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Exposure to Traffic-Related Air Pollutants in the Perinatal Period of Life in Relation to Respiratory Health in Infancy

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Abstract

The role of air pollution exposure on the development of asthma remains unclear. This can only be answered by prospective cohort studies. The authors give an overview of cohort studies focusing mainly on the role of early exposure, investigating the association between outdoor exposure early in life and respiratory or allergy symptoms in the growing children. Based on those studies, there is a suggestive evidence for a causal association between childhood asthma symptoms and exposure to traffic-related air pollutants.

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... For adult male and female patients, the total weight of the chemical variables in the occurrence of asthma ER visits is higher in the pollen season of Ambrosia compared to the pollen-free season ( Table 2). Some studies found that exposure to outdoor air pollutants may increase the risk of allergic airway diseases [11,[55][56][57][58]. This may be explained by the fact that air pollutants, especially burning of fossil fuels, can affect allergens. ...
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p>Joint effect of biological (pollen) and chemical air pollutants on asthma emergency room (ER) visits was analyzed for Szeged region of Southern Hungary. Our database of a nine-year period (1999-2007) includes daily number of asthma emergency room (ER) visits, and daily mean concentrations of CO, PM10, NO, NO2 , O3 and SO2 , furthermore two pollen variables (Ambrosia and total pollen excluding Ambrosia), as well. The analysis was performed for ER visits of asthma bronchiale using two age groups (adults and the elderly) of males and females for three seasons. Factor analysis was performed in order to clarify the relative importance of the pollutant variables affecting asthma ER visits. Asthma ER visits denote notably stronger associations with the pollutants in adult male than in adult female patients both for the pollen season of Ambrosia and the pollen-free season. Furthermore, adults are substantially more sensitive to severe asthma attack than the elderly for the season of total pollen excluding Ambrosia pollen. The joint effect of the chemical and pollen variables is the highest for the asthma ER cases in the pollen season of Ambrosia, basically due to the extra impact of the total pollen excluding Ambrosia pollen and partly due to Ambrosia pollen. A nonparametric regression technique was applied to discriminate between events of ER visit – no ER visit using pollen and chemical pollutants as explaining variables. Based on multiple correlations, the strongest relationships between ER visits and pollutants are observed during the pollen-free season. The elderly group with asthma bronchiale is characterized by weaker relationships between ER visits and pollutants compared to adults. Ratio of the number of correct decisions on the events of ER visit – no ER visit is lowest for the season of total pollen excluding Ambrosia pollen. Otherwise, similar conclusions hold as those received by multiple correlations.</p
... Environmental exposure to PM has been also associated with the increased risk of human skin diseases, especially atopic dermatitis, eczema and skin aging (Annesi-Maesano et al., 2007;Ngoc et al., 2017;Song et al., 2011). In addition, pre-and postneonatal exposure to PM has also been associated with increased vulnerability to the development of cardiorespiratory diseases (Brugha and Grigg, 2014;Kelishadi et al., 2011;Koppen et al., 2011). ...
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Children, an important vulnerable group, spend most of their time at schools (up to 10 h per day, mostly indoors) and the respective air quality may significantly impact on children health. Thus, this work reviews the published studies on children biomonitoring and environmental exposure to particulate matter (PM) and polycyclic aromatic hydrocarbons (PAHs) at school microenvironments (indoors and outdoors), major sources and potential health risks. A total of 28, 35, and 31% of the studies reported levels that exceeded the international outdoor ambient air guidelines for PM10, PM2.5, and benzo(a)pyrene, respectively. Indoor and outdoor concentrations of PM10 at European schools, the most characterized continent, ranged between 7.5 and 229 μg/m3 and 21–166 μg/ m3 , respectively; levels of PM2.5 varied between 4 and 100 μg/m3 indoors and 6.1–115 μg/m3 outdoors. Despite scarce information in some geographical regions (America, Oceania and Africa), the collected data clearly show that Asian children are exposed to the highest concentrations of PM and PAHs at school environments, which were associated with increased carcinogenic risks and with the highest values of urinary total monohydroxyl PAH metabolites (PAH biomarkers of exposure). Additionally, children attending schools in polluted urban and industrial areas are exposed to higher levels of PM and PAHs with increased concentrations of urinary PAH metabolites in comparison with children from rural areas. Strong evidences demonstrated associations between environmental exposure to PM and PAHs with several health outcomes, including increased risk of asthma, pulmonary infections, skin diseases, and allergies. Nevertheless, there is a scientific gap on studies that include the characterization of PM fine fraction and the levels of PAHs in the total air (particulate and gas phases) of indoor and outdoor air of school environments and the associated risks for the health of children. There is a clear need to improve indoor air quality in schools and to establish international guidelines for exposure limits in these environments.
... Recent studies, particularly in urban areas, have suggested a role of pollutants in the development of respiratory diseases (Chiusolo et al. 2011; Darrow et al. 2011; Namdeo et al. 2011). Evidence is emerging that traffic-related pollutants may contribute to the development of allergy (Kelly and Fussell 2011; Koppen et al. 2011). Furthermore, numerous epidemiological and experimental studies suggest an association between exposure to ambient NO 2 , O 3 and PM and an increased susceptibility to respiratory morbidity (Giovannini et al. 2010; Kim et al. 2011; Tramuto et al. 2011). ...
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The effect of biological (pollen) and chemical air pollutants on respiratory hospital admissions for the Szeged region in Southern Hungary is analysed. A 9-year (1999-2007) database includes-besides daily number of respiratory hospital admissions-daily mean concentrations of CO, PM10, NO, NO2, O3 and SO2. Two pollen variables (Ambrosia and total pollen excluding Ambrosia) are also included. The analysis was performed for patients with chronic respiratory complaints (allergic rhinitis or asthma bronchiale) for two age categories (adults and the elderly) of males and females. Factor analysis was performed to clarify the relative importance of the pollutant variables affecting respiratory complaints. Using selected low and high quantiles corresponding to probability distributions of respiratory hospital admissions, averages of two data sets of each air pollutant variable were evaluated. Elements of these data sets were chosen according to whether actual daily patient numbers were below or above their quantile value. A nonparametric regression technique was applied to discriminate between extreme and non-extreme numbers of respiratory admissions using pollen and chemical pollutants as explanatory variables. The strongest correlations between extreme patient numbers and pollutants can be observed during the pollen season of Ambrosia, while the pollen-free period exhibits the weakest relationships. The elderly group with asthma bronchiale is characterised by lower correlations between extreme patient numbers and pollutants compared to adults and allergic rhinitis, respectively. The ratio of the number of correct decisions on the exceedance of a quantile resulted in similar conclusions as those obtained by using multiple correlations.
