Air Temperature and Cardiovascular Mortality in Bavaria
Air Temperature and Cardiovascular Mortality in Bavaria
We examined the effects of air temperature on cause-specific cardiovascular mortality in Munich, Nuremberg and the Augsburg region, Germany, during the years 1990–2006. Low and high air temperatures showed associations with increased cause-specific cardiovascular mortality. We found strongest consistent risk estimates for very high 2-day average temperatures and mortality due to other heart diseases (including arrhythmias and heart failure) and cerebrovascular diseases.
Many investigators have reported U-shaped or J-shaped associations between temperature and mortality. This study confirmed these findings as we also found that high and low temperatures increased mortality. An increase in the 2-day average temperature from the 90th to the 99th centiles (representing high temperatures) resulted in an increase of cardiovascular mortality by 10% (95% CI 5% to 15%), which is about the same effects size compared with studies conducted in the Czech Republic (excess mortality for the 10% warmest days: 11.4% (95% CI 8.1% to 14.8%)) or in England and Wales during summer (increase of about 9.0% (95% CI 6.0% to 12.5%) per 5°C above the 93rd centile threshold of maximum temperature). In contrast with this study's findings, however, the study in Prague and Southern Bohemia did not show any associations with low temperatures.
Further, studies have observed that high temperatures affect mortality more immediately while cold effects are delayed and last for several days up to weeks. Consistently, we observed heat effects on the same day and or with a delay of 1 day, whereas cold effects only became predominant with longer time lags.
We found the strongest, consistent risk estimates in this study for heat and mortality due to other heart diseases (including arrhythmias and heart failure), heart failure and cerebrovascular diseases. Only very few studies have so far investigated temperature effects on these subcategories of cardiovascular mortality. Among others, studies were conducted in the Czech Republic, England and Wales. Overall, these studies also found comparable or slightly stronger effects of heat on these subcategories of cardiovascular mortality. For example, the study conducted in the Czech Republic found an excess mortality of 9.8% (95% CI 3.5% to 16.4%) for cerebrovascular disease mortality for the 10% warmest days.
As has been found in other studies people 75 years and older were most sensitive to effects of high, but also low temperatures. The elderly often suffer from multiple pre-existing chronic conditions and have physiological changes in thermoregulation and homoeostasis making them more vulnerable to temperature effects. Further, factors such as living conditions and family and/or social support can have impacts on high temperature-related effects on the elderly mortality.
We observed some heterogeneity in the associations between air temperature and cause-specific mortality for Munich, Nuremberg and the Augsburg region. Whereas, for example, for Munich and the Augsburg region effects of very low and very high temperatures on overall cardiovascular mortality could be seen, for Nuremberg only heat effects were observed. Heterogeneity between Munich, Nuremberg and the Augsburg region could be due to a lack of statistical power for Nuremberg and the Augsburg regions. Heterogeneity may also be partly attributed to differences in the proportion of specific causes of cardiovascular mortality in Nuremberg and the Augsburg region compared with Munich. Also, many other socioeconomic factors, such as lifestyle differences, occupation and economic status, or climatic conditions such as higher relative humidity may contribute to the differences in mortality; however, these issues need further investigations.
Heat can induce events such as heart failure or stroke. Proposed mechanisms between heat and cardiovascular mortality include increased surface blood circulation and sweating. This leads to increased cardiac work load, dehydration and salt depletion, haemoconcentration, elevated blood viscosity, and the risk of thrombosis. Also, heat stress was suggested to induce the release of interleukins modulating local and systemic acute inflammatory responses. These inflammatory responses can result in heart failure by increasing damage to heart tissue and inflammation.
Low air temperature can increase the sympathetic tone causing vasoconstriction and increases in heart rate and blood pressure, decreases in the ratio of myocardial oxygen supply to demand, myocardial ischaemia and angina pectoris or myocardial infarctions. Also, increases in fibrinogen, platelet counts and blood viscosity in association with cold temperatures have been shown which may promote thrombosis.
We selected daily mean air temperature as the exposure metric as it represents the exposure throughout the whole day and night and can, therefore, be straightforwardly interpreted, also with a policy context. Recent assessments compared mean air temperature with other temperature metrics and found that mean air temperature was either the best predictor of mortality or none of the temperature measures was superior over the others.
Strength of this study was the available data set with a large number of deaths which had high quality (no missing data for mortality). Moreover, the use of advanced statistical approaches, which can flexibly examine effects of temperature on mortality, allows for smooth and lagged effects of temperature at the same time. The multivariate meta-analysis used even allows combining city-specific smooth effect estimates. We also adjusted for a range of confounders including relative humidity, barometric pressure, influenza epidemics and air pollutants. Further, this study compared time series and case cross-over analyses to assess whether results using the two approaches are consistent and comparable.
A study limitation is the use of data on temperature and air pollution from fixed monitoring sites rather than measuring individual exposure. Such misclassification may be more pronounced among elderly people who spend a lot of their time indoors. This misclassification is assumed to be non-differential and should bias the effect estimates towards the null. Moreover, a recent study found that time series models using non-spatial temperatures were equally good at estimating the city-wide association between temperature and mortality as spatiotemporal models. Further, some disease misclassification of the death counts is possible, especially for the subcauses, but it is unlikely to be related to temperature. We only used data from Bavaria, Southern Germany, to examine the effects of temperature on mortality, so the findings may not be generalisable to other areas.
