Respiratory exposure to air pollutants is associated with cardiovascular morbidity and mortality and firefighters have been shown to be at an increased risk of work-related cardiovascular events. Wildland firefighters experience intermittent, intense exposure to biomass smoke. The aim of this study was to characterize the respiratory and systemic effects of smoke exposure in wildland firefighters. Seventeen seasonal firefighters from a northeastern Ontario community were recruited at the beginning of the fire season and baseline measurements obtained; postexposure measurements were made at various times within 16 d of firefighting. Spirometric measurements showed a transient decline in forced vital capacity within 7 d of fire exposure, not evident by 8–16 d. Induced sputum showed a significant increase in macrophages and epithelial cells within 7 d, with evidence that macrophages had internalized particles; such changes were not evident in the second week following exposure. Likewise, peripheral blood analysis revealed significant increases in erythrocytes, hemoglobin, monocytes, and platelets within the first week after fire exposure, which were diminished 8–16 d in postexposure group. We conclude that acute exposure to forest-fire smoke elicits transient inflammatory responses, both in the airways and systemically. Whether these changes contribute to the observed increased risk of cardiovascular events requires further study.
Air pollution is known to be associated with a variety of adverse health effects in humans. Epidemiological evidence clearly documents that air pollution exposure is associated with increased morbidity and mortality due to cardiovascular and respiratory causes [
Ambient air pollution arises from both natural and anthropogenic sources, and the contribution of forest fires to ambient air pollution has substantial public health relevance. The products of biomass combustion are numerous and can vary considerably depending on the nature of the fuel and burning conditions [
Given the high smoke exposures experienced by wildland firefighters and the epidemiological evidence supporting an association between cardiopulmonary effects and poor air quality, we hypothesized that inhalation exposure to smoke from forest fires would provoke an inflammatory response in the airways and stimulate changes in the peripheral blood consistent with increased cardiovascular risk. Swiston et al. have recently examined this issue in forest firefighters within the first day after exposure to biomass smoke [
Subjects were recruited from among wildland firefighters (“Fire Rangers”) employed by the Ontario Ministry of Natural Resources and based out of the Sudbury Fire Management Headquarters during the summers of 2006 and 2007; subject characteristics are summarized in Table
Subject characteristics.
Subject | Gender | Smoker | Age | Sampling days | Sampling days |
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1–7 | 8–16 | ||||
1 | F | 26 |
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2 | F | 28 |
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3 | M |
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30 |
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4 | F |
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19 |
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5 | M | 24 |
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6 | M | 31 |
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7 | M | 30 |
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8 | M | 30 |
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9 | M | 25 |
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10 | M | 20 |
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11 | M | 20 |
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12 | M | 26 |
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13 | M | 27 |
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14 | M | 27 |
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15 | F |
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24 |
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16 | M | 29 |
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17 | F | 30 |
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Note: 1–7 or 8–16 day samples provided by the same subject were not after the same fire exposure.
This study protocol was approved by the Laurentian University Ethics Board and all subjects provided written, informed consent to participate in the study.
Baseline (BL) measurements were made either before any exposure during the firefighting season or with at least 3 weeks since the previous fire exposure. During the active fire season, Fire Rangers returning from fire exposure contacted the research group for the postexposure (PE) measurements. Because the Fire Rangers were often flown to remote sites, the postexposure measurements were made between 1 and 16 d after exposure, depending on travel constraints. Pre- and postexposure measures were taken in the morning and included blood samples, induced sputum, and lung function, including forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC). A questionnaire was administered at the postexposure visit to obtain a qualitative determination of smoke exposure (including type, duration, and intensity of exposure), physical exertion during firefighting, and symptoms.
