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Exposure to Traffic and Early Life Respiratory Infection: A Cohort Study
Abstract
We examined whether proximity to a major roadway and traffic density around the home during pregnancy are associated with risk of early life respiratory infection in a pre-birth cohort in the Boston area. We geocoded addresses for 1,263 mother-child pairs enrolled during the first trimester of pregnancy in Project Viva during 1999–2002. We calculated distance from home to nearest major roadway and traffic density in a 100 m buffer around the home. We defined respiratory infection as maternal report of ≥1 doctor-diagnosed pneumonia, bronchiolitis, croup, or other respiratory infection from birth until the early childhood visit (median age 3.3). We used relative risk regression models adjusting for potential confounders to estimate associations between traffic exposures and risk of respiratory infection. Distance to roadway during pregnancy was associated with risk of respiratory infection. In fully adjusted models, relative risks (95% CI) for respiratory infection were: 1.30 (1.08, 1.55) for <100 m, 1.15 (0.93, 1.41) for 100 to <200 m, and 0.95 (0.84, 1.07) for 200 to <1,000 m compared with living ≥1,000 m away from a major roadway. Each interquartile range increase in distance to roadway was associated with an 8% (95% CI 0.87, 0.98) lower risk, and each interquartile range increase in traffic density was associated with a 5% (95% CI 0.98, 1.13) higher risk of respiratory infection. Our findings suggest that living close to a major roadway during pregnancy may predispose the developing lung to infection in early life. Pediatr Pulmonol. © 2014 Wiley Periodicals, Inc.
... The prenatal period represents a critical exposure window for air pollution effects on humans due to the plasticity and susceptibility of respiratory (Pinkerton and Joad, 2006), immune (Kuper et al., 2016;Palmer, 2011), and detoxification (McElroy et al., 1992) systems. Epidemiologic studies have shown prenatal exposure to outdoor air pollution to be associated with adverse respiratory health outcomes in childhood (Kim et al., 2018), including respiratory tract infections (Aguilera et al., 2013;Jedrychowski et al., 2013;Rice et al., 2015;Soh et al., 2018), impaired lung function performance (Bose et al., 2018;Bougas et al., 2018;Jedrychowski et al., 2010;Korten et al., 2017;Latzin et al., 2009;Morales et al., 2015), asthma (Jung et al., 2019;Subramanian and Khatri, 2019), and related allergic manifestations (Burbank et al., 2017;Cecchi et al., 2018;Deng et al., 2016). The biological mechanisms responsible for these long-lasting effects remain unclear, but disturbances in the developing immune system might play a key role (Ashley-Martin et al., 2016;Sun et al., 2020). ...
... Nevertheless, NK cells play an important role in the early response to viral infections (Abel et al., 2018) and can also inhibit allergic eosinophilic airway inflammation Simons et al., 2017). Thus, it is plausible that impairment of NK cell fetal development could mediate associations between prenatal exposure to air pollution and subsequent higher risk of respiratory infections (Rice et al., 2015;Soh et al., 2018) and asthma (Jung et al., 2019) in childhood. ...
... In contrast to our study, previous ones have examined percentages of immune cells and findings should be interpreted with caution because changes in frequencies could be the result of an immune compensation but not a real change in the absolute cell number (Rivino et al., 2004). Nevertheless, we hypothesize that a reduction in Tc cells, which are involved in the response to virus infections (Schmidt and Varga, 2018), may play a role in predisposing to higher risk of respiratory viral infection in infants associated with air pollution exposure as previously reported (Aguilera et al., 2013;Jedrychowski et al., 2013;Rice et al., 2015;Soh et al., 2018). ...
Background
Hazards of traffic-related air pollution (TRAP) on the developing immune system are poorly understood. We sought to investigate the effects of prenatal exposure to TRAP on cord blood immune cell distributions; and to identify gestational windows of susceptibility.
Methods
In-depth immunophenotyping of cord blood leukocyte and lymphocyte subsets was performed by flow cytometry in 190 newborns embedded in the Nutrition in Early Life and Asthma (NELA) birth cohort (2015–2018). Long-term (whole pregnancy and trimesters) and short-term (15-days before delivery) residential exposures to traffic-related nitrogen dioxide (NO2), particulate matter (PM2.5 and PM10), and ozone (O3) were estimated using dispersion/chemical transport modelling. Associations between TRAP concentrations and cord blood immune cell counts were assessed using multivariate Poisson regression models.
Results
Mean number of natural killer (NK) cells decreased 15% in relation to higher NO2 concentrations (≥36.4 μg/m3) during whole pregnancy (incidence relative risk (IRR), 0.85; 95% CI, 0.72, 0.99), with stronger associations in the first trimester. Higher PM2.5 concentrations (≥13.3 μg/m3) during whole pregnancy associated with a reduced mean number of cytotoxic T cells (IRR, 0.88; 95% CI, 0.78, 0.99). Newborns exposed to higher PM10 (≥23.6 μg/m3) and PM2.5 concentrations during the first and third trimester showed greater mean number of helper T type 1 (Th1) cells (P < 0.05). Decreased number of regulatory T (Treg) cells was associated with greater short-term NO2 (IRR, 0.90; 95% CI, 0.80, 1.01) and PM10 (IRR, 0.88; 95% CI, 0.77, 0.99) concentrations.
Conclusions
Prenatal exposure to TRAP, particularly in early and late gestation, impairs fetal immune system development through disturbances in cord blood leukocyte and lymphocyte distributions.
... Intrauterine exposure to both particulate matter with an aerodynamic diameter <2.5 mm (PM 2.5 ) and second-hand smoke (SHS) has been associated with increased risk of infantile eczema (Jedrychowski et al., 2011). Epidemiological studies have also shown significant associations between air pollution exposure in utero or during the first year of life and childhood pneumonia, bronchiolitis and ear infections (Soh et al., 2018;Kennedy et al., 2018;Rice et al., 2015), further highlighting potential susceptibility during this period. Exposure to air pollution prompts immediate immune responses (Carlsen et al., 2016;Adetona et al., 2013) and can modulate later immune expression (Yi et al., 2017;Rice et al., 2015). ...
... Epidemiological studies have also shown significant associations between air pollution exposure in utero or during the first year of life and childhood pneumonia, bronchiolitis and ear infections (Soh et al., 2018;Kennedy et al., 2018;Rice et al., 2015), further highlighting potential susceptibility during this period. Exposure to air pollution prompts immediate immune responses (Carlsen et al., 2016;Adetona et al., 2013) and can modulate later immune expression (Yi et al., 2017;Rice et al., 2015). It is therefore plausible that short-term exposure to air pollution in the critical first 1000 days of life, from conception to age 2 years, could affect later immunological function (Wopereis et al., 2014). ...
... For example, a Polish study suggested a dose-response relationship between in utero PM 2.5 exposure levels and the incidence of recurrent respiratory infections (!5 episodes of bronchitis and/or pneumonia) from birth to age 7 (OR 2.44; 95%CI, 1.12, 5.36) (Jedrychowski et al., 2013). Another study suggested that intrauterine exposure to traffic-related air pollution, estimated by proximity to a major roadway and traffic density, was associated with increased risk of childhood respiratory infection (Rice et al., 2015). A Chinese study suggested that intrauterine exposure to industrial air pollution was associated with increased risk of otitis media in children aged 3e4 years (Deng et al., 2017). ...
... Intrauterine exposure to both particulate matter with an aerodynamic diameter <2.5 mm (PM 2.5 ) and second-hand smoke (SHS) has been associated with increased risk of infantile eczema (Jedrychowski et al., 2011). Epidemiological studies have also shown significant associations between air pollution exposure in utero or during the first year of life and childhood pneumonia, bronchiolitis and ear infections (Soh et al., 2018;Kennedy et al., 2018;Rice et al., 2015), further highlighting potential susceptibility during this period. Exposure to air pollution prompts immediate immune responses (Carlsen et al., 2016;Adetona et al., 2013) and can modulate later immune expression (Yi et al., 2017;Rice et al., 2015). ...
... Epidemiological studies have also shown significant associations between air pollution exposure in utero or during the first year of life and childhood pneumonia, bronchiolitis and ear infections (Soh et al., 2018;Kennedy et al., 2018;Rice et al., 2015), further highlighting potential susceptibility during this period. Exposure to air pollution prompts immediate immune responses (Carlsen et al., 2016;Adetona et al., 2013) and can modulate later immune expression (Yi et al., 2017;Rice et al., 2015). It is therefore plausible that short-term exposure to air pollution in the critical first 1000 days of life, from conception to age 2 years, could affect later immunological function (Wopereis et al., 2014). ...
... For example, a Polish study suggested a dose-response relationship between in utero PM 2.5 exposure levels and the incidence of recurrent respiratory infections (!5 episodes of bronchitis and/or pneumonia) from birth to age 7 (OR 2.44; 95%CI, 1.12, 5.36) (Jedrychowski et al., 2013). Another study suggested that intrauterine exposure to traffic-related air pollution, estimated by proximity to a major roadway and traffic density, was associated with increased risk of childhood respiratory infection (Rice et al., 2015). A Chinese study suggested that intrauterine exposure to industrial air pollution was associated with increased risk of otitis media in children aged 3e4 years (Deng et al., 2017). ...
Background:
Evidence of health effects following early life exposure to short-to-medium duration of high pollution levels is extremely limited.
Objectives:
We aimed to evaluate the associations between: 1. intrauterine exposure to fine particulate matter (PM2.5) from coal mine fire emissions and the frequencies of general practitioner attendances and dispensations of prescribed asthma inhalers, steroid skin creams, and antibiotics during the first year of life; 2. infant exposure and those outcomes during the year following the fire.
Methods:
All participants were recruited from the Latrobe Valley of Victoria, Australia. Participants' 24-h average and hourly peak mine fire-specific PM2.5 exposures from 09/02/2014 to 31/03/2014 were estimated using chemical transport modelling. Outcome data were obtained from the Australian Medicare Benefits Schedule and Pharmaceutical Benefits Scheme from each child's birth to 31/12/2016. We used negative binomial and logistic regression models to independently assess risks of the outcomes associated with every 10 and 100 μg m-3 increase in average or peak PM2.5 exposure, respectively, while adjusting for potential confounders.
Results:
We included 286 of 311 children whose parents consented to be linked, comprising 77 with no exposure, 88 with intrauterine exposure and 121 with exposure in infancy. 10- and 100- μg m-3 increases in average and peak PM2.5 exposure during infancy were associated with greater incidence of antibiotics being dispensed during the year following the fire: the adjusted incidence rate ratios were 1.24 (95% CI 1.02, 1.50, p = 0.036) and 1.14 (1.00, 1.31, p = 0.048) respectively. No other significant associations were observed.
Conclusion:
Exposure to coal mine fire emissions during infancy was associated with increased dispensing of antibiotics. This could reflect increased childhood infections or increased prescriptions of antibiotics in the year following the fire.
... Previous studies have only considered average exposures to air pollution over the entire pregnancy, or at a single prenatal time point, and could, therefore, not provide insights into the critical exposure time windows for increased LRTIs risk. [5][6][7][8] Moreover, very few studies to date have evaluated the effect of air pollution exposure during specific trimesters on childhood LRTIs. [9][10][11] Particulate matter with an aerodynamic diameter of less than 2.5 μm (PM 2.5 ) exposure during second and first trimester increased bronchiolitis and bronchitis by 2 years 9 and current wheeze at 4 years, respectively. ...
... Although several prior studies have investigated the associations between air pollution exposure throughout pregnancy with LRTIs in children, [5][6][7][8] relatively few reports to date have evaluated the association between PM 2.5 exposure during each trimester of pregnancy and LRTIs. 9,10 A previous Singapore cohort study revealed an association between PM 2.5 exposure in the second trimester and bronchiolitis and bronchitis by 2 years of age. ...
Objectives:
To investigate the association between particulate matter with an aerodynamic diameter of less than 2.5 μm (PM2.5 ) exposure during each trimester of pregnancy and development of lower respiratory tract infections (LRTIs) during the first 3 years of life and whether GSTM1 gene polymorphisms modify these effects.
Methods:
This study included 1,180 mother-child pairs from the Cohort for Childhood Origin of Asthma and allergic diseases. The PM2.5 levels during pregnancy were estimated by residential address using land-use regression models based on a national monitoring system. A diagnosis of LRTIs was based on a parental report of a physician's diagnosis. Real-time polymerase chain reaction was used for GSTM1 genotyping.
