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Air Pollution in Infancy, Childhood and Young Adults

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Abstract

Children are particularly exposed to the effect of air pollution when compared to adults because of behavioural, environmental and physiological features. Exposure to air pollutants can start since foetal and early life, and the consequences on health can show up later in childhood or in adulthood with chronic or lifelong conditions. Although the effect on the respiratory tract secondary to acute and short-term exposure is known, constant exposure to background pollution can cause harmful effect on different organs and systems. As children develop and grow, the constant action of toxins coming from airborne compounds can cause inflammation, oxidative stress and immune responses that could lead to the onset of chronic diseases and to the exacerbation of subacute conditions

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... In un recentissimo articolo [6], Gonzales e Whalen (Texas Children's Hospital, Baylor College of Medicine, Houston, TX) analizzano lo stato dell'arte in termini di salute e qualità dell'aria, sottolineando alcuni dei problemi principali che possono colpire bambini esposti a inquinamento ambientale. Il problema è di massimo interesse dal momento che le fonti di inquinamento che possono impattare sulla qualità dell'aria sia all'esterno che all'interno degli edifici sono molteplici [Figura 2] e le peculiarità degli aspetti fisiologici, comportamentali e sociali dei bambini rendono questa categoria estremamente esposta agli agenti inquinanti aerei [7], molto più della controparte adulta della popolazione. L'esposizione a una scarsa qualità dell'aria è stata associata a diversi possibili effetti negativi sulla salute tra cui i più studiati sono gli apparati cardiovascolare e polmonare, il sistema nervoso, il sistema neurologico e il sistema endocrino. ...
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Le sfide in termini di salute globale poste dalla prima metà del ventunesimo secolo hanno imposto un cambiamento di pro-spettive di ciò che erano inizialmente stati definiti gli Obietti-vi di sviluppo del millennio (Millennium Development Goals o MDGs) e successivamente rivisitati come Obiettivi di svi-luppo sostenibile (Sustainable Development Goals o SGDs) [1]. Il terzo obiettivo in particolare [Figura 1], che definisce i termini in cui salute e benessere possano essere dei beni ac-cessibile a tutti, pone un particolare accento sulle condizioni che riguardano l'infanzia. La "costruzione" di un bambino Accanto alla riduzione della morbidità e mortalità sotto i cin-que anni di vita e il diritto all'accesso alle cure, viene eviden-ziata la necessità che i bambini crescano in un ambiente con-sono, privo di elementi nocivi che possano impattare sulla cre-scita e sullo sviluppo psicofisico. In quest'ottica, e superando il concetto di salute basata sulla sola assenza di malattia, diventa necessario individuare quali sono i fattori che possono alterare il sano sviluppo di un orga-nismo in crescita. I bambini quindi non possono che essere la somma di tutti i fattori che contribuiscono al processo che li porta a diventare individui adulti. Ogni mattone che va a costruire l'organismo completo ha un suo peso specifico e influenza, come in un castello di carte, tutta l'armonia dell'insieme. Tra gli altri, il miglioramento delle condizioni igienico-sanitarie, l'introduzione della cam-pagne vaccinali, l'accesso universale alle cure, il miglioramen-to della qualità dell'alimentazione, l'introduzione dell'educa-zione all'attività motoria e fisica e l'accesso ad ambienti cul-turalmente stimolanti sono elementi che hanno contribuito negli ultimi decenni a migliorare in termini generali la qualità della vita e della salute dei bambini [2-3], così come le attività di educazione sanitaria in contesti scolastici e non [4-5]. Il mosaico tuttavia non si può comporre se non si tiene in con-siderazione l'elemento ambiente, e in particolare la qualità dell'aria che i bambini respirano. La respirazione è uno dei processi che hanno reso possibile la vita sul pianeta Terra. I gas e gli elementi chimici che compon-gono l'aria, così come le particelle che viaggiano in sospensio-ne in essa, sono essi stessi mattoni che quotidianamente con-sentono all'individuo-e al bambino in particolare-di vivere e svilupparsi. Se gli alimenti si trasformano in proteine, strutture cellulari e tessuti, l'aria respirata diventa il carburante che consente alla macchina di funzionare. Contestualmente, qualunque impu-rità in grado di far inceppare il processo presente nell'aria può determinare gravi conseguenze sulla salute e sullo sviluppo del bambino. Cresco come respiro: qualità dell'aria, salute e malattia In un recentissimo articolo [6], Gonzales e Whalen (Texas Children's Hospital, Baylor College of Medicine, Houston, TX) analizzano lo stato dell'arte in termini di salute e quali-tà dell'aria, sottolineando alcuni dei problemi principali che possono colpire bambini esposti a inquinamento ambientale. Il problema è di massimo interesse dal momento che le fonti di inquinamento che possono impattare sulla qualità dell'aria sia all'esterno che all'interno degli edifici sono molteplici [Figu-ra 2] e le peculiarità degli aspetti fisiologici, comportamentali e sociali dei bambini rendono questa categoria estremamente esposta agli agenti inquinanti aerei [7], molto più della contro-parte adulta della popolazione. L'esposizione a una scarsa qualità dell'aria è stata associata a diversi possibili effetti negativi sulla salute tra cui i più stu-diati sono gli apparati cardiovascolare e polmonare, il sistema nervoso, il sistema neurologico e il sistema endocrino. Un crescente numero di evidenze scientifiche mostra una stret-ta correlazione tra sviluppo di tumori e inquinamento atmosfe-rico e tra sviluppo di processi infiammatori e stress ossidativo. In aggiunta lo stesso sviluppo fetale può essere fortemente compromesso dal tipo di sostanze inalate durante la gravi-danza, con risultati che possono portare anche all'aborto in selezionante circostanze. Un'ulteriore criticità riguarde-rebbe l'effetto che alcune so-stanze presenti nell'aria avreb-bero sulla lunghezza dei telo-meri, e nella duplicazione del DNA: alcuni studi [8-9] mo-strerebbero un accorciamen-to dei telomeri già in bambini in età scolare esposti cronica-mente a inquinamento dell'a-ria. A esso si assocerebbero cambiamenti epigenetici ca-paci di influenzare la funzio-ne mitocondriale e in genera-le il processo di sviluppo del feto e successivamente del bambino. In generale ogni tessuto in crescita, e in particolare il si-stema nervoso centrale, pos-sono essere colpiti dagli ef-fetti degli agenti inquinanti contenuti nell'aria, aumen-Figura 1. Obiettivi per lo sviluppo sostenibile come indicati dalla road map pubblicata dalle Nazioni Unite [12].
