bowel 

cancer (on the same side of the family) or one first-degree relative diagnosed under the 

age of 55 years. Because of their greater risk for cancer, screening is generally based on 

periodic (usually every five years) colonoscopy. 


151 


• 

The third category covers members of families with definite or suspected FAP or 

HNPCC. People with FAP usually have hundreds of small polyps throughout their 

bowel, some of which become malignant if not removed. HNPCC is not associated with 

polyposis but, like FAP, is caused by an inherited change in a gene. The place of genetic 

testing and recommendations about surveillance and prophylactic surgery are described 

in chapter 7 of the guidelines (ACN Revision Committee 2005). 

Detailed recommendations for surveillance by colonoscopy in those with past bowel 

cancer or adenoma are also set out in the Australian Cancer Network guidelines. 

Culturally appropriate communication 

Announcements made with the 2005/06 federal budget stated that Aboriginal and Torres 

Strait Islander communities will be invited to participate in the screening program from age 

45. The pilot evaluation showed that culturally and linguistically diverse communities and 

Aboriginal people and Torres Strait Islanders lacked awareness of bowel cancer screening 

issues. This was a major barrier against participation (Woolcott Research 2004). Culturally 

appropriate education and resources, as well as engagement with local health workers, will 

be needed to address the particular needs of these communities (Woolcott Research 2004) 

and to ensure that their participation, or non-participation, is based on informed choice. 


General practitioners (GPs) have an important role at critical points in the National Bowel 

Cancer Screening Program (DHA 2006). These include: 

• 

• 

• 

• 

• 

determining the appropriateness of screening for individual patients (e.g. those with 

significant co-morbidities, or those who’ve recently undergone screening outside the 

national program) 

assessing high-risk individuals and managing them according to National Health and 

Medical Research Council guidelines 

receiving FOBT results where the participant has nominated a GP 

managing participants with a positive FOBT 

notifying the central registry of outcomes. 

GPs also have an important role in recognising and assessing individuals with symptoms 

that could be related to cancer, and in whom diagnostic investigations (rather than 

screening) are required (ACN Revision Committee 2005; McMurrick, Dorien & Shapiro 

2006). Symptoms include: 

• 

• 

• 

• 

• 

bleeding from the back passage or any sign of blood in a bowel motion 

an unexplained and persistent change in bowel actions 

unexplained tiredness 

lower abdominal pain 

a persistent feeling of fullness. 

A recommendation from a GP has been shown to enhance participation rates in bowel 

cancer screening using FOBTs (Cole et al. 2002). It has been shown to be the most highly 

rated attribute that would encourage participation in bowel cancer screening (Salkeld et 

al. 2003). Over 90% of a population group surveyed responded that they would be likely or 

very likely to have an FOBT every two years if a doctor recommended this (Epidemiology 

Services Unit 2004). Pilot program invitees who did not participate indicated they were 


likely to do so if reinvited, especially if recommended by a GP (DHA 2005). Given this, it 

is not unreasonable to expect that a proactive approach by GPs in identifying their eligible 

patients and recommending their involvement in the screening program, may enhance 

participation rates. Whilst there is evidence that GPs support bowel cancer screening, GPs 

have also articulated a need for further education about this activity (Turner et al. 2006; 

Tong et al. 2004). 

It is anticipated that the national screening program will increase awareness of bowel 

cancer and bowel cancer screening in the broader population, including those not currently 

eligible for the screening program. GPs will be in a position to respond to this demand by 

managing patients according to current guidelines (RACGP 2005; ACN Revision Committee 

2005). 

Potential benefits and adverse effects of bowel 


Potential benefits 

As discussed earlier, bowel cancer screening using FOBTs has the potential to significantly 

reduce mortality from bowel cancer. Monitoring systems in South Australia found that only 

15% of bowel cancers are detected at the earliest point, Stage A (AHTAC 1997). Thus an 

important potential benefit of screening is to detect early stage, curable cancers in those 

without any clinical evidence of disease (ACN Revision Committee 2005). A screening 

program also has the potential to detect advanced adenomas, allowing them to be 

removed before progressing to bowel cancer. 

Thus, the benefits of bowel cancer screening are two-fold: providing opportunities for both 

prevention and early detection. It is predicted that a fully implemented screening program 

could save close to 2000 lives per year (Macrae 2005). 

Potential adverse effects 

Bowel cancer screening may result in adverse psychological and physical effects due to 

false positive tests. The potential adverse effects include anxiety induced by fear of having 

bowel cancer, anxiety related to diagnosis of lesions of doubtful clinical significance and 

complications of invasive diagnostic procedures (specifically colonoscopy). In several 

studies, anxiety due to positive test results was shown to decrease after investigation 

of the cause, with no evidence of long-term harm after screening (Lindholm et al. 1997; 

Wardle et al. 1999; Parker et al. 2002). The need to provide timely follow-up investigations 

following a positive result from an FOBT has important implications for the national 

program, as delays in the provision of colonoscopy may lead to high levels of anxiety. 

The most significant adverse effect is the potential for physical harm linked to exposure 

to colonoscopy. Colonoscopy is performed as a day case procedure and usually requires 

sedation. It can produce severe complications such as perforation, haemorrhage or death 

and carries a remote risk of transmitting infections. In a review of six prospective studies 

of colonoscopy, about one in 1000 patients suffered perforation, three in 1000 suffered 

major haemorrhage, and between one and three in 10,000 died as a result of the procedure 

(Winawer et al. 1997). In two more recent studies, the findings were similar, overall 

morbidity being 0.4% (Dafnis et al. 2001; Gatto et al. 2003). A review of a large Australian 

hospital experience supported the conclusions of these other studies and reported a 

mortality rate of 0.004% in outpatients having the procedure (Viiala et al. 2003). 


153 


Despite the possibility of adverse consequences of screening, distress generated by 

diagnosis of an advanced cancer when there has been no opportunity for early detection 

by screening also needs to be taken into consideration (ACN Revision Committee 2005). 


Randomised controlled trials at the population level indicate that screening tests for faecal 

occult blood reduce overall mortality from colorectal cancer in populations selected on the 

basis of age. These have shown benefit for people aged 45–50 years and upward. Costeffectiveness 

studies also demonstrate that age influences cost-effectiveness. Together 

with the observation that risk increases four-fold between ages of 40 and 50 years, these 

lead to the recommendation that screening of average risk people should commence at 

age 50 years (NHMRC 2005). 

Although the National Health and Medical Research Council guidelines do not suggest 

an upper age for screening, it is common for population-based screening programs to do 

so. There is no clear evidence on the best age to cease screening for bowel cancer. In the 

randomised controlled trials using FOBT, the upper age at the time of entry ranged from 

75 (Kronborg et al. 1996) to 80 years (Mandel et al. 1993). With increasing age, bowel 

cancer becomes more prevalent, but the potential for years of life saved through screening 

decreases. In addition, follow up colonoscopies may be less well tolerated among the 

elderly and participation is likely to drop off after the age of 70 (Hardcastle et al. 1996). 

Further cost-effectiveness research is needed to establish an appropriate upper age for the 

National Bowel Cancer Screening Program. 

Aims 

The Cancer Council aims to maximise participation of eligible people in the bowel cancer 

screening program and contribute to developments in knowledge to improve that program. 



Increased awareness among 

the general public and key 

health professional groups 

of the links between bowel 

cancer and nutrition, physical 

activity, obesity, alcohol 

consumption and smoking 

cessation 

A high-quality, well resourced 

national bowel cancer 

screening program capable 

of reaching 70% two-yearly 

participation of people over 

50 years of age by 2012 

154 Section Two: Screening to detect cancer early 

Advocate for a whole-of-government approach incorporating social 

marketing, policy reform and research, administered through a 

partnership involving all jurisdictions and peak health bodies (the 

success of the integrated National Tobacco Campaign of the late 1990s 

provides an excellent example on which to draw) 




Promote and/or develop primary health resources, specifically for 

general practice, to improve evidence-based interventions by health 

professionals 

Advocate for a whole-of-government agreement to a comprehensive, 

evidence-based screening program with adequate funding to reach the 

target population



A process of quality 

assurance and continuous 

improvement in the national 

bowel cancer screening 

program 

Sufficient workforce capacity 

to ensure colonoscopy wait 

times for a positive FOBT 

are under 30 days (for 

both screening program 

participants and those who 

have screened outside the 

program) 

Maximum participation of 

eligible people in bowel 


Referral to appropriate 

treatment services and 

collection of information 

about the outcome of 

treatment 

Advocate for the development of mandatory national training and 

accreditation standards for colonoscopy provision 

Advocate for government to build a formal, ongoing evaluation 

mechanism into the program to ensure regular monitoring and periodic 

evaluation. Evaluation should address: 

• overall outcomes relating to the impact of the program on bowel 

cancer mortality and morbidity 

• economic outcomes relating to the cost-effectiveness of the program 

and barriers to optimising participation among the target population 

• process outcomes relating to the performance of the program against 

its stated objectives 

• potential barriers to evaluation, notably fast-tracking cancer 

registrations to facilitate timely evaluation of program outcomes 

• sufficient resources to enable stated objectives to be achieved 

• periodic review of the target screening age group 

Support professionals such as general practitioners to contribute to the 

program’s efficiency and effectiveness 

Advocate for increase government funding and service redevelopment 

initiatives to increase colonoscopy capacity and ensure wait times are 

minimised 

Advocate for government support, including adequate funding, to 

ensure targets for participation are met, while maintaining a focus 

on equity and access. Priority should be given to maximising the 

participation of Australian Aboriginal and Torres Strait Islander 

communities and people of culturally and linguistically diverse (CALD) 

backgrounds, as they are likely to be under-screened 

Assist in developing tailored communications strategies, to promote and 

foster participation among specific population groups (e.g. Aboriginal 

and Torres Strait Islander and CALD communities) 

Recognising the importance of providing consistent high quality care for 

people diagnosed with bowel cancer in Australia: 

• support or advocate for examination of the extent to which people 

diagnosed in the screening program are being treated in accordance 

with the NHMRC Clinical practice guidelines for the prevention, early 

detection and management of colorectal cancer (2005) 

• 

encourage data collection that includes stage and outcome measures 

as well as qualitative information on patient experience 


155 


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McMurrick P, Dorien S & Shapiro J 2006. Bowel cancer: guide for the GP. Aust Fam Physician 35(4): 192–7. 

National Cancer Control Initiative (NCCI) 1999. Screening for early detection of colorectal cancer: a national 

initiative for the new millennium. Melbourne: NCCI. 

National Health and Medical Research Council (NHMRC) 2005. Clinical practice guidelines for the prevention, 

early detection and management of colorectal cancer. Canberra: NHMRC. 

National Health and Medical Research Council (NHMRC), Clinical Oncological Society of Australia (COSA) 

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colorectal cancer (CRC). Canberra: NHMRC. 

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Pinsky PF, Schoen RE, Weissfeld JL, Kramer B, Hayes RB & Yokochi L 2005. Variability in flexible 

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15 


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97(10): 2499–507. 

1 0 Section Two: Screening to detect cancer early

M e l a n o m a 

Melanoma in Australia 

Currently there is no conclusive scientific evidence 

that population screening for melanoma reduces 

mortality from this disease. 

Australia has the highest incidence of melanoma in the world. In 2005, an estimated 

10,014 Australians (5705 men and 4309 women) were diagnosed with melanoma. 

Excluding non-melanoma skin cancer, melanoma was the third most common cancer 

diagnosed in Australian women (after breast and colorectal cancer), and the third most 

common in Australian men (after prostate and colorectal cancer) in 2005. In 2005 there 

were 862 deaths from melanoma in men and 411 in women (ABS 2007). 

Can melanoma be prevented? 

Melanoma is potentially almost totally preventable. Exposure to excess ultraviolet (UV) 

radiation is the major environmental factor in its development and one which is amenable 

to behavioural intervention. More information on prevention of melanoma is included in the 

chapter on ultraviolet radiation. 

Screening tests for melanoma 

The screening tests proposed for early detection of melanoma include total body skin 

examination by a health care professional or skin self-examination. Detection of a 

suspicious lesion constitutes a positive screening test for which further investigation is 

required. Melanoma is confirmed by skin biopsy (ACN & NHMRC 1999). 

Skin examination by a GP or specialist 

Although differences have been reported between the effectiveness of specialists and 

GPs in detecting malignant melanoma (Morrison, O’Loughlin & Powell 2001), a systematic 

review concluded that there was insufficient evidence to prove an overall difference (Chen 

et al. 2001). Nevertheless, a number of studies have indicated that the benign-to-malignant 

ratio of pigmented skin lesions is very high (around 30:1) in the general practice setting in 

Australia (Del Mar et al. 1994; Marks et al. 1997). 

The ability of GPs to conduct screening for melanoma is an important pre-condition for the 

introduction of a screening program, but little information is available on this. In a large trial 

of population screening in Queensland using whole-body skin examinations, 2.5% of all 

suspicious skin lesions detected by GPs were confirmed as melanoma giving an estimated 

specificity of 86.1% (Aitken et al. 2006). The melanomas detected during that screening 

program tended to be less advanced, similar to results found in other screening programs 

(Geller et al. 2003). 

Another factor to be considered in screening for melanoma is the proportion of the 

body examined. Melanoma is more likely than non-melanoma skin cancers to appear on 


1 1 

M e l a n o m a

sites of the body not normally exposed to the sun. One study estimated that detection 

of melanomas was six times more likely with a total body skin examination (Rigel et al. 

1986), but a smaller subsequent study found little advantage in total body examination 

(De Rooij et al. 1996). While screening of visible areas of the body has been demonstrated 

to be well accepted (Girgis et al. 1996), a total body skin examination raises the issue of 

embarrassment as a barrier to repeated screening. However, a recent study found that only 

8% of participants said that they agreed or strongly agreed that having a skin examination 

would be embarrassing (Janda et al. 2004). 

A critical issue in regards to screening by GPs or specialists is to determine the 

significance of including relatively new diagnostic techniques in the screening process. 

Dermoscopy (surface microscopy) is a well-researched technique that uses inexpensive 

hand-held surface microscopes allowing a significant increased melanoma diagnostic 

ability in a specialist setting (Kittler et al. 2002). It has also been shown to improve the 

sensitivity for melanoma diagnosis by 38% in a study using Australian GPs (Westerhoff, 

McCarthy & Menzies 2000). There have been a number of computer programs developed 

to analyse digitalised dermoscopy images. These have been widely promoted by the 

manufacturers for use in the general community. However, they are still in the research 

and development phase and there are no data as yet to show they are superior to a welltrained 

and experienced clinician using dermoscopy. Trials using dermoscopy and handheld 

digital monitoring devices within general practice are currently underway in Western 

Australia. Further research is required to determine their value in community screening for 

melanoma. 

