Clinical Focus Review Jerrold H. Levy, M.D., F.A.H.A., F.C.C.M.

, Editor

Impact of Wildfire Smoke on Acute Illness

Fintan Hughes, M.B.B.Ch., B.A.O., Luke Parsons, Ph.D., Jerrold H. Levy, M.D., F.A.H.A., F.C.C.M., Drew Shindell, Ph.D.,
Brooke Alhanti, Ph.D., Tetsu Ohnuma, M.D., Ph.D., M.P.H., Prasad Kasibhatla, Ph.D., Hugh Montgomery, O.B.E., M.D.,
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Vijay Krishnamoorthy, M.D., M.P.H., Ph.D.

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H ealthcare professionals need to better understand

the health impacts of a warming planet. The fre-
quency and severity of extreme weather events (and
Wildfire smoke elicits oxidative stress and inflammatory
responses,9 and a significant mortality impact results from
short-term increases in PM exposure.10 Additionally, cer-
their health impacts) are rising (e.g., heatwaves, droughts, tain sociodemographic groups (e.g., young, elderly, obese,
floods, storms). So, too, are the frequency and severity and pregnant persons and those with preexisting cardio-
of wildfires. For example, Australia’s “Black Summer” pulmonary disease or of low socioeconomic status) are at
fires in 2019 and 2020 were estimated to be 30% more greater risk than others.11,12 In the United States, approxi-
likely due to human-caused increases in global surface mately 52% of all 24-h mean PM2.5 levels greater than 35
temperatures.1,2 Globally, 61% of countries experienced μg/m3 result from wildfire smoke exposure.13 Between
increased wildfires during 2018 to 2021 compared 2008 and 2012, 10.3 million U.S. residents were exposed
to 2001 to 2004, causing an additional 9.17 million to more than 10 days of wildfire smoke–induced pollution
person-days of smoke exposure annually.3 Despite this above the World Health Organization’s 24-h mean PM2.5
growing public health risk, data on its perioperative threshold of 25 μg/m3.14 Communities close to wildfires
impacts are lacking, as are guidelines on the manage- have even documented hourly PM2.5 concentrations as high
ment of exposed patients. as 6,106 μg/m3 and daily concentrations of 394 μg/m3.15,16
Air pollution from combustion contains fine particulate Such wildfire smoke is known to spread over large geo-
matter (PM) that is typically composed of carbon, sulfur, graphic regions; even populations thousands of miles down-
and nitrogen compounds. Exposure to this PM causes more wind of the fires have experienced health impacts.5,6 Given
death and disability worldwide than alcohol use, high- the broad cardio-respiratory impacts of wildfire smoke, it is
sodium diets, or fasting hyperglycemia.4 Consequently, the likely that a significant unmeasured impact on perioperative
World Health Organization (Geneva, Switzerland) recom- and critical care morbidity is being caused by smoke expo-
mends that exposure to mean 24-h concentrations of PM sure. Unrecognized subclinical exposure to smoke from dis-
with a diameter of 2.5 μm or less (PM2.5) not exceed 25 tant wildfires could play a role in the development of major
μg/m3. Wildfire smoke composition is influenced by the adverse cardiac events or postoperative respiratory com-
fire area, intensity, and materials burned. In addition to PM, promise. The increased obstetric risk affects mothers and
it contains gases, including carbon dioxide, sulfur dioxide, is then conferred to newborns through prematurity and
nitric oxide, ozone, polycyclic aromatic hydrocarbons, and low birth weight, with long-lasting health consequences,
volatile organic compounds (e.g., aldehydes and alkanes).5–7 including increased perioperative risk among those chil-
The latter elements may make wildfire smoke inhalation dren. As population exposure to wildfire smoke increases,
even more harmful than fossil fuel–derived PM. Further, there is a need for development of perioperative protocols
polyaromatic hydrocarbon components may be carcino- to guide the management of patients with overt or subclin-
genic in the long term.8 ical wildfire smoke exposure.

