Comprehensive evidence implies a higher social cost of CO2.

The social cost of carbon dioxide (SC-CO2) measures the monetized value of the damages to society caused by an incremental metric tonne of CO2 emissions and is a key metric informing climate policy. Used by governments and other decision-makers in benefit-cost analysis for over a decade, SC-CO2 estimates draw on climate science, economics, demography and other disciplines. However, a 2017 report by the US National Academies of Sciences, Engineering, and Medicine1 (NASEM) highlighted that current SC-CO2 estimates no longer reflect the latest research. The report provided a series of recommendations for improving the scientific basis, transparency and uncertainty characterization of SC-CO2 estimates. Here we show that improved probabilistic socioeconomic projections, climate models, damage functions, and discounting methods that collectively reflect theoretically consistent valuation of risk, substantially increase estimates of the SC-CO2. Our preferred mean SC-CO2 estimate is $185 per tonne of CO2 ($44-$413 per tCO2: 5%-95% range, 2020 US dollars) at a near-term risk-free discount rate of 2%, a value 3.6 times higher than the US government's current value of $51 per tCO2. Our estimates incorporate updated scientific understanding throughout all components of SC-CO2 estimation in the new open-source Greenhouse Gas Impact Value Estimator (GIVE) model, in a manner fully responsive to the near-term NASEM recommendations. Our higher SC-CO2 values, compared with estimates currently used in policy evaluation, substantially increase the estimated benefits of greenhouse gas mitigation and thereby increase the expected net benefits of more stringent climate policies.

Personal Interventions to Reduce Exposure to Outdoor Air Pollution.

Unhealthy levels of air pollution are breathed by billions of people worldwide, and air pollution is the leading environmental cause of death and disability globally. Efforts to reduce air pollution at its many sources have had limited success, and in many areas of the world, poor air quality continues to worsen. Personal interventions to reduce exposure to air pollution include avoiding sources, staying indoors, filtering indoor air, using face masks, and limiting physical activity when and where air pollution levels are elevated. The effectiveness of these interventions varies widely with circumstances and conditions of use. Compared with upstream reduction or control of emissions, personal interventions place burdens and risk of adverse unintended consequences on individuals. We review evidence regarding the balance of benefits and potential harms of personal interventions for reducing exposure to outdoor air pollution, which merit careful consideration before making public health recommendations with regard to who should use personal interventions and where, when, and how they should be used.

Assessing air quality index awareness and use in Mexico City.

BACKGROUND: The Mexico City Metropolitan Area has an expansive urban population and a long history of air quality management challenges. Poor air quality has been associated with adverse pulmonary and cardiac health effects, particularly among susceptible populations with underlying disease. In addition to reducing pollution concentrations, risk communication efforts that inform behavior modification have the potential to reduce public health burdens associated with air pollution. METHODS: This study investigates the utilization of Mexico's IMECA risk communication index to inform air pollution avoidance behavior among the general population living in the Mexico City Metropolitan Area. Individuals were selected via probability sampling and surveyed by phone about their air quality index knowledge, pollution concerns, and individual behaviors. RESULTS: The results indicated reasonably high awareness of the air quality index (53% of respondents), with greater awareness in urban areas, among older and more educated individuals, and for those who received air quality information from a healthcare provider. Additionally, behavior modification was less influenced by index reports as it was by personal perceptions of air quality, and there was no difference in behavior modification among susceptible and non-susceptible groups. CONCLUSIONS: Taken together, these results suggest there are opportunities to improve the public health impact of risk communication through an increased focus on susceptible populations and greater encouragement of public action in response to local air quality indices.

A joint ERS/ATS policy statement: what constitutes an adverse health effect of air pollution? An analytical framework.

The American Thoracic Society has previously published statements on what constitutes an adverse effect on health of air pollution in 1985 and 2000. We set out to update and broaden these past statements that focused primarily on effects on the respiratory system. Since then, many studies have documented effects of air pollution on other organ systems, such as on the cardiovascular and central nervous systems. In addition, many new biomarkers of effects have been developed and applied in air pollution studies.This current report seeks to integrate the latest science into a general framework for interpreting the adversity of the human health effects of air pollution. Rather than trying to provide a catalogue of what is and what is not an adverse effect of air pollution, we propose a set of considerations that can be applied in forming judgments of the adversity of not only currently documented, but also emerging and future effects of air pollution on human health. These considerations are illustrated by the inclusion of examples for different types of health effects of air pollution.

