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This JAMA Insights explores the adverse effects of wildfires on human health and health care systems and offers suggestions on how clinicians can help mitigate the health threats posed by wildfires.

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.

The Peak Design Ltd hyperspectral radiometer (HSR1) was tested at the Atmospheric Radiation Measurement (ARM) user facility Southern Great Plains (SGP) site in Lamont, Oklahoma, for 2 months from May to July 2022. The HSR1 is a prototype instrument that measures total (Ftotal) and diffuse (Fdiffuse) spectral irradiance from 360 to 1100 nm with a spectral resolution of 3 nm. The HSR1 spectral irradiance measurements are compared to nearby collocated spectral radiometers, including two multifilter rotating shadowband radiometers (MFRSRs) and the Shortwave Array Spectroradiometer–Hemispheric (SASHe) radiometer. The Ftotal at 500 nm for the HSR1 compared to the MFRSRs has a mean (relative) difference of 0.01 W m−2 nm−1 (1 %–2 %). The HSR1 mean Fdiffuse at 500 nm is smaller than the MFRSRs' by 0.03–0.04 (10 %) W m−2 nm−1. The HSR1 clear-sky aerosol optical depth (AOD) is also retrieved by considering Langley regressions and compared to collocated instruments such as the Cimel sunphotometer (CSPHOT), MFRSRs, and SASHe. The mean HSR1 AOD at 500 nm is larger than the CSPHOT's by 0.010 (8 %) and larger than the MFRSRs' by 0.007–0.017 (6 %–18 %). In general, good agreement between the HSR1 and other instruments is found in terms of the Ftotal, Fdiffuse, and AODs at 500 nm. The HSR1 quantities are also compared at other wavelengths to the collocated instruments. The comparisons are within ∼ 10 % for the Ftotal and Fdiffuse, except for 940 nm, where there is relatively larger disagreement. The AOD comparisons are within ∼ 10 % at 415 and 440 nm; however, a relatively larger disagreement in the AOD comparison is found for higher wavelengths.

PURPOSE: Exposures to ambient air pollutants may prime the lung enhancing risk of acute respiratory distress syndrome (ARDS) in sepsis. Our objective was to determine the association of short-, medium-, and long-term pollutant exposures and ARDS risk in critically ill sepsis patients. METHODS: We analyzed a prospective cohort of 1858 critically ill patients with sepsis, and estimated short- (3 days), medium- (6 weeks), and long- (5 years) term exposures to ozone, nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon monoxide (CO), particulate matter

IntroductionAir pollution is widely acknowledged as a significant factor in respiratory outcomes, including coughing, wheezing, emergency department (ED) visits, and even death. Although several literature reviews have confirmed the association between air pollution and respiratory outcomes, they often did not standardize associations across different studies and overlooked other increasingly impactful pollutants such as trace metals. Recognizing the importance of consistent comparison and emissions of non-exhaust particles from road traffic, this study aims to comprehensively evaluate the standardized effects of various criteria pollutants and trace metals on respiratory health.MethodsWe conducted a comprehensive meta-analysis of peer-reviewed journal articles on air pollution and respiratory outcomes published between 1 January 2000, and 1 June 2024. The study included children (age

Ground level ozone is a potent respiratory toxicant with decades of accumulated data demonstrating respiratory harms to children. Despite the ubiquity of ozone in the United States, impacting both urban and rural communities, the associated harms of exposure to this important air pollutant are often infrequently or inadequately covered during medical training including pulmonary specialization. Thus, many providers caring for childrens respiratory health may have limited knowledge of the harms which may result in reduced discussion of ozone pollution during clinical encounters. Further, the current US air quality standard for ozone does not adequately protect children. In this nonsystematic review, we present basic background information for healthcare providers caring for childrens respiratory health, review the US process for setting air quality standards, discuss the respiratory harms of ozone for healthy children and those with underlying respiratory disease, highlight the urgent need for a more protective ozone standard to adequately protect childrens respiratory health, review impacts of climate change on ozone levels, and provide information for discussion in clinical encounters.

Current American Thoracic Society (ATS) standards promote the use of race and ethnicity-specific reference equations for pulmonary function test (PFT) interpretation. There is rising concern that the use of race and ethnicity in PFT interpretation contributes to a false view of fixed differences between races and may mask the effects of differential exposures. This use of race and ethnicity may contribute to health disparities by norming differences in pulmonary function. In the United States and globally, race serves as a social construct that is based on appearance and reflects social values, structures, and practices. Classification of people into racial and ethnic groups differs geographically and temporally. These considerations challenge the notion that racial and ethnic categories have biological meaning and question the use of race in PFT interpretation. The ATS convened a diverse group of clinicians and investigators for a workshop in 2021 to evaluate the use of race and ethnicity in PFT interpretation. Review of evidence published since then that challenges current practice and continued discussion concluded with a recommendation to replace race and ethnicity-specific equations with race-neutral average reference equations, which must be accompanied with a broader re-evaluation of how PFTs are used to make clinical, employment, and insurance decisions. There was also a call to engage key stakeholders not represented in this workshop and a statement of caution regarding the uncertain effects and potential harms of this change. Other recommendations include continued research and education to understand the impact of the change, to improve the evidence for the use of PFTs in general, and to identify modifiable risk factors for reduced pulmonary function.

BackgroundEvidence in the literature suggests that air pollution exposures experienced prenatally and early in life can be detrimental to normal lung development, however the specific timing of critical windows during development is not fully understood.ObjectivesWe evaluated air pollution exposures during the prenatal and early-life period in association with lung function at ages 6-9, in an effort to identify potentially influential windows of exposure for lung development.MethodsOur study population consisted of 222 children aged 6-9 from the Fresno-Clovis metro area in California with spirometry data collected between May 2015 and May 2017. We used distributed-lag non-linear models to flexibly model the exposure-lag-response for monthly average exposure to fine particulate matter (PM2.5) and ozone (O3) during the prenatal months and first three years of life in association with forced vital capacity (FVC), and forced expiratory volume in the first second (FEV1), adjusted for covariates.ResultsPM2.5 exposure during the prenatal period and the first 3-years of life was associated with lower FVC and FEV1 assessed at ages 6-9. Specifically, an increase from the 5th percentile of the observed monthly average exposure (7.55 μg/m3) to the median observed exposure (12.69 μg/m3) for the duration of the window was associated with 0.42 L lower FVC (95% confidence interval (CI): -0.82, -0.03) and 0.38 L lower FEV1 (95% CI: -0.75, -0.02). The shape of the lag-response indicated that the second half of pregnancy may be a particularly influential window of exposure. Associations for ozone were not as strong and typically CIs included the null.ConclusionsOur findings indicate that prenatal and early-life exposures to PM2.5 are associated with decreased lung function later in childhood. Exposures during the latter months of pregnancy may be especially influential.