... For adult male and female patients, the total weight of the chemical variables in the occurrence of asthma ER visits is higher in the pollen season of Ambrosia compared to the pollen-free season (Tables 2a-2c). Some studies found that exposure to outdoor air pollutants may increase the risk of allergic airway diseases (de Marco et al., 2002;Yu et al., 2005;Pénard-Morand et al., 2005;Kelly and Fussell, 2011;Koppen et al., 2011). This may be explained by the fact that air pollutants, especially burning of fossil fuels, can affect allergens. ...
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Joint effect of biological (pollen) and chemical air pollutants on asthma emergency room (ER) visits was analyzed for Szeged region of Southern Hungary. Our database of a nine-year period (1999-2007) includes daily number of asthma emergency room (ER) visits, and daily mean concentrations of CO, PM(10), NO, NO(2), O(3) and SO(2), furthermore two pollen variables (Ambrosia and total pollen excluding Ambrosia), as well. The analysis was performed for ER visits of asthma bronchiale using two age groups (adults and the elderly) of males and females for three seasons. Factor analysis was performed in order to clarify the relative importance of the pollutant variables affecting asthma ER visits. Asthma ER visits denote notably stronger associations with the pollutants in adult male than in adult female patients both for the pollen season of Ambrosia and the pollen-free season. Furthermore, adults are substantially more sensitive to severe asthma attack than the elderly for the season of total pollen excluding Ambrosia pollen. The joint effect of the chemical and pollen variables is the highest for the asthma ER cases in the pollen season of Ambrosia, basically due to the extra impact of the total pollen excluding Ambrosia pollen and partly due to Ambrosia pollen. A nonparametric regression technique was applied to discriminate between events of ER visit-no ER visit using pollen and chemical pollutants as explaining variables. Based on multiple correlations, the strongest relationships between ER visits and pollutants are observed during the pollen-free season. The elderly group with asthma bronchiale is characterized by weaker relationships between ER visits and pollutants compared to adults. Ratio of the number of correct decisions on the events of ER visit-no ER visit is lowest for the season of total pollen excluding Ambrosia pollen. Otherwise, similar conclusions hold as those received by multiple correlations.
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Results from studies of traffic and childhood asthma have been inconsistent, but there has been little systematic evaluation of susceptible subgroups. In this study, we examined the relationship of local traffic-related exposure and asthma and wheeze in southern California school children (5-7 years of age). Lifetime history of doctor-diagnosed asthma and prevalent asthma and wheeze were evaluated by questionnaire. Parental history of asthma and child's history of allergic symptoms, sex, and early-life exposure (residence at the same home since 2 years of age) were examined as susceptibility factors. Residential exposure was assessed by proximity to a major road and by modeling exposure to local traffic-related pollutants. Residence within 75 m of a major road was associated with an increased risk of lifetime asthma [odds ratio (OR)=1.29; 95% confidence interval (CI), 1.01-1.86], prevalent asthma (OR=1.50; 95% CI, 1.16-1.95), and wheeze (OR=1.40; 95% CI, 1.09-1.78). Susceptibility increased in long-term residents with no parental history of asthma for lifetime asthma (OR=1.85; 95% CI, 1.11-3.09), prevalent asthma (OR=2.46; 95% CI, 0.48-4.09), and recent wheeze (OR=2.74; 95% CI, 1.71-4.39). The higher risk of asthma near a major road decreased to background rates at 150-200 m from the road. In children with a parental history of asthma and in children moving to the residence after 2 years of age, there was no increased risk associated with exposure. Effect of residential proximity to roadways was also larger in girls. A similar pattern of effects was observed with traffic-modeled exposure. These results indicate that residence near a major road is associated with asthma. The reason for larger effects in those with no parental history of asthma merits further investigation.
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Due to scientific interest on the one hand and political and regulatory obligations on the other hand the monitoring of ozone in the troposphere is an important issue. To this end, in Belgium as in many other countries, a fixed network of monitoring stations is operated. In order to estimate the ozone concentrations over the whole territory, a model is needed to spatially complement the sparse measurements. This paper describes the development of an interpolation scheme which is aimed at fast operational use. The model uses the population density as auxiliary data to remove a spatial trend due to titration by nitric oxide. The residuals are interpolated by kriging. As a benchmark the inverse distance weighting interpolation method is used with and without the detrending. The proposed model systematically improves the interpolation and makes a significant difference when estimating human exposure to ozone. It is generic in design, easy to implement and flexible to changes in the monitoring network.
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We previously reported an association between infant wheezing and residence < 100 m from stop-and-go bus and truck traffic. The use of a proximity model, however, may lead to exposure misclassification. Results obtained from a land use regression (LUR) model of exposure to truck and bus traffic are compared with those obtained with a proximity model. The estimates derived from the LUR model were then related to infant wheezing. We derived a marker of diesel combustion--elemental carbon attributable to traffic sources (ECAT)--from ambient monitoring results of particulate matter with aerodynamic diameter < 2.5 microm. We developed a multiple regression model with ECAT as the outcome variable. Variables included in the model were locations of major roads, bus routes, truck traffic count, and elevation. Model parameter estimates were applied to estimate individual ECAT levels at infants' homes. The levels of estimated ECAT at the monitoring stations ranged from 0.20 to 1.02 microg/m(3). A LUR model of exposure with a coefficient of determination (R(2)) of 0.75 was applied to infants' homes. The mean (+/- SD) ambient exposure of ECAT for infants previously categorized as unexposed, exposed to stop-and-go traffic, or exposed to moving traffic was 0.32 +/- 0.06, 0.42 +/- 0.14, and 0.49 +/- 0.14 microg/m(3), respectively. Levels of ECAT from 0.30 to 0.90 mug/m(3) were significantly associated with infant wheezing. The LUR model resulted in a range of ECAT individually derived for all infants' homes that may reduce the exposure misclassification that can arise from a proximity model.
