Impact of Wildfires on Cardiovascular Health

Abstract

Wildfire smoke (WFS) is a mixture of respirable particulate matter, environmental gases, and other hazardous pollutants that originate from the unplanned burning of arid vegetation during wildfires. The increasing size and frequency of recent wildfires has escalated public and occupational health concerns regarding WFS inhalation, by either individuals living nearby and downstream an active fire or wildland firefighters and other workers that face unavoidable exposure because of their profession. In this review, we first synthesize current evidence from environmental, controlled, and interventional human exposure studies, to highlight positive associations between WFS inhalation and cardiovascular morbidity and mortality. Motivated by these findings, we discuss preventative measures and suggest interventions to mitigate the cardiovascular impact of wildfires. We then review animal and cell exposure studies to call attention on the pathophysiological processes that support the deterioration of cardiovascular tissues and organs in response to WFS inhalation. Acknowledging the challenges of integrating evidence across independent sources, we contextualize laboratory-scale exposure approaches according to the biological processes that they model and offer suggestions for ensuring relevance to the human condition. Noting that wildfires are significant contributors to ambient air pollution, we compare the biological responses triggered by WFS to those of other harmful pollutants. We also review evidence for how WFS inhalation may trigger mechanisms that have been proposed as mediators of adverse cardiovascular effects upon exposure to air pollution. We finally conclude by highlighting research areas that demand further consideration. Overall, we aspire for this work to serve as a catalyst for regulatory initiatives to mitigate the adverse cardiovascular effects of WFS inhalation in the community and alleviate the occupational risk in wildland firefighters.

Keywords: epidemiological studies; in vitro techniques; models, animal; occupational health; public health; smoke inhalation injury.

Figure 1.. The inhalation of intricate wildfire emissions triggers cardiovascular responses of significance for both public and occupational health.

Wildfire emissions depend on fuel and combustion type but typically comprise particulate matter (segregated by size in ${PM}_{2.5}$, ${PM}_4$and ${PM}_{10}$), organic compounds (n-alkanes, aldehydes, polycyclic aromatic hydrocarbons or $PAHs$, methoxyphenols, levoglucosan), inorganic elements, and environmental gases. Exposure to wildfire smoke (WFS) raises concerns for both public and occupational health. WFS inhalation elicit responses in the autonomic nervous, respiratory, and cardiovascular systems that may either indirectly or directly impact cardiovascular function. Proposed cellular, molecular, and tissue mechanisms of action include: (1) Dysregulated autonomic control of cardiovascular homeostasis, (2) Spillover of signaling mediators into the bloodstream (3) $PM$ translocation into the bloodstream through alveolar-capillary interface. HRV, heart rate variability. BRS, baroreceptor reflex sensitivity. EV, extracellular vesicles.

Figure 2.. Epidemiological evidence generally associates instances of cardiovascular disease with air quality measurements.

Visual summary of positive (red) and null (blue) associations between clinical diagnosis of cardiovascular morbidity and mortality and either specific constituents of wildfire smoke (WFS, A) or the day when they manifest following a wildfire event (B). Color intensity increases with the number of environmental exposure studies that discuss each association or lack thereof. Data synthesized in figure from references (^{,,,,–,–,–,–}). Each row in the associations matrices either groups specific ICD codes (I00-I09: rheumatic heart disease, I10-I1A: hypertensive disease, I20-I25: ischemic heart disease, I26-I28: pulmonary vascular disease, I30-I5A: other forms of heart disease, I60-I69: cerebrovascular disease, I70-I99: diseases of the circulatory system), refers to out of hospital cardiac arrests (OHCA), or reports mortality. Columns in A are assigned to different components of wildfire smoke (particulate matter with diameter <2.5 μm: ${PM}_{2.5}$, particulate matter with diameter <10 μm: ${PM}_{10}$, black carbon: BC, carbon monoxide: $CO$, ozone: $O_3$, nitrogen dioxide: ${NO}_2$, sulfur dioxide: ${SO}_2$), temperature, and humidity. Columns in B represent the number of days since the wildfire event.

Figure 3.. Alternative study designs for in vivo and in vitro wildfire smoke (WFS) exposure.

Tight control over the experimental parameters facilitates the interpretation of cellular and tissue responses to exposure injury. Environmental WFS or lab-scale WFS generated from the combustion of wood may serve as stimuli for in vivo and in vitro models, as a whole or following isolation of $PM$. Additionally, serum from exposed animals may be added to the cell culture medium to capture circulating mediators of biological responses. Cell culture strategies include submerged endothelial cultures, submerged co-cultures of ALI-differentiated epithelial and endothelial cells, and co-cultures of ALI epithelial and submerged endothelial cells. Extracted $PM$ is deployed to mice via oropharyngeal aspiration. Exposure towers deliver lab-scale WFS to the mice, or animals may be housed in the environment nearby an active wildfire. ALI: air-liquid interface.