Changing incidence of non-melanoma skin cancer in New Zealand.
ABSTRACT Basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) are the commonest types of non-melanoma skin cancer (NMSC). The incidence of NMSC has been increasing globally with Australia recording a 1.5-fold increase over the last 17 years. The incidence of NMSC in New Zealand is currently unknown. Given that Australia and New Zealand share similar latitude, sun exposure levels, and other risk factors, it is conceivable this increase has also occurred in New Zealand. This study aimed to provide an analysis of the incidence of NMSC within the Central Region of New Zealand based on longitudinal data derived from pathology reports.
This retrospective study examined the pathology records of 26 411 patients who underwent surgical excision for 54 004 NMSC lesions which were histologically confirmed, over a 10-year period from 1 January, 1997 to 1 January, 2007, within the Central Region of New Zealand.
Over the study period, 50 411 primary NMSC lesions were excised. The age-standardized incidence for NMSC, BCC and SCC was 406, 299 and 118 per 100 000, respectively. Since 1999, the annual incidence of BCC and SCC has increased by 4.0% and 1.1%, respectively, with the greatest increases seen in the population over the age of 50 years.
New Zealand has one of the highest incidence of NMSC in the world. The high and increasing incidence of NMSC underscores the importance for the development and implementation of a national health-care delivery model, and a commitment to continued monitoring of the NMSC problem.
- SourceAvailable from: PubMed Central[Show abstract] [Hide abstract]
ABSTRACT: Incidence rates of skin cancer increase with decreasing latitude in Norway, as in many other countries with white populations. The latitudinal trends of the incidence rates of skin cancer were studied and compared with data for vitamin D-induced by UV and for vitamin D intake. The north-south gradient for CMM incidence rates on sun exposed skin is much smaller than those for BCC and SCC, and that for BCC is smaller than that for SCC. This indicates that SCC and BCC are mainly due to solar UVB, while UVA may play a significant role for CMM and a smaller role for BCC, since the north-south gradient of annual UVB fluences is larger than that of UVA fluences. However, there is an inverse latitudinal gradient of skin cancer in central Europe. This is probably due to a gradient of skin color, since white skin is an important determinant of increased risk of skin cancer. The role of vitamin D for skin cancer risk is difficult to evaluate, since serum levels of 25-hydroxyvitamin D, as well as vitamin D intakes, are widely different from country to country. Still, epidemiological evidence indicates a role: for melanomas arising on non-sun exposed body localizations (uveal melanomas, melanomas arising in the vulva and perianal/anorectal regions) there appears to be no latitudinal gradient, or, a negative gradient, i.e., increasing rates with decreasing latitude as would be expected if UV-generated vitamin D plays a protective role. Both skin cancer risk and vitamin D photosynthesis decrease with increasing skin darkness.Dermato-endocrinology. 01/2013; 5(1):186-91.
- [Show abstract] [Hide abstract]
ABSTRACT: Cutaneous squamous cell carcinoma (cSCC) constitutes the most common cancer capable of metastasis. While the latest version of the American Joint Committee on Cancer guidelines represents a significant step forward in accurate staging of cSCC, several proven independent risk factors remain excluded. We review the current literature on the incidence and proven independent risk factors of metastasis for cSCC and proposes their full inclusion in the staging system for primary lesions. J. Surg. Oncol. © 2014 Wiley Periodicals, Inc.Journal of Surgical Oncology 08/2014; · 2.84 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: Solar ultraviolet (UV) radiation is the main source of vitamin D production and is also the most important environmental risk factor for cutaneous malignant melanoma (CMM) development. In the present study the relationships between daily or seasonal UV radiation doses and vitamin D status, dietary vitamin D intake and CMM incidence rates at different geographical latitudes were investigated. North-South gradients of 25-hydroxyvitamin D (25(OH)D) generation and CMM induction were calculated, based on known action spectra, and compared with measured vitamin D levels and incidence rates of CMM. The relative roles of UVA and UVB in CMM induction are discussed. Latitudinal dependencies of serum 25(OH)D levels and CMM incidence rates can only partly be explained by ambient UV doses. The UV sensitivity is different among populations with different skin color. This is well known for CMM, but seems also to be true for vitamin D status. The fact that UV-induced vitamin D may reduce the risk of CMM complicates the discussion. To some extent high dietary vitamin D intake seems to compensate low UV doses.Dermato-endocrinology. 01/2013; 5(1):150-8.
