Ambient Air Pollution Exposure Research Articles

Ambient air pollution exposure and incidence of cataract surgery: The prospective 3City-Alienor study.

Cataract, the leading cause of blindness worldwide, is a multifactorial disease involving oxidative stress mechanisms. The aim of our study was to investigate the relationship between air pollution exposure and the incidence of cataract surgery. The 3C-Alienor study is a population-based cohort of residents of Bordeaux, France, aged 65 years or more, recruited in 1999-2000 and followed every 2-3 years until 2017. Cataract surgery was self-reported and checked at slit-lamp by trained professionals. Average air pollution exposure (particulate matter ≤2.5 μm (PM2.5), black carbon (BC), nitrogen dioxide (NO2)) in the 10 years preceding baseline was estimated at the participants' geocoded residential address, using temporally adjusted land use regression. Associations of 10-year average air pollution exposure with incidence of cataract were estimated using Cox proportional hazard models adjusted for confounders. The study included 829 subjects without cataract surgery prior to inclusion; the mean age at inclusion was 72.6 years (standard deviation (SD): 4.2) and 61% were women. The median (Interquartile-range (IQR)) follow-up duration was 14.1 (6.4) years during which 507 participants underwent cataract surgery. Exposure to a concentration ≥40 μg/m3 of NO2 (the current regulatory limit value in Europe) was associated with incident cataract surgery (HR = 1.46, CI (1.16, 1.84), p = 0.001). No statistically significant association was found with PM2.5 and BC. Long-term exposure to a NO2 concentration ≥ 40 μg/m3 was associated with an increased incidence of cataract surgery. Complying with current European air pollution standards could reduce cataract surgery costs and improve population quality of life.

Windows of susceptibility and joint effects of prenatal and postnatal ambient air pollution and temperature exposure on asthma and wheeze in Mexican children

IntroductionPrenatal and early-life exposure to air pollution and extreme temperatures are associated with childhood asthma and wheeze. However, potential windows of susceptibility and their sex-specific and interactive effects have not been fully elucidated. We aimed to identify critical windows of susceptibility and evaluate sex-specific effects in these associations, and evaluate exposure interactions. MethodsWe analyzed data from 468 mother–child pairs enrolled in the PROGRESS birth cohort in Mexico City. Daily residential levels of PM2.5, NO2, and temperature were generated from our validated spatiotemporally resolved models from conception to age 4 years. Childhood asthma and wheeze outcomes were collected at 4–6 and 7–8 years. Distributed lag nonlinear models (DLNMs) were used to identify susceptible windows for prenatal weekly-specific and postnatal monthly-specific associations of air pollution and temperature with respiratory outcomes adjusting for covariates. To evaluate sex-specific effects, DLNMs were stratified. Joint effects were assessed using relative excess risk due to interaction and attributable proportion. ResultsMid-gestation was a critical window for both PM2.5 (weeks 20–28, cumulative OR: 1.18 [95% CI: 1.01, 1.37]; weeks 19–26, cumulative OR: 1.18 [95% CI: 1.02, 1.36]) and NO2 (weeks 18–25, cumulative OR: 1.16 [95% CI: 1.02, 1.31]) exposure, associated with higher odds of wheeze. Postnatal exposure to PM2.5 and NO2 during the first year of life was also linked to higher odds of wheeze. The warmer and colder temperatures showed mixed effects on respiratory outcomes. We observed a synergistic interaction between high PM2.5 and high temperature exposure during the first year of life, associated with higher odds of current wheeze. The associations of prenatal air pollution and temperature exposure with respiratory outcomes were more pronounced in males. ConclusionsEarly-life air pollution exposure contributes to the development of childhood asthma and wheeze, while exposure to temperature showed mixed associations with respiratory outcomes.

Air pollution exposure in vitrified oocyte donors and male recipient partners in relation to fertilization and embryo quality.

