RESUMO
To date, no study has explored the extent to which genetic susceptibility modifies the effects of air pollutants on the risk of atrial fibrillation (AF). This study was designed to investigate the separate and joint effects of long-term exposure to air pollutants and genetic susceptibility on the risk of AF events. This study included 401,251 participants without AF at baseline from UK Biobank. We constructed a polygenic risk score and categorized it into three categories. Cox proportional hazards models were fitted to assess the separate and joint effects of long-term exposure to air pollutants and genetics on the risk of AF. Additionally, we further evaluated the effect modification of genetic susceptibility. The hazard ratios and corresponding 95% confidence intervals of incident AF for per interquartile range increase in particulate matter with an aerodynamic diameter smaller than 2.5 µm (PM2.5) or 10 µm (PM10), nitrogen dioxide (NO2), and nitrogen oxide (NOx) were 1.044 (1.025, 1.063), 1.063 (1.044, 1.083), 1.061 (1.042, 1.081), and 1.039 (1.023, 1.055), respectively. For the combined effects, participants exposed to high air pollutants levels and high genetic risk had approximately 149.2% (PM2.5), 181.7% (PM10), 170.2% (NO2), and 157.2% (NOx) higher risk of AF compared to those with low air pollutants levels and low genetic risk, respectively. Moreover, the significant additive interactions between PM10 and NO2 and genetic risk on AF risk were observed, with around 16.4% and 35.1% of AF risk could be attributable to the interactive effects. In conclusion, long-term exposure to air pollutants increases the risk of AF, particularly among individuals with high genetic susceptibility.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Fibrilação Atrial , Humanos , Fibrilação Atrial/etiologia , Fibrilação Atrial/genética , Dióxido de Nitrogênio/efeitos adversos , Dióxido de Nitrogênio/análise , Estudos Prospectivos , Predisposição Genética para Doença , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Material Particulado/efeitos adversos , Material Particulado/análise , Óxido NítricoRESUMO
BACKGROUND AND AIMS: Air pollutants are important contributors to cardiovascular diseases, but associations between long-term exposure to air pollutants and the risk of abdominal aortic aneurysm (AAA) are still unknown. METHODS: This study was conducted using a sample of 449 463 participants from the UK Biobank. Hazard ratios and 95% confidence intervals for the risk of AAA incidence associated with long-term exposure to air pollutants were estimated using the Cox proportional hazards model with time-varying exposure measurements. Additionally, the cumulative incidence of AAA was calculated by using the Fine and Grey sub-distribution hazards regression model. Furthermore, this study investigated the combined effects and interactions between air pollutants exposure and genetic predisposition in relation to the risk of AAA onset. RESULTS: Long-term exposure to particulate matter with an aerodynamic diameter <2.5â µm [PM2.5, 1.21 (1.16, 1.27)], particulate matter with an aerodynamic diameter <10â µm [PM10, 1.21 (1.16, 1.27)], nitrogen dioxide [NO2, 1.16 (1.11, 1.22)], and nitrogen oxides [NOx, 1.10 (1.05, 1.15)] was found to be associated with an elevated risk of AAA onset. The detrimental effects of air pollutants persisted even in participants with low-level exposure. For the joint associations, participants with both high levels of air pollutants exposure and high genetic risk had a higher risk of developing AAA compared with those with low concentrations of pollutants exposure and low genetic risk. The respective risk estimates for AAA incidence were 3.18 (2.46, 4.12) for PM2.5, 3.09 (2.39, 4.00) for PM10, 2.41 (1.86, 3.13) for NO2, and 2.01 (1.55, 2.61) for NOx. CONCLUSIONS: In this study, long-term air pollutants exposure was associated with an increased risk of AAA incidence.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Humanos , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Dióxido de Nitrogênio/análise , Estudos Prospectivos , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Material Particulado/efeitos adversos , Material Particulado/análise , Predisposição Genética para DoençaRESUMO