Changing incidence of non-melanoma skin cancer in New Zealandans_5583633..636
Nicholas D. L. Brougham,*† Elizabeth R. Dennett† and Swee T. Tan*†‡
*Wellington Regional Plastic, Maxillofacial and Burns Unit, Hutt Hospital, Lower Hutt, New Zealand
†Wellington School of Medicine and Health Sciences, University of Otago, Wellington, New Zealand
‡Gillies McIndoe Research Institute, Wellington, New Zealand
basal cell carcinoma, incidence, non-melanoma, skin
cancer, squamous cell carcinoma.
Professor Swee T. Tan, Wellington Regional Plastic,
Maxillofacial & Burns Unit, Hutt Hospital, Private Bag
31709, High St, Lower Hutt, New Zealand. Email:
N. D. L. Brougham MBChB; E. R. Dennett MBChB,
FRACS; S. T. Tan MBBS, FRACS, PhD.
Accepted for publication 21 June 2010.
Background: Basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) are
the commonest types of non-melanoma skin cancer (NMSC). The incidence of NMSC
has been increasing globally with Australia recording a 1.5-fold increase over the last
17 years. The incidence of NMSC in New Zealand is currently unknown. Given that
Australia and New Zealand share similar latitude, sun exposure levels, and other risk
factors, it is conceivable this increase has also occurred in New Zealand. This study
aimed to provide an analysis of the incidence of NMSC within the Central Region of
New Zealand based on longitudinal data derived from pathology reports.
Methods: This retrospective study examined the pathology records of 26 411 patients
who underwent surgical excision for 54 004 NMSC lesions which were histologically
confirmed, over a 10-year period from 1 January, 1997 to 1 January, 2007, within the
Central Region of New Zealand.
Results: Over the study period, 50 411 primary NMSC lesions were excised. The
age-standardized incidence for NMSC, BCC and SCC was 406, 299 and 118 per
100 000, respectively. Since 1999, the annual incidence of BCC and SCC has
increased by 4.0% and 1.1%, respectively, with the greatest increases seen in the
population over the age of 50 years.
Conclusion: New Zealand has one of the highest incidence of NMSC in the world.
The high and increasing incidence of NMSC underscores the importance for the
development and implementation of a national health-care delivery model, and a
commitment to continued monitoring of the NMSC problem.
Non-melanoma skin cancers (NMSC) are the most commonly diag-
nosed group of cancers in New Zealand.1,2In 2006, NMSC was
estimated to have cost the New Zealand health-care system NZ$58
million.3This represented 8% of total expenditure for the treatment
of all cancers, making it one of the most expensive cancers to treat.3,4
Despite its frequency and cost implications, the incidence of NMSC
within New Zealand is currently unknown.5In 1958, the New
Zealand Cancer Registry (NZCR) abandoned mandatory reporting
of the most common forms of NMSC, basal cell carcinoma (BCC)
and squamous cell carcinoma (SCC), because of incomplete report-
ing and a lack of resources to manage the large number of these
The incidence of NMSC has been increasing globally, with Aus-
tralia recently reporting a 1.5-fold increase over the past 17 years.7
Given that Australia and New Zealand share similar latitude, sun
exposure levels, population skin types and other risk factors, it is
conceivable that this increase may have also occurred within New
The lack of data on the incidence, particularly of BCC and SCC,
in New Zealand has prevented effective service planning and
delivery. This is reflected by the implementation of a variety of
unproven and inconsistent primary care models13for skin lesion
removal by different District Health Boards (DHBs) within the
Stronger epidemiological data is needed to support the implemen-
tation of an integrated and sustainable service that addresses New
Zealand’s NMSC burden.5This study aimed to provide an analysis
of the current incidence of NMSC based on longitudinal data derived
from pathology reports from within the Central Region of New
Zealand during the period 1997–2007.
