NO2 Exposure Research Articles

The Influence of Airborne Particulate Matter on the Risk of Gestational Diabetes Mellitus: A Large Retrospective Study in Chongqing, China.

Emerging research findings suggest that airborne particulate matter might be a risk factor for gestational diabetes mellitus (GDM). However, the concentration-response relationships and the susceptible time windows for different types of particulate matter may vary. In this retrospective analysis, we employ a novel robust approach to assess the crucial time windows regarding the prevalence of GDM and to distinguish the susceptibility of three GDM subtypes to air pollution exposure. This study included 16,303 pregnant women who received routine antenatal care in 2018-2021 at the Maternal and Child Health Hospital in Chongqing, China. In total, 2482 women (15.2%) were diagnosed with GDM. We assessed the individual daily average exposure to air pollution, including PM2.5, PM10, O3, NO2, SO2, and CO based on the volunteers' addresses. We used high-accuracy gridded air pollution data generated by machine learning models to assess particulate matter per maternal exposure levels. We further analyzed the association of pre-pregnancy, early, and mid-pregnancy exposure to environmental pollutants using a generalized additive model (GAM) and distributed lag nonlinear models (DLNMs) to analyze the association between exposure at specific gestational weeks and the risk of GDM. We observed that, during the first trimester, per IQR increases for PM10 and PM2.5 exposure were associated with increased GDM risk (PM10: OR = 1.19, 95%CI: 1.07~1.33; PM2.5: OR = 1.32, 95%CI: 1.15~1.50) and isolated post-load hyperglycemia (GDM-IPH) risk (PM10: OR = 1.23, 95%CI: 1.09~1.39; PM2.5: OR = 1.38, 95%CI: 1.18~1.61). Second-trimester O3 exposure was positively correlated with the associated risk of GDM, while pre-pregnancy and first-trimester exposure was negatively associated with the risk of GDM-IPH. Exposure to SO2 in the second trimester was negatively associated with the risk of GDM-IPH. However, there were no observed associations between NO2 and CO exposure and the risk of GDM and its subgroups. Our results suggest that maternal exposure to particulate matter during early pregnancy and exposure to O3 in the second trimester might increase the risk of GDM, and GDM-IPH is the susceptible GDM subtype to airborne particulate matter exposure.

Residential Nitrogen Dioxide Exposure and Cause-Specific Cerebrovascular Mortality: An Individual-Level, Case-Crossover Study.

Existing studies have already shown a connection between nitrogen dioxide (NO2) exposure and cerebrovascular mortality. However, the differential effects of NO2 on cerebrovascular disease and its subtypes remain unclear and require further exploration. Daily stroke mortality data between 2013 and 2021 in Shanghai, China were collected. Residential daily air pollution data for each decedent were predicted from a satellite model. An individual-level, time-stratified, case-crossover design was applied to examine the relationship between NO2 exposure and cerebrovascular mortality. A combination of conditional logistic regression and distributed lag models with a maximum lag of 7 days was used for data analysis. A total of 219,147 cases of cerebrovascular mortality were recorded. Among them, the proportion of sequelae of cerebrovascular disease, hemorrhagic stroke and ischemic stroke was 50.7%, 17.1% and 27.5%, respectively. The monotonic increases in mortality risks of cerebrovascular diseases, sequelae of cerebrovascular disease and ischemic stroke were observed, without any discernible thresholds. Each 10 μg/m3 increase in NO2 concentration was associated with increments of 3.62% [95% confidence interval (CI): 2.56%, 4.69%] for total cerebrovascular mortality, 4.29% (95% CI: 2.81%, 5.80%) for sequelae of cerebrovascular disease mortality and 4.30% (95% CI: 2.30%, 6.33%) for ischemic stroke mortality. No positive associations between NO2 exposure and hemorrhagic stroke mortality were observed. A greater risk of NO2 was observed in the warm season, in patients with less than 9 years of education and in those with single marital status. The effects of NO2 were robust to mutual adjustment of co-pollutants. Short-term exposures to NO2 may increase the risk of cerebrovascular mortality, specifically for ischemic stroke and sequelae of cerebrovascular disease.