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In the current issue of the European Respiratory Journal , Brauer et al. 1 report positive associations between markers of traffic-related air pollution and respiratory health outcomes, including asthma onset, incidence of wheeze, ear/nose/throat infections and serious colds or flu, in a large cohort of children 4 yrs of age. This study replicates and extends earlier findings on the same birth cohort at 2 yrs of age. Although a replication, the findings here are more compelling than the earlier study for a number of reasons. First, the effects are larger and more consistent than in the study of the children at 2 yrs of age. In the field of air pollution epidemiology, which closely links to government policy and regulation, concepts such as statistical significance take on a greater meaning, one that often goes beyond what epidemiologists and health scientists consider essential to interpreting results. The stronger and more consistent effects in the current study bolster a growing body of research suggesting that more refined exposure metrics associate with larger respiratory health effects in children, which are discussed hereafter. Secondly, and linked to the first point, the diagnostic accuracy of the conditions after the first 4 yrs of life is likely to be higher than in the first 2 yrs of life, again leading to greater confidence in the association. The relative consistency of the associations at 4 yrs of age compared with those at 2 yrs of age suggests that onset and persistence of respiratory disease formation begins at an early age and continues throughout the course …
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Few studies of air pollutants address morbidity in preschool children. In this study we evaluated bronchitis in children from two Czech districts: Teplice, with high ambient air pollution, and Prachatice, characterized by lower exposures. Our goal was to examine rates of lower respiratory illnesses in preschool children in relation to ambient particles and hydrocarbons. Air monitoring for particulate matter < 2.5 microm in diameter (PM(2.5)) and polycyclic aromatic hydrocarbons (PAHs) was conducted daily, every third day, or every sixth day. Children born May 1994 through December 1998 were followed to 3 or 4.5 years of age to ascertain illness diagnoses. Mothers completed questionnaires at birth and at follow-up regarding demographic, lifestyle, reproductive, and home environmental factors. Longitudinal multivariate repeated-measures analysis was used to quantify rate ratios for bronchitis and for total lower respiratory illnesses in 1,133 children. After adjustment for season, temperature, and other covariates, bronchitis rates increased with rising pollutant concentrations. Below 2 years of age, increments in 30-day averages of 100 ng/m(3) PAHs and of 25 microg/m(3) PM(2.5) resulted in rate ratios (RRs) for bronchitis of 1.29 [95 % confidence interval (CI), 1.07-1.54] and 1.30 (95% CI, 1.08-1.58), respectively; from 2 to 4.5 years of age, these RRs were 1.56 (95% CI, 1.22-2.00) and 1.23 (95% CI, 0.94-1.62), respectively. Ambient PAHs and fine particles were associated with early-life susceptibility to bronchitis. Associations were stronger for longer pollutant-averaging periods and, among children > 2 years of age, for PAHs compared with fine particles. Preschool-age children may be particularly vulnerable to air pollution-induced illnesses.
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There is limited evidence for the role of air pollution in the development and triggering of wheezing symptoms in young children. A study was undertaken to examine the effect of exposure to air pollution on wheezing symptoms in children under the age of 3 years with genetic susceptibility to asthma. Daily recordings of symptoms were obtained for 205 children participating in the birth cohort study Copenhagen Prospective Study on Asthma in Children and living in Copenhagen for the first 3 years of life. Daily air pollution levels for particulate matter <10 microm in diameter (PM(10)) and the concentrations of ultrafine particles, nitrogen dioxide (NO(2)), nitrogen oxide (NO(x)) and carbon monoxide (CO) were available from a central background monitoring station in Copenhagen. The association between incident wheezing symptoms and air pollution on the concurrent and previous 4 days was estimated by a logistic regression model (generalised estimating equation) controlling for temperature, season, gender, age, exposure to smoking and paternal history of asthma. Significant positive associations were found between concentrations of PM(10), NO(2), NO(x), CO and wheezing symptoms in infants (aged 0-1 year) with a delay of 3-4 days. Only the traffic-related gases (NO(2), NO(x)) showed significant effects throughout the 3 years of life, albeit attenuating after the age of 1 year. Air pollution related to traffic is significantly associated with triggering of wheezing symptoms in the first 3 years of life.
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This review summarizes the level of epidemiologic evidence for relationships between prenatal and/or early life exposure to environmental chemical contaminants and fetal, child, and adult health. Discussion focuses on fetal loss, intrauterine growth restriction, preterm birth, birth defects, respiratory and other childhood diseases, neuropsychological deficits, premature or delayed sexual maturation, and certain adult cancers linked to fetal or childhood exposures. Environmental exposures considered here include chemical toxicants in air, water, soil/house dust and foods (including human breast milk), and consumer products. Reports reviewed here included original epidemiologic studies (with at least basic descriptions of methods and results), literature reviews, expert group reports, meta-analyses, and pooled analyses. Levels of evidence for causal relationships were categorized as sufficient, limited, or inadequate according to predefined criteria. There was sufficient epidemiological evidence for causal relationships between several adverse pregnancy or child health outcomes and prenatal or childhood exposure to environmental chemical contaminants. These included prenatal high-level methylmercury (CH(3)Hg) exposure (delayed developmental milestones and cognitive, motor, auditory, and visual deficits), high-level prenatal exposure to polychlorinated biphenyls (PCBs), polychlorinated dibenzofurans (PCDFs), and related toxicants (neonatal tooth abnormalities, cognitive and motor deficits), maternal active smoking (delayed conception, preterm birth, fetal growth deficit [FGD] and sudden infant death syndrome [SIDS]) and prenatal environmental tobacco smoke (ETS) exposure (preterm birth), low-level childhood lead exposure (cognitive deficits and renal tubular damage), high-level childhood CH(3)Hg exposure (visual deficits), high-level childhood exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (chloracne), childhood ETS exposure (SIDS, new-onset asthma, increased asthma severity, lung and middle ear infections, and adult breast and lung cancer), childhood exposure to biomass smoke (lung infections), and childhood exposure to outdoor air pollutants (increased asthma severity). Evidence for some proven relationships came from investigation of relatively small numbers of children with high-dose prenatal or early childhood exposures, e.g., CH(3)Hg poisoning episodes in Japan and Iraq. In contrast, consensus on a causal relationship between incident asthma and ETS exposure came only recently after many studies and prolonged debate. There were many relationships supported by limited epidemiologic evidence, ranging from several studies with fairly consistent findings and evidence of dose-response relationships to those where 20 or more studies provided inconsistent or otherwise less than convincing evidence of an association. The latter included childhood cancer and parental or childhood exposures to pesticides. In most cases, relationships supported by inadequate epidemiologic evidence reflect scarcity of evidence as opposed to strong evidence of no effect. This summary points to three main needs: (1) Where relationships between child health and environmental exposures are supported by sufficient evidence of causal relationships, there is a need for (a) policies and programs to minimize population exposures and (b) population-based biomonitoring to track exposure levels, i.e., through ongoing or periodic surveys with measurements of contaminant levels in blood, urine and other samples. (2) For relationships supported by limited evidence, there is a need for targeted research and policy options ranging from ongoing evaluation of evidence to proactive actions. (3) There is a great need for population-based, multidisciplinary and collaborative research on the many relationships supported by inadequate evidence, as these represent major knowledge gaps. Expert groups faced with evaluating epidemiologic evidence of potential causal relationships repeatedly encounter problems in summarizing the available data. A major driver for undertaking such summaries is the need to compensate for the limited sample sizes of individual epidemiologic studies. Sample size limitations are major obstacles to exploration of prenatal, paternal, and childhood exposures during specific time windows, exposure intensity, exposure-exposure or exposure-gene interactions, and relatively rare health outcomes such as childhood cancer. Such research needs call for investments in research infrastructure, including human resources and methods development (standardized protocols, biomarker research, validated exposure metrics, reference analytic laboratories). These are needed to generate research findings that can be compared and subjected to pooled analyses aimed at knowledge synthesis.