Discussion
We examined the effects of air temperature on cause-specific cardiovascular mortality in Munich, Nuremberg and the Augsburg region, Germany, during the years 1990–2006. Low and high air temperatures showed associations with increased cause-specific cardiovascular mortality. We found strongest consistent risk estimates for very high 2-day average temperatures and mortality due to other heart diseases (including arrhythmias and heart failure) and cerebrovascular diseases.
Many investigators have reported U-shaped or J-shaped associations between temperature and mortality. This study confirmed these findings as we also found that high and low temperatures increased mortality. An increase in the 2-day average temperature from the 90th to the 99th centiles (representing high temperatures) resulted in an increase of cardiovascular mortality by 10% (95% CI 5% to 15%), which is about the same effects size compared with studies conducted in the Czech Republic (excess mortality for the 10% warmest days: 11.4% (95% CI 8.1% to 14.8%)) or in England and Wales during summer (increase of about 9.0% (95% CI 6.0% to 12.5%) per 5°C above the 93rd centile threshold of maximum temperature). In contrast with this study's findings, however, the study in Prague and Southern Bohemia did not show any associations with low temperatures.
Further, studies have observed that high temperatures affect mortality more immediately while cold effects are delayed and last for several days up to weeks. Consistently, we observed heat effects on the same day and or with a delay of 1 day, whereas cold effects only became predominant with longer time lags.
We found the strongest, consistent risk estimates in this study for heat and mortality due to other heart diseases (including arrhythmias and heart failure), heart failure and cerebrovascular diseases. Only very few studies have so far investigated temperature effects on these subcategories of cardiovascular mortality. Among others, studies were conducted in the Czech Republic, England and Wales. Overall, these studies also found comparable or slightly stronger effects of heat on these subcategories of cardiovascular mortality. For example, the study conducted in the Czech Republic found an excess mortality of 9.8% (95% CI 3.5% to 16.4%) for cerebrovascular disease mortality for the 10% warmest days.
As has been found in other studies people 75 years and older were most sensitive to effects of high, but also low temperatures. The elderly often suffer from multiple pre-existing chronic conditions and have physiological changes in thermoregulation and homoeostasis making them more vulnerable to temperature effects. Further, factors such as living conditions and family and/or social support can have impacts on high temperature-related effects on the elderly mortality.
We observed some heterogeneity in the associations between air temperature and cause-specific mortality for Munich, Nuremberg and the Augsburg region. Whereas, for example, for Munich and the Augsburg region effects of very low and very high temperatures on overall cardiovascular mortality could be seen, for Nuremberg only heat effects were observed. Heterogeneity between Munich, Nuremberg and the Augsburg region could be due to a lack of statistical power for Nuremberg and the Augsburg regions. Heterogeneity may also be partly attributed to differences in the proportion of specific causes of cardiovascular mortality in Nuremberg and the Augsburg region compared with Munich. Also, many other socioeconomic factors, such as lifestyle differences, occupation and economic status, or climatic conditions such as higher relative humidity may contribute to the differences in mortality; however, these issues need further investigations.
Heat can induce events such as heart failure or stroke. Proposed mechanisms between heat and cardiovascular mortality include increased surface blood circulation and sweating. This leads to increased cardiac work load, dehydration and salt depletion, haemoconcentration, elevated blood viscosity, and the risk of thrombosis. Also, heat stress was suggested to induce the release of interleukins modulating local and systemic acute inflammatory responses. These inflammatory responses can result in heart failure by increasing damage to heart tissue and inflammation.
Low air temperature can increase the sympathetic tone causing vasoconstriction and increases in heart rate and blood pressure, decreases in the ratio of myocardial oxygen supply to demand, myocardial ischaemia and angina pectoris or myocardial infarctions. Also, increases in fibrinogen, platelet counts and blood viscosity in association with cold temperatures have been shown which may promote thrombosis.
We selected daily mean air temperature as the exposure metric as it represents the exposure throughout the whole day and night and can, therefore, be straightforwardly interpreted, also with a policy context. Recent assessments compared mean air temperature with other temperature metrics and found that mean air temperature was either the best predictor of mortality or none of the temperature measures was superior over the others.
Strength of this study was the available data set with a large number of deaths which had high quality (no missing data for mortality). Moreover, the use of advanced statistical approaches, which can flexibly examine effects of temperature on mortality, allows for smooth and lagged effects of temperature at the same time. The multivariate meta-analysis used even allows combining city-specific smooth effect estimates. We also adjusted for a range of confounders including relative humidity, barometric pressure, influenza epidemics and air pollutants. Further, this study compared time series and case cross-over analyses to assess whether results using the two approaches are consistent and comparable.
A study limitation is the use of data on temperature and air pollution from fixed monitoring sites rather than measuring individual exposure. Such misclassification may be more pronounced among elderly people who spend a lot of their time indoors. This misclassification is assumed to be non-differential and should bias the effect estimates towards the null. Moreover, a recent study found that time series models using non-spatial temperatures were equally good at estimating the city-wide association between temperature and mortality as spatiotemporal models. Further, some disease misclassification of the death counts is possible, especially for the subcauses, but it is unlikely to be related to temperature. We only used data from Bavaria, Southern Germany, to examine the effects of temperature on mortality, so the findings may not be generalisable to other areas.
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