Impedance spectroscopy studies revealing the influence of ZnO-rGO heterojunction interface on NO2 sensing

Heterojunction interfaces play a very important role in improving the gas sensing properties. In our previous study through direct current (dc) measurements we showed that a synergetic balance of depletion width at ZnO-rGO interface with the Debye length leads to the improved selective NO2 response. In this paper, impedance spectroscopy is used to probe the NO2 sensing behaviour of ZnO-rGO heterostructure films as the processes of different time constants in gas/ solid interactions can be distinguished by varying the AC frequency. The Nyquist plots for ZnO-rGO films measured under ambient as well as after NO2 exposure shows that sensor response is governed by the variation in potential barrier of depletion region formed at the p-n junction between ZnO and rGO. To understand the adsorption mechanism, experimental response data measured at different NO2 concentrations were fitted using suitable adsorption kinetic models. Elovich model is found to be apt for lower concentrations where energetically different sites are involved in the adsorption process while higher concentrations are better modelled with pseudo first order kinetics that is independent of the surface coverage.

Association of prenatal exposure to PM2.5 and NO2 with gestational diabetes in Western New York

BackgroundAlthough many studies have examined the association between prenatal air pollution exposure and gestational diabetes (GDM), the relevant exposure windows remain inconclusive. We aim to examine the association between preconception and trimester-specific exposure to PM2.5 and NO2 and GDM risk and explore modifying effects of maternal age, pre-pregnancy body mass index (BMI), smoking, exercise during pregnancy, race and ethnicity, and neighborhood disadvantage. MethodsAnalyses included 192,508 birth records of singletons born to women without pre-existing diabetes in Western New York, 2004–2016. Daily PM2.5 and NO2 at 1-km2 grids were estimated from ensemble-based models. We assigned each birth with exposures averaged in preconception and each trimester based on residential zip-codes. We used logistic regression to examine the associations and distributed lag models (DLMs) to explore the sensitive windows by month. Relative excess risk due to interaction (RERI) and multiplicative interaction terms were calculated. ResultsGDM was associated with PM2.5 averaged in the first two trimesters (per 2.5 μg/m3: OR = 1.08, 95% CI: 1.01, 1.14) or from preconception to the second trimester (per 2.5 μg/m3: OR = 1.10, 95% CI: 1.03, 1.18). NO2 exposure during each averaging period was associated with GDM risk (per 10 ppb, preconception: OR = 1.10, 95% CI: 1.06, 1.14; first trimester: OR = 1.12, 95% CI: 1.08, 1.16; second trimester: OR = 1.10, 95% CI: 1.06, 1.14). In DLMs, sensitive windows were identified in the 5th and 6th gestational months for PM2.5 and one month before and three months after conception for NO2. Evidence of interaction was identified for pre-pregnancy BMI with PM2.5 (P-for-interaction = 0.023; RERI = 0.21, 95% CI: 0.10, 0.33) and with NO2 (P-for-interaction = 0.164; RERI = 0.16, 95% CI: 0.04, 0.27). ConclusionPM2.5 and NO2 exposure may increase GDM risk, and sensitive windows may be the late second trimester for PM2.5 and periconception for NO2. Women with higher pre-pregnancy BMI may be more susceptible to exposure effects.

Air pollution mortality benefits of sustained COVID-19 mobility restrictions in Australian cities

ObjectivesEmissions from road traffic, power generation and industry were substantially reduced during pandemic lockdown periods globally. Thus, we analysed reductions in traffic-related air pollution in Australian capital cities during March–April 2020 and then modelled the mortality benefits that could be realised if similar reductions were sustained by structural policy interventions. Study designSatellite, air pollution monitor and land use observations were used to estimate ground-level nitrogen dioxide (NO2) concentrations in all Australian capital cities during: (a) a typical year with no prolonged air pollution events; (b) a hypothetical sustained reduction in NO2 equivalent to the COVID-19 lockdowns. MethodsWe use the WHO recommended NO2 exposure-response coefficient for mortality (1.023, 95 % CI: 1.008–1.037, per 10 μg/m3 annual average) to assess gains in life expectancy and population-wide years of life from reduced exposure to traffic-related air pollution. ResultsWe attribute 1.1 % of deaths to anthropogenic NO2 exposures in Australian cities, corresponding to a total of 13,340 years of life lost annually. Although COVID-19-related reductions in NO2 varied widely between Australian cities during April 2020, equivalent and sustained reductions in NO2 emissions could reduce NO2-attributable deaths by 27 %, resulting in 3348 years of life gained annually. ConclusionsCOVID-19 mobility restrictions reduced NO2 emissions and population-wide exposures in Australian cities. When sustained to the same extent by policy interventions that reduce fossil fuel consumption by favouring the uptake of electric vehicles, active travel and public transport, the health, mortality and economic benefits will be measurable in Australian cities.

