Abstract:Background:Although it is well established that air pollutants can exacerbate asthma, the link with new asthma onset in children is less clear.Objective:We assessed the association between the onset of childhood asthma with both time of birth and time-varying exposures to outdoor air pollutants.Method:An open cohort of children born in the province of Québec, Canada, was created using linked medical–administrative databases. New cases of asthma were defined as one hospital discharge with a diagnosis of asthma … Show more
“…Figure 1 shows the flow of papers. A total of 42 studies met our inclusion criteria [31,32,33,34,36,37,38,39,40,41,42,43,44,45,46,47,48,50,51,52,58,67,68,69,70,71,72,73,74,75,76,77,78,79,80,81,82,83,84,85,86,87] (Table 1). …”
Section: Resultsmentioning
confidence: 99%
“…Ages of participants ranged from 1 to 18 years old and sample sizes ranged from 184 [69] to 1,133,938 [85]. Follow-up periods ranged from 1 to 16 years [47].…”
Background: Current levels of traffic-related air pollution (TRAP) are associated with the development of childhood asthma, although some inconsistencies and heterogeneity remain. An important part of the uncertainty in studies of TRAP-associated asthma originates from uncertainties in the TRAP exposure assessment and assignment methods. In this work, we aim to systematically review the exposure assessment methods used in the epidemiology of TRAP and childhood asthma, highlight recent advances, remaining research gaps and make suggestions for further research. Methods: We systematically reviewed epidemiological studies published up until 8 September 2016 and available in Embase, Ovid MEDLINE (R), and “Transport database”. We included studies which examined the association between children’s exposure to TRAP metrics and their risk of “asthma” incidence or lifetime prevalence, from birth to the age of 18 years old. Results: We found 42 studies which examined the associations between TRAP and subsequent childhood asthma incidence or lifetime prevalence, published since 1999. Land-use regression modelling was the most commonly used method and nitrogen dioxide (NO2) was the most commonly used pollutant in the exposure assessments. Most studies estimated TRAP exposure at the residential address and only a few considered the participants’ mobility. TRAP exposure was mostly assessed at the birth year and only a few studies considered different and/or multiple exposure time windows. We recommend that further work is needed including e.g., the use of new exposure metrics such as the composition of particulate matter, oxidative potential and ultra-fine particles, improved modelling e.g., by combining different exposure assessment models, including mobility of the participants, and systematically investigating different exposure time windows. Conclusions: Although our previous meta-analysis found statistically significant associations for various TRAP exposures and subsequent childhood asthma, further refinement of the exposure assessment may improve the risk estimates, and shed light on critical exposure time windows, putative agents, underlying mechanisms and drivers of heterogeneity.
“…Figure 1 shows the flow of papers. A total of 42 studies met our inclusion criteria [31,32,33,34,36,37,38,39,40,41,42,43,44,45,46,47,48,50,51,52,58,67,68,69,70,71,72,73,74,75,76,77,78,79,80,81,82,83,84,85,86,87] (Table 1). …”
Section: Resultsmentioning
confidence: 99%
“…Ages of participants ranged from 1 to 18 years old and sample sizes ranged from 184 [69] to 1,133,938 [85]. Follow-up periods ranged from 1 to 16 years [47].…”
Background: Current levels of traffic-related air pollution (TRAP) are associated with the development of childhood asthma, although some inconsistencies and heterogeneity remain. An important part of the uncertainty in studies of TRAP-associated asthma originates from uncertainties in the TRAP exposure assessment and assignment methods. In this work, we aim to systematically review the exposure assessment methods used in the epidemiology of TRAP and childhood asthma, highlight recent advances, remaining research gaps and make suggestions for further research. Methods: We systematically reviewed epidemiological studies published up until 8 September 2016 and available in Embase, Ovid MEDLINE (R), and “Transport database”. We included studies which examined the association between children’s exposure to TRAP metrics and their risk of “asthma” incidence or lifetime prevalence, from birth to the age of 18 years old. Results: We found 42 studies which examined the associations between TRAP and subsequent childhood asthma incidence or lifetime prevalence, published since 1999. Land-use regression modelling was the most commonly used method and nitrogen dioxide (NO2) was the most commonly used pollutant in the exposure assessments. Most studies estimated TRAP exposure at the residential address and only a few considered the participants’ mobility. TRAP exposure was mostly assessed at the birth year and only a few studies considered different and/or multiple exposure time windows. We recommend that further work is needed including e.g., the use of new exposure metrics such as the composition of particulate matter, oxidative potential and ultra-fine particles, improved modelling e.g., by combining different exposure assessment models, including mobility of the participants, and systematically investigating different exposure time windows. Conclusions: Although our previous meta-analysis found statistically significant associations for various TRAP exposures and subsequent childhood asthma, further refinement of the exposure assessment may improve the risk estimates, and shed light on critical exposure time windows, putative agents, underlying mechanisms and drivers of heterogeneity.