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Rationale: In vitro studies, animal experiments, and human exposure studies have shown how ambient air pollution increases the risk of atopic diseases. However, results derived from observational studies are inconsistent. Objectives: To assess the relationship between individual-based exposure to traffic-related air pollutants and allergic disease outcomes in a prospective birth cohort study during the first 6 years of life. Methods:We studied 2,860 children at the age of 4 years and 3,061 at the age of 6 years to investigate atopic diseases and allergic sensitization. Long-term exposure to particulate matter (PM2.5), PM2.5 absorbance, and long-term exposure to nitrogen dioxide (NO2) was assessed at residential addresses using geographic information systems based regression models and air pollution measurements. The distance to the nearest main road was used as a surrogate for traffic-related air pollutants. Measurements and Main Results: Strong positive associations were found between the distance to the nearest main road and asthmatic bronchitis, hay fever, eczema, and sensitization. A distance-dependent relationship could be identified, with the highest odds ratios (ORs) for children living less than 50 m from busy streets. For PM2.5 absorbance, statistically significant effects were found for asthmatic bronchitis (OR, 1.56; 95% confidence interval [CI], 1.03-2.37), hay fever (OR, 1.59; 95% CI, 1.11-2.27), and allergic sensitization to pollen (OR, 1.40; 95% CI, 1.20-1.64). NO2 exposure was associated with eczema, whereas no association was found for allergic sensitization. Conclusions: This study provides strong evidence for increased risk of atopic diseases and allergic sensitization when children are exposed to ambient particulate matter
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To analyze the relationship between levels of air pollution and number of children hospitalizations because of respiratory tract infection in Shenmu County, the data regarding meteorological factors, environmental pollutants, that is SO 2 and NO 2 , Particulate Matter 10 (PM10), and hospitalizations of children less than 16 years of age was collected during the time duration of November 2009 to October 2012. Using SAS 9.3, descriptive data analysis for meteorological and environmental factors and hospital admissions were performed along with main air pollutants determination. Using the statistical software R 3.0.1, a generalized additive Poisson regression model was established, the linear fitting models of the air pollutant concentrations and meteorological factors were introduced considering the lag effect, and the relative risk of the main atmospheric pollutants on children hospitalization was evaluated. The results showed that the primary air pollutant in Shenmu County is PM10 and its Pearson correlation coefficient with Air Pollution Index (API) is 0.917. After control of long term climate trend, “week day effect,” meteorological factors, and impact of other contaminants, it was found that, on the same day and during the lag of 1 to 10 days, PM10 concentrations had no significant effect on children hospitalization rate.
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Outdoor air pollution is one of the leading contributors to adverse respiratory health outcomes in urban areas around the world. Children are highly sensitive to the adverse effects of air pollution due to their rapidly growing lungs, incomplete immune and metabolic functions, patterns of ventilation and high levels of outdoor activity. The Children's Health Study (CHS) is a continuing series of longitudinal studies that first began in 1993 and has focused on demonstrating the chronic impacts of air pollution on respiratory illnesses from early childhood through adolescence. A large body of evidence from the CHS has documented that exposures to both regional ambient air and traffic-related pollutants are associated with increased asthma prevalence, new-onset asthma, risk of bronchitis and wheezing, deficits of lung function growth, and airway inflammation. These associations may be modulated by key genes involved in oxidative-nitrosative stress pathways via gene-environment interactions. Despite successful efforts to reduce pollution over the past 40 years, air pollution at the current levels still brings many challenges to public health. To further ameliorate adverse health effects attributable to air pollution, many more toxic pollutants may require regulation and control of motor vehicle emissions and other combustion sources may need to be strengthened. Individual interventions based on personal susceptibility may be needed to protect children's health while control measures are being implemented.
