Following the rapid growth in mobile

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1 CANCER Trends in incidence of primary brain cancer in New Zealand, 1995 to 2010 Stella J-H Kim, 1 Sally J. Ioannides, 1 J. Mark Elwood 1 Following the rapid growth in mobile phone use throughout the world in the 1990s, and several case-control studies including the Interphone studies, 1 the International Agency for Research on Cancer (IARC) classed radio-frequency exposures as a possible human carcinogen. 2 The epidemiological evidence is strongest for associations with glioma and acoustic neuroma, but generally indicates no increased risk of meningioma. 2 Evaluating the association between mobile phone usage and primary brain cancer incidence poses a challenge to researchers because, if there is an association, the induction and latency periods of any cancers produced are unknown. 3 Further, during the time in which mobile phone use dramatically increased, new and improved diagnostic technologies (CTs and MRIs) were increasingly used in most developed countries, which would improve the detection of brain cancers and thus lead to an increasing population incidence. 3 However, given the steep increase in exposure prevalence in mobile phone usage in the past three decades, as well as the limited number of other known environmental risk factors, 3 a clear increase in incidence of primary brain cancers should be observed if a substantial true association with mobile phone use exists, so long as an appropriate follow-up period is studied. 3 Many ecological studies have been undertaken in various countries to evaluate associations between the use of mobile phones and the incidence of primary brain cancer. The majority of previous studies have relied on data on mobile phone subscriptions Abstract Objective: Case-control studies have linked mobile phone use to an increased risk of glioma in the most exposed brain areas, the temporal and parietal lobes, although inconsistently. We examined time trends in the incidence rates of brain malignancies in New Zealand from 1995 to Methods: Data from the New Zealand Cancer Registry was used to calculate incidence rates of primary brain cancer, by age, gender, morphology and anatomical site. Log-linear regression analysis was used to assess trends in the annual incidence of primary brain cancer; annual percentage changes and their 95% confidence intervals were estimated. Results: No consistent increases in all primary brain cancer, glioma, or temporal or parietal lobe glioma were seen. At ages 10-69, the incidence of all brain cancers declined significantly. Incidence of glioma increased at ages over 70. Conclusion: In New Zealand, there has been no consistent increase in incidence rates of primary brain cancers. An increase in glioma at ages over 70 is likely to be due to improvements in diagnosis. As with any such studies, a small effect, or one with a latent period of more than 10 to 15 years, cannot be excluded. Key words: cancer epidemiology, brain cancer, trends, mobile phones to estimate the prevalence of mobile phone use and used cancer incidence data from large population-based cancer registries. The results of many previous ecological studies are summarised in the IARC report, 2 which concluded that the overall results of different time-trend analyses do not support the hypothesis that the increase in the use of mobile phones elevates the risk of primary brain cancer. Discussed within that report, Scandinavian 4-7 and American studies 8,9 found no evidence of an increase in incidence in primary brain cancers from the 1970s to the 2000s, in keeping with the growing number of people using mobile phones over this time period. An exception to this was the 20 to 29 year age group of women in the Inskip et al. study, 8 which showed a steady increasing trend in primary brain cancer incidence; however this was due to an increase in frontal lobe cancer, which is an anatomical site not thought to be highly exposed to radiation from mobile phone usage. A UK study found no increase in overall primary brain cancer trends between 1998 and 2007, but did find an increasing trend in temporal lobe tumour incidence in both men and women over the study period. 10 In Osaka, Japan, rates at ages increased from 1975 to 1988, and at ages 75+ increased until 1984, but then stabilised; these changes were attributed to diagnostic improvements. 11 A recent study in Australia based on clinical data showed some increases. 12,13 No increases were seen 1. Department of Epidemiology and Biostatistics, School of Population Health, University of Auckland, New Zealand Correspondence to: Professor Mark Elwood, University of Auckland, FMHS School of Population Health, Private Bag 92019, Auckland 1142, New Zealand; mark.elwood@auckland.ac.nz Submitted: May 2014; Revision requested: July 2014; Accepted: October 2014 The authors have stated they have no conflict of interest. Aust NZ J Public Health. 2015; 39:148-52; doi: / Australian and New Zealand Journal of Public Health 2015 vol. 39 no. 2