BACKGROUND: The extent to which genetic susceptibility modifies the associations between air pollutants and the risk of incident stroke is still unclear. This study was designed to investigate the separate and joint associations of long-term exposure to air pollutants and genetic susceptibility on stroke risk. METHODS: The participants of this study were recruited by the UK Biobank between 2006 and 2010. These participants were followed up from the enrollment until the occurrence of stroke events or censoring of data. Hazard ratios (HRs) and 95% CIs for stroke events associated with long-term exposure to air pollutants were estimated by fitting both crude and adjusted Cox proportional hazards models. Additionally, the polygenic risk score was calculated to estimate whether the polygenic risk score modifies the associations between exposure to air pollutants and incident stroke. RESULTS: A total of 502â 480 subjects were included in this study. After exclusion, 452â 196 participants were taken into the final analysis. During a median follow-up time of 11.7 years, 11â 334 stroke events were observed, with a mean age of 61.60 years, and men accounted for 56.2% of the total cases. Long-term exposures to particulate matter with an aerodynamic diameter smaller than 2.5 µm (adjusted HR, 1.70 [95% CI, 1.43-2.03]) or particulate matter with an aerodynamic diameter smaller than 10 µm (adjusted HR, 1.50 [95% CI, 1.36-1.66]), nitrogen dioxide (adjusted HR, 1.10 [95% CI, 1.07-1.12]), and nitrogen oxide (adjusted HR, 1.04 [95% CI, 1.02-1.05]) were pronouncedly associated with increased risk of stroke. Meanwhile, participants with high genetic risk and exposure to high air pollutants had ≈45% (31%, 61%; particulate matter with an aerodynamic diameter smaller than 2.5 µm), 48% (33%, 65%; particulate matter with an aerodynamic diameter smaller than 10 µm), 51% (35%, 69%; nitrogen dioxide), and 39% (25%, 55%; nitrogen oxide) higher risk of stroke compared with those with low genetic risk and exposure to low air pollutants, respectively. Of note, we observed additive and multiplicative interactions between genetic susceptibility and air pollutants on stroke events. CONCLUSIONS: Chronic exposure to air pollutants was associated with an increased risk of stroke, especially in populations at high genetic risk.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Acidente Vascular Cerebral , Masculino , Humanos , Pessoa de Meia-Idade , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Estudos de Coortes , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Dióxido de Nitrogênio/efeitos adversos , Exposição Ambiental/efeitos adversos , Material Particulado/efeitos adversos , Material Particulado/análise , Óxidos de Nitrogênio , Predisposição Genética para Doença , Óxido Nítrico , Acidente Vascular Cerebral/epidemiologia , Acidente Vascular Cerebral/genética , Acidente Vascular Cerebral/induzido quimicamenteRESUMO
BACKGROUND: Epidemiological evidence links a close correlation between long-term exposure to air pollutants and autoimmune diseases, while the causality remained unknown. METHODS: Two-sample Mendelian randomization (TSMR) was used to investigate the role of PM10, PM2.5, NO2, and NOX (N = 423,796-456,380) in 15 autoimmune diseases (N = 14,890-314,995) using data from large European GWASs including UKB, FINNGEN, IMSGC, and IPSCSG. Multivariable Mendelian randomization (MVMR) was conducted to investigate the direct effect of each air pollutant and the mediating role of common factors, including body mass index (BMI), alcohol consumption, smoking status, and household income. Transcriptome-wide association studies (TWAS), two-step MR, and colocalization analyses were performed to explore underlying mechanisms between air pollution and autoimmune diseases. RESULTS: In TSMR, after correction of multiple testing, hypothyroidism was causally associated with higher exposure to NO2 [odds ratio (OR): 1.37, p = 9.08 × 10-4] and NOX [OR: 1.34, p = 2.86 × 10-3], ulcerative colitis (UC) was causally associated with higher exposure to NOX [OR: 2.24, p = 1.23 × 10-2] and PM2.5 [OR: 2.60, p = 5.96 × 10-3], rheumatoid arthritis was causally associated with higher exposure to NOX [OR: 1.72, p = 1.50 × 10-2], systemic lupus erythematosus was causally associated with higher exposure to NOX [OR: 4.92, p = 6.89 × 10-3], celiac disease was causally associated with lower exposure to NOX [OR: 0.14, p = 6.74 × 10-4] and PM2.5 [OR: 0.17, p = 3.18 × 10-3]. The risky effects of PM2.5 on UC remained significant in MVMR analyses after adjusting for other air pollutants. MVMR revealed several common mediators between air pollutants and autoimmune diseases. Transcriptional analysis identified specific gene transcripts and pathways interconnecting air pollutants and autoimmune diseases. Two-step MR revealed that POR, HSPA1B, and BRD2 might mediate from air pollutants to autoimmune diseases. POR pQTL (rs59882870, PPH4=1.00) strongly colocalized with autoimmune diseases. CONCLUSION: This research underscores the necessity of rigorous air pollutant surveillance within public health studies to curb the prevalence of autoimmune diseases.
