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Lots of effects --> coughing, trouble breathing, wheezing, asthma attacks, irritated sinuses etc etc

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Be ready to protect yourself against smoke and ash before, during, and after a wildfire.

When wildfires burn near you, smoke can reach your community. Wildfire smoke is a mix of gases and fine particles from burning trees and plants, buildings, and other material. Wildfire smoke can make anyone sick, but people with asthma, Chronic Obstructive Pulmonary Disease ( COPD), or heart disease, or who are pregnant and children and responders are especially at risk.

Breathing in smoke can affect you right away, causing:

Coughing

Trouble breathing

Wheezing

Asthma attacks

Stinging eyes

Scratchy throat

Runny nose

Irritated sinuses

Headaches

Tiredness

Chest pain

Fast heartbeat

Be ready to protect yourself against smoke and ash before, during, and after a wildfire.

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Be ready to protect yourself against smoke and ash before, during, and after a wildfire.

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https://www.redcross.ca/how-we-help/emergencies-and-disasters-in-canada/get-help-disaster-relief-and-recovery/coping-with-crisis

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Every year millions of people suffer as a result of disasters and emergencies. Any significant loss results in a natural grieving process and all of us are affected by traumatic experiences in different ways.

Following an emergency or disaster, a person may experience a range of thoughts, feelings and behaviour that can be intense, confusing and frightening.

These experiences trigger responses that are both physical and psychological, which are expected reactions to abnormal events, and can include physical, emotional and behavioural reactions such as:

Sleeping problems

Headaches

Muscle tension and bodily pains

Fast heart beat

Nausea

Anxiety

Watchfulness

Poor concentration

Guilt

Sadness

Anger

Confusion

Having intrusive memories

Trying to avoid being reminded of the crisis

Some people also react by feeling numb or not feeling anything at all, by struggling with day-to-day decision making, or by isolating themselves from others. Some people increase their intake of alcohol, medicine or drugs to escape the pain they are feeling.

It may help to:

Maintain daily routines and do things that normally give you pleasure.

Eat healthy foods, get plenty of sleep and exercise if possible.

Visit with other people.

Accept support and assistance.

Allow yourself to feel sad and grieve.

Give someone a hug.

Take small steps.

Children's Reactions

After a stressful experience, including those involving loss, children's grief is often abrupt and they may switch quickly from intense grief reactions to play and having fun. Almost all children play, even if they have gone through an intense crisis event.
Younger children may:

Behave aggressively towards caregivers or other children.

Cling to their caregivers.

Show signs of separation anxiety.

Regress to the behaviour of younger children such as bedwetting, thumb sucking or not being able to sleep alone.

In such situations, stable and secure relationships and establishing predictable routines contribute to a supportive environment.

When to seek help:

The stress reactions may last several weeks. If your reactions persist and make it impossible to function normally over a long period of time, seek help. One option is to contact your local health facility or a local crisis support line.

You may also want to contact:

Useful Resources:

Guidebook for Wellbeing in Recovery

Coping With Crisis: Common reactions to stress and suggestions on how to cope

Guide to Disaster Recovery for Parents and Caregivers

Preparing for and Coping with Effects of a Disaster or Emergency

Moving Through Recovery: A Guide for Holidays

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Learn how to prepare for and recover emotionally from a disaster or emergency.

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National Centre for Epidemiology and Population Health, Research School of Population Health, The Australian National University, Canberra, ACT, Australia

Fenner School of Environment and Society, The Australian National University, Canberra, ACT, Australia

Departments of General Medicine and Infectious Diseases, The Canberra Hospital, Canberra, ACT, Australia

Centre for Mental Health Research, Research School of Population Health, The Australian National University, Canberra, ACT, Australia

Research School of Psychology, The Australian National University, Canberra, ACT, Australia

The 2019-20 bushfire season in south-eastern Australia was one of the most severe in recorded history. Bushfire smoke-related air pollution reached hazardous levels in major metropolitan areas, including the Australian Capital Territory (ACT), for prolonged periods of time. Bushfire smoke directly challenges human health through effects on respiratory and cardiac function, but can also indirectly affect health, wellbeing and quality of life. Few studies have examined the specific health effects of bushfire smoke, separate from direct effects of fire, and looked beyond physical health symptoms to consider effects on mental health and lifestyle in Australian communities. This paper describes an assessment of the health impacts of this prolonged exposure to hazardous levels of bushfire smoke in the ACT and surrounding area during the 2019-20 bushfire season. An online survey captured information on demographics, health (physical and mental health, sleep) and medical advice seeking from 2,084 adult participants (40% male, median age 45 years). Almost all participants (97%) experienced at least one physical health symptom that they attributed to smoke, most commonly eye or throat irritation, and cough. Over half of responders self-reported symptoms of anxiety and/or feeling depressed and approximately half reported poorer sleep. Women reported all symptoms more frequently than men. Participants with existing medical conditions or poorer self-rated health, parents and those directly affected by fire (in either the current or previous fire seasons) also experienced poorer physical, mental health and/or sleep symptoms. Approximately 17% of people sought advice from a medical health practitioner, most commonly a general practitioner, to manage their symptoms. This study demonstrated that prolonged exposure to bushfire smoke can have substantial effects on health. Holistic approaches to understanding, preventing and mitigating the effects of smoke, not just on physical health but on mental health, and the intersection of these, is important. Improved public health messaging is needed to address uncertainty about how individuals can protect their and their families health for future events. This should be informed by identifying subgroups of the population, such as those with existing health conditions, parents, or those directly exposed to fire who may be at a greater risk.

Introduction

During the summer of late 2019 and early 2020, extensive areas of south-eastern Australia experienced one of the most severe bushfire seasons in recorded history. Over 10 million hectares of land were burnt, and over 2,400 homes were destroyed in New South Wales (NSW) alone. Bushfire smoke-related air pollution reached hazardous levels in major metropolitan areas including Canberra, Australia's capital, in the Australian Capital Territory (ACT). Between 15 December and 15 February in the ACT, 27% of days ( n = 17/63 days) had air quality levels that were considered extremely poor (≥ 300 PM 2.5 μg/m ³) and on three quarters of days ( n = 47/63 days), air quality was classified as poor or worse (≥ 50 PM 2.5 μg/m ³) at one or more of Canberra's three air quality monitoring stations ( 1) [using thresholds defined by NSW Department of Planning, Industry and Environment ( 2)]. On the worst days, hourly levels reached well over 1000 PM 2.5 μg/m ³.

Bushfire is an inevitable and essential part of natural Australian ecosystems; however, the severity and duration of fire seasons are projected to increase globally with climate change ( 3). A recent study concluded that as a result of anthropogenic climate change, the prevalence of days of high-risk bushfire weather has increased, conservatively, by at least 30% since 1900 ( 4). As a result of predicted changes to bushfire patterns, the health and community impacts of bushfire are likely to increase unless effective adaptation measures are implemented. The public health impacts of bushfire extend beyond direct exposure to the fire itself, with increasing awareness of the effects of bushfire smoke-related air pollution ( 5). Smoke can travel long distances and affect large populations, even in urban areas geographically separated from fire ( 6). Bushfire smoke can have considerable impacts on health; it is estimated 340,000 deaths can be attributed to bushfire smoke globally each year ( 7). Fine particulate matter, i.e., particles <2.5 micrometers in diameter (PM 2.5), can adversely affect health via impaired respiratory and cardiac functioning, promotion of inflammation, and alteration of immune function ( 8, 9). Bushfire-related air pollution has also been associated with increases in mortality ( 10- 12) and the effects of smoke can be more severe in populations with particular vulnerability, such as those with pre-existing medical conditions including cardiovascular disease or respiratory conditions ( 13, 14).

In bushfire events, it can be difficult to separate the health effects associated with direct displacement, loss, or exposure to fire from those of bushfire smoke. Most studies examining the effects of bushfire smoke on health have used routinely collected health data such as emergency department presentations, hospital admissions and mortality ( 5), which are very likely to underestimate the effects on the population by capturing only those affected severely enough to require seeking secondary or tertiary-level health care. Prior studies have also focused primarily on physical health concerns, with few studies taking a holistic approach to the assessment of health by including measures of mental health and lifestyle in addition to physical health.

The 2019-20 bushfire season affecting south-eastern Australia elicited widespread public concern due to its duration, and uncertainty about potential immediate and long-lasting health effects of prolonged smoke exposure. In addition, individuals experienced considerable uncertainty about how to protect the health and wellbeing of themselves and their families during this period ( 15). A preliminary evaluation of the air pollution health burden in eastern Australia estimated that bushfire smoke was responsible for 417 (95% CI, 153-680) excess deaths, over 3,000 excess hospitalizations for cardiovascular (1,124; 95% CI, 211-2,047) and respiratory (2,027; 95% CI, 0-4,252) problems, and 1,305 (95% CI, 705-1,908) presentations to emergency departments with asthma ( 16). The total smoke-related physical health costs during the 2019-20 bushfire period have been estimated at AU$1.95 billion ( 17). The 2019-20 bushfires were of particular interest in the Canberra and surrounding community, as this area experienced a severe bushfire in January 2003. During this earlier disaster, almost 160,000 hectares of land were burnt, 448 houses were destroyed (and a much greater number damaged), over 5,000 people were evacuated, four people died and hundreds of people received medical care ( 18).

This paper presents the findings of a cross-sectional study examining the effects of prolonged exposure to hazardous levels of bushfire smoke-related air pollution on the physical health, mental health, and sleep patterns of residents of the ACT region during the 2019-20 bushfire season and how these vary by demographic and lifestyle factors.

Materials and Methods

Study Design

This cross-sectional survey asked participants about their experiences during a "period of interest" defined as 15 December 2019 to 15 February 2020, as this was the period during which the most significant levels of bushfire smoke-related air pollution (hereafter referred to as "smoke") affected the Canberra region.

Participant Recruitment

The survey was conducted over a six-week period in March and April 2020. The sampling frame included all adult residents of the ACT and immediately adjacent regions of NSW. Inclusion criteria were: aged 18 years or older, able to understand an online questionnaire in English, and a residential address defined by specific postcode areas constituting the ACT and immediately surrounding postcodes (2600-2612, 2614-2620, 2626, 2900-2906, 2911-2914).

Participants were recruited using three methods: (i) Letter-An invitation to complete the online survey was posted to a random selection of 10 000 addresses, selected from the ACTmapi database ("ACT Addressing" from ACTmapi ©Australian Capital Territory). Any addresses identified as non-residential (e.g., businesses, schools) were removed and replaced prior to the mail out; (ii) Panel-A representative population sample of participants recruited by an external company; (iii) General-A convenience sample of the population was recruited via social media, radio advertisements and word of mouth, including interest from local media.

Data Collection

Potential participants were invited to complete the online survey via REDCap electronic data capture tools hosted at Australian National University ( 19). The survey was available in English and in an online format only. Participants provided consent by submitting a completed survey. Two participants that received a letter mailout invitation and who did not have internet access completed the survey by phone with a study team member recording their responses.

The survey collected: postcode of residence, age (years), highest level of education achieved (no school qualification/ school or intermediate/ HSC or leaving certificate/ trade or apprenticeship/ certificate or diploma/ university or higher), tobacco smoking (never/past/current), rental status (renter/owner-occupier/other), pregnancy status (self/partner/none/not applicable), parental (yes/no and age of youngest child) or carer status (yes/no); previous medical diagnoses [asthma/chronic obstructive pulmonary disease (COPD-including emphysema and chronic bronchitis)]/allergies or hay fever/other respiratory disease (e.g., pleurisy, bronchiectasis, pulmonary fibrosis)/multiple sclerosis/arthritis/diabetes/other), engagement with a professional for a mental health concern during the last 12 months (yes/no) and self-rated health (poor/fair/good/very good/excellent); prior exposure to bushfire (no previous exposure to bushfire/been in an area with fire nearby/evacuated due to bushfire/experienced loss of or damage to property/had direct contact with bushfire (e.g.,firefighter or protecting property)/other) including whether this was during the 2003 Canberra bushfire (yes/no); direct exposure to bushfire in the current season (not affected/voluntarily relocated/forced to evacuate/damage to or loss of property/family or close friend affected/had to cancel or alter travel or holiday plans/ firefighter or first responder/other); effects of smoke on physical health (eye irritation or watery eyes/throat irritation or dry throat/cough/wheeze or whistling chest/sneezing/chest tightness or pain/breathlessness/headache/diarrhea or gastroenterological symptoms/other condition not listed), sleep (disrupted or poor sleep/fatigue or feeling tired) and mental health (anxiety/feeling depressed) symptoms and whether these were attributed to smoke (yes/no/unsure); health advice sought as a result of symptoms (yes/no, hospital inpatient/emergency department/general practitioner/specialist/24 h health advice hotline/pharmacist/mental health professional e.g., psychologist/other health professional).

Data Analysis

Data Management

Summary statistics were used to describe the study's participants ( Table 1) using demographic, health and lifestyle variables as described in Table 2. To explore physical health outcomes, data were divided into quartiles based on the cumulative number of physical health symptoms reported. A mental health outcome variable was created by including those who self-reported anxiety and/or feeling depressed as a result of smoke. Similarly, a sleep outcome variable was created by combining those who reported disrupted or poor sleep and/or fatigue or feeling tired. Although scaled, validated measures, especially of mental and physical health status, are generally preferable, this paper reports results of a rapid research response developed during the bushfire crisis, with the intention of reporting responses during or soon after the emergency in a way that would be helpful for future researchers and public health officials. Accordingly, our outcomes measures are brief assessments. They were developed from the research team's expertise in different contexts, and are based on our previous research ( 13, 15, 20).

Statistical Analysis

All analyses were conducted in Stata (v15.1, College Station, TX StataCorp LLC). Summary statistics were used to describe the study sample as detailed in Table 1. Number (%) were used to describe categorical variables and mean (SD) to describe continuous data. Descriptive statistics were calculated to examine the prevalence of self-reported physical health, sleep and mental health symptoms, overall and for men and women which were compared using Chi ² analyses. Ordinal logistic regression was used to identify factors (as per Table 2) that were associated with higher physical health symptoms. Bivariate analyses including age, gender and age*gender interaction were then conducted for factors for which p ≤ 0.1. Logistic regression was used to determine factors that were associated with either disrupted sleep or mental health symptoms. Similar bivariate analyses were conducted to develop sleep and mental health models. Summary statistics [n (%)] were used to describe sources of health advice sought, overall and separately for males and females, which were compared using Chi ² analyses.

Results

Population

A total of 2,095 completed responses to the survey were received; 644 (30.7%), 639 (30.5%), and 812 (38.8%) people recruited via the panel, letter and general recruitment methods respectively. This was a response rate of approximately 6.4% to the letter invitations, although many were returned to sender so it was unclear how many were undelivered. Eleven responses were excluded as the participant resided outside of the target area or did not provide a valid postcode. This resulted in a total sample of 2,084 responses that were included in subsequent analyses.

Participant characteristics are summarized in Table 1. Of the study participants, 40.2% were male, 59.6% were female, and 0.2% identified as being of another gender. The mean age of respondents was 45 years (median 45, range 18-85 years), approximately 10 years older than the median age of ACT residents. Approximately 13% of the sample had completed a high school certificate or less, 17% a trade, apprenticeship, certificate or diploma, and 70% had completed a University degree. This suggests that the sample included a greater proportion of women, was on average older, and more highly educated than the ACT population compared with data from the Australian Bureau of Statistics ( 21).

Approximately a quarter of respondents were parents, 15.4% were carers for one or more non-child dependents and 22% of participants rented their place of residence. Forty-three respondents (2.1%) were pregnant during the period of interest, 11% rated their own health as poor-fair (vs 89% good-excellent), 3% were current smokers, 25% were ex-smokers and 72% had never smoked. Over half of the sample (58%) had been directly affected by fire (not just smoke) during the 2019-20 bushfire season, with 8% of the total sample reporting being affected severely. Previous direct exposure to bushfire had been reported by 67% of the sample, 10.5% severely. For most participants (43% of the total sample), this exposure had been during the 2003 Canberra bushfire event.

Physical Health

Most participants (97.1%) reported experiencing at least one specified physical health symptom during the period of interest that they attributed to the smoke ( Table 3). The most common symptoms were eye irritation or watery eyes (73.1%), throat irritation or dry throat (70.4%) and cough (50.6%). A considerable proportion of people also reported experiencing headaches (38.2%), breathlessness (21.9%), sneezing (21%) or wheeze/whistling chest (19.9%). A small number of people (3.2%) also reported experiencing other (non-itemized) physical or mental health impacts of the smoke including asthma, bronchitis, itchy skin/rash, runny nose, sinusitis and mental trauma. Women reported all physical symptoms more frequently than men ( p <0.001 for all other than sneeze p <0.05) and had almost three times the odds of men of experiencing a greater number of physical health conditions as a result of exposure to smoke (2.92 ± 0.344, p <0.001) ( Table 4). After accounting for age and gender, those participants with poorer self-rated health (2.13 ± 0.344, p <0.001), a previous diagnosis of either a physical (2.18 ± 0.266, p <0.001) or mental health condition (1.64 ± 0.206, p <0.001), or were a past (but not current) smoker (1.83 ± 0.226; p <0.001), had greater odds of experiencing more physical symptoms. Any direct exposure with fire this season increased odds of experiencing a greater number of health symptoms (1.64 ± 0.186, p <0.001). The effect was strongest in those who had experienced more severe effects of bushfire compared to those who reported mild exposure to fire (2.47 ± 0.465 vs. 1.52 ± 0.178; p < 0.001). Previous fire exposure increased the odds of experiencing more physical health symptoms, whether this was defined as any previous exposure (1.55 ± 0.182, p <0.001), mild or severe exposure (1.51 ± 0.181; p = 0.001, 1.82 ± 0.345; p = 0.001, for mild and severe respectively) or as a cumulative measure (1.40 ± 0.121; p < 0.001). Having experienced the 2003 Canberra bushfires did not statistically increase the odds of experiencing a greater number of negative physical health symptoms (1.56 ± 0.447; p = 0.124). Parental, carer, pregnancy or education status were not associated with an increase in physical health symptoms.

Mental Health

Over 55% of responders self-reported symptoms of anxiety (45.3%) and/or feeling depressed (21.4%) as a result of the smoke ( Table 3). Women were more likely than men to report negative mental health outcomes (1.99 ± 0.192, p <0.001) which reflected increased symptoms of both anxiety (54.5 vs. 31.8%) and feelings of depression (25.5 vs. 15.5%). Poor mental health outcomes were associated with younger age groups (25-54 years groups). Bivariate models ( Table 5) identified parents (1.27 ± 0.142; p = 0.029), individuals with an existing physical (1.35 ± 0.138; p = 0.004) or mental health diagnosis (1.30 ± 0.164; p = 0.038), and those who had obtained a higher level of education (high school or lower vs. trade/diploma: 1.46 ± 0.257, p = 0.032 vs university: 1.42 ± 0.208; p = 0.015) had greater odds of experiencing negative mental health outcomes ( Table 5). Direct exposure to fire in the current season was associated with increased reported symptoms of anxiety and feeling depressed, according to all measures used (p ≤ 0.001). Of note, severe bushfire exposure had a stronger effect on mental health than mild exposure (1.87 ± 0.344 and 1.46 ± 0.148 for severe and mild, respectively). Exposure to fire in a previous season, including during the 2003 Canberra fires, was not associated with mental health outcomes.

Sleep

Half of survey respondents reported poorer sleep as a result of exposure to smoke ( Table 3). This was defined as either disrupted or poor sleep (37.2%) and/or fatigue or feeling tired (32.5%). Females were more likely to experience poorer sleep outcomes than men (1.75 ± 0.168, p <0.001). Odds of poor sleep outcomes were increased in younger age groups. When age and gender were accounted for, those with poorer self-rated health (2.01± 0.339; p <0.001), or a previous diagnosis of a physical health condition (1.34± 0.136; p <0.01) all had greater odds of experiencing smoke-attributed impairments in sleep ( Table 6). Direct exposure to fire in the current fire season increased the odds of poor sleep outcomes, irrespective of the measure used ( p < 0.001). This effect was more pronounced in those who had experienced more severe exposure (1.81 ± 0.326 vs. 1.34 ± 0.135 for mild vs. severe exposure, respectively). The odds of poor sleep outcomes were increased in the group who had experienced more severe exposures to fire in a previous season (1.82 ± 0.312; p < 0.001), and tended to be increased to a lesser extent in the group who had more mild experiences (1.29 ± 0.135; p = 0.014).

Medical Advice

Approximately 17% of people reported they sought advice from a health professional or medical facility in relation to their smoke-attributed symptoms ( Table 7). The most commonly accessed source was a general practitioner (13.2%), followed by pharmacist (3.6%) and mental health professional (2%). Females were more likely to have sought health advice than males (21 vs. 11%, p <0.001).