© 2010 The Authors
ANZ Journal of Surgery © 2010 Royal Australasian College of SurgeonsANZ J Surg 81 (2011) 633–636
Six of the DHBs within the Central Region of New Zealand –
Capital and Coast (Wellington), Mid Central (Palmerston North),
Whanganui, Wairarapa (Masterton), Hawkes Bay, and Hutt Valley –
were included in this study. In 2006, these DHBs collectively
serviced a population of 824 799.14
Pathology reports of 26 411 patients who were surgically treated
for 54 004 NMSC which were histologically confirmed, over a
10-year period from 1 January 1997 to 1 January 2007, were culled
from all public and private laboratories within the Central Region.
Cases identified by the pathology laboratories were imported into
a Microsoft Access database (Microsoft Corporation, Redmond,
Washington, USA). Records were replicated for cases where a single
pathology report described multiple specimens, allowing each speci-
men its own record.
The data was searched for patient demographics (sex, age and
domicile), diagnosis, anatomical site, completeness of excision and
other histology features such as differentiation and the presence
of lymphovascular or perineural invasion. Incisional biopsies, non-
cutaneous lesions, non-malignant precursor lesions and malignant
melanoma were excluded from the study. The specimens were
classified as a primary lesion, re-excision or metastasis. Data was
supplemented with information gathered during review of the
pathology reports and also review of the medical notes for lesions
recorded as metastasis. Information on the ethnicity of patients was
not contained within the pathology records, and hence the affected
population was not stratified according to ethnicity when generating
national estimates of NMSC cases.
Incidence was calculated by recording either the number of indi-
vidual patients treated, or the number of individual lesions excised
within a given year. Incidence was then generated using population
figures obtained from census data on the Statistics New Zealand
website.14To enable international comparison and comparison with
previous New Zealand studies, incidence was standardized to a
World and New Zealand population.14,15Incidence was reported for
NMSC (this includes Bowens Disease and rarer forms, e.g. Merkel
cell carcinoma) as well as for BCC and SCC.
lesions for each year in the study period were modelled using a
Poisson regression model within the statistical programmes SAS
version 9.1 (SAS, Cary, North Carolina, USA) to assess whether a
statistically significant trend was emerging. This model adjusted for
changes in both the age and sex of the population during the study
Strength of the trends was assessed using Chi-square. The differ-
ence in the mean ages at diagnosis was assessed using the unpaired
t-test. Calculation of the risk of developing NMSC up to 80 years of
age was done using a life-table method. Statistical significance was
achieved if P < 0.05.
Between 1 January 1997 and 1 January 2007, a total of 50 411
55% of whom were males. Multiple lesions at first presentation
with multiple lesions being similar for each histological type.
BCC and SCC constituted the majority of cases, representing 66%
and 27% of primary NMSC lesions, respectively. There was a sta-
tistically significant difference in the age of presentation for both
BCC (68 versus 67 years, P < 0.001) and SCC (72 versus 76 years,
P < 0.001) between males and females, respectively.
Incidence rates were calculated for both patient numbers and
lesion numbers. Table 1 shows the age-standardized patient inci-
dence rates. It can be seen that the incidence of patients with NMSC
increased with advancing age for both males and females with the
incidence being higher for men in every age group. Overall, BCC
was more common than SCC and developed earlier with a high
incidence first being observed in the 40–49 years age group.
Total lesion incidence for NMSC was 824/100 000. Based on
these incidence rates, it was estimated that in 2006, 24 103 patients,
or 0.6% of the total New Zealand population of 4 184 60014were
treated for 34 481 primary NMSC lesions. The risk of being treated
for any form of NMSC by the age of 80 years is 52% for males and
33% for females.
Table 2 reports trends in the annual incidence of patients with
primary SCC and BCC. Compared with SCC, the incidence of BCC
increased at a significantly faster rate, particularly among females.
The annual percentage change (increase) in NMSC incidence was
calculated at 4.1% per year (P < 0.001).