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The rubric complementary therapy covers a variety of approaches that may seem alike only in their being outside conventional care and training. We have asked experienced practitioners to present their own pieces of this jigsaw, realising that these clinical fragments, when seen together, create excitement but also confusion. Of course, this forum is not intended to be a comprehensive review of relevant complementary treatments, and often the individual approaches to clinical problems will appear totally unrelated, while their apparent effectiveness stretches the biomedical model and conventional research methodology beyond their capacity. With this in mind, we intend that forthcoming articles and reviews will expand on the therapies themselves, and discuss the evidence supporting them.
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The Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS) is a prospective birth cohort whose purpose is to determine if exposure to high levels of diesel exhaust particles (DEP) during early childhood increases the risk for developing allergic diseases. In order to estimate exposure to DEP, a land-use regression (LUR) model was developed using geographic data as independent variables and sampled levels of a marker of DEP as the dependent variable. A continuous wind direction variable was also created. The LUR model predicted 74% of the variability in sampled values with four variables: wind direction, length of bus routes within 300 m of the sample site, a measure of truck intensity within 300 m of the sampling site, and elevation. The LUR model was subsequently applied to all locations where the child had spent more than eight hours per week from through age three. A time-weighted average (TWA) microenvironmental exposure estimate was derived for four time periods: 0–6 months, 7–12 months, 13–24 months, 25–36 months. By age two, one third of the children were spending significant time at locations other than home and by 36 months, 39% of the children had changed their residential addresses. The mean cumulative DEP exposure estimate increased from age 6 to 36 months from 70 to 414 μg/m3-days. Findings indicate that using birth addresses to estimate a child's exposure may result in exposure misclassification for some children who spend a significant amount of time at a location with high exposure to DEP.
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The general public, especially patients with upper or lower respiratory symptoms, is aware from media reports that adverse respiratory effects can occur from air pollution. It is important for the allergist to have a current knowledge of the potential health effects of air pollution and how they might affect their patients to advise them accordingly. Specifically, the allergist-clinical immunologist should be keenly aware that both gaseous and particulate outdoor pollutants might aggravate or enhance the underlying pathophysiology of both the upper and lower airways. Epidemiologic and laboratory exposure research studies investigating the health effects of outdoor air pollution each have advantages and disadvantages. Epidemiologic studies can show statistical associations between levels of individual or combined air pollutants and outcomes, such as rates of asthma, emergency visits for asthma, or hospital admissions, but cannot prove a causative role. Human exposure studies, animal models, and tissue or cellular studies provide further information on mechanisms of response but also have inherent limitations. The aim of this rostrum is to review the relevant publications that provide the appropriate context for assessing the risks of air pollution relative to other more modifiable environmental factors in patients with allergic airways disease.
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Traffic-related air pollution (TAP) impairs respiratory health and could influence the development of allergies, as was demonstrated in urban areas with relatively high pollution. Whether eczema is affected by TAP was rarely investigated. To investigate whether exposure to TAP affects eczema and respiratory allergies also in small-town areas with lower concentrations of pollution. Between 1995 and 1999, we recruited 3390 newborns from small-town areas. Diagnoses and symptoms of eczema and respiratory allergies were recorded by annual questionnaires. Seventy-seven percent of families participated until the child's 6th birthday, when a clinical test for eczema and IgE-sensitization was performed. Individual exposure to traffic-related soot and NO(2) at the children's home addresses was determined by land-use-regression. We used Cox-regression/log-binomial-regression to determine its confounder-adjusted association with incidence and prevalence of eczema and respiratory allergies. The prevalence of eczema at age 6 was significantly higher in children who resided in areas where TAP was higher. The adjusted relative risk for doctor diagnosed eczema for instance was 1.69 (95% confidence interval 1.04-2.75) per 90%-range of soot concentration. Current eczema at the 6 year clinical investigation was likewise associated, children with parental allergies showed significantly stronger effects (p<0.05). Incidence of eczema was not affected. No associations between TAP and asthma, hay fever, or allergic sensitization emerged. Eczema was sensitive to TAP, effects emerged even in lower polluted small-town areas of Germany. They could be seen for prevalence but not incidence of eczema. This is equivalent to a longer duration of eczema in exposed children.
Article
The main goal of the paper was to assess the pattern of risk factors having an impact on the onset of early wheezing phenotypes in the birth cohort of 468 two-year olds and to investigate the severity of respiratory illness in the two-year olds in relation to both wheezing phenotypes, environmental tobacco smoke (ETS) and personal PM(2.5) exposure over pregnancy period (fine particulate matter). The secondary goal of the paper was to assess possible association of early persistent wheezing with the length of the baby at birth. Pregnant women were recruited from ambulatory prenatal clinics in the first and second trimester of pregnancy. Only women 18-35 years of age, who claimed to be non-smokers, with singleton pregnancies, without illicit drug use and HIV infection, free from chronic diseases were eligible for the study. In the statistical analysis of respiratory health of children multinomial logistic regression and zero-inflated Poisson regression models were used. Approximately one third of the children in the study sample experienced wheezing in the first 2 years of life and in about two third of cases (67%) the symptom developed already in the first year of life. The early wheezing was easily reversible and in about 70% of infants with wheezing the symptom receded in the second year of life. The adjusted relative risk ratio (RRR) of persistent wheezing increased with maternal atopy (RRR=3.05; 95%CI: 1.30-7.15), older siblings (RRR=3.05; 95%CI: 1.67-5.58) and prenatal ETS exposure (RRR=1.13; 95%CI: 1.04-1.23), but was inversely associated with the length of baby at birth (RRR=0.88; 95%CI: 0.76-1.01). The adjusted incidence risk ratios (IRR) of coughing, difficult breathing, runny/stuffy nose and pharyngitis/tonsillitis in wheezers were much higher than that observed among non-wheezers and significantly depended on prenatal PM(2.5) exposure, older siblings and maternal atopy. The study shows a clear inverse association between maternal age or maternal education and respiratory illnesses and calls for more research efforts aiming at the explanation of factors hidden behind proxy measures of quality of maternal care of babies. The data support the hypothesis that burden of respiratory symptoms in early childhood and possibly in later life may be programmed already in prenatal period when the respiratory system is completing its growth and maturation.