Particulate Air Pollution and Clinical Cardiovascular Disease Risk Factors.

BACKGROUND: Long-term exposure to ambient particulate matter (PM) air pollution is associated with increased cardiovascular disease (CVD); however, the impact of PM on clinical risk factors for CVD in healthy subjects is unclear. We examined the relationship of PM with levels of circulating lipids and blood pressure in the Third National Health and Nutrition Examination Survey (NHANES III), a large nationally representative US survey. METHODS: This study was based on 11,623 adult participants of NHANES III (1988-1994; median age 41.0). Serum lipids and blood pressure were measured during the NHANES III examination. Average exposure for 1988-1994 to particulate matter <10 µm in aerodynamic diameter (PM10) at the residences of participants was estimated based on measurements from US Environmental Protection Agency monitors. Multivariate linear regression was used to estimate the associations of PM10 with lipids and blood pressure. RESULTS: An interquartile range width increase in PM10 exposure (11.1 µg/m) in the study population was associated with 2.42% greater serum triglycerides (95% confidence interval: 1.09, 3.76); multivariate adjusted means of triglycerides according to increasing quartiles of PM10 were 137.6, 142.5, 142.6, and 148.9 mg/dl, respectively. An interquartile range width increase in PM10 was associated with 1.43% greater total cholesterol (95% confidence interval: 1.21, 1.66). These relationships with triglycerides and total cholesterol did not differ by age or region. Associations of PM10 with blood pressure were modest. CONCLUSIONS: Findings from this large, diverse study indicate that greater long-term PM10 exposure is associated with elevated serum triglycerides and total cholesterol, potentially mediating air pollution-related effects on CVD.

Resistin deficiency in mice has no effect on pulmonary responses induced by acute ozone exposure.

Acute exposure to ozone (O3), an air pollutant, causes pulmonary inflammation, airway epithelial desquamation, and airway hyperresponsiveness (AHR). Pro-inflammatory cytokines-including IL-6 and ligands of chemokine (C-X-C motif) receptor 2 [keratinocyte chemoattractant (KC) and macrophage inflammatory protein (MIP)-2], TNF receptor 1 and 2 (TNF), and type I IL-1 receptor (IL-1α and IL-1ß)-promote these sequelae. Human resistin, a pleiotropic hormone and cytokine, induces expression of IL-1α, IL-1ß, IL-6, IL-8 (the human ortholog of murine KC and MIP-2), and TNF. Functional differences exist between human and murine resistin; yet given the aforementioned observations, we hypothesized that murine resistin promotes O3-induced lung pathology by inducing expression of the same inflammatory cytokines as human resistin. Consequently, we examined indexes of O3-induced lung pathology in wild-type and resistin-deficient mice following acute exposure to either filtered room air or O3. In wild-type mice, O3 increased bronchoalveolar lavage fluid (BALF) resistin. Furthermore, O3 increased lung tissue or BALF IL-1α, IL-6, KC, TNF, macrophages, neutrophils, and epithelial cells in wild-type and resistin-deficient mice. With the exception of KC, which was significantly greater in resistin-deficient compared with wild-type mice, no genotype-related differences in the other indexes existed following O3 exposure. O3 caused AHR to acetyl-ß-methylcholine chloride (methacholine) in wild-type and resistin-deficient mice. However, genotype-related differences in airway responsiveness to methacholine were nonexistent subsequent to O3 exposure. Taken together, these data demonstrate that murine resistin is increased in the lungs of wild-type mice following acute O3 exposure but does not promote O3-induced lung pathology.

Effect of antigen sensitization and challenge on oscillatory mechanics of the lung and pulmonary inflammation in obese carboxypeptidase E-deficient mice.