Studies on air pollution and outcomes of in vitro fertilization (IVF) have focused on couples undergoing autologous IVF, in which it is challenging to disentangle maternal and paternal exposures during gametogenesis. We sought to evaluate the independent associations between air pollution exposure during oogenesis and spermatogenesis on fertilization and embryo quality in non-identified donor oocyte IVF cycles. Our study included 500 oocyte donors and 915 male recipient partners who contributed 1,095 oocyte thaw cycles (2008-2019). Daily ambient air pollutant exposure was estimated using spatio-temporal models based on residential address and averaged over folliculogenesis (i.e., three months prior to initiation of controlled ovarian stimulation), controlled ovarian stimulation, and spermatogenesis (i.e., 72days prior to oocyte thaw). We used multivariable generalized estimating equations to estimate the adjusted odds ratios (aOR) and 95% confidence intervals (CI) for an interquartile range increase in pollutant exposure in relation to the proportion of oocytes surviving thaw, oocytes fertilized, and usable embryos. Oocyte donors with higher exposure to organic carbon (OC) (aOR=0.86 95%CI 0.79,0.94) and particulate matter<10µm (aOR=0.69 95%CI 0.54,0.90) during folliculogenesis had a lower proportion of oocytes surviving thaw. During ovarian stimulation, higher particulate matter<2.5µm (aOR=0.78 95%CI 0.66, 0.91), nitrate (aOR=0.83 95% CI 0.69,0.99), and OC (aOR=0.86 95% CI 0.80,0.93) exposure was associated with a lower proportion of surviving oocytes while nitrogen dioxide (aOR=1.11 95%CI 1.00,1.23) and ozone (aOR=1.19 95%CI 1.04,1.37) exposure was associated with a higher proportion of fertilized oocytes and usable embryos. Elemental carbon (aOR=0.93 95%CI 0.87,1.00) and OC (aOR=0.95 95%CI 0.90,1.00) exposure during spermatogenesis was associated with a slightly lower proportion of usable embryos. On the day of oocyte thaw, higher ambient OC at the IVF clinic was associated with lower oocyte survival and higher ozone was associated with lower fertilization. Both maternal and paternal air pollution exposures during gametogenesis have independent, largely detrimental, effects on early embryological outcomes.

Association Between Long-Term Exposure to Ambient Air Pollution and Fasting Blood Glucose: A Systematic Review and Meta-Analysis

Increasing studies are indicating a potential association between ambient air pollution exposure and fasting blood glucose (FBG), an indicator of prediabetes and diabetes. However, there is inconsistency within the existing literature. The aim of this study was to summarize the associations of exposures to particulate matters (PMs) (with aerodynamic diameters of ≤1 μm (PM1), ≤2.5 μm (PM2.5), and ≤10 μm (PM10), respectively) and gaseous pollutants (sulfur dioxide (SO2), nitrogen dioxide (NO2) and ozone (O3)) with FBG based on the existing epidemiological research for a better understanding of the relationship between air pollution and diabetes. Up to 2 July 2024, we performed a comprehensive literature retrieval from various electronic databases (PubMed, Web of Science, Scopus, and Embase). Random-effect and fixed-effect models were utilized to estimate the pooled percent changes (%) and 95% confidence intervals (CIs). Then, subgroup meta-analyses and meta-regression analyses were applied to recognize the sources of heterogeneity. There were 33 studies eligible for the meta-analysis. The results showed that for each 10 μg/m3 increase in long-term exposures to PM1, PM2.5, PM10, and SO2, the pooled percent changes in FBG were 2.24% (95% CI: 0.54%, 3.96%), 1.72% (95% CI: 0.93%, 2.25%), 1.19% (95% CI: 0.41%, 1.97%), and 0.52% (95% CI:0.40%, 0.63%), respectively. Long-term exposures to ambient NO2 and O3 were not related to alterations in FBG. In conclusion, our findings support that long-term exposures to PMs of various aerodynamic diameters and SO2 are associated with significantly elevated FBG levels.

Climate Change Impacts on Respiratory Health: Bridging Inequalities in Children and Adults

Abstract Respiratory diseases rank as the third leading global cause of mortality, with climate change exacerbating their prevalence and severity. Wild fires, floods, extreme heat events, infectious diseases, urban air pollution and aeroallergen exposure contribute to respiratory health deterioration. Vulnerable populations, including individuals with pre-existing lung conditions and children, bear a disproportionate burden of these effects. We centrepiece the connection of climate change to respiratory health inequalities, while bridging the evidence gap regarding increasing extreme heat and cold events, ambient and indoor air pollution exposure with significant ramifications on respiratory health. Specifically, we will showcase research on the tailored, multidisciplinary NCD prevention package named FRESHAIR4Life, targeting air pollution exposure in mid- to late adolescents from disadvantaged populations. Given the high burden of non-communicable diseases (NCDs) and air pollution exposure as major contributors, urgent preventive interventions are required, particularly in disadvantaged populations. Initiating preventive interventions during adolescence is considered an optimal window of opportunity for long-term health benefits. Furthermore, we will present a robust evidence base delineating climate change’s impact on lung health among vulnerable European populations. We will discuss how narratives on climate-induced lung health issues are co-created with affected communities and stakeholders to facilitate policy translation. The aim of these presentations is to break silos among health professionals, fostering collaboration from the respiratory community to the public health community. Through lung health collaborations we seek to deepen understanding and catalyze action to address the intersection of climate change, respiratory health, and inequalities, ultimately working towards a healthier and more equitable health for all.