Self-examination 

Studies have shown a tendency by subjects to under-report or demonstrate poor selfassessment 

of pigmented skin lesions (Borland, Marks & Noy 1992; Hanrahan et al. 1995), 

which may have significant ramifications for self-referral to screening (Eiser et al. 2000; 

Melia et al. 2000). Most studies examining detection of melanoma have found that the 

majority of melanomas are first detected by the patient (Koh et al. 1992; McPherson et 

al. 2006). However, in one of these studies only about 4% of patients who detected the 

melanoma themselves did so during a deliberate skin self-examination (McPherson et al. 

2006). 

Rationale for screening for melanoma 

Interest in screening for melanoma is based on the potential for detection and treatment of 

significantly thinner melanomas, since people in whom thinner melanomas are detected 

and excised experience a better outcome than those detected with more advanced 

disease. 

For non-melanoma skin cancer, early detection of squamous cell carcinoma can also 

reduce the rate of deaths if treated early, while for basal cell carcinomas for which the rates 

of death are much lower, the benefits of screening would relate to reductions in illness, 

costs and inconvenience (NHMRC 1997). 

This discussion will focus on screening in relation to melanoma. 


Would screening be of benefit at this stage? 

Despite no formalised screening program in Australia, mortality from melanoma in younger 

cohorts is improving. This may reflect either earlier presentation of tumours or increased 

detection of clinically irrelevant indolent melanomas (AIHW & AACR 2004). 

Existing community awareness is leading to successful screening and early detection 

both at the request of individuals and opportunistically from their health care providers. 

To reduce mortality further, an organised screening program would need to significantly 

enhance early diagnosis beyond what is currently being achieved. 

An additional concern relates to rapidly growing melanoma. A recent study suggests that 

one-third of melanomas grow rapidly (at 0.5 mm or more of tumour thickness per month) 

(Liu et al 2006). These are unlikely to be detected early at an annual screening program. 

Evidence is insufficient at present to recommend for or against routine screening for 

melanoma of the general asymptomatic population. This is consistent with the current 

position of the US Preventive Services Task Force (AHRQ 2005). 

Aims 

The Cancer Council’s aims are to: 

• 

• 

encourage research to determine the impact of new diagnostic technologies 

(dermoscopy and digital monitoring) in general practice 

encourage further research to determine whether screening for melanoma in Australia 

would reduce illness and death and whether implementation would be practical and 

acceptable to the community. 

References 

Melanoma 

Agency for Healthcare Research and Quality (AHRQ) 2005. Guide to clinical preventive services. AHRQ 

Publication no. 05-0570, June 2005. Rockville MD: AHRQ. 

Aitken JF, Janda M, Elwood M, Youl PH, Ring IT & Lowe JB 2006. Clinical outcomes from skin screening 

clinics within a community-based melanoma screening program. J Am Acad Dermatol 54(1): 105–14. 


Australian Cancer Network (ACN) & National Health and Medical Research Council (NHMRC) 1999. Clinical 

practice guidelines for the management of cutaneous melanoma. Canberra: ACN. 



Borland R, Marks R & Noy S 1992. Public knowledge about characteristics of moles and melanomas. Aust J 

Public Health 16(4): 370–5. 

Chen SC, Bravata DM, Weil E & Olkin I 2001. A comparison of dermatologists’ and primary care physicians’ 

accuracy in diagnosing melanoma: a systematic review. Arch Dermatol 137(12): 1627–34. 

De Rooij MJ, Rampen FH, Schouten LJ & Neumann HA 1996. Total skin examination during screening for 

malignant melanoma does not increase the detection rate. Br J Dermatol 135(1): 42–5. 


1 3 

M e l a n o m a

Del Mar C, Green A, Cooney T, Cutbush K, Lawrie S & Adkins G 1994. Melanocytic lesions excised from the 

skin: what percentage are malignant? Aust J Public Health 18(2): 221–3. 

Eiser JR, Pendry L, Greaves CJ, Melia J, Harland C & Moss S 2000. Is targeted early detection for melanoma 

feasible? Self-assessment of risk and attitudes to screening. J Med Screen 7(4): 199–202. 

Geller AC, Zhang Z, Sober AJ, Halpern AC, Weinstock MA, Daniels S, Miller DR, Demierre MF, Brooks DR 

& Gilchrest BA 2003. The first 15 years of the American Academy of Dermatology skin cancer screening 

programs: 1985–1999. J Am Acad Dermatol 48(1): 34–41. 

Girgis A, Clarke P, Burton RC & Sanson-Fisher RW 1996. Screening for melanoma by primary health care 

physicians: a cost-effectiveness analysis. J Med Screen 3(1): 47–53. 

Hanrahan PF, Hersey P, Watson AB & Callaghan TM 1995. The effect of an educational brochure on 

knowledge and early detection of melanoma. Aust J Public Health 19: 270–4. 

Janda M, Elwood M, Ring IT, Firman DW, Lowe JB, Youl PH & Aitken JF 2004. Prevalence of skin screening 

by general practitioners in regional Queensland. Med J Aust 180(1): 10–15. 

Kittler H, Pehamberger H, Wolff K & Binder M 2002. Diagnostic accuracy of dermoscopy. Lancet Oncol 3(3): 

159–65. 

Koh HK, Miller DR, Geller AC, Clapp RW, Mercer MB & Lew RA 1992. Who discovers melanoma? J Am Acad 

Dermatol 26: 914–19. 

Liu W, Dowling JP, Murray WK, McArthur GA, Thompson JF, Wolfe R & Kelly JW 2006. Rate of growth in 

melanomas: characteristics and associations of rapidly growing melanomas. Arch Dermatol. 142: 1551–8. 

Marks R, Jolley D, McCormack C & Dorevitch AP 1997. Who removes pigmented skin lesions? J Am Acad 

Dermatol 36(5 Pt 1): 721–6. 

McPherson M, Elwood M, English DR, Baade PD, Youl PH & Aitken JF 2006. Presentation and detection of 

invasive melanoma in a high-risk population. J Am Acad Dermatol 54: 783–92. 

Melia J, Harland C, Moss S, Eiser JR & Pendry L 2000. Feasibility of targeted early detection for melanoma: a 

population-based screening study. Br J Cancer 82(9): 1605–9. 

Morrison A, O’Loughlin S & Powell FC 2001. Suspected skin malignancy: a comparison of diagnoses of 

family practitioners and dermatologists in 493 patients. Int J Dermatol 40(2): 104–7. 

National Health and Medical Research Council (NHMRC) 1997. Preventive interventions in primary health care: 

cardiovascular disease and cancer. Canberra: NHMRC. 

Rigel DS, Friedman RJ, Kopf AW, Weltman R, Prioleau PG, Safai B, Lebwohl MG, Eliezri Y, Torre DP & Binford 

RT, Jr. 1986. Importance of complete cutaneous examination for the detection of malignant melanoma. J Am 

Acad Dermatol 14(5 Pt 1): 857–60. 

Westerhoff K, McCarthy W & Menzies S 2000. Increase in the sensitivity for melanoma diagnosis by primary 

care physicians using skin surface microscopy. Br J Dermatol 143(5): 1016–20. 


P r o s t a t e c a n c e r 

Cancer of the prostate is a common and important 

health problem. Its early diagnosis and subsequent 

treatment present a dilemma for medical practitioners 

and consumers. Since advantages of testing and 

treatment are not clear-cut, individual men who 

decide to be tested for prostate cancer should be able 

to do so on the basis of informed consent, having 

access to full information about the potential benefits 

and risks associated with testing. Preliminary findings 

suggest that introduction of a national education 

program for general practitioners to improve decision- 

making relating to the use of prostate-specific antigen 

Prostate cancer in Australia 

testing would be cost-effective. 

In 2005, prostate cancer is projected to be the most common cancer (apart from nonmelanoma 

skin cancer) diagnosed in Australian men, with an estimated 12,529 new cases 

(AIHW, AACR, NCSG & McDermid 2005). 

Prostate cancer mainly affects men in older age groups. Over 85% of new cases and over 

96% of deaths occur in men over 60 years of age. It is rare in men under 45 years. 

Although the incidence of prostate cancer increases with age, the threat to life from 

prostate cancer decreases with age because the disease generally develops and 

progresses slowly. This means that men diagnosed with prostate cancer who are older 

than 75 years or have fewer than 10 years life expectancy are considered to be least at risk 

of dying of prostate cancer. 

Men who are diagnosed at an earlier age (e.g. in their 50s) are most at risk of dying from 

prostate cancer (Baade, Steginga et al. 2005). This is because it is probable that they will 

live long enough for their prostate cancer to progress to a life-threatening stage and are 

less likely to die from competing causes. It is also important to note that, irrespective of the 

risk it poses, a diagnosis of prostate cancer at any age can have a major impact on a man’s 

quality of life. 

The incidence of prostate cancer was relatively stable until 1989 but, between 1990 and 

1994, there was a dramatic rise in the number of new cases reported (AIHW & AACR 

2004). This has been attributed to increased detection of the disease due to many more 

investigations, particularly case-finding using PSA testing, which was introduced around 

1990 (see below). However, between 1994 and 1997 the age-standardised prostate cancer 

incidence rate fell by 30%. Since then, there has been little change between the 1998 and 

2005 rate, indicating that the surge-effect from the previously undetected cases has been 

accommodated and the practice of early detection has stabilised. 


1 5 

P r o s t a t e c a n c e r

The mortality rate from prostate cancer, which is significantly lower than the incidence rate, 

decreased by 1.9% per annum between 1991 and 2005, when 2,946 deaths were reported 

(ABS 2007). 

The burden of prostate cancer is likely to increase with the ageing of the Australian 

population, and this has major public health and economic implications (Weller et al. 1998). 

Can prostate cancer be prevented? 

The causes of prostate cancer are poorly understood. Geographical and racial differences 

in rates of prostate cancer provide compelling evidence that environmental and lifestyle 

factors are involved (Weller et al. 1998). Age and family history are the strongest risk 

factors in Australia. Researchers continue to examine other possible risk factors, including 

diet, weight and physical activity. An effective approach to primary prevention of prostate 

cancer has not yet been identified (Harris & Lohr 2002). 

Chemoprevention is being investigated but is not in routine use. A trial examining selenium 

and vitamin E (The SELECT trial) is in progress, with results not anticipated until 2013 

(Klein 2004). An analysis of the screening arm of the prostate, lung, colorectal and ovarian 

(PLCO) cancer trial does not show a benefit for supplementation with the micronutrient 

antioxidants vitamin E, beta-carotene and vitamin C (Kirsh et al. 2006). 

An Australian review noted that there is little evidence that could define risk groups 

sufficiently for targeted screening activities (Weller et al. 1998). One possible exception 

is men with a strong family history of prostate cancer. Men with a first-degree relative 

diagnosed with prostate cancer have a two-and-a-half times greater risk of being 

diagnosed, with some evidence that the risk is higher if the relative was diagnosed before 

the age of 60 years (Johns & Houlston 2003). The genetic basis has not been identified, 

though men carrying mutations of the breast cancer susceptibility genes BRCA1 or BRCA2 

gene have an increased risk of several types of cancer, including prostate cancer (Liede et 

al. 2000). The questions of whether, when and how often such people should be monitored 

have yet to be addressed. 

Tests for prostate cancer 

Prostate-specific antigen test 

The prostate-specific antigen (PSA) test is commonly used to try to detect prostate cancer. 

It measures the amount of PSA in blood. 

PSA levels can be raised due to a range of conditions. In studies of men aged 45 to 80 

years, 7% to 13% had a PSA level greater than 4 ng/ml; of these, 10% to 30% were 

identified as having prostate cancer on biopsy (USPSTF 2005). The level of PSA used to 

justify biopsy is commonly set at 4 ng/ml. Some have advocated a cut-off of 2.5 ng/ml 

(Punglia et al. 2003), since it is estimated that 25% to 30% of prostate cancers are detected 

with a PSA between 2.5 and 4 ng/ml (Pepe et al. 2006). However, increased sensitivity 

by use of a lower level will decrease specificity, leading to a higher rate of unnecessary 

biopsies and an increase in over-diagnosis (see below). 

Accuracy may be improved by taking into account a man’s age, since PSA levels increase 

with age due to benign enlargement of the prostate. It may also be improved by measuring 

the proportion of free to total or complexed PSA, since men with prostate cancer tend to 


have lower levels of free PSA than men who don’ t have prostate cancer. However, there is 

no consensus yet on either of these measurements (Harris & Lohr 2002; Stenman 1997). 

Digital rectal examination 

Another form of testing is digital rectal examination. This test involves manual examination 

of the prostate gland through the rectum. Some abnormalities may be felt but it is not 

possible to feel all of the prostate. A cancer that is in a part of the prostate gland out of the 

doctor’ s reach—estimated to be 25% to 35% of the prostate—may be missed (USPSTF 

2005). In addition, small (stage A or T1) cancers cannot be felt. Wide variations in reporting 

occur between doctors (AHTAC 1996). 

Transrectal ultrasound and biopsy 

Neither the PSA test nor DRE, alone or together, is a truly accurate test for prostate cancer. 

If abnormalities are detected by a PSA test or DRE, tissue specimens will be needed for 

diagnosis, usually via transrectal ultrasound (TRUS) imaging to permit spatial positioning of 

biopsy needles. The needle biopsy procedure involves eight to 10 or more cores of tissue 

being removed for examination under a microscope. Even though tissue is taken from a 

number of locations, and most malignant cancers will be detected, it is not possible to say 

with complete certainty that a negative result excludes the presence of cancer. The test 

carries risks of infection and bleeding (AHTAC 1996). 

Test limitations and implications 

The sensitivity and specificity of the screening tests available for prostate cancer cannot be 

determined with certainty (i.e. confirmed by pathology tests on tissue samples) because 

biopsies are generally not done on people with negative screening tests (USPSTF 2005). 

Only the positive predictive value—the probability of cancer when the test is positive—can 

be calculated with any confidence, but this also is subject to methodological difficulties 

from the needle biopsy (USPSTF 2005). 

A recent study where 2950 men with ‘normal’ PSA values (

Participants in the ERSPC trial completed a questionnaire on health before screening and 

then twice subsequently if they were diagnosed with prostate cancer. Mental and self-rated 

overall health worsened significantly immediately after diagnosis (P

• 

• 

a monitoring mechanism be put in place to ensure that the Australian Health Technology 

Advisory Committee position on screening is reviewed when significant developments 

occur 

a comprehensive education program on the risks and benefits of prostate cancer testing 

be introduced for GPs, their patients and the community. 

The Cancer Council Australia and state and territory cancer councils were active in the 

establishment in 1998 of the National Prostate Cancer Collaboration to foster clinical, 

laboratory and epidemiological research, as well as research and programs in education. In 

1999 the group became the Australian Prostate Cancer Collaboration. Its aim is to develop 

strategies for the control of prostate cancer to decrease mortality and increase quality of 

life. 