Assuntos
Poluentes Atmosféricos , Doenças Autoimunes , Estudo de Associação Genômica Ampla , Humanos , Doenças Autoimunes/genética , Poluentes Atmosféricos/efeitos adversos , Análise da Randomização Mendeliana , Predisposição Genética para Doença , Material Particulado/efeitos adversosRESUMO
BACKGROUND: Particulate matter exposure (PM) is a cause of aerodigestive disease globally. The destruction of the World Trade Center (WTC) exposed first responders and inhabitants of New York City to WTC-PM and caused obstructive airways disease (OAD), gastroesophageal reflux disease (GERD) and Barrett's Esophagus (BE). GERD not only diminishes health-related quality of life but also gives rise to complications that extend beyond the scope of BE. GERD can incite or exacerbate allergies, sinusitis, bronchitis, and asthma. Disease features of the aerodigestive axis can overlap, often necessitating more invasive diagnostic testing and treatment modalities. This presents a need to develop novel non-invasive biomarkers of GERD, BE, airway hyperreactivity (AHR), treatment efficacy, and severity of symptoms. METHODS: Our observational case-cohort study will leverage the longitudinally phenotyped Fire Department of New York (FDNY)-WTC exposed cohort to identify Biomarkers of Airway Disease, Barrett's and Underdiagnosed Reflux Noninvasively (BAD-BURN). Our study population consists of n = 4,192 individuals from which we have randomly selected a sub-cohort control group (n = 837). We will then recruit subgroups of i. AHR only ii. GERD only iii. BE iv. GERD/BE and AHR overlap or v. No GERD or AHR, from the sub-cohort control group. We will then phenotype and examine non-invasive biomarkers of these subgroups to identify under-diagnosis and/or treatment efficacy. The findings may further contribute to the development of future biologically plausible therapies, ultimately enhance patient care and quality of life. DISCUSSION: Although many studies have suggested interdependence between airway and digestive diseases, the causative factors and specific mechanisms remain unclear. The detection of the disease is further complicated by the invasiveness of conventional GERD diagnosis procedures and the limited availability of disease-specific biomarkers. The management of reflux is important, as it directly increases risk of cancer and negatively impacts quality of life. Therefore, it is vital to develop novel noninvasive disease markers that can effectively phenotype, facilitate early diagnosis of premalignant disease and identify potential therapeutic targets to improve patient care. TRIAL REGISTRATION: Name of Primary Registry: "Biomarkers of Airway Disease, Barrett's and Underdiagnosed Reflux Noninvasively (BADBURN)". Trial Identifying Number: NCT05216133 . Date of Registration: January 31, 2022.
Assuntos
Esôfago de Barrett , Biomarcadores , Bombeiros , Refluxo Gastroesofágico , Ataques Terroristas de 11 de Setembro , Humanos , Esôfago de Barrett/diagnóstico , Esôfago de Barrett/etiologia , Refluxo Gastroesofágico/diagnóstico , Biomarcadores/sangue , Estudos de Casos e Controles , Bombeiros/estatística & dados numéricos , Cidade de Nova Iorque , Exposição Ocupacional/efeitos adversos , Material Particulado/efeitos adversos , Material Particulado/análise , Estudos Observacionais como Assunto , MasculinoRESUMO
BACKGROUND: Short-term exposure to air pollution may trigger symptoms of drug-resistant tuberculosis (DR-TB) through stimulating lung tissue, damaging tracheobronchial mucosa, the key anti-mycobacterium T cell immune function, and production and release of inflammatory cytokines. OBJECTIVE: To investigate the association between acute exacerbations of DR-TB and short-term residential exposure to air pollutants (PM10, PM2.5, SO2, NO2, CO and O3) based on a large prospective cohort in Anhui Province, China. METHOD: Patients were derived from a prospective cohort study of DR-TB in Anhui Province. All DR-TB patients underwent drug-susceptibility testing and prefecture-level reference laboratories confirmed their microbiologies. The case-crossover design was performed to evaluate the association between the risk of acute exacerbations of DR-TB and short-term residential exposure to air pollution. RESULTS: Short-term NO2 exposure was significantly related to an elevated risk of first-time outpatient visit due to acute exacerbations of DR-TB(relative risk:1.159, 95% confidence interval:1.011 ~ 1.329). Stratification analyses revealed that the relationship between the risk of acute exacerbations and NO2 exposure was stronger in the elderly (age ≥ 65) DR-TB patients, and in individuals with a history of TB treatment. CONCLUSIONS: NO2 Exposure was significantly associated with an elevated risk of acute exacerbation of DR-TB in Anhui Province, China.
Assuntos
Poluentes Atmosféricos , Tuberculose Resistente a Múltiplos Medicamentos , Idoso , Humanos , Estudos Cross-Over , Dióxido de Nitrogênio , Estudos ProspectivosRESUMO
Upgrading to the CHINA 7 standard is crucial for managing air pollution from passenger vehicles in China. Meanwhile, China aims to achieve carbon neutrality by 2060, which necessitates large-scale replacement of gasoline vehicles with electric vehicles in the future. Consequently, the public might view upgrading gasoline vehicles to the CHINA 7 standard as redundant. However, the emission reduction benefits of upgrading standards in the context of uncertain electrification ambitions have not received adequate attention. Here, we show that upgrading standards will compensate for the absence of emissions reductions due to hindered electrification efforts. In the best scenario, China's CO2 emissions can be reduced to 0.047 Gt and NOx to 8.2 × 103 t in 2050. In nonextreme electrification scenarios with CHINA 7 standard, the emission intensity reduction will remain the main driver for emission reductions, outweighing the electrification contribution. In extreme electrification scenarios, upgrading standards will tackle the increased emissions from plug-in hybrid electric vehicles. Our fleet-level results advocate for early standards upgrades to enhance resilience against air pollution risks arising from uncertainties in electrification. Our evidence from China, with one of the most stringent emission standards, can provide a reference point for the world on the upgrading passenger vehicle emission standard issue.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Emissões de Veículos/prevenção & controle , Emissões de Veículos/análise , Poluentes Atmosféricos/análise , Gasolina , Incerteza , Poluição do Ar/prevenção & controle , Poluição do Ar/análise , China , Veículos AutomotoresRESUMO
Ethylene oxide ("EtO") is an industrially made volatile organic compound and a known human carcinogen. There are few reliable reports of ambient EtO concentrations around production and end-use facilities, however, despite major exposure concerns. We present in situ, fast (1 Hz), sensitive EtO measurements made during February 2023 across the southeastern Louisiana industrial corridor. We aggregated mobile data at 500 m spatial resolution and reported average mixing ratios for 75 km of the corridor. Mean and median aggregated values were 31.4 and 23.3 ppt, respectively, and a majority (75%) of 500 m grid cells were above 10.9 ppt, the lifetime exposure concentration corresponding to 100-in-one million excess cancer risk (1 × 10-4). A small subset (3.3%) were above 109 ppt (1000-in-one million cancer risk, 1 × 10-3); these tended to be near EtO-emitting facilities, though we observed plumes over 10 km from the nearest facilities. Many plumes were highly correlated with other measured gases, indicating potential emission sources, and a subset was measured simultaneously with a second commercial analyzer, showing good agreement. We estimated EtO for 13 census tracts, all of which were higher than EPA estimates (median difference of 21.3 ppt). Our findings provide important information about EtO concentrations and potential exposure risks in a key industrial region and advance the application of EtO analytical methods for ambient sampling and mobile monitoring for air toxics.