Ambient air pollution exposure is associated with liver fat and stiffness in Latino youth with a more pronounced effect in those with PNPLA3 genotype and more advanced liver disease

BackgroundExposure to ambient air pollutants has emerged as a risk for metabolic-dysfunction associated steatotic liver disease (MASLD). ObjectivesWe sought to examine associations between short-term (prior month) and long-term (prior year) ambient air pollution exposure with hepatic fat fraction (HFF) and liver stiffness in Latino youth with obesity. A secondary aim was to investigate effect modification by patatin-like phospholipase domain-containing protein 3 (PNPLA3) genotype and liver disease severity. MethodsData was analyzed from 113 Latino youth (age 11–19) with obesity in Southern California. Individual exposure to particulate matter with aerodynamic diameter ≤ 2.5μm (PM2.5), ≤ 10μm (PM10), nitrogen dioxide (NO2), 8-hour maximum ozone (8hrMax-O3), 24-hr O3, and redox-weighted oxidative capacity (Oxwt) were estimated using residential address histories and United States Environmental Protection Agency air quality observations. HFF and liver stiffness were measured using magnetic resonance imaging. Linear models were used to determine associations between short-term and long-term exposure to air pollutants with HFF and liver stiffness. Modification by PNPLA3 and liver disease severity was then examined. ResultsShort-term exposure to 8hrMax-O3 was positively associated with HFF. Relationships between air pollution exposure and HFF were not impacted by PNPLA3 genotype or liver disease severity. Long-term exposure to 8hrMax-O3 and Oxwt were positively associated with liver stiffness. Associations between air pollution exposure and liver stiffness depended on PNPLA3 genotype, such that individuals with GG genotypes exhibited stronger, more positive relationships between short-term exposure to PM10, 8hrMax-O3, 24-hr O3, and Oxwt and liver stiffness than individuals with CC/CG genotypes. In addition, relationships between short-term exposure to NO2 and liver stiffness were stronger in those with severe liver disease. DiscussionAir pollution exposure may be a risk factor for liver disease among Latino youth with obesity, particularly in those with other preexisting risks for liver damage.

Outdoor Air Pollution Relates to Amygdala Subregion Volume and Apportionment in Early Adolescents.

Outdoor air pollution is associated with an increased risk for psychopathology. Although the neural mechanisms remain unclear, air pollutants may impact mental health by altering limbic brain regions, such as the amygdala. Here, we examine the association between ambient air pollution exposure and amygdala subregion volumes in 9-10-year-olds. Cross-sectional Adolescent Brain Cognitive Development SM (ABCD) Study ® data from 4,473 participants (55.4% male) were leveraged. Air pollution was estimated for each participant's primary residential address. Using the probabilistic CIT168 atlas, we quantified total amygdala and 9 distinct subregion volumes from T1- and T2-weighted images. First, we examined how criteria pollutants (i.e., fine particulate matter [PM 2.5 ], nitrogen dioxide, ground-level ozone) and 15 PM 2.5 components related with total amygdala volumes using linear mixed-effect (LME) regression. Next, partial least squares correlation (PLSC) analyses were implemented to identify relationships between co-exposure to criteria pollutants as well as PM 2.5 components and amygdala subregion volumes. We also conducted complementary analyses to assess subregion apportionment using amygdala relative volume fractions (RVFs). No significant associations were detected between pollutants and total amygdala volumes. Using PLSC, one latent dimension (LD) (52% variance explained) captured a positive association between calcium and several basolateral subregions. LDs were also identified for amygdala RVFs (ranging from 30% to 82% variance explained), with PM 2.5 and component co-exposure associated with increases in lateral, but decreases in medial and central, RVFs. Fine particulate and its components are linked with distinct amygdala differences, potentially playing a role in risk for adolescent mental health problems.