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Children's urban air pollution exposures result in systemic and brain inflammation and the early hallmarks of Alzheimer's disease (AD). The apolipoprotein E (APOE) ε4 allele is the most prevalent genetic risk for AD. We assessed whether APOE in healthy children modulates cognition, olfaction, and metabolic brain indices. The Wechsler Intelligence Scale for Children (WISC-R) and the University of Pennsylvania Smell Identification Test were administered to 50 Mexico City Metropolitan Area children (13.4 ± 4.8 years, 28 APOE ε3 and 22 APOE ε4). N-acetylaspartate (NAA)/creatine (Cr), choline (Cho)/Cr, myo-inositol (mI)/Cr, and NAA/mI were calculated using proton magnetic resonance spectroscopy in the white matter of the frontal and parietal lobes, hippocampus, and pons. APOE ε4 versus ε3 children had a reduced NAA/Cr ratio in the right frontal white matter and decrements on attention, short-term memory, and below-average scores in Verbal and Full Scale IQ (>10 points). APOE modulated the group effects between WISC-R and left frontal and parietal white matter, and hippocampus metabolites. Soap was the predominantly failed odor AD-related item in urban children and in APOE ε4 versus ε3 carriers strongly correlated with left hippocampus mI/Cr ratio. APOE modulates responses to air pollution on the developing brain. APOE ε4 carriers could have a higher risk of developing early AD if they reside in a polluted environment. APOE, cognition, and olfaction testing and targeted magnetic resonance spectroscopy may contribute to the assessment of urban children and their results could provide new paths toward the unprecedented opportunity for early neuroprotection and AD prevention.
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Indoor air pollution (IAP) is a key contributor to the global burden of disease mainly in developing countries. The use of solid fuel for cooking and heating is the main source of IAP in developing countries, accounting for an estimated 3.5 million deaths and 4.5% of Disability-Adjusted Life Years in 2010. Other sources of IAP include indoor smoking, infiltration of pollutants from outdoor sources and substances emitted from an array of human utilities and biological materials. Children are among the most vulnerable groups for adverse effects of IAP. The respiratory system is a primary target of air pollutants resulting in a wide range of acute and chronic effects. The spectrum of respiratory adverse effects ranges from mild subclinical changes and mild symptoms to life threatening conditions and even death. However, IAP is a modifiable risk factor having potential mitigating interventions. Possible interventions range from simple behavior change to structural changes and from shifting of unclean cooking fuel to clean cooking fuel. Shifting from use of solid fuel to clean fuel invariably reduces household air pollution in developing countries, but such a change is challenging. This review aims to summarize the available information on IAP exposure during childhood and its effects on respiratory health in developing countries. It specifically discusses the common sources of IAP, susceptibility of children to air pollution, mechanisms of action, common respiratory conditions, preventive and mitigating strategies.
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Introduction Genotoxic biomarkers have been studied largely in adult population, but few studies so far have investigated them in children exposed to air pollution. Children are a high-risk group as regards the health effects of air pollution and some studies suggest that early exposure during childhood can play an important role in the development of chronic diseases in adulthood. The objective of the project is to evaluate the associations between the concentration of urban air pollutants and biomarkers of early biological effect in children, and to propose a model for estimating the global risk of early biological effects due to air pollutants and other factors in children. Methods and analysis Two biomarkers of early biological effects, DNA damage by the comet assay and the micronuclei (MN) test, will be investigated in oral mucosa cells of 6–8-year-old children. Concurrently, some toxic airborne pollutants (polycyclic aromatic hydrocarbon (PAH) and nitro-PAH) and in vitro air mutagenicity and toxicity in ultra-fine air particulates (PM0.5) will be evaluated. Furthermore, demographic and socioeconomic variables, other sources of exposures to air pollutants and lifestyle variables will be assessed by a structured questionnaire. The associations between sociodemographic, environmental and other exposure variables and biomarkers of early biological effect using univariate and multivariate models will be analysed. A tentative model for calculating the global absolute risk of having early biological effects caused by air pollution and other variables will be proposed. Ethics and dissemination The project has been approved by the Ethics Committees of the local Health Authorities. The results will be communicated to local Public Health Agencies, for supporting educational programmes and health policy strategies. LIFE+2012 Environment Policy and Governance. LIFE12 ENV/IT/000614.
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Background Air pollution has many negative health effects on the general population, especially children, subjects with underlying chronic disease and the elderly. The aims of this study were to evaluate the effects of traffic-related pollution on the exacerbation of asthma and development of respiratory infections in Italian children suffering from asthma or wheezing compared with healthy subjects and to estimate the association between incremental increases in principal pollutants and the incidence of respiratory symptoms. Methods This prospective study enrolled 777 children aged 2 to 18 years (375 with recurrent wheezing or asthma and 402 healthy subjects). Over 12 months, parents filled out a daily clinical diary to report information about respiratory symptoms, type of medication used and healthcare utilization. Clinical data were combined with the results obtained using an air pollution monitoring system of the five most common pollutants. Results Among the 329 children with recurrent wheezing or asthma and 364 healthy subjects who completed follow-up, children with recurrent wheezing or asthma reported significantly more days of fever (p = 0.005) and cough (p < 0.001), episodes of rhinitis (p = 0.04) and tracheitis (p = 0.01), asthma attacks (p < 0.001), episodes of pneumonia (p < 0.001) and hospitalizations (p = 0.02). In the wheezing/asthma cohort, living close to the street with a high traffic density was a risk factor for asthma exacerbations (odds ratio [OR] = 1.79; 95% confidence interval [CI], 1.13-2.84), whereas living near green areas was found to be protective (OR = 0.50; 95% CI, 0.31 -0.80). An increase of 10 μg/m3 of particulates less than 10 microns in diameter (PM10) and nitrogen dioxide (NO2) increased the onset of pneumonia only in wheezing/asthmatic children (continuous rate ratio [RR] = 1.08, 95% CI: 1.00-1.17 for PM10; continuous RR = 1.08, 95% CI: 1.01-1.17 for NO2). Conclusions There is a significant association between traffic-related pollution and the development of asthma exacerbations and respiratory infections in children born to atopic parents and in those suffering from recurrent wheezing or asthma. These findings suggest that environmental control may be crucial for respiratory health in children with underlying respiratory disease.
