Environmental risk factors for cancers of the brain and nervous system: the use of ecological data to generate hypotheses.
BACKGROUND
There is a public health need to balance timely generation of hypotheses with cautious causal inference. For rare cancers this is particularly challenging because standard epidemiological study designs may not be able to elucidate causal factors in an early period of newly emerging risks. Alternative methodologies need to be considered for generating and shaping hypotheses prior to definitive investigation.


OBJECTIVE
To evaluate whether open-access databases can be used to explore links between potential risk factors and cancers at an ecological level, using the case study of brain and nervous system cancers as an example.


METHODS
National age-adjusted cancer incidence rates were obtained from the GLOBOCAN 2008 resource and combined with data from the United Nations Development Report and the World Bank list of development indicators. Data were analysed using multivariate regression models.


RESULTS
Cancer rates, potential confounders and environmental risk factors were available for 165 of 208 countries. 2008 national incidences of brain and nervous system cancers were associated with continent, gross national income in 2008 and Human Development Index Score. The only exogenous risk factor consistently associated with higher incidence was the penetration rate of mobile/cellular telecommunications subscriptions, although other factors were highlighted. According to these ecological results the latency period is at least 11-12 years, but probably more than 20 years. Missing data on cancer incidence and for other potential risk factors prohibit more detailed investigation of exposure-response associations and/or explore other hypotheses.


CONCLUSIONS
Readily available ecological data may be underused, particularly for the study of risk factors for rare diseases and those with long latencies. The results of ecological analyses in general should not be overinterpreted in causal inference, but equally they should not be ignored where alternative signals of aetiology are lacking.
Centre for Occupational and Environmental Health, Institute for Population Health, Manchester Academic Health Sciences Centre, The University of Manchester, Manchester, UK. frank.devocht@manchester.ac.uk
Frank
F
de Vocht
Kimberly
K
Hannam
Iain
I
Buchan
D001921:Brain / Q000473:pathology*; D001932:Brain Neoplasms / Q000453:epidemiology / Q000209:etiology*; D040421:Cell Phone; D016543:Central Nervous System Neoplasms; D015986:Confounding Factors, Epidemiologic; D016208:Databases, Factual; D004463:Ecology; D060733:Electromagnetic Radiation; D004781:Environmental Exposure / Q000009:adverse effects*; D004812:Epidemiologic Methods; D014943:Global Health; D006801:Humans; D015994:Incidence; D007182:Income; D015999:Multivariate Analysis; D012307:Risk Factors