Early life air pollution exposures and thyroid function in children: A prospective cohort study

Studies on early life ambient air pollution exposures and childhood thyroid function are scarce. This study aimed to evaluate the relationships between early life fine particulate matter (≤2.5 μm; PM2.5) and nitrogen dioxide (NO2) exposures and thyroid function in children. We measured the levels of thyrotropin, triiodothyronine, and free thyroxine in children (n = 684) residing in a rural Korean area at age 2, 4, 6, or 8 years from 2012 to 2020 in the Environment and Development of Children cohort. The relationship between residential average exposure levels of PM2.5 and NO2 during pregnancy and 1-year average levels before visit and thyroid function during childhood were analyzed. Inverse association between increases of 10 μg/m3 in PM2.5 during the first trimester and thyrotropin levels at aged 4 (β, −0.12; 95% CI: −0.22, −0.02) and 6 years (β, −0.16; 95% CI: −0.26, −0.06) were observed. No association was found between PM2.5 exposure during the second and third trimester and childhood TSH levels. Childhood PM2.5 exposure was positively associated with thyrotropin rise at aged 4 (β, 0.2; 95% CI: 0.06, 0.35) and 6 years (β, 0.16; 95% CI: 0.02, 0.29) and inversely related with free thyroxine levels at aged 8 years (β, −0.04; 95% CI: −0.07, −0.01). No relationship between NO2 exposure and thyroid function was found. In conclusion, association between PM2.5 exposure and childhood thyrotropin levels varied depending on exposure timing. Early gestational exposure showed an inverse relationship, whereas childhood exposure were positively associated with childhood thyrotropin levels. The long-term effects of early life air pollution exposure and underlying mechanisms should be investigated in future studies.

Exposure to Air Pollutants and Myocardial Infarction Incidence: A UK Biobank Study Exploring Gene-Environment Interaction.

Unraveling gene-environment interaction can provide a novel insight into early disease prevention. Nevertheless, current understanding of the interplay between genetic predisposition and air pollution in relation to myocardial infarction (MI) risk remains limited. Furthermore, the potential long-term influence of air pollutants on MI incidence risk warrants more conclusive evidence in a community population. We investigated interactions between genetic predisposition and exposure to air pollutants on MI incidence. This study incorporated a sample of 456,354 UK Biobank participants and annual mean air pollution (, , , and ) from the UK Department for Environment, Food and Rural Affairs (2006-2021). The Cox proportional hazards model was employed to explore MI incidence after chronic air pollutants exposure. By quantifying genetic risk through the calculation of polygenic risk score (PRS), this study further examined the interactions between genetic risk and exposure to air pollutants in the development of MI on both additive and multiplicative scales. Among 456,354 participants, 9,114 incident MI events were observed during a median follow-up of 12.08 y. Chronic exposure to air pollutants was linked with an increased risk of MI occurrence. Specifically, the hazard ratios (per interquartile range) were 1.12 (95% CI: 1.10, 1.13) for , 1.20 (95% CI: 1.19, 1.22) for , 1.13 (95% CI: 1.12, 1.15) for , and 1.12 (95% CI: 1.11, 1.13) for . In terms of the joint effects, participants with high PRS and high level of air pollution exposure exhibited the greatest risk of MI among all study participants ( to 324%). Remarkably, both multiplicative and additive interactions were detected in the ambient air pollutants exposure and genetic risk on the incidence of MI. There were interactions between exposure to ambient air pollutants and genetic susceptibility on the risk of MI onset. Moreover, the joint effects of these two exposures were greater than the effect of each factor alone. https://doi.org/10.1289/EHP14291.

Ambient Air Pollution Exposure and Outcomes in Patients Receiving Lung Transplant

Elevated ambient fine particulate matter (PM2.5) air pollution exposure has been associated with poor health outcomes across several domains, but its associated outcomes among lung transplant recipients are poorly understood. To investigate whether greater PM2.5 exposure at the zip code of residence is associated with a higher hazard for mortality and graft failure in patients with lung transplants. This retrospective cohort study used panel data provided by the United Network for Organ Sharing, which includes patients receiving transplants across all active US lung transplant programs. Adult patients who received lung transplants between May 2005 and December 2016 were included, with a last follow-up of September 10, 2020. Data were analyzed from September 2022 to May 2023. Zip code-level annual PM2.5 exposure was constructed using previously published North American estimates. The primary outcome was time to death or lung allograft failure after lung transplant. A gamma shared frailty Cox proportional hazards model was used to produce unadjusted and adjusted hazard ratios (HRs) to estimate the association of zip code PM2.5 exposure at the time of transplant with graft failure or mortality. Among 18 265 lung transplant recipients (mean [SD] age, 55.3 [13.2] years; 7328 female [40.2%]), the resident zip code's annual PM2.5 exposure level was greater than or equal to the Environmental Protection Agency (EPA) standard of 12μg/m3 for 1790 patients (9.8%) and less than the standard for 16 475 patients (90.2%). In unadjusted analysis, median graft survival was 4.87 years (95% CI, 4.57-5.23 years) for recipients living in high PM2.5 areas and 5.84 years (95% CI, 5.71-5.96 years) for recipients in the low PM2.5 group. Having an annual PM2.5 exposure level greater than or equal to the EPA standard 12 μg/m3 was associated with an increase in the hazard of death or graft failure (HR, 1.11; 95% CI, 1.05-1.18; P < .001) in the unadjusted analysis and after adjusting for covariates (HR, 1.08; 95% CI, 1.01-1.15; P = .02). Each 1 μg/m3 increase in exposure was associated with an increase in the hazard of death or graft failure (adjusted HR, 1.01; 95% CI, 1.00-1.02; P = .004) when treating PM2.5 exposure as a continuous variable. In this study, elevated zip code-level ambient PM2.5 exposure was associated with an increased hazard of death or graft failure in lung transplant recipients. Further study is needed to better understand this association, which may help guide risk modification strategies at individual and population levels.

