Search

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.

Background: Inhalation of ambient levels of ozone causes airway inflammation and epithelial injury. Methods: To examine the responses of airway cells to ozone-induced oxidative injury, 19 subjects (7 with asthma) were exposed to clean air (0ppb), medium (1

© 2015 Bates et al.Background: Results have been conflicting whether long-term ambient hydrogen sulfide (H2S) affects lung function or is a risk factor for asthma or chronic obstructive pulmonary disease (COPD). Rotorua city, New Zealand, has the world's l

© 2015, Public Health Services, US Dept of Health and Human Services. All rights reserved.Background: Although pesticide use is widespread, the possible effect of early-life exposure to organophosphate (OP) on pediatric respiratory health is not well descr

© 2015 Public Health Services, US Dept of Health and Human Services. All rights reserved.Background: With 40% of the world’s population relying on solid fuel, household air pollution (HAP) represents a major preventable risk factor for COPD (chronic obstru

Background: With an increase in indoor smoking bans, many smokers smoke outside establishments and near their entrances, which has become a public health concern. Objectives: We characterized the exposure of nonsmokers to secondhand smoke (SHS) outside a r

Occupational medicine physicians are frequently asked to establish cancer causation in patients with both workplace and non-workplace exposures. This is especially difficult in cases involving beryllium for which the data on human carcinogenicity are limited and controversial. In this report we present the case of a 73-year-old former technician at a government research facility who was recently diagnosed with lung cancer. The patient is a former smoker who has worked with both beryllium and asbestos. He was referred to the University of California, San Francisco, Occupational and Environmental Medicine Clinic at San Francisco General Hospital for an evaluation of whether past workplace exposures may have contributed to his current disease. The goal of this paper is to provide an example of the use of data-based risk estimates to determine causation in patients with multiple exposures. To do this, we review the current knowledge of lung cancer risks in former smokers and asbestos workers, and evaluate the controversies surrounding the epidemiologic data linking beryllium and cancer. Based on this information, we estimated that the patient's risk of lung cancer from asbestos was less than his risk from tobacco smoke, whereas his risk from beryllium was approximately equal to his risk from smoking. Based on these estimates, the patient's workplace was considered a probable contributing factor to his development of lung cancer.

Occupational asthma is the most common form of occupational lung disease in the developed world at the present time. In this review, the epidemiology, pathogenesis/mechanisms, clinical presentations, management, and prevention of occupational asthma are discussed. The population attributable risk of asthma due to occupational exposures is considerable. Current understanding of the mechanisms by which many agents cause occupational asthma is limited, especially for low-molecular-weight sensitizers and irritants. The diagnosis of occupational asthma is generally established on the basis of a suggestive history of a temporal association between exposure and the onset of symptoms and objective evidence that these symptoms are related to airflow limitation. Early diagnosis, elimination of exposure to the responsible agent, and early use of inhaled steroids may play important roles in the prevention of long-term persistence of asthma. Persistent occupational asthma is often associated with substantial disability and consequent impacts on income and quality of life. Prevention of new cases is the best approach to reducing the burden of asthma attributable to occupational exposures. Future research needs are identified.

Asthma is a clinical condition characterized by intermittent respiratory symptoms, nonspecific airway hyperresponsiveness, and reversible airway obstruction. Although the pathogenesis of asthma is incompletely understood, it is clear that airway inflammation is a paramount feature of the condition. Because inhalation of ozone by normal, healthy subjects causes increased airway responsiveness and inflammation, it is somewhat surprising that most controlled human exposure studies that have involved asthmatic subjects have not shown them to be especially sensitive to ozone. The acute decrement in lung function that is the end point traditionally used to define sensitivity to ozone in these studies may be due more to neuromuscular mechanisms limiting deep inspiration than to bronchoconstriction. The frequency of asthma attacks following ozone exposures may be a more relevant end point. Epidemiologic studies, rather than controlled human exposure studies, are required to determine whether ozone pollution increases the risk of asthma exacerbations. Asthma affects approximately 10 million people in the United States and, thus, the answer to this question is of considerable public health importance. Both the prevalence and severity of asthma appear to be increasing in many countries. Although increased asthma morbidity and mortality are probably of multifactorial etiology, a contributory role of urban air pollution is plausible. The epidemiologic database to support an association between asthma and ozone exposure is limited, but the results of several studies suggest such an association. Some potential approaches to further investigation of the relationship between asthma and ozone, including those that would link controlled human exposures to population-based studies, are considered.