Assuntos
Monitoramento Ambiental , Óxido de Etileno , Louisiana , Monitoramento Ambiental/métodos , Humanos , Poluentes Atmosféricos/análiseRESUMO
Plug-in electric vehicles (PEVs) can reduce air emissions when charged with clean power, but prior work estimated that in 2010, PEVs produced 2 to 3 times the consequential air emission externalities of gasoline vehicles in PJM (the largest US regional transmission operator, serving 65 million people) due largely to increased generation from coal-fired power plants to charge the vehicles. We investigate how this situation has changed since 2010, where we are now, and what the largest levers are for reducing PEV consequential life cycle emission externalities in the near future. We estimate that PEV emission externalities have dropped by 17% to 18% in PJM as natural gas replaced coal, but they will remain comparable to gasoline vehicle externalities in base case trajectories through at least 2035. Increased wind and solar power capacity is critical to achieving deep decarbonization in the long run, but through 2035 we estimate that it will primarily shift which fossil generators operate on the margin at times when PEVs charge and can even increase consequential PEV charging emissions in the near term. We find that the largest levers for reducing PEV emissions over the next decade are (1) shifting away from nickel-based batteries to lithium iron phosphate, (2) reducing emissions from fossil generators, and (3) revising vehicle fleet emission standards. While our numerical estimates are regionally specific, key findings apply to most power systems today, in which renewable generators typically produce as much output as possible, regardless of the load, while dispatchable fossil fuel generators respond to the changes in load.
Assuntos
Poluição do Ar , Gasolina , Humanos , Gasolina/análise , Emissões de Veículos/prevenção & controle , Emissões de Veículos/análise , Centrais Elétricas , Políticas , Carvão Mineral , Gás Natural , Veículos AutomotoresRESUMO
OBJECTIVES: To estimate the number of deaths and the cost of deaths attributable to wood heater smoke in the Australian Capital Territory. STUDY DESIGN: Rapid health impact assessment, based on fine particulate matter (PM2.5 ) data from three outdoor air pollution monitors and published exposure-response functions for natural cause mortality attributed to PM2.5 exposure. SETTING: Australian Capital Territory (population, 2021: 454 000), 2016-2018, 2021, and 2022 (2019 and 2020 excluded because of the impact of extreme bushfires on air quality). MAIN OUTCOME MEASURES: Proportion of PM2.5 exposure attributable to wood heaters; numbers of deaths and associated cost of deaths (based on the value of statistical life: $5.3 million) attributable to wood heater smoke. RESULTS: Wood heater emissions contributed an estimated 1.16-1.73 µg/m3 to the annual mean PM2.5 concentration during the three colder years (2017, 2018, 2021), or 17-25% of annual mean exposure, and 0.72 µg/m3 (15%) or 0.89 µg/m3 (13%) during the two milder years (2016, 2022). Using the most conservative exposure-response function, the estimated annual number of deaths attributable to wood heater smoke was 17-26 during the colder three years and 11-15 deaths during the milder two years. Using the least conservative exposure-response function, an estimated 43-63 deaths per year (colder years) and 26-36 deaths per year (milder years) were attributable to wood heater smoke. The estimated annual equivalent cost of deaths was $57-136 million (most conservative exposure-response function) and $140-333 million (least conservative exposure-response function). CONCLUSIONS: The estimated annual number of deaths in the ACT attributable to wood heater PM2.5 pollution is similar to that attributed to the extreme smoke of the 2019-20 Black Summer bushfires. The number of wood heaters should be reduced by banning new installations and phasing out existing units in urban and suburban areas.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Humanos , Fumaça/efeitos adversos , Poluentes Atmosféricos/análise , Território da Capital Australiana , Madeira/efeitos adversos , Madeira/química , Avaliação do Impacto na Saúde , Austrália/epidemiologia , Poluição do Ar/efeitos adversos , Material Particulado/efeitos adversos , Exposição Ambiental/efeitos adversosRESUMO
Limiting the negative impact of climate change on nature and humans is one of the most pressing issues of the 21st century. Meanwhile, people in modern society spend most of the day indoors. It is therefore surprising that comparatively little attention has been paid to indoor human exposure in relation to climate change. Heat action plans have now been designed in many regions to protect people from thermal stress in their private homes and in public buildings. However, in order to be able to plan effectively for the future, reliable information is required about the long-term effects of climate change on indoor air quality and climate. The Indoor Air Quality Climate Change (IAQCC) model is an expediant tool for estimating the influence of climate change on indoor air quality. The model follows a holistic approach in which building physics, emissions, chemical reactions, mold growth and exposure are combined with the fundamental parameters