Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 133
Filtrar
1.
Sci Total Environ ; 804: 150091, 2021 Sep 04.
Artigo em Inglês | MEDLINE | ID: mdl-34517316

RESUMO

BACKGROUND: Ambient air pollution exposure has been associated with higher mortality risk in numerous studies. We assessed potential variability in the magnitude of this association for non-accidental, cardiovascular disease, respiratory disease, and lung cancer mortality in a country-wide administrative cohort by exposure assessment method and by adjustment for geographic subdivisions. METHODS: We used the Belgian 2001 census linked to population and mortality register including nearly 5.5 million adults aged ≥30 (mean follow-up: 9.97 years). Annual mean concentrations for fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC) and ozone (O3) were assessed at baseline residential address using two exposure methods; Europe-wide hybrid land use regression (LUR) models [100x100m], and Belgium-wide interpolation-dispersion (RIO-IFDM) models [25x25m]. We used Cox proportional hazards models with age as the underlying time scale and adjusted for various individual and area-level covariates. We further adjusted main models for two different area-levels following the European Nomenclature of Territorial Units for Statistics (NUTS); NUTS-1 (n = 3), or NUTS-3 (n = 43). RESULTS: We found no consistent differences between both exposure methods. We observed most robust associations with lung cancer mortality. Hazard Ratios (HRs) per 10 µg/m3 increase for NO2 were 1.060 (95%CI 1.042-1.078) [hybrid LUR] and 1.040 (95%CI 1.022-1.058) [RIO-IFDM]. Associations with non-accidental, respiratory disease and cardiovascular disease mortality were generally null in main models but were enhanced after further adjustment for NUTS-1 or NUTS-3. HRs for non-accidental mortality per 5 µg/m3 increase for PM2.5 for the main model using hybrid LUR exposure were 1.023 (95%CI 1.011-1.035). After including random effects HRs were 1.044 (95%CI 1.033-1.057) [NUTS-1] and 1.076 (95%CI 1.060-1.092) [NUTS-3]. CONCLUSION: Long-term air pollution exposure was associated with higher lung cancer mortality risk but not consistently with the other studied causes. Magnitude of associations varied by adjustment for geographic subdivisions, area-level socio-economic covariates and less by exposure assessment method.

2.
BMJ ; 374: n1904, 2021 09 01.
Artigo em Inglês | MEDLINE | ID: mdl-34470785

RESUMO

OBJECTIVE: To investigate the associations between air pollution and mortality, focusing on associations below current European Union, United States, and World Health Organization standards and guidelines. DESIGN: Pooled analysis of eight cohorts. SETTING: Multicentre project Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE) in six European countries. PARTICIPANTS: 325 367 adults from the general population recruited mostly in the 1990s or 2000s with detailed lifestyle data. Stratified Cox proportional hazard models were used to analyse the associations between air pollution and mortality. Western Europe-wide land use regression models were used to characterise residential air pollution concentrations of ambient fine particulate matter (PM2.5), nitrogen dioxide, ozone, and black carbon. MAIN OUTCOME MEASURES: Deaths due to natural causes and cause specific mortality. RESULTS: Of 325 367 adults followed-up for an average of 19.5 years, 47 131 deaths were observed. Higher exposure to PM2.5, nitrogen dioxide, and black carbon was associated with significantly increased risk of almost all outcomes. An increase of 5 µg/m3 in PM2.5 was associated with 13% (95% confidence interval 10.6% to 15.5%) increase in natural deaths; the corresponding figure for a 10 µg/m3 increase in nitrogen dioxide was 8.6% (7% to 10.2%). Associations with PM2.5, nitrogen dioxide, and black carbon remained significant at low concentrations. For participants with exposures below the US standard of 12 µg/m3 an increase of 5 µg/m3 in PM2.5 was associated with 29.6% (14% to 47.4%) increase in natural deaths. CONCLUSIONS: Our study contributes to the evidence that outdoor air pollution is associated with mortality even at low pollution levels below the current European and North American standards and WHO guideline values. These findings are therefore an important contribution to the debate about revision of air quality limits, guidelines, and standards, and future assessments by the Global Burden of Disease.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Poluição do Ar/efeitos adversos , Doenças Cardiovasculares/mortalidade , Exposição Ambiental/efeitos adversos , Doenças não Transmissíveis/mortalidade , Europa (Continente) , Humanos
3.
Psychon Bull Rev ; 2021 Sep 28.
Artigo em Inglês | MEDLINE | ID: mdl-34582031

RESUMO

Here, we present two case studies of extremely long-term retention. In the first, Richard C. Atkinson (RCA) had learned word sequences during experiments for his dissertation. Sixty-seven years later, RCA relearned the same words either in the original order or in a scrambled order. RCA reported no conscious awareness that the words were those used in the dissertation, but his relearning was considerably better for the words in the original order. In the second case study, Denis Cousineau had searched displays of objects for the presence of a target. The targets and foils had been novel at the beginning of training, and his search rate improved markedly over about 70 sessions. After 22 years, retraining showed retention of much of this gain in rate of search, and the rate was markedly faster than search for new objects with the same structure as the trained set. We consider interpretations of these case studies for our understanding of long-term retention.