Results:
Higher PM2.5 exposure during the third trimester was associated with LRTIs at 1 year of age (aRR, 1.06; 95% CI, 1.00-1.13). This result did not change after adjusting for PM2.5 exposures during the first and second trimesters (aRR, 1.06; 95% CI, 0.99-1.13). This association was significant after adjusting for PM2.5 exposures during first year of age (aRR, 1.08; 95% CI, 1.02-1.15) and exposures to NO2 and ozone at the third trimester (aRR, 1.07; 95% CI, 1.00-1.16). In addition, PM2.5 exposure during the third trimester increased the risk of LRTIs at 1 year of age in cases with the GSTM1 null genotype (aRR, 1.26; 95% CI, 1.01-1.57; P for interaction .20).
Conclusion:
Higher PM2.5 exposure during the third trimester of pregnancy may increase the susceptibility to LRTIs at 1 year of age. This effect is modified by GSTM1 gene polymorphisms.
... 13 The effect of air pollution exposure during pregnancy on respiratory health and allergic responses early in life has been examined by several studies with large heterogeneity. [14][15][16][17][18][19] Some studies report associations of prenatal air pollution exposure with LRTI in early childhood. [14][15][16][17] Other studies have found no support for an association between air pollution exposure and LRTI in early childhood. ...
... [14][15][16][17][18][19] Some studies report associations of prenatal air pollution exposure with LRTI in early childhood. [14][15][16][17] Other studies have found no support for an association between air pollution exposure and LRTI in early childhood. 18 19 In addition, there are animal exposure studies that have identified both anatomic/mechanical and immunological mechanisms by which air pollution exposure may increase susceptibility of the respiratory system to infections. ...
Objectives
It is unclear whether maternal air pollution exposure during pregnancy induces changes in the developing respiratory system of a child and whether it has consequences for respiratory health in early childhood. We investigated associations between exposure to moderate levels of air pollution during pregnancy and early childhood lower respiratory tract infections (LRTI) and wheezing.
Methods
This study used a subgroup of 17 533 participants in the Norwegian Mother and Child Cohort Study. Air pollution levels at residential addresses were estimated using land use regression models, and back-extrapolated to the period of each pregnancy. Information on LRTI and wheezing and lifestyle factors was collected from questionnaires completed by mothers during pregnancy and when the child was 6 and 18 months of age.
Results
Moderate mean levels of NO2 (13.6 µg/m³, range 0.01–60.4) exposure at residential address during pregnancy were not statistically associated with LRTI and wheezing. No association was found per 10 µg/m³ change in NO2 exposure and LRTI before the age of 6 months (adjusted risk ratio (RR) 0.99; 95% CI 0.84 to 1.17), or between 6 and 18 months of age (adjusted RR 1.05; 95% CI 0.94 to 1.16). Similarly, we found no association per 10 µg/m³ change in NO2 exposure and wheezing between 6 and 18 months of age (adjusted RR 1.02; 95% CI 0.97 to 1.07).
Conclusions
There were no statistically significant associations for moderate levels of pregnancy NO2 exposure and respiratory health outcomes during early childhood in overall analyses.
... Our mechanistic findings align with the results of a recent, 10year retrospective cohort study that examined whether proximity to a major roadway and traffic density around the home during pregnancy was associated with risk of early life respiratory infection in a pre-birth cohort in the Boston area (Rice et al., 2015). In that study, addresses for 1263 mother-child pairs were geo-coded subsequent to enrollment during the first trimester of pregnancy in a study known as "Project Viva" that was conducted from 1992 to 2002. ...
... Strikingly, each interquartile range increase in distance to roadway was associated with an 8% (95% CI 0.87, 0.98) lower risk, and each interquartile range increase in traffic density was associated with a 5% (95% CI 0.98, 1.13) higher risk of respiratory infection. These findings are the first to suggest that living close to a major roadway during pregnancy may predispose the developing lung to infection in early life (Rice et al., 2015). ...
... Distance is readily determined using a geographic information system (GIS) if the residential or school address is known. [54][55][56] The advantages of this approach are its low cost, straightforward calculation, and ability to estimate exposures for large numbers of participants at their current address or historically. However, it does not consider traffic composition (i.e., petrol vs. diesel) or volume (i.e., vehicles/day) on roads, both of which can affect exposure to air pollutants. ...
... Traffic density is another proxy for TRAP and is derived by counting the numbers and types of vehicles on roads within a specified distance of an address and the length of those roads. 55 Traffic density can offer an improved ability to capture variability in TRAP compared with distance to road estimates. 57 However, it is dependent on the availability of relevant traffic volume data for all subjects, which is often difficult to acquire across large areas. ...
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.
... The study also found IRR =1. 53 42 Rosa et al also studied prenatal exposure to PAH. The authors reported no association with asthma at 5-6 years of age. ...
... The results suggest that living near a large highway during pregnancy increases the risk of respiratory infections during the first years of life. 53 Among the prospective birth cohorts, a study conducted by Aguilera et al in four regions of Spain described an increased risk of respiratory infections and ear infections following increased NO 2 exposure and, to a lesser extent, following exposure to benzene during the first years of life. An increase in NO 2 exposure of 10 μg/m 3 during pregnancy was associated with an increased risk of lower respiratory tract infection (relative risk [RR] =1.05; 95% CI: 0.98-1.12). ...
Exposure to atmospheric pollutants in both open and closed environments is a major cause of morbidity and mortality that may be both controlled and minimized. Despite growing evidence, several controversies and disagreements exist among the studies that have analyzed the effects of prenatal pollutant exposure. This review article aims to analyze primary scientific evidence of the effects of air pollution during pregnancy and the impact of these effects on the fetus, infant health, and in particular, the respiratory system. We performed a review of articles from the PubMed and Web of Science databases that were published in English within the past 5 years, particularly those related to birth cohorts that began in pregnancy with follow-up until the first years of life. The largest reported effects are associated with prenatal exposure to particulate matter, nitrogen dioxide, and tobacco smoke. The primary effects affect birth weight and other parameters of fetal biometry. There is strong evidence regarding the impact of pollutants on morbidity secondary to respiratory problems. Growing evidence links maternal smoking to childhood asthma and wheezing. The role of passive maternal smoking is less clear. Great heterogeneity exists among studies. There is a need for additional studies on birth cohorts to monitor the relationship between the exposure of pregnant women to pollutants and their children’s progress during the first years of life.
... exposure of macrophages to BaP led to a decrease in the potential for activation of the CD32 receptor (FcγRII) by immunoglobulin G (IgG) by approximately 30% and disrupted macrophage functions such as phagocytosis and the generation of an oxidative burst, thereby increasing the risk of infection [19]. A large-scale ten-year cohort study conducted between 1992 and 2002 involving 1263 pregnant women and their children assessed whether the distance between a pregnant woman's residence and a road with high traffic intensity was related to the risk of respiratory tract infection in newborns [20]. The study showed a relationship between distance from the road and estimated that the average risk of infection decreased by 8% for each additional 100 meters from the street. ...
Background: Benzo(a)pyrenes are organic compounds from the polycyclic aromatic hydrocarbons group known for their carcinogenic properties. Benzo(a)pyrenes form from incomplete combustion of organic matter, such as biomass or fossil fuels. Aim of the study: To investigate whether respiratory diseases and malignant neoplasm-related deaths correlate with air concentrations of benzo(a)pyrene in European countries. Material and methods: Publicly available data regarding benzo(a)pyrene concentration were obtained from the EUROSTAT database and divided by territory based on the nomenclature for territorial units for statistics 2 (NUTS2). Diseases were defined using the International Classification of Diseases 10th revision (ICD-10). Results: There was a positive correlation of medium effect (r = 0.442; p < 0.001) between the annual mean benzo(a)pyrene concentration and deaths due to malignant neoplasms, with the strongest correlation being malignant bladder neoplasms (r = 0.502; p < 0.001). There was also a positive correlation of a moderately weak effect (r = 0.221; p = 0.002) between the annual mean concentration of benzo(a)pyrene and deaths due to respiratory diseases, with the strongest correlation for pneumonia of various etiologies, which had a positive correlation of medium effect (r = 0.496; p < 0.001). Linear regression models showed that reducing the concentration of benzo(a)pyrene by 1 ng/m3 will reduce the frequency of deaths due to malignant laryngeal neoplasms by 0.816 per 1000 residents, malignant bladder neoplasms by 1.41 per 1000 residents, and deaths due to pneumonia by 11.26 per 1000 residents. Conclusions: We found that benzo(a)pyrene concentration had a moderate correlation with death due to respiratory diseases and malignant neoplasms. More in-depth studies regarding other factors, such as patient age, are needed.
... A study investigating a bushfire in Canada also found that physician visits for acute URTIs and acute bronchitis in children under 10 years old were higher in the month following the fire than before or during, which could indicate delayed health responses (Mahsin et al., 2022). In terms of chronic exposure, a study conducted in a Boston pre-birth cohort of 1263 mother-child pairs found that distance to roadway in the prenatal and postnatal periods was inversely related to doctor-diagnosed respiratory infections, including croup, in the first years of life (Rice et al., 2015). A multicohort European study found inconsistent results, as increases in urban PM exposure were associated with pneumonia cases, but not with otitis media or croup in the first three years of life (MacIntyre et al., 2014). ...
Background:
Due to climate change, landscape fires account for an increasing proportion of air pollution emissions, and their impacts on primary and pharmaceutical care are little understood.
Objectives:
To evaluate associations between exposure in two early life periods to severe levels of PM2.5 from a mine fire, background PM2.5, and primary and pharmaceutical care.
Methods:
We linked records of births, general practitioner (GP) presentations and prescription dispensing for children born in the Latrobe Valley, Australia, 2012-2014, where a severe mine fire occurred in February-March 2014 in an area with otherwise low levels of ambient PM2.5. We assigned modelled exposure estimates for fire-related (cumulative over the fire and peak 24-hour average) and annual ambient PM2.5 to residential address. Associations with GP presentations and dispensing of prescribed medications in the first two years of life (exposure in utero) and in the two years post-fire (exposure in infancy) were estimated using two-pollutant quasi-Poisson regression models.
Results:
Exposure in utero to fire-related PM2.5 was associated with an increase in systemic steroid dispensing (Cumulative: IRR = 1.11, 95%CI = 1.00-1.24 per 240 μg/m3; Peak: IRR = 1.15, 95%CI = 1.00-1.32 per 45 μg/m3), while exposure in infancy was associated with antibiotic dispensing (Cumulative: IRR = 1.05, 95%CI = 1.00-1.09; Peak: IRR = 1.06, 95%CI = 1.00-1.12). Exposure in infancy to ambient PM2.5, despite relatively low levels from a global perspective (Median = 6.1 μg/m3), was associated with an increase in antibiotics (IRR = 1.10, 95%CI = 1.01-1.19 per 1.4 μg/m3) and in GP presentations (IRR = 1.05, 95%CI = 1.00-1.11), independently from exposure to the fire. We also observed differences in associations between sexes with GP presentations (stronger in girls) and steroid skin cream dispensing (stronger in boys).
Discussion:
Severe medium-term concentrations of PM2.5 were linked with increased pharmaceutical treatment for infections, while chronic low levels were associated with increased prescriptions dispensed for infections and primary care usage. Our findings also indicated differences between sexes.
... Several studies link acute exposure to PM air pollution with premature mortality and morbidity, but questions remain about which species and sources in the vast PM mix are responsible for the health effects observed. Although a few studies exist on the effects of species and sources in U.S. cities [65], European cities-with a higher proportion of diesel engines and denser urban populations-have not been well characterized, with only a few examples available for short-term studies including sources or PM chemical components [45,66,67]. Similarly, the risks of long-term exposures are often based on ambient air pollution levels and on results from cohort studies, not including information on specific sources or chemical components [68]. ...
Vehicular traffic is one of the major sources of air pollution in European cities. This work aims to understand which characteristics of the urban environment could influence mobility-related air pollution, quantify the health impacts of exposure to traffic-derived PM2.5 and NO2 concentrations, and assess the potential health benefits expected from traffic interventions. The health benefits modeled are intended to provide a set of comparable data to support decision-makers and encourage informed decision-making to design healthier cities. Targeting a large geographical coverage, 12 European cities from 9 countries were comparatively assessed in terms of mean daily traffic volume/area, the number of public transport stops/area, and the percentage of green and outdoor leisure areas, among other urban indicators. This was implemented using an open-source data mining tool, which was seen as a useful engine to identify potential strategies to improve air quality. The comparison of urban indicators in the selected cities evidenced two trends: (a) cities with the most heterogeneous distribution of public transport stops, as an indicator of poor accessibility, are also those with the lowest proportion of km dedicated to cycleways and footways, highlighting the need in these cities for more sustainable mobility management; and (b) the percentage of green and outdoor leisure areas may influence the share of journeys by bicycle, pointing out that promoting the perception of green routes is relevant to enhance the potential of active transport modes. Socioeconomic factors can be key determinants of the urban indicators and would need further consideration. For the health impact assessment (HIA), two baseline scenarios were evaluated and compared. One is based on mean annual traffic contributions to PM2.5 concentrations in each target city (ranging between 1.9 and 13 µg/m3), obtained from the literature, and the second is grounded on mean annual NO2 concentrations at all available traffic and urban background stations within each city (17.2–83.5 µg/m3), obtained from the European Environment Agency database. The intervention scenarios modeled were designed based on traffic mitigation strategies in the literature, and set to ranges of 6–50% in traffic-derived PM2.5 concentrations and of 4–12.5% in NO2 concentrations. These scenarios could result in only a 1.7% (0.6–4%) reduction in premature mortality due to exposure to traffic-derived PM2.5, and 1.0% (0.4–2%) due to exposure to NO2, as the mean for all the cities. This suggests that more ambitious pollution abatement strategies should be targeted.