BackgroundBecause fine particulate matter [PM, with aerodynamic diameter ≤2.5μm (PM2.5)] is a ubiquitous environmental exposure, small changes in cognition associated with PM2.5 exposure could have great societal costs. Prior studies have demonstrated a relationship between in utero PM2.5 exposure and cognitive development in urban populations, but it is not known whether these effects are similar in rural populations and whether they persist into late childhood.ObjectivesIn this study, we tested for associations between prenatal PM2.5 exposure and both full-scale and subscale measures of IQ among a longitudinal cohort at age 10.5 y.MethodsThis analysis used data from 568 children enrolled in the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS), a birth cohort study in California's agricultural Salinas Valley. Exposures were estimated at residential addresses during pregnancy using state of the art, modeled PM2.5 surfaces. IQ testing was performed by bilingual psychometricians in the dominant language of the child.ResultsA 3-μg/m3 higher average PM2.5 over pregnancy was associated with -1.79 full-scale IQ points [95% confidence interval (CI): -2.98, -0.58], with decrements specifically in Working Memory IQ (WMIQ) and Processing Speed IQ (PSIQ) subscales [WMIQ -1.72 (95% CI: -2.98, -0.45) and PSIQ -1.19 (95% CI: -2.54, 0.16)]. Flexible modeling over the course of pregnancy illustrated mid-to-late pregnancy (months 5-7) as particularly susceptible times, with sex differences in the timing of susceptible windows and in which subscales were most affected [Verbal Comprehension IQ (VCIQ) and WMIQ in males; and PSIQ in females].DiscussionWe found that small increases in outdoor PM2.5 exposure in utero were associated with slightly lower IQ in late childhood, robust to many sensitivity analyses. In this cohort there was a larger effect of PM2.5 on childhood IQ than has previously been observed, perhaps due to differences in PM composition or because developmental disruption could alter the cognitive trajectory and thus appear more pronounced as children get older. https://doi.org/10.1289/EHP10812.

Microbial fuel cell technology addresses both issues in finding new ways to clean water systems while harnessing electricity. Several studies suggest that a single large-scale MFC is proven to be inefficient and expensive. Therefore, producing small-scale MFCs is focused on investigation to provide an efficient system and cost-effective approach. This study used 3D-printed MFCs using a spongy electrode design to produce a modern approach to modifying electrode capacity in energy generation. Furthermore, the study identifies the electrical conductivity of the spongy electrode by determining the voltage generated and power density by stacked MFCs in series, parallel, and hybrid configurations. The MFCs generate a maximum voltage of 633 mV and a current of 14.22 . One way to reduce the effects of voltage reversal in the MFC system is the application of hybrid connection circuits. Parallel-series hybrid connection possesses stable voltage generation of 250−300 𝑚𝑉 with the highest current generation of 115.20 𝜇𝐴. At the same time, the Series-Parallel Connection generates the highest voltage and current of 259 mV and 30 , respectively. The spongy electrode design and hybrid connection produced a maximum power and current density of 29.30 μW⁄m2 and 279.41 μA⁄m2 obtained from a different connection of pure parallel and 28P-2S hybrid connection. Furthermore, water quality parameters were examined (pH, TDS, ORP, and COD), that the MFCs design is efficient in wastewater treatment, with a %COD removal of 95.24% efficiency, reduced ORP from +48.00 mV to -7.00 mV, and the TDS concentration from 270 ppm to 239 ppm.

The Social Teachings of the Church define work as a “human act” (opus humanum), an “arduous good” (bonum arduum), and an expression of the intrinsic value and dignity of the human person. The right to work is not only granted by the State but rather a disposition of the value possessed by a person in fulfilling his/her “destiny and vocation” as a rational and autonomous being. However, the breakthroughs of modernity dichotomized the established value of humanity and his work. Artificial Intelligence (AI) is on the way to altering this essential relationship, giving priority to Machine Intelligence (MI). This admiration of humanity for the proliferation of technical advances lurks a certain danger, “a danger as such” if I may use Heidegger’s term. The danger is not only the possible displacements of humanity in his/her work but rather an alienated individual stripped of his/her worth and dignity as a person who is the sole object of work. This paper argues that (1) the human person remains the indispensable subject of work and (2) artificial intelligence is problematic. To facilitate the said discourse, the work of John Paul II “Laborem Exercems” (John Paul II, 1981), shall be the guide in exploring the issue.

Atopic dermatitis (AD) has increased in prevalence to become the most common inflammatory skin condition globally, and geographic variation and migration studies suggest an important role for environmental triggers. Air pollution, especially due to industrialization and wildfires, may contribute to the development and exacerbation of AD. We provide a comprehensive, multidisciplinary review of existing molecular and epidemiologic studies on the associations of air pollutants and AD symptoms, prevalence, incidence, severity, and clinic visits. Cell and animal studies demonstrated that air pollutants contribute to AD symptoms and disease by activating the aryl hydrocarbon receptor pathway, promoting oxidative stress, initiating a proinflammatory response, and disrupting the skin barrier function. Epidemiologic studies overall report that air pollution is associated with AD among both children and adults, though the results are not consistent among cross-sectional studies. Studies on healthcare use for AD found positive correlations between medical visits for AD and air pollutants. As the air quality worsens in many areas globally, it is important to recognize how this can increase the risk for AD, to be aware of the increased demand for AD-related medical care, and to understand how to counsel patients regarding their skin health. Further research is needed to develop treatments that prevent or mitigate air pollution-related AD symptoms.

BackgroundAmbient air pollutant (AAP) exposure is associated with adverse pregnancy outcomes, such as preeclampsia, preterm labor, and low birth weight. Previous studies have shown methylation of immune genes associate with exposure to air pollutants in pregnant women, but the cell-mediated response in the context of typical pregnancy cell alterations has not been investigated. Pregnancy causes attenuation in cell-mediated immunity with alterations in the Th1/Th2/Th17/Treg environment, contributing to maternal susceptibility. We recruited women (n = 186) who were 20 weeks pregnant from Fresno, CA, an area with chronically elevated AAP levels. Associations of average pollution concentration estimates for 1 week, 1 month, 3 months, and 6 months prior to blood draw were associated with Th cell subset (Th1, Th2, Th17, and Treg) percentages and methylation of CpG sites (IL4, IL10, IFNγ, and FoxP3). Linear regression models were adjusted for weight, age, season, race, and asthma, using a Q value as the false-discovery-rate-adjusted p-value across all genes.ResultsShort-term and mid-term AAP exposures to fine particulate matter (PM2.5), nitrogen dioxide (NO2) carbon monoxide (CO), and polycyclic aromatic hydrocarbons (PAH456) were associated with percentages of immune cells. A decrease in Th1 cell percentage was negatively associated with PM2.5 (1 mo/3 mo: Q