This article has been selected for the Anesthesiology CME Program (www.asahq.org/JCME2024OCT). Learning objectives and disclosure and ordering information can be found in
the CME section at the front of this issue. Peter Nagele, M.D., M.Sc., served as Handling Editor for this article.
Submitted for publication October 15, 2023. Accepted for publication June 4, 2024. Published online first on August 6, 2024.
Fintan Hughes, M.B.B.Ch., B.A.O.: Department of Anesthesiology, Duke University School of Medicine, Durham, North Carolina.
Luke Parsons, Ph.D.: Global Science, Nature Conservancy and Nicholas School of the Environment, Duke University, Durham, North Carolina.
Jerrold H. Levy, M.D., F.A.H.A., F.C.C.M.: Departments of Anesthesiology and Surgery (Cardiothoracic), Duke University School of Medicine, Durham, North Carolina.
Drew Shindell, Ph.D.: Nicholas School of the Environment, Duke University, Durham, North Carolina.
Brooke Alhanti, Ph.D.: Duke Clinical Research Institute, Duke University, Durham, North Carolina.
Tetsu Ohnuma, M.D., Ph.D., M.P.H.: Department of Anesthesiology, Duke University School of Medicine, Durham, North Carolina.
Prasad Kasibhatla, Ph.D.: Nicholas School of the Environment, Duke University, Durham, North Carolina.
Hugh Montgomery, O.B.E., M.D.: Department of Intensive Care Medicine, University College London, London, United Kingdom.
Vijay Krishnamoorthy, M.D., M.P.H., Ph.D.: Department of Anesthesiology, Duke University School of Medicine, Durham, North Carolina.
Copyright © 2024 American Society of Anesthesiologists. All Rights Reserved. Anesthesiology 2024; 141:779–89. DOI: 10.1097/ALN.0000000000005115

A nesthesiology, V 141 • NO 4 October 2024 779

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<zdoi;10.1097/ALN.0000000000005115>
 Clinical Focus Review

Mechanisms of Health Impacts reduced among healthy middle-aged subjects in response

to controlled exposure to both fine (PM2.5) and ultrafine
Once inhaled, wildfire smoke PM directly stimulates airway
PM (0.1 μm, or PM0.1).23,24
and alveolar inflammation. Beyond these directly exposed
tissues, wildfire smoke impacts organs through three pri-
mary mechanisms: autonomic dysregulation, a cascade
Inflammation and Oxidative Stress
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of inflammation and oxidative stress (from the pulmo- Wood smoke exposure causes inflammation of the pulmo-
nary vasculature), and direct translocation of PM into the nary and systemic vascular endothelium, lipid peroxidation,
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bloodstream. Collectively, this exposure results in systemic and systemic oxidative stress. Wildfire smoke (especially
inflammation, platelet activation, and endothelial dysfunc- through its metallic components) induces oxidative stress
tion (fig. 1). through redox cycling mechanisms25 and triggers a vast
inflammatory response in the pulmonary circulation, which
Autonomic Dysfunction and Hypertension initiates a systemic inflammatory response resulting in
end-organ damage (table 1).
Inhalation of PM stimulates respiratory C-nerve fibers
and rapidly adapting pulmonary receptors in the bron-
chial tree, resulting in vagal afferent signaling. This
Translocation into the Bloodstream
increase in parasympathetic tone is contrasted by a sim- Fire-derived PM (especially ultrafine particulate matter,
ilarly associated reduction in carotid baroreceptors’ sen- or PM0.1) and gases cross the alveolar–capillary membrane
sitivity.17,18 The overall result appears to be sympathetic to enter the bloodstream and reach the heart, peripheral
stimulation, with increased circulating concentrations of vessels, and other organs, where they induce endothelial
noradrenaline, renin, angiotensin II, and aldosterone.19 activation and platelet aggregation.34 Metallic PM compo-
Adults exposed to either ambient wildfire or wood nents stimulate platelet activation and aggregation.35 Such
smoke in a laboratory setting experience significant and effects are accompanied by a fibrinolytic response char-
reproducible increases in blood pressure.20 Even tran- acterized by increased plasminogen activator inhibitor-
sient PM2.5 exposure increases systolic, diastolic, and 1 and decreased tissue plasminogen activator. When
mean blood pressure for 12 h or more.20,21 Long-term combined with endothelial cell damage, a prothrom-
PM exposure is associated with a 41% increased risk botic state is promoted. In a laboratory setting, NADPH
of hypertension.22 Additionally, heart rate variability is oxidase inhibitors alleviated PM2.5-induced endothelial