... Epidemiological studies link in utero exposure to traffic-related air pollutants (TRAP) with increased risk of lower respiratory infections, impaired lung function, and asthma in childhood. [1][2][3] Although the mechanisms of these long-lasting effects are not fully understood, it is likely that a reshaped development of the immune system response may play a key role. 4 Asthma and allergies are characterized by diverse clinical phenotypes that result from an exacerbated immune response to diverse stimuli in susceptible individuals. ...
Background
Outdoor air pollution may disturb immune system development. We investigated whether gestational exposure to traffic‐related air pollutants (TRAP) is associated with unstimulated cytokine profiles in newborns.
Methods
Data come from 235 newborns of the NELA cohort. Innate response–related cytokines (IL‐6, IFN‐α, IL1‐β, and TNF‐α), Th1‐related (IFN‐γ and IL‐2), Th2‐related (IL‐4, IL‐5, and IL‐13), Th17‐related (IL‐17 and IL‐23), and immunomodulatory cytokine IL‐10 were quantified in the supernatant of unstimulated whole umbilical cord blood cells after 7 days of culture using the Luminex technology. Dispersion/chemical transport modeling was used to estimate long‐term (whole pregnancy and trimesters) and short‐term (15 days before delivery) residential exposures to traffic‐related nitrogen dioxide (NO2), particulate matter (PM2.5 and PM10), and ozone (O3). We fitted multivariable logistic regression, Bayesian kernel machine regression (BKMR), and weighted quantile sum (WQS) regression models.
Results
NO2 during the whole pregnancy increased the odds of detection of IL‐1β (OR per 10 µg/m³ increase = 1.37; 95% CI, 1.02, 1.85) and IL‐6 (OR per 10 µg/m³ increase = 1.32; 95% CI 1.00, 1.75). Increased odds of detected concentrations of IL‐10 was found in newborns exposed during whole pregnancy to higher levels of NO2 (OR per 10 µg/m³ increase = 1.30; 95% CI 0.99, 1.69), PM10 (OR per 10 µg/m³ increase = 1.49; 95% CI 0.95, 2.33), and PM2.5 (OR per 5 µg/m³ increase = 1.56; 95% CI 0.97, 2.51). Exposure to O3 during the whole pregnancy increased the odds of detected IL‐13 (OR per 10 µg/m³ increase = 1.22; 95% CI 1.01, 1.49). WQS model revealed first and third trimesters of gestation as windows of higher susceptibility.
Conclusions
Gestational exposure to TRAP may increase detection of pro‐inflammatory, Th2‐related, and T regulatory cytokines in newborns. These changes might influence immune system responses later in life.
... For non-BPD cohorts, exposure to ambient air pollutants has been associated with asthma development, asthma symptoms and asthma exacerbations. [24][25][26][27][28][29][30][31] Moreover, home-based measurements of nitrogen dioxide (NO 2 ) and other pollutants with indoor sources have been associated with asthma symptom severity 25 32-34 in children, even at modest levels of exposure. 33 Across many locations, indoor exposure to environmental pollutants has been associated with increased incident asthma diagnosis, 35 asthma symptoms 33 36 and asthma severity 32 in children. ...
Introduction
Almost half of all school-age children with bronchopulmonary dysplasia (BPD) have asthma-like symptoms and more suffer from lung function deficits. While air pollution and indoor respiratory irritants are known to affect high-risk populations of children, few studies have objectively evaluated environmental contributions to long-term respiratory morbidity in this population. This study aimed to examine the role of indoor environmental exposures on respiratory morbidity in children with BPD.
Methods and analysis
The Air quality, Environment and Respiratory Ouctomes in BPD (AERO-BPD) study is a prospective, single-centre observational study that will enrol a unique cohort of 240 children with BPD and carefully characterise participants and their indoor home environmental exposures. Measures of indoor air quality constituents will assess the relationship of nitrogen dioxide (NO 2 ), particulate matter (PM 2.5 ), nitric oxide (NO), temperature and humidity, as well as dust concentrations of allergens, with concurrently measured respiratory symptoms and lung function.
Adaptations to the research protocol due to the SARS-CoV-2 pandemic included remote home environment and participant assessments.
Ethics and dissemination
Study protocol was approved by the Boston Children’s Hospital Committee on Clinical Investigation. Dissemination will be in the form of peer-reviewed publications and participant information products.
Trial registration number
NCT04107701 .
... Epidemiological studies show significant associations between exposure to air pollutants (e.g. PM, polycyclic aromatic hydrocarbons -PAHs) in utero or during the first year of life and childhood LRIs (Jedrychowski et al. 2005(Jedrychowski et al. , 2013Rice et al. 2015;Kennedy et al. 2018;Soh et al. 2018). Nevertheless, there are no published studies on the effects of prenatal exposure to ambient pollutants to bacterial infections of airways, although indirect evidence can be obtained from recent studies (Claude et al. 2012;Shao et al. 2020). ...
The World Health Organization attributed more than four million premature deaths to ambient air pollution in 2016. Numerous epidemiologic studies demonstrate that acute respiratory tract infections and exacerbations of pre-existing chronic airway diseases can result from exposure to ambient (outdoor) air pollution. In this context, the atmosphere contains both chemical and microbial pollutants (bioaerosols), whose impact on human health remains unclear. Therefore, this review: summarises the findings from recent studies on the association between exposure to air pollutants—especially particulate matter and ozone—and onset or exacerbation of respiratory infections (e.g. pneumonia, cystic fibrosis lung infection, and tuberculosis); discusses the mechanisms underlying the relationship between air pollution and respiratory bacterial infections, which is necessary to define prevention and treatment strategies; demonstrates the relevance of air pollution modelling in investigating and preventing the impact of exposure to air pollutants on human health; and outlines future actions required to improve air quality and reduce morbidity and mortality related to air pollution.
... Nevertheless, relatively few studies examined the effect of intrauterine exposure to pollution and early life respiratory infections [1,20]. Some have found an association between prenatal exposure to PM and respiratory infections in children [1,21,22] while others did not find any association between the two, specifically for exposure to nitrogen dioxide (NO 2 ) during pregnancy [23]. ...
Background:
Lower respiratory tract infections (LRTI) in early life, including pneumonia, bronchitis and bronchiolitis, can lead to decreased lung function, persistent lung damage and increased susceptibility to various respiratory diseases such as asthma. In-utero exposure to particulate matter (PM) during pregnancy may disrupt biological mechanisms that regulate fetal growth, maturation and development. We aimed to estimate the association between intrauterine exposure to PM of size < 2.5 μm in diameter (PM2.5) and incidence of LRTIs during the first year of life.
Methods:
A retrospective population-based cohort study in a population of mothers and infants born in Soroka University Medical Center (SUMC) in the years 2004-2012. All infants < 1 year old that were hospitalized due to LRTIs were included. The main exposure assessment was based on a hybrid model incorporating daily satellite-based predictions at 1 km2 spatial resolution. Data from monitoring stations was used for imputation of main exposure and other pollutants. Levels of environmental exposures were assigned to subjects based on their residential addresses and averaged for each trimester. Analysis was conducted by a multivariable generalized estimating equation (GEE) Poisson regression. Data was analyzed separately for the two main ethnic groups in the region, Jewish and Arab-Bedouin.
Results:
The study cohort included 57,331 deliveries that met the inclusion criteria. Overall, 1871 hospitalizations of infants < 1 year old due to pneumonia or bronchiolitis were documented. In a multivariable analysis, intrauterine exposure to high levels of PM2.5 (> 24 μg/m3) in the first and second trimesters was found to be adversely associated with LRTIs in the Arab-Bedouin population (1st trimester, RR = 1.31, CI 95% 1.08-1.60; 2nd trimester: RR = 1.34, CI 95% 1.09-1.66).
Conclusion:
Intrauterine exposure to high levels of PM2.5 is associated with a higher risk of hospitalizations due to lower respiratory tract infections in Arab-Bedouin infants.
... Rice e cols. 32 examinaram a associação entre a exposição pré-natal à poluição do ar relacionada ao tráfego e o risco de infecção respiratória (incluindo pneumonia, bronquiolite e crupe) no início da vida, e verificaram que morar próximo a uma estrada principal durante a gravidez aumentava o risco de infecções respiratórias no início da vida. ...
... Rice e cols. 32 examinaram a associação entre a exposição pré-natal à poluição do ar relacionada ao tráfego e o risco de infecção respiratória (incluindo pneumonia, bronquiolite e crupe) no início da vida, e verificaram que morar próximo a uma estrada principal durante a gravidez aumentava o risco de infecções respiratórias no início da vida. ...
... The strongest associations have been with postneonatal respiratory mortality, [32][33][34] which in part may be related to respiratory infections that have links to pollution. 35 Air pollution may be a "second hit" in newborns who are susceptible to infection because of their immature immune systems. Postnatal diesel pollution exposure also has been found to attenuate the lung's immune response to respiratory infection and to augment the inflammatory response, which likely results in a worse course of illness. ...
Air pollution poses a great environmental risk to health. Outdoor fine particulate matter (PM2.5) exposure is the fifth leading risk factor for death in the world, accounting for 4.2 million deaths and more than a hundred million disability-adjusted-life-years lost according to the Global Burden of Disease Report. The World Health Organization attributes 3.8 million additional deaths to Indoor air pollution. Air pollution can harm acutely, usually manifested by respiratory or cardiac symptoms, as well as chronically, potentially affecting every organ in the body. It can cause, complicate, or exacerbate many adverse health conditions. Tissue damage may result directly from pollutant toxicity, because fine and ultrafine particles can gain access to organs, or indirectly through systemic inflammatory processes. Susceptibility is partly under genetic and epigenetic regulation. Although air pollution affects people of all regions, ages, and social groups, it is likely to cause greater illness in those with heavy exposure and greater susceptibility. Persons are more vulnerable to air pollution if they have other illnesses or less social support. Harmful effects occur on a continuum of dosage and even at levels below air quality standards previously considered to be safe.
... There is a growing public health concern that residential proximity to roadways during pregnancy may adversely affect offspring health. Although evidence remains mixed, several recent epidemiological studies have linked prenatal residential proximity to major roadways with a wide range of health problems, including reduced fetal growth (Fleisch et al. 2015), higher systolic blood pressure in newborns (van Rossem et al. 2015), as well as adverse respiratory health (Rice et al. 2014) and cognitive impairment during early and midchildhood (Harris et al. 2015;Yorifuji et al. 2016). However, the identification of intermediate biomarkers linking roadway proximity to health outcomes has been impeded due to their inability to capture and reflect fetal responses to environmental stressors at critical prenatal exposure windows. ...
Background:
Epigenetic variability is hypothesized as a regulatory pathway through which prenatal exposures may influence child development and health.
Objective:
We sought to examine the associations of residential proximity to roadways at birth and epigenome-wide DNA methylation. We also assessed associations of differential methylation with child cognitive outcomes.
Methods:
We estimated residential proximity to roadways at birth using a geographic information system (GIS) and cord blood methylation using Illumina's HumanMethylation450-array in 482 mother-child pairs in Project Viva. We identified individual CpGs associated with residential-proximity-to-roadways at birth using robust linear regression [[Formula: see text]]. We also estimated association between proximity-to-roadways at birth and methylation of the same sites in blood samples collected at age 7-11 y ([Formula: see text]). We ran the same analyses in the Generation R Study for replication ([Formula: see text]). In Project Viva, we investigated associations of differential methylation at birth with midchildhood cognition using linear regression.
Results:
Living closer to major roadways at birth was associated with higher cord blood (and-more weakly-midchildhood blood) methylation of four sites in LAMB2. For each halving of residential-proximity-to-major-roadways, we observed a 0.82% increase in DNA methylation at cg05654765 [95% confidence interval (CI): (0.54%, 1.10%)], 0.88% at cg14099457 [95% CI: (0.56%, 1.19%)], 0.19% at cg03732535 [95% CI: (0.11%, 0.28)], and 1.08% at cg02954987 [95% CI: (0.65%, 1.51%)]. Higher cord blood methylation of these sites was associated with lower midchildhood nonverbal cognitive scores. Our results did not replicate in the Generation R Study.
