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1.
Sci Total Environ ; 757: 143960, 2021 Feb 25.
Artigo em Inglês | MEDLINE | ID: mdl-33321334

RESUMO

Previous studies have suggested an increased risk of depression related to air pollutants. This study investigated the relationship of air pollutant exposure and meteorological factors with depression. The Korean National Health Insurance Service-Health Screening Cohort from 2002 to 2013 was analyzed. In total, 25,589 depression participants were 1:4 matched with 102,356 control participants for age, sex, income, and region of residence. Depression was defined based on a diagnosis (ICD-10: F31-33) by a psychiatric physician. Meteorological factors and air pollutants including sulfur dioxide (SO2) (ppm), nitrogen dioxide (NO2) (ppm), ozone (O3) (ppm), carbon monoxide (CO) (ppm), and particulate matter with an aerodynamic diameter <10 µm (PM10) (µg/m3) during the 30 days and 365 days before the index date were analyzed for associations with depression using conditional logistic regression. Subgroup analyses were performed according to age, sex, income, and region of residence. The odds ratios (ORs) for depression were 1.05 (95% CI = 1.02-1.08) at 365 days for 1 h less of sunshine. The ORs for depression were 1.02 (95% CI = 1.01-1.03) and 1.03 (95% CI = 1.00-1.05) at 30 days and 365 days for PM10 (10 µg/m3), respectively. The ORs for depression were 1.18 (95% CI = 1.04-1.35) and 1.25 (95% CI = 1.07-1.47) at 30 days and 365 days for CO (ppm), respectively. In the subgroup analyses, the overall results were consistent. However, statistical significance diminished in the younger, high-income, and urban resident subgroups. Both short- and long-term exposure to PM10 and CO and a reduced duration of sunshine were related to an increased risk of depression.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Ozônio , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Estudos de Casos e Controles , Depressão/epidemiologia , Exposição Ambiental , Humanos , Dióxido de Nitrogênio/efeitos adversos , Dióxido de Nitrogênio/análise , Ozônio/efeitos adversos , Material Particulado/efeitos adversos , Material Particulado/análise , Dióxido de Enxofre/análise , Luz Solar
2.
Environ Health ; 19(1): 81, 2020 07 08.
Artigo em Inglês | MEDLINE | ID: mdl-32641060

RESUMO

BACKGROUND: Inconclusive evidence has suggested a possible link between air pollution and central nervous system (CNS) tumors. We investigated a range of air pollutants in relation to types of CNS tumors. METHODS: We identified all (n = 21,057) intracranial tumors in brain, meninges and cranial nerves diagnosed in Denmark between 1989 and 2014 and matched controls on age, sex and year of birth. We established personal 10-year mean residential outdoor exposure to particulate matter < 2.5 µm (PM2.5), nitrous oxides (NOX), primary emitted black carbon (BC) and ozone. We used conditional logistic regression to calculate odds ratios (OR) linearly (per interquartile range (IQR)) and categorically. We accounted for personal income, employment, marital status, use of medication as well as socio-demographic conditions at area level. RESULTS: Malignant tumors of the intracranial CNS was associated with BC (OR: 1.034, 95%CI: 1.005-1.065 per IQR. For NOx the OR per IQR was 1.026 (95%CI: 0.998-1.056). For malignant non-glioma tumors of the brain we found associations with PM2.5 (OR: 1.267, 95%CI: 1.053-1.524 per IQR), BC (OR: 1.049, 95%CI: 0.996-1.106) and NOx (OR: 1.051, 95% CI: 0.996-1.110). CONCLUSION: Our results suggest that air pollution is associated with malignant intracranial CNS tumors and malignant non-glioma of the brain. However, additional studies are needed.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Neoplasias Encefálicas/epidemiologia , Exposição Ambiental/efeitos adversos , Material Particulado/efeitos adversos , Adulto , Idoso , Idoso de 80 Anos ou mais , Poluição do Ar/efeitos adversos , Neoplasias Encefálicas/induzido quimicamente , Estudos de Casos e Controles , Dinamarca/epidemiologia , Feminino , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Óxido Nitroso/efeitos adversos , Ozônio/efeitos adversos , Fatores de Risco , Fuligem/efeitos adversos
3.
Artigo em Inglês | MEDLINE | ID: mdl-32471209

RESUMO

Although hospital length of stay (LOS) has been identified as a proxy measure of healthcare expenditures in the United States, there are limited studies investigating the potentially important association between outdoor air pollution and LOS for pediatric asthma. This study aims to examine the effect of ambient air pollution on LOS among children with asthma in South Texas. It included retrospective data on 711 children aged 5-18 years old admitted for asthma to a pediatric tertiary care hospital in South Texas between 2010 and 2014. Air pollution data including particulate matter (PM2.5) and ozone were collected from the U.S. Centers for Disease Control and Prevention. The multivariate binomial logistic regression analyses were performed to determine the association between each air pollutant and LOS, controlling for confounders. The regression models showed the increased ozone level was significantly associated with prolonged LOS in the single- and two-pollutant models (p < 0.05). Furthermore, in the age-stratified models, PM2.5 was positively associated with LOS among children aged 5-11 years old (p < 0.05). In conclusion, this study revealed a concerning association between ambient air pollution and LOS for pediatric asthma in South Texas.