Discussion

The extreme 2019-20 Australian bushfire season increased the burden on the health system ( 22). The current study indicates substantial self-reported effects of bushfire smoke on the ACT community's physical, mental health and sleep patterns, with almost all respondents reporting at least one negative health effect during this time. The most common symptoms (eye and throat irritation, cough) were consistent with other studies ( 23) and the known short-term effects of exposure to very high levels of PM 2.5. Bushfire smoke-related air pollution reached hazardous levels in the ACT over a longer period and to higher levels than previously reported in other areas of south eastern Australia ( 23, 24). In the current ACT study, 97% of the sample reported at least one smoke-related health symptom, whereas prevalence of similar health conditions was 65.1% in the Hunter-New England area ( 25, 26), and 16.1% in a control population located in Hobart, Tasmania that was not affected by smoke.

The smoke-attributable health burden experienced in the ACT region is higher than other studies of the health effects of smoke ( 23). Other studies have relied on emergency presentations or hospital records to identify those experiencing negative health outcomes ( 8, 27- 30), but the current study drew on self-reported effects from community members, only ~1% of whom presented at a hospital. Presentation measures only capture medical conditions severe enough for individuals to seek clinical care, therefore underestimating the total health burden. These measures may also miss mental health conditions, for which support may be sought elsewhere. The extent to which this study documents smoke effects is significant and concerning. The prevalence of health conditions for which formal medical advice was not sought highlights the importance of interventions to better prepare people on ways to reduce exposure during periods of hazardous air pollution and when to seek help. Barriers to accessing medical and psychological care were not investigated in this study, but future studies should examine this. Further epidemiological studies that accurately measure individual smoke exposure will be able to better characterize specific health impacts of severe smoke, or thresholds for these, and give more accurate advice about how and when individuals should protect their health.

Smoke exposure is known to exacerbate existing health conditions ( 14). Our finding that participants with an existing health condition had greater odds of experiencing more smoke-related health issues is consistent with this. Similarly, poorer self-rated health was associated with increases in both physical health and sleep-related symptoms. Sleep problems have been associated with both physical and mental health problems ( 31, 32) and physical and mental health are also strongly linked ( 33, 34). Future studies ought to examine the inter-relatedness of these health outcomes ( 14).

Several studies demonstrate the lasting psychological effects of bushfire exposure, including increased rates of depression, post-traumatic stress disorder (PTSD), and increased drug and alcohol use ( 35, 36). A year after fires in an Australian community, twice as many people (42%) were classified as "potential psychiatric cases" than in an unexposed comparison population ( 37). Most people do not develop psychological conditions following a natural disaster ( 38), but it is important to identify those at risk of doing so and to provide the support they require. Future research should also consider community factors such as community cohesion, competence and support ( 39) that may influence individual wellbeing, rather than focus solely on individual-level variables.

Women and men may experience, respond to, and recover from bushfires differently ( 40, 41). For example, women are more likely to report higher rates of PTSD ( 42, 43), and men to report an increase in alcohol abuse after experiencing bushfires ( 40, 44). In the current study, women reported higher rates of all physical health symptoms, poorer sleep, and mental health issues. Gender differences have been attributed to biological, social or situational factors ( 38, 40, 45).

Longer term mental health outcomes for communities exposed to bushfire are generally good, although a significant minority may experience persistent difficulties and vulnerability may increase with cumulative trauma exposures ( 44). In our study, previous exposure to fire was associated with greater odds of reporting poorer physical health outcomes and sleep disturbance, but not with mental health outcomes. More disrupted sleep for people who had previously been directly exposed to a bushfire event is possible, as the smoke may have triggered memories of that event. Direct exposure to fire is inherently difficult to understand as exposure severity and personal experience vary among individuals. To investigate this, we explored this measure in several ways-by assessing a binary (yes/no) response, a cumulative measure of the number of effects identified, or a ranking measure, in which some experiences were weighted more strongly than others. Unsurprisingly, people who were directly affected by fire had increased odds of physical, sleep, and negative mental health outcomes. For all of these outcomes, the pattern of relationship was similar, with higher odds ratios in the group ranked severe, compared to the mild group. The different ways of measuring exposure were all statistically significant, suggesting the link between direct experience of bushfire with adverse health outcomes is robust. In contrast, the cumulative measure showed consistently weaker odds ratios compared to other measures. This poses questions about the level of detail needed in measuring people's objective and subjective experience with bushfire, whether there are severity of impact thresholds for concern, and how a single measure might account for different experiences of a similar event (for example voluntary vs. forced evacuation). The complexity of this issue warrants more detailed study.

Although participants in this study were asked to focus on the effects of smoke (and not fire) specifically, it is likely some people were unable to separate the effects of smoke from other factors, such as heat stress or the direct effects of fire. Also, this study coincided with the early stages of the COVID-19 pandemic in Australia, and participants may have been unable to disentangle their feelings of distress and anxiety about the bushfires from the uncertainty of the developing pandemic.

During the 2019-20 bushfire season, there was community concern about whether smoke exposure would have long-term effects on health ( 46). This continues to be an area that is not well understood as only limited studies have explored long-lasting or delayed effects of smoke on health. Some have identified increased incidence of influenza ( 47) and impaired lung function ( 48) for months to years after a fire event. Canberra had experienced a severe bushfire in January 2003 and a survey 3 years after this disaster found that for over half the survey respondents (56.4%, n = 272) the bushfire did not have a lasting effect on their overall health and 2.5% (n = 12) reported that their overall health was better than before ( 18). However, 40.9% (n = 197) reported a lasting negative effect of the bushfire on their overall health. As such, we hypothesized that community members who had been exposed to the 2003 bushfires in Canberra may have been at greater risk of negative health effects during the 2019-20 fire season, particularly regarding negative mental health outcomes. However, this was not evident from our results, perhaps indicating that people were resilient and had had sufficient time to resolve any adverse reactions to the 2003 fires. Further longitudinal research is needed to understand the long-lasting, as well as the acute, health effects of bushfire and smoke exposure.

Rapid research during or immediately following natural disasters is challenging ( 49, 50). Here, a survey was designed to be deployed quickly to capture a broad snapshot of a population's health in response to a bushfire smoke event. Online data collection was suitable for a wide range of the population, but not when such as electricity or internet services are interrupted. The use of multiple sampling approaches captured experiences from a broad cross-section of the population, though the sample is not representative of the whole population as some groups such as the elderly, those with no fixed address, or those for whom English is not their primary language, may have been missed or underrepresented. Further, the focus here was on rapid and easy to measure self-report items with good face validity, rather than on more sophisticated measures of key constructs such as mental health. Despite these limitations, important trends concerning health and lifestyle burdens were identified, presenting an effective way to screen for specific areas or groups requiring more detailed examination. This method should, though, be refined to focus on the most pertinent and useful information to ensure ease of completion and associated rapid delivery of appropriate support and services to communities.

Conclusions

Bushfire smoke can have considerable and underestimated effects on physical and mental health, beyond those associated with direct contact with fire and the acute effects of smoke inhalation. Greater understanding of mental health and long-term health effects is needed, particularly for at-risk groups, including parents, those with existing health conditions, or those who had previous exposure to fire and smoke. Improved public health communication is needed to strengthen individuals' ability to prevent harm and protect the health of themselves and their families for future events.

Data Availability Statement

The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.

Ethics Statement

The studies involving human participants were reviewed and approved by Human Research Ethics Committee of the Australian National University (protocol number: 2020/029). The patients/participants provided their written informed consent to participate in this study.

Author Contributions

RR, AS, AC, BC, AL, JL, JR, ST, SV, and IW contributed to the conception and design of the study. ST and RR obtained ethics approval, conducted data collection, and database management. RR was responsible for data analysis and drafting of manuscript. All authors contributed to manuscript revision, read, and approved the submitted version.

Funding

This research was funded by the Australian National University College of Health and Medicine. AC is supported by a National Health and Medical Research Council (NHMRC) Fellowship 1173146.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher's Note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Acknowledgments

The authors would like to thank the community members who participated in this study.

References

17. Johnston FH, Borchers-Arriagada N, Morgan GG, Jalaludin B, Palmer AJ, Williamson GJ, et al. Unprecedented health costs of smoke-related PM 2.5 from the 2019-20 Australian megafires. Nature Sustainability. (2021) 4:42-7. doi: 10.1038/s41893-020-00610-5

CrossRef Full Text | Google Scholar

25. Moberley S, Carlson S, Durrheim D, Dalton C. Flutracking: Weekly online community-based surveillance of influenza-like illness in Australia, 2017 Annual Report. Communicable Diseases Intelligence. (2019) 43. doi: 10.33321/cdi.2019.43.31

48. Orr A, AL Migliaccio C, Buford M, Ballou S, Migliaccio CT. Sustained effects on lung function in community members following exposure to hazardous PM 2.5 levels from wildfire smoke. Toxics. (2020) 8:53. doi: 10.3390/toxics8030053

50. Kessler RC, Keane TM, Mokdad A, Ursano RJ, Zaslavsky AM. Feature Paper: Methodological issues in post-disaster mental health needs assessment research. Peachtree City, Georgia: Conference on Health Survey Research Methods. (2007). p. 33.
Google Scholar

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Frontiers | Physical and Mental Health Effects of Bushfire and Smoke in the Australian Capital Territory 2019-20

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The 2019-20 bushfire season in south-eastern Australia was one of the most severe in recorded history. Bushfire smoke-related air pollution reached hazard...

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Exposure to wildfire smoke has been shown to increase cardiovascular-related health issues such as:

acute myocardial infarction

cardiovascular mortality

cardiovascular emergency department visits and hospitalization

cardiac arrest

heart failure

endothelial dysfunction

Alpo Vuorio, Budowle, B., Raal, F., & Kovanen, P. T. (2023). Wildfire smoke exposure and cardiovascular disease—should statins be recommended to prevent cardiovascular events? Frontiers in Cardiovascular Medicine, 10. https://doi.org/10.3389/fcvm.2023.1259162

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Increased levels of PTSD, anxiety, and depression. https://globalnews.ca/news/9912490/natural-disasters-wildfires-canada-mental-health/#:~:text=Many%20studies%20have%20shown%20there,7%20through%2012%20remained%20traumatized.

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Whether it's the raging wildfires forcing thousands to evacuate their homes in western and northern Canada, or deadly floods striking the east coast, those caught up in natural disasters face more than immediate physical challenges: They also bear emotional and psychological trauma that can last well beyond the events themselves, mental health experts warn.

But people can take steps to manage the effects and protect their mental health.

"During a natural disaster, we see an initial immediate concern for physical safety, which is incredibly important," said Julia Payson, executive director of the Canadian Mental Health Association, Vernon, B.C. branch.

"What often comes later - or even concurrently, but is put aside - is the mental health impact of these disasters, whether it's the direct impact of being under an evacuation order or being in the vicinity of these alerts and fires."

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Those impacts can persist for years, she added.

Payson, who lives in Vernon, said the ongoing wildfires in the province have led many people to feel a rollercoaster of emotions including anxiety, fear, sadness, numbness and anger, which she describes as typical responses amid such destruction.

"The range of emotions that you feel when there are fires nearby is intense... You alternate between wanting to know what is happening and wanting to just tune out a lot of the news," Payson said.

"We've watched some of these fires move really quickly. You feel relief when a fire stops moving towards you, but you know that often it's because it's moving somewhere else. So then you're dealing with the guilt of that."

As climate change continues to make wildfires, flooding and heat waves more frequent and severe, Health Canada has warned of increased risks to the mental health and well-being of many people in the country. Those reactions can include feelings of hopelessness, a lack of community and even heightened suicide ideation or attempts.

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Mental health symptoms to watch for

Dr. Jude Mary Cénat, professor in the School of Psychology at the University of Ottawa, said that after a natural disaster, many people will experience unwanted upsetting memories, as well as flashbacks, nightmares and emotional distress.

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"Some will try and avoid those feelings, thoughts, events and places that remind them of the natural disaster," he said.

Substance abuse can also be a symptom, said Nicole Sadler, a clinical psychologist based in Australia, who has studied the mental effects of natural disasters.

She said the mental health fallout from a disaster, such as wildfire, can be short-term, lasting a few days or weeks. For some, the effects may last for months, or even years.

"They might have trouble sleeping, they might feel very agitated. They might feel that it's difficult to really feel like there's a sense of safety and security in their life," Sadler said.

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"And of course, that comes from not just the impact of the disaster itself, but perhaps their communities being impacted, their job, their livelihood."

There's also been a link between natural disasters and post-traumatic stress disorder (PTSD), she said, clarifying that this is observed only ain minority of people.

Many studies have shown there are increased levels of post-traumatic stress, depression and anxiety after disasters, such as wildfires.

For example, a 2019 study out of the University of Alberta found that 18 months after the 2016 Fort McMurray wildfires, many students in Grades 7 through 12 remained traumatized. More than one in three students were suffering from PTSD, 31 per cent cited depression and 15 per cent said they had probable alcohol or substance use disorders.

Sadler cited another study that looked at the impact of the destructive bushfires in New South Wales during 2019-20 on children. The study revealed that in communities significantly impacted by wildfires, children's school grades suffered while instances of financial strain and domestic violence within households were reported.

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How to protect your mental health

Cénat said letting people know that their feelings following a natural disaster are normal is a cornerstone of restoring their mental health.

"It is normal to feel psychological distress because you lost your home, you lost your environment. Your children cannot be in that same school they were in for the last two years," he said. "Normalize the symptoms and then help people know what they can do to overcome to heal from the symptoms."

Maintaining social connections and reaching out for help is another important step, Sadler said.

"One of the best indicators of recovery from something big like a natural disaster is the quality of someone's social connections... doing those things that get back a sense of routine, a sense of not being overwhelmed," she said.

This includes engaging in activities like getting back into a social routine, getting your children back in school, or going to church.

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She said it's also important to provide "self-care," such as taking a mental break from the stress of what is happening around the world.

"And doing all those basic things that we know look after your mental health and well-being, trying to get enough sleep, making sure that you're eating as properly as you can, trying to get a little bit of exercise, and talking to other people about what's happened for you, talking to people that you trust, people that you feel safe with," she stressed.

Regardless of what we are exposed to, she said humans are "resilient" and there is always hope for recovery.

"For most of us, we won't need formal support to do that, we won't need formal counselling. We can do this in the context of our communities, of our own coping support and banding togetherand supporting each other," Sadler said.

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But if you are worried about yourself or someone else, there are services people can use for mental health support.

In Canada, for example, the Red Cross offers a list of services. For immediate assistance anywhere in Canada, call Talk Suicide Canada to connect to a crisis responder at 1-833-456-4566.

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Anxiety, depression and anger: The mental health impacts of natural disasters | Globalnews.ca

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Natural disasters can have a big impact on a person's mental well-being. Experts say it's important to maintain self-care and stay connected to your community for support.

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irritate eyes, lungs, throat and sinuses

increase the risk of heart attacks

trigger headaches and allergies

reduce lung function, especially in children

trigger asthma attacks

worsen COPD

worsen pneumonia

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Forest fires are often a concern in Canada, especially during dry, hot summers. People all over Canada may be affected by the smoke from forest fires. The Canadian Lung Association urges those with lung disease such as asthma and COPD to monitor their breathing and avoid exposure to smoke. If breathing problems develop, refer to your action plan or call your health-care provider.

What type of health effects can be caused by forest fire smoke?

For someone without lung problems, wood smoke can:

irritate eyes, lungs, throat and sinuses

increase the risk of heart attacks

trigger headaches and allergies

reduce lung function, especially in children

For someone with lung disease, wood smoke can cause all of the above sooner and it can:

trigger asthma attacks

worsen COPD

worsen pneumonia

** Symptoms of worsening lung problems include increased cough, chest discomfort, wheeze and shortness of breath.

If you or someone you love experiences an asthma emergency or a COPD lung attack, call 911 and go to the nearest emergency department right away. Do not drive yourself. Take your fast acting (rescue) inhaler as necessary on your way to the hospital.

What can you do to prevent problems when there is wood smoke in the air?
General recommendations for everyone to avoid forest fire smoke:

Remain indoors.

Keep doors, windows and fireplace dampers shut.

Use air conditioners on the recirculation setting so outside air will not be moved inside.

Refrain from exercising outdoors.

Take extra precaution with children, who are more susceptible to smoke because their breathing systems are still developing and they breathe in more air (and therefore more smoke) than adults.

Older adults are more likely to have heart or lung disease, which can make them more susceptible to smoke. Extra precaution should also be taken during forest fire season.

Keep your windows and vents closed while driving. Again, only use air conditioning in the "recirculate" setting.

Pay attention to air quality reports on the local news channel or these websites:

Remember: dust masks will not protect your lungs from the fine particles in smoke. If you have lung disease, you should:

Always keep your lung disease well-managed and under good control before forest fires can cause a problem.

Follow your action plan developed with your doctor. If you don't have a written asthma action plan, print one and ask your doctor to fill it in.

Use your rescue medication if you need it.

Talk to your doctor ahead of the forest fire season to know what to do before there is a problem.

People using home oxygen should not make any changes to the oxygen - call your doctor if you have questions or concerns.

If breathing symptoms are not relieved by the usual medicines, seek medical attention. Symptoms to watch for include: increased wheeze, cough, shortness of breath, and chest heaviness.

Make sure your medications are up-to-date and filled. Everyone with Asthma or COPD should have a fast acting (rescue) inhaler with them at all times. Learn how to take your inhaler using the best techniques.

If you live in an area that you might need to evacuate due to forest fires or wild fires, be prepared. Pack an emergency kit which includes extra medications. Learn more from the Government of Canada on how to prepare for a wildfire.

For more information please call our toll-free number 1-866-717-2673 to speak with one of our certified respiratory educators:

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Forest fires are often a concern in Canada, especially during dry, hot summers. People all over Canada may be affected by the smoke from forest fires. The Canadian Lung Association urges those with lung disease such as asthma and COPD to monitor their breathing and avoid exposure to smoke.

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Mao, W., Adu, M., Eboreime, E., Shalaby, R., Nkire, N., Agyapong, B., Pazderka, H., Obuobi-Donkor, G., Owusu, E., Oluwasina, F., Zhang, Y., & Agyapong, V. I. O. (2022). Post-Traumatic Stress Disorder, Major Depressive Disorder, and Wildfires: A Fifth-Year Postdisaster Evaluation among Residents of Fort McMurray. International Journal of Environmental Research and Public Health, 19(15), 9759-. https://doi.org/10.3390/ijerph19159759

# data[].attributes.subject
Mao, W., Adu, M., Eboreime, E., Shalaby, R., Nkire, N., Agyapong, B., Pazderka, H., Obuobi-Donkor, G., Owusu, E., Oluwasina, F., Zhang, Y., & Agyapong, V. I. O. (2022). Post-Traumatic Stress Disorder, Major Depressive Disorder, and Wildfires: A Fifth-Year Postdisaster Evaluation among Residents of Fort McMurray. International Journal of Environmental Research and Public Health, 19(15), 9759-. https://doi.org/10.3390/ijerph19159759

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The findings of this quantitative cross-sectional survey found that 5 years following the Fort McMurray Wildfire back in 2016 , 45% of participants still experience MDD and 39.6% of first respondent suffered from PTSD

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Scoping Review of the effects of wildfires

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Scoping Review of the effects of wildfires

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BMC Public Health 22, Article number: 2274 (2022) Cite this article

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Abstract

Background

Smoke from wildfires is a growing public health risk due to the enormous amount of smoke-related pollution that is produced and can travel thousands of kilometers from its source. While many studies have documented the physical health harms of wildfire smoke, less is known about the effects on mental health and well-being. Understanding the effects of wildfire smoke on mental health and well-being is crucial as the world enters a time in which wildfire smoke events become more frequent and severe. We conducted a scoping review of the existing information on wildfire smoke's impact on mental health and well-being and developed a model for understanding the pathways in which wildfire smoke may contribute to mental health distress.

Methods

We conducted searches using PubMed, Medline, Embase, Google, Scopus, and ProQuest for 1990-2022. These searches yielded 200 articles. Sixteen publications met inclusion criteria following screening and eligibility assessment. Three more publications from the bibliographies of these articles were included for a total of 19 publications.

Results

Our review suggests that exposure to wildfire smoke may have mental health impacts, particularly in episodes of chronic and persistent smoke events, but the evidence is inconsistent and limited. Qualitative studies disclose a wider range of impacts across multiple mental health and well-being domains. The potential pathways connecting wildfire smoke with mental health and well-being operate at multiple interacting levels including individual, social and community networks, living and working conditions, and ecological levels.