Table 1 Patient age-standardized incidence of BCC, SCC and NMSC (per 100 000)
Age (years) SCC
FemaleMaleTotal MaleTotalMale Total
Age-standardized Incidence (World)
Age-standardized Incidence (NZ)
Estimated Number of Patients with NMSC
Risk to 80 (%)
SCC, squamous cell carcinoma; BCC, basal cell carcinoma; NMSC, non-melanoma skin cancer.
Brougham et al.
© 2010 The Authors
ANZ Journal of Surgery © 2010 Royal Australasian College of Surgeons
We have estimated that in 2006, 0.6% of the population of New
Zealand were treated surgically for NMSC, making it the most
prevalent cancer in New Zealand.6,14This estimate does not include
those patients treated non-surgically with radiotherapy, curettage,
cryotherapy or pharmacologic therapy. The age-standardized inci-
dence of NMSC reported here is among the highest in the world,
greater than all other international epidemiological studies with the
exception of population-based surveys from Australia.7,16–20
Approximately, 30% of the Central Region is made up from
darker skinned, Ma ¯ori, Pacific Island and Asian residents who have
a considerably lower incidence of NMSC.1,21,22It is conceivable that
fair-skinned Caucasian’s are disproportionately over-represented
in the amount of NMSC treated during this study. However, the lack
of data on ethnicity contained within the pathology records hampers
an accurate analysis of the true incidence of NMSC among the
The overall incidence of both BCC and SCC increased over the
study period. While increases in the incidence for both BCC and
SCC among older patients were the greatest, the rapid rise of the
incidence of BCC among females aged 40–50 years is most alarm-
ing. This is in contrast with other international epidemiological
studies showing stabilization of the incidence among this age
group.7,8,23This increase in the incidence in the Central Region may
be due to a combination of negative sun exposure behaviour during
this cohort’s childhood and adolescence, as well as depletion of
atmospheric ozone levels.
The major determinant of lifetime risk for NMSC is sun exposure
during childhood and adolescence.24,25Ozone levels have been
decreasing since the 1970s, while skin cancer prevention campaigns
despite ozone depletion, means this cohort would have experienced
greater levels of exposure during their childhood and adolescence.
This, however, does not fully explain the difference in the incidence
the desirability for tanned skin is greater among young females, as is
their confusion over the effectiveness of sunscreen.27–29This might
leading to the increased incidence of BCC as adults.
The overall increase in the incidence of SCC over the study period
was smaller than that for BCC. This is consistent with studies in
other countries over a similar period.8,23Only men aged over 80
years showed an increase in the incidence of SCC. One potential
explanation for the difference in the incidence trend between SCC
and BCC may be that doctors within the Central Region were
actively treating precursor solar keratoses. A large number of histo-
logically confirmed solar keratoses were noted during the study
period. This early intervention could have resulted in a decrease in
the incidence of SCC. In contrast, BCC does not have specific
precursor lesions which received active intervention.Another possi-
bility is the regular application of sunscreen, which even during
adulthood has been shown to reduce the incidence of SCC, but not
BCC.30The disparity in the incidence trend of BCC and that of SCC
could therefore be due to actual changes in preventative behaviours
of adults within the Central Region with more people regularly
This study represents the first attempt in New Zealand to docu-
ment the changing incidence of NMSC and quantify the burden to
the New Zealand health system. During this study, we encountered
several formats for the pathology reports. Only one laboratory data-
base included separated pathology reports for each lesion for
patients having multiple lesions excised. None of the laboratories
could provide records specifically identifying the different types of
NMSC treated. It is clear that a standardized method of reporting for
NMSC by all laboratories in New Zealand is needed. The pathology
report should include a synoptic summary of common key informa-
tion for each lesion, such as the diagnosis, size, anatomical location,
excision margin, differentiation, and presence of lymphovascular or
perineural invasion, entered into individual fields. This would allow
analysis of the incidence of NMSC, and facilitate future audits.
