Heat Waves and Pollution Can Increase MI Risk

Quick Takes

  • Exposure to extreme heat can accelerate the body’s thermoregulatory system by increasing cardiac output; whereas extreme cold increases cardiac workload by stimulating the sympathetic nervous system and renin-angiotensin system resulting in vasoconstriction, increase in blood pressure and viscosity, and decrease in plasma volume.
  • The risk of MI is doubled during heat waves in the setting of fine particle pollution (PM2.5) ≥37.5 µg/m3, especially in women and adults >80 years of age.
  • Extreme cold waves combined with PM2.5 do not significantly increase the risk of MI.

Study Questions:

How does the combination of extreme temperatures and pollution increase the risk of myocardial infarction (MI)?


This population-based case-crossover study of 202,678 MI deaths in the Jiangsu province, China between 2015–2020 evaluated the association of extreme temperatures (heat wave: daily maximum air temperature ≥35°C for >3 consecutive days, and cold spell: daily minimum air temperature <4°C dropping >8°C within 48 hours) and fine particulate matter pollution (PM2.5) to the incidence of MI mortality. Conditional logistic regression models were applied to perform exposure-response analyses to MI mortality to estimate relative excess odds.


The odds ratio of MI mortality associated with heat wave and cold spell ranged from 1.18 (95% confidence interval, 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. Heat waves, especially with longer durations, and PM2.5 had a significant synergistic interaction on MI mortality (relative excess odds due to interaction >0, proportion attributable to interaction >0, and synergy index >1). Findings suggest 2.8% of the MI deaths were attributable to combined exposure to extreme temperatures 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 extreme temperatures and PM2.5. The interactive effects of extreme temperatures or PM2.5 on MI mortality did not vary across sex, age, or socioeconomic status.


Exposure to extreme temperatures and PM2.5 is significantly associated with an increased risk for MI mortality, especially for women and older adults. In addition, heat waves combined with pollution triggers increase MI mortality rates during longer durations of high intensity as compared to cold spells.


This study found a significant synergistic interaction of heat wave and PM2.5 on MI mortality that may be resultant to thermoregulatory responses that accelerate the uptake of PM2.5 through sweating, elevating skin blood flow, insensible water loss, and minute ventilation. During prolonged heat waves, thermoregulation is triggered; thereby, increasing systemic inflammation, oxidative stress, endothelial dysfunction, direct cytotoxic effects, and potentially myocardial ischemia. Although this study found lesser risk for MI mortality during cold spells, extremely low temperatures can activate both the sympathetic nervous system and the renin-angiotensin system to provoke vasoconstriction, increase blood pressure and viscosity, and decrease plasma volume; consequently, increasing cardiac workload. In addition to women and older adults being at higher risk, various patients including those with heart failure, hypertension, anemia, and inflammatory diseases may also be at higher risk. As global climate changes are evolving, clinicians need to promote surveillance for patients that are vulnerable to extreme temperature and PM2.5 exposure to mitigate environmental stressors that may double their MI mortality risk.

Clinical Topics: Acute Coronary Syndromes, Geriatric Cardiology, Heart Failure and Cardiomyopathies, Prevention, Stress

Keywords: Acute Coronary Syndrome, Air Pollution, Angiotensins, Blood Pressure, Body Temperature Regulation, Climate Change, Cold Temperature, Environmental Pollution, Extreme Heat, Geriatrics, Hot Temperature, Inflammation, Myocardial Ischemia, Myocardial Infarction, Oxidative Stress, Particulate Matter, Patient Care Team, Primary Prevention, Renin-Angiotensin System, Socioeconomic Factors, Sweating, Temperature, Vasoconstriction, Viscosity

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