Conclusions:
Our discovery results must be interpreted with caution, given that they were not replicated in a separate cohort. However, living close to major roadways at birth was associated with cord blood methylation of sites in LAMB2-a gene known to be linked to axonal development-in our U.S. cohort. Higher methylation of these sites associated with lower nonverbal cognitive scores at age 7-11 y in the same children. https://doi.org/10.1289/EHP2034.
... Due to their size, inhalation rates, incomplete development of the respiratory and immune systems, and time spent outdoors, children are more vulnerable to urban air pollutants than adults 5 . Recent epidemiologic evidence suggests traffic-related air pollution may be a risk factor for respiratory infections and related comorbidities in infants and children [6][7][8][9][10][11][12] . Secondary pollutants including ozone and particulate matter were found to be significantly associated with increased risk for bronchitis, pneumonia, and otitis media in a case crossover study of Georgia pediatric emergency department visits during 2002-2008 13 . ...
Background:
Exposure to pollution from motor vehicles in early life may increase susceptibility to common pediatric infections.
Methods:
We estimated associations between residential exposure to primary fine particulate matter (PM2.5), nitrogen oxides (NOx), and carbon monoxide (CO) from traffic during the first year of life and incident pneumonia, bronchiolitis, and otitis media events by age two years in 22,441 children from the Kaiser Air Pollution and Pediatric Asthma Study, a retrospective birth cohort of children born during 2000-2010 and insured by Kaiser Permanente Georgia. Time to first clinical diagnosis of each outcome was defined using medical records. Exposure to traffic pollutants was based on observation-calibrated estimates from A Research LINE-source dispersion model for near surface releases (RLINE) and child residential histories. Associations were modeled using Cox proportional hazards models, with exposure as a continuous linear variable, a natural-log transformed continuous variable, and categorized by quintiles.
Results:
During follow-up 2,181 children were diagnosed with pneumonia, 5,533 with bronchiolitis, and 14,373 with otitis media. We observed positive associations between early-life traffic exposures and all three outcomes; confidence intervals were widest for pneumonia as it was the least common outcome. For example, adjusted hazard ratios for a 1-unit increase in NOx on the natural log scale (a 2.7-fold increase) were 1.19 (95% CI 1.12, 1.27) for bronchiolitis, 1.17 (1.12, 1.22) for otitis media, and 1.08 (0.97, 1.20) for pneumonia.
Conclusions:
Our results provide evidence for modest, positive associations between exposure to traffic emissions and common pediatric infections during early childhood.
... Epidemiological studies have demonstrated associations of TRAP with exacerbations of respiratory symptoms, decreased lung function, and the development of asthma [12][13][14][15][16]. Infantile bronchiolitis and wheezing can lead to the subsequent development of childhood asthma [17,18], and they have also been associated with air pollution [19][20][21][22]. There is evidence that early-life exposure to TRAP may increase the risk of respiratory infection in infants [23]. ...
Objective:
This study examined the role of exposure to traffic-related air pollution (TRAP) on susceptibility to asthma in children with past episodes of bronchiolitis.
Methods:
The baseline data included 2,627 school children aged 6-14 years who had participated in the longitudinal follow-up survey of the Children's Health and Environmental Research of Korea. Lifetime wheezing, past episodes of bronchiolitis, and doctor-diagnosed asthma were evaluated using an International Study of Asthma and Allergies in Childhood questionnaire. We used generalized linear regression with binomial distribution to calculate the relative risk (RR) between TRAP, assessed by proximity to a main road and the total length of roads, and asthma.
Results:
Compared with the subjects who had less than 100 m of road length within 200-m radius from their home, those with more than 500 m of road length had significantly increased odds for infantile bronchiolitis (adjusted OR [aOR]: 1.57, 95% confidence interval [CI]: 1.01-2.42). Positive exposure-response relationships were found between residential proximity to the main road and asthma (aOR: 1.79, 95% CI: 1.05-3.06; <75 m vs. >700 m from a main road, P for the trend = 0.02). Closer residential proximity to the main road (<75 m) and bronchiolitis combined increased the risks of newly diagnosed asthma (adjusted RR: 3.62, 95% CI: 1.07-12.26) compared with those without bronchiolitis and living ≥ 75 m away from the main road.
Conclusions:
TRAP appeared to be associated with an increased asthma among children with bronchiolitis, indicating the importance of modifying effects of bronchiolitis in asthma pathogenesis.
The association of air pollution and greenspace with respiratory pathogen acquisition and respiratory health was investigated in a community-based birth-cohort of 158 Australian children. Weekly nasal swabs and daily symptom-diaries were collected for 2-years, with annual reviews from ages 3-7-years. Annual exposure to fine-particulate-matter (PM2.5), nitrogen-dioxide (NO2), and normalised-difference-vegetation-index (NDVI) was estimated for pregnancy and the first 2-years-of-life. We examined rhinovirus, any respiratory virus, Streptococcus pneumoniae, Moraxella catarrhalis, and Haemophilus influenzae detections in the first 3-months-of-life, age at initial pathogen detection, wheezing in the first 2-years, and asthma at ages 5-7-years. Our findings suggest that higher NDVI was associated with fewer viral and M. catarrhalis detections in the first 3-months, while increased PM2.5 and NO2 were linked to earlier symptomatic rhinovirus and H. influenzae detections, respectively. However, no associations were observed with wheezing or asthma. Early-life exposure to air pollution and greenspace may influence early-life respiratory pathogen acquisition and illness. .
Lifelong respiratory health is rooted in the structural and functional development of the respiratory system in early life. Exposures and interventions antenatally through childhood can influence lung development into young adulthood, the life stage with the highest achievable lung function. Because early respiratory health sets the stage for adult lung function trajectories and risk of developing chronic obstructive pulmonary disease, understanding how to promote lung health in children will have far reaching personal and population benefits. To achieve this, it is critical to have accurate and precise measures of structural and functional lung development that track throughout life stages. From this foundation, evaluation of environmental, genetic, metabolic, and immune mechanisms involved in healthy lung development can be investigated. These goals require the involvement of general pediatricians, pediatric subspecialists, patients, and researchers to design and implement studies that are broadly generalizable and applicable to otherwise healthy and chronic disease populations. This National Institutes of Health workshop report details the key gaps and opportunities regarding lung function and structure.
Background:
Childhood wheezing is a highly heterogeneous condition with incomplete understanding of the characteristics of wheeze trajectories, particularly for persistent wheeze.
Objective:
To characterise predictors and allergic comorbidities of distinct wheeze trajectories in a multi-ethnic Asian cohort.
Methods:
A total of 974 mother-child pairs from the prospective XXX cohort were included in this study. Wheeze and allergic comorbidities in the first eight years of life were assessed using the modified ISAAC questionnaires and skin prick tests. Group-based trajectory modelling was used to derive wheeze trajectories and regression was used to assess associations with predictive risk factors and allergic comorbidities.
Results:
Four wheeze trajectories were derived: early onset with rapid remission from age 3 years (4.5%), late onset peaking at age 3 years and rapidly remitting from 4 years (8.1%), persistent with steady increase to age 5 years and high wheeze occurrence until 8 years (4.0%) and no/low wheeze (83.4%). Early onset wheezing was associated with respiratory infections during infancy and linked to subsequent non-allergic rhinitis throughout childhood. Late onset and persistent wheeze shared similar origins characterized by parent-reported viral infections in later childhood. However, persistent wheeze was generally more strongly associated with a family history of allergy, parent-reported viral infections in later childhood and allergic comorbidities as compared to late onset wheeze.
Conclusion:
The timing of viral infection occurrence may determine the type of wheeze trajectory development in children. Children with family history of allergy and viral infections in early life may be predisposed to persistent wheeze development and the associated comorbidities early allergic sensitization and eczema.
Background
Nearly 40% of the world’s population is exposed daily to household air pollution. The relative impact of prenatal and postnatal household air pollution exposure on early childhood pneumonia, a leading cause of mortality, is unknown.
Research Question
Are prenatal and/or postnatal household air pollution associated with pneumonia risk in the first year of life?
Study Design and Methods
The Ghana Randomized Air Pollution and Health Study (GRAPHS) enrolled 1,414 non-smoking, pregnant women prior to 24 weeks gestation with prospective follow-up to child age one. We measured 72-hour personal household air pollution exposures, indexed by carbon monoxide (CO), four times prenatally and three times postnatally. Weekly fieldworker surveillance identified ill-appearing children for physician pneumonia assessment. We employed quasi-Poisson models to examine associations between prenatal and postnatal CO and physician-diagnosed pneumonia and severe pneumonia. Sex-specific effects were examined.
Results
Of the 1,306 live births, 1,141 infants were followed with 55,605 child-weeks of fieldworker surveillance. The estimated risk for pneumonia and severe pneumonia in the first year of life increased by 10% (RR 1.10, 95% CI 1.04-1.16) and 15% (RR 1.15, 95% CI 1.03-1.28), respectively, per 1ppm increase in average prenatal CO exposure and by 6% (RR 1.06, 95% CI 0.99, 1.13) per 1ppm increase in average postnatal CO exposure. Females appeared more vulnerable.
Interpretation
Prenatal household air pollution exposure increased risk for pneumonia and severe pneumonia in the first year of life. Clean burning interventions may be most effective when begun prenatally.
Objectives
To examine the association among acute bronchiolitis-related hospitalisation in children, meteorological variation and outdoor air pollution.
Methods
We obtained the daily counts of acute bronchiolitis-related admission of children≤2 years old from all public hospitals, meteorological data and outdoor air pollutants’ concentrations between 1 January 2008 and 31 December 2017 in Hong Kong. We used quasi-Poisson generalised additive models together with distributed lag non-linear models to estimate the associations of interest adjusted for confounders.
Results
A total of 29 688 admissions were included in the analysis. Increased adjusted relative risk (ARR) of acute bronchiolitis-related hospitalisation was associated with high temperature (ambient temperature and apparent temperature) and was marginally associated with high vapour pressure, a proxy for absolute humidity. High concentration of NO 2 was associated with elevated risk of acute bronchiolitis admission; the risk of bronchiolitis hospitalisation increased statistically significantly with cumulative NO 2 exposure over the range 66.2–119.6 µg/m ³ . For PM 10 , the significant effect observed at high concentrations appears to be immediate but not long lasting. For SO 2 , ARR increased as the concentration approached the 75th percentile and then decreased though the association was insignificant.
Conclusions
Acute bronchiolitis-related hospitalisation among children was associated with temperature and exposure to NO 2 and PM 10 at different lag times, suggesting a need to adopt sustainable clean air policies, especially to target pollutants produced by motor vehicles, to protect young children’s health.
Increased global industrialisation has increased air pollution resulting in 3 million annual deaths globally. Air pollutants could have different health effects, so specific models to identify the different immune effects are needed. The aim of this study was to determine the immune effects and lung function of acute exposure to two different pollution sources using a mouse model. Three intranasal challenges with either urban dust or diesel particulate matter resulted in significant (P < 0.001) immune cell infiltration into the lung, which was mostly because of an increased (P < 0.001) percentage of neutrophils. We found that exposure to either urban dust or diesel particulate matter significantly increased the lung tissue concentration of the neutrophil chemoattractant cytokine CXCL5 when compared with naïve controls. Urban dust challenge also significantly increased the concentration of the proinflammatory cytokine CCL20, but diesel particulate matter did not. Urban dust challenge significantly (P < 0.001) decreased tissue compliance and ability to stretch, and increased total airways constriction) and lung tissue stiffness. In comparison, diesel particulate matter exposure slightly, but significantly (P = 0.022) increased tissue compliance and did not affect other lung function parameters. Although both urban dust and diesel particulate matter induced immune cell infiltration into the lung resulting in lung inflammation, their detrimental effects on cytokine production and lung function were quite different. This may be attributed to the variation in particulates that comprise these pollutants that directly interact with the lung tissue and consequently elicit a different functional response.
Objective:
To use spatial analysis methodology to analyze residential and school proximity to major roadways and pediatric asthma morbidity.
Methods:
The School Inner-City Asthma Study (n=350) recruited school-aged children with asthma. Each participant's school and home addresses were geocoded and distances from major roadways were measured to calculate a composite measurement accounting for both home and school traffic exposure. Generalized estimated equation models were clustered by subject and adjusted for age, race/ethnicity, gender, income, environmental tobacco smoke, controller medication, upper respiratory tract infections and seasonality.