Previous studies of air pollution and respiratory disease often relied on aggregated or lagged acute respiratory disease outcome measures, such as emergency department (ED) visits or hospitalizations, which may lack temporal and spatial resolution. This study investigated the association between daily air pollution exposure and respiratory symptoms among participants with asthma and chronic obstructive pulmonary disease (COPD), using a unique dataset passively collected by digital sensors monitoring inhaled medication use. The aggregated dataset comprised 456,779 short-acting beta-agonist (SABA) puffs across 3,386 people with asthma or COPD, between 2012 and 2019, across the state of California. Each rescue use was assigned space–time air pollution values of nitrogen dioxide (NO2), fine particulate matter with diameter ≤ 2.5 µm (PM2.5) and ozone (O3), derived from highly spatially resolved air pollution surfaces generated for the state of California. Statistical analyses were conducted using linear mixed models and random forest machine learning. Results indicate that daily air pollution exposure is positively associated with an increase in daily SABA use, for individual pollutants and simultaneous exposure to multiple pollutants. The advanced linear mixed model found that a 10-ppb increase in NO2, a 10 μg m−3 increase in PM2.5, and a 30-ppb increase in O3 were respectively associated with incidence rate ratios of SABA use of 1.025 (95 % CI: 1.013–1.038), 1.054 (95 % CI: 1.041–1.068), and 1.161 (95 % CI: 1.127–1.233), equivalent to a respective 2.5 %, 5.4 % and 16 % increase in SABA puffs over the mean. The random forest machine learning approach showed similar results.This study highlights the potential of digital health sensors to provide valuable insights into the daily health impacts of environmental exposures, offering a novel approach to epidemiological research that goes beyond residential address. Further investigation is warranted to explore potential causal relationships and to inform public health strategies for respiratory disease management.

Introduction Traumatic rib fractures present a considerable risk to patient well-being, contributing to morbidity and mortality in trauma patients. To address the risks associated with rib fractures, evidence-based interventions have been implemented, including effective pain management, pulmonary hygiene, and early walking. Vancouver General Hospital, a level 1 trauma center in British Columbia, Canada, developed a comprehensive multidisciplinary chest trauma clinical practice guideline (CTCPG) to optimize the management of patients with rib fractures. This prospective cohort study aimed to assess the impact of the CTCPG on pain management interventions and patient outcomes.Methods The study involved patients admitted between January 1, 2021 and December 31, 2021 (post-CTCPG cohort) and a historical control group admitted between November 1, 2018 and December 31, 2019 (pre-CTCPG cohort). Patient data were collected from patient charts and the British Columbia Trauma Registry, including demographics, injury characteristics, pain management interventions, and relevant outcomes.Results Implementation of the CTCPG resulted in an increased use of multimodal pain therapy (99.4% vs 96.1%; p=0.03) and a significant reduction in the incidence of delirium in the post-CTCPG cohort (OR 0.43, 95% CI 0.21 to 0.80, p=0.0099). There were no significant differences in hospital length of stay, ICU (intensive care unit) days, non-invasive positive pressure ventilation requirement, ventilator days, pneumonia incidence, or mortality between the two cohorts.Discussion Adoption of a CTCPG improved chest trauma management by enhancing pain management and reducing the incidence of delirium. Further research, including multicenter studies, is warranted to validate these findings and explore additional potential benefits of the CTCPG in the management of chest trauma patients.Level of evidence IIb.

BackgroundExposure to ozone (O3) is associated with increased risk of exacerbations of asthma, but the underlying mechanisms are not well studied.ObjectiveWe sought to determine whether O3 exposure would enhance airway inflammatory responses to allergen and the GSTM1-null genotype would modulate this enhancement.MethodsIn a crossover design, 10 asthmatic participants (5 with GSTM1-null genotype) who had specific sensitization to Dermatophagoides pteronyssinus (DP) were exposed to 160 ppb O3 or filtered air (FA) control for 4 hours on 2 separate days at least 3 weeks apart. At 20 hours after exposure, endobronchial challenge with DP allergen, and sham normal saline (NS) instillation, were performed in separate bronchi. Six hours later, a second bronchoscopy was performed to collect bronchoalveolar lavage (BAL) from the DP- and NS-challenged segments for analyses of inflammatory biomarkers. Linear regression compared cell and cytokine responses across the 4 exposure groups (FA-NS, O3-NS, FA-DP, O3-DP). Effect modification by GSTM1 genotype was assessed in stratified regressions.ResultsBAL eosinophil counts were increased in segments challenged with DP compared to sham-challenged segments (P < .01). DP challenge compared to sham also caused a significant increase in BAL concentrations of the TH2 cytokines IL-4, IL-5, IL-10, and IL-13 (P < .03 for all comparisons). O3 exposure did not significantly affect BAL cells or cytokine after DP challenge. Compared to GSTM1-present participants, GSTM1-null participants had significantly lower eosinophil (P < .041) and IL-4 (P < .014) responses to DP challenge after O3 exposure.ConclusionsWhile O3 did not cause a clear differential effect on airway inflammatory responses to allergen challenge, those responses did appear to be modulated by the antioxidant enzyme, GSTM1.

Previous studies have reported associations between air pollution and COVID-19 morbidity and mortality, but most have limited their exposure assessment to a large area, have not used individual-level variables, nor studied infections. We examined 3.1 million SARS-CoV-2 infections and 49,691 COVID-19 deaths that occurred in California from February 2020 to February 2021 to evaluate risks associated with long-term neighborhood concentrations of particulate matter less than 2.5 μm in diameter (PM2.5). We obtained individual address data on SARS-CoV-2 infections and COVID-19 deaths and assigned 2000-2018 1km-1km gridded PM2.5 surfaces to census block groups. We included individual covariate data on age and sex, and census block data on race/ethnicity, air basin, Area Deprivation Index, and relevant comorbidities. Our analyses were based on generalized linear mixed models utilizing a Poisson distribution. Those living in the highest quintile of long-term PM2.5 exposure had risks of SARS-CoV-2 infections 20% higher and risks of COVID-19 mortality 51% higher, compared to those living in the lowest quintile of long-term PM2.5 exposure. Those living in the areas of highest long-term PM2.5 exposure were more likely to be Hispanic and more vulnerable, based on the Area Deprivation Index. The increased risks for SARS-CoV-2 Infections and COVID-19 mortality associated with highest long-term PM2.5 concentrations at the neighborhood-level in California were consistent with a growing body of literature from studies worldwide, and further highlight the importance of reducing levels of air pollution to protect public health.