of temperature and humidity. The features of the model have already been presented in an earlier publication, and it is now used for the expected climatic conditions in Central Europe, taking into account various shared socioeconomic pathway (SSP) scenarios up to the year 2100. For the test house examined in this study, the concentrations of pollutants in the indoor air will continue to rise. At the same time, the risk of mold growth also increases (the mold index rose from 0 to 4 in the worst case for very sensitive material). The biggest problem, however, is protection against heat and humidity. Massive structural improvements are needed here, including insulation, ventilation, and direct sun protection. Otherwise, the occupants will be exposed to increasing thermal discomfort, which can also lead to severe heat stress indoors.
Assuntos
Poluição do Ar em Ambientes Fechados , Poluição do Ar , Humanos , Mudança Climática , Poluição do Ar em Ambientes Fechados/análise , Umidade , VentilaçãoRESUMO
Urban greening can improve cities' air quality by filtering the main gaseous pollutants such as tropospheric ozone (O3). However, the pollutant removal capacity offered by woody species strongly depends on eco-physiological and morphological traits. Woody species with higher stomatal conductance (gs) can remove more gases from the atmosphere, but other species can worsen air quality due to high O3 forming potential (OFP), based on their emitting rates of biogenic volatile organic compounds (bVOCs) and Leaf Mass per Area (LMA). Presently, there is a lack of data on eco-physiological (gs, bVOCs emissions) and foliar traits (LMA) for several ornamental species used in urban greening programs, which does not allow assessment of their O3 removal capacity and OFP. This study aimed to (i) parameterize gs, assess bVOCs emissions and LMA of 14 ornamental woody species commonly used in Mediterranean urban greening, and (ii) model their Net O3 uptake. The gs Jarvis model was parameterized considering various environmental conditions alongside isoprene and monoterpene foliar bVOCs emission rates trapped in the field and quantified by gas chromatography-mass spectrometry. The results are helpful for urban planning and landscaping; suggesting that Catalpa bignonioides and Gleditsia triacanthos have excellent O3 removal capacity due to their high maximum gs (gmax) equal to 0.657 and 0.597 mol H2O m-2 s-1. Regarding bVOCs, high isoprene (16.75 µg gdw-1 h-1) and monoterpene (13.12 µg gdw-1 h-1) emission rates were found for Rhamnus alaternus and Cornus mas. In contrast, no bVOCs emissions were detected for Camellia sasanqua and Paulownia tomentosa. In conclusion, 11 species showed a positive Net O3 uptake, while the use of large numbers of R. alaternus, C. mas, and Chamaerops humilis for urban afforestation planning are not recommended due to their potential to induce a deterioration of outdoor air quality.
Assuntos
Poluentes Atmosféricos , Ozônio , Compostos Orgânicos Voláteis , Ozônio/análise , Poluentes Atmosféricos/análise , Compostos Orgânicos Voláteis/análise , Compostos Orgânicos Voláteis/metabolismo , Folhas de Planta/metabolismo , Monitoramento Ambiental/métodosRESUMO
Past studies support the hypothesis that the prenatal period influences childhood growth. However, few studies explore the joint effects of exposures that occur simultaneously during pregnancy. To explore the feasibility of using mixtures methods with neighborhood-level environmental exposures, we assessed the effects of multiple prenatal exposures on body mass index (BMI) from birth to age 24 months. We used data from two cohorts: Healthy Start (n = 977) and Maternal and Developmental Risks from Environmental and Social Stressors (MADRES; n = 303). BMI was measured at delivery and 6, 12, and 24 months and standardized as z-scores. We included variables for air pollutants, built and natural environments, food access, and neighborhood socioeconomic status (SES). We used two complementary statistical approaches: single-exposure linear regression and quantile-based g-computation. Models were fit separately for each cohort and time point and were adjusted for relevant covariates. Single-exposure models identified negative associations between NO2 and distance to parks and positive associations between low neighborhood SES and BMI z-scores for Healthy Start participants; for MADRES participants, we observed negative associations between O3 and distance to parks and BMI z-scores. G-computations models produced comparable results for each cohort: higher exposures were generally associated with lower BMI, although results were not significant. Results from the g-computation models, which do not require a priori knowledge of the direction of associations, indicated that the direction of associations between mixture components and BMI varied by cohort and time point. Our study highlights challenges in assessing mixtures effects at the neighborhood level and in harmonizing exposure data across cohorts. For example, geospatial data of neighborhood-level exposures may not fully capture the qualities that might influence health behavior. Studies aiming to harmonize geospatial data from different geographical regions should consider contextual factors when operationalizing exposure variables.
