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.

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

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. To determine health impacts from ambient air pollution concentrations in the United States that exceed the levels recommended by the American Thoracic Society.

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.

Comprehensive evidence implies a higher social cost of CO.

The social cost of carbon dioxide (SC-CO) measures the monetized value of the damages to society caused by an incremental metric tonne of CO 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-CO estimates draw on climate science, economics, demography and other disciplines. However, a 2017 report by the US National Academies of Sciences, Engineering, and Medicine (NASEM) highlighted that current SC-CO estimates no longer reflect the latest research.

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

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. 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.

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.

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.

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

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/m and 25 μg/m for long- and short-term fine particulate matter (PM) 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.

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.

Personal Interventions for Reducing Exposure and Risk for Outdoor Air Pollution: An Official American Thoracic Society Workshop Report.

Poor air quality affects the health and wellbeing of large populations around the globe. Although source controls are the most effective approaches for improving air quality and reducing health risks, individuals can also take actions to reduce their personal exposure by staying indoors, reducing physical activity, altering modes of transportation, filtering indoor air, and using respirators and other types of face masks. A synthesis of available evidence on the efficacy, effectiveness, and potential adverse effects or unintended consequences of personal interventions for air pollution is needed by clinicians to assist patients and the public in making informed decisions about use of these interventions.

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-CO) have generally been made in isolation from health experts and have never been rigorously evaluated. Version 3.

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.

Evaluating the U.S. Air Quality Index as a risk communication tool: Comparing associations of index values with respiratory morbidity among adults in California.

Background: The Air Quality Index (AQI) in the United States is widely used to communicate daily air quality information to the public. While use of the AQI has led to reported changes in individual behaviors, such behavior modifications will only mitigate adverse health effects if AQI values are indicative of public health risks. Few studies have assessed the capability of the AQI to accurately predict respiratory morbidity risks.

Air Pollution Monitoring for Health Research and Patient Care. An Official American Thoracic Society Workshop Report.

Air quality data from satellites and low-cost sensor systems, together with output from air quality models, have the potential to augment high-quality, regulatory-grade data in countries with monitoring networks and provide much-needed air quality information in countries without them. Each of these technologies has strengths and limitations that need to be considered when integrating them to develop a robust and diverse global air quality monitoring network. To address these issues, the American Thoracic Society, the U.

PM2.5 air pollution and cause-specific cardiovascular disease mortality.

Background: Ambient air pollution is a modifiable risk factor for cardiovascular disease, yet uncertainty remains about the size of risks at lower levels of fine particulate matter (PM2.5) exposure which now occur in the USA and elsewhere.

Methods: We investigated the relationship of ambient PM2.

Trends in Excess Morbidity and Mortality Associated with Air Pollution above American Thoracic Society-Recommended Standards, 2008-2017.

Air quality improvements are increasingly difficult to come by as modern pollution control technologies and measures have been widely implemented in the United States. Although there have been dramatic improvements in air quality over the last several decades, it is important to evaluate changes in the health impacts of air pollution for a more recent time period to better understand the current trajectory of air quality improvements. To provide county-level estimates of annual air pollution-related health outcomes across the United States and to evaluate these trends from 2008 to 2017, presented as part of the annual American Thoracic Society (ATS)/Marron Institute "Health of the Air" report.

A Novel Environmental Justice Indicator for Managing Local Air Pollution.

Environmental justice efforts in the United States seek to provide equal protection from environmental hazards, such as air pollution, to all groups, particularly among traditionally disadvantaged populations. To accomplish this objective, the U.S.

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.

Chemokine (C-C Motif) Receptor-Like 2 is not essential for lung injury, lung inflammation, or airway hyperresponsiveness induced by acute exposure to ozone.

Inhalation of ozone (O), a gaseous air pollutant, causes lung injury, lung inflammation, and airway hyperresponsiveness. Macrophages, mast cells, and neutrophils contribute to one or more of these sequelae induced by O Furthermore, each of these aforementioned cells express chemokine (C-C motif) receptor-like 2 (Ccrl2), an atypical chemokine receptor that facilitates leukocyte chemotaxis. Given that Ccrl2 is expressed by cells essential to the development of O-induced lung pathology and that chemerin, a Ccrl2 ligand, is increased in bronchoalveolar lavage fluid (BALF) by O, we hypothesized that Ccrl2 contributes to the development of lung injury, lung inflammation, and airway hyperresponsiveness induced by O To that end, we measured indices of lung injury (BALF protein, BALF epithelial cells, and bronchiolar epithelial injury), lung inflammation (BALF cytokines and BALF leukocytes), and airway responsiveness to acetyl--methylcholine chloride (respiratory system resistance) in wild-type and mice genetically deficient in Ccrl2 (Ccrl2-deficient mice) 4 and/or 24 hours following cessation of acute exposure to either filtered room air (air) or O In air-exposed mice, BALF chemerin was greater in Ccrl2-deficient as compared to wild-type mice.

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.

Plasminogen activator inhibitor-1 does not contribute to the pulmonary pathology induced by acute exposure to ozone.

Expression of plasminogen activator inhibitor (PAI)-1, the major physiological inhibitor of fibrinolysis, is increased in the lung following inhalation of ozone (O), a gaseous air pollutant. PAI-1 regulates expression of interleukin (IL)-6, keratinocyte chemoattractant (KC), and macrophage inflammatory protein (MIP)-2, which are cytokines that promote lung injury, pulmonary inflammation, and/or airway hyperresponsiveness following acute exposure to O Given these observations, we hypothesized that PAI-1 contributes to the severity of the aforementioned sequelae by regulating expression of IL-6, KC, and MIP-2 following acute exposure to O To test our hypothesis, wild-type mice and mice genetically deficient in PAI-1 (PAI-1-deficient mice) were acutely exposed to either filtered room air or O (2 ppm) for 3 h. Four and/or twenty-four hours following cessation of exposure, indices of lung injury [bronchoalveolar lavage fluid (BALF) protein and epithelial cells], pulmonary inflammation (BALF IL-6, KC, MIP-2, macrophages, and neutrophils), and airway responsiveness to aerosolized acetyl-β-methylcholine chloride (respiratory system resistance) were measured in wild-type and PAI-1-deficient mice.