Conclusions

Priorities for future research include: 1) applying more rigorous methods; 2) differentiating between mental illness and emotional well-being; 3) studying chronic, persistent or repeated smoke events; 4) identifying the contextual factors that set the stage for mental health and well-being effects, and 5) identifying the causal processes that link wildfire smoke to mental health and well-being effects. The pathways model can serve as a basis for further research and knowledge synthesis on this topic. Also, it helps public health, community mental health, and emergency management practitioners mitigate the mental health and well-being harms of wildfire smoke.

Peer Review reports

Background

Climate change is leading to increased frequency, duration, and severity of wildfires, with longer fire seasons too [ 1, 2, 3, 4, 5]. Wildfires are a growing public health risk due to the enormous amount of smoke related pollution produced, including carbon monoxide, nitrous oxide, volatile organic compounds and particulate matter less than 2.5 μm in diameter (PM 2.5), which are mixtures of solid and liquid particles that are suspended in the air. Wildfire smoke can travel thousands of kilometers from the source polluting the air over distant populations for weeks and months [ 6]. For example, long-range transport of pollutants from Canadian forest fires contributed to peak PM 2.5 and PM ₁₀ values of 200 and 650 μg/m ³ in Baltimore, Maryland [ 7]. These levels were 17 times higher than the U.S. Environmental Protection Agency's National Ambient Air Quality standard for PM 2.5 and four times higher than the PM ₁₀ standard. Wildfire smoke episodes are expected to increase as climate change brings warming temperatures and drier weather, leading to more smoke events even several thousand miles away from the source fires. Climate change models predict a 55% increase in wildfire-related pollution from PM 2.5 (under Representative Concentration Pathway [RCP] 4.5) to a 190% increase (under RCP 8.5) [ 8].

Many studies have examined and documented the physical health harms of wildfire smoke exposure including cardiovascular, respiratory, and neuro-cognitive effects [ 9]. Studies are also documenting these effects occur far from the wildfire. Cardiorespiratory hospitalization rates increased across the mid-Atlantic and Northeastern United States from fires thousands of kilometers away in Quebec Province, Canada [ 10]. O'Dell and colleagues reported that while most large fires occur in the western U.S., a majority of the attributable mortality and asthma morbidity occurs in the eastern U.S., due to the higher population density there [ 11]. Over 1.4 million wildfires have occurred in the U.S. since 2000, causing more than 15,000 fatalities per year due to harmful emissions [ 8]. These harms are unevenly distributed across subpopulations, with children, the elderly, women, racial and ethnic minorities, those living in low socioeconomic areas, and those with preexisting comorbidities at greatest risk [ 12, 13, 14, 15, 16, 17, 18]. Research has not adequately elucidated the mechanisms for these differences in effects [ 18]. While the increased risk faced by children and the elderly may be imparted by physical and physiological susceptibility, disparities experienced across lines of social advantage and disadvantage may result from constructed social and environmental reasons [ 19]. In one intriguing study, Shrestha and colleagues investigated indoor and outdoor levels of PM2.5 in low-income homes at the wildland-urban interface in Colorado on days when ambient air pollution was elevated from short- and long-range wildfire smoke [ 20]. Controlling for indoor impacts from cooking, indoor/outdoor ratios of PM 2.5 were slightly less than one, indicating only slightly higher levels outdoors than indoors due to the use of open windows in these homes for ventilation. The authors hypothesized that poorer quality and older construction and lack of air conditioning, all related to lower socioeconomic status, were associated with these higher rates of indoor air pollution. Rural and Indigenous communities are also at heightened risk for health and well-being impacts of exposure to wildfire smoke [ 21, 22] possibly due to closer proximity to wildfires [ 23], longer residential tenure in smoke-exposed geographies, reduced access to services, and higher levels of comorbidities [ 24]. In Canada, approximately 60% of First Nation reserves are located within regions that are at high risk from wildfire events [ 25].

The increasing intensity of wildfire events and duration of wildfire seasons, combined with current and anticipated wildfire-related health impacts underscores the importance of understanding the full range of potential health effects including impacts on mental health and well-being [ 26]. Herein, we define mental health following the American Psychological Association as "a state of mind characterized by emotional well-being, good behavioral adjustment, relative freedom from anxiety and disabling symptoms, and a capacity to establish constructive relationships and cope with the ordinary demands and stresses of life" [ 27]. The mental health effects of climate change generally, and wildfire smoke specifically, have not been adequately examined compared to physical health endpoints. Studies documenting the risk of adverse mental health consequences after experiencing a wildfire have focused on the traumatic experience of being in a life-threatening experience, losing property, the stress of evacuation, and the stress of recovery [ 28]. Less attention has focused on the effects of smoke on mental health and well-being. Exploring this relationship is even more pertinent considering the growing body of research documenting the negative effects of air pollution on mental health, including depression, anxiety, suicide, and psychological distress [ 29, 30, 31, 32, 33, 34, 35]. Understanding these effects of wildfire smoke is crucial as the world enters a time in which wildfire smoke events can spread hundreds of miles past the immediate burn for prolonged periods of time and the interconnection between the physical and mental well-being effects of smoke is increasingly recognized [ 36].

We conducted a scoping review on the impacts of wildfire smoke on mental health and well-being. Our aim was to review the existing information on wildfire smoke's impact on mental health and well-being and to develop a model for understanding the ways in which wildfire smoke may contribute to mental health distress. For the purposes of this review, wildfire smoke (referred to as bushfire smoke in some contexts) was defined broadly as smoke from the landscape including both wild lands and agricultural lands. This broad definition encompasses various sources of smoke including from forests and peatland fires. It permitted a more wide-ranging and comprehensive review of the literature and was made necessary by existing studies' broad definitions.

Methods

We followed the five phase process outlined by Arksey and O'Malley for conducting scoping reviews [ 37] which includes: (1) identifying the research objectives/questions, (2) identifying relevant publications, (3) selection of publications, (4) data charting, and (5) collating, summarizing, and reporting the results.

Librarians at the U.S. National Academies of Science, Engineering, and Medicine and Lakehead University conducted systematic electronic database searches using Google, Scopus, PubMed, Medline, Embase and ProQuest Research Library from January 1990 to February 2022 to identify scientific papers, journal articles, book chapters, and reports related to mental health and well-being impacts of wildfire smoke exposure [ 38]. This date range was selected to "balance feasibility with breadth and comprehensiveness" as outlined by Levac [ 38] and based on our general knowledge of the scholarly research in this realm (it is noteworthy that only one article identified in our database searches was published between 1990 and 2004, justifying this decision [ 39]). The search was conducted using a combination of multiple keywords including "environmental exposure", "smoke", "mental health", "depression", "anxiety", "psychological symptoms", and "psychological distress". The search was limited to studies in the English language. After duplicates were removed, titles, abstracts and full texts were screened for relevance. Exclusion criteria were applied (see Table 1). Importantly, publications that did not explicitly examine the relationship between mental health and/or well-being and wildfire smoke events/exposures were excluded (i.e., exclusive focus on wildfire evacuations without smoke exposure). Questionable cases were resolved through discussion among the authors. In all cases, we searched the citations of final eligible articles to ensure the inclusion of all the relevant articles. Lastly, we contacted experts to locate unpublished reports from the gray literature. All evaluation of results from these studies was based on the authors' interpretation of the reported findings in each paper.

Table 1 Inclusion and exclusion criteria used in review

The database searches yielded a total of 200 articles (see Fig. 1). After title, abstract and full text screening and eligibility assessment, we identified 16 studies for inclusion and added three more studies from the bibliographies of these publications for a total of 19.

Flow diagram of records identified through database searches, relevance and eligibility screening, and hand searches

A data extraction form, which included 17 items (publication year, main objective(s), methodology overview, exposure data, outcome data, publication type, study design, study population (or unit), sample size, study country, geographic scope, summary of results, mental health/well-being outcomes, emotional impacts, notes about moderators/mediators/pathways, implications/recommended actions, and future research recommendations) was used to structure and support knowledge synthesis. The data charting process was conducted independently by each author and all ambiguities regarding the results and interpretation considered for the final scoping review were discussed among the authors. A short narrative summary of each of the 19 publications was written to further contribute to synthesis. Also, after completing the data charting and narrative synthesis of the 19 publications, the authors met to discuss the potential pathways between wildfire smoke exposure and mental health and well-being and to codevelop the proposed model presented in our results. The authors self-identify as a U.S. white, able-bodied man and a Canadian white settler, able-bodied woman.

Results

The results of this scoping review represent key findings and insights relevant to the impacts of wildfire smoke on mental health and well-being. In the sub-sections below, findings from our analysis of 19 articles are presented. First, we summarize key characteristics of the publications, then we summarize and synthesize the set of studies using quantitative data followed by a summary of the qualitative, mixed methods, and literature review studies. Finally, we provide a model of the potential multiple interacting pathways between wildfire smoke exposure and mental health and well-being.

General characteristics of the publications

Overall, we found that the literature on wildfire smoke and mental health and well-being is growing, characterized by a diversity of study designs and methods, and predominantly taking place in North America and Australia. Table 2 displays the author, date, study objective(s), study design, and mental health and well-being outcomes measured or discussed for all studies included in this review.

Table 2 Summary of 19 studies included in the review

There was an overall increasing trend in the number of publications over time, with 70% published since 2014. Although we searched for publications from 1990 onwards, we only found one published between 1990 and 2004. In terms of geography, the countries which were most represented were Australia ( n = 4), Canada ( n = 5), and the USA ( n = 3) highlighting that most of the literature is situated within high-income countries. Middle-income countries represented, all located within Southeast Asia, included Singapore ( n = 2) and Malaysia ( n = 1); there were no low-income countries represented. Geographic scope of the publications included local/community ( n = 6), regional ( n = 9), national ( n = 1) and international ( n = 3).

Of the 19 publications, 15 were original empirical research, one was a report, and three presented findings from literature review processes. Among the original empirical research publications, nine publications collected and analyzed quantitative data, five qualitative data, and one used mixed methods [the Hazelwood Mine Fire Inquiry [ 44] was a report that also utilized mixed methods]. A diversity of methods and designs were used in the publications. Ecological and cross-sectional study designs using surveys were common among the quantitative publications; semi-structured interviews were used in all five of the publications that collected qualitative data.

Regarding smoke exposure data among the nine studies using quantitative methods, four publications characterized exposure based on population/community exposure to wildfire smoke events (e.g., assumed smoke exposure because of proximity to fire events), three publications used self-reported measures of exposure (e.g., self-reported wildfire exposure as none, mild or severe), and two studies used outdoor air quality monitoring data. With respect to the outcome data for the quantitative studies, most measured mental health and well-being outcomes with self-reported data (five of nine), three used administrative data (e.g., emergency room data, prescription data), and one publication used a physiological measure.

Summary of publications using quantitative data

We reviewed nine quantitative studies. Three studies used administrative data to measure mental health outcomes [ 39, 41, 43]. Duclos compared emergency room visits in six California counties during a wildfire to visits during two reference periods (a year before and two weeks before the fire) [ 37]. There was a statistically significant increase in visits for asthma, COPD and other conditions such as laryngitis but the increase in mental health conditions was not statistically significant ( p = 0.4). Smoke exposure was not specifically assessed or extracted from the medical record and the authors reported that air monitoring could not be quantified reliably for the exposed counties.

Moore analyzed physician billing records to study the relationship between increases in PM 2.5 and PM ₁₀ from wildfires in two regions of Canada and physician visits for physical and mental health complaints [ 41]. There was a positive association between wildfire particulate matter and increased weekly rates of physician visits for respiratory complaints in one of the two regions. Increased rates of visits for cardiovascular and mental illnesses were detected before, during and after the fires and the authors felt they could not be ascribed to the fires. Similarly, Caamano-Isorna analyzed a database of pharmaceuticals prescribed by primary care doctors to study the association of the 2006 wildfires in Galicia, north-west Spain, with respiratory and mental health effects, using the consumption in that region of drugs for obstructive airway diseases and anxiolytics-hypnotics as indicators [ 43]. The study found a significant increase in anxiolytic-hypnotics consumption among men from exposed municipalities; it did not assess smoke exposure independently of fire exposure or other wildfire-related experiences.

Rodney's study surveyed Australian residents of thirty-one postal codes that had experienced high levels of smoke-related air pollution from the 2019-2020 Australian Capital Territory bushfire season [ 6]. Outcomes included self-reported physical health, mental health, and sleep patterns and whether they attributed their symptoms to smoke. Participants were recruited by letters posted to homes, from a pre-existing population panel, and by social media, radio advertisements, and word of mouth. The response rate for the letter invitations was 6.4%. 45.3% reported anxiety due to the smoke and 21.4% reported feeling depressed because of the smoke. Negative mental health symptoms were more common among women and 25-54 year olds. Bivariate models disclosed greater odds of mental health symptoms among parents, persons with pre-existing physical health diagnoses, persons with pre-existing mental health diagnoses, and persons reporting direct exposure to the current fires. Over 37% of respondents reported disrupted or poor sleep which was positively associated in bivariate analyses with females, younger age groups, pre-existing physical diagnoses, direct exposure to the current fires, and direct exposure to previous bushfires.

Two studies employing a trauma mental health framework included questions about wildfire smoke exposure as an indicator of a perceived threat to the safety of participants or their families [ 40, 42]. McDermott conducted a study on posttraumatic stress disorder and general psychopathology in children and adolescents following wildfires in the Australian Capital Territory in 2003 [ 40]. Children and adolescents who saw smoke scored significantly higher on components of the Strengths and Difficulties Questionnaire, a screening instrument for child and adolescent mental health in which higher scores are predictive of psychiatric diagnoses. In the trauma mental health framework, the authors considered witnessing smoke to be an indicator of a perceived threat to the child and adolescent participants or their family, thereby affecting their stress and emotional well-being. In Marshall's trauma mental health study of evacuees of a 2003 Southern California wildfire, difficulty breathing due to smoke or ashes along with house or property damage and physical injury to self or loved one were predictors of a probable PTSD or major depression diagnosis [ 42]. After adjusting for demographic characteristics, difficulty breathing due to smoke exposure was no longer a predictor of probable mental health diagnosis.

Three studies focusing on the smoke and air pollution from annual forest fires caused by agricultural land clearing techniques and burning of tropical peatland, called "haze", reported adverse effects on mental health and well-being [ 36, 45, 50]. Ho studied acute psychological symptoms due to short-term exposure to haze during the 2013 Southeast Asian Haze Crisis [ 36]. Singapore participants were recruited during a week when the Pollution Standard Index (PSI) reached 401 on a scale of 0-500, with > 300 defined as hazardous for health. Participants were a snowball sample of mainly students aged 18-29 years old. The total on the Impact of Events Scale-Revised (IES-R) score was 18.47 (S.D. = 11.69) consistent with mild to moderate psychological stress (primarily intrusion symptoms and hyper-arousal symptoms) but below the threshold of acute stress reaction syndrome at a score of 33. The participants' intrusion symptoms included recurrent thinking about haze, negative feelings from reminders of the haze, dreams about haze, and recurrent mental pictures of haze. The arousal scores included irritability, being easily startled, insomnia, poor concentration, and physical reactions after reminders of the haze. Perceiving a lower level of PSI as dangerous was associated with higher IES-R total scores (β = − 2.734, SE = 1.374, R ² = 0.013, p = 0.047), mean intrusion score (β = − 0.162, SE = 0.074, R ² = 0.016, p = 0.029), and mean hyperarousal score (β = − 0.217, SE = 0.087, R ² = 0.020, p = 0.013). The total number of physical symptoms was associated with the mean avoidance score (β = 0.048, SE = 0.011, R2 = 0.061, p < 0.001), mean intrusion score (β = 0.075,SE = 0.013, R ² = 0.095, p < 0.001), mean hyperarousal score (β = 0.075,SE = 0.013, R ² = 0.095, p < 0.001), total mean IES-R score (β = 0.080, SE = 0.011, R ² = 0.153, p < 0.001), and total IES-R score (β = 0.080, SE = 0.011, R ² = 0.153, p < 0.001).

Tan and colleagues studied the effect of haze exposure on cerebral hemodynamics also during the 2013 Southeast Asian Haze Crisis in Singapore [ 50]. The authors hypothesized that vasoactive substances in the haze would cause cerebral vasculature vasodilation which might lead to psychosomatic symptoms (sore throat, nausea, anxiety, insomnia, poor appetite, headache, neck stiffness, cough, sputum, breathlessness, runny nose, joint pain, rash, lethargy, itching, and watery eyes) [ 50]. Cerebral hemodynamics (pulsatility index, resistivity index), blood pressure, and symptoms were measured before and immediately after participants were exposed to 30 minutes of outdoor haze. Haze exposure caused modest, significant changes in cerebral hemodynamics. Moreover, participants with one or more new psychosomatic symptoms after haze exposure had pronounced changes in cerebral hemodynamics that were not observed among asymptomatic volunteers, leading the investigators to postulate a differential susceptibility to the vasoactive effects of haze on cerebral vasculature.

In the third study of haze in Southeast Asia, De Pretto et al. surveyed two sets of residents of Kuala Lumpur, Malaysia in 2014 about their knowledge, concerns, and practices in relation to haze: amateur athletes taking part in a duathlon and members of the general public in a shopping mall [ 45]. Concern was high in most participants: 70% of persons surveyed reported sadness in response to haze conditions, 80% reported feeling sad because of "the negative effects on the natural environment" and 79% reported being afraid for their health. Concern was significantly higher among participants from the duathlon event than among shopping mall respondents (3.94 ± 0.4 vs. 3.80 ± 0.5; p < 0.05). In analyses of covariance conducted to test the effect of the different variables simultaneously, parenthood (t = 2.90, df = 294, p < 0.05) and age (t = 3.35, df = 294, p < 0.05) were associated with higher concern. There was a weak positive correlation between greater knowledge about the haze and greater concerns (r = 0.15, t = 2.6, df = 300, p < 0.05).

Summary of publications using qualitative data, mixed-methods and literature reviews

As outlined above, our review included five publications using qualitative data, three literature reviews, and two mixed-methods publications (one empirical study and one report). These publications provide a deeper understanding of the lived experiences of the mental health and well-being impacts of wildfire smoke exposure and a more fulsome understanding of the myriad ways that exposure to smoke may affect mental health and well-being beyond clinical diagnostic outcomes and categories.

Three of the qualitative publications examined mental health and well-being impacts in Indigenous communities in Canada and provide intriguing insights into how long periods of smoke events, along with evacuations, can affect mental health and well-being. These studies are particularly valuable given that Indigenous communities, which are commonly located in forest ecosystems prone to wildfire, are at heightened risk of exposure to wildfire and smoke events [ 54]. Importantly, these communities are also at risk of repeated exposures over time and cumulative impacts associated with smoke exposure along with wildfire evacuation processes and face structural and systematic racism and marginalization [ 49]. Mottershead et al. worked with the Dene Tha' First Nation to explore the wildfire evacuation experience, to identify factors that helped and hindered the evacuation process, and to examine how the evacuation process affected evacuees, including mental health and well-being [ 51]. The study was part of a larger project and partnership called the First Nations Wildfire Evacuation Partnership and used a community-based case-study approach. Drawing on individual and group semi-structured interviews with 31 community members, authors reported that the evacuation experience and being confined indoors due to wildfire smoke led to feelings of frustration, isolation, stress, and depression for residents while they awaited updates and for the fire to be contained. Some community members noted that stress lasted beyond the evacuation and wildfire event with longer term consequences for mental health and well-being. Also noteworthy, having limited information overall and about smoke exposure and air quality beyond visual observation exacerbated mental and emotional health impacts. The authors also report that the following factors contributed to the communities' adaptation to the wildfire event and evacuation: strong leadership, keeping families together, providing social support, and using familiar host communities.

Dodd et al's 2018 study examined the impact of prolonged wildfire smoke events on mental health and well-being throughout the summer of 2014 in the Northwest Territories [ 48]. Based on 30 interviews with community members, community leadership, Elders, and other relevant key informants (e.g., local physician and public health official), the research team found that prolonged and persistent smoke exposure had wide-ranging effects on mental and emotional well-being. The majority of those interviewed reported "a direct connection between the wildfires and smoke and a decrease in their mental and emotional health." [ 48]. Elevated feelings of fear, anger, depression, stress, isolation, hopelessness and uncertainty were frequently expressed. Being confined to home and disruptions to land-based activities led to isolation from community and family which exacerbated feelings of loneliness, stress, and anxiety. Personal and community isolation were the most commonly expressed consequences associated with living through the "summer of smoke" [ 48]. Persons who depended on the land for supplementing their food also experienced increased food insecurity. Relatedly, lack of outdoor physical activity was a mental health stressor and the physical symptoms of smoke exposure impeded such activities. The emotional and mental impacts of being separated from the land, outdoor activities, food sources and livelihoods, along with dislocation due to evacuations, are succinctly described by research participants in the following quotations and align with the concept of solastalgia:

It was the lost summer...the attachment to the land and place, what it does, and when you get alienated, you know, from that place...it takes a deep, emotional toll, if not a spiritual toll

As another respondent said:

It was like we didn't have a summer, for me, because, usually we get outside, we do things on the water...we enjoy being in the North. We enjoy being outside. We enjoy the environment. We enjoy cooking. Everything that's outside, we enjoy, and, I feel like I lost that...that impacts you emotionally and mentally

Findings also illustrate community resilience [conceptualized as how communities avoid, reduce, or cope with the damages caused by disasters, and how they recover with minimal social disruption] and a strong sense of community in response to the prolonged wildfire events, smoke exposure, and wildfire evacuations.

