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1.
Artigo em Inglês | MEDLINE | ID: mdl-34417545

RESUMO

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 (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)). RESULTS: HDL 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. 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.

2.
Chest ; 2021 Aug 10.
Artigo em Inglês | MEDLINE | ID: mdl-34389296

RESUMO

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 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. 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.

5.
Ann Am Thorac Soc ; 18(6): 921-930, 2021 06.
Artigo em Inglês | MEDLINE | ID: mdl-33938390

RESUMO

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.


Assuntos
Poluição do Ar , Incêndios , Incêndios Florestais , Adulto , Criança , Humanos , Políticas , Fumaça/efeitos adversos , Estados Unidos/epidemiologia
6.
J Expo Sci Environ Epidemiol ; 31(3): 503-513, 2021 05.
Artigo em Inglês | MEDLINE | ID: mdl-33859340

RESUMO

BACKGROUND: Preterm 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. OBJECTIVE: We 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. METHODS: We 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. RESULTS: Our 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. SIGNIFICANCE: These 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.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Nascimento Prematuro , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , California/epidemiologia , Feminino , Humanos , Recém-Nascido , Exposição Materna/efeitos adversos , Material Particulado/efeitos adversos , Material Particulado/análise , Gravidez , Nascimento Prematuro/induzido quimicamente , Nascimento Prematuro/epidemiologia , Estudos Retrospectivos , Fatores Socioeconômicos
7.
JAMA Dermatol ; 157(6): 658-666, 2021 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-33881450

RESUMO

Importance: Air pollution is a worldwide public health issue that has been exacerbated by recent wildfires, but the relationship between wildfire-associated air pollution and inflammatory skin diseases is unknown. Objective: To assess the associations between wildfire-associated air pollution and clinic visits for atopic dermatitis (AD) or itch and prescribed medications for AD management. Design, Setting, and Participants: This cross-sectional time-series study assessed the associations of air pollution resulting from the California Camp Fire in November 2018 and 8049 dermatology clinic visits (4147 patients) at an academic tertiary care hospital system in San Francisco, 175 miles from the wildfire source. Participants included pediatric and adult patients with AD or itch from before, during, and after the time of the fire (October 2018 through February 2019), compared with those with visits in the same time frame of 2015 and 2016, when no large wildfires were near San Francisco. Data analysis was conducted from November 1, 2019, to May 30, 2020. Exposures: Wildfire-associated air pollution was characterized using 3 metrics: fire status, concentration of particulate matter less than 2.5 µm in diameter (PM2.5), and satellite-based smoke plume density scores. Main Outcomes and Measures: Weekly clinic visit counts for AD or itch were the primary outcomes. Secondary outcomes were weekly numbers of topical and systemic medications prescribed for AD in adults. Results: Visits corresponding to a total of 4147 patients (mean [SD] age, 44.6 [21.1] years; 2322 [56%] female) were analyzed. The rates of visits for AD during the Camp Fire for pediatric patients were 1.49 (95% CI, 1.07-2.07) and for adult patients were 1.15 (95% CI, 1.02-1.30) times the rate for nonfire weeks at lag 0, adjusted for temperature, relative humidity, patient age, and total patient volume at the clinics for pediatric patients. The adjusted rate ratios for itch clinic visits during the wildfire weeks were 1.82 (95% CI, 1.20-2.78) for the pediatric patients and 1.29 (95% CI, 0.96-1.75) for adult patients. A 10-µg/m3 increase in weekly mean PM2.5 concentration was associated with a 7.7% (95% CI, 1.9%-13.7%) increase in weekly pediatric itch clinic visits. The adjusted rate ratio for prescribed systemic medications in adults during the Camp Fire at lag 0 was 1.45 (95% CI, 1.03-2.05). Conclusions and Relevance: This cross-sectional study found that short-term exposure to air pollution due to the wildfire was associated with increased health care use for patients with AD and itch. These results may provide a better understanding of the association between poor air quality and skin health and guide health care professionals' counseling of patients with skin disease and public health practice.

8.
Emerg Infect Dis ; 27(5): 1266-1273, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33755007

RESUMO

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.