Latino construction workers in the U.S. have faced a disproportionate risk for COVID-19 infection in the workplace. Prior studies have focused on quantifying workplace risk for COVID-19 infection; few have captured workers' experiences and perspectives. This study describes COVID-19-related workplace risks from the perspectives of Latino construction workers. We conducted a qualitative study using semi-structured phone interviews with Latino construction workers from the Fruitvale District of Oakland, California. Twenty individuals were interviewed from December 2020 to March 2021. Nearly all participants (19/20) were Spanish-speaking men; mean age 42.6 years. The majority were low-income and over one-third did not have health insurance. Participants worked in varied construction-related jobs ranging from demolition to office work; additionally, four were day laborers, and three belonged to a labor union. We identified four major themes with public health policy and workplace safety implications: (1) Major concern about the risk of SARS-CoV-2 infection for family health and economic wellbeing; (2) Clarity about mask use and social distancing but not disclosure; (3) Variability in access to additional resources provided by employers; and (4) Uncertainty around structural support for SARS-CoV-2 quarantine/isolation. Our findings provide further evidence from workers' own perspectives of the major gaps experienced during the pandemic in workplace protections and resources.

BackgroundPrevious research has revealed links between air pollution exposure and metabolic syndrome in adults; however, these associations are less explored in children.ObjectiveThis study aims to investigate the association between traffic-related air pollutants (TRAP) and biomarkers of metabolic dysregulation, oxidative stress, and lung epithelial damage in children.MethodsWe conducted cross-sectional analyses in a sample of predominantly Latinx, low-income children (n = 218) to examine associations between air pollutants (nitrogen dioxide (NO2), nitrogen oxides (NOx), elemental carbon, polycyclic aromatic hydrocarbons, carbon monoxide (CO), fine particulates (PM2.5)) and biomarkers of metabolic function (high-density lipoprotein (HDL), hemoglobin A1c (HbA1c), oxidative stress (8-isoprostane), and lung epithelial damage (club cell protein 16 (CC16)).ResultsHDL cholesterol showed an inverse association with NO2 and NOx, with the strongest relationship between HDL and 3-month exposure to NO2 (-15.4 mg/dL per IQR increase in 3-month NO2, 95% CI = -27.4, -3.4). 8-isoprostane showed a consistent pattern of increasing values with 1-day and 1-week exposure across all pollutants. Non-significant increases in % HbA1c were found during 1-month time frames and decreasing CC16 in 3-month exposure time frames.ConclusionOur results suggest that TRAP is significantly associated with decreased HDL cholesterol in longer-term time frames and elevated 8-isoprostane in shorter-term time frames. TRAP could have the potential to influence lifelong metabolic patterns, through metabolic effects in childhood.

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.

Ocean surface radiation measurement best practices have been developed as a first step to support the interoperability of radiation measurements across multiple ocean platforms and between land and ocean networks. This document describes the consensus by a working group of radiation measurement experts from land, ocean, and aircraft communities. The scope was limited to broadband shortwave (solar) and longwave (terrestrial infrared) surface irradiance measurements for quantification of the surface radiation budget. Best practices for spectral measurements for biological purposes like photosynthetically active radiation and ocean color are only mentioned briefly to motivate future interactions between the physical surface flux and biological radiation measurement communities. Topics discussed in these best practices include instrument selection, handling of sensors and installation, data quality monitoring, data processing, and calibration. It is recognized that platform and resource limitations may prohibit incorporating all best practices into all measurements and that spatial coverage is also an important motivator for expanding current networks. Thus, one of the key recommendations is to perform interoperability experiments that can help quantify the uncertainty of different practices and lay the groundwork for a multi-tiered global network with a mix of high-accuracy reference stations and lower-cost platforms and practices that can fill in spatial gaps.

Global warming and climate change have increased the pollen burden and the frequency and intensity of wildfires, sand and dust storms, thunderstorms, and heatwaves—with concomitant increases in air pollution, heat stress, and flooding. These environmental stressors alter the human exposome and trigger complex immune responses. In parallel, pollutants, allergens, and other environmental factors increase the risks of skin and mucosal barrier disruption and microbial dysbiosis, while a loss of biodiversity and reduced exposure to microbial diversity impairs tolerogenic immune development. The resulting immune dysregulation is contributing to an increase in immune-mediated diseases such as asthma and other allergic diseases, autoimmune diseases, and cancer. It is now abundantly clear that multisectoral, multidisciplinary, and transborder efforts based on Planetary Health and One Health approaches (which consider the dependence of human health on the environment and natural ecosystems) are urgently needed to adapt to and mitigate the effects of climate change. Key actions include reducing emissions and improving air quality (through reduced fossil fuel use), providing safe housing (e.g., improving weatherization), improving diets (i.e., quality and diversity) and agricultural practices, and increasing environmental biodiversity and green spaces. There is also a pressing need for collaborative, multidisciplinary research to better understand the pathophysiology of immune diseases in the context of climate change. New data science techniques, biomarkers, and economic models should be used to measure the impact of climate change on immune health and disease, to inform mitigation and adaptation efforts, and to evaluate their effectiveness. Justice, equity, diversity, and inclusion (JEDI) considerations should be integral to these efforts to address disparities in the impact of climate change.

Background: Diesel exhaust and respirable dust exposures in the mining industry have not been studied in depth with respect to non-malignant respiratory disease including chronic obstructive pulmonary disease (COPD), with most available evidence coming from other settings. Objectives: To assess the relationship between occupational diesel exhaust and respirable dust exposures and COPD mortality, while addressing issues of survivor bias in exposed miners. Methods: The study population consisted of 11,817 male workers from the Diesel Exhaust in Miners Study II, followed from 1947 to 2015, with 279 observed COPD deaths. We fit Cox proportional hazards models for the relationship between respirable elemental carbon (REC) and respirable dust (RD) exposure and COPD mortality. To address healthy worker survivor bias, we leveraged the parametric g-formula to assess effects of hypothetical interventions on both exposures. Results: Cox models yielded elevated estimates for the associations between average intensity of REC and RD and COPD mortality, with hazard ratios (HR) corresponding to an interquartile range width increase in exposure of 1.46 (95 % confidence interval (CI): 1.12, 1.91) and 1.20 (95 % CI: 0.96, 1.49), respectively for each exposure. HRs for cumulative exposures were negative for both REC and RD. Based on results from the parametric g-formula, the risk ratio (RR) for COPD mortality comparing risk under an intervention eliminating REC to the observed risk was 0.85 (95 % CI: 0.55, 1.06), equivalent to an attributable risk of 15 %. The corresponding RR comparing risk under an intervention eliminating RD to the observed risk was 0.93 (95 % CI: 0.56, 1.31). Conclusions: Our findings, based on data from a cohort of nonmetal miners, are suggestive of an increased risk of COPD mortality associated with REC and RD, as well as evidence of survivor bias in this population leading to negative associations between cumulative exposures and COPD mortality in traditional regression analysis.