Christianson et al. also conducted semi-structured interviews ( n = 35) to learn about experiences of evacuations due to a wildfire and smoke event that occurred in May 2011 in Whitefish Lake First Nation 459 (Alberta, Canada) [ 49]. Although most mental health and well-being consequences reported in this publication were linked specifically to the community evacuation process, participants shared that exposure to smoke heightened feelings of concern, fear, and distress. Seeing smoke in the sky, which is very common in summer months for Whitefish Lake residents, triggered emotional impacts and feelings of concern and fear after returning to the community underscoring the recurring and lasting effects [ 49]. Several studies in our review describe how persons experiencing wildfire events had recurring negative thoughts about their experiences when confronted with reminders like the smell of smoke and images of smoke [ 40, 47, 49, 55].

Humphreys et al. used focus groups and interviews to describe how extreme and persistent smoke events impact mental health and well-being in rural communities in Washington state (USA) [ 21]. Participants discussed a diversity of emotional impacts and responses associated with persistent smoke events including worry, stress, guilt, depression, lack of motivation, hopelessness, and helplessness. Interestingly, those who left the community during smoke events also reported feeling stress as well as guilt. The authors argue that the impacts of wildfire smoke on mental health and well-being may be particularly problematic in rural communities, which tend to be "dependent on contributions of nature to people's quality of life" [ 21]. When discussing pathways leading to anxiety, stress, and depression, key factors included experiencing physical health effects (such as respiratory effects), isolation, and lack of physical exercise. This study also examined how community members coped with these impacts and possible actions to mitigate well-being impacts in future wildfire events. Findings highlighted the need for stress reduction activities and support groups, a community clean air space to facilitate gathering and address social isolation, resources dedicated to strengthening social connections in rural communities, community air quality monitoring, and free air filters (particularly for low-income groups).

Heaney, Vincent, and Reid reported on literature review processes related to wildfire smoke and mental health and being [ 9, 46, 52]. Heaney synthesized current evidence pertaining to optimal public communication strategies used in smoke-related disasters using a scoping review methodology [ 52]. The authors reviewed 67 articles that focused on health communication and/or adverse health effects of smoke exposure in the context of wildfire (bushfire) smoke events. Only 8 of 67 articles in the review made the connection between wildfire smoke events and psychosocial and mental health effects specifically. The authors emphasize that smoke exposure is usually associated with mild psychological distress, that isolation is a common precipitating factor, and that effective health communication may help reduce mental health consequences [ 52]. They also highlight that "... it is difficult to differentiate the psychological impacts specifically related to smoke exposure from other potentially traumatizing factors like forced evacuation from home, an approaching fire front, or the loss of loved ones and belongings".

The literature review from Reid and colleagues [ 9], aimed to assess the evidence of health effects from exposure to wildfire smoke (respiratory, cardiovascular, mental, and perinatal health specifically) and to identify susceptible populations using a modified systematic review methodology (based on Woodruff and Sutton) [ 56]. Studies that were reviewed were assessed for risk of bias based on considerations of sample size, study exposure assessment methods, controlling for potential confounding factors, and use of objective outcome measures. They found six studies that investigated the association between wildfire smoke exposure and objective mental health impacts and outcomes. Two studies were assessed as low potential for bias (which we also describe above); Duclos [ 39] and Moore [ 41]. The review highlighted the lack of rigorous research on the association between wildfire smoke and mental health outcomes and highlighted the "lack of information about which populations are most susceptible to wildfire smoke exposure and associated health impacts".

Vincent et al's literature review focused on wildland firefighter sleep and associated impacts on safety and health (including mental health) illustrating that wildland firefighters who are constantly exposed to smoke, noise and heat may experience impaired sleep quality and quantity which may have physiological and cognitive effects [ 46]. Pelletier also focused specifically on the health of wildland firefighters [ 53]. This study used a survey and semi-structured interviews with wildland firefighters and related personnel to identify health research priorities among this subgroup with heightened vulnerability to health impacts of wildfire smoke. The effects of exposures on fatigue and sleep, stress, and overall mental health (78%) were identified as key research priorities, along with long term health impacts generally.

Finally, two publications included in our review focused on the Hazelwood Mine Fire, a 45 day-long mine fire sparked by a nearby bushfire which led to persistently elevated air pollution and dramatic, thick plumes of ash and smoke covering nearby towns [ 44]. The Hazelwood Mine Fire Inquiry used a Rapid Health Risk Assessment approach and gathered qualitative and quantitative data to generate a comprehensive after event report and to examine the health effects that the smoke and ash produced [ 44]. Due to the fire and smoke event, families had to move away, wear masks and staying indoors to reduce smoker exposure. Also, schools relocated and businesses closed down. The assessment of psychological impacts stated:

Many community members have developed levels of anxiety and depression, which they attribute to the mine fire. Issues raised by community members at community consultations included concern about evident smoke and ash and the generally unpleasant environment during the mine fire, and also the unknown long-term impact of the mine fire to their health. A number of individuals advised that they were afraid to leave their home for the period of time that the mine fire was burning. Many residents also suffered anxiety and stress from disrupted family life, the loss of enjoyment of their home and neighborhood, the smell in the air, and because they could not go outside.... The Board also heard evidence about the broader social effects of the Hazelwood mine fire. Concerns were expressed during community consultations about the potential for an increase in family violence in the short to medium-term as a result of stress caused by the mine fire. Professor Campbell advised the Board that the whole community, especially young children, are at risk of psychosocial impacts as a result of the emergency, including an increased risk of family violence, drug and alcohol abuse, depression and anxiety, post-traumatic stress disorders and phobias. (Part 4, page 318)

The Hazelwood Mine Fire Inquiry emphasized that the community was highly concerned about the long-term physical and mental health impacts of smoke and ash exposure associated with the fire [ 44]. A phenomenological analysis of school relocation due to the Hazelwood Mine Fire by Berger et al. supports the report's findings and describes elevated anxiety among students and increases in stress and violence in the home [ 47].

Pathways between wildfire smoke exposure and mental health and well-being

The publications we reviewed provide insights into underlying pathways which may connect smoke exposure with adverse mental health and well-being. We identified potential mechanisms operating at several levels including the Individual, Social and community networks, Living and working conditions, and Ecological levels (Fig. 2) These levels are nested and interactively influence mental health and well-being. Mechanisms can cross between multiple levels and can influence mental health and well-being differently, based on cumulative and intersectional experiences. The interplay and interaction between these mechanisms may be complex and vary in different communities, people, and situations. Our model is adapted from Lawrance and colleagues [ 57], which was based on Dahlgren and Whitehead, Bronfenbrenner's Ecological Systems Theory and the Lancet Commission for Global Mental Health and Sustainable Development [ 58, 59, 60]. The model is based on limited evidence since the number of publications in our review is small and a heterogeneous mix of populations, outcomes, and study types. However, it illustrates the need for future research to consider the variety of mechanisms and interconnected levels by which wildfire smoke may harm mental health and well-being.

Potential pathways between wildfire smoke exposure and mental health and well-being

Individual level mechanisms include physiological and physical mechanisms such as diminished sleep quantity and quality [ 6, 46, 53], changes in cerebral perfusion [ 50], physical symptoms from the smoke [ 6, 21, 36, 48], food insecurity [ 48], and reductions in outdoor physical activity [ 48]. The individual level also includes psychological and emotional mechanisms, such as previous negative physical harms from the smoke, perceived risk of danger [ 36], and negative reminders from smoke [ 36, 40, 47, 49, 55]. These are nested in social and community network factors including isolation from people [ 21, 46, 48, 51, 52] and reduced summertime outdoor activity brought on by smoke [ 48], the potential for family stress and violence that may occur [ 44], and risk communications from authorities that may be limited or inadequate [ 36, 51, 52].

The individual level and social and community level factors are placed in the context of living and working conditions such as home evacuations [ 6, 26, 49, 49, 51, 55], school relocations [ 44, 47], and reductions in access to one's livelihood [ 21, 44, 48] particularly for outdoor workers and people in the recreation and tourism industries. All of this occurs in the ecological context of increasing and possibly yearly, repeated and prolonged smoke events and the feeling of a loss of nature that occurs [ 21, 44, 48]. As authors have noted, it is challenging to tease out the mental health impact of exposure to wildfire smoke from the impact of evacuation and traumatic experiences such as an approaching fire front and lack of information or poor communication from government agencies [ 6, 52]. Though these proposed pathways arose from our review they must be considered preliminary and hypothetical.

Discussion

We provide a scoping review examining how wildfire smoke may affect mental health and well-being. With coverage of the global, quantitative and qualitative literature spanning outcomes, our study offers the most comprehensive review of research on the mental health and well-being consequences and pathways to date.

Compared to the understanding of the physical health impacts of wildfire smoke exposure, the understanding of the mental health impacts of wildfire smoke is in its infancy. Our review suggests that exposure to wildfire smoke may have mental health impacts, particularly in episodes of chronic and persistent smoke events, but the evidence is inconsistent and limited. The knowledge and evidence gaps alongside the growing risks of exposure and impacts underscore the importance of additional research in this realm.

Reviewing the quantitative research, overall, we concur with Reid that methodological limitations make it difficult to reach a conclusion from these studies [ 9]. Studies of comparable events such as seasonal haze do find an association [ 36, 45, 50] but also have a likelihood of bias due to their non-random samples. Studies applying a trauma framework do not provide sufficient information to assess the association [ 40, 42]. Moreover, it is difficult to tease out the differential impacts of exposure to wildfire smoke from other frightening and traumatic experiences such as witnessing fire or an evacuation. Short term exposures like those studied by Moore and Duclos may not have a mental health impact [ 39, 41]. Also, using administrative health data may limit detection in rural communities where population density and both mental healthcare seeking and access are low.

The quantitative empirical studies were further limited by their methods of exposure determinations and measurement of mental health outcomes. It is challenging to accurately assess exposure, and many studies relied on self-reported exposure or duration of time exposure. For example, a limitation of both Moore's and Caamano-Isorno's studies is that the exposure classifications are crude and non-specific [ 41, 43]. All residents in the population are assumed to be equally exposed during the fire period which is not likely the case. None of the quantitative studies adequately examined the characteristics differentiating vulnerable and susceptible sub-groups though Reid's literature review study did aim to identify susceptible populations [ 9]. Also relevant, the long-term mental health and well-being impacts of wildfire smoke, and the impacts of exposure to multiple events, are inadequately understood in the existing literature.

Qualitative studies provide a richer sense of the topic and a more fulsome understanding of lived experiences. In Dodd's study conducted after a wildfire season with over 40 days of smoke, affected residents far from the fires said it was like they lost their summer [ 48]. People reported isolation from others, less community participation, loss of nature, and worsened mental health.

The learning from qualitative research allows a more nuanced understanding of the social well-being, emotional well-being and spiritual impacts of wildfire smoke events and exposures. Qualitative research provides outcomes of importance beyond diagnostic codes and categories which are inherently limited in information and meaning, and likely less prevalent. It provides an opportunity for cultural framing of mental health. By avoiding the pathologizing framework of mental health diagnoses it also allows more stakeholders to engage, for instance first responders and community members who may not want to be pathologized as traumatized [ 42]. Qualitative research is well suited to community participatory research methods and greater community ownership over the research process and results. Understanding wildfires, particularly smoke but any of the issues examined here, as lived experiences invites greater discourse.

Our model of the potential pathways between smoke exposure and mental health and well-being effects is a contribution that scientists can use to connect the lessons of past studies with future research. The mechanisms proposed are supported by research in similar fields uncovering the biological and non-biological channels through which non-wildfire related air pollution leads to mental health problems. The population mental health effects of urban fine particulate air pollution (PM 2.5 and PM ₁₀) from industrial and motor vehicle emissions is documented [ 61, 62]. A study in Belgium found that the association between air pollution derived PM 2.5 and generalized anxiety disorder was partially mediated by a difference in physical activity and Wang reported the association between PM 2.5 and depression was mediated by physical activity [ 30, 36]. Inhaled pollution activates biological pathways implicated in the development of depression [ 61, 62] and wildfires may have worse toxicities; for example, the particulate matter in wildfire smoke may be more toxic to lung tissue than particulate matter from ambient air pollution [ 63, 64]. While concentrations of fine particulate matter from U.S. anthropogenic sources are decreasing due to reduced industrial emissions, climate model simulations predict a 55% increase in wildfire-related PM 2.5,-making the study of wildfire smoke's mental health effects all the more important [ 8]. As regulations seek to further reduce anthropogenic sources of emissions, wildfire smoke may become the major source of ambient air pollution in regions of the continental United States [ 8, 65]. Air pollution studies also suggest that psychological factors can moderate vulnerability to the negative effects of environmental pollutants on health and physiology [ 64, 66, 67]. We suggest that living under the lockdowns of the COVID-19 pandemic may have given readers some sense of what this is like; the isolation from community and the dread that leaving the house to go into the world outside is fundamentally dangerous might sum up the isolating and fearsome experience of the pandemic and persistent wildfire smoke events.

Implications for future research

Our review suggests many priorities for future research. We recommend more rigorous methods to generate more robust conclusions about the mental health and well-being impacts of wildfire smoke exposure. For example, improved epidemiological studies that accurately measure individual and population smoke exposure are needed to better characterize specific health impacts. The reviewed wildfire research used self-reported exposure or spatially and temporally resolved models of exposure to outdoor wildfire smoke levels as proxies for exposure, without accounting for the effects of pollutant transfer indoors. Advances in the measurement of wildfire smoke and air quality are needed to address the existing limitations in exposure assessment [ 68]. Wildfire smoke exposure accounting for indoor and outdoor chemical and particulate matter concentrations can improve this exposure characterization. Emerging technologies in ground-level monitoring of air quality alongside innovations in wearable sensors that reduce the potential of misclassification bias in exposure assessment present opportunities for addressing existing gaps and limitations in the existing research. Another priority is research differentiating between mental illness or probable mental illness on the one hand and emotional well-being on the other. Quality of life should also be studied as an outcome. Current research is mostly from the global north (United States, Canada, Australia) with only three studies published from the global south. Studies conducted in the global south are urgently needed where fuel types may differ, susceptible populations may differ, fires frequently extend for long times, and interventions to protect mental health and well-being may differ [ 69]. For example, seasonal "haze" is created by wildland fires due to slash-and-burn techniques for clearing agricultural lands in South Asia, where the cultural framing of mental health and well-being may differ compared to the global north and where mental health resources are in short supply.

At the same time, more work is needed to identify the contextual factors that set the stage for mental health and well-being effects and the pathways and mechanisms that link wildfire smoke to mental health and well-being effects. Our proposed pathways model can be used to inform future data collection investigating how smoke harms mental health and well-being. Since reducing the factors and their interactions may also positively influence mental health, the model can be used to understand which protective factors mitigate against mental health and well-being harms. Still, missing from the research is anything more than a preliminary understanding of which pathways may be important in different populations and contexts. This includes identifying susceptible populations and a better understanding of the mechanisms and risk factors underlying the associations. Additional contextual factors that should be considered are socioeconomic disadvantage, marginalization, and housing attributes that influence the indoor accumulation of wildfire smoke. The specific groups studied in the papers we reviewed included fire-fighters, Indigenous communities (in Canada), and residents of rural communities. Further research is needed to uncover other mechanisms and mediators that may explain mental health and well-being effects in other groups, such as age (particularly children) and gender groups. Finally, studies to date have focused mainly on the Individual level and Social and community network level. Additional factors that may influence risk and impact such as experiences of systemic racism and community cohesion should be considered in future research.

The accelerating increase in wildfires and population smoke exposures calls for new priorities and approaches, too. Wildfires are becoming chronic, multi-week events, as was seen in Australia in 2019 and California in 2020 [ 21]. Residents of rural areas in Washington state (USA) call the summer wildfire smoke season the "Fifth Season" "when smoke from wildfires blankets North Central Washington for weeks or even months at a time." [ 70] As outlined in the Hazelwood Mine Fire inquiry, the long term adverse effects of exposure to smoke, including mental health impacts, are of great concern to the community [ 44]. This parallels studies on emotional distress brought on by chronic industrial and vehicular air-pollution. But the only studies that considered chronic exposure have been qualitative; longitudinal studies particularly of cumulative and chronic exposures are required [ 44, 47, 48, 51].

Finally, we found only one study that addressed community response to chronic wildfire smoke [ 21]. Needed are studies identifying actions, strategies, and interventions individuals, families and communities use to cope with wildfire smoke events such as community gathering spaces, community monitoring, and clean air spaces [ 21]. Participatory research, that engages with at-risk and affected communities throughout the research process in meaningful ways, is particularly well-suited to identifying solutions and interventions. Understanding the mediators of mental health effects can be useful to intervention development too. For example, Ho suggests in their study of the psychological impact of haze that reducing physical symptoms from smoke and addressing its perceived danger through updates, education and regular communications may help reduce psychological stress [ 36]. Motterhead similarly found that limited official communications about smoke exposure and air quality exacerbated mental and emotional health impacts, further underscoring the need for updated communications (and community based air quality monitoring) [ 51]. More rapid research conducted during and directly after events can address these topics.

Although this paper presents results from a comprehensive, transparent, and repeatable scoping review process, there are limitations that should be recognized when interpreting the findings and considering implications. First, our review only searched for and therefore only includes English language papers. This may have influenced our finding papers mainly from the countries of the global north. Similarly, only a few studies centered the perspectives of Indigenous First Nation communities so the results reflect primarily a Western-centric, high-income country perspective of mental health and well-being. We set the start date for our search in 1990 due to constraints of time and resources for the review. Including earlier years in our literature search could add to the available data and enrich the results. However, our inclusion of only one paper from the decade 1990 to 2004 suggests that papers before 1990 are unlikely. Any variability in the outcomes we found may be influenced by the heterogeneity of the populations studied, variability of the wildfire smoke exposures, and the range of health outcomes studied. Also, because we used a scoping review process, we did not assess the quality of articles included in our review [ 37]. The qualitative research we reviewed provided a contextual exploration of the possible pathways, still we recognize that these study findings may not be generalizable to all communities.

Conclusion

We provide the first scoping review ever conducted examining how wildfire smoke may affect mental health and well-being. We identified potential pathways for mental health and well-being impacts that exist on multiple levels. These pathways that we organized in a nested model can guide researchers in their future data gathering. They provide a conceptual framework for future knowledge synthesis efforts in this topic. Also, they may be helpful to public health, community mental health, and emergency management practitioners seeking to mitigate the harms of wildfire smoke on mental health and well-being. Future studies should focus on the chronic, persistent or repeated smoke events. More research is required beyond those of richer Northern countries and across cultures with different understandings of mental health, available resources, and needs for intervention. Well-being and quality of life should also be studied as an outcome. This can be addressed best in large longitudinal cohort studies that monitor the trajectories and long-term impacts of susceptible populations. The data and key findings of this report highlight gaps in the literature and suggest areas for theoretical, methodological, and empirical advances for wildfire smoke and mental health research.

Availability of data and materials

The datasets used and analyzed during the current study are available from the corresponding author on reasonable request.

References

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Acknowledgments

We are pleased to acknowledge Brigitte Champaigne-Klassen for the design of our Fig. 2, Kris Eclarino and May M.T. Kyaw for data abstraction, and librarian Debra Gold for her assistance with electronic database searches.

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Authors and Affiliations

1. David Geffen School of Medicine at UCLA, UCLA Fielding School of Public Health, Center for Healthy Climate Solutions and Center for Public Health and Disasters, 1100 Glendon Avenue, Suite 850-878, Los Angeles, CA, 90024, USA

David P. Eisenman

2. Lakehead University Department of Health Sciences, 955 Oliver Road, Thunder Bay, ON, P7B 5E1, Canada

Lindsay P. Galway

Contributions

DPE conceived and led the study. DPE and LPG directed the search and data abstraction, and participated in all data extraction. DPE and LPG wrote the manuscript text and prepared all figures and tables. All authors read and approved the final manuscript.

