Effects of Wildfire Smoke on Volatile Organic Compound (VOC) and PM_2.5 Composition in a United States Intermountain Western Valley and Estimation of Human Health Risk

Abstract

With a warmer and drier climate, there has been an increase in wildfire events in the Northwest U.S., posing a potential health risk to downwind communities. The Lewis–Clark Valley (LCV), a small metropolitan area on the Washington/Idaho border in the United States Intermountain West region, was studied over the time period of 2017–2018. The main objective was to determine the community’s exposure to particulate matter (PM_2.5) and volatile organic compounds (VOCs) during wildfire smoke events and to estimate the associated health risk. VOCs were analyzed previously in the LCV using sorbent tube sampling and thermal-desorption gas-chromatography mass-spectrometry (TD-GC-MS) during several local smoke events in the 2017–2018 fire seasons. PM_2.5 measurements were obtained from nearby agency monitors. PM_2.5 reached up to 200 µg/m³ in 2017 and over 100 µg/m³ in 2018 in the LCV, and has been observed to be increasing at a rate of 0.10 µg m⁻³/yr over the past two decades. Benzene, a carcinogen and air toxic, was measured with concentrations up to 11 µg/m³, over ten times the normal level in some instances, in the LCV. The health risk in the LCV from benzene was calculated at seven extra cancers per million for lifetime exposure and thirteen extra cancers per million considering all air toxics measured. The other cities monitored showed similar lifetime cancer risk, due to benzene of about 6–7 extra cancers per million. This work is important, as it measures ground-level exposures of VOCs and demonstrates decreases in PM_2.5 air quality over time in the region.

1. Introduction

Wildfires have become increasingly prevalent in the Western United States (U.S.) due to climate change, prolonged droughts, and land-use practices [1,2,3,4]. During 1984–2011, large U.S. wildfires increased at the rate of seven fires per year, or 355 square kilometers per year [5]. In the Western U.S., from 1950 until 2019, wildfire frequency and annual area burned followed an exponential growth, and mega-fires have doubled [6]. The forecast for large, simultaneous fires in the west is also increasing [7]. In the Western United States, the number of rain-wetting days between May and September from 1984 to 2015 exhibited a decreasing trend, which has been directly correlated to an increase in forested area burned [8]. Anthropogenic climate impacts have led to an excess of 4.2 million hectares of additional area burned within Western United States forests [9].

As the frequency and area of wildfires escalate, their associated emissions have surged to the forefront of environmental and public health concerns. Biomass burning (BB) contributes to the majority of carbonaceous fine aerosol emissions, and is the second largest source of trace gases in the atmosphere [10]. These emissions lead to the formation of secondary organic aerosols, as well as downwind ozone formation [11]. Studies have shown high concentrations of various VOCs, including alkenes, benzene, furans, phenols, and sulfur-containing compounds in wildfire smoke [12,13,14,15,16]. Fine particulate matter (PM_2.5) has been shown to be increasing in the Northwest U.S., at a rate of 0.21 (±0.12) µg m⁻³/yr, while it is on a downward trend for the rest of the country [17]. Most data to date show health effects from particulates and smoke but overlook ground-level speciated gas components. These can be just as important in human health.

Both primary and secondary biomass-burning emissions have been shown to be harmful to human health. Exposure to benzene, a trace gas emitted through biomass burning, can lead to acute lymphoblastic leukemia and chronic myeloid leukemia, as well as chromosomal damage in humans [18,19]. Exposure to PM_2.5 can exacerbate pre-existing respiratory illnesses such as asthma and emphysema [20]. These particles are so small that they make their way into the lung tissue, eventually leading to alveolar wall corrosion [21]. While this decreases overall pulmonary function, it also leads to the formation of lung cancers and adenocarcinoma [22]. A study conducted by the American Cancer Society found that with each increase of 10 µg m⁻³ in the PM_2.5 concentration, mortality due to lung cancer increases by 8% [23]. Models predict a 2.8% increase in overall mortality from short-term exposures for each additional 10 µg m⁻³ in the PM_2.5 concentration [24]. Large cities and urban centers can pose a human health risk to their respective populations due to air pollution, but rural and small urban areas have been frequently overlooked with respect to air pollution from trace gases or particulates. These rural or small urban areas, which have less pollution due to numbers of people and transportation, tend to be impacted during winter months, due to biomass burning for heating homes and during summer/early fall, due to agriculture or wildfire smoke events [25]. Although some studies and regional monitoring have been conducted during wildfire seasons [13,16,26,27,28], there is generally a lack of information from these less populated areas, due to minimal or non-existent ground-based monitoring.