Fig. 1. The mechanisms by which wildfire smoke inhalation causes systemic health impacts. IL, interleukin; TNF-α, tumor necrosis factor-α;
TLR, Toll-like receptor. Created with BioRender.com.

780 A nesthesiology 2024; 141:779–89 Hughes et al.

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 Wildfires and Perioperative Health Impacts

dysfunction.27 Merely 3 h of exposure to wood smoke ventricular dysfunction and right atrial stretch, causing
increases circulating concentrations of endothelial intra-atrial conduction abnormalities.58
adhesion molecules, intracellular adhesion molecule-
1, and vascular cell adhesion molecule-1 in healthy Heart Failure. Through high sympathetic tone, systemic
adults,30 while its gaseous components induce a pro- inflammation, and endothelial injury, wildfire smoke
atherosclerotic vascular response.36
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may drive myocardial injury, resulting in decompensa-

tion of existing heart failure. Both pulmonary artery
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pressures and right ventricular afterload are increased

Specific Disease Processes
by exposure to ambient PM, while increased arterial
Cardiovascular Disease vasoconstriction elevates left ventricular afterload.
When combined with PM-induced blunting of urinary
Myocardial Infarction. The impact of PM on cardiovascu-
sodium excretion, wildfire smoke markedly increases
lar disease is well established37 (table 2). The combination
the demand on a failing heart and can precipitate
of endothelial injury, platelet activation, and coagulation
decompensation.59–62
increases the risk of acute coronary syndromes. Similarly,
elevations in sympathetic tone and systemic inflammation
Stroke. Stroke is the second-leading cause of death and the
increase the risk of myocardial infarction. This association
third-leading cause of disability worldwide. PM-induced
between the incidence of myocardial infarction and PM
hypertension, atrial fibrillation, platelet aggregation, and
concentration has been described across age ranges and
oxidative stress increase stroke risk.63 Ambient PM ranks
geographies.53–55 Similarly, PM concentrations greater than
fourth among 19 stroke risk factors summarized by the
8 μg/m3 resulting from forest fires increase cardiovascular
Global Burden of Diseases Study in 2019.64
mortality.56

Arrhythmias. Driven by circulating inflammatory cytokines, Insulin Resistance. PM exposure is associated with insulin
oxidative stress, and increased sympathetic tone, short- resistance and impaired pancreatic β-cell function, major
term increases in PM concentrations raise the risk of new- risk factors for cardiac disease. With a 2-month lag, lower
onset atrial fibrillation.56,57 Over a longer time, PM-induced insulin sensitivity and higher fasting glucose concentrations
inflammatory fibrosis, progressive atrial remodeling, were observed after high PM exposure in 1,000 Mexican-
and increased pulmonary artery pressures lead to right American patients.65 In Eastern China, short-term PM

Table 1. Oxidative Stress and Inflammatory Response to Particulate Matter Exposure