Assuntos
Poluição do Ar/efeitos adversos , Asma , Exposição Ambiental/efeitos adversos , Tempo de Internação , Adolescente , Poluição do Ar/análise , Asma/epidemiologia , Criança , Pré-Escolar , Exposição Ambiental/análise , Feminino , Humanos , Masculino , Ozônio/efeitos adversos , Ozônio/análise , Material Particulado/efeitos adversos , Material Particulado/análise , Estudos Retrospectivos , Texas/epidemiologia
4.
Rev Mal Respir ; 37(5): 389-398, 2020 May.
Artigo em Francês | MEDLINE | ID: mdl-32278507

RESUMO

Few studies have examined the effects of air pollution in diffuse interstitial lung disease and they have focused on small numbers of patients. Most data are available in idiopathic pulmonary fibrosis and studies suggest that the level of exposure to pollutants may influence the development of acute exacerbations (ozone and NO2), their incidence (NO2), decline in respiratory function (PM10) and death (PM10 and PM2.5). Several studies show an increase in the incidence of rheumatoid arthritis in people living near busy roads. In systemic scleroderma, hypersensitivity pneumonitis and sarcoidosis although negative effects of pollution have been reported the data are insufficient to be conclusive. Nevertheless, the observed effects of air pollution are consistent with those described for other chronic respiratory diseases. Exposure to pollution induces oxidative stress, chronic inflammation and shortening of telomeres, which are all mechanisms described in fibrogenesis. New epidemiological studies are needed with individual measurements of exposure to outdoor and indoor pollution, as well as fundamental studies to clarify the effect of pollution on fibrogenesis.


Assuntos
Poluição do Ar/efeitos adversos , Doenças Pulmonares Intersticiais/etiologia , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/toxicidade , Poluição do Ar/estatística & dados numéricos , Alveolite Alérgica Extrínseca/epidemiologia , Alveolite Alérgica Extrínseca/etiologia , Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/etiologia , Exposição Ambiental/efeitos adversos , Humanos , Fibrose Pulmonar Idiopática/epidemiologia , Fibrose Pulmonar Idiopática/etiologia , Incidência , Doenças Pulmonares Intersticiais/epidemiologia , Doenças Pulmonares Intersticiais/fisiopatologia , Ozônio/efeitos adversos , Material Particulado/efeitos adversos , Fenômenos Fisiológicos Respiratórios/efeitos dos fármacos , Fatores de Risco
5.
Environ Geochem Health ; 42(10): 3303-3316, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32328899

RESUMO

As the pollution of fine particulate matter (≤ 2.5 µg/m3 in aerodynamic diameter; PM2.5) and ozone (O3) is becoming more and more serious in developing countries, we, hereby, investigated the effects of PM2.5, constituents of PM2.5 and O3 on the lung function of children in Tianjin, China. The lung functions of 198 pupils from nine primary schools in Tianjin were examined (repeated five times) during the months of October to December in 2016, 2017 and 2018, respectively. And the mixed-effect models were used to evaluate the effects of air pollutants. A 10 µg/m3 increase in PM2.5 and O3-8h might lead to reductions of forced vital capacity (FVC) in 1.03% (- 1.87 to - 0.19%) and 21.09% (- 25.54 to - 16.58%), respectively, while a 10 ng/m3 increment in ANY might account for the 166.44% (- 221.32 to - 112.31%) decreases in FVC. PM2.5 and O3-8h might be more harmful to the lung functions of female students and participants with PS exposure at home. And the main sources of pollution resulting in the decrease in pulmonary function might be traffic pollution and coal combustion.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Exposição Ambiental/efeitos adversos , Pulmão/efeitos dos fármacos , Ozônio/efeitos adversos , Material Particulado/efeitos adversos , Capacidade Vital/efeitos dos fármacos , Adolescente , Poluentes Atmosféricos/análise , Criança , China , Exposição Ambiental/análise , Feminino , Humanos , Masculino , Ozônio/análise , Material Particulado/análise
6.
Environ Int ; 138: 105676, 2020 05.
Artigo em Inglês | MEDLINE | ID: mdl-32217428