Household air pollution is a leading risk factor for morbidity and premature mortality. Numerous cookstoves have been developed to reduce household air pollution, but it is unclear whether such cookstoves meaningfully improve health. In a controlled exposure study with a crossover design, we assessed the effect of pollution emitted from multiple cookstoves on acute differences in blood lipids and inflammatory biomarkers. Participants (n = 48) were assigned to treatment sequences of exposure to air pollution emitted from five cookstoves and a filtered-air control. Blood lipids and inflammatory biomarkers were measured before and 0, 3, and 24 hours after treatments. Many of the measured outcomes had inconsistent results. However, compared to control, intercellular adhesion molecule-1 was higher 3 hours after all treatments, and C-reactive protein and serum amyloid-A were higher 24 hours after the highest treatment. Our results suggest that short-term exposure to cookstove air pollution can increase inflammatory biomarkers within 24 hours.

SETTING: Household air pollution (HAP) and chronic obstructive pulmonary disease (COPD) are both major public health problems, reported to cause around 4 million and 3 million deaths every year, respectively. The great majority of these deaths, as well as the burden of disease during life is felt by people in low- and middle-income countries (LMICs).OBJECTIVE and DESIGN: The extent to which HAP causes COPD is controversial; we therefore undertook this review to offer a viewpoint on this from the Global Initiative for COPD (GOLD).RESULTS: We find that while COPD is well-defined in many studies on COPD and HAP, there are major limitations to the definition and measurement of HAP. It is thus difficult to disentangle HAP from other features of poverty that are themselves associated with COPD. We identify other limitations to primary research studies, including the use of cross-sectional designs that limit causal inference.CONCLUSION: There is substantial preventable morbidity and mortality associated with HAP, COPD and poverty, separately and together. Although it may not be possible to define clear causal links between HAP and COPD, there is a clear urgency to reduce the avoidable burden of disease these inflict on the world´s poor.

Previous studies have shown associations between air pollutants and low birth weight. However, few studies assess whether poverty and race/ethnicity are effect modifiers for this relationship. We used publicly available data on 7785 California census tracts from the California Communities Environmental Health Screening Tool (CalEnviroScreen). Multivariable linear regression was used to examine the association between outdoor PM2.5 and low birth weight (LBW), including stratification by poverty and race/ethnicity (as a proxy for experienced racism). A 1 µg m-3 increase in PM2.5 was associated with a 0.03% (95% CI: 0.01, 0.04) increase in the percentage of LBW infants in a census tract. The association between PM2.5 and LBW was stronger in census tracts with the majority living in poverty (0.06% increase; 95% CI: 0.03, 0.08) compared to those with fewer people living in poverty (0.02% increase; 95% CI: 0.00, 0.03). Our results show that exposure to outdoor PM2.5 is associated with a small increase in the percentage of LBW infants in a census tract, with a further increase in tracts with high poverty. The results for effect modification by race/ethnicity were less conclusive.

Women and children in rural regions of low-income countries are exposed to high levels of household air pollution (HAP) as they traditionally tend to household chores such as cooking with biomass fuels. Early life exposure to air pollution is associated with aeroallergen sensitization and developing allergic diseases at older ages. This prospective cohort study assigned HAP-reducing chimney stoves to 557 households in rural Guatemala at different ages of the study children. The children's air pollution exposure was measured using personal CO diffusion tubes. Allergic outcomes at 4-5 years old were assessed using skin prick tests and International Study of Asthma and Allergies in Childhood (ISAAC)-based questionnaires. Children assigned to improved stoves before 6 months old had the lowest HAP exposure compared to the other groups. Longer exposure to the unimproved stoves was associated with higher risks of maternal-reported allergic asthma (OR = 2.42, 95% CI: 1.11-5.48) and rhinitis symptoms (OR = 2.01, 95% CI: 1.13-3.58). No significant association was found for sensitization to common allergens such as dust mites and cockroaches based on skin prick tests. Reducing HAP by improving biomass burning conditions might be beneficial in preventing allergic diseases among children in rural low-income populations.

BACKGROUND: The greatest burden of chronic respiratory disease is in low- and middle-income countries, with recent population-based studies reporting substantial levels of obstructive and restrictive lung function.OBJECTIVE: To characterise the common chronic respiratory diseases encountered in hospital outpatient clinics in three African countries.METHODS This was a cross-sectional study of consecutive adult patients with chronic respiratory symptoms (>8 weeks) attending hospital outpatient departments in Ethiopia, Kenya and Sudan. Patients were assessed using a respiratory questionnaire, spirometry and chest radiography. The diagnoses of the reviewing clinicians were ascertained.RESULT: A total of 519 patients (209 Kenya, 170 Ethiopia, 140 Sudan) participated; the mean age was 45.2 years (SD 16.2); 53% were women, 83% had never smoked. Reviewing clinicians considered that 36% (95% CI 32-40) of patients had asthma, 25% (95% CI 21-29) had chronic bronchitis, 8% (95% CI 6-11) chronic obstructive pulmonary disease (COPD), 5% (95% CI 4-8) bronchiectasis and 4% (95% CI 3-6) post-TB lung disease. Spirometry consistent with COPD was present in 35% (95% CI 30-39). Restriction was evident in 38% (95% CI 33-43). There was evidence of sub-optimal diagnosis of asthma and COPD.CONCLUSION: In Ethiopia, Kenya and Sudan, asthma, COPD and chronic bronchitis account for the majority of diagnoses in non-TB patients with chronic respiratory symptoms. The suboptimal diagnosis of these conditions will require the widespread use of spirometry.

BackgroundOzone effects on lung function are particularly important to understand in the context of the air pollution-health outcomes epidemiologic literature, given the complex relationships between ozone and other air pollutants with known lung function effects.Research questionWhat has been learned about the association between ozone exposures and lung function from epidemiology studies published from 2013 through 2020?Study design and methodsOn March 18, 2018, and September 8, 2020, PubMed was searched using the terms health AND ozone, filtering to articles in English and about humans, from 2013 or later. An additional focused review searching for ozone AND (lung function OR FEV1OR FVC) was performed June 26, 2021. Articles were selected for this review if they reported a specific relationship between a lung function outcome and ozone exposure.ResultsOf 3,271 articles screened, 53 ultimately met criteria for inclusion. A systematic review with assessment of potential for bias was conducted, but a meta-analysis was not carried out because of differences in exposure duration and outcome quantification. Consistent evidence exists of small decreases in children's lung function, even associated with very low levels of short-term ozone exposure. The effects on adult lung function from exposure to low-level, short-term ozone are less clear, although ozone-associated decrements may occur in the elderly. Finally, long-term ozone exposure decreases both lung function and lung function growth in children, although few new studies have examined long-term ozone and lung function in adults.InterpretationMuch of this literature involves concentrations below the current US Environmental Protection Agency's National Ambient Air Quality Standard of 70 parts per billion over an 8-h averaging time, suggesting that this current standard may not protect children adequately from ozone-related decrements in lung function.