Results:
The majority of participants (62%) attended schools within 100 meters from major roadways and 40% also resided within 100 meters of major roadways. In multivariate analyses, major roadway proximity was independently associated with increased asthma symptom days. Above a threshold of 100 meters, children had 29% less odds of a symptom day over the past 2 weeks for each 100 meter increase in distance from major roadway (OR 0.71; 95% CI:0.58-0.87; p <0.01). Children farther from a major roadway also had significantly less reported health care utilization (OR 0.63; 95% CI: 0.47-0.85; p<0.01); and significantly less likely to have poor asthma control (OR 0.80; 95% CI: 0.69-0.94; p< 0.01). There was not a meaningful association between distance to major roadway and lung function outcomes.
Conclusions:
Proximity to major roadway, a composite measurement of home and school exposure, primarily driven by home exposure, was associated with greater asthma morbidity. More studies are needed to evaluate the independent effect of school distance to roadway on asthma morbidity.
We studied whether ambient air pollution is associated with interstitial lung abnormalities (ILAs) and high attenuation areas (HAAs), which are qualitative and quantitative measurements of subclinical interstitial lung disease (ILD) on computed tomography (CT).
We performed analyses of community-based dwellers enrolled in the Multi-Ethnic Study of Atherosclerosis (MESA) study. We used cohort-specific spatio-temporal models to estimate ambient pollution (fine particulate matter (PM 2.5 ), nitrogen oxides (NO x ), nitrogen dioxide (NO 2 ) and ozone (O 3 )) at each home. A total of 5495 participants underwent serial assessment of HAAs by cardiac CT; 2671 participants were assessed for ILAs using full lung CT at the 10-year follow-up. We used multivariable logistic regression and linear mixed models adjusted for age, sex, ethnicity, education, tobacco use, scanner technology and study site.
The odds of ILAs increased 1.77-fold per 40 ppb increment in NO x (95% CI 1.06 to 2.95, p = 0.03). There was an overall trend towards an association between higher exposure to NO x and greater progression of HAAs (0.45% annual increase in HAAs per 40 ppb increment in NO x ; 95% CI −0.02 to 0.92, p = 0.06). Associations of ambient fine particulate matter (PM 2.5 ), NO x and NO 2 concentrations with progression of HAAs varied by race/ethnicity (p = 0.002, 0.007, 0.04, respectively, for interaction) and were strongest among non-Hispanic white people.
We conclude that ambient air pollution exposures were associated with subclinical ILD.
Background:
Ambient and home exposure to nitrogen dioxide (NO2) causes asthma symptoms and decreased lung function in children with asthma. Little is known about the health effects of school classroom pollution exposure.
Objective:
We aimed to determine the effect of indoor classroom NO2 on lung function and symptoms of inner-city schoolchildren with asthma.
Methods:
Children enrolled in the School Inner City Asthma Study were followed for one academic year. Subjects performed spirometry and fractional exhaled nitric oxide (FeNO) twice during the school year, at school. Classroom NO2 was collected by passive sampling for 1 week periods, twice per year coinciding with lung function testing. Generalized estimating equation models assessed lung function and symptom relationships with the temporally nearest classroom NO2 level.
Results:
NO2 mean values were 11.1ppb (range 4.3 - 29.7ppb). In total, exposure data was available for 296 subjects; 188 with complete spirometry data. Above a threshold of 8ppb NO2, and after adjusting for race and season (spirometry standardized by age, height, and gender), NO2 was highly associated with airflow obstruction such that each 10ppb rise in NO2 was associated with a 5% decline in FEV1/FVC (β: -0.05, 95% confidence interval (CI) [-0.08, -0.02], p=0.01). FEF25-75% predicted was also inversely associated with higher NO2 exposure (β: -22.8, 95%CI [-36.0, -9.7], p=0.01). There was no significant association of NO2 with FEV1% predicted, FeNO or asthma symptoms. Additionally, there was no effect modification of atopy on lung function or symptom outcomes.
Conclusion:
In children with asthma, indoor classroom NO2 may be associated with increased airflow obstruction.
Objective:
To study the correlation between the levels of environmental pollutants and the number of paediatric consultations related to respiratory disease in Primary Health Care.
Patients and methods:
An ecological study is performed, in which the dependent variable analysed was the number of paediatric consultations in an urban Primary Health Care centre in Madrid over a 3 year period (2013-2015), and specifically the consultations related to bronchiolitis, recurrent bronchospasm, and upper respiratory diseases. The independent variables analysed were the levels of environmental pollutants. Coefficients of correlation and multiple lineal regressions were calculated. An analysis has been carried out comparing the average of paediatric consultations when the levels of nitrogen dioxide (NO2) were higher and lower than 40μg/m(3.) RESULTS: During the period of the study, there were a total of 52,322 paediatric consultations in the health centre, of which 6,473 (12.37%) were related to respiratory diseases. A positive correlation was found between SO2, CO, NOx and NO2 and benzene levels and paediatric consultations related to respiratory diseases, and a negative correlation with temperature. The number of consultations was significantly higher when NO2 levels exceeded 40μg/m(3). In the multiple lineal regression (P=.0001), the correlation was only positive between consultations and NO2 levels (3.630, 95% CI: 0.691-6.570), and negative with temperature (-5,957, 95% CI: -8.665 to -3.248).
Conclusions:
NO2 environmental pollution is related to an increase in respiratory diseases in children. Paediatricians should contribute to promote an improvement in urban air quality as a significant preventive measure.
Use of wood for residential heating is regaining popularity in developed countries. Currently, over 11 million US homes are heated with a wood stove. Although wood stoves reduce heating costs, wood smoke may adversely impact child health through the emission of gaseous and particulate air pollutants. Our purpose is to raise awareness of this environmental health issue among pediatricians. To summarize the state of the science, we performed a narrative review of articles published in PubMed and Web of Science. We identified 36 studies in developed countries that reported associations of household wood stove use and/or community wood smoke exposure with pediatric health outcomes. Studies primarily investigated respiratory outcomes, with no evaluation of cardiometabolic or neurocognitive health. Studies found community wood smoke exposure to be consistently associated with adverse pediatric respiratory health. Household wood stove use was less consistently associated with respiratory outcomes. However, studies of household wood stoves always relied on participant self-report of wood stove use, while studies of community wood smoke generally assessed air pollution exposure directly and more precisely in larger study populations. In most studies, important potential confounders, such as markers of socioeconomic status, were unaccounted for and may have biased results. We conclude that studies with improved exposure assessment, that measure and account for confounding, and that consider non-respiratory outcomes are needed. While awaiting additional data, pediatricians can refer patients to precautionary measures recommended by the US Environmental Protection Agency (EPA) to mitigate exposure. These include replacing old appliances with EPA-certified stoves, properly maintaining the stove, and using only dry, well-seasoned wood. In addition, several studies have shown mechanical air filters to effectively reduce wood stove pollution exposure in affected homes and communities.
BACKGROUND: The most common cause of hospitalization for children younger than age one is bronchiolitis. Several prenatal and environmental risk factors may affect the incidence of hospitalization for bronchiolitis. The aim of this study was to investigate the relation between exposure to vehicular traffic and the incidence of hospitalization for bronchiolitis in children during their first year of life in Italy. METHODS: A multicenter prospective birth cohort study, where equal numbers of newborns of 33-34, 35-37 and .38 wGA were recruited at birth (1814 children) in 30 Italian neonatology units. Two interviewer-administered questionnaires were used to collect data. The first interview was carried out at the end of the Italian epidemic season. The second interview was carried out when the child was one year old. Data on possible prenatal, perinatal, and postnatal/environmental risk factors and on vehicular traffic density in the zone of residence were collected. On each interview, parents were also asked about any hospitalizations of the child. The outcome measure was the hospitalization for bronchiolitis (International Health Service ICD-9 code 466). RESULTS: Univariate analysis demonstrated that exposure to air pollution due to vehicular traffic, was significantly associated with an increased risk of hospitalization for bronchiolitis. The adjusted risk from logistic regression model confirmed that children exposed to air pollution due to vehicular traffic were at increased risk of hospitalization for bronchiolitis. CONCLUSIONS: Exposure to air pollution due to vehicular traffic may increase the risk of hospitalization for bronchiolitis in the first year of life.
Viral bronchiolitis is a common clinical syndrome affecting infants and young children. Concern about its associated morbidity and cost has led to a large body of research that has been summarised in systematic reviews and integrated into clinical practice guidelines in several countries. The evidence and guideline recommendations consistently support a clinical diagnosis with the limited role for diagnostic testing for children presenting with the typical clinical syndrome of viral upper respiratory infection progressing to the lower respiratory tract. Management is largely supportive, focusing on maintaining oxygenation and hydration of the patient. Evidence suggests no benefit from bronchodilator or corticosteroid use in infants with a first episode of bronchiolitis. Evidence for other treatments such as hypertonic saline is evolving but not clearly defined yet. For infants with severe disease, the insufficient available data suggest a role for high-flow nasal cannula and continuous positive airway pressure use in a monitored setting to prevent respiratory failure.
Background:
The most common cause of hospitalization for children younger than age one is bronchiolitis. Several prenatal and environmental risk factors may affect the incidence of hospitalization for bronchiolitis.
Aim:
To investigate the relation between exposure to vehicular traffic and the incidence of hospitalization for bronchiolitis in children during their first year of life in Italy.
Study design:
Multicenter prospective birth cohort study.
Subjects:
Equal numbers of newborns of 33-34, 35-37 and ≥38 wGA were recruited at birth (1,814 children) in 30 Italian neonatology units. Two interviewer-administered questionnaires were used to collect data. The first interview was carried out at the end of the Italian epidemic season. The second interview was carried out when the child was one year old. Data on possible prenatal, perinatal, and postnatal/environmental risk factors and on vehicular traffic density in the zone of residence were collected. On each interview, parents were also asked about any hospitalizations of the child.
Outcome measures:
Hospitalization for bronchiolitis (International Health Service ICD-9 code 466).
Results:
Univariate analysis demonstrated that exposure to air pollution due to vehicular traffic, was significantly associated with an increased risk of hospitalization for bronchiolitis. The adjusted risk from logistic regression model confirmed that children exposed to air pollution due to vehicular traffic were at increased risk of hospitalization for bronchiolitis.
Conclusions:
Exposure to air pollution due to vehicular traffic may increase the risk of hospitalization for bronchiolitis in the first year of life.
Background: Prenatal and early-life periods may be critical windows for harmful effects of air pollution on infant health.
Objectives: We studied the association of air pollution exposure during pregnancy and the first year of life with respiratory illnesses, ear infections, and eczema during the first 12–18 months of age in a Spanish birth cohort of 2,199 infants.
Methods: We obtained parentally reported information on doctor-diagnosed lower respiratory tract infections (LRTI) and parental reports of wheezing, eczema, and ear infections. We estimated individual exposures to nitrogen dioxide (NO2) and benzene with temporally adjusted land use regression models. We used log-binomial regression models and a combined random-effects meta-analysis to estimate the effects of air pollution exposure on health outcomes across the four study locations.
Results: A 10-µg/m3 increase in average NO2 during pregnancy was associated with LRTI [relative risk (RR) = 1.05; 95% CI: 0.98, 1.12] and ear infections (RR = 1.18; 95% CI: 0.98, 1.41). The RRs for an interquartile range (IQR) increase in NO2 were 1.08 (95% CI: 0.97, 1.21) for LRTI and 1.31 (95% CI: 0.97, 1.76) for ear infections. Compared with NO2, the association for an IQR increase in average benzene exposure was similar for LRTI (RR = 1.06; 95% CI: 0.94, 1.19) and slightly lower for ear infections (RR = 1.17; 95% CI: 0.93, 1.46). Associations were slightly stronger among infants whose mothers spent more time at home during pregnancy. Air pollution exposure during the first year was highly correlated with prenatal exposure, so we were unable to discern the relative importance of each exposure period.
Conclusions: Our findings support the hypothesis that early-life exposure to ambient air pollution may increase the risk of upper and lower respiratory tract infections in infants.