4.
Lancet Planet Health ; 5(9): e620-e632, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-34508683

RESUMO

BACKGROUND: Long-term exposure to outdoor air pollution increases the risk of cardiovascular disease, but evidence is unclear on the health effects of exposure to pollutant concentrations lower than current EU and US standards and WHO guideline limits. Within the multicentre study Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), we investigated the associations of long-term exposures to fine particulate matter (PM2·5), nitrogen dioxide (NO2), black carbon, and warm-season ozone (O3) with the incidence of stroke and acute coronary heart disease. METHODS: We did a pooled analysis of individual data from six population-based cohort studies within ELAPSE, from Sweden, Denmark, the Netherlands, and Germany (recruited 1992-2004), and harmonised individual and area-level variables between cohorts. Participants (all adults) were followed up until migration from the study area, death, or incident stroke or coronary heart disease, or end of follow-up (2011-15). Mean 2010 air pollution concentrations from centrally developed European-wide land use regression models were assigned to participants' baseline residential addresses. We used Cox proportional hazards models with increasing levels of covariate adjustment to investigate the association of air pollution exposure with incidence of stroke and coronary heart disease. We assessed the shape of the concentration-response function and did subset analyses of participants living at pollutant concentrations lower than predefined values. FINDINGS: From the pooled ELAPSE cohorts, data on 137 148 participants were analysed in our fully adjusted model. During a median follow-up of 17·2 years (IQR 13·8-19·5), we observed 6950 incident events of stroke and 10 071 incident events of coronary heart disease. Incidence of stroke was associated with PM2·5 (hazard ratio 1·10 [95% CI 1·01-1·21] per 5 µg/m3 increase), NO2 (1·08 [1·04-1·12] per 10 µg/m3 increase), and black carbon (1·06 [1·02-1·10] per 0·5 10-5/m increase), whereas coronary heart disease incidence was only associated with NO2 (1·04 [1·01-1·07]). Warm-season O3 was not associated with an increase in either outcome. Concentration-response curves indicated no evidence of a threshold below which air pollutant concentrations are not harmful for cardiovascular health. Effect estimates for PM2·5 and NO2 remained elevated even when restricting analyses to participants exposed to pollutant concentrations lower than the EU limit values of 25 µg/m3 for PM2·5 and 40 µg/m3 for NO2. INTERPRETATION: Long-term air pollution exposure was associated with incidence of stroke and coronary heart disease, even at pollutant concentrations lower than current limit values. FUNDING: Health Effects Institute.

5.
J. pediatr. (Rio J.) ; 97(4): 420-425, July-Aug. 2021. tab
Artigo em Inglês | LILACS-Express | LILACS | ID: biblio-1287045

RESUMO

Abstract Objective This study aimed to investigate human adenovirus 36 (Adv36) as an associated factor for adiposity in children and adolescents aged 9-12 years. Methods This was a case-control study comparing overweight (cases) and eutrophic (controls) children and adolescents aged 9-12 years based on their body mass index in relation to human adenovirus 36 serology. Human adenovirus 36-specific neutralizing antibodies were assessed using the serum neutralization assay, and a questionnaire regarding the subjects' personal backgrounds, breastfeed history, age of starting daycare, and eating and exercise habits was also applied. Results A total of 101 (51, eutrophic; 50, overweight) children were included in the study. The Adv36 seropositivity rate was of 15.8%, which increased the chance of being overweight by 3.17 times (p = 0.049). Enrollment in a full-time daycare center before the age of 24 months increased the chance of being overweight by 2.78 times (p = 0.027). Metabolic parameters (total cholesterol and blood glucose) were insignificantly different among children who were seropositive or seronegative for human adenovirus 36. Conclusion This study concluded that excessive weight was positively associated with seropositivity for human adenovirus 36. Early enrollment in a full-time daycare was also an associated factor for obesity. Such data, confirmed in new studies, reinforces the role of human adenovirus 36 in the increase of childhood adiposity.