RESUMO

BACKGROUND: High-income nations have the highest rates of inflammatory bowel disease (IBD). The incidence of pediatric-onset IBD is increasing faster than IBD diagnosed in older individuals. Previous epidemiological studies have shown that air pollution might be a risk factor for development of earlier-onset IBD, but results remain mixed. OBJECTIVES: The objective of this study was to evaluate the associations between maternal and early-life exposures to nitrogen dioxide (NO2), fine particulate matter (PM2.5), ozone (O3,) and oxidant capacity (Ox) and risk of pediatric-onset IBD diagnosis. METHODS: We conducted a retrospective cohort study using linked population-based health administrative data. Singleton livebirths in Ontario, Canada between April 1st, 1991 and March 31st, 2014 were included. We investigated the association between weekly exposures during pregnancy and annual exposures from birth until the age of 18 years, and IBD diagnosed <18 years of age using Cox proportional hazards models. We reported hazard ratios (HR) and 95% confidence intervals (CI) for an associated increase in the interquartile range (IQR) of each pollutant. Models were mutually adjusted for exposures in both prenatal and postnatal periods, as well as for sex, rurality of residence at birth, maternal IBD, and neighborhood income. RESULTS: 2,218,789 newborns were included in this study, of whom 2491 developed IBD during follow-up. Increased associations with pediatric-onset IBD were noted for childhood exposure to Ox (HR 1.08, 95% CI 1.01-1.16). IBD development was also associated with Ox during the second trimester (HR 1.21, 95% CI 1.03-1.42), but not the overall pregnancy period (HR 1.12, 95% CI 0.79-1.59). There were no associations of IBD with exposure to NO2, PM2.5, or O3. DISCUSSION: Exposure to Ox during childhood was associated with IBD < 18 years. This suggests that air pollution may impact the developing child physiology in such a way that leads to early onset of IBD.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Doenças Inflamatórias Intestinais , Ozônio , Adolescente , Idoso , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Criança , Estudos de Coortes , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Feminino , Humanos , Recém-Nascido , Doenças Inflamatórias Intestinais/epidemiologia , Doenças Inflamatórias Intestinais/etiologia , Dióxido de Nitrogênio/análise , Ontário/epidemiologia , Ozônio/efeitos adversos , Ozônio/análise , Material Particulado/efeitos adversos , Material Particulado/análise , Gravidez , Estudos Retrospectivos
7.
Artigo em Inglês | MEDLINE | ID: mdl-32210080

RESUMO

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death globally and ozone exposure is a main cause of its disease burden. However, studies on COPD hospitalizations from short-term ambient level ozone exposure have not generated consensus results. To address the knowledge gap, comprehensive and systematic searches in several databases were conducted using specific keywords for publications up to February 14, 2020. Random-effect models were used to derive overall excess risk estimates between short-term ambient-level ozone exposure and COPD hospitalizations. The influence analyses were used to test the robustness of the results. Both meta-regression and subgroup analyses were used to explore the sources of heterogeneity and potential modifying factors. Based on the results from 26 eligible studies, the random-effect model analyses show that a 10 µg/m3 increase in maximum 8-h ozone concentration was associated with 0.84% (95% CI: 0.09%, 1.59%) higher COPD hospitalizations. The estimates were higher for warm season and multiple-day lag but lower for old populations. Results from subgroup analyses also indicate a multiple-day lag trend and bigger significant health effects during longer day intervals. Although characteristics of individual studies added modest heterogeneity to the overall estimates, the results remained robust during further analyses and exhibited no evidence of publication bias. Our systematic review and meta-analysis indicate that short-term ambient level ozone exposure was associated with increased risk of COPD hospitalizations. The significant association with multiple-day lag trend indicates that a multiple-day exposure metric should be considered for establishing ambient ozone quality and exposure standards for improvement of population health. Future investigations and meta-analysis studies should include clinical studies as well as more careful lag selection protocol.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Hospitalização , Ozônio/efeitos adversos , Doença Pulmonar Obstrutiva Crônica , Exposição Ambiental/efeitos adversos , Humanos , Doença Pulmonar Obstrutiva Crônica/induzido quimicamente , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Estações do Ano
8.
Artigo em Inglês | MEDLINE | ID: mdl-32012989

RESUMO

Birth season is an important factor that reflects prenatal nutritional conditions during early development, and which might have lifelong impacts on health. Moreover, ambient ozone pollution has been considered an important environmental risk factor for hypertension. However, whether birth season affects vulnerability to the effect of ambient ozone exposure on late-life hypertension is still unknown. A flexible case-crossover design was used to explore the effect of ambient ozone exposure on the disease burden of hypertension using years of life lost (YLL) in the elderly population in a coastal city in South China from 2013 to 2016. The influence of birth season was also explored. Ozone exposure was significantly associated with increased YLL from hypertension. The association was higher in the elderly individuals who were born in autumn than in those born in other seasons. Specifically, every 10 µg/m3 increase in ozone was associated with 0.68 (95% CI: 0.27, 1.10) YLL from hypertension in the elderly population born in autumn, while nonsignificant associations were found for those born in other seasons. The birth season, which affects the nutritional condition during early development, could affect vulnerability to the effect of ambient ozone exposure on the disease burden of hypertension in late life. The findings highlighted the importance of taking birth season into consideration when exploring the hypertensive effects of ozone exposure.


Assuntos
Poluição do Ar/efeitos adversos , Exposição Ambiental/efeitos adversos , Hipertensão/epidemiologia , Ozônio/efeitos adversos , Estações do Ano , Idoso , China/epidemiologia , Estudos Cross-Over , Humanos , Material Particulado
9.
BMJ ; 368: m108, 2020 02 10.
Artigo em Inglês | MEDLINE | ID: mdl-32041707

