Effects Of Air Pollution Exposure Research Articles

Effects of Air Pollution on Respiratory Events and Pain Crises among Children with Sickle Cell Disease in New York City.

The disease burden of sickle cell disease (SCD) is highest among U.S. Black and Hispanic populations, who are often disproportionately represented in communities with poor air quality. There is limited data on the effects of air pollution exposure and social environmental factors on health outcomes in children with SCD. The objective of our study was to examine the associations between air pollution exposure and acute respiratory and vaso-occlusive pain crises (VOCs), and further study the associations stratifying by asthma status and neighborhood disadvantages. We conducted a retrospective study collecting data on outpatient sick and ED visits, and hospital admissions for respiratory events (i.e., respiratory tract infections, asthma exacerbation, acute chest syndrome), and hospitalizations for VOCs among children with SCD in a tertiary care center in New York City (NYC) from 2015-2018. Modeled data from the NYC Community Air Survey data using home addresses estimated street-level, annual-average exposure to air pollution (i.e., black carbon (BC), fine particulate matter (PM2.5), and nitrogen dioxide (NO2)). The area deprivation index (ADI): continuous national ranking percentile (1-100) was used, representing a composite index for neighborhood-level social disadvantage. We further dichotomized study participants at the upper tertile (high vs. low ADI). Multivariable Poisson regression in generalized estimating equation (GEE) models were used to estimate relative risks (RR), after adjusting for potential covariates. A total of 114 children with SCD were included in this study and had between 1-4 annual repeated measures of annual average air pollutants over a total of 425 visits. Overall, there were no significant associations between air pollution levels and acute respiratory and VOCs among children with SCD and when stratified by asthma status. We found significant interactions between air pollution levels and the continuous ADI variable on respiratory outpatient and frequent respiratory outpatient/ED visits (p<0.1). When stratified by high ADI, increased exposure to PM2.5 was significantly associated with more frequent respiratory outpatient/ED visits among children residing in higher ADI neighborhoods (RR (95% CI)= 1.13 (1.01, 1.27), p<0.05), but not among those in lower ADI neighborhoods. Increased exposure to NO2 was associated with more outpatient respiratory events for children in high ADI neighborhoods (RR (95%CI= 2.74 (1.24, 6.08), p<0.05), compared with low ADI neighborhoods. Air pollution exposures increased respiratory complications among children with SCD living in deprived neighborhoods.

A novel concern from two sample Mendelian randomization study: The effects of air pollution exposure on the cardiovascular, respiratory, and nervous system

BackgroundCardiovascular, respiratory, and nervous system diseases have high morbidity and mortality rates, but the causal relationship between air pollution and these diseases remains controversial. MethodsWe conducted a large-scale genome-wide association (GWAS) study using Mendelian randomization (MR) to investigate the association between air pollution like Nitrogen dioxide (NO2), Nitrogen oxides (NOX), Particulate matter with diameter<2.5μm (PM2.5), Particulate matter with diameter<10μm (PM10) and cardiovascular, respiratory, and nervous system diseases, including acute myocardial infarction, heart failure, asthma, chronic obstructive pulmonary disease (COPD), pneumonia, stroke and Parkinson's disease. This study included 337,199 patients with acute myocardial infarction, 178,726 patients with heart failure, 463,010 patients with asthma, 462,933 patients with COPD, 486,484 patients with pneumonia, 484,598 patients with stroke, and 482,730 patients with Parkinson's disease. All genetic tools were identified from GWAS. The association effects of environmental pollution and these diseases were investigated using MR analysis, sensitivity analysis with heterogeneity, pleiotropy test, and leave-one-out test. ResultsOur MR analysis showed the association between NOX and the development of COPD and stroke (Odds ratio (OR)=1.010, 95 % Confidence interval (CI): 1.000～1.020, P=0.046; OR=1.017, 95 %CI:1.003–1.031, P=0.019), the association between PM2.5 and the development of asthma, COPD and stroke (OR=1.013, 95 %CI:1.003–1.024, P=0.011; OR=1.010, 95 %CI:1.000–1.019, P=0.035; OR=1.019, 95 %CI:1.004–1.033, P=0.012). No significant associations were found between the rest of the air pollution exposures and diseases. Leave-one-out sensitivity analysis showed stable results. ConclusionsThe study clarifies the relationship between air pollution and cardiovascular, respiratory, and nervous system diseases, providing valuable evidence for environmental pollution prevention and population health monitoring, and provides a clear direction and evidence for the subsequent investigation of the association between air pollution and diseases.

Air pollutants, genetic susceptibility and the risk of schizophrenia: large prospective study.