Article
To determine the impact of environmental exposures (diesel exhaust particle [DEP], environmental tobacco smoke [ETS], and mold) that may contribute to oxidative stress on persistent wheezing in the Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS) birth cohort and to determine how the impact of these exposures is modified by the GST-P1 Ile105Val polymorphism. A land-use regression model was used to derive an estimate of each child's DEP exposure. ETS exposure was determined by questionnaire data. Each child's home was evaluated for visible mold by a trained professional. Children in the CCAAPS cohort were genotyped for the GST-P1 polymorphism (n = 570). Persistent wheezing was defined as wheezing at both 12 and 24 months. High DEP exposure conferred increased risk for wheezing phenotypes but only among the Val(105) allele carriers. Infants with multiple exposures were significantly more likely to persistently wheeze despite their genotype. There is evidence for an environmental effect of DEP among carriers of the GST-P1 Val(105) allele in the development of persistent wheezing in children. The protective effect of the GST-P1 Ile(105) genotype may be overwhelmed by multiple environmental exposures that converge on oxidative stress pathways.
Article
The increasing number of population-based and epidemiologic associations between oxidant pollutant exposures and cardiopulmonary disease exacerbation, decrements in pulmonary function, and mortality underscores the important detrimental effects of oxidants on public health. Because inhaled oxidants initiate a number of pathologic processes, including inflammation of the airways, which may contribute to the pathogenesis and/or exacerbation of airways disease, it is critical to understand the mechanisms through which exogenous and endogenous oxidants interact with molecules in the cells, tissues, and epithelial lining fluid of the lung. Furthermore, it is clear that interindividual variation in response to a given exposure also exists across an individual lifetime. Because of the potential impact that oxidant exposures may have on reproductive outcomes and infant, child, and adult health, identification of the intrinsic and extrinsic factors that may influence susceptibility to oxidants remains an important issue. In this review, we discuss mechanisms of oxidant stress in the lung, the role of oxidants in lung disease pathogenesis and exacerbation (eg, asthma, chronic obstructive pulmonary disease, and acute respiratory distress syndrome), and the potential risk factors (eg, age, genetics) for enhanced susceptibility to oxidant-induced disease.
Article
Many young children wheeze during viral respiratory infections, but the pathogenesis of these episodes and their relation to the development of asthma later in life are not well understood. In a prospective study, we investigated the factors affecting wheezing before the age of three years and their relation to wheezing at six years of age. Of 1246 newborns in the Tucson, Arizona, area enrolled between May 1980 and October 1984, follow-up data at both three and six years of age was available for 826. For these children, assessments in infancy included measurement of cord-serum IgE levels (measured in 750 children), pulmonary-function testing before any lower respiratory illness had occurred (125), measurement of serum IgE levels at nine months of age (672), and questionnaires completed by the children's parents when the children were one year old (800). Assessments at six years of age included measurement of serum IgE levels (in 460), pulmonary-function testing (526), and skin allergy testing (629). At the age of six years, 425 children (51.5 percent) had never wheezed, 164 (19.9 percent) had had at least one lower respiratory illness with wheezing during the first three years of life but had no wheezing at six years of age, 124 (15.0 percent) had no wheezing before the age of three years but had wheezing at the age of six years, and 113 (13.7 percent) had wheezing both before three years of age and at six years of age. The children who had wheezing before three years of age but not at the age of six had diminished airway function (length-adjusted maximal expiratory flow at functional residual capacity [Vmax FRC]) both before the age of one year and at the age of six years, were more likely than the other children to have mothers who smoked but not mothers with asthma, and did not have elevated serum IgE levels or skin-test reactivity. Children who started wheezing in early life and continued to wheeze at the age of six were more likely than the children who never wheezed to have mothers with a history of asthma (P < 0.001), to have elevated serum IgE levels (P < 0.01), to have normal lung function in the first year of life, and to have elevated serum IgE levels (P < 0.001) and diminished values for VmaxFRC (P < 0.01) at six years of age. The majority of infants with wheezing have transient conditions associated with diminished airway function at birth and do not have increased risks of asthma or allergies later in life. In a substantial minority of infants, however, wheezing episodes are probably related to a predisposition to asthma.
Article
The prevalence of allergic diseases has been on the rise for the last 200 years, when hay fever, an easy and obvious-to-recognize illness, was virtually unknown in Europe and North America. Genetic factors are unlikely to explain these rapid increases. Among the potential environmental factors, exposure to ambient air pollution has been intensely debated. Besides passive smoking, which has convincingly been shown to increase the risk for asthma and bronchial hyperresponsiveness among exposed children, the evidence to suggest that outdoor pollution to sulfur dioxide, particulate matter, diesel exhaust, and ozone is causally related with the inception of allergic diseases is poor. Rather, factors associated with the lifestyle of populations or families, such as socioeconomic status, allergen exposure, sibship size, early childhood infections, dietary habits, and growing up in anthroposophic families or a farming environment, may prove to be of greater relevance. The future challenge is to tackle the complex interplay between environmental factors and genetic determinants that will eventually contribute to a better understanding and to better prevention strategies for such multifactorial conditions as asthma and allergies.
Article
Atopy is a major risk factor for the development of asthma. Immune processes that lead to the development of antigen-specific IgE are essential to the development of atopy. This review examines the immune processes that are candidate targets for modulation by environmental agents; environmental and lifestyle factors that have been suggested as modulators of the development of atopy; and the impact of known environmental agents on atopic processes in the airway. The most important periods of immune development with regard to expression of atopy are likely during gestation and early childhood. A better understanding of which environmental agents are important, as well as the period of life during which these agents may exert an important effect, is essential to devising rational environmental avoidance strategies for at-risk populations.