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Negative associations between bone turnover markers and bone mineral density have been reported. In order to study the association between ambient air pollution and bone turnover markers, as indicators of bone loss, we investigated associations between land-use regression modeled air pollution (NO2, PM2.5 mass, PM2.5-10 [coarse particles], PM10 mass and PM2.5 absorbance) and bone turnover markers in 2264 children aged 10 years. Serum osteocalcin and C-terminal telopeptide of type I collagen (CTx), measured by Modular-System (Roche), were the two bone turnover markers considered in this analysis. In total population, NO2, PM2.5-10 and PM10 mass exposure were positively and significantly associated with both osteocalcin and CTx. A 2.5 (95% CI: 0.6, 4.4) ng/ml increase in osteocalcin and a 24.0 (95% CI: 6.7, 41.3) ng/L increase in CTx were observed per IQR (6.7 μg/m3) increase in NO2, independent of socioeconomic status, sex, age, pubertal status, fasting status and total physical activity. The estimated coefficients were 3.0 (95% CI: 0.1, 5.8) for osteocalcin and 32.3 (95% CI: 6.1, 58.5) for CTx with PM2.5-10; 3.2 (95% CI: 0.0, 6.4) for osteocalcin and 30.7 (95% CI: 1.7, 59.7) for CTx with PM10. Children living close to a major road (≤ 350 m) had higher levels of both osteocalcin (1.4 [-1.2, 4.0] ng/ml) and CTx (16.2 [-7.4, 39.8] ng/L). The adverse impact of ambient air pollution on bone turnover rates observed in one of the study areas showed stimulation of more such studies.
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Reduction of indoor air pollution (IAP) exposure from solid fuel use is a potentially important intervention for childhood pneumonia prevention. This review updates a prior meta-analysis and investigates whether risk varies by etiological agent and pneumonia severity among children aged less than 5 years who are exposed to unprocessed solid fuels. Searches were made of electronic databases (including Africa, China and Latin America) without language restriction. Search terms covered all sources of IAP and wide-ranging descriptions of acute lower respiratory infections, including viral and bacterial agents. From 5317 studies in the main electronic databases (plus 307 African and Latin American, and 588 Chinese studies, in separate databases), 25 were included in the review and 24 were suitable for meta-analysis. Due to substantial statistical heterogeneity, random effects models were used. The overall pooled odds ratio was 1.78 (95% confidence interval, CI: 1.45-2.18), almost unchanged at 1.79 (95% CI: 1.26-2.21) after exclusion of studies with low exposure prevalence (
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To determine the acute effects of ozone exposure, the authors conducted a short follow-up study of respiratory illness in a population of 111 preschool children frequently exposed to ozone levels that regularly exceed 0. 120 parts per million (ppm). The children attended a private kindergarten in the southwestern part of Mexico City. Parents completed a questionnaire on demographic data, medical history, and potential sources of indoor air pollution. To determine the relation of ozone and respiratory-related school absenteeism, the authors used a logistic regression model for longitudinal data. During the 3-month follow-up, 50% of the children had at least one respiratory-related absenteeism period, and 11. 7% had two or more. Children exposed for 2 consecutive days to high ozone levels (≥0. 13 ppm)had a 20% increment in the risk of respiratory illness. For children exposed for 2 consecutive days to a high ozone level and the previous day to low temperature (≤5. 1°C), the risk reached 40% (odds ratio=1. 44, 95% confidence interval 1. 37–1.52). This study suggests that ozone exposure might be positively associated with the risk of respiratory illness in children and that it may have an interactive effect with low temperature exposure. Am J Epidemiol 1992; 136: 1524–31
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Background The fall peak in childhood asthma exacerbations is thought to be related to an increase in viral infections and allergen exposure when children return to school. Whether the seasonality of asthma attacks among children from different geographic regions follows similar trends is unclear. Objective To compare seasonal trends in asthma exacerbations among school-age children who lived in different geographic locations, with different climates, within the United States. Methods Hospital billing data bases were examined to determine the monthly number of school-age children who were hospitalized or treated in the emergency department (ED) for asthma exacerbations. Data from four cities within three states were compared. Climate data were obtained from archives of the National Climate Data Center, U.S. Department of Commerce. Results An annual peak in asthma exacerbations was observed during the fall months (September through November) among children who lived in Charlottesville, Virginia, as well as throughout the state of Virginia. An increase in exacerbations, which peaked in November, was observed for exacerbations among children who lived in Tucson, Arizona, and Yuma, Arizona. In contrast, exacerbations among children from New Orleans, Louisiana, increased in September but remained elevated throughout the school year. Although there was annual variation in the frequency of exacerbations over time, the seasonal patterns observed remained similar within the locations from year to year. A nadir in the frequency of attacks was observed during the summer months in all the locations. Conclusion Seasonal peaks for asthma exacerbations varied among the children who lived in geographic locations with different climates, and were not restricted to the beginning of the school year.