Assuntos
COVID-19 , Coccidioidomicose , Coinfecção , Idoso , Coccidioidomicose/epidemiologia , Grupos Étnicos , Humanos , Grupos Minoritários , Pandemias , SARS-CoV-2 , Estados Unidos/epidemiologia
9.
Sci Rep ; 11(1): 4067, 2021 02 18.
Artigo em Inglês | MEDLINE | ID: mdl-33603036

RESUMO

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 < 0.0001). Both B cells (est = - 0.19) and CD4+ cells (est = 0.16) were associated with 1 day NO2 exposure (P ≤ 0.031), whereas CD4+ and CD8+ cells were associated with chronic exposure to PAH456, NOx and/or NO2 (P ≤ 0.038 for all). Finally, diastolic BP (DBP) was inversely associated with long-term exposures to both CO and PAH456, and both systolic and pulse pressure were associated with short-term NO2 and chronic NOx exposure. Our findings demonstrate links between air pollution exposure and methylation of immunoregulatory genes, immune cell profiles and blood pressure, suggesting that even at a young age, the immune and cardiovascular systems are negatively impacted by exposure to air pollution.

10.
Environ Res ; 195: 110870, 2021 04.
Artigo em Inglês | MEDLINE | ID: mdl-33587949

RESUMO

BACKGROUND: Metabolic 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. OBJECTIVES: To 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. METHODS: We 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. RESULTS: The 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. DISCUSSION: Our 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.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Adulto , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Pressão Sanguínea , Criança , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Feminino , Glucose , Humanos , Masculino , Estresse Oxidativo , Material Particulado/análise , Material Particulado/toxicidade
11.
J Expo Sci Environ Epidemiol ; 31(1): 1-20, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-32952154

RESUMO

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.


Assuntos
Poluição do Ar , Incêndios Florestais , Criança , Exposição Ambiental , Humanos , Saúde Pública , Fumaça/efeitos adversos
12.
Sci Total Environ ; 760: 144296, 2021 Mar 15.
Artigo em Inglês | MEDLINE | ID: mdl-33341613

RESUMO

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.


Assuntos
COVID-19 , Coronavirus , Bombeiros , Humanos , SARS-CoV-2 , Fumaça/efeitos adversos
13.
J Am Coll Cardiol ; 76(24): 2878-2894, 2020 12 15.
Artigo em Inglês | MEDLINE | ID: mdl-33303078

RESUMO

Fine particulate air pollution <2.5 µm in diameter (PM2.5) is a major environmental threat to global public health. Multiple national and international medical and governmental organizations have recognized PM2.5 as a risk factor for cardiopulmonary diseases. A growing body of evidence indicates that several personal-level approaches that reduce exposures to PM2.5 can lead to improvements in health endpoints. Novel and forward-thinking strategies including randomized clinical trials are important to validate key aspects (e.g., feasibility, efficacy, health benefits, risks, burden, costs) of the various protective interventions, in particular among real-world susceptible and vulnerable populations. This paper summarizes the discussions and conclusions from an expert workshop, Reducing the Cardiopulmonary Impact of Particulate Matter Air Pollution in High Risk Populations, held on May 29 to 30, 2019, and convened by the National Institutes of Health, the U.S. Environmental Protection Agency, and the U.S. Centers for Disease Control and Prevention.


Assuntos
Poluição do Ar/efeitos adversos , Cardiopatias/prevenção & controle , Pneumopatias/prevenção & controle , Material Particulado/efeitos adversos , Ensaios Clínicos como Assunto , Educação , Cardiopatias/etiologia , Humanos , Pneumopatias/etiologia
14.
Clin Chest Med ; 41(4): 771-776, 2020 12.
Artigo em Inglês | MEDLINE | ID: mdl-33153694

RESUMO

Catastrophic wildfires are increasing around the globe as climate change continues to progress. Another risk factor for large wildfires in the western United States is a legacy of fire suppression that has allowed overgrowth of underbrush and small trees in forests where periodic lightning-sparked wildfires are part of the natural ecosystem. Wildfire smoke contains CO2, CO, NOx, particulate matter, complex hydrocarbons (including polycyclic aromatic hydrocarbons), and irritant gases, including many of the same toxic and carcinogenic substances as cigarette smoke. The public need clear and consistent messaging to understand that wildland fire smoke poses a health risk.