The Lewis–Clark Valley (LCV) is a small urban area located along the Northern Idaho–Eastern Washington border with a combined population of about fifty thousand. Wildfire smoke can travel short or long distances and remain stagnant in the LCV for several days or weeks. This leads to spikes in PM_2.5 concentrations, at times raising the air quality index to unhealthy and very hazardous levels, as seen in the last decade [28]. While wildfire smoke does have an impact on the area, it is not the lone source of air pollution. There are various industrial sources within the valley which contribute to the local air pollution, including a Kraft process pulp paper mill. The authors have assessed the valley’s emissions and health risk in the past, but without particular focus on wildfire smoke impacts [29]. The Nez Perce Tribe conducted a study on various volatile organic compounds such as benzene and formaldehyde [30,31]. Benzene levels in the LCV were found to be greater than the national mean , while formaldehyde was found to be decreasing over time [30,31]. Health risks attributed to the local pollution were seen as low risk, ranging from 2 to 11 extra cancers per million [29]. In these studies, health risk attributed to wildfire smoke in the LCV has not been reported.

This current work aimed to determine the impact that wildfire smoke has on the concentration of volatile organic compounds (VOCs) and PM_2.5 in the Lewis–Clark Valley and nearby cities of Coeur d’Alene, Boise and Spokane. Specifically, how did two major smoke events in the summers of 2017–2018 affect health risk, based on these exposures to the communities? VOC concentrations obtained previously during this time from thermal-desorption gas-chromatography mass-spectrometry (TD-GC-MS) by the coauthors [29] were used with PM_2.5 values to classify wildfire smoke versus normal air-quality days. Human health risk due to benzene and other elevated air toxic exposure in wildfire smoke was determined. PM_2.5 trends over the past 23 years in the LCV were also investigated. This work addresses the impact of ground-level VOCs and PM_2.5 from wildfire smoke on these communities in the Northwest, where smoke influence is growing at the greatest rate [17].

2. Materials and Methods

2.1. Volatile Organic Compound (VOC) Data

VOC concentration data used in this study were obtained previously by the coauthors [29]. In brief, Markes International (Bridgend, UK) dual sorbent tubes (Tenax^®TA-Sulficarb) were used for weekly active sampling at 10 sites in the LCV in 2017–2018 (Figure 1a), and Markes Tenax^®TA sorbent tubes were used for biweekly-to-monthly passive sampling at LCV and three other cities: Boise, ID, Coeur d’Alene, ID and Spokane, WA in 2018 only (Figure 1b) [29]. Analysis of 50 VOCs using thermal-desorption gas-chromatography mass-spectrometry followed U.S. EPA Methods TO-17 and 325 [29,32,33,34]. Benzene, ethylbenzene and xylenes were analyzed additionally in passive samples, as these uptake rates were available [35]. This dataset of VOCs is available in Scott et al. as Supplement Materials [29]. For this current study, 337 samples from June to early October 2017–2108 were utilized for the smoke and health risk analysis.

2.2. PM_2.5 Data

Daily mean particulate matter data (PM_2.5) were obtained from the monitoring sites of the Idaho Department of Environmental Quality and/or Washington Department of Ecology through the U.S. EPA Air Quality System [28]. The monitoring sites were matched to the closest VOC sites and are as follows: Lewiston–Sunset Park, Boise–St. Luke’s in Meridian, Coeur d’Alene–Lancaster Road, and Spokane–Augusta Ave (Figure 1b) [28]. PM_2.5 data were taken the same day and same hour for comparison with active VOC samples from 2017 to 2018. Passive samples of VOCs were of two-week to monthly duration and were compared to daily mean PM_2.5 levels averaged during the respective time period. In addition, the daily mean PM_2.5 record from 2000 to 2023 was utilized to observe longer term trends in the LCV [28].

Direct observation of wildfire smoke during grab sampling, as well as observation of PM_2.5 levels, were used to designate smoke-impacted samples. For the background observation designation, daily mean PM_2.5 was below 25 µg/m³, while biomass burning levels were considered above this threshold during the summer/early fall months (June–October), unless smoke was directly observed. For reference, the regulatory daily 24 h PM_2.5 standard is 35 µg/m³, and the annual is 9 µg/m³ [36]. Student t-tests of differences of standard deviation and means (95% confidence level) were performed on VOCs that had at least 20% detection, to determine differences in background versus smoke samples. Correlations between PM_2.5 and VOCs were also calculated with both the background (BG) and smoke samples (BB), and tested for significance (95% confidence level) using the critical values for the correlation coefficients.

