Wildfire smoke, a potential infectious agent

18 December 2020

Published by https://science.sciencemag.org/

USA – Wildfires over the past 3 years have resulted in lengthy episodes of smoke inundation across major metropolitan areas in Australia, Brazil, and the United States. In 2020, air quality across the western United States reached and sustained extremely unhealthy to hazardous levels for successive weeks from August through November. Although the pulmonary and cardiovascular consequences of human exposure to smoke particulate matter are extensively researched, there remains little recognition or monitoring of a smoke component with potentially important health repercussions: microbes.

Wildland fire is a source for bioaerosols that differ in composition and concentration from those found under background conditions, and most of these microbes in smoke are viable (12). Bioaerosols, composed of fungal and bacterial cells and their metabolic by-products, are known to affect human health (3). At the same time, respiratory allergic and inflammatory diseases, including asthma and bronchitis, are exacerbated by exposure to wildfire smoke (4). However, the risk of infection to the upper and lower respiratory tract after exposure to wildfire smoke is frequently overlooked (5). Smoke-related immunologic deficits and inflammatory responses may exacerbate the effects of inhalation of airborne microbial particulates and toxicants in smoke. The intersection of these epidemiological trends and smoke microbial content has yet to be addressed in public health and atmospheric sciences, despite compelling overlaps of increasing mycoses rates and increasing wildfire smoke in some locations (e.g., aspergillosis, invasive mold infections, and coccidioidomycosis in the western United States) (6).

Smoke plume temperatures are determined by fire behavior and meteorological factors and can exceed presumed temperature tolerances of some microbial organisms. However, a high degree of variability in fuels, ambient air mixing, and fire behavior results in a range of biologic niches and responses, especially at smaller scales (7). The energy release during a wildland fire varies in space and time by orders of magnitude (7), so that microscopic-scale biota likely experience considerable heterogeneity in heat transfer and may escape the duration of high temperature that leads to mortality. In addition to species-specific resistance to heat, this may help explain why some soil-dwelling microbes appear tolerant of, and even proliferate under, high temperatures following high-intensity and/or high-severity wildfire (8). Pyrogenic carbon produced by wildland fire provides temporary habitat for soil microbes and could potentially function similarly in air for microbes aerosolized from soils and both living and dead plant materials: Microbial cells have been found to associate positively with particulate matter (1). Particulate matter in smoke confers attenuation of ultraviolet-B (UV-B) by 80% and UV-A by up to 74%—radiation that would otherwise decrease bioaerosol viability (9). Additionally, water vapor is a product of biomass combustion and may also play a role in vectoring microbes from the combustion zone into a smoke column, limiting desiccation of entrained organisms.

Microbes may also be drawn into convective columns from outside the combustion zone. For example, a plume from the El Portal wildfire in Yosemite National Park, California, caused updraft winds of 13.5 m s−1 (10), whereas dry spore–discharging fungi can be emitted from soils with surface winds of only ∼1 m s−1 (11). Once aerosolized, microbes, spores, or fungal conidia <5 µm in aerodynamic diameter have the potential to travel hundreds of miles, depending on fire behavior and atmospheric conditions, and are eventually deposited or inhaled downwind of a fire. Smoke emissions from high-intensity, large wildfires have been transported across continents, increasing particulate matter concentrations in distant locations (12). The consequences for more immediate populations, such as firefighters on the front line who often spend up to 14 consecutive days in smoky conditions, are likely greater given that microbial concentration in smoke is higher near the source of a fire (see the figure) (2). For example, the U.S. Centers for Disease Control and Prevention counts firefighting as an at-risk profession for coccidioidomycosis, an infection caused by a pathogenic fungus well known to be aerosolized when soils are disturbed.

So far, studies measuring smoke transport of microbes have been limited to direct measures during prescribed fires (12) and indirect measures of microbes or their chemical indicators in distal smoke-polluted air (13). Even in low-intensity prescribed fires, microbial cell counts from smoke averaged 6.7 × 104 cells m−3, approximately five times that of background concentrations (1.3 × 104 cells m−3), and equivalent to ∼7.2 × 109 cells m−2 burned area (1). The estimated lowest cell counts leading to reduced airway conductance, function, and inflammation effect in nonsensitive populations range from 1 × 104 to 1 × 105 m−3 for aerosolized fungal spores (14). Therefore, the potential for wildland fire’s microbial content to affect humans who breathe in smoke, especially from high-emissions wildfires or for multiple weeks, is appreciable. How far and which microbes are transported in smoke under various conditions are critical unknowns, but the relevance of these questions is increasing with longer wildfire seasons and higher severity trends.

Addressing these unknowns will require a multidisciplinary approach representing expertise in fire ecology, environmental microbiology, epidemiology, public health and infectious disease, and atmospheric sciences. The knowledge gained has the potential to answer questions about the consequences of wildland fire specific to each of these disciplines. For example, what roles does fire play in the spread of disease, and can natural reservoirs and affected populations be linked through smoke to predict public health problems before they occur? Exploration of infections and indicators such as antibiotic use in populations subjected to known amounts and durations of wildfire smoke is a promising first direction.

Given that climate change impacts on wildfire are predicted to lead to total emissions (greenhouse and trace gases plus particulate matter) increases of 19 to 101% in California alone through 2100 (15), it is important that atmospheric and public health sciences expand their perspectives to include the potential impact of smoke’s microbial cargo on human populations. This is especially relevant where smoky skies are more likely to be a seasonal norm rather than a rare event.

References and Notes

Acknowledgments: We thank J. Andrew, D. Vuono, M. Pingree, A. Watts, and J. Smith for their insights.

View Abstract

Print Friendly, PDF & Email
WP-Backgrounds Lite by InoPlugs Web Design and Juwelier Schönmann 1010 Wien