Assuntos
Saúde Pública/normas , Incêndios Florestais/estatística & dados numéricos , Humanos
15.
Circulation ; 142(23): e432-e447, 2020 12 08.
Artigo em Inglês | MEDLINE | ID: mdl-33147996

RESUMO

In 2010, the American Heart Association published a statement concluding that the existing scientific evidence was consistent with a causal relationship between exposure to fine particulate matter and cardiovascular morbidity and mortality, and that fine particulate matter exposure is a modifiable cardiovascular risk factor. Since the publication of that statement, evidence linking air pollution exposure to cardiovascular health has continued to accumulate and the biological processes underlying these effects have become better understood. This increasingly persuasive evidence necessitates policies to reduce harmful exposures and the need to act even as the scientific evidence base continues to evolve. Policy options to mitigate the adverse health impacts of air pollutants must include the reduction of emissions through action on air quality, vehicle emissions, and renewable portfolio standards, taking into account racial, ethnic, and economic inequality in air pollutant exposure. Policy interventions to improve air quality can also be in alignment with policies that benefit community and transportation infrastructure, sustainable food systems, reduction in climate forcing agents, and reduction in wildfires. The health care sector has a leadership role in adopting policies to contribute to improved environmental air quality as well. There is also potentially significant private sector leadership and industry innovation occurring in the absence of and in addition to public policy action, demonstrating the important role of public-private partnerships. In addition to supporting education and research in this area, the American Heart Association has an important leadership role to encourage and support public policies, private sector innovation, and public-private partnerships to reduce the adverse impact of air pollution on current and future cardiovascular health in the United States.


Assuntos
Poluição do Ar/efeitos adversos , Poluição do Ar/prevenção & controle , American Heart Association , Doenças Cardiovasculares/prevenção & controle , Guias de Prática Clínica como Assunto/normas , Política Pública , Poluentes Atmosféricos/efeitos adversos , Doenças Cardiovasculares/epidemiologia , Disparidades em Assistência à Saúde , Humanos , Material Particulado/efeitos adversos , Estados Unidos/epidemiologia
16.
Artigo em Inglês | MEDLINE | ID: mdl-33167314

RESUMO

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 <2.5 µm in diameter (PM2.5) concentration from 16 ground-level monitoring stations in the San Francisco Bay Area and smoke plume density from satellite imagery for the 2017-2018 California wildfire seasons. We tested for trends and calculated bootstrapped differences in the median PM2.5 concentrations by plume density category on a 0-3 scale. The median PM2.5 concentrations for categories 0, 1, 2, and 3 were 16, 22, 25, and 63 µg/m3, respectively, and there was much variability in PM2.5 concentrations within each category. A case study of the Camp Fire illustrates that in San Francisco, PM2.5 concentrations reached their maximum many days after the peak for plume density scores. We found that air pollution characterization by satellite imagery did not precisely align with ground-level PM2.5 concentrations. Public health practitioners should recognize the need to combine multiple sources of data regarding smoke patterns when developing public guidance to limit the health effects of wildfire smoke.


Assuntos
Poluentes Atmosféricos/análise , Poluição do Ar/estatística & dados numéricos , Monitoramento Ambiental , Incêndios Florestais , Poluição do Ar/análise , Humanos , Material Particulado/análise , São Francisco , Fumaça/análise , Astronave
17.
Glob Heart ; 15(1): 11, 2020 02 07.
Artigo em Inglês | MEDLINE | ID: mdl-32489784

RESUMO

Background: Exposure to household air pollution (HAP) from cooking with biomass fuel affects billions of people. We hypothesized that HAP from woodsmoke, compared to other household fuels, was associated with adverse cardiovascular outcomes, of which there have been few studies. Methods: A cross-sectional study was completed in 299 females aged 40-70 years in Kaski District, Nepal, during 2017-18. All participants underwent a standard 12-lead ECG, ankle and brachial systolic blood pressure measurement, and 2D color and Doppler echocardiography. Current stove type was confirmed by inspection. Blood pressure, height, and weight were measured using a standardized protocol. Hypertension was defined as ≥140/90 mmHg or prior diagnosis. Hemoglobin A1c (HbA1c) was obtained, with diabetes mellitus defined as a prior diagnosis or HbA1C ≥ 6.5%. We used adjusted linear and logistic multivariable regressions to examine the relationship of stove type with cardiac structure and function. Results: The majority of women primarily used liquified petroleum gas (LPG) stoves (65%), while 12% used biogas, and 23% used wood-burning cook-stoves. Prevalence of major cardiovascular risk factors was 35% with hypertension, 19% with diabetes mellitus, and 15% current smokers. After adjustment, compared to LPG, wood stove use was associated with increased indexed left atrial volume (ß = 3.15, 95% CI 1.22 to 5.09) and increased indexed left ventricular end diastolic volume (ß = 7.97, 95% CI 3.11 to 12.83). There was no association between stove type and systemic hypertension, left ventricular mass, systolic dysfunction, diastolic dysfunction, pulmonary hypertension, abnormal ankle-brachial index, or clinically significant ECG abnormalities. Conclusion: Biomass fuel use was associated with increased indexed left atrial volume and increased indexed left ventricular diastolic volume in Nepali women, suggesting subclinical adverse cardiac remodeling from HAP in this cross-sectional study. We did not find evidence of an association with hypertension or typical cardiac sequelae of hypertension. Future studies to confirm these results are needed.