6.
Cochrane Database Syst Rev ; 8: CD013441, 2021 08 09.
Artigo em Inglês | MEDLINE | ID: mdl-34368949

RESUMO

BACKGROUND: More than 90% of the global population lives in areas exceeding World Health Organization air quality limits. More than four million people each year are thought to die early due to air pollution, and poor air quality is thought to reduce an average European's life expectancy by one year. Individuals may be able to reduce health risks through interventions such as masks, behavioural changes and use of air quality alerts. To date, evidence is lacking about the efficacy and safety of such interventions for the general population and people with long-term respiratory conditions. This topic, and the review question relating to supporting evidence to avoid or lessen the effects of air pollution, emerged directly from a group of people with chronic obstructive pulmonary disease (COPD) in South London, UK. OBJECTIVES: 1. To assess the efficacy, safety and acceptability of individual-level interventions that aim to help people with or without chronic respiratory conditions to reduce their exposure to outdoor air pollution. 2. To assess the efficacy, safety and acceptability of individual-level interventions that aim to help people with chronic respiratory conditions reduce the personal impact of outdoor air pollution and improve health outcomes. SEARCH METHODS: We identified studies from the Cochrane Airways Trials Register, Cochrane Central Register of Controlled Trials, and other major databases. We did not restrict our searches by date, language or publication type and included a search of the grey literature (e.g. unpublished information). We conducted the most recent search on 16 October 2020. SELECTION CRITERIA: We included randomised controlled trials (RCTs) and non-randomised studies (NRS) that included a comparison treatment arm, in adults and children that investigated the effectiveness of an individual-level intervention to reduce risks of outdoor air pollution. We included studies in healthy individuals and those in people with long-term respiratory conditions. We excluded studies which focused on non-respiratory long-term conditions, such as cardiovascular disease. We did not restrict eligibility of studies based on outcomes. DATA COLLECTION AND ANALYSIS: We used standard Cochrane methods. Two review authors independently selected trials for inclusion, extracted study characteristics and outcome data, and assessed risk of bias using the Cochrane Risk of Bias tool for RCTs and the Risk Of Bias In Non-randomised Studies - of Interventions (ROBINS-I) as appropriate. One review author entered data into the review; this was spot-checked by a second author. We planned to meta-analyse results from RCTs and NRS separately, using a random-effects model. This was not possible, so we presented evidence narratively. We assessed certainty of the evidence using the GRADE approach. Primary outcomes were: measures of air pollution exposure; exacerbation of respiratory conditions; hospital admissions; quality of life; and serious adverse events. MAIN RESULTS: We identified 11 studies (3372 participants) meeting our inclusion criteria (10 RCTs and one NRS). Participants' ages ranged from 18 to 74 years, and the duration of studies ranged from 24 hours to 104 weeks. Six cross-over studies recruited healthy adults and five parallel studies included either people with pre-existing conditions (three studies) or only pregnant women (two studies). Interventions included masks (e.g. an N95 mask designed to filter out airborne particles) (five studies), an alternative cycle route (one study), air quality alerts and education (five studies). Studies were set in Australia, China, Iran, the UK, and the USA. Due to the diversity of study designs, populations, interventions and outcomes, we did not perform any meta-analyses and instead summarised results narratively. We judged both RCTs and the NRS to be at risk of bias from lack of blinding and lack of clarity regarding selection methods. Many studies did not provide a prepublished protocol or trial registration. From five studies (184 participants), we found that masks or altered cycle routes may have little or no impact on physiological markers of air pollution exposure (e.g. blood pressure and heart rate variability), but we are very uncertain about this estimate using the GRADE approach. We found conflicting evidence regarding health care usage from three studies of air pollution alerts, with one non-randomised cross-over trial (35 participants) reporting an increase in emergency hospital attendances and admissions, but the other two randomised parallel trials (1553 participants) reporting little to no difference. We also gave the evidence for this outcome a very uncertain GRADE rating. None of our included trials reported respiratory exacerbations, quality of life or serious adverse events. Secondary outcomes were not well reported, but indicated inconsistent impacts of air quality alerts and education interventions on adherence, with some trials reporting improvements in the intervention groups and others reporting little or no difference. Symptoms were reported by three trials, with one randomised cross-over trial (15 participants) reporting a small increase in breathing difficulties associated with the mask intervention, one non-randomised cross-over trial (35 participants) reporting reduced throat and nasal irritation in the lower-pollution cycle route group (but no clear difference in other respiratory symptoms), and another randomised parallel trial (519 participants) reporting no clear difference in symptoms between those who received a smog warning and those who did not. AUTHORS' CONCLUSIONS: The lack of evidence and study diversity has limited the conclusions of this review. Using a mask or a lower-pollution cycle route may mitigate some of the physiological impacts from air pollution, but evidence was very uncertain. We found conflicting results for other outcomes, including health care usage, symptoms and adherence/behaviour change. We did not find evidence for adverse events. Funders should consider commissioning larger, longer studies, using high-quality and well-described methods, recruiting participants with pre-existing respiratory conditions. Studies should report outcomes of importance to people with respiratory conditions, such as exacerbations, hospital admissions, quality of life and adverse events.

7.
Int J Cancer ; 149(11): 1887-1897, 2021 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-34278567

RESUMO

Particulate matter air pollution and diesel engine exhaust have been classified as carcinogenic for lung cancer, yet few studies have explored associations with liver cancer. We used six European adult cohorts which were recruited between 1985 and 2005, pooled within the "Effects of low-level air pollution: A study in Europe" (ELAPSE) project, and followed for the incidence of liver cancer until 2011 to 2015. The annual average exposure to nitrogen dioxide (NO2 ), particulate matter with diameter <2.5 µm (PM2.5 ), black carbon (BC), warm-season ozone (O3 ), and eight elemental components of PM2.5 (copper, iron, zinc, sulfur, nickel, vanadium, silicon, and potassium) were estimated by European-wide hybrid land-use regression models at participants' residential addresses. We analyzed the association between air pollution and liver cancer incidence by Cox proportional hazards models adjusting for potential confounders. Of 330 064 cancer-free adults at baseline, 512 developed liver cancer during a mean follow-up of 18.1 years. We observed positive linear associations between NO2 (hazard ratio, 95% confidence interval: 1.17, 1.02-1.35 per 10 µg/m3 ), PM2.5 (1.12, 0.92-1.36 per 5 µg/m3 ), and BC (1.15, 1.00-1.33 per 0.5 10-5 /m) and liver cancer incidence. Associations with NO2 and BC persisted in two-pollutant models with PM2.5 . Most components of PM2.5 were associated with the risk of liver cancer, with the strongest associations for sulfur and vanadium, which were robust to adjustment for PM2.5 or NO2 . Our study suggests that ambient air pollution may increase the risk of liver cancer, even at concentrations below current EU standards.