Rationale: The Southeast Asian tuberculosis burden is high, and it remains unclear if urban indoor air pollution in this setting is exacerbating the epidemic. Objectives: To determine the associations of latent tuberculosis with common urban indoor air pollution sources (secondhand smoke, indoor motorcycle emissions, and cooking) in Southeast Asia. Methods: We enrolled child household contacts of patients with microbiologically confirmed active tuberculosis in Vietnam, from July 2017 to December 2019. We tested children for latent tuberculosis and evaluated air pollution exposures with questionnaires and personal aerosol sampling. We tested hypotheses using generalized estimating equations. Measurements and Main Results: We enrolled 72 patients with tuberculosis (27% with cavitary disease) and 109 of their child household contacts. Latent tuberculosis was diagnosed in 58 (53%) household contacts at baseline visit. Children experienced a 2.56-fold increased odds of latent tuberculosis for each additional household member who smoked (95% confidence interval, 1.27-5.16). Odds were highest among children exposed to indoor smokers and children

BackgroundIn Sub-Saharan Africa cross-sectional studies report a high prevalence of abnormal lung function indicative of chronic respiratory disease. The natural history and health impact of this abnormal lung function in low-and middle-income countries is largely unknown.MethodsA cohort of 1481 adults representative of rural Chikwawa in Malawi were recruited in 2014 and followed-up in 2019. Respiratory symptoms and health-related quality of life (HRQoL) were quantified. Lung function was measured by spirometry.Findings1232 (83%) adults participated; spirometry was available for 1082 (73%). Mean (SD) age 49.5 (17.0) years, 278(23%) had ever smoked, and 724 (59%) were women. Forced expiratory volume in one second (FEV1) declined by 53.4 ml/year (95% CI: 49.0, 57.8) and forced vital capacity (FVC) by 45.2 ml/year (95% CI: 39.2, 50.5) . Chronic airflow obstruction increased from 9.5% (7.6, 11.6%) in 2014 to 17.5% (15.3, 19.9%) in 2019. There was no change in diagnosed asthma or in spirometry consistent with asthma or restriction. Rate of FEV1 decline was not associated with diagnosed Chronic obstructive pulmonary disease (COPD), asthma, or spirometry consistent with asthma, COPD, or restriction. HRQoL was adversely associated with respiratory symptoms (dyspnoea, wheeze, cough), previous tuberculosis, declining FEV1 and spirometry consistent with asthma or restriction. These differences exceeded the minimally important difference.InterpretationIn this cohort, the increasing prevalence of COPD is associated with the high rate of FEV1 decline and lung function deficits present before recruitment. Respiratory symptoms and sub-optimal lung function are independently associated with reduced HRQoL.

Background: Cooking-related biomass smoke is a major source of household air pollution (HAP) and an important health hazard. Prior studies identified associations between HAP exposure and childhood stunting; less is known for underweight and wasting. Few studies had personal HAP measurements. Methods: 557 households in rural Guatemala were enrolled in the CRECER study, the follow-up study of the RESPIRE randomized intervention trial. They were assigned to three groups that received chimney stoves at different ages of the study children. Multiple personal carbon monoxide (CO) exposure measurements were used as proxies for HAP exposures. Children’s heights and weights were measured from 24 to 60 months of age. Height-for-age z-score (HAZ), weight-for-age z-score (WAZ), and weight-for-height z-score (WHZ) were calculated based on the World Health Organization’s Multicentre Growth Reference Study. HAZ, WAZ, and WHZ below −2 were classified as stunting, underweight, and wasting, respectively. Generalized linear models and mixed effects models were applied. Results: 541 children had valid anthropometric data, among whom 488 (90.2 %) were stunted, 192 (35.5 %) were underweight, and 2 (0.3 %) were wasted. A 1 ppm higher average CO exposure was associated with a 0.21 lower HAZ (95 % CI: 0.17–0.25), a 0.13 lower WAZ (95 % CI: 0.10–0.17) and a 0.06 lower WHZ (95 % CI: 0.02–0.10).The associations for HAZ were stronger among boys (coefficient = −0.29, 95 % CI: −0.35 – −0.22) than among girls (coefficient = −0.15, 95 % CI: −0.20 – −0.10). A 1 ppm-year higher cumulative CO exposure was associated with a higher risk of moderate stunting among boys (OR = 1.27, 95 % CI: 1.05-1.59), but not among girls. Discussion: In this rural Guatemalan population, higher HAP exposure was associated with lower HAZ and WAZ. The associations between HAP and HAZ/stunting were stronger among boys. Reducing HAP might benefit childhood somatic growth in rural populations of low-income countries.

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.

BackgroundPreterm birth is the leading cause of perinatal morbidity and mortality in the U.S. and disparities among racial and ethnic groups persist. While etiologies of preterm birth have not been fully elucidated, it is probable that environmental and social factors play a role.ObjectiveWe hypothesized that there is an interactive association between exposure to fine particulate matter (PM2.5) or ozone (O3) and neighborhood socioeconomic factors that increase the risk of preterm birth.MethodsWe conducted a retrospective study using geocoded birth certificate data between 2007 and 2011, daily ambient air quality data on PM2.5 and O3, and American Community Survey (2007-2011 5-year estimates) data to assess census tract-level socioeconomic factors in California urban counties.ResultsOur study found a small positive association between maternal exposures to PM2.5 and O3 and preterm birth that varied by gestational exposure period. In mixed-effects models, we found an increase in the risk of preterm birth for a one-unit change in PM2.5 averaged across the entire pregnancy (AOR = 1.02, 95% CI: 1.01, 1.02) and O3 during 3-months pre-pregnancy (AOR = 1.03, 95% CI: 1.02, 1.04). Interaction between census tract-level factors and air pollutants showed an increase in the risk of preterm birth among mothers living in higher socioeconomic areas, though, a fixed cohort bias sensitivity analysis showed these associations were not significant.SignificanceThese findings substantiate previous studies that showed associations between air pollution and preterm birth, even as pollution levels have decreased. This study has important implications for policy decisions and may help inform research on potential mechanisms of preterm birth.