“…Multiple population studies have shown an association between exposure to air pollutants and increased risk of asthma (89–92). An increased risk of developing asthma associated with self-reported or assumed “low-level or moderate irritant exposures” has also been suggested from epidemiologic studies, and has been listed as possible IIA in the European Academy of Allergy and Clinical Immunology Task Force statement on IIA (4), with examples given as work as cleaners or work with pesticides, and in the wood industry.…”
The Sixth Jack Pepys Workshop on Asthma in the Workplace focused on six key themes regarding the recognition and assessment of work-related asthma and airway diseases: (1) cleaning agents and disinfectants (including in swimming pools) as irritants and sensitizers: how to evaluate types of bronchial reactions and reduce risks; (2) population-based studies of occupational obstructive diseases: use of databanks, advantages and pitfalls, what strategies to deal with biases and confounding?; (3) damp environments, dilapidated buildings, recycling processes, and molds, an increasing problem: mechanisms, how to assess causality and diagnosis; (4) diagnosis of occupational asthma and rhinitis: how useful are recombinant allergens (component-resolved diagnosis), metabolomics, and other new tests?; (5) how does exposure to gas, dust, and fumes enhance sensitization and asthma?; and (6) how to determine probability of occupational causality in chronic obstructive pulmonary disease: epidemiological and clinical, confirmation, and compensation aspects. A summary of the presentations and discussion is provided in this proceedings document. Increased knowledge has been gained in each topic over the past few years, but there remain aspects of controversy and uncertainty requiring further research.
“…A large number of epidemiological studies have linked exposure to PM with a variety of adverse health effects including respiratory and cardiovascular diseases, and mortality [1][2][3]. Children are particularly susceptible; exposure to PM 2.5 (PM with aerodynamic diameter ≤2.5 µm) early in life can lead to the onset of asthma [4], wheeze [5], and decreased lung function [6].…”
Recent use of satellite observations of aerosol optical depth (AOD) to characterize surface concentrations of particulate matter (PM) air pollution has proven extremely valuable in estimating exposures for health effects studies. While the spatial resolutions of satellite data provide far better coverage than existing fixed site surface monitoring stations, they are not able to capture atmospheric processes such as dilution of primary pollutants that vary at small spatial scales. As a result, small-scale variability due to highly localized sources such as traffic may be poorly represented, which in turn may lead to exposure measurement error in epidemiological analyses. Using a fixed spatial grid representing 4.4 km Multiangle Imaging SpectroRadiometer (MISR) aerosol observations, we examined the spatial variability in fine and coarse mode PM (PM 2.5 and PM 2.5-10 respectively) measured at ground monitors from a unique spatially-dense sampling campaign in Southern California. We found that while the variance in measured PM 2.5 differed seasonally (warm 6.82 µg 2 /m 6 and cool 24.5 µg 2 /m 6 ) across the study region, the average subgrid (<4.4 km) variance did not (warm 2.03 µg 2 /m 6 and cool 2.43 µg 2 /m 6 ) and was significantly smaller. On the other hand, ground monitor PM 2.5-10 concentrations showed large variance in warm (18.6 µg 2 /m 6 ) and cool (20.6 µg 2 /m 6 ) seasons, as well as seasonal differences in subgrid variance (warm 8.90 µg 2 /m 6 and cool 3.28 µg 2 /m 6 ). Geostatistical analysis of the semivariance as a function of distance indicated that variability in measured PM 2.5 and PM 2.5-10 concentrations was relatively constant for spatial scales of one to five kilometers, but there was evidence of small-scale (~500 m) variability in PM 2.5-10 concentrations in the cool season. The lack of small-scale spatial variability in the warm season was likely due to large photochemical contributions to regional PM 2.5 , and greater regional contributions to PM 2.5-10 from windblown dust. In contrast, in the cool season there tends to be greater localized concentrations from primary traffic sources due to stronger nocturnal inversions and delayed morning winds reducing dilution that contribute to greater spatial heterogeneity. Overall, these results suggest that regional contributions tend to dominate PM 2.5 , and spatial resolutions of satellite observations including the 4.4 km MISR and 3 km MODIS aerosol products aptly capture relevant spatial variability. Coarse PM 2.5-10 can have seasonally dependent localized contributions, leading to small-scale variability below current satellite aerosol product resolutions.
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