Evidence linking air pollutants and the risk of schizophrenia remains limited and inconsistent, and no studies have investigated the joint effect of air pollutant exposure and genetic factors on schizophrenia risk. To investigate how exposure to air pollution affects schizophrenia risk and the potential effect modification of genetic susceptibility. Our study was conducted using data on 485 288 participants from the UK Biobank. Cox proportional hazards models were used to estimate the schizophrenia risk as a function of long-term air pollution exposure presented as a time-varying variable. We also derived the schizophrenia polygenic risk score (PRS) utilising data provided by the UK Biobank, and investigated the modification effect of genetic susceptibility. During a median follow-up period of 11.9 years, 417 individuals developed schizophrenia (mean age 55.57 years, s.d. = 8.68; 45.6% female). Significant correlations were observed between long-term exposure to four air pollutants (PM2.5; PM10; nitrogen oxides, NOx; nitrogen dioxide, NO2) and the schizophrenia risk in each genetic risk group. Interactions between genetic factors and the pollutants NO2 and NOx had an effect on schizophrenia events. Compared with those with low PRS and low air pollution, participants with high PRS and high air pollution had the highest risk of incident schizophrenia (PM2.5: hazard ratio = 6.25 (95% CI 5.03-7.76); PM10: hazard ratio = 7.38 (95% CI 5.86-9.29); NO2: hazard ratio = 6.31 (95% CI 5.02-7.93); NOx: hazard ratio = 6.62 (95% CI 5.24-8.37)). Long-term exposure to air pollutants was positively related to the schizophrenia risk. Furthermore, high genetic susceptibility could increase the effect of NO2 and NOx on schizophrenia risk.

Ambient Air Pollution Exposure and Adverse Outcomes Among Medicare Beneficiaries With Heart Failure.

Exposure to fine particulate matter (<2.5 um, particulate matter with an aerodynamic diameter <2.5 microns [PM2.5]) has been implicated in atherogenesis. Limited data in animal studies suggest that PM2.5 exposure leads to myocardial fibrosis and increased incidence of heart failure (HF). Whether PM2.5 is associated with adverse outcomes in patients with preexisting HF has not been widely studied. In this retrospective cohort study, Medicare patients hospitalized with first HF between 2013 and 2020 were identified from the Medicare Provider Analysis and Review Part A 100% files. Patients were linked with integrated estimates of ambient PM2.5 obtained at 1×1 km using the zip code of participants' residence. The study outcomes were all-cause death, HF, and all-cause readmissions burden. A total of 2 599 525 patients were included in this study, with 6 321 731 person-years of follow-up. Mean PM2.5 was 7.3±1.7 μg/m3. Each interquartile range of PM2.5 was associated with 0.9% increased hazard of all-cause death, 4.5% increased hazard of first HF readmission, 3.1% increased risk of HF hospitalization burden, and 5.2% increase in all-cause readmission burden, after adjusting for 11 sociodemographic and medical factors. Subgroup analyses showed that the effects were more pronounced at levels <7 μg/m3 and in patients aged <75 years, Asians, and those residing in rural areas. Ambient air pollution is associated with higher risk of adverse events in Medicare beneficiaries with established HF. These associations persist below the National Air Quality Standards (12 μg/m3), supporting that no threshold effect exists for health effects of air pollution exposure.

Male-biased vulnerability of mouse brain tryptophan/kynurenine and glutamate systems to adolescent exposures to concentrated ambient ultrafine particle air pollution

Air pollution (AP) exposures have been associated with numerous neurodevelopmental and psychiatric disorders, including autism spectrum disorder, attention deficit hyperactivity disorder and schizophrenia, all male-biased disorders with onsets from early life to late adolescence/early adulthood. While prior experimental studies have focused on effects of AP exposures during early brain development, brain development actually extends well into early adulthood. The current study in mice sought to extend the understanding of developmental brain vulnerability during adolescence, a later but significant period of brain development and maturation to the ultrafine particulate (UFPs) component of AP, considered its most reactive component. Additionally, it examined adolescent response to UFPs when preceded by earlier developmental exposures, to ascertain the trajectory of effects and potential enhancement or mitigation of adverse consequences. Outcomes focused on shared features associated with multiple neurodevelopmental disorders. For this purpose, C57Bl/6 J mice of both sexes were exposed to ambient concentrated UFPs or filtered air from PND (postnatal day) 4–7 and PND10–13, and again at PND39–42 and 45–49, resulting in 3 exposure postnatal/adolescent treatment groups per sex: Air/Air, Air/UFP, and UFP/UFP. Features common to neurodevelopmental disorders were examined at PND50. Mass exposure concentration from postnatal exposure averaged 44.34 μg/m3 and the adolescent exposure averaged 49.18 μg/m3. Male brain showed particular vulnerability to UFP exposures in adolescence, with alterations in frontal cortical and striatal glutamatergic and tryptophan/serotonergic neurotransmitters and concurrent reductions in levels of astrocytes in corpus callosum and in serum cytokine levels, with combined exposures resulting in significant reductions in corpus callosum myelination and serum corticosterone. Reductions in serum corticosterone in males correlated with reductions in neurotransmitter levels, and reductions in striatal glutamatergic function specifically correlated with reductions in corpus callosum astrocytes. UFP-induced changes in neurotransmitter levels in males were mitigated by prior postnatal exposure, suggesting potential adaptation, whereas reductions in corticosterone and in corpus callosum neuropathological effects were further strengthened by combined postnatal and adolescent exposures. UFP-induced changes in females occurred primarily in striatal dopamine systems and as reductions in serum cytokines only in response to combined postnatal and adolescent exposures. Findings in males underscore the importance of more integrated physiological assessments of mechanisms of neurotoxicity. Further, these findings provide biological plausibility for an accumulating epidemiologic literature linking air pollution to neurodevelopmental and psychiatric disorders. As such, they support a need for consideration of the regulation of the UFP component of air pollution.