8.
Eur Respir J ; 57(6)2021 06.
Artigo em Inglês | MEDLINE | ID: mdl-34088754

RESUMO

BACKGROUND: Long-term exposure to ambient air pollution has been linked to childhood-onset asthma, although evidence is still insufficient. Within the multicentre project Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), we examined the associations of long-term exposures to particulate matter with a diameter <2.5 µm (PM2.5), nitrogen dioxide (NO2) and black carbon (BC) with asthma incidence in adults. METHODS: We pooled data from three cohorts in Denmark and Sweden with information on asthma hospital diagnoses. The average concentrations of air pollutants in 2010 were modelled by hybrid land-use regression models at participants' baseline residential addresses. Associations of air pollution exposures with asthma incidence were explored with Cox proportional hazard models, adjusting for potential confounders. RESULTS: Of 98 326 participants, 1965 developed asthma during a mean follow-up of 16.6 years. We observed associations in fully adjusted models with hazard ratios of 1.22 (95% CI 1.04-1.43) per 5 µg·m-3 for PM2.5, 1.17 (95% CI 1.10-1.25) per 10 µg·m-3 for NO2 and 1.15 (95% CI 1.08-1.23) per 0.5×10-5 m-1 for BC. Hazard ratios were larger in cohort subsets with exposure levels below the European Union and US limit values and possibly World Health Organization guidelines for PM2.5 and NO2. NO2 and BC estimates remained unchanged in two-pollutant models with PM2.5, whereas PM2.5 estimates were attenuated to unity. The concentration-response curves showed no evidence of a threshold. CONCLUSIONS: Long-term exposure to air pollution, especially from fossil fuel combustion sources such as motorised traffic, was associated with adult-onset asthma, even at levels below the current limit values.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Asma , Adulto , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Criança , Exposição Ambiental/análise , Europa (Continente) , Humanos , Incidência , Material Particulado/análise , Suécia
9.
Environ Health ; 20(1): 54, 2021 05 07.
Artigo em Inglês | MEDLINE | ID: mdl-33962646

RESUMO

BACKGROUND: Although the associations of outdoor air pollution exposure with mortality and hospital admissions are well established, few previous studies have reported on primary care clinical and prescribing data. We assessed the associations of short and long-term pollutant exposures with General Practitioner respiratory consultations and inhaler prescriptions. METHODS: Daily primary care data, for 2009-2013, were obtained from Lambeth DataNet (LDN), an anonymised dataset containing coded data from all patients (1.2 million) registered at general practices in Lambeth, an inner-city south London borough. Counts of respiratory consultations and inhaler prescriptions by day and Lower Super Output Area (LSOA) of residence were constructed. We developed models for predicting daily PM2.5, PM10, NO2 and O3 per LSOA. We used spatio-temporal mixed effects zero inflated negative binomial models to investigate the simultaneous short- and long-term effects of exposure to pollutants on the number of events. RESULTS: The mean concentrations of NO2, PM10, PM2.5 and O3 over the study period were 50.7, 21.2, 15.6, and 49.9 µg/m3 respectively, with all pollutants except NO2 having much larger temporal rather than spatial variability. Following short-term exposure increases to PM10, NO2 and PM2.5 the number of consultations and inhaler prescriptions were found to increase, especially for PM10 exposure in children which was associated with increases in daily respiratory consultations of 3.4% and inhaler prescriptions of 0.8%, per PM10 interquartile range (IQR) increase. Associations further increased after adjustment for weekly average exposures, rising to 6.1 and 1.2%, respectively, for weekly average PM10 exposure. In contrast, a short-term increase in O3 exposure was associated with decreased number of respiratory consultations. No association was found between long-term exposures to PM10, PM2.5 and NO2 and number of respiratory consultations. Long-term exposure to NO2 was associated with an increase (8%) in preventer inhaler prescriptions only. CONCLUSIONS: We found increases in the daily number of GP respiratory consultations and inhaler prescriptions following short-term increases in exposure to NO2, PM10 and PM2.5. These associations are more pronounced in children and persist for at least a week. The association with long term exposure to NO2 and preventer inhaler prescriptions indicates likely increased chronic respiratory morbidity.


Assuntos
Poluentes Atmosféricos/análise , Modelos Estatísticos , Nebulizadores e Vaporizadores/estatística & dados numéricos , Dióxido de Nitrogênio/análise , Visita a Consultório Médico/estatística & dados numéricos , Ozônio/análise , Material Particulado/análise , Prescrições/estatística & dados numéricos , Adolescente , Adulto , Idoso , Criança , Pré-Escolar , Clínicos Gerais , Humanos , Lactente , Recém-Nascido , Exposição por Inalação , Londres , Pessoa de Meia-Idade , Atenção Primária à Saúde , Doenças Respiratórias/diagnóstico , Doenças Respiratórias/tratamento farmacológico , Adulto Jovem
10.
Environ Health Perspect ; 129(4): 47009, 2021 04.
Artigo em Inglês | MEDLINE | ID: mdl-33844598

RESUMO

BACKGROUND: Inconsistent associations between long-term exposure to particles with an aerodynamic diameter ≤2.5 µm [fine particulate matter (PM2.5)] components and mortality have been reported, partly related to challenges in exposure assessment. OBJECTIVES: We investigated the associations between long-term exposure to PM2.5 elemental components and mortality in a large pooled European cohort; to compare health effects of PM2.5 components estimated with two exposure modeling approaches, namely, supervised linear regression (SLR) and random forest (RF) algorithms. METHODS: We pooled data from eight European cohorts with 323,782 participants, average age 49 y at baseline (1985-2005). Residential exposure to 2010 annual average concentration of eight PM2.5 components [copper (Cu), iron (Fe), potassium (K), nickel (Ni), sulfur (S), silicon (Si), vanadium (V), and zinc (Zn)] was estimated with Europe-wide SLR and RF models at a 100×100 m scale. We applied Cox proportional hazards models to investigate the associations between components and natural and cause-specific mortality. In addition, two-pollutant analyses were conducted by adjusting each component for PM2.5 mass and nitrogen dioxide (NO2) separately. RESULTS: We observed 46,640 natural-cause deaths with 6,317,235 person-years and an average follow-up of 19.5 y. All SLR-modeled components were statistically significantly associated with natural-cause mortality in single-pollutant models with hazard ratios (HRs) from 1.05 to 1.27. Similar HRs were observed for RF-modeled Cu, Fe, K, S, V, and Zn with wider confidence intervals (CIs). HRs for SLR-modeled Ni, S, Si, V, and Zn remained above unity and (almost) significant after adjustment for both PM2.5 and NO2. HRs only remained (almost) significant for RF-modeled K and V in two-pollutant models. The HRs for V were 1.03 (95% CI: 1.02, 1.05) and 1.06 (95% CI: 1.02, 1.10) for SLR- and RF-modeled exposures, respectively, per 2 ng/m3, adjusting for PM2.5 mass. Associations with cause-specific mortality were less consistent in two-pollutant models. CONCLUSION: Long-term exposure to V in PM2.5 was most consistently associated with increased mortality. Associations for the other components were weaker for exposure modeled with RF than SLR in two-pollutant models. https://doi.org/10.1289/EHP8368.

