The rapid rise in asthma during the 1980s and 1990s1 was too abrupt to be explained solely by change in prevalence of genetic variations. Changing environmental exposures appear to be relevant to the high prevalence of asthma
in the Western world,2 PD173955? although some exposures are likely to be effective via epigenetic mechanisms.3 Many environmental exposures have been linked to asthma causation, including allergens,4 smoking,5 dietary factors6 and respiratory infections.7 Recently, evidence has emerged to suggest that asthma causation may involve interactions between different environmental exposures8 9 and/or environmental exposures and atopy.10 Owing to the many challenges of relating even a single exposure to asthma causation, there is very little synthesis in the literature of multiple environmental exposures
and asthma causation. The Environmental Determinants of Public Health in Scotland (EDPHiS) was commissioned in 2009 to quantify the evidence on the connections between the environment and key aspects of health of children in order to inform the development of public policy. Asthma was identified as a priority along with obesity, unintentional injury and mental health. The overall aim of this systematic review was to capture all of the literature associating early environmental exposures and asthma development in children up to 9 years of age; this cut-off was chosen to avoid the effects of puberty and active smoking on asthma causation. A recent paper describes associations between environmental exposures and asthma control and exacerbation.11 Our specific aims were (1)
to describe the magnitude of association between the development of asthma and environmental exposures and (2) to explore evidence of interactions between environmental exposures. Methods Study design A workshop attended by senior researchers from government and academia, and health practitioners and policy professionals identified environmental influences Entinostat considered important on causation and exacerbation of asthma (previously described,11 box 1). By extrapolation from approaches to assessment of causation in workplace exposures for compensation purposes (http://iiac.independent.gov.uk/about/index.shtm), we considered an exposure that increased the risk for asthma by at least twofold as having at least a modest effect size.
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