2.3. Health Risk Calculations

The health risks of exposure to VOCs in smoke were determined by use of U.S. EPA exposure methods [37,38]. This approach used the upper confidence limit (UCL), exposure concentration multiplied by a risk factor for selected compounds. The unit risk factors and risk categories were available through the Integrated Risk Information System [39]. The following equations were used in calculating risk [37]:

$$Risk=EC\times IUR$$

(1)

where EC is the exposure concentration in μg/m³, calculated by Equation (2),

$$EC={\displaystyle \frac{\sum (CA\times ET\times EF\times ED)}{AT}}$$

(2)

and IUR is the inhalation unit risk in (μg/m³)⁻¹, or the lifetime risk for an individual exposed to 1 µg/m³ of developing cancer. CA is the measured concentration in µg/m³, which was taken as the UCL or the upper confidence limit (95%) of the chemical, ET is the exposure time (h/day), or 24 h/day (residential), EF is the exposure frequency (days/year), 30 days for smoke and 320 days for background, totaling 350/year (residential), ED is the exposure duration (years), 26 years (residential) or 70 years (lifetime), and AT is the averaging time (h) = 70 years × 365 days/year × 24 h/day = 6 × 10⁵ h (expected lifetime) [38]. For benzene, risk factor = EC (μg/m³) × (7.8 × 10⁻⁶ m³/μg), where the upper estimate of IUR is used [39]. For multiple VOCs measured, a cumulative cancer risk was based on the summation of the individual risks.

For non-carcinogenic VOCs, a hazard quotient (HQ) was calculated, based on the inhalation chronic reference concentration (RfC) in (μg/m³), where EC was calculated using ET of 24 h, ED of 30 days for smoke and 335 days for background, and ED of 26 and 70 years for residential and lifetime exposures [37]:

$$HQ={\displaystyle \frac{EC}{RfC}}$$

(3)

Specifically, the HQ was used to assess the non-carcinogenic effects from compounds like benzene and toluene. An HQ greater than one indicates that estimated exposure may cause non-carcinogenic health effects [37]. If the HQ is less than one, then non-carcinogenic health effects should not be likely to occur. The hazard index (HI) is the sum of HQs of each compound [37].

3. Results/Discussion

3.1. Observed Smoke Events and PM_2.5 Trends

Both in the summers of 2017 and 2018, biomass burning events were observed in the LCV. Air quality was poor, and at times was at the very unhealthy-to-hazardous level in and nearby the LCV. One example is shown on 7 September 2017, in Figure 2, when a severe biomass burning event was taking place in the Northwest U.S. During the two summer seasons of 2017–2018, 245 background samples and 92 smoke samples were taken in the LCV. For longer-term trends outside of this time period, particulate matter was investigated. Figure 3 demonstrates PM_2.5 changes over the past 23 years in the LCV [28]. The horizontal line is the 24-h average air-quality standard of 35 µg/m³ [36]. There is an increasing trend, with a slope of 0.10 µg m^−3/yr during this time. This value is comparable to the 0.21 µg m^−3/yr that McClure and Jaffe reported for the Northwest [17]. From 2012 to 2023, there were eight years that had summer spikes of PM_2.5 > 35 µg/m³, compared to 2000–2011, where only 2006 had a small spike above this level.

3.2. Concentrations of VOCs and PM_2.5 in Wildfire Smoke in LCV

The most concentrated and/or most detected VOCs of those measured during the June–October periods are shown in

Table 1. 2017–2018 statistics divided by year, background (BG) and smoke or biomass burning (BB). Compounds with statistically significant increases from BG to BB are indicated (*). All concentrations are in µg/m³. % ND is the percent of non-detects, Min–Max is the range of observations, (S) is mean ± standard deviation, and UCL is upper confidence limit (95%).