Age and sex differences in the effects of short- and long-term exposure to air pollution on endothelial dysfunction

BackgroundThe effects of air pollution on endothelial function remain unclear across populations. We aimed to use brachial artery flow-mediated dilatation (FMD) to identify demographic differences in the effects of air pollution exposure on endothelial dysfunction.MethodsWe measured FMD in 850 participants from October 2016 to January 2020. Location-specific concentrations of fine particulate matter < 2.5 μm aerodynamic diameter (PM2.5), inhalable particulate matter < 10 μm aerodynamic diameter (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3) measured by fixed ambient air monitoring stations were collected for short- and long-term exposure assessment. Multiple linear regression models and restricted cubic splines were used to assess the associations before and after stratification by age and sex.ResultsThis study eventually included 828 participants [551 (66.5%) younger than 65 years and 553 (66.8%) men]. Each 10 µg/m3 increase in 7-day exposure to PM2.5 and PM10 was significantly linearly associated with a 0.07% (β = -0.07, 95% CI: -0.13 to -0.004) and 0.05% (β = -0.05, 95% CI: -0.10 to -0.004) decrease in FMD in the fully adjusted model. After full adjustment, long-term exposure to all air pollutants was significantly associated with impaired FMD. Each 10 µg/m3 increase in long-term exposure to PM2.5 and PM10 was significantly associated with a -0.18% (95% CI: -0.34 to -0.03) and − 0.23% (95% CI: -0.40 to -0.06) change in FMD, respectively. After stratification, the associations of lower FMD with long-term exposure to PM2.5, PM10, SO2, NO2, and CO significantly persisted in men and participants younger than 65 years instead of women or older participants. For short-term exposure, we observed differences consistent with long-term exposure and a stronger effect of 7-day exposure to SO2 in men due to a significant interaction effect.ConclusionShort- and long-term exposure to different air pollutants are strongly associated with decreased endothelial function, and susceptibility to air pollution varies significantly with age and sex.

Beneficial effect of residential greenness on sperm quality and the role of air pollution: A multicenter population-based study

BackgroundPoor sperm quality is a major cause of male infertility. However, evidence remains scarce on how greenness affects male sperm quality. ObjectivesTo assess the associations of residential greenness with male sperm quality and the modification effect of air pollution exposure on the relationship. MethodsA total of 78,742 samples from 33,184 sperm donors from 6 regions across China during 2014–2020 were included and analyzed. Individual residential greenness exposures of study subjects were estimated using the Normalized Difference Vegetation Index (NDVI) during the entire (0–90 lag days) and two key stages (0–37, and 34–77 lag days) of sperm development. Contemporaneous personal exposure levels to air pollutants were estimated using a spatio-temporal deep learning method. Linear mixed models were employed to assess the impact of greenspace in relation to sperm quality. The modification effect of air pollution on the greenspace-sperm quality relationship was also estimated. ResultsPer IQR increment in NDVI exposure throughout spermatogenesis were statistically associated with increasing sperm count by 0.0122 (95 % CI: 0.0007, 0.0237), progressive motility by 0.0162 (95 % CI: 0.0045, 0.0280), and total motility by 0.0147 (95 % CI: 0.0014, 0.0281), respectively. Similar results were observed when the model added air pollutants (PM1, PM2.5 or O3) for adjustment. Additionally, specific air pollutants, including PM1, PM2.5, and O3, were found to modify this association. Notably, the protective effects of greenness exposure were more pronounced at higher concentrations of PM1 and PM2.5 and lower concentrations of O3 (all Pinteraction < 0.05). Statistically significant positive effects of NDVI were observed on sperm motility in early spermatogenesis and sperm count in late spermatogenesis. ConclusionsExposure to residential greenness may have beneficial effects on sperm quality and air pollution modifies their relationship. These findings highlight the importance of adopting adaptable urban greenspace planning and policies to safeguard male fertility against environmental factors.