2 Cancer Incidence trends of primary brain cancer from 1986 to 1998 in a previous study in New Zealand (NZ). 14 The present study was undertaken to assess if there had been any increase in more recent years in NZ. Methods Data Collection Incidence data on brain cancers, including the brain, meninges, central nervous system and cranial nerves, diagnosed between 1995 and 2010 inclusive were requested from the NZ Cancer Registry. The included ICD-10 codes were: C70.0, C70.1 and C70.9 for malignant neoplasms of meninges, C71.0, C71.1, C71.2, C71.3, C71.4, C71.5, C71.6, C71.7, C71.8 and C71.9 for malignant neoplasms of the brain, C72.0 and C72.1 for cancer of the central nervous system and C72.2, C72.3, C72.4 and C72.5 for cancer of the cranial nerves. Tumour types excluded from the study were histologically benign tumours of the brain, meninges and head and neck, tumours with unknown or uncertain classification, and metastatic tumours. Collected data included information on site, morphology, gender, ethnicity, domicile code, diagnosis date, date of birth, extent of disease, basis of disease, laboratory code and date of death. Estimated resident population data were taken from the Statistics NZ website. 15 Data Analysis The population was divided into fiveyear age sub-groups, and sub-groups 0-9 years, years and 70+ years were also assessed. Population estimates by fiveyear age groups, sex, and individual year from 1995 to 2010 were used. 15 Within the years age group, sub-groups of years, years, and years were analysed separately. Within these groups, direct age-standardisation used the World Health Organization s standard population. 16 Morphology was analysed by all morphologies or glioma alone. Anatomical sites were analysed by all sites of brain cancer, brain cancers in the temporal or parietal lobe only and all other anatomical sites. Temporal and parietal lobe sites were examined separately as they are located in the area of maximum exposure to radio-frequency energy emitted from mobile phones. 17 A log linear regression model was used to analyse trends, and annual percentage changes and 95% confidence intervals were calculated. Cases in children aged 0-9 years were excluded from the trend analyses as they represent a different spectrum of primary brain cancer pathology than adults. Results There were 4,212 eligible cases (2,433 in males, 1,779 in females) at all ages diagnosed in the 15-year period in an average NZ population of 4.36 million in 2010, 15 giving age-standardised rates (WHO world standard) of 6.74 in males, and 4.49 in females per 100,000. Of these, 3,684 tumours were gliomas (87%), 461 (10.9%) were neoplasms not otherwise specified, 49 (1.2%) were meningiomas, and 18 (0.4%) were neuroepitheliomatous neoplasms. The most common anatomical site recorded was brain unspecified (1,451, 34.4%), followed by frontal lobe (1,041, 24.7%), temporal lobe (787, 18.7%), parietal lobe (698, 16.6%), occipital lobe (148, 3.5%), meninges (54, 1.3%) and cranial nerves (33, 0.8%). Rates by age, sex, and major subtype are shown in Table 1. The incidence rates of all primary brain cancers for the period demonstrated a bimodal pattern, with a peak among children aged 5-9 years, lower rates at ages 15-24, and the highest rates at ages or Males had higher incidence rates than females at all ages except and 15-19; both the childhood and the age 60s peaks are greater in males. Brain tumours at ages under 10 (n=247) have quite different pathologies and so were excluded from further analyses. The time trends in annual incidence rates were also assessed. For ages 10-69, for all brain cancers, a significant decreasing trend in yearly incidence rates was observed, with an annual percentage change (APC) of (95% CI to -0.16). This decrease was more pronounced for men, -1.19% (95% CI to -0.03), than for women, for whom it was not significant; APC -0.30% (95% CI to 0.89). The trends assessed by sex, age group, morphology and anatomical site are shown in Table 2. In the age group years, a non-statistically significant downward trend in parietal and temporal lobe gliomas was observed for both genders combined, APC -0.39% (95% CI to ), and for males, APC -0.70% (95% CI to 0.87). For women, a small non-statistically significant upward trend was seen, APC 0.35% (95% CI to 2.35); (Figure 1). Analysis of narrower age