2017	Background Samples (n = 125)				Biomass Burning Samples (n = 44)
Compound	% ND	Min–Max	Mean ± S	UCL	% ND	Min–Max	Mean ± S	UCL
Benzene *	5	0.02–3.42	0.45 ± 0.54	0.67	0	0.18–11.46	2.14 ± 2.30	2.89
Benzene, propyl- *	75	0.02–0.61	0.05 ± 0.10	0.09	39	0.02–0.56	0.10 ± 0.12	0.18
Dichlorodifluoromethane *	0	2.51–17.87	6.31 ± 2.91	6.75	0	5.49–12.90	8.71 ± 1.32	9.04
Ethylbenzene *	32	0.01–2.55	0.20 ± 0.38	0.34	5	0.01–1.78	0.42 ± 0.44	0.71
m,p-Xylene *	10	0.02–12.31	0.88 ± 1.71	1.55	2	0.02–6.25	1.50 ± 1.60	2.50
Naphthalene *	79	0.01–0.89	0.05 ± 0.12	0.08	59	0.01–0.89	0.12 ± 0.18	0.18
p-cymene *	61	0.01–1.24	0.14 ± 0.25	0.19	7	0.01–2.57	0.49 ± 0.49	0.65
Phenol *	63	0.02–4.58	0.26 ± 0.62	0.32	2	0.02–2.37	0.66 ± 0.43	0.79
Trichloromonofluoromethane *	1	0.01–4.73	0.97 ± 0.62	1.07	0	0.37–2.69	1.21 ± 0.56	1.35
Benzene, 1,2,4 trimethyl	85	0.06–4.16	0.22 ± 0.57	0.34	70	0.06–0.74	0.13 ± 0.14	0.17
Dimethyl sulfide	50	0.02–40.55	1.99 ± 5.80	3.97	41	0.02–54.99	3.28 ± 8.77	7.49
Disulfide, dimethyl	78	0.01–25.57	0.56 ± 3.12	1.80	68	0.01–5.64	0.27 ± 0.87	0.75
Mesitylene	67	0.02–1.15	0.08 ± 0.17	0.15	50	0.02–0.73	0.11 ± 0.15	0.16
Methylene chloride	6	0.02–2.32	0.17 ± 0.21	0.19	0	0.08–1.71	0.23 ± 0.24	0.29
Tetrachloroethylene	74	0.01–1.85	0.07 ± 0.23	0.16	45	0.01–0.62	0.10 ± 0.14	0.19
Toluene	1	0.01–41.95	1.99 ± 5.57	4.17	0	0.21–12.8	2.98 ± 2.92	3.75
Trichloromethane	29	0.01–1.55	0.14 ± 0.22	0.23	20	0.01–1.13	0.21 ± 0.23	0.29
2018	Background Samples (n = 120)				Biomass Burning Samples (n = 48)
Compound	% ND	Min–Max	Mean ± S	UCL	% ND	Min–Max	Mean ± S	UCL
Benzene *	0	0.09–1.26	0.44 ± 0.23	0.48	0	0.23–5.12	1.42 ± 1.53	2.38
Ethylbenzene *	42	0.01–1.14	0.09 ± 0.14	0.14	19	0.01–0.62	0.21 ± 0.20	0.27
m,p-Xylene *	22	0.02–5.09	0.35 ± 0.58	0.55	12	0.02–2.32	0.54 ± 0.47	0.69
Naphthalene *	78	0.01–0.36	0.03 ± 0.05	0.04	65	0.01–0.37	0.08 ± 0.12	0.11
p-cymene *	40	0.01–0.80	0.14 ± 0.18	0.21	21	0.01–2.16	0.38 ± 0.48	1.17
Toluene *	1	0.01–3.93	0.65 ± 0.59	0.75	0	0.15–4.49	1.51 ± 1.44	2.32
Benzene, propyl-	84	0.02–0.31	0.03 ± 0.04	0.05	65	0.02–0.14	0.04 ± 0.04	0.05
Carbon Tetrachloride	47	0.03–0.50	0.22 ± 0.18	0.25	79	0.03–0.46	0.10 ± 0.14	0.13
Dichlorodifluoromethane	0	3.83–5.97	4.70 ± 0.38	4.76	0	3.95–5.50	4.59 ± 0.40	4.69
Dimethyl sulfide	15	0.02–16.00	1.75 ± 3.30	3.07	12	0.02–13.88	2.45 ± 3.37	10.33
Disulfide, dimethyl	85	0.01–5.25	0.25 ± 0.91	0.10	75	0.01–3.34	0.16 ± 0.53	0.43
Methylene chloride	2	0.02–0.71	0.20 ± 0.08	0.21	0	0.10–0.25	0.18 ± 0.03	0.19
Tetrachloroethylene	72	0.01–0.47	0.05 ± 0.08	0.05	71	0.01–0.34	0.03 ± 0.06	0.02
Trichloromethane	8	0.01–3.33	0.25 ± 0.39	0.40	17	0.01–1.07	0.23 ± 0.23	0.48
Trichloromonofluoromethane	0	0.29–2.40	1.33 ± 0.40	1.39	0	0.52–2.11	1.37 ± 0.35	1.46

. Benzene, toluene, ethylbenzene and m,p-xylene (BTEX) were all elevated in smoke compared to the background samples, with 2017 means of 2.14, 2.98, 0.42, and 1.50 µg/m³ and 2018 means of 1.42, 1.51, 0.21, and 0.54 µg/m³, respectively (Table 1). Other elevated hydrocarbons included naphthalene, p-cymene, and phenol (Table 1).