Article
Background: Evidence linking long-term exposure to outdoor air pollution with allergic rhinitis (AR) in children is scare, and the role of components of air pollution and timing of exposure remains unclear. Objective: To assess the association of pre- and post-natal exposure to air pollution with life-time prevalence of AR in preschool children. Methods: We conducted a cohort study of 2598 children aged 3-6 years in Changsha, China. The lifetime prevalence of AR was assessed by a questionnaire administered by parents. Children's exposures to dioxide nitrogen (NO2), sulfur dioxide (SO2) and particulate matter with an aerodynamic diameter ≤ 10 μm (PM10) during different pre- and post-natal timing windows were estimated using the measured concentrations at monitoring stations. The odds ratio (OR) and 95% confidence interval (CI) of childhood AR for exposure to different air pollutants during different timing windows were assessed by logistic regression model in terms of an interquartile range (IQR) increase in exposure level. Results: Life-time prevalence of AR in preschool children (7.3%) was associated with both pre- and post-natal exposure to traffic-related air pollution (TRAP), but only significant during the third trimester of pregnancy with adjusted OR = 1.40 (95% CI: 1.08-1.82) for a 15 μg/m3 increase in NO2 and during the first-year of life with adjusted OR = 1.36 (95% CI: 1.03-1.78) and 1.54 (95% CI: 1.07-2.21) respectively for 11 and 12 μg/m3 increase in NO2 and PM10. The association of early life exposure to TRAP with childhood AR was robust by adjusting for other air pollutants and timing windows. Sensitivity analysis indicated that the association was higher in the children who are male, young, with genetic predisposition by parental atopy, and living in damp houses. Conclusion: Early life exposure to traffic-related air pollutant during pregnancy and first-year of life may contribute to childhood AR.
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Background A broad literature base provides evidence of association between air pollution and paediatric asthma. Socioeconomic status (SES) may modify these associations; however, previous studies have found inconsistent evidence regarding the role of SES. Methods Effect modification of air pollution–paediatric asthma morbidity by multiple indicators of neighbourhood SES was examined in Atlanta, Georgia. Emergency department (ED) visit data were obtained for 5–18 years old with a diagnosis of asthma in 20-county Atlanta during 2002–2008. Daily ZIP Code Tabulation Area (ZCTA)-level concentrations of ozone, nitrogen dioxide, fine particulate matter and elemental carbon were estimated using ambient monitoring data and emissions-based chemical transport model simulations. Pollutant–asthma associations were estimated using a case-crossover approach, controlling for temporal trends and meteorology. Effect modification by ZCTA-level (neighbourhood) SES was examined via stratification. Results We observed stronger air pollution–paediatric asthma associations in ‘deprivation areas’ (eg, ≥20% of the ZCTA population living in poverty) compared with ‘non-deprivation areas’. When stratifying analyses by quartiles of neighbourhood SES, ORs indicated stronger associations in the highest and lowest SES quartiles and weaker associations among the middle quartiles. Conclusions Our results suggest that neighbourhood-level SES is a factor contributing vulnerability to air pollution-related paediatric asthma morbidity in Atlanta. Children living in low SES environments appear to be especially vulnerable given positive ORs and high underlying asthma ED rates. Inconsistent findings of effect modification among previous studies may be partially explained by choice of SES stratification criteria, and the use of multiplicative models combined with differing baseline risk across SES populations.
Article
Objective: To investigate associations between exposure to air pollution and child and adolescent mental health. Design: Observational study. Setting: Swedish National Register data on dispensed medications for a broad range of psychiatric disorders, including sedative medications, sleeping pills and antipsychotic medications, together with socioeconomic and demographic data and a national land use regression model for air pollution concentrations for NO2, PM10 and PM2.5. Participants: The entire population under 18 years of age in 4 major counties. We excluded cohort members whose parents had dispensed a medication in the same medication group since the start date of the register. The cohort size was 552 221. Main outcome measures: Cox proportional hazards models to estimate HRs and their 95% CIs for the outcomes, adjusted for individual-level and group-level characteristics. Results: The average length of follow-up was 3.5 years, with an average number of events per 1000 cohort members of 21. The mean annual level of NO2 was 9.8 g/m3. Children and adolescents living in areas with higher air pollution concentrations were more likely to have a dispensed medication for a psychiatric disorder during follow-up (HR=1.09, 95% CI 1.06 to 1.12, associated with a 10 g/m3 increase in NO2). The association with NO2 was clearly present in 3 out of 4 counties in the study area; however, no statistically significant heterogeneity was detected. Conclusion: There may be a link between exposure to air pollution and dispensed medications for certain psychiatric disorders in children and adolescents even at the relatively low levels of air pollution in the study regions. The findings should be corroborated by others.
Article
Rationale: Individuals with asthma chronic obstructive pulmonary disease (COPD) overlap syndrome (ACOS), have more rapid decline in lung function, more frequent exacerbations and poorer quality of life than those with asthma or COPD alone. Air pollution exposure is a known risk factor for asthma and COPD; however, its role in ACOS is not as well understood. Objectives: To determine if individuals with asthma exposed to higher levels of air pollution have an increased risk of ACOS. Methods: Individuals who resided in Ontario, Canada aged ≥18 years in 1996 with incident asthma between 1996 and 2009 and participated in the Canadian Community Health Survey (CCHS) were identified and followed until 2014 to determine the development of ACOS. Data on exposures to fine particulate matter (PM2.5) and ozone (O3) were obtained from fixed monitoring sites. Associations between air pollutants and ACOS were evaluated using Cox regression models. Measurements and main results: Of the 6,040 adults with incident asthma who completed the CCHS, 630 were identified as ACOS cases. Compared to non-ACOS, the ACOS population had later onset of asthma, higher proportion of mortality, and more frequent ED visits prior to COPD diagnosis. The adjusted hazard ratios (HR) of ACOS and cumulative exposures to PM2.5 (per 10 µg/m(3)) and O3 (per 10 ppb) were 2.78 (CI: 1.62-4.78) and 1.31 (CI: 0.71-2.39) respectively. Conclusions: Individuals exposed to higher levels of air pollution had nearly 3-fold greater odds of developing ACOS. Minimizing exposure to high levels of air pollution may decrease the risk of ACOS.