groups (10-29 years, years, years) showed few consistent results (Table 2). There was a significant increase in all brain tumours in females aged 30-49, and this was most marked for glioma of the parietal and temporal lobes (APC 3.63, 95% CI 1.21 to 6.10); but in males in this age group a nonsignificant decline was seen. In younger subjects, aged 10-29, rates of all brain tumours declined over time, significantly for both sexes combined (APC -3.91), and the decline appeared greater for gliomas of the parietal and temporal lobes (APC 6.32), but Table 1: Numbers and rates per 100,000 of brain cancers by age, sex, and major subtype, New Zealand (16 years). Male Female All Glioma All Glioma all sites all sites temporal +parietal all sites all sites temporal +parietal Age group N rate N rate N rate N rate N rate N rate All ages Age- stand 1,648 2, ,547 2, ,107 1, ,011 1, Age-stand = age standardised to the WHO world standard population vol. 39 no. 2 Australian and New Zealand Journal of Public Health 149

3 Kim, Ioannides and Elwood Article these estimates are based on small numbers. At ages years non-significant declines were seen. In the 70+ age group, there was a decreasing trend in the incidence of all brain tumours in females, APC % (95% CI to -0.05), however, there was a non-statistically significant increasing trend for males, APC 0.56% (95% CI to 2.63). A significant increasing trend in the incidence of glioma was seen in males (APC 2.98, 95% CI 0.31 to 5.72), and a smaller and non-significant increase occurred in females; but in both, the increase was no greater for gliomas in the temporal and parietal lobes. Discussion areas of the brain are more highly exposed to radio-frequency energy than other brain sites when using cell phones, the increases in the incidence of glioma originating in the temporal or parietal lobes should be greater than the increase in glioma of all sites. Such trends were not consistently observed. For glioma of all sites, and glioma of the temporal or parietal lobe, the year age group showed no significant trends, with small decreases in females and small increases in males. By age group, significant decreases were seen at ages in both sexes combined, but based on small numbers. At ages in females, there was a significant increase in all glioma, and a greater increase in glioma of the temporal and parietal lobes; but the rates were decreasing in males of that age, and in females in the adjacent age groups. Other studies of trends in brain cancer incidence in adults apart from the most elderly have been inconsistent. A previous study in NZ 14 showed no change from 1986 Figure 1: Trends in incidence of temporal or parietal lobe glioma for males (M) and females (F) aged years during in New Zealand. Age-standardised rates For all primary brain cancer, at ages there was a decreasing trend in incidence from 1995 to 2010 in NZ. This was greater in males, and was greatest at ages Decreases were seen in each age and sex group assessed, except one: incidence increased in females aged If there were a substantial causal relationship between mobile phone usage and primary brain cancer, increasing trends in incidence of glioma in both males and females should be observed. Also, since temporal and parietal Incidence per 100,000 p yrs Year of diagnosis M F Table 2: Annual percentage changes (APC) of age-standardized primary brain cancer incidence by sex, age group, morphology and site, New Zealand, Age group Male Female All genders Total cases years Glioma + temporal & parietal 1,648 1, years Glioma + temporal & parietal years Glioma + temporal & parietal years Glioma + temporal & parietal years Glioma + temporal & parietal Results in bold are statistically significant. 95% limits not calculated due to the small number of cases. APC 95% Lower 95% Upper Total cases APC 95% Lower 1,107 1, % Upper Total cases APC 95% Lower ,755 2, ,574 1, , % Upper Australian and New Zealand Journal of Public Health 2015 vol. 39 no. 2

4 Cancer Incidence trends of primary brain cancer to 1998 in the incidence rates for primary brain cancers overall, or in the temporal and parietal lobes. The International Agency for Research on Cancer (IARC) 2 reviewed 13 studies published up to 2011, showing inconsistent trends between subtypes and subsites. Subsequent to the IARC review, generally stable trends of glioma have been reported from the US 18 and from the Nordic countries, 4 while a steady increase in all brain tumours was seen in Shanghai, China, from 1983 to An overall increase in malignant, but not in benign, tumours from 2000 to 2008 was seen in data from 24 neurological centres in New South Wales and the Australian Capital Territory; this is reported as being mainly in the 65+ age group, but the data shows that their rate of increase was not higher than in younger adults; 12 the authors note their results differ from those of population-based registries. In the same study, decreases were seen for acoustic neuroma (Schwannoma). 