Air pollution and survival in patients with malignant mesothelioma and asbestos-related lung cancer: a follow-up study of 1591 patients in South Korea

BackgroundDespite significant advancements in treatments such as surgery, radiotherapy, and chemotherapy, the survival rate for patients with asbestos-related cancers remains low. Numerous studies have provided evidence suggesting that air pollution induces oxidative stress and inflammation, affecting acute respiratory diseases, lung cancer, and overall mortality. However, because of the high case fatality rate, there is limited knowledge regarding the effects of air pollution exposures on survival following a diagnosis of asbestos-related cancers. This study aimed to determine the effect of air pollution on the survival of patients with malignant mesothelioma and asbestos-related lung cancer.MethodsWe followed up with 593 patients with malignant mesothelioma and 998 patients with lung cancer identified as asbestos victims between 2009 and 2022. Data on five air pollutants—sulfur dioxide, carbon monoxide, nitrogen dioxide, fine particulate matter with a diameter < 10 μm, and fine particulate matter with a diameter < 2.5 μm—were obtained from nationwide atmospheric monitoring stations. Cox proportional hazard models were used to estimate the association of cumulative air pollutant exposure with patient mortality, while adjusting for potential confounders. Quantile-based g-computation was used to assess the combined effect of the air pollutant mixture on mortality.ResultsThe 1-, 3-, and 5-year survival rates for both cancer types decreased with increasing exposure to all air pollutants. The estimated hazard ratios rose significantly with a 1-standard deviation increase in each pollutant exposure level. A quartile increase in the pollutant mixture was associated with a 1.99-fold increase in the risk of malignant mesothelioma-related mortality (95% confidence interval: 1.62, 2.44). For lung cancer, a quartile increase in the pollutant mixture triggered a 1.87-fold increase in the mortality risk (95% confidence interval: 1.53, 2.30).ConclusionThese findings support the hypothesis that air pollution exposure after an asbestos-related cancer diagnosis can negatively affect patient survival.

Risk/benefit trade-off of habitual physical activity and air pollution on mortality: A large-scale prospective analysis in the UK Biobank

BackgroundPrevious observational studies have indicated associations of physical activity (PA) and air pollution with mortality. A few studies have evaluated air pollution and PA interactions for health. Still, the trade-off between the harmful effects of air pollution exposure and the protective effects of PA remains controversial and unclear. ObjectiveThis study aimed to investigate the joint association of air pollution and PA with mortality risks. MethodsThis prospective cohort study included 322,092 participants from 2006 to 2010 and followed up to 2021 in the UK Biobank study. The concentrations of air pollutants (2006–2010), including particulate matter (PM) with diameters <=2.5 mm (PM2.5), <=10 mm (PM10), and between 2.5 and 10 mm (PM2.5–10), and nitrogen oxides (NO2 and NOx) were obtained. Information on PA measured by the International Physical Activity Questionnaire short form (2006–2010) and wrist-worn accelerometer (2013–2015) were collected. All-cause and cause-specific mortalities were recorded. Cox proportional hazard models were used to investigate the associations of air pollution exposure and PA with mortality risks. The additive and multiplicative interactions were also examined. ResultsDuring a mean follow-up of 11.83 years, 16629 deaths were recorded. Compared with participants reporting low PA, higher PA was negatively associated with all-cause [hazard ratio (HR), 0.74; 95% CI, 0.71–0.78], cancer (HR, 0.85; 95% CI, 0.80–0.90), CVD (HR, 0.79; 95% CI, 0.71–0.87), and respiratory disease-specific mortality (HR, 0.51; 95% CI, 0.44–0.60). Exposure to PM2.5 (HR, 1.05; 95% CI, 1.00–1.09) and NOx (HR, 1.06; 95% CI, 1.02–1.10) was connected with increased all-cause mortality risk, and significant PM2.5-associated elevated risks for CVD mortality and NOx-associated elevated risks for respiratory disease mortality were observed. No obvious interaction between PA and PM2.5 or NOx exposure was detected. ConclusionsOur study provides additional evidence that higher PA and lower air pollutant levels are independently connected with reduced mortality risk. The benefits of PA are not significantly affected by long-term air pollution exposure, indicating PA can be recommended to prevent mortality regardless of air pollution levels. Our findings highlight the importance of public health policies and interventions facilitating PA and reducing air pollution in reducing mortality risks and maximizing health benefits. Future investigation is urgently needed to identify these findings in areas with severe air pollution conditions.