Although halogenated air toxics were measured, these were not statistically increased in wildfire smoke and/or were not believed to come from wildfire sources, as they are anthropogenic. The 2017 means of VOCs in smoke samples were higher compared to 2018, and this was also seen in PM_2.5 levels, indicating a more severe fire season in the LCV (Table 1, Figure 4). Benzene time-series are plotted with PM_2.5 for each year, in Figure 4. Two large wildfire smoke events, as evidence by the maximum benzene and PM_2.5 levels in Figure 4, peaked on 5 September 2017 (11.46 µg/m³ benzene, 211 µg/m³ PM_2.5) and 20 August 2018 (4.22 µg/m³ benzene, 109 µg/m³ PM_2.5).

Benzene and PM_2.5 behaved very similarly to each other during the biomass-burning smoke episodes. This relationship supports the fact that the benzene increases were a result of the wildfire smoke. BTEX distributions for background and wildfire smoke or biomass burning samples are shown in Figure 5. All species were elevated in smoke samples, with 2017 showing higher means than 2018, and all the differences from background were statistically significant, except toluene in 2017. Local emissions of benzene (and BTEX) including automobiles and industry, were captured in background samples, but there was a five-fold increase in the 2017 mean values of benzene in smoke (biomass burning) vs. background samples (Table 1). Sources of other VOCs in the LCV, such as trichloromethane and dimethyl sulfide, were appointed to the paper mill, and still others to secondary formation, traffic and biogenic sources [29,30]. However, an in-depth analysis of sources other than biomass burning is not the focus here.

Several species were correlated with PM_2.5 in the smoke samples versus the background (

Table 2. Coefficient of determination values for VOCs with PM_2.5 in both background (BG) and biomass burning (BB) samples from 2017 to 2018. Values are significant at the 95% confidence level are indicated (*) and bolded values are strong correlations over 0.5. The strongest correlations are with PM_2.5 and benzene, followed by naphthalene and p-cymene.

	PM2.5 BG	PM2.5 BB
Benzene	0.09 *	0.69 *
Benzene, 1,2,4 trimethyl	0.00	0.03
Benzene, propyl-	0.03 *	0.25 *
Carbon Tetrachloride	0.03 *	0.03
Dichlorodifluoromethane	0.01 *	0.02
Dimethyl sulfide	0.05	0.00
Disulfide, dimethyl	0.00 *	0.04 *
Ethylbenzene	0.02 *	0.29 *
m,p-Xylene	0.02 *	0.09 *
Mesitylene	0.02 *	0.04 *
Methylene chloride	0.01	0.00
Naphthalene	0.01	0.56 *
p-cymene	0.11 *	0.54 *
Phenol	0.00	0.01
Tetrachloroethylene	0.02 *	0.01
Toluene	0.02 *	0.39 *
Trichloromethane	0.13 *	0.00
Trichloromonofluoromethane	0.01 *	0.01

). Benzene and PM_2.5 were correlated in smoke samples with R² value of 0.69, as shown in Figure 6a and Table 2. In fact, the slope of benzene to PM_2.5 was 0.024 µg/m³ benzene: µg/m³ PM_2.5 or 7.5 ppb benzene: 1000 µg/m³ PM_2.5. This was comparable to the ratios of benzene to PM₁ of 9.2 ppb benzene : 1000 µg/m³ PM_2.5 found in the WE-CAN airborne study [13]. The non-benzene BTEX compounds did not correlate as well to PM_2.5, with R² values of 0.39, 0.29, and 0.08, respectively, as they were elevated on both background and smoky days (Table 2). This suggests multiple sources, and correlations may be related to the particulate matter from industrial sources and traffic. In addition, naphthalene and p-cymene were moderately correlated to PM_2.5 with R² of 0.56 and 0.54 (Table 2). Naphthalene is a known combustion byproduct and p-cymene is a monoterpene of biogenic origin. Dimethyl disulfide (DMDS) was not observed in each sample, and its R² with PM_2.5 was low (0.04). Dimethyl sulfide (DMS) was observed at high levels in both background and smoke events, due to the location of a local paper mill in Lewiston [29]. DMS did not have a correlation with PM_2.5 (0), even though it has been shown to be emitted from biomass burning [41]. It is likely that the wildfire smoke was aged and DMS and DMDS decayed in this smoke before it got to the region, since the lifetime of these compounds are a day or less.

BTEX species were also correlated to each other in smoke samples. Benzene and toluene correlation is shown in Figure 6b, with R² of 0.76 for smoke samples, and R² reduced to 0.31 for background samples. The slope was higher for biomass burning (BB) samples as well, showing benzene levels increasing in smoke rather than without. Smoke (BB) samples were expected to have a higher benzene/toluene (B/T) ratio compared to traffic emissions, and aged samples from either source should also have higher B/T ratios compared to samples closer to source, as toluene will react in the atmosphere more quickly with OH radicals, one of the main sinks [42]. The B/T (mole/mole) ratio was on average 1.18 +/−0.70 (range 0.12–3.27) in BB samples, and 0.94 ± 1.02 (range 0.02–11.04) in BG samples. These values are consistent with other studies reporting B/T ratios greater than one for smoke samples [43,44,45] and less than one for traffic [44].