The association between air pollution and dementia: results from the Cognitive Function and Ageing Study II and Wales

AbstractBackgroundAir pollution has been recognised as one of the key modifiable risk factors for dementia. In the UK, there is a lack of evidence from population‐based cohort studies including older people from different backgrounds and living environments. Using two multicentre ageing cohorts in England and Wales, the aim of this study is to investigate the potential impact of air pollution on dementia in later life.MethodThis study was based on the Cognitive Function and Ageing Study (CFAS) II (2008‐2011) and Wales (2011‐2013), two longitudinal studies of people aged 65 or above across five centres in England (Cambridgeshire, Newcastle upon Tyne, Nottingham) and Wales (Gwynedd, Neath Port Talbot). A two‐year follow‐up wave was carried out for both studies. Dementia was identified using the Geriatric Mental State and its diagnostic algorithm, Automated Geriatric Examination for Computer Assisted Taxonomy (GMS‐AGEACT). Based on the participants’ postcodes at the baseline, exposure to four air pollutants in 2012, including nitrogen dioxide (NO2), ozone (O3), particulate matter with a diameter ≤10 microns (PM10) and ≤2.5 microns (PM2.5), was estimated using the Community Multiscale Air Quality pollution modelling at a resolution of 20×20 m. Multistate modelling was used to investigate the effects of air pollution exposure on risk of developing dementia over the follow‐up period, incorporating mortality (from national death certification) and adjusting for age, sex, education, study centre and area deprivation.ResultAmong the 11329 participants in CFAS II (N = 7753) and Wales (N = 3576), the median exposure was 17.7 (IQR = 11.6) µg/m3 for NO2, 43.8 (IQR = 11.1) µg/m3 for O3, 15.5 (IQR = 3.1) µg/m3 for PM10 and 10.1 (IQR = 2.8) µg/m3 for PM2.5 and large variation was observed across the five centres. Per unit increase in NO2 exposure was associated with a higher risk of dementia in CFAS II (HR: 1.07; 95%CI: 1.03, 1.12) but not the Welsh cohort (HR: 0.93; 95%CI: 0.86, 1.00) after adjustment. For the other air pollutants, the associations were unclear.ConclusionOur study suggests limited evidence for the impacts of air pollution on dementia. Other environmental factors may influence individual exposure to air pollution and altogether have a complex effect on cognitive health in later life.

Association between gestational exposure and risk of orofacial clefts: a systematic review and meta-analysis

BackgroundThe occurrence of orofacial Clefts (OFCs) is a congenital disease caused by many factors. According to recent studies, air pollution has a strong correlation with the occurrence of OFCs. However, there are still some controversies about the current research results, and there is no relevant research to review the latest results in recent years.ObjectiveIn this paper, the authors conducted a systematic review and meta-analysis to explore the correlation between ambient air pollution and the occurrence of neonatal OFCs deformity.MethodsWe searched Pubmed, Web of science, and Embase databases from the establishment of the database to May 2023. We included observational studies on the relationship between prenatal exposure to fine particulate matter 2.5 (PM2.5), fine particulate matter 10 (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), ozone (O3), carbon monoxide (CO) and the risk of cleft lip (CL), cleft palate (CP), cleft lip with or without palate (CL/P). the Newcastle-Ottawa quality assessment scale (NOS) was used to evaluate the quality of the literature. Funnel plot and Egger’s regression were used to verify the publication bias. Random effect model or fixed effect model was used to estimate the combined relative risk (RR) and 95% confidence interval (95%CI).ResultsA total of eleven studies were included in this study, including four cohort studies and seven case-control studies, including 22,453 cases of OFCs. Ten studies had low risk of bias and only one study had high risk of bias. Three studies reported that PM2.5 was positively correlated with CL and CP, with a combined RR and 95%CI of 1.287(1.174,1.411) and 1.267 (1.105,1.454). Two studies reported a positive correlation between O3 and CL, with a combined RR and 95%CI of 1.132(1.047,1.225). Two studies reported a positive correlation between PM10 and CL, with a combined RR and 95%CI of 1.108 (1.017,1.206). No association was found between SO2, CO, NO2 exposure during pregnancy and the risk of OFCs.ConclusionThe results of this study showed that there was a significant statistical correlation between exposure to PM10, PM2.5, O3 and the risk of OFCs in the second month of pregnancy. Exposure assessment, research methods and mechanisms need to be further explored.