Cell Type or Biochemical

Exposure Population Molecule Effect Significance

Wood smoke26 Isolated pulmonary Superoxide dismutase 1 Upregulation Antioxidant enzyme and heat shock protein that upregulate in
vascular endothelium Heme oxygenase 1 Upregulation response to high levels of oxidative stress
PM2.527 Human umbilical vein Endothelin-1 Activation Demonstrative of endothelial dysregulation; inducing processes
endothelial cells NADPH oxidase Upregulation of vasoconstriction, oxidative stress, thrombogenesis, and
Protein kinase B/ endothelial Increase atherosclerosis
nitric oxide synthase pathway
Inducible nitric oxide synthase Increase
Asymmetric dimethylarginine Increase
Wood smoke28 Human monocytes Tumor necrosis factor-α Increase Cytokines that upregulate inflammation through the innate
Interleukin-1b Increase immune response
Interleukin-8 Increase
PM1029 Alveolar macrophages and Toll-like receptors 2–4 Expression and Activation leads to phagocytosis and immunomodulation in
airway epithelial cells activation macrophages, and mast cell activation
Wood smoke30 Healthy volunteers Intracellular adhesion molecule 1 No change Cellular adhesion molecules and cytokines involved in innate and
L-selectin adaptive immune responses
Interleukins 6 and 8
Occupational Healthy firefighters 8-Isoprostane Increase Marker of lipid peroxidation in oxidative stress
wood smoke31
Occupational Healthy firefighters Sputum granulocytes Increase Markers of acute inflammation
wildfire Circulating white blood cells Increase
smoke32 Circulating band cells Increase
PM2.533 Healthy volunteers Clara cell protein Increase Marker of lung epithelial injury

PM, particulate matter; PM2.5, particulate matter with a diameter of 2.5 μm or less; PM10, particulate matter with a diameter of 10 μm or less.

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 Clinical Focus Review

Table 2. Selected Studies Investigating Clinical Impacts of Wildfire Smoke and Particulate Matter Exposure

Disease Process Region Date Population Effect Size for PM2.5 Exposure

Myocardial infarction38 International 2001–2018 2,250,473 patients RR, 1.02 (95% CI, 1.01–1.03) per 10 μg/m3
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meta-analysis
Atrial fibrillation39 Beijing, China 2013–2014 100 patients RR, 1.038 (95% CI, 1.014–1.062) per 10 μg/m3
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Atrial fibrillation40 Yancheng, China 2015–2020 15,171 inpatients RR, 1.028 (95% CI, 1.013–1.042) per 10 μg/m3
Atrial fibrillation41 Seoul, South 2007–2015 1137 emergency depart- RR, 1.045 (95% CI, 1.002–1.089) per 10 μg/m3
Korea ment visits
Cardiac arrhythmia42 South Korea 2002–2016 178,780 men OR, 1.27 (95% CI, 1.15–1.40) per 10 μg/m3
Heart failure43 International 1981–2005 1,520,099 hospital Attributable risk, 2.1% (admission)
meta-analysis encounters Attributable risk, 1.6% (mortality)
Ischemic stroke44 China 2013–2017 117,338,867 hospital 0.20% per 10 μg/m3
admissions
Transient ischemic attack44 China 2013–2017 117,338,867 hospital 0.33% per 10 μg/m3
admissions
Ischemic stroke45 Beijing, China 2014–2018 315,499 admissions 0.22% (95% CI, 0.12–0.33%) per 10 μg/m3
Deep vein thrombosis46 USA 2000–2008 435,413 admissions 0.68% per 10 µg/m3
Pulmonary embolism46 USA 2000–2008 435,413 admissions 0.59% per 10 µg/m3
Asthma47 Colorado, USA 2011–2014 446,106 emergency OR, 1.081 (95% CI, 1.058–1.105) per 1 μg/m3*
department admission
Combined respiratory Colorado, USA 2011–2014 446,106 emergency OR, 1.021 (95% CI, 1.012–1.031) per 1 μg/m3*
disease47 department admission
Asthma48 Oregon, USA 5-month fire season in 2013 2,490 patients OR, 1.089 (95% CI, 1.043–1.136) per 10 µg/m3*
Asthma49 California, USA 2008 102,311 patients RR, 1.07 (95% CI, 1.05–1.10) per 5 µg/m3 (hospital
admission)
RR, 1.06 (95% CI, 1.05–1.07) per 5 µg/m3 (ED presentation)
Asthma50 New South Wales, 1994–2007 3,141,017 admissions OR, 1.12 (95% CI, 1.05–1.19) when PM > 99th percentile
Australia
COPD50 New South Wales, 1994–2007 3,141,017 admissions OR, 1.13 (95% CI, 1.05–1.22) when PM > 99th percentile
Australia
Asthma51 California, USA 2003 40,856 admissions OR, 1.34 (95% CI, 1.13–1.57) during smoke exposure
COPD mortality52 Washington state, 2006–2017 170,965 deaths OR, 1.14 (95% CI, 1.02–1.26) when PM > 20.4
USA
All-cause respiratory mor- Washington state, 2006–2017 170,965 deaths OR, 1.35 (95% CI, 1.09–1.67) when PM > 20.4
tality (ages 45–64 yr)52 USA
*Wildfire-specific.
COPD, chronic obstructive pulmonary disease; OR, odds ratio; PM, particulate matter; PM2.5, particulate matter with a diameter of 2.5 μm or less; RR, relative risk.