Atopic, obese asthmatics exhibit airway obstruction with variable degrees of eosinophilic airway inflammation. We previously reported that mice obese as a result of a genetic deficiency in either leptin (ob/ob mice) or the long isoform of the leptin receptor (db/db mice) exhibit enhanced airway obstruction in the presence of decreased numbers of bronchoalveolar lavage fluid (BALF) eosinophils compared with lean, wild-type mice following antigen (ovalbumin; OVA) sensitization and challenge. To determine whether the genetic modality of obesity induction influences the development of OVA-induced airway obstruction and OVA-induced pulmonary inflammation, we examined indices of these sequelae in mice obese as a result of a genetic deficiency in carboxypeptidase E, an enzyme that processes prohormones and proneuropeptides involved in satiety and energy expenditure (Cpe(fat) mice). Accordingly, Cpe(fat) and lean, wild-type (C57BL/6) mice were sensitized to OVA and then challenged with either aerosolized PBS or OVA. Compared with genotype-matched, OVA-sensitized and PBS-challenged mice, OVA sensitization and challenge elicited airway obstruction and increased BALF eosinophils, macrophages, neutrophils, IL-4, IL-13, IL-18, and chemerin. However, OVA challenge enhanced airway obstruction and pulmonary inflammation in Cpe(fat) compared with wild-type mice. These results demonstrate that OVA sensitization and challenge enhance airway obstruction in obese mice regardless of the genetic basis of obesity, whereas the degree of OVA-induced pulmonary inflammation is dependent on the genetic modality of obesity induction. These results have important implications for animal models of asthma, as modeling the pulmonary phenotypes for subpopulations of atopic, obese asthmatics critically depends on selecting the appropriate mouse model.

Adverse Health Impacts of Outdoor Air Pollution, Including from Wildland Fires, in the United States: "Health of the Air," 2018-2020.

Rationale: Adverse health impacts from outdoor air pollution occur across the United States, but the magnitude of these impacts varies widely by geographic region. Ambient pollutant concentrations, emission sources, baseline health conditions, and population sizes and distributions are all important factors that need to be taken into account to quantify local health burdens. Objectives: To determine health impacts from ambient air pollution concentrations in the United States that exceed the levels recommended by the American Thoracic Society. Methods: Using a methodology that has been well established in previous "Health of the Air" reports, this study provides policy-relevant estimates for every monitored county and city in the United States for the adverse health impacts of outdoor pollution concentrations using U.S. Environmental Protection Agency design values for years 2018-2020. Additionally, for the first time, the report includes adverse birth outcomes as well as estimates of health impacts specifically attributable to wildland fires using an exposure dataset generated through Community Multiscale Air Quality simulations. Results: The adverse health burdens attributable to air pollution occur across the entire age spectrum, including adverse birth outcomes (10,660 preterm and/or low-weight births; 95% confidence interval [CI], 3,180-18,330), in addition to mortality impacts (21,300 avoidable deaths; 95% CI, 16,180-26,200), lung cancer incidence (3,000 new cases; 95% CI, 1,550-4,390), multiple types of cardiovascular and respiratory morbidity (748,660 events; 95% CI, 326,050-1,057,080), and adversely impacted days (52.4 million days; 95% CI, 7.9-92.4 million days). Two different estimates of mortality impacts from wildland fires were created based on assumptions regarding the underlying toxicity of particles from wildland fires (low estimate of 4,080 deaths, 95% CI, 240-7,890; middle estimate of 28,000 deaths, 95% CI, 27,300-28,700). Conclusions: This year's report identified sizable health benefits that would be expected to occur across the United States with compliance with more health-protective air quality standards such as those recommended by the American Thoracic Society. This study also indicates that a large number of excess deaths are attributable to emissions from wildland fires; air quality management strategies outside what is required by the Clean Air Act will be needed to best address this important source of air pollution and its associated health risks.

Indoor Air Sources of Outdoor Air Pollution: Health Consequences, Policy, and Recommendations: An Official American Thoracic Society Workshop Report.

Indoor sources of air pollution worsen indoor and outdoor air quality. Thus, identifying and reducing indoor pollutant sources would decrease both indoor and outdoor air pollution, benefit public health, and help address the climate crisis. As outdoor sources come under regulatory control, unregulated indoor sources become a rising percentage of the problem. This American Thoracic Society workshop was convened in 2022 to evaluate this increasing proportion of indoor contributions to outdoor air quality. The workshop was conducted by physicians and scientists, including atmospheric and aerosol scientists, environmental engineers, toxicologists, epidemiologists, regulatory policy experts, and pediatric and adult pulmonologists. Presentations and discussion sessions were centered on 1) the generation and migration of pollutants from indoors to outdoors, 2) the sources and circumstances representing the greatest threat, and 3) effective remedies to reduce the health burden of indoor sources of air pollution. The scope of the workshop was residential and commercial sources of indoor air pollution in the United States. Topics included wood burning, natural gas, cooking, evaporative volatile organic compounds, source apportionment, and regulatory policy. The workshop concluded that indoor sources of air pollution are significant contributors to outdoor air quality and that source control and filtration are the most effective measures to reduce indoor contributions to outdoor air. Interventions should prioritize environmental justice: Households of lower socioeconomic status have higher concentrations of indoor air pollutants from both indoor and outdoor sources. We identify research priorities, potential health benefits, and mitigation actions to consider (e.g., switching from natural gas to electric stoves and transitioning to scent-free consumer products). The workshop committee emphasizes the benefits of combustion-free homes and businesses and recommends economic, legislative, and education strategies aimed at achieving this goal.