Recent reports suggest that GPs are poorly resourced to assist their patients making an 

informed choice on prostate cancer testing. Only half or less of the GPs who responded 

to a survey were aware of guidelines published by the Royal Australasian College of 

General Practitioners and The Cancer Council Australia—both of which recommend against 

population screening (Ward, Young & Sladden 1998). 

A meeting about informed choice for prostate cancer testing in general practice (Pinnock 

2004) reported that: 

• 

• 

• 

• 

• 

• 

studies on how patients make medical decisions indicate that non-systematic factors 

such as old beliefs, anecdotes and salient experiences are more common than a 

systematic weighing up of pros and cons (see also Farrell, Murphy & Schneider 2002; 

Steginga et al. 2002) 

testing is often requested for medico-legal reasons. The process and content of an 

informed choice discussion needs to reflect medico-legal obligations 

criteria have been developed to assess which decision aids are likely to be most 

effective in helping patients become informed and make decisions 

the barriers GPs face in fully informing patients with diverse backgrounds and 

knowledge need to be better understood 

particular skills are needed in order to communicate complex issues such as uncertainty 

and risk to patients 

complicating factors are men’s lack of access to primary care services, particularly 

in rural areas, poor general knowledge of male health in the community and high 

prevalence of anxiety about urinary symptoms. 

Preliminary findings suggest that the introduction of a national education program for 

GPs to improve decision-making relating to the use of PSA testing would be cost effective 

(Stone et al. 2005). Evaluations of the GP education workshops have shown that as 

participants’ knowledge about PSA testing and level of understanding increased, they were 

more likely to initiate discussions with patients about the risks and benefits of testing, and 

they were more confident in doing so (Metcalfe et al. 2006; Steginga et al. 2005). 


1 


Potential benefits and adverse effects of prostate 


Refer to the introduction to Section Two for the World Health Organization criteria that 

need to be satisfied before population screening for a disease may be introduced. Central 

to this is the need for evidence that screening for the disease, with subsequent early 

treatment, is effective in improving health outcomes. In relation to prostate cancer, the 

question is whether detection of tumours using currently available tests will result in 

benefits for most patients. 

The difficulty regarding early detection of prostate cancer is that first, depending on the 

age of the patient, many cancers found through screening will not be life threatening. 

Second, it is currently not possible to distinguish with certainty those cancers that will be 

life threatening. It has been estimated that prostate cancer is present in 30% to 40% of 

men aged more than 50 years, but only one in four of these cancers will result in clinical 

symptoms and one in 14 will cause death (Weller et al. 1998). 

Would population screening be of benefit at this stage? 

The current state of knowledge does not satisfy the World Health Organization criterion 

that there should be an accepted treatment for patients with recognised disease. It is 

possible that intervention through early detection will cause more harm than good, for 

example in the risks posed by treatment (see below). 

The problem of over-diagnosis 

A major concern with screening is that it will diagnose cancers which, if left undetected, 

would never have caused morbidity or mortality. This is known as over-diagnosis. One 

estimate using mathematical modelling puts the over-diagnosis rate as high as 50% 

(Draisma et al. 2003). It has been estimated that most prostate cancer detected by 

commonly promoted testing strategies would not have caused morbidity or mortality 

(McGregor et al. 1998; Draisma et al. 2003). Over-diagnosis results in unnecessary 

treatment with high risks of urinary incontinence, bowel problems (especially following 

radiation) and erectile dysfunction (Begg et al. 2002). 

Prostate cancer treatment issues 

The major treatment options following detection of prostate cancer are active treatment 

(surgical removal of the prostate or radiation therapy) or observational treatment (watchful 

waiting) (AHTAC 1996). 

Our knowledge of which prostate cancers are life threatening and which are not is limited. 

In the European Randomised study of screening for prostate cancer, the patients in the 

Rotterdam section were screened by PSA, DRE and transrectal ultrasound. A subset of 

patients who would have qualified for a surveillance program were identified: those with 

a Gleason score less than or equal to 3+3, PSA density less than 0.2 and a maximum PSA 

level of 15 ng/ml. Those who met the above arbitrary criteria who chose watchful waiting 

did not do worse than those who had active treatment at a mean follow-up to 80.8 months 

(Roemeling et al. 2006). 

Limitations of studies comparing the effectiveness of treatments occur because most 

information on treatment by surgical removal of the prostate comes from uncontrolled 

case series and cohort studies that indicate survival following surgery is high. However, 


ecause surgical patients are usually younger and have less advanced disease, it is difficult 

to separate out the effects of treatment efficacy and selection bias. 

In practice there is a wide variation in treatment decisions. Treatments for early prostate 

cancer differ in the proportion of patients who are likely to experience side effects such as 

erectile problems, incontinence and bowel symptoms. 

Current clinical practice supports active intervention, particularly among men whose life 

expectancy exceeds 10 years with aggressive and early onset of disease. 

Randomised controlled trials comparing options are difficult to conduct, but a recent study 

compared watchful waiting with immediate radical prostatectomy in 695 men with newly 

diagnosed early stage prostate cancer. Prostatectomy led to a significant reduction in 

both metastatic disease and disease-specific mortality, and, after eight to 10 years, overall 

mortality (Holmberg et al. 2002; Bill-Axelson et al. 2005). 

Radiation therapy is widely practised in Australia, particularly among older patients and 

those with more aggressive or later stage (high-risk) cancers. Newer techniques, delivering 

radiation therapy aimed at increasing the radiation dose while minimising effects on 

adjacent tissues, are becoming increasingly available. An analysis of 60,290 men with low 

and moderate grade organ-confined prostate cancer, on the National Cancer Institute’s 

Surveillance, Epidemiology and End Results (SEER) Program showed better survival for 

men under and over 60 years if they received surgery or brachytherapy rather no definitive 

treatment (Tward et al 2006). 

Because it has not been possible to prove definitively that treatments differ in effectiveness 

(NHMRC 2003), the incorporation of patient preference into treatment decisions is widely 

endorsed (Weller et al. 1998; NHMRC & ACN 2003). 

Aims 

The Cancer Council Australia supports: 

• 

• 

• 

• 

• 

advocating for and contributing expert advice to the development of decision-making 

tools for informed choice about prostate cancer testing, for medical practitioners and 

consumers, based on the best available evidence 

contributing to the development and implementation of community education relating 

to the prostate and prostate cancer 

monitoring and supporting research on population screening and testing for prostate 

cancer to inform the development of policy and communication strategies 

seeking opportunities to work with health related agencies, health professionals and 

consumers to increase understanding of the prostate and prostate cancer 

addressing the issues which cause inequities in access and outcomes in prostate 

cancer, such as living in rural and remote Australia, by developing models where 

information and multidisciplinary care can be accessed by those groups. 


1 1 


References 

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Australian Health Technology Advisory Committee (AHTAC) 1996. Prostate cancer screening: summary of 

the review prepared by the Australian Health Technology Advisory Committee. Canberra: Commonwealth 

Department of Health and Family Services. 






National Cancer Strategies Group (NCSG) & McDermid I 2005. Cancer incidence projections Australia, 2002 to 

2011. Canberra: AIHW. 

Baade PD, Steginga SK, et al. 2005. Communicating prostate cancer risk: what should we be telling our 

patients. Med J Aust 182: 472–5. 

Bangma CH, Kranse R, Blijenberg BG & Schroder FH 1995. The value of screening tests in the detection 

of prostate cancer. Part II: Retrospective analysis of free/total prostate-specific analysis ratio, age-specific 

reference ranges, and PSA density. Urology 46(6): 779–84. 

Begg CB, Riedel ER, Bach PB, Kattan MW, Schrag D, Warren JL & Scardino PT 2002. Variations in morbidity 

after radical prostatectomy. N Engl J Med 346(15): 1138–44. 

Bill–Axelson A, Holmberg L, Ruutu M, Haggman M, Andersson S-O, Bratell S, Spangberg A, Busch C, 

Nording S, Garmo H, Palmgren J, Adami H-O, Norlen BJ & Johansson J-E 2005. Radical prostatectomy 

versus watchful waiting in early prostate cancer. N Engl J Med 352(19): 1977–84. 

Ciatto S, Bonardi R, Lombardi C, Cappelli G, Castagnoli A, D’Agata A, Zappa M & Gervasi G 2001. Predicting 

prostate biopsy outcome by findings at digital rectal examination, transrectal ultrasonography, PSA, PSA 

density and free-to-total PSA ratio in a population-based screening setting. Int J Biol Markers 16(3): 179–82. 

Coory MD & Baade PD 2005. Urban–rural differences in prostate cancer mortality, radical prostatectomy and 

prostate-specific antigen testing in Australia. Med J Aust 182(3): 112–15. 

Draisma G, Boer R, Otto SJ, Cruijsen van der I, Damhuis RA, Schroder FH & de Koning HJ 2003. Lead times 

and overdetection due to prostate-specific antigen screening: estimates from the European Randomized 

Study of Screening for Prostate Cancer. J Natl Cancer Inst 95(12): 868–78. 

Farrell MH, Murphy MA & Schneider CE 2002. How underlying patient beliefs can affect physician–patient 

communication about prostate-specific antigen testing. Eff Clin Pract 5(3): 120–9. 

Gattellari M & Ward JE 2005. Men’s reactions to disclosed and undisclosed opportunistic PSA screening for 

prostate cancer. Med J Aust 182(8): 386–9. 

Harris R & Lohr KN 2002. Screening for prostate cancer: an update of the evidence for the US Preventive 

Services Task Force. Ann Intern Med 137(11): 917–29. 

Holmberg L, Bill-Axelson A, Helgesen F, Salo JO, Folmerz P, Haggman M, Andersson SO, Spangberg A, 

Busch C, Nordling S, Palmgren J, Adami HO, Johansson JE, Norlen BJ & The Scandinavian Prostatic Cancer 

Group Study Number 4 2002. A randomized trial comparing radical prostatectomy with watchful waiting in 

early prostate cancer. N Engl J Med 347(11): 781–9. 

Johns LE & Houlston RS 2003. A systematic review and meta-analysis of familial prostate cancer risk. BJU Int 

91(9): 789–94. 

Kirsh VA, Hayes RB, Mayne ST, Chatterjee N, Subar AF, Dixon LB, Albanes D, Andriole GL, Urban DA & Peters 

U 2006. Supplemental and dietary vitamin E, beta-carotene, and vitamin C intakes and prostate cancer risk. J 



Klein EA 2004. Selenium and vitamin E cancer prevention trial. Ann N Y Acad Sci 1031: 234–41. 

Korfage IJ, de Koning HJ, Roobol M, Schroder FH & Essink-Bot ML 2006. Prostate cancer diagnosis: the 

impact on patients’ mental health. Eur J Cancer 42(2): 165–170. 

Kupelian P, Kuban D, Thames H, Levy L, Horwitz E, Martinez A, Michalski J, Pisansky T, Sandler H, Shipley W, 

Zelefsky M & Zietman A 2005. Improved biochemical relapse-free survival with increased external radiation 

doses in patients with localized prostate cancer: the combined experience of nine institutions in patients 

treated in 1994 and 1995. Int J Radiat Oncol Biol Phys 61(2): 415–19. 

Liede A, Metcalfe K, Hanna D, Hoodfar E, Snyder C, Durham C, Lynch HT & Narod SA 2000. Evaluation of 

the needs of male carriers of mutations in BRCA1 or BRCA2 who have undergone genetic counseling. Am J 

Hum Genet 67(6): 1494–504. 

Luo LY, Shan SJ, Elliott MB, Soosaipillai A & Diamandis EP 2006. Purification and characterization of human 

kallikrein 11, a candidate prostate and ovarian cancer biomarker, from seminal plasma. Clin Cancer Res 12(3 

Pt 1): 742–50. 

McGregor M, Hanley JA, Boivin JF & McLean RG 1998. Screening for prostate cancer: estimating the 

magnitude of overdetection. Can Med Assoc J 159(11): 1368–72. 

Metcalfe R, Russell R, McAvoy B, Tse J, Sutherland G & Hoey L 2006. Promoting shared decision making and 

informed choice for the early detection of prostate cancer: Development and evaluation of a GP education 

program. Cancer Forum 30(1): 38–42. 

National Health and Medical Research Council (NHMRC) & Australian Cancer Network (ACN) 2003. Clinical 

practice guidelines: evidence–based information and recommendations for the management of localised 

prostate cancer. Canberra: NHMRC. 

Pepe P, Panella P, D’Arrigo L, Savoca F, Pennisi M & Aragona F 2006. Should men with serum prostatespecific 

antigen < or =4 ng/ml and normal digital rectal examination undergo a prostate biopsy? A literature 

review. Oncology 70(2): 81–9. 

Pinnock CB 2004. PSA testing in general practice: can we do more now? Med J Aust 180(8): 379–81. 

Pinnock CB, Weller DP & Marshall VR 1998. Self-reported prevalence of prostate-specific antigen testing in 

South Australia: a community study. Med J Aust 169(1): 25–8. 

Potosky AL, Davis WW, Hoffman RM, Stanford JL, Stephenson RA, Penson DF & Harlan LC 2004. Five-year 

outcomes after prostatectomy or radiotherapy for prostate cancer: the prostate cancer outcomes study. J 


Punglia RS, D’Amico AV, Catalona WJ, Roehl KA & Kuntz KM 2003. Effect of verification bias on screening 

for prostate cancer by measurement of prostate-specific antigen. N Engl J Med 349(4): 335–42. 

Roemeling S, Roobol MJ, Postma R, Gosselaar C, van der Kwast TH, Bangma CH & Schroder FH 2006. 

Management and survival of screen-detected prostate cancer patients who might have been suitable for 

active surveillance. Eur Urol 50(3): 475–82. 

Schroder FH, Kranse R, Rietbergen J, Hoedemaeke R & Kirkels W 1999. The European Randomized Study 

of Screening for Prostate Cancer (ERSPC): an update. Members of the ERSPC, Section Rotterdam. Eur Urol 

35(5–6): 539–43. 

Selley S, Donovan J, Faulkner A, Coast J & Gillatt D 1997. Diagnosis, management and screening of early 

localised prostate cancer. Health Technol Assess 1(2): 1–96. 

Smith DP & Armstrong BK 1998. Prostate-specific antigen testing in Australia and association with prostate 

cancer incidence in New South Wales. Med J Aust 169(1): 17–20. 

Steginga SK, Occhipinti S, Gardiner RA, Yaxley J & Heathcote P 2002. Making decisions about treatment for 

localized prostate cancer. BJU Int 89(3): 255–60. 