Causal effects of exposure to ambient air pollution on cancer risk: Insights from genetic evidence

Air pollution has been increasingly linked to cancer risk. However, the genetic causality between air pollution and cancer risk remains poorly understood. To elucidate the potential roles of air pollution (NOx, NO2, PM2.5, PM course, and PM10) in the risk of 18 specific-site cancers, large-scale genome-wide association studies with a novel Mendelian randomization (MR) method were employed. Our MR analyses revealed significant associations between certain air pollutants and specific types of cancer. Specifically, a positive association was observed between NOx exposure and squamous cell lung cancer (OR: 1.96, 95%CI: 1.07–3.59, p = 0.03) as well as esophageal cancer (OR: 1.002, 95%CI: 1.001–1.003, p = 0.005). Genetically predicted NO2 exposure was found to be a risk factor for endometrial cancer (OR 1.41, 95%CI: 1.03–1.94, p = 0.03) and ovarian cancer (OR: 1.49, 95%CI: 1.14–1.95, p = 0.0037). Additionally, genetically predicted PM2.5 exposure was associated with an increased risk of ER+ breast cancer (OR: 1.24, 95%CI: 1.03–1.5, p = 0.02) and ER- breast cancer (OR: 2.57, 95%CI: 1.05–6.3, p = 0.04). PM course exposure was identified as a risk factor for glioma (OR: 487.28, 95%CI: 13.08–18,153, p = 0.0008), while PM10 exposure exerted a detrimental effect on mesothelioma (OR: 114.75, 95%CI: 1.14–11,500.11, p = 0.04) and esophageal cancer (OR: 1.01, 95%CI: 1.007–1.02, p = 0.03). These findings underscored the importance of mitigating air pollution to reduce the burden of cancer and highlight the need for further investigations to elucidate the underlying mechanisms involved in these associations.

Short-Term Exposure to Nitrogen Dioxide Modifies Genetic Predisposition in Blood Lipid and Fasting Plasma Glucose: A Pedigree-Based Study.

(1) Background: Previous studies suggest that exposure to nitrogen dioxide (NO2) has a negative impact on health. But few studies have explored the association between NO2 and blood lipids or fasting plasma glucose (FPG), as well as gene-air pollution interactions. This study aims to fill this knowledge gap based on a pedigree cohort in southern China. (2) Methods: Employing a pedigree-based design, 1563 individuals from 452 families participated in this study. Serum levels of triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDLC), high-density lipoprotein cholesterol (HDLC), and FPG were measured. We investigated the associations between short-term NO2 exposure and lipid profiles or FPG using linear mixed regression models. The genotype-environment interaction (GenoXE) for each trait was estimated using variance component models. (3) Results: NO2 was inversely associated with HDLC but directly associated with TG and FPG. The results showed that each 1 μg/m3 increase in NO2 on day lag0 corresponded to a 1.926% (95%CI: 1.428-2.421%) decrease in HDLC and a 1.400% (95%CI: 0.341-2.470%) increase in FPG. Moreover, we observed a significant genotype-NO2 interaction with HDLC and FPG. (4) Conclusion: This study highlighted the association between NO2 exposure and blood lipid profiles or FPG. Additionally, our investigation suggested the presence of genotype-NO2 interactions in HDLC and FPG, indicating potential loci-specific interaction effects. These findings have the potential to inform and enhance the interpretation of studies that are focused on specific gene-environment interactions.

Exploring the association between air pollution and Parkinson's disease or Alzheimer's disease: a Mendelian randomization study.

