It is important to emphasize that the temporal association of environmental exposures with illness onset does not imply causality. For example, certain exposures, such as trauma or weight training, could have occurred after the onset of illness as a consequence of the first unrecognized symptoms of disease, such as fatigue or muscle weakness. Rather, exposures with temporal relationships to disease onset, as were seen in this hypothesisgenerating study, constitute a first step for determining which factors may trigger the onset of illness and warrant further investigation. Additional support for a relationship between these exposures and disease pathogenesis could be provided by dechallenge data, which did not exist in this cohort-based study, from laboratory investigations and from case-controlled epidemiological studies [43] . A case-control study by Pachman et al. [19] did not find any significant differences in pesticide use, psychological stress or exposure to animals in 80 JDM patients within 6 months of illness onset compared with 63 age-matched geographically similar healthy controls with similar school or daycare experiences, nor was parvovirus found to be an aetiological factor in recent-onset JDM patients compared with age-, genderand race-matched controls [44] . However, both of those studies may not been adequately powered to detect differences between the cases and controls. Also, the extent of matching of controls may have obscured differences with JDM patients. For example, in the parvovirus study [44] , the controls were age, race and gender matched to patients, but they were not geographically matched, whereas in the study of Pachman et al. [19] , the healthy controls, frequently age-matched classmates and neighbours, may have been geographically overmatched, but they were not gender or race matched. An appropriately powered prospective case-controlled study is needed to confirm the observations from this and other previous reports.