Steginga SK, Pinnock C, Baade PD, Jackson C, Green A, Preston J, Heathcote P & McAvoy B 2005. An 

educational workshop on the early detection of prostate cancer. Aust Fam Physician 34(10): 889–91. 

Stenman UH 1997. Prostate-specific antigen, clinical use and staging: an overview. Br J Urol 79 (1 Suppl): 

S53–60. 


1 3 


Stone CA, May FW, Pinnock CB, Elwood M & Rowett DS 2005. Prostate cancer, the PSA test and academic 

detailing in Australian general practice: an economic evaluation. Aust N Z J Public Health 29: 349–57. 

Thompson IM, Pauler DK, Goodman PJ, Tangen CM, Lucia MS, Parnes HL, Minasian LM, Ford LG, Lippman 

SM, Crawford ED, Crowley JJ & Coltman CA Jr 2004. Prevalence of prostate cancer among men with a 

prostate-specific antigen level < or =4.0 ng per milliliter. N Engl J Med 350(22): 2239–46. 

Tward JD, Lee CM, Pappas LM, Szabo A, Gaffney DK & Shrieve DC 2006. Survival of men with clinically 

localized prostate cancer treated with prostatectomy, brachytherapy, or no definitive treatment: impact of age 

at diagnosis. Cancer 107(10): 2392–400. 

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Agency for Healthcare Research and Quality. 

Ward J, Young J & Sladden M 1998. Australian general practitioners’ views and use of tests to detect early 

prostate cancer. Aust N Z J Public Health 22: 374–80. 

Ward JE, Hughes AM, Hirst GH & Winchester L 1997. Men’s estimates of prostate cancer risk and selfreported 

rates of screening. Med J Aust 167(5): 250–3. 

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AHTAC report. Unpublished document on behalf of the Australian Cancer Network. Adelaide: Department of 

Evidence-based Care and General Practice, Flinders University of South Australia. 


Section Three: 

Immunisation 

www.cancer.org.au

H u m a n p a p i l l o m a v i r u s 

HPV 

1 Section Three: Immunisation 

Prophylactic vaccination against human papilloma 

virus (HPV) 16/18 has the potential to prevent up 

to 70% of cervical cancers. The National Cervical 

Screening Program has been effective at reducing 

cervical cancer incidence and mortality, and the 

vaccine offers the potential to further decrease the 

incidence of and mortality from this disease. 

Species specific papilloma viruses infect a range of animals including humans. Over 100 

different types of HPV have been identified. The majority of HPV types infect only epithelial 

cells of the skin and mucosa. Most produce no evident disease. Some HPV types have 

been associated with anogenital and aerodigestive diseases (Baseman & Koutsky 2005). 

Some produce proliferative lesions (warts) of skin and genital skin, and these tend to be 

grouped as low and high risk based on their potential to cause malignancy. 

There are in excess of 40 anogenital HPV types, about 15 of which are oncogenic (high 

risk) (Schiffman & Kjaer 2003). Anogenital HPVs are the most common sexually transmitted 

infections. 

Transmission 

Genital HPVs are primarily transmitted through sexual contact (genital-genital or genital 

anal), though this need not include penetrative sexual intercourse. Other modes of 

transmission, including perinatal, digital, oral and autoinoculation, are less common 

(IARC 1995). HPV infections are thought to be established in the basal epithelium through 

abrasion or microtrauma of the superficial epithelium (Lowy & Schiller 2006). In sexually 

active adults acquisition of HPV is common. Prevalence among sexually active young 

women is high at around 20% to 25% (Ho et al 1998). Repeated testing of teenagers over a 

three-year period has documented a cumulative prevalence rate of 44% (95% CI, 40 to 48) 

(Woodman et al 2001). Infection may be with one or more HPV subtypes and these may 

change over time (NHMRC 2005). 

The link between HPV infection and cancer 

HPV infections can induce the development of either benign or malignant lesions. Benign 

lesions include non-genital and anogenital skin warts, oral and laryngeal papillomas 

and anogenital mucosal condylomata (Lowy & Schiller 2006). Persistent infection with 

high-risk HPVs are generally subclinical, but can result in the development of a range of 

anogenital tumours including cancers of the cervix, anus, penis, vulva and vagina (Lowy 

& Schiller 2006). It has been estimated that HPV infections are present in over 80% of 

anal cancers (Frisch et al. 1999, Daling et al. 2004), 40% of penile cancers, 40% of vulval 

and vaginal cancers, and nearly 100% of cervical cancers (Parkin 2006). An association of 

HPV infection with squamous cell carcinomas of the head and neck has been established 

and HPV infection is thought to contribute to 3% and 12% of cancers of the mouth and 

oro-pharynx respectively (Parkin 2006). The role of HPV infection in the development of

epithelial carcinomas of the bladder, oesophagus and lung is being studied (Persing & 

Prendergast 1999). 

The role of HPV infection in the aetiology of a range of anogenital and other cancers has 

been demonstrated. However, the HPV vaccines currently available have principally been 

tested for and aimed at reducing cervical cancer incidence. The following summary will 

focus on HPV infection and cervical cancer. 

HPV and cervical cancer 

The association between HPV and cervical cancer was not determined until the 1970s, 

and it wasn’t until the mid-1990s that the primary role of HPV in the development of 

cervical cancer was definitely confirmed (Eurogin 2003). Research has now distinguished 

between high-risk (oncogenic) and low-risk (non-oncogenic) types of HPV, and persistent 

infection with high-risk types of HPV is now recognised to be a necessary precursor to the 

development of cervical cancer (Nobbenhuis et al. 1999). 

Oncogenic and non-oncogenic HPVs cause low-grade squamous intraepithelial lesions 

(LSIL) of the cervix (Baseman & Koutsky 2005). It was believed that the development of 

cervical cancer involved progression from low to moderate to high-grade intraepithelial 

lesions (HSIL). However, natural history studies suggest that low and high-grade cervical 

lesions are distinct HPV processes (Baseman & Koutsky 2005). LSIL represent the transient 

appearance of viral infection where the HPV-infected epithelium undergoes differentiation 

and maturation and displays minor cellular abnormalities (Baseman & Koutsky 2005). 

Longitudinal studies were conducted in Brazil (Schlecht et al, 2003) and the Netherlands 

(Nobbenhuis et al. 2001) to examine the natural history of low grade cervical neoplasia. 

Schlecht et al. (2003) reported that, in the absence of intervention, only a minority of LSIL 

progressed to HSIL (mean progression time 86.4 months, 95% CI, 81.9 to 90.9), with the 

majority (78%) of LSIL regressing in less than one year (mean regression time 10.5 months, 

95% CI, 8.1 to 12.9). The regression rates reported by the Dutch (Nobbenhuis et al, 2001) 

were slightly lower, 37.2% (95% CI, 24.8 to 49.6) at 12 months, and 54.9% (95% CI, 41.9 

to 67.9) at 24 months, which probably reflects their stricter definition of regression (two 

negative follow-up Pap tests). 

HSIL occurs when HPV infects immature cells and prevents maturation and differentiation, 

resulting in the replication of immature cells and the accrual of genetic changes that can 

lead to cervical cancer (Baseman & Koutsky 2005). Cervical screening data shows the 

incidence of HSIL is 0.7% (VCCR 2005) and is most commonly found amongst women in 

their twenties, declining rapidly with age (NHMRC 2005). In an unscreened population, it 

is estimated that between one third and two thirds of women will develop cervical cancer 

after HSIL, although the time to development of cancer is variable. (Schiffman & Kjaer 

2003) The world age standardised incidence rate of cervical cancer is 26.9 per 100,000, 

peaking at age 54 years (Gustafsson et al. 1997). 

It is estimated that it takes an average of 10 years from HPV infection to malignant 

progression (Schiffman & Kjaer 2003). The steps involved in HPV-induced cervical 

carcinogenesis include HPV infection, HPV persistence, progression to precancer and 

invasion (Schiffman & Kjaer 2003). Most HPV infections are transient and clearance of 

HPV infection and regression of precancerous changes can occur (Schiffman & Kjaer 

2003). The majority of type-specific HPV infection clears within two years (Richardson et al. 

2003). The mean time for regression of precancerous changes is longer in women infected 

with high-risk HPV types (mean duration of regression 13.8 – 17.1 months) compared to 

low-risk HPV types (mean duration of regression 7.7 – 8.9 months) (Schlecht et al. 2003). 

Precancerous changes also persist longer and progress faster in women infected with 

high-risk HPVs (Schlecht et al. 2003), and those with HIV infection (Ferenczy et al. 2003). 


1 

H u m a n p a p i l l o m a v i r u s

The impact 

About 70% of invasive cervical cancers are caused by HPV 16 and 18 (Munoz et al. 2003) 

and about 90% of genital warts are caused by HPV 6 or 11 (Von Krogh 2001). 

Cervical cancer is the second most common cancer, and the third most common cause of 

cancer deaths in women worldwide (Figure 3.1). Eighty per cent of cervical cancer cases 

occur in the developing world (Jones 1999). 

Figure 3.1 Female cancer incidence and mortality worldwide: leading sites of new cancer and cancer 

death 2002 

Breast 

Cervix uteri 

Colon and rectum 

Lung 

Stomach 

Ovary etc. 

Corpus uteri 

Liver 

Oesophagus 

Leukaemia 

Non-Hodgkin lymphoma 

Pancreas 

Thyroid 

Oral cavity 

Melanoma of skin 

Brain, nervous system 

Kidney etc. 

Bladder 

Multiple myeloma 

Nasopharynx 

Other pharynx 

Hodgkin lymphoma 

Larynx 

Mortality 

Incidence 

0 5 10 15 20 25 30 35 40 

Age-standardised rate per 100,000 women 

Source: Ferlay et al. 2004 

In 2005 in Australia, there were 610 estimated cases of cervical cancer (AIHW 2006) 

and there were 212 deaths in 2004 (AIHW 2005), making cervical cancer the 12th most 

common cause of cancer in women and 16th most common cause of cancer death (AIHW 

& AACR 2004). Approximately 80% of cervical cancers occur in less developed countries 

and this is largely attributable to the absence of organised population-based cervical cancer 

screening programs (Monsonego et al. 2004). HPV has been identified in 99.7% of cervical 

cancer specimens (Walboomers et al. 1999). The estimated lifetime risk for women of one 

or more genital HPV infection is 75%. 

Worldwide there are estimated to be 326 million adult women who are infected with HPV. 

In comparison, there are approximately 450,000 new cases of cervical cancer worldwide 

each year (Bosch 2000); thus, HPV is considered necessary but not sufficient for the 

development of cervical cancers. 

1 Section Three: Immunisation

The challenge 

Stigmatisation of cervical cancer as a sexually transmitted disease 

HPV is a sexually transmitted infection and most individuals become infected with HPV 

within two to five years of initiating sexual activity (Wright et al. 2006). Risk factors for HPV 

transmission include age at first sexual intercourse, age of the woman and her partner, 

the number of sexual partners and other surrogate indicators for the likelihood that a 

sexual partner is infected with HPV (Schlecht et al. 2003). Prophylactic vaccines must be 

administered to individuals prior to virus exposure. This ideally prevents the establishment 

of the HPV infection by eliminating the virus at the time of, or shortly after, exposure to 

HPV. This is achieved by stimulating the immune system to produce neutralising antibodies 

that bind to certain areas of the virus, preventing it from attaching to the host cell (Devaraj, 

Gillison & Wu 2003). 

Parents may be reluctant to involve their young daughters in a vaccination program 

that is linked to sexual activity. However, cervical cancer should be considered as a rare 

complication of oncogenic HPV infection rather than as a sexually transmitted disease. 

Overall, the impact of the HPV vaccines on cervical cancer will be influenced by uptake 

of the vaccine by the population. In turn, the uptake of the vaccines will be influenced by 

perceived benefits and risks. Therefore communication strategies with health professionals, 

parents, women and adolescents which are sensitive to culture, religion and age are 

required to support uptake of the HPV vaccine. 

Encouraging high levels of uptake in the indigenous community 

Immunisation should positively impact on under-screened groups and populations with 

a higher incidence of cervical cancer. In Australia, Aboriginal women are more than four 

times more likely to die of cervical cancer than other Australian women (AIHW 2006). 

This difference is in part due to lower participation of this group in the National Cervical 

Screening Program. Vaccinating Aboriginal girls and women should reduce the incidence 

and mortality from cervical cancer but this will require better understanding of their barriers 

to participation. Targeted efforts are required for this at-risk population. 

Confusion about the importance of continuing to screen 

Confusion about HPV vaccination and cervical screening may lessen compliance with 

cervical screening in the vaccinated population. The currently available vaccines target 

only two or four of the 40 HPV types infecting the anogenital tract, therefore effective 

communication strategies will be required to ensure women still participate in the National 

Cervical Screening Program. 

The duration and scope of protection provided by the vaccine is unknown 

Current level 1 evidence supports the delivery of the vaccine to young women who have 

not yet commenced sexual activity and have therefore not yet been infected with the virus. 

The level of protection provided to older, sexually active women or boys is under evaluation 

in clinical trials (Kahn & Burk 2007). As this information becomes available, changes may 

need to be made to the delivery of the vaccine and the communication strategy. 


1 



National Cervical Screening Program 

Between 1991 and 2002 the incidence of cervical cancer almost halved among women 

aged 20 to 69 (AIHW 2006) and the mortality from cervical cancer in Australia is among 

the lowest in the world. The decline in incidence and mortality, in part, is attributable to the 

success of the National Cervical Screening Program (see pages 138 to 144). 

Prophylactic vaccine 

Prophylactic vaccination against HPV 16/18 has the potential to prevent up to 70% of 

cervical cancers. While the National Cervical Screening Program has been effective at 

reducing cervical cancer incidence and mortality, the vaccine offers the potential to further 

decrease the incidence of and mortality from this disease. Internationally the greatest 

impact of the vaccine will be in countries without an organised screening program, in 

conditions of nutrient deficiency and where HIV is endemic (Gravitt & Shah 2005). 

Two HPV L1 VLP vaccines have been developed commercially. Cervarix is a bivalent HPV 

16/18 vaccine developed by GlaxoSmithKline. The vaccine is given as an intra-muscular 

injection in a three-step protocol at zero, one and six month intervals (Stanley, Lowy & 

Frazer 2006). Gardasil, developed by Merck and Co. Inc., is a quadrivalent HPV 16/18/6/11 

L1 VLP vaccine delivered by an intra-muscular injection at zero, two and six month 

intervals (Stanley, Lowy & Frazer 2006). 