Article
Little is known about the effect of exposure to air pollution during exercise or time spent outdoors on the development of asthma. We investigated the relation between newly-diagnosed asthma and team sports in a cohort of children exposed to different concentrations and mixtures of air pollutants. 3535 children with no history of asthma were recruited from schools in 12 communities in southern California and were followed up for up to 5 years. 265 children reported a new diagnosis of asthma during follow-up. We assessed risk of asthma in children playing team sports at study entry in six communities with high daytime ozone concentrations, six with lower concentrations, and in communities with high or low concentrations of nitrogen dioxide, particulate matter, and inorganic-acid vapour. In communities with high ozone concentrations, the relative risk of developing asthma in children playing three or more sports was 3.3 (95% CI 1.9-5.8), compared with children playing no sports. Sports had no effect in areas of low ozone concentration (0.8, 0.4-1.6). Time spent outside was associated with a higher incidence of asthma in areas of high ozone (1.4, 1.0-2.1), but not in areas of low ozone. Exposure to pollutants other than ozone did not alter the effect of team sports. Incidence of new diagnoses of asthma is associated with heavy exercise in communities with high concentrations of ozone, thus, air pollution and outdoor exercise could contribute to the development of asthma in children.
Article
Despite the important contribution of traffic sources to urban air quality, relatively few studies have evaluated the effects of traffic-related air pollution on health, such as its influence on the development of asthma and other childhood respiratory diseases. We examined the relationship between traffic-related air pollution and the development of asthmatic/allergic symptoms and respiratory infections in a birth cohort (n approximately 4,000) study in The Netherlands. A validated model was used to assign outdoor concentrations of traffic-related air pollutants (nitrogen dioxide, particulate matter less than 2.5 micro m in aerodynamic diameter, and "soot") at the home of each subject of the cohort. Questionnaire-derived data on wheezing, dry nighttime cough, ear, nose, and throat infections, skin rash, and physician-diagnosed asthma, bronchitis, influenza, and eczema at 2 years of age were analyzed in relation to air pollutants. Adjusted odds ratios for wheezing, physician-diagnosed asthma, ear/nose/throat infections, and flu/serious colds indicated positive associations with air pollutants, some of which reached borderline statistical significance. No associations were observed for the other health outcomes analyzed. Sensitivity analyses generally supported these results and suggested somewhat stronger associations with traffic, for asthma that was diagnosed before 1 year of age. These findings are subject to confirmation at older ages, when asthma can be more readily diagnosed.
Article
The health effects of air pollution have been subject to intense study in recent years. Exposure to pollutants such as airborne particulate matter and ozone has been associated with increases in mortality and hospital admissions due to respiratory and cardiovascular disease. These effects have been found in short-term studies, which relate day-to-day variations in air pollution and health, and long-term studies, which have followed cohorts of exposed individuals over time. Effects have been seen at very low levels of exposure, and it is unclear whether a threshold concentration exists for particulate matter and ozone below which no effects on health are likely. In this review, we discuss the evidence for adverse effects on health of selected air pollutants.
Article
Automobile exhaust is considered to be a potential risk factor for respiratory diseases. To investigate the effects of traffic-related air pollution on respiratory symptoms among children who lived near trunk roads, we conducted a cohort study on 2,506 schoolchildren in eight different communities in Japan. Over that four-year period, the prevalence of asthma was higher among girls who lived less than 50 m from trunk roads (roadside areas) than among girls in the other areas studied. Testing for trends showed that the prevalence of asthma among girls increased significantly with increases in the concentration of air pollution in each area. Among boys, the prevalence of asthma did not differ in relation to the distance from roads, although the rate was higher in urban areas than in rural areas. The incidence of asthma during the follow-up period significantly increased among boys living in roadside areas relative to rural areas (odds ratio = 3.75; 95% confidence interval: 1.00-14.06). Among girls, the incidence of asthma also increased (odds ratio = 4.06; 95% confidence interval:0.91-18.10), although the risk was not significant. These findings suggest that traffic-related air pollution may be of particular importance in the development of asthma among children living near major trunk roads with heavy traffic.
Article
The effects of air pollution on asthmatic symptoms were assessed in a prospective cohort study of 3,049 schoolchildren in 8 different communities in Japan. Respiratory symptoms in these children were evaluated by questionnaires every year from the 1st through the 6th grades. The prevalence of asthma among the 1st graders was strongly associated with a history of allergic or respiratory diseases, but it was not associated with concentrations of air pollution. During the follow-up period, incidence rates of asthma were associated significantly with atmospheric concentrations of nitrogen dioxide. Particulate matter less than 10 microm in diameter (PM10) was also associated with a higher incidence of asthma, although the association was not significant. These findings suggest that air pollution, including nitrogen dioxide, may be an important factor in the development of asthma among children in urban districts.
Article
The prevalence and incidence of allergic diseases have increased in Europe during the last decades, as in most industrialized countries in other parts of the world. Persistent exposure to traffic related air pollution and especially particulate matter from motor vehicles has often been discussed as one of the factors responsible for this increase. This view seems to be supported by recent human and animal laboratory-based studies, which have shown that particulate pollutants, and in particular diesel exhaust particles, can enhance allergic inflammation and induce the development of allergic immune responses. However, the results from epidemiologic research provide a more complex picture. It has been clearly shown in many studies that traffic related air pollution contributes to increased mortality risk; in particular in relation to cardiopulmonary causes. Traffic related air pollution also increases the risk of non-allergic respiratory symptoms and disease. However, for allergic symptoms and illnesses like asthma, allergic rhinitis, atopic dermatitis, wheeze, and allergic sensitization less consistent results have been found. This is the reason why the World Health Organisation concludes cautiously that traffic related air pollution may increase the risk of allergy development and may exacerbate symptoms in particular in susceptible subgroups. This review concentrates on recent epidemiologic studies on the long-term effects of exposure to traffic related air pollution on allergic disease in Europe. In conclusion, the evidence for an increased risk for asthma and hay fever still is weak but seems to be strengthened a little. However, many questions are left open.
Article
Few studies have characterized the atopic profile of toddler-aged children with recurrent wheezing at high risk of the development of persistent asthma. Objective We sought to determine the atopic profile of toddler-aged children with frequent wheeze at high risk for the development of persistent asthma who either had a parental history of asthma, a personal history of atopic dermatitis, or both. Participants enrolled in the Prevention of Early Asthma in Kids study (n = 285) on the basis of a modified Asthma Predictive Index were characterized on the basis of allergy and asthma questionnaire responses and allergy skin puncture test results. The majority of the children (60.7%, n = 148) were sensitized to either food or aeroallergens. Male children were significantly more likely to be sensitized to aeroallergens ( P = .03) and to have a blood eosinophil level of 4% or greater ( P = .03) and a total serum IgE level of greater than 100 IU/mL ( P = .0004). Additionally, eosinophilia and total serum IgE level had the strongest correlation with aeroallergen sensitization. The high prevalence of aeroallergen sensitization in this high-risk cohort suggests that aeroallergens might have an important role in the early development of asthma. As such, the Prevention of Early Asthma in Kids cohort appears to be an appropriate cohort in which to test whether early intervention with an inhaled corticosteroid can significantly attenuate, or perhaps even prevent, the allergic march from the initial stages of allergic sensitization to the subsequent development of asthma in toddlers with episodic wheezing.