RESUMO

OBJECTIVE: To assess short term mortality risks and excess mortality associated with exposure to ozone in several cities worldwide. DESIGN: Two stage time series analysis. SETTING: 406 cities in 20 countries, with overlapping periods between 1985 and 2015, collected from the database of Multi-City Multi-Country Collaborative Research Network. POPULATION: Deaths for all causes or for external causes only registered in each city within the study period. MAIN OUTCOME MEASURES: Daily total mortality (all or non-external causes only). RESULTS: A total of 45 165 171 deaths were analysed in the 406 cities. On average, a 10 µg/m3 increase in ozone during the current and previous day was associated with an overall relative risk of mortality of 1.0018 (95% confidence interval 1.0012 to 1.0024). Some heterogeneity was found across countries, with estimates ranging from greater than 1.0020 in the United Kingdom, South Africa, Estonia, and Canada to less than 1.0008 in Mexico and Spain. Short term excess mortality in association with exposure to ozone higher than maximum background levels (70 µg/m3) was 0.26% (95% confidence interval 0.24% to 0.28%), corresponding to 8203 annual excess deaths (95% confidence interval 3525 to 12 840) across the 406 cities studied. The excess remained at 0.20% (0.18% to 0.22%) when restricting to days above the WHO guideline (100 µg/m3), corresponding to 6262 annual excess deaths (1413 to 11 065). Above more lenient thresholds for air quality standards in Europe, America, and China, excess mortality was 0.14%, 0.09%, and 0.05%, respectively. CONCLUSIONS: Results suggest that ozone related mortality could be potentially reduced under stricter air quality standards. These findings have relevance for the implementation of efficient clean air interventions and mitigation strategies designed within national and international climate policies.


Assuntos
Poluição do Ar/efeitos adversos , Exposição Ambiental/efeitos adversos , Saúde Global/estatística & dados numéricos , Mortalidade , Ozônio/efeitos adversos , Poluição do Ar/análise , Cidades/estatística & dados numéricos , Mudança Climática/mortalidade , Exposição Ambiental/normas , Política Ambiental , Humanos , Cooperação Internacional , Ozônio/análise , Estações do Ano
10.
Int J Health Plann Manage ; 35(1): 79-103, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31149758

RESUMO

This study aims to examine the correlations between air pollution and dynamic stroke mortality, which is defined as the daily real-time number of deaths from stroke. Death data were obtained from daily medical records of 7230 incidents from the Center for Disease Control and Prevention in the Longquanyi District of China from 2016 to 2017. Air pollution data were obtained from environmental monitoring stations in the Longquanyi District. Time series analysis using generalized additive Poisson regression models was applied, and single-pollutant and two-pollutant adjusted models were utilized. Furthermore, categories based on gender, age, and meteorological factors were considered in the analysis. The results indicated that PM2.5, PM10, O3 , and CO had significant effects on dynamic stroke mortality, which were stronger for older people and during the cold season. This study helps hospital managers, patients, and governments seeking to prevent and control the effects of air pollution on the risks of stroke.


Assuntos
Poluição do Ar/efeitos adversos , Acidente Vascular Cerebral/epidemiologia , Fatores Etários , Idoso , Poluição do Ar/estatística & dados numéricos , Monóxido de Carbono/efeitos adversos , Monóxido de Carbono/análise , China/epidemiologia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Ozônio/efeitos adversos , Ozônio/análise , Material Particulado/efeitos adversos , Material Particulado/análise , Distribuição de Poisson , Fatores de Risco , Estações do Ano , Fatores Sexuais , Acidente Vascular Cerebral/etiologia
11.
Biol Sex Differ ; 10(1): 54, 2019 12 02.
Artigo em Inglês | MEDLINE | ID: mdl-31791410

RESUMO

BACKGROUND: Exposure to air pollution and high levels of noise have both been independently associated with the development of adverse pregnancy outcomes including low birth weight. However, exposure to such environmental stressors rarely occurs in isolation and is often co-localized, especially in large urban areas. METHODS: The purpose of this study was to compare the effects of combined exposure to noise (N) or ozone (O3), compared to either exposure alone. Long-Evans dams were exposed to air or 0.4 ppm ozone for 4 h on gestation day (GD) 5 and 6, coinciding with implantation receptivity. A subset of dams from each exposure group was further exposed to intermittent white noise (~ 85 dB) throughout the dark cycle following each inhalation exposure (n = 14 - 16/group). Uterine artery ultrasound was performed on GD 15 and 21. Fetal growth characteristics and indicators of placental nutrient status were measured at GD 21. RESULTS: Exposure to ozone + quiet (O3 + Q) conditions reduced uterine arterial resistance at GD 15 compared to air + quiet (A + Q) exposure, with no further reduction by GD 21. By contrast, exposure to air + noise (A + N) significantly increased uterine arterial resistance at both GD 15 and 21. Notably, while peri-implantation exposure to O3 + Q conditions reduced male fetal weight at GD 21, this effect was not observed in the air + noise (A + N) or the ozone + noise (O3 + N) exposure groups. Fetal weight in female offspring was not reduced by ozone exposure alone (O3 + Q), nor was it affected by air + noise (A + N) or by combined ozone + noise (O3 + N) exposure. CONCLUSIONS: These data indicate that exposure to ozone and noise differentially impact uterine blood flow, particularly at mid-gestation, with only ozone exposure being associated with sex-dependent fetal growth retardation in male offspring.