Unlike all other types of cancer in New Zealand that are registered
by cancer registry which collects pathological and demographic
data, there is no simple way to document the incidence of NMSC
because of the nature and number of cases. Like the cancer registry
our study does not account for NMSC treated without pathological
confirmation, making estimates of the true incidence of NMSC
conservative. A 2003 study in the United Kingdom shows that 13%
of NMSC cases treated by General Practice have no matching
histological records.31Future New Zealand surveys such as the one
in Australia by Staples et al.7that rely on patient recall of NMSC
This study has shown one of the highest incidences of NMSC
in the world. This high and increasing incidence underscores the
Table 2 Trends in patient incidence for primary BCC and SCC by age and sex 1997–2007
Age (years)BCC SCC
Male FemaleMale Female
APCP valueAPCP valueAPCP value APCP value
SCC, squamous cell carcinoma; BCC, basal cell carcinoma; APC, annual percentage change.
Non-melanoma skin cancer in New Zealand
© 2010 The Authors
ANZ Journal of Surgery © 2010 Royal Australasian College of Surgeons
importance of continued community education about the risks of sun
exposure and for the development and implementation of a sound
national health-care delivery model to address and treat the problem.
We feel that New Zealand should also follow Australia’s lead in
committing to continue to monitor the incidence of NMSC.
We wish to thank Dr Karen Wood at Aotea Pathology, Dr Bruce
Lockett at Medlab Central, and Dr Helen Brasch at Hutt Hospital,
for their support and advice. We would also like to acknowledge
Messrs Chris Lewer, Niven Paine, Andrew Crooke, Glenn Knight,
Gavin Teahan and Adrian Lumsden, for all their help in extracting
the pathology data needed for this project. We are indebted to Mr
Raymond Cooper for his considerable contribution in creating the
database used for this project. We also thank Ms Cherise Tan for her
assistance in the entry of the database.We are grateful to Mr Gordon
Purdie from the Wellington School of Medicine & Health Sciences,
for his biostatistical advice. Finally, we would like to thank Ms Jyoti
Rauniyar for her valuable input in the preparation of this manuscript.
Aspects of this research were funded by grants from the Recon-
structive Plastic Surgery Research Foundation, the Wellington
Regional Plastic Surgery Unit Research & Education Trust, the
Henry Cotton CharitableTrust, and the New Zealand Cancer Society
1. Freeman NR, Fairbrother GE, Rose RJ. Survey of skin cancer incidence
in the Hamilton area. N Z Med. J. 1982; 95: 529–33.
2. McAvoy B, Davis P, Raymont A, Gribben B. TheWaikato Medical Care
(WaiMedCa) Survey 1992–1992. N Z Med. J. 2009; 107: 388–433.
3. O’Dea D, Cancer Society of New Zeland. The Cost of Skin Cancer to
New Zealand. 2009.
4. Ministry of Health. Health Sector Expenditure on Cancer Council. New
Zealand Health Information Service, 2009.
5. Brougham NDL, Tan ST, Dennett ER. Non-melanoma skin cancers in
New Zealand – a neglected problem. N Z Med. J. 2010; 123: 59–65.
6. Ministry of Health. Cancer: New Registrations and Deaths 2004.
New Zealand Health Information Service, 2007. [Cited January
2010.] Available from URL: http://www.moh.govt.nz/moh.nsf/Files/
7. Staples MP, Elwood M, Burton RC et al. Non-melanoma skin cancer in
Australia: the 2002 national survey and trends since 1985. Med. J. Aust.
2006; 184: 6–10.
8. Holme SA, Malinovszky K, Roberts DL. Changing trends in non-
melanoma skin cancer in South Wales, 1988–1998. Br. J. Dermatol.
2000; 143: 1224–9.
9. Hannuksela-Svahn A, Pukkala E, Karvonen J. Basal cell skin carcinoma
and other nonmelanoma skin cancers in Finland from 1956 through
1995. Arch. Dermatol. 1999; 135: 781–6.
10. Kricker A, Armstrong BK, English DR. Sun exposure and non-
melanocytic skin cancer. Cancer Causes Control 1994; 5: 367–92.
11. Armstrong BK, Kricker A. Epidemiology of sun exposure and skin
cancer. Cancer Surv. 1996; 26: 133–53.
12. Giles GG, Marks R, Foley P. Incidence of non-melanocytic skin cancer
treated in Australia. Br. Med. J. (Clin Res Ed). 1988; 296: 13–7.