Article
The aim of our study was to evaluate any effects in red blood cells in children exposed to air pollution. The subjects were 354 pupils, aged 11-14 years, living for more than ten years in the same home. The exposed group of children (n=215) were attending school in a city area with a high level of air pollution, while the children in the comparison group (n=139), designated the non-exposed group, were attending school in an area with a lower level of air pollution. The mean value of hemoglobin (g/mL) for exposed children was 10.97±0.38 and for non-exposed children 11.09±0.78. The diagnosis of iron deficiency anemia was made using the pre-defined criteria. The air concentrations of black smoke, nitrogen dioxide, sulfur dioxide and lead in sediment matter were determined from 1990 to 2000. The red blood cell count and average of hemoglobin blood levels of exposed children differ significantly from those of the non-exposed (P<0.001). There was also a significant difference in the prevalence of anemia in children exposed to higher concentrations of air pollutants (RR=3.76; 95% CI:2.06-6.88). These findings suggest that air pollution could have negative effects on red blood cells in children.
Article
Air pollution (indoors and outdoors) is a major issue in public health as epidemiological studies have highlighted its numerous detrimental health consequences (notably, respiratory and cardiovascular pathological conditions). Over the past 15years, air pollution has also been considered a potent environmental risk factor for neurological diseases and neuropathology. This review examines the impact of air pollution on children's brain development and the clinical, cognitive, brain structural and metabolic consequences. Long-term potential consequences for adults' brains and the effects on multiple sclerosis (MS) are also discussed. One challenge is to assess the effects of lifetime exposures to outdoor and indoor environmental pollutants, including occupational exposures: how much, for how long and what type. Diffuse neuroinflammation, damage to the neurovascular unit, and the production of autoantibodies to neural and tight-junction proteins are worrisome findings in children chronically exposed to concentrations above the current standards for ozone and fine particulate matter (PM2.5), and may constitute significant risk factors for the development of Alzheimer's disease later in life. Finally, data supporting the role of air pollution as a risk factor for MS are reviewed, focusing on the effects of PM10 and nitrogen oxides.
Article
Objective: To evaluate the association between household air pollution (HAP) with lower respiratory tract illness (LRTI) in children younger than 5 years old and adverse pregnancy outcomes. Study design and setting: This retrospective cohort study took place in two cities in Patagonia. Using systemic random sampling, we selected households in which at least one child <5 years had lived and/or a child had been born alive or stillborn. Trained interviewers administered the questionnaire. Results: We included 926 households with 695 pregnancies and 1,074 children. Household cooking was conducted indoors in ventilated rooms and the use of wood as the principal fuel for cooking was lower in Temuco (13% vs 17%). In exposed to biomass fuel use, the adjusted OR for LRTI was 1.87 (95% CI 0.98-3.55; p = 0.056) in Temuco and 1.12 (95% CI 0.61-2.05; p = 0.716) in Bariloche. For perinatal morbidity, the OR was 3.11 (95% CI 0.86-11.32; p = 0.084) and 1.41 (95% CI 0.50-3.97; p = 0.518), respectively. However, none of the effects were statistically significant (p >0.05) CONCLUSION: The use of biomass fuel to cook in traditional cookstoves in ventilated dwellings may increase the risk of perinatal morbidity and LRTI. This article is protected by copyright. All rights reserved.
