Campfire Smoke as a Plausible Trigger for Vasospastic Angina: Insights From a Case Report

Introduction

Vasospastic angina (VSA), also known as variant angina or Prinzmetal angina, is characterized by sudden chest pain due to coronary artery vasospasms, leading to a transient reduced coronary perfusion [1]. The prevalence of VSA remains inadequately characterized [2]. This condition is underdiagnosed, and it can occur in patients with or without coronary atherosclerosis [3].

The diagnosis includes nitrate-responsive chest pain, transient ischemic changes on electrocardiogram (ECG), and angiographic evidence of a coronary artery spasm [2]. VSA is also associated with serious adverse events, including myocardial infarction, arrhythmia, and death [4,5]. Management of VSA involves the use of vasodilator medications, as well as the identification and avoidance of known triggers [2]. Risk factors of VSA include tobacco smoking [6–9], migraine, and Raynaud’s phenomenon [10,11]. Various other factors may contribute as triggers VSA, such as mental stress [12], allergies [13], magnesium deficiency [14], alcohol consumption [15], recreational drugs (eg, amphetamine, cocaine, marijuana), and certain medications such as beta-blockers, ergot alkaloids [3,16], and immune checkpoint inhibitors [17]. Several studies reported associations between angina pectoris and exposure to particulate matter (PM2.5 or 10) [18–21]. However, there is a lack of studies specifically investigating VSA and air pollution [22,23]. To our knowledge, no case report describes VSA potentially triggered by exposure to campfire smoke. This report describes the case of 45-year-old man who developed chest pain following exposure to campfire smoke, with subsequent clinical evaluation leading to a diagnosis of VSA.

Case Report

A 45-year-old White man presented with frequent episodes of chest pain at rest. He was known to have eczema, dyslipidemia, and occasional gastroesophageal reflux. He reported a history of viral meningitis at the age of 4 years. He was also a heterozygous carrier of the PABN1 oculopharyngeal muscular dystrophy gene. He was not known to have migraine issues or any anxiety disorder. He had smoked cigarettes at approximately 7 pack-years between the ages of 14 to 22, when he stopped smoking altogether. He consumed approximately 1 to 2 glasses of alcohol per day since 2001 and did not use drugs. An environmental allergy to Gramineae was confirmed in adulthood by skin prick testing. He also has a history of food allergies (fish and shellfish) diagnosed in childhood, which have not been re-evaluated in adulthood. Apart from occasional use of Cetirizine per os for seasonal allergies, he was not taking any other medications or natural products. The patient’s mother had oculopharyngeal muscular dystrophy, and his father had Raynaud’s disease. Both of his parents had coronary artery disease. His paternal grandfather had scleroderma. His maternal grandfather had arrhythmia, and he died at the age of 75 following a pacemaker malfunction. The patient lived in an urban center and worked at home. He resided close to a highway in a house dating from the late 1800s, which had been completely renovated over 5 years ago. There was no history of water damage in his home. His house was heated by electricity, and was without a fireplace. Two air exchangers with HEPA filters were installed in his home. The filters were regularly changed. The floors were covered in wood or concrete, with no carpet. The patient had no pets.

The patient’s chest pain began in September 2022 following a weekend stay of 3 days in a campground in the national park of Mont-Tremblant (Quebec, Canada) from Friday, September 9 to Sunday, September 11, 2022. The campground had approximately 150 camping spots and campfires were lit every day by campers. Outdoor temperatures ranged from 9°C in the morning to a maximum of 27°C at midday. There was no rain during the stay. Winds reached a maximum speed of 5.6 km/h [24]. A governmental expert study conducted between August and October 2023 at the same campground evaluated fine particulate (PM2.5) exposure associated with campfire activity [25]. The study area included the campground where the patient stayed. To minimize bias from individual campfire smoke plumes, sampling equipment was placed near restroom facilities. The patient was camping in the central-southern portion of the campground, which was within the monitored zone. The study found that exposure to fine particles was highest on Fridays, Saturdays, and Sundays between 5: 30 p.m. and 11: 30 p.m. During this period, the maximum 10-minute PM2.5 concentration reached 217 μg/m3, the 90th percentile of 10-minute averages was 144 μg/m3, and the mean concentration over that time window was 78 μg/m3. Daily 24 h averages were lower, with 3 days during the sampling period where levels were above 30 μg/m3. The patient was likely exposed to comparable environmental conditions during his stay the year prior [24,26].