exposure positively correlated with increased fasting blood increased by 85% in richer counties but by 124% in poor
glucose, especially in patients older than 65 yr.66 counties.69

Respiratory Disease Obstetric and Neonatal Risk

Wildfire smoke causes lung inflammation, with alveolar Black carbon, a component of PM2.5, translocates into
macrophages and monocytes mounting a local immune the systemic circulation and deposits in placental tissue.
response, resulting in direct tissue damage, impaired gas A two-photon microscopy study assessing black carbon
exchange, and airway irritation. Increases in both emer- load in placental villous tissue demonstrated that the pla-
gency department presentations and hospital admissions cental barrier is permeable to air pollution components,
for asthma and chronic obstructive pulmonary disease which would allow pollution to reach the fetal circula-
result from exposure (table 2). Generally, finer particles tion.70 There is concern that the same processes of inflam-
are more toxic than coarser particles, and wildfire PM mation, oxidative stress, and endothelial dysfunction
appears more toxic than urban PM.67 Between 2013 and may also affect the maternal–fetal unit. Evidence sug-
2018 in Nevada, wildfire smoke resulted in a 6.1% higher gests a dose-dependent placental inflammatory response
incidence of asthma presentations compared to similar lev- to wildfire smoke exposure.71 Placental inflammation is
els of PM originating from nonwildfire sources.68 These strongly associated with preeclampsia and adverse birth
effects are also modified by social factors. For example, outcomes, including preterm birth, low birth weight,
North Carolina asthma emergency department visits strat- and neonatal morbidity72–74 (table 3). Likewise, oxidative
ified by socioeconomic status show that per 100 μg/m3 of stress–induced vascular and endothelial dysfunction are
peat smoke PM2.5 exposure, emergency department visits associated with preterm birth, hypertensive disorders of

782 A nesthesiology 2024; 141:779–89 Hughes et al.

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 Wildfires and Perioperative Health Impacts