The correlation between air pollution and neurodegenerative diseases has garnered growing attention. Although observational studies have indicated a potential link between air pollution and neurodegenerative disease, establishing a causal relationship remains uncertain. To address this gap, we performed a two-sample Mendelian randomization analysis utilizing genetic instruments. This analysis aimed to investigate the causal connections between PM2.5, PM10, NO2, and NOX exposure and the occurrence of Parkinson's disease (PD) and Alzheimer's disease (AD). We implemented a series of filtering steps to identify suitable genetic instruments that demonstrated significant associations (P < 5 × 10-8) with PM2.5, PM10, NO2, and NOX. These instruments were derived from a comprehensive genome-wide association study (GWAS) encompassing up to 456,380 participants in the UK Biobank. To obtain summary statistics for PD (N = 482,730) and AD risk (N = 63,926), we utilized the most recent GWAS datasets available. For our primary analysis, we employed the inverse-variance weighted approach for two-sample MR. A multivariable MR (MVMR) was also performed to verify the impact of air pollution exposure on the risk of PD and AD. To ensure the robustness of our findings, sensitivity analyses and heterogeneity assessments were performed. In two-sample MR, by employing the inverse-variance weighted method, our result suggested that genetically NO2 exposure showed a significant association with an elevated risk of PD (OR = 4.07, 95% CI: 1.13 to 19.62, P = 0.034) and genetically PM10 exposure exhibited a significant association with a heightened risk of AD (OR = 1.93, 95% CI: 1.03-3.59, P = 0.040). Further MVMR analysis demonstrated that the causal effect between NO2 and PD disappeared (OR = 3.489, 95% CI: 0.01 to 2.1e + 03, P = 0.703), and only PM10 was associated with an increased risk of AD (OR = 6.500, 95% CI: 1.10 to 38.51, P = 0.039). Sensitivity analysis showed no detectable heterogeneity and pleiotropy (P > 0.05). Our findings demonstrate that NO2 and PM10 exposure may contribute to a risk of PD and AD, respectively. Future research is necessary to elucidate potential physiopathological mechanisms.

Reconsidering gas as clean energy: Switching to electricity for household cooking to reduce NO2-attributed disease burden

Nitrogen dioxide (NO2) is a prevalent air pollutant in urban areas, originating from outdoor sources, household gas consumption, and secondhand smoke. The limited evaluation of the disease burden attributable to NO2, encompassing different health effects and contributions from various sources, impedes our understanding from a public health perspective. Based on modeled NO2 exposure concentrations, their exposure–response relationships with lung cancer, chronic obstructive pulmonary disease, and diabetes mellitus, and baseline disability-adjusted life years (DALYs), we estimated that 1,675 (655–2,624) thousand DALYs were attributable to NO2 in urban China in 2019 [138 (54–216) billion Chinese yuan (CNY) economic losses]. The transition from gas to electricity for household cooking was estimated to reduce the attributable economic losses by 35%. This reduction falls within the range of reductions achieved when outdoor air meets the World Health Organization interim target 3 and air quality guidelines for annual NO2, highlighting the significance of raising awareness of gas as a polluting household energy for cooking. These findings align with global sustainable development initiatives, providing a sustainable solution to promote public health while potentially mitigating climate change.

Simultaneous decreases in NO2 levels and disparities in California during the COVID-19 pandemic

This study investigated the changes in nitrogen dioxide (NO2) air pollution levels and their disparities in California, U.S. during the pandemic of coronavirus disease 2019 (COVID-19). From pre-COVID (February 11–March 10, 2020) to peri-COVID (March 22–April 21, 2020) periods, ground-level measured NO2 concentrations decreased by 6.9 ppb (54.2%) on average across California. Our novel statistical approach showed that the meteorology-adjusted NO2 concentrations declined to a smaller extent (4.3 ppb, 34.4%), implying that the meteorological parameters helped reduce NO2 concentrations along with lockdown-related NOx emission reductions. In addition, satellite TROPOspheric Monitoring Instrument (TROPOMI) tropospheric NO2 data demonstrated substantial decreases in NO2 levels in urban (49.7% versus 16.5% in rural areas) and high-traffic (50.1%) areas. On average, 32.8%, 62.8%, and 14.9% higher TROPOMI NO2 levels were identified for socially vulnerable populations, as defined by the CalEnviroScreen 3.0, race/ethnicity, and educational attainment, respectively. The NO2 exposure differences generally decreased as average TROPOMI NO2 levels decreased during the pandemic (Pearson correlations = 0.61–0.95). From pre- to peri-COVID periods, the decreasing NO2 disparities were pronounced in relation to race/ethnicity [from 39.0 (78.6%) to 10.4 (36.7%) μmol/m2]. Despite the remaining NO2 disparities during the pandemic, our findings indicated that the mitigation of NO2 disparities (particularly racial inequity) would be achievable by the continued regulatory actions emphasizing the reduction of traffic-related NOx emissions such as electrification of passenger cars and diesel trucks.