Early studies have shown the HPV vaccines to be safe and well tolerated (Giles & Garland 

2006). Results demonstrate that both vaccines are effective at protecting against persistent 

cervical HPV 16/18 infection and associated disease (Stanley, Lowy & Frazer 2006). Trials 

have shown almost universal seroconversion in vaccinated subjects (Giles & Garland 

2006) and 100% efficacy for preventing persistent infection. The quadrivalent vaccine 

was shown to confer additional protection in women against HPV 6/11-induced mucosal 

and cutaneous genital disease (Stanley, Lowy & Frazer 2006). The vaccines have been 

shown to be safe and effective in preventing infection with HPV 16 and 18. The duration of 

protection conferred by the vaccine beyond five years is under evaluation in clinical trials 

(Kahn & Burk 2007). 

In the short term the impact of the HPV vaccines will be a reduction in cervical dysplasia. 

The long-term impact is a reduction in the incidence and mortality from cervical cancer. 

Taken together this translates to a reduction in treatment costs as well as psychological 

and medical morbidity (Lowy & Schiller 2006). 

The impact of the vaccine on other anogenital cancers and aero-digestive cancers is not 

presently known. 

The prophylactic vaccine and the development of therapeutic vaccines together with 

emerging new technologies in screening present the opportunity to progressively reduce 

HPV-associated malignancy and in doing so significantly decrease the burden of cervical 

cancer on the community (Roden & Wu 2003). 

Therapeutic vaccine 

Worldwide it is estimated that there are 100 million women infected with high-risk HPV 

types, and five million women have persistent infections which may result in anogenital 

cancers (Giles & Garland 2006). 

1 0 Section Three: Immunisation

The goals of a therapeutic vaccine could include: clearing an existing HPV infection, 

preventing the development and progression of lesions, and eliminating existing lesions 

and possibly cancers (Devaraj, Gillison & Wu 2003). 

When available, the impact of the therapeutic vaccine will include less invasive and 

disfiguring treatment options for women with pre-existing HPV lesions (Brinkman et al. 

2005), potentially lessening the treatment costs and psychosocial impact on women. 

However such vaccines are at least 10 years from market. 


In 2006 the Therapeutics Goods Administration approved the quadrivalent HPV vaccine 

Gardasil for use in women aged nine to 26 and males aged nine to 15 . 

Since April 2007, free HPV vaccination in Australia has been provided through schoolbased 

programs to girls aged between 12 and 18. From July 2007 until 30 June 2009, the 

HPV vaccine will be made available through general practitioners and other immunisation 

providers for females aged 12 to 18 who did not receive the vaccine through the schoolbased 

program. Females aged 18 to 26 are eligible to receive the free vaccine, however, 

the full course of three doses must be completed before the end of June 2009. Under the 

National HPV Vaccination Program the HPV vaccine is not funded for males and is not 

available as a PBS product. 

In 2007 the TGA approved the bivalent vaccine Cervarix for use in women aged 12 to 45 

– this vaccine is not available as part of the free vaccination program and is not available as 

a PBS product. 

Aims 

As the prophylactic HPV vaccine is made available in Australia there are a number of public 

health challenges which need to be addressed. 

What needs to be achieved How The Cancer Council Australia and its members (the state 

and territory cancer councils) will do this 

Maximised uptake of the 

prophylactic vaccine and effective 

communication 

Immunisation of populations with 

higher incidences and poorer 

outcomes 

Promote uptake of the vaccine and compliance with the 

vaccination schedule among adolescent girls and young women 

Devise a clear and culturally and age-sensitive communication 

strategy 

Communicate information about HPV in a way which meets the 

information needs of the public and health professionals 

Provide information in a culturally sensitive manner 

Focus on strategies to facilitate vaccination among Aboriginal 

women, who have a higher incidence of and mortality from cervical 

cancer than the rest of the Australian population, and recent 

immigrants from high prevalence countries. 


1 1 


What needs to be achieved How The Cancer Council Australia and its members (the state 

and territory cancer councils) will do this 

Ensure that the National Cervical 

Screening Program continues to 

have high participation by relevant 

women 

1 2 Section Three: Immunisation 

Communicate clearly about the role of cervical screening in 

vaccinated women, to limit confusion and prevent reduced 

compliance with screening 

Devise approaches to managing different screening schedules, if 

changes in the frequency of screening are indicated for vaccinated 

women 

Monitor and evaluate the program Set up data processes to capture and monitor vaccination data 

Match vaccination data with screening program data and state 

cancer registries 

Research on therapeutic vaccine Advocate for continued research on the application and effect of 

therapeutic vaccines on regression of lesions and cancers. Studies 

on the acceptability of a vaccine as treatment also need to be 

undertaken 

Further research Advocate for further research in: 

• vaccine efficacy and booster requirements 

• two versus three doses 

• epidemiology and vaccination of boys – issue of herd immunity 

• infant vaccination efficacy 

• adult vaccination efficacy 

• uptake and acceptability of the vaccine in non-English speaking 

communities 

• barriers to screening 

• most effective way of screening for cervical cancer in a 

vaccinated population 

• genotype replacement over time 

References 

Australian Institute of Health and Welfare (AIHW) 2006. Cervical screening in Australia 

2003–2004. AIHW cat. no. 28; Cancer Series no. 33. Canberra: AIHW. 

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1 3 


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1 5 


H e p a t i t i s B 

Introduction 

At least 25% of those with chronic hepatitis B 

infection will develop hepatocellular cancer 

The hepatitis B virus (also known as HBV) was discovered in the 1960s; however, chronic 

hepatitis B infection (also known as CHB) was suspected as a cause of liver cancer from 

the early 1940s (Heymann 2004). 

Hepatitis B is a hepadnavirus that contains partially double-stranded DNA (Heymann 2004). 

The outer surface of the virus contains the hepatitis B surface antigen (HBsAg). Other 

important antigenic components are the hepatitis B core antigen (HBcAg), and hepatitis 

B e antigen (HBeAg). These antigenic components form the foundation of serological 

diagnosis of hepatitis B infection and immunity (Heymann 2004). 

Hepatitis B replicates almost exclusively in the liver but very high concentrations of 

virus are released into the blood, so that most tissues and body fluids are infectious. 

Transmission occurs through percutaneous or mucous membrane contact with infected 

blood or body fluids. This can occur by needle/syringe sharing, sexual intercourse and 

even in household settings, possibly through the use of shared objects, such as razor 

blades, where infectious virus has been shown to persist for up to a week (Lavanchy 

2004; Previsani, Lavanchy & Zuckerman 2004; Tawk et al. 2006a). The major mode 

of transmission on a global level is from mother to child, around the time of birth. If a 

pregnant woman has active or chronic hepatitis B infection and presence of HBeAg 

(indicating higher levels of hepatitis B viral load), the risk of infection in her newborn infant 

is 90% (Previsani, Lavanchy & Zuckerman 2004). During much of the last century, blood 

transfusions were a potential source of hepatitis B but the Australian Red Cross Blood 

Service has routinely screened all donated blood products and organ donors for a number 

of viruses, including hepatitis B, which has been screened for since 1975. 

Hepatitis B infection causes symptomatic acute hepatitis in approximately 30% to 50% of 

adults, but in young children, particularly those aged less than one year, infection is usually 

asymptomatic (Heymann 2004). The incubation period is 45 to 180 days and the period of 

communicability extends from several weeks before the onset of acute illness usually to 

the end of the period of acute illness. 

Acute illness is indistinguishable from other forms of hepatitis and symptoms include 

fever, jaundice, malaise, anorexia, nausea and vomiting, abdominal pain, myalgia and the 

passage of dark-coloured urine and light-coloured stools. During recovery, malaise and 

fatigue may persist for many weeks. Fulminant hepatitis, which occurs in approximately 

1% of cases, is a clinical syndrome of sudden onset occurring in people without preexisting 

liver disease, and results in severe impairment of liver function, sometimes with 

cerebral oedema and encephalopathy.

Chronic hepatitis B infection occurs when the immune response fails to clear acute 

infection. Markers of chronic hepatitis B infection are the persistence of HBsAg, with or 

without HBeAg, for more than six months after initial infection. This is further determined 

by the presence of hepatitis B DNA. Chronic infection occurs in 1% to 5% of adults, but 

is more common in immunocompromised persons and considerably more common in 

infants infected around the time of birth (up to 90%) (Heymann 2004; Lavanchy 2004; 

Ocama, Opio & Lee 2005; Previsani, Lavanchy & Zuckerman 2004). People with chronic 

hepatitis B infection, particularly those who are HBeAg positive, can transmit hepatitis B to 

others via the routes discussed above. 

The complications of chronic hepatitis B infection include progression to cirrhosis in up to 

30% of cases (Fattovich et al. 2004; Villeneuve 2005). Cirrhosis is a serious liver disease 

associated with chronic and often widespread destruction of liver substance occurring 

over a period of several years. Because liver inflammation can be totally symptomless, 

progression of inflammation to cirrhosis can occur without the knowledge of the patient. 

Chronic hepatitis B infection is the major cause of hepatocellular carcinoma (HCC) 

worldwide (Lavanchy 2005; WHO 2004). 

Australia 

Hepatitis B infection is a notifiable condition in Australia. There are two case definitions 

applied to notifications of hepatitis B: incident and unspecified. 

• 

• 

Incident hepatitis B is recorded when there is no evidence of hepatitis B infection in 

the past 24 months and serological markers such as HBsAg and IgM core antigen are 

present or hepatitis B DNA and IgM core antibodies are present. In 2005, 245 cases 

of incident hepatitis B were reported to the National Notifiable Diseases Surveillance 

System (NNDSS 2007). Of the people with incident hepatitis B notified in 2005, 46% 

reported injecting drug use exposure and 34% reported sexual exposure (NNDSS 2007). 

Unspecified hepatitis B, defined where a person does not meet the criteria for a 

newly acquired hepatitis B infection but has laboratory evidence of hepatitis B infection, 

accounted for 6396 notifications in 2005 (NNDSS 2007). 

The Northern Territory has the highest reported rates of incident and unspecified 

notifications of hepatitis B; chronic hepatitis B infection is considered endemic in 

Aboriginal and Torres Strait Islander communities. Studies undertaken in the mid-1990s 

indicated that up to 25% of rural Aboriginal populations were HBsAg positive (Fisher & 

Huffam 2003; O’Sullivan et al. 2004; Wood et al. 2005). A large proportion of chronic 

hepatitis B infection cases occur among people born in Asia and the Pacific Islands and 

also among people born in other hepatitis B-endemic areas such as the Middle East, 

Mediterranean and central or northern Africa (O’Sullivan et al. 2004; Tawk et al. 2006a), 

with the vast majority of these cases presumed to have been acquired overseas. In 

addition, Australian and overseas-born children of parents from these hepatitis B endemic 

regions, who were born prior to the introduction of the universal infant hepatitis B 

vaccination program in Australia, are at an increased risk of acquiring hepatitis B, either 

perinatally or through horizontal transmission. 


1 

H e p a t i t i s B

Figure 3.1 shows the number of incident hepatitis B notifications from 1993 to 2006 (mean 

notifications per year = 315) and Figure 3.2 shows the number of unspecified notifications 

from 1991 to 2006, total over 90,000 notifications during those 15 years (NNDSS 2007). 

Figure 3.1 Incident hepatitis B notifications 1993–2006 

Number 

450 

400 

350 

300 

250 

200 

150 

100 

50 

0 

1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 

Year 

Source: NNDSS 2007 

Figure 3.2 Unspecified hepatitis B notifications, 1991–2006 

Number 

10000 

9000 

8000 

7000 

6000 

5000 

4000 

3000 

2000 

1000 

0 

Source: NNDSS 2007 

1 Section Three: Immunisation 

1991 1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 

Year

Global 

Globally, an estimated two to three billion people have been infected with hepatitis B and 

of these, more than 400 million suffer from chronic hepatitis B infection (Goldstein et al. 

2005; Lavanchy 2004; Lavanchy 2005; WHO 2004). At least 25% of those with chronic 

hepatitis B infection will develop hepatocellular cancer (HCC), making HCC the tenth 

leading cause of death worldwide (Ghany & Doo 2004; Lavanchy 2004; Lavanchy 2005; 

Previsani, Lavanchy & Zuckerman 2004). 

Over 75% of people with chronic hepatitis B infection reside in the Asia-Pacific region 

(Lesmana et al. 2006). Within this region is the Western Pacific Region, which consists 

of 37 countries, including Australia (WHO 2004). Australia, New Zealand and Japan are 

all considered low prevalence countries (Clements et al. 2006; Lesmana et al. 2006). In 

the Western Pacific Region, hepatitis B seroprevalence estimates range from less than 

1% to 20%. China has the highest prevalence and accounts for more than a third of the 

global burden of chronic hepatitis B infection. Vietnam, Taiwan and the Philippines also 

report hepatitis B seroprevalence rates of up to 20% (Clements et al. 2006; Lesmana et al. 

2006). There are approximately 280,000 deaths in the Western Pacific Region each year 

attributable to complications arising from hepatitis B infection. Over 90% of these deaths 

are due to hepatitis B acquired decades earlier at birth or during childhood (Clements et 

al. 2006). Hepatitis B vaccination has been introduced into the Western Pacific Region to 

improve hepatitis B control in this region. 

The link between hepatitis B infection and cancer 

An association between chronic liver damage from any cause and hepatocellular 

carcinoma (HCC) was well known before the discovery of hepatitis B (Kew 2002). It was 

obvious that countries with very high chronic infectious hepatitis rates were also among 

those with the highest prevalence of HCC (Bosch & Ribes 2002). The introduction of 

serologic tests for hepatitis B in the late 1960s further supported the connection between 

chronic hepatitis B infection and HCC. In 1994 hepatitis B was classified as a carcinogen 

by the International Agency for Research on Cancer (IARC 1997). Case–control studies 

from various regions of the world have consistently demonstrated that chronic hepatitis 

B infection is more common among HCC cases than controls (IARC 1997). A number of 

studies have demonstrated the geographic coincidence between hepatitis B endemicity 

and HCC prevalence (Beasley et al. 1981; Chan et al. 2004; Craxi & Camma 2005; 

Heymann 2004; Lee, Hsieh & Ko 2003; Lok 2004). 

Multiple factors appear to play a role in the progression of chronic hepatitis B infection 

to HCC, with chronic inflammation and cytokine effect playing a major role in the 

development of fibrosis and ongoing hepatocyte generation. Hepatitis B DNA has also 

been demonstrated to be integrated into cellular DNA in samples of HCC (Brechot 2004; 

Chang et al. 2005; Hayashi & Di Bisceglie 2005). Various other viral factors associated 

with HCC development include the hepatitis B genotype, viral mutations and high viral 

load (Brechot 2004; Chan et al. 2004; Chen et al. 2006; McGlynn & London 2005; Tang et 

al. 2004; Yu et al. 2005). The direct involvement of the hepatitis B virus in carcinogenesis 

has now been shown to be related to expression of several hepatitis B proteins (Bonilla & 

Roberts 2005; Brechot 2004). The product of the HB X gene, the X protein, has multiple 

oncogenic effects. The hepatitis B X gene transactivates other genes, including those 

involved in cell turnover, and is found in an integrated form in almost all hepatitis B-related 

cancers. More rapid progression may occur in the presence of environmental carcinogens 

such as aflatoxins in the diet. However, people with chronic hepatitis B infection from 

endemic regions retain their high risk of HCC even if they migrate to countries with low 

levels of environmental carcinogens. Women are less likely to maintain persistent hepatitis 


1 

H e p a t i t i s B

B infection than men, or to develop HCC if they remain carriers through middle age. 