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A substantial proportion of the global burden of disease is directly or indirectly attributable to exposure to air pollution. Exposures occurring during the periods of organogenesis and rapid lung growth during fetal development and early post-natal life are especially damaging. In this State of the Art review, we discuss air toxicants impacting on children's respiratory health, routes of exposure with an emphasis on unique pathways relevant to young children, methods of exposure assessment and their limitations and the adverse health consequences of exposures. Finally, we point out gaps in knowledge and research needs in this area. A greater understanding of the adverse health consequences of exposure to air pollution in early life is required to encourage policy makers to reduce such exposures and improve human health. Pediatr Pulmonol. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
Article
Although ambient air pollution has been linked to reduced lung function in healthy children, longitudinal analyses of pollution effects in asthmatic patients are lacking. We sought to investigate pollution effects in a longitudinal asthma study and effect modification by controller medications. We examined associations of lung function and methacholine responsiveness (PC20) with ozone, carbon monoxide (CO), nitrogen dioxide, and sulfur dioxide concentrations in 1003 asthmatic children participating in a 4-year clinical trial. We further investigated whether budesonide and nedocromil modified pollution effects. Daily pollutant concentrations were linked to ZIP/postal code of residence. Linear mixed models tested associations of within-subject pollutant concentrations with FEV1 and forced vital capacity (FVC) percent predicted, FEV1/FVC ratio, and PC20, adjusting for seasonality and confounders. Same-day and 1-week average CO concentrations were negatively associated with postbronchodilator percent predicted FEV1 (change per interquartile range, -0.33 [95% CI, -0.49 to -0.16] and -0.41 [95% CI, -0.62 to -0.21], respectively) and FVC (-0.19 [95% CI, -0.25 to -0.07] and -0.25 [95% CI, -0.43 to -0.07], respectively). Longer-term 4-month CO averages were negatively associated with prebronchodilator percent predicted FEV1 and FVC (-0.36 [95% CI, -0.62 to -0.10] and -0.21 [95% CI, -0.42 to -0.01], respectively). Four-month averaged CO and ozone concentrations were negatively associated with FEV1/FVC ratio (P < .05). Increased 4-month average nitrogen dioxide concentrations were associated with reduced postbronchodilator FEV1 and FVC percent predicted. Long-term exposures to sulfur dioxide were associated with reduced PC20 (percent change per interquartile range, -6% [95% CI, -11% to -1.5%]). Treatment augmented the negative short-term CO effect on PC20. Air pollution adversely influences lung function and PC20 in asthmatic children. Treatment with controller medications might not protect but rather worsens the effects of CO on PC20. This clinical trial design evaluates modification of pollution effects by treatment without confounding by indication. Copyright © 2015 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
Article
Little information exists regarding the effect of interaction of obesity and long-term air pollution exposure on children's blood pressure and hypertension in areas with high levels of air pollution. The aim of this study is to assess effect modification by obesity on the association between exposure and blood pressure in Chinese children. We studied 9,354 Chinese children, ages 5-17 years old, from 24 elementary schools and 24 middle schools in the Seven Northeastern Cities during 2012-2013. Four-year average concentrations of particles with an aerodynamic diameter ≤10 µm (PM10), sulfur dioxide, nitrogen dioxides, and ozone (O3) were measured at the monitoring stations in the 24 districts. We used generalized additive models and two-level logistic regression models to examine the health effects. Consistent interactions were found between exposure and obesity on blood pressure and hypertension. The association between exposure and hypertension was consistently larger for overweight/obese children than for children with normal-weight, with odds ratios for hypertension ranging from 1.16 per 46.3μg/m for O3 (95% confidence interval [CI] = 1.12, 1.20) to 2.91 per 30.6μg/m for PM10 (95% CI = 2.32, 3.64), and estimated increases in mean systolic and diastolic blood pressure ranging from 0.57 mmHg (95% CI = 0.36, 0.78) and 0.63 mmHg (95% CI = 0.46, 0.81) per 46.3 μg/m for O3 to 4.04 mmHg (95% CI = 3.00, 5.09) and 2.02 mmHg (95% CI = 1.14, 2.89) per 23.4 μg/m for sulfur dioxide. Obesity amplifies the association of long-term air pollution exposure with blood pressure and hypertension in Chinese children.
Article
To compare the differences of children's health in different area, and to confirm if the prevalence of respiratory diseases and symptoms among children are closely associated with the air pollution. A cross-sectional study was conducted in an urban area A and a suburban area B with different levels of air pollution in Beijing. Using a cluster sampling method, we recruited 4 564 children from 3 primary schools in urban A and 4 primary schools in suburban B. Respiratory symptoms were investigated using an international standardized questionnaire including characteristics of children, living conditions, respiratory diseases and symptoms and situation of parents. The concentrations of air pollutants for recent five years were obtained from Reports on the Quality of the Beijing Environment. SPSS 16.0 was used to analyze data. The prevalence of cough, persistent cough, phlegm, persistent phlegm, wheeze and asthma in A area were higher than those in B area [(62.2% vs. 59.9%), (6.3% vs. 3.1%), (42.4% vs. 37.4%),(3.6% vs. 2.4%),(13.3% vs. 9.9%)and(9.5% vs. 5.4%)]. Except for cough, cough with cold, cough without cold, the prevalence of respiratory diseases and symptoms in A area were significantly higher than those in B area (P<0.05). Logistic regression analysis showed the prevalence of persistent cough, phlegm without cold, asthma in A area were significantly higher than those in B area (P<0.05). Respiratory diseases and symptoms among school-age children were closely associated with the level of air pollution.
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“The sick-building syndrome” (WHO) is reported with increasing intensity in non-industrial places of work, such as schools, kindergartens, and offices, all of which have a heavy load of traffic (people). The construction of these buildings (e.g. flat roofs) often leads to water damage with subsequent microbial growth. Further, reduced cleaning budgets in connection with the wide use of needle-felt carpets, as well as ventilation systems not regularly maintained, will lead to pollution by dust and microorganisms. A systematic registration of dust and microbial parameters has been carried out since 1980 in buildings with indoor climate complaints, m order to elucidate the possible influence of these factors.