Short-term exposure to ambient air pollution and hospital admissions for angina among older adults in South China

Ambient air pollution has been linked to an increased risk of various acute cardiovascular outcomes; however, its effects on hospital admissions for angina are yet to be evaluated. We conducted a time-stratified case-crossover study with conditional logistic regression models among 46,687 adults 60 years or older who were admitted to hospital for angina in Guangzhou, China during 2016–2019 to investigate the association of exposure to ambient particulate matter with an aerodynamic diameter ≤2.5 μm (PM2.5), particulate matter with an aerodynamic diameter ≤10 μm (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3) with hospital admissions for angina. Daily residential air pollutant exposures were extracted from a grid dataset. Each 10 μg/m3 increase of lag 0-day exposure to PM10, SO2, NO2, CO, and O3 was significantly associated with a 0.80% (95% confidential interval: 0.32%, 1.28%), 4.04% (0.34%, 7.89%), 2.47% (1.81%, 3.12%), 0.13% (0.07%, 0.19%), and −0.38% (−0.74%, −0.01%) increase in odds of admission, respectively. The association for NO2 exposure remained stable, while the associations for PM10, SO2, CO, and O3 became insignificant with adjustment for other air pollutants. The association for NO2 exposure was stronger in cool season. We estimated that up to 9.12% of angina admissions were attributable to NO2 exposure. Our findings suggest that ambient NO2 may trigger hospital admissions for angina in Chinese older adults, which highlights the importance to prevent angina by reducing individual NO2 exposures.

Ethnoracial Disparities in Nitrogen Dioxide Pollution in the United States: Comparing Data Sets from Satellites, Models, and Monitors.

In the United States (U.S.), studies on nitrogen dioxide (NO2) trends and pollution-attributable health effects have historically used measurements from in situ monitors, which have limited geographical coverage and leave 66% of urban areas unmonitored. Novel tools, including remotely sensed NO2 measurements and estimates of NO2 estimates from land-use regression and photochemical models, can aid in assessing NO2 exposure gradients, leveraging their complete spatial coverage. Using these data sets, we find that Black, Hispanic, Asian, and multiracial populations experience NO2 levels 15-50% higher than the national average in 2019, whereas the non-Hispanic White population is consistently exposed to levels that are 5-15% lower than the national average. By contrast, the in situ monitoring network indicates more moderate ethnoracial NO2 disparities and different rankings of the least- to most-exposed ethnoracial population subgroup. Validating these spatially complete data sets against in situ observations reveals similar performance, indicating that all these data sets can be used to understand spatial variations in NO2. Integrating in situ monitoring, satellite data, statistical models, and photochemical models can provide a semiobservational record, complete geospatial coverage, and increasingly high spatial resolution, enhancing future efforts to characterize, map, and track exposure and inequality for highly spatially heterogeneous pollutants like NO2.

Study on revision of standard limits for nitrogen dioxide in "Standards for indoor air quality（GB/T 18883-2022）" in China

Nitrogen dioxide (NO2) is an important indoor air pollutant, with both outdoor and indoor sources contributing to indoor NO2 exposure levels. Considering the association of high NO2 exposure with adverse health effects, the Standards for indoor air quality (GB/T 18883-2022) have been revised to further restrict indoor NO2 limit values. The 1-h average concentration limit value for NO2 has been reduced from 0.24 mg/m3 to 200 μg/m3.This study analyzed the technical contents related to the determination of the limits of indoor NO2 in Standards for Indoor Air Quality (GB/T 18883-2022), including source, exposure level, health effects, and the process and evidence basis for determining the limit value. It also proposed prospects for the direction for the implementation of the indoor NO2 standard.