Acid fog is complex and contains multiple stimuli that may be capable of inducing bronchoconstriction. These stimuli include sulfuric and niric acids, the principal inorganic acids present; sulfites, formed in the atmosphere as a reaction product of sulfur dioxide and water droplets; fog water itself, a hypoosmolar aerosol; the organic acid hydroxymethanesulfonate, the bisulfite adduct of formaldehyde; and gaseous pollutants, e.g., sulfur dioxide, oxides of nitrogen, ozone. Given this complexity, evaluation of the respiratory health effects of naturally occurring acid fog requires assessment of the bronchoconstrictor potency of each component stimulus and possible interactions among these stimuli. We summarize the results of three studies that involve characterization of the bronchoconstrictor potency of acid fog stimuli and/or their interaction in subjects with asthma. The results of the first study indicate that titratable acidity appears to be a more important stimulus to bronchoconstriction than is pH. The results of the second study demonstrate that sulfite species are capable of inducing bronchoconstriction, especially when inhaled at acid pH. The results of the third study suggest that acidity can potentiate hypoosmolar fog-induced bronchoconstriction.

Context: Biomass serves as a major fuel source for > 50% of the world's population. The global burden of disease attributed to indoor air pollution from biomass combustion accounts for approximately 3% of worldwide disability-adjusted life-years lost. This is due to pneumonia in children and chronic obstructive pulmonary disease and lung cancer in women. Case Presentation: A 53-year-old man from Mexico was referred to the pulmonary clinic for evaluation of chronic productive cough and pulmonary nodules. In his youth, he worked at a charcoal plant in Mexico, where he burned wood and was exposed to massive amounts of smoke. His evaluation revealed thickened bronchovascular bundles with nodules on thoracic computed tomography, dark black plaques in large airways on bronchoscopy, and carbon-laden macrophages and fibrotic scars on lung biopsy. Discussion: The patient was diagnosed with 'hut lung,' a term that refers to the noninfectious, nonmalignant respiratory manifestations of chronic, high-level exposures to biomass smoke. This is the first reported case of hut lung associated with charcoal production. This case highlights that histopathologic abnormalities of the lung parenchyma may be present in patients with only mild symptoms and that clinical progression is likely a function of both the duration and intensity of exposure. Relevance to Clinical Practice: As residents of lesser developed countries continue to be exposed to high levels of biomass smoke at work or at home and continue to immigrate to developed countries, it is important that health care providers in developed countries be aware of biomass-smoke-related pulmonary disease. Key words: biomass combustion, domestically acquired particulate lung disease, hut lung, indoor air pollution, wood smoke. [ABSTRACT FROM AUTHOR]

Despite numerous published studies, debate continues regarding the risk of developing lung cancer among men exposed occupationally to asbestos, particularly those without radiographic or functional evidence of asbestosis. The beta-Carotene and Retinol Efficacy Trial (CARET), a study of vitamin supplementation for chemoprevention of lung cancer, has followed 4,060 heavily exposed US men for 9-17 years. Lung cancer incidence for 1989-2002 was analyzed using a stratified proportional hazards model. The study confirmed excessive rates of lung cancer among men with radiographic asbestosis. Comparison of study arms revealed a strong, unanticipated synergy between radiographic profusion category and the active intervention. In the large subgroup of men with normal lung parenchyma on chest radiograph at baseline, there was evidence of exposure-related lung cancer risk: Men with more than 40 years' exposure in high-risk trades had a risk approximately fivefold higher than men with 5-10 years, after adjustment for covariates. The effect in these men was independent of study intervention arm, but pleural plaques on the baseline radiograph and abnormal baseline flow rate were strong independent predictors of subsequent lung cancer. Residual confounding by subclinical asbestosis, exposure to unmeasured lung carcinogens, or differences in smoking are unlikely to explain these observations better than a carcinogenic effect of asbestos per se. [ABSTRACT FROM AUTHOR]