Reducing Indoor Particulate Air Pollution Improves Student Test Scores: A Randomized Double-Blind Crossover Study.

Short-term exposure to air pollution is associated with a decline in cognitive function. Standardized test scores have been employed to evaluate the effects of air pollution exposure on cognitive performance. Few studies aimed to prove whether air pollution is responsible for reduced test scores; none have implemented a "gold-standard" method for assessing the association such as a randomized, double-blind intervention. This study used a "gold-standard" method─randomized, double-blind crossover─to assess whether reducing short-term indoor particle concentrations results in improved test scores in college students in Tianjin, China. Participants (n = 162) were randomly assigned to one of two similar classrooms and completed a standardized English test on two consecutive weekends. Air purifiers with active or sham (i.e., filter removed) particle filtration were placed in each classroom. The filtration mode was switched between the two test days. Linear mixed-effect models were used to evaluate the effect of the intervention mode on the test scores. The results show that air purification (i.e., reducing PM) was significantly associated with increases in the z score for combined (0.11 [95%CI: 0.02, 0.21]) and reading (0.11 [95%CI: 0.00, 0.22]) components. In conclusion, a short-term reduction in indoor particle concentration led to improved test scores in students, suggesting an improvement in cognitive function.

The changing health effects of air pollution exposure for respiratory diseases: a multicity study during 2017–2022

BackgroundMultifaceted SARS-CoV-2 interventions have modified exposure to air pollution and dynamics of respiratory diseases. Identifying the most vulnerable individuals requires effort to build a complete picture of the dynamic health effects of air pollution exposure, accounting for disparities across population subgroups.MethodsWe use generalized additive model to assess the likely changes in the hospitalisation and mortality rate as a result of exposure to PM2.5 and O3 over the course of COVID-19 pandemic. We further disaggregate the population into detailed age categories and illustrate a shifting age profile of high-risk population groups. Additionally, we apply multivariable logistic regression to integrate demographic, socioeconomic and climatic characteristics with the pollution-related excess risk.ResultsOverall, a total of 1,051,893 hospital admissions and 34,954 mortality for respiratory disease are recorded. The findings demonstrate a transition in the association between air pollutants and hospitalisation rates over time. For every 10 µg/m3 increase of PM2.5, the rate of hospital admission increased by 0.2% (95% CI: 0.1–0.7%) and 1.4% (1.0–1.7%) in the pre-pandemic and dynamic zero-COVID stage, respectively. Conversely, O3-related hospitalization rate would be increased by 0.7% (0.5–0.9%) in the pre-pandemic stage but lowered to 1.7% (1.5–1.9%) in the dynamic zero-COVID stage. Further assessment indicates a shift of high-risk people from children and young adolescents to the old, primarily the elevated hospitalization rates among the old people in Lianyungang (RR: 1.53, 95%CI: 1.46, 1.60) and Nantong (RR: 1.65, 95%CI: 1.57, 1.72) relative to those for children and young adolescents. Over the course of our study period, people with underlying diseases would have 26.5% (22.8–30.3%) and 12.7% (10.8–14.6%) higher odds of having longer hospitalisation and over 6 times higher odds of deaths after hospitalisation.ConclusionsOur estimates provide the first comprehensive evidence on the dynamic pollution-health associations throughout the pandemic. The results suggest that age and underlying diseases collectively determines the disparities of pollution-related health effect across population subgroups, underscoring the urgency to identifying the most vulnerable individuals to air pollution.

AIR POLLUTION BY FINE PARTICULATE MATERIAL ON HOSPITALIZATION FOR RESPIRATORY DISEASES IN THE ELDERLY

Objective: To analyze the effects of air pollution exposure on hospitalizations for respiratory diseases in the elderly. Methods: this was an ecological time series study in Cuiabá, Mato Grosso, during the years 2015 and 2016. Daily levels of fine particulate matter PM2.5 and carbon monoxide were estimated and made available by the National Institute for Space Research. Variables related to temperature, relative humidity and adjustments for temporal trend, seasonality and calendar effects were included in the stochastic model of the ARIMA class (integrated autoregressive moving averages). Results: During the period selected for data collection, there were 1556 hospitalizations for respiratory diseases in Cuiabá. It was verified with this study that the number of cases of respiratory hospitalizations in the elderly was higher between the months of May and September 2015, despite a smaller number of occurrences, in the same period of 2016. As for the monthly average number of hospitalizations of elderly people aged 60 or over, these ranged from 41 hospitalizations in December 2016 to 103 hospitalizations in May 2015. Conclusion: The present study found an association between an increase in PM2.5 and a greater number of hospitalizations of elderly people with 60 years or older due to respiratory diseases. These results are consistent with some other studies found in other investigations on the subject.