A genome-wide gene-environmental interaction study identified novel loci for the relationship between ambient air pollution exposure and depression, anxiety

BackgroundGenetic factors and environmental exposures, including air pollution, contribute to the risk of depression and anxiety. While the association between air pollution and depression and anxiety has been established in the UK Biobank, there has been limited research exploring this relationship from a genetic perspective. MethodsBased on individual genotypic and phenotypic data from a cohort of 104,385 participants in the UK Biobank, a polygenic risk score for depression and anxiety was constructed to explore the joint effects of nitric oxide (NO), nitrogen dioxide (NO2), particulate matter (PM) with a diameter of ⩽2.5 μm (PM2.5) and 2.5–10 μm (PMcoarse) with depression and anxiety by linear and logistic regression models. Subsequently, a genome-wide gene-environmental interaction study (GWEIS) was performed using PLINK 2.0 to identify the genes interacting with air pollution for depression and anxiety. ResultsA substantial risk of depression and anxiety development was detected in participants exposed to the high air pollution concomitantly with high genetic risk. GWEIS identified 166, 23, 18, and 164 significant candidate loci interacting with NO, NO2, PM2.5, and PMcoarse for Patient Health Questionnaire-9 (PHQ-9) score, and detected 44, 10, 10, and 114 candidate loci associated with NO, NO2, PM2.5, and PMcoarse for General Anxiety Disorder (GAD-7) score, respectively. And some significant genes overlapped among four air pollutants, like TSN (rs184699498, PNO2 = 3.47 × 10−9; rs139212326, PPM2.5 = 1.51 × 10−8) and HSP90AB7P(rs150987455, PNO2 = 1.63 × 10−11; rs150987455, PPM2.5 = 7.64 × 10−11), which were common genes affecting PHQ-9 score for both NO2 and PM2.5. ConclusionOur study identified the joint effects of air pollution with genetic susceptibility on the risk of depression and anxiety, and provided several novel candidate genes for the interaction, contributing to an understanding of the genetic architecture of depression and anxiety.

Exposure to ambient particulate matter and ovarian reserve impairment among reproductive age women in China

Ovarian aging, characterized by a decline in ovarian reserve, is a critical concern in female reproductive health. However, the evidence linking ambient air pollution exposure with ovarian reserve impairment remains limited. We aimed to estimate the association between exposure to fine particulate matter (PM2.5) and respirable particulate matter (PM10) and key indicators of ovarian reserve, including antral follicle count (AFC), ovarian volume (OV), anti-Müllerian hormone (AMH), follicle-stimulating hormone (FSH), estradiol (E2), luteinizing hormone (LH), FSH/LH ratio, and inhibin B (INHB). The cohort consisted of women attending an infertility clinic at the Tongji Reproductive and Environmental (TREE) study between 2018 and 2020. We used multivariate linear and Poisson regression models to estimate the association between PM2.5 and PM10 exposure and these ovarian reserve indicators. Our results showed that PM2.5 and PM10 exposure were associated with a reduction in AFC and an increase in E2 levels, highlighting the adverse effects of ambient air pollution on ovarian reserve. Our findings have important public health implications, emphasizing the urgent need for interventions to safeguard female reproductive health and reduce exposure to ambient air pollution.