Studies suggest childhood exposure to environmental tobacco smoke (ETS) leads to increased incidence of infections of the lower respiratory tract. The objective of this study was to determine whether perinatal exposure to ETS increases the incidence, morbidity and severity of respiratory influenza infection and whether a secondary bacterial challenge at the peak of a pre-existing viral infection creates an enhanced host-pathogen susceptibility to an opportunistic infection. Timed-pregnant female Balb/c mice were exposed to either ETS for 6 h/day, 7 d/week beginning on gestation day 14 and continuing with the neonates to 6 weeks of age. Control animals were exposed to filtered air (FA). At the end of exposure, mice were intranasally inoculated with a murine-adapted influenza A. One week later, an intranasal inoculation of S. aureus bacteria was administered. The respective treatment groups were: bacteria only, virus only or virus+bacteria for both FA and ETS-exposed animals for a total of six treatment groups. Animal behavior and body weights were documented daily following infection. Mice were necropsied 1-day post-bacterial infection. Bronchoalveolar lavage fluid (BALF) cell analysis demonstrated perinatal exposure to ETS, compared to FA, leads to delayed but enhanced clinical symptoms and enhanced total cell influx into the lungs associated with viral infection followed by bacterial challenge. Viral infection significantly increases the number of neutrophils entering the lungs following bacterial challenge with either FA or ETS exposure, while the influx of lymphocytes and monocytes is significantly enhanced only by perinatal ETS exposure. There is a significant increase in peribronchiolar inflammation following viral infection in pups exposed to ETS compared with pups exposed to FA, but no change is noted in the degree of lung injury between FA and ETS-exposed animals following bacterial challenge. The data suggests perinatal exposure to ETS alters the response of neonates to the timing and severity of infection as well as ETS alters the pattern of inflammation and cellular influx into the lungs due to viral and bacterial infection.
Passive smoke exposure increases the risk of lower respiratory infection (LRI) in infants, but the extensive literature on this association has not been systematically reviewed for nearly ten years. The aim of this paper is to provide an updated systematic review and meta-analysis of studies of the association between passive smoking and LRI, and with diagnostic subcategories including bronchiolitis, in infants aged two years and under.
We searched MEDLINE and EMBASE (to November 2010), reference lists from publications and abstracts from major conference proceedings to identify all relevant publications. Random effect pooled odds ratios (OR) with 95% confidence intervals (CI) were estimated.
We identified 60 studies suitable for inclusion in the meta-analysis. Smoking by either parent or other household members significantly increased the risk of LRI; odds ratios (OR) were 1.22 (95% CI 1.10 to 1.35) for paternal smoking, 1.62 (95% CI 1.38 to 1.89) if both parents smoked, and 1.54 (95% CI 1.40 to 1.69) for any household member smoking. Pre-natal maternal smoking (OR 1.24, 95% CI 1.11 to 1.38) had a weaker effect than post-natal smoking (OR 1.58, 95% CI 1.45 to 1.73). The strongest effect was on bronchiolitis, where the risk of any household smoking was increased by an OR of 2.51 (95% CI 1.96 to 3.21).
Passive smoking in the family home is a major influence on the risk of LRI in infants, and especially on bronchiolitis. Risk is particularly strong in relation to post-natal maternal smoking. Strategies to prevent passive smoke exposure in young children are an urgent public and child health priority.
Murine models demonstrate a synergistic production of reactive oxygen species on coexposure to diesel exhaust particles and endotoxin.
It was hypothesized that coexposure to traffic-related particles and endotoxin would have an additive effect on persistent wheezing during early childhood.
Persistent wheezing at age 36 months was assessed in the Cincinnati Childhood Allergy and Air Pollution Study, a high-risk birth cohort. A time-weighted average exposure to traffic-related particles was determined by applying a land-use regression model to the homes, day cares, and other locations where children spent time from birth through age 36 months. Indoor levels of endotoxin were measured from dust samples collected before age 12 months. The relationship between dichotomized ( or=75th percentile) traffic-related particle and endotoxin exposure and persistent wheezing, controlling for potential covariates, was examined.
Persistent wheezing at age 36 months was significantly associated with exposure to increased levels of traffic-related particles before age 12 months (OR = 1.75; 95% confidence interval, 1.07-2.87). Coexposure to endotoxin had a synergistic effect with traffic exposure on persistent wheeze (OR = 5.85; 95% confidence interval, 1.89-18.13) after adjustment for significant covariates.
The association between traffic-related particle exposure and persistent wheezing at age 36 months is modified by exposure to endotoxin. This finding supports prior toxicological studies demonstrating a synergistic production of reactive oxygen species after coexposure to diesel exhaust particles and endotoxin. The effect of early versus later exposure to traffic-related particles, however, remains to be studied because of the high correlation between exposure throughout the first 3 years of life.
There are at least three mechanisms by which alveolar macrophages play a critical role in protecting the lung from bacterial or viral infections: production of inflammatory cytokines that recruit and activate lung phagocytes, production of antimicrobial reactive oxidant species, and production of interferon (an antiviral agent). In this article we summarize data concerning the effect of exposure to diesel exhaust particles on these alveolar macrophage functions and the role of adsorbed organic chemicals compared to the carbonaceous core in the toxicity of diesel particles. In vitro exposure of rat alveolar macrophages to diesel exhaust particles decreased the ability of lipopolysaccharide (LPS), a bacterial product] to stimulate the production of inflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha). Methanol extract exhibited this potential but methanol-washed diesel particles did not. Exposure of rats to diesel exhaust particles by intratracheal instillation also decreased LPS-induced TNF-alpha and IL-1 production from alveolar macrophages. In contrast, carbon black did not exhibit this inhibitory effect. Exposure of rats to diesel exhaust particles by inhalation decreased the ability of alveolar macrophages to produce antimicrobial reactive oxidant species in response to zymosan (a fungal component). In contrast, exposure to coal dust increased zymosan-stimulated oxidant production. In vivo exposure to diesel exhaust particles but not to carbon black decreased the ability of the lungs to clear bacteria. Inhalation exposure of mice to diesel exhaust particles but not to coal dust depressed the ability of the lung to produce the antiviral agent interferon and increased viral multiplication in the lung. These results support the hypothesis that exposure to diesel exhaust particles increases the susceptibility of the lung to infection by depressing the antimicrobial potential of alveolar macrophages. This inhibitory effect appears to be due to adsorbed organic chemicals rather than the carbonaceous core of the diesel particles.
Motor vehicle emissions usually constitute the most significant source of ultrafine particles (diameter <0.1 microm) in an urban environment, yet little is known about the concentration and size distribution of ultrafine particles in the vicinity of major highways. In the present study, particle number concentration and size distribution in the size range from 6 to 220 nm were measured by a condensation particle counter (CPC) and a scanning mobility particle sizer (SMPS), respectively. Measurements were taken 30, 60, 90, 150, and 300 m downwind, and 300 m upwind, from Interstate 405 at the Los Angeles National Cemetery. At each sampling location, concentrations of CO, black carbon (BC), and particle mass were also measured by a Dasibi CO monitor, an aethalometer, and a DataRam, respectively. The range of average concentration of CO, BC, total particle number, and mass concentration at 30 m was 1.7-2.2 ppm, 3.4-10.0 microg/m3, 1.3-2.0 x 10(5)/cm3, and 30.2-64.6 microg/m3, respectively. For the conditions of these measurements, relative concentrations of CO, BC, and particle number tracked each other well as distance from the freeway increased. Particle number concentration (6-220 nm) decreased exponentially with downwind distance from the freeway. Data showed that both atmospheric dispersion and coagulation contributed to the rapid decrease in particle number concentration and change in particle size distribution with increasing distance from the freeway. Average traffic flow during the sampling periods was 13,900 vehicles/hr. Ninety-three percent of vehicles were gasoline-powered cars or light trucks. The measured number concentration tracked traffic flow well. Thirty meters downwind from the freeway, three distinct ultrafine modes were observed with geometric mean diameters of 13, 27, and 65 nm. The smallest mode, with a peak concentration of 1.6 x 10(5)/cm3, disappeared at distances greater than 90 m from the freeway. Ultrafine particle number concentration measured 300 m downwind from the freeway was indistinguishable from upwind background concentration. These data may be used to estimate exposure to ultrafine particles in the vicinity of major highways.
Fully understanding the determinants and sequelae of fetal growth requires a continuous measure of birth weight adjusted for gestational age. Published United States reference data, however, provide estimates only of the median and lowest and highest 5th and 10th percentiles for birth weight at each gestational age. The purpose of our analysis was to create more continuous reference measures of birth weight for gestational age for use in epidemiologic analyses.
We used data from the most recent nationwide United States Natality datasets to generate multiple reference percentiles of birth weight at each completed week of gestation from 22 through 44 weeks. Gestational age was determined from last menstrual period. We analyzed data from 6,690,717 singleton infants with recorded birth weight and sex born to United States resident mothers in 1999 and 2000.
Birth weight rose with greater gestational age, with increasing slopes during the third trimester and a leveling off beyond 40 weeks. Boys had higher birth weights than girls, later born children higher weights than firstborns, and infants born to non-Hispanic white mothers higher birth weights than those born to non-Hispanic black mothers. These results correspond well with previously published estimates reporting limited percentiles.
Our method provides comprehensive reference values of birth weight at 22 through 44 completed weeks of gestation, derived from broadly based nationwide data. Other approaches require assumptions of normality or of a functional relationship between gestational age and birth weight, which may not be appropriate. These data should prove useful for researchers investigating the predictors and outcomes of altered fetal growth.
Ambient air pollutant exposure has been linked to childhood respiratory disease, but infants have received little study. The authors tested the hypotheses that subchronic and chronic exposure to fine particulate matter (particulate matter < or = 2.5 microm in aerodynamic diameter (PM2.5)), nitrogen dioxide, carbon monoxide, and ozone increases risk of severe infant bronchiolitis requiring hospitalization. Study subjects were derived from linked birth-hospital-discharge records of infants born in 1995-2000 in the South Coast Air Basin of California. Cases with a hospital discharge for bronchiolitis in infancy were matched to 10 age- and gestational-age-matched controls. Exposures in the month prior to hospitalization (subchronic) and mean lifetime exposure (chronic) referenced to the case diagnosis date were assessed on the basis of data derived from the California Air Resources Board. In conditional logistic regression, only subchronic and chronic PM2.5 exposures were associated with increased risk of bronchiolitis hospitalization after adjustment for confounders (per 10-microg/m3 increase, adjusted odds ratio = 1.09 (95% confidence interval: 1.04, 1.14) for both). Ozone was associated with reduced risk in the single-pollutant model, but this relation did not persist in multipollutant models including PM2.5. These unique US data suggest that infant bronchiolitis may be added to the list of adverse effects of PM2.5 exposure.
Long-term exposure to particulate air pollution has been associated with an increased risk of dying from cardiopulmonary and ischemic heart disease, yet few studies have evaluated cardiovascular end points other than mortality. We investigated the relationship between long-term exposure to traffic and occurrence of acute myocardial infarction (AMI) in a case-control study.
A total of 5,049 confirmed cases of AMI were identified between 1995 and 2003 as part of the Worcester Heart Attack Study, a community-wide study examining changes over time in the incidence of AMI among greater Worcester, Massachusetts, residents. Population controls were selected from Massachusetts resident lists. We used cumulative traffic within 100 m of subjects' residence and distance from major roadway as proxies for exposure to traffic-related air pollution. We estimated the relationship between exposure to traffic and occurrence of AMI using logistic regression, and we adjusted for the following potential confounders: age, sex, section of the study area, point sources emissions of particulate matter with aerodynamic diameter < 2.5 microm, area socioeconomic characteristics, and percentage of open space.
An increase in cumulative traffic near the home was associated with a 4% increase in the odds of AMI per interquartile range [95% confidence interval (CI), 2-7%], whereas living near a major roadway was associated with a 5% increase in the odds of AMI per kilometer (95% CI, 3-6%).
These results provide support for an association between long-term exposure to traffic and the risk of AMI.
There has been growing interest among exposure assessors, epidemiologists, and policymakers in the concept of "hot spots", or more broadly, the "spatial extent" of impacts from traffic-related air pollutants. This review attempts to quantitatively synthesize findings about the spatial extent under various circumstances.
We include both the peer-reviewed literature and government reports, and focus on four significant air pollutants: carbon monoxide, benzene, nitrogen oxides, and particulate matter (including both ultrafine particle counts and fine particle mass). From the identified studies, we extracted information about significant factors that would be hypothesized to influence the spatial extent within the study, such as the study type (e.g., monitoring, air dispersion modeling, GIS-based epidemiological studies), focus on concentrations or health risks, pollutant under study, background concentration, emission rate, and meteorological factors, as well as the study's implicit or explicit definition of spatial extent. We supplement this meta-analysis with results from some illustrative atmospheric dispersion modeling.