Assuntos
Poluição do Ar/efeitos adversos , Desenvolvimento Fetal , Retardo do Crescimento Fetal/etiologia , Ruído/efeitos adversos , Ozônio/efeitos adversos , Caracteres Sexuais , Animais , Exposição Ambiental/efeitos adversos , Feminino , Retardo do Crescimento Fetal/fisiopatologia , Masculino , Ratos Long-Evans , Fluxo Sanguíneo Regional , Artéria Uterina/fisiologia
12.
Sci Rep ; 9(1): 17925, 2019 11 29.
Artigo em Inglês | MEDLINE | ID: mdl-31784596

RESUMO

Agonists of ß2 adrenergic receptors (ß2AR) and glucocorticoid receptors (GR) are prescribed to treat pulmonary diseases. Since ozone effects are mediated through the activation of AR and GR, we hypothesized that the treatment of rats with relevant therapeutic doses of long acting ß2AR agonist (LABA; clenbuterol; CLEN) and/or GR agonist (dexamethasone; DEX) would exacerbate ozone-induced pulmonary and systemic changes. In the first study, male 12-week-old Wistar-Kyoto rats were injected intraperitoneally with vehicle (saline), CLEN (0.004 or 0.02 mg/kg), or DEX (0.02 or 0.1 mg/kg). Since dual therapy is commonly used, in the second study, rats received either saline or combined CLEN + DEX (each at 0.005 or 0.02 mg/kg) one day prior to and on both days of exposure (air or 0.8ppm ozone, 4 hr/day x 2-days). In air-exposed rats CLEN, DEX or CLEN + DEX did not induce lung injury or inflammation, however DEX and CLEN + DEX decreased circulating lymphocytes, spleen and thymus weights, increased free fatty acids (FFA) and produced hyperglycemia and glucose intolerance. Ozone exposure of vehicle-treated rats increased bronchoalveolar lavage fluid protein, albumin, neutrophils, IL-6 and TNF-α. Ozone decreased circulating lymphocytes, increased FFA, and induced hypeerglycemia  and glucose intolerance. Drug treatment did not reverse ozone-induced ventillatory changes, however, lung effects (protein and albumin leakage, inflammation, and IL-6 increase) were exacerbated by CLEN and CLEN + DEX pre-treatment in a dose-dependent manner (CLEN > CLEN + DEX). Systemic effects induced by DEX and CLEN + DEX but not CLEN in air-exposed rats were analogous to and more pronounced than those induced by ozone. These data suggest that adverse air pollution effects might be exacerbated in people receiving LABA or LABA plus glucocorticoids.


Assuntos
Agonistas de Receptores Adrenérgicos beta 2/farmacologia , Clembuterol/farmacologia , Dexametasona/farmacologia , Glucocorticoides/farmacologia , Pulmão/efeitos dos fármacos , Ozônio/farmacologia , Agonistas de Receptores Adrenérgicos beta 2/efeitos adversos , Animais , Clembuterol/efeitos adversos , Dexametasona/efeitos adversos , Interações Medicamentosas , Ácidos Graxos/metabolismo , Glucocorticoides/efeitos adversos , Glucose/metabolismo , Interleucina-6/metabolismo , Pulmão/metabolismo , Linfócitos/efeitos dos fármacos , Masculino , Ozônio/efeitos adversos , Ratos , Ratos Wistar , Baço/efeitos dos fármacos , Baço/metabolismo , Timo/efeitos dos fármacos , Timo/metabolismo , Fator de Necrose Tumoral alfa/metabolismo
13.
Front Immunol ; 10: 2890, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31867021

RESUMO

The respiratory effects of O3 are well established. High ambient O3 concentrations are associated with respiratory symptoms, declines in pulmonary function, asthma exacerbations, and even mortality. The metabolic effects of O3 are less well appreciated. Here we review data indicating that O3 exposure leads to glucose intolerance and hyperlipidemia, characteristics of the metabolic syndrome. We also review the role of stress hormones in these events. We describe how the metabolic effects of O3, including effects within the lungs, are exacerbated in the setting of the metabolic derangements of obesity and we discuss epidemiological data indicating an association between ambient O3 exposure and diabetes. We conclude by describing the role of the gut microbiome in the regulation of metabolism and by discussing data indicating a link between the gut microbiome and pulmonary responses to O3.


Assuntos
Metabolismo Energético , Exposição Ambiental , Ozônio , Animais , Suscetibilidade a Doenças , Metabolismo Energético/efeitos dos fármacos , Exposição Ambiental/efeitos adversos , Humanos , Síndrome Metabólica/etiologia , Síndrome Metabólica/metabolismo , Microbiota , Especificidade de Órgãos , Ozônio/efeitos adversos , Roedores/metabolismo
14.
Curr Med Sci ; 39(6): 1019-1028, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31845236

RESUMO

Gestational hypertension (GH) is a common complication during pregnancy. GH is regarded as a potential public health challenge for pregnant women and infants. Limited evidence has linked ambient air pollution to an increased GH risk. However, most of the studies were conducted in developed countries, with inconsistent results obtained. The present study was performed to explore whether exposure to particulate matters with an aerodynamic diameter < 2.5 (PM2.5) and ozone (O3) was related to elevated odds of GH in a Chinese population. This population-based cohort study involved 38 115 pregnant women in Wuhan, China. All information was collected from the Wuhan Maternal and Child Health Management Information System, using standardized quality control. The daily air pollutant data for PM2.5 and O3 were obtained from the 20 monitoring stations of the Wuhan Environmental Monitoring Center during 2014. The nearest monitor approach was applied to individual exposure assessment of PM2.5 and O3 for each participant. After adjusting for major confounders and other air pollutants, a 10 µg/m3 increase in PM2.5 and O3 concentrations was found to correlate to a 1.14-fold [95% confidence interval (95% CI): 1.09, 1.20] and a 1.05-fold (95% CI: 1.02, 1.07) increase in GH risk, respectively. Additionally, stronger relationships between GH risk and PM2.5 and O3 exposure were observed in women who conceived in winter and summer, respectively. These findings suggest that air pollutants may contribute to the development of GH.