11.
Int J Obes (Lond) ; 45(6): 1342-1356, 2021 06.
Artigo em Inglês | MEDLINE | ID: mdl-33753885

RESUMO

INTRODUCTION: Obesity has numerous etiologies and includes biological factors. Studies have demonstrated that the human adenovirus subtype 36 (Adv36) is an adipogenic agent and causes metabolic alterations. Study results on the prevalence of Adv36 and clinical effects in humans vary substantially. This was a systematic review to summarize the studies on the prevalence of Adv36 infection and its association with human obesity. METHODS: A systematic literature review was conducted using the preferred reporting items for systematic reviews and meta-analysis (PRISMA). Observational or experimental studies found in the Medline, Embase, LILACS, Science Direct and SciELO databases that presented results on the prevalence of Adv36 in humans were included. RESULTS: Thirty-seven studies were screened. A total of 10,300 adults aged 18-70 years and 4585 children and adolescents aged 3-18 years were assessed. The average prevalence of Adv36 among adults was 22.9%, ranging from 5.5% to 49.8%. Among children and adolescents, the average prevalence of Adv36 was 28.9%, ranging from 7.5% to 73.9%. There was a positive statistical relationship between Adv36 and weight gain, obesity, or metabolic changes in 31 studies. However, in four studies there was no association with obesity, and in one, no association was described. One of the studies showed an inverse correlation, i.e., Adv36 was a protective factor against obesity. CONCLUSION: Strong evidence suggested a positive association between viral infection and obesity. However, due to the multi-causality of obesity and heterogeneity of studies, diagnostic tests should be standardized and easily accessible by the population to estimate the overall prevalence of Adv36 infection and its association with obesity.

12.
Nutr Res ; 86: 60-67, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33551256

RESUMO

The dramatic increase of people affected by obesity worldwide seems to be influenced by external factors independent of eating habits, physical exercise, or genetic characteristics. There may be a number of such factors, but one hypothesis is that there is person-to-person transmission, causing an epidemic effect, as occurs with infectious diseases. In animal models, experimental infection with human adenovirus-36 (Adv36) causes obesity. Humans cannot be experimentally infected, but a number of studies found a correlation of positive serology for Adv36 with overweight/obesity in humans. In vitro studies have shown that Adv36 accelerates the differentiation and proliferation of preadipocytes into adipocytes and increases their lipid concentration. Another viral mechanism involved is the activation of a noninsulin-dependent process that increases glucose uptake, mainly in adipose tissue and muscle. The increased glucose, coupled with increased lipogenesis due to increased fatty acid synthase and the action of peroxisome proliferator-activated receptor gamma (PPAR-gamma) in stimulating adipocyte differentiation from adult stem cells enhances fat accumulation within the adipocytes. In studies conducted to date, the Adv36 E4 open reading frame 1 gene (E4orf1), which activates the glucose transporter protein isoform 4 (GLUT4) and glucose transporter protein isoform 1 (GLUT1) glucose transporters, appears to play a major role in the virus adipogenesis. The aim of this study was to review the pathophysiology of obesity and the role of Adv36.


Assuntos
Infecções por Adenovirus Humanos/fisiopatologia , Infecções por Adenovirus Humanos/virologia , Adenovírus Humanos/fisiologia , Obesidade/fisiopatologia , Obesidade/virologia , Infecções por Adenovirus Humanos/complicações , Infecções por Adenovirus Humanos/etiologia , Adipócitos/fisiologia , Adipogenia , Tecido Adiposo/metabolismo , Animais , Glucose/metabolismo , Transportador de Glucose Tipo 1/metabolismo , Transportador de Glucose Tipo 4/metabolismo , Humanos , Metabolismo dos Lipídeos , PPAR gama/metabolismo
13.
Environ Int ; 146: 106306, 2021 01.
Artigo em Inglês | MEDLINE | ID: mdl-33395948

RESUMO

INTRODUCTION: To characterize air pollution exposure at a fine spatial scale, different exposure assessment methods have been applied. Comparison of associations with health from different exposure methods are scarce. The aim of this study was to evaluate associations of air pollution based on hybrid, land-use regression (LUR) and dispersion models with natural cause and cause-specific mortality. METHODS: We followed a Dutch national cohort of approximately 10.5 million adults aged 29+ years from 2008 until 2012. We used Cox proportional hazard models with age as underlying time scale and adjusted for several potential individual and area-level socio-economic status confounders to evaluate associations of annual average residential NO2, PM2.5 and BC exposure estimates based on two stochastic models (Dutch LUR, European-wide hybrid) and deterministic Dutch dispersion models. RESULTS: Spatial variability of PM2.5 and BC exposure was smaller for LUR compared to hybrid and dispersion models. NO2 exposure variability was similar for the three methods. Pearson correlations between hybrid, LUR and dispersion modeled NO2 and BC ranged from 0.72 to 0.83; correlations for PM2.5 were slightly lower (0.61-0.72). In general, all three models showed stronger associations of air pollutants with respiratory disease and lung cancer mortality than with natural cause and cardiovascular disease mortality. The strength of the associations differed between the three exposure models. Associations of air pollutants estimated by LUR were generally weaker compared to associations of air pollutants estimated by hybrid and dispersion models. For natural cause mortality, we found a hazard ratio (HR) of 1.030 (95% confidence interval (CI): 1.019, 1.041) per 10 µg/m3 for hybrid modeled NO2, a HR of 1.003 (95% CI: 0.993, 1.013) per 10 µg/m3 for LUR modeled NO2 and a HR of 1.015 (95% CI: 1.005, 1.024) per 10 µg/m3 for dispersion modeled NO2. CONCLUSION: Air pollution was positively associated with natural cause and cause-specific mortality, but the strength of the associations differed between the three exposure models. Our study documents that the selected exposure model may contribute to heterogeneity in effect estimates of associations between air pollution and health.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Doenças Respiratórias , Adulto , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Estudos de Coortes , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Humanos , Dióxido de Nitrogênio/análise , Dióxido de Nitrogênio/toxicidade , Material Particulado/efeitos adversos , Material Particulado/análise
14.
Environ Int ; 147: 106371, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33422970