pregnancy, preeclampsia, and restricted fetal growth.87 In acetate exposure associated with electronic cigarette use
rabbit models, exposure to PM from fossil fuel combus- is mechanistically different from PM exposure, periopera-
tion decreased placental blood flow and increased umbili- tive guidelines on electronic cigarette smoke exposure may
cal artery resistance.88 form a useful starting point. Guidelines recommend that
PM exposure may also impact endocrine signaling; in patients are screened preoperatively for electronic cigarette
the second trimester, exposure among 222 mother–new- smoke exposure and recommend focused investigations
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born pairs was associated with differences in the cord blood for health impacts when the exposure is suspected.96 Such
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metabolites derived from the lipoxygenase pathways. These an approach could be taken in relation to wildfire smoke,
are key regulatory hormones for fetal metabolism and labor screening patients for risk of exposure based on their loca-
progression.89 Premature birth negatively impacts health tion. Passive cigarette smoke exposure has been associated
throughout a patient’s life,90 and wildfire smoke exposure is with increased acute respiratory distress syndrome develop-
consistently associated with increased rates of preterm birth. ment in septic patients.97 Similarly, pediatric patients with
A dose-dependent decrease in birth weight is observed chronic cigarette smoke exposure demonstrate increased
with respect to proximity to wildfires and the severity of rates of coughing, laryngospasm, and hypoxia when under-
smoke exposure. In vitro experimentation also shows that going procedural sedation.98 Linking wildfire smoke expo-
organogenesis, as well as migration and differentiation of sure data to perioperative outcomes datasets will likely
neural crest cells, are sensitive to oxidative stress.91 elucidate this relationship. Linking critical care outcome
registries or intensive care unit admissions datasets to
Pediatric Populations smoke exposure data will be helpful to identify the pro-
portion of patients whose critical illness is exacerbated by
Children are particularly vulnerable to PM pollution due
PM exposure.
to increased minute ventilation relative to body mass and
reduced efficiency of nasopharyngeal particle deposition.
This unique physiology results in a higher proportion of Wildfire-specific Smoke
particles reaching lung tissue92 (table 3). Since the mid- Many existing studies have determined exposure using total
1990s, pediatric asthma presentations have been shown to measured PM concentration, with some combining satellite
increase during wildfire smoke exposure.93 Furthermore, images of smoke clouds or seasonal smoke patterns to attri-
fire-derived ozone emissions account for more than 2,000 bute this measured PM to wildfire sources. Modern chemi-
annual pediatric emergency department visits for asthma in cal transport models allow the impacts of wildfire PM to be
the United States.94 studied in isolation.

Discussion Low-income Countries

A host of negative cardiopulmonary, obstetric, and neonatal Many of these existing data originate from relatively
outcomes result from wildfire smoke exposure, driving a high-income countries. A substantial portion of global
greater burden of comorbidities in the perioperative pop- wildfire smoke exposure occurs in Sub-Saharan Africa and
ulation. In addition, recent wildfire smoke exposure may South Asia, where access to healthcare and healthcare data
directly increase perioperative risk: adverse respiratory is limited. Data collected in low-resource settings would be
events affected 37% of children with a past medical history highly valuable in producing better estimates of the true
of reactive airway disease during healthy air periods but global burden of wildfire smoke impact.
affected 55% during periods with unhealthy air (1.50 [1.04
to 2.17]; P = 0.032).95 This finding may well represent just Nonlinear Modeling of High Smoke Concentrations
the tip of the iceberg, with wildfire smoke exposure being
Studies typically have included linear models reporting the
responsible for a significant perioperative morbidity burden.
odds ratio or relative risk of developing a clinical endpoint
Several key knowledge gaps are currently hampering our
for a given change in PM concentration, typically 1 or 10
understanding of this perioperative risk factor.
μg/m3. PM concentrations can exceed 500 μg/m3 in regions
close to fires, and it is not known whether the exposure–
Knowledge Gaps response function is linear at these concentrations. Studies
that explore the nonlinear effects of smoke exposure would
Broader Perioperative Impacts allow for more complete estimates of current and future
Data pertaining to perioperative risk from wildfires are health impacts. Developing such an exposure response
sparse. The Californian data from Marsh et al.95 were the function will allow health systems to prepare for future
first of their kind to bring this risk to light with a spe- impacts while providing vital data to guide policy decisions.
cific focus on pediatric respiratory complications. Given the Likewise, impacts of dynamic responses need to be studied
paucity of perioperative data, some insight may be gained (i.e., might a sudden but small rise be more acutely harmful
from tobacco literature. While the harm from vitamin E than a sustained higher concentration of toxicants?)