Lifetime exposure to air pollution and academic achievement: A nationwide cohort study in Denmark

Recent research suggests a link between air pollution and cognitive development in children, and studies on air pollution and academic achievement are emerging. We conducted a nationwide cohort study in Denmark to explore the associations between lifetime exposure to air pollution and academic performance in 9th grade. The study encompassed 785,312 children born in Denmark between 1989 and 2005, all of whom completed 9th-grade exit examinations. Using linear mixed models with a random intercept for each school, we assessed the relationship between 16 years of exposure to PM2.5, PM10, and gaseous pollutants and Grade Point Averages (GPA) in exit examinations, covering subjects such as Danish literature, Danish writing, English, mathematics, and natural sciences. The study revealed that a 5 µg/m3 increase in PM2.5 and PM10 was associated with a decrease of 0.99 (95 % Confidence Intervals: −1.05, −0.92) and 0.46 (−0.50, −0.41) in GPA, respectively. Notably, these negative associations were more pronounced in mathematics and natural sciences compared to language-related subjects. Additionally, girls and children with non-Danish mothers were found to be particularly susceptible to the adverse effects of air pollution exposure. These results underscore the potential long-term consequences of air pollution on academic achievement, emphasizing the significance of interventions that foster healthier environments for children's cognitive development.

Integrating Augmented In Situ Measurements and a Spatiotemporal Machine Learning Model To Back Extrapolate Historical Particulate Matter Pollution over the United Kingdom: 1980-2019.

Historical PM2.5 data are essential for assessing the health effects of air pollution exposure across the life course or early life. However, a lack of high-quality data sources, such as satellite-based aerosol optical depth before 2000, has resulted in a gap in spatiotemporally resolved PM2.5 data for historical periods. Taking the United Kingdom as an example, we leveraged the light gradient boosting model to capture the spatiotemporal association between PM2.5 concentrations and multi-source geospatial predictors. Augmented PM2.5 from PM10 measurements expanded the spatiotemporal representativeness of the ground measurements. Observations before and after 2009 were used to train and test the models, respectively. Our model showed fair prediction accuracy from 2010 to 2019 [the ranges of coefficients of determination (R2) for the grid-based cross-validation are 0.71-0.85] and commendable back extrapolation performance from 1998 to 2009 (the ranges of R2 for the independent external testing are 0.32-0.65) at the daily level. The pollution episodes in the 1980s and pollution levels in the 1990s were also reproduced by our model. The 4-decade PM2.5 estimates demonstrated that most regions in England witnessed significant downward trends in PM2.5 pollution. The methods developed in this study are generalizable to other data-rich regions for historical air pollution exposure assessment.

Associations between air pollution exposure and empirically derived subtypes of mild cognitive impairment in older women

AbstractBackgroundExposure to air pollution in older adulthood is a novel risk factor for mild cognitive impairment (MCI). MCI is a heterogenous construct with different subtypes likely reflecting different disease etiologies. Understanding if long‐term exposure to air pollution is differentially associated with MCI subtypes may provide insight into the neurotoxic effects of air pollution exposure on the aging brain.MethodParticipants included women from the Women’s Health Initiative Memory Study. Data from 651 women without dementia who screened positive for cognitive impairment on the modified mini‐mental state examination (3MS) and a randomly selected comparison sample of 2,560 women who were cognitively intact based on the 3MS were utilized. Participants were administered the 3MS annually (1996‐2008). Those who screened positive for cognitive impairment on the 3MS completed the Consortium to Establish a Registry for Alzheimer’s Disease (CERAD) cognitive battery and the Trailmaking Test parts A and B. Average annual levels of particulate matter of aerodynamic diameter&lt;2.5 (PM2.5) and nitrogen dioxide (NO2) were estimated at the participant’s residence using regionalized national universal kriging models and averaged over the 3‐year period before the cognitive assessment. Latent class structural equation models (SEM) were constructed to identify MCI subtypes. We then examined associations between air pollution exposure and latent class membership using multinomial regression while adjusting for demographic, lifestyle, and clinical confounders.ResultFour significant MCI subtypes were identified (Figure 1): multidomain MCI (n = 147; 23%), amnestic MCI (n = 141; 22%), dysnomic/dysexecutive MCI (n = 200; 31%), and subtle MCI (n = 163; 25%). Women living in locations with higher levels of PM2.5 (per interquartile range [IQR] = 3.93 µg/m3; OR = 1.28; p = .04) or NO2 (per IQR = 9.25 ppb; OR = 1.36; p = .02) were more likely to be classified as having subtle MCI compared to normal comparisons. One IQR increase in NO2 was also associated with increased likelihood of being classified with dysnomic/dysexecutive MCI (OR = 1.38; p = .003) compared to normal comparisons.ConclusionOur study illustrates that long‐term exposure to PM2.5 and NO2 may be associated with specific subtypes of MCI. Our findings provide further evidence that air pollution may exert neurotoxic effects on brain areas underlying executive function and language ability in older women.