The patient reported daily exposure to smoke from campfires and described the presence of a large amount of visible campfire smoke throughout the duration of his stay. He recalled experiencing irritation of the throat and the eyes, as well as headaches. Two days after his stay, he reported episodes of intense chest pain, described as a burning sensation. These episodes could last more than 20 minutes and occur up to 10 times a day, although their duration and frequency varied. The pain radiated up to the left shoulder and the jaw. Other symptoms that can accompany episodes include dyspnea and a feeling of impending doom. The episodes worsened at the end of the day and were triggered by physical effort, standing, cold, stress, fatigue, exposure to cooking smoke, eating, and allergies. Alcohol consumption and headaches were not identified as trigger factors. His pain could be partially reduced by lying on his back. He had no previous history of chest pain. He did not report any extraneous physical activity or exposure in the 2 days following the trip and prior to the onset of symptoms.

Further investigations were carried out. Exercise-stress electrocardiogram was clinically negative and showed baseline T inversion in V1–3. Coronary angiography showed normal coronary blood flow with no evidence of significant atherosclerotic disease. ECG findings were consistent with a normal sinus rhythm and no detectable anomalies. The stress test with ergotamine (60 mg) reproduced the patient’s typical chest pain, revealed up to 50% coronary vasospasm, and demonstrated ST-segment depression of up to 1 mm in leads V3 to V5. As can be seen in Figure 1, the acetylcholine provocation test induced even more pronounced ECG changes, with 3-mm ST-segment depression in anterior leads and up to 70% vasospasm, particularly evident in the left anterior descending artery. The typical intracoronary dose of acetylcholine used to provoke or reproduce vasospasm during diagnostic testing for VSA ranges from 20 to 100 μg, administered as a bolus over approximately 20 seconds to elicit a 90% vasospasm [27]. For this patient, only 6 ug was given and led to a 70% vasospasm with significant ST-segment depression and chest pain. This was promptly reversed with intracoronary nitroglycerin. Cardiac MRI showed normal myocardial volumes and thicknesses, and an absence of myocardial fibrosis. A PET scan showed no myocardial ischemia or necrotic sequelae. Left and right ventricular ejection fractions were 61% and 60%, respectively. A cardiac scan also showed a calcium score of 1.4 AU, placing the patient between the 50th and 75th percentile. A CT scan of the lung showed mild bi-apical fibronodular changes, bi-basilar subsegmental atelectasis, a benign-appearing intra-fissural nodule in the right major fissure, and a benign-appearing subpleural solid nodule measuring 2 mm in the basal left lower lobe. The patient had no magnesium deficiency. A rheumatology consultation did not suggest any evidence of rheumatologic disease. A positive anti-nuclear antibody (ANA) result of 1/640 and a ratio kappa/lambda light chain rising from 1.65 to 1.81 were found. However, by February 11, 2025, immunofluorescence on HEp-2 cells ANA was down to 1: 160.

A hematology consultation was requested to rule out monoclonal gammopathy. The rest of the investigations were normal, including anti-extractable nuclear antigen, rheumatoid factor, IgG and IgM anti-cardiolipins, anti-beta-2-glycoproteins, neutrophil cytoplasmic antibodies, a scleroderma panel, a cryoglobulin panel, and a myositis panel. There was no evidence of Raynaud’s disease on capillaroscopy. The diagnosis of VSA was later confirmed by an acetylcholine provocation test during a second coronography. The patient also had a spirometry test to rule out asthma, the result of which was equivocal (FEV1/FVC ratio of 69.5%, post-bronchodilator increase in FEV1 of 9.9% of the predicted value). A methacholine test was contraindicated due to the positive acetylcholine provocation test.

As stated by the American Heart Association, calcium channel blockers are the cornerstone of therapy for patients with coronary artery spasm [27]. Short-acting sublingual nitrates are effective for the acute relief of vasospastic episodes [2]. Nicorandil, a potassium channel opener, may also be beneficial in alleviating coronary spasm [27]. For this patient, the episodes improved partially with the use of sublingual and patch nitroglycerine. Oral nicorandil 20 mg twice daily was then started. He reported symptomatic improvement, with sublingual nitroglycerine intake reduced from 10 to 2 puffs daily. However, nicorandil was discontinued several months later following anal pain. Oral diltiazem was subsequently introduced. He also reduced his alcohol intake to between 0 and 3 glasses of alcohol per week.