Authors' information

DPE is a Professor-in-Residence in the David Geffen School of Medicine at UCLA and the Fielding School of Public Health where he co-directs the Center for Healthy Climate Solutions and directs the Center for Public Health and Disasters. LPG is an Associate Professor in The Faculty of Health and Behavioural Sciences at Lakehead University. She also holds a Canada Research Chair in Social-Ecological Health and co-leads the Confluence Co-laboratory.

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Correspondence to David P. Eisenman.

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Eisenman, D.P., Galway, L.P. The mental health and well-being effects of wildfire smoke: a scoping review. BMC Public Health 22, 2274 (2022). https://doi.org/10.1186/s12889-022-14662-z
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DOI: https://doi.org/10.1186/s12889-022-14662-z

Keywords

# data[].attributes.attachment_link.title
The mental health and well-being effects of wildfire smoke: a scoping review - BMC Public Health

# data[].attributes.attachment_link.description
Background Smoke from wildfires is a growing public health risk due to the enormous amount of smoke-related pollution that is produced and can travel thousands of kilometers from its source. While many studies have documented the physical health harms of wildfire smoke, less is known about the effects on mental health and well-being.

# data[].attributes.body
https://www.lung.org/blog/how-wildfires-affect-health#:~:text=They%20spread%20air%20pollution%20not,threats%20seriously%20and%20be%20prepared.

# data[].attributes.body
ischemic heart disease and stroke, is associated with increased levels of air pollutants. Wildfire events can cause an abrupt increase in ambient pollutants. Exposure to such short-term elevations are capable of evoking cardiac arrhythmias, worsening heart failure, and triggering atherosclerotic/ischemic cardiovascular complications,

# data[].attributes.body
Hypoxia (inhalation of carbon monoxide)

damage to mucosal structures in airway

edema of upper airways

bronchoconstriction

Acute respiratory failure

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Abstract

Smoke inhalation injury is a major determinant of morbidity and mortality in fire victims. It is a complex multifaceted injury affecting initially the airway; however, in short time, it can become a complex life-threatening systemic disease affecting every organ in the body. In this review, we provide a summary of the underlying pathophysiology of organ dysfunction and provide an up-to-date survey of the various critical care modalities that have been found beneficial in caring for these patients. Major pathophysiological change is development of edema in the respiratory tract. The tracheobronchial tree is injured by steam and toxic chemicals, leading to bronchoconstriction. Lung parenchyma is damaged by the release of proteolytic elastases, leading to release of inflammatory mediators, increase in transvascular flux of fluids, and development of pulmonary edema and atelectasis. Decreased levels of surfactant and immunomodulators such as interleukins and tumor-necrosis-factor-α accentuate the injury. A primary survey is conducted at the site of fire, to ensure adequate airway, breathing, and circulation. A good intravenous access is obtained for the administration of resuscitation fluids. Early intubation, preferably with fiberoptic bronchoscope, is prudent before development of airway edema. Bronchial hygiene is maintained, which involves therapeutic coughing, chest physiotherapy, deep breathing exercises, and early ambulation. Pharmacological agents such as beta-2 agonists, racemic epinephrine, N-acetyl cysteine, and aerosolized heparin are used for improving oxygenation of lungs. Newer agents being tested are perfluorohexane, porcine pulmonary surfactant, and ClearMate. Early diagnosis and treatment of smoke inhalation injury are the keys for better outcome.

Keywords: Burns, lung injury, smoke inhalation injury

INTRODUCTION

In major fire disasters such as 9/11 bombing of the World Trade Centre in New York, smoke inhalation injury was an important cause of mortality.[ 1] Smoke inhalation injury increases the mortality by 24 times in fire-related injuries[ 2] and is highlighted to be one of the most important risk factors increasing the morbidity and mortality.[ 2]

The objective of this article is to review the etiopathogenesis, early diagnosis, and latest management guidelines of smoke inhalation injury. This knowledge is important for anesthesiologists, emergency physicians, and critical care specialists, who are frequently involved in the care of these patients.

PATHOPHYSIOLOGY

Smoke inhalation injury is caused by the inspiration of steam, superheated gases, or toxic, often incomplete products of combustion. The heating capacity of steam is 4000 times that of hot dry air and thus causes tissue damage, even with momentary contact.[ 3] The various toxic compounds present in smoke are carbon monoxide (CO), hydrogen cyanide (HCN), phosgene, ammonia, sulfur dioxide, hydrogen sulfide (H ₂S), formaldehyde, and acrylonitriles.[ 3] Some of these superheated products of combustion are inhaled, causing thermal burns to the airway mucosa.[ 4] Particles larger than 10 μ in size are retained in the nasopharynx, but 1-2 μ sized particles can pass into the alveoli.[ 5]

Smoke inhalation results in three physiological types of injury: (a) thermal injury predominantly to the upper airway; (b) chemical injury to the upper and lower respiratory tract; and (c) systemic effects of the toxic gases such as CO and CN. Early deaths in fire are predominantly due to hypoxia, which results from a lethal synergistic effect of low oxygen (O ₂) levels (due to massive O ₂ consumption during combustion) and inhalation of high concentrations of CO and CN (resulting in inability to use O ₂ at tissue level).[ 6] The major pathophysiological change is edema formation in the respiratory system (airway and lungs).

The anatomical areas affected by the smoke inhalation are as follows.

Supraglottic area/upper airway

The oropharyngeal mucosal structures are damaged primarily by the heat transfer and secondarily via the release of chemical mediators [ Figure 1 ].[ 4, 7] Thermal injury releases substance P, calcitonin gene-related peptide, eicosanoids, neural endopeptidase, and interleukin-8 (IL-8), which attract polymorphonuclear cells and release proteases, thus further aggravating the inflammation.[ 7] There is marked swelling of the tongue, epiglottis, and glottis. This leads to increased edema in the upper airway and can lead to airway compromise. Thermal injury rarely occurs below the vocal cords because high blood flow in the upper airway cools it efficiently.[ 4, 8]

Tracheobronchial tree/lower airway and lungs

The chemicals present in smoke lead to inflammation and edema of the tracheobronchial tree.[ 3, 7, 8] Within 3 h of smoke inhalation injury, the bronchial blood circulation is increased by 10-20 times due to increased cardiac output and hypermetabolic response.[ 9] The upper and lower airways become characteristically hyperemic.[ 8, 9] The blood flow is increased by 4-6 times in the lungs.[ 9] This increase in bronchial blood flow leads to edema of the airway, fluid exudation, and flux of inflammatory mediators. Ligation of bronchial circulation attenuates the lung edema after smoke inhalation injury in ovine models.[ 10] The circulation of inflammatory mediators increases the permeability of the bronchial vasculature and pulmonary transvascular fluid flux exacerbating the pulmonary edema.[ 10]

All the variables of Starling equation favoring pulmonary edema are activated.[ 11] The microvascular hydrostatic pressure is increased, interstitial hydrostatic pressure is decreased, interstitial oncotic pressure is increased, and the reflection coefficient is decreased, leading to pulmonary edema.[ 11] There is disruption of the ciliary mucosa and sloughing of the bronchial columnar epithelium, which leads to obstruction of the airway and alveoli [ Figure 2 ].[ 9, 12] The leakage of plasma-rich fluid contains procoagulants that accentuate solidification of the cast. This bronchial occlusion increases the risk of infection in lungs. The toxic chemicals present in smoke decrease the surfactant levels, resulting in widespread micro-atelectasis and ventilation-perfusion mismatch.[ 13, 14, 15]

The pathophysiological details of airway and lung injury are shown in Figure 3 . The irritants present in smoke stimulate sensory nerve endings of the tracheobronchial tree, releasing neuropeptides which cause bronchoconstriction and activate nitric oxide synthase (NOS).[ 13, 14] The arginine levels are decreased in the burn victim, which cause NOS to produce reactive oxygen species (ROS) [ Figure 3 ].[ 15] ROS react with NO to form reactive nitrogen species (RNS).[ 13, 14] ROS and RNS increase the capillary permeability and hydrostatic pressure of the bronchial microvasculature [ Figure 3 ].[ 13, 14] There is an increase in neutrophil infiltration, resulting in pulmonary interstitial edema and marked reduction in lung compliance.[ 13, 14] Neutrophils are activated to release the proteolytic enzymes (such as elastase), which damage lung parenchyma.[ 13, 14] The biomarkers of acute lung injury (such as IL-6, IL-8, IL-10, and tumor-necrosis-factor [TNF]-alpha) are increased in most of the victims of smoke inhalation injury.[ 13, 14] There is increased risk of developing acute respiratory distress syndrome, which subsequently leads to acute respiratory failure. The repair enzyme polyADP-ribose polymerase (PARP) is activated, depleting ATP, resulting in cellular dysfunction and apoptosis [ Figure 3 ].[ 16] Increased production of NO inhibits the hypoxic pulmonary vasoconstriction,[ 17] further aggravating the hypoxia resulting from airspace obliteration.

SYSTEMIC CHANGES

Burn injury leads to cytokine-mediated inflammatory response at both the site of burn and even distant site. Sepsis, loss of proteins, and immunodeficiency result, which further aggravate the injury.[ 18] The CO and CN poisoning further compounds hypoxia by affecting the O ₂ transport or utilization.[ 6]

Carbon monoxide poisoning

Asphyxia from CO toxicity is the main cause of rapid death among the victims of fire.[ 6] As O ₂ is consumed, incomplete combustion predominates, generating CO.[ 19] CO and O ₂ compete for the O ₂-binding sites on hemoglobin (Hb) with an avidity of 250:1. The lower the partial pressure of O ₂ (pO ₂), the greater the success of CO in occupying the O ₂-binding sites. The binding of CO shifts the oxyhemoglobin (O ₂ Hb) dissociation curve to the left, increasing binding affinity of O ₂ to Hb; thus, requiring a greater degree of tissue hypoxia before O ₂ can be offloaded. Finally, CO binds to intracellular cytochromes (a and a ₃), resulting in an inability of the tissues to use oxidative energy pathways.[ 19] The net effect is widespread asphyxia, which is out of proportion to the pO ₂ measured by blood gases. The restricted O ₂ delivery predominantly affects the organs which have a high rate of O ₂ utilization, such as brain and heart.[ 6, 19]

The clinical manifestations of CO toxicity often vary with the concentration of blood carboxyhemoglobin (COHb) [ Table 1 ].[ 19] The survivors develop long-term neurologic and affective sequelae.[ 19] CO poisoning is diagnosed by a history of CO exposure, an increase in COHb levels, and ruling out the other causes of symptoms/signs. Pulse oximetry and arterial blood gases may be otherwise normal early in the course of treatment as they cannot differentiate between O ₂ Hb and COHb. Pulse oximetry gives falsely high readings. Newer generation pulse oximeters such as Masimo Rad 7 or Rainbows measure specifically HbCO (and also methemoglobin) and will therefore detect the CO poisoning early.[ 20]

Table 1

Hydrogen cyanide poisoning

CN inhibits mitochondrial cytochrome C oxidase, a component of the respiratory chain, thus inhibiting oxidative phosphorylation and causing tissue hypoxia because of inability to use the delivered O ₂.[ 21, 22] CN poisoning affects the central nervous system, respiratory system, and cardiovascular system, proportionate to the concentration of cyanide inhaled.[ 21, 22] The symptoms of CN toxicity vary from tachycardia, tachypnea, dyspnea, drowsiness, and headache at low concentration to cardiac arrhythmias, hypotension, convulsions, paralysis, cardiorespiratory collapse, and coma at high concentration (>100 ppm).[ 21, 22] Blood cyanide levels can be measured to confirm exposure to CN.[ 21, 22]

COMPLICATIONS OF INHALATION INJURY

The victims of smoke inhalation injury can develop acute respiratory distress syndrome and respiratory failure needing ventilator support[ 23] and placing them at risk for ventilator-associated complications such as barotrauma and pneumonia.[ 24] Infectious complications such as tracheobronchitis, bronchiectasis, bronchiolitis obliterans, and pneumonia can develop in 38%-60% of the victims, after 3-10 days of smoke inhalation injury,[ 25] and are associated with a mortality of up to 60%.[ 25]

The airway may remain hyperreactive for up to 6 months after extubation. Damage to the larynx by inhaled toxins or prolonged intubation can cause persistent hoarseness or dysphonia.[ 26] The injury to epithelium of upper airway from initial injury can cause tracheoesophageal fistula, tracheomalacia, late subglottic stenosis, or tracheobronchial polyps.[ 26] Smoke inhalation injury leads to severe restrictive ventilatory dysfunction, mild obstructive ventilatory dysfunction, and reduced diffusing capacity,[ 27] which may persist for many months.

DIAGNOSIS OF SMOKE INHALATION INJURY

Smoke inhalation injury is diagnosed by a combination of history of exposure to fire and smoke, physical examination, fiberoptic bronchoscopy (FOB) (carbonaceous debris, erythema, ulceration), laboratory investigations, and radiological tests (chest computed tomographic [CT] scan).[ 28, 29, 30, 31, 32]

History

The history should be obtained regarding the source of combustion, duration of exposure to smoke, time elapsed since injury, and manner of exposure to smoke (open or enclosed space, such as house fires/industrial accidents).[ 28, 29, 30, 31, 32]

Signs/symptoms of inhalation injury

Shortly, after fire exposure, there may be only a few symptoms/signs of airway damage. This is not reassuring as life-threatening airway and lung impairment may follow quickly. Early clues of smoke inhalation injury are facial burns, hoarse voice, singed nasal hair, carbonaceous sputum, and soot/carbonaceous material in the oral cavity.[ 28, 29, 30, 31, 32] Facial/oral edema, stridor, wheezing, dyspnea, and cyanosis are the signs of advanced damage.[ 28, 29, 30, 31, 32]

Investigations

The baseline tests include complete blood count, serum electrolytes, creatinine, arterial blood gases, electrocardiogram, and chest X-ray. A toxicology screen for prescribed and street drugs should be supplemented with fire-specific toxins such as blood cyanide and COHb.[ 19, 22] The chest radiograph appears normal initially, but later, it may reveal atelectasis, consolidation, and/or pulmonary edema.[ 28, 29, 30, 31, 32] Chest CT scan may reveal ground-glass opacities in peribronchial distribution, within a few hours of inhalation injury.[ 33] Chest CT scan is helpful to rule out smoke inhalation injury in case of any doubt in diagnosis and can identify the extent of injury to the distal airway, which is missed by FOB.[ 33]

Grading of severity

FOB is used to assess the severity of smoke inhalation injury, which correlates with clinical signs/symptoms.[ 35] Bronchial wall thickness measured by chest CT scan correlates with the severity of smoke inhalation injury.[ 36] Plasma COHb, airway neutrophilia, and cytokine release also correlate with the severity of smoke inhalation injury.[ 37] The PaO ₂/FiO ₂ ratio is a very good indicator of the prognosis and severity of smoke inhalation injury.[ 38]

MANAGEMENT

The victim should be immediately evacuated from the site of fire and decontaminated using full isolation precautions.[ 39] All clothing as well as rings, watch, and jewelry should be removed as soon as possible, as they may be contaminated by toxins (such as HCN), or may retain heat, and produce a tourniquet-like effect in the event of swelling.[ 39]

Advanced trauma guidelines should be followed, and a primary survey should be performed to identify any immediate life-threatening conditions (under "airway-breathing-circulation" scheme).[ 32] Definitive airway may be difficult to obtain in the field, depending on the skill level of the first responder and the degree of airway edema. Repeated failed attempts at intubation may result in upper airway trauma, exacerbation of edema, initiation of bleeding, and total loss of airway patency.[ 32] For victims without evidence of impending airway compromise at the scene, it would seem prudent to delay intervention until the patient arrives at the hospital and has access to advanced airway management tools and expertise. For victims with signs or symptoms of airway compromise from inhalation injury at the scene, the decision regarding airway management is more difficult. If necessary, bag-mask ventilation with humidified O ₂ may provide a bridge to deliver the patient to hospital, when the transport time is short. Intravenous (IV) access should be obtained and fluid infusion started at the scene.[ 39] Later, a secondary survey should be performed to obtain information regarding medical history, medications, allergies, and concomitant injuries.[ 31, 32, 39] A thorough physical examination, including neurological assessment, is advocated.[ 31, 32, 39]

Airway management

The patency of airway is at risk with time as is the maintenance of ventilation and oxygenation. The need for an advanced airway is difficult to predict as airway patency can decrease with even minimal appearing airway burn and small skin surface burns; the rate of encroachment of the airway may vary as well.[ 40, 41] Progressive edema results from local trauma, skin burns, and large volumes of fluid used for resuscitation. Edema usually increases progressively in the first 72 h.[ 30, 41] If endotracheal intubation is delayed, intubation is rendered difficult due to edematous tissue that swells the tongue and epiglottis, fills in aryepiglottic folds, and obscures arytenoid eminences and interarytenoid areas.[ 30, 41]

There should be frequent reevaluation of the airway, and we need to keep a high index of suspicion for airway compromise. Regardless of initial symptoms, the best strategy is to have a low threshold for intubation.[ 30, 40, 41] It is best to intubate early when swelling is least and the patient is still physiologically intact. The indications of endotracheal intubation are airway obstruction, severe cognitive impairment (Glasgow coma scale ≤8), major cutaneous burn (≥40%), where there is a high risk of impending airway obstruction (such as moderate-to-severe facial burn, oropharyngeal burn, and airway injury seen on endoscopy).[ 40] Absence of history/signs of smoke inhalation injury on FOB, and burn site distant from the airway are reassuring to wait.

Awake FOB is preferred at our institute, as the patient stays awake and breathes spontaneously and the airway remains patent [ Figure 4 ]. Use of videolaryngoscope for intubation is also emerging as a promising technique. Mask ventilation may also be difficult, resulting in "Can't Ventilate Can't Intubate" situation. All remaining alternatives such as supraglottic airways, cricothyrotomy, and tracheostomy are much more difficult in burn victims than in nonburn patients.[ 42] Safdarjung Hospital difficult airway algorithm in smoke inhalation injury is depicted in Figure 4 .

Bronchial hygiene therapy

Bronchial hygiene consists of therapeutic coughing, chest physiotherapy, deep breathing exercises, suctioning of the airway, and early ambulation.[ 28, 29, 30, 44] The victim should be placed 30°-45° head-up to attenuate the upper airway edema and minimize the pressure of abdominal contents on the diaphragm. The management strategy targets decreasing airway edema/hyperemia, treatment of bronchospasm, attenuation of mucus secretion, and lysis of the casts in the airway.[ 28, 29, 30, 44]

Therapeutic coughing

Cough impairment can lead to retained secretions, which can exacerbate bronchial obstruction, atelectasis, and pneumonia.[ 30] The goal of therapeutic coughing is to remove excess mucus or fibrin casts from the tracheobronchial tree. Repeating therapeutic coughing and deep breathing every 2 h effectively removes the secretions.[ 28, 29, 30, 44]

Chest physiotherapy

Chest physiotherapy, in the form of gravity-assisted drainage of secretions from the bronchial tree, is achieved by chest percussion and vibration.[ 44] The victim should be turned from one side to another, every 4 h, to mobilize the secretions [ Table 2 ].[ 28, 29, 30] Early ambulation is encouraged to prevent respiratory complications.[ 28, 29, 30, 44]

Table 2

PHARMACOLOGICAL AGENTS

Beta-2 agonists and muscarinic antagonist

The inhaled irritants in smoke cause severe bronchospasm, which is treated with inhaled beta-agonists such as albuterol, levalbuterol, or salbutamol.[ 45, 46] Aerosolized sympathomimetics relax bronchial smooth muscles and stimulate mucociliary clearance.[ 45, 46] This decreases the resistance of the airway and improves dynamic compliance of the lungs.[ 45, 46] The β ₂-agonists also have an anti-inflammatory action, reflected by attenuation of inflammatory mediators, such as histamine, leukotrienes, and TNF-α.[ 45, 46] Attenuation in pulmonary vascular permeability, pulmonary edema, and peak airway pressures, with improvement of oxygenation (PaO ₂/FiO ₂ ratio), has been reported with the use of nebulized albuterol (20 or 40 mg/h) in ovine model.[ 45] Tiotropium, a muscarinic receptor antagonist, has been reported to improve P aO ₂/F iO ₂ ratio and decrease the peak airway pressure after smoke inhalation injury.[ 47]

N-Acetyl cysteine

N-Acetyl cysteine (NAC) has pulmonary antioxidant and mucolytic properties.[ 50] NAC releases sulfhydryl radical, which breaks the disulfide bonds in mucoprotein (mucus).[ 50] NAC stimulates production of glutathione, which protects cells from free radicals and ROS.[ 50] NAC is an irritant to respiratory tract and can cause bronchospasm; hence, we mix NAC (0.5 ml) with a bronchodilator (0.5 ml salbutamol) in 4 ml normal saline for nebulization.[ 50]

Aerosolized heparin and antithrombin

Smoke inhalation injury has procoagulant activity; therefore, aerosolized administration of anticoagulants is beneficial.[ 51] Aerosolized heparin prevents inspissation of secretions, improves microcirculation by breaking fibrin component of the bronchial cast,[ 52] and has been found to reduce mortality in preclinical and clinical studies of smoke inhalation injury.[ 53, 54, 55] Administration of nebulized heparin 5000 units (in 3 ml) and alternating it with 4 ml of 20% nebulized NAC every 4 h is beneficial [ Table 2 ].[ 53, 54, 55] This combination has been reported to significantly improve pulmonary function, oxygenation, and survival rates in patients of smoke inhalation injury.[ 53, 54, 55]

Heparin exerts its anticoagulant effect by binding to antithrombin, and its effect is limited in antithrombin deficiency.[ 56] Antithrombin deficiency is common after burn injury and correlates significantly with increased mortality rate and longer hospital stay.[ 56, 57] Antithrombin has anticoagulant and anti-inflammatory activity by inhibiting transduction of inflammatory signal.[ 57] In ovine model, combined nebulization of heparin and recombinant human antithrombin improved the pulmonary function after smoke inhalation injury by dissolving bronchial casts and decreasing the airway obstruction.[ 57] This improves lung oxygenation (PaO ₂:FiO ₂ ratio) and decreases the incidence of pneumonia.[ 58]

BRONCHOALVEOLAR LAVAGE

FOB-guided bronchoalveolar lavage is very useful for removal of secretions and casts, if chest physiotherapy and pharmacological agents fail.[ 28, 29, 30, 54] In victims of smoke inhalation injury, removal of obstructing airway cast improves the oxygenation.[ 59]

The smoke inhalation injury treatment protocol being followed at Safdarjung Hospital is illustrated in Table 2 .