RESUMO

BACKGROUND: We evaluated methods for the analysis of multi-level survival data using a pooled dataset of 14 cohorts participating in the ELAPSE project investigating associations between residential exposure to low levels of air pollution (PM2.5 and NO2) and health (natural-cause mortality and cerebrovascular, coronary and lung cancer incidence). METHODS: We applied five approaches in a multivariable Cox model to account for the first level of clustering corresponding to cohort specification: (1) not accounting for the cohort or using (2) indicator variables, (3) strata, (4) a frailty term in frailty Cox models, (5) a random intercept under a mixed Cox, for cohort identification. We accounted for the second level of clustering due to common characteristics in the residential area by (1) a random intercept per small area or (2) applying variance correction. We assessed the stratified, frailty and mixed Cox approach through simulations under different scenarios for heterogeneity in the underlying hazards and the air pollution effects. RESULTS: Effect estimates were stable under approaches used to adjust for cohort but substantially differed when no adjustment was applied. Further adjustment for the small area grouping increased the effect estimates' standard errors. Simulations confirmed identical results between the stratified and frailty models. In ELAPSE we selected a stratified multivariable Cox model to account for between-cohort heterogeneity without adjustment for small area level, due to the small number of subjects and events in the latter. CONCLUSIONS: Our study supports the need to account for between-cohort heterogeneity in multi-center collaborations using pooled individual level data.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Estudos de Coortes , Exposição Ambiental/análise , Humanos , Material Particulado/análise
15.
Environ Res ; 193: 110568, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33278469

RESUMO

BACKGROUND: An association between long-term exposure to fine particulate matter (PM2.5) and lung cancer has been established in previous studies. PM2.5 is a complex mixture of chemical components from various sources and little is known about whether certain components contribute specifically to the associated lung cancer risk. The present study builds on recent findings from the "Effects of Low-level Air Pollution: A Study in Europe" (ELAPSE) collaboration and addresses the potential association between specific elemental components of PM2.5 and lung cancer incidence. METHODS: We pooled seven cohorts from across Europe and assigned exposure estimates for eight components of PM2.5 representing non-tail pipe emissions (copper (Cu), iron (Fe), and zinc (Zn)), long-range transport (sulfur (S)), oil burning/industry emissions (nickel (Ni), vanadium (V)), crustal material (silicon (Si)), and biomass burning (potassium (K)) to cohort participants' baseline residential address based on 100 m by 100 m grids from newly developed hybrid models combining air pollution monitoring, land use data, satellite observations, and dispersion model estimates. We applied stratified Cox proportional hazards models, adjusting for potential confounders (age, sex, calendar year, marital status, smoking, body mass index, employment status, and neighborhood-level socio-economic status). RESULTS: The pooled study population comprised 306,550 individuals with 3916 incident lung cancer events during 5,541,672 person-years of follow-up. We observed a positive association between exposure to all eight components and lung cancer incidence, with adjusted HRs of 1.10 (95% CI 1.05, 1.16) per 50 ng/m3 PM2.5 K, 1.09 (95% CI 1.02, 1.15) per 1 ng/m3 PM2.5 Ni, 1.22 (95% CI 1.11, 1.35) per 200 ng/m3 PM2.5 S, and 1.07 (95% CI 1.02, 1.12) per 200 ng/m3 PM2.5 V. Effect estimates were largely unaffected by adjustment for nitrogen dioxide (NO2). After adjustment for PM2.5 mass, effect estimates of K, Ni, S, and V were slightly attenuated, whereas effect estimates of Cu, Si, Fe, and Zn became null or negative. CONCLUSIONS: Our results point towards an increased risk of lung cancer in connection with sources of combustion particles from oil and biomass burning and secondary inorganic aerosols rather than non-exhaust traffic emissions. Specific limit values or guidelines targeting these specific PM2.5 components may prove helpful in future lung cancer prevention strategies.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Neoplasias Pulmonares , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Exposição Ambiental/análise , Europa (Continente)/epidemiologia , Humanos , Incidência , Neoplasias Pulmonares/induzido quimicamente , Neoplasias Pulmonares/epidemiologia , Material Particulado/análise
16.
Environ Int ; 146: 106249, 2021 01.
Artigo em Inglês | MEDLINE | ID: mdl-33197787