At the beginning of August 2023, he went hiking in the forest during a trip, staying at a cottage for 14 days at Saint-Donat (Quebec, Canada) (07/28-08/10/2023). After a hike, he reported an increase in the frequency of chest pain episodes. He indicated that there was some smoke outside due to forest fires. Nicorandil treatment was restarted. Allergy investigations were subsequently carried out, and he was later put on a Gramineae desensitization protocol. Constant use of Cetirizine also helped reduce episodes of pain. An experimental use of L-arginine 1000 mg PO BID was also started, but did not lead to any clinical improvement.

Discussion

This case report highlights the plausible role of environmental triggers of VSA symptoms, specifically campfire smoke, underscoring the need for a deeper understanding of the multifactorial contributors of VSA. This 45-year-old man developed VSA symptoms 2 days after a 3-day in a campground where he was exposed to smoke from campfires. Wood combustion is a source of ambient air pollution, emitting various pollutants such as PM10 and PM2.5 [28]. Although the patient’s exposure to smoke could not be quantified due to the absence of air quality data for this campsite in 2022, insights can be drawn from the 2023 ambient air quality expert report conducted at the same location. This report revealed frequent peaks in fine particulate matter concentrations attributable to campfires, particularly during evenings and weekends [25]. These values may underestimate the patient’s true exposure, as they are derived from fixed monitoring stations that reflect the cumulative impact of all campfire sources. The patient’s movement within the campground likely resulted in higher exposure to localized plumes from individual campfires. The patient was not typically exposed to outdoor air pollution levels as high as those occasionally recorded at the campground. In comparison, the yearly average PM2.5 concentration in Montréal (Quebec, Canada) in 2022 was 7.2 μg/m3 [29].

Significant exposure to air pollution poses a serious threat to public health, as it has been linked to a wide range of health issues [30]. In 2016, it was estimated that PM2.5 caused 8.42 million deaths worldwide, resulting in 163.68 million years of life lost [31]. To date, health risks, including cardiovascular effects, remain even when PM2.5 concentrations are below the limits established by the World Health Organization (WHO) and the US Environmental Protection Agency [32–35]. There is growing evidence that both acute and chronic exposure to particulate matter contribute to cardiovascular morbidity and mortality [18,32,36–39]. More specifically, research has also shown associations between exposure to air pollution and angina pectoris. A recent Chinese time series analysis demonstrated that short-term exposure to PM2.5 increased the risk of angina hospitalization, with the highest increase at a cumulative lag period of 0 to 7 days (RR: 1.042; 95% CI: 1.017–1.068) [21]. A large Chinese case-crossover study also showed that exposure to extremely heavy PM2.5 pollution events (PM2.5 concentration ≥150 μg/m3) lasting 3 days was associated with increased hospital admissions for angina pectoris (OR: 1.112, 95% CI: 1.095–1.130) [20]. Moreover, a Canadian longitudinal cohort study showed that for every 10 μg/m3 increase in PM2.5, the prevalence rate of angina pectoris increased by 1.20 (95% CI: 1.09–1.31) [19]. However, in the 3 previous studies, the type of angina was not specified, nor was the presence of significant coronary artery disease among patients. Only 2 studies focusing specifically on coronary vasospasm and air pollution were identified. An Italian study investigated the effect of chronic air pollution on coronary vasomotor disorders in patients presenting with non-obstructive coronary artery disease and myocardial ischemia or infarction. Among 287 patients undergoing an acetylcholine provocation test, exposure to PM2.5 (OR: 4.568; 95% CI: 2.758–7.566) and PM 10 (OR: 1.676; 95% CI: 1.056–2.662) were found to be independent predictors of a positive provocation test result [22]. Finally, a South Korean study assessed local air pollution concentrations within 72 h of hospital admission and coronary artery spasm following an acetylcholine provocation test among 5822 patients with typical or atypical chest pain without significant coronary disease. The study reported a positive correlation between the incidence of coronary artery spasm and the levels and duration of PM10 exposure [23].

