Climate Change: Effects of Heat and Wildfire Smoke on Cardiovascular Disease

Heat and Cardiovascular Disease

In 2022 there were 1,714 heat-related deaths in the United States.  By 2023, the number of heat-related deaths grew to 2,300.  To date, 2024 has been one of the hottest years on record and this will likely result in even more deaths.  

Studies show that for every 1°C increase in temperature above reference temperatures there is an associated 2.1 percent increase in cardiovascular disease related mortality and a 0.5 percent increase in cardiovascular disease related morbidity. Humidity worsens the effects of heat.  

Several pathophysiological mechanisms can explain the associations between heat exposure and cardiovascular events. Heat exposure increases skin blood flow and sweating to lower the body’s core temperature. In response, the sympathetic nervous system is activated to maintain cardiac output through a compensatory increase in cardiac workloads, with increases in heart rate and stroke volume. Peripheral vasodilatation and dehydration might also cause drops in blood pressure. Hemoconcentration and prothrombotic conditions due to decreased plasma volume because of sweating, and increases in circulating levels of platelets, red blood cells, and blood viscosity also occur.

Additionally, heat stress has been shown to induce the release of cytokines such as interleukin 1 and interleukin 6, which modulate local and systemic inflammatory responses that can lead to endothelial dysfunction. The heat-related inflammatory response might be further exaggerated by a bacterial infection following gastrointestinal ischemia and intestinal hyperpermeability, which is due to decreased splanchnic blood flow to maintain blood pressure during heat exposure, as well as release of heat shock at proteins.

Congestive heart failure (CHF) has been identified as an independent prognostic factor in heatstroke-related deaths. Patients with CHF lack the ability to compensate for the increased cardiovascular demands induced by heat exposure. Increased cardiac strain and output, arrhythmias, and peripheral edema may render CHF patients vulnerable to heat-related sudden death and in-hospital mortality. In CHF patients, higher temperatures were associated with increased levels of B-type natriuretic peptide and C-reactive protein, both of which are predictors of CHF prognosis and severity.

In the past 20 years, there has been a 54 percent increase in heat-related mortality among persons older than 65 years of age, with more than one-third of all global warm-season, heat-related deaths attributable to climate change.  

Several physiological changes from the aging process raise the predisposition of older people to heat-related circulatory collapse. Aging causes reductions in evaporative cooling efficiency due to decreased overall sweat production, exacerbated by the fact that elders are less able to redirect blood flow away from the deep splanchnic vasculature to the skin for cooling. Also, there is a reduction in surface thermoreceptor density in older adults. Aging is also associated with weaker contractile force of the heart in response to heat, making older hearts less capable of maintaining sufficient cardiac output in response to drops in blood pressure and left ventricular preload. Many chronic diseases are exacerbated or triggered by exposure to heat, including ischemic heart disease, cardiac dysrhythmias, ischemic stroke, asthma and chronic obstructive pulmonary disease, respiratory tract infections, hyperglycemia, kidney failure, and neuropsychiatric disorders.

Smoke and CV Disease

With climate change, wildland fires have occurred more frequently and with increased intensity.  

Wildfire smoke is a complex mixture of particulate matter (PM), gases such as carbon monoxide, nitrogen oxide, and volatile and semi-volatile organic compounds. Epidemiological studies have consistently found an association between exposure to wildfire smoke (typically monitored as the PM concentration) and increased respiratory morbidity and mortality. However, now there are increasing studies that link wildfire smoke exposure and adverse cardiovascular effects.  

According to the Journal of American Heart Association, exposure to heavy smoke during wildfires raised the risk of out-of-hospital cardiac arrests up to 70 percent. Wildfire smoke exposure was also associated with increased rates of emergency room visits, for ischemic heart disease, dysrhythmia, heart failure, pulmonary embolism and stroke. ER visits increased 42 percent for MI and 22 percent for ischemic heart disease within a day of exposure to dense wildfire smoke. This increase was most notable for adults aged 65 and older.

The knowledge of mechanisms underlying air pollution–mediated systemic CV risk is still evolving but can be encapsulated into six broad secondary “effector” pathways. These include:

• Endothelial barrier dysfunction/disruption
• Inflammation, involving both innate and adaptive immune components
• Prothrombotic pathways
• Autonomic imbalance favoring sympathetic tone via afferent pathways the upper airways and/or lung
• Central nervous system effects on metabolism and hypothalamic-pituitary-adrenal axis activation
• Epigenomic changes. 

Many of these pathways are interdependent, can cross-react (e.g., “feed-forward” and amplify each other) with considerable overlap, and underlying susceptibility and other baseline risk factors may be required to unmask disease.  

Some pathways have more relevance to short-term exposures (e.g., autonomic imbalance, heightened thrombosis potential) and likely factor most in a triggering role. Others likely play a more long-term role. 

But what are the primary initiating pathways of secondary effects? Among the three primary initiating pathways are:

• Oxidative stress
• Direct translocation, or effects of particles and secondary mediators formed in response to air pollution effects that may then mediate systemic effects. 

Of note, neural reflexes triggered by the sensing of inhaled particles in the lungs by various receptors (perhaps without a prerequisite for the generation of oxidative stress) may also be considered important. For a more thorough discussion of each of these triggers, see Rajagopalan s. et al.  

PLEASE NOTE: The ACOI 2024 Annual Convention will have two speakers on Climate and Health. I will be presenting on prioritizing health in a changing climate, and MarkAlain Déry, DO, MPH, FACOI will address the impact of climate change on the proliferation of infectious diseases.

References:  

Badger M. The Intersection of Geriatrics, Climate Change, and Wilderness Medicine: Education is Critical. Wilderness and Environmental Medicine. 2024. DOI: 10.1177/10806032241245399.

Bourdrel et al. Cardiovascular Effects of Air Pollution. Archives of Cardiovascular Disease: 2017; 110; 634-642.

Million Hearts and Climate campaign- https://millionhearts.hhs.gov/about-million-hearts/building-communities/climate-change-ccc.html

Rajagopalan s. et al. JAmCardiol. 2018; 72(17):2054-70

Note: The views expressed in this article are the author’s own and do not necessarily represent the views of ACOI.