Recent and forecasted increases in coccidioidomycosis incidence in California linked to hydroclimatic swings.

Coccidioidomycosis, or Valley fever, is an infectious disease caused by inhalation of Coccidioides spp., fungi found primarily in soils of the southwestern United States. Prior work showed that coccidioidomycosis cases in California sharply increase by nearly 2-fold following wet winters that occur one- and two-years following drought. Statewide drought between 2020-2022 followed by heavy precipitation during the 2022-2023 winter raised concerns over potential increases in coccidioidomycosis cases in the fall of 2023, prompting California Department of Public Health (CDPH) to issue public health alerts. As anticipated, California saw a near record number of cases in 2023, with 9,054 provisional cases reported. During the 2023-2024 California wet season, precipitation was 115% the long-term average, furthering concerns about continued high coccidioidomycosis risk. We developed an ensemble model to forecast coccidioidomycosis cases in California in 2024-2025. Using this model, we predicted a total of 11,846 cases (90% PI: 10,056-14,094) in California between April 1, 2023, and March 31, 2024, encompassing the preliminary state report of 10,593. Our model forecasted 12,244 cases statewide between April 1, 2024, and March 31, 2025 - a 62% increase over the cases reported during the same period two years prior, and on par with the high incidence seen in 2023. The Southern San Joaquin Valley (5,398 cases, 90% PI: 4,556-6,442), Southern Coast (3,322, 90% PI: 2,694-3,961), and Central Coast (1,207 cases, 90% PI: 867-1,585) regions are expected to see the largest number of infections. Our model forecasts that disease incidence will exhibit pronounced seasonality, particularly in endemic regions, with cases rising in June and peaking in November at 1,411 (90% PI: 815-2,172) cases statewide - 98% higher than the peak two years prior (714) and nearly as high as the peak in 2023 (1,462). Near-term forecasts have the potential to inform public health messaging to enhance provider and patient awareness, encourage risk reduction practices, and improve recognition and management of coccidioidomycosis.

Examining air pollution exposure dynamics in disadvantaged communities through high-resolution mapping.

This study bridges gaps in air pollution research by examining exposure dynamics in disadvantaged communities. Using cutting-edge machine learning and massive data processing, we produced high-resolution (100 meters) daily air pollution maps for nitrogen dioxide (NO2), fine particulate matter (PM2.5), and ozone (O3) across California for 2012-2019. Our findings revealed opposite spatial patterns of NO2 and PM2.5 to that of O3. We also identified consistent, higher pollutant exposure for disadvantaged communities from 2012 to 2019, although the most disadvantaged communities saw the largest NO2 and PM2.5 reductions and the advantaged neighborhoods experienced greatest rising O3 concentrations. Further, day-to-day exposure variations decreased for NO2 and O3. The disparity in NO2 exposure decreased, while it persisted for O3. In addition, PM2.5 showed increased day-to-day variations across all communities due to the increase in wildfire frequency and intensity, particularly affecting advantaged suburban and rural communities.

Wildfires and Human Health.

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.

Long-term air pollution exposure and the risk of primary graft dysfunction after lung transplantation.

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.

Health effects of air pollution on respiratory symptoms: A longitudinal study using digital health sensors.

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.

Household Air Pollution Interventions to Improve Health in Low- and Middle-Income Countries: An Official American Thoracic Society Research Statement.

Background: An estimated 3 billion people, largely in low- and middle-income countries, rely on unclean fuels for cooking, heating, and lighting to meet household energy needs. The resulting exposure to household air pollution (HAP) is a leading cause of pneumonia, chronic lung disease, and other adverse health effects. In the last decade, randomized controlled trials of clean cooking interventions to reduce HAP have been conducted. We aim to provide guidance on how to interpret the findings of these trials and how they should inform policy makers and practitioners.Methods: We assembled a multidisciplinary working group of international researchers, public health practitioners, and policymakers with expertise in household air pollution from within academia, the American Thoracic Society, funders, nongovernmental organizations, and global organizations, including the World Bank and the World Health Organization. We performed a literature search, convened four sessions via web conference, and developed consensus conclusions and recommendations via the Delphi method.Results: The committee reached consensus on 14 conclusions and recommendations. Although some trials using cleaner-burning biomass stoves or cleaner-cooking fuels have reduced HAP exposure, the committee was divided (with 55% saying no and 45% saying yes) on whether the studied interventions improved measured health outcomes.Conclusions: HAP is associated with adverse health effects in observational studies. However, it remains unclear which household energy interventions reduce exposure, improve health, can be scaled, and are sustainable. Researchers should engage with policy makers and practitioners working to scale cleaner energy solutions to understand and address their information needs.

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

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

Diesel exhaust and respiratory dust exposure in miners and chronic obstructive pulmonary disease (COPD) mortality in DEMS II.

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.

Biomass smoke exposure and somatic growth among children: The RESPIRE and CRECER prospective cohort studies in rural Guatemala.

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.

Exposure to ambient air pollutants and acute respiratory distress syndrome risk in sepsis.

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 < 2.5 µm (PM2.5), and PM < 10 µm (PM10) 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 SO2, NO2, and PM2.5 were associated with ARDS risk (SO2: 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; NO2: 1.36 (1.06, 1.74); p = 0.04, PM2.5: 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 SO2, PM2.5, and NO2 are associated with increased ARDS risk in sepsis, representing potentially modifiable environmental risk factors for sepsis-associated ARDS.

Impact of Global Climate Change on Pulmonary Health: Susceptible and Vulnerable Populations.

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.

Race and Ethnicity in Pulmonary Function Test Interpretation: An Official American Thoracic Society Statement.

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.

Cognitive Development and Prenatal Air Pollution Exposure in the CHAMACOS Cohort.

BACKGROUND: Because 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. OBJECTIVES: In 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. 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 PM2.5 surfaces. IQ testing was performed by bilingual psychometricians in the dominant language of the child. RESULTS: A 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]. DISCUSSION: We 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.