Letter to the Editor

Wildfire smoke and respiratory symptoms in patients with chronic obstructive pulmonary disease

Climate change has been deemed the biggest global health threat of the 21st century. One consequence of climate change is the increasing frequency and severity of forest fires. Smoke from wildfires has the ability to negatively impact air quality over large distances. The aim of this study was to examine the association that air quality had on emergency department visits for cardiac, respiratory and psychiatric/behavioral health chief complaints during forest fire season in Vancouver, British Columbia.

The study period was January 1, 2009 – December 31, 2019. Forest fire season was defined as April 1- September 30. Air quality (measured by PM2.5 in ug/m³) was obtained from the Vancouver International Airport (YVR) Air Quality station. Emergency department visit data (CEDIS triage complaint) was acquired from a regional emergency department database. A generalized linear mixed model with Poisson link function was used to determine the relative risk (as a percentage) for respiratory, cardiac and psychiatric/behavioral health CEDIS triage complaints associated with a 10 unit increase in PM2.5.

PM2.5 during forest fire season was significantly associated with emergency department visits for respiratory chief complaints. For every 10 ug/m³ increase in PM2.5, there was a 4.61% (95% CI: 3.07, 6.17) increase in relative risk of respiratory chief complaints presenting to emergency departments. No association was found between PM2.5 and cardiac or psychiatric/behavioral health chief complaints during forest fire season or non-forest fire season. During non-forest fire season, PM2.5 was found to be negatively associated with respiratory (-3.57, 95% CI: -5.44, -1.66) and cardiac chief complaints (-2.77, 95% CI: -4.16, -1.47).

Our results indicate a probable association between air quality during forest fire season and emergency department visits for respiratory chief complaints. This provides further illustration of the widespread impact of climate change, and underscores the importance of efforts to address it.

Biomass burning (BB) has been considered as a major source for primary aerosols and gas pollutants in the atmosphere, but the influence of atmospheric aging processes on the chemical compositions of BB aerosols remains unclear. In this study, a combustion chamber and an oxidation flow reactor were combined to simulate fresh and 7-day aged PM_2.5 from burning of rice, maize, and wheat straws in a laboratory. The emission factors (EFs) of PM_2.5 mass, carbonaceous species (i.e. organic carbon (OC) and elemental carbon (EC)), and water-soluble inorganic ions in both fresh and 7-day aged samples were determined. The EFs of PM_2.5, OC, EC, and ions were 7.2–45, 2.8–24, 0.3–0.8, and 1.6–4.7 g kg⁻¹ in the fresh particles from the straws burning, and 12–63, 3.0–25, 0.3–1.3, and 4.1–13 g kg⁻¹ in the aged ones. Cl⁻ and K⁺ were the most abundant ions in the fresh samples. EFs of NO₃⁻ and NH₄⁺ were increased by 35–100 and 1.6–126 times, respectively, becoming the most abundant ions in the aged particles. By comparison with the results in experiments on 2-day aged specimens, we found a continuous formation of secondary aerosols in the atmospheric aging processes (especially for secondary inorganic ions), and that the deficit of anion equivalents increases with longer aging time. These results are valuable for studying the transportation effects of plumes from wildfires of forest and agriculture, or intensive domestic BB in some rural regions.

Overproduction of reactive oxygen species (ROS) induced by atmospheric particles and subsequent inflammatory responses are considered as one of the most important pathological mechanisms with regard to the adverse effects of air pollution exposure. In this study, fine particulate matter (PM_2.5) samples were collected at a rural site in Guanzhong Basin, Northwest China, in both summer (August 3–23, 2016) and winter (January 5–February 1, 2017). Then, human bronchial epithelial BEAS-2B cells were exposed to the PM_2.5, cultured for 24 h, and then assayed for particle-induced ROS and three inflammatory factors (tumor necrosis-α (TNF-α), interleukin-6 (IL-6), and interferon-γ (IFN-γ)) in vitro. The oxidative potential (OP) induced by winter PM_2.5 samples was higher than that induced by summertime samples, whereas inflammatory values showed contrasting seasonal variations. Both OP and inflammatory factors were significantly correlated with most chemical compounds in winter, but not in summer, which was thought to be related mainly to the higher contribution from secondary aerosols formed during the warm season. Source apportionment results showed secondary aerosols formation have significant contribution to OP of PM_2.5 in both seasons, but the dominant oxidation processes is different. Secondary nitrates-related process was the major contributors regulating the OP in winter; however, secondary sulfates formation were mainly responsible for the ROS responses in summer. For primary emission, biomass burning, rather than coal emission or vehicle exhaust, was the significant source for OP of PM_2.5 in winter. In most cases, the source contribution of each inflammatory factor was similar to that of the ROS. Our results highlighted the significant health risk of atmospheric aerosols from biomass burning in the rural regions of Guanzhong Basin, Northwest China.