Spirometry was performed with a MicroPlus handheld spirometer (MicroDirect, Lewiston, ME) according to the American Thoracic Society standards [
Sputum was induced by inhalation of a hypertonic saline mist and processed according to Pin et al. [
Complete blood counts (CBC), erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) measurements were performed by LifeLabs Medical Laboratory Services. Erythropoietin concentrations and CC16 levels were measured in serum in our laboratory using commercially available ELISA assays (R&D Systems, Minneapolis, USA, and ALPCO Diagnostics Salem, USA, resp.); the limits of detection of the assays were 2.5 ng/mL and 0.4 ng/mL, respectively. All samples were processed the same day. After processing, samples were sent to LifeLabs for analysis on the same day, and in-house samples were frozen at −80°C until all samples were collected and then analyzed together. None of the measurements of the samples were below the assay detection limits.
Data are expressed as mean ± SEM. Differences between baseline and postexposure firefighting values were evaluated using a paired
A total of 17 firefighters (12 male, 5 female) were enrolled in the study (Table
Firefighters perceived a relatively low level of smoke exposure: 80% of firefighters reported heavy smoke exposure for only a few seconds at a time, and less than 10% reported heavy smoke exposure for 10 min or longer (data not shown). When fighting a fire, subjects reported levels of exertion comparable to running 44% of the time and comparable to walking 56% of the time. All firefighters reported noticing gray/black-coloured sputum and nasal mucous after exposure. None reported injury or requirement for medical attention.
There were no significant changes in measured FEV1 within the first or the second week after exposure (PE) to firefighting (Figures
Spirometric measures were measured at baseline and at 1–7 d after exposure and at baseline and 8–16 d after exposure. FEV1 is shown in panels (a) (1–7 d) and (b) (8–16 d); FVC is shown in panels (c) (1–7 d) and (d) (8–16 d). Measures are expressed in liters (L) as mean ± SEM. There were no significant changes in FEV1 after fire exposure at either time point. There was a significant decrease in FVC in firefighters 1–7 d after fire exposure (*
Of the 14 subjects that provided measurements at baseline and within 1–7 d of return from fire, 10 fulfilled the criteria for the production of adequate sputum samples. Post-fire exposure, macrophage cell numbers increased significantly in the sputum (Figure
Induced sputum macrophage (a) and epithelial (b) cell counts at baseline and 1–7 days after fire exposure. There was a significant increase in macrophages (*
The number of inclusion low-positive macrophages increased from
Induced sputum and macrophage particle inclusion cell counts, at baseline and after 1–7 days after fire exposure. 200 macrophage cells were counted per slide and percentage of having zero, less than 20, or more than 20 particle inclusions. Solid bars represent cell counts for each category at baseline. Grey bars represent cell counts for each category after fire exposure. Inclusion negative macrophages significantly decreased 1–7 days after fire exposure (*
Of the 8 subjects that provided measurements at baseline and within 8–16 d of return from fire, 7 fulfilled the criteria for the production of adequate sputum samples. There were no measureable changes in macrophage, neutrophil, lymphocyte, eosinophil, or basophil cell. numbers nor in bronchial epithelial cells within 8–16 d of return from fire (data not shown). Likewise, there were no measureable changes in the inclusion negative, inclusion low-positive, or inclusion high-positive macrophages within 8–16 d following fire exposure (data not shown).
Circulating total red blood cells (RBC), total white blood cells (WBC) and leukocyte subsets, platelets, erythropoietin, ESR, and CRP levels were compared at baseline and at 1–7 d and at BL and within 8–16 d of return from fire exposure.
