Association of Exposure to Extreme Temperature Events and Fine Particulate Matter With Myocardial Infarction–Related Mortality
abstract
This abstract is available on the publisher's site.
Access this abstract nowBACKGROUND
Extreme temperature events (ETEs), including heat wave and cold spell, have been linked to myocardial infarction (MI) morbidity; however, their effects on MI mortality are less clear. Although ambient fine particulate matter (PM2.5) is suggested to act synergistically with extreme temperatures on cardiovascular mortality, it remains unknown if and how ETEs and PM2.5 interact to trigger MI deaths.
METHODS
A time-stratified case-crossover study of 202 678 MI deaths in Jiangsu province, China, from 2015 to 2020, was conducted to investigate the association of exposure to ETEs and PM2.5 with MI mortality and evaluate their interactive effects. On the basis of ambient apparent temperature, multiple temperature thresholds and durations were used to build 12 ETE definitions. Daily ETEs and PM2.5 exposures were assessed by extracting values from validated grid datasets at each subject's geocoded residential address. Conditional logistic regression models were applied to perform exposure-response analyses and estimate relative excess odds due to interaction, proportion attributable to interaction, and synergy index.
RESULTS
Under different ETE definitions, the odds ratio of MI mortality associated with heat wave and cold spell ranged from 1.18 (95% CI, 1.14-1.21) to 1.74 (1.66-1.83), and 1.04 (1.02-1.06) to 1.12 (1.07-1.18), respectively. Lag 01-day exposure to PM2.5 was significantly associated with an increased odds of MI mortality, which attenuated at higher exposures. We observed a significant synergistic interaction of heat wave and PM2.5 on MI mortality (relative excess odds due to interaction >0, proportion attributable to interaction >0, and synergy index >1), which was higher, in general, for heat wave with greater intensities and longer durations. We estimated that up to 2.8% of the MI deaths were attributable to exposure to ETEs and PM2.5 at levels exceeding the interim target 3 value (37.5 μg/m3) of World Health Organization air quality guidelines. Women and older adults were more vulnerable to ETEs and PM2.5. The interactive effects of ETEs or PM2.5 on MI mortality did not vary across sex, age, or socioeconomic status.
CONCLUSIONS
This study provides consistent evidence that exposure to both ETEs and PM2.5 is significantly associated with an increased odds of MI mortality, especially for women and older adults, and that heat wave interacts synergistically with PM2.5 to trigger MI deaths but cold spell does not. Our findings suggest that mitigating both ETE and PM2.5 exposures may bring health cobenefits in preventing premature deaths from MI.
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Additional Info
Disclosure statements are available on the authors' profiles:
Extreme Temperature Events, Fine Particulate Matter, and Myocardial Infarction Mortality
Circulation 2023 Jul 25;148(4)312-323, R Xu, S Huang, C Shi, R Wang, T Liu, Y Li, Y Zheng, Z Lv, J Wei, H Sun, Y LiuFrom MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
Extreme temperatures and PM2.5 particles are causing more myocardial infarction deaths
With global warming, extreme temperatures are now breaking new records and becoming more commonplace. Therefore, it is important that we understand how extreme temperatures affects the circulatory system.
The authors of this study from China examined over 200,000 myocardial infarction (MI)–related deaths and correlated these deaths to data on extreme temperatures and fine particulate matter (PM2.5). They found that with extreme heat, meaning above the 95 percentiles for temperatures, the rate of MI-related death increased from 18% to 74% And the pattern was clear — with higher temperatures and longer duration of exposure, the death rate shot up. For example, 4 days of high temperatures would have a higher rate of MI-related death than 3 days.
One theory is that, with high temperatures, there is massive vasodilation of the skin vasculature. This means that the heart has to pump extra hard to keep the pressure up in this dilated configuration. If the heart is not well or the coronaries cannot keep up with the oxygen demands of the heart, then, that would trigger an MI. Hence, this vasodilation might be something we need to watch out for. In addition, when the body cannot get rid of the heat anymore, overheating can cause vascular damage, inflammation, and even coagulation issues, which is another pathway that the authors pointed out that could be driving up the rate of MI-related mortality.
Interestingly, with cold temperatures, there was only a slight increase in the rate of MI-related mortality in the order of 4% to 12%. Perhaps, the vasoconstriction is easier to deal with than the massive vasodilation observed during the heat waves. However, living in Canada, I wonder whether the authors should be considering snow shoveling into the equation. Perhaps, it is not the cold temperature that is the real hazard but the physical exertion needed when shoveling that increases the risk. Perhaps, this theory could be the focus of a subsequent study.
As for the pollution data, the PM2.5, which are the 2.5 micron-sized air pollution particles, were associated with a significant increase in MI-related death rates. These particles are the perfect size because they end up depositing in the lungs and they can diffuse into blood vessels. Smaller particles stay floating in the air so they do not get deposited in the lung and larger particles are often trapped in the airways, and hence, these large particles have a hard time making it into the lungs. PM2.5 are perfect for getting deep into the lungs and then getting absorbed into our vasculature.
Unfortunately, burning fossil fuels and forest fires create a lot of chemicals that fit into the PM2.5 particle size range. These chemicals can cause damage to the vasculature, and by being foreign substances, can cause inflammation, which can increase the rate of MI, leading to MI-related deaths. Interestingly, manure and fertilizer can release ammonia into the air, which reacts with sulfur and nitrogen oxide, forming products like ammonium sulfate and nitrates, which can interact with soot and other compounds to create more toxic PM2.5 particles.
That is why in this study, the higher the PM2.5 exposure for more consecutive days, the higher the MI-related death rate.
When they combined extreme heat and high PM2.5, the researchers observed a significantly higher rate of MI-related death. Therefore, the combination of the two is deadly.
However, the graph that scared me the most, showed that just high PM2.5 with no extreme temperature event actually accounted for 40% to 60% of all MI-related deaths in this study. PM2.5 alone was associated with more than half of the deaths.
We should treat high blood pressure, increased cholesterol levels, diabetes, etc, but we need to pay attention to these environmental factors as well. Vulnerable people should be kept in cool places, and we need to try to reduce the PM2.5 exposure. For individuals that can afford it, air filtration is an option, but perhaps just using a mask might cut down the PM2.5 exposure enough to reduce the cardiovascular risk.
Remember we do not need to clean all the polluted air in order to win – we just need to reduce the amount patients inhale into their lungs.
Reference