Middle-term nitrogen dioxide exposure and electrocardiogram abnormalities: A nationwide longitudinal study

BackgroundRecently, professionals, such as those from the World Health Organization, have recommended a rigorous standard for nitrogen dioxide (NO2), a typical urban air pollutant affected by regular traffic emissions, based on its short-term and long-term cardiorespiratory effects. However, the association between middle-term NO2 exposure and cardiovascular disorders remains unknown. ObjectivesThis study was conducted to examine the relationship between NO2 exposure and its middle-term cardiovascular risks indicated by electrocardiogram (ECG) abnormalities. MethodWe included 61,094 subjects (132,249 visits) with repeated ECG observations based on longitudinal data from the China National Stroke Screening Survey (CNSSS). The NO2 exposure concentration was derived from a predictive model, measured as the monthly average concentration in the 6 months of preceding the ECG measurement. We used the generalized estimation equation to assess the association between NO2 exposure and ECG abnormalities. ResultFor each 10 µg/m3 increase in monthly average NO2 concentration, the odds ratio of ECG abnormalities was 1.10 (95% confidence interval [CI] 1.09–1.12) after multiple adjustments. Stratified regression analyses of urban and rural residents showed associations between middle-term NO2 exposure and ECG abnormalities in urban (OR 1.09 [95% CI 1.08–1.11]) and rural residents (OR 1.14 [95% CI 1.10–1.19]). The association was robust within different subpopulations. Associations generally remained statistically significant (OR 1.03 [95% CI 1.02–1.05]) after extra adjustment for PM2.5. Exposure-response relationship analysis revealed a nearly linear relationship between NO2 exposure and the risk for ECG abnormalities. ConclusionUsing the variation in ECG signals as a potentially reversible indicator for subclinical risk in cardiovascular systems, our study provides additional evidence on the increased risk posed by middle-term NO2 exposure. Our study showed that policies controlling for NO2 concentrations are beneficial to prevent cardiovascular diseases among Chinese adults.

Weekly prenatal PM2.5 and NO2 exposures in preterm, early term, and full term infants: Decrements in birth weight and critical windows of susceptibility

BackgroundPrevious studies have observed associations between birth weight and prenatal air pollution exposure, but there is not consensus on timing of critical windows of susceptibility. ObjectiveWe estimated the difference in birth weight among preterm, early term and full term births associated with weekly exposure to PM2.5 and NO2 throughout gestation. MethodsWe included all singleton live births in the Lower Peninsula of Michigan (United States) between 2007 and 2012 occurring at or after 32 weeks gestational age (n = 497,897). Weekly ambient PM2.5 and NO2 concentrations were estimated at maternal residences using 1-km gridded data from ensemble-based models. We utilized a distributed lag nonlinear model to estimate the difference in birth weight associated with weekly exposures from the last menstrual period (week 0) through 31 weeks gestation for preterm births; through 36 weeks gestation for early term births; and through 38 weeks gestation for full term births. ResultsIn single-pollutant models, a 5 μg/m3 increase in PM2.5 exposure was associated with a reduction in birth weight among preterm births (−37.1 g [95% confidence interval [CI]: 60.8 g, −13.5 g]); early term births (−13.5 g [95% CI: 26.2 g, −0.67 g]); and full term births (−8.23 g [95% CI: 15.8 g, −0.68 g])]. In single-pollutant models, a 10 ppb increase in NO2 exposure was associated with a −11.7 g (95% CI: 14.46 g, −8.92 g) decrement in birth weight among full term births only. In models co-adjusted for PM2.5 and NO2, PM2.5 exposure was associated with reduced birth weight among preterm births (−36.9 g [95% CI: 61.9 g, −11.8 g]) and NO2 exposure was associated with reduced birth weight among full term births (−11.8 g [95% CI: 14.7 g, −8.94 g]). The largest decrements in birth weight were associated with PM2.5 exposure between approximately 10 and 26 weeks of pregnancy; for NO2 exposure, the largest decrements in birth weight in full term births were associated with exposure between weeks 6–18. ConclusionWe observed the largest and most persistent adverse associations between PM2.5 exposure and birth weight in preterm infants, and between NO2 exposure and birth weight in full term infants. Exposure during the first half of pregnancy had a greater impact on birthweight.

Assessment of the association between ambient air pollution and stillbirth in the UK: Results from a secondary analysis of the MiNESS case-control study.