13. Field B, Lespearance A, Bridges L. Central Region’s TechnicalAdvisory
Service Limited Skin Lesion Service Review Hutt Valley District Health
14. Statistics New Zealand. Estimated Subnational Population (RC,TA,AU)
by Age and Sex at 30 June 1996, 2001 and 2006. 2009. [Cited June
2010.] Available from URL: http://wdmzpub01.stats.govt.nz/wds/
15. Ahmad OB, Boschi-Pinto C, Lopez AD, Murray CJL. WHO Age-
standardisation of rates: A new WHO standard. 2009. [Cited January
2010.] Available from URL: http://www.who.int/healthinfo/paper31.pdf
16. Ridky TW. Nonmelanoma skin cancer. J. Am. Acad. Dermatol. 2007;
17. Curado MP, Edwards B, Shin HR et al. International Agency For
Research on Cancer Cancer Incidence in Five Continents, Vol. IX. 2007
[Cited January 2010.] Available from URL: http://www.iarc.fr/en/
18. Buettner PG, Raasch BA. Incidence rates of skin cancer in Townsville,
Australia. [erratum appears in Int J Cancer 2001 Jul 15;93(2):302–3].Int.
J. Cancer 1998; 78: 587–93.
19. Green A, Battistutta D, Hart V et al. Skin cancer in a subtropical Aus-
tralian population: incidence and lack of association with occupation.
The Nambour Study Group. Am. J. Epidemiol. 1996; 144: 1034–40.
20. Diepgen TL, Mahler V. The epidemiology of skin cancer. Br. J. Derma-
tol. 2002; 146 (Suppl. 61): 1–6.
21. Yokota J, Sugimura T. Multiple steps in carcinogenesis involving alter-
ations of multiple tumor suppressor genes. FASEB J. 1993; 7: 920–5.
22. Statistics New Zealand. Ethnic Group (Total Responses), for the Census
Usually Resident Population Count, 2006. [Cited June 2010.] Avail-
23. Harris RB, Griffith K, Moon TE. Trends in the incidence of nonmela-
noma skin cancers in southeastern Arizona, 1985–1996. J. Am. Acad.
Dermatol. 2001; 45: 528–36.
24. World Health Organisation. World Health Organisation Sun Protection
and Schools: How to Make A Difference. 2003. [Cited March
2010.] Available from URL: http://www.who.int/uv/publications/en/
25. English DR, Armstrong BK, Kricker A et al. Demographic characteris-
tics, pigmentary and cutaneous risk factors for squamous cell carcinoma
of the skin: a case-control study. Int. J. Cancer. 1998; 76: 628–34.
26. Watts C, Reeder AI, Glasgow H. A Cover-Up Story: the Cancer Society
Melanoma Prevention Programme. In: McKenzie R, Reisinger A, Watts
C (eds). UV Radiation and Its Effects – An Update 2002. Wellington:
Royal Society of New Zealand, 2002; 1–3.
27. Robinson JK, Rigel DS, Amonette RA. Trends in sun exposure knowl-
edge, attitudes, and behaviors: 1986 to 1996. J. Am. Acad. Dermatol.
1997; 37: 179–86.
28. Livingston PM, White V, Hayman J, Dobbinson S. Sun exposure and
sun protection behaviours among Australian adolescents: trends over
time. Prev. Med. 2003; 37: 577–84.
29. Livingston PM, White V, Hayman J, Dobbinson S. Australian adoles-
cents’ sun protection behavior: who are we kidding? Prev. Med. 2007;
30. Green A, Williams G, Neale R et al. Daily sunscreen application and
betacarotene supplementation in prevention of basal-cell and squamous-
cell carcinomas of the skin: a randomised controlled trial. [see commen-
t][erratum appears in Lancet 1999 Sep 18;354(9183):1038]. Lancet.
1999; 354: 723–9.
31. Stefoski Mikeljevic J, Johnston C, Adamson PJ et al. How complete has
skin cancer registration been in the UK? A study fromYorkshire. Eur. J.
Cancer Prev. 2003; 12: 125–33.
Brougham et al.
© 2010 The Authors
ANZ Journal of Surgery © 2010 Royal Australasian College of Surgeons