3.3. Passive-Sampling Comparison between Cities

In order to better understand the long-term exposure of these compounds (versus a compilation of grab samples), passive samplers were used at four locations, with a sample taken for 2–4 weeks (Figure 1b). Only benzene, toluene and xylene were examined, as these compounds had available uptake rates on the Tenax^®TA sorbent when previously published [29,35]. These results are shown in Figure 7b. Smoke influence was present in August 2018 at all locations, consistent with the grab-sampling results of LCV.

The whole region experienced this smoke event, with highest levels of PM_2.5 in Spokane (185 µg/m³) and Coeur d’Alene (CDA) (154 µg/m³) on 19 August 2018. LCV peaked the next day at 109 µg/m³ and Boise did not have as much smoke, evidenced by PM_2.5 of 43 µg/m³ (Figure 7a). Benzene levels also had a peak in August 2018, coinciding with the smoke event, but had a second and higher peak in November in the northern sites (LCV, Spokane and CDA) (Figure 7b). This could be from the use of wood burning stoves and/or cold weather inversions, as the PM_2.5 also has a small increase during that time. In general, the Northwest region experienced similar values of PM_2.5, and benzene levels ranged from 0.2–1.1 µg/m³, which were slightly lower than the active samples (Figure 7b). This was likely due to the passive monthly averaging vs. the short-term active sampling.

3.4. Health Risk Assessment

Of the compounds measured, benzene was the biggest contribution to health risk (due to its carcinogenicity) aside from PM_2.5 in wildfire smoke. The inhalation unit risk (IUR) for benzene of 7.8 × 10⁻⁶ (µg/m³)⁻¹ was used in this analysis to err on the side of protection [39]. This corresponds to the risk of cancer when exposed to 1 µg/m³ of benzene throughout a lifetime. This level of benzene (1 µg/m³) is representative in the U.S. of an associated health risk of 1–10 × 10⁻⁶, according to the air toxic inventory and ambient air monitoring [46]. The background mean in this study was 0.26 and 0.30 µg/m³ for 2017 and 2018, respectively. The biomass burning event grab-sampling means for LCV was 2.62 µg/m³ and 1.73 µg/m³ for 2017 and 2018, about ten and six times that of the background, respectively. The corresponding cancer risk factors were 3 × 10⁻⁶ and 7 × 10⁻⁶ for residential and lifetime scenarios for benzene alone, and 5 × 10⁻⁶ and 13 × 10⁻⁶ when including trichloromethane (

Table 3. Cancer risk analysis of LCV, including smoke or biomass-burning exposures (BB) of 30 days and background (BG), repeated for 26 years (Residential) and 70 years (Lifetime). CA (measured concentration) is based on the upper confidence level of concentrations in µg/m³ obtained via active sampling. EC is the exposure concentration in µg/m³, calculated for both residential (Res) and lifetime (Life) scenarios. The inhalation unit risk (IUR) in (µg/m³)⁻¹ and the Reference Concentration (RfC) in µg/m³ were used for the Cancer Risk and Hazard Quotient (HQ) calculations, respectively [40]. Cancer risks and HQ are unitless.

Compound	CA BG	CA BB	EC BG Res	EC BB Res	EC BG Life	EC BB Life	IUR	RfC	Cancer Risk Res	Cancer Risk Life	HQ
Benzene	0.7	2.941	0.23	0.09	0.64	0.24	7.80 × 10−6	30	2 × 10−6	7 × 10−6	2.9 × 10−2
Trichloromethane	0.23	0.52	0.07	0.02	0.21	0.04	2.30 × 10−5	98	2 × 10−6	6 × 10−6	2.6 × 10−3
Methylene Chloride	0.22	0.33	0.07	0.01	0.20	0.03	1.00 × 10−8	600	8 × 10−10	2 × 10−9	3.8 × 10−4
Tetrachloroethylene	0.05	0.18	0.02	0.01	0.04	0.01	2.60 × 10−7	40	6 × 10−9	2 × 10−8	1.5 × 10−3
Benzene, 1,2,4 trimethyl	0.33	0.15	0.11	0.00	0.30	0.01	NA	60			5.2 × 10−3
Benzene, propyl	0.07	0.23	0.02	0.01	0.06	0.02	NA	1000			7.9 × 10−5
Ethylbenzene	0.31	0.57	0.10	0.02	0.29	0.05	NA	1000			3.3 × 10−4
Mesitylene	0.11	0.11	0.04	0.00	0.10	0.01	NA	60			1.9 × 10−3
Naphthalene	0.07	0.19	0.02	0.01	0.06	0.02	NA	3			2.5 × 10−2
Toluene	3.34	4.58	1.09	0.14	3.06	0.38	NA	5000			6.9 × 10−4
Xylene (m,p)	1.46	2.61	0.47	0.08	1.34	0.21	NA	100			1.6 × 10−2
Cumulative									5 × 10−6	1.3 × 10−5	8.3 × 10−2