Assuntos
Poluição do Ar/efeitos adversos , Biomassa , Cardiopatias/fisiopatologia , População Rural , Função Ventricular/fisiologia , Adulto , Idoso , Estudos Transversais , Ecocardiografia , Eletrocardiografia , Feminino , Cardiopatias/diagnóstico , Cardiopatias/epidemiologia , Humanos , Masculino , Pessoa de Meia-Idade , Morbidade/tendências , Nepal/epidemiologia , Fatores de Risco
18.
Environ Int ; 141: 105780, 2020 08.
Artigo em Inglês | MEDLINE | ID: mdl-32417614

RESUMO

RATIONALE: Chronic air pollutant exposure has been associated with development of Acute Respiratory Distress Syndrome (ARDS) in patients at risk, particularly from severe trauma. We recently reported that shorter peripheral blood leukocyte (PBL) telomere length (TL) was associated with worse outcomes and higher severity of ARDS in critically ill patients. Since most major air pollutants are potent oxidants that can induce cellular oxidative stress, and oxidative stress can accelerate telomere shortening, we hypothesized that higher levels of chronic air pollutant exposure would be associated with shorter telomere length in critically ill patients including patients with ARDS. METHODS: PBL-TL was measured in genomic DNA collected on the morning of ICU day 2 in 772 critically ill patients enrolled in a prospective observational study. Exposures to air pollutants including ozone (warm-season only), particulate matter < 2.5 µm (PM2.5), particulate matter < 10 µm (PM10), CO, NO2 and SO2, were estimated by weighted average of daily levels from all monitors within 50 km of each patient's residential address for the 3 years prior to admission. Associations of each air pollutant exposure and PBL-TL were investigated by multivariable linear regression models adjusting for age, ethnicity, sex, smoking history, alcohol abuse, insurance status, median household income, history of malignancy and APACHE II. RESULTS: Contrary to our hypothesis, TL increased across exposure quartiles in both ozone and PM2.5 analyses (p < 0.05). In a regression model controlling for potential confounders, long term ozone exposure was significantly associated with an increase in TL in the entire cohort (0.31 kb per 10 ppb), as well as in subgroups with sepsis, trauma and ARDS (all p < 0.05). In multivariable models, entire-year exposure to PM2.5, PM10, CO, NO2 and SO2 was not associated with TL after adjustment for potential confounders. In an analysis restricted to warm-season levels to assess the effect of seasonality, higher warm-season PM2.5 and CO exposures were independently associated with longer TL. CONCLUSIONS: Long-term exposure to ozone is associated with longer peripheral blood TL in critically ill patients. Further studies are needed to investigate the potential underlying mechanisms for this unexpected positive association between telomere length and air pollution exposure in critical illness.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Ozônio , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Estado Terminal , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Humanos , Ozônio/análise , Ozônio/toxicidade , Material Particulado/análise , Telômero
19.
Ann Am Thorac Soc ; 17(4): 387-398, 2020 04.
Artigo em Inglês | MEDLINE | ID: mdl-32233861