We examined whether the risk of stillbirth was related to ambient air pollution in a UK population. Prospective case-control study. Forty-one maternity units in the UK. Women who had a stillbirth ≥28 weeks' gestation (n = 238) and women with an ongoing pregnancy at the time of interview (n = 597). Secondary analysis of data from the Midlands and North of England Stillbirth case-control study only including participants domiciled within 20 km of fixed air pollution monitoring stations. Pollution exposure was calculated using pollution climate modelling data for NO2 , NOx and PM2.5 . The association between air pollution exposure and stillbirth risk was assessed using multivariable logistic regression adjusting for household income, maternal body mass index (BMI), maternal smoking, Index of Multiple Deprivation quintile and household smoking and parity. Stillbirth. There was no association with whole pregnancy ambient air pollution exposure and stillbirth risk, but there was an association with preconceptual NO2 exposure (adjusted odds ratio [aOR] 1.06, 95% CI 1.01-1.08 per microg/m3 ). Risk of stillbirth was associated with maternal smoking (aOR 2.54, 95% CI 1.38-4.71), nulliparity (aOR 2.16, 95% CI 1.55-3.00), maternal BMI (aOR 1.05, 95% CI 1.01-1.08) and placental abnormalities (aOR 4.07, 95% CI 2.57-6.43). Levels of ambient air pollution exposure during pregnancy in the UK, all of were beneath recommended thresholds, are not associated with an increased risk of stillbirth. Periconceptual exposure to NO2 may be associated with increased risk but further work is required to investigate this association.

Mitigation potential of local traffic interventions on paediatric asthma incidence in EU cities

Abstract Issue/Problem Motorised road traffic is a major contributor to Nitrogen Dioxide (NO2) emissions, contributing to the development and worsening of asthma. With a substantial and escalating prevalence of asthma in urban areas worldwide, this is an issue of public health significance. Description of the problem Deploying methods such as Random Forests and Boosted Regression Trees, this study aims to determine the potential reduction in paediatric asthma incidence in European cities that could be achieved through policy interventions targeting local traffic reductions, such as car-free days. Results In trafficked areas in European cities such as Brussels and Paris, up to 40% of asthma incidence can be attributed to NO2 exposure. Preliminary results show a potential reduction of 29% [95% CI: 20-34%], 21% [95% CI: 13-25%], and 12% [95% CI: 7-15 %] in paediatric asthma incidence in trafficked areas, central urban areas, and residential areas in Brussels, respectively. In Trafficked and Urban Background Areas in Paris, we found a potential reduction of 17% [95% CI: 11 -19%] and 13% [95% CI: 8-16%] in paediatric asthma incidence respectively. Trends and findings are consistent with several methodologies applied. Lessons Using real-world interventions such as car-free days is an innovative way to assess the mitigation potential of diseases associated with traffic. Our study highlights the public health significance of local traffic reduction policies in addressing asthma incidence in urban areas. The recommended public health actions include implementing policy interventions to reduce traffic levels and emissions in urban areas. These findings can be useful for other countries/settings facing similar issues with traffic-related air pollution and asthma incidence. The policy intervention can also positively impact other traffic-related health effects such as physical activity, noise, and availability of green spaces. Key messages • Local traffic reduction policies can significantly reduce (paediatric) asthma incidence in urban areas in large European Cities. • Reducing traffic levels reduces traffic-related air pollution and improves public health via pathways such as promoting physical activity, reducing noise, and increasing green space availability.

Short-term effects of ambient oxidation, and its interaction with fine particles on first-ever stroke: A national case-crossover study in China

Stroke is a significant global cause of disability and death, and its burden has been on the rise, while ambient air pollution has been conclusively linked to stroke incidence. However, knowledge about effects of atmospheric oxidation on stroke and its interactions with fine particles (PM2.5) are still limited. In this study, we investigated the short-term effects of ambient NO2, O3, and their combined oxidation (Owt) on first-ever stroke, based on data from the China National Stroke Screening Survey (CNSSS) conducted from 2013 to 2015. We found significant association between ambient NO2 exposure at lag0 day with first-ever stroke, with a 13.1 % (95 % CI: 3.5 %, 23.6 %) increase in the first-ever stroke risk per 10 μg/m3 exposure. We also found a significant interaction between NO2 and PM2.5 (p < 0.05): first-ever stroke risk increased 23.8 % (95 % CI: 9.6 %, 39.8 %) per 10 μg/m3 NO2 exposure in population exposed to higher PM2.5 concentrations, while no significant association was found in population exposed to lower PM2.5 concentrations. The results of stratified analyses indicated that physical inactivity enhanced the detrimental effects of O3 and Owt exposure, while smoking and transient ischemic attack (TIA) history enhanced the detrimental effects of NO2 exposure. However, TIA history appeared to mitigate the adverse effects of O3 exposure. This study is helpful to better understand the impact of ambient oxidation on stroke, as well as its interaction with PM2.5, and has implications for policies and standards for atmospheric protection and governance.