13 There are no clear causal factors that explain the overall downward trend seen here in the incidence of primary brain cancer in NZ. A decline seems unlikely to be due to late reporting or under-ascertainment, as cancer registration has generally improved over time. Classification issues between benign and malignant tumours may be possible: the NZ Cancer registry does not register benign tumours, so if some types previously regarded as malignant were more likely to be classified as benign, that would lead to a decrease in the recorded incidence of malignant tumours; however, we have no direct evidence of this. Changes in histology classification and localisation information may have accounted for decrease in the incidence of lesions with unspecified subtype or subsite; this would lead to an increase in specified lesions, so the lack of an upward trend in specified types and sites is seen in spite of any such influence. A major review in 2010 gives only ionising radiation as an established risk factor for glioma, apart from demographic factors and several genetic states However, an inverse (protective) effect of allergies, asthma, and elevated IgE is given as a probable risk factor, and has been shown in meta-analysis, 23 as has an inverse association with diabetes history. 24 Such associations could relate to a decrease in incidence; however, a large cohort study has shown increased risks of adult glioma associated with greater birth weight. 25 Tobacco smoking and alcohol consumption seem unrelated to glioma. 26 At ages over 70, the incidence of glioma increased in both sexes. The increase in glioma of the temporal and parietal lobes was less than the increase in all glioma, and the trend for brain cancers other than glioma showed a small decrease. An increased incidence of brain cancers or other intracranial tumours among the elderly is consistent with previous studies done in several countries, 10,12,13,27-30 and is likely to be related to improved diagnostic technologies. 27,28,30-33 Information on mobile phone usage over time is limited to the annual numbers of mobile phone subscribers in the whole population. 34 Although NZ was part of the Interphone study, 1 the numbers of controls were insufficient to give adequate data on population level exposures. Since mobile phone subscriptions do not necessarily describe the actual use of mobile phones, or the proportion of the population who use them extensively, the information needs to be interpreted with caution. In 1986, only about 0.2 % of the NZ population were subscribers to mobile phones; by 1995, this had risen to 9.5 %. 14 By the year 2000, there were 1,542,000 subscriptions to mobile phone companies, about 40% of the total population, and since 2007 there have been more mobile phone subscriptions than people in NZ. 35 The NZ National Household Use of Information and Communication Technology Survey shows mobile phone use by 80% of people aged over 15 in 2006, and 85% in 2009, with the highest usage rates at ages 15-44; but gives no comparison by sex. 34 The interpretation of time trends is limited by the lack of information on the latency period for non-ionising radiation exposure from mobile phones (if there is a causal relationship), the limited information on other risk factors, and documentation of the effects of improvements in diagnostic technologies and practices. However, it seems reasonable to conclude that mobile phone exposure has been high in NZ since about 2000, so if this caused a substantial increased risk of brain tumours with a latency of 10 years of less, an increase in incidence would be seen; in fact, at ages 10-69, there have been decreases in the incidence of these cancers. Conclusion This study shows no consistent increase in primary brain cancers over the period 1995 to 2010 in NZ and no consistent increasing trends in the incidence of gliomas occurring in temporal or parietal lobe of the brain were seen. This is despite high mobile phone prevalence since 2000 and so does not support the hypothesis that mobile phone usage increases the incidence of brain cancer in NZ, although it cannot exclude a small effect or a latency period greater than 10 years. Acknowledgements We thank the NZ Cancer Registry for the provision of anonymous data. This work was part of the BHSc dissertation by Ms Stella Kim for the University of Auckland. 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