Treatment of carbon monoxide poisoning

The half-time of elimination of COHb varies with concentration of O ₂ inhaled (320 min on room air; 74 min on 100% O ₂).[ 60] Hyperbaric O ₂ can reduce the half-life of COHb to 20 min.[ 19] A recent Cochrane review does not show any benefit of using hyperbaric O ₂ over normobaric O ₂ for the treatment of CO poisoning, thus leaving no highly effective treatment.[ 61]

The current limitation in hyperbaric O ₂ treatment is that hyperbaric chambers are not mobile, require considerable infrastructure, are very expensive to run and maintain, and are scarce, even in industrial countries (e.g., Canada has eight such facilities).[ 19] Even in institutions that house hyperbaric facilities, it takes from 90 min to 3 h after arrival of the patient to deploy. The latter is a severe limitation for treatment of CO poisoning. The greatest determinant of the reversibility of CO poisoning is not the high O ₂ partial pressure, but rather, how rapidly the elimination of CO can be implemented.[ 19]

A recent approach in eliminating CO is similar in concept to that of hemodialysis, cardiopulmonary bypass, and extracorporeal membrane oxygenation (ECMO).[ 62] In this approach, lung is used as the dialysis membrane and minute ventilation performs a function analogous to the flow of dialysate.[ 62, 63] As in extracorporeal methods, the ventilatory dialysate can be conditioned by the addition to CO ₂ to prevent hypocapnia despite high minute ventilation. This isocapnic hyperpnea is implemented by a device that delivers 100% O ₂ via a self-inflating bag and passively administers CO ₂ in proportion to ventilation that exceeds baseline ventilation (ClearMate™ Thornhill Medical Inc., Toronto, Canada), thus maintaining normocapnia independent of the minute ventilation.[ 63] The reduction in COHb is a rectangular hyperbolic function of minute ventilation. This implies that initial increase in minute ventilation results in steep reduction in half-life of COHb, approaching that of hyperbaric O ₂ with as little ventilation as about 15 L/min.[ 62, 63] The ClearMate™ is a portable device and takes minutes to set up and implement, making it available where there is no ready access to hyperbaric chambers, or during the preparation of the hyperbaric chamber, when available. Recent work has shown that such early intervention in severe CO poisoning results in three times faster recovery of consciousness, improved postrecovery quality of life, and reduction in the incidence of delayed neurological sequelae from 20% to 1%, independent of the use of hyperbaric O ₂.[ 63]

Treatment of cyanide poisoning

Administration of thiosulfate converts cyanide to thiocyanate, which is excreted by the kidneys. In a swine model of severe cyanide poisoning, sodium thiosulfate was found to be ineffective for CN-induced cardiac effects.[ 64] Hydroxocobalamin is a natural Vitamin B12 derivative, used as an antidote of CN poisoning.[ 65] It chelates CN to the nontoxic product cyanocobalamin (Vitamin B12).[ 65] Administration of 5 g hydroxocobalamin IV over 15 min in victims of smoke inhalation injury is associated with lower rate of pneumonia, faster weaning from the ventilator, and faster discharge from Intensive Care Unit and can be given empirically in victims of smoke inhalation injury.[ 65]

MECHANICAL VENTILATION

Indications

The indications of mechanical ventilation are presence of tachypnea, use of accessory muscles of respiration, upper airway edema, sternal retraction, respiratory rate >30/min, PaO ₂<65 mmHg, PaCO ₂>50 mmHg, and PaO ₂/FiO ₂ ratio <200.[ 30]

Strategy

The lungs are ventilated using small tidal volume (6-8 ml/kg) and high respiratory rate.[ 67] The goal is to maintain peak airway pressure <35 mmHg, plateau airway pressure <30 mmHg, PaCO ₂35-55 mmHg, and pH 7.25-7.45. FiO ₂ is adjusted to maintain PaO ₂ between 80 and 100 mmHg.[ 67] Optimal positive end-expiratory pressure may be administered to maintain the desired airway pressure, below which the alveoli collapse.[ 67]

Newer modes of ventilation

The newer modes of ventilation such as high-frequency percussive ventilation, high-frequency oscillatory ventilation, pressure control inverse ratio ventilation, and airway pressure release ventilation have proven to be beneficial in managing patients with smoke inhalation injury.[ 68, 69] High-frequency percussive ventilation has been reported to improve O ₂ and CO ₂ tension (increased PaO ₂/FiO ₂ ratio), decrease lung inflammation/injury/infection, and improve the lung compliance and survival rate in victims of smoke inhalation injury.[ 69] Simple prone positioning has also been found to improve oxygenation (PaO ₂/FiO ₂ ratio).[ 70]

Future therapies

The use of ECMO is beneficial for the victims who develop severe respiratory failure after smoke inhalation injury.[ 71] Blood is circulated through an extracorporeal cardiopulmonary bypass circuit, which facilitates gas exchange through a semipermeable membrane.[ 71] Hence, low FiO ₂ and decreased ventilatory pressure can be used to ventilate the injured lungs and thus prevent barotrauma.

Newer agents such as perfluorohexane and porcine pulmonary surfactant are being investigated for their beneficial role in attenuating the release of inflammatory mediators in the airway and lungs.[ 72, 73] In animal models, use of peroxynitrite decomposition catalyst, inducible NOS inhibitors, PARP inhibitors, Na ₂S (H ₂S donor), and inhalation of H ₂S are being studied for their role in attenuating the lung parenchymal injury.[ 74, 75]

Limitations

The major limitation of this review is that many treatment strategies have been tested in animals but still need clinical trials on human subjects before implementation into clinical practice.

CONCLUSION

Early diagnosis and treatment of smoke inhalation injury are the keys for better outcome. Clinical signs/symptoms, FOB, and chest CT scan are helpful in early diagnosis. Initial treatment is early airway management, treatment of CO and CN toxicity, IV fluid resuscitation, and supportive respiratory care.

Financial support and sponsorship

The study was supported by the Department of Anesthesia and Critical Care, Vardhaman Mahavir Medical College and Safdarjung Hospital, New Delhi - 110 029, India.

Conflicts of interest

The ClearMate™ was developed by JF, his coworkers, and students. JF is a shareholder in Thornhill Research Inc., a spin-off company from the University Health Network.

REFERENCES

35. Suri JC, Sen MK. Respiratory tract injury in burns. Principles and Practice of Burn Care. In: Sarabahi S, editor. 1st ed. New Delhi: Jaypee Brothers Medical Publishers Ltd; 2010. pp. 129-30. [ Google Scholar]

63. Wu W, Ma Y, Jiang F. A clinical study of treatment for delayed psychoneural sequela caused by acute CO poisoning with clear mate gas poisoning first aid ventilator. Chin J Hosp Pharm. 2016;36:425. [ Google Scholar]

69. Miller AC, Ferrada PA, Kadri SS, Nataraj-Bhandari K, Vahedian-Azimi A, Quraishi SA, et al. High-frequency ventilation modalities as salvage therapy for smoke inhalation-associated acute lung injury: A Systematic review. J Intensive Care Med. 2017:1-11-885066617714770. doi: 10.1177/0885066617714770. Epub ahead of print. [[ PubMed] Google Scholar]

Articles from Indian Journal of Critical Care Medicine : Peer-reviewed, Official Publication of Indian Society of Critical Care Medicine are provided here courtesy of Indian Society of Critical Care Medicine

# data[].attributes.attachment_link.title
Smoke Inhalation Injury: Etiopathogenesis, Diagnosis, and Management

# data[].attributes.attachment_link.description
Smoke inhalation injury is a major determinant of morbidity and mortality in fire victims. It is a complex multifaceted injury affecting initially the airway; however, in short time, it can become a complex life-threatening systemic disease affecting ...

# data[].attributes.body
Wildfire events can cause increased levels of air pollutants such as PM.

CVD, IHD and stroke is associated with increased levels of PM air pollutants.

Exposure to short-term elevations in PM levels can evoke

Cardiac arrhythmias

Worsening heart failure

Triggering atherosclerotic/ischemic cardiovascular complications (particularly in certain high-risk subpopulations)

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Abstract

In recent years, wildland fires have occurred more frequently and with increased intensity in many fire-prone areas. In addition to the direct life and economic losses attributable to wildfires, the emitted smoke is a major contributor to ambient air pollution, leading to significant public health impacts. Wildfire smoke is a complex mixture of particulate matter (PM), gases such as carbon monoxide, nitrogen oxide, and volatile and semi-volatile organic compounds. PM from wildfire smoke has a high content of elemental carbon and organic carbon, with lesser amounts of metal 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, previous reviews of the health effects of wildfire smoke exposure have not established a conclusive link between wildfire smoke exposure and adverse cardiovascular effects. In this review, we systematically evaluate published epidemiological observations, controlled clinical exposure studies, and toxicological studies focusing on evidence of wildfire smoke exposure and cardiovascular effects, and identify knowledge gaps. Improving exposure assessment and identifying sensitive cardiovascular endpoints will serve to better understand the association between exposure to wildfire smoke and cardiovascular effects and the mechanisms involved. Similarly, filling the knowledge gaps identified in this review will better define adverse cardiovascular health effects of exposure to wildfire smoke, thus informing risk assessments and potentially leading to the development of targeted interventional strategies to mitigate the health impacts of wildfire smoke.

Introduction

Wildland fires have been an important factor in shaping the landscape and controlling the biomes on Earth for millions of years [ 115]. Over recent decades, rapid growth of the wildland-urban interface and anthropogenic climate change have contributed to increased wildfire frequency and unprecedented intensity in many fire-prone regions [ 1, 22, 117, 163, 169]. In the western United States, summer wildfire frequency increased approximately eightfold between 1972 and 2018; resulting in a fivefold rise in the annual area burned [ 163]. Southeastern Australia is a densely populated region where large-scale wildfires have led to massive life and property loss [ 169]. Multiple forms of vegetation in wildlands, including trees, bushes, grass, and their partially decayed form "peat", fuel these fires, and smoke emitted from the combustion of these vegetations are referred to as wildfire smoke, with alternative names including "landscape fire smoke", "wildland fire smoke", "peat fire smoke", "forest fire smoke", and "biomass smoke" [ 30, 75, 156]. Wildfire smoke contains many air pollutants known to be detrimental to human health, such as particulate matter (PM) and volatile organic compounds (VOCs) [ 4, 30].

Wildfires impact public health since wildfire smoke presents a source of air pollution in neighboring and even more distant populated areas [ 30, 85]. Epidemiological studies estimate that the global mortality burden attributable to landscape fire smoke is approximately 339,000 deaths annually [ 75]. Between 2008 to 2012, about 10.3 million individuals in the United States were estimated to have experienced unhealthy air quality levels (average daily fire-PM 2.5 > 35 μg/m ³) associated with exposure to wildfire for more than 10 days [ 120]. Evidence also indicates an association between the long-distance transport of PM 2.5 resulting from wildfire smoke and the adverse health effects in susceptible populations thousands of miles away [ 84, 85].

As a leading cause of death worldwide [ 69], cardiovascular disease (CVD), especially ischemic heart disease (IHD) and stroke, has been shown to associate with increased levels of air pollutants such as PM [ 51]. Wildfire events can cause an abrupt increase in ambient PM 2.5 levels to more than 2000 μg/m ³ [ 3, 8]. Exposure to such short-term elevations in PM levels are capable of evoking cardiac arrhythmias, worsening heart failure, and triggering atherosclerotic/ischemic cardiovascular complications, particularly in certain high-risk subpopulations [ 29]. Biomass smoke has also been found to be comparable to tobacco smoke as a cardiovascular comorbidity factor among patients with COPD, suggesting the need to treat diseases associated with biomass combustion similarly to those associated with tobacco use [ 61].

Understanding whether wildfire smoke exposure increases cardiovascular risk is of utmost importance to provide scientific evidence to better inform policymaking to protect public health, especially in the most vulnerable segments of the population. Wildfire smoke exposure has been linked to increased hospitalization and emergency department (ED) visits for respiratory symptoms, exacerbation of asthma, and chronic obstructive pulmonary disease (COPD), but the association with elevated cardiovascular risks, primarily based on epidemiological studies, is less conclusive [ 4, 30, 123, 124]. In recent years, a growing number of observational and experimental studies have investigated cardiovascular effects of wildfire smoke and their associated mechanisms. The observational studies include studies focusing on wildfire smoke and also on household biomass smoke that can be important sources of evidence of an association with cardiovascular risk [ 47]. The experimental studies using wood smoke, are more likely to capture acute pathophysiological changes associated with wood smoke exposure, compared to the observational studies that are based on healthcare data such as hospitalizations and ED visits for acute cardiovascular symptoms [ 138]. In this review, we will systematically examine the evidence from these studies on the association between cardiovascular health impacts and wildfire smoke (including biomass smoke and wood smoke) exposure and their possible underlying mechanisms. This review will also identify knowledge gaps and point to possible directions for future research.

Literature search

Wildfire in this review is conceptualized within the definitions of landscape fires encompassing wild and prescribed forest fires, tropical deforestation fires, peat fires, agricultural burning, and grass fires. Wildfires release approximately 2 × 10 ¹² kg of carbon into the atmosphere annually [ 75, 156]. The main aim of this review is to examine evidence from the published peer-reviewed literature on the association between cardiovascular effects and exposure to wildfire smoke. Combustion of household biomass fuels for cooking and heating including wood, grass, and straw, which are also commonly found in wildfire scenarios, contributes to both indoor and ambient air pollution. In addition, a number of controlled human wood smoke exposure studies that are sufficiently powered to infer a causal relationship will be discussed in concert with both in vivo animal and in vitro toxicological experiments. Although the composition of household biomass smoke and experimental wood smoke is different from that of wildfire smoke, studies of biomass and experimental wood smoke provide important information that may be used to infer an association between cardiovascular effects and wildfire smoke and the associated mechanisms. Therefore, a number of household biomass smoke studies as well as clinical and experimental wood smoke studies will also be included to complement the wildfire studies in this review.

We searched peer-reviewed publications on the topic of wildfire smoke and cardiovascular health covering the period between 1980 and 2020. Terms including "forest fire smoke", "wildfire smoke", "biomass smoke", "wildland fire smoke", "peat fire smoke", "wood smoke", and "prescribed fire" have been employed interchangeably in the literature. Searches were performed using two engines, "PubMed" and "Web of Science". As shown in Fig. 1, searching "PubMed" and "Web of Science" yielded 949 and 866 results as of April 7th, 2020, respectively. After duplicate exclusion and title screening, 182 records in English language were assessed for their eligibility for further review. After excluding 31 letters or perspectives, 8 review articles, and 37 studies on coal or animal dung as combustion fuel or that did not specify the types of fuel, 108 publications were included for detailed review. These included 77 epidemiological studies which were further grouped into 48 wildfire smoke studies (Table 2 and Table S 1) and 29 indoor and ambient biomass smoke studies (Table S 2). Of the remaining 31 articles, 15 were controlled human exposure or interventional studies (Table S 3), 7 were in vivo animal studies (Table S 4), and 9 were in vitro studies (Table S 5).

Literature review flow chart

Composition of wildfire smoke

Wildfire smoke is complex physically and chemically, and its composition is determined by fuel type and combustion conditions [ 30, 83]. Wildfire smoke generally consists of coarse and fine PM, VOCs (e.g., aldehydes, n-alkanes), polycyclic aromatic hydrocarbons (PAHs), gases (e.g., CO, SO ₂, NO, NO ₂), and metals [ 155]. PM composition is a summation of the emitted mixture of compounds that is usually present as soot or oily substances high in elemental and organic carbon, and metallic compounds [ 155]. VOCs and gases are normally dispersed into the environment and they are able to react further photochemically to generate secondary organic aerosol (SOA), for example in situ ozone oxidation of alkanes in the ambient air, which can also be detrimental to human health [ 60, 113]. Clinical and toxicological studies offer a detailed opportunity to examine the chemical compositions of wood smoke, a major contributor of wildfire smoke, in a controlled experimental setting. The chemical composition of wood smoke in a laboratory setting is different from that of wildfire smoke in a natural environment where vegetation characteristics, combustion conditions, weather conditions, and the geographical area burnt are factors that add complexity relative to emissions from the combustion or pyrolysis of one or two types of wood in a controlled chamber environment. As summarized from these studies in Table 1, wood smoke, independently of fuel type and combustion conditions, is characterized by the presence of PM, gases, n-alkanes, PAHs, methoxyphenol compounds, levoglucosan, and metals species.

Table 1 Chemicals detected in wood smoke in laboratory studies

Most epidemiological studies in this review did not provide detailed chemical profiles of the wildfire smoke studied. Instead, they employed large-scale air pollution data derived from local air quality monitoring stations or satellite imagery obtained during wildfire seasons that feature elevated levels of PM 2.5 and/or PM ₁₀, with a few studies also relying on the concentrations of other index air pollutants such as SO ₂, oxides of nitrogen (NO x), CO, and ozone [ 2, 28, 37, 43, 45, 92, 126]. In all cases, wildfire events dramatically elevated ambient air pollutant levels. For example, the peak levels of PM 2.5 and PM ₁₀ during wildfire days were approximately 10 times higher than those in non-fire days in Sydney, Australia [ 94]. Efforts have also been made specifically to address the role of organic compounds in epidemiology by using environmental markers of PAHs such as delta-C [ 18, 19, 38, 45, 127]. Delta-C is based on a calculation of the difference between light absorption of ultraviolet black carbon (BC), measured at 370 nm and BC 880 nm with a two-wavelength aethalometer [ 38], and was used for source apportionment for wood smoke [ 159]. Studies have employed urinary 1-hydroxypyrene (1-OHP), a metabolic biomarker of PAHs [ 14, 131, 132] as an index of exposure, and found that the urinary 1-OHP levels measured in a group of Mexican women who were exposed to indoor biomass smoke can be 11 times above the mean reported for the general population [ 132]. In addition, measurement of levoglucosan, a sugar anhydride byproduct of pyrolysis of cellulose was utilized as a relative indicator of exposure to products of pyrolysis from burning biomass [ 55].

Cardiovascular effects of wildfire smoke

Epidemiological studies

Wildfire events are normally transient in nature and, therefore, pose a challenge to the implementation of prospective cohort or case-control epidemiological study designs that require long-term exposure observations. A significant challenge is the lack of clear definition of the timeline that corresponds to the PM measurements, for instance, whether it represent 3-day averages, 24 h averages or one-hour daily peak averages. Instead, cross-sectional, case crossover time-series, population-based cohort, or ecological study designs are commonly employed to assess the possible association between wildfire smoke exposure and cardiovascular risk in epidemiological studies as summarized in Table 2 and Table S 1. Most of these studies have found that certain populations are at a higher risk of acute adverse cardiovascular effects due to wildfire smoke exposure.