Assuntos
Índice de Massa Corporal , Exposição Ambiental , Humanos , Feminino , Lactente , Gravidez , Masculino , Estudos de Coortes , Recém-Nascido , Pré-Escolar , Características de Residência , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Adulto , Fatores Socioeconômicos , Saúde da Criança , Poluentes Atmosféricos/análiseRESUMO
RATIONALE: Air pollution and extreme temperature and humidity are risk factors for lung dysfunction, but their interactions are not clearly understood. OBJECTIVES: To assess the impact of exposure to air pollutants and meteorological factors on lung function, and the contribution of their interaction to the overall effect. METHODS: The peak expiratory flow rates of 135 participants were repeatedly measured during up to four visits. Two weeks before each visit, the concentrations of gaseous pollutants and 19 fine particle components, and the temperature and relative humidity, were continuously monitored in the community where they lived. A Bayesian Kernel machine regression model was used to explore the non-linear exposure-response relationships of the peak expiratory flow rate with pollutant exposure and meteorological factors, and their interactions. MEASUREMENTS AND MAIN RESULTS: Increased temperature and relative humidity could exacerbate pollutant-associated decline in the peak expiratory flow rate, although their associations with lung dysfunction disappeared after adjustment for pollutant exposure. For example, declines of peak expiratory flow rate associated with interquartile range increase of 3-day cadmium exposure were -0.03 and -0.07 units, when temperature was at 0.1 and 19.5 °C, respectively. Decreased temperature were associated with declines of peak expiratory flow rate after adjustment for pollutant exposure, and had interaction with pollutant exposure on lung dysfunction. CONCLUSIONS: High temperature, low temperature, and high humidity were all high-risk factors for lung dysfunction, and their interactions with pollutant levels contributed greatly to the overall effects.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Poluentes Ambientais , Humanos , Idoso , Umidade , Temperatura , Teorema de Bayes , Material Particulado/toxicidade , Material Particulado/análise , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Poluição do Ar/análise , Poluentes Atmosféricos/toxicidade , Poluentes Atmosféricos/análise , Pulmão/químicaRESUMO
BACKGROUND: Air pollution is one of the most serious environmental risks to mortality of stroke. However, there exists a noteworthy knowledge gap concerning the different stroke subtypes, causes of death, the susceptibility of stroke patient, and the role of greenness in this context. METHODS: We analyzed data from an ecological health cohort, which included 334,261 patients aged ≥40 years with stroke (comprising 288,490 ischemic stroke and 45,771 hemorrhagic stroke) during the period 2013-2019. We used Cox proportional hazards models with time-varying exposure to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) to assess the associations of annual average fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3) with both all-cause and cause-specific mortality. Additionally, we conducted analyses to examine the effect modification by greenness and identify potential susceptibility factors through subgroup analyses. RESULT: In multivariable-adjusted models, long-term exposure to PM2.5 and NO2 was associated with increased risk of all-cause mortality (HR: 1.038, 95% CI: 1.029-1.047 for PM2.5; HR: 1.055, 95% CI: 1.026-1.085 for NO2, per 10 µg/m3, for ischemic stroke patients; similar for hemorrhagic stroke patients). Gradually increasing effect sizes were shown for CVD mortality and stroke mortality. The HRs of mortality were slightly weaker with high versus low vegetation exposure. Cumulative exposures increased the HRs of pollutant-related mortality, and greater greenness decreased this risk. Two subtypes of stroke patients exhibited diverse patterns of benefit. CONCLUSION: Increasing residential greenness attenuates the increased risk of mortality with different patterns due to chronic air pollutants for ischemic and hemorrhagic stroke, offering valuable insights for precise tertiary stroke prevention strategies.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Acidente Vascular Cerebral Hemorrágico , AVC Isquêmico , Material Particulado , Humanos , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/efeitos adversos , Masculino , Idoso , Feminino , Pessoa de Meia-Idade , Material Particulado/análise , Material Particulado/efeitos adversos , Estudos de Coortes , AVC Isquêmico/mortalidade , Acidente Vascular Cerebral Hemorrágico/mortalidade , Acidente Vascular Cerebral Hemorrágico/induzido quimicamente , Acidente Vascular Cerebral Hemorrágico/epidemiologia , Poluição do Ar/efeitos adversos , Exposição Ambiental/efeitos adversos , Ozônio/análise , Ozônio/efeitos adversos , Dióxido de Nitrogênio/análise , Adulto , Idoso de 80 Anos ou mais , Acidente Vascular Cerebral/mortalidadeRESUMO