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784
Table 3. Selected Studies Investigating Obstetric, Neonatal, and Pediatric Impacts of Wildfire Smoke, and Particulate Matter Exposure

Clinical Endpoint Exposure Region Date Population Effect Size

Gestational hypertension75 Mean PM2.5 across all three trimesters Colorado, USA 2007–2015 535,895 OR, 1.204 (95% CI, 1.083–1.339) per 1 μg/m3
Preeclampsia76 Mean PM2.5 during weeks 10–14 of gestation Southern Israel 2004–2016 133,197 HR, 1.04 (95% CI, 1.00–1.09) per 10 μg/m3
Preeclampsia76 Mean PM2.5 during first 25 weeks’ gestation Southern Israel 2004–2016 133,197 HR, 2.08 (95% CI, 1.10–3.94) per 10 μg/m3
Premature birth (<37 weeks)75 Mean PM2.5 during the second trimester Colorado, USA 2007–2015 535,895 OR, 1.13 (95% CI, 1.09–1.18) per 1 μg/m3
Clinical Focus Review

Premature birth (<37 weeks)77 Days of wildfire smoke during second trimester California, USA 2006–2012 3,002,014 0.83% increase in risk per day
Premature birth (<37 weeks)77 Days of wildfire smoke during third trimester California, USA 2006–2012 3,002,014 0.68% increase in risk per day
Premature birth (<37 weeks)77 Days of wildfire smoke during entire pregnancy California, USA 2006–2012 3,002,014 0.49% increase in risk per day
Premature birth (<37 weeks)78 Smoke exposure from Camp Fire event California, USA 2018 68,006 RR, 1.25 (95% CI, 1.22–1.28) per 1 μg/m3
Premature birth (<37 weeks)79 Exposure to wildfire smoke wave during first trimester Brazil 2001–2018 190,911 OR, 1.41 (95% CI, 1.31–1.51)
Premature birth (20–27 weeks)80 For 3 months following severe bushfires Victoria, Australia 2009 73,831 50% increase
Premature birth (<37 weeks)81 PM2.5 during entire pregnancy Canada 2005–2012 818,400 OR, 1.04 (95% CI, 1.024–1.056) per interquartile range
Birth weight75 Mean PM2.5 across all three trimesters Colorado, USA 2007–2015 535,895 –5.7g per 1 ug/m3 PM2.5
Birth weight82 Exposure to smoke plume Colorado, USA 2007–2013 135,676 3.8% lower
Birth weight <2,500 g82 Exposure to smoke plume Colorado, USA 2007–2013 135,676 3.4% increased incidence
Birth weight <2,500 g83 Mean PM2.5 during first trimester Brazil 2001–2018 1,602,417 18.6% increased incidence
Birth weight <500 g80 For 3 months following severe bushfires Victoria, Australia 2009 73,831 50% increased incidence
Congenital heart disease84 Mean PM2.5 during the second month of pregnancy Wuhan, China 2011–2013 105,988 OR, 1.10 (95% CI, 1.03–1.18) per 10 μg/m3
Gastroschisis85 Second trimester wildfire smoke exposure California, USA 2007–2010 844,384 RR, 1.28 (95% CI, 1.07–1.54)
Gastroschisis85 Third trimester wildfire smoke exposure California, USA 2007–2010 844,384 RR, 2.17 (95% CI, 1.42–3.52)
Pediatric emergency department presentation for Wildfire-exposed zip codes San Diego, USA 2007 25,992 RR, 1.34 (95% CI, 1.18–1.52)
respiratory conditions86
Pediatric emergency department presentation for Wildfire-exposed zip codes San Diego, USA 2007 25,992 RR, 2.12 (95% CI, 1.57–2.86)
asthma86
Pediatric perioperative adverse respiratory events95 Elective surgery during periods of wildfire smoke exposure California, USA 2018 625 RR, 1.5 (95% CI, 1.03–2.17)

A nesthesiology 2024; 141:779–89

HR, hazard ratio; OR, odds ratio; PM, particulate matter; PM2.5, particulate matter with a diameter of 2.5 μm or less; RR, relative risk.