Introduction: Air 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., Methods: We 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 < 18 years), adults (age ≥ 18 years), and all age groups exposed to criteria pollutants established by the US Environmental Protection Agency National Ambient Air Quality Standards and over 10 trace metals. Using databases, such as PubMed, MEDLINE, Web of Science Core Collection, and Google Scholar, we identified 579 relevant articles. After rigorous screening and quality assessment using the Newcastle-Ottawa Scale, 50 high-quality studies were included. We converted various reported outcomes (e.g., odds ratios, relative risk, and percent increase) to a standardized odds ratio (OR) for comparability and performed meta-analyses using R 4.4.0 and related packages, ensuring the robustness of our findings., Results: Our meta-analysis indicated significant associations between air pollutants and respiratory outcomes. For particulate matter with diameter ≤ 2.5 μm (PM 2.5 ), the overall ORs for children, adults, and combined age groups were 1.31, 1.10, and 1.26, respectively, indicating a consistent positive association. Similar positive associations were observed for particulate matter with diameter ≤ 10 μm (PM 10 ) and other pollutants, with children showing higher susceptibility than adults. The analysis of trace metals also showed significant associations; however, these findings require cautious interpretation due to the small number of studies., Conclusion: Our study supports associations between air pollutants, including non-exhaust trace metals, and respiratory outcomes across different age groups. The findings underscore the need for stringent environmental health policies and further research, especially in regions with higher pollution levels. The future studies should consider long-term and short-term exposures separately and include diverse populations to improve the accuracy and generalizability of the results., Competing Interests: MB is a Propeller Health and ResMed employee and receives salary and stock. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision., (Copyright © 2024 Su, Aslebagh, Shahriary, Barrett and Balmes.)

Background: Primary graft dysfunction (PGD) contributes substantially to both short- and long-term mortality after lung transplantation, but the mechanisms that lead to PGD are not well understood. Exposure to ambient air pollutants is associated with adverse events during waitlisting for lung transplantation and chronic lung allograft dysfunction, but its association with PGD has not been studied. We hypothesized that long-term exposure of the lung donor and recipient to high levels of ambient air pollutants would increase the risk of PGD in lung transplant recipients., Methods: Using data from 1428 lung transplant recipients and their donors enrolled in the Lung Transplant Outcomes Group observational cohort study, we evaluated the association between the development of PGD and zip-code-based estimates of long-term exposure to 6 major air pollutants (ozone, nitrogen dioxide, sulfur dioxide, carbon monoxide, particulate matter 2.5, and particulate matter 10) in both the lung donor and the lung recipient. Exposure estimates used daily EPA air pollutant monitoring data and were based on the geographic centroid of each subject's residential zip code. Associations were tested in both univariable and multivariable models controlling for known PGD risk factors., Results: We did not find strong associations between air pollutant exposures in either the donor or the recipient and PGD., Conclusions: Exposure to ambient air pollutants, at the levels observed in this study, may not be sufficiently harmful to prime the donor lung or the recipient to develop PGD, particularly when considering the robust associations with other established PGD risk factors., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

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., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier Ltd.)

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.

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 (NO 2 ), sulfur dioxide (SO 2 ), carbon monoxide (CO), particulate matter < 2.5 μm (PM 2.5 ), and PM < 10 μm (PM 10 ) using weighted averages of daily levels from monitors within 50 km of subjects' residences. Subjects were followed for 6 days for ARDS by the Berlin Criteria. The association between each pollutant and ARDS was determined using multivariable logistic regression adjusting for preselected confounders. In 764 subjects, we measured plasma concentrations of inflammatory proteins at presentation and tested for an association between pollutant exposure and protein concentration via linear regression., Results: ARDS developed in 754 (41%) subjects. Short- and long-term exposures to SO 2 , NO 2 , and PM 2.5 were associated with ARDS risk (SO 2 : odds ratio (OR) for the comparison of the 75-25th long-term exposure percentile 1.43 (95% confidence interval (CI) 1.16, 1.77); p < 0.01; NO 2 : 1.36 (1.06, 1.74); p = 0.04, PM 2.5 : 1.21 (1.04, 1.41); p = 0.03). Long-term exposures to these three pollutants were also associated with plasma interleukin-1 receptor antagonist and soluble tumor necrosis factor receptor-1 concentrations., Conclusion: Short and long-term exposures to ambient SO 2 , PM 2.5 , and NO 2 are associated with increased ARDS risk in sepsis, representing potentially modifiable environmental risk factors for sepsis-associated ARDS., (© 2023. Springer-Verlag GmbH Germany, part of Springer Nature.)