Interactive effect of air pollution and genetic risk of depression on processing speed by resting-state functional connectivity of occipitoparietal network

BackgroundAir pollution, a reversible environmental factor, was significantly associated with the cognitive domains that are impaired in major depressive disorder (MDD), notably processing speed. Limited evidence explores the interactive effect of air pollution and the genetic risk of depression on cognition. This cross-sectional study aims to extend the research by specifically examining how this interaction influences depression-related cognitive impairment and resting-state brain function.MethodsEligible participants were 497 healthy adult volunteers (48.7% males, mean age 24.5) living in Beijing for at least 1 year and exposed to relatively high air pollution from the local community controlling for socioeconomic and genomic. Six months’ ambient air pollution exposures were assessed based on residential addresses using monthly averages of fine particulate matter with a diameter of less than or equal to 2.5 μm (PM2.5). A cross-sectional analysis was conducted using functional magnetic resonance imaging (fMRI) and cognitive performance assessments. The polygenic risk score (PRS) of MDD was used to estimate genetic susceptibility.ResultsUsing a general linear model and partial least square regression, we observed a negative association between resting-state local connectivity in precuneus and PRS-by-PM2.5 interactive effect (PFWE = 0.028), indicating that PM2.5 exposure reduced the spontaneous activity in precuneus in individuals at high genetic risk for MDD. DNA methylation and gene expression of the SLC30A3 gene, responsible for maintaining zinc-glutamate homeostasis, was suggestively associated with this local connectivity. For the global functional connectivity, the polygenic risk for MDD augmented the neural impact of PM2.5 exposure, especially in the frontal-parietal and frontal-limbic regions of the default mode network (PFDR < 0.05). In those genetically predisposed to MDD, increased PM2.5 exposure positively correlated with resting-state functional connectivity between the left angular gyrus and left cuneus gyrus. This connectivity was negatively associated with processing speed.ConclusionsOur cross-sectional study suggests that air pollution may be associated with an increased likelihood of cognitive impairment in individuals genetically predisposed to depression, potentially through alterations in the resting-state function of the occipitoparietal and default mode network.

Assessment of short-term effects of ambient air pollution exposure on osteoarthritis outpatient visits

The association of short-term ambient air pollution exposure with osteoarthritis (OA) outpatient visits has been unclear and no study has assessed the modifying roles of district-level characteristics in the association between ambient air pollution exposure and OA outpatient visits. We investigated the cumulative associations of ambient air pollution exposure with daily OA outpatient visits and vulnerable factors influencing the associations using data from 16 districts of Beijing, China during 2013–2019. A total of 18,351,795 OA outpatient visits were included in the analyses. An increase of 10 μg/m3 in fine particulate matter (PM2.5), inhalable particulate matter (PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2), maximum 8-hour moving-average ozone (8 h-O3), and 0.1 mg/m3 in carbon monoxide (CO) at representative lag days were associated with significant increases of 0.31 %, 0.06 %, 0.77 %, 0.87 %, 0.30 %, and 0.48 % in daily OA outpatient visits, respectively. Considerable OA outpatient visits were attributable to short-term ambient air pollution exposure. In addition, low temperature and high humidity aggravated ambient air pollution associated OA outpatient visits. District-level characteristics, such as population density, green coverage rate, and urbanization rate modified the risk of OA outpatient visits associated with air pollution exposure. These findings highlight the significance of controlling ambient air pollution during the urbanization process, which is useful in policy formation and implementation.

Is Medium-term Exposure to Ambient Air Pollution a Risk Factor for Parkinson’s Disease?

ObjectivesThis study used Census data from Northern Ireland linked to administrative data on prescriptions between 2010 and 2016, to examine the association between ambient air pollution exposure and the risk of Parkinson’s Disease (PD) onset. It contributes to this literature by providing new evidence in a comparatively low pollution context, using rich and nationally representative cohort data with comprehensive information on Parkinson’s Disease medications dispensed over an extended period. ApproachWe estimated Cox Proportional Hazards models for the association between pollution exposure and PD onset as proxied by first receipt of PD medication, controlling extensively for potentially confounding factors at the neighbourhood, household, and individual levels. Estimates are presented in the form of hazard ratios for the effect of medium-term PM2.5 exposure on the risk of PD onset. ResultsThere was a clear unadjusted association between medium-term exposure to ambient pollution and the risk of developing PD, with those experiencing higher exposures being at greater risk. Once individual, household and neighbourhood confounders were adjusted for, however, we found no evidence supporting such associations. However, there was evidence of a positive association with both PM2.5 and NO2 exposure for sub-samples by age and education. ConclusionsThis study contributes to an emerging literature examining the association between ambient PM2.5 pollution and onset of PD. Despite finding an unconditional association, we find no evidence for an association once individual, family and contextual characteristics are controlled for, at least in the relatively low-pollution context of Northern Ireland.

