Outdoor air pollution exposure and the risk of asthma and wheezing in the offspring

Hua, Lei; Ju, Liangliang; Xu, Hanbing; Li, Changlian; Sun, Shuai; Zhang, Qi; Cao, Jiyu; Ding, Rui

doi:10.1007/s11356-022-23094-6

Cited by 8 publications

(4 citation statements)

References 70 publications

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“…The oldest review 37 focused on asthma in children from postnatal exposure. The other recent review 45 on childhood asthma included studies only on maternal exposure during pregnancy, with the effect estimate for the entire pregnancy close to the null, and we have decided not to recommend it for HRA.…”

Section: Resultsmentioning

confidence: 99%

Choices of morbidity outcomes and concentration–response functions for health risk assessment of long-term exposure to air pollution

Forastiere,

Spadaro,

Ancona

et al. 2024

Environmental Epidemiology

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Background: Air pollution health risk assessment (HRA) has been typically conducted for all causes and cause-specific mortality based on concentration–response functions (CRFs) from meta-analyses that synthesize the evidence on air pollution health effects. There is a need for a similar systematic approach for HRA for morbidity outcomes, which have often been omitted from HRA of air pollution, thus underestimating the full air pollution burden. We aimed to compile from the existing systematic reviews and meta-analyses CRFs for the incidence of several diseases that could be applied in HRA. To achieve this goal, we have developed a comprehensive strategy for the appraisal of the systematic reviews and meta-analyses that examine the relationship between long-term exposure to particulate matter with an aerodynamic diameter smaller than 2.5 µm (PM2.5), nitrogen dioxide (NO2), or ozone (O3) and incidence of various diseases. Methods: To establish the basis for our evaluation, we considered the causality determinations provided by the US Environmental Protection Agency Integrated Science Assessment for PM2.5, NO2, and O3. We developed a list of pollutant/outcome pairs based on these assessments and the evidence of a causal relationship between air pollutants and specific health outcomes. We conducted a comprehensive literature search using two databases and identified 75 relevant systematic reviews and meta-analyses for PM2.5 and NO2. We found no relevant reviews for long-term exposure to ozone. We evaluated the reliability of these studies using an adaptation of the AMSTAR 2 tool, which assesses various characteristics of the reviews, such as literature search, data extraction, statistical analysis, and bias evaluation. The tool’s adaptation focused on issues relevant to studies on the health effects of air pollution. Based on our assessment, we selected reviews that could be credible sources of CRF for HRA. We also assessed the confidence in the findings of the selected systematic reviews and meta-analyses as the sources of CRF for HRA. We developed specific criteria for the evaluation, considering factors such as the number of included studies, their geographical distribution, heterogeneity of study results, the statistical significance and precision of the pooled risk estimate in the meta-analysis, and consistency with more recent studies. Based on our assessment, we classified the outcomes into three lists: list A (a reliable quantification of health effects is possible in an HRA), list B+ (HRA is possible, but there is greater uncertainty around the reliability of the CRF compared to those included on list A), and list B− (HRA is not recommended because of the substantial uncertainty of the CRF). Results: In our final evaluation, list A includes six CRFs for PM2.5 (asthma in children, chronic obstructive pulmonary disease, ischemic heart disease events, stroke, hypertension, and lung cancer) and three outcomes for NO2 (asthma in children and in adults, and acute lower respiratory infections in children). Three additional outcomes (diabetes, dementia, and autism spectrum disorders) for PM2.5 were included in list B+. Recommended CRFs are related to the incidence (onset) of the diseases. The International Classification of Diseases, 10th revision codes, age ranges, and suggested concentration ranges are also specified to ensure consistency and applicability in an HRA. No specific suggestions were given for ozone because of the lack of relevant systematic reviews. Conclusion: The suggestions formulated in this study, including CRFs selected from the available systematic reviews, can assist in conducting reliable HRAs and contribute to evidence-based decision-making in public health and environmental policy. Future research should continue to update and refine these suggestions as new evidence becomes available and methodologies evolve.

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Section: Resultsmentioning

confidence: 99%

Choices of morbidity outcomes and concentration–response functions for health risk assessment of long-term exposure to air pollution

Forastiere,

Spadaro,

Ancona

et al. 2024

Environmental Epidemiology

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“…These findings demonstrate the potential for additive effects of maternal asthma exposure when coupled with PM exposure. Independently, studies have shown in both humans and animal models that PM exposure during pregnancy can increase the susceptibility of offspring developing asthma [ 49 , 84 , 123 ]. This increased susceptibility of asthma in offspring is also seen in children of asthmatic mothers [ 71 , 85 ] (Mattes et al 2013), suggesting the potential for systemic immune dysfunction when these two stimuli are combined during pregnancy.…”

Section: Discussionmentioning

confidence: 99%

Characterizing the neuroimmune environment of offspring in a novel model of maternal allergic asthma and particulate matter exposure