). Trichloromethane (chloroform) is not associated with wildfires, but with the paper mill emissions in this region [29]. Non-cancer risk was calculated for the smoke and background exposures for all VOCs with an available chronic inhalation reference concentration (RfC) [39]. The resulting HQ values were under 1, with highest values for benzene and naphthalene of about 0.03 each, and HI of 0.08 (Table 3). This suggests there was a low probability of a non-cancer health event occurring. Each VOC has specific target organs, and the results may or may not be summative, as this is beyond the scope of our analysis.

When considering the monthly passive samples obtained, the benzene range of 0.22–0.56 µg/m³ translates to a cancer risk of 2 × 10⁻⁶ and 5 × 10⁻⁶ for residential and lifetime scenarios in the LCV (

Table 4. Comparison of health risk during smoke events for LCV and three cities in 2018, using the upper confidence level of benzene concentrations in µg/m³ obtained via passive sampling (CA). BG represents background and BB represents smoke or biomass-burning samples. EC is the exposure concentration in µg/m³, calculated for both residential (Resident) and lifetime scenarios. The inhalation unit risk (IUR) of 7.8 × 10⁻⁶ (µg/m³)⁻¹ and the Reference Concentration (RfC) of 30 µg/m³ were used for the Cancer Risk calculations, and Hazard Quotient (HQ), respectively [40]. Cancer risks and HQ are unitless.

Site	CA BG	CA BB	EC BG Resident	EC BB Resident	EC BG Lifetime	EC BB Lifetime	Cancer Risk Resident	Cancer Risk Lifetime	HQ
LCV	0.69	1.15	0.23	0.04	0.61	0.09	2 × 10−6	5 × 10−6	0.02
Boise	0.78	0.56	0.25	0.02	0.68	0.05	2 × 10−6	6 × 10−6	0.02
Coeur d’Alene	0.91	0.69	0.30	0.02	0.80	0.06	2 × 10−6	7 × 10−6	0.03
Spokane	0.97	0.82	0.32	0.03	0.85	0.07	3 × 10−6	7 × 10−6	0.03

). This was slightly less than the analysis of the grab sampling, and the sampling size was smaller at n = 13 (monthly samples). The other cities sampled were about the same risk, with Spokane having 3 × 10⁻⁶ and 7 × 10⁻⁶ cancer risk (residential, lifetime), and Boise and Coeur d’Alene (CDA) both with 2 × 10⁻⁶ residential cancer risk and 6 × 10⁻⁶ and 7 × 10⁻⁶ lifetime cancer risk, respectively (Table 4). The HI was about the same for all of the areas, ranging from 0.02 to 0.03 for lifetime exposure to benzene.

The health implication found was that wildfire smoke events increase the lifetime cancer risk to the community by up to seven extra cancers per million in the LCV, and this is similar to surrounding areas in the Northwest.

Although the health risk due to PM_2.5 is a bit more complex, a 2.8% increase in mortality for every 10 µg/m³ increase in PM_2.5 was estimated for short-term exposures [24]. For the smoke events observed in this study, increases of up to 200 µg/m³ would imply a 56% increase in mortality associated with such events. While this seems large, it warrants epidemiological studies to further study the severity of such events.

3.5. Comparison with Previous Works

The co-authors’ earlier health risk assessment in the LCV (due to local pollution sources) showed cancer risk from VOCs to be in the range of 2–11 extra cancers per million [29]. The current analysis confirms that, with 2–13 extra cancers per million using the background and smoke criteria versus aggregating the VOCs without this distinction. Miller et al. [26] studied benzene and other VOCs in 2019 emissions in the LCV, as well as in Boise and Spokane, with a cancer risk of only one extra cancer per million due to benzene, since 2019 had much less smoke impact than in 2017–2018, studied here. Another study in the region was closer to the wildfires themselves, and this estimated cancer risk to be 1–19 extra cancers per million, due to benzene alone, which again, is comparable [45]. Few other studies have focused on VOCs in wildfire smoke and assessed cancer risk. O’Dell et al. [13] used ratios of benzene and other air toxics with PM_2.5 at higher altitude, to estimate risk at ground levels, in the range of 2–10 extra cancers per million in Idaho/Eastern Washington during 2018. This was comparable to the present study. Navarro et al. [47] used the benzene-to-PM₁ ratios observed by O’Dell et al. [13] to estimate exposure concentrations of fire fighters in the Western U.S. The ratio of Benzene to PM_2.5 found in this study was 7.5 ppb:1000 µg/m³ compared to 9.2 ppb:1000 µg/m³ [13,47]. The benzene levels measured by Navarro et al. [47] on the front lines were much higher than in the communities, and these were closer to levels observed by Dickinson et al. [45], which were also close to the fires. Jin et al. [16] and Wang et al. [48] observed benzene to be about 1 µg/m³ in wildfire smoke. These results and others are summarized in