We found that pollutant characteristics and background concentrations best explained variability in previously published spatial extent estimates, with a modifying influence of local meteorology, once some extreme values based on health risk estimates were removed from the analysis. As hypothesized, inert pollutants with high background concentrations had the largest spatial extent (often demonstrating no significant gradient), and pollutants formed in near-source chemical reactions (e.g., nitrogen dioxide) had a larger spatial extent than pollutants depleted in near-source chemical reactions or removed through coagulation processes (e.g., nitrogen oxide and ultrafine particles). Our illustrative dispersion model illustrated the complex interplay of spatial extent definitions, emission rates, background concentrations, and meteorological conditions on spatial extent estimates even for non-reactive pollutants. Our findings indicate that, provided that a health risk threshold is not imposed, the spatial extent of impact for mobile sources reviewed in this study is on the order of 100-400 m for elemental carbon or particulate matter mass concentration (excluding background concentration), 200-500 m for nitrogen dioxide and 100-300 m for ultrafine particle counts.
First, to allow for meaningful comparisons across studies, it is important to state the definition of spatial extent explicitly, including the comparison method, threshold values, and whether background concentration is included. Second, the observation that the spatial extent is generally within a few hundred meters for highway or city roads demonstrates the need for high resolution modeling near the source. Finally, our findings emphasize that policymakers should be able to develop reasonable estimates of the "zone of influence" of mobile sources, provided that they can clarify the pollutant of concern, the general site characteristics, and the underlying definition of spatial extent that they wish to utilize.
Our goal was to evaluate the relationship between cause-specific postneonatal infant mortality and chronic early-life exposure to particulate matter and gaseous air pollutants across the United States.
We linked county-specific monitoring data for particles with aerodiameter of < or = 2.5 microm (PM2.5) and < or = 10 microm (PM10), ozone, sulfur dioxide, and carbon monoxide to birth and death records for infants born from 1999 to 2002 in U.S. counties with > 250,000 residents. For each infant, we calculated the average concentration of each pollutant over the first 2 months of life. We used logistic generalized estimating equations to estimate odds ratios of postneonatal mortality for all causes, respiratory causes, sudden infant death syndrome (SIDS), and all other causes for each pollutant, controlling for individual maternal factors (race, marital status, education, age, and primiparity), percentage of county population below poverty, region, birth month, birth year, and other pollutants. This analysis includes about 3.5 million births, with 6,639 postneonatal infant deaths.
After adjustment for demographic and other factors and for other pollutants, we found adjusted odds ratios of 1.16 [95% confidence interval (CI), 1.06-1.27] for a 10-mug/m3 increase in PM10 for respiratory causes and 1.20 (95% CI, 1.09-1.32) for a 10-ppb increase in ozone and deaths from SIDS. We did not find relationships with other pollutants and for other causes of death (control category).
This study supports particulate matter air pollution being a risk factor for respiratory-related postneonatal mortality and suggests that ozone may be associated with SIDS in the United States.
Chronic exposure to air pollution has been associated with adverse effects on children's lung growth.
We analyzed the effects of chronic exposure to urban levels of particulate matter (PM) on selected phases of mouse lung development.
The exposure occurred in two open-top chambers (filtered and nonfiltered) placed 20 m from a street with heavy traffic in São Paulo, 24 hours/day for 8 months. There was a significant reduction of the levels of PM(2.5) inside the filtered chamber (filtered = 2.9 +/- 3.0 microg/m(3), nonfiltered = 16.8 +/- 8.3 microg/m(3); P = 0.001). At this exposure site, vehicular sources are the major components of PM(2.5) (PM <or= 2.5 microm). Exposure of the parental generation in the two chambers occurred from the 10th to the 120th days of life. After mating and birth of offspring, a crossover of mothers and pups occurred within the chambers, resulting in four groups of pups: nonexposed, prenatal, postnatal, and pre+postnatal. Offspring were killed at the age of 15 (n = 42) and 90 (n = 35) days; lungs were analyzed by morphometry for surface to volume ratio (as an estimator of alveolization). Pressure-volume curves were performed in the older groups, using a 20-ml plethysmograph.
Mice exposed to PM(2.5) pre+postnatally presented a smaller surface to volume ratio when compared with nonexposed animals (P = 0.036). The pre+postnatal group presented reduced inspiratory and expiratory volumes at higher levels of transpulmonary pressure (P = 0.001). There were no differences among prenatal and postnatal exposure and nonexposed animals.
Our data provide anatomical and functional support to the concept that chronic exposure to urban PM affects lung growth.
Over the last decades many epidemiologic studies considered the morbidity patterns for respiratory diseases and lung function of children in the context of ambient air pollution usually measured in the postnatal period. The main purpose of this study is to assess the impact of prenatal exposure to fine particulate matter (PM(2.5)) on the recurrent broncho-pulmonary infections in early childhood. The study included 214 children who had measurements of personal prenatal PM(2.5) exposure and regularly collected data on the occurrence of acute bronchitis and pneumonia diagnosed by a physician from birth over the seven-year follow-up. The effect of prenatal exposure to PM(2.5) was adjusted in the multivariable logistic models for potential confounders, such as prenatal and postnatal ETS (environmental tobacco smoke), city residence area as a proxy of postnatal urban exposure, children's sensitization to domestic aeroallergens, and asthma. In the subgroup of children with available PM(2.5) indoor levels, the effect of prenatal exposure was additionally adjusted for indoor exposure as well. The adjusted odds ratio (OR) for incidence of recurrent broncho-pulmonary infections (five or more spells of bronchitis and/or pneumonia) recorded in the follow-up significantly correlated in a dose-response manner with the prenatal PM(2.5) level (OR=2.44, 95%CI: 1.12-5.36). In conclusion, the study suggests that prenatal exposure to PM(2.5) increases susceptibility to respiratory infections and may program respiratory morbidity in early childhood. The study also provides evidence that the target value of 20μg/m(3) for the 24-h mean level of PM(2.5) protects unborn babies better than earlier established EPA guidelines.
Historic air pollution episodes of the 1950s led to acute increases in infant mortality, and some recent epidemiologic studies suggest that infant or child mortality may still result from air pollution at current levels. To investigate the evidence for such an association, we conducted a time-series study of infant mortality in the southwestern part of Mexico City in the years 1993 to 1995 using mortality data from death registrations and air pollution measurements from a monitoring station we operated. Excess infant mortality was associated with the level of fine particles in the days before death, with the strongest association observed for the average concentration of fine particles during the period 3 to 5 days previously: a 10-[mu]g m-3 increase in the mean level of fine particles during these 3 days was associated with a 6.9% excess of infant deaths (95% confidence interval 2.5-11.3%). Infant mortality was also associated with the levels of nitrogen dioxide and ozone 3 to 5 days before death, but not as consistently as with particles.
(C) 1999 Lippincott Williams & Wilkins, Inc.
Low birth weight and preterm birth have a substantial public health impact. Studies examining their association with outdoor air pollution were identified using searches of bibliographic databases and reference lists of relevant papers. Pooled estimates of effect were calculated, heterogeneity was quantified, meta-regression was conducted and publication bias was examined. Sixty-two studies met the inclusion criteria. The majority of studies reported reduced birth weight and increased odds of low birth weight in relation to exposure to carbon monoxide (CO), nitrogen dioxide (NO(2)) and particulate matter less than 10 and 2.5 microns (PM(10) and PM(2.5)). Effect estimates based on entire pregnancy exposure were generally largest. Pooled estimates of decrease in birth weight ranged from 11.4 g (95% confidence interval -6.9-29.7) per 1 ppm CO to 28.1g (11.5-44.8) per 20 ppb NO(2), and pooled odds ratios for low birth weight ranged from 1.05 (0.99-1.12) per 10 μg/m(3) PM(2.5) to 1.10 (1.05-1.15) per 20 μg/m(3) PM(10) based on entire pregnancy exposure. Fewer effect estimates were available for preterm birth and results were mixed. Pooled odds ratios based on 3rd trimester exposures were generally most precise, ranging from 1.04 (1.02-1.06) per 1 ppm CO to 1.06 (1.03-1.11) per 20 μg/m(3) PM(10). Results were less consistent for ozone and sulfur dioxide for all outcomes. Heterogeneity between studies varied widely between pollutants and outcomes, and meta-regression suggested that heterogeneity could be partially explained by methodological differences between studies. While there is a large evidence base which is indicative of associations between CO, NO(2), PM and pregnancy outcome, variation in effects by exposure period and sources of heterogeneity between studies should be further explored.
The relationship between residential proximity to roadway and long-term survival after acute myocardial infarction (AMI) is unknown. We investigated the association between distance from residence and major roadway and 10-year all-cause mortality after AMI in the Determinants of Myocardial Infarction Onset Study (Onset Study), hypothesizing that living closer to a major roadway at the time of AMI would be associated with increased risk of mortality.
The Onset Study enrolled 3886 individuals hospitalized for AMI in 64 centers across the United States from 1989 to 1996. Institutionalized patients, those providing only post office boxes, and those whose addresses could not be geocoded were excluded, leaving 3547 patients eligible for analysis. Addresses were geocoded, and distance to the nearest major roadway was assigned. Cox regression was used to calculate hazard ratios, with adjustment for personal characteristics (age, sex, race, education, marital status, distance to nearest acute care hospital), clinical characteristics (smoking, body mass index, comorbidities, medications), and neighborhood-level characteristics derived from US Census block group data (household income, education, urbanicity). There were 1071 deaths after 10 years of follow-up. In the fully adjusted model, compared with living >1000 m, hazard ratios (95% confidence interval) for living ≤100 m were 1.27 (1.01-1.60), for 100 to ≤200 m were 1.19 (0.93-1.60), and for 200 to ≤1000 m were 1.13 (0.99-1.30) (P(trend)=0.016).
In this multicenter study, living close to a major roadway at the time of AMI was associated with increased risk of all-cause 10-year mortality; this relationship persisted after adjustment for individual and neighborhood-level covariates.
Data regarding the influence of ambient air pollution on infant bronchiolitis are few.
We evaluated the impact of several air pollutants and their sources on infant bronchiolitis.
Infants in the Georgia Air Basin of British Columbia with an inpatient or outpatient clinical encounter for bronchiolitis (n = 11,675) were matched on day of birth to as many as 10 control subjects. Exposure to particulate matter with a diameter of 2.5 mum or less (PM(2.5)), PM(10), NO(2)/NO, SO(2), CO, and O(3) were assessed on the basis of a regional monitoring network. Traffic exposure was assessed using regionally developed land use regression (LUR) models of NO(2), NO, PM(2.5), and black carbon as well as proximity to highways. Exposure to wood smoke and industrial emissions was also evaluated. Risk estimates were derived using conditional logistic regression and adjusted for infant sex and First Nations (Canadian government term for recognized aboriginal groups) status and for maternal education, age, income-level, parity, smoking during pregnancy, and initiation of breastfeeding.
An interquartile increase in lifetime exposure to NO(2), NO, SO(2), CO, wood-smoke exposure days, and point source emissions score was associated with increased risk of bronchiolitis (e.g., adjusted odds ratio [OR(adj)] NO(2), 95% confidence interval [CI], 1.12, 1.09-1.16; OR(adj) wood smoke, 95% CI, 1.08, 1.04-1.11). Infants who lived within 50 meters of a major highway had a 6% higher risk (1.06, 0.97-1.17). No adverse effect of increased exposure to PM(10), PM(2.5), or black carbon, was observed. Ozone exposure was negatively correlated with the other pollutants and negatively associated with the risk of bronchiolitis.
Air pollutants from several sources may increase infant bronchiolitis requiring clinical care. Traffic, local point source emissions, and wood smoke may contribute to this disease.
Few studies investigate the impact of air pollution on the leading cause of infant morbidity, acute bronchiolitis. We investigated the influence of PM2.5 and other metrics of traffic-derived air pollution exposure using a matched case-control dataset derived from 1997 to 2003 birth and infant hospitalization records from the Puget Sound Region, Washington State. Mean daily PM2.5 exposure for 7, 30, 60 and lifetime days before case bronchiolitis hospitalization date were derived from community monitors. A regional land use regression model of NO2 was applied to characterize subject's exposure in the month prior to case hospitalization and lifetime average before hospitalization. Subject's residential proximity within 150 m of highways, major roadways, and truck routes was also assigned. We evaluated 2604 (83%) cases and 23,354 (85%) controls with information allowing adjustment for mother's education, mother's smoking during pregnancy, and infant race/ethnicity. Effect estimates derived from conditional logistic regression revealed very modest increased risk and were not statistically significant for any of the exposure metrics in fully adjusted models. Overall, risk estimates were stronger when restricted to bronchiolitis cases attributed to respiratory syncytial virus (RSV) versus unspecified and for longer exposure windows. The adjusted odds ratio (ORadj) and 95% confidence interval per 10 mcg/m3 increase in lifetime PM2.5 was 1.14, 0.88-1.46 for RSV bronchiolitis hospitalization. This risk was also elevated for infants who resided within 150 m of a highway (ORadj 1.17, 0.95-1.44). This study supports a developing hypothesis that there may be a modest increased risk of bronchiolitis attributable to chronic traffic-derived particulate matter exposure particularly for infants born just before or during peak RSV season. Future studies are needed that can investigate threshold effects and capture larger variability in spatial contrasts among populations of infants.