BACKGROUND AND OBJECTIVE: When multiple complex air pollutants are combined in real-world settings, the reliability of estimating the effect of a single pollutant is questionable. This study aimed to investigate the combined effects of changes in air pollutants on small airway dysfunction (SAD). METHODS: We analysed Korea National Health and Nutrition Examination Survey (KNHANES) V-VIII database from 2010 to 2018 to elucidate the associations between annual changes in air pollutants over a previous 5-year period and small airway function. We estimated the annual concentrations of five air pollutants: NO2, O3, PM2.5, SO2 and CO. Forced expiratory flow between 25% and 75% of vital capacity (FEF25%-75%) <65% was defined as SAD. Using the quantile generalized-Computation (g-Computation) model, the combined effect of the annual changes in different air pollutants was estimated. RESULTS: A total of 29,115 individuals were included. We found significant associations between SAD and the quartiles of annual changes in NO2 (OR = 1.10, 95% CI = 1.08-1.12), O3 (OR = 1.03, 95% CI = 1.00-1.05), PM2.5 (OR = 1.03, 95% CI = 1.00-1.05), SO2 (OR = 1.04, 95% CI = 1.02-1.08) and CO (OR = 1.16, 95% CI = 1.12-1.19). The combined effect of the air pollutant changes was significantly associated with SAD independent of smoking (OR = 1.31, 95% CI = 1.26-1.35, p-value <0.001), and this trend was consistently observed across the entire study population and various subgroup populations. As the estimated risk of SAD, determined by individual-specific combined effect models, increased and the log odds for SAD increased linearly. CONCLUSION: The combined effect of annual changes in multiple air pollutant concentrations were associated with an increased risk of SAD.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Humanos , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Material Particulado/efeitos adversos , Material Particulado/análise , Dióxido de Nitrogênio/efeitos adversos , Dióxido de Nitrogênio/análise , Inquéritos Nutricionais , Reprodutibilidade dos Testes , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , China/epidemiologiaRESUMO
BACKGROUND: Air pollution and obstructive sleep apnea (OSA) are both linked with cardiovascular co-morbidities and share similar pathophysiological mechanisms. A causal association between the two has been postulated. However, the results of the studies on this topic are conflicting mainly because of the lack of adjustment for important confounders such as seasonality and temperature. We aimed to evaluate if such an association exists in a highly polluted area like Lombardy region (Italy) when accounting for all confounders. METHODS: Data of adult patients seen at the Sleep Disorder Centre in Milan from 2010 to 2020 were analysed and the main polygraphic data were retrieved. Air pollutant concentrations of the following pollutants NO2, O3, PM2.5, and PM10 were collected through monitoring stations. RESULTS: A total of 3493 patients were included: males (2358, 67.5%) mean age 60.1 (SD = 14.3) years, BMI 29.2 (6.2) kg/m2, mean AHI 16.5 (18.1) events/h. After adjusting for all confounders, in the multivariable analysis, the only associations that remained significant were long-term exposure to O3 with indexes of OSA severity (AHI and ODI) but only in spring. Furthermore, a positive association was seen between long-term exposure to PM10 and ODI but in springtime only. CONCLUSION: The findings of the current study does not support an association between fine particulate matter and OSA severity.
Assuntos
Poluentes Atmosféricos , Síndromes da Apneia do Sono , Apneia Obstrutiva do Sono , Masculino , Adulto , Humanos , Pessoa de Meia-Idade , Material Particulado/efeitos adversos , Material Particulado/análise , Exposição Ambiental/análise , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Apneia Obstrutiva do Sono/epidemiologiaRESUMO
BACKGROUND: Depression is a global health priority. Maintaining and delaying depressive symptoms in older adults is a key to healthy aging. This study aimed to identify depressive symptom trajectories, predictors and mortality, while also exploring the relationship between air quality and depressive symptoms in older adults in the Hong Kong community over 14 years. METHODS: This study is a longitudinal study in Hong Kong. The target population was community-dwelling older adults over age 65. Depressive symptoms were measured by the Geriatric Depression Scale (GDS-15). Group-based trajectory model was used to identify heterogeneity in longitudinal changes over 14 years and examine the associations between baseline variables and trajectories for different cohort members using multinomial logistic regression. The Kaplan-Meier method was employed to conduct survival analysis and explore the variations in survival probabilities over time among different trajectory group. Linear mixed model was used to explore the relationship between air quality and depressive symptoms. RESULTS: A total of 2828 older adults were included. Three different trajectories of depressive symptoms in older people were identified: relatively stable (15.4%), late increase (67.1%) and increase (17.5%). Female, more number of chronic diseases, poor cognitive function, and poor health-related quality of life (HRQOL) were significantly associated with other less favorable trajectories compared with participants with stable levels of depressive symptoms. The late increase group had a lower mortality rate than the relatively stable and increased groups. Lower baseline ambient air pollutant exposure to NO2 over 14 years was significantly associated with fewer depressive symptoms. CONCLUSIONS: In this study, we found that a late increase in depressive symptoms was the predominant trend in older Chinese people in Hong Kong. Poorer HRQOL was predictive of less favorable trajectories of depressive symptoms. Ambient air pollution was associated with depressive symptoms. This novel observation strengthens the epidemiological evidence of longitudinal changes in depressive symptoms and associations with late-life exposure to air pollution.