RESUMO

BACKGROUND/AIM: Ambient air pollution has been associated with lung cancer, but the shape of the exposure-response function - especially at low exposure levels - is not well described. The aim of this study was to address the relationship between long-term low-level air pollution exposure and lung cancer incidence. METHODS: The "Effects of Low-level Air Pollution: a Study in Europe" (ELAPSE) collaboration pools seven cohorts from across Europe. We developed hybrid models combining air pollution monitoring, land use data, satellite observations, and dispersion model estimates for nitrogen dioxide (NO2), fine particulate matter (PM2.5), black carbon (BC), and ozone (O3) to assign exposure to cohort participants' residential addresses in 100 m by 100 m grids. We applied stratified Cox proportional hazards models, adjusting for potential confounders (age, sex, calendar year, marital status, smoking, body mass index, employment status, and neighborhood-level socio-economic status). We fitted linear models, linear models in subsets, Shape-Constrained Health Impact Functions (SCHIF), and natural cubic spline models to assess the shape of the association between air pollution and lung cancer at concentrations below existing standards and guidelines. RESULTS: The analyses included 307,550 cohort participants. During a mean follow-up of 18.1 years, 3956 incident lung cancer cases occurred. Median (Q1, Q3) annual (2010) exposure levels of NO2, PM2.5, BC and O3 (warm season) were 24.2 µg/m3 (19.5, 29.7), 15.4 µg/m3 (12.8, 17.3), 1.6 10-5m-1 (1.3, 1.8), and 86.6 µg/m3 (78.5, 92.9), respectively. We observed a higher risk for lung cancer with higher exposure to PM2.5 (HR: 1.13, 95% CI: 1.05, 1.23 per 5 µg/m3). This association was robust to adjustment for other pollutants. The SCHIF, spline and subset analyses suggested a linear or supra-linear association with no evidence of a threshold. In subset analyses, risk estimates were clearly elevated for the subset of subjects with exposure below the EU limit value of 25 µg/m3. We did not observe associations between NO2, BC or O3 and lung cancer incidence. CONCLUSIONS: Long-term ambient PM2.5 exposure is associated with lung cancer incidence even at concentrations below current EU limit values and possibly WHO Air Quality Guidelines.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Neoplasias Pulmonares , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Exposição Ambiental/análise , Europa (Continente)/epidemiologia , Humanos , Neoplasias Pulmonares/induzido quimicamente , Neoplasias Pulmonares/epidemiologia , Material Particulado/análise
17.
Environ Int ; 146: 106267, 2021 01.
Artigo em Inglês | MEDLINE | ID: mdl-33276316

RESUMO

BACKGROUND: Air pollution has been suggested as a risk factor for chronic obstructive pulmonary disease (COPD), but evidence is sparse and inconsistent. OBJECTIVES: We examined the association between long-term exposure to low-level air pollution and COPD incidence. METHODS: Within the 'Effects of Low-Level Air Pollution: A Study in Europe' (ELAPSE) study, we pooled data from three cohorts, from Denmark and Sweden, with information on COPD hospital discharge diagnoses. Hybrid land use regression models were used to estimate annual mean concentrations of particulate matter with a diameter < 2.5 µm (PM2.5), nitrogen dioxide (NO2), and black carbon (BC) in 2010 at participants' baseline residential addresses, which were analysed in relation to COPD incidence using Cox proportional hazards models. RESULTS: Of 98,058 participants, 4,928 developed COPD during 16.6 years mean follow-up. The adjusted hazard ratios (HRs) and 95% confidence intervals for associations with COPD incidence were 1.17 (1.06, 1.29) per 5 µg/m3 for PM2.5, 1.11 (1.06, 1.16) per 10 µg/m3 for NO2, and 1.11 (1.06, 1.15) per 0.5 10-5m-1 for BC. Associations persisted in subset participants with PM2.5 or NO2 levels below current EU and US limit values and WHO guidelines, with no evidence for a threshold. HRs for NO2 and BC remained unchanged in two-pollutant models with PM2.5, whereas the HR for PM2.5 was attenuated to unity with NO2 or BC. CONCLUSIONS: Long-term exposure to low-level air pollution is associated with the development of COPD, even below current EU and US limit values and possibly WHO guidelines. Traffic-related pollutants NO2 and BC may be the most relevant.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Doença Pulmonar Obstrutiva Crônica , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Estudos de Coortes , Exposição Ambiental/análise , Europa (Continente)/epidemiologia , Humanos , Incidência , Material Particulado/análise , Material Particulado/toxicidade , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Doença Pulmonar Obstrutiva Crônica/etiologia , Suécia
18.
Eur Respir J ; 2020 Dec 10.
Artigo em Inglês | MEDLINE | ID: mdl-33303534

RESUMO

BACKGROUND: Long-term exposure to ambient air pollution has been linked to childhood-onset asthma, while evidence is still insufficient. Within the multicentre project "Effects of Low-Level Air Pollution: A Study in Europe" (ELAPSE), we examined the associations of long-term exposures to particulate matter with diameter<2.5 µm (PM2.5), nitrogen dioxide (NO2), and black carbon (BC) with asthma incidence in adults. METHODS: We pooled data from three cohorts in Denmark and Sweden with information on asthma hospital diagnoses. The average concentrations of air pollutants in 2010 were modelled by hybrid land use regression models at participants' baseline residential addresses. Associations of air pollution exposures with asthma incidence were explored with Cox proportional hazard models, adjusting for potential confounders. RESULTS: Of 98 326 participants, 1965 developed asthma during a 16.6 years mean follow-up. We observed associations in fully adjusted models with hazard ratios and 95% confidence intervals of 1.22 (1.04-1.43) per 5 µg·m-3 for PM2.5, 1.17 (1.10-1.25) per 10 µg·m-3 for NO2, and 1.15 (1.08-1.23) per 0.5 10-5 m-1 for BC. Hazard ratios were larger in cohort subsets with exposure levels below the EU and US limit values and possibly WHO guidelines for PM2.5 and NO2. NO2 and BC estimates remained unchanged in two-pollutant models with PM2.5, whereas PM2.5 estimates were attenuated to unity. The concentration response curves showed no evidence of a threshold. CONCLUSIONS: Long-term exposure to air pollution, especially from fossil fuel combustion sources such as motorised traffic, was associated with adult-onset asthma, even at levels below the current limit values.