Although the pathophysiological pathways linking air pollution to cardiovascular outcomes have mostly been explored in the context of atherosclerotic cardiovascular disease [34,36,40–42], they can also provide a mechanistic basis for air pollution as a trigger of coronary vasospasm. The minute size of PM2.5 particles emitted from wood fires may enable them to circumvent the respiratory system’s defense mechanisms and infiltrate the systemic circulation. Once in the bloodstream, PM2.5 initiates a cascade of biological responses that collectively enhance vasoreactivity. Central to these processes are inflammation and oxidative stress responses [22,34,42–45]. PM2.5 exposure stimulates the production of reactive oxygen species and pro-inflammatory mediators, which contribute to endothelial dysfunction. This dysfunction results in an imbalance between vasoconstrictive and vasodilatory factors [40,42–46]. Specifically, the bioavailability and production of nitric oxide, a key vasodilator, are reduced, while levels of endothelin-1, a potent vasoconstrictor, are increased [22,23,34,40,43,44,46,47]. Another pathway involves autonomic nervous system hyperactivation. Exposure to air pollution has been associated with dysregulation of autonomic balance and activation of the hypothalamic-pituitary-adrenal (HPA) axis, leading to increased sympathetic and reduced parasympathetic activity [22,34,42,44,48–50]. This dysregulation has been associated with higher levels of circulating stress hormones, increased blood pressure, and reduced cardiac rate variability, which could play a part in the pathogenesis of coronary vasomotor disorder.

In addition to smoke exposure, other factors could have contributed to the triggering of VSA in our patient. Notably, he had a confirmed environmental allergy to Gramineae and a history of food allergies (eg, fish and shellfish) and identified allergies as one of several recurring triggers of his chest pain episodes. In the context of allergic sensitization, mast cell activation can lead to the release of vasoactive and pro-inflammatory mediators such as histamine, which induces coronary vasoconstrictions [13,51]. This mechanism has been proposed in the context of allergic angina, also known as Kounis syndrome, which has been reported in several case studies of coronary artery vasospasm triggered by acute allergic reaction [52]. As described earlier, the pathophysiological mechanisms in our patient are likely different from those underlying Kounis syndrome. To our knowledge, no case report describes VSA potentially triggered by exposure to campfire smoke or similar environmental air pollution, highlighting the novelty of our report. Our patient also reported a past smoking history. Smoking is recognized as a contributing factor to coronary artery spasm, primarily due to its role in endothelial function impairment and increase in oxidative stress [53]. However, since he had stopped smoking more than 20 years ago, it is less probable that it was the primary trigger, although persistent vascular alterations cannot be fully excluded [54]. Furthermore, potential genetic susceptibility may have contributed to the VSA, given the role of genetically-influenced mechanisms such as endothelial dysfunction, oxidative stress, and vascular hyperreactivity. A large nationwide cohort study in Sweden demonstrated a significantly increased familial risk of VSA [55]. Furthermore, a genome-wide association study among Japanese women identified a single-nucleotide polymorphism (SNP rs10498345) in a gene significantly associated with coronary spasm [56]. It remains unknown whether this polymorphism or similar ones play a comparable role in White men like this patient. Although rheumatologists ruled out an autoimmune disorder, the borderline elevated ANA levels and increased kappa/lambda light chain ratio may suggest an underlying autoimmune process that has not yet fully manifested and could have contributed to the VSA.

This case report should be interpreted with caution. Given the single-patient nature of this report, the clinical observations and potential implications should not be generalized without further investigation through multiple case reports, case-control studies, or cohort studies. Moreover, while epidemiologic studies have observed an association between particulate pollution and VSA, and a temporal link appears evident in this case, further research is needed to clarify the role of particulate pollution in the causal pathway leading to VSA. VSA is a multifactorial condition, and while campfire smoke cannot be identified as a direct cause, further research is needed to determine whether it can act as a trigger in individuals with an underlying predisposition. Data on the occupancy level of the campsite, allergen levels, and air quality during the patient’s camping stay in September 2022 were not available. Although an expert report documented elevated PM2.5 concentrations on weekends in September 2023, these findings may not accurately reflect the conditions in 2022. Nonetheless, the exposures were most likely similar, given that the measurements were performed during the same period of the year and under very similar environmental conditions.

Conclusions

This case report highlights the need for more studies to assess whether exposure to air pollution could be a trigger for VSA. Given that VSA is a multifactorial condition, it is also essential to consider additional variables such as the patient’s lifestyle, dietary habits, and medication use, which can also influence disease onset and severity. Despite the availability of various treatment options, including lifestyle changes and pharmacotherapy for patients with VSA, actively identifying and avoiding exposures to vasospasm triggers are crucial preventive strategies from a public health perspective.