15) 144 Discussion

15).144 Discussion selleck screening library The aim of this systematic review was to provide an overview of the literature describing associations between environmental exposures in early life and asthma outcomes by 9 years of age. This review is mostly based on observational studies and is likely to be influenced by submission bias (where investigators do not submit papers that find no associations which challenge current paradigms) and/or publication bias. In addition, reverse causation or confounding may explain some associations reported, for example, postnatal exposures to antibiotics, paracetamol

and perhaps pets. Moreover, observational studies cannot prove causation and most intervention studies found no effect on outcome even where studies indicated a potentially important mechanism, for example, HDM interventions. Given these caveats, we believe that three major conclusions can be

drawn. First, there was a moderately strong level of evidence (ie, RCT, systematic review or meta-analysis) for the presence of associations between most exposures and asthma risk but the literature remains relatively deficient for exposures to infection and domestic combustion (both of which are likely to be important on a global basis). Second, where associations were present, these were of small-moderate effect size by our predefined standard. Third, we identified interactions between exposures (most commonly SHS) and/or atopy which increased the risk of that exposure being associated with asthma. Given

that there is no prospect of a cure for asthma, modification of the environment in early life currently offers the best hope of reducing the burden of asthma in the population and an overview of all exposures such as we present here may be of use to policymakers, healthcare workers and lobbying groups. There is no single exposure which seems likely to cause asthma and even ‘single’ exposures are invariably contaminated by other exposures. There was consistent evidence in the literature for associations between exposures to SHS, inhaled chemicals, mould, respiratory viruses, ambient air pollutants and maternal dietary components, and increased asthma risk. However, each of these is a complex GSK-3 exposure and there was evidence of interaction between all these exposures. There is evidence that asthma risk may be related to diversity of exposure to fungus and not exposure per se145 and our findings are consistent with this idea. There were inconsistent associations between asthma and exposures to pets, breast feeding and infant diet when considered separately but those intervention studies where asthma risk was successfully reduced often included modifications to some or all of these exposures.

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