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Information on the long-term effects of different air pollutant levels on lung function is relatively lacking in Asia and still inconclusive in the world. Age differential effects of air pollution are not known. To assess the acute and subchronic effects of ambient air pollution on lung function and compared among children of different ages. From April to May 2011, a nationwide study was conducted on schoolchildren aged 6-15 years in 44 schools of 24 districts in Taiwan. Spirograms were obtained from 1494 non-asthmatic children. Air pollution data were retrieved from air monitoring stations within one kilometre of the schools. Using three-level hierarchical linear models, individual lung function was fitted to air pollution, with adjustments for demographics, indoor exposures, outdoor activity, and districts. Lung function changes per inter-quartile increase of the past two-months average levels of particulate matter <2.5μm (PM2.5) and ozone (12μg/m(3), 32-44 and 6.7ppb, 32-38, respectively) were -103 and -142ml on FVC, -86 and -131 on FEV1, and -102 and -188ml/s on MMEF, respectively. Lag-1-day ozone exposure was associated with decreased MMEF. In children aged 6-10, PM2.5 was associated with decreased FEV1/FVC and MMEF/FVC ratios. In children aged 6-15 years, sub-chronic exposure to ambient PM2.5 and ozone leads to reduced lung capacity, whereas acute exposure to ozone decreases mid-expiratory flow. In children aged 6-10 years, additional airway obstructive patterns in lung function may be associated with PM2.5 exposure. Copyright © 2014 Elsevier Inc. All rights reserved.
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Upper and lower respiratory infections are common in early childhood and may be exacerbated by air pollution. We investigated short-term changes in ambient air pollutant concentrations, including speciated particulate matter less than 2.5 μm in diameter (PM2.5), in relation to emergency department (ED) visits for respiratory infections in young children. Daily counts of ED visits for bronchitis and bronchiolitis (n = 80,399), pneumonia (n = 63,359), and upper respiratory infection (URI) (n = 359,246) among children 0-4 years of age were collected from hospitals in the Atlanta, Georgia, area for the period 1993-2010. Daily pollutant measurements were combined across monitoring stations using population weighting. In Poisson generalized linear models, 3-day moving average concentrations of ozone, nitrogen dioxide, and the organic carbon fraction of particulate matter less than 2.5 μm in diameter (PM2.5) were associated with ED visits for pneumonia and URI. Ozone associations were strongest and were observed at low (cold-season) concentrations; a 1-interquartile range increase predicted a 4% increase (95% confidence interval: 2%, 6%) in visits for URI and an 8% increase (95% confidence interval: 4%, 13%) in visits for pneumonia. Rate ratios tended to be higher in the 1- to 4-year age group compared with infants. Results suggest that primary traffic pollutants, ozone, and the organic carbon fraction of PM2.5 exacerbate upper and lower respiratory infections in early life, and that the carbon fraction of PM2.5 is a particularly harmful component of the ambient particulate matter mixture.
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Millions of children are exposed to concentrations of air pollutants, including fine particulate matter (PM2.5), above safety standards. Mexico City Metropolitan Area (MCMA) megacity children show an early brain imbalance in oxidative stress, inflammation, innate and adaptive immune response-associated genes, and blood-brain barrier breakdown. We investigated serum and cerebrospinal fluid (CSF) antibodies to neural and tight junction proteins and environmental pollutants in 139 children ages 11.91 ± 4.2 y with high versus low air pollution exposures. We also measured metals in serum and CSF. MCMA children showed significantly higher serum actin IgG, occludin/zonulin 1 IgA, IgG, myelin oligodendrocyte glycoprotein IgG and IgM (p < 0.01), myelin basic protein IgA and IgG, S-100 IgG and IgM, and cerebellar IgG (p < 0.001). Serum IgG antibodies to formaldehyde, benzene, and bisphenol A, and concentrations of Ni and Cd were significantly higher in exposed children (p < 0.001). CSF MBP antibodies and nickel concentrations were higher in MCMA children (p = 0.03). Air pollution exposure damages epithelial and endothelial barriers and is a robust trigger of tight junction and neural antibodies. Cryptic 'self' tight junction antigens can trigger an autoimmune response potentially contributing to the neuroinflammatory and Alzheimer and Parkinson's pathology hallmarks present in megacity children. The major factor determining the impact of neural antibodies is the integrity of the blood-brain barrier. Defining the air pollution linkage of the brain/immune system interactions and damage to physical and immunological barriers with short and long term neural detrimental effects to children's brains ought to be of pressing importance for public health.
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Background: Genetic and environmental factors are believed to contribute to the development of autism, but relatively few studies have considered potential environmental risks. Here, we examine risks for autism in children related to in utero exposure to monitored ambient air toxics from urban emissions. Methods: Among the cohort of children born in Los Angeles County, California, 1995-2006, those whose mothers resided during pregnancy in a 5-km buffer around air toxics monitoring stations were included (n = 148,722). To identify autism cases in this cohort, birth records were linked to records of children diagnosed with primary autistic disorder at the California Department of Developmental Services between 1998 and 2009 (n = 768). We calculated monthly average exposures during pregnancy for 24 air toxics selected based on suspected or known neurotoxicity or neurodevelopmental toxicity. Factor analysis helped us identify the correlational structure among air toxics, and we estimated odds ratios (ORs) for autism from logistic regression analyses. Results: Autism risks were increased per interquartile range increase in average concentrations during pregnancy of several correlated toxics mostly loading on 1 factor, including 1,3-butadiene (OR = 1.59 [95% confidence interval = 1.18-2.15]), meta/para-xylene (1.51 [1.26-1.82]), other aromatic solvents, lead (1.49 [1.23-1.81]), perchloroethylene (1.40 [1.09-1.80]), and formaldehyde (1.34 [1.17-1.52]), adjusting for maternal age, race/ethnicity, nativity, education, insurance type, parity, child sex, and birth year. Conclusions: Risks for autism in children may increase following in utero exposure to ambient air toxics from urban traffic and industry emissions, as measured by community-based air-monitoring stations.