An ecological study of infant mortality and air pollution was conducted in the Czech Republic. Routinely collected data on infant mortality and air pollution in the period 1986-88 were analysed for the 46 of the 85 districts in the republic for which both were available. The independent effects of total suspended particulates (TSP-10), sulphur dioxide (SO2), and oxides of nitrogen (NOx) adjusted for district socioeconomic characteristics, such as income, car ownership, and abortion rate, were estimated by logistic regression. We found weak positive associations between neonatal mortality and quintile of TSP-10 and SO2. Stronger adjusted effects were seen for postneonatal mortality, with a consistent increase in risk from the lowest to the highest TSP-10 quintile (p < 0.001). Weaker and less consistent evidence of a positive association with NOx (p = 0.061) was observed. The strongest effects were seen for postneonatal respiratory mortality, which increased consistently from lowest to highest TSP-10 quintile (p = 0.013). There was also a suggestion of a positive association with SO2 (p = 0.062). The highest to lowest quintile risk ratios for postneonatal respiratory mortality were 2.41 (95% Cl 1.10-5.28) for TSP-10, 3.91 (0.90-16.9) for SO2, and 1.20 (0.37-3.91) NOx. The specificity of the association between air pollution quintile (especially TSP-10) and postneonatal respiratory mortality is consistent with the known effects of air pollution on respiratory disease morbidity in children. These ecological associations require confirmation in an individually based study.
A diary study on a random sample of 625 Swiss children aged 0 to 5 yr was conducted in two cities in Switzerland to investigate the association between air pollution and respiratory symptoms. Total suspended particulates (TSP), SO2 and NO2 were measured by city monitor. In addition, passive samplers inside and outside the home measured NO2 concentration during the 6 wk each child was on the diary. Diaries were filled out by parents, and 20% were validated with the attending pediatrician's case notes. Incidence and duration of symptom episodes were examined separately. The study included any episode, episodes of coughing without runny nose, upper respiratory episodes, and episodes of breathing difficulty. In regressions using 6-wk average pollution that controlled for medical history, NO2 measured outdoors but not indoors was associated with the duration of any symptom. Total suspended particulates were a more significant predictor of duration of any symptom than NO2. The 6-wk average TSP was significantly associated with incidence of coughing episodes and marginally significant as a predictor of upper respiratory episodes. Previous day's TSP was a significant predictor of incidence of upper respiratory symptoms. Annual average of NO2 was associated with the duration of any episode and of upper respiratory episodes. We conclude that the incidence and duration of respiratory symptom episodes are likely associated with particulate concentrations and duration may be associated with NO2.
We evaluated whether sidestream smoke (SS) exposure in utero and/or postnatally causes airway obstruction and hyperresponsiveness, and whether the effect is associated with neuroendocrine cell hyperplasia. Pregnant Sprague-Dawley rats were exposed to filtered air (FA) or to SS (total suspended particulate concentration, 1.00 +/- 0.07 mg/m3, CO, 4.9 +/- 0.7 ppm; nicotine, 344 +/- 85 micrograms/m3; mean +/- SD) for 4 hr/day, 7 days/week from Day 3 of gestation until birth and then their female pups were exposed to either FA or SS for 7-10 weeks postnatally. This resulted in four exposure conditions: in utero FA followed by postnatal FA (FA/FA), in utero FA followed by postnatal SS (FA/SS), in utero SS followed by postnatal FA (SS/FA), and in utero SS followed by postnatal SS (SS/SS). The lungs from the pups (n = 6-8 of each exposure combination) were then placed in an isolated buffer-perfused system where transpulmonary pressure, airflow, and pulmonary artery pressure (Ppa) were measured while increasing doses of methacholine were injected into the pulmonary artery. Three lungs from each group were then fixed in 1% paraformaldehyde and neuroendocrine cells were identified immunohistochemically using antibodies to neuron-specific enolase. As compared to lungs from FA/FA-exposed rats, lungs from SS/SS-exposed rats exhibited 24% lower Cdyn (p = 0.0006, ANOVA), greater reactivity to methacholine (p = 0.0001, repeated measures ANOVA), and more neuroendocrine cells per centimeter basal lamina (p = 0.0006, ANOVA). Lungs from SS/FA- or FA/SS-exposed rats were not different from lungs from FA/FA-exposed rats in any of these parameters. We conclude that exposure to SS both pre- and postnatally (but not only pre- or only postnatally) results in lungs which are less compliant, more reactive to methacholine, and have a greater number of neuroendocrine cells.
This work presents the results of a time series study relating air pollution and respiratory mortality in children under 5 years of age in the metropolitan area of São Paulo, Brazil. Daily records of mortality (excluding neonatal mortality) for the period May 1990 to April 1991 were collected along with daily records of relative humidity, temperature, SO2, CO, particulates (PM10), O3, and NOx concentrations. Using multiple regression methods we demonstrated a significant association between mortality due to respiratory diseases and the NOx levels. After controlling for weather and season effects, the odds of dying due to respiratory diseases, considering the mean levels of NOx in São Paulo, was estimated at 1.3 (+/- 0.13). This result is in accord with previous animal studies conducted by our group and indicates that air pollution in São Paulo has reached levels high enough to have adverse health effects on the exposed population.
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.
Although epidemiologic data strongly suggest a role for inhaled environmental pollutants in modulating the susceptibility to respiratory infection in humans, the underlying cellular and molecular mechanisms have not been well studied in experimental systems. The current study assessed the impact of inhaled diesel engine emissions (DEE) on the host response in vivo to a common pediatric respiratory pathogen, respiratory syncytial virus (RSV). Using a relatively resistant mouse model of RSV infection, prior exposure to either 30 microg/m3 particulate matter (PM) or 1,000 microg/m3 PM of inhaled DEE (6 h/d for seven consecutive days) increased lung inflammation to RSV infection as compared with air-exposed RSV-infected C57Bl/6 mice. Inflammatory cells in bronchoalveolar lavage fluid were increased in a dose-dependent manner with regard to the level of DEE exposure, concomitant with increased levels of inflammatory mediators. Lung histology analysis indicated pronounced peribronchial and peribronchiolar inflammation concordant with the level of DEE exposure during infection. Mucous cell metaplasia was markedly increased in the airway epithelium of DEE-exposed mice following RSV infection. Interestingly, both airway and alveolar host defense and immunomodulatory proteins were attenuated during RSV infection by prior DEE exposure. DEE-induced changes in inflammatory and lung epithelial responses to infection were associated with increased RSV gene expression in the lungs following DEE exposure. These findings are consistent with the concept that DEE exposure modulates the lung host defense to respiratory viral infections and may alter the susceptibility to respiratory infections leading to increased lung disease.
To investigate perinatal predictors of newborn blood pressure.
Among 1059 mothers and their newborn infants participating in Project Viva, a US cohort study of pregnant women and their offspring, we obtained five systolic blood pressure readings on a single occasion in the first few days of life. Using multivariate linear regression models, we examined the extent to which maternal age and other pre- and perinatal factors predicted newborn blood pressure level.
Mean (SD) maternal age was 32.0 (5.2) years, and mean (SD) newborn systolic blood pressure was 72.6 (9.0) mm Hg. A multivariate model showed that for each 5-year increase in maternal age, newborn systolic blood pressure was 0.8 mm Hg higher (95% CI, 0.2, 1.4). In addition to maternal age, independent predictors of newborn blood pressure included maternal third trimester blood pressure (0.9 mm Hg [95% CI, 0.2, 1.6] for each increment in maternal blood pressure); infant age at which we measured blood pressure (2.4 mm Hg [95% CI 1.7, 3.0] for each additional day of life); and birth weight (2.9 mm Hg [95% CI, 1.6, 4.2] per kg).
Higher maternal age, maternal blood pressure, and birth weight were associated with higher newborn systolic blood pressure. Whereas blood pressure later in childhood predicts adult hypertension and its consequences, newborn blood pressure may represent different phenomena, such as pre- and perinatal influences on cardiac structure and function.
Relative risk is usually the parameter of interest in epidemiologic and medical studies. In this paper, the author proposes a modified Poisson regression approach (i.e., Poisson regression with a robust error variance) to estimate this effect measure directly. A simple 2-by-2 table is used to justify the validity of this approach. Results from a limited simulation study indicate that this approach is very reliable even with total sample sizes as small as 100. The method is illustrated with two data sets.
To examine associations between birth weight and air pollution among full-term infants in California.
We matched exposure data collected from air pollution monitors for small particles (PM(2.5)) and carbon monoxide (CO) to California birth records for singleton births delivered at 40 weeks' gestation in 2000 using the locations of the monitors and mother's residence. Pollution measurements collected within 5 miles of the mother's residence, averaged for the time period corresponding to the duration of pregnancy and each trimester, were used as exposure variables. Logistic and linear regression models were used to estimate the associations between the pollution measures and 2 pregnancy outcomes: small for gestational age (SGA) and birth weight. Variations of the models were used to examine the robustness of the findings.
The adjusted odds ratio for SGA for exposure in the highest compared with lowest quartile of PM(2.5) was 1.26 (95% confidence interval [CI]: 1.03-1.50). We found no association between CO and birth weight or SGA after controlling for maternal factors and PM(2.5) (mean birth weight difference: 2.6 g; 95% CI: -20.6 to 25.8). The difference in mean birth weight for infants with a 9-month exposure in the highest quartile of PM(2.5) compared with that of infants who were exposed in the lowest quartile was -36.1 g (95% CI: -16.5 g to -55.8 g); this difference was similar after controlling for CO. We did not find PM(2.5) exposure during a particular trimester most important for assessing birth weight; trimester-level associations were similar to those found using the 9-month exposure variable.
We found an increased odds of SGA and a small difference in mean birth weight between infants with the highest and lowest exposures to PM(2.5) but not CO. These findings have important implications for infant health because of the ubiquitous exposure to fine particulate air pollution across the United States.
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.
Respiratory syncytial virus (RSV) is one of the most common respiratory pathogens in infants and young children. It is not known why some previously healthy infants, when in contact with RSV, develop bronchiolitis whereas others have only mild symptoms. Our study aimed to evaluate the possible association between emergency hospital visits for bronchiolitis and air pollution in the Paris region during four winter seasons. We included children under the age of 3 years who attended emergency room services for bronchiolitis (following standardized definition) during the period 1997-2001. Two series of data from 34 hospitals, the daily number of emergency hospital consultations (n=50857) and the daily number of hospitalizations (n=16588) for bronchiolitis, were analyzed using alternative statistical methods; these were the generalized additive model (GAM) and case-crossover models. After adjustments for public holidays, holidays and meteorological variables the case-crossover model showed that PM10, BS, SO2 and NO2 were positively associated with both consultations and hospitalizations. GAM models, adjusting for long-term trend, seasonality, holiday, public holiday, weekday and meteorological variables, gave similar results for SO2 and PM10. This study shows that air pollution may act as a trigger for the occurrence of acute severe bronchiolitis cases.
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.
Exposure to environmental tobacco smoke (ETS) during fetal development and early postnatal life is perhaps the most ubiquitous and hazardous of children's environmental exposures. The developing lung is highly susceptible to ETS. A large body of literature links both prenatal maternal smoking and children's ETS exposure to decreased lung growth. This review summarizes the state of the knowledge, including both human epidemiology and laboratory animal experiments, linking ETS, lung development, and respiratory outcomes. Important issues discussed include lung development and lung function and asthma in relation to ETS exposure during critical windows of growth. Prenatal exposure to ETS is associated with impaired lung function and increased risk of developing asthma, whereas postnatal exposure mainly acts to trigger respiratory symptoms and asthma attacks, but it also plays an important role in the occurrence of asthma in children. This review provides evidence that avoidance of ETS exposure both before and after birth is beneficial to long-term respiratory health, because airway function in later life is believed to be largely determined by lung development occurring in utero and in early infancy.
Chronic exposure to ambient levels of urban particles affects mouse lung development
- T Mauad
- Dhrf Rivero
- R C De Oliveira
- F C Lichtenfels Aj De
- E T Guimarães
- P A De Andre
- D I Kasahara
- S Bueno Hm De
- Phn Saldiva
Mauad T, Rivero DHRF, de Oliveira RC, Lichtenfels AJ de FC,
Guimarães ET, de Andre PA, Kasahara DI, Bueno HM de S,
Saldiva PHN. Chronic exposure to ambient levels of urban
particles affects mouse lung development. Am J Respir Crit Care
Med 2008;178:721-728.
A nearly continuous measure of birth weight for gestational age using a United States national reference
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