As fossil fuel combustion continues to power the global economy, the rate of climate change is accelerating, causing severe respiratory health impacts and large disparities in the degree of human suffering. Hotter and drier climates lead to longer and more severe wildland fire seasons, impairing air quality around the globe. Hotter temperatures lead to higher amounts of ozone and particles, causing the exacerbation of chronic respiratory diseases and premature mortality. Longer pollen seasons and higher pollen concentrations provoke allergic airway diseases. In arid regions, accelerated land degradation and desertification are promoting dust pollution and impairing food production and nutritional content that are essential to respiratory health. Extreme weather events and flooding impede healthcare delivery and can lead to poor indoor air quality due to mold overgrowth. Climate and human activities that harm the environment and ecosystem may also affect the emergence and spread of viral infections, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and associated morbidity and mortality exacerbated by air pollution. Children and elderly individuals are more susceptible to the adverse health effects of climate change. Geographical and socioeconomic circumstances, together with a decreased capacity to adapt, collectively increase vulnerability to the adverse effects of climate change. Successful mitigation of anthropogenic climate change is dependent on the commitment of energy-intensive nations to manage greenhouse gas emissions, as well as societal support and response to aggravating factors. In this review, we focus on the respiratory health impacts of global climate change, with an emphasis on susceptible and vulnerable populations and low- and middle-income countries.

Background: Evidence 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., Objectives: We 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., Methods: Our 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 (PM 2.5 ) and ozone (O 3 ) 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 (FEV 1 ), adjusted for covariates., Results: PM 2.5 exposure during the prenatal period and the first 3-years of life was associated with lower FVC and FEV 1 assessed at ages 6-9. Specifically, an increase from the 5th percentile of the observed monthly average exposure (7.55 μg/m 3 ) to the median observed exposure (12.69 μg/m 3 ) 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 FEV 1 (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., Conclusions: Our findings indicate that prenatal and early-life exposures to PM 2.5 are associated with decreased lung function later in childhood. Exposures during the latter months of pregnancy may be especially influential., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Andreas Neophytou reports financial support was provided by National Institute of Environmental Health Sciences. John R. Balmes, Liza Lutzker, Stephanie Holm, Elizabeth M. Noth, Sadie Costello, Tim Tyner, Ellen Eisen, Kari C. Nadeau, S Katharine Hammond reports financial support was provided by National Institute of Environmental Health Sciences. John R. Balmes reports a relationship with California Air Resources Board that includes: board membership., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Background: Because fine particulate matter [PM, with aerodynamic diameter ≤ 2.5 μ m ( PM 2.5 )] is a ubiquitous environmental exposure, small changes in cognition associated with PM 2.5 exposure could have great societal costs. Prior studies have demonstrated a relationship between in utero PM 2.5 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., Objectives: In this study, we tested for associations between prenatal PM 2.5 exposure and both full-scale and subscale measures of IQ among a longitudinal cohort at age 10.5 y., Methods: This 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 PM 2.5 surfaces. IQ testing was performed by bilingual psychometricians in the dominant language of the child., Results: A 3 - μ g / m 3 higher average PM 2.5 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]., Discussion: We found that small increases in outdoor PM 2.5 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 PM 2.5 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.

Rationale: Wildfires are a significant cause of exposure to ambient air pollution in the United States and other settings. Although indoor air pollution is a known contributor to tuberculosis reactivation and progression, it is unclear whether ambient pollution exposures, including wildfire smoke, similarly increase risk. Objectives: To determine whether tuberculosis diagnosis was associated with recent exposure to acute outdoor air pollution events, including those caused by wildfire smoke. Methods: We conducted a case-crossover analysis of 6,238 patients aged ⩾15 years diagnosed with active tuberculosis disease between 2014 and 2019 in 8 California counties. Using geocoded address data, we characterized individuals' daily exposure to <2.5 μm-diameter particulate matter (PM 2.5 ) during counterfactual risk periods 3-6 months before tuberculosis diagnosis (hazard period) and the same time 1 year previously (control period). We compared the frequency of residential PM 2.5 exposures exceeding 35 μg/m 3 (PM 2.5 events) overall and for wildfire-associated and nonwildfire events during individuals' hazard and control periods. Measurements and Main Results: In total, 3,139 patients experienced 1 or more PM 2.5 events during the hazard period, including 671 experiencing 1 or more wildfire-associated events. Adjusted odds of tuberculosis diagnosis increased by 5% (95% confidence interval, 3-6%) with each PM 2.5 event experienced over the 6-month observation period. Each wildfire-associated PM 2.5 event was associated with 23% (19-28%) higher odds of tuberculosis diagnosis in this time window, whereas no association was apparent for nonwildfire-associated events. Conclusions: Residential exposure to wildfire-associated ambient air pollution is associated with an increased risk of active tuberculosis diagnosis.