Prenatal exposure to ambient air pollution and persistent postpartum depression

BackgroundAmbient air pollution during pregnancy has been linked with postpartum depression up to 12 months, but few studies have investigated its impact on persistent depression beyond 12 months postpartum. This study aimed to evaluate prenatal ambient air pollution exposure and the risk of persistent depression over 3 years after childbirth and to identify windows of susceptibility. MethodsThis study included 361 predominantly low-income Hispanic/Latina participants with full-term pregnancies in the Maternal and Developmental Risks from Environmental and Social Stressors (MADRES) cohort. We estimated daily residential PM2.5, PM10, NO2, and O3 concentrations throughout 37 gestational weeks using inverse-distance squared spatial interpolation from monitoring data and calculated weekly averaged levels. Depression was assessed by the 20-item Center for Epidemiologic Studies-Depression (CES-D) scale at 12, 24, and 36 months postpartum, with persistent postpartum depression defined as a CES-D score ≥16 at any of these timepoints. We performed robust Poisson log-linear distributed lag models (DLM) via generalized estimating equations (GEE) to estimate the adjusted risk ratio (RR). ResultsDepression was observed in 17.8 %, 17.5 %, and 13.4 % of participants at 12, 24, and 36 months, respectively. We found one IQR increase (3.9 ppb) in prenatal exposure to NO2 during the identified sensitive window of gestational weeks 13–29 was associated with a cumulative risk ratio of 3.86 (95 % CI: 3.24, 4.59) for persistent depression 1–3 years postpartum. We also found one IQR increase (7.4 μg/m3) in prenatal exposure to PM10 during gestation weeks 12–28 was associated a cumulative risk ratio of 3.88 (95 % CI: 3.04, 4.96) for persistent depression. No clear sensitive windows were identified for PM2.5 or O3. ConclusionsMid-pregnancy PM10 and NO2 exposures were associated with nearly 4-fold increased risks of persistent depression after pregnancy, which has critical implications for prevention of perinatal mental health outcomes.

Ambient air pollution, low-grade inflammation, and lung function: Evidences from the UK Biobank

The associations of ambient air pollution exposure and low-grade inflammation with lung function remain uncertain. In this study, 276,289 subjects were enrolled in the UK Biobank. Individual exposure to ambient air pollution (including nitrogen dioxide [NO2], nitrogen oxides [NOx]), and particulate matter [PM2.5, PM10, PMcoarse]) were estimated by using the land-use regression model. Forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1) were tested, and low-grade inflammation score (INFLA score) was calculated for each subject. In this cross-sectional study, the median concentrations of air pollution were 9.89 µg/m3 for PM2.5, 15.98 µg/m3 for PM10, 6.09 µg/m3 for PMcoarse, 25.60 µg/m3 for NO2, and 41.46 µg/m3 for NOx, respectively. We observed that PM2.5, PM10, PMcoarse, NO2, NOx was negatively associated with lung function. Besides, significant positive associations between PM exposure and low-grade inflammation were noted. Per interquartile range (IQR) increase in PM2.5, PM10, and PMcoarse was related to higher INFLA score, and the β (95 % CI) was 0.06 (0.03, 0.08), 0.03 (0.02, 0.05), and 0.03 (0.01, 0.04), respectively. Additionally, we found significant negative associations between INFLA scores and lung function. One-unit increase in INFLA score was linked with 12.41- and 11.31-ml decreases in FVC and FEV1, respectively. Compared with individuals with low air pollution exposure and low INFLA scores, participants with high air pollution and high INFLA scores had the lowest FVC and FEV1. Additionally, we observed that INFLA scores could modify the relationships of PM2.5, NO2, and NOx with FVC and FEV1 (Pinteraction <0.05). The negative impact of air pollutants on lung function was more pronounced in subjects with high INFLA scores in comparison to those with low INFLA scores. In conclusion, we demonstrated negative associations between ambient air pollution and lung function, and the observed associations were strengthened and modified by low-grade inflammation.

The effects of ambient air pollution exposure on Thoroughbred racehorse performance.

Limited research exists on impacts of air pollution on non-human mammals, particularly animal athletes such as Thoroughbred racehorses. Athletes have a greater risk of exposure as heightened exertion and increased airflow carry more pollutants deeper into the respiratory tract. To provide insights into the impact of ambient air pollution, particularly fine particulate matter (PM2.5), on race speed. Retrospective observational study. Data were obtained from The Jockey Club Information Systems, covering 31 407 winning races by Thoroughbred horses in California spanning 10 years (2011-2020) and evaluated the association between air pollution and winning race speeds. For race days, we collected PM2.5 data from the nearest U.S. Environmental Protection Agency (EPA) monitoring site within 100 km of each racetrack (n = 12). We assessed the associations between daily average PM2.5 concentrations and speed of winning horses with linear mixed effects regression. We adjusted for horse characteristics, race-related covariates, temporal indicators (e.g., year), other air pollutants and temperature. We conducted sensitivity analyses by adjusting extreme air pollution days by reassigning values to the 95th percentile value and conducting linear mixed effects regression on series of datasets with incremental cutpoints of PM2.5. In the cutpoint analysis, we found that for PM2.5 between 4 and 23.6 μg/m3, speed decreased 0.0008 m/s (95% CI: -0.0014562 to -0.00018) for every 1 μg/m3 increase of PM2.5. Limitations include the use of offsite monitors leading to imprecise exposure measurements, not using training practice data, and generalisability as the study focuses on California racetracks. This study highlights the need to create advisories to safeguard the performance of horses during periods of poor air quality. Further research is recommended to explore additional factors influencing the relationship between air pollution and equine welfare.