Biomass burning (BB) including forest, bush, prescribed fires, agricultural fires, residential wood combustion, and power generation has long been known to affect climate, air quality and human health. With this work we supply a systematic review on the health effects of BB emissions in the framework of the WHO activities on air pollution. We performed a literature search of online databases (PubMed, ISI, and Scopus) from year 1980 up to 2020. A total of 81 papers were considered as relevant for mortality and morbidity effects. High risk of bias was related with poor estimation of BB exposure and lack of adjustment for important confounders. PM10 and PM2.5 concentrations originating from BB were associated with all-cause mortality: the meta-analytical estimate was equal to 1.31% (95% CI 0.71, 1.71) and 1.92% (95% CI −1.19, 5.03) increased mortality per each 10 μg m⁻³ increase of PM10 and PM2.5, respectively. Regarding cardiovascular mortality 8 studies reported quantitative estimates. For smoky days and for each 10 μg m⁻³ increase in PM2.5 concentrations, the risk of cardiovascular mortality increased by 4.45% (95% CI 0.96, 7.95) and by 3.30% (95% CI −1.97, 8.57), respectively. Fourteen studies evaluated whether respiratory morbidity was adversely related to PM2.5 (9 studies) or PM10 (5 studies) originating from BB. All found positive associations. The pooled effect estimates were 4.10% (95% CI 2.86, 5.34) and 4.83% (95% CI 0.06, 9.60) increased risk of total respiratory admissions/emergency visits, per 10 μg m^-3 increases in PM2.5 and PM10, respectively. Regarding cardiovascular morbidity, sixteen studies evaluated whether this was adversely related to PM2.5 (10 studies) or PM10 (6 studies) originating from BB. They found both positive and negative results, with summary estimates equal to 3.68% (95% CI −1.73, 9.09) and 0.93% (95% CI −0.18, 2.05) increased risk of total cardiovascular admissions/emergency visits, per 10 μg m⁻³ increases in PM2.5 and PM10, respectively. To conclude, a significant number of studies indicate that BB exposure is associated with all-cause and cardiovascular mortality and respiratory morbidity.

Biomass burning (BB) has an important impact on local/regional air quality and human health in China, but most previous studies overlooked the influence of atmospheric aging processes on cytotoxicity and chemical composition of BB aerosols. In this study, we combined a combustion chamber and an oxidation flow reactor to generate fresh and aged BB PM_2.5. Human bronchial epithelial BEAS-2B cells were exposed to PM_2.5 preparation for 24 h, and then determined for particle-induced reactive oxygen species (ROS) in vitro. The particle-induced ROS production increased by 11 %–64 % after two days of aging, suggesting an enhancement of in vitro-induced oxidative stress (OS) of aged BB particles. Chemical analysis showed that organic matter (OM) was the dominant component with no changes in relative abundance for the fresh and aged BB particles. Organic polycyclic aromatic compounds and some metals showed strong correlations with ROS in fresh particles, indicating the important effects of these harmful components on the OS of fresh BB aerosols. However, such correlations were not found for the aged particles, which is possibly related to the loss of non- or low-toxic semivolatile compounds and the formation of secondary harmful OM (such as some N-containing organic compounds) during the atmospheric aging processes.

Understanding the effect of wildfire smoke exposure on human health represents a unique interdisciplinary challenge to the scientific community. Population health studies indicate that wildfire smoke is a risk to human health and increases the healthcare burden of smoke-impacted areas. However, wildfire smoke composition is complex and dynamic, making characterization and modeling difficult. Furthermore, current efforts to study the effect of wildfire smoke are limited by availability of air quality measures and inconsistent air quality reporting among researchers. To help address these issues, we conducted a substantive review of wildfire smoke effects on population health, wildfire smoke exposure in occupational health, and experimental wood smoke exposure. Our goal was to evaluate the current literature on wildfire smoke and highlight important gaps in research. In particular we emphasize long-term health effects of wildfire smoke, recovery following wildfire smoke exposure, and health consequences of exposure in children.