Article
The occurrence of asthma and allergic diseases has continued to increase in the United States and worldwide, despite general improvements in air quality over the past 40 years. This observation has led many to question whether air quality is truly a significant risk factor in the development and exacerbation of asthma and whether further improvement in air quality is likely to result in improved health outcomes. However, epidemiologic studies have shown that levels of pollutants of less than the current ambient air quality standards still result in exacerbations of asthma and are associated with other morbidities as well. Specific locations, such as living near a roadway, might pose a special exposure risk. Genetic factors almost certainly play a role in determining susceptibility to pollutants, such as including those involved with antioxidant defenses. The best studied of these in the context of air pollution risks are glutathione-S-transferase polymorphisms. Irrespective of whether pollutants contribute to the development of asthma or the well-documented increases in asthma results in more people having pollutant-induced disease, poor air quality in many places remains a significant problem for patients with asthma and allergic disease. A number of public health, pharmaceutical, and nutriceutical interventions might mitigate the effects of pollutant exposure and deserve further study.
Article
A growing body of research supports the role of outdoor air pollutants in acutely aggravating chronic diseases in children, and suggests that the pollutants may have a role in the development of these diseases. This article reviews the biologic basis of children's unique vulnerability to highly prevalent outdoor air pollutants, with a special focus on ozone, respirable particulate matter (PM 2.5 [<2.5 microm in diameter] and PM 10 [<10 microm in diameter]), lead, sulfur dioxide, carbon monoxide, and nitrogen oxides. We also summarize understanding regarding health effects and molecular mechanisms of action. Practitioners can significantly reduce morbidity in children and other vulnerable populations by advising families to minimize pollutant exposures to children with asthma, or at a broader level by educating policymakers about the need to act to reduce pollutant emissions. Management of children with asthma must expand beyond preventing exposures to agents that directly cause allergic reactions (and therefore can be diagnosed by means of skin tests) and must focus more attention on agents that cause a broad spectrum of nonspecific, generalized inflammation, such as air pollution.
Article
Many studies showing effects of traffic-related air pollution on health rely on self-reported exposure, which may be inaccurate. We estimated the association between self-reported exposure to road traffic and respiratory symptoms in preschool children, and investigated whether the effect could have been caused by reporting bias. In a random sample of 8700 preschool children in Leicestershire, UK, exposure to road traffic and respiratory symptoms were assessed by a postal questionnaire (response rate 80%). The association between traffic exposure and respiratory outcomes was assessed using unconditional logistic regression and conditional regression models (matching by postcode). Prevalence odds ratios (95% confidence intervals) for self-reported road traffic exposure, comparing the categories 'moderate' and 'dense', respectively, with 'little or no' were for current wheezing: 1.26 (1.13-1.42) and 1.30 (1.09-1.55); chronic rhinitis: 1.18 (1.05-1.31) and 1.31 (1.11-1.56); night cough: 1.17 (1.04-1.32) and 1.36 (1.14-1.62); and bronchodilator use: 1.20 (1.04-1.38) and 1.18 (0.95-1.46). Matched analysis only comparing symptomatic and asymptomatic children living at the same postcode (thus exposed to similar road traffic) showed similar ORs, suggesting that parents of children with respiratory symptoms reported more road traffic than parents of asymptomatic children. Our study suggests that reporting bias could explain some or even all the association between reported exposure to road traffic and disease. Over-reporting of exposure by only 10% of parents of symptomatic children would be sufficient to produce the effect sizes shown in this study. Future research should be based only on objective measurements of traffic exposure.
Article
To estimate long-term exposure to traffic-related air pollutants on an individual basis and to assess adverse health effects using a combination of air pollution measurement data, data from geographical information systems (GIS) and questionnaire data. 40 measurement sites in the city of Munich, Germany were selected at which to collect particulate matter with a 50% cut-off aerodynamic diameter of 2.5 microm (PM2.5) and to measure PM2.5 absorbance and nitrogen dioxide (NO2). A pool of GIS variables (information about street length, household and population density and land use) was collected for the Munich metropolitan area and was used in multiple linear regression models to predict traffic-related air pollutants. These models were also applied to the birth addresses of two birth cohorts (German Infant Nutritional Intervention Study (GINI) and Influence of Life-style factors on the development of the Immune System and Allergies in East and West Germany (LISA)) in the Munich metropolitan area. Associations between air pollution concentrations at birth address and 1-year and 2-year incidences of respiratory symptoms were analysed. The following means for the estimated exposures to PM2.5, PM2.5 absorbance and NO2 were obtained: 12.8 microg/m3, 1.7x10(-5) m(-1) and 35.3 mug/m3, respectively. Adjusted odds ratios (ORs) for wheezing, cough without infection, dry cough at night, bronchial asthma, bronchitis and respiratory infections indicated positive associations with traffic-related air pollutants. After controlling for individual confounders, significant associations were found between the pollutant PM2.5 and sneezing, runny/stuffed nose during the first year of life (OR 1.16, 95% confidence interval 1.01 to 1.34) Similar effects were observed for the second year of life. These findings are similar to those from our previous analysis that were restricted to a subcohort in Munich city. The extended study also showed significant effects for sneezing, running/stuffed nose. Additionally, significant associations were found between NO2 and dry cough at night (or bronchitis) during the first year of life. The variable "living close to major roads" (<50 m), which was not analysed for the previous inner city cohort with birth addresses in the city of Munich, turned out to increase the risk of wheezing and asthmatic/spastic/obstructive bronchitis. Effects on asthma and hay fever are subject to confirmation at older ages, when these outcomes can be more validly assessed.
Article
A growing body of evidence has been generated indicating that the fetus, infant, and young child are especially susceptible to environmental toxicants as diverse as polycyclic aromatic hydrocarbons (PAHs), pesticides, lead, mercury, polychlorinated biphenyls (PCBs), and environmental tobacco smoke (ETS). Exposures to these toxicants may be related to the increases in recent decades in childhood asthma, cancer, and developmental disability. The Columbia Center for Children's Environmental Health (CCCEH), located in New York City, has developed four cohorts around the world to elucidate the relationships between these exposures and childhood illness. This article summarizes the recent findings from the Center's projects in the context of current research in children's environmental health.