Associations between Changes in Exposure to Air Pollutants due to Relocation and the Incidence of 14 Major Disease Categories and All-Cause Mortality: A Natural Experiment Study.

Though observational studies have widely linked air pollution exposure to various chronic diseases, evidence comparing different exposures in the same people is limited. This study examined associations between changes in air pollution exposure due to relocation and the incidence and mortality of 14 major diseases. We included 50,522 participants enrolled in the UK Biobank from 2006 to 2010. Exposures to particulate matter with a diameter (), particulate matter with a diameter (), nitrogen oxides (), nitrogen dioxide (), and sulfur dioxide () were estimated for each participant based on their residential address and relocation experience during the follow-up. Nine exposure groups were classified based on changes in long-term exposures due to residential mobility. Incidence and mortality of 14 major diseases were identified through linkages to hospital inpatient records and death registries. Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for incidence and mortality of the 14 diseases of interest. During a median follow-up of 12.6 years, 29,869 participants were diagnosed with any disease of interest, and 3,144 died. Significantly increased risk of disease and all-cause mortality was observed among individuals who moved from a lower to higher air polluted area. Compared with constantly low exposure, moving from low to moderate exposure was associated with increased risk of all 14 diseases but not for all-cause mortality, with adjusted HRs (95% CIs) ranging from 1.18 (1.05, 1.33) to 1.48 (1.30, 1.69); moving from low to high areas increased risk of all 14 diseases: infections [1.37 (1.19, 1.58)], blood diseases [1.57 (1.34, 1.84)], endocrine diseases [1.77 (1.50, 2.09)], mental and behavioral disorders [1.93 (1.68, 2.21)], nervous system diseases [1.51 (1.32, 1.74)], ocular diseases [1.76 (1.56, 1.98)], ear disorders [1.58 (1.35, 1.86)], circulatory diseases [1.59 (1.42, 1.78)], respiratory diseases [1.51 (1.33, 1.72)], digestive diseases [1.74 (1.58, 1.92)], skin diseases [1.39 (1.22, 1.58)], musculoskeletal diseases [1.62 (1.45, 1.81)], genitourinary diseases [1.54 (1.36, 1.74)] and cancer [1.42 (1.24, 1.63)]. We observed similar associations for and with 14 diseases (but not with all-cause mortality); increases in and were positively associated with 14 diseases and all-cause mortality. This study supports potential associations between ambient air pollution exposure and morbidity as well as mortality. Findings also emphasize the importance of maintaining consistently low levels of air pollution to protect the public's health. https://doi.org/10.1289/EHP14367.

Ambient Air Pollution and Depressed Mood in the National Longitudinal Study of Adolescent to Adult Health (Add Health) Wave IV.

Depression is a major contributor to the global burden of disease. There is limited understanding of how environmental exposures may contribute to depression etiology. We used Wave IV of the National Longitudinal Study of Adolescent to Adult Health (Add Health) to examine associations between low-level ambient air pollution exposure and depressed mood in a generally healthy population of over 10,000 24-32 year olds. Annual mean PM2.5 levels in the 2008-2009 study were close to the current U.S. standard. In fully adjusted quasi-binomial logistic regression models, there were no meaningful associations between IQR increases in air pollutant and change in depressed mood status regardless of specific pollutant or moving average lags. In interaction effects models, an IQR increase in lag day 0-30 PM2.5 resulted in 1.20 (95% CI, 1.02-1.41) times higher likelihood of having depressed mood, but only for persons with chronic lung disease (interaction P=0.04); the association was null for participants without chronic lung disease (OR 0.98, 95% CI, 0.91, 1.05). Our findings suggest that among persons with a lifetime history of chronic lung disease, greater exposure to even low-level PM2.5, PM10, and sulfate may be associated with modest increases in the likelihood of having depressed mood.