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.

Background: Exposure to ozone (O 3 ) is associated with increased risk of exacerbations of asthma, but the underlying mechanisms are not well studied., Objective: We sought to determine whether O 3 exposure would enhance airway inflammatory responses to allergen and the GSTM1-null genotype would modulate this enhancement., Methods: In a crossover design, 10 asthmatic participants (5 with GSTM1-null genotype) who had specific sensitization to Dermatophagoides pteronyssinus (DP) were exposed to 160 ppb O 3 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, O 3 -NS, FA-DP, O 3 -DP). Effect modification by GSTM1 genotype was assessed in stratified regressions., Results: BAL 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 T H 2 cytokines IL-4, IL-5, IL-10, and IL-13 ( P < .03 for all comparisons). O 3 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 O 3 exposure., Conclusions: While O 3 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., Competing Interests: Disclosure of potential conflict of interest: The authors declare that they have no relevant conflicts of interest.

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 PM 2.5 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 PM 2.5 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 PM 2.5 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 PM 2.5 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.

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 (PM 2.5 ). We obtained individual address data on SARS-CoV-2 infections and COVID-19 deaths and assigned 2000-2018 1km-1km gridded PM 2.5 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 PM 2.5 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 PM 2.5 exposure. Those living in the areas of highest long-term PM 2.5 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 PM 2.5 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., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2022 The Authors. Published by Elsevier Ltd.)

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.

Background: Previous research has revealed links between air pollution exposure and metabolic syndrome in adults; however, these associations are less explored in children., Objective: This 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., Methods: We conducted cross-sectional analyses in a sample of predominantly Latinx, low-income children (n = 218) to examine associations between air pollutants (nitrogen dioxide (NO 2 ), nitrogen oxides (NO x ), elemental carbon, polycyclic aromatic hydrocarbons, carbon monoxide (CO), fine particulates (PM 2.5 )) 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))., Results: HDL cholesterol showed an inverse association with NO 2 and NO x , with the strongest relationship between HDL and 3-month exposure to NO 2 (-15.4 mg/dL per IQR increase in 3-month NO 2 , 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., Conclusion: Our 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., (© 2021. The Author(s).)

Background: The cardiovascular effects of ozone exposure are unclear. Using measurements from the 87 participants in the Multicenter Ozone Study of oldEr Subjects (MOSES), we examined whether personal and ambient pollutant exposures before the controlled exposure sessions would be associated with adverse changes in pulmonary and cardiovascular function., Methods: We used mixed effects linear regression to evaluate associations between increased personal exposures and ambient pollutant concentrations in the 96 h before the pre-exposure visit, and 1) biomarkers measured at pre-exposure, and 2) changes in biomarkers from pre-to post-exposure., Results: Decreases in pre-exposure forced expiratory volume in 1 s (FEV 1 ) were associated with interquartile-range increases in concentrations of particulate matter ≤2.5 μm (PM 2.5 ) 1 h before the pre-exposure visit (-0.022 L; 95% CI -0.037 to -0.006; p = 0.007), carbon monoxide (CO) in the prior 3 h (-0.046 L; 95% CI -0.076 to -0.016; p = 0.003), and nitrogen dioxide (NO 2 ) in the prior 72 h (-0.030 L; 95% CI -0.052 to -0.008; p = 0.007). From pre-to post-exposure, increases in FEV 1 were marginally significantly associated with increases in personal ozone exposure (0.010 L; 95% CI 0.004 to 0.026; p = 0.010), and ambient PM 2.5 and CO at all lag times. Ambient ozone concentrations in the prior 96 h were associated with both decreased pre-exposure high frequency (HF) heart rate variability (HRV) and increases in HF HRV from pre-to post-exposure., Conclusions: We observed associations between increased ambient PM 2.5 , NO 2 , and CO levels and reduced pulmonary function, and increased ambient ozone concentrations and reduced HRV. Pulmonary function and HRV increased across the exposure sessions in association with these same pollutant increases, suggesting a "recovery" during the exposure sessions. These findings support an association between short term increases in ambient PM 2.5 , NO 2 , and CO and decreased pulmonary function, and increased ambient ozone and decreased HRV., (Copyright © 2021. Published by Elsevier Inc.)

Background: Ozone 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 Question: What has been learned about the association between ozone exposures and lung function from epidemiology studies published from 2013 through 2020?, Study Design and Methods: On 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 FEV 1 OR 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., Results: Of 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., Interpretation: Much 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., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)