Article
Few studies have addressed associations between traffic-related air pollution and respiratory disease in young children. The present authors assessed the development of asthmatic/allergic symptoms and respiratory infections during the first 4 yrs of life in a birth cohort study (n = approximately 4,000). Outdoor concentrations of traffic-related air pollutants (nitrogen dioxide PM(2.5), particles with a 50% cut-off aerodynamic diameter of 2.5 mum and soot) were assigned to birthplace home addresses with a land-use regression model. They were linked by logistic regression to questionnaire data on doctor-diagnosed asthma, bronchitis, influenza and eczema and to self-reported wheeze, dry night-time cough, ear/nose/throat infections and skin rash. Total and specific immunoglobulin (Ig)E to common allergens were measured in a subgroup (n = 713). Adjusted odds ratios (95% confidence intervals) per interquartile pollution range were elevated for wheeze (1.2 (1.0-1.4) for soot), doctor-diagnosed asthma (1.3 (1.0-1.7)), ear/nose/throat infections (1.2 (1.0-1.3)) and flu/serious colds (1.2 (1.0-1.4)). No consistent associations were observed for other end-points. Positive associations between air pollution and specific sensitisation to common food allergens (1.6 (1.2-2.2) for soot), but not total IgE, were found in the subgroup with IgE measurements. Traffic-related pollution was associated with respiratory infections and some measures of asthma and allergy during the first 4 yrs of life.
Article
Whether local exposure to major roadways adversely affects lung-function growth during the period of rapid lung development that takes place between 10 and 18 years of age is unknown. This study investigated the association between residential exposure to traffic and 8-year lung-function growth. In this prospective study, 3677 children (mean age 10 years [SD 0.44]) participated from 12 southern California communities that represent a wide range in regional air quality. Children were followed up for 8 years, with yearly lung-function measurements recorded. For each child, we identified several indicators of residential exposure to traffic from large roads. Regression analysis was used to establish whether 8-year growth in lung function was associated with local traffic exposure, and whether local traffic effects were independent of regional air quality. Children who lived within 500 m of a freeway (motorway) had substantial deficits in 8-year growth of forced expiratory volume in 1 s (FEV(1), -81 mL, p=0.01 [95% CI -143 to -18]) and maximum midexpiratory flow rate (MMEF, -127 mL/s, p=0.03 [-243 to -11), compared with children who lived at least 1500 m from a freeway. Joint models showed that both local exposure to freeways and regional air pollution had detrimental, and independent, effects on lung-function growth. Pronounced deficits in attained lung function at age 18 years were recorded for those living within 500 m of a freeway, with mean percent-predicted 97.0% for FEV1 (p=0.013, relative to >1500 m [95% CI 94.6-99.4]) and 93.4% for MMEF (p=0.006 [95% CI 89.1-97.7]). Local exposure to traffic on a freeway has adverse effects on children's lung development, which are independent of regional air quality, and which could result in important deficits in attained lung function in later life.
Article
Epidemiological studies that have investigated the association between air pollution and atopy have found inconsistent results. Furthermore, often exposure to outdoor air pollution has had limited quality, and more individual exposure is needed. To investigate the relations between early and lifetime exposure to residential outdoor air pollution and allergen sensitization in 9-10-year-old children in Oslo, Norway. Sensitization to common allergens was measured by skin prick tests (SPTs), which were performed in 2244 children who had lived in Oslo since birth. Several definitions of positive SPT were used. Information on potential confounding variables was collected by a parental questionnaire. Exposure to outdoor air pollution was assessed by the EPISODE dispersion model, which calculates hourly concentrations of nitrogen dioxide (NO2), particulate matter (PM) with aerodynamic diameter <10 microm (PM10) and <2.5 microm (PM2.5), respectively. We found no associations between long-term air pollution exposure and sensitization to any allergen, any indoor or any pollen allergen. However, lifetime air pollution exposure was associated with sensitization to the house dust mite Dermatophagoides farinae. One interquartile increase of lifetime exposure to NO2, PM10 and PM2.5 was associated with 1.88 (adjusted odds ratio) (1.02, 3.47) [95% confidence interval (CI)], 1.61 (0.96, 2.72) and 1.46 (0.96, 2.22), respectively, for D. farinae. Lifetime exposure was also associated with sensitization to cat in a subpopulation. Both associations diminished after adjusting for a contextual socio-economic factor. Long-term exposure to traffic-related pollutants was generally not associated with allergen sensitization in 9-10-year-old Oslo children. However, lifetime exposure was associated with sensitization to D. farinae, and with sensitization to cat in a subpopulation, which may be explained by socio-economic confounding or multiple comparisons. The air pollution levels in Oslo may be too low to reveal associations with sensitization.
Article
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. 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. 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 (PM(2.5)), PM(2.5) absorbance, and long-term exposure to nitrogen dioxide (NO(2)) 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. 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 PM(2.5) 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). NO(2) exposure was associated with eczema, whereas no association was found for allergic sensitization. This study provides strong evidence for increased risk of atopic diseases and allergic sensitization when children are exposed to ambient particulate matter.
Article
Urban air pollution can trigger asthma symptoms in children, but there is conflicting evidence on effects of long-term exposure on lung function, onset of airway disease and allergic sensitization. The spatial distribution of nitrogen oxides from traffic (traffic-NOx) and inhalable particulate matter from traffic (traffic-PM10) in the study area was assessed with emission databases and dispersion modeling. Estimated levels were used to assign first-year exposure levels for children in a prospective birth cohort (n = 4089), by linking to geocoded home addresses. Parents in 4 Swedish municipalities provided questionnaire data on symptoms and exposures when the children were 2 months and 1, 2, and 4-year-old. At 4 years, 73% of the children underwent clinical examination including peak expiratory flow and specific IgE measurements. Exposure to air pollution from traffic during the first year of life was associated with an excess risk of persistent wheezing (odds ratio [OR] for 44 microg/m3 [5th-95th percentile] difference in traffic-NOx = 1.60; 95% confidence interval [CI] = 1.09-2.36). Similar results were found for sensitization (measured as specific IgE) to inhalant allergens, especially pollen (OR for traffic-NOx = 1.67; 95% CI = 1.10-2.53), at the age of 4 years. Traffic-related air pollution exposure during the first year of life was also associated with lower lung function at 4 years of age. Results were similar using traffic-NOx and traffic-PM10 as indicators. Exposure to moderate levels of locally emitted air pollution from traffic early in life appears to influence the development of airway disease and sensitization in preschool children.