Tamayo,

Osman,

Schwartzer

et al. 2023

J Neuroinflammation

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Inflammation during pregnancy is associated with an increased risk for neurodevelopmental disorders (NDD). Increased gestational inflammation can be a result of an immune condition/disease, exposure to infection, and/or environmental factors. Epidemiology studies suggest that cases of NDD are on the rise. Similarly, rates of asthma are increasing, and the presence of maternal asthma during pregnancy increases the likelihood of a child being later diagnosed with NDD such as autism spectrum disorders (ASD). Particulate matter (PM), via air pollution, is an environmental factor known to worsen the symptoms of asthma, but also, PM has been associated with increased risk of neuropsychiatric disorders. Despite the links between asthma and PM with neuropsychiatric disorders, there is a lack of laboratory models investigating combined prenatal exposure to asthma and PM on offspring neurodevelopment. Thus, we developed a novel mouse model that combines exposure to maternal allergic asthma (MAA) and ultrafine iron-soot (UIS), a common component of PM. In the current study, female BALB/c mice were sensitized for allergic asthma with ovalbumin (OVA) prior to pregnancy. Following mating and beginning on gestational day 2 (GD2), dams were exposed to either aerosolized OVA to induce allergic asthma or phosphate buffered saline (PBS) for 1 h. Following the 1-h exposure, pregnant females were then exposed to UIS with a size distribution of 55 to 169 nm at an average concentration of 176 ± 45 μg/m3) (SD), or clean air for 4 h, over 8 exposure sessions. Offspring brains were collected at postnatal days (P)15 and (P)35. Cortices and hippocampal regions were then isolated and assessed for changes in cytokines using a Luminex bead-based multiplex assay. Analyses identified changes in many cytokines across treatment groups at both timepoints in the cortex, including interleukin-1 beta (IL-1β), and IL-17, which remained elevated from P15 to P35 in all treatment conditions compared to controls. There was a suppressive effect of the combined MAA plus UIS on the anti-inflammatory cytokine IL-10. Potentially shifting the cytokine balance towards more neuroinflammation. In the hippocampus at P15, elevations in cytokines were also identified across the treatment groups, namely IL-7. The combination of MAA and UIS exposure (MAA–UIS) during pregnancy resulted in an increase in microglia density in the hippocampus of offspring, as identified by IBA-1 staining. Together, these data indicate that exposure to MAA, UIS, and MAA–UIS result in changes in the neuroimmune environment of offspring that persist into adulthood.

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“…These findings demonstrate the potential for additive effects of maternal asthma exposure when coupled with PM exposure. Independently, studies have shown in both humans and animal models that PM exposure during pregnancy can increase the susceptibility of offspring developing asthma ( Mortimer et al, 2008 ; Wang et al, 2013 ; Hua et al, 2023 ). This increased susceptibility of asthma in offspring is also seen in children of asthmatic mothers ( Martel et al, 2009 ; Mattes et al, 2013 ; Murphy 2022 ), suggesting the potential for systemic immune disfunction when these two stimuli are combined during pregnancy.…”

Section: Discussionmentioning

confidence: 99%

Characterizing the Neuroimmune Environment of Offspring in a Novel Model of Maternal Allergic Asthma and Particulate Matter Exposure

Tamayo

Schwartzer

Pinkerton

et al. 2023

Preprint

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Autism spectrum disorders (ASD) are neurodevelopmental disorders characterized by the presence of decreased social interactions and an increase in stereotyped and repetitive behaviors. Epidemiology studies suggest that cases of ASD are on the rise. Similarly, rates of asthma are increasing, and the presence of maternal asthma during pregnancy increases the likelihood of a child being later diagnosed with ASD. Particulate matter (PM), via air pollution, is an environmental factor known to worsen the symptoms of asthma, but also, PM has been associated with increased risk of neuropsychiatric disorders including ASD. Despite the links between asthma and PM with neuropsychiatric disorders, there is a lack of laboratory models investigating combined prenatal exposure to asthma and PM on offspring neurodevelopment. Thus, we developed a novel mouse model that combines exposure to maternal allergic asthma (MAA) and ultrafine iron-soot (UIS), a common component of PM. In the current study, female BALB/c mice were primed for allergic asthma with ovalbumin (OVA) prior to pregnancy. Following mating and beginning on gestational day 2 (GD2), dams were exposed to either aerosolized OVA or phosphate buffered saline (PBS) for 1 hour. Following the 1-hour exposure, pregnant females were then exposed to UIS or clean air for 4 hours. Offspring brains were collected at postnatal days (P)15 and (P)35. Cortices and hippocampal regions were then isolated and assessed for changes in cytokines using a Luminex bead-based multiplex assay. Analyses identified changes in many cytokines across treatment groups at both timepoints in the cortex, including interleukin-1 beta (IL-1β), IL-2, IL-13, and IL-17, which remained elevated from P15 to P35 in all treatment conditions compared to controls. In the hippocampus at P15, elevations in cytokines were also identified across the treatment groups, namely interferon gamma (IFNγ) and IL-7. The combination of MAA and UIS exposure (MAA-UIS) during pregnancy resulted in an increase in microglia density in the hippocampus of offspring, as identified by IBA-1 staining. Together, these data indicate that exposure to MAA, UIS, and MAA-UIS result in changes in the neuroimmune environment of offspring that persist into adulthood.

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Outdoor air pollution exposure and the risk of asthma and wheezing in the offspring

Cited by 8 publications

References 70 publications

Choices of morbidity outcomes and concentration–response functions for health risk assessment of long-term exposure to air pollution

Choices of morbidity outcomes and concentration–response functions for health risk assessment of long-term exposure to air pollution

Characterizing the neuroimmune environment of offspring in a novel model of maternal allergic asthma and particulate matter exposure

Characterizing the Neuroimmune Environment of Offspring in a Novel Model of Maternal Allergic Asthma and Particulate Matter Exposure

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