Endogenous osteopontin promotes ozone-induced neutrophil recruitment to the lungs and airway hyperresponsiveness to methacholine.

Inhalation of ozone (O3), a common environmental pollutant, causes pulmonary injury, pulmonary inflammation, and airway hyperresponsiveness (AHR) in healthy individuals and exacerbates many of these same sequelae in individuals with preexisting lung disease. However, the mechanisms underlying these phenomena are poorly understood. Consequently, we sought to determine the contribution of osteopontin (OPN), a hormone and a pleiotropic cytokine, to the development of O3-induced pulmonary injury, pulmonary inflammation, and AHR. To that end, we examined indices of these aforementioned sequelae in mice genetically deficient in OPN and in wild-type, C57BL/6 mice 24 h following the cessation of an acute (3 h) exposure to filtered room air (air) or O3 (2 parts/million). In wild-type mice, O3 exposure increased bronchoalveolar lavage fluid (BALF) OPN, whereas immunohistochemical analysis demonstrated that there were no differences in the number of OPN-positive alveolar macrophages between air- and O3-exposed wild-type mice. O3 exposure also increased BALF epithelial cells, protein, and neutrophils in wild-type and OPN-deficient mice compared with genotype-matched, air-exposed controls. However, following O3 exposure, BALF neutrophils were significantly reduced in OPN-deficient compared with wild-type mice. When airway responsiveness to inhaled acetyl-ß-methylcholine chloride (methacholine) was assessed using the forced oscillation technique, O3 exposure caused hyperresponsiveness to methacholine in the airways and lung parenchyma of wild-type mice, but not OPN-deficient mice. These results demonstrate that OPN is increased in the air spaces following acute exposure to O3 and functionally contributes to the development of O3-induced pulmonary inflammation and airway and lung parenchymal hyperresponsiveness to methacholine.

Respiratory Health Impacts of Outdoor Air Pollution and the Efficacy of Local Risk Communication in Quito, Ecuador.

Relatively few studies on the adverse health impacts of outdoor air pollution have been conducted in Latin American cities, whose pollutant mixtures and baseline health risks are distinct from North America, Europe, and Asia. This study evaluates respiratory morbidity risk associated with ambient air pollution in Quito, Ecuador, and specifically evaluates if the local air quality index accurately reflects population-level health risks. Poisson generalized linear models using air pollution, meteorological, and hospital admission data from 2014 to 2015 were run to quantify the associations of air pollutants and index values with respiratory outcomes in single- and multi-pollutant models. Significant associations were observed for increased respiratory hospital admissions and ambient concentrations of fine particulate matter (PM2.5), ozone (O3), nitrogen dioxide (NO2), and sulfur dioxide (SO2), although some of these associations were attenuated in two-pollutant models. Significant associations were also observed for index values, but these values were driven almost entirely by daily O3 concentrations. Modifications to index formulation to more fully incorporate the health risks of multiple pollutants, particularly for NO2, have the potential to greatly improve risk communication in Quito. This work also increases the equity of the existing global epidemiological literature by adding new air pollution health risk values from a highly understudied region of the world.

Communicating respiratory health risk among children using a global air quality index.