Table 5. Summary of results from biomass-burning VOC measurements in the Western U.S. region, including the current study. Benzene levels were reported in both µg/m³ and ppb, for comparison across studies. Cancer risk is unitless.

Biomass-Burning Study	Study Area	Main Pollutant(s)	Benzene Levels Measured	Cancer Health Risk (Per Million)
Current study	Northwest U.S., LCV (ground level)	BTEX	0.02–11 µg/m3 (0.06–3.6 ppb)	2–13
Dickinson et al., 2022 [45]	Northwest U.S. (ground level, near fires)	BTEX	0.06–80 µg/m3 0.02–25 ppb	1–19
O’Dell et al., 2020 [13]	Western U.S. (airborne)	Benzene, Acrolein, Formaldehyde	0.1–10 µg/m3 0.03–3 ppb)	2–10
Navarro et al., 2021 [47]	Western U.S. (ground-level estimates)	Benzene, Acrolein, Formaldehyde	4.5–19 µg/m3 1.4–6 ppb	NA
Wang et al., 2024 [48]	Northern California, U.S. (ground level)	BTEX	1 ± 0.2 µg/m3 0.3 ± 0.06 ppb	NA
Jin et al., 2023 [16]	Western U.S. (airborne, ground level)	BTEX, Formaldehyde, Acetaldehyde	0.03–0.96 µg/m3 0.01–0.3 ppb	NA

. In addition to the levels of VOCs, PM_2.5 trends over time in the LCV of 0.10 µg m⁻³/yr are in the range of McClure and Jaffe’s analysis of the Northwest U.S. increases of 0.21 ± 0.12 µg m⁻³/yr [17].

3.6. Limitations

The lifetime risk for increased benzene exposure due to wildfire smoke was elevated for LCV residents. However, acute and sub-chronic problems may occur as a result of wildfire smoke. This analysis did not consider the PM_2.5 health effects, which can also contribute to illness. In addition, these were calculated risks of cancer and non-cancer events, due to increased air toxics during wildfire smoke episodes. There are many other potential causes of cancer, and this study only addressed the air toxics that were measured. Not all mass of smoke was accounted for in the sampling methods. Thus, this is likely an underestimate of the total health risk via all exposures and mechanisms.

Uncertainties were estimated at 10% for the original VOC measurements, as well as using the upper confidence limit (UCL) in the risk calculations for the exposure concentration calculations. The risk analysis used a value for IUR which was the upper limit (7.8 × 10⁻⁶ (µg/m³)⁻¹, where the lower limit was reported as 2.2 × 10⁻⁶ (µg/m³)⁻¹, about a third of the value used in this study [40].

4. Conclusions

This study focused on the impact of wildfire smoke on VOCs in a small metropolitan, intermountain valley in the Western U.S. and surrounding cities from 2017 to 2018. Wildfire smoke events occurred in the Lewis–Clark Valley (LCV) in September 2017 and August 2018, which elevated PM_2.5 and VOCs well above the background levels.

The key findings were the following:

• Wildfire smoke events lasted up to 30 days and PM_2.5 daily exposures spiked up to 200 µg/m³.
• Several VOCs were elevated in 2017–2018 smoke events, including air toxics (means in µg/m³): benzene (1.78), toluene (2.25), ethylbenzene (0.32), xylenes (1.02), phenol (0.66), and p-cymene (0.87).
• The lifetime hazard index of the LCV smoke exposures was below one, and considered low risk for non-cancer health events.
• There was an associated risk of 6–7 extra cancers per million in the LCV and Boise, Coeur d’Alene and Spokane, due to lifetime benzene exposure from smoke.
• Combined with other pollutants in the background air, the total cancer health risk of VOCs measured in the LCV was up to 13 extra cancers per million, which was consistent with an earlier study of the region [29].
• PM_2.5 have increased in the LCV by 0.10 µg/m³/yr over the past 23 years, showing the impact of wildfires on the region.

This work is important, as it assessed air toxic and PM_2.5 exposure at the ground level, where communities were exposed, in the Northwest U.S. region, which has been plagued by wildfire smoke events in the past decade.