The incidence of HCC is two to four times greater in men than in women. This may be 

explained, in part, by the fact that males are generally more likely to be co-infected with 

hepatitis C, consume alcohol and smoke cigarettes (McGlynn & London 2005). 

The greatly increased risk of developing HCC associated with chronic hepatitis B infection 

was unequivocally demonstrated by surveys of middle-aged male civil servants in Taiwan 

(Beasley et al. 1981). In this study, 22,707 men were prospectively followed for HBsAg 

status and mortality. Forty-one subjects died from HCC and all but one were HBsAg 

negative. A similar increase in risk for people with chronic hepatitis B infection has been 

reported from many different countries, with both high and low overall adult hepatitis B 

prevalence rates. The risk of HCC from chronic hepatitis B infection is far higher than that 

observed among individuals with liver cirrhosis from other causes (Cantarini et al. 2006). 

The impact 

Worldwide, there were more than 600,000 deaths due to primary liver cancer in 2002 

(Perz et al. 2006). Among primary liver cancers worldwide, hepatocellular carcinoma (HCC) 

represents the major histologic type and is likely to account for 70% to 85% of cases 

(Perz et al. 2006). HCC is the tenth leading cause of death from any condition and is the 

fifth most common malignancy in males and the eighth in females (Lavanchy 2004; WHO 

2004). Hepatitis B and C infections account for an estimated 78% of HCC globally (53% 

and 25%, respectively); however, the relative percentage of HCC cases linked to hepatitis B 

(and/or hepatitis C) varies by geographic setting. In addition to HCC, an estimated 446,000 

cirrhosis deaths related to hepatitis B and C occurred in 2002 (Perz et al. 2006). The lifetime 

risk of death from hepatitis B-related HCC or cirrhosis is estimated to be 25% for a person 

who becomes chronically infected during childhood (Bonilla & Roberts 2005; Roberts & 

Kemp 2007). 

Data on the incidence and mortality from primary liver cancers in Australia are shown 

in Tables 3.1 and 3.2 below. The majority of liver cancers are HCC (as determined by 

ICD-10 code C22.0), but these data include other tumours such as cholangiocarcinoma, 

hepatoblastoma and tumours without histological confirmation. These data demonstrate 

the increase in primary liver cancers between 2001 and 2005, similar to that reported 

elsewhere (Amin et al. 2007) and to what has been seen in the past two decades, when the 

incidence of HCC almost doubled in both men (from 2.06 to 3.97 per 100,000) and women 

(from 0.57 to 0.99 per 100,000) from 1978 to 1997 (Law et al. 2000). 

Precise information regarding the number of cases of HCC due to hepatitis B infection 

Australia-wide is not available. However, a recent longitudinal study in NSW using data 

linkage found that of 2072 cases of HCC identified from 1990 to 2002, 323 (15.6%), 267 

(12.9%) and 18 (0.8%) were linked to hepatitis B, hepatitis C and hepatitis B/hepatitis C coinfection 

notifications respectively (Amin et al. 2007). A younger age at diagnosis of HCC 

and birth outside of Australia (particularly Asia) were associated with hepatitis B-linked 

cases. However, the rates of hepatitis B and C infection among people with HCC in this 

study may have been underestimated due to limitations of the data used in the analysis 

and factors such as underreporting and testing of hepatitis B and C infection, particularly 

in earlier years. A smaller Victorian study of 96 people with cirrhosis who had developed 

HCC reported that approximately 15% were HBsAg positive (and 30% hepatitis C antibody 

positive) (Kemp et al. 2005). 


The rise in HCC is thought to be associated with a number of factors, many of which are 

related to hepatitis B (and hepatitis C) infection. An analysis of HCC epidemiology in an 

Australian tertiary hospital from 1975–2002 reported that between 1995 and 2002, people 

with HCC were more likely to be male, aged less than 64 years, non-Caucasian and born 

overseas, in comparison to patients with HCC between 1975 and 1983 (Roberts & Kemp 

2007). This is consistent with an increase in the average age of immigrants from highrisk 

hepatitis B endemic countries, bringing more individuals into the age groups at risk. 

Secondly, the prevalence of chronic hepatitis C has risen in Australia and is associated 

with HCC cases. Co-infection with hepatitis C and hepatitis B is known to increase the 

risk of developing HCC (Amin et al. 2006a; Amin et al. 2006b; Amin et al. 2007). A recent 

Australian study describing cancer incidence in people with hepatitis B, hepatitis C or a 

co-infection with both viruses found that the risk of HCC was 20 to 30 times greater than in 

the uninfected population (Amin et al. 2006a). 

Although in developed countries the mean duration from onset of chronic hepatitis B 

infection to the diagnosis of HCC is 35 years (Craxi & Camma 2005), in countries where 

hepatitis B is highly endemic, HCC can develop in children and across all age groups but is 

uncommon before the age of 30 (Lavanchy 2005; McGlynn & London 2005; Raza, Clifford 

& Franceschi 2007; Villeneuve 2005). Given that since 1991 there have already been over 

90,000 chronic hepatitis B infection cases notified in Australia, the future burden of HCC 

will continue for many years to come, before the impact of the universal hepatitis B vaccine 

on HCC will become apparent. 

Table 3.1 Incidence data for primary liver cancers from 2005 compared with 2001 # 

New cases ASR* % change ASR 

(last 10 years) 

% of all 

cancer 

% increase in cases 

2001–2005 

Male 718 7.4 +2.9% 1.3% 62% 

Female 261 2.2 +4.8% 0.6% 53% 

*ASR = age standardised rate per 100,000 (Australian 2001 population standard) 

# Includes intrahepatic bile duct cancer 

Source: AIHW et al. 2005 

Table 3.2 Mortality data for primary liver cancers # 

Deaths ASR* % change p.a. ASR (last 10 years) 

Male 596 6.1 +1.9% 

Female 346 2.9 +4.6% 

*ASR = age standardised rate per 100,000 (Australian 2001 population standard) 

# Includes intrahepatic bile duct cancer 


In 2001, the direct costs of managing people with chronic hepatitis B infection in Australia 

were estimated to range from $1233 for a person with non-cirrhotic chronic hepatitis B 

infection to $144,392 for a person requiring a liver transplant. Direct costs for HCC were 

$11,753 and the average cost for palliative care for a person with chronic hepatitis B 

infection and HCC was $6307 (Butler et al. 2004). 


1 1 

H e p a t i t i s B

The challenge 

Hepatitis B is transmitted through percutaneous or mucous membrane contact with 

infected blood or body fluids: in healthcare and other settings, by needle/syringe sharing, 

in sexual intercourse and possibly through the sharing of household items, such as razor 

blades. Worldwide, transmission is most common from mother to child, around the time 

of birth. The challenge is to protect against transmission wherever possible. Prevention 

measures are described below. 


Vaccination 

The hepatitis B vaccine has been available for over 20 years and was the world’s first 

cancer prevention vaccine (Beasley et al. 1983; van der Sande et al. 2006). In the early 

1980s, a plasma-derived hepatitis B vaccine prepared from the inactivated plasma of 

people with chronic hepatitis B infection was used in Australia and internationally. In the 

late 1980s, a hepatitis B vaccine manufactured by recombinant DNA technology became 

available and replaced the plasma-derived vaccine in most countries, including Australia 

(Yu, Cheung & Keeffe 2004). The gene for the major ‘surface’ antigen (HBsAg) of the 

hepatitis B virus is expressed in yeast cells. The hepatitis B vaccines currently available 

in Australia are monovalent, meaning the vaccine only contains hepatitis B antigen, 

or combination vaccines that contain hepatitis B antigen and other antigens such as 

diphtheria, tetanus, pertussis, Haemophilus influenzae type B, poliomyelitis and hepatitis A 

antigens (NHMRC 2008). 

In Australia during the early 1980s, hepatitis B vaccination was initially administered to 

at-risk groups such as healthcare workers. In 1987, hepatitis B vaccination of infants born 

to mothers who were hepatitis B surface-antigen-positive commenced. In 1997, routine 

adolescent hepatitis B vaccination was introduced, followed by universal infant vaccination 

in May 2000. The adolescent program will continue until all children born since 2000 reach 

adolescence (NHMRC 2008; Williams 2002). 

The Australian National Immunisation Program currently includes a single dose of hepatitis 

B vaccine at birth or up to eight days of age followed by three doses of hepatitis B vaccine 

at two, four and either six or 12 months of age. Adolescents aged between 12 and 15 

years receive either a two-dose schedule (adult dose vaccine) administered at a 0 and four- 

(or six-) month interval; or a three-dose schedule (paediatric dose vaccine) at 0, one- and 

six-monthly intervals, predominantly through school-based programs. Adults receive a 

three-dose schedule of hepatitis B vaccine administered at 0, one and six-monthly intervals 

(AHC 2006; Yuen et al. 2004). 

Hepatitis B vaccines are recommended in adults (or those not previously immunised) in the 

following at-risk groups (NHMRC 2008; Williams 2002): 

• 

• 

• 

• 

• 

household contacts of people with acute and chronic hepatitis B 

sexual contacts of people with acute and chronic hepatitis B 

people on haemodialysis, people who are HIV-positive and other adults with impaired 

immunity 

injecting drug users 

recipients of concentrated blood products 


• 

• 

• 

• 

• 

• 

• 

• 

• 

• 

people with chronic liver disease and/or hepatitis C (who are seronegative for 

hepatitis B) 

residents and staff of facilities for people with intellectual disabilities 

people adopting children from overseas 

liver transplant recipients (who are seronegative for hepatitis B) 

inmates and staff of long-term correctional facilities 

healthcare workers, ambulance personnel, dentists, embalmers, tattooists and bodypiercers 

police, members of the armed forces and emergency services staff if at risk of exposure 

to body fluids 

funeral workers and other workers who have regular contact with human tissue, blood 

or body fluids and/or used needles or syringes 

people travelling to regions of intermediate or high endemicity, either long term or for 

frequent short terms 

sex industry workers. 

Although vaccine-induced antibody levels decline with time and may become 

undetectable, booster doses are not recommended in immuno-competent individuals after 

a primary course, as there is good evidence that a completed primary course of hepatitis 

B vaccination provides long-lasting protection (NHMRC 2008; Williams 2002). This applies 

to children and adults, including those at risk of occupational exposure, such as healthcare 

workers and dentists (Fitzsimons et al. 2005; Petersen et al. 2004). 

During the late 1980s, perinatal transmission of hepatitis B was recognised as the major 

factor leading to virus persistence and chronic liver disease and HCC. Vaccination of 

newborn infants of mothers with chronic hepatitis B infection was shown to be effective in 

reducing viral transmission, especially if combined with administration of ‘hyperimmune’ 

hepatitis B immunoglobulin (HBIG) at birth. Hepatitis B vaccine given in combination with 

one dose of HBIG to babies within 12–24 hours after birth is around 85% to 95% effective 

in preventing hepatitis B infection (Beasley et al. 1983; Chang & Chen 2002; Kripke 2007; 

Lee et al. 2006; Petersen et al. 2004; WHO 2004; Yu, Cheung & Keeffe 2004). In Australia, 

all antenatal women are tested for hepatitis B or the hepatitis B status of mother is 

determined upon presentation in labour if unknown. Infants born to hepatitis B surfaceantigen-positive 

mothers or those of unknown status should receive HBIG at birth as well 

as the hepatitis B vaccine. 

The effect of vaccination on carriage rates in vaccinated age cohorts has been reported 

in many countries (Chang 2003; Chang et al. 2005; Chang & Chen 2002; Clements et al. 

2006; Chen 2005; Yu, Cheung & Keeffe 2004). More time must elapse before these cohorts 

reach the age of greatest HCC prevalence, but already some countries with previously 

very high HCC rates, such as Taiwan, have observed statistically significant reductions in 

young, vaccinated age groups (Chang & Chen 2002; Yuen et al. 2004). Taiwan introduced 

a universal hepatitis B vaccination program for infants in 1984; while HCC is uncommon in 

children, the reported incidence of HCC fell by 75% in children aged six to nine years who 

were born after the program started (Chang 2003; Lee, Hsieh & Ko 2003). 

The use of the hepatitis B vaccine and HBIG has been shown to be cost effective even 

in countries such as Australia with a low prevalence of hepatitis B. In the late 1990s, the 

World Health Organization advised the introduction of universal vaccination for all infants 

born in countries where the prevalence of chronic hepatitis B infection exceeded 2%. 

However, universal hepatitis B vaccination has been undertaken only sporadically in many 


1 3 

H e p a t i t i s B

countries, primarily due to limited resources. Data from the World Health Organization 

in 2005 indicate that although 158 out of 192 (82%) of member states had introduced a 

routine infant immunisation program, only 119 countries could report coverage of three 

doses at levels greater than 80% (ACT-HBV APSCM 2006; WHO 2004). As such, hepatitis 

B and its complications remain a global concern (WHO 2004). 

Other interventions 

Transmission of hepatitis B in healthcare settings has been greatly reduced by screening 

of blood donations prior to transfusion or manufacture of blood products, and screening 

of organ donors prior to transplant (Hilleman 2003). In addition, the use of standard 

precautions in the clinical setting to minimise transmission of blood-borne viruses and 

other infection control measures—such as the use of disposable equipment, sterilisation of 

multi-use equipment and the correct disposal of sharps, body fluids and other body parts— 

has further minimised the risk of hepatitis B transmission in the healthcare setting. 

Treatment of chronic hepatitis B infection, cirrhosis and HCC 

The medical treatment of people with established chronic hepatitis B infection is targeted 

at reducing the hepatitis B replication, which in turn can potentially prevent or slow 

progression to cirrhosis and HCC. 

In a very small percentage of people with chronic hepatitis B infection, there may be 

resolution of the infection. The choice of therapy varies, depending on the viral load 

and extent of hepatic damage; however, the ultimate aim of treatment is sustained viral 

suppression that results in normal ALT levels, a decrease in hepatitis B DNA and prevention 

of the sequelae of infection (ACT-HBV APSCM 2006; Okanoue & Minami 2006). Nucleoside 

analogue drugs such as lamivudine and entecavir suppress hepatitis B virus replication 

very effectively, although emergence of resistance is a serious problem, particularly in the 

case of lamivudine (ACT-HBV APSCM 2006; Fung & Lok 2004; Locarnini & Omata 2006). 