Air pollution poses a serious threat to children's respiratory health around the world. Satellite remote-sensing technology and air quality models can provide pollution data on a global scale, necessary for risk communication efforts in regions without ground-based monitoring networks. Several large centers, including NASA, produce global pollution forecasts that may be used alongside air quality indices to communicate local, daily risk information to the public. Here we present a health-based, globally applicable air quality index developed specifically to reflect the respiratory health risks among children exposed to elevated outdoor air pollution. Additive, excess-risk air quality indices were developed using 51 different coefficients derived from time-series health studies evaluating the impacts of ambient fine particulate matter, nitrogen dioxide, and ozone on children's respiratory morbidity outcomes. A total of four indices were created which varied based on whether or not the underlying studies controlled for co-pollutants and in the adjustment of excess risks of individual pollutants. Combined with historical estimates of air pollution provided globally at a 25 × 25 km2 spatial resolution from the NASA's Goddard Earth Observing System composition forecast (GEOS-CF) model, each of these indices were examined in a global sample of 664 small and 140 large cities for study year 2017. Adjusted indices presented the most normal distributions of locally-scaled index values, which has been shown to improve associations with health risks, while indices based on coefficients controlling for co-pollutants had little effect on index performance. We provide the steps and resources need to apply our final adjusted index at the local level using freely-available forecasting data from the GEOS-CF model, which can provide risk communication information for cities around the world to better inform individual behavior modification to best protect children's respiratory health.

Excess Morbidity and Mortality Associated with Air Pollution above American Thoracic Society Recommended Standards, 2017-2019.

Rationale: Over the past year, the American Thoracic Society (ATS), led by its Environmental Health Policy Committee, has reviewed the most current air quality scientific evidence and has revised their recommendations to 8 µg/m3 and 25 µg/m3 for long- and short-term fine particulate matter (PM2.5) and reaffirmed the recommendation of 60 ppb for ozone to protect the American public from the known adverse health effects of air pollution. The current U.S. Environmental Protection Agency (EPA) standards, in contrast, expose the American public to pollution levels that are known to result in significant morbidity and mortality. Objectives: To provide county-level estimates of annual air pollution-related health outcomes across the United States using the most recent federal air quality data, and to support the ATS's recent update to the long-term PM2.5 recommended standard. This study is presented as part of the annual ATS/Marron Institute "Health of the Air" report. Methods: Daily air pollution values were obtained from the EPA's air quality system for monitored counties in the United States from 2017-2019. Concentration-response functions used in the EPA's regulatory review process were applied to pollution increments corresponding to differences between the rolling 3-year design values and ATS-recommended levels for long-term PM2.5 (8 µg/m3), short-term PM2.5 (25 µg/m3), and ground-level ozone (O3; 60 ppb). Health impacts were estimated at the county level in locations with valid monitoring data. Results: Meeting ATS recommendations throughout the country prevents an estimated 14,650 (95% confidence interval [CI], 8,660-22,610) deaths; 2,950 (95% CI, 1,530-4,330) lung cancer incidence events; 33,100 (95% CI, 7,300-71,000) morbidities, and 39.8 million (95% CI, 14.6-63.3 million) impacted days annually. This prevents 11,850 more deaths; 2,580 more lung cancer incidence events; 25,400 more morbidities; and 27.2 million more impacted days than meeting EPA standards alone. Conclusions: Significant health benefits to be gained by U.S. communities that work to meet ATS-recommended air quality standards have now been identified under scenarios meeting the new ATS recommendation for long-term PM2.5 (8 µg/m3). The "Health of the Air" report presents an opportunity for air quality managers to quantify local health burdens and EPA officials to update their standards to reflect the latest science.

Global Health Impacts for Economic Models of Climate Change: A Systematic Review and Meta-Analysis.

Rationale: Avoiding excess health damages attributable to climate change is a primary motivator for policy interventions to reduce greenhouse gas emissions. However, the health benefits of climate mitigation, as included in the policy assessment process, have been estimated without much input from health experts. Objectives: In accordance with recommendations from the National Academies in a 2017 report on approaches to update the social cost of greenhouse gases (SC-GHG), an expert panel of 26 health researchers and climate economists gathered for a virtual technical workshop in May 2021 to conduct a systematic review and meta-analysis and recommend improvements to the estimation of health impacts in economic-climate models. Methods: Regionally resolved effect estimates of unit increases in temperature on net all-cause mortality risk were generated through random-effects pooling of studies identified through a systematic review. Results: Effect estimates and associated uncertainties varied by global region, but net increases in mortality risk associated with increased average annual temperatures (ranging from 0.1% to 1.1% per 1°C) were estimated for all global regions. Key recommendations for the development and utilization of health damage modules were provided by the expert panel and included the following: not relying on individual methodologies in estimating health damages; incorporating a broader range of cause-specific mortality impacts; improving the climate parameters available in economic models; accounting for socioeconomic trajectories and adaptation factors when estimating health damages; and carefully considering how air pollution impacts should be incorporated in economic-climate models. Conclusions: This work provides an example of how subject-matter experts can work alongside climate economists in making continued improvements to SC-GHG estimates.