Assuntos
Hipertensão Induzida pela Gravidez/epidemiologia , Ozônio/efeitos adversos , Material Particulado/análise , Adulto , Estudos de Coortes , Feminino , Humanos , Hipertensão Induzida pela Gravidez/induzido quimicamente , Idade Materna , Tamanho da Partícula , Material Particulado/efeitos adversos , Gravidez , Estações do Ano , Adulto Jovem
15.
Environ Int ; 133(Pt A): 105110, 2019 12.
Artigo em Inglês | MEDLINE | ID: mdl-31610366

RESUMO

BACKGROUND: Ambient air pollution and maternal diabetes may affect common biological pathways underlying adverse neurodevelopmental effects. However, joint effects of maternal diabetes and air pollution on autism spectrum disorder (ASD) have not been studied. OBJECTIVE: We evaluated whether prenatal and early-life air pollution exposure interacts with maternal diabetes status to affect ASD risk. METHODS: This retrospective cohort study included 246,420 singleton children born in Kaiser Permanente Southern California hospitals in 1999-2009. Children were followed from birth until age 5, during which 2471 ASD cases were diagnosed. Ozone (O3), particulate matter < 2.5 µm (PM2.5) and <10 µm in aerodynamic diameter, and nitrogen dioxide measured at regulatory air monitoring stations were interpolated to estimate exposures during preconception and each pregnancy trimester, and first year of life at each child's birth address. Hazard ratios (HRs) for ASD were estimated adjusting for birth year, KPSC service areas, and relevant maternal and child characteristics. For each exposure window, interactions were tested between pollutants and a 4-category maternal diabetes variable (none, GDM ≥ 24 and <24 weeks' gestation, and pre-existing type 2 diabetes). For an exposure window with statistically significant global interaction between pollutant and diabetes (p < 0.05), pollutant-associated HRs were estimated separately for each category of maternal diabetes. RESULTS: There were associations of ASD with preconception, first and third trimesters, and first year of life PM2.5, but not with other pollutants. There were, however, interactions of maternal diabetes with first trimester and first year of life O3. Increased ASD risk was associated with first trimester O3 among mothers with GDM < 24 weeks' gestation [adjusted HR 1.50 per 15.7 ppb O3 (95% CI: 1.08-2.09)]. No O3 associations with ASD were observed in other categories of maternal diabetes. CONCLUSIONS: GDM onset early in pregnancy may increase children's susceptibility to prenatal O3-associated ASD risk. These novel findings merit further investigation.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Transtorno do Espectro Autista/etiologia , Diabetes Gestacional/etiologia , Exposição Materna , Adulto , Poluentes Atmosféricos/análise , California , Pré-Escolar , Estudos de Coortes , Diabetes Mellitus Tipo 2/complicações , Feminino , Humanos , Lactente , Recém-Nascido , Masculino , Dióxido de Nitrogênio/análise , Ozônio/efeitos adversos , Ozônio/análise , Material Particulado/efeitos adversos , Material Particulado/análise , Gravidez , Trimestres da Gravidez , Modelos de Riscos Proporcionais , Estudos Retrospectivos
16.
J Plant Res ; 132(6): 789-811, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31628563

RESUMO

The study aimed to assess response of juvenile progeny of seven forest tree species, Pinus sylvestris, Picea abies, Betula pendula, Alnus glutinosa, Populus tremula, Quercus robur and Fraxinus excelsior, and their populations to different combinations of climate change-related multiple stressors, simulated in a phytotron under elevated CO2 concentration: (1) heat + elevated humidity (HW); (2) heat + frost + drought (HFD); (3) heat + elevated humidity + increased UV-B radiation doses + elevated ozone concentration (HWUO); and (4) heat + frost + drought + increased UV-B radiation doses + elevated ozone concentration (HFDUO). Effects of the complex treatments, species and species-by-treatment interaction were highly significant in most of the growth, physiological and biochemical traits studied, indicating general and species-specific responses to the applied treatments. For deciduous trees, height increment was much higher under HW treatment than in ambient conditions (control) indicating a positive effect of elevated temperature and better water and CO2 availability. HFD treatment caused reduction of height increment in comparison to HW treatment in most species except for Q. robur and F. excelsior which benefited from lower humidity. Treatments HWUO and HFDUO have caused substantial damages to leaves in fast growing deciduous P. tremula, A. glutinosa and B. pendula, and resulted in their lower height increment than in HW treatment, although it was the same or even higher than that in the control. Rates of photosynthesis in most of the tree species were greatest in HFD treatment. A lower photosynthetic rate (compared to control) was observed in B. pendula, P. tremula and F. excelsior in HW treatment, and in most species-in HWUO treatment. Compared to control, intrinsic water use efficiency in all treatments was significantly lower in P. tremula, A. glutinosa and F. excelsior and higher in conifers P. sylvestris and P. abies. Significant population-by-treatment interactions found for most traits showed variation in response of populations, implying that this reflects adaptive potential of each tree species. The observed responses may not always be considered as adaptive as deteriorating growth of some populations or species may lead to loss of their competitiveness thus compromising regeneration and natural successions.


