Has the incidence of brain cancer risen in Australia since the introduction of mobile phones 29 years ago?

Cancer epidemiology · 2016 · No effect · Low evidence

← Research stream

No effectLow evidencePaper 4861

Study snapshot

PublicationCancer epidemiology · 2016

Study typeecological

Reported directionNo effect

Evidence ratingLow

Abstract

BACKGROUND: Mobile phone use in Australia has increased rapidly since its introduction in 1987 with whole population usage being 94% by 2014. We explored the popularly hypothesised association between brain cancer incidence and mobile phone use. STUDY METHODS: Using national cancer registration data, we examined age and gender specific incidence rates of 19,858 male and 14,222 females diagnosed with brain cancer in Australia between 1982 and 2012, and mobile phone usage data from 1987 to 2012. We modelled expected age specific rates (20-39, 40-59, 60-69, 70-84 years), based on published reports of relative risks (RR) of 1.5 in ever-users of mobile phones, and RR of 2.5 in a proportion of 'heavy users' (19% of all users), assuming a 10-year lag period between use and incidence. SUMMARY ANSWERS: Age adjusted brain cancer incidence rates (20-84 years, per 100,000) have risen slightly in males (p<0.05) but were stable over 30 years in females (p>0.05) and are higher in males 8.7 (CI=8.1-9.3) than in females, 5.8 (CI=5.3-6.3). Assuming a causal RR of 1.5 and 10-year lag period, the expected incidence rate in males in 2012 would be 11.7 (11-12.4) and in females 7.7 (CI=7.2-8.3), both p<0.01; 1434 cases observed in 2012, vs. 1867 expected. Significant increases in brain cancer incidence were observed (in keeping with modelled rates) only in those aged ≥70 years (both sexes), but the increase in incidence in this age group began from 1982, before the introduction of mobile phones. Modelled expected incidence rates were higher in all age groups in comparison to what was observed. Assuming a causal RR of 2.5 among 'heavy users' gave 2038 expected cases in all age groups. LIMITATIONS: This is an ecological trends analysis, with no data on individual mobile phone use and outcome. WHAT THIS STUDY ADDS: The observed stability of brain cancer incidence in Australia between 1982 and 2012 in all age groups except in those over 70 years compared to increasing modelled expected estimates, suggests that the observed increases in brain cancer incidence in the older age group are unlikely to be related to mobile phone use. Rather, we hypothesize that the observed increases in brain cancer incidence in Australia are related to the advent of improved diagnostic procedures when computed tomography and related imaging technologies were introduced in the early 1980s.

Machine Enhanced Logic

AI evidence extraction

Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.

Study typeecological

Effect directionno_effect

PopulationAustralia (national population; brain cancer cases 1982–2012)

Sample size34080

ExposureRF · Population mobile phone use data 1987–2012; models assumed 10-year lag

Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

Using Australian national cancer registry data (1982–2012) and mobile phone usage data (1987–2012), age-adjusted brain cancer incidence rose slightly in males but was stable in females. Modelled expected incidence assuming causal relative risks (RR=1.5 for ever-users; RR=2.5 for 19% heavy users) and a 10-year lag exceeded observed incidence (e.g., 1434 observed vs 1867 expected cases in 2012 under RR=1.5). Increases were observed mainly in those aged ≥70 years, but the rise began before mobile phone introduction.

Outcomes measured

Brain cancer incidence (age- and gender-specific incidence rates; age-adjusted incidence per 100,000)

Limitations

Ecological trends analysis; no individual-level mobile phone use or outcome data
Expected rates were based on assumed relative risks from published reports and an assumed 10-year lag period

View raw extracted JSON

{
  "study_type": "ecological",
  "exposure": {
    "band": "RF",
    "source": "mobile phone",
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": "Population mobile phone use data 1987–2012; models assumed 10-year lag"
  },
  "population": "Australia (national population; brain cancer cases 1982–2012)",
  "sample_size": 34080,
  "outcomes": [
    "Brain cancer incidence (age- and gender-specific incidence rates; age-adjusted incidence per 100,000)"
  ],
  "main_findings": "Using Australian national cancer registry data (1982–2012) and mobile phone usage data (1987–2012), age-adjusted brain cancer incidence rose slightly in males but was stable in females. Modelled expected incidence assuming causal relative risks (RR=1.5 for ever-users; RR=2.5 for 19% heavy users) and a 10-year lag exceeded observed incidence (e.g., 1434 observed vs 1867 expected cases in 2012 under RR=1.5). Increases were observed mainly in those aged ≥70 years, but the rise began before mobile phone introduction.",
  "effect_direction": "no_effect",
  "limitations": [
    "Ecological trends analysis; no individual-level mobile phone use or outcome data",
    "Expected rates were based on assumed relative risks from published reports and an assumed 10-year lag period"
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "mobile phones",
    "brain cancer",
    "incidence trends",
    "Australia",
    "ecological study",
    "cancer registry",
    "heavy users",
    "lag period"
  ],
  "suggested_hubs": [
    {
      "slug": "mobile-phones-brain-cancer",
      "weight": 0.95,
      "reason": "Assesses national brain cancer incidence trends in relation to mobile phone uptake and modelled risk assumptions."
    }
  ]
}

AI can be wrong. Always verify against the paper.

AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.

Identifiers and source

DOI: 10.1016/j.canep.2016.04.010
PubMed: 27156022

Read the original paper →

Related papers

← Back to the Research Library