Health Impacts of Climate Change as Contained in Economic Models Estimating the Social Cost of Carbon Dioxide.

The health impacts of climate change are substantial and represent a primary motivating factor to mitigate climate change. However, the health impacts in economic models that estimate the social cost of carbon dioxide (SC-CO2) have generally been made in isolation from health experts and have never been rigorously evaluated. Version 3.10 of the Framework for Uncertainty, Negotiation and Distribution (FUND) model was used to estimate the health-based portion of current SC-CO2 estimates across low-, middle-, and high-income regions. In addition to the base model, three additional experiments assessed the sensitivity of these estimates to changes in the socio-economic assumptions in the model. Economic impacts from adverse health outcomes represent ∼8.7% of current SC-CO2 estimates. The majority of these health impacts (74%) were attributable to diarrhea mortality (from both low- and high-income regions) followed by diarrhea morbidity (12%) and malaria mortality (11%); no other health impact makes a meaningful contribution to SC-CO2 estimates in current economic models. The results of the socio-economic experiments show that the health-based portion of SC-CO2 estimates are highly sensitive to assumptions regarding income elasticity of health effects, income growth, and use of equity weights. Improving the health-based portion of SC-CO2 estimates could have substantial impacts on magnitude of the SC-CO2. Incorporating additional health impacts not previously included in estimates of SC-CO2 will be a critical component of model updates. This effort will be most successful through coordination between economists and health researchers and should focus on updating the form and function of concentration-response functions.

Augmenting the Standard Operating Procedures of Health and Air Quality Stakeholders With NASA Resources.

The combination of air quality (AQ) data from satellites and low-cost sensor systems, along with output from AQ models, have the potential to augment high-quality, regulatory-grade data in countries with in situ monitoring networks and provide much needed AQ information in countries without them, including Low and Moderate Income Countries (LMICs). We demonstrate the potential of free and publicly available USA National Aeronautics and Space Administration (NASA) resources, which include capacity building activities, satellite data, and global AQ forecasts, to provide cost-effective, and reliable AQ information to health and AQ professionals around the world. We provide illustrative case studies that highlight how global AQ forecasts along with satellite data may be used to characterize AQ on urban to regional scales, including to quantify pollution concentrations, identify pollution sources, and track the long-range transport of pollution. We also provide recommendations to data product developers to facilitate and broaden usage of NASA resources by health and AQ stakeholders.

Respiratory Impacts of Wildland Fire Smoke: Future Challenges and Policy Opportunities. An Official American Thoracic Society Workshop Report.

Wildland fires are diminishing air quality on a seasonal and regional basis, raising concerns about respiratory health risks to the public and occupational groups. This American Thoracic Society (ATS) workshop was convened in 2019 to meet the growing health threat of wildland fire smoke. The workshop brought together a multidisciplinary group of 19 experts, including wildland fire managers, public health officials, epidemiologists, toxicologists, and pediatric and adult pulmonologists. The workshop examined the following four major topics: 1) the science of wildland fire incidence and fire management, 2) the respiratory and cardiovascular health effects of wildland fire smoke exposure, 3) communication strategies to address these health risks, and 4) actions to address wildland fire health impacts. Through formal presentations followed by group discussion, workshop participants identified top priorities for fire management, research, communication, and public policy to address health risks of wildland fires. The workshop concluded that short-term exposure to wildland smoke causes acute respiratory health effects, especially among those with asthma and chronic obstructive pulmonary disease. Research is needed to understand long-term health effects of repeated smoke exposures across fire seasons for children, adults, and highly exposed occupational groups (especially firefighters). Other research priorities include fire data collection and modeling, toxicology of different fire fuel sources, and the efficacy of health protective measures to prevent respiratory effects of smoke exposure. The workshop committee recommends a unified federal response to the growing problem of wildland fires, including investment in fire behavior and smoke air quality modeling, research on the health impacts of smoke, and development of robust clinical and public health communication tools.