PEG-interferon suppresses hepatitis B replication in a majority of individuals and achieves 

sustained virological control (ongoing low or undetectable levels of hepatitis B viraemia) in 

about a third (ACT-HBV APSCM 2006; Farrell & Teoh 2006; Ghany & Doo 2004; Hoofnagle 

et al. 2007). Virological control, whether spontaneous or after treatment, greatly reduces 

the subsequent risk of HCC; however, it has no effect on the course of established liver 

cancer. As most people with chronic hepatitis B infection are completely asymptomatic, 

a policy of monitoring and treating those with the highest risk of HCC (e.g. those with 

hepatitis B viral load above 2000 IU/mL and age above 40 years) may be the most effective 

strategy. This would require effective screening and detection programs to identify people 

with chronic hepatitis B infection. 

Treatment of HCC itself is difficult because of the multifocal nature of the tumour and 

its inaccessibility. Techniques for destruction of tumour nodules depend on accurate 

localisation, and, although they do prolong life, they are seldom curative. Unfortunately 

blood tests for tumour markers have not proved reliable as screening tests, and effective 

chemotherapy is still lacking (Hilleman 2003; Kemp et al. 2005; O’Brien, Kirk & Zhang 

2004). Imaging techniques have been employed to monitor known carriers, especially 

those who have developed cirrhosis and/or are entering middle age. Liver transplantation 

and removal of the entire liver is regarded as the most likely treatment to achieve cure, but 

prior spread beyond the liver may already have occurred and this has proved difficult to 

assess (Kemp et al. 2005). 



The bleak outcome of HCC makes prevention an especially desirable public and personal 

health policy. Prevention of persistent hepatitis B infection by universal infant vaccination 

is clearly the most significant measure, and since 2000 it has achieved global acceptance 

and support (Hipgrave, Maynard & Biggs 2006; WHO 2004). It will be many years before 

this is manifested in a falling prevalence of HCC. In the meantime, treatment of established 

hepatitis B infection and reduction of exposure to other factors that increase the risk of 

developing chronic liver disease, such as alcohol and aflatoxins, can reduce the proportion 

of infected people who develop chronic liver disease and HCC. The appropriate schedules 

for early tumour detection in people with established cirrhosis have yet to be established in 

Australia and there are also ongoing evaluations of different methods of surgical treatment 

(Roberts & Kemp 2007). 

Primary prevention of hepatitis B by vaccination is now provided for all Australian infants 

as part of the National Immunisation Program described above. This provides optimum 

protection against infection in early life, when the likelihood of developing persistent 

infection is very high, and also provides ongoing immunity into adolescence and adult life. 

Uptake of hepatitis B vaccine in Australian children is very good, with three-dose coverage 

reported in 94.7% of infants aged 12 months and 95.9% of children aged two years (ACIR 

2006). 

However, despite good vaccine coverage in infants, children and school-based delivery to 

unimmunised adolescent groups in Australia, hepatitis B vaccination has been consistently 

underused by adults in high-risk groups who would not have been targeted by universal 

infant and childhood immunisation because of their age (Tawk et al. 2006b; Yuen et al. 

2004). Low vaccine uptake rates among high-risk adults have generally been due to a 

lack of awareness, failure to identify and offer vaccination to at-risk persons, the cost 

of accessing the hepatitis B vaccine and failure to complete a course of the hepatitis 

B vaccine. At-risk groups, in particular people from culturally and language diverse 

communities, Indigenous Australians, injecting drug users, inmates of correctional facilities 

and men who have sex with men, need to have ready access to hepatitis B vaccines, 

potentially via targeted campaigns. 

There is evidence that universal immunisation of infants and children in Australia is having 

an impact, with the number of cases of acute hepatitis B declining between 2001 and 

2006 from 415 to 295 (from 2.1 to 1.6 per 100,000 population) (NHMRC 2008). It is likely 

that these declining rates also reflect changing practices among other risk groups, such 

as sex workers and intravenous drug users. However, while incident hepatitis B may 

have declined as a result of vaccination, the impact from the pool of people with chronic 

hepatitis B infection—many of whom may not be recognised as such—is still to be felt. 

It will be several more decades before they reach middle age, when HCC is most likely 

to develop. In most high prevalence countries, vaccination was introduced even more 

recently so that adult immigrants from these countries still have high hepatitis B carriage 

rates (Farrell & Teoh 2006; Tawk et al. 2006a; Tawk et al. 2006b). This means that for many 

years to come the pool of adult hepatitis B carriers in Australia will be relatively static or 

may even grow, as will the prevalence of hepatitis B-related HCC. 

There are two options for reducing the disease burden from those with established chronic 

hepatitis B infection. The first is to treat people with chronic hepatitis B infection before 

they develop cirrhosis. There is good evidence that the risk of HCC is greatly reduced if 

viral replication is controlled either spontaneously or with treatment. Although between 

0.5% and 1% of the adult population have chronic hepatitis B infection with detectable 

virus in their blood, a minority are aware of their infected status or assessed for treatment 

(Gidding et al. 2007; O’Sullivan et al. 2004; Wood et al. 2005). Apart from antenatal 


1 5 

H e p a t i t i s B

screening, case finding has not been promoted as a public health priority, and there is 

generally no systematic arrangement for referral and assessment of individuals who are 

found to be HBsAg positive in the course of ordinary medical care, although many of these 

are notified under the current laboratory-based reporting system. Cost–benefit analyses of 

hepatitis B treatment strategies do not yet include the expense of case finding, and there 

is debate in the literature about the benefit of treatment of non-cirrhotic patients, whose 

infection may clear spontaneously over time. 

The second option for reducing the disease burden of HCC is to institute screening for 

cancer nodules in the livers of people with established cirrhosis. If small and single, the 

nodules can be treated by resection of the affected lobe of the liver. If large or multiple, 

injection of the lesions with cytotoxic drugs may prolong life (Craxi & Camma 2005; 

Hilleman 2003; Kemp et al. 2005). In summary, the current approaches to secondary 

prevention of HCC in those with established hepatitis B infection have not yet attained a 

sufficiently firm scientific basis to justify their introduction on a nationwide scale. 

In 2006, the Australian Hepatitis Council issued a position paper outlining a number of 

actions that members believe are necessary to address hepatitis B in Australia. These 

include (ACT-HBV ANZLC 2007; AHC 2006): 

• 

• 

• 

• 

• 

the development and implementation of a national hepatitis B strategy 

the development of health maintenance and support resources for people with chronic 

hepatitis B infection 

broad research that encompasses both the social and health impacts of hepatitis B 

infection 

representation of people living with chronic hepatitis B infection on any national 

strategic council and an ongoing campaign to raise awareness of hepatitis B 

vaccinations and treatment among high-risk groups. 

Despite the gains that will be made through universal vaccination of infants, many further 

measures require consideration in an overall strategy to reduce the future burden of 

disease from HCC 

. 


Aims 

What needs to be achieved How Cancer Council Australia and its members (the state and 



link between hepatitis B 

Infection and liver cancer 

among those at high risk 

and key health professional 

groups 

Immunisation of populations 

with higher incidences and 

poorer outcomes 

Monitor and evaluate the 

vaccination program 

Effective coordinated policy 

to support development 

and implementation of 

a National Hepatitis B 

Strategy 

Timely evaluation of new 

technologies 

Monitor and clarify best evidence on the relationship between hepatitis B 

and liver cancer causation 

Ensure key messages are promoted to those at high risk and relevant 

health professionals via publications, presentations, programs, media 

statements and wherever opportunities arise 

Promote and/or develop primary health resources, specifically for general 

practice, to improve evidence-based interventions by health professionals 

in the field of hepatitis B prevention and treatment. 

Advocate for and support screening and vaccination among recent 

immigrants from high prevalence countries and for Indigenous 

Australians. 

Advocate to government for funding and establishment of data processes 

to capture and monitor vaccination data at a National level 

Match vaccination data with screening program data and state cancer 

registries 


relationship between HBV infection and cancer in the Australian context 

Identify, analyse and advocate for evidence-based policy initiatives to 

reduce alcohol consumption in populations at risk for hepatitis B related 

disease 

Monitor development of relevant new technologies, (such as ultrasound 

and MRI), advocate for rapid evaluation of their relevance and adoption 

of those that are positively evaluated 

Further research Support and conduct high quality epidemiological research further 

clarifying the relationship between chronic hepatitis B infection and 

cancer in the Australian population. 

Support and conduct high-quality behavioural research to determine: 

• the barriers and enabling factors for people from target at-risk 

populations to participation in a HBV monitoring and HCC prevention 

program 

• whether increased knowledge about the link between hepatitis B virus 

infection and liver cancer can affect behaviour 

• 

identify key messages for social marketing campaigns about hepatitis 

B vaccination, early liver disease diagnosis and management (including 

responsible use of alcohol). 


1 

H e p a t i t i s B

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H e p a t i t i s B

List of contributors

Authors 

Dr Cleola Anderiesz BSc (Hons), PhD, Grad 

Cert H.Ec (HPV chapter) 

Kate Broun BAppSci (Health Promotion) 

(Hons) (Cervical cancer chapter) 

Manager 

PapScreen Victoria 

Kathy Chapman BSc, MNutrDiet* (Nutrition 

and Obesity chapters) 

Nutrition Program Manager 


Dr Tanya Chikritzhs PhD, Post GradDip (Epi 

& Biostats), BA (Hons) (Alcohol chapter) 

Senior Research Fellow 

National Drug Research Institute 

Curtin University 

Professor Yvonne Cossart (Hepatitis B 

chapter) 

Bosch Professor 

Department of Infectious Diseases and 

Immunology 

The University of Sydney 

Alison Evans PhD (Breast cancer chapter) 

Acting Deputy Director 

National Breast Cancer Centre 

Associate Professor Dorota Gertig MBBS, 

MHSC, ScD, FAFPHM (Principles of 

Screening chapter) 

Medical Director 

Victorian Cervical Cytology Registry 

Paul Grogan* (Tobacco chapter) 

Advocacy Manager 

The Cancer Council Australia 

Dr Jane Jeffs BAppSc (Med Lab Sc), PhD, 

MASM (Hepatitis B chapter) 

Immunisation Handbook and Policy 

Coordinator 

The Children’s Hospital at Westmead 

Tracey Johnston BA (Hons) (Breast cancer 

chapter) 

Communications Officer 

BreastScreen Victoria Coordination Unit 

Ellen Kerrins BN (UNSW), RN, Post Grad 

OncNsg* (Prostate cancer chapter) 

Group Executive 

Cancer Control Programs 


Dr Simone Lee BSc, MND, PhD (Nutrition 

chapter) 

Coordinator Public Health Nutrition 

Cancer Prevention Unit 


Dr Kristine Macartney BMedSci, MBBS 

(Hons), MD, FABP (USA) (Hepatitis B 

chapter) 

Deputy Director, Policy Support 

The National Centre for Immunisation 

Research and Surveillance (NCIRS) 

Postgraduate Clinical Fellow, Department of 

Infectious Diseases and Microbiology 

The Children’s Hospital at Westmead 

Professor Ian Olver MD, PhD, CMin, FRACP, 

FAChPM, MRACMA* (Prostate cancer 

chapter) 

Chief Executive Officer 


Alison Peipers BEd, GradDipTEFL* (Bowel 

cancer chapter) 

Deputy Director 

Cancer Education Unit 


Steve Pratt APD, MAAESS, BSc (Human 

Movement), BSc (Nutrition and Food 

Science), GradDip (Dietetics), GradCert 

(Food Technology) (Physical activity 

chapter) 

Nutrition and Physical Activity Coordinator 


Craig Sinclair BEd (Sec), PostGrad Rec, 

PostGrad OrgBehav, MPPM* (Ultraviolet 

radiation and Melanoma chapters) 

Director 



Professor James St John MD, FRCP, FRACP 

(Bowel cancer chapter) 

Honorary Senior Associate 


Anita Tang BA, MALP* (Tobacco chapter) 

Director, Health Strategies 


Susan Upham (Physical activity chapter) 

GP Education Project Coordinator 



203 

L i s t o f c o n t r i b u t o r s

Noni Walker MPH, BSc, Postgraduate 

Diploma in Nutrition and Dietetics (Tobacco 

chapter) 

Walker Shanley Consultancy 

*Members of The Cancer Council Australia’s 

Public Health Committee 2006–07 

Contributors/reviewers 

Professor Annie S Anderson BSc, PhD, SRD 

Centre for Public Health Nutrition Research 

Department of Medicine 

University of Dundee 

Sandy Angus BSSc* 

Senior Project Officer (Indigenous), 

Queensland Cervical Screening Program 

Cancer Screening Services Unit 

Population Health/Public Health Services 

Unit 

Queensland Health 

Gaël Castillo Bachelor of Business Systems 

Office of the Director 


Professor Simon Chapman PhD 

Director of Research 

School of Public Health A27 

University of Sydney 

Professor Kate Conigrave FAChAM, 

FAFPHM, PhD 

Staff Specialist 

Drug Health Services 

Royal Prince Alfred Hospital 

Conjoint Associate Professor 

School of Public Health and Departments of 

Psychological Medicine and Medicine 

University of Sydney 

Kay Coppa RN, GradDipHealthScience 

(Primary Health Care), MPH 

Skin Cancer Prevention Manager 


Levinia Crooks BA (Hons), DipEd 


Australasian Society for HIV Medicine 

(ASHM) 

Levinia Crooks BA (Hons), DipEd 


Australasian Society for HIV Medicine 

(ASHM) 

204 National Cancer Prevention Policy 2007 – 09 

Professor Chris Del Mar MA, MB BChir, 

MD, FRACGP, FAFPHM 

Dean, Faculty of Health Sciences and 

Medicine 

Bond University 

Associate Professor Greg Dore BSc, MBBS, 

PhD, FRACP, MPH 

Head, Viral Hepatitis Clinical Research 

Program 

National Centre In HIV Epidemiology and 

Clinical Research 

University of New South Wales 

Associate Professor Peter Foley BMedSc, 

MBBS (Monash), MD (Melbourne), FACD 

Department of Medicine (Dermatology) 

The University of Melbourne 

St Vincent’s Hospital Melbourne 

Dr Linda Foreman MBBS, MPH, FRACGP* 

General Practitioner, Chandlers Hill Surgery 

GP Advisor 


Professor Ian Frazer FAA, MB, ChB, MD 

Director, Diamantina Institute for Cancer, 

Immunology and Metabolic Medicine 

The University of Queensland 

Susan Greenbank BAppSci (Health 

Promotion)* 

Manager, Prevention and Early Detection 

Unit 


Professor Mark Harris MBBS, DRACOG, 

FRACGP, MD 

Professor of General Practice 

Executive Director, Centre for Primary 

Health Care and Equity 

School of Public Health and Community 

Medicine 

University of NSW 

Darlene Henning BA (Psychology) 