BackgroundMetabolic syndrome increases the risk of cardiovascular disease in adults. Antecedents likely begin in childhood and whether childhood exposure to air pollution plays a contributory role is not well understood.ObjectivesTo assess whether children's exposure to air pollution is associated with markers of risk for metabolic syndrome and oxidative stress, a hypothesized mediator of air pollution-related health effects.MethodsWe studied 299 children (ages 6-8) living in the Fresno, CA area. At a study center visit, questionnaire and biomarker data were collected. Outcomes included hemoglobin A1c (HbA1c), urinary 8-isoprostane, systolic blood pressure (SBP), and BMI. Individual-level exposure estimates for a set of four pollutants that are constituents of traffic-related air pollution (TRAP) - the sum of 4-, 5-, and 6-ring polycyclic aromatic hydrocarbon compounds (PAH456), NO2, elemental carbon, and fine particulate matter (PM2.5) - were modeled at the primary residential location for 1-day lag, and 1-week, 1-month, 3-month, 6-month, and 1-year averages prior to each participant's visit date. Generalized additive models were used to estimate associations between each air pollutant exposure and outcome.ResultsThe study population was 53% male, 80% Latinx, 11% Black and largely low-income (6% were White and 3% were Asian/Pacific Islander). HbA1c percentage was associated with longer-term increases in TRAP; for example a 4.42 ng/m3 increase in 6-month average PAH456 was associated with a 0.07% increase (95% CI: 0.01, 0.14) and a 3.62 μg/m3 increase in 6-month average PM2.5 was associated with a 0.06% increase (95% CI: 0.01, 0.10). The influence of air pollutants on blood pressure was strongest at 3 months; for example, a 6.2 ppb increase in 3-month average NO2 was associated with a 9.4 mmHg increase in SBP (95% CI: 2.8, 15.9). TRAP concentrations were not significantly associated with anthropometric or adipokine measures. Short-term TRAP exposure averages were significantly associated with creatinine-adjusted urinary 8-isoprostane.DiscussionOur results suggest that both short- and longer-term estimated individual-level outdoor residential exposures to several traffic-related air pollutants, including ambient PAHs, are associated with biomarkers of risk for metabolic syndrome and oxidative stress in children.

BACKGROUND: Scientific understanding of indoor air pollution is predominately based on research carried out in cities in high-income countries (HICs). Less is known about how pollutant concentrations change over the course of a typical day in cities in low- and middle-income countries (LMICs).OBJECTIVE: To understand how concentrations of fine particulate matter smaller than 2.5 microns in diameter (PM2.5) change over the course of the day outdoors (across a range of countries) and indoors (using measurements from Dhaka, Bangladesh).DESIGN: Data on PM2.5 concentrations were gathered from 779 households in Dhaka as part of the MCLASS II (Muslim Communities Learning About Second-hand Smoke in Bangladesh) project, and compared to outdoor PM2.5 concentrations to determine the temporal variation in exposure to air pollution. Hourly PM2.5 data from 23 cities in 14 LMICs, as well as London (UK), Paris (France) and New York (NY, USA), were extracted from publicly available sources for comparison.RESULTS: PM2.5 in homes in Dhaka demonstrated a similar temporal pattern to outdoor measurements, with greater concentrations at night than in the afternoon. This pattern was also evident in 19 of 23 LMIC cities.CONCLUSION: PM2.5 concentrations are greater at night than during the afternoon in homes in Dhaka. Diurnal variations in PM2.5 in LMICs is substantial and greater than in London, Paris or New York. This has implications for public health community approaches to health effects of air pollution in LMICs.

Throughout the United States, wildland firefighters respond to wildfires, performing arduous work in remote locations. Wildfire incidents can be an ideal environment for the transmission of infectious diseases, particularly for wildland firefighters who congregate in work and living settings. In this review, we examine how exposure to wildfire smoke can contribute to an increased likelihood of SARS-CoV-2 infection and severity of coronavirus disease (COVID-19). Human exposure to particulate matter (PM), a component of wildfire smoke, has been associated with oxidative stress and inflammatory responses; increasing the likelihood for adverse respiratory symptomology and pathology. In multiple epidemiological studies, wildfire smoke exposure has been associated with acute lower respiratory infections, such as bronchitis and pneumonia. Co-occurrence of SARS-CoV-2 infection and wildfire smoke inhalation may present an increased risk for COVID-19 illness in wildland firefighters due to PM based transport of SARS CoV-2 virus and up-regulation of angiotensin-converting enzyme II (ACE-2) (i.e. ACE-2 functions as a trans-membrane receptor, allowing the SARS-CoV-2 virus to gain entry into the epithelial cell). Wildfire smoke exposure may also increase risk for more severe COVID-19 illness such as cytokine release syndrome, hypotension, and acute respiratory distress syndrome (ARDS). Current infection control measures, including social distancing, wearing cloth masks, frequent cleaning and disinfecting of surfaces, frequent hand washing, and daily screening for COVID-19 symptoms are very important measures to reduce infections and severe health outcomes. Exposure to wildfire smoke may introduce additive or even multiplicative risk for SARS-CoV-2 infection and severity of disease in wildland firefighters. Thus, additional mitigative measures may be needed to prevent the co-occurrence of wildfire smoke exposure and SARS-CoV-2 infection.

Ambient air pollution exposure is associated with cardiovascular dysregulation and immune system alterations, yet no study has investigated both simultaneously in children. Understanding the multifaceted impacts may provide early clues for clinical intervention prior to actual disease presentation. We therefore determined the associations between exposure to multiple air pollutants and both immunological outcomes (methylation and protein expression of immune cell types associated with immune regulation) and cardiovascular outcomes (blood pressure) in a cohort of school-aged children (6-8 years; n = 221) living in a city with known elevated pollution levels. Exposure to fine particular matter (PM2.5), carbon monoxide (CO), and ozone (O3) was linked to altered methylation of most CpG sites for genes Foxp3, IL-4, IL-10 and IFN-g, all involved in immune regulation (e.g. higher PM2.5 exposure 1 month prior to the study visit was independently associated with methylation of the IL-4 CpG24 site (est = 0.16; P = 0.0095). Also, immune T helper cell types (Th1, Th2 and Th17) were associated with short-term exposure to PM2.5, O3 and CO (e.g. Th1 cells associated with PM2.5 at 30 days: est = - 0.34, P

Wildfire smoke is an increasing environmental health threat to which children are particularly vulnerable, for both physiologic and behavioral reasons. To address the need for improved public health messaging this review summarizes current knowledge and knowledge gaps in the health effects of wildfire smoke in children, as well as tools for public health response aimed at children, including consideration of low-cost sensor data, respirators, and exposures in school environments. There is an established literature of health effects in children from components of ambient air pollution, which are also present in wildfire smoke, and an emerging literature on the effects of wildfire smoke, particularly for respiratory outcomes. Low-cost particulate sensors demonstrate the spatial variability of pollution, including wildfire smoke, where children live and play. Surgical masks and respirators can provide limited protection for children during wildfire events, with expected decreases of roughly 20%  and 80% for surgical masks and N95 respirators, respectively. Schools should improve filtration to reduce exposure of our nation's children to smoke during wildfire events. The evidence base described may help clinical and public health authorities provide accurate information to families to improve their decision making.

