In this analysis of over 7,000 patients, we found that higher ambient temperature transiently increased the risk of headache requiring emergency department evaluation, with approximate 7.5% higher risk for each 5°C increment in temperature. There was also some evidence for higher risk with lower barometric pressure in the 48 to 72 hours before hospital presentation for cases not diagnosed as migraine. We did not find clear association of ambient air pollutants with risk.
Migraine and other headache syndromes have long been linked to weather conditions, particularly with changes in barometric pressure.4,5
In fact, an association with weather conditions has been suggested as a diagnostic symptom specific to migraine relative to other forms of headache.28
However, this association was not borne out in a large case-crossover study of migraines in Ottawa,7
and a large study of headaches not coded as migraines in Montreal also found an association solely with barometric pressure.6
These results together with ours suggest that the association of headache with barometric pressure is unlikely to be a useful diagnostic marker specific for migraine.
We also found a strong association of headache with ambient temperature, regardless of the discharge diagnosis coded. The one previous large case-crossover study of migraines did not find such an association but examined only a single temperature cutpoint of 19.6°C.7
However, other studies have found generally higher rates of migraine in warmer seasons,29–31
despite an association of higher temperature with lower blood pressure.32,33
Whether higher temperature is also associated with a greater likelihood of triggering the more common headaches that do not result in emergency department evaluation will require additional study.
There is growing interest in air pollution as a trigger of a variety of acute health conditions. Air pollution represents a complex mix of pollutants, including both coarse and fine particles and gaseous constituents. Two common pollutant gases, sulfur and nitrogen dioxides, were positively associated with emergency visits for nonmigraine headache in similar time-series studies in Ottawa and Montreal, with higher risks seen across multiple lag scales.6,18
Our results tend to support the higher risk associated with NO2
exposure, where higher risk was seen specifically for headaches not diagnosed as migraine.
We anticipated that PM2.5
might have the strongest association with headache, as they appear to induce sympathetic nervous system activation (best studied in relation to heart rate variability34
), pulmonary and subsequently systemic inflammation,35,36
and vascular endothelial injury.37,38
They have also been most closely associated with triggering cardiovascular events.39
In the one previous large-scale study of headaches, PM2.5
only increased risk on a lag 2 scale, with a generally weaker effect than observed for gaseous pollutants.6
Given the marked effects of fine particulate matter observed in previous studies of cardiovascular disease, the role of these particles as a trigger of headache clearly merits additional study.
It is also important to recognize the expected magnitude of effect when considering the lack of statistical association between pollutants and risk in our study. In general, previous case-crossover studies of fine particulate air pollution and cardiovascular conditions such as ischemic stroke9
have demonstrated approximately 1% higher risk (i.e., relative risk of 1.01) with an interquartile range increment similar to that used here. The precision of our estimates was generally insufficient to exclude an effect of that magnitude, and hence we cannot rule out an association that, albeit small in magnitude, could have far-reaching public health implications.
The clinical and public health implications of our findings even for temperature may differ to some degree. Our results suggest that an increase in temperature of 5°C would confer a short-term 7.5% increase in risk. This magnitude of excess risk is obviously modest and may not be an important factor in the clinical management of individual patients, given the many other potential triggers of migraine that patients may face. At the same time, every member of a given geographic region is repeatedly exposed to this excess risk, and hence the public health impact of triggering migraine by rising ambient temperatures may be greater than exposures that confer a higher relative risk but to a much smaller number of potentially exposed patients.
This study has several potential limitations, most of which were likely to have potentially biased our results toward the null. First, we relied upon headaches classified by emergency department physicians, and hence misclassification of some admissions—and particularly for comparisons of cases coded as migraine or not40
—is likely. Second, we relied upon use of a central ambient monitor rather than personal exposure measures, although levels of SO2
in particular tend to be spatially homogenous within our region of study. Third, we had highly accurate information on the time of hospital presentation but not about the timing of actual symptom onset, and hence could not account for the variable duration of time that patients experienced headaches before evaluation. Finally, because this study relied upon patients seen for headaches requiring emergency evaluation, we cannot distinguish whether observed increases in risk related to temperature or barometric pressure reflect changes in the incidence of headaches or in their severity.