RESUMO

Although it is well accepted that air pollution exposure exacerbates preexisting airway disease, it has not been firmly established that long-term pollution exposure increases the risk of new-onset asthma or chronic obstruction pulmonary disease (COPD). This Workshop brought together experts on mechanistic, epidemiological, and clinical aspects of airway disease to review current knowledge regarding whether air pollution is a causal factor in the development of asthma and/or COPD. Speakers presented recent evidence in their respective areas of expertise related to air pollution and new airway disease incidence, followed by interactive discussions. A writing committee summarized their collective findings. The Epidemiology Group found that long-term exposure to air pollution, especially metrics of traffic-related air pollution such as nitrogen dioxide and black carbon, is associated with onset of childhood asthma. However, the evidence for a causal role in adult-onset asthma or COPD remains insufficient. The Mechanistic Group concluded that air pollution exposure can cause airway remodeling, which can lead to asthma or COPD, as well as asthma-like phenotypes that worsen with long-term exposure to air pollution, especially fine particulate matter and ozone. The Clinical Group concluded that air pollution is a plausible contributor to the onset of both asthma and COPD. Available evidence indicates that long-term exposure to air pollution is a cause of childhood asthma, but the evidence for a similar determination for adult asthma or COPD remains insufficient. Further research is needed to elucidate the exact biological mechanism underlying incident childhood asthma, and the specific air pollutant that causes it.


Assuntos
Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Asma/etiologia , Doença Pulmonar Obstrutiva Crônica/etiologia , Adulto , Fatores Etários , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Asma/fisiopatologia , Causalidade , Criança , Exposição Ambiental/efeitos adversos , Humanos , Ozônio/toxicidade , Material Particulado/análise , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Sociedades Médicas , Poluição Relacionada com o Tráfego/efeitos adversos , Estados Unidos
20.
Ann Am Thorac Soc ; 17(5): 563-572, 2020 05.
Artigo em Inglês | MEDLINE | ID: mdl-32125874

RESUMO

Rationale: In a previous trial (MOSES [Multicenter Ozone Study of oldEr Subjects]), 3 hours of controlled ozone (O3) exposure caused concentration-related reductions in lung function with evidence of airway inflammation and injury, but without convincing evidence of effects on cardiovascular function. However, the subjects' exposures to indoor and outdoor air pollution in the hours and days before each controlled O3 exposure may have modified biomarker responses to the controlled O3 exposures.Objectives: We sought to determine whether personal measures of nitrogen dioxide (NO2) and O3, or ambient concentrations of O3, particulate matter ≤2.5 µm in aerodynamic diameter, NO2, carbon monoxide (CO), and sulfur dioxide (SO2) in the 72 and 96 hours before the exposure visit modified biomarker responses to controlled O3 exposure.Methods: MOSES subjects were exposed for 3 hours in random order to clean air containing 0 ppb O3, 70 ppb O3, or 120 ppm O3, alternating 15 minutes of moderate exercise with 15 minutes of rest. Cardiovascular and pulmonary endpoints (biomarkers of autonomic function, repolarization, ST segment change, arrhythmia, prothrombotic vascular status, systemic inflammation, vascular function, pulmonary function, oxidative stress, and lung injury) were measured on the day before, the day of, and up to 22 hours after each exposure. We evaluated whether ambient pollutant concentrations in the 96 hours before the pre-exposure visit modified pre- to post-exposure lung function biomarker responses to the controlled O3 exposures, using tertiles of passive personal exposure samplers (PES) of O3 and NO2, ambient air pollutant concentrations, and mixed effects linear regression. We also similarly explored the effect modification of controlled O3 effects on biomarkers of other MOSES outcome groups in the same way. Although we used P < 0.01 to define statistical significance, we did not formally correct for multiple comparisons.Results: The effects of MOSES controlled O3 exposures on forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) were modified by ambient NO2 and CO, and PES NO2. Reductions in FEV1 and FVC were observed only when these concentrations were in the "medium" or "high" tertile in the 72 hours before the pre-exposure visit. There was no such modification of the effect of controlled O3 exposure on any other cardiopulmonary outcome group.Conclusions: Reductions in markers of lung function, but not other pathways, by the MOSES controlled O3 exposure were modified by ambient NO2 and CO, and PES NO2, and these reductions were observed only when these pollutant concentrations were elevated in the hours and days before the pre-exposure visit.Clinical trial registered with ClinicalTrials.gov (NCT01487005).


Assuntos
Poluentes Atmosféricos/efeitos adversos , Inflamação/induzido quimicamente , Exposição por Inalação/efeitos adversos , Pulmão/fisiopatologia , Ozônio/efeitos adversos , Idoso , Biomarcadores/sangue , Feminino , Humanos , Inflamação/sangue , Modelos Lineares , Masculino , Pessoa de Meia-Idade , Dióxido de Nitrogênio/análise , Material Particulado/análise , Estudos Prospectivos , Testes de Função Respiratória
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