Effects of Air Pollution on Respiratory Events and Pain Crises Among Children with Sickle Cell Disease in New York City

Introduction: Sickle cell disease (SCD) has the highest U.S. disease burden among Black and Hispanic populations, who more commonly live in urban areas with poor ambient air quality. The effect of air pollution exposure and social environmental factors on health outcomes in SCD have not been extensively studied, especially among children, and may further contribute to health disparities. Objectives: This study aims to examine the associations between air pollution exposure and acute respiratory and pain events and to determine whether neighborhood-level social disadvantage would modify their associations. Methods: We collected retrospective data on unscheduled outpatient visits, emergency department (ED) visits, and hospital admissions for respiratory events (i.e., respiratory tract infections, asthma exacerbation, acute chest syndrome) and vaso-occlusive pain crises requiring hospitalization (VOCs) for children with SCD in a tertiary care center in New York City (NYC) from 2015-2018. A total of 114 children with SCD (Table 1) were included in this study and had between 1-4 annual repeated measures of annual average air pollutants (i.e., black carbon (BC), fine particulate matter (PM 2.5), and nitrogen dioxide (NO 2)) with a total of 425 visits. Using home addresses, modeled data from the NYC Community Air Survey data were used to estimate street-level, annual average exposure to air pollution. The area deprivation index (ADI), a composite index of neighborhood-level social disadvantage, was dichotomized at the upper tertile (higher vs lower). Multivariable Poisson regression in generalized estimating equation (GEE) models were used to estimate relative risks (RR), after adjusting for potential covariates. Results: Overall, there were no significant associations between air pollution levels and acute respiratory and pain events among children with SCD. When stratified by ADI, increased exposure to PM 2.5 and NO 2, but not BC, was significantly associated with more frequent respiratory outpatient and ED visits among children residing in higher ADI neighborhoods (RR (95%CI)= 1.13 (1.00, 1.28) and 1.43 (1.01, 2.02) for PM 2.5 and NO 2, respectively, p&amp;lt;0.05 for all), but not among those in lower ADI neighborhoods (P-value for interaction=0.2 and 0.02 for PM 2.5 and NO 2, respectively) (Figure 1). Associations of air pollution with hospital admissions and VOCs were not observed for neither high ADI nor low ADI neighborhoods (p-value&amp;gt;0.05). Conclusions: Exposure to air pollutants increased respiratory complications among children living in deprived neighborhoods.

Neurodevelopmental consequences of gestational exposure to particulate matter 10: Ultrasonic vocalizations and gene expression analysis using a bayesian approach

Air pollution has been associated with a wide range of health issues, particularly regarding cardio-respiratory diseases. Increasing evidence suggests a potential link between gestational exposure to environmental pollutants and neurodevelopmental disorders such as autism spectrum disorder. The respiratory pathway is the most commonly used exposure model regarding PM due to valid and logical reasons. However, PM deposition on food (vegetables, fruits, cereals, etc.) and water has been previously described. Although this justifies the need of unforced, oral models of exposure, preclinical studies using oral exposure are uncommon. Specifically, air pollution can modify normal brain development at genetic, cellular, and structural levels. The present work aimed to investigate the effects of oral gestational exposure to particulate matter (PM) on ultrasonic vocalizations (USV). To this end, pregnant rats were exposed to particulate matter during gestation. The body weight of the pups was monitored until the day of recording the USVs. The results revealed that the exposed group emitted more USV calls when compared to the control group. Furthermore, the calls from the exposed group were longer in duration and started earlier than those from the non-exposed group. Gene expression analyses showed that PM exposure down-regulates the expression of Gabrg2 and Maoa genes in the brain, but no effect was detected on glutamate or other neurotransmission systems. These findings suggest that gestational exposure to PM10 may be related to social deficits or other phenomena that can be analyzed with USV. In addition, we were able to detect abnormalities in the expression of genes related to different neurotransmitter systems, such as the GABAergic and monoaminergic systems. Further research is needed to fully understand the possible effects of air pollutant exposure on neurodevelopmental disorders as well as the way in which these effects are linked to differences in neurotransmission systems.