Coordinator, General Practice Program 



Dr Chris Karapetis MBBS, FRACP, MMedSc 

Senior Consultant Medical Oncologist 

Department of Medical Oncology, Flinders 

Medical Centre 

And Senior Lecturer, Flinders University

Associate Professor John Kelly MDBS, 

FACD 

Head, Victorian Melanoma Service 

The Alfred 

Rachel Laws BSc (Nutrition), MSc (Nutrition 

& Dietetics) 

Research Fellow 

UNSW Research Centre for Primary Health 

Care & Equity 

School of Public Health & Community 

Medicine 

UNSW 

Professor Evie Leslie BAppSci (Phys Ed), 

MHN, PhD 

Associate Professor of Public Health 

Deakin University 

Dr Rosemary Lester MBBS, MPH, MS 

(Epid), FAFPHM 

Assistant Director, Public Health Branch 

Communicable Disease Control Unit 

Department of Human Services 

Belinda Lowcay BBehavSc* 

Primary Health Care Coordinator 

Cancer Prevention Unit 


Jane Martin BA (Hons), MPH 

Senior Policy Adviser 

Obesity Policy Coalition (The Cancer Council 

Victoria, Diabetes Victoria and Deakin 

University) 

Rosemary Moore 

Editor, Publications Unit 


Jennifer Muller 

Senior Director 

Cancer Screening Services Unit 

Queensland Health 

Meg Murchland BA (Lib & Inf Mgmt), 

GDPH 

Cancer Control Programs Information 

Officer 


Carole Pinnock PhD 

Chair, Education Committee 

Australian Prostate Cancer Collaboration 

Principal Research Scientist, Urology Unit 

Repatriation General Hospital, Daws Park, 

South Australia 

Dorothy Reading BA, DipEd* 

Senior Strategic Consultant 


And Chair, Public Health Committee 


Lesley Rowlands MPH 

Research Assistant 

Victorian Cytology Service 

Dr Marion Saville MBChB, Am Bd (Anat 

Path & Cytopath), FIAC, Grad Dip Med 

(Clin Epi) 

Director, Victorian Cytology Service 

Terry Slevin BA (Hons), MPH 

Director, Education and Research 


Associate Professor Suzanne Steginga PhD 

Director of Community Services and 

Research Programs 


Philippa Thomson BA, BEd 

Research Administrative Assistant, 

Research Management Unit 


Vicky Thursfield 

Information Manager, Cancer Epidemiology 

Centre 


Dr Justin Tse MBBS, MMed, FRACGP 

Sub-dean, Royal Melbourne Hospital 

Clinical School 

Royal Melbourne Hospital 

The University of Melbourne 

Elmer V Villanueva MD, ScM, FRIPH 

Epidemiologist 

National Breast Cancer Centre 

Dr Vicky White 

Deputy Director, Centre for Behavioural 

Research in Cancer 



205 

L i s t o f c o n t r i b u t o r s

Index

A 

alcohol 107 – 119 

aims of The Cancer Council 

Australia 116 

alcohol-related health impacts 

deaths 111 

disease burden 

how disease burden is calculated 

110 

economic costs 111 

social costs 111 

alcohol control measures 107, 

113 

access 113 

community interventions 113 

media / advertising 113 

National Alcohol Strategy 113, 

116 

NHMRC guidelines 107 

pricing 113 

primary care / GPs 113 

public safety 113 

reports and guidelines 

Alcohol guidelines for Australians 

107, 116 

GP guidelines 115 

Lifescripts 116 

NHMRC dietary guidelines 

115, 116 

surveys and reports 

ASSAD 112 

link between alcohol and 

cancer 

and smoking 108 

cancer types 108 

bowel/colorectal cancer 108, 

146 

breast cancer 108 

evidence for other cancers 109 

larynx 107 

liver 107 

mouth 107 

oesophagus 107 

other diseases 107 

pharynx 107 

women and risk 107 

prevalence of risky, high-risk 

and binge drinking 112 

Aboriginal and Torres Strait 

Islander peoples 112 

adults 112 

drinking trends 113 

teenagers 112 

B 

bowel cancer 145 – 160 


Australia 154, 155 

benefits and risk from bowel 

screening 153 

colonoscopy complications 

124, 153 

detecting advanced adenoma 

153 

false positive results 153 

psychological effects 153, 154 

reduce mortality 153 

deaths 145 

detection and screening 147 

colonoscopy 149, 150, 153 

faecal occult blood tests 148, 

151 

role of general practice 146, 

152, 153 

screening rationale 147 

sigmoidoscopy 149 

incidence 145 



men 145 

women 145 

national bowel cancer 

screening program 123, 

150, 151 



pilot program 150 


153 

screening for people at 

increased risk 151, 152 

who should be screened? 150, 

154 

prevention 145 

aspirin 146 

Clinical practice guidelines 

146 

preventable risk factors 146 

risk factors 145 

advanced adenoma 145 

alcohol 146 

chronic inflammatory bowel 

disease 145 

Clinical practice guidelines 

146 

family history 145 

FAP 146 

HNPCC 146 

nutrition 146 

obesity and overweight 74 

personal history of bowel 

cancer 145 

reducing risk through physical 

activity 74 

breast cancer 126 – 137 



benefits and risks from breast 

screening 124, 132 

DCIS ‘over-diagnosis’ 132 

false negative and false positive 

results 124 

psychological effects 132 

reducing deaths 132 

deaths 126 

detection and screening 

breast awareness 129 

effectiveness 129 

breast self-examination 129 


clinical breast examination 

129 


mammography 128 


role of general practice 131 

incidence 126 

national breast cancer 

screening program 123 

BreastScreen Australia performance 

130 


133 


risk factors 127 

alcohol 127 

being female 127 


gene variations 127 

HRT 127 

increasing age 127 

obesity and overweight (postmenopause) 

74 

other risk factors 127 

reducing risk with physical 

activity 74 

C 

cervical cancer 138 – 144 


20 

I n d e x


Australia 143 

benefits and risks from cervical 

screening 141 

false negative and false positive 

results 142 

reducing deaths 141 

causes / risk factors 138 

antibodies for Chlamydia or 

herpes 138 

HPV 138, 139 

immunosuppression 138 

oral contraceptives 138 

pregnancies 138 

smoking 138 

detection and screening 

other screening technologies 

139, 140 

Pap test 139 

national cervical cancer 

screening program 123, 

140 

changes to guidelines 141 



142 

vaccine 9, 139 

H 

hepatitis B 9, 109, 186 

human papilloma virus 9, 138, 

139, 140, 141, 143 

M 

melanoma 161 – 164 


Australia 163 

deaths 161 

detection and screening 161 

dermoscopy 162 

rationale for screening for 

melanoma 162 


162 

self-examination 162 

skin examination by doctor 161 

incidence 161 

insufficient evidence for 

population screening 

123, 163 


N 

nutrition 52 – 70 



improving nutrition: approaches 

and programs 59 

behavioural interventions 60 

economic benefits 57 

environmental interventions 60 

general practice 62 

programs 

Eat Well Australia 63 

Healthy Weight 2008 63 

specific cancer prevention 

interventions 61 

statewide programs 61 

reports and regulation 

Australian Guide to Healthy 

Eating 64 

Children’s Television Standards 

63 

Food Standards Code 63 

National Nutrition Survey 

57 

NHMRC dietary guidelines 

64 

UICC cancer prevention 

strategies 64 

WHO Global Strategy on 

diet 63 

improving nutrition: barriers to 

effective interventions 



current consumption trends 58 

disadvantaged groups 59 

link between poor nutrition and 

cancer 52 

bowel cancer 146 

deaths 57 

dietary fat 55 

dietary supplements 56 



fibre 55 

fish 55 

fruit and vegetables 53, 54, 55 

meat 55 

salt 56 

20 National Cancer Prevention Policy 2007 – 09 

O 

selenium 56 

overweight and obesity 86 – 106 


Australia 99 

approaches and programs to 

help prevent overweight 

and obesity 93, 94 

body mass index (BMI) 86 

children and adolescents 86 

childcare 95 

children 86, 93 

addressing the obesogenic 

environment 94 

families 95 

food industry 95, 96 

individual behaviour change 

95 

life course approach 93 

media / advertising 95 

neighbourhoods 95 

policy 96 

primary care / GPs 95 

public health interventions 97 

reports 

Acting on Australia’s weight 

98 

Eat well Australia 98 

GP guidelines 97 

Healthy weight 2008 98 

Lifescripts 97 

National physical activity for 

health action plan 98 

Overweight and obesity in 

adults 97 

Overweight and obesity in 

children and adolescents 

97 

WHO Global Strategy 98 

schools 95 

tax on soft drinks 96 

waist circumference measurement 

86, 87 

workplaces 95 

burden of disease 14, 89 

deaths 89 

economic costs 87, 89, 90 


quality of life 90 

link between overweight and 

obesity and cancer 

bowel / colon cancer 146

east cancer (post-menopause) 

87, 88 

cancer types 86, 88 

colon cancer 86, 87, 88 

endometrial cancer 86, 87, 88 

gall bladder cancer 86, 87, 88 

kidney cancer 86, 87, 88 

oesophageal cancer 86, 87, 88 

weight loss and reduction in 

cancer risk 88 

prevalence of overweight and 

obesity 

‘epidemic’ in Australia 8, 86 



adults 86, 90 

children 86, 87, 91 


Middle Eastern origin 86, 92 

rural communities 92 

southern European origin 86, 

92 

P 

physical activity 71 – 85 



approaches and programs 

to encourage physical 

activity 



Australia’s physical activity 

recommendations for 12- 

18 year olds 80 

Australia’s physical activity 

recommendations for 5-12 

year olds 80 

Be Active Australia 76 

childcare 78 

community environments and 

organisations 76 

disadvantaged people 80 

GPs 77, 78 

health services 77 

National physical activity 

guidelines for Australians 

80, 81 

national programs 75 

population trends in physical 

activity 75, 76 

schools 78 

strategies 

communications and media 

79 

GPs 79 

research 79 

workplaces 78, 79 

links between physical activity 

and cancer prevention 

75 

breast cancer 73, 74, 75, 80 

colon cancer 73, 80 

other cancers 74 

links between physical 

inactivity and cancer 

71, 73 

bowel / colon cancer 146 

breast cancer 71 

colon cancer 71 

how physical activity is measured 

72 

overweight and obesity 71 

types of cancer 71 

prostate cancer 165 – 174 


Australia 171 

benefits and risk from prostate 

screening (potential) 170 

difficulty of distinguishing lifethreatening 

cancers 170 

over-diagnosis 170 

treatment issues 170, 171 

causes / risk factors 166 

age 166 


deaths 165, 166 

detection 166 

digital rectal examination 167 

future screening prospects 

168 

PSA 166, 167 

test limitations 167, 168 

who has been tested? 168 


transrectal ultrasound and 

biopsy 167 

incidence 165 

insufficient evidence for 

population screening 

123, 168, 170 


chemoprevention 166 

S 

screening 

economic issues 125 

informed consent 124 

potential harms 124 

principles 122 

WHO criteria 122 

T 

tobacco 12 – 40 


Australia 34, 35, 36, 37 

link between tobacco and 

cancer 13 

anal cancer 15 

bladder cancer 15 

bowel / colorectal cancer 15 

cervical cancer 15 

kidney cancer 15 

laryngeal cancer 15 

lung cancer 15 

oesophageal cancer 15 

oral cancers 15 

other diseases 14, 19 

pancreatic cancer 15 

passive smoking and cancer 

13 

penis cancer 15 

stomach cancer 15 

types of cancer associated 

with tobacco 13, 15 

bowel cancer 146 

vulval cancer 15 

smoking prevalence 15, 17 



adults 27 

country of birth 17 

socially disadvantaged 16, 18 

teenagers 17 

tobacco control: barriers to 


attitudes that undermine effective 

intervention 18, 19 

tobacco industry 12, 19 

tobacco control measures 9, 12 


Islander peoples 26, 32 

disadvantaged people 31, 32 

economic benefits 19, 20 

funding 21 

health warnings 26 

history of policy in Australia 

26 

litigation 24 


20 

I n d e x

preventing smoking uptake 31 

price increases 24 

product regulation 22, 23, 24, 

28, 29 

programs 

National Tobacco Campaign 

22, 27, 32 

National Tobacco Strategy 

24, 28, 30, 33 

Quit 30 

Smoke-free 30 

reports and legislation 

health surveys 15 

International Tobacco 

Control Policy Evaluation 

Study 32 

National Drug Strategy 

Household Survey 32 

National Tobacco Strategy 

21 

Tobacco Advertising Prohibition 

Act 22, 23, 27, 33 

Tobacco control: a blue 

chip investment in public 

health 34 

Trade Practices Act 34 

WHO Framework Convention 

on Tobacco Control 

23, 33 

smoke-free environments 25, 

28 

smoking cessation aids 25 

workplace development 33 

workplaces 26 

tobacco related health impacts 

chronic disease 14 

deaths 13, 14, 17, 18 



U 

ultraviolet radiation 41 – 50 


Australia 47, 48, 49 

link between UV radiation and 

skin cancer 41 

adult exposure 42 

basal cell carcinoma 41 

incidence 44 

childhood exposure 41 

impact of ozone depletion 42 

melanoma 41 

incidence 43 

screening 46 

solariums 42 

squamous cell carcinoma 41 

incidence 44 

skin cancer: barriers to 


absence of a national program 

46 

concerns about vitamin D 

deficiency 42, 45 

desirability of a tan 45 

growth in solarium industry 44 

skin cancer prevention 

approaches and 

programs 41, 46, 47 

changing adolescents’ attitudes 

45 

Slip! Slop! Slap! 41 

sunscreen 42 

upskilling GPs 45, 47 

UV Alert 45 

210 National Cancer Prevention Policy 2007 – 09

The National Cancer Prevention Policy 2007–09 advocates for a concerted and 

comprehensive national approach to the prevention of cancer in Australia. 

Preventing cancer means that the pain, inconvenience and distress of cancer are 

avoided—not only for people with disease, but also for their families and friends. Our 

health system also benefits; resources and time can be allocated elsewhere as the 

burden of treating this disease reduces. 

This policy has been carefully researched and reviewed. International knowledge about 

risk is presented, along with evidence of effective interventions and strategies relevant to 

the Australian context. We outline program structures that could be suitable for helping a 

wide range of people. 

We recommend actions for a national impact. For these actions to be effective, the 

cancer councils and government need to bring together our strengths—our capacities to 

lead, implement and resource. 

www.cancer.org.au

National Cancer Prevention Policy - Tobacco Control Supersite

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