Table 2 A summary of epidemiological studies of the association between wildfire smoke exposure and cardiovascular effects

Cardiovascular morbidity

Of the 48 wildfire epidemiological studies, 38 are on cardiovascular morbidity (Table 2 and S 1), and most outcomes focus on ED visits and hospitalizations for cardiovascular symptoms and illness, for which extensive data are available from hospitals and governmental health agencies. Twenty-five of the 38 studies have reported a positive association between wildfire smoke exposure and increased healthcare needs for CVD.

Wildfire smoke exposures were categorized based on exposure time or location. Employing a time-series study design, researchers in Australia stratified continuous air pollution data into different exposure doses in order to compare the healthcare needs between non-smoky days and smoky days when either PM 2.5 or PM ₁₀ concentrations exceeded 99% of the days during the entire time series. They found that increased ED visits for CVD (e.g., IHD, arrhythmias) were associated with elevated levels of PM ₁₀ and PM 2.5 on smoky days [ 37, 76]. Lee et al. [ 86] demonstrated that during the 1999 forest fire near the Hoopa Valley Indian reservation in California, daily PM ₁₀ levels were significant predictors of the number of patients seeking care for circulatory and respiratory illnesses among residents of Hoopa and nearby communities. A recent study found that out-of-hospital cardiac arrest risk was significantly elevated in association with heavy smoke during wildfire events in California between 2015 to 2017 [ 77]. Rappold and colleagues employed a population-based cohort study design and discovered that, compared with wildfire-free counties, there was an increased number of ED visits for cardiovascular illness in counties impacted by exposure to smoke from a peat bog wildfire in North Carolina in 2008, with the association being more prominent for the elderly population [ 121]. Parthum et al. [ 114] investigated effects of another peatland fire in Virginia in 2008 and found that the fire event significantly contributed to 32 and 33 more ED visits for congestive heart failure (CHF) and cardiopulmonary symptoms respectively, compared with those on non-fire days.

Continuous air pollution data, such as ambient concentration of PM 2.5 levels, were also commonly directly employed in the analyses. Similar to the North Carolina peat wildfire study [ 121], a 10 μg/m ³ increase in 24-h PM 2.5 during peat fires was correlated with increased risk of hypertension in adults, and of all-cause cardiac outcomes in youth [ 149]. Haikerwal et al., reported that an interquartile range increase of 9.04 μg/m ³ in PM 2.5 over a 2-day moving average during the 2006-2007 wildfire season in Victoria, Australia, was significantly associated with a 6.98% increase in risk of out-of-hospital cardiac arrests, with the strongest associations observed among men and older adults, and was also associated with an increased risk for IHD-related ED visits (2.07%) and hospitalizations (1.86%), particularly among women and the elderly [ 64]. In addition to PM 2.5, the same group found that the ambient levels of PM ₁₀ and CO were also correlated with a 48-h lag to an elevated incidence of increased out-of-hospital cardiac arrests among men during the wildfire events, although PM 2.5 was still the main contributor of these effects [ 43]. A larger scale study in the Greater Sydney Metropolitan area from 2004 to 2015 showed similar results, specifically that a 10 μg/m ³ increase in PM 2.5 resulting from the wildfire smoke was positively associated with the number of same-day emergency ambulance dispatches responding to calls for cardiac arrest, stroke, and chest pain [ 133].

In contrast, 13 of the 38 studies reported null associations between cardiovascular healthcare needs and wildfire smoke exposure. During a 2003 forest fire event in British Columbia Canada, despite significant increases in physician visits for respiratory complaints, the physician visits for CVD were not significantly increased by forest fire smoke containing a peak of 200 μg/m ³ PM ₁₀ and 250 μg/m ³ PM 2.5 [ 103]. Similar to the British Columbia study, Henderson and colleagues employed a population-based cohort methodology and multiple exposure assessment metrics, including tapered element oscillating microbalance measurements, a CALPUFF dispersion model, and a SMOKE exposure metric. Despite more novel methods, they reached the same conclusion that no significant association were observed between PM ₁₀ exposure and cardiovascular hospital admissions [ 67, 68]. Null cardiovascular results were also reported in the USA [ 8, 40, 41, 88, 123, 124, 137, 147] and in Australia [ 94, 104], in spite of the presence of strong links to the incidence of respiratory diseases [ 8, 40, 41, 104, 137, 147].

Cardiovascular mortality

Among the 10 epidemiological studies investigating the association between exposure to wildfire smoke and cardiovascular mortality, eight found a positive association. Using satellite-derived estimates and atmospheric modeling for exposure categorization, wildfire contributed to 200 days per year in which the World Health Organization's 24-h PM 2.5 interim air quality target was exceeded in Southeast Asia between 1997 and 2006, leading to an estimated 2% annual increase in adult cardiovascular mortality [ 92]. Similarly, smoky days with PM ₁₀ higher than 8 μg/m ³ based on satellite data, were significantly related to increased cardiovascular mortality, during forest fire episodes in several Mediterranean cities in 2003-2010 [ 48]. A recent study from Indonesia found that peatland fire smoke contributed to an annual average of 26 μg/m ³ PM 2.5 per year, and was associated with excess mortality due to respiratory or cardiovascular causes [ 153]. In addition to PM, other meteorological conditions, such as high temperature, were determined to be co-contributors to the association between increased cardiovascular mortality and wildfire events [ 143].

As with the morbidity studies discussed above, null associations have also been reported in a couple of cardiovascular mortality studies. One study showed that the daily cardiorespiratory mortality was not associated with same-day wildfire smoke containing peak PM ₁₀ and PM 2.5 levels of 372 and 200 μg/m ³, respectively [ 157]. Another study also reported no significant associations between increased PM ₁₀ levels during biomass fires and cardiovascular mortality, even though there was a significant finding for respiratory mortality among people who were ≥ 75 years old [ 87]. Some authors argue that the mortality impact of short-term increases in PM due to wildfire would not be expected to be limited to 1 day but show a lag several days later [ 157], and this could explain the lack of a relationship between wildfire smoke exposures and cardiovascular mortality.

Occupational exposure to wildfire smoke

Firefighters are a special group of workers who are likely to be exposed to high levels of air pollutants during wildfire events [ 110, 125]. Hejl et al. [ 66] showed that firefighters exposed to up to 1306 μg/m ³ PM 2.5 during firefighting had increased serum markers of inflammation (IL-8) and altered vascular function (ICAM1, VCAM1). Another study showed that elevated mean augmentation index, an indicator of arterial stiffness, was linked to urinary levoglucosan levels among wildfire firefighters [ 55]. These pathophysiological changes may lead to higher risks of adverse cardiovascular outcomes among firefighters due to exposure to wildfire smoke. Navarro found that firefighters who worked 49 days per year were exposed to a mean concentration of PM ₄ at 510 μg/m ³ during wildland firefighting activities. They estimated that the increased PM exposure was associated with increased risk of lung cancer as well as CVD-related mortality [ 107].

Indoor and ambient biomass smoke

While the focus of this review is on wildfire smoke, there are 29 studies (Table S 2) examining the health impacts of indoor or ambient exposure to biomass smoke from household fuel combustion for cooking or heating using wood, grass, or straw. Using a cohort study design, researchers identified differences among cardiovascular outcomes between cohorts exposed to biomass smoke and control groups. Compared with those using cleaner fuels, biomass use in Peruvian households was associated with significantly higher levels of indoor PM 2.5 concentrations, which were, in turn, associated with increased carotid intima media thickness, elevated prevalence of carotid plaques, and higher systolic blood pressure (SBP) [ 112]. Similarly, the use of biomass fuel for cooking was associated with elevations in SBP, diastolic blood pressure (DBP), and mean arterial pressure, with a stronger association observed among older populations in China [ 21, 42]. In addition to PM 2.5, one study in Western Kenya showed that smoke from the incomplete combustion of locally acquired wood contained high levels of household CO, which was a driver of an association with heart abnormalities detected by echocardiography [ 5]. A cross-sectional study in Turkey reported that long-term exposure to indoor biomass smoke was associated with systolic and diastolic biventricular dysfunction, as well as increased pulmonary artery systolic pressure [ 80]. However, some studies have found no significant association between increased cardiovascular risk and indoor exposure to biomass smoke [ 33, 101, 102, 142]. Indoor biomass combustion contributes to ambient air pollution, which has also been linked to increased incidence of cardiovascular outcomes. A 10 μg/m ³ increase in ambient PM 2.5 levels due to wood combustion for winter heating in Tasmania, Australia was significantly associated with an increased rate of hospitalization for heart failure [ 72]. Domestic wood combustion for heating in Central Launceston, Australia was associated with increased levels of ambient PM ₁₀ and increased cardiovascular mortality; the effects were mitigated by intervention to reduce wood smoke production [ 74]. It is important to note that smoke emitted from household combustion of biomass is not equal to wildfire smoke; therefore, caution is advised when interpreting results from these biomass smoke studies.

Vulnerable populations

It is known that certain subpopulations are more susceptible to health impacts of exposure to air pollution, including children, the elderly, the obese, pregnant women, people with low socio-economic status (SES), and those with underlying lung and heart diseases [ 79, 96]. These subpopulations are also more susceptible to wildfire smoke exposure, especially the elderly, pregnant women, and those with lower SES.

The elderly are more likely to seek healthcare (i.e. ED visits, hospitalizations) due to cardiovascular issues, such as IHD, CHF, cardiac arrest and acute myocardial infarction (MI), during wildfire season [ 64, 76, 77, 105, 118]. Many more studies are in agreement with this finding, with small variations of the age at which these effects are evident. Exposure to high PM 2.5 levels were strongly associated with increased rates of acute MI among people > 75 years old [ 109], and with increases in ED visits for cardiovascular dysfunction (e.g. IHD, dysrhythmia, heart failure, stroke and MI) among people > 65 years old [ 126, 161]. In addition, meteorological factors such as low ambient temperature positively modified the association between increases in 3-day average PM 2.5 levels and increased risk of MI among the elderly (≥ 65 years old) during biomass fire periods [ 160]. Interestingly, a few studies revealed the possibility that wildfire emissions can impact the health of more remote elderly populations after long-distance transport of the particles. The 2002 Quebec forest fires in Canada significantly increased average PM 2.5 levels during hazy days to 53 μg/m ³ from 21.5 μg/m ³ on clear days in the United States. Compared with the clear days, the rate of hospitalizations for both respiratory and cardiovascular illness were increased during the hazy days among the elderly [ 85]. Similar evidence was found in a Finnish study which reported that a 10 μg/m ³ increase in PM 2.5, attributed to a long-range transport from vegetation fires, was associated with all-cardiovascular mortality especially among population > 65 years old [ 84].

Pregnant women are also susceptible to wildfire smoke exposure. Abdo and colleagues examined the impact of wildfire smoke on hypertension during pregnancy and reported that a 1 μg/m ³ increase in PM 2.5 exposure to wildfire smoke over the full gestation or during the 1st and 2nd trimester was positively associated with gestational hypertension, in addition to adverse effects on premature birth and decreased birth weight in newborns [ 2]. Using delta-C as an environmental marker for wood combustion, Assibey-Mensah and colleagues first discovered that each 0.52 μg/m ³ increase in delta-C concentration during the 7th and 8th gestational month was associated with an elevated risk of hypertensive disorders of pregnancy [ 18]. They also report that exposure to wood smoke-sourced fine PM was positively associated with an increased risk of early onset of preeclampsia during pregnancy [ 19].

Health disparity was another risk factor that may render certain subpopulations more susceptible to wildfire smoke-associated cardiovascular effects. A study showed that indigenous people in Darwin, Australia were more likely to be admitted to the hospital for IHD and respiratory illnesses during vegetation fire season when there were significantly increased levels of PM ₁₀ [ 65, 73]. Jones and colleagues indicated that low SES may increase the risk of out-of-hospital cardiac arrest due to wildfire smoke exposure during wildfire events in California [ 77]. Rappold and colleagues compared the ED visits due to wildfire smoke between top- and bottom-ranked counties in North Carolina stratified by socioeconomic factor and found that increased ED visits for asthma and CHF were significantly higher in the low SES counties, 85 and 124% respectively, per 100 μg/m ³ increase in PM 2.5 [ 118].

Cigarette smoking may increase the susceptibility to adverse health impacts of wildfire smoke among smokers. Cigarette smoking is an established risk factor for cardiovascular disease [ 9] and there is a positive interaction between cigarette smoking and PM 2.5 for cardiovascular mortality [ 152]. It is likely that smoking or history of cigarette smoking may increase wildfire smoke-induced cardiovascular morbidity; however, to our knowledge, no studies have specifically investigated such an interaction. Nonetheless, many studies do consider smoking and smoking history as a co-variate on the association between wildfire smoke exposure and cardiovascular diseases [ 18, 118].

Limitations of epidemiological studies of the effects of wildfire smoke

As shown in Table 3, a number of studies showed positive association between wildfire smoke exposure and cardiovascular endpoints while several presented null associations. The inconsistency of the findings might result from differences in study design, endpoint choices, case count, and exposure assessment.

Table 3 Characteristics of the studies reviewed

Some epidemiological studies employed an integrated approach to include large-scale healthcare and mortality data that may not be representative of the whole population. Some studies noted that null findings for cardiovascular effects were partly attributed to the low cardiovascular case counts, leading to wide confidence intervals, relative to respiratory case counts [ 8]. Outcomes based on healthcare needs for cardiovascular issues are likely to limit the investigations to certain susceptible subpopulations, while omitting healthier subgroups who may have developed small but significant pathophysiological effects, involving oxidative stress and inflammation.

Epidemiological studies are also prone to exposure misclassification due to their dependence on the use of exposure data from air quality monitoring stations or satellite images [ 85]. The broad approach applies exposure data based on smoky days, smoky area, scale of burnt forests, or air pollutant levels for the entire region [ 48, 54, 118], but does not consider individual-specific differences such as activity level, time spent indoors versus outdoors, and wind direction changes that may drastically affect the actual concentration of wildfire smoke. Total suspended particle levels from a study on biomass smoke derived from agricultural combustion of sugar cane, for example, may not specify particulate size information that is toxicologically relevant [ 16]. It has been shown that the amount of wood combustion in a city does not necessarily guarantee that the measured PM ₁₀ levels are representative of wood smoke exposure [ 44, 135].

Exposure misclassification can also be due to data quality factors or variations in the statistical methods used to process the data. Several studies surveyed in this review failed to distinguish between PM from wildfire smoke or background urban PM, while a few studies subtracted the background levels [ 10, 84, 85, 111]. In addition, fire intensity does not necessarily correspond to smoke levels and thus is not a sound metric for smoke exposure assessment [ 10]. The PM 2.5 results based on modeled air pollution level seem to vary from model to model. Yao et al. [ 165] found that even though close in values, modeled PM 2.5 concentrations, but not the measured levels, were associated with increased physician visits for cardiovascular disease on smoky days during the forest fire seasons of 2003 through 2010 in British Columbia, Canada. Gan and colleagues estimated PM 2.5 concentrations based on both satellite and in situ data using three distinct methods: the Weather Research and Forecasting with Chemistry chemical-weather model, the Kriged interpolation of PM 2.5 data from of in situ surface monitors, and a geographically weighted regression. The three models overall generated consistent PM 2.5 exposure levels, but there were some significant differences among specific locations where the models were used, resulting in varying conclusions regarding the associations [ 53].

A majority (42 out of 48) of the wildfire smoke epidemiological studies reviewed (Table S 1) utilized PM as an exposure metric for wildfire smoke in a variety of timelines and size fractions, and only 6 studies examined measured levels of gases (e.g. O ₃, CO) and volatile organic compounds (e.g. levoglucosan). Null findings between exposure to wildfire smoke and cardiovascular health effects may be due to the lack of accounting for gases, VOCs, PAHs and SOA, as well as cumulative exposure and co-exposures. While monitoring gaseous components from wildfire smoke can be challenging, some studies did propose indirect methodology including the environmental markers such as delta-C and metabolic markers such as 1-OHP for exposure assessment of PAHs from wildfire smoke [ 12, 13, 45]. However, such methods may not best represent exposure to organic compounds due to the low correlation between these markers and the actual air pollutant levels. For example, in one study the Pearson correlation factor between the delta-C levels and ambient PM 2.5 levels was only R = 0.26 [ 18].

Some other limitations are identified in epidemiological studies that may lead to bias when interpreting results from these studies. For example, one study did not adequately account for important covariates such as temperature, humidity, and time trends [ 126]. Another study may have low power to detect an effect as it claims a positive finding with only a correlation between 2-day exposure and 2-day mortality data [ 157]. In addition, the choice of groups compared is questionable in this study, where frequency of pulmonary hypertension among women exposed to biomass smoke was higher than that among men who were cigarette smokers [ 141]. All the limitations discussed here may contribute the inconclusive results of a positive association between wildfire smoke exposure and cardiovascular effects in epidemiological studies.

Controlled clinical exposure studies

Controlled clinical exposure studies complement the cardiovascular mortality and morbidity observations in epidemiology as they offer a chance to examine the associated pathophysiological changes. As shown in Table 3 and S 3, wood smoke used in clinical and experimental studies in laboratory settings may not represent wildfire smoke entirely. In a clinical chamber setting, it is possible to maintain a relatively consistent wood smoke concentration, coupled with controllable environmental conditions such as temperature, humidity, and barometric pressure. In addition, chamber studies also allow researchers to characterize the chemical composition of the wood smoke (Table 1) and potentially investigate their roles in the cardiovascular effects. Low or moderate exercise can be introduced in the study protocols to increase the ventilatory rate to simulate physical activity in the vicinity of a wildland fire. The randomization and crossover design utilized in the chamber studies significantly reduce the influence of confounding covariates and are statistically efficient [ 25]. These considerations in clinical exposure studies significantly avoid exposure misclassification and provide much higher confidence in the causal inference of observed associations between wood smoke exposure and cardiovascular effects. These studies often purposely focus on the combustion of a single type or source of combustion material (e.g., red oak from a single tree or neighboring trees harvested from a single location) in order to minimize variability in the exposures from subject to subject.

Most clinical wood smoke exposure studies conducted to date have investigated pulmonary function, respiratory inflammation and systemic inflammatory responses, while about a dozen included cardiovascular endpoints or markers related to vascular pathophysiology. Commonly investigated cardiovascular endpoints include heart rate variability (HRV), vascular function, blood pressure, circulating endothelial adhesion molecules (e.g. ICAM1, VCAM1 and p-selectin), and coagulation proteins (vWF, tPA, and D-dimer). HRV is a reflection of the autonomic nervous system control on the heart and is quantified in the time domain with measurements of the time interval between consecutive heartbeats, and in the frequency domain, which measures the absolute or relative amount of signal energy within component bands [ 154]. An optimal level of HRV is associated with cardiac health; decreased HRV among healthy individuals is reported as a risk factor of cardiovascular morbidity and mortality [ 151]. Controlled chamber exposure to air pollutants, such as concentrated ambient fine and ultrafine PM, can significantly decrease HRV among middle-aged healthy subjects [ 150]. In one study, 14 subjects underwent a 3-h controlled exposure to a mean PM ₁ concentration at 314 μg/m ³ of wood smoke generated through pyrolysis of birch wood with intermittent moderate exercise (an average minute ventilation of 20 L/min/m ² body surface area (BSA)). The authors found that HRV markers in the time domain, including standard deviation of successive NN intervals (SDNN), root-mean square of successive NN interval differences (RMSSD), and the proportion of NN50 divided by the total number of NN (R-R) intervals (pNN50), were significantly decreased 1-h after wood smoke exposure compared to filtered air [ 154]. In another study, 43 subjects participated in various training exercises that included activities to extinguish fires fueled by either wood alone or by wood and household materials (mattress). They found that firefighting activity was associated with decreased HRV and microvascular function measured as reactive hyperemia index [ 14]. On the other hand, a few studies have reported no significant changes in HRV following exposure to red oak wood smoke (485 ± 84 μg/m ³) [ 57, 58], or to Danish beech wood smoke (13, 222, and 385 μg/m ³) [ 24].

Several studies investigated changes in vascular function and blood pressure post exposure to wood smoke. Exposure to birch wood smoke significantly increased heart rate and central arterial stiffness, though not blood pressure [ 154]. After 1-h exposure to wood smoke measured as PM ₁ at about 1000 μg/m ³ of birch wood smoke with intermittent exercise (average minute ventilation target 20 L/min/m ² BSA), 16 male firefighters showed significantly increased blood carboxyhemoglobin and increased vasodilatory response to bradykinin infusion compared with controls exposed to clean air, but no change in arterial pressure or pulse wave velocity [ 71]. The concentrations of the endothelial adhesion molecules ICAM1 and VCAM1 showed changes in the blood of healthy adults following a 3-h resting exposure to wood smoke corresponding to start-up and burn-out phases [ 144]. A few other studies failed to find any positive effects on vascular endpoints, but did report that blood markers related to vascular pathophysiology, such as coagulation factors, lipid peroxidation and oxidative stress, were significantly increased after wood smoke exposure [ 20, 50].