19.
Environ Sci Technol ; 54(24): 15698-15709, 2020 12 15.
Artigo em Inglês | MEDLINE | ID: mdl-33237771

RESUMO

We developed Europe-wide models of long-term exposure to eight elements (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) in particulate matter with diameter <2.5 µm (PM2.5) using standardized measurements for one-year periods between October 2008 and April 2011 in 19 study areas across Europe, with supervised linear regression (SLR) and random forest (RF) algorithms. Potential predictor variables were obtained from satellites, chemical transport models, land-use, traffic, and industrial point source databases to represent different sources. Overall model performance across Europe was moderate to good for all elements with hold-out-validation R-squared ranging from 0.41 to 0.90. RF consistently outperformed SLR. Models explained within-area variation much less than the overall variation, with similar performance for RF and SLR. Maps proved a useful additional model evaluation tool. Models differed substantially between elements regarding major predictor variables, broadly reflecting known sources. Agreement between the two algorithm predictions was generally high at the overall European level and varied substantially at the national level. Applying the two models in epidemiological studies could lead to different associations with health. If both between- and within-area exposure variability are exploited, RF may be preferred. If only within-area variability is used, both methods should be interpreted equally.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Monitoramento Ambiental , Europa (Continente) , Modelos Lineares , Material Particulado/análise , Zinco/análise
20.
Environ Int ; 144: 105998, 2020 11.
Artigo em Inglês | MEDLINE | ID: mdl-33032072

RESUMO

BACKGROUND: WHO has published several volumes of Global Air Quality Guidelines to provide guidance on the health risks associated with exposure to outdoor air pollution. As new scientific evidence is generated, air quality guidelines need to be periodically revised and, where necessary, updated. OBJECTIVES: The aims of the study were 1) to summarise the available evidence on the effect of long-term exposure to ozone (O3) and nitrogen dioxide (NO2) on mortality; 2) and to assess concentration response functions (CRF), their shape and the minimum level of exposures measured in studies to support WHO's update of the global air quality guidelines. DATA SOURCES: We conducted a systematic literature search of the Medline, Embase and Web of Science databases following a protocol proposed by WHO and applied Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) guidelines for reporting our results. STUDY ELIGIBILITY CRITERIA: Cohort studies in human populations (including sub-groups at risk) exposed to long-term concentrations of NO2 and O3. Outcomes assessed were all-cause, respiratory, Chronic Obstructive Pulmonary Disease (COPD) and Acute Lower Respiratory Infection (ALRI) mortality. STUDY APPRAISAL AND SYNTHESIS METHODS: Studies included in the meta-analyses were assessed using a new Risk of Bias instrument developed by a group of experts convened by WHO. Study results are presented in forest plots and quantitative meta-analyses were conducted using random effects models. The certainty of evidence was assessed using a newly developed adaptation of GRADE. RESULTS: The review identified 2068 studies of which 95 were subject to full-text review with 45 meeting the inclusion criteria. An update in September 2018 identified 159 studies with 1 meeting the inclusion criteria. Of the 46 included studies, 41 reported results for NO2 and 20 for O3. The majority of studies were from the USA and Europe with the remainder from Canada, China and Japan. Forty-two studies reported results for all-cause mortality and 22 for respiratory mortality. Associations for NO2 and mortality were positive; random-effects summary relative risks (RR) were 1.02 (95% CI: 1.01, 1.04), 1.03 (1.00, 1.05), 1.03 (1.01, 1.04) and 1.06 (1.02, 1.10) per 10 µg/m3 for all-cause (24 cohorts), respiratory (15 cohorts), COPD (9 cohorts) and ALRI (5 cohorts) mortality respectively. The review identified high levels of heterogeneity for all causes of death except COPD. A small number of studies investigated the shape of the concentration-response relationship and generally found little evidence to reject the assumption of linearity across the concentration range. Studies of O3 using annual metrics showed the associations with all-cause and respiratory mortality were 0.97 (0.93, 1.02) and 0.99 (0.89, 1.11) per 10 µg/m3 respectively. For studies using peak O3 metrics, the association with all-cause mortality was 1.01 (1.00, 1.02) and for respiratory mortality 1.02 (0.99, 1.05), each per 10 µg/m3. The review identified high levels of heterogeneity. Few studies investigated the shape of the concentration-response relationship. Certainty in the associations (adapted GRADE) with mortality was rated low to moderate for each exposure-outcome pair, except for NO2 and COPD mortality which was rated high. LIMITATIONS: The substantial heterogeneity for most outcomes in the review requires explanation. The evidence base is limited in terms of the geographical spread of the study populations and, for some outcomes, the small number of independent cohorts for meta-analysis precludes meaningful meta-regression to explore causes of heterogeneity. Relatively few studies assessed specifically the shape of the CRF or multi-pollutant models. CONCLUSIONS: The short-comings in the existing literature base makes determining the precise nature (magnitude and linearity) of the associations challenging. Certainty of evidence assessments were moderate or low for both NO2 and O3 for all causes of mortality except for NO2 and COPD mortality where the certainty of the evidence was judged as high.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Canadá , China , Europa (Continente) , Humanos , Japão , Dióxido de Nitrogênio/análise , Dióxido de Nitrogênio/toxicidade
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...