BackgroundExposure to household air pollution from solid fuel combustion for cooking and heating is an important risk factor for premature death and disability worldwide. Current evidence supports an association of ambient air pollution with cardiovascular disease but is limited for household air pollution and for cardiac function. Controlled exposure studies can complement evidence provided by field studies.ObjectivesTo investigate effects of short-term, controlled exposures to emissions from five cookstoves on measures of cardiac function.MethodsForty-eight healthy adults (46% female; 20-36 years) participated in six, 2-h exposures ('treatments'), including emissions from five cookstoves and a filtered-air control. Target fine particulate matter (PM2.5) exposure-concentrations per treatment were: control, 0 µg/m3; liquefied petroleum gas, 10 µg/m3; gasifier, 35 µg/m3; fan rocket, 100 µg/m3; rocket elbow, 250 µg/m3; and three stone fire, 500 µg/m3. Participants were treated in a set (pre-randomized) sequence as groups of 4 to minimize order bias and time-varying confounders. Heart rate variability (HRV) and cardiac repolarization metrics were calculated as 5-min means immediately and at 3 h following treatment, for analysis in linear mixed-effects models comparing cookstove to control.ResultsShort-term differences in SDNN (standard deviation of duration of all NN intervals) and VLF (very-low frequency power) existed for several cookstoves compared to control. While all cookstoves compared to control followed a similar trend for SDNN, the greatest effect was seen immediately following three stone fire (β = -0.13 ms {%}; 95% confidence interval = -0.22, -0.03%), which reversed in direction at 3 h (0.03%; -0.06, 0.13%). VLF results were similar in direction and timing to SDNN; however, other HRV or cardiac repolarization results were not similar to those for SDNN.DiscussionWe observed some evidence of short-term, effects on HRV immediately following cookstove treatments compared to control. Our results suggest that cookstoves with lower PM2.5 emissions are potentially capable of affecting cardiac function, similar to stoves emitting higher PM2.5 emissions.

Pollution from landscape fires, which are increasing with climate change, leads to babies being born with lower birthweights in low- and middle-income countries.

BackgroundThough SARS-CoV-2 outbreaks have been documented in occupational settings and in-person essential work has been suspected as a risk factor for COVID-19, occupational differences in excess mortality have, to date, not been examined. Such information could point to opportunities for intervention, such as vaccine prioritization or regulations to enforce safer work environments.Methods and findingsUsing autoregressive integrated moving average models and California Department of Public Health data representing 356,188 decedents 18-65 years of age who died between January 1, 2016 and November 30, 2020, we estimated pandemic-related excess mortality by occupational sector and occupation, with additional stratification of the sector analysis by race/ethnicity. During these first 9 months of the COVID-19 pandemic, working-age adults experienced 11,628 more deaths than expected, corresponding to 22% relative excess and 46 excess deaths per 100,000 living individuals. Sectors with the highest relative and per-capita excess mortality were food/agriculture (39% relative excess; 75 excess deaths per 100,000), transportation/logistics (31%; 91 per 100,000), manufacturing (24%; 61 per 100,000), and facilities (23%; 83 per 100,000). Across racial and ethnic groups, Latino working-age Californians experienced the highest relative excess mortality (37%) with the highest excess mortality among Latino workers in food and agriculture (59%; 97 per 100,000). Black working-age Californians had the highest per-capita excess mortality (110 per 100,000), with relative excess mortality highest among transportation/logistics workers (36%). Asian working-age Californians had lower excess mortality overall, but notable relative excess mortality among health/emergency workers (37%), while White Californians had high per-capita excess deaths among facilities workers (70 per 100,000).ConclusionsCertain occupational sectors are associated with high excess mortality during the pandemic, particularly among racial and ethnic groups also disproportionately affected by COVID-19. In-person essential work is a likely venue of transmission of coronavirus infection and must be addressed through vaccination and strict enforcement of health orders in workplace settings.

We review the interaction between coronavirus disease (COVID-19) and coccidioidomycosis, a respiratory infection caused by inhalation of Coccidioides fungal spores in dust. We examine risk for co-infection among construction and agricultural workers, incarcerated persons, Black and Latino populations, and persons living in high dust areas. We further identify common risk factors for co-infection, including older age, diabetes, immunosuppression, racial or ethnic minority status, and smoking. Because these diseases cause similar symptoms, the COVID-19 pandemic might exacerbate delays in coccidioidomycosis diagnosis, potentially interfering with prompt administration of antifungal therapies. Finally, we examine the clinical implications of co-infection, including severe COVID-19 and reactivation of latent coccidioidomycosis. Physicians should consider coccidioidomycosis as a possible diagnosis when treating patients with respiratory symptoms. Preventive measures such as wearing face masks might mitigate exposure to dust and severe acute respiratory syndrome coronavirus 2, thereby protecting against both infections.

The American Thoracic Society Core Curriculum updates clinicians annually in adult and pediatric pulmonary disease, medical critical care, and sleep medicine, in a 3- to 4-year recurring cycle of topics. These topics will be presented at the 2020 International Conference. Below is the pediatric pulmonary medicine core, including pediatric hypoxemic respiratory failure; modalities in noninvasive management of chronic respiratory failure in childhood; surgical and nonsurgical management of congenital lung malformations; an update on smoke inhalation lung injury; an update on vaporizers, e-cigarettes, and other electronic delivery systems; pulmonary complications of sarcoidosis; pulmonary complications of congenital heart disease; and updates on the management of congenital diaphragmatic hernia.

Fine particulate air pollution

Wildfires, which are becoming more frequent and intense in many countries, pose serious threats to human health. To determine health impacts and provide public health messaging, satellite-based smoke plume data are sometimes used as a proxy for directly measured particulate matter levels. We collected data on particulate matter

BackgroundAmbient environmental pollutants have been shown to adversely affect respiratory health in susceptible populations. However, the role of simultaneous exposure to multiple diverse environmental pollutants is poorly understood.ObjectiveWe applied a multidomain, multipollutant approach to assess the association between pediatric lung function measures and selected ambient air pollutants and pesticides.MethodsUsing data from the US EPA and California Pesticide Use Registry, we reconstructed three months prior exposure to ambient air pollutants ((ozone (O3), nitrogen dioxide (NO2), particulate matter with a median aerodynamic diameter