In a clinical study that included six different cookstoves that represent different combustion conditions, 48 subjects each underwent 2-h wood smoke exposures over six sessions at PM 2.5 doses ranging from 0 to 500 μg/m ³. Overall, the results showed that mean SBP, but not DBP, was 2 to 3 mmHg higher for all but one stove emission. All cookstove treatments also marginally increased pulse wave velocity and central augmentation index after 24 h compared to control. These results raised concerns that even low level PM 2.5 from the most efficient cookstove can pose adverse cardiovascular effects [ 49, 158]. Similar reductions of cardiovascular effects associated with use of efficient energy usage to reduce indoor biomass smoke levels were also found in other observational studies [ 6, 34, 164].

In vivo animal studies

As with clinical exposure studies, wood smoke used in the animal studies surveyed was derived from the combustion of one or two types of wood. The exposure methodology was either inhalation by animals breathing spontaneously in a small chamber, or intratracheal instillation of an extract prepared from condensed wood smoke. As summarized in Table S 4, several studies have shown that exposure to wood smoke leads to increased cardiovascular risk in animals. Kim and colleagues established an in vivo model wherein female CD-1 mice were exposed to 100 μg peat smoke condensate from different combustion stages (smoldering vs. near-extinguished) through oropharyngeal aspiration. The mice exposed to the smoke produced during the smoldering-stage showed significantly decreased cardiac function and increased post-ischemic cardiac death in an experimentally induced ischemia model [ 82]. Another study demonstrated that Sprague-Dawley (SD) rats exposed to peat fire smoke extracts through oropharyngeal aspiration showed significantly higher end-systolic volume and pulmonary artery blood flow acceleration/ejection time ratios. Though minimal immune cell changes were observed in the bronchoalveolar lavage fluid (BALF), high doses of peat smoke PM extract (350 μg per animal) led to altered regulation of ventricular ejection and filling volumes, affecting blood flow in the pulmonary circulation [ 148]. In a study investigating the cardiometabolic responses to a high fat diet, rats exposed to peat fire smoke for 1 h showed increases in serum high-density lipoprotein (HDL) and total cholesterol, as well as increased isovolumic heart relaxation time after high fat food challenge, compared to values seen in control rats exposed to filtered air [ 93].

On the other hand, Reed and colleagues did not find any significant changes in cardiovascular markers among different animal strains (F344 rats, SHR rats, A/J mice, and C57BL/6 mice) after subchronic exposure to mixed oak wood smoke [ 122]. The animals in this study were whole-body exposed to different concentrations of wood smoke particulates (30, 100, 300, and 1000 μg/m ³) for 6 h per day, 7 days a week for either 1 week or 6 months. The investigators evaluated cardiovascular function using electrocardiograms. No consistent changes were apparent under the wood smoke exposure conditions of this study, although increases in platelet numbers and decreases in blood urea nitrogen and serum alanine aminotransferase were reported [ 122]. Animal studies have also shown that the toxicity of wood smoke depends on the wood type as well as the combustion conditions, with wood smoke from either smoldering or flaming oak showing weaker effects relative to smoke produced by the burning of a few other wood types [ 81, 83, 140]. More details on how composition of wood smoke will affect its toxicity will be discussed in the next section.

Mechanisms of cardiovascular impacts of wildfire smoke

As summarized in Table 3, in vivo animal and in vitro studies may often be challenging to interpret in a clinical context, as exposure dose and duration may be difficult to compare with real world conditions impacting public health. However, these studies provide insight into underlying pathophysiological mechanisms. In this section, we will focus on evidence from the literature including controlled human exposure studies, in vivo animal studies and in vitro studies to discuss the possible mechanisms of wildfire smoke induced cardiovascular effects.

Several hypotheses have been proposed regarding the biological mechanisms underlying the health effects of air pollution. Among them are three principal pathways supported by evidence from epidemiological, clinical and toxicological studies [ 108, 146]. First, air pollutants can directly interact with neural receptors in the respiratory system and activate the autonomic nervous system, which has an impact on the heart rhythm and blood pressure. Second, pulmonary exposure to air pollutants produces oxidative stress and local and systemic inflammation, leading to lipid peroxidation, increased platelet activation and thrombosis, inflammation of vascular endothelia, and increased vasomotor tone. Lastly, small molecules of air pollutants, such as ultrafine PM and gases, may translocate through alveolar membranes and cause cardiovascular effects, including endothelial activation and injury [ 30, 99, 116]. There is limited research conducted directly on the mechanisms of cardiovascular effects caused by wildfire smoke, but after reviewing direct and indirect evidence from the literature, we postulate possible mechanistic pathways of cardiovascular effects induced by exposure to wildfire smoke based on these three notions (Fig. 2).

Schematic pathway showing proposed pathophysiological mechanisms of cardiovascular effects induced by wildfire smoke exposure. Wildfire smoke contains PM, gases, PAHs, and VOCs, etc. These components may affect the cardiovascular system through inhalational route, with a contribution from dermal exposure. Wildfire smoke can cause cardiovascular effects through three possible pathways: activation of autonomic reflex, oxidative stress and systemic inflammation, and direct interaction with the vasculature. Abbreviations: BP: blood pressure, CO: carbon monoxide, EV: extracellular vesicle, HRV: heart rate variability, miRNA: microRNAs, NO x: oxides of nitrogen, PAHs: polycyclic aromatic hydrocarbons, PM: particulate matter, ROS: reactive oxygen species

Autonomic nervous system imbalance

As discussed earlier, wood smoke exposure under controlled conditions can significantly decrease HRV (i.e., SDNN, RMSSD, pNN50), a commonly examined endpoint of autonomic nervous system function [ 14, 154]. Inhalation of air pollutants, such as wildfire smoke, triggers autonomic reflexes in pulmonary receptors, baroreceptors, and chemoreceptors, leading to altered functional outcomes in the cardiovascular system [ 116].

Vagal sensory nerves and neural receptors in the respiratory system function to maintain normal respiratory physiology and pulmonary defense, and are sensitive to various environmental irritants [ 95]. These respiratory receptors include those found on unmyelinated C fibers (e.g., TRPA1, TRPV1, and J receptors), rapidly adapting pulmonary receptors (RAR), and slowly adapting pulmonary receptors (SAR) [ 116, 162]. Although not tested in wildfire smoke, studies of individual components present in wildfire smoke have shown potential to activate these receptors. For example, inhalation of high levels of ozone or volatile aldehydes can cause cardiovascular and pulmonary injury through activation of the TRPA1 receptor in humans and animals [ 28, 35, 62].

Activated sensory nerves send signals to the central nervous system, leading to modulation of the baroreceptor reflex that controls blood pressure and normal cardiovascular function [ 36]. In addition, these sensory nerves signal to the carotid body chemoreceptors located at the bifurcation of the carotid artery to maintain homeostasis of O ₂, CO ₂, pH, temperature and blood pressure [ 91]. Multiple studies have reported significant changes in blood pressure following exposure to wildfire smoke or wood smoke in humans in epidemiological and clinical studies [ 21, 32, 49, 167]. Wildfire smoke components, including PM, ozone, and SO ₂, have been shown to significantly decrease baroreflex sensitivity or affect the activity of chemoreceptors in the carotid body [ 116, 130]. Nevertheless, more research is needed to directly investigate the role of autonomic nerves in the control of the cardiovascular effects of wildfire smoke exposure.

Oxidative stress and systemic inflammation

Oxidative stress is believed to be a key mechanism by which exposure to air pollution causes cardiovascular morbidity and mortality [ 97]. Components of wildfire smoke particles such as metals, are known to induce oxidative stress through redox and non-redox cycling mechanisms [ 57, 58, 59, 134].

Cultured human pulmonary artery endothelial cells exposed to 40 μg/ml of wood smoke condensate for 1-4 h showed increased production of reactive oxygen species (ROS), loss of mitochondrial membrane potential, increased expression of the mitochondrial apoptosis regulator Bcl-2-associated X protein (BAX), DNA fragmentation, and increased mRNA expression of superoxide dismutase 1 (SOD1) and heme oxygenase 1 (HMOX1) [ 89]. The antioxidant n-acetylcysteine was shown to reverse the oxidative stress state and restore depleted intracellular glutathione levels following wood smoke exposure [ 89]. Wood smoke particles from smoldering red oak also induced significant increases in ROS detected using the non-specific sensor 2′,7′ -dichlorofluorescein diacetate [ 57, 58]. Though Miousse et al. did not find any significant changes in ROS following biomass smoke exposure, mRNA expression of catalase and HMOX1 was significantly increased at 24 or 72 h compared to controls in an in vitro study [ 100].

Wood smoke-induced oxidative stress can cause a disruption of the cell cycle and cellular apoptosis. In RAW264.7 cells, birch wood smoke extract suspended in cell culture media at 15-300 μg/ml decreased cellular metabolism and increased the number of cells entering the subG1 phase of the cell cycle after 24-h exposure [ 106]. Similarly, after 40-h exposure to 40 μg/cm ² of wood smoke extract, THP-1 cells entered S/G2 phase of the cell cycle, indicating decreased proliferation [ 23]. Studies have also shown evidence of cytotoxicity from exposure to wood smoke by using lactate dehydrogenase (LDH) release assay [ 57, 58, 100, 106] or MTT assay [ 168], although the positive results were not present in all studies partly due to different wood type, cell line, and doses and exposure duration.

Inhaled particulates elicit inflammatory responses in the lung, and a sufficient particle dose, reactivity, or lack of clearance may lead to a "spill-over" of inflammatory responses into the blood causing systemic inflammation [ 139, 146]. Clinical wood smoke exposure studies have consistently found significantly elevated blood markers of inflammation, including interleukin 1 beta (IL-1β), IL-6, IL-8, C-C motif chemokine ligand 2 (CCL2), clara cell protein 16 (CC16), and tumor necrosis factor α (TNFα) [ 50, 57, 58, 63, 144, 145]. In vivo animal studies also offered insights on wood smoke exposure induced inflammatory responses locally and systemically. Exposure of BALB/c mice to an organic wood smoke extract from emissions derived from spruce combustion significantly increased inflammatory responses (COX-2, MPO) in both respiratory and cardiovascular systems [ 46]. Serum collected from C57BL/6 mice exposed to oak wood smoke (PM 2.5 at 380 μg/m ³) for 24 h was able to induce pro-inflammatory responses (IL-6 and CXCL1), and elevated expression of adhesion molecules (VCAM1 and ICAM1) in murine endothelial cells [ 15]. Wood smoke produced from smoldering fire generated higher levels of aerosolized endotoxin and potently induced cytokine levels, neutrophil influx, and intracellular ROS production in mouse lavage fluid relative to emissions produced at the near-extinguishing stage [ 82]. In vitro toxicological investigations have yielded similarly consistent inflammatory responses caused by exposure to wood smoke extract across different experimental cell lines, exposure time, and doses [ 23, 57, 58, 90, 106].

Recent research has pointed to extracellular vesicle (EV) microRNAs (miRNA) released by exposed cells into the circulation, which may facilitate cell-to-cell communications and play a role in air-pollution induced cardiovascular effects. Studies have shown that exposure to PM 2.5 or ozone, two important components of wildfire smoke, was associated with an altered profile of miRNA targets such as miR-126, miR-19b, miR-150, miR-155, miR-191, and let-7a in human circulation [ 31, 128]. Many of these miRNA targets were associated with cardiovascular pathophysiology [ 129]. In terms of wildfire smoke, Ruiz-Vera and colleagues found that the expression of plasma miR-126 and miR-155 was significantly higher in women exposed to wood smoke compared to those using liquid petroleum gas (LPG), a cleaner form of fuel. In addition, there was a significant association between miR-126 and miR-155 expression levels and urinary 1-OHP concentrations, an indicator of PAH exposure [ 131].

Distinguishing between the effects of particles and absorbed volatile components

Studies show that UFPs with a mean aerodynamic diameter < 100 nm may translocate into the blood circulation through the alveolar-capillary barrier, reaching the heart and peripheral blood vessels [ 52, 136]. A more recent study found that nano-sized particles could be detected in surgical specimens of the carotid artery of animals and in the blood and urine of healthy human volunteers following acute inhalation of the particles [ 98]. Ultrafine wildfire smoke PM might have the same potential to cross the epithelial barrier to enter the pulmonary circulation.

In addition, when wildfire smoke particles deposit in the alveolar region, the majority of their available PAH-load may rapidly detach from the particles, and transfer across the epithelial barrier and diffuse into the bloodstream in an unmetabolized state [ 56, 70]. Interestingly, an in vitro study has shown that wood smoke-induced proinflammatory responses and cytotoxicity were mainly determined by the organic fraction, rather than the washed particulates [ 23]. In addition to the particulates, gaseous components of wood smoke including SO ₂, ammonia, NO x, and CO were found to be important contributors to the pro-atherosclerotic vascular response to air pollution exposure in mice [ 140]. A series of studies testing the chemical components of wood smoke generated from different kinds of biomass (red oak, pocosin peat, ponderosa pine needles, lodgepole pine, eucalyptus) at different combustion stage (smoldering versus flaming) showed different acute pulmonary toxicity and mutagenicity in mice [ 81, 83].

Research needs

A growing number of studies have implicated exposure to wildfire smoke as a risk factor for CVD. However, significant knowledge gaps regarding the association remain. Future epidemiological studies would benefit from improved exposure assessments and the implementation of more sensitive indicators of cardiovascular dysfunction. Similarly, the development of new methodologies could allow researchers to acquire individualized wildfire smoke exposure assessment, capturing more accurate exposure data [ 26, 27]. In addition to index air pollutants, future studies should also consider the impact of VOCs, which may be an important driver of wildfire smoke effects. Besides large-scale morbidity and mortality data, the identification of sensitive biomarkers should warrant information on the early onset of injury and on the underlying mechanisms of cardiovascular effects induced by wildfire smoke exposure. Since the direct evidence is lacking, more research is needed on how wildfire smoke exposure induces cardiovascular effects through the autonomic nervous system and directly impacts the vasculature. Novel mechanistic concepts including the role played by circulating miRNAs and cell-free DNA in the circulation on endothelial activation and injury should also be investigated.

There is also a geographical disparity in terms of the number of studies representing different regions. Among the wildlife smoke epidemiological studies presented in Table S 1, 29 studies are from North America, 1 from South America, 9 from Australia, 3 from Southeast Asia, and 6 from Europe. However, there were no studies from Africa where Savanna fires are common and intensification of wildfire frequency and scale is projected for the future [ 11, 39]. More wildfire smoke studies should be carried out in these underrepresented regions where the public health system is more vulnerable, especially under the circumstances of global warming and increased wildland-urban interface.

Data should serve as the scientific backbone for policymaking in public health issues. As wildfire events are likely to occur more frequently in the foreseeable future, scientific efforts should be directing attention to the possible interventional approaches to reduce wildfire smoke induced health effects. Physical methods such as HEPA-equipped air purifiers, have showed promise in reducing exposure to wildfire smoke or wood smoke, leading to reduced inflammation and improved vascular function [ 7, 78]. A wildfire smoke forecast that triggers interventions to reduce personal exposure at lower PM 2.5 threshold could be beneficial to reduce respiratory and cardiovascular health burdens [ 119]. In addition, comprehensive public health measures, such as Rule 4901, to reduce wood smoke exposure have been shown to lead to reductions in cardiovascular cases and IHD cases among those 65 years and older [ 166]. More research on the effectiveness of these strategies and applicability at a larger population scale is warranted to generate more robust data for informed public health decisions.

Conclusion

This review finds that wildfire smoke contributes to high levels of air pollutants, including coarse and fine PM, gases, PAHs and VOCs, during wildfire events. Exposure to these pollutants, with most evidence derived from studies of wildfire smoke PM, is a risk factor for adverse cardiovascular effects, especially among susceptible populations, including the elderly, pregnant women, and those with low SES. The young and healthy may also develop biological responses including systemic inflammation and vascular activation. The limited understanding between exposure to the gaseous components of wildfire smoke and the cardiovascular effects warrants more research. We have also discussed the importance of more accurate exposure assessment and measurement of more sensitive cardiovascular endpoints in future epidemiological studies. Clinical and toxicological research have highlighted several possible mechanisms of wildfire smoke-induced cardiovascular effects including systemic inflammation and oxidative stress, autonomic nervous system imbalance, release of EV mediators into the circulation, and direct interaction of translocated smoke components into the circulation. As large-scale wildfire events will likely occur more frequently in the future, more research is needed to understand and intervene in the cardiovascular effects of wildfire. With science-guided policy decisions, we may diminish the adverse impacts of wildfires through reducing exposure levels, mitigating toxicity, and protecting the most vulnerable.

Availability of data and materials

All data reviewed and described is either included in this manuscript or available online in the relevant publications.

Abbreviations

BALF:

Bronchial alveolar fluid

BAX:

Bcl-2-associated X protein

BC:

Black carbon

BSA:

Body surface area

CCL2:

C-C motif chemokine ligand 2

CC16:

Clara cell protein 16

CHF:

Congestive heart failure

CO:

Carbon monoxide

COPD:

Chronic obstructive pulmonary disease

COX-2:

Cyclooxygenase-2

CVD:

Cardiovascular disease

CXCL1:

C-X-C motif chemokine ligand 1

DBP:

Diastolic blood pressure

ED:

Emergency department

EV:

Extracellular vesicles

HDL:

High-density lipoprotein

HMOX1:

Heme oxygenase 1

HRV:

Heart rate variability

ICAM1:

Intercellular Adhesion Molecule 1

IL:

Interleukin

IHD:

Ischemic heart disease

LDH:

Lactate Dehydrogenase

LPG:

Liquid petroleum gas

MI:

Myocardial infarction

MIP-2:

Macrophage inflammatory protein 2

miRNA:

MicroRNA

MMP9:

Matrix metallopeptidase 9

MPO:

Myeloperoxidase

NAC:

N-acetylcysteine

NO:

Nitric oxide

NO₂ :

Nitrogen dioxide

PAHs:

Polycyclic aromatic hydrocarbons

PM:

Particulate matter

pNN50:

Proportion of NN50 divided by the total number of NN (R-R) intervals

RAR:

Rapidly adapting pulmonary receptors

RMSSD:

Root-mean square of successive NN interval differences

ROS:

Reactive oxygen species

SAR:

Slowly adapting pulmonary receptors

SBP:

Systolic blood pressure

SDNN:

Standard deviation of successive NN intervals

SES:

Socio-economic status

SO₂ :

Sulfur dioxide

SOA:

Secondary organic aerosol

SOD:

Superoxide dismutase

TNFα:

Tumor necrosis factor α

tPA:

Tissue plasminogen activator

TRPA1:

Transient receptor potential ankyrin 1

TRPV1:

Transient receptor potential vanilloid 1

UFPs:

Ultrafine particles (< 100 nm diameter)

VCAM1:

Vascular Cell Adhesion Molecule 1

VOCs:

Volatile organic compounds

vWF:

Von Willebrand factor

1-OHP:

1-Hydroxypyrene

# data[].attributes.attachment_link.title
Cardiovascular health impacts of wildfire smoke exposure - Particle and Fibre Toxicology

# data[].attributes.attachment_link.description
In recent years, wildland fires have occurred more frequently and with increased intensity in many fire-prone areas. In addition to the direct life and economic losses attributable to wildfires, the emitted smoke is a major contributor to ambient air pollution, leading to significant public health impacts.

# data[].attributes.headline
Acute stress disorder or post traumatic stress disorder may become a complication due to most subjects who are exposed to wildfires failing to recognize the mental health factors that may be associated (Caamano-Isorna et al. 2011, p.2-3) . Caamano-Isorna., Figueiras, A., Montes-Martinez, A., Taracido, M., Pineiro-Lamas, M. (2011). Respiratory and mental health effects of wildfires: an ecological study in Galician municipalities (north-west Spain).Environmental Health, 10, pp. 1-9.

# data[].attributes.subject
Acute stress disorder or post traumatic stress disorder may become a complication due to most subjects who are exposed to wildfires failing to recognize the mental health factors that may be associated (Caamano-Isorna et al. 2011, p.2-3) . Caamano-Isorna., Figueiras, A., Montes-Martinez, A., Taracido, M., Pineiro-Lamas, M. (2011). Respiratory and mental health effects of wildfires: an ecological study in Galician municipalities (north-west Spain).Environmental Health, 10, pp. 1-9.