Wildland fire smoke and human health

Abstract

The natural cycle of landscape fire maintains the ecological health of the land, yet adverse health effects associated with exposure to emissions from wildfire produce public health and clinical challenges. Systematic reviews conclude that a positive association exists between exposure to wildfire smoke or wildfire particulate matter (PM2.5) and all-cause mortality and respiratory morbidity. Respiratory morbidity includes asthma, chronic obstructive pulmonary disease (COPD), bronchitis and pneumonia. The epidemiological data linking wildfire smoke exposure to cardiovascular mortality and morbidity is mixed, and inconclusive. More studies are needed to define the risk for common and costly clinical cardiovascular outcomes. Susceptible populations include people with respiratory and possibly cardiovascular diseases, middle-aged and older adults, children, pregnant women and the fetus. The increasing frequency of large wildland fires, the expansion of the wildland-urban interface, the area between unoccupied land and human development; and an increasing and aging U.S. population are increasing the number of people at-risk from wildfire smoke, thus highlighting the necessity for broadening stakeholder cooperation to address the health effects of wildfire. While much is known, many questions remain and require further population-based, clinical and occupational health research. Health effects measured over much wider geographical areas and for longer periods time will better define the risk for adverse health outcomes, identify the sensitive populations and assess the influence of social factors on the relationship between exposure and health outcomes. Improving exposure models and access to large clinical databases foreshadow improved risk analysis facilitating more effective risk management. Fuel and smoke management remains an important component for protecting population health. Improved smoke forecasting and translation of environmental health science into communication of actionable information for use by public health officials, healthcare professionals and the public is needed to motivate behaviors that lower exposure and protect public health, particularly among those at high risk.

Keywords: Air pollution; Health effects; Particulate matter, PM(2.5); Smoke; Wildfire emissions.

Conflict of interest statement

The author declares no competing financial interest.

Published by Elsevier B.V.

Figures

Figure 1. Global fire map corresponding to September 8 to 17, 2015.

The global fire map (https://lance.modaps.eosdis.nasa.gov/cgi-bin/imagery/firemaps.cgi?period=2015251–2015260) reports the location of fires detected by MODIS (Moderate Resolution Image Spectroradiometer) on board NASA’s Terra and Aqua research satellites and shows the global expanse of wildfires. Each colored dot indicates a location where MODIS detected a fire during the 10-day period. Red dots indicate low fire counts, whereas yellow dots indicate larger numbers of fires. Global mortality from wildfire smoke is estimated to be 339,000 deaths annually (Johnson et al., 2012).

Figure 2. Cardiovascular health effects during wildfires in Victoria, Australia, December 1, 2006 to January 31, 2007.

The upper panel shows the percent change in out-of-hospital cardiac arrest (OHCA) and the lower panel ischemic heart disease (IHD) hospitalizations for a 9µg/m3 interquartile range increase in wildfire-PM2.5 exposure. Lag 0: effect occurs on the day of exposure. Lag 0 to 1: Health effects occur on the day of exposure and a day after exposure. [Adapted from Haikerwal et al., 2015].

Figure 3. Toxicology of Wildland Fire Emissions.

Murine lungs were exposed to fine (blue bars) and coarse (orange bars) PM collected at the 2008 Pocosin Lakes National Wildlife Refuge fire and endotoxin in the presence and absence of polymixin B (PMB) an antibiotic that binds endotoxin and blocks the effect of endotoxin, a key component of the outer membrane of Gram-negative bacteria. Murine lungs responded with an inflammatory response to exposure to endotoxin (Gray bar) as shown by the increase in the pro-inflammatory cytokine TNF-alpha. The effect of endotoxin was blocked by the addition of polymixin B. Coarse PM (orange bars) induced a pro-inflammatory response as indicated by the increased TNF-alpha, an effect blocked by polymyxin B. Inhibition of the TNF-alpha response by polymyxin B confirms that endotoxin probably plays a role in the inflammatory response induced by the coarse PM fraction. By contrast fine PM (blue bars) did not induce an inflammatory response in this model. (Kim et al., 2014)

Figure 4. Satellite image showing the location of Evans Road Fire in the Pocosin Lakes National Wildlife Refuge, NC in 2008.

www.fws.gov/pocosinlakes/news/ERF/news-erf-out.html

Figure 5.

Left-hand panel. Annual average daily fire- PM2.5 footprint by counties of continental U.S. and perimeters of area burned by large fires in black between 2008 and 2012. Right-hand panel. Number of days with fire-PM2.5 above 35 μg/m3 by counties of continental U.S.. Adapted from Rappold et al., 2017.

Figure 6.. Chronic obstructive pulmonary disease prevalence by county in the U.S. in 2014.

Age-standardized prevalence of chronic obstructive pulmonary disease (COPD) among adults aged ≥ 18 years. Source: CDC, Behavioral Risk Factor Surveillance System, 2014, Census 2010, ACS 2010–2014. www.cdc.gov/copd/pdfs/COPD_cnty2014_saeColor_2.pdf

Figure 7.. Community Health-Vulnerability Index

Adapted from Rappold et al., 2017.

Figure 8.

Clinical and Sub-Clinical Impacts of Wildfire Smoke or PM2.5