Assuntos
Mudança Climática , Secas , Temperatura Alta/efeitos adversos , Ozônio/efeitos adversos , Árvores/fisiologia , Raios Ultravioleta , Tempo (Meteorologia) , Dióxido de Carbono/análise , Especificidade da Espécie
17.
BMC Public Health ; 19(1): 1366, 2019 Oct 24.
Artigo em Inglês | MEDLINE | ID: mdl-31651288

RESUMO

BACKGROUND: Many studies have reported the impact of air pollution on cardiovascular disease (CVD), but few of these studies were conducted in severe haze-fog areas. The present study focuses on the impact of different air pollutant concentrations on daily CVD outpatient visits in a severe haze-fog city. METHODS: Data regarding daily air pollutants and outpatient visits for CVD in 2013 were collected, and the association between six pollutants and CVD outpatient visits was explored using the least squares mean (LSmeans) and logistic regression. Adjustments were made for days of the week, months, air temperature and relative humidity. RESULTS: The daily CVD outpatient visits for particulate matter (PM10 and PM2.5), sulphur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3) in the 90th-quantile group were increased by 30.01, 29.42, 17.68, 14.98, 29.34%, and - 19.87%, respectively, compared to those in the <10th-quantile group. Odds ratios (ORs) and 95% confidence intervals (CIs) for the increase in daily CVD outpatient visits in PM10 300- and 500-µg/m3, PM2.5 100- and 300-µg/m3 and CO 3-mg/m3 groups were 2.538 (1.070-6.020), 7.781 (1.681-36.024), 3.298 (1.559-6.976), 8.72 (1.523-49.934), and 5.808 (1.016-33.217), respectively, and their corresponding attributable risk percentages (AR%) were 60.6, 87.15, 69.68, 88.53 and 82.78%, respectively. The strongest associations for PM10, PM2.5 and CO were found only in lag 0 and lag 1. The ORs for the increase in CVD outpatient visits per increase in different units of the six pollutants were also analysed. CONCLUSIONS: All five air pollutants except O3 were positively associated with the increase in daily CVD outpatient visits in lag 0. The high concentrations of PM10, PM2.5 and CO heightened not only the percentage but also the risk of increased daily CVD outpatient visits. PM10, PM2.5 and CO may be the main factors of CVD outpatient visits.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Doenças Cardiovasculares/terapia , Ambulatório Hospitalar/estatística & dados numéricos , Adulto , Idoso , Monóxido de Carbono/efeitos adversos , Monóxido de Carbono/análise , Doenças Cardiovasculares/epidemiologia , China/epidemiologia , Cidades , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Dióxido de Nitrogênio/efeitos adversos , Dióxido de Nitrogênio/análise , Ozônio/efeitos adversos , Ozônio/análise , Material Particulado/efeitos adversos , Material Particulado/análise , Dióxido de Enxofre/efeitos adversos , Dióxido de Enxofre/análise , Adulto Jovem
18.
Artigo em Inglês | MEDLINE | ID: mdl-31547235

RESUMO

Since the 2000s, air pollution has generally continued to decrease in the U.S. To investigate preterm birth (PTB) risk associated with air pollutants in two consecutive pregnancies, we estimated exposures using modified Community Multiscale Air Quality models linked to the NICHD Consecutive Pregnancy Study. Electronic medical records for delivery admissions were available for 50,005 women with singleton births in 20 Utah-based hospitals between 2002-2010. We categorized whole pregnancy average exposures as high (>75th percentile), moderate (25-75) and low (<25). Modified Poisson regression estimated second pregnancy PTB risk associated with persistent high and moderate exposure, and increasing or decreasing exposure, compared to persistent low exposure. Analyses were adjusted for prior PTB, interpregnancy interval and demographic and clinical characteristics. Second pregnancy PTB risk was increased when exposure stayed high for sulfur dioxide (32%), ozone (17%), nitrogen oxides (24%), nitrogen dioxide (43%), carbon monoxide (31%) and for particles < 10 microns (29%) versus consistently low exposure. PTB risk tended to increase to a lesser extent for repeated PTB (19-21%) than for women without a prior PTB (22-79%) when exposure increased or stayed high. Area-level changes in air pollution exposure appear to have important consequences in consecutive pregnancies with increasing exposure associated with higher risk.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Monóxido de Carbono/efeitos adversos , Exposição Ambiental/estatística & dados numéricos , Dióxido de Nitrogênio/efeitos adversos , Óxidos de Nitrogênio/efeitos adversos , Ozônio/efeitos adversos , Nascimento Prematuro/induzido quimicamente , Dióxido de Enxofre/efeitos adversos , Adulto , Poluentes Atmosféricos/análise , Monóxido de Carbono/análise , Feminino , Humanos , Recém-Nascido , Dióxido de Nitrogênio/análise , Óxidos de Nitrogênio/análise , Ozônio/análise , Material Particulado/efeitos adversos , Material Particulado/análise , Gravidez , Medição de Risco , Fatores de Risco , Dióxido de Enxofre/análise , Utah
19.
Sci Total Environ ; 692: 713-722, 2019 Nov 20.
Artigo em Inglês | MEDLINE | ID: mdl-31539979