Total RBC measured at baseline and 1–7 d after return from firefighting significantly increased after fire exposure (Figure
Blood cell counts measured at baseline and 1–7 d after exposure and baseline and 8–16 d after exposure. Erythrocytes are shown in panels (a) (1–7 d) and (b) (8–16 d); monocytes in panels (c) (1–7 d) and (d) (8–16 d); and platelets in panels (e) (1–7 d) and (f) (8–16 d). Measures are expressed in cells/L as mean
No significant changes were observed in any of the peripheral blood measures in the second week after exposure (Figures
Inhalation of air pollution not only induces airway inflammation but has systemic effects as well, which are thought to be responsible for the increased risk of adverse cardiovascular events associated with air pollution exposure observed epidemiologically [
Recently, Swiston et al. [
A small decline in forced vital capacity with exposure to forest fire within 7 days was detected. This was not accompanied by a decline in FEV1. Several other studies have shown a similar decline in pulmonary function, but in conjunction with a decline in FEV1 [
Analysis of induced sputum samples indicated clearly that occupational exposure to biomass smoke elicits airway inflammatory responses in this population, with an increase in the fraction of airway macrophages, an increase in macrophages with evidence of particle assimilation, and an increase in airway epithelial cell shedding within 7 days following smoke exposure. Epithelial desquamation is commonly detected in airway inflammatory diseases [
In addition to increased circulating monocytes, we also measured increased numbers of circulating platelets within 7 days of firefighting, which remained elevated in most subjects between 8 and 16 d. This is a novel finding and highlights the link between smoke inhalation and the possibility of enhancing hemostasis. Platelets have an important role in the progression of atherosclerosis and the pathophysiology of cardiovascular events [
Blood analysis also showed increases in red blood cell numbers and hemoglobin levels within 7 days of firefighting. This is most likely due to exposure to carbon monoxide in firefighters and likely reflects an erythrogenic response to the formation of carboxyhemoglobin and subsequent mild hypoxia. We investigated this possibility by measuring erythropoietin in our serum sample but did not observe any changes in serum erythropoietin; since the half-life of this cytokine is only 3.5 h however, this is not unexpected. Like monocytes and platelet numbers, increased red blood cells are also independently associated with risk of cardiovascular events [
We would note three limitations with this study. First, we were unable to directly measure the amount of smoke inhaled by our subjects, so we relied upon the firefighters’ qualitative report of smoke exposure and inhalation and an analysis of macrophage particle inclusion in the sputum. Other investigators have examined the relationships between subjective self-reports of smoke exposure and measured levels of PM2.5 [
Second, we did not exclude participants who smoked. Given that only 3 of the 17 subjects were smokers it was not feasible to do a subgroup analysis for the smokers, and indeed we acknowledge that smoking could have influenced measures of relevance. That being said, when excluding the 3 smokers from the data, we found that for most measures significant statistical difference remained. For three measures, statistical significance was lost, specifically, FVC (
Lastly, although male and female subjects were both included in this study, the majority of our subjects were male, and the relatively small number of subjects means that subgroup analysis by sex/gender was not feasible. As expected, the FEV1, FVC, and red blood cell indices in female subjects were lower than in male subjects at baseline (data not shown), but it should be noted that these were all within the predicted normal ranges. Previous studies have suggested that sex/gender is not a significant covariate for changes in spirometric measures associated with exposure to smoke from wildland fires [
In summary, the present study has shown that healthy, seasonal, wildland firefighters exposed to biomass smoke mount a pulmonary and systemic inflammatory response that is sustained through the first week following exposure but diminishes within the second week. Examining wildland firefighters’ physiological responses to smoke inhalation provides an opportunity to better understand the effects of biomass air pollution on humans as well as the occupational health risks of firefighters in general. The present results provide a plausible mechanism implicating exposure to inhaled pollutants in the increased risk of cardiovascular events seen in firefighters, which Kales et al. suggested was attributable to poor cardiovascular fitness [
The authors declare that there is no conflict of interests regarding the publication of this paper.
The authors thank Ted Shannon and the Ministry of Natural Resources based out of the Sudbury Fire Management Headquarters for their cooperation, which allowed this study to be completed, as well as the Ontario Fire Rangers that donated their time and consented to participate in this study. The authors are also grateful to Patricia Woloshyn for her technical and administrative contributions to this research. This study was funded by the Laurentian University Research Fund and the Northern Ontario School of Medicine.