Long-term air pollution exposure, habitual physical activity, and incident chronic kidney disease

Both air pollution and physical inactivity contribute to the increased risk of incident chronic kidney disease (CKD). However, the detrimental effects of air pollution exposure could be augmented by an elevated intake of air pollutants during exercise. In the present study, we analyzed 367,978 participants who were CKD-free at baseline (2006–2010) based on the UK Biobank. Air pollutants included fine particulate matter (PM2.5 and PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOX). Physical activity (PA) was obtained by the self-reported questionnaire. Using Cox proportional hazards models, hazard ratios (HRs) for incident CKD related to air pollution, PA, and incident CKD were evaluated. During a median of 12.4 years of follow-up, 14,191 incident CKD events were documented. High PM2.5, PM10, NO2, and NOX increased CKD risks by 11 %, 15 %, 14 %, and 12 %, respectively, while moderate and high PA reduced CKD risks by 18 % and 22 %, respectively. Participants with high PA and low air pollution exposure had 29 %, 31 %, 30 %, and 30 % risks of incident CKD than those with low PA and high air pollution exposure for the four air pollutants, with multivariable-adjusted HRs of 0.71 (95 % confidence intervals [CI]: 0.65–0.76) for PM2.5, 0.69 (95 % CI: 0.64–0.75) for PM10, 0.70 (95 % CI: 0.64–0.75) for NO2, and 0.70 (95 % CI: 0.64–0.75) for NOX. No clear interactions were observed between each air pollutant exposure and PA (all P for interaction > 0.05). The findings that reducing air pollution exposure and increasing PA were both independently correlated with a diminished risk of incident CKD suggest that PA could be targeted to prevent CKD generally regardless of air pollution levels. Further research is needed in areas polluted moderately and severely to examine our findings.

The mediation effect of lipids, blood pressure and BMI between air pollutant mixture and atherosclerotic cardiovascular disease: The CHCN-BTH cohort study

BackgroundThe combine effect of air pollutant mixture on atherosclerotic cardiovascular disease (ASCVD) remain undefined. This study aims to explore the association between long-term exposure of air pollutants and ASCVD, focusing on the mediating role of lipids, blood pressure and BMI. MethodsThis study was based on the CHCN-BTH cohort study. The annual concentrations of air pollutants and PM2.5 constituents were sourced from in the Tracking Air Pollution in China (TAP) and ChinaHighAirPollutants (CHAP) datasets from 2014 to 2019. A Cox mixed-effects model was used to investigate the associations between long-term exposure of air pollutants and ASCVD. The combined impact of the air pollutant mixture was assessed using Quantile g-Computation. Stratified, sensitivity, and mediation analyses were conducted. ResultsA total of 27,134 participants aged 18–80 were recruited in the present study. We found that each IQR increase of PM2.5, PM1, NO2, O3, BC, SO42-, and OM were significantly associated with the incidence of ASCVD, the hazard ratios (HRs) and 95 % confidence interval (CI) were 1.55 (1.35, 1.78), 1.46 (1.27, 1.67), 1.30 (1.21, 1.39), 1.66 (1.41,1.95), 2.14 (1.63, 2.83), 1.65 (1.25, 2.17) and 1.92(1.52, 2.45), respectively. The combined effect of air pollutant mixture on ASCVD was 1.79 (1.46, 2.20), PM2.5 contributed 83.3 % to this combined effect. Mediation effect models suggested that air pollutants and ASCVD might be mediated through SBP, DBP, HDL-C, LDL-C, hsCRP and BMI (mediation proportion range from 1.3 % to 26.1 %), Notably, HDL-C played mediation roles of 11.3 % (7.0 %, 18.4), 26.1 % (17.7 %, 38.1 %) and 25.4 % (15.4, 47.7 %) in the effects of long-term exposure to PM2.5, PM1 and OM on ASCVD, respectively. ConclusionsLong-term, high-level air pollutant exposure was significantly associated with an elevated risk of ASCVD, particularly for PM2.5. Blood pressure, lipids and BMI, especially HDL-C, may mediate the effects of air pollutants exposure on ASCVD.

The effect of air pollution exposure on the risk of outpatient visits for periodontitis: a time-series study

ABSTRACT This study aimed to determine if air pollution affected the risk of periodontitis outpatient visits. We collected the records of 56,456 periodontitis outpatient visits in Hefei, China, from January 1, 2014 to December 31, 2021. The relationship between air pollution and periodontitis outpatient visits was evaluated using distributed lag nonlinear and generalized linear models. Additional analyses were performed, stratifying the data by age, season, and sex. Subgroup analyses showed a significantly higher risk of periodontitis outpatient visits due to NO2 exposure during the warm season compared with the cold season. Moreover, O3 exposure was associated with a lower risk of periodontitis outpatient visits in the cold season. The findings suggest that NO2 exposure is associated with an increased risk of periodontitis outpatient visits, whereas O3 exposure is associated with a decreased risk of periodontitis outpatient visits. Season is found to be an effect modifier in these associations.