RESUMO

Nocturnal transpiration may be a key factor influencing water use in plants. Tropospheric ozone (O3) and availability of nutrients such as nitrogen (N) and phosphorus (P) in the soil can affect daytime water use through stomata, but the combined effects of O3, N and P on night-time stomatal conductance (gs) are not known. We investigated the effects of O3 and soil availability of N and P on nocturnal gs and the dynamics of stomatal response after leaf severing in an O3-sensitive poplar clone (Oxford) subjected to combined treatments over a growing season in an O3 free air controlled exposure (FACE) facility. The treatments were two soil N levels (0 and 80 kg N ha-1; N0 and N80), three soil P levels (0, 40 and 80 kg P ha-1; P0, P40 and P80) and three O3 levels (ambient concentration, AA [35.0 ppb as hourly mean]; 1.5 × AA; 2.0 × AA). The analysis of stomatal dynamics after leaf severing suggested that O3 impaired stomatal closure execution. As a result, nocturnal gs was increased by 2.0 × AA O3 in August (+39%) and September (+108%). Night-time gs was correlated with POD0 (phytotoxic O3 dose) and increased exponentially after 40 mmol m-2 POD0. Such increase of nocturnal gs was attributed to the emission of ethylene due to 2.0 × AA O3 exposure, while foliar abscisic acid (ABA) or indole-3-acetic acid (IAA) did not affect gs at night. Interestingly, the O3-induced stomatal opening at night was limited by N treatments in August, but not limited in September. Phosphorus decreased nocturnal gs, although P did not modify the O3-induced stomatal dysfunction. The results suggest that the increased nocturnal gs may be associated with a need to improve N acquisition to cope with O3 stress.


Assuntos
Nitrogênio/fisiologia , Ozônio/efeitos adversos , Fósforo/fisiologia , Estômatos de Plantas/efeitos dos fármacos , Populus/efeitos dos fármacos , Ritmo Circadiano , Fertilizantes/análise , Itália , Estômatos de Plantas/fisiologia , Populus/fisiologia
20.
PLoS One ; 14(9): e0222601, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31553765

RESUMO

The evidence that exposure to ozone air pollution causes acute cardiovascular effects is mixed. We postulated that exposure to ambient levels of ozone would increase blood markers of systemic inflammation, prothrombotic state, oxidative stress, and vascular dysfunction in healthy older subjects, and that absence of the glutathione S-transferase Mu 1 (GSTM1) gene would confer increased susceptibility. This double-blind, randomized, crossover study of 87 healthy volunteers 55-70 years of age was conducted at three sites using a common protocol. Subjects were exposed for 3 h in random order to 0 parts per billion (ppb) (filtered air), 70 ppb, and 120 ppb ozone, alternating 15 min of moderate exercise and rest. Blood was obtained the day before, approximately 4 h after, and approximately 22 h after each exposure. Linear mixed effect and logistic regression models evaluated the impact of exposure to ozone on pre-specified primary and secondary outcomes. The definition of statistical significance was p<0.01. There were no effects of ozone on the three primary markers of systemic inflammation and a prothrombotic state: C-reactive protein, monocyte-platelet conjugates, and microparticle-associated tissue factor activity. However, among the secondary endpoints, endothelin-1, a potent vasoconstrictor, increased from pre- to post-exposure with ozone concentration (120 vs 0 ppb: 0.07 pg/mL, 95% confidence interval [CI] 0.01, 0.14; 70 vs 0 ppb: -0.03 pg/mL, CI -0.09, 0.04; p = 0.008). Nitrotyrosine, a marker of oxidative and nitrosative stress, decreased with increasing ozone concentrations, with marginal significance (120 vs 0 ppb: -41.5, CI -70.1, -12.8; 70 vs 0 ppb: -14.2, CI -42.7, 14.2; p = 0.017). GSTM1 status did not modify the effect of ozone exposure on any of the outcomes. These findings from healthy older adults fail to identify any mechanistic basis for the epidemiologically described cardiovascular effects of exposure to ozone. The findings, however, may not be applicable to adults with cardiovascular disease.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Endotélio Vascular/efeitos dos fármacos , Inflamação/induzido quimicamente , Estresse Oxidativo/efeitos dos fármacos , Ozônio/efeitos adversos , Trombose/induzido quimicamente , Idoso , Biomarcadores/sangue , Proteína C-Reativa/análise , Estudos Cross-Over , Relação Dose-Resposta a Droga , Método Duplo-Cego , Feminino , Humanos , Inflamação/sangue , Exposição por Inalação/efeitos adversos , Masculino , Pessoa de Meia-Idade , Ativação Plaquetária/efeitos dos fármacos
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