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Hughes et al.
 Wildfires and Perioperative Health Impacts

Perioperative Needs Conclusions

The health impact of wildfire smoke is just one symptom
Guidelines for Acute and Subclinical Exposure of a far broader systemic problem in the human ecosystem.
Although a broad array of pathophysiologic mechanisms Through changes in surface temperatures, rainfall patterns,
of smoke exposure has been described, it is challenging wind speed, and relative humidity, the adverse effects of
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to identify a targeted intervention for exposed individu- wildfires will increase as we continue warming the planet
als, and thus there are no established treatments or prac- through the combustion of fossil fuels (e.g., gasoline, natural
0hCywCX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC1y0abggQZXdgGj2MwlZLeI= on 04/23/2025

tice guidelines. No randomized controlled trials have gas, oil, coal, and diesel).As leaders in the perioperative space
investigated treatment of PM or wildfire smoke expo- (the most carbon-intensive area of healthcare), anesthesiol-
sure. Instead, care is typically supportive and defined by ogists can lead the charge in rapidly reducing healthcare-
the presenting pathology. Emergency medicine guide- related greenhouse gas emissions and those across society.
lines do exist regarding smoke inhalation but are not spe- Moreover, the healthcare industry has a global market more
cific to wildfires. These guidelines focus on supportive than three times the value of the fossil fuel industry. If lever-
respiratory care with high-flow oxygen and bronchodi- aged effectively through coordinated action, the economic
lators as needed, testing for carbon monoxide toxicity, might of the healthcare community and academic institu-
and administration of thromboprophylaxis. Perioperative tions could reduce future damage to human health caused
wildfire smoke exposure protocols should consider the by the continued use of fossil fuels. As the window to limit
need for additional thromboprophylaxis, the need for global warming to 1.5° or 2°C closes, clinicians should act
antihypertensives in the acute setting, the role of addi- urgently and decisively to safeguard human health.
tional hemodynamic monitoring among those with
heart failure, the role of bronchodilators or other airway Research Support
clearance interventions, and risk stratification for obstet-
ric patients. Dr. Montgomery is partly funded through the United
Kingdom National Institute for Health Research’s
Procedure Timing to Mitigate Risk Comprehensive Biomedical Research Center at University
College London Hospitals (London, United Kingdom).
Modern weather forecasting allows for accurate smoke
This work was funded by a grant from Duke University
plume spread prediction, which facilitates targeted air
(Durham, North Carolina).
pollution warning systems. If research reveals increased
perioperative complications after smoke exposure, then
changes could be made in the scheduling of surgical cases Competing Interests
in high-risk patients at times of high smoke exposure. Dr. Montgomery is cochair of the Lancet Countdown
Reactive airway disease or obstructive lung diseases typi- on Health and Climate Change and is a member of other
cally present on lag days 0 to 2.47 Hypertension develops organizations that address this issue. Dr. Montgomery is
within hours and can resolve after 12 h.63 Downstream cofounder of a nonprofit company to help decarbonize
cardiac effects are variable in timing and peak between healthcare. Dr. Shindell is a consultant for the Institute for
days 0 and 6 across different studies.38 These risk peaks Governance and Sustainable Development. Dr. Levy has
typically span 1 day, and in the few studies that employ received funding from Merck, Octapharma, and Werfen
longer time series, the effects were not significant during unrelated to this work. The other authors declare no com-
a 7-day window. While some patients present at lag day 0, peting interests.
within hours of smoke exposure, others will present sev-
eral days into the exposure. As a period of PM exposure Correspondence
persists, the risk of health impacts increases. Beyond day
Address correspondence to Dr. Krishnamoorthy: vijay.
15, the exposure response curves for cardiovascular and
[email protected]
respiratory admissions become nonlinear and appear to
plateau.99 During periods of heavy smoke, high hourly
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