Assuntos
Poluição do Ar , Depressão , População do Leste Asiático , Idoso , Feminino , Humanos , Poluição do Ar/efeitos adversos , Estudos de Coortes , Depressão/diagnóstico , Depressão/epidemiologia , Depressão/psicologia , Hong Kong/epidemiologia , Estudos Longitudinais , Qualidade de Vida , MasculinoRESUMO
BACKGROUND: Acute otitis media (AOM) is a prevalent childhood acute illness, with 13.6 million pediatric office visits annually, often stemming from upper respiratory tract infections (URI) and affected by environmental factors like air pollution and cold seasons. METHODS: Herein, we made use of territory-wide hospitalization data to investigate the relationships between meteorological factors, air pollutants, influenza infection, and AOM for children observed from 1998 to 2019 in Hong Kong. Quasi-Poisson generalized additive model, combined with a distributed-lag non-linear model, was employed to examine the relationship between weekly AOM admissions in children and weekly influenza-like illness-positive (ILI +) rates, as well as air pollutants (i.e., oxidant gases, sulfur dioxide, and fine particulate matter), while accounting for meteorological variations. RESULTS: There were 21,224 hospital admissions due to AOM for children aged ≤ 15 years throughout a 22-year period. The cumulative adjusted relative risks (ARR) of AOM were 1.15 (95% CI, 1.04-1.28) and 1.07 (95% CI, 0.97-1.18) at the 95th percentile concentration of oxidant gases (65.9 ppm) and fine particulate matter (62.2 µg/m3) respectively, with reference set to their medians of concentration. The ARRs exhibited a monotone increasing trend for all-type and type-specific ILI + rates. Setting the reference to zero, the cumulative ARRs of AOM rose to 1.42 (95% CI, 1.29-1.56) at the 95th percentile of ILI + Total rate, and to 1.07 (95% CI, 1.01-1.14), 1.19 (95% CI, 1.11-1.27), and 1.22 (95% CI, 1.13-1.32) for ILI + A/H1N1, A/H3N2, and B, respectively. CONCLUSIONS: Our findings suggested that policy on air pollution control and influenza vaccination for children need to be implemented, which might have significant implications for preventing AOM in children.
Assuntos
Poluentes Atmosféricos , Hospitalização , Influenza Humana , Otite Média , Estações do Ano , Humanos , Otite Média/epidemiologia , Influenza Humana/epidemiologia , Hospitalização/estatística & dados numéricos , Pré-Escolar , Criança , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/efeitos adversos , Lactente , Hong Kong/epidemiologia , Feminino , Masculino , Adolescente , Doença Aguda , Material Particulado/análise , Material Particulado/efeitos adversos , Poluição do Ar/efeitos adversos , Poluição do Ar/análiseRESUMO
BACKGROUND: Respiratory conditions and health symptoms associated with air pollution in children are a major public health concern, as their immune systems and lungs are not yet fully developed. This study aimed to assess self-reported respiratory conditions and health symptoms associated with air pollution sources amongst children aged six years and below in Melusi informal settlement, Tshwane Metropolitan Municipality, South Africa. METHODS: With a quantitative cross-sectional study design, parents/caregivers of children aged six years and below (n = 300) from eight Early Childhood Development Centres were invited to participate in the study. This study employed complete sampling, and data was collected using the modified International Study of Asthma and Allergies in Children. The chi-square and multiple logistic regression models were used to analyze data, with p < 0.05 in the adjusted odds ratios considered as being statistically significant. RESULTS: Three models were run to examine the predictors of wheezing in the past 12 months, dry cough, and itchy-watery eyes. The model for asthma was excluded, as only seven participants reported having asthma. Wheeze in the past 12 months was associated with participants living in the area for more than three years (OR 2.96 95%CI: 1.011-8.674). Furthermore, having a dog in the house in the past 12 months was associated with wheeze in the past 12 months (OR 5.98 95%CI: 2.107-16.967). There was an association between duration of stay in a residence and dry cough prevalence (OR 5.63 95%CI: 2.175-14.584). Trucks always or frequently passing near homes was associated with itchy-watery eyes (OR 3.27 95%CI: 1.358-7.889). 59% (59%) of participants perceived the indoor air quality in their homes to be good, while 6% perceived it as poor. In contrast, 36% of participants perceived the outdoor air quality to be good, and 19.7% perceived it as poor. CONCLUSION: The association between perceived air pollution exposure, self-reported respiratory conditions, and health symptoms amongst children is complex. Further research is required to better understand the multifaceted nature of air pollution and its impact on the health of children.